Posterior epistaxis, which is bleeding from the back of the nose, is typically caused by bleeding from the sphenopalatine artery or its branches. The most common surgical treatment for posterior epistaxis involves tying off the sphenopalatine artery. It is important to note that there is some disagreement in the literature regarding the exact location of the bleeding, with some sources referring to Woodruff’s plexus. However, cadaveric studies suggest that Woodruff’s plexus is more likely a venous anastomosis rather than an arterial one involving branches of the sphenopalatine artery.

Further Reading:

Epistaxis, or nosebleed, is a common condition that can occur in both children and older adults. It is classified as either anterior or posterior, depending on the location of the bleeding. Anterior epistaxis usually occurs in younger individuals and arises from the nostril, most commonly from an area called Little’s area. These bleeds are usually not severe and account for the majority of nosebleeds seen in hospitals. Posterior nosebleeds, on the other hand, occur in older patients with conditions such as hypertension and atherosclerosis. The bleeding in posterior nosebleeds is likely to come from both nostrils and originates from the superior or posterior parts of the nasal cavity or nasopharynx.

The management of epistaxis involves assessing the patient for signs of instability and implementing measures to control the bleeding. Initial measures include sitting the patient upright with their upper body tilted forward and their mouth open. Firmly pinching the cartilaginous part of the nose for 10-15 minutes without releasing the pressure can also help stop the bleeding. If these measures are successful, a cream called Naseptin or mupirocin nasal ointment can be prescribed for further treatment.

If bleeding persists after the initial measures, nasal cautery or nasal packing may be necessary. Nasal cautery involves using a silver nitrate stick to cauterize the bleeding point, while nasal packing involves inserting nasal tampons or inflatable nasal packs to stop the bleeding. In cases of posterior bleeding, posterior nasal packing or surgery to tie off the bleeding vessel may be considered.

Complications of epistaxis can include nasal bleeding, hypovolemia, anemia, aspiration, and even death. Complications specific to nasal packing include sinusitis, septal hematoma or abscess, pressure necrosis, toxic shock syndrome, and apneic episodes. Nasal cautery can lead to complications such as septal perforation and caustic injury to the surrounding skin.

In children under the age of 2 presenting with epistaxis, it is important to refer them for further investigation as an underlying cause is more likely in this age group.

According to Public Health England, there is no recommended exclusion period for viral or bacterial conjunctivitis from school, nursery, or childminders, unless there is an outbreak or cluster of cases.

Addison’s disease occurs when the adrenal cortex is destroyed. The anterior pituitary gland produces and releases adrenocorticotropic hormone (ACTH), not the posterior pituitary gland. The adrenal cortex is responsible for producing cortisol, not the adrenal medulla.

Further Reading:

Addison’s disease, also known as primary adrenal insufficiency or hypoadrenalism, is a rare disorder caused by the destruction of the adrenal cortex. This leads to reduced production of glucocorticoids, mineralocorticoids, and adrenal androgens. The deficiency of cortisol results in increased production of adrenocorticotropic hormone (ACTH) due to reduced negative feedback to the pituitary gland. This condition can cause metabolic disturbances such as hyperkalemia, hyponatremia, hypercalcemia, and hypoglycemia.

The symptoms of Addison’s disease can vary but commonly include fatigue, weight loss, muscle weakness, and low blood pressure. It is more common in women and typically affects individuals between the ages of 30-50. The most common cause of primary hypoadrenalism in developed countries is autoimmune destruction of the adrenal glands. Other causes include tuberculosis, adrenal metastases, meningococcal septicaemia, HIV, and genetic disorders.

The diagnosis of Addison’s disease is often suspected based on low cortisol levels and electrolyte abnormalities. The adrenocorticotropic hormone stimulation test is commonly used for confirmation. Other investigations may include adrenal autoantibodies, imaging scans, and genetic screening.

Addisonian crisis is a potentially life-threatening condition that occurs when there is an acute deficiency of cortisol and aldosterone. It can be the first presentation of undiagnosed Addison’s disease. Precipitating factors of an Addisonian crisis include infection, dehydration, surgery, trauma, physiological stress, pregnancy, hypoglycemia, and acute withdrawal of long-term steroids. Symptoms of an Addisonian crisis include malaise, fatigue, nausea or vomiting, abdominal pain, fever, muscle pains, dehydration, confusion, and loss of consciousness.

There is no fixed consensus on diagnostic criteria for an Addisonian crisis, as symptoms are non-specific. Investigations may include blood tests, blood gas analysis, and septic screens if infection is suspected. Management involves administering hydrocortisone and fluids. Hydrocortisone is given parenterally, and the dosage varies depending on the age of the patient. Fluid resuscitation with saline is necessary to correct any electrolyte disturbances and maintain blood pressure. The underlying cause of the crisis should also be identified and treated. Close monitoring of sodium levels is important to prevent complications such as osmotic demyelination syndrome.

Cobblestoning and rose thorn ulcers are visual characteristics seen in radiological images of individuals with Crohn’s disease. Cobblestoning occurs when there are linear ulcerations running both lengthwise and widthwise, creating a cobblestone-like appearance on the intestinal wall. This effect is enhanced by the presence of nodular wall swelling, and when barium enters the deep crevices of the ulcers, it further accentuates the cobblestone pattern.

Further Reading:

Inflammatory bowel disease (IBD) is a chronic condition characterized by inflammation of the intestinal tract and an imbalance of the intestinal microbiota. The two main forms of IBD are Crohn’s disease and ulcerative colitis (UC). In some cases, it is not possible to differentiate between Crohn’s disease and UC, and the term inflammatory bowel disease type-unclassified may be used.

Crohn’s disease is a chronic, relapsing-remitting inflammatory disease that can affect any part of the gastrointestinal tract, from the mouth to the anus. It most commonly involves the ileum and colon. The inflammation in Crohn’s disease affects all layers of the intestinal wall, leading to complications such as strictures, fistulas, and adhesions. Risk factors for developing Crohn’s disease include a family history, smoking, infectious gastroenteritis, appendicectomy, and the use of NSAIDs and oral contraceptive drugs. Symptoms of Crohn’s disease can vary but often include diarrhea, abdominal pain, weight loss, and perianal disease. Extraintestinal features, such as arthritis, erythema nodosum, and uveitis, can also occur.

Ulcerative colitis is a chronic, relapsing-remitting inflammatory disease that primarily affects the large bowel. The inflammation in UC is limited to the intestinal mucosa and does not involve skip lesions like in Crohn’s disease. Risk factors for developing UC include a family history, not smoking, and no appendix. Symptoms of UC include bloody diarrhea, urgency, tenesmus, and abdominal pain. Extraintestinal features, such as arthritis and uveitis, can also occur. Complications of UC include toxic megacolon, bowel obstruction, bowel perforation, strictures, fistula formation, anemia, malnutrition, and colorectal cancer.

Diagnosing IBD involves various investigations, including blood tests, stool microscopy and culture, fecal calprotectin testing, endoscopy with biopsy, and imaging modalities such as CT and MR enterography. The management of Crohn’s disease and UC is complex and may involve corticosteroids, immunosuppressive drugs, biologic therapy, surgery, and nutritional support. Patients with IBD should also be monitored for nutritional deficiencies, colorectal cancer, and osteoporosis.

According to the latest guidelines from NICE, it is recommended that adult patients who are undergoing treatment for acute leukaemia, stem cell transplants, or solid tumours and are expected to experience significant neutropenia as a result of chemotherapy, should be offered prophylaxis with a fluoroquinolone such as ciprofloxacin (500 mg taken orally twice daily) during the period when neutropenia is expected. This is to help prevent the occurrence of neutropenic sepsis, a serious infection that can occur in cancer patients with low levels of neutrophils.

Reference:
NICE guidance: ‘Neutropenic sepsis: prevention and management of neutropenic sepsis in cancer patients’

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This leads to the accumulation of urea and other waste products in the body, as well as disturbances in fluid balance and electrolyte levels. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease. It is a relatively common condition, with approximately 15% of adults admitted to hospitals in the UK developing AKI.

AKI is categorized into three stages based on specific criteria. In stage 1, there is a rise in creatinine levels of 26 micromol/L or more within 48 hours, or a rise of 50-99% from baseline within 7 days (1.5-1.99 times the baseline). Additionally, a urine output of less than 0.5 mL/kg/hour for more than 6 hours is indicative of stage 1 AKI.

Stage 2 AKI is characterized by a creatinine rise of 100-199% from baseline within 7 days (2.0-2.99 times the baseline), or a urine output of less than 0.5 mL/kg/hour for more than 12 hours.

In stage 3 AKI, there is a creatinine rise of 200% or more from baseline within 7 days (3.0 or more times the baseline). Alternatively, a creatinine rise to 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours, or a rise of 50% or more within 7 days, is indicative of stage 3 AKI. Additionally, a urine output of less than 0.3 mL/kg/hour for 24 hours or anuria (no urine output) for 12 hours also falls under stage 3 AKI.

A threatened miscarriage is characterized by bleeding in the first trimester of pregnancy, but without the passing of any products of conception and with a closed cervical os. The main features of a threatened miscarriage include vaginal bleeding, often in the form of brown discharge or spotting, minimal abdominal pain, and a positive pregnancy test. It is important for stable patients who are more than 6 weeks pregnant and experiencing bleeding in early pregnancy, without any signs of an ectopic pregnancy, to seek follow-up care at an early pregnancy assessment unit (EPAU).

Generally speaking, if a child shows clinical signs of dehydration but does not exhibit shock, it can be assumed that they are 5% dehydrated. On the other hand, if shock is also present, it can be assumed that the child is 10% dehydrated or more. To put it in simpler terms, 5% dehydration means that the body has lost 5 grams of fluid per 100 grams of body weight, which is equivalent to 50 milliliters per kilogram of fluid. Similarly, 10% dehydration implies a loss of 100 milliliters per kilogram of fluid.

The clinical features of dehydration are summarized below:

Dehydration (5%):
– The child appears unwell
– The heart rate may be normal or increased (tachycardia)
– The respiratory rate may be normal or increased (tachypnea)
– Peripheral pulses are normal
– Capillary refill time (CRT) is normal or slightly prolonged
– Blood pressure is normal
– Extremities feel warm
– Decreased urine output
– Reduced skin turgor
– Sunken eyes
– Depressed fontanelle
– Dry mucous membranes

Clinical shock (10%):
– The child appears pale, lethargic, and mottled
– Tachycardia (increased heart rate)
– Tachypnea (increased respiratory rate)
– Weak peripheral pulses
– Prolonged CRT
– Hypotension (low blood pressure)
– Extremities feel cold
– Decreased urine output
– Decreased level of consciousness

Hyperkalemia is a condition where the level of potassium in the blood is higher than normal, specifically greater than 5.5 mmol/l. It can be categorized as mild, moderate, or severe depending on the potassium level. Mild hyperkalemia is when the potassium level is between 5.5-5.9 mmol/l, moderate hyperkalemia is between 6.0-6.4 mmol/l, and severe hyperkalemia is above 6.5 mmol/l. The most common cause of hyperkalemia is renal failure, which can be acute or chronic. Other causes include acidosis, adrenal insufficiency, cell lysis, and excessive potassium intake.

In the treatment of hyperkalemia, calcium plays a crucial role. It works by counteracting the harmful effects of high potassium levels on the heart by stabilizing the cardiac cell membrane. Calcium acts quickly, with its effects seen within 15 minutes, but its effects are relatively short-lived. It is considered a first-line treatment for arrhythmias and significant ECG abnormalities caused by hyperkalemia. However, it is rare to see arrhythmias occur at potassium levels below 7.5 mmol/l.

It’s important to note that calcium does not lower the serum level of potassium. Therefore, when administering calcium, other therapies that actually help lower potassium levels, such as insulin and salbutamol, should also be used. Insulin and salbutamol are effective in reducing serum potassium levels.

When choosing between calcium chloride and calcium gluconate, calcium chloride is preferred when hyperkalemia is accompanied by hemodynamic compromise. This is because calcium chloride contains three times more elemental calcium than an equal volume of calcium gluconate.

This patient is displaying symptoms and signs that are consistent with a vestibular schwannoma, which is also known as an acoustic neuroma. A vestibular schwannoma typically affects the 5th and 8th cranial nerves and is characterized by the following classic presentations: gradual deterioration of hearing in one ear, facial numbness and tingling, tinnitus, and vertigo. It is also possible for the patient to have a history of headaches, and in rare cases, the 7th, 9th, and 10th cranial nerves may be affected. It is recommended that this patient be referred to either an ENT specialist or a neurosurgeon for further assessment, including an MRI of the internal auditory meatus. The main treatment options for vestibular schwannoma include surgery, radiotherapy, and stereotactic radiosurgery.

Renal colic, also known as ureteric colic, refers to a sudden and intense pain in the lower back caused by a blockage in the ureter, which is the tube that carries urine from the kidney to the bladder. This condition is commonly associated with the presence of a urinary tract stone.

The main symptoms of renal or ureteric colic include severe abdominal pain on one side, starting in the lower back or flank and radiating to the groin or genital area in men, or to the labia in women. The pain comes and goes in spasms, lasting for minutes to hours, with periods of no pain or a dull ache. Nausea, vomiting, and the presence of blood in the urine are often accompanying symptoms.

People experiencing renal or ureteric colic are usually restless and unable to find relief by lying still, which helps to distinguish this condition from peritonitis. They may have a history of previous episodes and may also present with fever and sweating if there is an associated urinary infection. Some individuals may complain of painful urination, frequent urination, and straining when the stone reaches the junction between the ureter and the bladder, as the stone irritates the detrusor muscle.

In terms of pain management, the first-line treatment for adults, children, and young people with suspected renal colic is a non-steroidal anti-inflammatory drug (NSAID), which can be administered through various routes. If NSAIDs are contraindicated or not providing sufficient pain relief, intravenous paracetamol can be offered as an alternative. Opioids may be considered if both NSAIDs and intravenous paracetamol are contraindicated or not effective in relieving pain. Antispasmodics should not be given to individuals with suspected renal colic.

For more detailed information, you can refer to the NICE guidelines on the assessment and management of renal and ureteric stones.

Infectious mononucleosis, also known as glandular fever, is a condition that is not clearly defined in medical literature. It is characterized by symptoms such as a sore throat, swollen tonsils with a whitish coating, enlarged lymph nodes in the neck, fatigue, and an enlarged liver and spleen. This condition is caused by a specific virus.

Further Reading:

Glandular fever, also known as infectious mononucleosis or mono, is a clinical syndrome characterized by symptoms such as sore throat, fever, and swollen lymph nodes. It is primarily caused by the Epstein-Barr virus (EBV), with other viruses and infections accounting for the remaining cases. Glandular fever is transmitted through infected saliva and primarily affects adolescents and young adults. The incubation period is 4-8 weeks.

The majority of EBV infections are asymptomatic, with over 95% of adults worldwide having evidence of prior infection. Clinical features of glandular fever include fever, sore throat, exudative tonsillitis, lymphadenopathy, and prodromal symptoms such as fatigue and headache. Splenomegaly (enlarged spleen) and hepatomegaly (enlarged liver) may also be present, and a non-pruritic macular rash can sometimes occur.

Glandular fever can lead to complications such as splenic rupture, which increases the risk of rupture in the spleen. Approximately 50% of splenic ruptures associated with glandular fever are spontaneous, while the other 50% follow trauma. Diagnosis of glandular fever involves various investigations, including viral serology for EBV, monospot test, and liver function tests. Additional serology tests may be conducted if EBV testing is negative.

Management of glandular fever involves supportive care and symptomatic relief with simple analgesia. Antiviral medication has not been shown to be beneficial. It is important to identify patients at risk of serious complications, such as airway obstruction, splenic rupture, and dehydration, and provide appropriate management. Patients can be advised to return to normal activities as soon as possible, avoiding heavy lifting and contact sports for the first month to reduce the risk of splenic rupture.

Rare but serious complications associated with glandular fever include hepatitis, upper airway obstruction, cardiac complications, renal complications, neurological complications, haematological complications, chronic fatigue, and an increased risk of lymphoproliferative cancers and multiple sclerosis.

Insect removal from the ear can be quite challenging due to the distress it causes the patient and the inevitable movement of the insect during the process.

To begin, it is important to make the patient comfortable by providing analgesia. In some cases, inhaled Entonox can be helpful, and if the patient is extremely distressed or experiencing significant discomfort, sedation may be necessary.

The first step in the removal process involves immobilizing or killing the insect to prevent further movement and potential damage within the ear. This can be achieved using options such as microscope immersion oil, mineral oil, or lidocaine solution.

Once the insect is confirmed to be dead, the actual removal can be performed using forceps or the highly effective Frazier suction technique. After inspecting the ear and ensuring the insect is no longer alive, connect the Frazier suction device to low continuous suction and slowly insert it into the patient’s external ear canal. By occluding the insufflation port, the contents of the ear canal can be suctioned out. Once no more liquid returns, withdraw the catheter and verify that the insect has been successfully removed.

Methanol poisoning is linked to an increase in anion gap acidosis.

Further Reading:

Arterial blood gases (ABG) are an important diagnostic tool used to assess a patient’s acid-base status and respiratory function. When obtaining an ABG sample, it is crucial to prioritize safety measures to minimize the risk of infection and harm to the patient. This includes performing hand hygiene before and after the procedure, wearing gloves and protective equipment, disinfecting the puncture site with alcohol, using safety needles when available, and properly disposing of equipment in sharps bins and contaminated waste bins.

To reduce the risk of harm to the patient, it is important to test for collateral circulation using the modified Allen test for radial artery puncture. Additionally, it is essential to inquire about any occlusive vascular conditions or anticoagulation therapy that may affect the procedure. The puncture site should be checked for signs of infection, injury, or previous surgery. After the test, pressure should be applied to the puncture site or the patient should be advised to apply pressure for at least 5 minutes to prevent bleeding.

Interpreting ABG results requires a systematic approach. The core set of results obtained from a blood gas analyser includes the partial pressures of oxygen and carbon dioxide, pH, bicarbonate concentration, and base excess. These values are used to assess the patient’s acid-base status.

The pH value indicates whether the patient is in acidosis, alkalosis, or within the normal range. A pH less than 7.35 indicates acidosis, while a pH greater than 7.45 indicates alkalosis.

The respiratory system is assessed by looking at the partial pressure of carbon dioxide (pCO2). An elevated pCO2 contributes to acidosis, while a low pCO2 contributes to alkalosis.

The metabolic aspect is assessed by looking at the bicarbonate (HCO3-) level and the base excess. A high bicarbonate concentration and base excess indicate alkalosis, while a low bicarbonate concentration and base excess indicate acidosis.

Analyzing the pCO2 and base excess values can help determine the primary disturbance and whether compensation is occurring. For example, a respiratory acidosis (elevated pCO2) may be accompanied by metabolic alkalosis (elevated base excess) as a compensatory response.

The anion gap is another important parameter that can help determine the cause of acidosis. It is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium.

Sodium bicarbonate is used to treat severe TCA toxicity by reducing the risk of seizures and arrhythmia. The goal is to increase the serum pH to a range of 7.45 to 7.55 through alkalinisation.

Further Reading:

Tricyclic antidepressant (TCA) overdose is a common occurrence in emergency departments, with drugs like amitriptyline and dosulepin being particularly dangerous. TCAs work by inhibiting the reuptake of norepinephrine and serotonin in the central nervous system. In cases of toxicity, TCAs block various receptors, including alpha-adrenergic, histaminic, muscarinic, and serotonin receptors. This can lead to symptoms such as hypotension, altered mental state, signs of anticholinergic toxicity, and serotonin receptor effects.

TCAs primarily cause cardiac toxicity by blocking sodium and potassium channels. This can result in a slowing of the action potential, prolongation of the QRS complex, and bradycardia. However, the blockade of muscarinic receptors also leads to tachycardia in TCA overdose. QT prolongation and Torsades de Pointes can occur due to potassium channel blockade. TCAs can also have a toxic effect on the myocardium, causing decreased cardiac contractility and hypotension.

Early symptoms of TCA overdose are related to their anticholinergic properties and may include dry mouth, pyrexia, dilated pupils, agitation, sinus tachycardia, blurred vision, flushed skin, tremor, and confusion. Severe poisoning can lead to arrhythmias, seizures, metabolic acidosis, and coma. ECG changes commonly seen in TCA overdose include sinus tachycardia, widening of the QRS complex, prolongation of the QT interval, and an R/S ratio >0.7 in lead aVR.

Management of TCA overdose involves ensuring a patent airway, administering activated charcoal if ingestion occurred within 1 hour and the airway is intact, and considering gastric lavage for life-threatening cases within 1 hour of ingestion. Serial ECGs and blood gas analysis are important for monitoring. Intravenous fluids and correction of hypoxia are the first-line therapies. IV sodium bicarbonate is used to treat haemodynamic instability caused by TCA overdose, and benzodiazepines are the treatment of choice for seizure control. Other treatments that may be considered include glucagon, magnesium sulfate, and intravenous lipid emulsion.

There are certain things to avoid in TCA overdose, such as anti-arrhythmics like quinidine and flecainide, as they can prolonged depolarization.

In an elderly patient with a history of gradual decline accompanied by high blood sugar levels, excessive thirst, and recent infection, the most likely diagnosis is hyperosmolar hyperglycemic state (HHS). This condition can be life-threatening, with a mortality rate of approximately 50%. Common symptoms include dehydration, elevated blood sugar levels, altered mental status, and electrolyte imbalances. About half of the patients with HHS also experience hypernatremia.

To calculate the serum osmolality, the formula is 2(K+ + Na+) + urea + glucose. In this case, the serum osmolality is 364 mmol/l, indicating a high level. It is important to discontinue the use of metformin in this patient due to the risk of metformin-associated lactic acidosis (MALA). Additionally, an intravenous infusion of insulin should be initiated.

The treatment goals for HHS are to address the underlying cause and gradually and safely:
– Normalize the osmolality
– Replace fluid and electrolyte losses
– Normalize blood glucose levels

If significant ketonaemia is present (3β-hydroxybutyrate is more than 1 mmol/L), it indicates a relative lack of insulin, and insulin should be administered immediately. However, if significant ketonaemia is not present, insulin should not be started.

Patients with HHS are at a high risk of thromboembolism, and it is recommended to routinely administer low molecular weight heparin. In cases where the serum osmolality exceeds 350 mmol/l, full heparinization should be considered.

Cerebral edema is the most significant complication of diabetic ketoacidosis (DKA), leading to death in many cases. It occurs in approximately 0.2-1% of DKA cases. The high blood glucose levels cause an osmolar gradient, resulting in the movement of water from the intracellular fluid (ICF) to the extracellular fluid (ECF) space and a decrease in cell volume. When insulin and intravenous fluids are administered to correct the condition, the effective osmolarity decreases rapidly, causing a reversal of the fluid shift and the development of cerebral edema.

Cerebral edema is associated with a higher mortality rate and poor neurological outcomes. To prevent its occurrence, it is important to slowly normalize osmolarity over a period of 48 hours, paying attention to glucose and sodium levels, as well as ensuring proper hydration. Monitoring the child for symptoms such as headache, recurrent vomiting, irritability, changes in Glasgow Coma Scale (GCS), abnormal slowing of heart rate, and increasing blood pressure is crucial.

If cerebral edema does occur, it should be treated with either a hypertonic (3%) saline solution at a dosage of 3 ml/kg or a mannitol infusion at a dosage of 250-500 mg/kg over a 20-minute period.

In addition to cerebral edema, there are other complications associated with DKA in children, including cardiac arrhythmias, pulmonary edema, and acute renal failure.

The Parkinson-plus syndromes are a group of neurodegenerative disorders that share similar features with Parkinson’s disease but also have additional clinical characteristics that set them apart from idiopathic Parkinson’s disease (iPD). These syndromes include Multiple System Atrophy (MSA), Progressive Supranuclear Palsy (PSP), Corticobasal degeneration (CBD), and Dementia with Lewy Bodies (DLB).

Multiple System Atrophy (MSA) is a less common condition than iPD and PSP. It is characterized by the loss of cells in multiple areas of the nervous system. MSA progresses rapidly, often leading to wheelchair dependence within 3-4 years of diagnosis. Some distinguishing features of MSA include autonomic dysfunction, bladder control problems, erectile dysfunction, blood pressure changes, early-onset balance problems, neck or facial dystonia, and a high-pitched voice.

To summarize the distinguishing features of the Parkinson-plus syndromes compared to iPD, the following table provides a comparison:

iPD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Typically starts at rest on one side of the body
– Levodopa response: Excellent response
– Mental changes: Depression
– Balance/falls: Late in the disease
– Common eye abnormalities: Dry eyes, trouble focusing

MSA:
– Symptom onset: Both sides equally affected
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

PSP:
– Symptom onset: Both sides equally affected
– Tremor: Less common, if present affects both sides
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Personality changes, depression
– Balance/falls: Within 1 year
– Common eye abnormalities: Dry eyes, difficulty in looking downwards

CBD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

Orthostatic hypotension is a condition where patients feel lightheaded and may experience tunnel vision when they stand up from a lying down position. These symptoms are often worse in the morning. The patient’s history of recurrent episodes after being in a supine position for a long time strongly suggests orthostatic hypotension. There are no signs of epilepsy, such as deja-vu or jambs vu prodrome, tongue biting, loss of bladder or bowel control, or postictal confusion. The normal ECG and consistent timing of symptoms make postural orthostatic tachycardia syndrome (PAF) less likely. There are no neurological deficits to suggest a transient ischemic attack (TIA). The prodromal symptoms, such as tunnel vision and lightheadedness, align more with orthostatic hypotension rather than vasovagal syncope, which typically occurs after long periods of standing and is characterized by feeling hot and sweaty. Although carotid sinus syndrome could be considered as a differential diagnosis, as the patient’s head turning on getting out of bed may trigger symptoms, it is not one of the options.

Further Reading:

Blackouts, also known as syncope, are defined as a spontaneous transient loss of consciousness with complete recovery. They are most commonly caused by transient inadequate cerebral blood flow, although epileptic seizures can also result in blackouts. There are several different causes of blackouts, including neurally-mediated reflex syncope (such as vasovagal syncope or fainting), orthostatic hypotension (a drop in blood pressure upon standing), cardiovascular abnormalities, and epilepsy.

When evaluating a patient with blackouts, several key investigations should be performed. These include an electrocardiogram (ECG), heart auscultation, neurological examination, vital signs assessment, lying and standing blood pressure measurements, and blood tests such as a full blood count and glucose level. Additional investigations may be necessary depending on the suspected cause, such as ultrasound or CT scans for aortic dissection or other abdominal and thoracic pathology, chest X-ray for heart failure or pneumothorax, and CT pulmonary angiography for pulmonary embolism.

During the assessment, it is important to screen for red flags and signs of any underlying serious life-threatening condition. Red flags for blackouts include ECG abnormalities, clinical signs of heart failure, a heart murmur, blackouts occurring during exertion, a family history of sudden cardiac death at a young age, an inherited cardiac condition, new or unexplained breathlessness, and blackouts in individuals over the age of 65 without a prodrome. These red flags indicate the need for urgent assessment by an appropriate specialist.

There are several serious conditions that may be suggested by certain features. For example, myocardial infarction or ischemia may be indicated by a history of coronary artery disease, preceding chest pain, and ECG signs such as ST elevation or arrhythmia. Pulmonary embolism may be suggested by dizziness, acute shortness of breath, pleuritic chest pain, and risk factors for venous thromboembolism. Aortic dissection may be indicated by chest and back pain, abnormal ECG findings, and signs of cardiac tamponade include low systolic blood pressure, elevated jugular venous pressure, and muffled heart sounds. Other conditions that may cause blackouts include severe hypoglycemia, Addisonian crisis, and electrolyte abnormalities.

Diabetic amyotrophy, also referred to as proximal diabetic neuropathy, is the second most prevalent form of diabetic neuropathy. It typically begins with discomfort in the buttocks, hips, or thighs and is often initially experienced on one side. The pain may start off as mild and gradually progress or it can suddenly manifest, as seen in this case. Subsequently, weakness and wasting of the proximal muscles in the lower limbs occur, making it difficult for the patient to transition from sitting to standing without assistance. Reflexes in the affected areas can also be impacted. Good control of blood sugar levels, physiotherapy, and lifestyle adjustments can reverse diabetic amyotrophy.

Peripheral neuropathy is the most common type of diabetic neuropathy and typically manifests as pain or loss of sensation in the feet or hands.

Autonomic neuropathy leads to changes in digestion, bowel and bladder function, sexual response, and perspiration. It can also affect the cardiovascular system, resulting in rapid heart rates and orthostatic hypotension.

Focal neuropathy causes sudden weakness in a single nerve or group of nerves, resulting in pain, sensory loss, or muscle weakness. Any nerve in the body can be affected.

Blood transfusion is a potentially life-saving treatment that can provide great clinical benefits. However, it also carries several risks and potential problems. These include immunological complications, administration errors, infections, immune dilution, and transfusion errors. While there have been improvements in safety procedures and efforts to minimize the use of transfusion, errors and serious adverse reactions still occur and often go unreported.

One rare complication of blood transfusion is transfusion-associated graft-vs-host disease (TA-GVHD). This condition typically presents with fever, rash, and diarrhea 1-4 weeks after the transfusion. Laboratory findings may show pancytopenia and abnormalities in liver function. Unlike GVHD after marrow transplantation, TA-GVHD leads to severe marrow aplasia with a mortality rate exceeding 90%. Unfortunately, there are currently no effective treatments available for this condition, and survival is rare, with death usually occurring within 1-3 weeks of the first symptoms.

During a blood transfusion, viable T lymphocytes from the donor are transfused into the recipient’s body. In TA-GVHD, these lymphocytes engraft and react against the recipient’s tissues. However, the recipient is unable to reject the donor lymphocytes due to factors such as immunodeficiency, severe immunosuppression, or shared HLA antigens. Supportive management is the only option for TA-GVHD.

The following summarizes the main complications and reactions that can occur during a blood transfusion:

Complication Features Management
Febrile transfusion reaction
– Presents with a 1-degree rise in temperature from baseline, along with chills and malaise.
– Most common reaction, occurring in 1 out of 8 transfusions.
– Usually caused by cytokines from leukocytes in transfused red cell or platelet components.
– Supportive management, with the use of paracetamol for symptom relief.

Acute haemolytic reaction
– Symptoms include fever, chills, pain at the transfusion site, nausea, vomiting, and dark urine.
– Often accompanied by a feeling of ‘impending doom’.
– Most serious type of reaction, often due to ABO incompatibility caused by administration errors.
– Immediate action required: stop the transfusion, administer IV fluids, and consider diuretics if necessary.

Delayed haemolytic reaction
– Typically occurs 4-8 days after a blood transfusion.
– Symptoms include fever, anemia and/or hyperbilirubinemia

Extradural hematoma is most frequently caused by injury to the middle meningeal artery. This artery is particularly susceptible to damage as it passes behind the pterion.

Further Reading:

Extradural haematoma (EDH) is a collection of blood that forms between the inner surface of the skull and the outer layer of the dura, the dura mater. It is typically caused by head trauma and is often associated with a skull fracture, with the pterion being the most common site of injury. The middle meningeal artery is the most common source of bleeding in EDH.

Clinical features of EDH include a history of head injury with transient loss of consciousness, followed by a lucid interval and gradual loss of consciousness. Other symptoms may include severe headache, sixth cranial nerve palsies, nausea and vomiting, seizures, signs of raised intracranial pressure, and focal neurological deficits.

Imaging of EDH typically shows a biconvex shape and may cause mass effect with brain herniation. It can be differentiated from subdural haematoma by its appearance on imaging.

Management of EDH involves prompt referral to neurosurgery for evacuation of the haematoma. In some cases with a small EDH, conservative management may be considered. With prompt evacuation, the prognosis for EDH is generally good.

Metformin is a type of biguanide medication that, when taken alone, does not lead to low blood sugar levels (hypoglycemia). However, it can potentially worsen hypoglycemia when used in combination with other drugs like sulphonylureas.

Gliclazide, on the other hand, is a sulphonylurea medication known to cause hypoglycemia. Pioglitazone, a thiazolidinedione drug, is also recognized as a cause of hypoglycemia.

It’s important to note that Actrapid and Novomix are both forms of insulin, which can also result in hypoglycemia.

To ensure prompt response in case of an adverse reaction, it is important to have adrenaline, antihistamine, and steroid readily available when administering Zagreb antivenom.

Further Reading:

Snake bites in the UK are primarily caused by the adder, which is the only venomous snake species native to the country. While most adder bites result in minor symptoms such as pain, swelling, and inflammation, there have been cases of life-threatening illness and fatalities. Additionally, there are instances where venomous snakes that are kept legally or illegally also cause bites in the UK.

Adder bites typically occur from early spring to late autumn, with the hand being the most common site of the bite. Symptoms can be local or systemic, with local symptoms including sharp pain, tingling or numbness, and swelling that spreads proximally. Systemic symptoms may include spreading pain, tenderness, inflammation, regional lymph node enlargement, and bruising. In severe cases, anaphylaxis can occur, leading to symptoms such as nausea, vomiting, abdominal pain, diarrhea, and shock.

It is important for clinicians to be aware of the potential complications and complications associated with adder bites. These can include acute renal failure, pulmonary and cerebral edema, acute gastric dilatation, paralytic ileus, acute pancreatitis, and coma and seizures. Anaphylaxis symptoms can appear within minutes or be delayed for hours, and hypotension is a critical sign to monitor.

Initial investigations for adder bites include blood tests, ECG, and vital sign monitoring. Further investigations such as chest X-ray may be necessary based on clinical signs. Blood tests may reveal abnormalities such as leukocytosis, raised hematocrit, anemia, thrombocytopenia, and abnormal clotting profile. ECG changes may include tachyarrhythmias, bradyarrhythmias, atrial fibrillation, and ST segment changes.

First aid measures at the scene include immobilizing the patient and the bitten limb, avoiding aspirin and ibuprofen, and cleaning the wound site in the hospital. Tetanus prophylaxis should be considered. In cases of anaphylaxis, prompt administration of IM adrenaline is necessary. In the hospital, rapid assessment and appropriate resuscitation with intravenous fluids are required.

Antivenom may be indicated in cases of hypotension, systemic envenoming, ECG abnormalities, peripheral neutrophil leucocytosis, elevated serum creatine kinase or metabolic acidosis, and extensive or rapidly spreading local swelling. Zagreb antivenom is commonly used in the UK, with an initial dose of 8 mL.

Sickle-cell disease is a blood disorder that is inherited in an autosomal recessive manner. It is characterized by the production of abnormal red blood cells that have a sickle shape. These abnormal cells are triggered by various factors such as low oxygen levels, dehydration, stress, and infection. The disease is caused by a specific mutation in the beta-globin chain of hemoglobin, resulting in the substitution of glutamic acid with valine at the sixth position. The gene responsible for this mutation is located on chromosome 11.

On the other hand, sickle-cell trait refers to the carrier state of the disease. Individuals with sickle-cell trait have one normal allele and one abnormal allele. Both alleles are co-dominant, meaning that both normal and abnormal hemoglobin are produced. As a result, individuals with sickle-cell trait do not experience the same severity of symptoms as those with sickle-cell disease.

When both parents are carriers of the sickle-cell trait, there is a 50% chance that their child will also be an unaffected carrier, a 25% chance that the child will be unaffected, and a 25% chance that the child will develop sickle-cell disease. This is because the inheritance of the disease follows the principles of autosomal recessive inheritance.

Several studies have shown that elevating the head by 20-30 degrees is beneficial for increasing oxygen levels compared to lying flat on the back.

Further Reading:

Rapid sequence induction (RSI) is a method used to place an endotracheal tube (ETT) in the trachea while minimizing the risk of aspiration. It involves inducing loss of consciousness while applying cricoid pressure, followed by intubation without face mask ventilation. The steps of RSI can be remembered using the 7 P’s: preparation, pre-oxygenation, pre-treatment, paralysis and induction, protection and positioning, placement with proof, and post-intubation management.

Preparation involves preparing the patient, equipment, team, and anticipating any difficulties that may arise during the procedure. Pre-oxygenation is important to ensure the patient has an adequate oxygen reserve and prolongs the time before desaturation. This is typically done by breathing 100% oxygen for 3 minutes. Pre-treatment involves administering drugs to counter expected side effects of the procedure and anesthesia agents used.

Paralysis and induction involve administering a rapid-acting induction agent followed by a neuromuscular blocking agent. Commonly used induction agents include propofol, ketamine, thiopentone, and etomidate. The neuromuscular blocking agents can be depolarizing (such as suxamethonium) or non-depolarizing (such as rocuronium). Depolarizing agents bind to acetylcholine receptors and generate an action potential, while non-depolarizing agents act as competitive antagonists.

Protection and positioning involve applying cricoid pressure to prevent regurgitation of gastric contents and positioning the patient’s neck appropriately. Tube placement is confirmed by visualizing the tube passing between the vocal cords, auscultation of the chest and stomach, end-tidal CO2 measurement, and visualizing misting of the tube. Post-intubation management includes standard care such as monitoring ECG, SpO2, NIBP, capnography, and maintaining sedation and neuromuscular blockade.

Overall, RSI is a technique used to quickly and safely secure the airway in patients who may be at risk of aspiration. It involves a series of steps to ensure proper preparation, oxygenation, drug administration, and tube placement. Monitoring and post-intubation care are also important aspects of RSI.

Hypothermia can cause various changes in an electrocardiogram (ECG). These changes include a slower heart rate (bradycardia), the presence of Osborn Waves (also known as J waves), a prolonged PR interval, a widened QRS complex, and a prolonged QT interval. Additionally, the ECG may show artifacts caused by shivering, as well as the presence of ventricular ectopics. In severe cases, hypothermia can lead to cardiac arrest, which may manifest as ventricular tachycardia (VT), ventricular fibrillation (VF), or asystole.

Further Reading:

Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, the basal metabolic rate decreases and cell signaling between neurons decreases, leading to reduced tissue perfusion. This can result in decreased myocardial contractility, vasoconstriction, ventilation-perfusion mismatch, and increased blood viscosity. Symptoms of hypothermia progress as the core temperature drops, starting with compensatory increases in heart rate and shivering, and eventually leading to bradyarrhythmias, prolonged PR, QRS, and QT intervals, and cardiac arrest.

In the management of hypothermic cardiac arrest, ALS should be initiated with some modifications. The pulse check during CPR should be prolonged to 1 minute due to difficulty in obtaining a pulse. Rewarming the patient is important, and mechanical ventilation may be necessary due to stiffness of the chest wall. Drug metabolism is slowed in hypothermic patients, so dosing of drugs should be adjusted or withheld. Electrolyte disturbances are common in hypothermic patients and should be corrected.

Frostbite refers to a freezing injury to human tissue and occurs when tissue temperature drops below 0ºC. It can be classified as superficial or deep, with superficial frostbite affecting the skin and subcutaneous tissues, and deep frostbite affecting bones, joints, and tendons. Frostbite can be classified from 1st to 4th degree based on the severity of the injury. Risk factors for frostbite include environmental factors such as cold weather exposure and medical factors such as peripheral vascular disease and diabetes.

Signs and symptoms of frostbite include skin changes, cold sensation or firmness to the affected area, stinging, burning, or numbness, clumsiness of the affected extremity, and excessive sweating, hyperemia, and tissue gangrene. Frostbite is diagnosed clinically and imaging may be used in some cases to assess perfusion or visualize occluded vessels. Management involves moving the patient to a warm environment, removing wet clothing, and rapidly rewarming the affected tissue. Analgesia should be given as reperfusion is painful, and blisters should be de-roofed and aloe vera applied. Compartment syndrome is a risk and should be monitored for. Severe cases may require surgical debridement of amputation.

Calcium-channel blocker overdose is a serious condition that can be life-threatening. The most dangerous types of calcium channel blockers in overdose are verapamil and diltiazem. These medications work by binding to the alpha-1 subunit of L-type calcium channels, which prevents the entry of calcium into cells. These channels are important for the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

When managing a patient with calcium-channel blocker overdose, it is crucial to follow the standard ABC approach for resuscitation. If there is a risk of life-threatening toxicity, early intubation and ventilation should be considered. Invasive blood pressure monitoring is also necessary if hypotension and shock are developing.

The specific treatments for calcium-channel blocker overdose primarily focus on supporting the cardiovascular system. These treatments include:

1. Fluid resuscitation: Administer up to 20 mL/kg of crystalloid solution.

2. Calcium administration: This can temporarily increase blood pressure and heart rate. Options include 10% calcium gluconate (60 mL IV) or 10% calcium chloride (20 mL IV) via central venous access. Repeat boluses can be given up to three times, and a calcium infusion may be necessary to maintain serum calcium levels above 2.0 mEq/L.

3. Atropine: Consider administering 0.6 mg every 2 minutes, up to a total of 1.8 mg. However, atropine is often ineffective in these cases.

4. High dose insulin – euglycemic therapy (HIET): The use of HIET in managing cardiovascular toxicity has evolved. It used to be a last-resort measure, but early administration is now increasingly recommended. This involves giving a bolus of short-acting insulin (1 U/kg) and 50 mL of 50% glucose IV (unless there is marked hyperglycemia). Therapy should be continued with a short-acting insulin/dextrose infusion. Glucose levels should be monitored frequently, and potassium should be replaced if levels drop below 2.5 mmol/L.

5. Vasoactive infusions: Catecholamines such as dopamine, adrenaline, and/or noradrenaline can be titrated to achieve the desired inotropic and chronotropic effects.

6. Sodium bicarbonate: Consider using sodium bicarbonate in cases where a severe metabolic acidosis develops.

The British Thoracic Society (BTS) advises that chest drains should be inserted within the safe triangle to minimize the risk of harm to underlying structures and prevent damage to muscle and breast tissue, which can result in unsightly scarring. The safe triangle is defined by the base of the axilla, the lateral border of the latissimus dorsi, the lateral border of the pectoralis major, and the 5th intercostal space.

There are several potential complications associated with the insertion of small-bore chest drains. These include puncture of the intercostal artery, accidental perforation of organs due to over-introduction of the dilator into the chest cavity, hospital-acquired pleural infection caused by a non-aseptic technique, inadequate stay suture that may lead to the chest tube falling out, and tube blockage, which may occur more frequently compared to larger bore Argyle drains.

For more information on this topic, please refer to the British Thoracic Society pleural disease guidelines.

Malignant otitis externa, also known as necrotising otitis externa, is a severe infection that affects the external auditory canal and spreads to the temporal bone and nearby tissues, leading to skull base osteomyelitis. The primary cause of this condition is usually an infection by Pseudomonas aeruginosa. It is commonly observed in older individuals with diabetes.

Further Reading:

Otitis externa is inflammation of the skin and subdermis of the external ear canal. It can be acute, lasting less than 6 weeks, or chronic, lasting more than 3 months. Malignant otitis externa, also known as necrotising otitis externa, is a severe and potentially life-threatening infection that can spread to the bones and surrounding structures of the ear. It is most commonly caused by Pseudomonas aeruginosa.

Symptoms of malignant otitis externa include severe and persistent ear pain, headache, discharge from the ear, fever, malaise, vertigo, and profound hearing loss. It can also lead to facial nerve palsy and other cranial nerve palsies. In severe cases, the infection can spread to the central nervous system, causing meningitis, brain abscess, and sepsis.

Acute otitis externa is typically caused by Pseudomonas aeruginosa or Staphylococcus aureus, while chronic otitis externa can be caused by fungal infections such as Aspergillus or Candida albicans. Risk factors for otitis externa include eczema, psoriasis, dermatitis, acute otitis media, trauma to the ear canal, foreign bodies in the ear, water exposure, ear canal obstruction, and long-term antibiotic or steroid use.

Clinical features of otitis externa include itching of the ear canal, ear pain, tenderness of the tragus and/or pinna, ear discharge, hearing loss if the ear canal is completely blocked, redness and swelling of the ear canal, debris in the ear canal, and cellulitis of the pinna and adjacent skin. Tender regional lymphadenitis is uncommon.

Management of acute otitis externa involves general ear care measures, optimizing any underlying medical or skin conditions that are risk factors, avoiding the use of hearing aids or ear plugs if there is a suspected contact allergy, and avoiding the use of ear drops if there is a suspected allergy to any of its ingredients. Treatment options include over-the-counter acetic acid 2% ear drops or spray, aural toileting via dry swabbing, irrigation, or microsuction, and prescribing topical antibiotics with or without a topical corticosteroid. Oral antibiotics may be prescribed in severe cases or for immunocompromised individuals.

Follow-up is advised if symptoms do not improve within 48-72 hours of starting treatment, if symptoms have not fully resolved

Calcium-channel blocker overdose is a serious matter and should be regarded as potentially life-threatening. Verapamil and diltiazem are the two most dangerous types of calcium channel blockers when taken in excess. They work by attaching to the alpha-1 subunit of L-type calcium channels, which stops calcium from entering the cells. These channels play a crucial role in the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

Tetracycline antibiotics, such as tetracycline and doxycycline, have the potential to cause staining on permanent teeth while they are still forming beneath the gum line. This staining occurs when the drug becomes calcified within the tooth during its development. It is important to note that children are vulnerable to tetracycline-related tooth staining until approximately the age of 8. Additionally, pregnant women should avoid taking tetracycline as it can affect the development of teeth in the unborn child.

Lithium is a commonly prescribed medication for bipolar disorder, as it helps stabilize mood. The recommended therapeutic range for lithium levels is typically between 0.4 and 0.8 mmol/l, although this range may vary depending on the laboratory. For maintenance therapy and treatment in older individuals, the lower end of the range is usually targeted. Toxic effects of lithium are typically observed when levels exceed 1.5 mmol/l. It is important to monitor lithium levels one week after starting therapy and after any dosage adjustments.

One potential side effect of lithium is the development of nephrogenic diabetes insipidus, a condition that affects the kidneys’ ability to concentrate urine. However, lithium does not cause diabetes mellitus. Another known side effect is hypothyroidism, which is a decrease in thyroid hormone production, but it does not lead to hyperthyroidism, an overactive thyroid.

Signs of lithium toxicity include nausea, vomiting, diarrhea, tremors, ataxia (loss of coordination), confusion, increased muscle tone, clonus (repetitive, involuntary muscle contractions), nephrogenic diabetes insipidus, convulsions, coma, and renal failure. It is crucial to be aware of these symptoms and seek medical attention if they occur.

Pericardial friction rub is a common finding in pericarditis and is often described as a sound similar to squeaking leather. This patient exhibits symptoms that are consistent with acute pericarditis, including flu-like illness with muscle pain and fatigue, chest pain that worsens when lying down and improves when sitting up or leaning forward, and the presence of a pleural rub. The gradual onset of symptoms rules out conditions like pulmonary embolism or acute myocardial ischemia. It is important to note that while the pericardial rub is often considered part of the classic triad of clinical features, it is only present in about one-third of patients. Additionally, the rub may come and go, so repeated examinations may increase the chances of detecting this sign.

Further Reading:

Pericarditis is an inflammation of the pericardium, which is the protective sac around the heart. It can be acute, lasting less than 6 weeks, and may present with chest pain, cough, dyspnea, flu-like symptoms, and a pericardial rub. The most common causes of pericarditis include viral infections, tuberculosis, bacterial infections, uremia, trauma, and autoimmune diseases. However, in many cases, the cause remains unknown. Diagnosis is based on clinical features, such as chest pain, pericardial friction rub, and electrocardiographic changes. Treatment involves symptom relief with nonsteroidal anti-inflammatory drugs (NSAIDs), and patients should avoid strenuous activity until symptoms improve. Complicated cases may require treatment for the underlying cause, and large pericardial effusions may need urgent drainage. In cases of purulent effusions, antibiotic therapy is necessary, and steroid therapy may be considered for pericarditis related to autoimmune disorders or if NSAIDs alone are ineffective.

The zone of hyperaemia, located at the outermost part of the burn, experiences heightened tissue perfusion. Typically, this area will return to its normal tissue state.

Burn injuries can be classified based on their type (degree, partial thickness or full thickness), extent as a percentage of total body surface area (TBSA), and severity (minor, moderate, major/severe). Severe burns are defined as a >10% TBSA in a child and >15% TBSA in an adult.

When assessing a burn, it is important to consider airway injury, carbon monoxide poisoning, type of burn, extent of burn, special considerations, and fluid status. Special considerations may include head and neck burns, circumferential burns, thorax burns, electrical burns, hand burns, and burns to the genitalia.

Airway management is a priority in burn injuries. Inhalation of hot particles can cause damage to the respiratory epithelium and lead to airway compromise. Signs of inhalation injury include visible burns or erythema to the face, soot around the nostrils and mouth, burnt/singed nasal hairs, hoarse voice, wheeze or stridor, swollen tissues in the mouth or nostrils, and tachypnea and tachycardia. Supplemental oxygen should be provided, and endotracheal intubation may be necessary if there is airway obstruction or impending obstruction.

The initial management of a patient with burn injuries involves conserving body heat, covering burns with clean or sterile coverings, establishing IV access, providing pain relief, initiating fluid resuscitation, measuring urinary output with a catheter, maintaining nil by mouth status, closely monitoring vital signs and urine output, monitoring the airway, preparing for surgery if necessary, and administering medications.

Burns can be classified based on the depth of injury, ranging from simple erythema to full thickness burns that penetrate into subcutaneous tissue. The extent of a burn can be estimated using methods such as the rule of nines or the Lund and Browder chart, which takes into account age-specific body proportions.

Fluid management is crucial in burn injuries due to significant fluid losses. Evaporative fluid loss from burnt skin and increased permeability of blood vessels can lead to reduced intravascular volume and tissue perfusion. Fluid resuscitation should be aggressive in severe burns, while burns <15% in adults and <10% in children may not require immediate fluid resuscitation. The Parkland formula can be used to calculate the intravenous fluid requirements for someone with a significant burn injury.

TBSA, or Total Body Surface Area, is a method commonly used to estimate the size of small burns and very large burns by including the area of unburnt skin. However, it is not considered a reliable method for medium-sized burns.

Further Reading:

Burn injuries can be classified based on their type (degree, partial thickness or full thickness), extent as a percentage of total body surface area (TBSA), and severity (minor, moderate, major/severe). Severe burns are defined as a >10% TBSA in a child and >15% TBSA in an adult.

When assessing a burn, it is important to consider airway injury, carbon monoxide poisoning, type of burn, extent of burn, special considerations, and fluid status. Special considerations may include head and neck burns, circumferential burns, thorax burns, electrical burns, hand burns, and burns to the genitalia.

Airway management is a priority in burn injuries. Inhalation of hot particles can cause damage to the respiratory epithelium and lead to airway compromise. Signs of inhalation injury include visible burns or erythema to the face, soot around the nostrils and mouth, burnt/singed nasal hairs, hoarse voice, wheeze or stridor, swollen tissues in the mouth or nostrils, and tachypnea and tachycardia. Supplemental oxygen should be provided, and endotracheal intubation may be necessary if there is airway obstruction or impending obstruction.

The initial management of a patient with burn injuries involves conserving body heat, covering burns with clean or sterile coverings, establishing IV access, providing pain relief, initiating fluid resuscitation, measuring urinary output with a catheter, maintaining nil by mouth status, closely monitoring vital signs and urine output, monitoring the airway, preparing for surgery if necessary, and administering medications.

Burns can be classified based on the depth of injury, ranging from simple erythema to full thickness burns that penetrate into subcutaneous tissue. The extent of a burn can be estimated using methods such as the rule of nines or the Lund and Browder chart, which takes into account age-specific body proportions.

Fluid management is crucial in burn injuries due to significant fluid losses. Evaporative fluid loss from burnt skin and increased permeability of blood vessels can lead to reduced intravascular volume and tissue perfusion. Fluid resuscitation should be aggressive in severe burns, while burns <15% in adults and <10% in children may not require immediate fluid resuscitation. The Parkland formula can be used to calculate the intravenous fluid requirements for someone with a significant burn injury.

The diagnostic criteria for hypertrophic pyloric stenosis (HPS) on ultrasound are as follows: the thickness of the pyloric muscle should be greater than 3 mm, the longitudinal length of the pylorus should be greater than 15-17 mm, the volume of the pylorus should be greater than 1.5 cm3, and the transverse diameter of the pylorus should be greater than 13 mm.

Further Reading:

Pyloric stenosis is a condition that primarily affects infants, characterized by the thickening of the muscles in the pylorus, leading to obstruction of the gastric outlet. It typically presents between the 3rd and 12th weeks of life, with recurrent projectile vomiting being the main symptom. The condition is more common in males, with a positive family history and being first-born being additional risk factors. Bottle-fed children and those delivered by c-section are also more likely to develop pyloric stenosis.

Clinical features of pyloric stenosis include projectile vomiting, usually occurring about 30 minutes after a feed, as well as constipation and dehydration. A palpable mass in the upper abdomen, often described as like an olive, may also be present. The persistent vomiting can lead to electrolyte disturbances, such as hypochloremia, alkalosis, and mild hypokalemia.

Ultrasound is the preferred diagnostic tool for confirming pyloric stenosis. It can reveal specific criteria, including a pyloric muscle thickness greater than 3 mm, a pylorus longitudinal length greater than 15-17 mm, a pyloric volume greater than 1.5 cm3, and a pyloric transverse diameter greater than 13 mm.

The definitive treatment for pyloric stenosis is pyloromyotomy, a surgical procedure that involves making an incision in the thickened pyloric muscle to relieve the obstruction. Before surgery, it is important to correct any hypovolemia and electrolyte disturbances with intravenous fluids. Overall, pyloric stenosis is a relatively common condition in infants, but with prompt diagnosis and appropriate management, it can be effectively treated.

The flight of ideas observed in mania is considered a type of thought disorder. The primary clinical characteristics of mania include changes in mood, behavior, speech, and thought.

In terms of mood, individuals experiencing mania often exhibit an elated mood and a sense of euphoria. They may also display irritability and hostility instead of their usual amiability. Additionally, there is an increase in enthusiasm.

Regarding behavior, individuals in a manic state tend to be overactive and have heightened energy levels. They may lose their normal social inhibitions and engage in more risk-taking behaviors. This can also manifest as increased sexual promiscuity and libido, as well as an increased appetite.

In terms of speech, individuals with mania often speak in a pressured and rapid manner. Their conversations may be cheerful, and they may engage in rhyming or punning.

Lastly, in terms of thought, the flight of ideas is a prominent feature of mania and is classified as a thought disorder. Individuals may experience grandiose delusions and have an inflated sense of self-esteem. They may also struggle with poor attention and concentration.

Overall, mania is characterized by a range of symptoms that affect mood, behavior, speech, and thought.

Patients with head injuries who show any signs of basal skull fracture, such as haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, or Battle’s sign, should undergo urgent CT imaging. Additionally, the following indications also warrant a CT scan: a Glasgow Coma Scale (GCS) score of less than 13 on initial assessment in the emergency department (ED), a GCS score of less than 15 at 2 hours after the injury on assessment in the ED, suspected open or depressed skull fracture, post-traumatic seizure, new focal neurological deficit, greater than 1 episode of vomiting, or the patient being on anticoagulation. If any of these signs are present, a CT scan should be performed within 1 hour, except for patients on anticoagulation who should have a CT scan within 8 hours if they do not have any other signs. However, if patients on anticoagulation do have any of the other signs, the CT scan should be performed within 1 hour.

Further Reading:

Indications for CT Scanning in Head Injuries (Adults):
– CT head scan should be performed within 1 hour if any of the following features are present:
– GCS < 13 on initial assessment in the ED
– GCS < 15 at 2 hours after the injury on assessment in the ED
– Suspected open or depressed skull fracture
– Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign)
– Post-traumatic seizure
– New focal neurological deficit
– > 1 episode of vomiting

Indications for CT Scanning in Head Injuries (Children):
– CT head scan should be performed within 1 hour if any of the features in List 1 are present:
– Suspicion of non-accidental injury
– Post-traumatic seizure but no history of epilepsy
– GCS < 14 on initial assessment in the ED for children more than 1 year of age
– Paediatric GCS < 15 on initial assessment in the ED for children under 1 year of age
– At 2 hours after the injury, GCS < 15
– Suspected open or depressed skull fracture or tense fontanelle
– Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign)
– New focal neurological deficit
– For children under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head

– CT head scan should be performed within 1 hour if none of the above features are present but two or more of the features in List 2 are present:
– Loss of consciousness lasting more than 5 minutes (witnessed)
– Abnormal drowsiness
– Three or more discrete episodes of vomiting
– Dangerous mechanism of injury (high-speed road traffic accident, fall from a height.

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

Acne conglobata is an extremely severe form of acne where acne nodules come together and create sinuses. Acne fulminans, on the other hand, is a rare and severe complication of acne conglobata that is accompanied by systemic symptoms. It is linked to elevated levels of androgenic hormones, specific autoimmune conditions, and a genetic predisposition.

The typical clinical characteristics of acne fulminans are as follows:

– Sudden and abrupt onset
– Inflammatory and ulcerated nodular acne primarily found on the chest and back
– Often painful lesions
– Ulcers on the upper trunk covered with bleeding crusts
– Severe acne scarring
– Fluctuating fever
– Painful joints and arthropathy
– General feeling of illness (malaise)
– Loss of appetite and weight loss
– Enlarged liver and spleen (hepatosplenomegaly)

It is crucial to refer patients immediately for a specialist evaluation and hospital admission. Treatment options for acne fulminans include systemic corticosteroids, dapsone, ciclosporin, and high-dose intravenous antibiotics.

Early signs of local anaesthetic systemic toxicity (LAST) can include numbness around the mouth and tongue, a metallic taste in the mouth, feeling lightheaded or dizzy, and experiencing visual and auditory disturbances. LAST is a rare but serious complication that can occur when administering anesthesia. It is important for healthcare providers to be aware of the signs and symptoms of LAST, as early recognition can lead to better outcomes. Additionally, hyperventilation can temporarily lower calcium levels, which can cause numbness around the mouth.

Further Reading:

Local anaesthetics, such as lidocaine, bupivacaine, and prilocaine, are commonly used in the emergency department for topical or local infiltration to establish a field block. Lidocaine is often the first choice for field block prior to central line insertion. These anaesthetics work by blocking sodium channels, preventing the propagation of action potentials.

However, local anaesthetics can enter the systemic circulation and cause toxic side effects if administered in high doses. Clinicians must be aware of the signs and symptoms of local anaesthetic systemic toxicity (LAST) and know how to respond. Early signs of LAST include numbness around the mouth or tongue, metallic taste, dizziness, visual and auditory disturbances, disorientation, and drowsiness. If not addressed, LAST can progress to more severe symptoms such as seizures, coma, respiratory depression, and cardiovascular dysfunction.

The management of LAST is largely supportive. Immediate steps include stopping the administration of local anaesthetic, calling for help, providing 100% oxygen and securing the airway, establishing IV access, and controlling seizures with benzodiazepines or other medications. Cardiovascular status should be continuously assessed, and conventional therapies may be used to treat hypotension or arrhythmias. Intravenous lipid emulsion (intralipid) may also be considered as a treatment option.

If the patient goes into cardiac arrest, CPR should be initiated following ALS arrest algorithms, but lidocaine should not be used as an anti-arrhythmic therapy. Prolonged resuscitation may be necessary, and intravenous lipid emulsion should be administered. After the acute episode, the patient should be transferred to a clinical area with appropriate equipment and staff for further monitoring and care.

It is important to report cases of local anaesthetic toxicity to the appropriate authorities, such as the National Patient Safety Agency in the UK or the Irish Medicines Board in the Republic of Ireland. Additionally, regular clinical review should be conducted to exclude pancreatitis, as intravenous lipid emulsion can interfere with amylase or lipase assays.

Hypothermia occurs when the core body temperature drops below 35°C. It is categorized as mild (32-35°C), moderate (28-32°C), or severe (<28°C). Rescuers at the scene can use the Swiss staging system to describe the condition of victims. The stages range from clearly conscious and shivering to unconscious and not breathing, with death due to irreversible hypothermia being the most severe stage. There are several risk factors for hypothermia, including environmental exposure, unsatisfactory housing, poverty, lack of cold awareness, drugs, alcohol, acute confusion, hypothyroidism, and sepsis. The clinical features of hypothermia vary depending on the severity. At 32-35°C, symptoms may include apathy, amnesia, ataxia, and dysarthria. At 30-32°C, there may be a decreased level of consciousness, hypotension, arrhythmias, respiratory depression, and muscular rigidity. Below 30°C, ventricular fibrillation may occur, especially with excessive movement or invasive procedures. Diagnosing hypothermia involves checking the core temperature using an oesophageal, rectal, or tympanic probe with a low reading thermometer. Rectal and tympanic temperatures may lag behind core temperature and are unreliable in hypothermia. Various investigations should be carried out, including blood tests, blood glucose, amylase, blood cultures, arterial blood gas, ECG, chest X-ray, and CT head if there is suspicion of head injury or CVA. The management of hypothermia involves supporting the ABCs, treating the patient in a warm room, removing wet clothes and drying the skin, monitoring the ECG, providing warmed, humidified oxygen, correcting hypoglycemia with IV glucose, and handling the patient gently to avoid VF arrest. Rewarming methods include passive Rewarming with warm blankets or Bair hugger/polythene sheets, surface Rewarming with a water bath, core Rewarming with heated, humidified oxygen or peritoneal lavage, and extracorporeal Rewarming via cardiopulmonary bypass for severe hypothermia/cardiac arrest. In the case of hypothermic cardiac arrest, CPR should be performed with chest compressions and ventilations at standard rates.

Slapped cheek syndrome, also known as fifth disease or erythema infectiosum, is caused by parvovirus B19. It is most commonly seen in children aged 4-12, but can affect individuals of any age. In the UK, the peak occurrence of this condition is in April and May. Slapped cheek syndrome is contagious, with the period of infectivity occurring before the appearance of the characteristic rash. The rash itself is painless.

Diagnosing slapped cheek syndrome is typically based on clinical presentation, characterized by the sudden onset of bright red cheeks resembling a slap mark. In some cases, a faint rash may also appear on other parts of the body. The rash usually lasts for a few days, but in rare instances, it may persist for a few weeks. Treatment for this condition is usually focused on managing symptoms. Additional symptoms that may accompany the rash include a mild fever and joint pain.

While slapped cheek syndrome is generally mild and resolves on its own, certain groups of individuals require extra caution. Pregnant women, for instance, are at an increased risk of miscarriage if exposed to fifth disease. Patients with sickle cell disease or weakened immune systems also need to take extra precautions.

The use of tetracyclines is not recommended during pregnancy as it can have harmful effects on the developing fetus. When taken during the second half of pregnancy, tetracyclines may lead to permanent yellow-grey discoloration of the teeth and enamel hypoplasia. Children affected by this may also be more prone to cavities. Additionally, tetracyclines have been associated with congenital defects, problems with bone growth, and liver toxicity in pregnant women.

Here is a list outlining the commonly encountered drugs that can have adverse effects during pregnancy:

ACE inhibitors (e.g. ramipril): If taken in the second and third trimesters, ACE inhibitors can cause reduced blood flow, kidney failure, and a condition called oligohydramnios.

Aminoglycosides (e.g. gentamicin): Aminoglycosides can cause ototoxicity, leading to hearing loss in the fetus.

Aspirin: High doses of aspirin can result in first trimester abortions, delayed labor, premature closure of the fetal ductus arteriosus, and a condition called fetal kernicterus. However, low doses (e.g. 75 mg) do not pose significant risks.

Benzodiazepines (e.g. diazepam): When taken late in pregnancy, benzodiazepines can cause respiratory depression in the newborn and a withdrawal syndrome.

Calcium-channel blockers: If taken in the first trimester, calcium-channel blockers can cause abnormalities in the fingers and toes. If taken in the second and third trimesters, they can lead to fetal growth retardation.

Carbamazepine: Carbamazepine has been associated with a condition called hemorrhagic disease of the newborn and an increased risk of neural tube defects.

Chloramphenicol: Chloramphenicol can cause a condition known as grey baby syndrome in newborns.

Corticosteroids: If taken in the first trimester, corticosteroids may increase the risk of orofacial clefts in the fetus.

Danazol: When taken in the first trimester, danazol can cause masculinization of the female fetuses genitals.

Finasteride: Pregnant women should avoid handling finasteride tablets as the drug can be absorbed through the skin and affect the development of male sex organs in the fetus.

Haloperidol: If taken during the first trimester, this medication may increase the risk of limb malformations. If taken during the third trimester, it can lead to an increased risk of extrapyramidal symptoms in the newborn.

Adrenaline can be given in cases of life-threatening anaphylactic reactions, even if there are certain conditions that may make it less advisable. These conditions include coronary artery disease, uncontrolled hypertension, serious ventricular arrhythmias, and the second stage of labor. Despite these relative contraindications, adrenaline may still be administered to address the immediate danger posed by anaphylaxis.

According to NICE, the presence of certain clinical features in a child between three months and five years old may indicate a urinary tract infection (UTI). These features include vomiting, poor feeding, lethargy, irritability, abdominal pain or tenderness, and urinary frequency or dysuria. For more information on this topic, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

Conn’s syndrome, also known as primary hyperaldosteronism, is often characterized by hypertension along with hypokalaemia and hypernatraemia. On the other hand, Addison’s disease typically leads to hypotension, hyponatremia, and hyperkalaemia. Hyponatraemia is commonly associated with pituitary adenoma, while acute renal failure (ARF) is characterized by elevated levels of urea and creatinine, and hyperkalaemia is frequently observed in ARF.

Further Reading:

Hyperaldosteronism is a condition characterized by excessive production of aldosterone by the adrenal glands. It can be classified into primary and secondary hyperaldosteronism. Primary hyperaldosteronism, also known as Conn’s syndrome, is typically caused by adrenal hyperplasia or adrenal tumors. Secondary hyperaldosteronism, on the other hand, is a result of high renin levels in response to reduced blood flow across the juxtaglomerular apparatus.

Aldosterone is the main mineralocorticoid steroid hormone produced by the adrenal cortex. It acts on the distal renal tubule and collecting duct of the nephron, promoting the reabsorption of sodium ions and water while secreting potassium ions.

The causes of hyperaldosteronism vary depending on whether it is primary or secondary. Primary hyperaldosteronism can be caused by adrenal adenoma, adrenal hyperplasia, adrenal carcinoma, or familial hyperaldosteronism. Secondary hyperaldosteronism can be caused by renal artery stenosis, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, or cor pulmonale.

Clinical features of hyperaldosteronism include hypertension, hypokalemia, metabolic alkalosis, hypernatremia, polyuria, polydipsia, headaches, lethargy, muscle weakness and spasms, and numbness. It is estimated that hyperaldosteronism is present in 5-10% of patients with hypertension, and hypertension in primary hyperaldosteronism is often resistant to drug treatment.

Diagnosis of hyperaldosteronism involves various investigations, including U&Es to assess electrolyte disturbances, aldosterone-to-renin plasma ratio (ARR) as the gold standard diagnostic test, ECG to detect arrhythmia, CT/MRI scans to locate adenoma, fludrocortisone suppression test or oral salt testing to confirm primary hyperaldosteronism, genetic testing to identify familial hyperaldosteronism, and adrenal venous sampling to determine lateralization prior to surgery.

Treatment of primary hyperaldosteronism typically involves surgical adrenalectomy for patients with unilateral primary aldosteronism. Diet modification with sodium restriction and potassium supplementation may also be recommended.

Addison’s disease is primarily caused by tuberculosis, making it the most prevalent factor worldwide.

Further Reading:

Addison’s disease, also known as primary adrenal insufficiency or hypoadrenalism, is a rare disorder caused by the destruction of the adrenal cortex. This leads to reduced production of glucocorticoids, mineralocorticoids, and adrenal androgens. The deficiency of cortisol results in increased production of adrenocorticotropic hormone (ACTH) due to reduced negative feedback to the pituitary gland. This condition can cause metabolic disturbances such as hyperkalemia, hyponatremia, hypercalcemia, and hypoglycemia.

The symptoms of Addison’s disease can vary but commonly include fatigue, weight loss, muscle weakness, and low blood pressure. It is more common in women and typically affects individuals between the ages of 30-50. The most common cause of primary hypoadrenalism in developed countries is autoimmune destruction of the adrenal glands. Other causes include tuberculosis, adrenal metastases, meningococcal septicaemia, HIV, and genetic disorders.

The diagnosis of Addison’s disease is often suspected based on low cortisol levels and electrolyte abnormalities. The adrenocorticotropic hormone stimulation test is commonly used for confirmation. Other investigations may include adrenal autoantibodies, imaging scans, and genetic screening.

Addisonian crisis is a potentially life-threatening condition that occurs when there is an acute deficiency of cortisol and aldosterone. It can be the first presentation of undiagnosed Addison’s disease. Precipitating factors of an Addisonian crisis include infection, dehydration, surgery, trauma, physiological stress, pregnancy, hypoglycemia, and acute withdrawal of long-term steroids. Symptoms of an Addisonian crisis include malaise, fatigue, nausea or vomiting, abdominal pain, fever, muscle pains, dehydration, confusion, and loss of consciousness.

There is no fixed consensus on diagnostic criteria for an Addisonian crisis, as symptoms are non-specific. Investigations may include blood tests, blood gas analysis, and septic screens if infection is suspected. Management involves administering hydrocortisone and fluids. Hydrocortisone is given parenterally, and the dosage varies depending on the age of the patient. Fluid resuscitation with saline is necessary to correct any electrolyte disturbances and maintain blood pressure. The underlying cause of the crisis should also be identified and treated. Close monitoring of sodium levels is important to prevent complications such as osmotic demyelination syndrome.

Ketamine should not be used in children under 12 months old due to the increased risk of laryngospasm and airway complications. The Royal College of Emergency Medicine advises against using ketamine in children under 1 year old in the emergency department, and it should only be administered by experienced clinicians in children aged 5 and under. Ketamine may cause a slight increase in blood pressure and heart rate, making it a suitable option for those with low blood pressure. However, it is contraindicated in individuals with malignant hypertension (blood pressure above 180 mmHg). Please refer to the notes below for additional contraindications.

Further Reading:

Procedural sedation is commonly used by emergency department (ED) doctors to minimize pain and discomfort during procedures that may be painful or distressing for patients. Effective procedural sedation requires the administration of analgesia, anxiolysis, sedation, and amnesia. This is typically achieved through the use of a combination of short-acting analgesics and sedatives.

There are different levels of sedation, ranging from minimal sedation (anxiolysis) to general anesthesia. It is important for clinicians to understand the level of sedation being used and to be able to manage any unintended deeper levels of sedation that may occur. Deeper levels of sedation are similar to general anesthesia and require the same level of care and monitoring.

Various drugs can be used for procedural sedation, including propofol, midazolam, ketamine, and fentanyl. Each of these drugs has its own mechanism of action and side effects. Propofol is commonly used for sedation, amnesia, and induction and maintenance of general anesthesia. Midazolam is a benzodiazepine that enhances the effect of GABA on the GABA A receptors. Ketamine is an NMDA receptor antagonist and is used for dissociative sedation. Fentanyl is a highly potent opioid used for analgesia and sedation.

The doses of these drugs for procedural sedation in the ED vary depending on the drug and the route of administration. It is important for clinicians to be familiar with the appropriate doses and onset and peak effect times for each drug.

Safe sedation requires certain requirements, including appropriate staffing levels, competencies of the sedating practitioner, location and facilities, and monitoring. The level of sedation being used determines the specific requirements for safe sedation.

After the procedure, patients should be monitored until they meet the criteria for safe discharge. This includes returning to their baseline level of consciousness, having vital signs within normal limits, and not experiencing compromised respiratory status. Pain and discomfort should also be addressed before discharge.

Trichomonas vaginalis (TV) is a highly prevalent sexually transmitted disease that affects individuals worldwide. This disease is caused by a parasitic protozoan organism that can survive without the presence of mitochondria or peroxisomes. The risk of contracting TV increases with the number of sexual partners one has. It is important to note that men can also be affected by this disease, experiencing conditions such as prostatitis or urethritis.

The clinical features of TV can vary. Surprisingly, up to 70% of patients may not exhibit any symptoms at all. However, for those who do experience symptoms, they may notice a frothy or green-yellow discharge with a strong odor. Other symptoms may include vaginitis and inflammation of the cervix, which can give it a distinctive strawberry appearance. In pregnant individuals, TV can lead to complications such as premature labor and low birth weight.

Diagnosing TV can sometimes occur incidentally during routine smear tests. However, if a patient is symptomatic, the diagnosis is typically made through vaginal swabs for women or penile swabs for men. Treatment for TV usually involves taking metronidazole, either as a 400 mg dose twice a day for 5-7 days or as a single 2 g dose. It is worth noting that the single dose may have more gastrointestinal side effects. Another antibiotic option is tinidazole.

One of the diagnostic criteria for ARDS is the presence of hypoxemia. Other criteria include the onset of symptoms within 7 days of a clinical insult or new/worsening respiratory symptoms, bilateral opacities on chest X-ray that cannot be fully explained by other conditions, and respiratory failure that cannot be fully attributed to cardiac failure or fluid overload.

Further Reading:

ARDS is a severe form of lung injury that occurs in patients with a predisposing risk factor. It is characterized by the onset of respiratory symptoms within 7 days of a known clinical insult, bilateral opacities on chest X-ray, and respiratory failure that cannot be fully explained by cardiac failure or fluid overload. Hypoxemia is also present, as indicated by a specific threshold of the PaO2/FiO2 ratio measured with a minimum requirement of positive end-expiratory pressure (PEEP) ≥5 cm H2O. The severity of ARDS is classified based on the PaO2/FiO2 ratio, with mild, moderate, and severe categories.

Lung protective ventilation is a set of measures aimed at reducing lung damage that may occur as a result of mechanical ventilation. Mechanical ventilation can cause lung damage through various mechanisms, including high air pressure exerted on lung tissues (barotrauma), over distending the lung (volutrauma), repeated opening and closing of lung units (atelectrauma), and the release of inflammatory mediators that can induce lung injury (biotrauma). These mechanisms collectively contribute to ventilator-induced lung injury (VILI).

The key components of lung protective ventilation include using low tidal volumes (5-8 ml/kg), maintaining inspiratory pressures (plateau pressure) below 30 cm of water, and allowing for permissible hypercapnia. However, there are some contraindications to lung protective ventilation, such as an unacceptable level of hypercapnia, acidosis, and hypoxemia. These factors need to be carefully considered when implementing lung protective ventilation strategies in patients with ARDS.

Stevens-Johnson syndrome is a severe and potentially deadly form of erythema multiforme. It can be triggered by anything that causes erythema multiforme, but it is most commonly seen as a reaction to medication within 1-3 weeks of starting treatment. Initially, there may be symptoms like fever, fatigue, joint pain, and digestive issues, followed by the development of severe mucocutaneous lesions that are blistering and ulcerating.

Stevens-Johnson syndrome and toxic epidermal necrolysis are considered to be different stages of the same mucocutaneous disease, with toxic epidermal necrolysis being more severe. The extent of epidermal detachment is used to differentiate between the two. In Stevens-Johnson syndrome, less than 10% of the body surface area is affected by epidermal detachment, while in toxic epidermal necrolysis, it is greater than 30%. An overlap syndrome occurs when detachment affects between 10-30% of the body surface area.

Several drugs can potentially cause Stevens-Johnson syndrome and toxic epidermal necrolysis, including tetracyclines, penicillins, vancomycin, sulphonamides, NSAIDs, and barbiturates.

Glandular fever, also known as infectious mononucleosis, can lead to a rare but potentially life-threatening complication called splenic rupture. Although splenomegaly (enlarged spleen) is common in glandular fever, it often does not cause any symptoms and cannot be felt during a physical examination. However, this increases the risk of splenic rupture, which can occur spontaneously or with minimal trauma. The spleen typically reaches its maximum size around two weeks into the illness before gradually shrinking. To prevent splenic rupture, patients are advised to avoid heavy lifting and contact sports for at least one month from the onset of the illness. Other complications of glandular fever include prolonged fatigue, mild hepatitis leading to jaundice, thrombocytopenia (low platelet count) with an increased risk of bleeding, neurological conditions such as Guillain-Barré syndrome, optic neuritis, Bell’s palsy, myocarditis, and nephritis.

Further Reading:

Glandular fever, also known as infectious mononucleosis or mono, is a clinical syndrome characterized by symptoms such as sore throat, fever, and swollen lymph nodes. It is primarily caused by the Epstein-Barr virus (EBV), with other viruses and infections accounting for the remaining cases. Glandular fever is transmitted through infected saliva and primarily affects adolescents and young adults. The incubation period is 4-8 weeks.

The majority of EBV infections are asymptomatic, with over 95% of adults worldwide having evidence of prior infection. Clinical features of glandular fever include fever, sore throat, exudative tonsillitis, lymphadenopathy, and prodromal symptoms such as fatigue and headache. Splenomegaly (enlarged spleen) and hepatomegaly (enlarged liver) may also be present, and a non-pruritic macular rash can sometimes occur.

Glandular fever can lead to complications such as splenic rupture, which increases the risk of rupture in the spleen. Approximately 50% of splenic ruptures associated with glandular fever are spontaneous, while the other 50% follow trauma. Diagnosis of glandular fever involves various investigations, including viral serology for EBV, monospot test, and liver function tests. Additional serology tests may be conducted if EBV testing is negative.

Management of glandular fever involves supportive care and symptomatic relief with simple analgesia. Antiviral medication has not been shown to be beneficial. It is important to identify patients at risk of serious complications, such as airway obstruction, splenic rupture, and dehydration, and provide appropriate management. Patients can be advised to return to normal activities as soon as possible, avoiding heavy lifting and contact sports for the first month to reduce the risk of splenic rupture.

Rare but serious complications associated with glandular fever include hepatitis, upper airway obstruction, cardiac complications, renal complications, neurological complications, haematological complications, chronic fatigue, and an increased risk of lymphoproliferative cancers and multiple sclerosis.

Thiazide diuretics, like bendroflumethiazide and hydrochlorothiazide, have the potential to raise levels of uric acid in the blood, which can worsen gout symptoms in individuals who are susceptible to the condition.

Other medications, such as diuretics, beta-blockers, ACE inhibitors, and non-losartan ARBs, are also linked to an increased risk of gout.

On the other hand, calcium-channel blockers like amlodipine and verapamil, as well as losartan, have been found to lower uric acid levels and are associated with a reduced risk of gout.

The patient’s history aligns with a generalized tonic-clonic seizure. The observer of the incident provided a detailed description, which is crucial in diagnosing epilepsy.

Diagnosing epilepsy can sometimes rely solely on the patient’s history. It is common to ask the patient to maintain a seizure diary to identify patterns and potential triggers. Additionally, EEG tests, along with an MRI scan or CT scan of the brain, can provide further insight into the type and possible cause of the seizures.

The patient is currently taking 20 mg of Atorvastatin once daily. They do not have a history of heart disease, vascular disease, or stroke. Their blood pressure is 148/92 mmHg, pulse rate is 86 bpm, and respiration rate is 1.

Further Reading:

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting around 5% of patients over the age of 70-75 years and 10% of patients aged 80-85 years. While AF can cause palpitations and inefficient cardiac function, the most important aspect of managing patients with AF is reducing the increased risk of stroke.

AF can be classified as first detected episode, paroxysmal, persistent, or permanent. First detected episode refers to the initial occurrence of AF, regardless of symptoms or duration. Paroxysmal AF occurs when a patient has 2 or more self-terminating episodes lasting less than 7 days. Persistent AF refers to episodes lasting more than 7 days that do not self-terminate. Permanent AF is continuous atrial fibrillation that cannot be cardioverted or if attempts to do so are deemed inappropriate. The treatment goals for permanent AF are rate control and anticoagulation if appropriate.

Symptoms of AF include palpitations, dyspnea, and chest pain. The most common sign is an irregularly irregular pulse. An electrocardiogram (ECG) is essential for diagnosing AF, as other conditions can also cause an irregular pulse.

Managing patients with AF involves two key parts: rate/rhythm control and reducing stroke risk. Rate control involves slowing down the irregular pulse to avoid negative effects on cardiac function. This is typically achieved using beta-blockers or rate-limiting calcium channel blockers. If one drug is not effective, combination therapy may be used. Rhythm control aims to restore and maintain normal sinus rhythm through pharmacological or electrical cardioversion. However, the majority of patients are managed with a rate control strategy.

Reducing stroke risk in patients with AF is crucial. Risk stratifying tools, such as the CHA2DS2-VASc score, are used to determine the most appropriate anticoagulation strategy. Anticoagulation is recommended for patients with a score of 2 or more. Clinicians can choose between warfarin and novel oral anticoagulants (NOACs) for anticoagulation.

Before starting anticoagulation, the patient’s bleeding risk should be assessed using tools like the HAS-BLED score or the ORBIT tool. These tools evaluate factors such as hypertension, abnormal renal or liver function, history of bleeding, age, and use of drugs that predispose to bleeding.

This ECG indicates changes that are consistent with an acute inferoposterior myocardial infarction (MI). There is ST elevation in leads I, II, aVF, and V6, along with reciprocal ST depression in leads V1-V4 and aVR. Additionally, there are tall dominant R waves in leads V2-V3 and upright T waves in leads V2-V3. Based on these findings, the most likely vessel involved in this case is the right coronary artery.

To summarize the vessels involved in different types of myocardial infarction see below:
ECG Leads – Location of MI | Vessel involved
V1-V3 – Anteroseptal | Left anterior descending
V3-V4 – Anterior | Left anterior descending
V5-V6 – Anterolateral | Left anterior descending / left circumflex artery
V1-V6 – Extensive anterior | Left anterior descending
I, II, aVL, V6 – Lateral | Left circumflex artery
II, III, aVF – Inferior | Right coronary artery (80%), Left circumflex artery (20%)
V1, V4R – Right ventricle | Right coronary artery
V7-V9 – Posterior | Right coronary artery

Urgent laparotomy is necessary in cases of penetrating abdominal trauma when certain indications are present. These indications include peritonism, the presence of free air under the diaphragm on an upright chest X-ray, evisceration, hypotension or signs of unstable blood flow, a gunshot wound that has penetrated the peritoneum or retroperitoneum, gastrointestinal bleeding following penetrating trauma, genitourinary bleeding following penetrating trauma, the presence of a penetrating object that is still in place (as removal may result in significant bleeding), and the identification of free fluid on a focused assessment with sonography for trauma (FAST) or a positive diagnostic peritoneal lavage (DPL).

Further Reading:

Abdominal trauma can be classified into two categories: blunt trauma and penetrating trauma. Blunt trauma occurs when compressive or deceleration forces are applied to the abdomen, often resulting from road traffic accidents or direct blows during sports. The spleen and liver are the organs most commonly injured in blunt abdominal trauma. On the other hand, penetrating trauma involves injuries that pierce the skin and enter the abdominal cavity, such as stabbings, gunshot wounds, or industrial accidents. The bowel and liver are the organs most commonly affected in penetrating injuries.

When it comes to imaging in blunt abdominal trauma, there are three main modalities that are commonly used: focused assessment with sonography in trauma (FAST), diagnostic peritoneal lavage (DPL), and computed tomography (CT). FAST is a non-invasive and quick method used to detect free intraperitoneal fluid, aiding in the decision on whether a laparotomy is needed. DPL is also used to detect intraperitoneal blood and can be used in both unstable blunt abdominal trauma and penetrating abdominal trauma. However, it is more invasive and time-consuming compared to FAST and has largely been replaced by it. CT, on the other hand, is the gold standard for diagnosing intra-abdominal pathology and is used in stable abdominal trauma patients. It offers high sensitivity and specificity but requires a stable and cooperative patient. It also involves radiation and may have delays in availability.

In the case of penetrating trauma, it is important to assess these injuries with the help of a surgical team. Penetrating objects should not be removed in the emergency department as they may be tamponading underlying vessels. Ideally, these injuries should be explored in the operating theater.

In summary, abdominal trauma can be classified into blunt trauma and penetrating trauma. Blunt trauma is caused by compressive or deceleration forces and commonly affects the spleen and liver. Penetrating trauma involves injuries that pierce the skin and commonly affect the bowel and liver. Imaging modalities such as FAST, DPL, and CT are used to assess and diagnose abdominal trauma, with CT being the gold standard. Penetrating injuries should be assessed by a surgical team and should ideally be explored in the operating theater.

Cauda equina syndrome (CES) is a rare but serious complication that can occur when a disc ruptures. This happens when the material from the disc is pushed into the spinal canal and puts pressure on the bundle of nerves in the lower back and sacrum. As a result, individuals may experience loss of control over their bladder and bowel functions.

There are certain red flags that may indicate the presence of CES. These include experiencing sciatica on both sides of the body, having severe or worsening neurological issues in both legs (such as significant weakness in knee extension, ankle eversion, or foot dorsiflexion), difficulty starting urination or a decreased sensation of urinary flow, loss of sensation in the rectum, experiencing numbness or tingling in the perianal, perineal, or genital areas (also known as saddle anesthesia or paresthesia), and having a lax anal sphincter.

Conus medullaris syndrome (CMS) is a condition that affects the conus medullaris, which is located above the cauda equina at the T12-L2 level. Unlike CES, CMS primarily causes back pain and may have less noticeable nerve root pain. The main symptoms of CMS are urinary retention and constipation.

To confirm a diagnosis of CES and determine the level of compression and any underlying causes, an MRI scan is considered the gold-standard investigation. In cases where an MRI is not possible or contraindicated, a CT myelogram or standard CT scans can be helpful. However, plain radiographs have limited value and may only show significant degenerative or traumatic bone diseases.

The percentage of patients who survive to hospital discharge after experiencing an out of hospital cardiac arrest.

Further Reading:

Cardiopulmonary arrest is a serious event with low survival rates. In non-traumatic cardiac arrest, only about 20% of patients who arrest as an in-patient survive to hospital discharge, while the survival rate for out-of-hospital cardiac arrest is approximately 8%. The Resus Council BLS/AED Algorithm for 2015 recommends chest compressions at a rate of 100-120 per minute with a compression depth of 5-6 cm. The ratio of chest compressions to rescue breaths is 30:2.

After a cardiac arrest, the goal of patient care is to minimize the impact of post cardiac arrest syndrome, which includes brain injury, myocardial dysfunction, the ischaemic/reperfusion response, and the underlying pathology that caused the arrest. The ABCDE approach is used for clinical assessment and general management. Intubation may be necessary if the airway cannot be maintained by simple measures or if it is immediately threatened. Controlled ventilation is aimed at maintaining oxygen saturation levels between 94-98% and normocarbia. Fluid status may be difficult to judge, but a target mean arterial pressure (MAP) between 65 and 100 mmHg is recommended. Inotropes may be administered to maintain blood pressure. Sedation should be adequate to gain control of ventilation, and short-acting sedating agents like propofol are preferred. Blood glucose levels should be maintained below 8 mmol/l. Pyrexia should be avoided, and there is some evidence for controlled mild hypothermia but no consensus on this.

Post ROSC investigations may include a chest X-ray, ECG monitoring, serial potassium and lactate measurements, and other imaging modalities like ultrasonography, echocardiography, CTPA, and CT head, depending on availability and skills in the local department. Treatment should be directed towards the underlying cause, and PCI or thrombolysis may be considered for acute coronary syndrome or suspected pulmonary embolism, respectively.

Patients who are comatose after ROSC without significant pre-arrest comorbidities should be transferred to the ICU for supportive care. Neurological outcome at 72 hours is the best prognostic indicator of outcome.

Traumatic aortic rupture is a relatively common cause of sudden death following major trauma, especially high-speed road traffic accidents (RTAs). It is estimated that 15-20% of deaths from RTAs are due to this injury. If the aortic rupture is promptly recognized and treated, patients who survive the initial injury can fully recover.

Surviving patients often have an incomplete laceration near the ligamentum arteriosum of the aorta. The continuity is maintained by either an intact adventitial layer or a contained mediastinal hematoma, which prevents immediate exsanguination and death.

Detecting traumatic aortic rupture can be challenging as many patients do not exhibit specific symptoms, and other injuries may also be present, making the diagnosis unclear.

Chest X-ray findings can aid in the diagnosis and include fractures of the 1st and 2nd ribs, a grossly widened mediastinum, a hazy left lung field, obliteration of the aortic knob, deviation of the trachea to the right, presence of a pleural cap, elevation and rightward shift of the right mainstem bronchus, depression of the left mainstem bronchus, obliteration of the space between the pulmonary artery and aorta, and deviation of the esophagus (or NG tube) to the right.

Helical contrast-enhanced CT scanning is highly sensitive and specific for detecting aortic rupture, but it should only be performed on hemodynamically stable patients.

Treatment options include primary repair or resection of the torn segment with replacement using an interposition graft. Endovascular repair is also now considered an acceptable alternative approach.

Chronic myeloid leukaemia (CML) is a type of blood disorder that arises from an abnormal pluripotent haemopoietic stem cell. The majority of CML cases, more than 80%, are caused by a cytogenetic abnormality called the Philadelphia chromosome. This abnormality occurs when there is a reciprocal translocation between the long arms of chromosomes 9 and 22.

CML typically develops slowly over a period of several years, known as the chronic stage. During this stage, patients usually do not experience any symptoms, and it is often discovered incidentally through routine blood tests. Around 90% of CML cases are diagnosed during this stage. In the bone marrow, less than 10% of the white cells are immature blasts.

Symptoms start to appear when the CML cells begin to expand, which is known as the accelerated stage. Approximately 10% of cases are diagnosed during this stage. Between 10 and 30% of the blood cells in the bone marrow are blasts at this point. Common clinical features during this stage include tiredness, fatigue, fever, night sweats, abdominal distension, left upper quadrant pain (splenic infarction), splenomegaly (enlarged spleen), hepatomegaly (enlarged liver), easy bruising, gout (due to rapid cell turnover), and hyperviscosity (which can lead to complications like stroke, priapism, etc.).

In some cases, a small number of patients may present with a blast crisis, also known as the blast stage. During this stage, more than 30% of the blood cells in the bone marrow are immature blast cells. Patients in this stage are generally very ill, experiencing severe constitutional symptoms such as fever, weight loss, and bone pain, as well as infections and bleeding tendencies.

Laboratory findings in CML include a significantly elevated white cell count (often greater than 100 x 109/l), a left shift with an increased number of immature leukocytes, mild to moderate normochromic, normocytic anaemia, variable platelet counts (low, normal, or elevated), presence of the Philadelphia chromosome in more than 80% of cases, and elevated levels of serum uric acid and alkaline phosphatase.

To calculate the total fluid requirement over 24 hours, you need to multiply the TBSA (Total Body Surface Area) by the weight in kilograms. In this particular case, the calculation would be 4 multiplied by 20 multiplied by 80, resulting in a total of 6400 milliliters.

Further Reading:

Burn injuries can be classified based on their type (degree, partial thickness or full thickness), extent as a percentage of total body surface area (TBSA), and severity (minor, moderate, major/severe). Severe burns are defined as a >10% TBSA in a child and >15% TBSA in an adult.

When assessing a burn, it is important to consider airway injury, carbon monoxide poisoning, type of burn, extent of burn, special considerations, and fluid status. Special considerations may include head and neck burns, circumferential burns, thorax burns, electrical burns, hand burns, and burns to the genitalia.

Airway management is a priority in burn injuries. Inhalation of hot particles can cause damage to the respiratory epithelium and lead to airway compromise. Signs of inhalation injury include visible burns or erythema to the face, soot around the nostrils and mouth, burnt/singed nasal hairs, hoarse voice, wheeze or stridor, swollen tissues in the mouth or nostrils, and tachypnea and tachycardia. Supplemental oxygen should be provided, and endotracheal intubation may be necessary if there is airway obstruction or impending obstruction.

The initial management of a patient with burn injuries involves conserving body heat, covering burns with clean or sterile coverings, establishing IV access, providing pain relief, initiating fluid resuscitation, measuring urinary output with a catheter, maintaining nil by mouth status, closely monitoring vital signs and urine output, monitoring the airway, preparing for surgery if necessary, and administering medications.

Burns can be classified based on the depth of injury, ranging from simple erythema to full thickness burns that penetrate into subcutaneous tissue. The extent of a burn can be estimated using methods such as the rule of nines or the Lund and Browder chart, which takes into account age-specific body proportions.

Fluid management is crucial in burn injuries due to significant fluid losses. Evaporative fluid loss from burnt skin and increased permeability of blood vessels can lead to reduced intravascular volume and tissue perfusion. Fluid resuscitation should be aggressive in severe burns, while burns <15% in adults and <10% in children may not require immediate fluid resuscitation. The Parkland formula can be used to calculate the intravenous fluid requirements for someone with a significant burn injury.

The top priority when dealing with suspected epiglottitis is to assess and secure the airway. This is especially important in patients who have not been vaccinated against Haemophilus influenzae type b (HiB), as they are at risk for complications from this infection. Classic signs of epiglottitis include tripod positioning, drooling, stridor, and a muffled voice. It is crucial to avoid agitating patients, particularly children, during examination or procedures, as this can trigger laryngospasm and potentially lead to airway obstruction. In such cases, it is recommended to call in senior ENT and anaesthetic support to perform laryngoscopy and be prepared for intubation or tracheostomy if necessary to address any airway compromise. If the patient is in a critical condition, securing the airway through intubation becomes the top priority.

Further Reading:

Epiglottitis is a rare but serious condition characterized by inflammation and swelling of the epiglottis, which can lead to a complete blockage of the airway. It is more commonly seen in children between the ages of 2-6, but can also occur in adults, particularly those in their 40s and 50s. Streptococcus infections are now the most common cause of epiglottitis in the UK, although other bacterial agents, viruses, fungi, and iatrogenic causes can also be responsible.

The clinical features of epiglottitis include a rapid onset of symptoms, high fever, sore throat, painful swallowing, muffled voice, stridor and difficulty breathing, drooling of saliva, irritability, and a characteristic tripod positioning with the arms forming the front two legs of the tripod. It is important for healthcare professionals to avoid examining the throat or performing any potentially upsetting procedures until the airway has been assessed and secured.

Diagnosis of epiglottitis is typically made through fibre-optic laryngoscopy, which is considered the gold standard investigation. Lateral neck X-rays may also show a characteristic thumb sign, indicating an enlarged and swollen epiglottis. Throat swabs and blood cultures may be taken once the airway is secured to identify the causative organism.

Management of epiglottitis involves assessing and securing the airway as the top priority. Intravenous or oral antibiotics are typically prescribed, and supplemental oxygen may be given if intubation or tracheostomy is planned. In severe cases where the airway is significantly compromised, intubation or tracheostomy may be necessary. Steroids may also be used, although the evidence for their benefit is limited.

Overall, epiglottitis is a potentially life-threatening condition that requires urgent medical attention. Prompt diagnosis, appropriate management, and securing the airway are crucial in ensuring a positive outcome for patients with this condition.

Recognizing the extent of blood loss based on vital sign and mental status abnormalities is a crucial skill. The Advanced Trauma Life Support (ATLS) classification for hemorrhagic shock correlates the amount of blood loss with expected physiological responses in a healthy individual weighing 70 kg. In terms of body weight, the total circulating blood volume accounts for approximately 7%, which is roughly equivalent to five liters in an average 70 kg male patient.

The ATLS classification for hemorrhagic shock is as follows:

CLASS I:
– Blood loss: Up to 750 mL
– Blood loss (% blood volume): Up to 15%
– Pulse rate: Less than 100 beats per minute (bpm)
– Systolic blood pressure: Normal
– Pulse pressure: Normal (or increased)
– Respiratory rate: 14-20 breaths per minute
– Urine output: Greater than 30 mL/hr
– CNS/mental status: Slightly anxious

CLASS II:
– Blood loss: 750-1500 mL
– Blood loss (% blood volume): 15-30%
– Pulse rate: 100-120 bpm
– Systolic blood pressure: Normal
– Pulse pressure: Decreased
– Respiratory rate: 20-30 breaths per minute
– Urine output: 20-30 mL/hr
– CNS/mental status: Mildly anxious

CLASS III:
– Blood loss: 1500-2000 mL
– Blood loss (% blood volume): 30-40%
– Pulse rate: 120-140 bpm
– Systolic blood pressure: Decreased
– Pulse pressure: Decreased
– Respiratory rate: 30-40 breaths per minute
– Urine output: 5-15 mL/hr
– CNS/mental status: Anxious, confused

CLASS IV:
– Blood loss: More than 2000 mL
– Blood loss (% blood volume): More than 40%
– Pulse rate: More than 140 bpm
– Systolic blood pressure: Decreased
– Pulse pressure: Decreased
– Respiratory rate: More than 40 breaths per minute
– Urine output: Negligible
– CNS/mental status: Confused, lethargic

Traumatic aortic rupture, also known as traumatic aortic disruption or transection, occurs when the aorta is torn or ruptured due to physical trauma. This condition often leads to sudden death because of severe bleeding. Motor vehicle accidents and falls from great heights are the most common causes of this injury.

The patients with the highest chances of survival are those who have an incomplete tear near the ligamentum arteriosum of the proximal descending aorta, close to where the left subclavian artery branches off. The presence of an intact adventitial layer or contained mediastinal hematoma helps maintain continuity and prevents immediate bleeding and death. If promptly identified and treated, survivors of these injuries can recover. In cases where traumatic aortic rupture leads to sudden death, approximately 50% of patients have damage at the aortic isthmus, while around 15% have damage in either the ascending aorta or the aortic arch.

Initial chest X-rays may show signs consistent with a traumatic aortic injury. However, false-positive and false-negative results can occur, and sometimes there may be no abnormalities visible on the X-ray. Some of the possible X-ray findings include a widened mediastinum, hazy left lung field, obliteration of the aortic knob, fractures of the 1st and 2nd ribs, deviation of the trachea to the right, presence of a pleural cap, elevation and rightward shift of the right mainstem bronchus, depression of the left mainstem bronchus, obliteration of the space between the pulmonary artery and aorta, and deviation of the esophagus or NG tube to the right.

A helical contrast-enhanced CT scan of the chest is the preferred initial investigation for suspected blunt aortic injury. It has proven to be highly accurate, with close to 100% sensitivity and specificity. CT scanning should be performed liberally, as chest X-ray findings can be unreliable. However, hemodynamically unstable patients should not be placed in a CT scanner. If the CT results are inconclusive, aortography or trans-oesophageal echo can be performed for further evaluation.

Immediate surgical intervention is necessary for these injuries. Endovascular repair is the most common method used and has excellent short-term outcomes. Open repair may also be performed depending on the circumstances. It is important to control heart rate and blood pressure during stabilization to reduce the risk of rupture. Pain should be managed with appropriate analgesic

The size of the cannula used for IV fluid infusion determines the maximum flow rate. For a 20g cannula, the maximum flow rate is around 60 ml per minute. As a result, the fastest infusion time through a 20g cannula is approximately 15 minutes for a maximum volume of 1000 ml.

Further Reading:

Peripheral venous cannulation is a procedure that should be performed following established guidelines to minimize the risk of infection, injury, extravasation, and early failure of the cannula. It is important to maintain good hand hygiene, use personal protective equipment, ensure sharps safety, and employ an aseptic non-touch technique during the procedure.

According to the National Institute for Health and Care Excellence (NICE), the skin should be disinfected with a solution of 2% chlorhexidine gluconate and 70% alcohol before inserting the catheter. It is crucial to allow the disinfectant to completely dry before inserting the cannula.

The flow rates of IV cannulas can vary depending on factors such as the gauge, color, type of fluid used, presence of a bio-connector, length of the cannula, and whether the fluid is drained under gravity or pumped under pressure. However, the following are typical flow rates for different gauge sizes: 14 gauge (orange) has a flow rate of 270 ml/minute, 16 gauge (grey) has a flow rate of 180 ml/minute, 18 gauge (green) has a flow rate of 90 ml/minute, 20 gauge (pink) has a flow rate of 60 ml/minute, and 22 gauge (blue) has a flow rate of 36 ml/minute. These flow rates are based on infusing 1000 ml of normal saline under ideal circumstances, but they may vary in practice.

Traumatic aortic rupture is a relatively common cause of sudden death following major trauma, especially high-speed road traffic accidents (RTAs). It is estimated that 15-20% of deaths from RTAs are due to this injury. If the aortic rupture is promptly recognized and treated, patients who survive the initial injury can fully recover.

Surviving patients often have an incomplete laceration near the ligamentum arteriosum of the aorta. The continuity is maintained by either an intact adventitial layer or a contained mediastinal hematoma, which prevents immediate exsanguination and death.

Detecting traumatic aortic rupture can be challenging as many patients do not exhibit specific symptoms, and other injuries may also be present, making the diagnosis unclear.

Chest X-ray findings can aid in the diagnosis and include fractures of the 1st and 2nd ribs, a grossly widened mediastinum, a hazy left lung field, obliteration of the aortic knob, deviation of the trachea to the right, presence of a pleural cap, elevation and rightward shift of the right mainstem bronchus, depression of the left mainstem bronchus, obliteration of the space between the pulmonary artery and aorta, and deviation of the esophagus (or NG tube) to the right.

Helical contrast-enhanced CT scanning is highly sensitive and specific for detecting aortic rupture, but it should only be performed on hemodynamically stable patients.

Treatment options include primary repair or resection of the torn segment with replacement using an interposition graft. Endovascular repair is also now considered an acceptable alternative approach.

Golfer’s elbow, also known as medial epicondylitis, is a condition characterized by inflammation and pain in the flexor tendons that attach to the medial epicondyle. It is commonly caused by repetitive strain, with golf being a frequent culprit. Similarly, tennis elbow, or lateral epicondylitis, occurs when the same strain and inflammation affect the tendons at the lateral epicondyle. In both cases, pain can be worsened by resisted wrist extension. Treatment involves avoiding activities that trigger symptoms and using non-steroidal anti-inflammatory drugs for flare-ups. In more severe cases, steroid injections may be necessary.

Ulnar neuritis presents with symptoms such as hand clumsiness, muscle weakness, and wasting in the muscles supplied by the ulnar nerve. Patients may also experience numbness or tingling in the little finger and medial half of the ring finger. This condition is caused by narrowing of the ulnar groove and can be associated with risk factors like osteoarthritis, trauma, and rheumatoid arthritis. Nerve conduction studies may be recommended, and surgical decompression may be necessary.

De Quervain’s tenosynovitis occurs when there is inflammation of the tendon sheaths for the thumb extensor and abductor muscles. This leads to pain over the radial styloid, which worsens with forced adduction and flexion of the thumb. Treatment options include anti-inflammatory medications, thumb splints, and steroid injections.

Bursitis can develop from repeated pressure on the olecranon, resulting in swelling and discomfort in that area. Aspiration of fluid may be performed to rule out conditions like gout or sepsis. If these conditions are ruled out, bursitis often resolves on its own.

Activated charcoal should be given to patients who have ingested paracetamol and meet two criteria: they must present within one hour of ingestion, and they must have taken a dose of paracetamol that is equal to or greater than 150 mg/kg. The recommended dose of activated charcoal is 50g, which is typically administered as 300ml. It is important to note that the dose criteria of 150 mg/kg is based on the amount of paracetamol reported by the patient, not on paracetamol levels, which should not be assessed until at least four hours after ingestion.

Further Reading:

Paracetamol poisoning occurs when the liver is unable to metabolize paracetamol properly, leading to the production of a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI). Normally, NAPQI is conjugated by glutathione into a non-toxic form. However, during an overdose, the liver’s conjugation systems become overwhelmed, resulting in increased production of NAPQI and depletion of glutathione stores. This leads to the formation of covalent bonds between NAPQI and cell proteins, causing cell death in the liver and kidneys.

Symptoms of paracetamol poisoning may not appear for the first 24 hours or may include abdominal symptoms such as nausea and vomiting. After 24 hours, hepatic necrosis may develop, leading to elevated liver enzymes, right upper quadrant pain, and jaundice. Other complications can include encephalopathy, oliguria, hypoglycemia, renal failure, and lactic acidosis.

The management of paracetamol overdose depends on the timing and amount of ingestion. Activated charcoal may be given if the patient presents within 1 hour of ingesting a significant amount of paracetamol. N-acetylcysteine (NAC) is used to increase hepatic glutathione production and is given to patients who meet specific criteria. Blood tests are taken to assess paracetamol levels, liver function, and other parameters. Referral to a medical or liver unit may be necessary, and psychiatric follow-up should be considered for deliberate overdoses.

In cases of staggered ingestion, all patients should be treated with NAC without delay. Blood tests are also taken, and if certain criteria are met, NAC can be discontinued. Adverse reactions to NAC are common and may include anaphylactoid reactions, rash, hypotension, and nausea. Treatment for adverse reactions involves medications such as chlorpheniramine and salbutamol, and the infusion may be stopped if necessary.

The prognosis for paracetamol poisoning can be poor, especially in cases of severe liver injury. Fulminant liver failure may occur, and liver transplant may be necessary. Poor prognostic indicators include low arterial pH, prolonged prothrombin time, high plasma creatinine, and hepatic encephalopathy.

Beta-blockers, like bisoprolol, and verapamil have a strong negative effect on the force of ventricular contraction. When these medications are taken together, they can significantly reduce ventricular contraction and lead to a slow heart rate, known as bradycardia. Additionally, the risk of developing AV block is increased. In certain situations, this combination can result in severe low blood pressure or even a complete absence of heart rhythm, known as asystole. Therefore, it is important to avoid using these medications together to prevent these potentially dangerous effects.

Bronchiolitis is primarily caused by the respiratory syncytial virus (RSV), while whooping cough is caused by pertussis.

Further Reading:

Croup, also known as laryngotracheobronchitis, is a respiratory infection that primarily affects infants and toddlers. It is characterized by a barking cough and can cause stridor (a high-pitched sound during breathing) and respiratory distress due to swelling of the larynx and excessive secretions. The majority of cases are caused by parainfluenza viruses 1 and 3. Croup is most common in children between 6 months and 3 years of age and tends to occur more frequently in the autumn.

The clinical features of croup include a barking cough that is worse at night, preceded by symptoms of an upper respiratory tract infection such as cough, runny nose, and congestion. Stridor, respiratory distress, and fever may also be present. The severity of croup can be graded using the NICE system, which categorizes it as mild, moderate, severe, or impending respiratory failure based on the presence of symptoms such as cough, stridor, sternal/intercostal recession, agitation, lethargy, and decreased level of consciousness. The Westley croup score is another commonly used tool to assess the severity of croup based on the presence of stridor, retractions, air entry, oxygen saturation levels, and level of consciousness.

In cases of severe croup with significant airway obstruction and impending respiratory failure, symptoms may include a minimal barking cough, harder-to-hear stridor, chest wall recession, fatigue, pallor or cyanosis, decreased level of consciousness, and tachycardia. A respiratory rate over 70 breaths per minute is also indicative of severe respiratory distress.

Children with moderate or severe croup, as well as those with certain risk factors such as chronic lung disease, congenital heart disease, neuromuscular disorders, immunodeficiency, age under 3 months, inadequate fluid intake, concerns about care at home, or high fever or a toxic appearance, should be admitted to the hospital. The mainstay of treatment for croup is corticosteroids, which are typically given orally. If the child is too unwell to take oral medication, inhaled budesonide or intramuscular dexamethasone may be used as alternatives. Severe cases may require high-flow oxygen and nebulized adrenaline.

When considering the differential diagnosis for acute stridor and breathing difficulty, non-infective causes such as inhaled foreign bodies

Full thickness burns are devoid of pain as they result in the complete destruction of the superficial nerve endings. These burns usually display characteristics such as a lack of sensation, a coloration of the burnt skin in shades of white, brown, or black, a texture that is waxy or leathery, and a dry appearance without any blistering.

Further Reading:

Burn injuries can be classified based on their type (degree, partial thickness or full thickness), extent as a percentage of total body surface area (TBSA), and severity (minor, moderate, major/severe). Severe burns are defined as a >10% TBSA in a child and >15% TBSA in an adult.

When assessing a burn, it is important to consider airway injury, carbon monoxide poisoning, type of burn, extent of burn, special considerations, and fluid status. Special considerations may include head and neck burns, circumferential burns, thorax burns, electrical burns, hand burns, and burns to the genitalia.

Airway management is a priority in burn injuries. Inhalation of hot particles can cause damage to the respiratory epithelium and lead to airway compromise. Signs of inhalation injury include visible burns or erythema to the face, soot around the nostrils and mouth, burnt/singed nasal hairs, hoarse voice, wheeze or stridor, swollen tissues in the mouth or nostrils, and tachypnea and tachycardia. Supplemental oxygen should be provided, and endotracheal intubation may be necessary if there is airway obstruction or impending obstruction.

The initial management of a patient with burn injuries involves conserving body heat, covering burns with clean or sterile coverings, establishing IV access, providing pain relief, initiating fluid resuscitation, measuring urinary output with a catheter, maintaining nil by mouth status, closely monitoring vital signs and urine output, monitoring the airway, preparing for surgery if necessary, and administering medications.

Burns can be classified based on the depth of injury, ranging from simple erythema to full thickness burns that penetrate into subcutaneous tissue. The extent of a burn can be estimated using methods such as the rule of nines or the Lund and Browder chart, which takes into account age-specific body proportions.

Fluid management is crucial in burn injuries due to significant fluid losses. Evaporative fluid loss from burnt skin and increased permeability of blood vessels can lead to reduced intravascular volume and tissue perfusion. Fluid resuscitation should be aggressive in severe burns, while burns <15% in adults and <10% in children may not require immediate fluid resuscitation. The Parkland formula can be used to calculate the intravenous fluid requirements for someone with a significant burn injury.

According to the latest guidelines from NICE, it is recommended that adult patients who are undergoing treatment for acute leukaemia, stem cell transplants, or solid tumours and are expected to experience significant neutropenia as a result of chemotherapy, should be offered prophylaxis with a fluoroquinolone such as ciprofloxacin (500 mg taken orally twice daily) during the period when neutropenia is expected. This is to help prevent the occurrence of neutropenic sepsis, a serious infection that can occur in cancer patients with low levels of neutrophils.

Reference:
NICE guidance: ‘Neutropenic sepsis: prevention and management of neutropenic sepsis in cancer patients’

This patient is diagnosed with Krukenberg tumors, also known as carcinoma microcellulare. These tumors are ovarian malignancies that have spread from a primary site. The most common source of these tumors is gastric adenocarcinoma, which aligns with the patient’s history of weight loss, dysphagia, and intermittent vomiting.

Other primary cancers that can serve as the origin for Krukenberg tumors include colorectal carcinoma, breast cancer, lung cancer, contralateral ovarian carcinoma, and cholangiocarcinoma.

During an ultrasound, a solid and well-defined ovarian mass is typically observed, often affecting both ovaries. Further evaluation through a CT scan or MRI can provide additional helpful information. A biopsy is necessary to confirm the diagnosis, and histological examination will reveal the presence of mucin-secreting signet-rings.

Ectopic production of ACTH is linked to small-cell lung cancer and can lead to Cushing’s syndrome. It can also be observed in cases of pancreatic cancer and thymoma.

Hypertrophic pulmonary osteoarthropathy (HPOA) is characterized by the presence of periostitis, arthritis, and finger clubbing. On plain X-ray, subperiosteal new bone formation can be detected. This condition primarily affects the long bones and often causes pain. It is most commonly associated with squamous cell lung cancer and pulmonary adenocarcinoma.

Gynaecomastia, which is the enlargement of breast tissue in males, can occur as a result of squamous cell lung cancer. In these cases, it tends to be accompanied by pain.

Rarely, squamous cell lung cancer can cause ectopic production of TSH, leading to hyperthyroidism.

Carcinoid syndrome is a condition that arises from carcinoid tumors, which secrete serotonin and kallikreins. This syndrome manifests as episodes of flushing, diarrhea, and bronchospasm. Additionally, 50% of patients develop a secondary restrictive cardiomyopathy. Carcinoid tumors can occur in various locations, with the small intestine being the most common site. Other locations include the lungs (bronchial adenoma), rectum, appendix, and stomach.

Anaemia can be categorized based on the size of red blood cells. Microcytic anaemia, characterized by a mean corpuscular volume (MCV) of less than 80 fl, can be caused by various factors such as iron deficiency, thalassaemia, anaemia of chronic disease (which can also be normocytic), sideroblastic anaemia (which can also be normocytic), lead poisoning, and aluminium toxicity (although this is now rare and mainly affects haemodialysis patients).

On the other hand, normocytic anaemia, with an MCV ranging from 80 to 100 fl, can be attributed to conditions like haemolysis, acute haemorrhage, bone marrow failure, anaemia of chronic disease (which can also be microcytic), mixed iron and folate deficiency, pregnancy, chronic renal failure, and sickle-cell disease.

Lastly, macrocytic anaemia, characterized by an MCV greater than 100 fl, can be caused by factors such as B12 deficiency, folate deficiency, hypothyroidism, reticulocytosis, liver disease, alcohol abuse, myeloproliferative disease, myelodysplastic disease, and certain drugs like methotrexate, hydroxyurea, and azathioprine.

It is important to understand the different causes of anaemia based on red cell size as this knowledge can aid in the diagnosis and management of this condition.

A massive haemothorax occurs when more than 1500 mL of blood, which is about 1/3 of the patient’s blood volume, rapidly accumulates in the chest cavity. The classic signs of a massive haemothorax include decreased chest expansion, decreased breath sounds, and dullness to percussion. Both tension pneumothorax and massive haemothorax can cause decreased breath sounds, but they can be differentiated through percussion. Hyperresonance indicates tension pneumothorax, while dullness suggests a massive haemothorax.

The first step in managing a massive haemothorax is to simultaneously restore blood volume and decompress the chest cavity by inserting a chest drain. In most cases, the bleeding in a haemothorax has already stopped by the time management begins, and simple drainage is sufficient. It is important to use a chest drain of adequate size (preferably 36F) to ensure effective drainage of the haemothorax without clotting.

If 1500 mL of blood is immediately drained or if the rate of ongoing blood loss exceeds 200 mL per hour for 2-4 hours, early thoracotomy should be considered.

Statins, although generally safe and well-tolerated, can cause myopathy and myotoxicity. This range of muscle-related side effects can vary from mild muscle pain to the most severe case of rhabdomyolysis, which can lead to kidney failure, blood clotting issues, and even death.

The different levels of myotoxicity associated with statins are as follows:
– Myalgia: muscle symptoms without an increase in creatine kinase (CK) levels.
– Asymptomatic myopathy: elevated CK levels without muscle symptoms.
– Myositis: muscle symptoms with CK levels elevated less than 10 times the upper limit of normal.
– Rhabdomyolysis: muscle symptoms with CK levels elevated more than 10 times the upper limit of normal, potentially leading to myoglobinuria (presence of myoglobin in urine) and renal failure.

Most statins are broken down by the cytochrome P450 enzyme system. When taken with drugs that strongly inhibit this system, the concentration of statins in the blood can significantly increase. This, in turn, raises the risk of myopathy. A well-known example of this is the combination of statins with macrolide antibiotics like erythromycin and clarithromycin. Co-prescribing these drugs with statins has been linked to a higher risk of myopathy, hospitalization due to rhabdomyolysis, acute kidney injury, and increased mortality rates.

Blood transfusion is a crucial treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion use, errors and adverse reactions still occur.

Delayed haemolytic transfusion reactions (DHTRs) typically occur 4-8 days after a blood transfusion, but can sometimes manifest up to a month later. The symptoms are similar to acute haemolytic transfusion reactions but are usually less severe. Patients may experience fever, inadequate rise in haemoglobin, jaundice, reticulocytosis, positive antibody screen, and positive Direct Antiglobulin Test (Coombs test). DHTRs are more common in patients with sickle cell disease who have received frequent transfusions.

These reactions are caused by the presence of a low titre antibody that is too weak to be detected during cross-match and unable to cause lysis at the time of transfusion. The severity of DHTRs depends on the immunogenicity or dose of the antigen. Blood group antibodies associated with DHTRs include those of the Kidd, Duffy, Kell, and MNS systems. Most DHTRs have a benign course and do not require treatment. However, severe haemolysis with anaemia and renal failure can occur, so monitoring of haemoglobin levels and renal function is necessary. If an antibody is detected, antigen-negative blood can be requested for future transfusions.

Here is a summary of the main transfusion reactions and complications:

1. Febrile transfusion reaction: Presents with a 1-degree rise in temperature from baseline, along with chills and malaise. It is the most common reaction and is usually caused by cytokines from leukocytes in transfused red cell or platelet components. Supportive treatment with paracetamol is helpful.

2. Acute haemolytic reaction: Symptoms include fever, chills, pain at the transfusion site, nausea, vomiting, and dark urine. It is the most serious type of reaction and often occurs due to ABO incompatibility from administration errors. The transfusion should be stopped, and IV fluids should be administered. Diuretics may be required.

3. Delayed haemolytic reaction: This reaction typically occurs 4-8 days after a blood transfusion and presents with fever, anaemia, jaundice and haemoglobuinuria. Direct antiglobulin (Coombs) test positive. Due to low titre antibody too weak to detect in cross-match and unable to cause lysis at time of transfusion. Most delayed haemolytic reactions have a benign course and require no treatment. Monitor anaemia and renal function and treat as required.

The use of antibiotics can impact the effectiveness of warfarin and other coumarin anticoagulants. This can lead to changes in the International Normalized Ratio (INR) and, in severe cases, increase the risk of bleeding. Some antibiotics, such as chloramphenicol, ciprofloxacin, co-trimoxazole, doxycycline, erythromycin, macrolides (e.g., clarithromycin), metronidazole, ofloxacin, and sulphonamide, are known to enhance the anticoagulant effect of warfarin. However, cefalexin is considered relatively safe and is the most suitable option in this situation.

An overdose of Amitriptyline can lead to the development of an anticholinergic toxidrome. This toxidrome is characterized by various symptoms, which can be remembered using the phrase ‘mad as a hatter, hot as hell, red as a beat, dry as a bone, and blind as a bat’. Some of these symptoms include a dry mouth and an elevated body temperature.

Further Reading:

Tricyclic antidepressant (TCA) overdose is a common occurrence in emergency departments, with drugs like amitriptyline and dosulepin being particularly dangerous. TCAs work by inhibiting the reuptake of norepinephrine and serotonin in the central nervous system. In cases of toxicity, TCAs block various receptors, including alpha-adrenergic, histaminic, muscarinic, and serotonin receptors. This can lead to symptoms such as hypotension, altered mental state, signs of anticholinergic toxicity, and serotonin receptor effects.

TCAs primarily cause cardiac toxicity by blocking sodium and potassium channels. This can result in a slowing of the action potential, prolongation of the QRS complex, and bradycardia. However, the blockade of muscarinic receptors also leads to tachycardia in TCA overdose. QT prolongation and Torsades de Pointes can occur due to potassium channel blockade. TCAs can also have a toxic effect on the myocardium, causing decreased cardiac contractility and hypotension.

Early symptoms of TCA overdose are related to their anticholinergic properties and may include dry mouth, pyrexia, dilated pupils, agitation, sinus tachycardia, blurred vision, flushed skin, tremor, and confusion. Severe poisoning can lead to arrhythmias, seizures, metabolic acidosis, and coma. ECG changes commonly seen in TCA overdose include sinus tachycardia, widening of the QRS complex, prolongation of the QT interval, and an R/S ratio >0.7 in lead aVR.

Management of TCA overdose involves ensuring a patent airway, administering activated charcoal if ingestion occurred within 1 hour and the airway is intact, and considering gastric lavage for life-threatening cases within 1 hour of ingestion. Serial ECGs and blood gas analysis are important for monitoring. Intravenous fluids and correction of hypoxia are the first-line therapies. IV sodium bicarbonate is used to treat haemodynamic instability caused by TCA overdose, and benzodiazepines are the treatment of choice for seizure control. Other treatments that may be considered include glucagon, magnesium sulfate, and intravenous lipid emulsion.

There are certain things to avoid in TCA overdose, such as anti-arrhythmics like quinidine and flecainide, as they can prolonged depolarization.

Pericarditis refers to the inflammation of the pericardium, which can be caused by various factors such as infections (typically viral, like coxsackie virus), drug-induced reactions (e.g. isoniazid, cyclosporine), trauma, autoimmune conditions (e.g. SLE), paraneoplastic syndromes, uremia, post myocardial infarction (known as Dressler’s syndrome), post radiotherapy, and post cardiac surgery.

The clinical presentation of pericarditis often includes retrosternal chest pain that worsens with lying flat and improves when sitting forwards, along with shortness of breath, rapid heartbeat, and the presence of a pericardial friction rub.

Characteristic electrocardiogram (ECG) changes associated with pericarditis typically show widespread concave or ‘saddle-shaped’ ST elevation, widespread PR depression, reciprocal ST depression and PR elevation in aVR (and sometimes V1), and sinus tachycardia is commonly observed.

Patients who have taken an overdose of tricyclic antidepressants (TCAs) should not be given phenytoin.

Further Reading:

Tricyclic antidepressant (TCA) overdose is a common occurrence in emergency departments, with drugs like amitriptyline and dosulepin being particularly dangerous. TCAs work by inhibiting the reuptake of norepinephrine and serotonin in the central nervous system. In cases of toxicity, TCAs block various receptors, including alpha-adrenergic, histaminic, muscarinic, and serotonin receptors. This can lead to symptoms such as hypotension, altered mental state, signs of anticholinergic toxicity, and serotonin receptor effects.

TCAs primarily cause cardiac toxicity by blocking sodium and potassium channels. This can result in a slowing of the action potential, prolongation of the QRS complex, and bradycardia. However, the blockade of muscarinic receptors also leads to tachycardia in TCA overdose. QT prolongation and Torsades de Pointes can occur due to potassium channel blockade. TCAs can also have a toxic effect on the myocardium, causing decreased cardiac contractility and hypotension.

Early symptoms of TCA overdose are related to their anticholinergic properties and may include dry mouth, pyrexia, dilated pupils, agitation, sinus tachycardia, blurred vision, flushed skin, tremor, and confusion. Severe poisoning can lead to arrhythmias, seizures, metabolic acidosis, and coma. ECG changes commonly seen in TCA overdose include sinus tachycardia, widening of the QRS complex, prolongation of the QT interval, and an R/S ratio >0.7 in lead aVR.

Management of TCA overdose involves ensuring a patent airway, administering activated charcoal if ingestion occurred within 1 hour and the airway is intact, and considering gastric lavage for life-threatening cases within 1 hour of ingestion. Serial ECGs and blood gas analysis are important for monitoring. Intravenous fluids and correction of hypoxia are the first-line therapies. IV sodium bicarbonate is used to treat haemodynamic instability caused by TCA overdose, and benzodiazepines are the treatment of choice for seizure control. Other treatments that may be considered include glucagon, magnesium sulfate, and intravenous lipid emulsion.

There are certain things to avoid in TCA overdose, such as anti-arrhythmics like quinidine and flecainide, as they can prolonged depolarization.

The effects of adrenaline on alpha-adrenergic receptors result in the narrowing of blood vessels throughout the body, leading to increased pressure in the coronary and cerebral arteries. On the other hand, the effects of adrenaline on beta-adrenergic receptors enhance the strength of the heart’s contractions and increase the heart rate, which can potentially improve blood flow to the coronary and cerebral arteries. However, it is important to note that these positive effects may be counteracted by the simultaneous increase in oxygen consumption by the heart, the occurrence of abnormal heart rhythms, reduced oxygen levels due to abnormal blood flow patterns, impaired small blood vessel function, and worsened heart function following a cardiac arrest.

This child has been clinically diagnosed with measles. The typical presentation includes a high fever accompanied by symptoms of a runny nose and sensitivity to light. Conjunctivitis, or pink eye, is often present as well. The associated rash is a widespread red rash with raised bumps. Koplik spots, which are white lesions on the inside of the cheeks, are a telltale sign of measles.

According to Public Health England, it is recommended that children with measles stay away from school, nursery, or childminders for four days starting from when the rash first appears.

For more information, you can refer to the Guidance on Infection Control in Schools and other Childcare Settings.
https://www.publichealth.hscni.net/sites/default/files/Guidance_on_infection_control_in%20schools_poster.pdf

This individual has a typical history for a transient ischaemic attack (TIA). According to the NICE recommendations, it is advised to offer aspirin (300 mg daily) to individuals who have experienced a suspected TIA, unless there are contraindications. This treatment should be started immediately. It is also important to refer individuals who have had a suspected TIA for specialist assessment and investigation, with the aim of being seen within 24 hours of symptom onset. Scoring systems, such as ABCD2, should not be used to assess the risk of subsequent stroke or determine the urgency of referral for individuals with a suspected or confirmed TIA. Secondary prevention measures, in addition to aspirin, should be offered as soon as possible after the diagnosis of TIA is confirmed.

In terms of imaging, it is not recommended to offer CT brain scanning to individuals with a suspected TIA, unless there is clinical suspicion of an alternative diagnosis that CT could detect. After a specialist assessment in the TIA clinic, MRI (including diffusion-weighted and blood-sensitive sequences) may be considered to determine the area of ischaemia, detect haemorrhage, or identify alternative pathologies. If an MRI is performed, it should ideally be done on the same day as the assessment. Carotid imaging is also important for everyone with a TIA who is considered a candidate for carotid endarterectomy, and this should be done urgently.

to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old: diagnosis and initial management.

Low-velocity gunshot wounds to the abdomen result in tissue damage through laceration and cutting. On the other hand, high-velocity gunshot wounds transfer a greater amount of kinetic energy to the abdominal viscera. These types of wounds can cause more extensive damage in the surrounding area of the missile’s path due to temporary cavitation.

When patients experience penetrating abdominal trauma as a result of gunshot wounds, certain organs are more commonly injured. The small bowel is affected in approximately 50% of cases, followed by the colon in 40% of cases. The liver is injured in around 30% of cases, while abdominal vascular structures are affected in about 25% of cases.

Please note that these statistics have been obtained from the most recent edition of the ATLS manual.

Pelvic inflammatory disease (PID) is an infection that affects the upper female reproductive tract, including the uterus, fallopian tubes, and ovaries. It is typically caused by an ascending infection from the cervix. The most common culprits are sexually transmitted diseases like chlamydia and gonorrhea, with chlamydia being the most prevalent infection seen in UK genitourinary medicine clinics.

PID can often be asymptomatic, but when symptoms do occur, they may include lower abdominal pain and tenderness, fever, painful urination, painful intercourse, purulent vaginal discharge, abnormal vaginal bleeding, and tenderness in the cervix and adnexa. It’s important to note that symptoms of ectopic pregnancy can be mistaken for PID, so a pregnancy test should always be conducted in patients with suspicious symptoms.

To investigate a potential case of PID, endocervical swabs are taken to test for chlamydia and gonorrhea using nucleic acid amplification tests. It is recommended to start empirical antibiotic treatment as soon as a presumptive diagnosis of PID is made, without waiting for swab results.

Mild to moderate cases of PID can usually be managed in primary care or outpatient settings. However, patients with severe disease should be admitted to the hospital for intravenous antibiotics. Signs of severe disease include a fever above 38°C, signs of a tubo-ovarian abscess, signs of pelvic peritonitis, or concurrent pregnancy.

The current recommended treatment for outpatient cases of PID is a single intramuscular dose of ceftriaxone 500 mg, followed by oral doxycycline 100 mg twice daily and oral metronidazole 400 mg twice daily for 14 days. An alternative regimen is oral ofloxacin 400 mg twice daily and oral metronidazole 400 mg twice daily for 14 days.

For severely ill patients in the inpatient setting, initial treatment consists of intravenous doxycycline, a single-dose of intravenous ceftriaxone, and intravenous metronidazole. Afterward, the treatment is switched to oral doxycycline and metronidazole to complete a 14-day course.

If a patient fails to respond to treatment, laparoscopy is necessary to confirm the diagnosis or consider alternative diagnoses.

Nitrofurantoin is currently the preferred antibiotic for treating uncomplicated urinary tract infections in non-pregnant women. However, antibiotic resistance is becoming a significant concern in the management of urinary tract infections and pyelonephritis in the UK. In England, the resistance of E. coli (the main bacteria causing these infections) to certain antibiotics is as follows:

Trimethoprim: 30.3% (varies between areas from 27.1% to 33.4%)
Co-amoxiclav: 19.8% (varies between areas from 10.8% to 30.7%)
Ciprofloxacin: 10.6% (varies between areas from 7.8% to 13.7%)
Cefalexin: 9.9% (varies between areas from 8.1% to 11.4%)

Rapid tranquillisation involves the administration of medication through injection when oral medication is not feasible or appropriate and immediate sedation is necessary. The current guidelines from NICE recommend two options for rapid tranquillisation in adults: intramuscular lorazepam alone or a combination of intramuscular haloperidol and intramuscular promethazine. The choice of medication depends on various factors such as advanced statements, potential intoxication, previous responses to these medications, interactions with other drugs, and existing physical health conditions or pregnancy.

If there is insufficient information to determine the appropriate medication or if the individual has not taken antipsychotic medication before, intramuscular lorazepam is recommended. However, if there is evidence of cardiovascular disease or a prolonged QT interval, or if an electrocardiogram has not been conducted, the combination of intramuscular haloperidol and intramuscular promethazine should be avoided, and intramuscular lorazepam should be used instead.

If there is a partial response to intramuscular lorazepam, a second dose should be considered. If there is no response to intramuscular lorazepam, then intramuscular haloperidol combined with intramuscular promethazine should be considered. If there is a partial response to this combination, a further dose should be considered.

If there is no response to intramuscular haloperidol combined with intramuscular promethazine and intramuscular lorazepam has not been used yet, it should be considered. However, if intramuscular lorazepam has already been administered, it is recommended to arrange an urgent team meeting to review the situation and seek a second opinion if necessary.

After rapid tranquillisation, the patient should be closely monitored for any side effects, and their vital signs should be regularly checked, including heart rate, blood pressure, respiratory rate, temperature, hydration level, and level of consciousness. These observations should be conducted at least hourly until there are no further concerns about the patient’s physical health.

For more information, refer to the NICE guidance on violence and aggression: short-term management in mental health, health, and community settings.

The fascia iliaca compartment is a space within the body that has specific boundaries. It is located at the front of the hip and is surrounded by various muscles and structures. The anterior limit of this compartment is formed by the posterior surface of the fascia iliaca, which covers the iliacus muscle. Additionally, the medial reflection of this fascia covers every surface of the psoas major muscle. On the posterior side, the limit is formed by the anterior surface of the iliacus muscle and the psoas major muscle. The medial boundary is the vertebral column, while the cranially lateral boundary is the inner lip of the iliac crest. This compartment is also continuous with the space between the quadratus lumborum muscle and its fascia in a cranio-medial direction.

The fascia iliaca compartment is important because it allows for the deposition of local anesthetic in sufficient volumes. This can be achieved through a straightforward injection, which targets the femoral and lateral femoral cutaneous nerves. These nerves supply sensation to the medial, anterior, and lateral thigh. Occasionally, the obturator nerve is also blocked, although this can vary from person to person.

To perform a fascia iliaca compartment block (FICB), specific landmarks need to be identified. An imaginary line is drawn between the anterior superior iliac spine (ASIS) and the pubic tubercle. This line is then divided into thirds. The injection entry point is marked 1 cm caudal (inferior) from the junction of the lateral and middle third.

However, there are certain contraindications to performing a FICB. These include patient refusal, anticoagulation or bleeding disorders, allergy to local anesthetics, previous femoral bypass surgery, and infection or inflammation over the injection site.

As with any medical procedure, there are potential complications associated with a FICB. These can include intravascular injection, local anesthetic toxicity, allergy to the local anesthetic, temporary or permanent nerve damage, infection, and block failure. It is important for healthcare professionals to be aware of these risks and take appropriate precautions when performing a FICB.

Conjunctivitis is the most frequent occurrence of Chlamydia trachomatis infection in newborns. Ophthalmia neonatorum refers to any cause of conjunctivitis during the newborn period, regardless of the specific organism responsible. Chlamydia is now the leading cause, accounting for up to 40% of cases. Neisseria gonorrhoea, on the other hand, only accounts for less than 1% of reported cases. The remaining cases are caused by non-sexually transmitted bacteria like Staphylococcus, Streptococcus, Haemophilus species, and viruses.

Gonorrhoeal ophthalmia neonatorum typically presents within 1 to 5 days after birth. It is characterized by intense redness and swelling of the conjunctiva, eyelid swelling, and a severe discharge of pus. Corneal ulceration and perforation may also be present.

Chlamydial ophthalmia neonatorum, on the other hand, usually appears between 5 to 14 days after birth. It is characterized by a gradually increasing watery discharge that eventually becomes purulent. The inflammation in the eyes is usually less severe compared to gonococcal infection, and there is a lower risk of corneal ulceration and perforation.

The second most common manifestation of Chlamydia trachomatis infection in newborns is pneumonia. Approximately 5-30% of infected neonates will develop pneumonia. About half of these infants will also have a history of ophthalmia neonatorum.

The Severity of Alcohol Dependence Questionnaire (SADQ) is a brief, self-administered questionnaire consisting of 20 items. It was developed by the World Health Organisation with the aim of assessing the severity of alcohol dependence. Another assessment tool recommended by NICE is the Leeds Dependence Questionnaire (LDQ), which is a self-completion questionnaire comprising of 10 items. The LDQ is designed to measure dependence on various substances. Both the SADQ and LDQ are considered useful in evaluating the severity of alcohol misuse.

NICE suggests the use of specific assessment tools to effectively evaluate the nature and severity of alcohol misuse. The AUDIT is recommended for identification purposes and as a routine outcome measure. For assessing the severity of dependence, the SADQ or LDQ are recommended. To evaluate the severity of withdrawal symptoms, the Clinical Institute Withdrawal Assessment of Alcohol Scale, revised (CIWA-Ar) is recommended. Lastly, the APQ is recommended for assessing the nature and extent of problems arising from alcohol misuse.

to the NICE guidance on the diagnosis, assessment, and management of harmful drinking and alcohol dependence.

According to the ALS algorithm, the main drugs used during CPR are oxygen, adrenaline, and amiodarone. Adrenaline is administered every 3-5 minutes as per the 2021 UK ALS algorithm. Amiodarone is given after 3 shocks.

Further Reading:

In the event of an adult experiencing cardiorespiratory arrest, it is crucial for doctors to be familiar with the Advanced Life Support (ALS) algorithm. They should also be knowledgeable about the proper technique for chest compressions, the appropriate rhythms for defibrillation, the reversible causes of arrest, and the drugs used in advanced life support.

During chest compressions, the rate should be between 100-120 compressions per minute, with a depth of compression of 5-6 cm. The ratio of chest compressions to rescue breaths should be 30:2. It is important to change the person giving compressions regularly to prevent fatigue.

There are two shockable ECG rhythms that doctors should be aware of: ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT). These rhythms require defibrillation.

There are four reversible causes of cardiorespiratory arrest, known as the 4 H’s and 4 T’s. The 4 H’s include hypoxia, hypovolemia, hypo or hyperkalemia or metabolic abnormalities, and hypothermia. The 4 T’s include thrombosis (coronary or pulmonary), tension pneumothorax, tamponade, and toxins. Identifying and treating these reversible causes is crucial for successful resuscitation.

When it comes to resus drugs, they are considered of secondary importance during CPR due to the lack of high-quality evidence for their efficacy. However, adrenaline (epinephrine) and amiodarone are the two drugs included in the ALS algorithm. Doctors should be familiar with the dosing, route, and timing of administration for both drugs.

Adrenaline should be administered intravenously at a concentration of 1 in 10,000 (100 micrograms/mL). It should be repeated every 3-5 minutes. Amiodarone is initially given at a dose of 300 mg, either from a pre-filled syringe or diluted in 20 mL of Glucose 5%. If required, an additional dose of 150 mg can be given by intravenous injection. This is followed by an intravenous infusion of 900 mg over 24 hours. The first dose of amiodarone is given after 3 shocks.

This infant is displaying prolonged jaundice and failure to thrive. Prolonged jaundice is defined as jaundice that persists beyond the first 14 days of life. Neonatal jaundice can be divided into two categories: unconjugated hyperbilirubinemia, which can be either physiological or pathological, and conjugated hyperbilirubinemia, which is always pathological.

Causes of prolonged unconjugated hyperbilirubinemia include breast milk jaundice, infections (particularly urinary tract infections), haemolysis (most commonly rhesus haemolytic disease), hypothyroidism, hereditary disorders (such as Crigler-Najjar syndrome), and galactosemia.

Causes of prolonged conjugated hyperbilirubinemia include biliary atresia, choledochal cysts, and neonatal hepatitis. Conjugated hyperbilirubinemia often presents with symptoms such as failure to thrive, easy bruising or bleeding tendency, dark urine, and pale, chalky stools.

In this case, the jaundice is clearly conjugated, and the only cause of prolonged conjugated hyperbilirubinemia listed is biliary atresia. To evaluate conjugated hyperbilirubinemia, an ultrasound of the bile ducts and gallbladder should be performed. If dilatation is observed, it may indicate the presence of choledochal cysts, which should be further investigated with a cholangiogram. If the bile ducts and gallbladder appear normal or are not visualized, a radionuclide scan is often conducted. The absence of excretion on the scan is consistent with biliary atresia.

Biliary atresia is a condition characterized by progressive destruction or absence of the extrahepatic biliary tree and intrahepatic biliary ducts. It is a rare condition, occurring in approximately 1 in 10-15,000 live births in the western world. Infants with biliary atresia typically exhibit jaundice early on, and their stools are pale while their urine is dark starting from the second day of life. If left untreated, the condition will progress to chronic liver failure, leading to portal hypertension and hepatosplenomegaly. Without treatment, death is inevitable.

ATLS guidelines now suggest administering only 1 liter of crystalloid fluid during the initial assessment. If patients do not respond to the crystalloid, it is recommended to quickly transition to blood products. Studies have shown that infusing more than 1.5 liters of crystalloid fluid is associated with higher mortality rates in trauma cases. Therefore, it is advised to prioritize the early use of blood products and avoid large volumes of crystalloid fluid in trauma patients. In cases where it is necessary, massive transfusion should be considered, defined as the transfusion of more than 10 units of blood in 24 hours or more than 4 units of blood in one hour. For patients with evidence of Class III and IV hemorrhage, early resuscitation with blood and blood products in low ratios is recommended.

Based on the findings of significant trials, such as the CRASH-2 study, the use of tranexamic acid is now recommended within 3 hours. This involves administering a loading dose of 1 gram intravenously over 10 minutes, followed by an infusion of 1 gram over eight hours. In some regions, tranexamic acid is also being utilized in the prehospital setting.

The symptoms and signs of strokes can vary depending on which blood vessel is affected. Here is a summary of the main symptoms based on the territory affected:

Anterior cerebral artery: This can cause weakness on the opposite side of the body, with the leg and shoulder being more affected than the arm, hand, and face. There may also be minimal loss of sensation on the opposite side of the body. Other symptoms can include difficulty speaking (dysarthria), language problems (aphasia), apraxia (difficulty with limb movements), urinary incontinence, and changes in behavior and personality.

Middle cerebral artery: This can lead to weakness on the opposite side of the body, with the face and arm being more affected than the leg. There may also be a loss of sensation on the opposite side of the body. Depending on the dominant hemisphere of the brain, there may be difficulties with expressive or receptive language (dysphasia). In the non-dominant hemisphere, there may be neglect of the opposite side of the body.

Posterior cerebral artery: This can cause a loss of vision on the opposite side of both eyes (homonymous hemianopia). There may also be defects in a specific quadrant of the visual field. In some cases, there may be a syndrome affecting the thalamus on the opposite side of the body.

It’s important to note that these are just general summaries and individual cases may vary. If you suspect a stroke, it’s crucial to seek immediate medical attention.

The risk of primary spontaneous pneumothorax is associated with smoking tobacco and increases as the duration of exposure and daily consumption rise. The changes caused by smoking in the small airways may contribute to the development of local emphysema, leading to the formation of bullae. In this case, the patient does not have any clinical features or significant risk factors for the other conditions mentioned. Therefore, primary spontaneous pneumothorax is the most probable diagnosis.

The most probable diagnosis in this case is septic arthritis, which occurs when an infectious agent invades a joint and causes pus formation. The clinical features of septic arthritis include pain in the affected joint, redness, warmth, and swelling of the joint, and difficulty in moving the joint. Patients may also experience fever and overall feeling of being unwell.

The most common cause of septic arthritis is Staphylococcus aureus, but other bacteria can also be responsible. These include Streptococcus spp., Haemophilus influenzae, Neisseria gonorrhoea (typically seen in sexually active young adults with macules or vesicles on the trunk), and Escherichia coli (common in intravenous drug users, the elderly, and seriously ill individuals).

According to the current recommendations by NICE (National Institute for Health and Care Excellence) and the BNF (British National Formulary), the treatment for septic arthritis involves using specific antibiotics. Flucloxacillin is the first-line choice, but if a patient is allergic to penicillin, clindamycin can be used instead. If there is suspicion of MRSA (Methicillin-resistant Staphylococcus aureus), vancomycin is recommended. In cases where gonococcal arthritis or Gram-negative infection is suspected, cefotaxime is the preferred antibiotic.

The suggested duration of treatment for septic arthritis is 4-6 weeks, although it may be longer if the infection is complicated.

Discitis is an infection that affects the space between the intervertebral discs in the spine. This condition can have serious consequences, including the formation of abscesses and sepsis. The most common cause of discitis is usually Staphylococcus aureus, but other organisms like Streptococcus viridans and Pseudomonas aeruginosa may be responsible in certain cases, especially in immunocompromised individuals and intravenous drug users. Gram-negative organisms like Escherichia coli and Mycobacterium tuberculosis can also cause discitis, particularly in cases of Pott’s disease.

There are several risk factors that increase the likelihood of developing discitis. These include having undergone spinal surgery (which occurs in about 1-2% of patients post-operatively), having an immunodeficiency, being an intravenous drug user, being under the age of eight, having diabetes mellitus, or having a malignancy.

The typical symptoms of discitis include back or neck pain (which occurs in over 90% of cases), pain that often wakes the patient from sleep, fever (present in 60-70% of cases), and neurological deficits (which can occur in up to 50% of cases). In children, a refusal to walk may also be a symptom.

When diagnosing discitis, magnetic resonance imaging (MRI) is the preferred imaging modality due to its high sensitivity and specificity. It is important to image the entire spine, as discitis often affects multiple levels. Plain radiographs are not very sensitive to the early changes of discitis and may appear normal for 2-4 weeks. Computed tomography (CT) scanning is also not very sensitive in detecting discitis.

Treatment for discitis involves hospital admission for intravenous antibiotics. Before starting the antibiotics, it is recommended to send three sets of blood cultures and a full set of blood tests, including a C-reactive protein (CRP) test, to the laboratory.

A typical antibiotic regimen for discitis would include intravenous flucloxacillin 2 g every 6 hours as the first-line treatment if there is no penicillin allergy. Intravenous vancomycin may be used if the infection was acquired in the hospital, if there is a high risk of methicillin-resistant Staphylococcus aureus (MRSA) infection, or if there is a documented penicillin allergy.

The Health Protection (Notification) Regulations currently require the reporting of certain diseases. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ Disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, SARS, scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

Acute bacterial prostatitis is a sudden inflammation of the prostate gland, which can be either focal or diffuse and is characterized by the presence of pus. The most common organisms that cause this condition include Escherichia coli, Streptococcus faecalis, Staphylococcus aureus, and Neisseria gonorrhoea. The infection usually reaches the prostate through direct extension from the posterior urethra or urinary bladder, but it can also spread through the blood or lymphatics. In some cases, the infection may originate from the rectum.

According to the National Institute for Health and Care Excellence (NICE), acute prostatitis should be suspected in men who present with a sudden onset of feverish illness, which may be accompanied by rigors, arthralgia, or myalgia. Irritative urinary symptoms like dysuria, frequency, urgency, or acute urinary retention are also common. Perineal or suprapubic pain, as well as penile pain, low back pain, pain during ejaculation, and pain during bowel movements, can occur. A rectal examination may reveal an exquisitely tender prostate. A urine dipstick test showing white blood cells and a urine culture confirming urinary infection are also indicative of acute prostatitis.

The current recommendations by NICE and the British National Formulary (BNF) for the treatment of acute prostatitis involve prescribing an oral antibiotic for a duration of 14 days, taking into consideration local antimicrobial resistance data. The first-line antibiotics recommended are Ciprofloxacin 500 mg twice daily or Ofloxacin 200 mg twice daily. If these are not suitable, Trimethoprim 200 mg twice daily can be used. Second-line options include Levofloxacin 500 mg once daily or Co-trimoxazole 960 mg twice daily, but only when there is bacteriological evidence of sensitivity and valid reasons to prefer this combination over a single antibiotic.

For more information, you can refer to the NICE Clinical Knowledge Summary on acute prostatitis.

Ascending cholangitis occurs when there is an infection in the common bile duct, usually caused by a stone that has led to a blockage of bile flow. This condition is known as choledocholithiasis. The typical symptoms of ascending cholangitis are jaundice, fever (often accompanied by chills), and pain in the upper right quadrant of the abdomen. It is important to note that ascending cholangitis is a serious medical emergency that can be life-threatening, as patients often develop sepsis. Approximately 10-20% of patients may also experience altered mental status and low blood pressure due to septic shock. When these additional symptoms are present along with the classic triad of symptoms (Charcot’s triad), it is referred to as Reynold’s pentad. Urgent biliary drainage is the recommended treatment for ascending cholangitis. While a high white blood cell count is commonly seen in this condition, it is not considered part of Reynold’s pentad.

The four essential elements for effective procedural sedation are analgesia, anxiolysis, sedation, and amnesia. According to the Royal College of Emergency Medicine (RCEM), it is important to prioritize pain management before sedation, using appropriate analgesics based on the patient’s pain level. Non-pharmacological methods should be considered to reduce anxiety, such as creating a comfortable environment and involving supportive family members. The level of sedation required should be determined in advance, with most procedures in the emergency department requiring moderate to deep sedation. Lastly, providing a degree of amnesia will help minimize any unpleasant memories associated with the procedure.

Further Reading:

Procedural sedation is commonly used by emergency department (ED) doctors to minimize pain and discomfort during procedures that may be painful or distressing for patients. Effective procedural sedation requires the administration of analgesia, anxiolysis, sedation, and amnesia. This is typically achieved through the use of a combination of short-acting analgesics and sedatives.

There are different levels of sedation, ranging from minimal sedation (anxiolysis) to general anesthesia. It is important for clinicians to understand the level of sedation being used and to be able to manage any unintended deeper levels of sedation that may occur. Deeper levels of sedation are similar to general anesthesia and require the same level of care and monitoring.

Various drugs can be used for procedural sedation, including propofol, midazolam, ketamine, and fentanyl. Each of these drugs has its own mechanism of action and side effects. Propofol is commonly used for sedation, amnesia, and induction and maintenance of general anesthesia. Midazolam is a benzodiazepine that enhances the effect of GABA on the GABA A receptors. Ketamine is an NMDA receptor antagonist and is used for dissociative sedation. Fentanyl is a highly potent opioid used for analgesia and sedation.

The doses of these drugs for procedural sedation in the ED vary depending on the drug and the route of administration. It is important for clinicians to be familiar with the appropriate doses and onset and peak effect times for each drug.

Safe sedation requires certain requirements, including appropriate staffing levels, competencies of the sedating practitioner, location and facilities, and monitoring. The level of sedation being used determines the specific requirements for safe sedation.

After the procedure, patients should be monitored until they meet the criteria for safe discharge. This includes returning to their baseline level of consciousness, having vital signs within normal limits, and not experiencing compromised respiratory status. Pain and discomfort should also be addressed before discharge.

Patients who have myxoedema coma usually show symptoms such as lethargy, bradycardia, hypothermia, worsening mental state, seizures, and/or coma. This patient has hypothyroidism and takes thyroxine regularly, which aligns with the signs and symptoms of myxoedema coma. It is worth noting that infections often act as a trigger, and this patient has developed a cough in the last week.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

Calcium-channel blocker overdose is a serious condition that should always be taken seriously as it can be potentially life-threatening. The two most dangerous types of calcium channel blockers in overdose are verapamil and diltiazem. These medications work by binding to the alpha-1 subunit of L-type calcium channels, which prevents the entry of calcium into the cells. These channels play a crucial role in the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

Significant toxicity can occur with the ingestion of more than 10 tablets of verapamil (160 mg or 240 mg immediate or sustained-release capsules) or diltiazem (180 mg, 240 mg or 360 mg immediate or sustained-release capsules). In children, even 1-2 tablets of immediate or sustained-release verapamil or diltiazem can be harmful. Symptoms usually appear within 1-2 hours of taking standard preparations, but with slow-release versions, the onset of severe toxicity may be delayed by 12-16 hours, with peak effects occurring after 24 hours.

The main clinical manifestations of calcium-channel blocker overdose include nausea and vomiting, low blood pressure, slow heart rate and first-degree heart block, heart muscle ischemia and stroke, kidney failure, pulmonary edema, and high blood sugar levels.

When managing a patient with calcium-channel blocker overdose, certain bedside investigations are crucial. These include checking blood glucose levels, performing an electrocardiogram (ECG), and obtaining an arterial blood gas sample. Additional investigations that can provide helpful information include assessing urea and electrolyte levels, conducting a chest X-ray to check for pulmonary edema, and performing an echocardiography.

The administration of IV drugs (adrenaline and amiodarone) should be delayed until the core body temperature of patients with severe hypothermia reaches above 30°C, as recommended by the resus council.

Further Reading:

Cardiopulmonary arrest is a serious event with low survival rates. In non-traumatic cardiac arrest, only about 20% of patients who arrest as an in-patient survive to hospital discharge, while the survival rate for out-of-hospital cardiac arrest is approximately 8%. The Resus Council BLS/AED Algorithm for 2015 recommends chest compressions at a rate of 100-120 per minute with a compression depth of 5-6 cm. The ratio of chest compressions to rescue breaths is 30:2.

After a cardiac arrest, the goal of patient care is to minimize the impact of post cardiac arrest syndrome, which includes brain injury, myocardial dysfunction, the ischaemic/reperfusion response, and the underlying pathology that caused the arrest. The ABCDE approach is used for clinical assessment and general management. Intubation may be necessary if the airway cannot be maintained by simple measures or if it is immediately threatened. Controlled ventilation is aimed at maintaining oxygen saturation levels between 94-98% and normocarbia. Fluid status may be difficult to judge, but a target mean arterial pressure (MAP) between 65 and 100 mmHg is recommended. Inotropes may be administered to maintain blood pressure. Sedation should be adequate to gain control of ventilation, and short-acting sedating agents like propofol are preferred. Blood glucose levels should be maintained below 8 mmol/l. Pyrexia should be avoided, and there is some evidence for controlled mild hypothermia but no consensus on this.

Post ROSC investigations may include a chest X-ray, ECG monitoring, serial potassium and lactate measurements, and other imaging modalities like ultrasonography, echocardiography, CTPA, and CT head, depending on availability and skills in the local department. Treatment should be directed towards the underlying cause, and PCI or thrombolysis may be considered for acute coronary syndrome or suspected pulmonary embolism, respectively.

Patients who are comatose after ROSC without significant pre-arrest comorbidities should be transferred to the ICU for supportive care. Neurological outcome at 72 hours is the best prognostic indicator of outcome.

Onchocerciasis is a parasitic disease caused by the filarial nematode Onchocerca volvulus. It is transmitted through the bites of infected blackflies of Simulium species, which carry immature larval forms of the parasite from human to human.

In the human body, the larvae form nodules in the subcutaneous tissue, where they mature to adult worms. After mating, the female adult worm can release up to 1000 microfilariae a day.

Onchocerciasis is currently endemic in 30 African countries, Yemen, and a few isolated regions of South America. Approximately 37 million people worldwide are currently infected.

Symptoms start to occur around a year after the patient is infected. The earliest symptom is usually an intensely itchy rash. Various skin manifestations occur, including scattered, red, pruritic papules (acute papular onchodermatitis), larger, chronic, hyperpigmented papules (chronic papular onchodermatitis), lichenified, oedematous, hyperpigmented papules and plaques (lichenified onchodermatitis), areas of skin atrophy with loss of elasticity (‘Lizard skin’), and depigmented areas with a ‘leopard skin’ appearance, usually on the shins.

Ocular involvement provides the common name associated with onchocerciasis, river blindness, and it can involve any part of the eye. Almost a million people worldwide have at least a partial degree of vision loss caused by onchocerciasis. Initially, there may be intense watering, a foreign body sensation, and photophobia. This can progress to conjunctivitis, iridocyclitis, and chorioretinitis. Secondary glaucoma and optic atrophy may also occur.

In a number of countries, onchocerciasis has been controlled through the spraying of blackfly breeding sites with insecticide. The drug ivermectin is the preferred treatment for onchocerciasis.

In this scenario, there are similarities between hypothyroidism and perimenopause in terms of their features. However, the most frequent cause of experiencing these symptoms together is depression. Therefore, it is necessary to delve deeper into this woman’s mood to rule out depression and provide appropriate management.

To exclude hypothyroidism as a potential cause, a TSH blood test should be conducted. Additionally, it is important to inquire about other symptoms that may align with early menopause.

Non-invasive ventilation is recommended for patients with hypercapnia and acidosis. Respiratory acidosis, indicated by a pH level below 7.35, is a strong indication for the use of BiPAP. However, patients with a pH level of 7.25 or lower may not respond well to non-invasive ventilation and should be considered for intensive care unit (ITU) treatment. Another criterion for the use of BiPAP is hypercapnia, which is characterized by an arterial pCO2 level greater than 6.0 KPa.

Further Reading:

Mechanical ventilation is the use of artificial means to assist or replace spontaneous breathing. It can be invasive, involving instrumentation inside the trachea, or non-invasive, where there is no instrumentation of the trachea. Non-invasive mechanical ventilation (NIV) in the emergency department typically refers to the use of CPAP or BiPAP.

CPAP, or continuous positive airways pressure, involves delivering air or oxygen through a tight-fitting face mask to maintain a continuous positive pressure throughout the patient’s respiratory cycle. This helps maintain small airway patency, improves oxygenation, decreases airway resistance, and reduces the work of breathing. CPAP is mainly used for acute cardiogenic pulmonary edema.

BiPAP, or biphasic positive airways pressure, also provides positive airway pressure but with variations during the respiratory cycle. The pressure is higher during inspiration than expiration, generating a tidal volume that assists ventilation. BiPAP is mainly indicated for type 2 respiratory failure in patients with COPD who are already on maximal medical therapy.

The pressure settings for CPAP typically start at 5 cmH2O and can be increased to a maximum of 15 cmH2O. For BiPAP, the starting pressure for expiratory pressure (EPAP) or positive end-expiratory pressure (PEEP) is 3-5 cmH2O, while the starting pressure for inspiratory pressure (IPAP) is 10-15 cmH2O. These pressures can be titrated up if there is persisting hypoxia or acidosis.

In terms of lung protective ventilation, low tidal volumes of 5-8 ml/kg are used to prevent atelectasis and reduce the risk of lung injury. Inspiratory pressures (plateau pressure) should be kept below 30 cm of water, and permissible hypercapnia may be allowed. However, there are contraindications to lung protective ventilation, such as unacceptable levels of hypercapnia, acidosis, and hypoxemia.

Overall, mechanical ventilation, whether invasive or non-invasive, is used in various respiratory and non-respiratory conditions to support or replace spontaneous breathing and improve oxygenation and ventilation.

Pick’s disease is a rare neurodegenerative disorder that leads to a gradual decline in cognitive function known as frontotemporal dementia. One of the key features of this condition is the accumulation of tau proteins in neurons, forming silver-staining, spherical aggregations called Pick bodies.

Typically, Pick’s disease manifests between the ages of 40 and 60. Initially, individuals may experience changes in their personality, such as disinhibition, tactlessness, and vulgarity. They may also exhibit alterations in their moral values and attempt to distance themselves from their family. Concentration problems, over-activity, pacing, and wandering are also common symptoms during this stage.

What sets Pick’s disease apart from Alzheimer’s disease is that the personality changes occur before memory loss. As the disease progresses, patients will experience deficits in intellect, memory, and language.

On the other hand, Lewy body dementia (LBD) is characterized by the presence of Lewy bodies, which are different from the Pick bodies seen in Pick’s disease.

Flumazenil is a specific antagonist for benzodiazepines that can be beneficial in certain situations. It acts quickly, taking less than 1 minute to take effect, but its effects are short-lived and only last for less than 1 hour. The recommended dosage is 200 μg every 1-2 minutes, with a maximum dose of 3mg per hour.

It is important to avoid using Flumazenil if the patient is dependent on benzodiazepines or is taking tricyclic antidepressants. This is because it can trigger a withdrawal syndrome in these individuals, potentially leading to seizures or cardiac arrest.

There are two scoring systems that NICE recommends for assessing sore throat: the Centor Clinical Prediction Score and the FeverPAIN Score.

The Centor Clinical Prediction Score was initially developed as a tool to determine the likelihood of a group A beta-haemolytic Streptococcus (GABHS) infection in adults with a sore throat. It was created and tested in US Emergency Departments, specifically for adults.

The Centor score evaluates patients based on several criteria, with one point given for each positive criterion. These criteria include a history of fever (temperature above 38°C), the presence of exudate or swelling on the tonsils, tender or swollen anterior cervical lymph nodes, and the absence of cough.

According to the current NICE guidance, the Centor score can be used to guide management in the following way:
– A score of 0 to 2 indicates a 3-17% likelihood of streptococcus isolation, and antibiotics are not recommended.
– A score of 3 to 4 suggests a 32-56% likelihood of streptococcus isolation, and immediate treatment with empirical antibiotics or a ‘backup prescription’ should be considered.

The diagnosis in this case is clearly gout. According to the guidelines from the European League Against Rheumatism (EULAR), the symptoms of acute pain, joint swelling, tenderness, and redness that worsen over a 6-12 hour period strongly suggest crystal arthropathy.

Checking serum urate levels to confirm hyperuricemia before starting treatment for acute gout attacks has little benefit and should not delay treatment. While these levels can be useful for monitoring treatment response, they often decrease during an acute attack and can even be normal. If levels are checked and found to be normal during the attack, they should be rechecked once the attack has resolved.

The first-line treatment for acute gout attacks is non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen. However, caution should be exercised when using NSAIDs in patients with a history of hypertension. Since this patient has had difficulty controlling their blood pressure and remains hypertensive, it would be wise to avoid NSAIDs in this case.

Colchicine is an effective alternative for treating gout, although it may take longer to take effect. It is often used in patients who cannot take NSAIDs due to contraindications such as hypertension or a history of peptic ulcer disease. Therefore, it is the most suitable choice for this patient.

During an acute gout attack, allopurinol should not be used as it can prolong the attack and even trigger another acute episode. However, in patients already taking allopurinol, it should be continued, and the acute attack should be treated with NSAIDs or colchicine as appropriate.

Febuxostat (Uloric) is another option for managing chronic gout, but like allopurinol, it should not be used for acute episodes.

Bartter’s syndrome is a rare genetic defect that affects the ascending limb of the loop of Henle. This condition is characterized by low blood pressure and a hypokalemic alkalosis, which means there is a decrease in potassium levels in the blood.

Hyperkalemia, on the other hand, is defined as having a plasma potassium level greater than 5.5 mmol/L. There are various non-drug factors that can cause hyperkalemia, such as renal failure, excessive potassium supplementation, Addison’s disease (adrenal insufficiency), congenital adrenal hyperplasia, renal tubular acidosis (type 4), rhabdomyolysis, burns and trauma, and tumor lysis syndrome. Additionally, acidosis can also contribute to the development of hyperkalemia.

In addition to these non-drug causes, certain medications can also lead to hyperkalemia. These include ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium. It is important to be aware of these potential causes and to monitor potassium levels in order to prevent and manage hyperkalemia effectively.

Pyloric stenosis, a condition characterized by narrowing of the pylorus (the opening between the stomach and small intestine), often leads to an electrolyte imbalance. This imbalance typically presents as hypochloremia (low chloride levels), hypokalemia (low potassium levels), and metabolic alkalosis (an increase in blood pH). To confirm the diagnosis, it is recommended to perform U&Es (tests to measure electrolyte levels) and a venous blood gas analysis. The electrolyte abnormalities observed in pyloric stenosis are primarily caused by the loss of hydrogen and chloride ions through vomiting. While urine is usually alkaline in this condition, severe dehydration can lead to paradoxical aciduria, where hydrogen ions are preferentially secreted instead of potassium ions to prevent further decrease in potassium levels.

Further Reading:

Pyloric stenosis is a condition that primarily affects infants, characterized by the thickening of the muscles in the pylorus, leading to obstruction of the gastric outlet. It typically presents between the 3rd and 12th weeks of life, with recurrent projectile vomiting being the main symptom. The condition is more common in males, with a positive family history and being first-born being additional risk factors. Bottle-fed children and those delivered by c-section are also more likely to develop pyloric stenosis.

Clinical features of pyloric stenosis include projectile vomiting, usually occurring about 30 minutes after a feed, as well as constipation and dehydration. A palpable mass in the upper abdomen, often described as like an olive, may also be present. The persistent vomiting can lead to electrolyte disturbances, such as hypochloremia, alkalosis, and mild hypokalemia.

Ultrasound is the preferred diagnostic tool for confirming pyloric stenosis. It can reveal specific criteria, including a pyloric muscle thickness greater than 3 mm, a pylorus longitudinal length greater than 15-17 mm, a pyloric volume greater than 1.5 cm3, and a pyloric transverse diameter greater than 13 mm.

The definitive treatment for pyloric stenosis is pyloromyotomy, a surgical procedure that involves making an incision in the thickened pyloric muscle to relieve the obstruction. Before surgery, it is important to correct any hypovolemia and electrolyte disturbances with intravenous fluids. Overall, pyloric stenosis is a relatively common condition in infants, but with prompt diagnosis and appropriate management, it can be effectively treated.

Osteoporosis is a condition characterized by weak and brittle bones, making them more prone to fractures. In this case, the patient’s sudden onset of central back pain and the X-ray findings of anterior wedging of the L2 vertebra suggest the possibility of undiagnosed osteoporosis.

One correct statement about osteoporosis is that it is defined as a T-score of less than -2.5. The T-score is a measure of bone density and is used to diagnose osteoporosis. A T-score of -2.5 or lower indicates a significant decrease in bone density and an increased risk of fractures.

Skeletal scintigraphy is not used to diagnose osteoporosis. Instead, it is commonly used to evaluate for other conditions such as bone infections or tumors.

The pubic rami is not the most common site for osteoporotic fractures. Osteoporotic fractures commonly occur in the spine (vertebral fractures), hip, and wrist.

Osteoporosis is not characterized by increased bone turnover in focal areas of the axial skeleton with a lytic phase followed by a rapid increase in bone formation by osteoblasts in the sclerotic phase. This description is more consistent with a condition called Paget’s disease of bone.

The prevalence of osteoporosis is not approximately 10% at 50 years of age. The prevalence of osteoporosis increases with age, and it is estimated that around 50% of women and 25% of men over the age of 50 will experience an osteoporotic fracture in their lifetime.

Further Reading:

Fragility fractures are fractures that occur following a fall from standing height or less, and may be atraumatic. They often occur in the presence of osteoporosis, a disease characterized by low bone mass and structural deterioration of bone tissue. Fragility fractures commonly affect the wrist, spine, hip, and arm.

Osteoporosis is defined as a bone mineral density (BMD) of 2.5 standard deviations below the mean peak mass, as measured by dual-energy X-ray absorptiometry (DXA). Osteopenia, on the other hand, refers to low bone mass between normal bone mass and osteoporosis, with a T-score between -1 to -2.5.

The pathophysiology of osteoporosis involves increased osteoclast activity relative to bone production by osteoblasts. The prevalence of osteoporosis increases with age, from approximately 2% at 50 years to almost 50% at 80 years.

There are various risk factors for fragility fractures, including endocrine diseases, GI causes of malabsorption, chronic kidney and liver diseases, menopause, immobility, low body mass index, advancing age, oral corticosteroids, smoking, alcohol consumption, previous fragility fractures, rheumatological conditions, parental history of hip fracture, certain medications, visual impairment, neuromuscular weakness, cognitive impairment, and unsafe home environment.

Assessment of a patient with a possible fragility fracture should include evaluating the risk of further falls, the risk of osteoporosis, excluding secondary causes of osteoporosis, and ruling out non-osteoporotic causes for fragility fractures such as metastatic bone disease, multiple myeloma, osteomalacia, and Paget’s disease.

Management of fragility fractures involves initial management by the emergency clinician, while treatment of low bone density is often delegated to the medical team or general practitioner. Management considerations include determining who needs formal risk assessment, who needs a DXA scan to measure BMD, providing lifestyle advice, and deciding who requires drug treatment.

Medication for osteoporosis typically includes vitamin D, calcium, and bisphosphonates. Vitamin D and calcium supplementation should be considered based on individual needs, while bisphosphonates are advised for postmenopausal women and men over 50 years with confirmed osteoporosis or those taking high doses of oral corticosteroids.

Cytochrome p450 enzyme inducers have the ability to hinder the effects of warfarin, leading to a decrease in INR levels. To remember the commonly encountered cytochrome p450 enzyme inducers, the mnemonic PC BRASS can be utilized. Each letter in the mnemonic represents a specific inducer: P for Phenytoin, C for Carbamazepine, B for Barbiturates, R for Rifampicin, A for Alcohol (chronic ingestion), S for Sulphonylureas, and S for Smoking. These inducers can have an impact on the effectiveness of warfarin and should be taken into consideration when prescribing or using this medication.

There are two scoring systems that NICE recommends for assessing sore throat: the Centor Clinical Prediction Score and the FeverPAIN Score.

The Centor Clinical Prediction Score was initially developed as a tool to determine the likelihood of a group A beta-haemolytic Streptococcus (GABHS) infection in adults with a sore throat. This score was created and tested in US Emergency Departments, specifically for adult patients.

The Centor score evaluates patients based on several criteria, with one point given for each positive criterion. These criteria include a history of fever (temperature above 38°C), the presence of exudate or swelling on the tonsils, tender or swollen anterior cervical lymph nodes, and the absence of cough.

According to the current NICE guidance, the Centor score can be used to guide management in the following way:
– A score of 0 to 2 indicates a 3-17% likelihood of streptococcus isolation, and antibiotics are not recommended.
– A score of 3 to 4 indicates a 32-56% likelihood of streptococcus isolation, and immediate treatment with empirical antibiotics or a backup prescription should be considered.

By utilizing these scoring systems, healthcare professionals can make more informed decisions regarding the management and treatment of patients with sore throat.

When patients have calcaneal fractures, it is important to evaluate them for any additional injuries that may be present. These can include vertebral fractures, fractures in the opposite calcaneus, and injuries to the cuboid bone.

Further Reading:

Calcaneus fractures are a common type of lower limb and joint injury. The calcaneus, or heel bone, is the most frequently fractured tarsal bone. These fractures are often intra-articular, meaning they involve the joint. The most common cause of calcaneus fractures is a fall or jump from a height.

When assessing calcaneus fractures, X-rays are used to visualize the fracture lines. Two angles are commonly assessed to determine the severity of the fracture. Böhler’s angle, which measures the angle between two tangent lines drawn across the anterior and posterior borders of the calcaneus, should be between 20-40 degrees. If it is less than 20 degrees, it indicates a calcaneal fracture with flattening. The angle of Gissane, which measures the depression of the posterior facet of the subtalar joint, should be between 120-145 degrees. An increased angle of Gissane suggests a calcaneal fracture.

In the emergency department, the management of a fractured calcaneus involves identifying the injury and any associated injuries, providing pain relief, elevating the affected limb(s), and referring the patient to an orthopedic specialist. It is important to be aware that calcaneus fractures are often accompanied by other injuries, such as bilateral fractures of vertebral fractures.

The definitive management of a fractured calcaneus can be done conservatively or through surgery, specifically open reduction internal fixation (ORIF). The orthopedic team will typically order a CT or MRI scan to classify the fracture and determine the most appropriate treatment. However, a recent UK heel fracture trial suggests that in most cases, ORIF does not improve fracture outcomes.

Recurrent or chronic tonsillitis is a clear indication for tonsillectomy, which is the surgical removal of the palatine tonsils. One common complication of this procedure is bleeding, which occurs in approximately 0.5-2% of cases. The bleeding that occurs after tonsillectomy is typically venous in nature and most frequently originates from the external palatine vein. This vein drains the lateral tonsillar region and ultimately empties into the facial vein. Additionally, bleeding can also arise from the tonsillar branch of the facial artery, which supplies the inferior pole of the palatine tonsil.

Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

Patients who experience bleeding after a tonsillectomy should be treated with two primary medications. The first is IV tranexamic acid, which is given to all patients. The second is a topical vasoconstrictor, such as co-phenylcaine spray or adrenaline-soaked gauze/cotton buds. However, the use of topical vasoconstrictors is typically reserved for patients with severe bleeding until they can be reviewed by a senior medical professional or transferred to the operating theatre. Patients with mild or occasional bleeding may be instructed to gargle with hydrogen peroxide regularly during their hospital stay.

Further Reading:

Tonsillectomy is a common procedure performed by ENT surgeons in the UK, with over 50,000 surgeries performed each year. While it is considered routine, there are risks of serious complications, including post-tonsillectomy bleeding. Approximately 5% of patients experience bleeding after the procedure, with most cases being self-limiting. However, severe bleeding can lead to hypovolemia and airway obstruction from clots, which can be life-threatening.

Post-tonsillectomy bleeding can be classified as primary (reactive) or secondary (delayed). Primary bleeding occurs within 24 hours of the procedure, while secondary bleeding occurs more than 24 hours post-procedure. Secondary bleeding is often caused by factors such as sloughing of eschar, trauma from solid food ingestion, tonsil bed infection, postoperative NSAID usage, or unknown causes.

Patients may present with symptoms such as vomiting blood, coughing up blood, tasting blood in the throat, finding blood on pillows or bed sheets, or excessive swallowing (especially in children). It is important for clinicians to assess the severity of blood loss, although it can be challenging to accurately estimate in children.

The ABCDE approach should be used to assess patients, with a focus on airway compromise, hemodynamic instability, and evidence of bleeding. Clinicians may use a head torch to identify any bleeding points, which may be actively bleeding or appear as fresh red clots. It is important to note that the tonsillar fossa may appear white or yellow, which is a normal postoperative finding.

Investigations such as a full blood count, coagulation profile, group and save, and venous blood gas may be performed to assess the patient’s condition. Senior support from ENT or anesthesiology should be called if there is active bleeding.

Management of post-tonsillectomy bleeding includes positioning the patient upright and keeping them calm, establishing intravenous access, administering fluids and blood products as needed, and administering tranexamic acid to stop bleeding. Bleeding points may require gentle suction removal of fresh clots, and topical medications such as Co-phenylcaine spray or topical adrenaline may be applied to the oropharynx. All patients with post-tonsillectomy bleeding should be assessed by ENT and observed for a prolonged period, typically 12-24 hours.

If bleeding remains uncontrolled, the patient should be kept nil by mouth in preparation for surgery, and early intervention.

According to NICE guidelines, when evaluating patients with acute upper GI bleeding, it is recommended to use the Blatchford score during the initial assessment and the full Rockall score after endoscopy. The Rockall score is specifically designed to assess the risk of re-bleeding or death in these patients. If a patient’s post-endoscopic Rockall score is less than 3, they are considered to have a low risk of re-bleeding or death and may be eligible for early discharge.

Further Reading:

Upper gastrointestinal bleeding (UGIB) refers to the loss of blood from the gastrointestinal tract, occurring in the upper part of the digestive system. It can present as haematemesis (vomiting blood), coffee-ground emesis, bright red blood in the nasogastric tube, or melaena (black, tarry stools). UGIB can lead to significant hemodynamic compromise and is a major health burden, accounting for approximately 70,000 hospital admissions each year in the UK with a mortality rate of 10%.

The causes of UGIB vary, with peptic ulcer disease being the most common cause, followed by gastritis/erosions, esophagitis, and other less common causes such as varices, Mallory Weiss tears, and malignancy. Swift assessment, hemodynamic resuscitation, and appropriate interventions are essential for the management of UGIB.

Assessment of patients with UGIB should follow an ABCDE approach, and scoring systems such as the Glasgow-Blatchford bleeding score (GBS) and the Rockall score are recommended to risk stratify patients and determine the urgency of endoscopy. Transfusion may be necessary for patients with massive hemorrhage, and platelet transfusion, fresh frozen plasma (FFP), and prothrombin complex concentrate may be offered based on specific criteria.

Endoscopy plays a crucial role in the management of UGIB. Unstable patients with severe acute UGIB should undergo endoscopy immediately after resuscitation, while all other patients should undergo endoscopy within 24 hours of admission. Endoscopic treatment of non-variceal bleeding may involve mechanical methods of hemostasis, thermal coagulation, or the use of fibrin or thrombin with adrenaline. Proton pump inhibitors should only be used after endoscopy.

Variceal bleeding requires specific management, including the use of terlipressin and prophylactic antibiotics. Oesophageal varices can be treated with band ligation or transjugular intrahepatic portosystemic shunts (TIPS), while gastric varices may be treated with endoscopic injection of N-butyl-2-cyanoacrylate or TIPS if bleeding is not controlled.

For patients taking NSAIDs, aspirin, or clopidogrel, low-dose aspirin can be continued once hemostasis is achieved, NSAIDs should be stopped in patients presenting with UGIB.

Spontaneous bacterial peritonitis (SBP) is a sudden bacterial infection of the fluid in the abdomen. It typically occurs in patients with high blood pressure in the portal vein, and about 70% of cases are seen in patients with severe liver disease. In any given year, around 30% of patients with fluid buildup in the abdomen will develop SBP.

SBP can present with a wide range of symptoms, so it’s important to be vigilant when caring for patients with fluid buildup in the abdomen, especially if there is a sudden decline in their condition. Some patients may not show any symptoms at all.

Common clinical features of SBP include fever (80% of cases), abdominal pain (70% of cases), worsening or unexplained confusion due to liver dysfunction, diarrhea, nausea and vomiting, and bowel obstruction.

There are several factors that increase the risk of developing SBP, including severe liver disease (Child-Pugh class C), gastrointestinal bleeding, urinary tract infection, excessive growth of bacteria in the intestines, presence of indwelling lines such as central venous catheters or urinary catheters, previous episodes of SBP, and low levels of protein in the fluid buildup in the abdomen.

To diagnose SBP, a procedure called abdominal paracentesis is performed to collect fluid from the abdomen. The following findings on fluid analysis strongly suggest SBP: total white blood cell count in the fluid greater than 500 cells/µL, total neutrophil count in the fluid greater than 250 cells/µL, lactate level in the fluid higher than 25 mg/dL, pH of the fluid below 7.35, and presence of bacteria on Gram-stain.

Patients with SBP should be admitted to the hospital and treated with broad-spectrum antibiotics. The preferred antibiotic is an intravenous third-generation cephalosporin, such as Ceftriaxone. If the patient is allergic to beta-lactam antibiotics, ciprofloxacin can be considered as an alternative. Administration of intravenous albumin has been shown to reduce the risk of kidney failure and death.

Urinary tract stones form when the concentration of salt and minerals in the urine becomes too high. These stones can be classified into five types based on their mineral composition and how they develop.

The most common type of stone is the calcium stone, which can be further divided into calcium oxalate and calcium phosphate stones. These account for 60-80% of all urinary tract stones.

Another type is the struvite or magnesium ammonium phosphate stone, making up about 10-15% of cases. Uric acid stones, also known as urate stones, occur in 3-10% of cases.

Cystine stones are less common, accounting for less than 2% of urinary tract stones. Finally, there are drug-induced stones, which are caused by certain medications such as triamterene, protease inhibitors like indinavir sulphate, and sulfa drugs. These account for approximately 1% of cases.

By understanding the different types of urinary tract stones, healthcare professionals can better diagnose and treat patients with this condition.

Anticholinergic drugs work by blocking the effects of acetylcholine, a neurotransmitter, in both the central and peripheral nervous systems. These drugs are commonly used in clinical practice and include antihistamines, typical and atypical antipsychotics, anticonvulsants, antidepressants, antispasmodics, antiemetics, antiparkinsonian agents, antimuscarinics, and certain plants. When someone ingests an anticholinergic drug, they may experience a toxidrome, which is characterized by an agitated delirium and various signs of acetylcholine receptor blockade in the central and peripheral systems.

The central effects of anticholinergic drugs result in an agitated delirium, which is marked by fluctuating mental status, confusion, restlessness, visual hallucinations, picking at objects in the air, mumbling, slurred speech, disruptive behavior, tremor, myoclonus, and in rare cases, coma or seizures. On the other hand, the peripheral effects can vary and may include dilated pupils, sinus tachycardia, dry mouth, hot and flushed skin, increased body temperature, urinary retention, and ileus.

Placental abruption, also known as abruptio placentae, occurs when the placental lining separates from the wall of the uterus before delivery and after 20 weeks of gestation.

In the early stages, there may be no symptoms, but typically abdominal pain and vaginal bleeding develop. Approximately 20% of patients experience a concealed placental abruption, where the haemorrhage is confined within the uterine cavity and the amount of blood loss can be significantly underestimated.

The clinical features of placental abruption include sudden onset abdominal pain (which can be severe), variable vaginal bleeding, severe or continuous contractions, abdominal tenderness, and an enlarged, tense uterus. The foetus often shows signs of distress, such as reduced movements, increased or decreased fetal heart rate, decreased variability of fetal heart rate, and late decelerations.

In contrast, placenta praevia is painless and the foetal heart is generally normal. The degree of obstetric shock is usually proportional to the amount of vaginal blood loss. Another clue that the cause of bleeding is placenta praevia rather than placental abruption is that the foetus may have an abnormal presentation or lie.

The symptoms and signs of strokes can vary depending on which blood vessel is affected. Here is a summary of the main symptoms based on the territory affected:

Anterior cerebral artery: This can cause weakness on the opposite side of the body, with the leg and shoulder being more affected than the arm, hand, and face. There may also be minimal loss of sensation on the opposite side of the body. Other symptoms can include difficulty speaking (dysarthria), language problems (aphasia), apraxia (difficulty with limb movements), urinary incontinence, and changes in behavior and personality.

Middle cerebral artery: This can lead to weakness on the opposite side of the body, with the face and arm being more affected than the leg. There may also be a loss of sensation on the opposite side of the body. Depending on the dominant hemisphere of the brain, there may be difficulties with expressive or receptive language (dysphasia). In the non-dominant hemisphere, there may be neglect of the opposite side of the body.

Posterior cerebral artery: This can cause a loss of vision on the opposite side of both eyes (homonymous hemianopia). There may also be defects in a specific quadrant of the visual field. In some cases, there may be a syndrome affecting the thalamus on the opposite side of the body.

It’s important to note that these are just general summaries and individual cases may vary. If you suspect a stroke, it’s crucial to seek immediate medical attention.

CAGE, AUDIT, and T-ACE are all tools used to screen for alcohol misuse. The CAGE tool is the most commonly used by clinicians and consists of four simple questions. It is easy to remember and effective in identifying potential alcohol-related issues. The CAGE questionnaire asks if the individual has ever felt the need to cut down on their drinking, if others have criticized their drinking, if they have felt guilty about their drinking, and if they have ever had a drink first thing in the morning to alleviate a hangover or calm their nerves. A score of 2 or 3 suggests a high likelihood of alcoholism, while a score of 4 is almost diagnostic.

T-ACE is specifically designed to screen for alcohol abuse in pregnant women. It helps identify potential issues and allows for appropriate intervention and support.

The AUDIT tool is a more comprehensive questionnaire consisting of 10 points. It is typically used after initial screening and provides a more detailed assessment of alcohol consumption and potential dependency. The AUDIT-C, a simplified version of the AUDIT tool, is often used in primary care settings. It consists of three questions and is a quick and effective way to assess alcohol-related concerns.

While asking patients about their alcohol intake can provide some insight into excessive drinking, the screening tools are specifically designed to assess alcohol dependence and hazardous drinking. They offer a more comprehensive evaluation and help healthcare professionals identify individuals who may require further intervention or support.

It is important to note that advising patients on the harmful effects of alcohol is a valuable component of brief interventions. However, it is not as effective as using screening tools to identify potential alcohol-related issues.

Vestibular neuronitis is believed to occur when the vestibular nerve becomes inflamed, often following a viral infection like a cold. This condition causes a constant feeling of dizziness, which can worsen with head movements. On the other hand, BPPV (benign paroxysmal positional vertigo) is characterized by brief episodes of vertigo lasting around 10-20 seconds, triggered by specific head movements. To diagnose BPPV, the Dix-Hallpike test is performed, and a positive result is indicated by a specific type of eye movement called nystagmus. In contrast, vestibular neuritis typically presents with horizontal nystagmus that only occurs in one direction.

Further Reading:

Vestibular neuritis, also known as vestibular neuronitis, is a condition characterized by sudden and prolonged vertigo of peripheral origin. It is believed to be caused by inflammation of the vestibular nerve, often following a viral infection. It is important to note that vestibular neuritis and labyrinthitis are not the same condition, as labyrinthitis involves inflammation of the labyrinth. Vestibular neuritis typically affects individuals between the ages of 30 and 60, with a 1:1 ratio of males to females. The annual incidence is approximately 3.5 per 100,000 people, making it one of the most commonly diagnosed causes of vertigo.

Clinical features of vestibular neuritis include nystagmus, which is a rapid, involuntary eye movement, typically in a horizontal or horizontal-torsional direction away from the affected ear. The head impulse test may also be positive. Other symptoms include spontaneous onset of rotational vertigo, which is worsened by changes in head position, as well as nausea, vomiting, and unsteadiness. These severe symptoms usually last for 2-3 days, followed by a gradual recovery over a few weeks. It is important to note that hearing is not affected in vestibular neuritis, and symptoms such as tinnitus and focal neurological deficits are not present.

Differential diagnosis for vestibular neuritis includes benign paroxysmal positional vertigo (BPPV), labyrinthitis, Meniere’s disease, migraine, stroke, and cerebellar lesions. Management of vestibular neuritis involves drug treatment for nausea and vomiting associated with vertigo, typically through short courses of medication such as prochlorperazine or cyclizine. If symptoms are severe and fluids cannot be tolerated, admission and administration of IV fluids may be necessary. General advice should also be given, including avoiding driving while symptomatic, considering the suitability to work based on occupation and duties, and the increased risk of falls. Follow-up is required, and referral is necessary if there are atypical symptoms, symptoms do not improve after a week of treatment, or symptoms persist for more than 6 weeks.

The prognosis for vestibular neuritis is generally good, with the majority of individuals fully recovering within 6 weeks. Recurrence is thought to occur in 2-11% of cases, and approximately 10% of individuals may develop BPPV following an episode of vestibular neuritis. A very rare complication of vestibular neuritis is ph

If you have missed one pill, which means it has been 48-72 hours since you took the last pill in your current packet or you started the first pill in a new packet 24-48 hours late, you need to take the missed pill as soon as you remember. Make sure to continue taking the remaining pills at your usual time. Emergency contraception is generally not necessary in this situation, but it may be worth considering if you have missed pills earlier in the packet or during the last week of the previous packet.

According to the current recommendations by NICE, it is advised to consider gastro-protection for patients who meet more than one of the following criteria: using the highest recommended dose of an NSAID, being 65 years or older, having a history of peptic ulcer or gastrointestinal bleeding, taking medications that increase the risk, using low dose aspirin, anticoagulants, corticosteroids, or anti-depressants including SSRIs and SNRIs, requiring prolonged NSAID usage, having osteoarthritis or rheumatoid arthritis at any age, or experiencing long-term back pain if older than 45.

If gastro-protection is necessary, it is recommended to choose either omeprazole 20 mg daily or lansoprazole 15-30 mg daily as the preferred PPIs.

In the case of this patient, they are currently taking 400 mg of ibuprofen three times a day, which is within the maximum recommended dose of 2.4 g daily. Therefore, there is no need for gastro-protection based on the dosage of ibuprofen alone. Additionally, factors such as co-prescription of codeine, a raised BMI, and a family history of peptic ulceration would also not warrant the need for gastro-protection.

For more information, you can refer to the NICE Clinical Knowledge Summary on prescribing issues with NSAIDs.

Anaemia can be categorized based on the size of red blood cells. Microcytic anaemia, characterized by a mean corpuscular volume (MCV) of less than 80 fl, can be caused by various factors such as iron deficiency, thalassaemia, anaemia of chronic disease (which can also be normocytic), sideroblastic anaemia (which can also be normocytic), lead poisoning, and aluminium toxicity (although this is now rare and mainly affects haemodialysis patients).

On the other hand, normocytic anaemia, with an MCV ranging from 80 to 100 fl, can be attributed to conditions like haemolysis, acute haemorrhage, bone marrow failure, anaemia of chronic disease (which can also be microcytic), mixed iron and folate deficiency, pregnancy, chronic renal failure, and sickle-cell disease.

Lastly, macrocytic anaemia, characterized by an MCV greater than 100 fl, can be caused by factors such as B12 deficiency, folate deficiency, hypothyroidism, reticulocytosis, liver disease, alcohol abuse, myeloproliferative disease, myelodysplastic disease, and certain drugs like methotrexate, hydroxyurea, and azathioprine.

It is important to understand the different causes of anaemia based on red cell size as this knowledge can aid in the diagnosis and management of this condition.

When performing CPR on patients with severe hypothermia, it is recommended to limit defibrillation attempts to three. Hypothermia is characterized by a core temperature below 35ºC, with mild hypothermia ranging from 32-35ºC, moderate hypothermia from 30-32ºC, and severe hypothermia below 30ºC. This condition often occurs after drowning. If the individual’s core body temperature is below 30°C, it is advised to administer a maximum of three shocks using the highest output of the defibrillator.

Further Reading:

Cardiopulmonary arrest is a serious event with low survival rates. In non-traumatic cardiac arrest, only about 20% of patients who arrest as an in-patient survive to hospital discharge, while the survival rate for out-of-hospital cardiac arrest is approximately 8%. The Resus Council BLS/AED Algorithm for 2015 recommends chest compressions at a rate of 100-120 per minute with a compression depth of 5-6 cm. The ratio of chest compressions to rescue breaths is 30:2.

After a cardiac arrest, the goal of patient care is to minimize the impact of post cardiac arrest syndrome, which includes brain injury, myocardial dysfunction, the ischaemic/reperfusion response, and the underlying pathology that caused the arrest. The ABCDE approach is used for clinical assessment and general management. Intubation may be necessary if the airway cannot be maintained by simple measures or if it is immediately threatened. Controlled ventilation is aimed at maintaining oxygen saturation levels between 94-98% and normocarbia. Fluid status may be difficult to judge, but a target mean arterial pressure (MAP) between 65 and 100 mmHg is recommended. Inotropes may be administered to maintain blood pressure. Sedation should be adequate to gain control of ventilation, and short-acting sedating agents like propofol are preferred. Blood glucose levels should be maintained below 8 mmol/l. Pyrexia should be avoided, and there is some evidence for controlled mild hypothermia but no consensus on this.

Post ROSC investigations may include a chest X-ray, ECG monitoring, serial potassium and lactate measurements, and other imaging modalities like ultrasonography, echocardiography, CTPA, and CT head, depending on availability and skills in the local department. Treatment should be directed towards the underlying cause, and PCI or thrombolysis may be considered for acute coronary syndrome or suspected pulmonary embolism, respectively.

Patients who are comatose after ROSC without significant pre-arrest comorbidities should be transferred to the ICU for supportive care. Neurological outcome at 72 hours is the best prognostic indicator of outcome.

The supraspinatus muscle is a small muscle located in the upper back. It extends from the supraspinatus fossa of the scapula to the greater tubercle of the humerus. This muscle is part of the rotator cuff, along with three other muscles. The supraspinatus muscle is innervated by the suprascapular nerve, which also innervates the infraspinatus muscle. The suprascapular nerve originates from the upper trunk of the brachial plexus.

The main function of the supraspinatus muscle is to assist the deltoid muscle in abducting the arm at the shoulder joint. Specifically, it is responsible for the initial 15 degrees of arm abduction. Beyond this range, the deltoid muscle takes over as the primary abductor.

In addition to its role in arm movement, the supraspinatus muscle works together with the other rotator cuff muscles to stabilize the shoulder joint. It helps keep the humeral head in the glenoid fossa and counteracts the downward gravitational forces exerted on the shoulder joint by the weight of the arm.

One common test used to assess the supraspinatus muscle is called the empty can test. During this test, the patient is positioned either standing or sitting, with their arms raised parallel to the ground in the scapular plane. The arm is then internally rotated fully, with the thumb facing downward. The clinician applies downward pressure on either the wrists or the elbow, while the patient resists this pressure. If the patient experiences weakness, pain, or both during this resistance, it indicates a possible tear in the supraspinatus tendon or muscle, or a suprascapular nerve neuropathy.

Acute bacterial prostatitis is a sudden inflammation of the prostate gland, which can be either focal or diffuse and is characterized by the presence of pus. The most common organisms that cause this condition include Escherichia coli, Streptococcus faecalis, Staphylococcus aureus, and Neisseria gonorrhoea. The infection usually reaches the prostate through direct extension from the posterior urethra or urinary bladder, but it can also spread through the blood or lymphatics. In some cases, the infection may originate from the rectum.

According to the National Institute for Health and Care Excellence (NICE), acute prostatitis should be suspected in men who present with a sudden onset of feverish illness, which may be accompanied by rigors, arthralgia, or myalgia. Irritative urinary symptoms like dysuria, frequency, urgency, or acute urinary retention are also common. Perineal or suprapubic pain, as well as penile pain, low back pain, pain during ejaculation, and pain during bowel movements, can occur. A rectal examination may reveal an exquisitely tender prostate. A urine dipstick test showing white blood cells and a urine culture confirming urinary infection are also indicative of acute prostatitis.

The current recommendations by NICE and the British National Formulary (BNF) for the treatment of acute prostatitis involve prescribing an oral antibiotic for a duration of 14 days, taking into consideration local antimicrobial resistance data. The first-line antibiotics recommended are Ciprofloxacin 500 mg twice daily or Ofloxacin 200 mg twice daily. If these are not suitable, Trimethoprim 200 mg twice daily can be used. Second-line options include Levofloxacin 500 mg once daily or Co-trimoxazole 960 mg twice daily, but only when there is bacteriological evidence of sensitivity and valid reasons to prefer this combination over a single antibiotic.

For more information, you can refer to the NICE Clinical Knowledge Summary on acute prostatitis.

Tryptase levels can be a valuable tool in diagnosing anaphylaxis. During an anaphylactic reaction, mast cell tryptase is released and can be measured in the blood. Research suggests that tryptase levels reach their highest point in the blood within 1 minute to 6 hours after the reaction begins, typically peaking around 1-2 hours after the onset of symptoms. This information is crucial for diagnosing and treating anaphylaxis, especially in cases where the diagnosis is uncertain. It’s important to note that tryptase levels may return to normal within 6 hours, so the timing of blood samples is crucial. The current recommendation is to take three tryptase level measurements: one as soon as resuscitation begins, another 1-2 hours after symptoms start, and a third 24 hours later or during the recovery period. It’s worth mentioning that some individuals may have elevated baseline tryptase levels, which should be taken into consideration during the diagnosis process.

Further Reading:

Anaphylaxis is a severe and life-threatening hypersensitivity reaction that can have sudden onset and progression. It is characterized by skin or mucosal changes and can lead to life-threatening airway, breathing, or circulatory problems. Anaphylaxis can be allergic or non-allergic in nature.

In allergic anaphylaxis, there is an immediate hypersensitivity reaction where an antigen stimulates the production of IgE antibodies. These antibodies bind to mast cells and basophils. Upon re-exposure to the antigen, the IgE-covered cells release histamine and other inflammatory mediators, causing smooth muscle contraction and vasodilation.

Non-allergic anaphylaxis occurs when mast cells degrade due to a non-immune mediator. The clinical outcome is the same as in allergic anaphylaxis.

The management of anaphylaxis is the same regardless of the cause. Adrenaline is the most important drug and should be administered as soon as possible. The recommended doses for adrenaline vary based on age. Other treatments include high flow oxygen and an IV fluid challenge. Corticosteroids and chlorpheniramine are no longer recommended, while non-sedating antihistamines may be considered as third-line treatment after initial stabilization of airway, breathing, and circulation.

Common causes of anaphylaxis include food (such as nuts, which is the most common cause in children), drugs, and venom (such as wasp stings). Sometimes it can be challenging to determine if a patient had a true episode of anaphylaxis. In such cases, serum tryptase levels may be measured, as they remain elevated for up to 12 hours following an acute episode of anaphylaxis.

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.

This patient has developed Wernicke’s encephalopathy, a condition that is associated with alcohol abuse and other causes of thiamine deficiency. It is important to note that the infusion of glucose-containing intravenous fluids without thiamine in a patient with chronic thiamine deficiency can trigger Wernicke’s encephalopathy. In this particular case, it seems that this is what has occurred.

Wernicke’s encephalopathy is typically characterized by a triad of symptoms, which include acute confusion, ophthalmoplegia, and ataxia. Additionally, other possible features of this condition may include papilloedema, hearing loss, apathy, dysphagia, memory impairment, and hypothermia. It is also common for peripheral neuropathy, primarily affecting the legs, to occur in the majority of cases.

This condition is characterized by the presence of acute capillary haemorrhages, astrocytosis, and neuronal death in the upper brainstem and diencephalon. These abnormalities can be visualized through MRI scanning, although CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will go on to develop a Korsakoff psychosis. This condition is characterized by retrograde amnesia, an inability to form new memories, disordered time perception, and confabulation.

Patients who are suspected to have Wernicke’s encephalopathy should be promptly treated with parenteral thiamine (such as Pabrinex) for a minimum of 5 days. Following the parenteral therapy, oral thiamine should be administered.

Gout and pseudogout are both characterized by the presence of crystal deposits in the joints that are affected. Gout occurs when urate crystals are deposited, while pseudogout occurs when calcium pyrophosphate crystals are deposited. Under a microscope, these crystals can be distinguished by their appearance. Urate crystals are needle-shaped and negatively birefringent, while calcium pyrophosphate crystals are brick-shaped and positively birefringent.

Gout can affect any joint in the body, but it most commonly manifests in the hallux metatarsophalangeal joint, which is the joint at the base of the big toe. This joint is affected in approximately 50% of gout cases. On the other hand, pseudogout primarily affects the larger joints, such as the knee.

The diving reflex occurs when the face comes into contact with cold water, leading to apnoea, bradycardia, and peripheral vasoconstriction. This response helps decrease the workload on the heart, lower oxygen demand in the heart muscle, and ensure adequate blood flow to the brain and vital organs. The trigeminal nerve (CN V) is responsible for transmitting sensory information, while the vagus nerve (CN X) primarily controls the motor response. This reflex is more prominent in young children and is believed to contribute to their improved survival rates in prolonged submersion in cold water.

Further Reading:

Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid. It can be classified as cold-water or warm-water drowning. Risk factors for drowning include young age and male sex. Drowning impairs lung function and gas exchange, leading to hypoxemia and acidosis. It also causes cardiovascular instability, which contributes to metabolic acidosis and cell death.

When someone is submerged or immersed, they will voluntarily hold their breath to prevent aspiration of water. However, continued breath holding causes progressive hypoxia and hypercapnia, leading to acidosis. Eventually, the respiratory center sends signals to the respiratory muscles, forcing the individual to take an involuntary breath and allowing water to be aspirated into the lungs. Water entering the lungs stimulates a reflex laryngospasm that prevents further penetration of water. Aspirated water can cause significant hypoxia and damage to the alveoli, leading to acute respiratory distress syndrome (ARDS).

Complications of drowning include cardiac ischemia and infarction, infection with waterborne pathogens, hypothermia, neurological damage, rhabdomyolysis, acute tubular necrosis, and disseminated intravascular coagulation (DIC).

In children, the diving reflex helps reduce hypoxic injury during submersion. It causes apnea, bradycardia, and peripheral vasoconstriction, reducing cardiac output and myocardial oxygen demand while maintaining perfusion of the brain and vital organs.

Associated injuries with drowning include head and cervical spine injuries in patients rescued from shallow water. Investigations for drowning include arterial blood gases, chest X-ray, ECG and cardiac monitoring, core temperature measurement, and blood and sputum cultures if secondary infection is suspected.

Management of drowning involves extricating the patient from water in a horizontal position with spinal precautions if possible. Cardiovascular considerations should be taken into account when removing patients from water to prevent hypotension and circulatory collapse. Airway management, supplemental oxygen, and ventilation strategies are important in maintaining oxygenation and preventing further lung injury. Correcting hypotension, electrolyte disturbances, and hypothermia is also necessary. Attempting to drain water from the lungs is ineffective.

Patients without associated physical injury who are asymptomatic and have no evidence of respiratory compromise after six hours can be safely discharged home. Ventilation strategies aim to maintain oxygenation while minimizing ventilator-associated lung injury.

Pelvic inflammatory disease (PID) is a pelvic infection that affects the upper female reproductive tract, including the uterus, fallopian tubes, and ovaries. It is typically caused by an ascending infection from the cervix and is commonly associated with sexually transmitted diseases like chlamydia and gonorrhea. In the UK, genital Chlamydia trachomatis infection is the most common cause of PID seen in genitourinary medicine clinics.

PID can often be asymptomatic, but when symptoms are present, they may include lower abdominal pain and tenderness, fever, painful urination, painful intercourse, purulent vaginal discharge, abnormal vaginal bleeding, and tenderness in the cervix and adnexa. It is important to note that symptoms of ectopic pregnancy can be similar to those of PID, so a pregnancy test should be conducted for all patients with suspicious symptoms.

To investigate a possible case of PID, endocervical swabs should be taken to test for C. trachomatis and N. gonorrhoeae using nucleic acid amplification tests if available. Mild to moderate cases of PID can usually be managed in primary care or outpatient settings, while patients with severe disease should be admitted to the hospital for intravenous antibiotics. Signs of severe disease include a fever above 38°C, signs of a tubo-ovarian abscess, signs of pelvic peritonitis, or concurrent pregnancy.

Empirical antibiotic treatment should be initiated as soon as a presumptive diagnosis of PID is made clinically, without waiting for swab results. The current recommended outpatient treatment for PID is a single intramuscular dose of ceftriaxone 500 mg, followed by oral doxycycline 100 mg twice daily and oral metronidazole 400 mg twice daily for 14 days. An alternative regimen is oral ofloxacin 400 mg twice daily and oral metronidazole 400 mg twice daily for 14 days.

For severely ill patients in the inpatient setting, initial treatment includes intravenous doxycycline, a single-dose of intravenous ceftriaxone, and intravenous metronidazole. This is then followed by a switch to oral doxycycline and metronidazole to complete a 14-day treatment course. If a patient fails to respond to treatment, laparoscopy is necessary to confirm the diagnosis or consider alternative diagnoses.

When giving chest compressions to an adult, it is important to compress the sternum to a depth of 5-6 cm. The resuscitation council updated their guidance in 2015 and now recommends a ratio of 30 chest compressions to 2 rescue breaths. It is worth noting that according to the algorithm, checking for a pulse is no longer necessary in the latest BLS sequence. The chest compressions should be administered at a rate of 100-120 per minute, with a ratio of 30 compressions to 2 rescue breaths.

Further Reading:

Cardiopulmonary arrest is a serious event with low survival rates. In non-traumatic cardiac arrest, only about 20% of patients who arrest as an in-patient survive to hospital discharge, while the survival rate for out-of-hospital cardiac arrest is approximately 8%. The Resus Council BLS/AED Algorithm for 2015 recommends chest compressions at a rate of 100-120 per minute with a compression depth of 5-6 cm. The ratio of chest compressions to rescue breaths is 30:2.

After a cardiac arrest, the goal of patient care is to minimize the impact of post cardiac arrest syndrome, which includes brain injury, myocardial dysfunction, the ischaemic/reperfusion response, and the underlying pathology that caused the arrest. The ABCDE approach is used for clinical assessment and general management. Intubation may be necessary if the airway cannot be maintained by simple measures or if it is immediately threatened. Controlled ventilation is aimed at maintaining oxygen saturation levels between 94-98% and normocarbia. Fluid status may be difficult to judge, but a target mean arterial pressure (MAP) between 65 and 100 mmHg is recommended. Inotropes may be administered to maintain blood pressure. Sedation should be adequate to gain control of ventilation, and short-acting sedating agents like propofol are preferred. Blood glucose levels should be maintained below 8 mmol/l. Pyrexia should be avoided, and there is some evidence for controlled mild hypothermia but no consensus on this.

Post ROSC investigations may include a chest X-ray, ECG monitoring, serial potassium and lactate measurements, and other imaging modalities like ultrasonography, echocardiography, CTPA, and CT head, depending on availability and skills in the local department. Treatment should be directed towards the underlying cause, and PCI or thrombolysis may be considered for acute coronary syndrome or suspected pulmonary embolism, respectively.

Patients who are comatose after ROSC without significant pre-arrest comorbidities should be transferred to the ICU for supportive care. Neurological outcome at 72 hours is the best prognostic indicator of outcome.

The most likely diagnosis in this case is Goodpasture’s syndrome, which is a rare autoimmune vasculitic disorder. It is characterized by a triad of symptoms including pulmonary hemorrhage, glomerulonephritis, and the presence of anti-glomerular basement membrane (Anti-GBM) antibodies. Goodpasture’s syndrome is more commonly seen in men, particularly in smokers. There is also an association with certain HLA types, specifically HLA-B7 and HLA-DRw2.

The clinical features of Goodpasture’s syndrome include constitutional symptoms such as fever, fatigue, nausea, and weight loss. Patients may also experience haemoptysis or pulmonary hemorrhage, chest pain, breathlessness, and inspiratory crackles at the lung bases. Anemia due to intrapulmonary bleeding, arthralgia, rapidly progressive glomerulonephritis, haematuria, hypertension, and hepatosplenomegaly (rarely) may also be present.

Blood tests will reveal an iron deficiency anemia, elevated white cell count, and renal impairment. Elisa for Anti-GBM antibodies is highly sensitive and specific, but it is not widely available. Approximately 30% of patients may also have circulating antineutrophilic cytoplasmic antibodies (ANCAs), although these are not specific for Goodpasture’s syndrome and can be found in other conditions such as Wegener’s granulomatosis.

Diagnosis is typically confirmed through renal biopsy, which can detect the presence of anti-GBM antibodies. The management of Goodpasture’s syndrome involves a combination of plasmapheresis to remove circulating antibodies and the use of corticosteroids or cyclophosphamide.

It is important to note that this patient’s history is inconsistent with a diagnosis of pulmonary embolism, as renal impairment, haematuria, and the presence of ANCAs and anti-GBM antibodies would not be expected. While pulmonary hemorrhage and renal impairment can occur in systemic lupus erythematosus, these are uncommon presentations, and the presence of ANCAs and anti-GBM antibodies would also be inconsistent with this diagnosis.

Churg-Strauss syndrome can present with pulmonary hemorrhage, and c-ANCA may be present, but patients typically have a history of asthma, sinusitis, and eosinophilia. Wegener’s granulomatosis can present similarly to Goodpasture’s syndrome,

Le Fort fractures are intricate fractures of the midface, which involve the maxillary bone and the surrounding structures. These fractures can occur in a horizontal, pyramidal, or transverse direction. The distinguishing feature of Le Fort fractures is the separation of the pterygomaxillary due to trauma. They make up approximately 10% to 20% of all facial fractures and can have severe consequences, both in terms of potential life-threatening situations and disfigurement.

The causes of Le Fort fractures vary depending on the type of fracture. Common mechanisms include motor vehicle accidents, sports injuries, assaults, and falls from significant heights. Patients with Le Fort fractures often have concurrent head and cervical spine injuries. Additionally, they frequently experience other facial fractures, as well as neuromuscular injuries and dental avulsions.

The specific type of fracture sustained is determined by the direction of the force applied to the face. Le Fort type I fractures typically occur when a force is directed downward against the upper teeth. Le Fort type II fractures are usually the result of a force applied to the lower or mid maxilla. Lastly, Le Fort type III fractures are typically caused by a force applied to the nasal bridge and upper part of the maxilla.

Transfusion-associated circulatory overload (TACO) is a reaction that occurs when a large volume of blood is infused rapidly. It is the second leading cause of deaths related to transfusions, accounting for about 20% of all fatalities.

TACO typically happens in patients with limited cardiac reserve or chronic anemia who receive a fast blood transfusion. Elderly individuals, infants, and severely anemic patients are particularly vulnerable.

The common signs of TACO include acute respiratory distress, rapid heartbeat, high blood pressure, the appearance of acute or worsening fluid accumulation in the lungs on a chest X-ray, and evidence of excessive fluid retention.

The B-type natriuretic peptide (BNP) can be a helpful diagnostic tool for TACO. Usually, the BNP level is elevated to at least 1.5 times the baseline before the transfusion.

In many cases, simply slowing down the rate of transfusion, positioning the patient upright, and administering diuretics will be sufficient. In more severe cases, the transfusion should be stopped, and non-invasive ventilation may be considered.

Aortic regurgitation is a condition where the aortic valve fails to close tightly, resulting in the backflow of blood from the aorta into the left ventricle during ventricular diastole. This valvular lesion presents with various clinical symptoms and signs.

The clinical symptoms of aortic regurgitation include exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. These symptoms are experienced by patients during physical activity, while lying flat, and during episodes of sudden nighttime breathlessness, respectively.

On the other hand, the clinical signs of aortic regurgitation can be observed during physical examination. These signs include a collapsing pulse, widened pulse pressure, hyperkinetic laterally displaced apex beat, and a thrill in the aortic area. Additionally, an early diastolic murmur can be heard, which is loudest at the lower left sternal edge when the patient is sitting forward and exhaling.

Aortic regurgitation is also associated with several eponymous signs, which are named after the physicians who first described them. These signs include Corrigan’s sign, which is characterized by visible and forceful neck pulsation. De Musset’s sign refers to head nodding in time with the heartbeat. Quincke’s sign is the observation of visible nail bed capillary pulsation. Duroziez’s sign is the presence of a diastolic murmur heard proximal to femoral artery compression. Traube’s sign is the perception of a pistol shot sound over the femoral arteries. The Lighthouse sign is the blanching and flushing of the forehead. Becker’s sign is the pulsation seen in retinal vessels. Rosenbach’s sign is the presence of a pulsatile liver. Lastly, Muller’s sign refers to pulsations of the uvula.

In summary, aortic regurgitation is a valvular lesion that leads to the incomplete closure of the aortic valve. It manifests with various clinical symptoms, signs, and eponymous findings, which can be identified through careful examination and observation.

Ondansetron is a medication that works by blocking serotonin receptors in the body. It is commonly used as a first-line treatment for postoperative nausea and vomiting (PONV), which can occur after procedures done under sedation or anesthesia.

Further Reading:

postoperative nausea and vomiting (PONV) is a common occurrence following procedures performed under sedation or anesthesia. It can be highly distressing for patients. Several risk factors have been identified for PONV, including female gender, a history of PONV or motion sickness, non-smoking status, patient age, use of volatile anesthetics, longer duration of anesthesia, perioperative opioid use, use of nitrous oxide, and certain types of surgery such as abdominal and gynecological procedures.

To manage PONV, antiemetics are commonly used. These medications work by targeting different receptors in the body. Cyclizine and promethazine are histamine H1-receptor antagonists, which block the action of histamine and help reduce nausea and vomiting. Ondansetron is a serotonin 5-HT3 receptor antagonist, which blocks the action of serotonin and is effective in preventing and treating PONV. Prochlorperazine is a dopamine D2 receptor antagonist, which blocks the action of dopamine and helps alleviate symptoms of nausea and vomiting. Metoclopramide is also a dopamine D2 receptor antagonist and a 5-HT3 receptor antagonist, providing dual action against PONV. It is also a 5-HT4 receptor agonist, which helps improve gastric emptying and reduces the risk of PONV.

Assessment and management of PONV involves a comprehensive approach. Healthcare professionals need to assess the patient’s risk factors for PONV and take appropriate measures to prevent its occurrence. This may include selecting the appropriate anesthesia technique, using antiemetics prophylactically, and providing adequate pain control. In cases where PONV does occur, prompt treatment with antiemetics should be initiated to alleviate symptoms and provide relief to the patient. Close monitoring of the patient’s condition and response to treatment is essential to ensure effective management of PONV.

Urinary retention can be caused by various drug classes. One such class is 5α-reductase inhibitors like finasteride, which are prescribed to alleviate obstructive symptoms caused by an enlarged prostate. Some commonly known drugs that can lead to urinary retention include alcohol, anticholinergics, decongestants (such as phenylephrine and pseudoephedrine), disopyramide, antihistamines (like diphenhydramine and phenergan), and amphetamines.

Further Reading:

Urinary retention is the inability to completely or partially empty the bladder. It is commonly seen in elderly males with prostate enlargement and acute retention. Symptoms of acute urinary retention include the inability to void, inability to empty the bladder, overflow incontinence, and suprapubic discomfort. Chronic urinary retention, on the other hand, is typically painless but can lead to complications such as hydronephrosis and renal impairment.

There are various causes of urinary retention, including anatomical factors such as urethral stricture, bladder neck contracture, and prostate enlargement. Functional causes can include neurogenic bladder, neurological diseases like multiple sclerosis and Parkinson’s, and spinal cord injury. Certain drugs can also contribute to urinary retention, such as anticholinergics, opioids, and tricyclic antidepressants. In female patients, specific causes like organ prolapse, pelvic mass, and gravid uterus should be considered.

The pathophysiology of acute urinary retention can involve factors like increased resistance to flow, detrusor muscle dysfunction, bladder overdistension, and drugs that affect bladder tone. The primary management intervention for acute urinary retention is the insertion of a urinary catheter. If a catheter cannot be passed through the urethra, a suprapubic catheter can be inserted. Post-catheterization residual volume should be measured, and renal function should be assessed through U&Es and urine culture. Further evaluation and follow-up with a urologist are typically arranged, and additional tests like ultrasound may be performed if necessary. It is important to note that PSA testing is often deferred for at least two weeks after catheter insertion and female patients with retention should also be referred to urology for investigation.

Dermovate (Clobetasol propionate) is a strong steroid used for treating skin conditions. It is important to continue using emollients alongside steroid treatment. If the flare-ups are not effectively controlled by steroids, Tacrolimus can be considered as a secondary treatment option.

Further Reading:

Eczema is a chronic inflammatory skin disease characterized by dry, itchy skin with eczematous lesions. It often follows a chronic relapsing course and can lead to chronic skin changes such as lichenification and pigment changes. The term eczema is often used interchangeably with dermatitis, but strictly speaking, dermatitis refers to inflammation of the skin while eczema refers to specific conditions where skin inflammation is a feature.

Atopic eczema, also known as atopic dermatitis, is the most common type of eczema. It is usually first diagnosed in young children, with 90% of cases diagnosed before the age of 5. However, it can affect individuals of any age. Symptoms often improve as patients progress into their teens and adulthood. Around 10-20% of children are affected by atopic eczema, but only 3% of adults experience symptoms.

The exact cause of atopic eczema is not fully understood, but it is believed to be multifactorial, with both genetic and environmental factors playing a role. Genetic defects in genes that aid in the functioning of the skin barrier have been identified, which may predispose individuals to breaks in the skin barrier and increased exposure to antigens. Environmental factors such as pollution, allergen exposure, climate, and others also contribute to the development of the disease.

Diagnosing atopic eczema involves assessing the presence of key clinical features, such as pruritus (itching), eczema/dermatitis in a pattern appropriate for age, early age of onset, and personal or family history of atopy. Various diagnostic criteria have been established to aid in the diagnosis, including those set out by the American Academy of Dermatology and the UK working party.

The severity of atopic eczema can vary, and treatment options depend on the severity. Mild cases may be managed with emollients (moisturizers) and mild potency topical corticosteroids. Moderate cases may require moderate potency topical corticosteroids, topical calcineurin inhibitors, and bandages. Severe cases may necessitate the use of potent topical corticosteroids, topical calcineurin inhibitors, bandages, phototherapy, and systemic therapy.

In addition to medical treatment, identifying and avoiding triggers is an important aspect of managing atopic eczema. Common triggers include irritants, contact allergens, certain foods, skin infections, inhalant triggers, stress and infection.

This individual has presented with haemoptysis and a purpuric rash, alongside a history of asthma and allergic rhinitis. Blood tests have revealed elevated inflammatory markers, pronounced eosinophilia, and acute renal failure. The most likely diagnosis in this case is Churg-Strauss syndrome.

Churg-Strauss syndrome is a rare autoimmune vasculitis that affects small and medium-sized blood vessels. The American College of Rheumatology has established six criteria for diagnosing Churg-Strauss syndrome. The presence of at least four of these criteria is highly indicative of the condition:

1. Asthma (wheezing, expiratory rhonchi)
2. Eosinophilia of more than 10% in peripheral blood
3. Paranasal sinusitis
4. Pulmonary infiltrates (which may be transient)
5. Histological confirmation of vasculitis with extravascular eosinophils
6. Mononeuritis multiplex or polyneuropathy

Churg-Strauss syndrome can affect various organ systems, with the most common clinical features including:

– Constitutional symptoms: fever, fatigue, weight loss, and arthralgia
– Respiratory symptoms: asthma, haemoptysis, allergic rhinitis, and sinusitis
– Cardiovascular symptoms: heart failure, myocarditis, and myocardial infarction
– Gastrointestinal symptoms: gastrointestinal bleeding, bowel ischaemia, and appendicitis
– Dermatological symptoms: purpura, livedo reticularis, and skin nodules
– Renal symptoms: glomerulonephritis, renal failure, and hypertension
– Neurological symptoms: mononeuritis multiplex

Investigations often reveal eosinophilia, anaemia, elevated CRP and ESR, elevated creatinine, and elevated serum IgE levels. Approximately 70% of patients test positive for p-ANCA.

The mainstay of treatment for Churg-Strauss syndrome is high-dose steroids. In cases with life-threatening complications, cyclophosphamide and azathioprine are often administered.

Polyarteritis nodosa is another vasculitic disorder that affects small and medium-sized blood vessels. It can impact the gastrointestinal tract, kidneys, skin, and joints, but it is not typically associated with rhinitis or asthma.

When performing Weber’s test, if the sound lateralizes to the unaffected side, it suggests sensorineural hearing loss in the opposite ear. For example, if the sound lateralizes to the left, it indicates sensorineural hearing loss in the right ear. On the other hand, if there is conductive hearing loss in the left ear, the sound will lateralize to the affected side. Additionally, a positive Rinne test result, where air conduction is greater than bone conduction, is typically seen in normal hearing and sensorineural loss. Conversely, a negative Rinne test result, where bone conduction is greater than air conduction, is expected in cases of conductive hearing loss. In summary, these test results can help identify the presence of sensorineural loss in the opposite ear.

Further Reading:

Hearing loss is a common complaint that can be caused by various conditions affecting different parts of the ear and nervous system. The outer ear is the part of the ear outside the eardrum, while the middle ear is located between the eardrum and the cochlea. The inner ear is within the bony labyrinth and consists of the vestibule, semicircular canals, and cochlea. The vestibulocochlear nerve connects the inner ear to the brain.

Hearing loss can be classified based on severity, onset, and type. Severity is determined by the quietest sound that can be heard, measured in decibels. It can range from mild to profound deafness. Onset can be sudden, rapidly progressive, slowly progressive, or fluctuating. Type of hearing loss can be either conductive or sensorineural. Conductive hearing loss is caused by issues in the external ear, eardrum, or middle ear that disrupt sound transmission. Sensorineural hearing loss is caused by problems in the cochlea, auditory nerve, or higher auditory processing pathways.

To diagnose sensorineural and conductive deafness, a 512 Hz tuning fork is used to perform Rinne and Weber’s tests. These tests help determine the type of hearing loss based on the results. In Rinne’s test, air conduction (AC) and bone conduction (BC) are compared, while Weber’s test checks for sound lateralization.

Cholesteatoma is a condition characterized by the abnormal accumulation of skin cells in the middle ear or mastoid air cell spaces. It is believed to develop from a retraction pocket that traps squamous cells. Cholesteatoma can cause the accumulation of keratin and the destruction of adjacent bones and tissues due to the production of destructive enzymes. It can lead to mixed sensorineural and conductive deafness as it affects both the middle and inner ear.

Parental responsibility encompasses the legal rights, duties, powers, responsibilities, and authority that a parent holds for their child. This includes the ability to provide consent for medical treatment on behalf of the child. Any individual with parental responsibility has the authority to give consent for their child. If a father meets any of the aforementioned criteria, he is considered to have parental responsibility. On the other hand, a mother is automatically granted parental responsibility for her child from the moment of birth.

Further Reading:

Patients have the right to determine what happens to their own bodies, and for consent to be valid, certain criteria must be met. These criteria include the person being informed about the intervention, having the capacity to consent, and giving consent voluntarily and freely without any pressure or undue influence.

In order for a person to be deemed to have capacity to make a decision on a medical intervention, they must be able to understand the decision and the information provided, retain that information, weigh up the pros and cons, and communicate their decision.

Valid consent can only be provided by adults, either by the patient themselves, a person authorized under a Lasting Power of Attorney, or someone with the authority to make treatment decisions, such as a court-appointed deputy or a guardian with welfare powers.

In the UK, patients aged 16 and over are assumed to have the capacity to consent. If a patient is under 18 and appears to lack capacity, parental consent may be accepted. However, a young person of any age may consent to treatment if they are considered competent to make the decision, known as Gillick competence. Parental consent may also be given by those with parental responsibility.

The Fraser guidelines apply to the prescription of contraception to under 16’s without parental involvement. These guidelines allow doctors to provide contraceptive advice and treatment without parental consent if certain criteria are met, including the young person understanding the advice, being unable to be persuaded to inform their parents, and their best interests requiring them to receive contraceptive advice or treatment.

Competent adults have the right to refuse consent, even if it is deemed unwise or likely to result in harm. However, there are exceptions to this, such as compulsory treatment authorized by the mental health act or if the patient is under 18 and refusing treatment would put their health at serious risk.

In emergency situations where a patient is unable to give consent, treatment may be provided without consent if it is immediately necessary to save their life or prevent a serious deterioration of their condition. Any treatment decision made without consent must be in the patient’s best interests, and if a decision is time-critical and the patient is unlikely to regain capacity in time, a best interest decision should be made. The treatment provided should be the least restrictive on the patient’s future choices.

The use of glucose infusion is not recommended due to its hypertonic nature, which can potentially increase the risk of extravasation injury.

Further Reading:

Diabetes Mellitus:
– Definition: a group of metabolic disorders characterized by persistent hyperglycemia caused by deficient insulin secretion, resistance to insulin, or both.
– Types: Type 1 diabetes (absolute insulin deficiency), Type 2 diabetes (insulin resistance and relative insulin deficiency), Gestational diabetes (develops during pregnancy), Other specific types (monogenic diabetes, diabetes secondary to pancreatic or endocrine disorders, diabetes secondary to drug treatment).
– Diagnosis: Type 1 diabetes diagnosed based on clinical grounds in adults presenting with hyperglycemia. Type 2 diabetes diagnosed in patients with persistent hyperglycemia and presence of symptoms or signs of diabetes.
– Risk factors for type 2 diabetes: obesity, inactivity, family history, ethnicity, history of gestational diabetes, certain drugs, polycystic ovary syndrome, metabolic syndrome, low birth weight.

Hypoglycemia:
– Definition: lower than normal blood glucose concentration.
– Diagnosis: defined by Whipple’s triad (signs and symptoms of low blood glucose, low blood plasma glucose concentration, relief of symptoms after correcting low blood glucose).
– Blood glucose level for hypoglycemia: NICE defines it as <3.5 mmol/L, but there is inconsistency across the literature.
– Signs and symptoms: adrenergic or autonomic symptoms (sweating, hunger, tremor), neuroglycopenic symptoms (confusion, coma, convulsions), non-specific symptoms (headache, nausea).
– Treatment options: oral carbohydrate, buccal glucose gel, glucagon, dextrose. Treatment should be followed by re-checking glucose levels.

Treatment of neonatal hypoglycemia:
– Treat with glucose IV infusion 10% given at a rate of 5 mL/kg/hour.
– Initial stat dose of 2 mL/kg over five minutes may be required for severe hypoglycemia.
– Mild asymptomatic persistent hypoglycemia may respond to a single dose of glucagon.
– If hypoglycemia is caused by an oral anti-diabetic drug, the patient should be admitted and ongoing glucose infusion or other therapies may be required.

Note: Patients who have a hypoglycemic episode with a loss of warning symptoms should not drive and should inform the DVLA.

The three sites most frequently used for IO access are the proximal tibia, distal tibia, and distal femur. The proximal tibia is located 2 cm below the tibial tuberosity, while the distal tibia is just above the medial malleolus. The distal femur site is situated 2 cm above the condyle in the midline. These sites are commonly chosen for IO access. However, there are also less commonly used sites such as the proximal humerus (above the surgical neck) and the iliac crest. It is important to note that the proximal humerus may be challenging to palpate in children and is typically not used in those under 5 years of age. Additionally, accessing the sternum requires a specialist device.

Further Reading:

Intraosseous (IO) cannulation is a technique used to gain urgent intravenous (IV) access in patients where traditional IV access is difficult to obtain. It involves injecting fluid or drugs directly into the medullary cavity of the bone. This procedure can be performed in both adult and pediatric patients and is commonly used in emergency situations.

There are different types of IO needles available, including manual IO needles and device-powered IO needles such as the EZ-IO. These tools allow healthcare professionals to access the bone and administer necessary medications or fluids quickly and efficiently.

The most commonly used sites for IO cannulation are the tibia (shinbone) and the femur (thighbone). In some cases, the proximal humerus (upper arm bone) may also be used. However, there are certain contraindications to IO cannulation that should be considered. These include fractures of the bone to be cannulated, overlying skin infections or a high risk of infection (such as burns), conditions like osteogenesis imperfecta or osteoporosis, ipsilateral vascular injury, and coagulopathy.

While IO cannulation is a valuable technique, there are potential complications that healthcare professionals should be aware of. These include superficial skin infections, osteomyelitis (infection of the bone), skin necrosis, growth plate injury (in pediatric patients), fractures, failure to access or position the needle correctly, extravasation (leakage of fluid or medication into surrounding tissues), and compartment syndrome (a rare but serious condition that can occur if there is an undiagnosed fracture).

Overall, IO cannulation is a useful method for gaining urgent IV access in patients when traditional methods are challenging. However, it is important for healthcare professionals to be aware of the potential complications and contraindications associated with this procedure.

Alzheimer’s disease, the leading cause of dementia, is characterized by the presence of beta-amyloid plaques and neurofibrillary tangles in the brain. These plaques are formed due to an excessive buildup of amyloid, which can be caused by either overproduction or impaired clearance of beta-amyloid. The accumulation of amyloid plaques leads to inflammation in the surrounding brain tissue, resulting in damage to neurons. Additionally, the abnormal phosphorylation of tau protein causes it to aggregate into neurofibrillary tangles within neurons. It is important to note that Lewy bodies, composed mainly of alpha-synuclein, are associated with diseases like Parkinson’s disease and dementia with Lewy bodies. Autoimmune diseases often involve the activation of autoreactive T-cells.

Further Reading:

Dementia is a progressive and irreversible clinical syndrome characterized by cognitive and behavioral symptoms. These symptoms include memory loss, impaired reasoning and communication, personality changes, and reduced ability to carry out daily activities. The decline in cognition affects multiple domains of intellectual functioning and is not solely due to normal aging.

To diagnose dementia, a person must have impairment in at least two cognitive domains that significantly impact their daily activities. This impairment cannot be explained by delirium or other major psychiatric disorders. Early-onset dementia refers to dementia that develops before the age of 65.

The most common cause of dementia is Alzheimer’s disease, accounting for 50-75% of cases. Other causes include vascular dementia, dementia with Lewy bodies, and frontotemporal dementia. Less common causes include Parkinson’s disease dementia, Huntington’s disease, prion disease, and metabolic and endocrine disorders.

There are several risk factors for dementia, including age, mild cognitive impairment, genetic predisposition, excess alcohol intake, head injury, depression, learning difficulties, diabetes, obesity, hypertension, smoking, Parkinson’s disease, low social engagement, low physical activity, low educational attainment, hearing impairment, and air pollution.

Assessment of dementia involves taking a history from the patient and ideally a family member or close friend. The person’s current level of cognition and functional capabilities should be compared to their baseline level. Physical examination, blood tests, and cognitive assessment tools can also aid in the diagnosis.

Differential diagnosis for dementia includes normal age-related memory changes, mild cognitive impairment, depression, delirium, vitamin deficiencies, hypothyroidism, adverse drug effects, normal pressure hydrocephalus, and sensory deficits.

Management of dementia involves a multi-disciplinary approach that includes non-pharmacological and pharmacological measures. Non-pharmacological interventions may include driving assessment, modifiable risk factor management, and non-pharmacological therapies to promote cognition and independence. Drug treatments for dementia should be initiated by specialists and may include acetylcholinesterase inhibitors, memantine, and antipsychotics in certain cases.

In summary, dementia is a progressive and irreversible syndrome characterized by cognitive and behavioral symptoms. It has various causes and risk factors, and its management involves a multi-disciplinary approach.

Femoral shaft fractures are quite common among children and have a significant impact on both the child and their family. It is important to carefully examine children with these fractures for any associated injuries, such as soft-tissue injury, head trauma, or additional fractures. In fact, up to 40% of children who experience a femoral shaft fracture due to high-energy trauma may have these associated injuries. Additionally, a thorough neurovascular examination should be conducted.

Rapidly immobilizing the limb is crucial for managing pain and limiting further blood loss from the fracture. For distal femoral shaft fractures, well-padded long leg splints with split plaster casts can be applied. However, for more proximal shaft fractures, long leg splints alone may not provide adequate control. In these cases, skin traction is a better option. Skin traction involves attaching a large foam pad to the patient’s lower leg using spray adhesive. A weight, approximately 10% of the child’s body weight, is then applied to the foam pad and allowed to hang over the foot of the bed. This constant longitudinal traction helps keep the bone fragments aligned.

When children experience severe pain, it is important to manage it aggressively yet safely. Immobilizing the fracture can provide significant relief. The Royal College of Emergency Medicine recommends other pain control measures for children, such as intranasal diamorphine (0.1 mg/kg in 0.2 ml sterile water), intravenous morphine (0.1-0.2 mg/kg), and oral analgesia (e.g., paracetamol 20 mg/kg, max 1 g, and ibuprofen 10 mg/kg, max 400 mg).

The subtraction of serial 7s is included in the 30-point Folstein mini-mental state examination (MMSE), but it is not included in the AMTS. The AMTS consists of ten questions that assess various cognitive abilities. These questions include asking about age, the nearest hour, the current year, the name of the hospital or location, the ability to recognize two people, date of birth, knowledge of historical events, knowledge of the present monarch or prime minister, counting backwards from 20 to 1, and recalling an address given earlier in the test. The AMTS is referenced in the RCEM syllabus under the topic of memory loss.

Corneal microdeposits are found in almost all individuals (over 90%) who have been taking amiodarone for more than six months, particularly at doses higher than 400 mg/day. These deposits generally do not cause any symptoms, although approximately 10% of patients may experience a perception of a ‘bluish halo’ around objects they see.

Amiodarone can also have other effects on the eye, but these are much less common, occurring in only 1-2% of patients. These effects include optic neuropathy, nonarteritic anterior ischemic optic neuropathy (N-AION), optic disc swelling, and visual field defects.

Post-traumatic stress disorder (PTSD) develops after experiencing an extremely threatening or catastrophic event that would cause distress in almost anyone. It is important to note that PTSD does not develop from everyday upsetting situations like divorce, job loss, or failing an exam.

The most common symptom of PTSD is re-experiencing the traumatic event involuntarily and vividly. This can manifest as flashbacks, nightmares, repetitive distressing images or sensations, and physical symptoms such as pain, sweating, nausea, or trembling. Other notable features of PTSD include avoidance, rumination, hyperarousal, emotional numbing, irritability, and insomnia.

It is common for individuals with PTSD to also experience other mental health problems such as depression, anxiety, phobias, self-harming behaviors, and substance abuse.

The recommended treatments for PTSD are Eye Movement Desensitization and Reprocessing (EMDR) and Trauma-focused Cognitive Behavioral Therapy (CBT). These treatments should be offered to individuals of all ages, regardless of the time that has passed since the traumatic event. Typically, 8-12 sessions are recommended, but more may be necessary in cases involving multiple traumas, chronic disability, comorbidities, or social problems.

This patient is likely experiencing an acute coronary syndrome, possibly a non-ST-elevation myocardial infarction (NSTEMI) or unstable angina. The troponin test will help confirm the diagnosis. The patient’s ECG showed ST depression in the inferior leads, but this normalized after treatment with GTN and morphine, ruling out a ST-elevation myocardial infarction (STEMI).

Immediate pain relief should be provided. GTN (sublingual or buccal) can be used, but intravenous opioids like morphine should be considered, especially if a heart attack is suspected.

Aspirin should be given to all patients with unstable angina or NSTEMI as soon as possible and continued indefinitely, unless there are contraindications like bleeding risk or aspirin hypersensitivity. A loading dose of 300 mg should be administered right after presentation.

Fondaparinux should be given to patients without a high bleeding risk, unless coronary angiography is planned within 24 hours of admission. Unfractionated heparin can be an alternative to fondaparinux for patients who will undergo coronary angiography within 24 hours. For patients with significant renal impairment, unfractionated heparin can also be considered, with dose adjustment based on clotting function monitoring.

Routine administration of oxygen is no longer recommended, but oxygen saturation should be monitored using pulse oximetry as soon as possible, preferably before hospital admission. Supplemental oxygen should only be offered to individuals with oxygen saturation (SpO2) below 94% who are not at risk of hypercapnic respiratory failure, aiming for a SpO2 of 94-98%. For individuals with chronic obstructive pulmonary disease at risk of hypercapnic respiratory failure, a target SpO2 of 88-92% should be achieved until blood gas analysis is available.

Bivalirudin, a specific and reversible direct thrombin inhibitor (DTI), is recommended by NICE as a possible treatment for adults with STEMI undergoing percutaneous coronary intervention.

For more information, refer to the NICE guidelines on the assessment and diagnosis of chest pain of recent onset.

A phaeochromocytoma is an uncommon functional tumor that develops from chromaffin cells in the adrenal medulla. Extra-adrenal paragangliomas, also known as extra-adrenal pheochromocytomas, are closely associated but less prevalent tumors that originate in the ganglia of the sympathetic nervous system. These tumors release catecholamines and result in a range of symptoms and indications linked to hyperactivity of the sympathetic nervous system.

Haloperidol should not be used in patients with Parkinson’s, Lewy body dementia, or prolonged QT syndrome. It is the first choice for controlling aggressive behavior in most patients with delirium, but lorazepam is preferred for patients with Parkinson’s, Lewy body dementia, prolonged QT syndrome, extrapyramidal side effects, or delirium due to alcohol withdrawal. Haloperidol can reduce the effectiveness of levodopa in Parkinson’s disease by blocking dopamine receptors in the corpus striatum, which can lead to worsened motor function, psychosis, or a combination of both.

Further Reading:

Delirium is an acute syndrome that causes disturbances in consciousness, attention, cognition, and perception. It is also known as an acute confusional state. The DSM-IV criteria for diagnosing delirium include recent onset of fluctuating awareness, impairment of memory and attention, and disorganized thinking. Delirium typically develops over hours to days and may be accompanied by behavioral changes, personality changes, and psychotic features. It often occurs in individuals with predisposing factors, such as advanced age or multiple comorbidities, when exposed to new precipitating factors, such as medications or infection. Symptoms of delirium fluctuate throughout the day, with lucid intervals occurring during the day and worse disturbances at night. Falling and loss of appetite are often warning signs of delirium.

Delirium can be classified into three subtypes based on the person’s symptoms. Hyperactive delirium is characterized by inappropriate behavior, hallucinations, and agitation. Restlessness and wandering are common in this subtype. Hypoactive delirium is characterized by lethargy, reduced concentration, and appetite. The person may appear quiet or withdrawn. Mixed delirium presents with signs and symptoms of both hyperactive and hypoactive subtypes.

The exact pathophysiology of delirium is not fully understood, but it is believed to involve multiple mechanisms, including cholinergic deficiency, dopaminergic excess, and inflammation. The cause of delirium is usually multifactorial, with predisposing factors and precipitating factors playing a role. Predisposing factors include older age, cognitive impairment, frailty, significant injuries, and iatrogenic events. Precipitating factors include infection, metabolic or electrolyte disturbances, cardiovascular disorders, respiratory disorders, neurological disorders, endocrine disorders, urological disorders, gastrointestinal disorders, severe uncontrolled pain, alcohol intoxication or withdrawal, medication use, and psychosocial factors.

Delirium is highly prevalent in hospital settings, affecting up to 50% of inpatients aged over 65 and occurring in 30% of people aged over 65 presenting to the emergency department. Complications of delirium include increased risk of death, high in-hospital mortality rates, higher mortality rates following hospital discharge, increased length of stay in hospital, nosocomial infections, increased risk of admission to long-term care or re-admission to hospital, increased incidence of dementia, increased risk of falls and associated injuries and pressure sores.

Due to the potentially life-threatening nature of the disease, it is crucial to initiate treatment without waiting for laboratory confirmation. Immediate administration of antibiotics is necessary.

In a hospital setting, the preferred agents for treatment are IV ceftriaxone (2 g for adults; 80 mg/kg for children) or IV cefotaxime (2 g for adults; 80 mg/kg for children). In the prehospital setting, IM benzylpenicillin can be given as an alternative. If there is a history of anaphylaxis to cephalosporins, chloramphenicol is a suitable alternative.

It is important to prioritize prompt treatment due to the severity of the disease. The recommended antibiotics should be administered as soon as possible to ensure the best possible outcome for the patient.

The timing of the initial rise, peak, and return to normality of various cardiac enzymes can serve as a helpful guide. Creatine kinase, the main cardiac isoenzyme, typically experiences an initial rise within 4-8 hours, reaches its peak at 18 hours, and returns to normal within 2-3 days. Myoglobin, which lacks specificity due to its association with skeletal muscle damage, shows an initial rise within 1-4 hours, peaks at 6-7 hours, and returns to normal within 24 hours. Troponin I, known for its sensitivity and specificity, exhibits an initial rise within 3-12 hours, reaches its peak at 24 hours, and returns to normal within 3-10 days. HFABP, or heart fatty acid binding protein, experiences an initial rise within 1.5 hours, peaks at 5-10 hours, and returns to normal within 24 hours. Lastly, LDH, predominantly found in cardiac muscle, shows an initial rise at 10 hours, peaks at 24-48 hours, and returns to normal within 14 days.

According to a Cochrane review conducted in 2008, it was discovered that approximately 80% of children experiencing acute otitis media were able to recover within a span of two days. However, the use of antibiotics only resulted in a reduction of pain for about 7% of children after the same two-day period. Furthermore, the administration of antibiotics did not show any significant impact on the rates of hearing loss, recurrence, or perforation. In cases where antibiotics are deemed necessary for children with otitis media, some indications include being under the age of two, experiencing discharge from the ear (otorrhoea), and having bilateral acute otitis media.

Wernicke’s encephalopathy is a condition that is linked to alcohol abuse and other causes of thiamine deficiency. It is commonly identified by the presence of three main symptoms: acute confusion, ophthalmoplegia (paralysis or weakness of the eye muscles), and ataxia (loss of coordination). Additional signs may include papilloedema (swelling of the optic disc), hearing loss, apathy, dysphagia (difficulty swallowing), memory impairment, and hypothermia. Most cases also involve peripheral neuropathy, primarily affecting the legs.

This condition is characterized by the occurrence of acute capillary hemorrhages, astrocytosis (abnormal increase in astrocytes, a type of brain cell), and neuronal death in the upper brainstem and diencephalon. These abnormalities can be detected through MRI scanning, while CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will develop a condition known as Korsakoff psychosis. This condition is characterized by retrograde amnesia (loss of memory for events that occurred before the onset of amnesia), an inability to form new memories, disordered perception of time, and confabulation (fabrication of false memories).

When Wernicke’s encephalopathy is suspected, it is crucial to administer parenteral thiamine (such as Pabrinex) for at least 5 days. Following the parenteral therapy, oral thiamine should be continued.

The count of lymphocytes, a type of white blood cell, can serve as an early indication of the level of radiation exposure. The severity of the exposure can be determined by observing the decrease in lymphocyte count, which is directly related to the amount of radiation absorbed by the body. Ideally, the count is measured 12 hours after exposure and then repeated every 4 hours initially to track the rate of decrease.

Further Reading:

Radiation exposure refers to the emission or transmission of energy in the form of waves or particles through space or a material medium. There are two types of radiation: ionizing and non-ionizing. Non-ionizing radiation, such as radio waves and visible light, has enough energy to move atoms within a molecule but not enough to remove electrons from atoms. Ionizing radiation, on the other hand, has enough energy to ionize atoms or molecules by detaching electrons from them.

There are different types of ionizing radiation, including alpha particles, beta particles, gamma rays, and X-rays. Alpha particles are positively charged and consist of 2 protons and 2 neutrons from the atom’s nucleus. They are emitted from the decay of heavy radioactive elements and do not travel far from the source atom. Beta particles are small, fast-moving particles with a negative electrical charge that are emitted from an atom’s nucleus during radioactive decay. They are more penetrating than alpha particles but less damaging to living tissue. Gamma rays and X-rays are weightless packets of energy called photons. Gamma rays are often emitted along with alpha or beta particles during radioactive decay and can easily penetrate barriers. X-rays, on the other hand, are generally lower in energy and less penetrating than gamma rays.

Exposure to ionizing radiation can damage tissue cells by dislodging orbital electrons, leading to the generation of highly reactive ion pairs. This can result in DNA damage and an increased risk of future malignant change. The extent of cell damage depends on factors such as the type of radiation, time duration of exposure, distance from the source, and extent of shielding.

The absorbed dose of radiation is directly proportional to time, so it is important to minimize the amount of time spent in the vicinity of a radioactive source. A lethal dose of radiation without medical management is 4.5 sieverts (Sv) to kill 50% of the population at 60 days. With medical management, the lethal dose is 5-6 Sv. The immediate effects of ionizing radiation can range from radiation burns to radiation sickness, which is divided into three main syndromes: hematopoietic, gastrointestinal, and neurovascular. Long-term effects can include hematopoietic cancers and solid tumor formation.

In terms of management, support is mainly supportive and includes IV fluids, antiemetics, analgesia, nutritional support, antibiotics, blood component substitution, and reduction of brain edema.