Whooping cough, also known as pertussis, is a respiratory infection caused by the bacteria Bordetella pertussis. It is transmitted through respiratory droplets and has an incubation period of about 7-21 days. This highly contagious disease can be passed on to around 90% of close household contacts.

To prevent the spread of whooping cough, Public Health England advises that children with the illness should stay away from school, nursery, or childminders for 48 hours after starting antibiotic treatment. If no antibiotic treatment is given, they should be kept away for 21 days from the onset of the illness. It’s important to note that even after treatment, non-infectious coughing may persist for several weeks.

For more information on how to control infections in schools and other childcare settings, you can refer to the guidance provided by Public Health England.

Phaeochromocytoma is characterized by certain clinical features, including paroxysmal hypertension, palpitations, headache, tremor, and profuse sweating. This patient exhibits paroxysmal symptoms that align with phaeochromocytoma, such as high blood pressure (systolic readings exceeding 220 mmHg are common), headache, sweating, and feelings of anxiety and fear. It is important to note that individuals with conditions like congenital adrenal hyperplasia, diabetes insipidus, and Addisonian crisis typically experience low blood pressure.

Further Reading:

Phaeochromocytoma is a rare neuroendocrine tumor that secretes catecholamines. It typically arises from chromaffin tissue in the adrenal medulla, but can also occur in extra-adrenal chromaffin tissue. The majority of cases are spontaneous and occur in individuals aged 40-50 years. However, up to 30% of cases are hereditary and associated with genetic mutations. About 10% of phaeochromocytomas are metastatic, with extra-adrenal tumors more likely to be metastatic.

The clinical features of phaeochromocytoma are a result of excessive catecholamine production. Symptoms are typically paroxysmal and include hypertension, headaches, palpitations, sweating, anxiety, tremor, abdominal and flank pain, and nausea. Catecholamines have various metabolic effects, including glycogenolysis, mobilization of free fatty acids, increased serum lactate, increased metabolic rate, increased myocardial force and rate of contraction, and decreased systemic vascular resistance.

Diagnosis of phaeochromocytoma involves measuring plasma and urine levels of metanephrines, catecholamines, and urine vanillylmandelic acid. Imaging studies such as abdominal CT or MRI are used to determine the location of the tumor. If these fail to find the site, a scan with metaiodobenzylguanidine (MIBG) labeled with radioactive iodine is performed. The highest sensitivity and specificity for diagnosis is achieved with plasma metanephrine assay.

The definitive treatment for phaeochromocytoma is surgery. However, before surgery, the patient must be stabilized with medical management. This typically involves alpha-blockade with medications such as phenoxybenzamine or phentolamine, followed by beta-blockade with medications like propranolol. Alpha blockade is started before beta blockade to allow for expansion of blood volume and to prevent a hypertensive crisis.

One of the clinical features of a tension pneumothorax is the deviation of the trachea away from the side where the pneumothorax is located. This particular feature is typically observed in cases of right-sided tension pneumothorax.

Further Reading:

A pneumothorax is an abnormal collection of air in the pleural cavity of the lung. It can be classified by cause as primary spontaneous, secondary spontaneous, or traumatic. Primary spontaneous pneumothorax occurs without any obvious cause in the absence of underlying lung disease, while secondary spontaneous pneumothorax occurs in patients with significant underlying lung diseases. Traumatic pneumothorax is caused by trauma to the lung, often from blunt or penetrating chest wall injuries.

Tension pneumothorax is a life-threatening condition where the collection of air in the pleural cavity expands and compresses normal lung tissue and mediastinal structures. It can be caused by any of the aforementioned types of pneumothorax. Immediate management of tension pneumothorax involves the ABCDE approach, which includes ensuring a patent airway, controlling the C-spine, providing supplemental oxygen, establishing IV access for fluid resuscitation, and assessing and managing other injuries.

Treatment of tension pneumothorax involves needle thoracocentesis as a temporary measure to provide immediate decompression, followed by tube thoracostomy as definitive management. Needle thoracocentesis involves inserting a 14g cannula into the pleural space, typically via the 4th or 5th intercostal space midaxillary line. If the patient is peri-arrest, immediate thoracostomy is advised.

The pathophysiology of tension pneumothorax involves disruption to the visceral or parietal pleura, allowing air to flow into the pleural space. This can occur through an injury to the lung parenchyma and visceral pleura, or through an entry wound to the external chest wall in the case of a sucking pneumothorax. Injured tissue forms a one-way valve, allowing air to enter the pleural space with inhalation but prohibiting air outflow. This leads to a progressive increase in the volume of non-absorbable intrapleural air with each inspiration, causing pleural volume and pressure to rise within the affected hemithorax.

The following list provides a summary of common causes for different acid-base disorders.

Respiratory alkalosis can be caused by hyperventilation, such as during periods of anxiety. It can also be a result of conditions like pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, or the early stages of aspirin overdose.

Respiratory acidosis is often associated with chronic obstructive pulmonary disease (COPD) or life-threatening asthma. It can also occur due to pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or other respiratory conditions.

Metabolic alkalosis can be caused by vomiting, potassium depletion (often due to diuretic usage), Cushing’s syndrome, or Conn’s syndrome.

Metabolic acidosis with a raised anion gap can occur due to lactic acidosis (such as in cases of hypoxemia, shock, sepsis, or infarction) or ketoacidosis (such as in diabetes, starvation, or alcohol excess). It can also be a result of renal failure or poisoning (such as in late stages of aspirin overdose, methanol or ethylene glycol ingestion).

Metabolic acidosis with a normal anion gap can be caused by conditions like renal tubular acidosis, diarrhea, ammonium chloride ingestion, or adrenal insufficiency.

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.

The most probable diagnosis in this case is vaginal thrush. Vaginal thrush is characterized by symptoms such as vulval irritation and itching, vulval redness, and a discharge that is often described as cheesy. Some women may also experience dysuria, which is pain or discomfort during urination, but without an increase in frequency or urgency. The recommended treatment for vaginal thrush is the use of antifungal agents, with topical azoles like clotrimazole or miconazole being commonly prescribed. It is important to note that breastfeeding patients should avoid taking oral terbinafine as it can pass into breast milk.

Hypothermic cardiac arrest is a rare situation that requires a tailored approach. Resuscitation is typically prolonged, but the prognosis for young, previously healthy individuals can be good. Hypothermic cardiac arrest may be associated with drowning. 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, basal metabolic rate falls and cell signaling between neurons decreases, leading to reduced tissue perfusion. Signs and symptoms of hypothermia progress as the core temperature drops, initially presenting as compensatory increases in heart rate and shivering, but eventually ceasing as the temperature drops into moderate hypothermia territory.

ECG changes associated with hypothermia include bradyarrhythmias, Osborn waves, prolonged PR, QRS, and QT intervals, shivering artifact, ventricular ectopics, and cardiac arrest. When managing hypothermic cardiac arrest, ALS should be initiated as per the standard ALS algorithm, but with modifications. It is important to check for signs of life, re-warm the patient, consider mechanical ventilation due to chest wall stiffness, adjust dosing or withhold drugs due to slowed drug metabolism, and correct electrolyte disturbances. The resuscitation of hypothermic patients is often prolonged and may continue for a number of hours.

Pulse checks during CPR may be difficult due to low blood pressure, and the pulse check is prolonged to 1 minute for this reason. Drug metabolism is slowed in hypothermic patients, leading to a build-up of potentially toxic plasma concentrations of administered drugs. Current guidance advises withholding drugs if the core temperature is below 30ºC and doubling the drug interval at core temperatures between 30 and 35ºC. Electrolyte disturbances are common in hypothermic patients, and it is important to interpret results keeping the setting in mind. Hypoglycemia should be treated, hypokalemia will often correct as the patient re-warms, ABG analyzers may not reflect the reality of the hypothermic patient, and severe hyperkalemia is a poor prognostic indicator.

Different warming measures can be used to increase the core body temperature, including external passive measures such as removal of wet clothes and insulation with blankets, external active measures such as forced heated air or hot-water immersion, and internal active measures such as inhalation of warm air, warmed intravenous fluids, gastric, bladder, peritoneal and/or pleural lavage and high volume renal haemofilter.

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.

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

Calcium is used to counteract the harmful effects of hyperkalaemia on the heart by stabilizing the cardiac cell membrane and preventing abnormal depolarization. It works quickly, usually within 15 minutes, but its effects are not long-lasting. Calcium is considered a first-line treatment for arrhythmias and significant ECG abnormalities caused by hyperkalaemia, such as widening of the QRS interval, loss of the P wave, and cardiac arrhythmias. However, arrhythmias are rare at potassium levels below 7.5 mmol/l.

It’s important to note that calcium does not lower the serum potassium level. Therefore, it should be used in conjunction with other therapies that actually help reduce potassium levels, such as insulin and salbutamol. If the pH is measured to be above 7.35 and the potassium level remains high despite nebulized salbutamol, the APLS guidelines recommend the administration of an insulin and glucose infusion.

The maximum dose of adrenaline is 2 mg/kg, regardless of its concentration or addition. However, when calculating the volume requirements, the concentration of adrenaline becomes a factor.

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.

Chlamydia trachomatis is a type of Gram-negative bacteria that is responsible for causing the sexually transmitted infection known as chlamydia. This bacterium is typically either coccoid or rod-shaped in its appearance.

There are various serological variants of C. trachomatis, and each variant is associated with different patterns of disease. Specifically, types D-K of this bacterium are responsible for causing genitourinary infections.

Chlamydia is the most commonly diagnosed sexually transmitted infection in the United Kingdom and is also the leading preventable cause of infertility worldwide. Interestingly, around 50% of men infected with chlamydia do not experience any symptoms, while at least 70% of infected women remain asymptomatic. However, if left untreated, chlamydia can lead to complications such as pelvic inflammatory disease, ectopic pregnancy, and tubal infertility in women. In men, it can result in proctitis, epididymitis, and epididymo-orchitis.

Addison’s disease, also known as adrenal insufficiency, is characterized by a gradual onset of symptoms over several weeks, although it can sometimes occur suddenly. The diagnosis of Addison’s disease can be challenging as its symptoms, such as fatigue, muscle pain, weight loss, and nausea, are non-specific. However, a key feature is low blood pressure. The disease is associated with changes in pigmentation, ranging from increased pigmentation due to elevated ACTH levels to the development of vitiligo caused by the autoimmune destruction of melanocytes.

Patients with Addison’s disease often exhibit hyponatremia (low sodium levels) and hyperkalemia (high potassium levels). If the patient is dehydrated, this may be reflected in elevated urea and creatinine levels. While hypercalcemia (high calcium levels) and hypoglycemia (low blood sugar levels) can occur in Addison’s disease, they are less common than hyponatremia and hyperkalemia.

In contrast, diabetes insipidus, characterized by normal or elevated sodium levels, does not cause pigmentation changes. Cushing’s syndrome, which results from excess steroid production, is almost the opposite of Addison’s disease, with hypertension (high blood pressure) and hypokalemia (low potassium levels) being typical symptoms. Phaeochromocytoma, on the other hand, is associated with episodes of high blood pressure and hyperglycemia (high blood sugar levels).

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.

De Quervain’s tenosynovitis is a condition characterized by inflammation and thickening of the sheath that contains the tendons of the extensor pollicis brevis and abductor pollicis longus. This leads to pain on the radial side of the wrist. It is more commonly observed in women, particularly those aged between 30 and 50 years. The condition is often associated with repetitive activities that involve pinching and grasping.

During examination, swelling and tenderness along the tendon sheath may be observed. The tendon sheath itself may also appear thickened. The most pronounced tenderness is usually felt over the tip of the radial styloid. A positive Finkelstein’s test, which involves flexing the wrist and moving it towards the ulnar side while the thumb is flexed across the palm, can help confirm the diagnosis.

Treatment for De Quervain’s tenosynovitis involves avoiding movements that can trigger symptoms and using a thumb splint to immobilize the thumb. In cases where symptoms persist, a local corticosteroid injection or surgical decompression may be considered.

Theophylline is a medication used to treat severe asthma. It is a bronchodilator that comes in modified-release forms, which can maintain therapeutic levels in the blood for 12 hours. Theophylline works by inhibiting phosphodiesterase and blocking the breakdown of cyclic AMP. It also competes with adenosine on A1 and A2 receptors.

Achieving the right dose of theophylline can be challenging because there is a narrow range between therapeutic and toxic levels. The half-life of theophylline can be influenced by various factors, further complicating dosage adjustments. It is recommended to aim for serum levels of 10-20 mg/l six to eight hours after the last dose.

Unlike many other medications, the specific brand of theophylline can significantly impact its effects. Therefore, it is important to prescribe theophylline by both its brand name and generic name.

Several factors can increase the half-life of theophylline, including heart failure, cirrhosis, viral infections, and certain drugs. Conversely, smoking, heavy drinking, and certain medications can decrease the half-life of theophylline.

There are several drugs that can either increase or decrease the plasma concentration of theophylline. Calcium channel blockers, cimetidine, fluconazole, macrolides, methotrexate, and quinolones can increase the concentration. On the other hand, carbamazepine, phenobarbitol, phenytoin, rifampicin, and St. John’s wort can decrease the concentration.

The clinical symptoms of theophylline toxicity are more closely associated with acute overdose rather than chronic overexposure. Common symptoms include headache, dizziness, nausea, vomiting, abdominal pain, rapid heartbeat, dysrhythmias, seizures, mild metabolic acidosis, low potassium, low magnesium, low phosphates, abnormal calcium levels, and high blood sugar.

Seizures are more prevalent in acute overdose cases, while chronic overdose typically presents with minimal gastrointestinal symptoms. Cardiac dysrhythmias are more common in chronic overdose situations compared to acute overdose.

Diabetic ketoacidosis (DKA) is a life-threatening condition that occurs when there is a lack of insulin, leading to an inability to process glucose. This results in high blood sugar levels and excessive thirst. As the body tries to eliminate the excess glucose through urine, dehydration becomes inevitable. Without insulin, the body starts using fat as its main energy source, which leads to the production of ketones and a buildup of acid in the blood.

The main characteristics of DKA are high blood sugar levels (above 11 mmol/l), the presence of ketones in the blood or urine, and acidosis (low bicarbonate levels and/or low venous pH). Symptoms of DKA include nausea, vomiting, excessive thirst, frequent urination, abdominal pain, signs of dehydration, a distinct smell of ketones on the breath, rapid and deep breathing, confusion or reduced consciousness, and cardiovascular symptoms like rapid heartbeat, low blood pressure, and shock.

To diagnose DKA, various tests should be performed, including blood glucose measurement, urine dipstick test (which shows high levels of glucose and ketones), blood ketone assay (more accurate than urine dipstick), complete blood count, and electrolyte levels. Arterial or venous blood gas analysis can confirm the presence of metabolic acidosis.

The management of DKA involves careful fluid administration and insulin replacement. Fluid boluses should only be given if there are signs of shock and should be administered slowly in 10 ml/kg increments. Once shock is resolved, rehydration should be done over 48 hours. The first 20 ml/kg of fluid given for resuscitation should not be subtracted from the total fluid volume calculated for the 48-hour replacement. In cases of hypotensive shock, consultation with a pediatric intensive care specialist may be necessary.

Insulin replacement should begin 1-2 hours after starting intravenous fluid therapy. A soluble insulin infusion should be used at a dosage of 0.05-0.1 units/kg/hour. The goal is to bring blood glucose levels close to normal. Regular monitoring of electrolytes and blood glucose levels is important to prevent imbalances and rapid changes in serum osmolarity. Identifying and treating the underlying cause of DKA is also crucial.

When calculating fluid requirements for children and young people with DKA, assume a 5% fluid deficit for mild-to-moderate cases (blood pH of 7.1 or above) and a 10% fluid deficit in severe DKA (indicated by a blood pH below 7.1). The total replacement fluid to be given over 48 hours is calculated as follows: Hourly rate = (deficit/48 hours) + maintenance per hour.

All of the mentioned medications are antiemetics that can be used to treat nausea. However, cyclizine would be the most appropriate choice as it also possesses anti-histamine properties, which can help alleviate symptoms of vertigo. Ondansetron is a specific 5HT3 antagonist that is particularly effective for patients undergoing cytotoxic treatment. Domperidone acts on the chemoreceptor trigger zone and is also highly beneficial for patients receiving cytotoxic treatment. Metoclopramide directly affects the gastrointestinal tract and is a useful anti-emetic for individuals with gastro-duodenal, hepatic, and biliary diseases. Haloperidol may be considered in end-of-life care situations where other medications have not yielded successful results.

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.

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.

There are two types of infectious agents that can lead to the development of a dendritic ulcer. The majority of cases (80%) are caused by the herpes simplex virus (type I), while the remaining cases (20%) are caused by the herpes zoster virus. To effectively treat this condition, the patient should follow a specific treatment plan. This includes applying aciclovir ointment topically five times a day for a duration of 10 days. Additionally, prednisolone 0.5% drops should be used 2-4 times daily. It is also recommended to take oral high dose vitamin C, as it has been shown to reduce the healing time of dendritic ulcers.

Traveller’s diarrhoea (TD) is a prevalent illness that affects travellers all around the world. It is estimated that up to 50% of Europeans who spend two or more weeks in developing regions experience TD. This condition is characterized by the passage of three or more loose stools within a 24-hour period. Typically, individuals with TD also experience abdominal cramps, nausea, and bloating.

In most cases of gastroenteritis, there is no need for stool microscopy and culture. However, it is advisable to arrange these tests if the patient has recently returned from overseas travel, is severely ill, has prolonged symptoms, comes from an institution, or works as a food handler.

Bacteria are responsible for approximately 80% of TD cases, while viruses and protozoa account for the remaining cases. The most common causative organism is Escherichia coli, with Enterohaemorrhagic Escherichia coli being the strain most likely to cause bloody diarrhoea.

Infective causes of bloody diarrhoea include Campylobacter jejuni, Shigella spp., Salmonella spp., Clostridium difficile, Yersinia spp., Schistosomiasis, and Amoebiasis (Entamoeba histolytica).

Patients who experience post-tonsillectomy bleeding, even if it stops, should be closely monitored and assessed by an ear, nose, and throat specialist before being discharged. It is important to note that minor bleeding episodes may occur before a more severe hemorrhage. Therefore, patients with post-tonsillectomy bleeds, even if they seem to have resolved, should be admitted to the hospital under the care of an ENT specialist.

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.

Indirect inguinal hernias have an elliptical shape, unlike direct hernias which are round. They are not easily reducible and do not reduce spontaneously when reclining. Unlike direct hernias that appear immediately, indirect hernias take longer to appear when standing. They are reduced superiorly and then superolaterally, while direct hernias reduce superiorly and posteriorly. Pressure over the deep inguinal ring helps control indirect hernias. However, they are more prone to strangulation due to the narrow neck of the deep inguinal ring.

The ulnar nerve provides innervation to several muscles in the hand. These include the palmar interossei, dorsal interossei, medial two lumbricals, and abductor digiti minimi. On the other hand, the median nerve innervates the opponens pollicis, lateral two lumbricals, and flexor pollicis brevis. Lastly, the radial nerve is responsible for innervating the extensor digitorum muscle.

A varicocele is a condition characterized by the presence of varicose veins in the pampiniform plexus of the cord and scrotum. It is more commonly observed in the left testis compared to the right and may be linked to infertility. The primary reason for this association is believed to be the elevated temperature of the testis caused by the presence of varicosities.

Typically, individuals with varicocele experience a dull ache in the testis, which tends to worsen after physical activity or towards the end of the day. The scrotum is often described as feeling like a bag of worms. While the varicocele cannot usually be detected when the patient is lying down, it can often be identified during examination while standing. It is felt as a poorly defined, non-transilluminable mass that is clearly separate from the testis and is located above and behind it. The dilation of the varicocele increases when the Valsalva maneuver is performed, and a cough impulse may also be present.

Conservative treatment is typically recommended for varicocele, with surgery being reserved for severe cases only.

According to NICE guidelines, amiodarone is recommended as the initial choice for pharmacological cardioversion of atrial fibrillation (AF) in individuals who have evidence of structural heart disease.

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.

Chancroid is a sexually transmitted infection caused by the bacteria Haemophilus ducreyi. It is not very common in the UK but is prevalent in Africa, Asia, and South America. HIV is often associated with chancroid, particularly in Africa where there is a 60% correlation.

The main symptom of chancroid is the development of painful ulcers on the genitalia. In women, these ulcers typically appear on the labia majora. Sometimes, kissing ulcers can form when ulcers are located on opposing surfaces of the labia. Painful swelling of the lymph nodes occurs in 30-60% of patients, and in some cases, these swollen nodes can turn into abscesses known as buboes.

The CDC recommends treating chancroid with a single oral dose of 1 gram of azithromycin or a single intramuscular dose of ceftriaxone. Alternatively, a 7-day course of oral erythromycin can be used. It’s important to note that Haemophilus ducreyi is resistant to several antibiotics, including penicillins, tetracyclines, trimethoprim, ciprofloxacin, aminoglycosides, and sulfonamides.

Possible complications of chancroid include extensive swelling of the lymph nodes, large abscesses and sinuses in the groin area, phimosis (a condition where the foreskin cannot be retracted), and superinfection with Fusarium spp. or Bacteroides spp.

Syphilis, caused by Treponema pallidum, presents with a painless ulcer called a chancre during its primary stage. This is different from chancroid, which causes painful ulcers. Chlamydia trachomatis can lead to lymphogranuloma venereum, where a painless genital ulcer may develop initially and go unnoticed. Granuloma inguinale, caused by Klebsiella granulomatis, causes painless nodules and ulcers on the genitals that eventually burst and create open, oozing lesions. Neisseria gonorrhoeae, on the other hand, typically causes vaginal or urethral discharge and is often asymptomatic, rather than causing genital ulceration.

Tonsillar herniation occurs when the cerebellar tonsils are pushed through the foramen magnum. This condition is characterized by a decrease in consciousness, respiratory arrest, and flaccid paralysis.

Further Reading:

Intracranial pressure (ICP) refers to the pressure within the craniospinal compartment, which includes neural tissue, blood, and cerebrospinal fluid (CSF). Normal ICP for a supine adult is 5-15 mmHg. The body maintains ICP within a narrow range through shifts in CSF production and absorption. If ICP rises, it can lead to decreased cerebral perfusion pressure, resulting in cerebral hypoperfusion, ischemia, and potentially brain herniation.

The cranium, which houses the brain, is a closed rigid box in adults and cannot expand. It is made up of 8 bones and contains three main components: brain tissue, cerebral blood, and CSF. Brain tissue accounts for about 80% of the intracranial volume, while CSF and blood each account for about 10%. The Monro-Kellie doctrine states that the sum of intracranial volumes is constant, so an increase in one component must be offset by a decrease in the others.

There are various causes of raised ICP, including hematomas, neoplasms, brain abscesses, edema, CSF circulation disorders, venous sinus obstruction, and accelerated hypertension. Symptoms of raised ICP include headache, vomiting, pupillary changes, reduced cognition and consciousness, neurological signs, abnormal fundoscopy, cranial nerve palsy, hemiparesis, bradycardia, high blood pressure, irregular breathing, focal neurological deficits, seizures, stupor, coma, and death.

Measuring ICP typically requires invasive procedures, such as inserting a sensor through the skull. Management of raised ICP involves a multi-faceted approach, including antipyretics to maintain normothermia, seizure control, positioning the patient with a 30º head up tilt, maintaining normal blood pressure, providing analgesia, using drugs to lower ICP (such as mannitol or saline), and inducing hypocapnoeic vasoconstriction through hyperventilation. If these measures are ineffective, second-line therapies like barbiturate coma, optimised hyperventilation, controlled hypothermia, or decompressive craniectomy may be considered.

According to the guidelines of the Difficult Airway Society, it is recommended to limit intubation attempts to a maximum of three. However, if the first three attempts are unsuccessful, a more experienced colleague may make a fourth attempt. If all four attempts are unsuccessful, the intubation should be declared as a failure.

Further Reading:

A difficult airway refers to a situation where factors have been identified that make airway management more challenging. These factors can include body habitus, head and neck anatomy, mouth characteristics, jaw abnormalities, and neck mobility. The LEMON criteria can be used to predict difficult intubation by assessing these factors. The criteria include looking externally at these factors, evaluating the 3-3-2 rule which assesses the space in the mouth and neck, assessing the Mallampati score which measures the distance between the tongue base and roof of the mouth, and considering any upper airway obstructions or reduced neck mobility.

Direct laryngoscopy is a method used to visualize the larynx and assess the size of the tracheal opening. The Cormack-Lehane grading system can be used to classify the tracheal opening, with higher grades indicating more difficult access. In cases of a failed airway, where intubation attempts are unsuccessful and oxygenation cannot be maintained, the immediate priority is to oxygenate the patient and prevent hypoxic brain injury. This can be done through various measures such as using a bag-valve-mask ventilation, high flow oxygen, suctioning, and optimizing head positioning.

If oxygenation cannot be maintained, it is important to call for help from senior medical professionals and obtain a difficult airway trolley if not already available. If basic airway management techniques do not improve oxygenation, further intubation attempts may be considered using different equipment or techniques. If oxygen saturations remain below 90%, a surgical airway such as a cricothyroidotomy may be necessary.

Post-intubation hypoxia can occur for various reasons, and the mnemonic DOPES can be used to identify and address potential problems. DOPES stands for displacement of the endotracheal tube, obstruction, pneumothorax, equipment failure, and stacked breaths. If intubation attempts fail, a maximum of three attempts should be made before moving to an alternative plan, such as using a laryngeal mask airway or considering a cricothyroidotomy.

Hereditary angioedema is a condition caused by a lack of C1 esterase inhibitor, a protein that is part of the complement system. It is typically inherited in an autosomal dominant manner. Symptoms usually start in childhood and continue sporadically into adulthood. Attacks can be triggered by minor surgical procedures, dental work, and stress. The main clinical signs of hereditary angioedema include swelling of the skin and mucous membranes, with the face, tongue, and extremities being the most commonly affected areas. There is often a tingling sensation before an attack, sometimes accompanied by a non-itchy rash.

Angioedema and anaphylaxis resulting from C1 esterase inhibitor deficiency do not respond to adrenaline, steroids, or antihistamines. Treatment requires the use of C1 esterase inhibitor concentrate or fresh frozen plasma, both of which contain C1 esterase inhibitor. In situations that may trigger an attack, short-term prophylaxis can be achieved by administering C1 esterase inhibitor or fresh frozen plasma infusions prior to the event. For long-term prevention, androgenic steroids like stanozolol or antifibrinolytic drugs such as tranexamic acid can be used.

Vomiting is a common occurrence during the early stages of pregnancy, typically happening between 7 and 12 weeks. However, there is a more severe condition called hyperemesis gravidarum, which involves uncontrollable and intense nausea and vomiting. This condition can lead to imbalances in fluids and electrolytes, significant ketonuria, malnutrition, and weight loss. It is relatively rare, affecting less than 1% of pregnancies.

For mild cases of nausea and vomiting in early pregnancy, dietary adjustments and non-pharmacological methods like consuming ginger or using P6 wrist acupressure can often provide relief.

In severe cases where heavy ketonuria and severe dehydration are present, hospital admission is usually necessary for intravenous fluid rehydration. The NICE Clinical Knowledge Summary (CKS) on nausea and vomiting in pregnancy recommends using oral promethazine, oral cyclizine, or oral prochlorperazine as the first-line treatment if an anti-emetic is needed. After 24 hours, the situation should be reassessed to determine if the initial treatment is effective. If not, a second-line drug like metoclopramide or ondansetron should be considered.

It’s important to exercise caution when using metoclopramide in patients under the age of 20 due to the increased risk of extrapyramidal side effects. Additionally, proton pump inhibitors (e.g., omeprazole) and histamine H2-receptor antagonists (e.g., ranitidine) can be beneficial for women experiencing significant dyspepsia alongside their nausea and vomiting.

For more information, refer to the NICE CKS on nausea and vomiting in pregnancy.

The best single test to evaluate thyroid function is TSH. Goitres can be associated with either hypothyroidism or hyperthyroidism, although hypothyroidism is more common. According to NICE guidelines, when there is suspicion of hypothyroidism, it is recommended to first check the TSH level. If the TSH level is above the normal range, then the free thyroxine (FT4) should be checked on the same sample. Similarly, in cases of suspected hyperthyroidism, it is advised to first check the TSH level. If the TSH level is below the normal range, then the free thyroxine (FT4) and free triiodothyronine (FT3) should be checked on the same sample.

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.

Hyperventilation leads to the constriction of blood vessels in the brain, which in turn reduces the flow and volume of blood in the brain, ultimately decreasing intracranial pressure (ICP). This is because hyperventilation lowers the levels of carbon dioxide (PaCO2) in the blood, resulting in an increase in pH and causing the arteries in the brain to constrict and reduce blood flow. As a result, cerebral blood volume and ICP decrease. The effects of hyperventilation are immediate, but they gradually diminish over a period of 6-24 hours as the brain adjusts its bicarbonate levels to normalize pH. However, caution must be exercised when discontinuing hyperventilation after a prolonged period, as the sudden increase in PaCO2 can lead to a rapid rise in cerebral blood flow and a detrimental increase in ICP.

Further Reading:

Intracranial pressure (ICP) refers to the pressure within the craniospinal compartment, which includes neural tissue, blood, and cerebrospinal fluid (CSF). Normal ICP for a supine adult is 5-15 mmHg. The body maintains ICP within a narrow range through shifts in CSF production and absorption. If ICP rises, it can lead to decreased cerebral perfusion pressure, resulting in cerebral hypoperfusion, ischemia, and potentially brain herniation.

The cranium, which houses the brain, is a closed rigid box in adults and cannot expand. It is made up of 8 bones and contains three main components: brain tissue, cerebral blood, and CSF. Brain tissue accounts for about 80% of the intracranial volume, while CSF and blood each account for about 10%. The Monro-Kellie doctrine states that the sum of intracranial volumes is constant, so an increase in one component must be offset by a decrease in the others.

There are various causes of raised ICP, including hematomas, neoplasms, brain abscesses, edema, CSF circulation disorders, venous sinus obstruction, and accelerated hypertension. Symptoms of raised ICP include headache, vomiting, pupillary changes, reduced cognition and consciousness, neurological signs, abnormal fundoscopy, cranial nerve palsy, hemiparesis, bradycardia, high blood pressure, irregular breathing, focal neurological deficits, seizures, stupor, coma, and death.

Measuring ICP typically requires invasive procedures, such as inserting a sensor through the skull. Management of raised ICP involves a multi-faceted approach, including antipyretics to maintain normothermia, seizure control, positioning the patient with a 30º head up tilt, maintaining normal blood pressure, providing analgesia, using drugs to lower ICP (such as mannitol or saline), and inducing hypocapnoeic vasoconstriction through hyperventilation. If these measures are ineffective, second-line therapies like barbiturate coma, optimised hyperventilation, controlled hypothermia, or decompressive craniectomy may be considered.

Triage is a crucial process that involves determining the priority of patients’ treatment based on the severity of their condition and their chances of recovery. Its purpose is to ensure that limited resources are used efficiently, maximizing the number of lives saved. During a major incident, primary triage takes place in the bronze area, which is located within the inner cordon.

In the context of a major incident, priorities are assigned numbers from 1 to 3, with 1 being the highest priority. These priorities are also color-coded for easy identification:
– P1: Immediate priority. This category includes patients who require immediate life-saving intervention to prevent death. They are color-coded red.
– P2: Intermediate priority. Patients in this group also require significant interventions, but their treatment can be delayed for a few hours. They are color-coded yellow.
– P3: Delayed priority. Patients in this category require medical treatment, but it can be safely delayed. This category also includes walking wounded individuals. The classification as P3 is based on the motor score of the Glasgow Coma Scale, which predicts a favorable outcome. They are color-coded green.

The fourth classification is for deceased individuals. It is important to identify and classify them to prevent the unnecessary use of limited resources on those who cannot be helped. Dead bodies should be left in their current location, both to avoid wasting resources and because the area may be considered a crime scene. Deceased individuals are color-coded black.

Acute pancreatitis is a frequently encountered and serious source of acute abdominal pain. It involves the sudden inflammation of the pancreas, leading to the release of enzymes that cause self-digestion of the organ.

The clinical manifestations of acute pancreatitis include severe epigastric pain, accompanied by feelings of nausea and vomiting. The pain may radiate to the T6-T10 dermatomes or even to the shoulder tip through the phrenic nerve if the diaphragm is irritated. Other symptoms may include fever or sepsis, tenderness in the epigastric region, jaundice, and the presence of Gray-Turner sign (bruising on the flank) or Cullen sign (bruising around the belly button).

The most common causes of acute pancreatitis are gallstones and alcohol consumption. Additionally, many cases are considered idiopathic, meaning the cause is unknown. To aid in remembering the various causes, the mnemonic ‘I GET SMASHED’ can be helpful. Each letter represents a potential cause: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion stings, Hyperlipidemia/hypercalcemia, ERCP (endoscopic retrograde cholangiopancreatography), and Drugs.

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

Unstable angina is characterized by the presence of one or more of the following symptoms: angina of effort occurring over a few days with increasing frequency, episodes of angina occurring recurrently and predictably without specific provocation, or an unprovoked and prolonged episode of cardiac chest pain. The electrocardiogram (ECG) may appear normal or show T-wave/ST-segment changes, and cardiac enzymes are typically within normal range.

On the other hand, stable angina is defined by central chest pain that is triggered by activities such as exercise and emotional stress. This pain may radiate to the jaw or left arm and is relieved by resting for a few minutes. It is usually brought on by a predictable amount of exertion.

Prinzmetal angina, although rare, is a variant of angina that primarily occurs at rest between midnight and early morning. The attacks can be severe and tend to happen in clusters. This type of angina is caused by coronary artery spasm, and patients may have normal coronary arteries.

Decubitus angina, on the other hand, is angina that occurs when lying down. It often develops as a result of cardiac failure due to an increased volume of blood within the blood vessels, which places additional strain on the heart.

Lastly, Ludwig’s angina is an extremely serious and potentially life-threatening cellulitis that affects the submandibular area. It most commonly arises from an infection in the floor of the mouth, which then spreads to the submandibular space.

Clostridium difficile infections can range in severity from mild to life-threatening. Mild or moderate severity infections are determined by the frequency of stool and white blood cell count. Severe or life-threatening infections are characterized by high fever, radiological signs, and evidence of organ dysfunction or sepsis.

In this case, the patient’s clinical features indicate a moderate severity C.diff infection. Moderate severity infections typically have an increased white blood cell count but less than 15 x 109/l. They are typically associated with 3-5 loose stools per day.

Further Reading:

Clostridium difficile (C.diff) is a gram positive rod commonly found in hospitals. Some strains of C.diff produce exotoxins that can cause intestinal damage, leading to pseudomembranous colitis. This infection can range from mild diarrhea to severe illness. Antibiotic-associated diarrhea is often caused by C.diff, with 20-30% of cases being attributed to this bacteria. Antibiotics such as clindamycin, cephalosporins, fluoroquinolones, and broad-spectrum penicillins are frequently associated with C.diff infection.

Clinical features of C.diff infection include diarrhea, distinctive smell, abdominal pain, raised white blood cell count, and in severe cases, toxic megacolon. In some severe cases, diarrhea may be absent due to the infection causing paralytic ileus. Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool. There are two types of exotoxins produced by C.diff, toxin A and toxin B, which cause mucosal damage and the formation of a pseudomembrane in the colon.

Risk factors for developing C.diff infection include age over 65, antibiotic treatment, previous C.diff infection, exposure to infected individuals, proton pump inhibitor or H2 receptor antagonist use, prolonged hospitalization or residence in a nursing home, and chronic disease or immunosuppression. Complications of C.diff infection can include toxic megacolon, colon perforation, sepsis, and even death, especially in frail elderly individuals.

Management of C.diff infection involves stopping the causative antibiotic if possible, optimizing hydration with IV fluids if necessary, and assessing the severity of the infection. Treatment options vary based on severity, ranging from no antibiotics for mild cases to vancomycin or fidaxomicin for moderate cases, and hospital protocol antibiotics (such as oral vancomycin with IV metronidazole) for severe or life-threatening cases. Severe cases may require admission under gastroenterology or GI surgeons.

Circumferential burns on the thorax can limit the expansion of the chest and hinder proper ventilation. When burns penetrate deeply, they can cause the formation of dead tissue called eschar, which is usually white or black in color. This eschar is contracted and inflexible compared to healthy tissue, leading to restricted movement and impaired breathing. In some cases, burns on the thorax can result in respiratory failure. Marjolin’s ulcer, a rare condition, refers to the development of squamous cell carcinoma in burnt or scarred tissue. Burn injuries often lead to the release of excess potassium into the bloodstream, which can cause hyperkalemia. Carbon monoxide poisoning typically occurs when someone inhales CO over a prolonged period, usually due to incomplete combustion of hydrocarbons. However, the history provided in this case does not align with prolonged exposure to carbon monoxide.

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.

Dressings that function as flutter valves are beneficial in the initial treatment of open pneumothorax. The first step involves applying an occlusive dressing that covers the wound, with one side intentionally left open to create a flutter-valve effect. Alternatively, a chest seal device can be used. The occlusive dressing should be square or rectangular in shape, with three sides securely sealed and one side left unsealed. When the patient inhales, the dressing is drawn against the chest wall, preventing air from entering the chest cavity. However, during exhalation, air can still escape through the open side of the dressing. Another option is to use a chest seal device that includes a built-in one-way (flutter) valve. Definitive management typically involves surgical intervention to repair the defect and address any other injuries. The Royal College of Emergency Medicine (RCEM) also recommends surgery as the definitive treatment, as inserting a chest drain may disrupt tissues that could otherwise be used to cover the defect with muscle flaps.

Further Reading:

An open pneumothorax, also known as a sucking chest wound, occurs when air enters the pleural space due to an open chest wound or physical defect. This can lead to ineffective ventilation, causing hypoxia and hypercarbia. Air can enter the pleural cavity passively or be sucked in during inspiration, leading to lung collapse on that side. Sucking wounds can be heard audibly as air passes through the chest defect, and entry wounds are usually visible.

To manage an open pneumothorax, respiratory compromise can be alleviated by covering the wound with a dressing or using a chest seal device. It is important to ensure that one side of the dressing is not occluded, allowing the dressing to function as a flutter valve and prevent significant air ingress during inspiration while allowing air to escape the pleural cavity. If tension pneumothorax is suspected after applying a dressing, the dressing may need to be temporarily removed for decompression.

Intubation and intermittent positive pressure ventilation (IPPV) can be used to ventilate the patient and alleviate respiratory distress. Definitive management involves either inserting a chest drain or surgically repairing the defect. Surgical repair is typically preferred, especially for large wounds.

Second degree frostbite is characterized by tissue necrosis that affects both the epidermis and a variable depth of the dermis. However, there is still some healthy dermis present, which allows for regeneration and recovery of the skin. This type of frostbite is often referred to as partial thickness. Clinically, it is observed as the formation of blisters filled with clear or milky fluid on the surface of the skin, accompanied by redness and swelling.

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.

Children who have been diagnosed with Rubella, also known as German measles, should be advised to stay away from school for a period of 5 days from the onset of the rash. It is important to be familiar with the guidelines for excluding children from school due to infectious diseases that present with a rash.

Further Reading:

Rubella, also known as German measles, is a viral infection caused by the togavirus. It used to be more common before the introduction of the MMR vaccine, but now it is rare. Outbreaks of rubella are more common during the winter and spring seasons. The incubation period for rubella is 14-21 days, and individuals are infectious from 7 days before symptoms appear to 4-5 days after the onset of the rash.

The features of rubella include a prodrome, which may include symptoms such as low-grade fever. The rash associated with rubella is maculopapular and initially appears on the face before spreading to the whole body. The rash usually fades by the 3-5 day. Lymphadenopathy, specifically suboccipital and postauricular, is also commonly seen in rubella cases.

Complications of rubella can include arthritis, thrombocytopenia, encephalitis, and myocarditis. However, these complications are rare. Rubella can be particularly dangerous if contracted during pregnancy, as it can lead to congenital rubella syndrome. The risk of fetal damage is highest during the first 8-10 weeks of pregnancy, with a risk as high as 90%. Fetal damage is rare after 16 weeks. Congenital rubella syndrome can result in various complications such as sensorineural deafness, congenital cataracts, congenital heart disease, growth retardation, hepatosplenomegaly, purpuric skin lesions, ‘salt and pepper’ chorioretinitis, microphthalmia, and cerebral palsy.

Diagnosis of rubella can be made by testing for raised IgM antibodies in women who have recently been exposed to the virus. Serological or PCR testing is the gold standard investigation for rubella. A testing kit can be obtained from the Local Health Protection Unit (HPU).

There is no specific treatment for rubella. Antipyretics can be used to manage fever. It is advised to exclude individuals with rubella from school for 5 days from the onset of the rash. Infection during pregnancy should prompt referral to obstetrics. Rubella is a notifiable disease, meaning that it requires notification of the local authority or UKHSA health protection team.

Atropine is a medication that slows down the movement of the digestive system and is not recommended for use in individuals with intestinal blockage. It works by blocking the effects of a neurotransmitter called acetylcholine, which is responsible for promoting gastrointestinal motility and the emptying of the stomach. Therefore, atropine should not be given to patients with gastrointestinal obstruction as it can further hinder the movement of the intestines.

Further Reading:

Types of Heart Block:

1. Atrioventricular (AV) Blocks:
– Disrupt electrical conduction between the atria and ventricles at the AV node.
– Three degrees of AV block: first degree, second degree (type 1 and type 2), and third degree (complete) AV block.

– First degree AV block: PR interval > 0.2 seconds.
– Second degree AV block:
– Type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs.
– Type 2 (Mobitz II): PR interval is constant, but the P wave is often not followed by a QRS complex.
– Third degree (complete) AV block: no association between the P waves and QRS complexes.

Features of complete heart block: syncope, heart failure, regular bradycardia (30-50 bpm), wide pulse pressure, JVP (jugular venous pressure) cannon waves in neck, variable intensity of S1.

2. Bundle Branch Blocks:
– Electrical conduction travels from the bundle of His to the left and right bundle branches.
– Diagnosed when the duration of the QRS complex on the ECG exceeds 120 ms.

– Right bundle branch block (RBBB).
– Left bundle branch block (LBBB).
– Left anterior fascicular block (LAFB).
– Left posterior fascicular block (LPFB).
– Bifascicular block.
– Trifascicular block.

ECG features of bundle branch blocks:
– RBBB: QRS duration > 120 ms, RSR’ pattern in V1-3 (M-shaped QRS complex), wide S wave in lateral leads (I, aVL, V5-6).
– LBBB: QRS duration > 120 ms, dominant S wave in V1, broad, notched (‘M’-shaped) R wave in V6, broad monophasic R wave in lateral leads (I, aVL, V5-6), absence of Q waves in lateral leads, prolonged R wave peak time > 60 ms in leads V5-6.

WiLLiaM MaRROW is a useful mnemonic for remembering the morphology of the QRS in leads V1 and V6 for LBBB.

The CIWA scale, also known as the Clinical Institute Withdrawal Assessment for Alcohol scale, is a scale consisting of ten items that is utilized in the evaluation and management of alcohol withdrawal. It is currently recommended by both NICE and the Royal College of Emergency Medicine for assessing patients experiencing acute alcohol withdrawal. The maximum score on the CIWA scale is 67, with scores indicating the severity of withdrawal symptoms. A score of less than 5 suggests mild withdrawal, while a score between 6 and 20 indicates moderate withdrawal. Any score above 20 is considered severe withdrawal. The ten items evaluated on the scale encompass common symptoms and signs of alcohol withdrawal, such as nausea/vomiting, tremors, sweating, anxiety, agitation, sensory disturbances, and cognitive impairments.

In addition to the CIWA scale, there are other screening tools available for assessing various conditions. The CAGE questionnaire is commonly used to screen for alcohol-related issues. The STEPI is utilized as a screening tool for early symptoms of the schizophrenia prodrome. The EPDS is an evidence-based questionnaire that can be employed to screen for postnatal depression. Lastly, the SCOFF questionnaire is a screening tool used to identify the possible presence of eating disorders.

For further information on the assessment and management of acute alcohol withdrawal, the NICE pathway is a valuable resource. The RCEM syllabus also provides relevant information on this topic. Additionally, the MHC1 module on alcohol and substance misuse offers further reading material for those interested in this subject.

Theophylline is a medication used to treat severe asthma. It is a bronchodilator that comes in modified-release forms, which can maintain therapeutic levels in the blood for 12 hours. Theophylline works by inhibiting phosphodiesterase and blocking the breakdown of cyclic AMP. It also competes with adenosine on A1 and A2 receptors.

Achieving the right dose of theophylline can be challenging because there is a narrow range between therapeutic and toxic levels. The half-life of theophylline can be influenced by various factors, further complicating dosage adjustments. It is recommended to aim for serum levels of 10-20 mg/l six to eight hours after the last dose.

Unlike many other medications, the specific brand of theophylline can significantly impact its effects. Therefore, it is important to prescribe theophylline by both its brand name and generic name.

Several factors can increase the half-life of theophylline, including heart failure, cirrhosis, viral infections, and certain drugs. Conversely, smoking, heavy drinking, and certain medications can decrease the half-life of theophylline.

There are several drugs that can either increase or decrease the plasma concentration of theophylline. Calcium channel blockers, cimetidine, fluconazole, macrolides, methotrexate, and quinolones can increase the concentration. On the other hand, carbamazepine, phenobarbitol, phenytoin, rifampicin, and St. John’s wort can decrease the concentration.

The clinical symptoms of theophylline toxicity are more closely associated with acute overdose rather than chronic overexposure. Common symptoms include headache, dizziness, nausea, vomiting, abdominal pain, rapid heartbeat, dysrhythmias, seizures, mild metabolic acidosis, low potassium, low magnesium, low phosphates, abnormal calcium levels, and high blood sugar.

Seizures are more prevalent in acute overdose cases, while chronic overdose typically presents with minimal gastrointestinal symptoms. Cardiac dysrhythmias are more common in chronic overdose situations compared to acute overdose.

Eclampsia is the most likely diagnosis in this case. It is characterized by the occurrence of one or more convulsions on top of pre-eclampsia. To control seizures in eclampsia, the recommended treatment is magnesium sulphate. The Collaborative Eclampsia Trial regimen should be followed for administering magnesium sulphate. Initially, a loading dose of 4 g should be given intravenously over 5 to 15 minutes. This should be followed by a continuous infusion of 1 g per hour for 24 hours. If the woman experiences another eclamptic seizure, the infusion should be continued for an additional 24 hours after the last seizure. In case of recurrent seizures, a further dose of 2-4 g should be administered intravenously over 5 to 15 minutes. It is important to note that the only cure for eclampsia is the delivery of the fetus and placenta. Once the patient is stabilized, she should be prepared for an emergency caesarean section.

This patient’s symptoms are consistent with a diagnosis of oesophageal candidiasis, which is commonly seen in patients undergoing treatment for haematopoietic or lymphatic malignancies.

The classic combination of symptoms associated with oesophageal candidiasis includes dysphagia, odynophagia, and retrosternal pain. This infection can be life-threatening and often requires hospital admission.

The recommended treatment for oesophageal candidiasis is as follows:

– First-line treatment involves taking oral fluconazole at a daily dose of 200-400 mg.
– If the patient is unable to tolerate oral treatment, intravenous fluconazole can be used instead.
– Second-line treatment options include oral itraconazole, oral posaconazole, or intravenous or oral voriconazole.

It is important to seek medical attention promptly for oesophageal candidiasis, as timely treatment is crucial in managing this potentially serious infection.

To treat low sodium levels, a solution of sodium chloride is administered. It is important to regularly monitor plasma sodium levels every 2 hours during this treatment, but it is crucial to avoid taking samples from the arm where the IV is inserted. The increase in serum sodium should not exceed 2 mmol/L per hour and should not exceed 8 to 10 mmol/L within a 24-hour period. Hypertonic saline is administered intravenously until neurological symptoms improve.

Further Reading:

Syndrome of inappropriate antidiuretic hormone (SIADH) is a condition characterized by low sodium levels in the blood due to excessive secretion of antidiuretic hormone (ADH). ADH, also known as arginine vasopressin (AVP), is responsible for promoting water and sodium reabsorption in the body. SIADH occurs when there is impaired free water excretion, leading to euvolemic (normal fluid volume) hypotonic hyponatremia.

There are various causes of SIADH, including malignancies such as small cell lung cancer, stomach cancer, and prostate cancer, as well as neurological conditions like stroke, subarachnoid hemorrhage, and meningitis. Infections such as tuberculosis and pneumonia, as well as certain medications like thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs), can also contribute to SIADH.

The diagnostic features of SIADH include low plasma osmolality, inappropriately elevated urine osmolality, urinary sodium levels above 30 mmol/L, and euvolemic. Symptoms of hyponatremia, which is a common consequence of SIADH, include nausea, vomiting, headache, confusion, lethargy, muscle weakness, seizures, and coma.

Management of SIADH involves correcting hyponatremia slowly to avoid complications such as central pontine myelinolysis. The underlying cause of SIADH should be treated if possible, such as discontinuing causative medications. Fluid restriction is typically recommended, with a daily limit of around 1000 ml for adults. In severe cases with neurological symptoms, intravenous hypertonic saline may be used. Medications like demeclocycline, which blocks ADH receptors, or ADH receptor antagonists like tolvaptan may also be considered.

It is important to monitor serum sodium levels closely during treatment, especially if using hypertonic saline, to prevent rapid correction that can lead to central pontine myelinolysis. Osmolality abnormalities can help determine the underlying cause of hyponatremia, with increased urine osmolality indicating dehydration or renal disease, and decreased urine osmolality suggesting SIADH or overhydration.

For the treatment of pregnant women with lower urinary tract infections (UTIs), it is recommended to provide them with an immediate prescription for antibiotics. It is important to consider their previous urine culture and susceptibility results, as well as any prior use of antibiotics that may have contributed to the development of resistant bacteria. Before starting antibiotics, it is advised to obtain a midstream urine sample from pregnant women and send it for culture and susceptibility testing.

Once the microbiological results are available, it is necessary to review the choice of antibiotic. If the bacteria are found to be resistant, it is recommended to switch to a narrow-spectrum antibiotic whenever possible. The choice of antibiotics for pregnant women aged 12 years and over is summarized below:

First-choice:
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days, if the estimated glomerular filtration rate (eGFR) is above 45 ml/minute.

Second-choice (if there is no improvement in lower UTI symptoms with the first-choice antibiotic for at least 48 hours, or if the first-choice is not suitable):
– Amoxicillin 500 mg taken orally three times daily for 7 days (only if culture results are available and show susceptibility).
– Cefalexin 500 mg taken twice daily for 7 days.

For alternative second-choice antibiotics, it is recommended to consult a local microbiologist and choose the appropriate antibiotics based on the culture and sensitivity results.

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.

Prolongation of the QT interval can lead to a dangerous ventricular arrhythmia called torsades de pointes, which can result in sudden cardiac death. There are several commonly used medications that are known to cause QT prolongation.

Low levels of potassium (hypokalaemia) and magnesium (hypomagnesaemia) can increase the risk of QT prolongation. For example, diuretics can interact with QT-prolonging drugs by causing hypokalaemia.

The QT interval varies with heart rate, and formulas are used to correct the QT interval for heart rate. Once corrected, it is referred to as the QTc interval. The QTc interval is typically reported on the ECG printout. A normal QTc interval is less than 440 ms.

If the QTc interval is greater than 440 ms but less than 500 ms, it is considered borderline. Although there may be some variation in the literature, a QTc interval within these values is generally considered borderline prolonged. In such cases, it is important to consider reducing the dose of QT-prolonging drugs or switching to an alternative medication that does not prolong the QT interval.

A prolonged QTc interval exceeding 500 ms is clinically significant and is likely to increase the risk of arrhythmia. Any medications that prolong the QT interval should be reviewed immediately.

Here are some commonly encountered drugs that are known to prolong the QT interval:

Antimicrobials:
– Erythromycin
– Clarithromycin
– Moxifloxacin
– Fluconazole
– Ketoconazole

Antiarrhythmics:
– Dronedarone
– Sotalol
– Quinidine
– Amiodarone
– Flecainide

Antipsychotics:
– Risperidone
– Fluphenazine
– Haloperidol
– Pimozide
– Chlorpromazine
– Quetiapine
– Clozapine

Antidepressants:
– Citalopram/escitalopram
– Amitriptyline
– Clomipramine
– Dosulepin
– Doxepin
– Imipramine
– Lofepramine

Antiemetics:
– Domperidone
– Droperidol
– Ondansetron/Granisetron

Others:
– Methadone
– Protein kinase inhibitors (e.g. sunitinib)

The first-rank symptoms of schizophrenia, as described by Kurt Schneider, include auditory hallucinations such as hearing 3rd person voices discussing the patient, experiencing thought echo, and receiving commentary on one’s actions. Additionally, passivity phenomena may occur, such as thought insertion, thought withdrawal, thought broadcast, and feelings of thoughts and actions being under external control. Delusions, which can be primary or secondary, are also common in schizophrenia.

On the other hand, chronic schizophrenia is characterized by negative symptoms. These include poor motivation and self-care, social withdrawal, depression, flat and blunted affect, emotional incongruity, decreased activity, and poverty of thought and speech. These symptoms are often present in individuals with chronic schizophrenia.

This man is experiencing an acute asthma episode. His initial peak flow is 55% of his best, indicating a moderate exacerbation according to the BTS guidelines. Acute asthma can be classified as moderate, acute severe, life-threatening, or near-fatal.

Moderate asthma is characterized by increasing symptoms and a peak expiratory flow rate (PEFR) between 50-75% of the individual’s best or predicted value. There are no signs of acute severe asthma in this case.

Acute severe asthma is identified by any one of the following criteria: a PEFR between 33-50% of the best or predicted value, a respiratory rate exceeding 25 breaths per minute, a heart rate over 110 beats per minute, or the inability to complete sentences in one breath.

Life-threatening asthma is indicated by any one of the following: a PEFR below 33% of the best or predicted value, oxygen saturation (SpO2) below 92%, arterial oxygen pressure (PaO2) below 8 kPa, normal arterial carbon dioxide pressure (PaCO2) between 4.6-6.0 kPa, a silent chest, cyanosis, poor respiratory effort, arrhythmia, exhaustion, altered conscious level, or hypotension.

Near-fatal asthma is characterized by elevated PaCO2 levels and/or the need for mechanical ventilation with increased inflation pressures.

Urinary alkalinisation aims to achieve a urinary pH of 7.5-8.5. This process helps enhance the elimination of salicylates. It is important to regularly monitor urinary pH, ideally on an hourly basis.

Further Reading:

Salicylate poisoning, particularly from aspirin overdose, is a common cause of poisoning in the UK. One important concept to understand is that salicylate overdose leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the overdose stimulates the respiratory center, leading to hyperventilation and respiratory alkalosis. However, as the effects of salicylate on lactic acid production, breakdown into acidic metabolites, and acute renal injury occur, it can result in high anion gap metabolic acidosis.

The clinical features of salicylate poisoning include hyperventilation, tinnitus, lethargy, sweating, pyrexia (fever), nausea/vomiting, hyperglycemia and hypoglycemia, seizures, and coma.

When investigating salicylate poisoning, it is important to measure salicylate levels in the blood. The sample should be taken at least 2 hours after ingestion for symptomatic patients or 4 hours for asymptomatic patients. The measurement should be repeated every 2-3 hours until the levels start to decrease. Other investigations include arterial blood gas analysis, electrolyte levels (U&Es), complete blood count (FBC), coagulation studies (raised INR/PTR), urinary pH, and blood glucose levels.

To manage salicylate poisoning, an ABC approach should be followed to ensure a patent airway and adequate ventilation. Activated charcoal can be administered if the patient presents within 1 hour of ingestion. Oral or intravenous fluids should be given to optimize intravascular volume. Hypokalemia and hypoglycemia should be corrected. Urinary alkalinization with intravenous sodium bicarbonate can enhance the elimination of aspirin in the urine. In severe cases, hemodialysis may be necessary.

Urinary alkalinization involves targeting a urinary pH of 7.5-8.5 and checking it hourly. It is important to monitor for hypokalemia as alkalinization can cause potassium to shift from plasma into cells. Potassium levels should be checked every 1-2 hours.

In cases where the salicylate concentration is high (above 500 mg/L in adults or 350 mg/L in children), sodium bicarbonate can be administered intravenously. Hemodialysis is the treatment of choice for severe poisoning and may be indicated in cases of high salicylate levels, resistant metabolic acidosis, acute kidney injury, pulmonary edema, seizures and coma.

The recommended dosage of buccal midazolam for treating a child experiencing seizures is 0.5 mg per kilogram of body weight.

Bronchiolitis is a common respiratory infection that primarily affects infants. It typically occurs between the ages of 3-6 months and is most prevalent during the winter months from November to March. The main culprit behind bronchiolitis is the respiratory syncytial virus, accounting for about 70% of cases. However, other viruses like parainfluenza, influenza, adenovirus, coronavirus, and rhinovirus can also cause this infection.

The clinical presentation of bronchiolitis usually starts with symptoms resembling a common cold, which last for the first 2-3 days. Infants may experience poor feeding, rapid breathing (tachypnoea), nasal flaring, and grunting. Chest wall recessions, bilateral fine crepitations, and wheezing may also be observed. In severe cases, apnoea, a temporary cessation of breathing, can occur.

Bronchiolitis is a self-limiting illness, meaning it resolves on its own over time. Therefore, treatment mainly focuses on supportive care. However, infants with oxygen saturations below 92% may require oxygen administration. If an infant is unable to maintain oral intake or hydration, nasogastric feeding should be considered. Nasal suction is recommended to clear secretions in infants experiencing respiratory distress due to nasal blockage.

It is important to note that there is no evidence supporting the use of antivirals (such as ribavirin), antibiotics, beta 2 agonists, anticholinergics, or corticosteroids in the management of bronchiolitis. These interventions are not recommended for this condition.

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

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.

Sexually transmitted eye infections can be quite severe and are often characterized by prolonged mucopurulent discharge. The two main causes of these infections are Chlamydia trachomatis and Neisseria gonorrhoea. Differentiating between the two can be done by considering certain features.

Chlamydia trachomatis infection typically presents with chronic low-grade irritation and mucous discharge that lasts for more than two weeks in sexually active individuals. Pre-auricular lymphadenopathy, or swelling of the lymph nodes in front of the ear, may also be present. Most cases of this infection are unilateral, affecting only one eye, but there is a possibility of it being bilateral, affecting both eyes.

On the other hand, Neisseria gonorrhoea infection tends to develop rapidly, usually within 12 to 24 hours. It is characterized by copious mucopurulent discharge, swelling of the eyelids, and tender preauricular lymphadenopathy. This type of infection carries a higher risk of complications, such as uveitis, severe keratitis, and corneal perforation.

Based on the patient’s symptoms, it appears that they are more consistent with a Chlamydia trachomatis infection, especially considering the slower and more gradual onset of their symptoms.

There is ongoing debate regarding the most effective antibiotic treatment for these infections. Some options include topical tetracycline ointment to be applied four times a day for six weeks, oral doxycycline to be taken twice a day for one to two weeks, oral azithromycin with a single dose of 1 gram followed by 500 mg orally for two days, or oral erythromycin to be taken four times a day for one week.

It is recommended to administer sodium chloride solution gradually over a period of 10-15 minutes. If the systolic does not respond adequately, the bolus dose may need to be repeated. It is important to note that patients with DKA often have a fluid deficit of more than 5 liters, which should be taken into consideration.

Further Reading:

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.

In pediatric patients who have sustained burns in a house fire, the presence of burns greater than 15% of the total body surface area should trigger the initiation of immediate fluid resuscitation.

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.

In infants who are less than 4 weeks old, it is recommended to measure their body temperature using an electronic thermometer placed in the armpit.

For children between the ages of 4 weeks and 5 years, there are several methods that can be used to measure body temperature. These include using an electronic thermometer in the armpit, a chemical dot thermometer in the armpit, or an infra-red tympanic thermometer.

It is important to note that measuring temperature orally or rectally should be avoided in this age group. Additionally, forehead chemical thermometers are not reliable and should not be used.

Glucagon may be an option for individuals experiencing anaphylaxis while taking beta blockers. However, it should not be chosen over Adrenaline as the primary treatment. Glucagon stimulates the production of cyclic AMP, which helps to increase heart contractility and heart rate, both of which are necessary during anaphylaxis. It is important to note that rapid administration of glucagon may lead to adverse effects such as nausea and vomiting.

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.
https://www.resus.org.uk/sites/default/files/2021-05/Emergency%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf

The recommended first line analgesics for mild pain are oral or rectal paracetamol and oral ibuprofen. When it comes to treating mild pain in children, it is best to consider either giving a loading dose of oral/rectal paracetamol at a rate of 20 mg/kg, followed by a maintenance dose of 15 mg/kg every 4-6 hours. Alternatively, oral ibuprofen can be administered at a rate of 10 mg/kg every 6-8 hours.

Further Reading:

Assessment and alleviation of pain should be a priority when treating ill and injured children, according to the RCEM QEC standards. These standards state that all children attending the Emergency Department should receive analgesia for moderate and severe pain within 20 minutes of arrival. The effectiveness of the analgesia should be re-evaluated within 60 minutes of receiving the first dose. Additionally, patients in moderate pain should be offered oral analgesia at triage or assessment.

Pain assessment in children should take into account their age. Visual analogue pain scales are commonly used, and the RCEM has developed its own version of this. Other indicators of pain, such as crying, limping, and holding or not-moving limbs, should also be observed and utilized in the pain assessment.

Managing pain in children involves a combination of psychological strategies, non-pharmacological adjuncts, and pharmacological methods. Psychological strategies include involving parents, providing cuddles, and utilizing child-friendly environments with toys. Explanation and reassurance are also important in building trust. Distraction with stories, toys, and activities can help divert the child’s attention from the pain.

Non-pharmacological adjuncts for pain relief in children include limb immobilization with slings, plasters, or splints, as well as dressings and other treatments such as reduction of dislocation or trephine subungual hematoma.

Pharmacological methods for pain relief in children include the use of anesthetics, analgesics, and sedation. Topical anesthetics, such as lidocaine with prilocaine cream, tetracaine gel, or ethyl chloride spray, should be considered for children who are likely to require venesection or placement of an intravenous cannula.

Procedural sedation in children often utilizes either ketamine or midazolam. When administering analgesia, the analgesic ladder should be followed as recommended by the RCEM.

Overall, effective pain management in children requires a comprehensive approach that addresses both the physical and psychological aspects of pain. By prioritizing pain assessment and providing appropriate pain relief, healthcare professionals can help alleviate the suffering of ill and injured children.

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.

Patients who have bradycardia and show ventricular pauses longer than 3 seconds on an electrocardiogram (ECG) are at a high risk of developing asystole. The following characteristics are indicators of a high risk for asystole: recent episodes of asystole, Mobitz II AV block, third-degree AV block (also known as complete heart block) with a broad QRS complex, and ventricular pauses longer than 3 seconds.

Further Reading:

Causes of Bradycardia:
– Physiological: Athletes, sleeping
– Cardiac conduction dysfunction: Atrioventricular block, sinus node disease
– Vasovagal & autonomic mediated: Vasovagal episodes, carotid sinus hypersensitivity
– Hypothermia
– Metabolic & electrolyte disturbances: Hypothyroidism, hyperkalaemia, hypermagnesemia
– Drugs: Beta-blockers, calcium channel blockers, digoxin, amiodarone
– Head injury: Cushing’s response
– Infections: Endocarditis
– Other: Sarcoidosis, amyloidosis

Presenting symptoms of Bradycardia:
– Presyncope (dizziness, lightheadedness)
– Syncope
– Breathlessness
– Weakness
– Chest pain
– Nausea

Management of Bradycardia:
– Assess and monitor for adverse features (shock, syncope, myocardial ischaemia, heart failure)
– Treat reversible causes of bradycardia
– Pharmacological treatment: Atropine is first-line, adrenaline and isoprenaline are second-line
– Transcutaneous pacing if atropine is ineffective
– Other drugs that may be used: Aminophylline, dopamine, glucagon, glycopyrrolate

Bradycardia Algorithm:
– Follow the algorithm for management of bradycardia, which includes assessing and monitoring for adverse features, treating reversible causes, and using appropriate medications or pacing as needed.
https://acls-algorithms.com/wp-content/uploads/2020/12/Website-Bradycardia-Algorithm-Diagram.pdf

Aortic dissection is a condition that occurs when the middle layer of the aorta, known as the tunica media, becomes weakened. This weakening leads to the development of cases of aortic dissection.

Further Reading:

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

Distinguishing between unstable angina and other acute coronary syndromes can be done by looking at normal troponin results. If serial troponin tests come back negative, it can rule out a diagnosis of myocardial infarction. Unstable angina is characterized by myocardial ischemia occurring at rest or with minimal exertion, without any acute damage or death of heart muscle cells. The patient in question shows ECG and biochemical features that align with this definition. Vincent’s angina, on the other hand, refers to an infection in the throat accompanied by ulcerative gingivitis.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

Plasmodium falciparum malaria is transmitted by female mosquitoes of the Anopheles genus. The Aedes genus, on the other hand, is responsible for spreading diseases like dengue fever and yellow fever. The parasite enters hepatocytes and undergoes asexual reproduction, resulting in the release of merozoites into the bloodstream. These merozoites then invade the red blood cells of the host. The incubation period for Plasmodium falciparum malaria ranges from 7 to 14 days.

The main symptom of malaria is known as the malarial paroxysm, which consists of a cyclical pattern of cold chills, followed by a stage of intense heat, and finally a period of profuse sweating as the fever subsides. However, some individuals may experience a continuous fever instead.

Currently, the recommended treatment for P. falciparum malaria is artemisinin-based combination therapy (ACT). This involves combining fast-acting artemisinin-based compounds with drugs from a different class. Companion drugs used in ACT include lumefantrine, mefloquine, amodiaquine, sulfadoxine/pyrimethamine, piperaquine, and chlorproguanil/dapsone. Artemisinin derivatives such as dihydroartemisinin, artesunate, and artemether are also used.

If artemisinin combination therapy is not available, oral quinine or atovaquone with proguanil hydrochloride can be used as an alternative. However, quinine is not well-tolerated for prolonged treatment and should be combined with another drug, typically oral doxycycline (or clindamycin for pregnant women and young children).

Severe or complicated cases of falciparum malaria require specialized care in a high dependency unit or intensive care setting. Intravenous artesunate is recommended for all patients with severe or complicated falciparum malaria, as well as those at high risk of developing severe disease (e.g., if more than 2% of red blood cells are parasitized) or if the patient is unable to take oral treatment. After a minimum of 24 hours of intravenous artesunate treatment and improvement in the patient’s condition, a full course of artemisinin combination therapy should be administered orally.

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 appropriate dosage of suxamethonium for rapid sequence intubation (RSI) in adults is between 1 and 1.5 milligrams per kilogram of body weight.

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.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This results in the accumulation of urea and other waste products in the body and disrupts the balance of fluids and electrolytes. 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.

The causes of AKI can be categorized into pre-renal, intrinsic renal, and post-renal factors. The majority of AKI cases that develop outside of healthcare settings are due to pre-renal causes, accounting for 90% of cases. These causes typically involve low blood pressure associated with conditions like sepsis and fluid depletion. Medications, particularly ACE inhibitors and NSAIDs, are also frequently implicated.

Pre-renal:
– Volume depletion (e.g., severe bleeding, excessive vomiting or diarrhea, burns)
– Oedematous states (e.g., heart failure, liver cirrhosis, nephrotic syndrome)
– Low blood pressure (e.g., cardiogenic shock, sepsis, anaphylaxis)
– Cardiovascular conditions (e.g., severe heart failure, arrhythmias)
– Renal hypoperfusion: NSAIDs, COX-2 inhibitors, ACE inhibitors or ARBs, abdominal aortic aneurysm
– Renal artery stenosis
– Hepatorenal syndrome

Intrinsic renal:
– Glomerular diseases (e.g., glomerulonephritis, thrombosis, hemolytic-uremic syndrome)
– Tubular injury: acute tubular necrosis (ATN) following prolonged lack of blood supply
– Acute interstitial nephritis due to drugs (e.g., NSAIDs), infection, or autoimmune diseases
– Vascular diseases (e.g., vasculitis, polyarteritis nodosa, thrombotic microangiopathy, cholesterol emboli, renal vein thrombosis, malignant hypertension)
– Eclampsia

Post-renal:
– Kidney stones
– Blood clot
– Papillary necrosis
– Urethral stricture
– Prostatic hypertrophy or malignancy
– Bladder tumor
– Radiation fibrosis
– Pelvic malignancy
– Retroperitoneal

The tricuspid valve is the most commonly affected valve in cases of infective endocarditis among intravenous drug users. This means that when IV drug users develop infective endocarditis, it is most likely to affect the tricuspid valve. On the other hand, in cases of native valve endocarditis and prosthetic valve endocarditis, the mitral valve is the valve that is most commonly affected.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

Respiratory alkalosis can be caused by hyperventilation, such as during periods of anxiety. It can also be a result of conditions like pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, or the early stages of aspirin overdose.

Respiratory acidosis is often associated with chronic obstructive pulmonary disease (COPD) or life-threatening asthma. Other causes include pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or certain medications.

Metabolic alkalosis can occur due to vomiting, potassium depletion (often caused by diuretic usage), Cushing’s syndrome, or Conn’s syndrome.

Metabolic acidosis with a raised anion gap can be caused by conditions like lactic acidosis (which can result from hypoxemia, shock, sepsis, or infarction) or ketoacidosis (commonly seen in diabetes, starvation, or alcohol excess). Other causes include renal failure or poisoning (such as late stages of aspirin overdose, methanol, or ethylene glycol).

Metabolic acidosis with a normal anion gap can be attributed to conditions like renal tubular acidosis, diarrhea, ammonium chloride ingestion, or adrenal insufficiency.

Here are some suggestions for managing breathlessness in the final days of life, as provided by NICE:

1. It is important to identify and treat any reversible causes of breathlessness in the dying person, such as pulmonary edema or pleural effusion.

2. Non-pharmacological methods can be considered for managing breathlessness in someone nearing the end of life. It is not recommended to start oxygen therapy as a routine measure. Oxygen should only be offered to individuals who are known or suspected to have symptomatic hypoxemia.

3. Breathlessness can be managed using different medications, including opioids, benzodiazepines, or a combination of both.

For more detailed information, you can refer to the NICE guidance on the care of dying adults in the last days of life. https://www.nice.org.uk/guidance/ng31

Transfusion transmitted bacterial infection is a rare complication that can occur during blood transfusion. It is more commonly associated with platelet transfusion, as platelets are stored at room temperature. Additionally, previously frozen components that are thawed using a water bath and red cell components stored for several weeks are also at a higher risk for bacterial infection.

Both Gram-positive and Gram-negative bacteria have been implicated in transfusion-transmitted bacterial infection, but Gram-negative bacteria are known to cause more severe illness and have higher rates of morbidity and mortality. Among the bacterial organisms, Yersinia enterocolitica is the most commonly associated with this type of infection. This particular organism is able to multiply at low temperatures and utilizes iron as a nutrient, making it well-suited for proliferation in blood stores.

The clinical features of transfusion-transmitted bacterial infection typically manifest shortly after the transfusion begins. These features include a high fever, chills and rigors, nausea and vomiting, tachycardia, hypotension, and even circulatory collapse.

If there is suspicion of a transfusion-transmitted bacterial infection, it is crucial to immediately stop the transfusion. Blood cultures and a Gram-stain should be requested to identify the specific bacteria causing the infection. Broad-spectrum antibiotics should be initiated promptly. Furthermore, the blood pack should be returned to the blood bank urgently for culture and Gram-stain analysis.

In cases where there are no contraindications, high-dose NSAIDs are the recommended initial treatment for acute gout. A commonly used and effective regimen is to administer a stat dose of Naproxen 750 mg, followed by 250 mg three times a day. It is important to note that Aspirin should not be used in gout as it hinders the urinary clearance of urate and interferes with the action of uricosuric agents. Instead, more appropriate choices include Naproxen, diclofenac, or indomethacin.

Allopurinol is typically used as a prophylactic measure to prevent future gout attacks by reducing serum uric acid levels. However, it should not be initiated during the acute phase of an attack as it can worsen the severity and duration of symptoms.

Colchicine works by binding to tubulin and preventing neutrophil migration into the joint. It is just as effective as NSAIDs in relieving acute gout attacks. Additionally, it has a role in prophylactic treatment if a patient cannot tolerate Allopurinol.

It is important to note that NSAIDs are contraindicated in patients with heart failure as they can lead to fluid retention and congestive cardiac failure. In such cases, Colchicine is the preferred treatment option for patients with heart failure or those who cannot tolerate NSAIDs.

First and foremost, the immediate concern is providing first aid for the wound. It is important to wash the wound with soap (or chlorhexidine) and water, while gently encouraging bleeding. It is crucial not to scrub or suck the wound. Additionally, if there are any splashes or body fluid that come into contact with the eyes or mouth, they should be thoroughly washed.

For all healthcare workers who experience a needlestick injury, it is necessary to have a baseline serum sample taken and stored. This should be arranged through occupational health. The subsequent management of the injury depends on the risk of blood-borne virus transmission. This risk is determined by factors such as the source patient’s history (e.g. IV drug use), the circumstances of the injury (e.g. visible blood on the device, use of personal protection equipment), and the healthcare worker’s own characteristics (e.g. response to hepatitis B vaccination).

If the patient consents after appropriate counseling, blood may be taken from the source patient for blood-borne virus testing. However, it is important to note that the injured healthcare worker should not be responsible for counseling and obtaining consent from the patient. Lastly, all needlestick injuries should be reported to the Health Protection Agency.

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.

Colonoscopy with histology is a useful tool in determining the extent and severity of ulcerative colitis. Chronic bloody diarrhea, lasting for more than four weeks, can be caused by various conditions. In this age group, the top differentials include inflammatory bowel disease (IBD) and infective causes such as C.diff and giardia. Other potential causes include drug use (such as laxatives and alcohol), hyperthyroidism (usually accompanied by other signs), coeliac disease (although blood in the stool is not a common symptom), and malabsorption syndromes like pancreatic insufficiency.

When IBD is suspected, fecal calprotectin is often tested and typically found to be elevated. This test is usually performed before colonoscopy and biopsy in individuals under 40 years old. However, in those over 40, a colonoscopy is often the initial investigation to assess for possible underlying malignancy. It is important to note that calprotectin is not specific to IBD and can also be elevated in other conditions such as infectious enteritis and colorectal neoplasia, which limits its diagnostic value. NICE guidelines advise against using calprotectin in individuals with bloody diarrhea.

Initial investigations for chronic bloody diarrhea should include thyroid function testing, coeliac screening, and stool analysis for microscopy and culture. It is worth noting that different hospitals may vary in the specific tests included in stool microscopy and culture, but most labs will typically test for ova, cysts, and parasites. Stool antigen tests are commonly used to detect H.pylori. Vitamin B12 testing may also be appropriate, although deficiency in this vitamin usually leads to a macrocytic anemia and is therefore unlikely to contribute significantly to the diagnosis.

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.

Dexamethasone is the preferred medication for treating Acute Mountain Sickness (AMS) and High Altitude Cerebral Edema (HACE). In cases of mild AMS, simply halting the ascent and giving the body time to acclimatize may be sufficient. However, if mild AMS persists or worsens, or if the patient experiences moderate to severe AMS, descending to a lower altitude is the most effective treatment, preferably with the addition of supplemental oxygen. Dexamethasone is the recommended medication for managing both AMS and HACE.

Further Reading:

High Altitude Illnesses

Altitude & Hypoxia:
– As altitude increases, atmospheric pressure decreases and inspired oxygen pressure falls.
– Hypoxia occurs at altitude due to decreased inspired oxygen.
– At 5500m, inspired oxygen is approximately half that at sea level, and at 8900m, it is less than a third.

Acute Mountain Sickness (AMS):
– AMS is a clinical syndrome caused by hypoxia at altitude.
– Symptoms include headache, anorexia, sleep disturbance, nausea, dizziness, fatigue, malaise, and shortness of breath.
– Symptoms usually occur after 6-12 hours above 2500m.
– Risk factors for AMS include previous AMS, fast ascent, sleeping at altitude, and age <50 years old.
– The Lake Louise AMS score is used to assess the severity of AMS.
– Treatment involves stopping ascent, maintaining hydration, and using medication for symptom relief.
– Medications for moderate to severe symptoms include dexamethasone and acetazolamide.
– Gradual ascent, hydration, and avoiding alcohol can help prevent AMS.

High Altitude Pulmonary Edema (HAPE):
– HAPE is a progression of AMS but can occur without AMS symptoms.
– It is the leading cause of death related to altitude illness.
– Risk factors for HAPE include rate of ascent, intensity of exercise, absolute altitude, and individual susceptibility.
– Symptoms include dyspnea, cough, chest tightness, poor exercise tolerance, cyanosis, low oxygen saturations, tachycardia, tachypnea, crepitations, and orthopnea.
– Management involves immediate descent, supplemental oxygen, keeping warm, and medication such as nifedipine.

High Altitude Cerebral Edema (HACE):
– HACE is thought to result from vasogenic edema and increased vascular pressure.
– It occurs 2-4 days after ascent and is associated with moderate to severe AMS symptoms.
– Symptoms include headache, hallucinations, disorientation, confusion, ataxia, drowsiness, seizures, and manifestations of raised intracranial pressure.
– Immediate descent is crucial for management, and portable hyperbaric therapy may be used if descent is not possible.
– Medication for treatment includes dexamethasone and supplemental oxygen. Acetazolamide is typically used for prophylaxis.

Gillick competence is a legal concept that determines whether a child under the age of 16 has the ability to give consent for their own medical treatment, even without parental consent or knowledge. This term originated in England and Wales and is commonly used in medical law. On the other hand, Fraser guidelines are specifically applied to situations involving advice and treatment related to a young person’s sexual health and contraception.

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 current guidelines from NICE provide recommendations for managing low back pain. It is suggested to consider using oral non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, while taking into account the potential risks of gastrointestinal, liver, and cardio-renal toxicity, as well as the person’s individual risk factors and age. When prescribing oral NSAIDs, it is important to conduct appropriate clinical assessments, monitor risk factors regularly, and consider the use of gastroprotective treatment. It is advised to prescribe the lowest effective dose of oral NSAIDs for the shortest duration possible. In cases where NSAIDs are contraindicated, not tolerated, or ineffective, weak opioids (with or without paracetamol) may be considered for managing acute low back pain. However, NICE does not recommend the use of paracetamol alone, opioids for chronic low back pain, serotonin reuptake inhibitors, serotonin-noradrenaline reuptake inhibitors, tricyclic antidepressants for non-neuropathic pain, anticonvulsants, or benzodiazepines for muscle spasm associated with acute low back pain. For more information, you can refer to the NICE guidance on low back pain and sciatica in individuals over 16 years old, as well as the NICE Clinical Knowledge Summary on low back pain without radiculopathy.

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.

The FeverPAIN score is a scoring system that is recommended by the current NICE guidelines for assessing acute sore throats. It consists of five items: fever in the last 24 hours, purulence, attendance within three days, inflamed tonsils, and no cough or coryza. Based on the score, different recommendations are given regarding the use of antibiotics.

If the score is 0-1, it is unlikely to be a streptococcal infection, with only a 13-18% chance of streptococcus isolation. Therefore, antibiotics are not recommended in this case. If the score is 2-3, there is a higher chance (34-40%) of streptococcus isolation, so delayed prescribing of antibiotics is considered, with a 3-day ‘back-up prescription’. If the score is 4 or higher, there is a 62-65% chance of streptococcus isolation, and immediate antibiotic use is recommended if the infection is severe. Otherwise, a 48-hour short back-up prescription is suggested.

The Fever PAIN score was developed from a study that included 1760 adults and children aged three and over. It was then tested in a trial that compared three different prescribing strategies: empirical delayed prescribing, using the score to guide prescribing, and combining the score with the use of a near-patient test (NPT) for streptococcus. The use of the score resulted in faster symptom resolution and a reduction in antibiotic prescribing, both by one third. However, the addition of the NPT did not provide any additional benefit.

Overall, the FeverPAIN score is a useful tool for assessing acute sore throats and guiding antibiotic prescribing decisions. It has been shown to be effective in reducing unnecessary antibiotic use and improving patient outcomes.

Many systemic illnesses have distinct dermatological associations. Some of these are listed below:

Addison’s disease is characterized by pigmentation and vitiligo.

Cushing’s disease is associated with pigmentation, striae, hirsutism, and acne.

Diabetes mellitus can cause necrobiosis lipoidica, which presents as shiny, yellowish plaques on the shin. It can also lead to xanthoma, a condition characterized by yellowish lipid deposits in the skin, and granuloma annulare, which manifests as palpable ring lesions on the hands, face, or feet.

Hyperlipidemia is linked to xanthoma and xanthomata, which are yellowish plaques on the eyelids.

Crohn’s disease is associated with erythema nodosum.

Ulcerative colitis can cause pyoderma gangrenosum and erythema nodosum.

Liver disease often presents with pruritus, spider naevi, and erythema.

Malignancy can lead to mycosis fungoides, a type of lymphoma that affects the skin. It is also associated with acanthosis nigricans, which is often seen in gastrointestinal malignancies.

Hypothyroidism is linked to alopecia, while thyrotoxicosis can cause both alopecia and pretibial myxedema.

Iodine deficiency is a widespread issue globally and is the leading cause of hypothyroidism worldwide. It is particularly prevalent in numerous African countries, as well as in developed nations such as Norway, Germany, Russia, and Ukraine. In the UK, however, autoimmune thyroiditis is the most common cause of hypothyroidism.

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.

Sexually transmitted eye infections can be quite severe and are often characterized by prolonged mucopurulent discharge. The two main causes of these infections are Chlamydia trachomatis and Neisseria gonorrhoea. Differentiating between the two can be done by considering certain features.

Chlamydia trachomatis infection typically presents with chronic low-grade irritation and mucous discharge that lasts for more than two weeks in sexually active individuals. Pre-auricular lymphadenopathy, or swelling of the lymph nodes in front of the ear, may also be present. Most cases of this infection are unilateral, affecting only one eye, but there is a possibility of it being bilateral, affecting both eyes.

On the other hand, Neisseria gonorrhoea infection tends to develop rapidly, usually within 12 to 24 hours. It is characterized by copious mucopurulent discharge, swelling of the eyelids, and tender preauricular lymphadenopathy. This type of infection carries a higher risk of complications, such as uveitis, severe keratitis, and corneal perforation.

Based on the patient’s symptoms, it appears that they are more consistent with a Chlamydia trachomatis infection, especially considering the slower and more gradual onset of their symptoms.

There is ongoing debate regarding the most effective antibiotic treatment for these infections. Some options include topical tetracycline ointment to be applied four times a day for six weeks, oral doxycycline to be taken twice a day for one to two weeks, oral azithromycin with a single dose of 1 gram followed by 500 mg orally for two days, or oral erythromycin to be taken four times a day for one week.

Urticaria is a condition characterized by a raised, itchy rash on the skin and mucous membranes. It can be localized or widespread and affects about 15% of people at some point in their lives. There are two forms of urticaria: acute and chronic, with the acute form being more common.

In about 50% of cases of acute urticaria, a specific trigger can be identified. Common triggers include allergies (such as foods, bites, stings, and drugs), skin contact with irritants (like chemicals, nettles, and latex), physical stimuli (such as firm rubbing, pressure, and extremes of temperature), and viral infections.

The main skin lesion seen in urticaria is called a wheal or wheel. Wheals typically have three characteristics: a central swelling that can be red or white in color, surrounded by a red area (known as the flare), and they are usually very itchy, sometimes accompanied by a burning sensation. Wheals are temporary and usually disappear within 1 to 24 hours, returning the skin to its normal appearance.

Wheals can vary in size, ranging from a few millimeters to lesions as large as 10 cm in diameter. They can appear as single lesions or multiple ones, and sometimes they merge together to form large patches. In some cases, urticaria can also cause swelling of the soft tissues in the eyelids, lips, and tongue, known as angioedema.

The Civil Contingencies Act 2004 establishes a framework for civil protection in the United Kingdom. This legislation categorizes local responders to major incidents into two groups, each with their own set of responsibilities.

Category 1 responders consist of organizations that play a central role in responding to most emergencies, such as the emergency services, local authorities, and NHS bodies. These Category 1 responders are obligated to fulfill a comprehensive range of civil protection duties. These duties include assessing the likelihood of emergencies occurring and using this information to inform contingency planning. They must also develop emergency plans, establish business continuity management arrangements, and ensure that information regarding civil protection matters is readily available to the public. Additionally, Category 1 responders are responsible for maintaining systems to warn, inform, and advise the public in the event of an emergency. They are expected to share information with other local responders to enhance coordination and efficiency. Furthermore, local authorities within this category are required to provide guidance and support to businesses and voluntary organizations regarding business continuity management.

On the other hand, Category 2 organizations, such as the Health and Safety Executive, transport companies, and utility companies, are considered co-operating bodies. While they may not be directly involved in the core planning work, they play a crucial role in incidents that impact their respective sectors. Category 2 responders have a more limited set of duties, primarily focused on cooperating and sharing relevant information with both Category 1 and Category 2 responders.

For more information on this topic, please refer to the Civil Contingencies Act 2004.

There is an increased risk of neural tube defects in women with epilepsy who take carbamazepine during pregnancy, ranging from 2 to 10 times higher. Additionally, there is a risk of haemorrhagic disease of the newborn associated with this medication. It is crucial to have discussions about epilepsy treatments with women of childbearing age during the planning stages so that they can start early supplementation of folic acid.

Below is a list outlining the most commonly encountered drugs that have adverse effects during pregnancy:

ACE inhibitors (e.g. ramipril): If given in the second and third trimester, these medications can cause hypoperfusion, renal failure, and the oligohydramnios sequence.

Aminoglycosides (e.g. gentamicin): These drugs can lead to ototoxicity and deafness in the fetus.

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

Benzodiazepines (e.g. diazepam): When given late in pregnancy, these medications can result in respiratory depression and a neonatal withdrawal syndrome.

Calcium-channel blockers: If given in the first trimester, these drugs can cause phalangeal abnormalities. If given in the second and third trimesters, they can lead to fetal growth retardation.

Carbamazepine: This medication is associated with haemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol: Use of this drug can cause grey baby syndrome in newborns.

Corticosteroids: If given in the first trimester, corticosteroids may cause orofacial clefts in the fetus.

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

Finasteride: Pregnant women should avoid handling finasteride tablets. Crushed or broken tablets can be absorbed through the skin and affect male sex organ development in the fetus.

Haloperidol: If given in the first trimester, haloperidol may cause limb malformations. In the third trimester, there is an increased risk of extrapyramidal symptoms in the neonate.

Heparin: Use of heparin during pregnancy is associated with an acceptable bleeding rate and a low rate of thrombotic recurrence in the mother.

It is unlikely that this patient has glandular fever, as school exclusion is not necessary for this condition. However, it is important to note that in the UK, school exclusion is not required for tonsillitis either. The only exception is if a child has tonsillitis and a rash consistent with scarlet fever, in which case exclusion is necessary for 24 hours after starting antibiotics. The child and parents should be provided with additional information about glandular fever (refer to the notes below).

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.

Blunt abdominal trauma often leads to injuries in certain organs. According to the latest edition of the ATLS manual, the spleen is the most frequently injured organ, with a prevalence of 40-55%. Following closely behind is the liver, which sustains injuries in about 35-45% of cases. The small bowel, although less commonly affected, still experiences injuries in approximately 5-10% of patients. It is worth noting that patients who undergo laparotomy for blunt trauma have a 15% incidence of retroperitoneal hematoma. These statistics highlight the significant impact of blunt abdominal trauma on organ health.

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.

Methaemoglobinaemia is a condition characterized by high levels of haemoglobin with iron in the ferric (Fe3+) state. This occurs when haemoglobin is oxidized from Fe2+ to Fe3+. Normally, NADH methaemoglobin reductase, also known as Cytochrome b5 reductase, regulates this process by transferring electrons from NADH to methaemoglobin, converting it back to haemoglobin. However, if there is a congenital or acquired dysfunction in the NADH methaemoglobin reductase enzyme system, it can lead to elevated levels of haemoglobin with iron in the Fe3+ state. Unfortunately, Fe3+ is unable to bind to haemoglobin.

Further Reading:

Methaemoglobinaemia is a condition where haemoglobin is oxidised from Fe2+ to Fe3+. This process is normally regulated by NADH methaemoglobin reductase, which transfers electrons from NADH to methaemoglobin, converting it back to haemoglobin. In healthy individuals, methaemoglobin levels are typically less than 1% of total haemoglobin. However, an increase in methaemoglobin can lead to tissue hypoxia as Fe3+ cannot bind oxygen effectively.

Methaemoglobinaemia can be congenital or acquired. Congenital causes include haemoglobin chain variants (HbM, HbH) and NADH methaemoglobin reductase deficiency. Acquired causes can be due to exposure to certain drugs or chemicals, such as sulphonamides, local anaesthetics (especially prilocaine), nitrates, chloroquine, dapsone, primaquine, and phenytoin. Aniline dyes are also known to cause methaemoglobinaemia.

Clinical features of methaemoglobinaemia include slate grey cyanosis (blue to grey skin coloration), chocolate blood or chocolate cyanosis (brown color of blood), dyspnoea, low SpO2 on pulse oximetry (which often does not improve with supplemental oxygen), and normal PaO2 on arterial blood gas (ABG) but low SaO2. Patients may tolerate hypoxia better than expected. Severe cases can present with acidosis, arrhythmias, seizures, and coma.

Diagnosis of methaemoglobinaemia is made by directly measuring the level of methaemoglobin using a co-oximeter, which is present in most modern blood gas analysers. Other investigations, such as a full blood count (FBC), electrocardiogram (ECG), chest X-ray (CXR), and beta-human chorionic gonadotropin (bHCG) levels (in pregnancy), may be done to assess the extent of the condition and rule out other contributing factors.

Active treatment is required if the methaemoglobin level is above 30% or if it is below 30% but the patient is symptomatic or shows evidence of tissue hypoxia. Treatment involves maintaining the airway and delivering high-flow oxygen, removing the causative agents, treating toxidromes and consider giving IV dextrose 5%.

Entonox is a combination of oxygen and nitrous oxide, with equal parts of each. Its primary effects are pain relief and a decrease in activity within the central nervous system. The exact mechanism of action is not fully understood, but it is believed to involve the modulation of enkephalins and endorphins in the central nervous system.

When inhaled, Entonox takes about 30 seconds to take effect and its effects last for approximately 60 seconds after inhalation is stopped. It is stored in cylinders that are either white or blue, with blue and white sections on the shoulders. Entonox has various uses, including being used alongside general anesthesia, as a pain reliever during labor, and for painful medical procedures.

There are some known side effects of Entonox, which include nausea and vomiting in about 15% of patients, dizziness, euphoria, and inhibition of vitamin B12 synthesis. It is important to note that there are certain situations where the use of Entonox is not recommended. These contraindications include reduced consciousness, diving injuries, pneumothorax, middle ear disease, sinus disease, bowel obstruction, documented allergy to nitrous oxide, hypoxia, and violent or disabled psychiatric patients.

Central retinal artery occlusion (CRAO) is characterized by sudden, painless, and unilateral loss of vision. The appearance of the retina in CRAO is distinct from that of CRVO. It shows a pale retina with narrowed blood vessels. A notable feature is the presence of a ‘cherry-red spot’ at the center of the macula, which is supplied by the underlying choroid. Additionally, examination often reveals an afferent pupillary defect.

On the other hand, branch retinal artery occlusion (BRAO) typically affects only one quadrant of the retina, leading to visual field deficits in that specific area rather than complete loss of vision.

Acute aortic dissection is characterized by the rapid formation of a false, blood-filled channel within the middle layer of the aorta. It is estimated to occur in 3 out of every 100,000 individuals per year.

Patients with aortic dissection typically experience intense chest pain that spreads to the area between the shoulder blades. The pain is often described as tearing or ripping and may also extend to the neck. Sweating, paleness, and rapid heartbeat are commonly observed at the time of presentation. Other possible symptoms include focal neurological deficits, weak pulses, fainting, and reduced blood flow to organs.

A significant difference in blood pressure between the arms, greater than 20 mmHg, is a highly sensitive indicator. If the dissection extends backward, it can involve the aortic valve, leading to the early diastolic murmur of aortic regurgitation.

Risk factors for aortic dissection include hypertension, atherosclerosis, aortic coarctation, the use of sympathomimetic drugs like cocaine, Marfan syndrome, Ehlers-Danlos syndrome, Turner’s syndrome, tertiary syphilis, and pre-existing aortic aneurysm.

Aortic dissection can be classified according to the Stanford classification system:
– Type A affects the ascending aorta and the arch, accounting for 60% of cases. These cases are typically managed surgically and may result in the blockage of coronary arteries and aortic regurgitation.
– Type B begins distal to the left subclavian artery and accounts for approximately 40% of cases. These cases are usually managed with medication to control blood pressure.

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.

The most frequent cause of non-allergic drug induced angioedema is ACE inhibitors. Symptoms usually appear several days to weeks after beginning the medication. It is important to note that penicillin and NSAIDs are the primary drug culprits for angioedema, but they trigger it through an IgE mediated allergic mechanism, resulting in both angioedema and urticaria. The onset of symptoms in these cases typically occurs within minutes to hours after exposure.

Further Reading:

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.

TSH-secreting pituitary adenoma is an uncommon cause of hyperthyroidism in the United Kingdom, accounting for only a small number of cases.

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.

Activated charcoal is a commonly utilized substance for decontamination in cases of poisoning. Its main function is to attract and bind molecules of the ingested toxin onto its surface.

Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. This powder is created by subjecting carbonaceous matter to high heat, a process known as pyrolysis, and then concentrating it with a solution of zinc chloride. Through this process, the activated charcoal develops a complex network of pores, providing it with a large surface area of approximately 3,000 m2/g. This extensive surface area allows it to effectively hinder the absorption of the harmful toxin by up to 50%.

The typical dosage for adults is 50 grams, while children are usually given 1 gram per kilogram of body weight. Activated charcoal can be administered orally or through a nasogastric tube. It is crucial to administer it within one hour of ingestion, and if necessary, a second dose may be repeated after one hour.

Whooping cough is a respiratory infection caused by the bacteria Bordetella pertussis. It is highly contagious and can be transmitted to about 90% of close household contacts. The Health Protection Agency has identified two priority groups for public health action in managing whooping cough contacts.

Group 1 consists of individuals who are at a higher risk of severe or complicated infection. This includes infants under one year old who have received less than three doses of the pertussis vaccine.

Group 2 consists of individuals who are at a higher risk of transmitting the infection to those in Group 1. This includes pregnant women who are at or beyond 32 weeks of gestation, healthcare workers who work with infants and pregnant women, individuals who work with infants too young to be vaccinated (under 4 months old), and individuals who share a household with infants too young to be vaccinated.

According to current guidance, antibiotic prophylaxis with a macrolide antibiotic, like erythromycin, should only be offered to close contacts if two criteria are met. First, the index case (the person with whooping cough) must have developed symptoms within the past 21 days. Second, there must be a close contact in one of the two priority groups.

If both criteria are met, all contacts, regardless of their vaccination status and age, should be offered chemoprophylaxis. In this case, the mother is in Group 2, so the current recommendation is that all household contacts, including the mother, father, and brother, should receive chemoprophylaxis.

Additionally, immunization or a booster dose should be considered for those who have been offered chemoprophylaxis, depending on their current vaccination status.

The caecum, positioned between the ileum and the ascending colon, serves as the closest segment of the large intestine. It can be found in the right iliac fossa, just below the ileocaecal junction. In case of enlargement, it can be detected through palpation. This structure is situated within the peritoneal cavity.

It is important to inform the police in cases of gunshot and deliberate knife wounds. Deliberate stabbings pose a risk of further attacks in the area and can endanger both the patient and the staff in the department. The General Medical Council (GMC) provides clear guidance supporting the need to involve the police in such situations.

According to the GMC, it is usually necessary to inform the police when a person presents with a gunshot wound. Even accidental shootings involving legally held firearms raise important issues for the police, such as firearms licensing. Similarly, the police should generally be informed when a person has been wounded in an attack involving a knife, blade, or any other sharp instrument. However, if a knife or blade injury appears to be accidental or a result of self-harm, it is not usually necessary to involve the police.

In cases where seeking consent to disclose personal information is not practical or appropriate, or if a patient refuses consent, it may be justified to disclose the information in the public interest. This is particularly true if failure to do so could expose others to a risk of death or serious harm.

Further Reading:

Principles of Medical Ethics:

1. Autonomy: Competent adults have the right to make informed decisions about their own medical care.
2. Beneficence: Healthcare professionals should take actions that serve the best interests of patients.
3. Non-maleficence: Healthcare professionals should not take actions that may injure or harm patients.
4. Justice: Healthcare professionals should take actions that are fair and equitable to both the individual and society as a whole.

Confidentiality:

1. Use minimum necessary personal information and consider anonymizing information if possible.
2. Manage and protect personal information to prevent improper access, disclosure, or loss.
3. Understand and adhere to information governance appropriate to your role.
4. Comply with the law when handling personal information.
5. Share relevant information for direct care unless the patient objects.
6. Obtain explicit consent to disclose identifiable information for purposes other than care or local clinical audit, unless required by law or justified in the public interest.
7. Inform patients about disclosures of personal information they would not reasonably expect, unless not practicable or undermines the purpose of the disclosure.
8. Support patients in accessing their information and respecting their legal rights.

Obtaining Patient’s Consent for Disclosure:

– Consent should be obtained for disclosing personal information for purposes other than direct care or local clinical audit, unless required by law or not appropriate or practicable.

Situations Where Patient Consent is Not Required for Disclosure:

– Adults at risk of or suffering abuse or neglect, as required by law.
– Adults lacking capacity, if neglect or harm is suspected, unless not overall beneficial to the patient.
– When required by law or approved through a statutory process.
– When justified in the public interest, such as for the prevention, detection, or prosecution of serious crime, patient’s fitness to drive, serious communicable disease, or posing a serious risk to others through being unfit for work.

Confidentiality Following a Patient’s Death:

– Respect the patient’s confidentiality even after their death.
– If the patient previously requested not to share personal information with those close to them, abide by their wishes.
– Be considerate, sensitive, and responsive to those close to the patient, providing as much information as possible.

The Law & Caldicott Guardians:

Data Protection Act:
– Sets rules and standards for the use and handling of personal data by organizations.
– Personal data must be used fairly, lawfully, transparently, and for specified purposes.
– Individuals have rights

Hyperkalaemia, a condition characterized by high levels of potassium in the blood, can be identified through specific changes seen on an electrocardiogram (ECG). One of these changes is the tenting of T-waves, where the T-waves become tall and pointed. Additionally, the P-wave, which represents atrial depolarization, may widen and flatten. Other ECG changes associated with hyperkalaemia include a prolonged PR interval, flat P-waves, wide P-waves, widened QRS complex, the appearance of a sine wave pattern, and the possibility of heart block.

Further Reading:

Vasoactive drugs can be classified into three categories: inotropes, vasopressors, and unclassified. Inotropes are drugs that alter the force of muscular contraction, particularly in the heart. They primarily stimulate adrenergic receptors and increase myocardial contractility. Commonly used inotropes include adrenaline, dobutamine, dopamine, isoprenaline, and ephedrine.

Vasopressors, on the other hand, increase systemic vascular resistance (SVR) by stimulating alpha-1 receptors, causing vasoconstriction. This leads to an increase in blood pressure. Commonly used vasopressors include norepinephrine, metaraminol, phenylephrine, and vasopressin.

Electrolytes, such as potassium, are essential for proper bodily function. Solutions containing potassium are often given to patients to prevent or treat hypokalemia (low potassium levels). However, administering too much potassium can lead to hyperkalemia (high potassium levels), which can cause dangerous arrhythmias. It is important to monitor potassium levels and administer it at a controlled rate to avoid complications.

Hyperkalemia can be caused by various factors, including excessive potassium intake, decreased renal excretion, endocrine disorders, certain medications, metabolic acidosis, tissue destruction, and massive blood transfusion. It can present with cardiovascular, respiratory, gastrointestinal, and neuromuscular symptoms. ECG changes, such as tall tented T-waves, prolonged PR interval, flat P-waves, widened QRS complex, and sine wave, are also characteristic of hyperkalemia.

In summary, vasoactive drugs can be categorized as inotropes, vasopressors, or unclassified. Inotropes increase myocardial contractility, while vasopressors increase systemic vascular resistance. Electrolytes, particularly potassium, are important for bodily function, but administering too much can lead to hyperkalemia. Monitoring potassium levels and ECG changes is crucial in managing hyperkalemia.

Croup, also known as laryngo-tracheo-bronchitis, is typically caused by the parainfluenza virus. Other viruses such as rhinovirus, influenza, and respiratory syncytial viruses can also be responsible. Before the onset of stridor, there is often a mild cold-like illness that lasts for 1-2 days. Symptoms usually reach their peak within 1-3 days, with the cough often being more troublesome at night. A milder cough may persist for another 7-10 days.

A distinctive feature of croup is a barking cough, but it does not indicate the severity of the condition. To reduce airway swelling, dexamethasone and prednisolone are commonly prescribed. If a child is experiencing vomiting, nebulized budesonide can be used as an alternative. However, it is important to note that steroids do not shorten the duration of the illness. In severe cases, nebulized adrenaline can be administered.

Hospitalization for croup is uncommon and typically reserved for children who are experiencing worsening respiratory distress or showing signs of drowsiness or agitation.

The desired core body temperature when cooling a patient with heat stroke is

Heat Stroke:
– Core temperature >40°C with central nervous system dysfunction
– Classified into classic/non-exertional heat stroke and exertional heat stroke
– Classic heat stroke due to passive exposure to severe environmental heat
– Exertional heat stroke due to strenuous physical activity in combination with excessive environmental heat
– Mechanisms to reduce core temperature overwhelmed, leading to tissue damage
– Symptoms include high body temperature, vascular endothelial surface damage, inflammation, dehydration, and renal failure
– Management includes cooling methods and supportive care
– Target core temperature for cooling is 38.5°C

Heat Exhaustion:
– Mild to moderate heat illness that can progress to heat stroke if untreated
– Core temperature elevated but <40°C
– Symptoms include nausea, vomiting, dizziness, and mild neurological symptoms
– Normal thermoregulation is disrupted
– Management includes moving patient to a cooler environment, rehydration, and rest

Other Heat-Related Illnesses:
– Heat oedema: transitory swelling of hands and feet, resolves spontaneously
– Heat syncope: results from volume depletion and peripheral vasodilatation, managed by moving patient to a cooler environment and rehydration
– Heat cramps: painful muscle contractions associated with exertion, managed with cooling, rest, analgesia, and rehydration

Risk Factors for Severe Heat-Related Illness:
– Old age, very young age, chronic disease and debility, mental illness, certain medications, housing issues, occupational factors

Management:
– Cooling methods include spraying with tepid water, fanning, administering cooled IV fluids, cold or ice water immersion, and ice packs
– Benzodiazepines may be used to control shivering
– Rapid cooling to achieve rapid normothermia should be avoided to prevent overcooling and hypothermia
– Supportive care includes intravenous fluid replacement, seizure treatment if required, and consideration of haemofiltration
– Some patients may require liver transplant due to significant liver damage
– Patients with heat stroke should ideally be managed in a HDU/ICU setting with CVP and urinary catheter output measurements

The ATLS guidelines categorize chest injuries in trauma into two groups: life-threatening injuries that require immediate identification and treatment in the primary survey, and potentially life-threatening injuries that should be identified and treated in the secondary survey.

During the primary survey, the focus is on identifying and treating life-threatening thoracic injuries. These include airway obstruction, tracheobronchial tree injury, tension pneumothorax, open pneumothorax, massive haemothorax, and cardiac tamponade. Prompt recognition and intervention are crucial in order to prevent further deterioration and potential fatality.

In the secondary survey, attention is given to potentially life-threatening injuries that may not be immediately apparent. These include simple pneumothorax, haemothorax, flail chest, pulmonary contusion, blunt cardiac injury, traumatic aortic disruption, traumatic diaphragmatic injury, and blunt oesophageal rupture. These injuries may not pose an immediate threat to life, but they still require identification and appropriate management to prevent complications and ensure optimal patient outcomes.

By dividing chest injuries into these two categories and addressing them in a systematic manner, healthcare providers can effectively prioritize and manage trauma patients, ultimately improving their chances of survival and recovery.

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.

Crohn’s disease is characterized by skip lesions, which are not present in ulcerative colitis. Unlike ulcerative colitis, Crohn’s disease causes inflammation throughout the entire thickness of the intestinal wall, not just the mucosa. Interestingly, smoking increases the risk of developing Crohn’s disease but decreases the risk of ulcerative colitis. Additionally, having an appendicectomy before adulthood is believed to protect against ulcerative colitis, whereas it actually increases the risk of developing Crohn’s disease for about 5 years after the surgery.

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.

When starting treatment with strong opioids for pain relief in palliative care, it is recommended to offer patients regular oral sustained-release or oral immediate-release morphine, depending on their preference. In addition, provide rescue doses of oral immediate-release morphine for breakthrough pain. For patients without renal or hepatic comorbidities, a typical total daily starting dose schedule of 20-30 mg of oral morphine is suggested, along with 5 mg of oral immediate-release morphine for rescue doses during the titration phase. It is important to adjust the dose until a good balance is achieved between pain control and side effects. If this balance is not reached after a few dose adjustments, it is advisable to seek specialist advice. Patients should be reviewed frequently, especially during the titration phase. For patients with moderate to severe renal or hepatic impairment, it is recommended to consult a specialist before prescribing strong opioids.

For maintenance therapy, oral sustained-release morphine is recommended as the first-line treatment for patients with advanced and progressive disease who require strong opioids. Transdermal patch formulations should not be routinely offered as first-line maintenance treatment unless oral opioids are not suitable. If pain remains inadequately controlled despite optimizing first-line maintenance treatment, it is important to review the analgesic strategy and consider seeking specialist advice.

When it comes to breakthrough pain, oral immediate-release morphine should be offered as the first-line rescue medication for patients on maintenance oral morphine treatment. Fast-acting fentanyl should not be offered as the first-line rescue medication. If pain continues to be inadequately controlled despite optimizing treatment, it may be necessary to seek specialist advice.

In cases where oral opioids are not suitable and analgesic requirements are stable, transdermal patches with the lowest acquisition cost can be considered. However, it is important to consult a specialist for guidance if needed. Similarly, for patients in whom oral opioids are not suitable and analgesic requirements are unstable, subcutaneous opioids with the lowest acquisition cost can be considered, with specialist advice if necessary.

For more information, please refer to the NICE Clinical Knowledge Summary: Opioids for pain relief in palliative care. https://www.nice.org.uk/guidance/cg140

The most probable diagnosis in this case is diabetic ketoacidosis (DKA). To confirm the diagnosis, it is necessary to establish that his blood glucose levels are elevated, he has significant ketonuria or ketonaemia, and that he is acidotic.

DKA is a life-threatening condition that occurs when there is a lack of insulin, leading to an inability to metabolize glucose. This results in high blood sugar levels and an osmotic diuresis, causing excessive thirst and increased urine production. Dehydration becomes inevitable when the urine output exceeds the patient’s ability to drink. Additionally, without insulin, fat becomes the primary energy source, leading to the production of large amounts of ketones and metabolic acidosis.

The key features of DKA include hyperglycemia (blood glucose > 11 mmol/l), ketonaemia (> 3 mmol/l) or significant ketonuria (> 2+ on urine dipstick), and acidosis (bicarbonate < 15 mmol/l and/or venous pH < 7.3). Clinical symptoms of DKA include nausea, vomiting, excessive thirst, excessive urine production, abdominal pain, signs of dehydration, a smell of ketones on breath (similar to pear drops), deep and rapid respiration (Kussmaul breathing), confusion or reduced consciousness, and tachycardia, hypotension, and shock. Investigations that should be performed include blood glucose measurement, urine dipstick (which will show marked glycosuria and ketonuria), blood ketone assay (more sensitive and specific than urine dipstick), blood tests (full blood count and urea and electrolytes), and arterial or venous blood gas analysis to assess for metabolic acidosis. The main principles of managing DKA are as follows: – Fluid boluses should only be given to reverse signs of shock and should be administered slowly in 10 ml/kg aliquots. If there are no signs of shock, fluid boluses should not be given, and specialist advice should be sought if a second bolus is required.
– Rehydration should be done with replacement therapy over 48 hours after signs of shock have been reversed.
– The first 20 ml/kg of fluid resuscitation should be given in addition to replacement fluid calculations and should not be subtracted from the calculations for the 48-hour fluid replacement.
– If a child in DKA shows signs of hypotensive shock, the use of inotropes may be considered.

In a child with a non-blanching rash, it is important to always consider the possibility of meningococcal septicaemia. This is especially true if the child appears unwell, has purpura (lesions larger than 2 mm in diameter), a capillary refill time of more than 3 seconds, or neck stiffness. In the UK, most cases of meningococcal septicaemia are caused by Neisseria meningitidis group B, although the vaccination program for Neisseria meningitidis group C has reduced the prevalence of this type. A vaccine for group B disease has now been introduced for children. It is also worth noting that Streptococcus pneumoniae can also cause meningitis.

In this particular case, the child is clearly very sick and showing signs of septic shock. It is crucial to administer a single dose of benzylpenicillin without delay and arrange for immediate transfer to the nearest Emergency Department via ambulance.

The recommended doses of benzylpenicillin based on age are as follows:
– Infants under 1 year of age: 300 mg of IM or IV benzylpenicillin
– Children aged 1 to 9 years: 600 mg of IM or IV benzylpenicillin
– Children and adults aged 10 years or older: 1.2 g of IM or IV benzylpenicillin.

Graphorrhoea is a communication disorder characterized by an excessive use of words and a tendency to ramble in written work. It is similar to word salad, but specifically occurs in written form. This condition is often observed in individuals with schizophrenia.

Blood transfusion is a crucial medical 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. One common adverse reaction is febrile transfusion reactions, which present as an unexpected rise in temperature during or after transfusion. This can be caused by cytokine accumulation or recipient antibodies reacting to donor antigens. Treatment for febrile transfusion reactions is supportive, and other potential causes should be ruled out.

Another serious complication is acute haemolytic reaction, which is often caused by ABO incompatibility due to administration errors. This reaction requires the transfusion to be stopped and IV fluids to be administered. Delayed haemolytic reactions can occur several days after a transfusion and may require monitoring and treatment for anaemia and renal function. Allergic reactions, TRALI (Transfusion Related Acute Lung Injury), TACO (Transfusion Associated Circulatory Overload), and GVHD (Graft-vs-Host Disease) are other potential complications that require specific management approaches.

In summary, blood transfusion carries risks and potential complications, but efforts have been made to improve safety procedures. It is important to be aware of these complications and to promptly address any adverse reactions that may occur during or after a transfusion.

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.

If a patient with breathing difficulty does not show improvement after removing the inner tracheostomy tube, it is recommended to use a suction catheter to remove any secretions. This can help clear any blockage caused by secretions or debris in or near the tube. If this does not improve the situation, the next step would be to deflate the cuff. If deflating the cuff stabilizes or improves the patient’s condition, it suggests that air can flow around the tube within the airway, indicating that the tracheostomy tube may be obstructed or displaced.

Further Reading:

Patients with tracheostomies may experience emergencies such as tube displacement, tube obstruction, and bleeding. Tube displacement can occur due to accidental dislodgement, migration, or erosion into tissues. Tube obstruction can be caused by secretions, lodged foreign bodies, or malfunctioning humidification devices. Bleeding from a tracheostomy can be classified as early or late, with causes including direct injury, anticoagulation, mucosal or tracheal injury, and granulation tissue.

When assessing a patient with a tracheostomy, an ABCDE approach should be used, with attention to red flags indicating a tracheostomy or laryngectomy emergency. These red flags include audible air leaks or bubbles of saliva indicating gas escaping past the cuff, grunting, snoring, stridor, difficulty breathing, accessory muscle use, tachypnea, hypoxia, visibly displaced tracheostomy tube, blood or blood-stained secretions around the tube, increased discomfort or pain, increased air required to keep the cuff inflated, tachycardia, hypotension or hypertension, decreased level of consciousness, and anxiety, restlessness, agitation, and confusion.

Algorithms are available for managing tracheostomy emergencies, including obstruction or displaced tube. Oxygen should be delivered to the face and stoma or tracheostomy tube if there is uncertainty about whether the patient has had a laryngectomy. Tracheostomy bleeding can be classified as early or late, with causes including direct injury, anticoagulation, mucosal or tracheal injury, and granulation tissue. Tracheo-innominate fistula (TIF) is a rare but life-threatening complication that occurs when the tracheostomy tube erodes into the innominate artery. Urgent surgical intervention is required for TIF, and management includes general resuscitation measures and specific measures such as bronchoscopy and applying direct digital pressure to the innominate artery.

The typical range for the partial pressure of carbon dioxide (pCO2) is 4.4-6.4 kilopascals (kPa). In terms of arterial blood gas (ABG) results, the normal range for pO2 (partial pressure of oxygen) is 10-14.4 kPa or 70-100 millimeters of mercury (mmHg). The normal range for pCO2 is 4.4-6.4 kPa or 35-45 mmHg. Additionally, the normal range for bicarbonate levels is 23-28 millimoles per liter (mmol/L).

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.

The NICE guidelines for suspected deep vein thrombosis (DVT) suggest considering the possibility of DVT if typical symptoms and signs are present, particularly if the person has risk factors like previous venous thromboembolism and immobility.

Typical signs and symptoms of DVT include unilateral localized pain (often throbbing) that occurs during walking or bearing weight, as well as calf swelling (or, less commonly, swelling of the entire leg). Other signs to look out for are tenderness, skin changes such as edema, redness, and warmth, and vein distension.

To rule out other potential causes for the symptoms and signs, it is important to conduct a physical examination and review the person’s general medical history.

When assessing leg and thigh swelling, it is recommended to measure the circumference of the leg 10 cm below the tibial tuberosity and compare it with the unaffected leg. A difference of more than 3 cm between the two legs increases the likelihood of DVT.

Additionally, it is important to check for edema and dilated collateral superficial veins on the affected side.

To assess the likelihood of DVT and guide further management, the two-level DVT Wells score can be used.

For more information, you can refer to the NICE Clinical Knowledge Summary on deep vein thrombosis.

This patient is experiencing a reactionary haemorrhage following their recent dental extraction.

There are three types of haemorrhage that can occur after a dental extraction. The first is immediate haemorrhage, which happens at the time of extraction. The second is reactionary haemorrhage, which occurs 2-3 hours after the extraction when the vasoconstrictor effects of the local anaesthetic wear off. The third is secondary haemorrhage, which typically happens at 48-72 hours and occurs if the clot becomes infected.

To manage this situation, the first step is to clean and rinse the mouth, removing any excessive clot. Then, a square of gauze should be rolled up into a pledgelet that is approximately twice the size of the bleeding socket and inserted. The patient should be instructed to bite down on it to apply pressure for about 10-20 minutes.

If the bleeding continues after this initial management, the area should be anaesthetised using lidocaine with adrenaline. Following the anaesthesia, a horizontal mattress suture should be inserted, pulling the gum over the bone edges tightly enough to blanch them. It is important to refer the patient to the on-call dental surgeon at this point.

There are several risk factors for dental haemorrhage, including hypertension, the use of anticoagulants such as warfarin, and hereditary bleeding disorders like von Willebrand disease or haemophilia.

The most probable diagnosis in this case is a subarachnoid haemorrhage (SAH).

When assessing patients who present with an SAH, there may be focal neurological signs that can indicate the potential location of the aneurysm. Common sites for aneurysms include the bifurcation of the middle cerebral artery, the junction of the anterior communicating cerebral artery, and the junction of the posterior communicating artery with the internal carotid artery. If there is complete or partial palsy of the oculomotor nerve, it suggests the rupture of a posterior communicating artery aneurysm.

While hypertension is a risk factor for SAH, a significant increase in blood pressure may occur as a reflex response following the haemorrhage.

The first-line investigation for SAH is a CT head scan, which can detect over 95% of cases if performed within the first 24 hours. The sensitivity of the scan increases to nearly 100% if done within 6 hours of symptom onset. If the CT head scan is negative and there are no contraindications, a lumbar puncture (LP) should be performed to diagnose SAH. It is recommended to perform the LP at least 12 hours after the onset of headache. It is important to note that approximately 3% of patients with a negative CT scan will be confirmed to have had an SAH after undergoing an LP.

This patient is displaying symptoms and signs that are consistent with a diagnosis of acute pyelonephritis. Additionally, they are showing signs of sepsis, which indicates a more serious illness or condition. Therefore, it would be advisable to admit the patient for inpatient treatment.

According to the recommendations from the National Institute for Health and Care Excellence (NICE), patients with pyelonephritis should be admitted if it is severe or if they exhibit any signs or symptoms that suggest a more serious condition, such as sepsis. Signs of sepsis include significant tachycardia, hypotension, or breathlessness, as well as marked signs of illness like impaired level of consciousness, profuse sweating, rigors, pallor, or significantly reduced mobility. A temperature greater than 38°C or less than 36°C is also indicative of sepsis.

NICE also advises considering referral or seeking specialist advice for individuals with acute pyelonephritis if they are significantly dehydrated or unable to take oral fluids and medicines, if they are pregnant, if they have a higher risk of developing complications due to known or suspected abnormalities of the genitourinary tract or underlying diseases like diabetes mellitus or immunosuppression, or if they have recurrent episodes of urinary tract infections (UTIs).

For non-pregnant women and men, the recommended choice of antibacterial therapy is as follows: oral first-line options include cefalexin, ciprofloxacin, or co-amoxiclav (taking into account local microbial resistance data), and trimethoprim if sensitivity is known. Intravenous first-line options are amikacin, ceftriaxone, cefuroxime, ciprofloxacin, or gentamicin if the patient is severely unwell or unable to take oral treatment. Co-amoxiclav may be used if given in combination or if sensitivity is known. Antibacterials may be combined if there are concerns about susceptibility or sepsis. For intravenous second-line options, it is recommended to consult a local microbiologist.

For pregnant women, the recommended choice of antibacterial therapy is cefalexin for oral first-line treatment. If the patient is severely unwell or unable to take oral treatment, cefuroxime is the recommended intravenous first-line option.

The initial indication of progressive compression on the oculomotor nerve is the dilation of the pupil. In cases where the oculomotor nerve is being compressed, the outer parasympathetic fibers are typically affected before the inner motor fibers. These parasympathetic fibers are responsible for stimulating the constriction of the pupil. When they are disrupted, the sympathetic stimulation of the pupil is unopposed, leading to the dilation of the pupil (known as mydriasis or blown pupil). This symptom is usually observed before the drooping of the eyelid (lid ptosis) and the downward and outward positioning of the eye.

Further Reading:

Intracranial pressure (ICP) refers to the pressure within the craniospinal compartment, which includes neural tissue, blood, and cerebrospinal fluid (CSF). Normal ICP for a supine adult is 5-15 mmHg. The body maintains ICP within a narrow range through shifts in CSF production and absorption. If ICP rises, it can lead to decreased cerebral perfusion pressure, resulting in cerebral hypoperfusion, ischemia, and potentially brain herniation.

The cranium, which houses the brain, is a closed rigid box in adults and cannot expand. It is made up of 8 bones and contains three main components: brain tissue, cerebral blood, and CSF. Brain tissue accounts for about 80% of the intracranial volume, while CSF and blood each account for about 10%. The Monro-Kellie doctrine states that the sum of intracranial volumes is constant, so an increase in one component must be offset by a decrease in the others.

There are various causes of raised ICP, including hematomas, neoplasms, brain abscesses, edema, CSF circulation disorders, venous sinus obstruction, and accelerated hypertension. Symptoms of raised ICP include headache, vomiting, pupillary changes, reduced cognition and consciousness, neurological signs, abnormal fundoscopy, cranial nerve palsy, hemiparesis, bradycardia, high blood pressure, irregular breathing, focal neurological deficits, seizures, stupor, coma, and death.

Measuring ICP typically requires invasive procedures, such as inserting a sensor through the skull. Management of raised ICP involves a multi-faceted approach, including antipyretics to maintain normothermia, seizure control, positioning the patient with a 30º head up tilt, maintaining normal blood pressure, providing analgesia, using drugs to lower ICP (such as mannitol or saline), and inducing hypocapnoeic vasoconstriction through hyperventilation. If these measures are ineffective, second-line therapies like barbiturate coma, optimised hyperventilation, controlled hypothermia, or decompressive craniectomy may be considered.

Thought echo is a phenomenon where a patient perceives their own thoughts as if they are being spoken out loud. When there is a slight delay in this perception, it is referred to as echo de la pensée. On the other hand, when the thoughts are heard simultaneously, it is known as Gedankenlautwerden.

Women have three options when requesting emergency contraception. The first option is Levonelle 1.5 mg, which contains levonorgestrel and can be used up to 72 hours after unprotected sexual intercourse (UPSI). If vomiting occurs within 2 hours of taking the tablet, another one should be given. Levonelle mainly works by preventing ovulation.

The second option is ulipristal acetate, the newest treatment available. It can be used up to 120 hours after UPSI. If vomiting occurs within 3 hours of ingestion, another tablet should be given. Ulipristal acetate also works by inhibiting ovulation. However, it should be avoided in patients taking enzyme-inducing drugs, those with severe hepatic impairment, or those with severe asthma requiring oral steroids.

The third option is the copper IUD, which can be fitted up to 5 days after UPSI or ovulation, whichever is longer. The failure rate of the copper IUD is less than 1 in 1000, making it 10-20 times more effective than oral emergency contraceptive options. It is important to note that Levonelle and ulipristal may be less effective in women with higher BMIs.

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.

This patient’s Child Pugh score is 9. The Child Pugh score is a scoring system used to assess the severity of liver disease and the prognosis of patients with cirrhosis. It takes into account five variables: bilirubin levels, albumin levels, INR (international normalized ratio), ascites, and hepatic encephalopathy. Each variable is assigned a score from 1 to 3, with 3 indicating the most severe impairment.

In this case, the patient’s bilirubin level is 45 µmol/l, which corresponds to a score of 2. The albumin level is 27 g/l, which also corresponds to a score of 3. The INR is 1.9, which corresponds to a score of 2. The presence of moderate ascites indicates a score of 3. Finally, the patient has moderate hepatic encephalopathy, which corresponds to a score of 3.

Adding up the scores for each variable, we get a total score of 13. This indicates that the patient has moderate to severe liver disease and a poorer prognosis.

Further Reading:
Cirrhosis is a condition where the liver undergoes structural changes, resulting in dysfunction of its normal functions. It can be classified as either compensated or decompensated. Compensated cirrhosis refers to a stage where the liver can still function effectively with minimal symptoms, while decompensated cirrhosis is when the liver damage is severe and clinical complications are present.

Cirrhosis develops over a period of several years due to repeated insults to the liver. Risk factors for cirrhosis include alcohol misuse, hepatitis B and C infection, obesity, type 2 diabetes, autoimmune liver disease, genetic conditions, certain medications, and other rare conditions.

The prognosis of cirrhosis can be assessed using the Child-Pugh score, which predicts mortality based on parameters such as bilirubin levels, albumin levels, INR, ascites, and encephalopathy. The score ranges from A to C, with higher scores indicating a poorer prognosis.

Complications of cirrhosis include portal hypertension, ascites, hepatic encephalopathy, variceal hemorrhage, increased infection risk, hepatocellular carcinoma, and cardiovascular complications.

Diagnosis of cirrhosis is typically done through liver function tests, blood tests, viral hepatitis screening, and imaging techniques such as transient elastography or acoustic radiation force impulse imaging. Liver biopsy may also be performed in some cases.

Management of cirrhosis involves treating the underlying cause, controlling risk factors, and monitoring for complications. Complications such as ascites, spontaneous bacterial peritonitis, oesophageal varices, and hepatic encephalopathy require specific management strategies.

Overall, cirrhosis is a progressive condition that requires ongoing monitoring and management to prevent further complications and improve outcomes for patients.

This patient exhibits signs of potentially life-threatening asthma. In adults, acute severe asthma is characterized by a peak expiratory flow (PEF) of 33-50% of the best or predicted value, a respiratory rate exceeding 25 breaths per minute, a heart rate over 110 beats per minute, and an inability to complete sentences in one breath. On the other hand, life-threatening asthma is indicated by a PEF below 33% of the best or predicted value, a blood oxygen saturation (SpO2) below 92%, a partial pressure of oxygen (PaO2) below 8 kPA, a normal partial pressure of carbon dioxide (PaCO2) within the range of 4.6-6.0 kPa, a silent chest, cyanosis, poor respiratory effort, exhaustion, altered consciousness, and hypotension.

To address acute asthma in adults, the recommended drug doses include administering 5 mg of salbutamol through an oxygen-driven nebulizer, delivering 500 mcg of ipratropium bromide via an oxygen-driven nebulizer, providing 40-50 mg of prednisolone orally, administering 100 mg of hydrocortisone intravenously, and infusing 1.2-2 g of magnesium sulfate intravenously over a period of 20 minutes.

According to the current Advanced Life Support (ALS) guidelines, it is advisable to seek senior advice before considering the use of intravenous aminophylline in cases of severe or life-threatening asthma. If used, a loading dose of 5 mg/kg should be given over 20 minutes, followed by a continuous infusion of 500-700 mcg/kg/hour. To prevent toxicity, it is important to maintain serum theophylline levels below 20 mcg/ml.

In situations where inhaled therapy is not feasible, intravenous salbutamol can be considered, with a slow administration of 250 mcg. However, it should only be used when a patient is receiving bag-mask ventilation.

It is worth noting that there is currently no evidence supporting the use of leukotriene receptor antagonists, such as montelukast, or Heliox in the management of acute severe or life-threatening asthma.

For further information, please refer to the BTS/SIGN Guideline on the Management of Asthma.

Desmopressin, a common treatment for cranial diabetes insipidus (DI) following pituitary surgery, can often lead to hyponatremia as a side effect. Therefore, it is important for patients to have their electrolyte levels regularly monitored. Symptoms of hyponatremia may include nausea, vomiting, headache, confusion, lethargy, fatigue, restlessness, irritability, muscle weakness or spasms, seizures, and drowsiness (which can progress to coma in severe cases).

Further Reading:

Diabetes insipidus (DI) is a condition characterized by either a decrease in the secretion of antidiuretic hormone (cranial DI) or insensitivity to antidiuretic hormone (nephrogenic DI). Antidiuretic hormone, also known as arginine vasopressin, is produced in the hypothalamus and released from the posterior pituitary. The typical biochemical disturbances seen in DI include elevated plasma osmolality, low urine osmolality, polyuria, and hypernatraemia.

Cranial DI can be caused by various factors such as head injury, CNS infections, pituitary tumors, and pituitary surgery. Nephrogenic DI, on the other hand, can be genetic or result from electrolyte disturbances or the use of certain drugs. Symptoms of DI include polyuria, polydipsia, nocturia, signs of dehydration, and in children, irritability, failure to thrive, and fatigue.

To diagnose DI, a 24-hour urine collection is done to confirm polyuria, and U&Es will typically show hypernatraemia. High plasma osmolality with low urine osmolality is also observed. Imaging studies such as MRI of the pituitary, hypothalamus, and surrounding tissues may be done, as well as a fluid deprivation test to evaluate the response to desmopressin.

Management of cranial DI involves supplementation with desmopressin, a synthetic form of arginine vasopressin. However, hyponatraemia is a common side effect that needs to be monitored. In nephrogenic DI, desmopressin supplementation is usually not effective, and management focuses on ensuring adequate fluid intake to offset water loss and monitoring electrolyte levels. Causative drugs need to be stopped, and there is a risk of developing complications such as hydroureteronephrosis and an overdistended bladder.

The current recommendations from NICE for managing warfarin in the presence of bleeding or an abnormal INR are as follows:

In cases of major active bleeding, regardless of the INR level, the first step is to stop administering warfarin. Next, 5 mg of vitamin K (phytomenadione) should be given intravenously. Additionally, dried prothrombin complex concentrate, which contains factors II, VII, IX, and X, should be administered. If dried prothrombin complex is not available, fresh frozen plasma can be given at a dose of 15 ml/kg.

If the INR is greater than 8.0 and there is minor bleeding, warfarin should be stopped. Slow injection of 1-3 mg of vitamin K can be given, and this dose can be repeated after 24 hours if the INR remains high. Warfarin can be restarted once the INR is less than 5.0.

If the INR is greater than 8.0 with no bleeding, warfarin should be stopped. Oral administration of 1-5 mg of vitamin K can be given, and this dose can be repeated after 24 hours if the INR remains high. Warfarin can be restarted once the INR is less than 5.0.

If the INR is between 5.0-8.0 with minor bleeding, warfarin should be stopped. Slow injection of 1-3 mg of vitamin K can be given, and warfarin can be restarted once the INR is less than 5.0.

If the INR is between 5.0-8.0 with no bleeding, one or two doses of warfarin should be withheld, and the subsequent maintenance dose should be reduced.

For more information, please refer to the NICE Clinical Knowledge Summary on the management of warfarin therapy and the BNF guidance on the use of phytomenadione.

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.

Sexually transmitted eye infections can be quite severe and are often characterized by prolonged mucopurulent discharge. There are two main causes of these infections: Chlamydia trachomatis and Neisseria gonorrhoea. Differentiating between the two can be done by considering certain features.

Chlamydia trachomatis infection typically presents with chronic low-grade irritation and mucous discharge that lasts for more than two weeks in sexually active individuals. It may also be accompanied by pre-auricular lymphadenopathy. This type of infection is usually unilateral but can sometimes affect both eyes.

On the other hand, Neisseria gonorrhoea infection tends to develop rapidly, usually within 12 to 24 hours. It is characterized by copious mucopurulent discharge, eyelid swelling, and tender preauricular lymphadenopathy. This type of infection carries a higher risk of complications, such as uveitis, severe keratitis, and corneal perforation.

Based on the patient’s symptoms, it appears that they are more consistent with a Neisseria gonorrhoea infection. The rapid onset, copious discharge, and tender preauricular lymphadenopathy are indicative of this type of infection.

Treatment for gonococcal conjunctivitis in adults is typically based on limited research. However, a study has shown that all 12 patients responded well to a single 1 g intramuscular injection of ceftriaxone, along with a single episode of ocular lavage with saline.

In summary, sexually transmitted eye infections can be caused by either Chlamydia trachomatis or Neisseria gonorrhoea. Differentiating between the two is important in order to provide appropriate treatment. The patient in this case exhibits symptoms that align more closely with a Neisseria gonorrhoea infection, which carries a higher risk of complications. Treatment options for gonococcal conjunctivitis are limited, but a single injection of ceftriaxone has shown positive results in previous studies.

N-acetylcysteine (NAC) enhances the production of glutathione, a substance that helps in the detoxification process. Specifically, NAC aids in the conjugation of NAPQI, a harmful metabolite of paracetamol, with glutathione, thereby neutralizing its toxicity.

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.

According to the 2021 resus council guidelines, when administering an IV fluid challenge to a child with anaphylaxis, the recommended dose is 10 ml/kg. It is important to note that prior to the update, the advised dose was 20 ml/kg. In an exam, if you are provided with the child’s weight, you may be required to calculate the volume requirement.

Further Reading:

Anaphylaxis is a severe and life-threatening allergic reaction that affects the entire body. It is characterized by a rapid onset and can lead to difficulty breathing, low blood pressure, and loss of consciousness. In paediatrics, anaphylaxis is often caused by food allergies, with nuts being the most common trigger. Other causes include drugs and insect venom, such as from a wasp sting.

When treating anaphylaxis, time is of the essence and there may not be enough time to look up medication doses. Adrenaline is the most important drug in managing anaphylaxis and should be administered as soon as possible. The recommended doses of adrenaline vary based on the age of the child. For children under 6 months, the dose is 150 micrograms, while for children between 6 months and 6 years, the dose remains the same. For children between 6 and 12 years, the dose is increased to 300 micrograms, and for adults and children over 12 years, the dose is 500 micrograms. Adrenaline can be repeated every 5 minutes if necessary.

The preferred site for administering adrenaline is the anterolateral aspect of the middle third of the thigh. This ensures quick absorption and effectiveness of the medication. It is important to follow the Resuscitation Council guidelines for anaphylaxis management, as they have recently been updated.

In some cases, 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. This can help confirm the diagnosis and guide further management.

Overall, prompt recognition and administration of adrenaline are crucial in managing anaphylaxis in paediatrics. Following the recommended doses and guidelines can help ensure the best outcomes for patients experiencing this severe allergic reaction.

The most probable diagnosis in this case is anterior uveitis, which refers to inflammation of the iris. It typically presents with symptoms such as a painful and red eye, sensitivity to light, excessive tearing, and decreased visual clarity. The photo above shows a possible indication of this condition, with the presence of pus in the front chamber of the eye, known as hypopyon.

Anterior uveitis can have various causes, including idiopathic cases where no specific cause is identified. Other potential triggers include trauma, chronic joint diseases like spondyloarthropathies and juvenile chronic arthritis, inflammatory bowel disease, psoriasis, sarcoidosis, and infections such as Lyme disease, tuberculosis, leptospirosis, herpes simplex virus (HSV), and varicella-zoster virus (VZV). Additionally, certain malignancies like non-Hodgkin lymphoma, ocular melanoma, and retinoblastoma can be associated with anterior uveitis.

It is worth noting that there is a strong link between the HLA-B27 genotype and anterior uveitis, with approximately 50% of patients having this genetic marker. In this particular case, the likely underlying diagnosis is ankylosing spondylitis, a condition characterized by chronic pain and stiffness in the mid-spine area and sacroiliitis. It is important to mention that around 30% of men with unilateral uveitis will be found to have ankylosing spondylitis.

The mortality rate linked to sepsis can vary depending on various factors such as the patient’s age, overall health, and the severity of the infection. However, on average, the mortality rate for sepsis is estimated to be around 30%.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

A needle cricothyroidotomy is a procedure used in emergency situations to provide oxygenation when intubation and oxygenation are not possible. It is typically performed when a patient cannot be intubated or oxygenated. There are certain conditions that make this procedure contraindicated, such as local infection, distorted anatomy, previous failed attempts, and swelling or mass lesions.

To perform a needle cricothyroidotomy, the necessary equipment should be assembled and prepared. The patient should be positioned supine with their neck in a neutral position. The neck should be cleaned in a sterile manner using antiseptic swabs. If time allows, the area should be anesthetized locally. A 12 or 14 gauge over-the-needle catheter should be assembled to a 10 mL syringe.

The cricothyroid membrane, located between the thyroid and cricoid cartilage, should be identified anteriorly. The trachea should be stabilized with the thumb and forefinger of one hand. Using the other hand, the skin should be punctured in the midline with the needle over the cricothyroid membrane. The needle should be directed at a 45° angle caudally while negative pressure is applied to the syringe. Needle aspiration should be maintained as the needle is inserted through the lower half of the cricothyroid membrane, with air aspiration indicating entry into the tracheal lumen.

Once the needle is in place, the syringe and needle should be removed while the catheter is advanced to the hub. The oxygen catheter should be attached and the airway secured. It is important to be aware of possible complications, such as technique failure, cannula obstruction or dislodgement, injury to local structures, and surgical emphysema if high flow oxygen is administered through a malpositioned cannula.

Calcium is effective in treating hyperkalaemia by counteracting the harmful effects on the heart caused by high levels of potassium. It achieves this by stabilizing the cardiac cell membrane and preventing unwanted depolarization. The onset of action is rapid, typically within 15 minutes, but the effects do not last for a long duration. Calcium is considered the first-line treatment for severe hyperkalaemia (potassium levels above 7 mmol/l) and when significant ECG abnormalities are present, such as widened QRS interval, loss of P wave, or cardiac arrhythmias. However, if the ECG only shows peaked T waves, calcium is usually not recommended.

It is important to note that calcium does not directly affect the serum potassium levels. Therefore, when administering calcium, it should be accompanied by other therapies that actively lower the serum potassium levels, such as insulin and salbutamol.

When hyperkalaemia is accompanied by hemodynamic compromise, calcium chloride is preferred over calcium gluconate. This is because calcium chloride contains approximately three times more elemental calcium than an equal volume of calcium gluconate.

Alzheimer’s disease is the most prevalent type of dementia, making up around 55-60% of all cases. In the UK, the occurrence of Alzheimer’s disease is approximately 5 per 1000 person-years, and the likelihood of developing it increases with age.

The highest amount of Prilocaine that can be administered without adrenaline is 6 mg per kilogram of body weight. However, if Prilocaine is used in combination with adrenaline, the maximum dose increases to 8mg per kilogram.

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.

Infantile hypertrophic pyloric stenosis is a condition characterized by the thickening and enlargement of the smooth muscle in the antrum of the stomach, leading to the narrowing of the pyloric canal. This narrowing can easily cause obstruction. It is a relatively common condition, occurring in about 1 in 500 live births, and is more frequently seen in males than females, with a ratio of 4 to 1. It is most commonly observed in first-born male children, although it can rarely occur in adults as well.

The main symptom of infantile hypertrophic pyloric stenosis is vomiting, which typically begins between 2 to 8 weeks of age. The vomit is usually non-bilious and forcefully expelled. It tends to occur around 30 to 60 minutes after feeding, leaving the baby hungry despite the vomiting. In some cases, there may be blood in the vomit. Other clinical features include persistent hunger, dehydration, weight loss, and constipation. An enlarged pylorus, often described as olive-shaped, can be felt in the right upper quadrant or epigastric in approximately 95% of cases. This is most noticeable at the beginning of a feed.

The typical acid-base disturbance seen in this condition is hypochloremic metabolic alkalosis. This occurs due to the loss of hydrogen and chloride ions in the vomit, as well as decreased secretion of pancreatic bicarbonate. The increased bicarbonate ions in the distal tubule of the kidney lead to the production of alkaline urine. Hyponatremia and hypokalemia are also commonly present.

Ultrasound scanning is the preferred diagnostic tool for infantile hypertrophic pyloric stenosis, as it is reliable and easy to perform. It has replaced barium studies as the investigation of choice.

Initial management involves fluid resuscitation, which should be tailored to the weight and degree of dehydration. Any electrolyte imbalances should also be corrected.

The definitive treatment for this condition is surgical intervention, with the Ramstedt pyloromyotomy being the procedure of choice. Laparoscopic pyloromyotomy is also an effective alternative if suitable facilities are available. The prognosis for infants with this condition is excellent, as long as there is no delay in diagnosis and treatment initiation.

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.

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. When we say 5% dehydration, it means that the body has lost 5 grams of fluid per 100 grams of body weight, which is equivalent to 50 ml of fluid per kilogram. Similarly, 10% dehydration implies a fluid loss of 100 ml per kilogram of body weight.

In the case of this child, who is 5% dehydrated, we can estimate that she has lost 50 ml of fluid per kilogram. Considering her weight of 8 kilograms, her estimated fluid loss would be 400 ml.

The clinical features of dehydration and shock are summarized below:

Dehydration (5%):
– The child appears unwell
– Normal heart rate or tachycardia
– Normal respiratory rate or tachypnea
– Normal peripheral pulses
– Normal or mildly prolonged capillary refill time (CRT)
– Normal blood pressure
– Warm extremities
– Decreased urine output
– Reduced skin turgor
– Sunken eyes
– Depressed fontanelle
– Dry mucous membranes

Clinical shock (10%):
– Pale, lethargic, mottled appearance
– Tachycardia
– Tachypnea
– Weak peripheral pulses
– Prolonged capillary refill time (CRT)
– Hypotension
– Cold extremities
– Decreased urine output
– Decreased level of consciousness

The lingual nerve, a branch of the mandibular division of the trigeminal nerve, provides sensory innervation to the front two-thirds of the tongue and the floor of the mouth. It also carries fibers of the chorda tympani, a branch of the facial nerve, which returns taste information from the front two-thirds of the tongue. The diagram below illustrates the relationships of the lingual nerve in the oral cavity.

The most common cause of lingual nerve injuries is wisdom tooth surgery. Approximately 2% of wisdom tooth extractions result in temporary injury, while permanent damage occurs in 0.2% of cases. Additionally, the nerve can be harmed during dental injections for local anesthesia.

The anterior superior alveolar nerve, a branch of the maxillary division of the trigeminal nerve, provides sensation to the incisor and canine teeth.

The inferior alveolar nerve, another branch of the mandibular division of the trigeminal nerve, supplies sensation to the lower teeth.

The zygomatic nerve, a branch of the maxillary division of the trigeminal nerve, offers sensation to the skin over the zygomatic and temporal bones.

Lastly, the mylohyoid nerve is a motor nerve that supplies the mylohyoid and the anterior belly of the digastric.

To control nosebleeds, it is recommended to have the patient sit upright with their upper body tilted forward and their mouth open. Apply firm pressure to the cartilaginous part of the nose, just in front of the bony septum, and hold it for 10-15 minutes without releasing the pressure.

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.

Hyperpyrexia and hypoglycemia are more frequently observed in children than in adults due to salicylate poisoning. Both adults and children may experience common clinical manifestations such as nausea, vomiting, tinnitus, deafness, sweating, dehydration, hyperventilation, and cutaneous flushing. However, it is important to note that xanthopsia is associated with digoxin toxicity, not salicylate poisoning.

The supraspinatus tendon passes through a narrow space located between the underside of the acromion and acromioclavicular joint, as well as the head of the humerus. When the tendon becomes trapped in this space, it can cause pain and restrict movement, especially during overhead activities. This condition is known as subacromial impingement.

Impingement can occur due to various factors, such as thickening of the tendon caused by partial tears, inflammation, or degeneration. It can also be a result of the space narrowing due to osteoarthritis of the acromioclavicular joint or the presence of bone spurs. Some individuals may have a naturally downward sloping acromion, which makes them more susceptible to impingement.

Certain professions that involve a significant amount of overhead work, like plasterers, builders, and decorators, are particularly prone to developing subacromial impingement.

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.

Congenital adrenal hyperplasia (CAH) is a group of inherited disorders that are caused by autosomal recessive genes. The majority of affected patients, over 90%, have a deficiency of the enzyme 21-hydroxylase. This enzyme is encoded by the 21-hydroxylase gene, which is located on chromosome 6p21 within the HLA histocompatibility complex. The second most common cause of CAH is a deficiency of the enzyme 11-beta-hydroxylase. The condition is rare, with an incidence of approximately 1 in 500 births in the UK. It is more prevalent in the offspring of consanguineous marriages.

The deficiency of 21-hydroxylase leads to a deficiency of cortisol and/or aldosterone, as well as an excess of precursor steroids. As a result, there is an increased secretion of ACTH from the anterior pituitary, leading to adrenocortical hyperplasia.

The severity of CAH varies depending on the degree of 21-hydroxylase deficiency. Female infants often exhibit ambiguous genitalia, such as clitoral hypertrophy and labial fusion. Male infants may have an enlarged scrotum and/or scrotal pigmentation. Hirsutism, or excessive hair growth, occurs in 10% of cases.

Boys with CAH often experience a salt-losing adrenal crisis at around 1-3 weeks of age. This crisis is characterized by symptoms such as vomiting, weight loss, floppiness, and circulatory collapse.

The diagnosis of CAH can be made by detecting markedly elevated levels of the metabolic precursor 17-hydroxyprogesterone. Neonatal screening is possible, primarily through the identification of persistently elevated 17-hydroxyprogesterone levels.

In infants presenting with a salt-losing crisis, the following biochemical abnormalities are observed: hyponatremia (low sodium levels), hyperkalemia (high potassium levels), metabolic acidosis, and hypoglycemia.

Boys experiencing a salt-losing crisis will require fluid resuscitation, intravenous dextrose, and intravenous hydrocortisone.

Affected females will require corrective surgery for their external genitalia. However, they have an intact uterus and ovaries and are capable of having children.

The long-term management of both sexes involves lifelong replacement of hydrocortisone (to suppress ACTH levels).

Acute limb ischaemia refers to a sudden reduction in blood flow to a limb, which puts the limb at risk of tissue death. This condition is most commonly caused by either a sudden blockage of a previously partially blocked artery by a blood clot or by an embolus that travels from another part of the body. Acute limb ischaemia is considered a medical emergency, and if not promptly treated with surgery to restore blood flow, it can lead to extensive tissue damage within six hours.

The classic signs of acute limb ischaemia are often described using the 6 Ps:
– Pain that is constant and persistent
– Absence of pulses in the ankle
– Pallor, cyanosis, or mottling of the skin
– Loss of power or paralysis in the affected limb
– Paraesthesia or reduced sensation, leading to numbness
– Feeling cold in the affected limb

It is important to be able to distinguish between ischaemia caused by a blood clot and ischaemia caused by an embolus. The following highlights the main differences:
Embolus Thrombus
– Onset is sudden, occurring within seconds to minutes – Onset is gradual, taking hours to days
– Ischaemia is usually severe due to the lack of collateral circulation – Ischaemia is less severe due to the presence of collateral circulation
– There is typically no history of claudication, and pulses may still be present in the other leg – There is often a history of claudication, and pulses may also be absent in the other leg
– Skin changes, such as marbling, may be visible in the feet. This can appear as a fine reticular blanching or mottling in the early stages, progressing to coarse, fixed mottling
– Skin changes are usually absent in cases of thrombus-induced ischaemia.

Atropine acts as a blocker for muscarinic acetylcholine receptors, making it an antagonist. It is commonly administered during peri-arrest bradycardia. In adults, a dose of 500 mcg is given every 3-5 minutes, with a maximum total dose of 3mg. On the other hand, the initial intravenous dose of amiodarone is 300 mg. Amiodarone works by prolonging repolarization and decreasing myocardial excitability. Additionally, lidocaine functions by blocking sodium channels.

Further Reading:

In the management of respiratory and cardiac arrest, several drugs are commonly used to help restore normal function and improve outcomes. Adrenaline is a non-selective agonist of adrenergic receptors and is administered intravenously at a dose of 1 mg every 3-5 minutes. It works by causing vasoconstriction, increasing systemic vascular resistance (SVR), and improving cardiac output by increasing the force of heart contraction. Adrenaline also has bronchodilatory effects.

Amiodarone is another drug used in cardiac arrest situations. It blocks voltage-gated potassium channels, which prolongs repolarization and reduces myocardial excitability. The initial dose of amiodarone is 300 mg intravenously after 3 shocks, followed by a dose of 150 mg after 5 shocks.

Lidocaine is an alternative to amiodarone in cardiac arrest situations. It works by blocking sodium channels and decreasing heart rate. The recommended dose is 1 mg/kg by slow intravenous injection, with a repeat half of the initial dose after 5 minutes. The maximum total dose of lidocaine is 3 mg/kg.

Magnesium sulfate is used to reverse myocardial hyperexcitability associated with hypomagnesemia. It is administered intravenously at a dose of 2 g over 10-15 minutes. An additional dose may be given if necessary, but the maximum total dose should not exceed 3 g.

Atropine is an antagonist of muscarinic acetylcholine receptors and is used to counteract the slowing of heart rate caused by the parasympathetic nervous system. It is administered intravenously at a dose of 500 mcg every 3-5 minutes, with a maximum dose of 3 mg.

Naloxone is a competitive antagonist for opioid receptors and is used in cases of respiratory arrest caused by opioid overdose. It has a short duration of action, so careful monitoring is necessary. The initial dose of naloxone is 400 micrograms, followed by 800 mcg after 1 minute. The dose can be gradually escalated up to 2 mg per dose if there is no response to the preceding dose.

It is important for healthcare professionals to have knowledge of the pharmacology and dosing schedules of these drugs in order to effectively manage respiratory and cardiac arrest situations.

Wernicke’s encephalopathy is a condition that is commonly associated with alcohol abuse and other causes of thiamine deficiency. It is characterized by a triad of symptoms, including acute confusion, ophthalmoplegia (paralysis or weakness of the eye muscles), and ataxia (loss of coordination). Additional features may include papilloedema (swelling of the optic disc), hearing loss, apathy, dysphagia (difficulty swallowing), memory impairment, and hypothermia. Most cases also involve peripheral neuropathy, which typically affects the legs.

The condition is caused by capillary hemorrhages, astrocytosis (abnormal increase in astrocytes, a type of brain cell), and neuronal death in the upper brainstem and diencephalon. These changes can be visualized using MRI scanning, although CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will develop 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 time perception, and confabulation (fabrication of false memories).

Patients suspected of having Wernicke’s encephalopathy should receive parenteral thiamine (such as Pabrinex) for at least 5 days. Oral thiamine should be administered after the parenteral therapy.

It is important to note that in patients with chronic thiamine deficiency, the infusion of glucose-containing intravenous fluids without thiamine can trigger the development of Wernicke’s encephalopathy.

The following provides a summary of common causes for different acid-base disorders.

Respiratory alkalosis can be caused by hyperventilation, such as during periods of anxiety. It can also be a result of conditions like pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, or the early stages of aspirin overdose.

Respiratory acidosis, on the other hand, is often associated with chronic obstructive pulmonary disease (COPD), life-threatening asthma, pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or other respiratory conditions.

Metabolic alkalosis can occur due to vomiting, potassium depletion (often caused by diuretic usage), Cushing’s syndrome, or Conn’s syndrome.

Metabolic acidosis with a raised anion gap can be caused by lactic acidosis (such as in cases of hypoxemia, shock, sepsis, or infarction), ketoacidosis (such as in diabetes, starvation, or alcohol excess), renal failure, or poisoning (such as in late stages of aspirin overdose, methanol or ethylene glycol ingestion).

Lastly, metabolic acidosis with a normal anion gap can be a result of conditions like diarrhea, ammonium chloride ingestion, or adrenal insufficiency.

The second heart sound (S2) is created by vibrations produced when the aortic and pulmonary valves close. It marks the end of systole. It is normal to hear a split in the sound during inspiration.

A loud S2 can be associated with certain conditions such as systemic hypertension (resulting in a loud A2), pulmonary hypertension (resulting in a loud P2), hyperdynamic states (like tachycardia, fever, or thyrotoxicosis), and atrial septal defect (which causes a loud P2).

On the other hand, a soft S2 can be linked to decreased aortic diastolic pressure (as seen in aortic regurgitation), poorly mobile cusps (such as calcification of the aortic valve), aortic root dilatation, and pulmonary stenosis (which causes a soft P2).

A widely split S2 can occur during deep inspiration, right bundle branch block, prolonged right ventricular systole (seen in conditions like pulmonary stenosis or pulmonary embolism), and severe mitral regurgitation. However, in the case of atrial septal defect, the splitting is fixed and does not vary with respiration.

Reversed splitting of S2, where P2 occurs before A2 (paradoxical splitting), can occur during deep expiration, left bundle branch block, prolonged left ventricular systole (as seen in hypertrophic cardiomyopathy), severe aortic stenosis, and right ventricular pacing.

Myxoedema coma is a condition characterized by severe hypothyroidism, leading to a state of metabolic decompensation and changes in mental status. Patients with myxoedema coma often experience electrolyte disturbances such as hypoglycemia and hyponatremia. In addition, laboratory findings typically show elevated levels of TSH, as well as low levels of T4 and T3. Other expected findings include hypoxemia and hypercapnia.

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.

The clinical symptoms of mitral stenosis include shortness of breath, which tends to worsen during exercise and when lying flat. Tiredness, palpitations, ankle swelling, cough, and haemoptysis are also common symptoms. Chest discomfort is rarely reported.

The clinical signs of mitral stenosis can include a malar flush, an irregular pulse if atrial fibrillation is present, a tapping apex beat that can be felt as the first heart sound, and a left parasternal heave if there is pulmonary hypertension. The first heart sound is often loud, and a mid-diastolic murmur can be heard.

The mid-diastolic murmur of mitral stenosis is a rumbling sound that is best heard at the apex, in the left lateral position during expiration, using the bell of the stethoscope.

Mitral stenosis is typically caused by rheumatic heart disease, and it is more common in females, with about two-thirds of patients being female.

The FeverPAIN score is a scoring system that is recommended by the current NICE guidelines for assessing acute sore throats. It consists of five items: fever in the last 24 hours, purulence, attendance within three days, inflamed tonsils, and no cough or coryza. Based on the score, different recommendations are given regarding the use of antibiotics.

If the score is 0-1, it is unlikely to be a streptococcal infection, with only a 13-18% chance of streptococcus isolation. Therefore, antibiotics are not recommended in this case. If the score is 2-3, there is a higher chance (34-40%) of streptococcus isolation, so delayed prescribing of antibiotics is considered, with a 3-day ‘back-up prescription’. If the score is 4 or higher, there is a 62-65% chance of streptococcus isolation, and immediate antibiotic use is recommended if the infection is severe. Otherwise, a 48-hour short back-up prescription is suggested.

The Fever PAIN score was developed from a study that included 1760 adults and children aged three and over. It was then tested in a trial that compared three different prescribing strategies: empirical delayed prescribing, using the score to guide prescribing, and combining the score with the use of a near-patient test (NPT) for streptococcus. The use of the score resulted in faster symptom resolution and a reduction in antibiotic prescribing, both by one third. However, the addition of the NPT did not provide any additional benefit.

Overall, the FeverPAIN score is a useful tool for assessing acute sore throats and guiding antibiotic prescribing decisions. It has been shown to be effective in reducing unnecessary antibiotic use and improving patient outcomes.

Q fever is a highly contagious infection caused by Coxiella burnetii, which can be transmitted from animals to humans. It is commonly observed as an occupational disease among individuals working in farming, slaughterhouses, and animal research. Approximately 50% of cases do not show any symptoms, while those who are affected often experience flu-like symptoms such as headache, fever, muscle pain, diarrhea, nausea, and vomiting.

In some cases, patients may develop an atypical pneumonia characterized by a dry cough and minimal chest signs. Q fever can also lead to hepatitis and enlargement of the liver (hepatomegaly), although jaundice is not commonly observed. Typical blood test results for Q fever include an elevated white cell count (30-40%), ALT/AST levels that are usually 2-3 times higher than normal, increased ALP levels (70%), reduced sodium levels (30%), and reactive thrombocytosis.

It is important to check patients for heart murmurs and signs of valve disease, as these conditions increase the risk of developing infective endocarditis. Treatment for Q fever typically involves a two-week course of doxycycline.

Bronchiolitis is a respiratory infection that primarily affects infants aged 2 to 6 months. It is typically caused by a viral infection, with respiratory syncytial virus (RSV) being the most common culprit. RSV infections are most prevalent during the winter months, from November to March. In fact, bronchiolitis is the leading cause of hospitalization among infants in the UK.

The symptoms of bronchiolitis include poor feeding (consuming less than 50% of their usual intake in the past 24 hours), lethargy, a history of apnea, a respiratory rate exceeding 70 breaths per minute, nasal flaring or grunting, severe chest wall recession, cyanosis (bluish discoloration of the skin), and low oxygen saturation levels. For children aged 6 weeks and older, oxygen saturation levels below 90% indicate a need for medical attention. For babies under 6 weeks or those with underlying health conditions, oxygen saturation levels below 92% require medical attention.

To confirm the diagnosis of bronchiolitis, a nasopharyngeal aspirate can be taken for rapid testing of RSV. This test is useful in preventing unnecessary further testing and allows for the isolation of the infected infant.

Most infants with bronchiolitis experience a mild, self-limiting illness that does not require hospitalization. Treatment primarily focuses on supportive measures, such as ensuring adequate fluid and nutritional intake and controlling the infant’s temperature. The illness typically lasts for 7 to 10 days.

However, hospital referral and admission are recommended in cases of poor feeding, lethargy, a history of apnea, a respiratory rate exceeding 70 breaths per minute, nasal flaring or grunting, severe chest wall recession, cyanosis, and oxygen saturation levels below 94%. If hospitalization is necessary, treatment involves supportive measures, supplemental oxygen, and nasogastric feeding as needed. There is limited or no evidence supporting the use of antibiotics, antivirals, bronchodilators, corticosteroids, hypertonic saline, or adrenaline nebulizers for the treatment of bronchiolitis.

This presentation strongly suggests a diagnosis of whooping cough, which is an infection of the upper respiratory tract caused by the bacteria Bordetella pertussis. The disease is highly contagious and is transmitted through respiratory droplets. The incubation period is typically 7-21 days, and it is estimated that about 90% of close household contacts will become infected.

The clinical course of whooping cough can be divided into two stages. The first stage, known as the catarrhal stage, is similar to a mild respiratory infection with symptoms such as low-grade fever and a runny nose. A cough may be present, but it is usually mild compared to the second stage. This phase typically lasts about a week.

The second stage, called the paroxysmal stage, is characterized by the development of a distinctive cough. The coughing occurs in spasms, often preceded by an inspiratory whoop sound. These spasms are followed by a series of rapid, hacking coughs. Patients may experience vomiting and may develop subconjunctival hemorrhages and petechiae. Between spasms, patients generally feel well and there are usually no abnormal chest findings. This stage can last up to 3 months, with a gradual recovery over this period. The later stages of this phase are sometimes referred to as the convalescent stage.

Complications of whooping cough can include secondary pneumonia, rib fractures, pneumothorax, hernias, syncopal episodes, encephalopathy, and seizures.

Public Health England (PHE) provides recommendations for testing for whooping cough based on the age of the patient, time since onset of illness, and severity of presentation. For infants under 12 months of age, hospitalised patients should undergo PCR testing, while non-hospitalised patients within two weeks of onset should be tested using culture of a nasopharyngeal swab or aspirate. Non-hospitalised patients presenting over two weeks after onset should be investigated with serology for anti-pertussis toxin IgG antibody levels.

For children over 12 months of age and adults, patients within two weeks of onset should be tested using culture of a nasopharyngeal swab or aspirate. Patients aged 5 to 16 who have not received the vaccine within the last year and present over two weeks after onset should have oral fluid testing for anti-pertussis toxin IgG antibody levels.

Based on the Lund and Browder chart, the total percentage of burns is calculated as 3 since it affects one side of both hands.

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.

Acute epiglottitis is inflammation of the epiglottis, which can be life-threatening if not treated promptly. When the soft tissues surrounding the epiglottis are also affected, it is called acute supraglottitis. This condition is most commonly seen in children between the ages of 3 and 5, but it can occur at any age, with adults typically presenting in their 40s and 50s.

In the past, Haemophilus influenzae type B was the main cause of acute epiglottitis, but with the introduction of the Hib vaccination, it has become rare in children. Streptococcus spp. is now the most common causative organism. Other potential culprits include Staphylococcus aureus, Pseudomonas spp., Moraxella catarrhalis, Mycobacterium tuberculosis, and the herpes simplex virus. In immunocompromised patients, Candida spp. and Aspergillus spp. infections can occur.

The typical symptoms of acute epiglottitis include fever, sore throat, painful swallowing, difficulty swallowing secretions (especially in children who may drool), muffled voice, stridor, respiratory distress, rapid heartbeat, tenderness in the front of the neck over the hyoid bone, ear pain, and swollen lymph nodes in the neck. Some patients may also exhibit the tripod sign, where they lean forward on outstretched arms to relieve upper airway obstruction.

To diagnose acute epiglottitis, fibre-optic laryngoscopy is considered the gold standard investigation. However, this procedure should only be performed by an anaesthetist in a setting prepared for intubation or tracheostomy in case of airway obstruction. Other useful tests include a lateral neck X-ray to look for the thumbprint sign, throat swabs, blood cultures, and a CT scan of the neck if an abscess is suspected.

When dealing with a case of acute epiglottitis, it is crucial not to panic or distress the patient, especially in pediatric cases. Avoid attempting to examine the throat with a tongue depressor, as this can trigger spasm and worsen airway obstruction. Instead, keep the patient as calm as possible and immediately call a senior anaesthetist, a senior paediatrician, and an ENT surgeon. Nebulized adrenaline can be used as a temporary measure if there is critical airway obstruction.

The Apgar score is a straightforward way to evaluate the well-being of a newborn baby right after birth. It consists of five criteria, each assigned a score ranging from zero to two. Typically, the assessment is conducted at one and five minutes after delivery, with the possibility of repeating it later if the score remains low. A score of 7 or higher is considered normal, while a score of 4-6 is considered fairly low, and a score of 3 or below is regarded as critically low. To remember the five criteria, you can use the acronym APGAR:

Appearance
Pulse rate
Grimace
Activity
Respiratory effort

The Apgar score criteria are as follows:

Score of 0:
Appearance (skin color): Blue or pale all over
Pulse rate: Absent
Reflex irritability (grimace): No response to stimulation
Activity: None
Respiratory effort: Absent

Score of 1:
Appearance (skin color): Blue at extremities (acrocyanosis)
Pulse rate: Less than 100 per minute
Reflex irritability (grimace): Grimace on suction or aggressive stimulation
Activity: Some flexion
Respiratory effort: Weak, irregular, gasping

Score of 2:
Appearance (skin color): No cyanosis, body and extremities pink
Pulse rate: More than 100 per minute
Reflex irritability (grimace): Cry on stimulation
Activity: Flexed arms and legs that resist extension
Respiratory effort: Strong, robust cry

DKA is characterized by three main symptoms: high blood sugar levels (hyperglycemia), an acidic pH in the body (acidosis), and an increased presence of ketones in the blood (ketonaemia).

Further Reading:

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.