Acute limb ischaemia refers to a sudden decrease 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 partially blocked artery or an embolus from another part of the body. It is considered a surgical emergency, as without surgical intervention, the limb can experience extensive tissue necrosis within six hours.

The typical signs of acute limb ischaemia are often described using the 6 Ps: constant and persistent pain, absence of pulses in the ankle, paleness or cyanosis of the limb, loss of power or paralysis, reduced sensation or numbness, and a sensation of coldness. The leading cause of acute limb ischaemia is a sudden blockage of a previously narrowed artery (60% of cases). The second most common cause is an embolism (30%), which can originate from sources such as a blood clot in the heart or a prosthetic heart valve. It is important to differentiate between these two causes, as the treatment and prognosis differ.

Other potential causes of acute limb ischaemia include trauma, Raynaud’s syndrome, iatrogenic injury, popliteal aneurysm, aortic dissection, and compartment syndrome. If acute limb ischaemia is suspected, it is crucial to seek immediate assessment by a vascular surgeon. Patients with suspected peripheral arterial disease should undergo an ankle brachial pressure index (ABPI) measurement. If there is uncertainty in the diagnosis, urgent arteriography may be necessary.

The management of acute limb ischaemia in secondary care depends on factors such as the type and location of the blockage, duration of ischaemia, presence of other medical conditions, type of conduit (artery or graft), risks associated with treatment, and viability of the limb. Possible interventions include percutaneous catheter-directed thrombolytic therapy, surgical embolectomy, and endovascular revascularisation if the limb is still viable. If the limb is at immediate or marginal risk, the choice between surgical or endovascular techniques will depend on factors such as time to revascularisation and the severity of sensory and motor deficits. In cases where the limb is unsalvageable, amputation may be necessary to prevent further complications and potential multi organ damage.

Erythroderma is a condition characterized by widespread redness affecting more than 90% of the body surface. It is also known as exfoliative erythroderma due to the presence of skin exfoliation. Another term used to describe this condition is the red man syndrome.

The clinical features of exfoliative erythroderma include the rapid spread of redness to cover more than 90% of the body surface. Scaling of the skin occurs between days 2 and 6, leading to thickening of the skin. Despite the skin feeling hot, patients often experience a sensation of coldness. Keratoderma, which is the thickening of the skin on the palms and soles, may develop. Over time, erythema and scaling of the scalp can result in hair loss. The nails may become thickened, ridged, and even lost. Lymphadenopathy, or enlarged lymph nodes, is a common finding. In some cases, the patient’s overall health may be compromised.

Exfoliative erythroderma can be caused by various factors, including eczema (with atopic dermatitis being the most common underlying cause), psoriasis, lymphoma and leukemia (with cutaneous T-cell lymphoma and Hodgkin lymphoma being the most common malignant causes), certain drugs (more than 60 drugs have been implicated, with sulphonamides, isoniazid, penicillin, antimalarials, phenytoin, captopril, and cimetidine being the most commonly associated), idiopathic (unknown cause), and rare conditions such as pityriasis rubra pilaris and pemphigus foliaceus. Withdrawal of corticosteroids, underlying infections, hypocalcemia, and the use of strong coal tar preparations can also precipitate exfoliative erythroderma.

Potential complications of exfoliative erythroderma include dehydration, hypothermia, cardiac failure, overwhelming secondary infection, protein loss and edema, anemia (due to loss of iron, B12, and folate), and lymphadenopathy.

Management of exfoliative erythroderma should involve referring the patient to the medical on-call team and dermatology for admission. It is important to keep the patient warm and start intravenous fluids, such as warmed 0.9% saline. Applying generous amounts of emollients and wet dressings can help alleviate

There is a significant link between methotrexate and the development of pulmonary fibrosis. While there have been instances of pulmonary fibrosis occurring as a result of infliximab, this particular side effect is more commonly associated with methotrexate use.

Methotrexate can also cause other side effects such as nausea and vomiting, abdominal pain, gastrointestinal bleeding, dizziness, stomatitis, hepatotoxicity, neutropenia, and pneumonitis.

A Focussed Assessment with Sonography for Trauma (FAST) scan is a point-of-care ultrasound examination conducted when a trauma patient arrives. Its primary purpose is to identify the presence of intra-abdominal free fluid, which is typically assumed to be haemoperitoneum in the context of trauma. This information helps healthcare providers make decisions regarding further management of the patient.

The sensitivity of FAST scanning for detecting intraperitoneal fluid is approximately 90%, while its specificity is around 95%. However, its sensitivity for detecting solid organ injuries is much lower. As a result, FAST scanning has largely replaced diagnostic peritoneal lavage as the preferred initial method for assessing haemoperitoneum.

During a standard FAST scan, four regions are assessed. The first is the subxiphoid transverse view, which is used to check for pericardial effusion and left lobe liver injuries. The second is the longitudinal view of the right upper quadrant, which helps identify right liver injuries, right kidney injuries, and fluid in the hepatorenal recess (Morison’s pouch). The third is the longitudinal view of the left upper quadrant, which is used to assess for splenic injury and left kidney injury. Lastly, the transverse and longitudinal views of the suprapubic region are examined to assess the bladder and fluid in the pouch of Douglas.

In addition to the standard FAST scan, an extended FAST or eFAST may also be performed. This involves examining the left and right thoracic regions to assess for the presence of pneumothorax and haemothorax.

The hepatorenal recess is the deepest part of the peritoneal cavity when a patient is lying flat. Therefore, it is the most likely area for fluid to accumulate in a supine position.

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.

When someone takes too much paracetamol, it can harm their liver cells and the tubules in their kidneys. This is because paracetamol produces a harmful substance called NAPQI, which is normally combined with glutathione. However, when there is too much NAPQI, it can cause damage and death to liver and kidney cells.

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.

Otoliths are commonly found in the inferior semicircular canal of patients, while their presence in the anterior semicircular canal is extremely uncommon.

Further Reading:

Benign paroxysmal positional vertigo (BPPV) is a common cause of vertigo, characterized by sudden dizziness and vertigo triggered by changes in head position. It typically affects individuals over the age of 55 and is less common in younger patients. BPPV is caused by dysfunction in the inner ear, specifically the detachment of otoliths (calcium carbonate particles) from the utricular otolithic membrane. These loose otoliths move through the semicircular canals, triggering a sensation of movement and resulting in conflicting sensory inputs that cause vertigo.

The majority of BPPV cases involve otoliths in the posterior semicircular canal, followed by the inferior semicircular canal. BPPV in the anterior semicircular canals is rare. Clinical features of BPPV include vertigo triggered by head position changes, such as rolling over in bed or looking upwards, accompanied by nausea. Episodes of vertigo typically last 10-20 seconds and can be diagnosed through positional nystagmus, which is a specific eye movement, observed during diagnostic maneuvers like the Dix-Hallpike maneuver.

Hearing loss and tinnitus are not associated with BPPV. The prognosis for BPPV is generally good, with spontaneous resolution occurring within a few weeks to months. Symptomatic relief can be achieved through the Epley maneuver, which is successful in around 80% of cases, or patient home exercises like the Brandt-Daroff exercises. Medications like Betahistine may be prescribed but have limited effectiveness in treating BPPV.

In patients of this age who have experienced a change in bowel habit, rectal bleeding, and weight loss, the most probable diagnosis is colorectal carcinoma. Considering the patient’s history and examination findings, the other options in this question are significantly less likely. It is crucial to refer this patient promptly to a specialized team that focuses on the treatment of lower gastrointestinal cancer.

Aminoglycosides have the ability to pass through the placenta and can lead to damage to the 8th cranial nerve in the fetus, resulting in permanent bilateral deafness.

ACE inhibitors, such as ramipril, can cause hypoperfusion, renal failure, and the oligohydramnios sequence if given in the 2nd and 3rd trimesters.

Aminoglycosides, like gentamicin, can cause ototoxicity and deafness in the fetus.

High doses of aspirin can lead to 1st 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, including diazepam, when administered late in pregnancy, can result in respiratory depression and a neonatal withdrawal syndrome.

Calcium-channel blockers, if given in the 1st trimester, can cause phalangeal abnormalities. If given in the 2nd and 3rd trimesters, they can lead to fetal growth retardation.

Carbamazepine can cause hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol is associated with grey baby syndrome.

Corticosteroids, if given in the 1st trimester, may cause orofacial clefts.

Danazol, if given in the 1st trimester, can cause masculinization of the female fetuses genitals.

Finasteride should not be handled by pregnant women as crushed or broken tablets can be absorbed through the skin and affect male sex organ development.

Haloperidol, if given in the 1st trimester, may cause limb malformations. If given in the 3rd trimester, there is an increased risk of extrapyramidal symptoms in the neonate.

Heparin can lead to maternal bleeding and thrombocytopenia.

Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate.

Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability.

Lithium, if given in the 1st trimester, poses a risk of fetal cardiac malformations.

Biliary colic occurs when a gallstone temporarily blocks either the cystic duct or Hartmann’s pouch, causing the gallbladder to contract. The blockage is relieved when the stone either falls back into the gallbladder or passes through the duct.

Located at the junction of the gallbladder’s neck and the cystic duct, there is a protrusion in the gallbladder wall known as Hartmann’s pouch. This is the most common site for gallstones to become stuck and cause cholestasis.

Patients experiencing biliary colic typically present with intermittent, cramp-like pain in the upper right quadrant of the abdomen. The pain can last anywhere from 15 minutes to 24 hours and is often accompanied by feelings of nausea and vomiting. It is not uncommon for the pain to radiate to the right scapula area.

Dementia with Lewy bodies (DLB) is characterized by several key features, including spontaneous fluctuations in cognitive abilities, visual hallucinations, and Parkinsonism. Visual hallucinations are particularly prevalent in DLB and Parkinson’s disease dementia, which are considered to be part of the same spectrum. While visual hallucinations can occur in other forms of dementia, they are less frequently observed.

Further Reading:

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

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

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

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

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

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

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

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

Lidocaine works by blocking voltage-gated sodium channels. These channels are responsible for the propagation of action potentials in nerve fibers. By blocking these channels, lidocaine prevents the influx of sodium ions into the nerve cells, thereby inhibiting the generation and conduction of nerve impulses. This results in local anesthesia, as the transmission of pain signals from the skin to the brain is effectively blocked.

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.

The Seidel test is a method used to assess ocular trauma. The procedure involves applying a 10% fluorescein strip to the affected area and examining it using a cobalt blue filter. If there is a corneal laceration with leakage of aqueous fluid, the dye will be diluted by the fluid, resulting in a visible stream.

In addition to the Seidel test, there are several other important steps to be taken during an eye examination for trauma. These include inspecting the overall appearance of the eye, examining the lids and peri-orbital bones, assessing visual acuity in both eyes, testing visual fields by confrontation, evaluating eye movements, measuring pupil size and response to light and accommodation, checking for foreign bodies using a slit lamp, performing fundoscopy and assessing the red reflex.

The Amsler grid test is a useful tool for detecting central visual field defects and aiding in the diagnosis of age-related macular degeneration. A positive Amsler test is indicated by the appearance of curved or wavy lines on the grid.

Tonometry is a technique used to measure intraocular pressure (IOP), which is helpful in diagnosing glaucoma.

Retinal photography is a sophisticated imaging process that involves using a digital camera to capture detailed pictures of the retina. It is primarily used to document the health of various structures in the eye, such as the optic nerve, posterior pole, macula, retina, and its blood vessels. However, it is not typically used as part of the initial evaluation for trauma.

Eye pH measurement is a valuable tool in evaluating chemical eye injuries.

Septic arthritis occurs when an infectious agent invades a joint, causing it to become purulent. The main symptoms of septic arthritis include pain in the affected joint, redness, warmth, and swelling of the joint, and difficulty moving the joint. Patients may also experience fever and systemic upset. The most common cause of septic arthritis is Staphylococcus aureus, but other bacteria such as Streptococcus spp., Haemophilus influenzae, Neisseria gonorrhoea, and Escherichia coli can also be responsible.

According to the current recommendations by NICE and the BNF, the initial treatment for septic arthritis is flucloxacillin. However, if a patient is allergic to penicillin, clindamycin can be used instead. If there is a suspicion of MRSA infection, vancomycin is the recommended choice. In cases where gonococcal arthritis or a Gram-negative infection is suspected, cefotaxime is the preferred treatment. The suggested duration of treatment is typically 4-6 weeks, although it may be longer if the infection is complicated.

The preferred imaging method for unstable patients with blunt abdominal trauma is FAST scanning (Focused Assessment with Sonography in Trauma). It has replaced DPL as the imaging modality of choice. It is important to note that the primary purpose of a FAST scan is to detect intraperitoneal fluid, assumed to be blood, and guide the decision on whether a laparotomy is necessary. In this case, a CT scan is not recommended as the patient is unstable with tachycardia and hypotension. While CT is the most diagnostically accurate imaging technique, it requires a stable and cooperative patient.

Further Reading:

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

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

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

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

Croup is identified by a distinct cough that sounds like a seal barking. This type of cough is commonly seen in patients within the typical age range for croup. Along with the barking cough, the patient may also experience hoarseness, stridor (a high-pitched sound during breathing), and respiratory distress. While there may be a history of a foreign body in the upper airway, it is not always present. The symptoms of an upper respiratory tract infection prior to the onset of croup do not align with a foreign body diagnosis. Additionally, there is no mention of a rash, which would be indicative of measles.

Further Reading:

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

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

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

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

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

When treating adults with bradycardia, a maximum of 6 doses of atropine 500 mcg can be administered. Each dose is given intravenously every 3-5 minutes. The total dose should not exceed 3mg.

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

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.

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.

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.

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.

A recent audit conducted by the Royal College of Emergency Medicine (RCEM) in 2018 revealed a concerning decline in the standards of pain management for children with fractured limbs in Emergency Departments (EDs). The audit found that the majority of patients experienced longer waiting times for pain relief compared to previous years. Shockingly, more than 1 in 10 children who presented with significant pain due to a limb fracture did not receive any pain relief at all.

To address this issue, the Agency for Health Care Policy and Research (AHCPR) in the USA recommends following the ABCs of pain management for all patients, including children. This approach involves regularly asking about pain, systematically assessing it, believing the patient and their family in their reports of pain and what relieves it, choosing appropriate pain control options, delivering interventions in a timely and coordinated manner, and empowering patients and their families to have control over their pain management.

The RCEM has established standards that require a child’s pain to be assessed within 15 minutes of their arrival at the ED. This is considered a fundamental standard. Various rating scales are available for assessing pain in children, with the choice depending on the child’s age and ability to use the scale. These scales include the Wong-Baker Faces Pain Rating Scale, Numeric rating scale, and Behavioural scale.

To ensure timely administration of analgesia to children in acute pain, the RCEM has set specific standards. These standards state that 100% of patients in severe pain should receive appropriate analgesia within 60 minutes of their arrival or triage, whichever comes first. Additionally, 75% should receive analgesia within 30 minutes, and 50% within 20 minutes.

The diagnosis in this case is clearly gout. According to the guidelines from the European League Against Rheumatism (EULAR), the development of sudden joint pain accompanied by swelling, tenderness, and redness, which worsens over a period of 6-12 hours, strongly suggests crystal arthropathy.

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

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

Colchicine is an effective alternative for treating gout, although it may take longer to take effect. It is often used in patients who cannot take NSAIDs due to contraindications, such as hypertension or a history of peptic ulcer disease. It’s important to note that colchicine can have effects on the bone marrow, leading to an increase in neutrophils and a decrease in platelets. Therefore, it should not be used in patients with blood disorders, as is the case with this patient.

Allopurinol should not be used during an acute gout attack as it can prolong the attack and even trigger another acute attack. If a patient is already taking allopurinol, it should be continued, and the acute attack should be treated with NSAIDs, colchicine, or corticosteroids as appropriate.

Corticosteroids are an effective alternative for managing acute gout in patients who cannot take NSAIDs or colchicine. They can be administered orally, intramuscularly, intravenously, or directly into the affected joint. In this patient’s case, using corticosteroids would be the safest and most reasonable treatment option.

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 most probable diagnosis in this case is idiopathic intracranial hypertension, also known as benign intracranial hypertension or pseudotumour cerebri. This condition typically affects overweight women in their 20s and 30s.

The clinical features of idiopathic intracranial hypertension include:
– Headache: The headache is usually worse in the morning and evenings, relieved by standing, and worsened when lying down. It can also be aggravated by coughing and sneezing. Some patients may experience pain around the shoulder girdle.
– Nausea and vomiting
– Visual field defects: These develop gradually over time.
– 6th nerve palsy and diplopia
– Bilateral papilloedema

To investigate this condition, the patient should undergo a CT scan and/or MRI of the brain, as well as a lumbar puncture to measure the opening pressure and analyze the cerebrospinal fluid (CSF).

The primary treatment goal for idiopathic intracranial hypertension is to prevent visual loss. This can be achieved through one of the following strategies:
– Repeated lumbar puncture to control intracranial pressure (ICP)
– Medical treatment with acetazolamide
– Surgical decompression of the optic nerve sheath

Haemothorax often leads to reduced or absent air entry, a dull percussion sound, and decreased fremitus on the affected side. Commonly observed symptoms in patients with haemothorax include decreased or absent air entry, a dull percussion note when the affected side is tapped, reduced fremitus on the affected side, and in cases of massive haemothorax, tracheal deviation away from the affected side. Other signs that may be present include a rapid heart rate (tachycardia), rapid breathing (tachypnoea), low blood pressure (hypotension), and signs of shock.

Further Reading:

Haemothorax is the accumulation of blood in the pleural cavity of the chest, usually resulting from chest trauma. It can be difficult to differentiate from other causes of pleural effusion on a chest X-ray. Massive haemothorax refers to a large volume of blood in the pleural space, which can impair physiological function by causing blood loss, reducing lung volume for gas exchange, and compressing thoracic structures such as the heart and IVC.

The management of haemothorax involves replacing lost blood volume and decompressing the chest. This is done through supplemental oxygen, IV access and cross-matching blood, IV fluid therapy, and the insertion of a chest tube. The chest tube is connected to an underwater seal and helps drain the fluid, pus, air, or blood from the pleural space. In cases where there is prompt drainage of a large amount of blood, ongoing significant blood loss, or the need for blood transfusion, thoracotomy and ligation of bleeding thoracic vessels may be necessary. It is important to have two IV accesses prior to inserting the chest drain to prevent a drop in blood pressure.

In summary, haemothorax is the accumulation of blood in the pleural cavity due to chest trauma. Managing haemothorax involves replacing lost blood volume and decompressing the chest through various interventions, including the insertion of a chest tube. Prompt intervention may be required in cases of significant blood loss or ongoing need for blood transfusion.

If deflating the cuff does not improve the stability of a tracheostomy patient, it is recommended to remove the tracheostomy tube. Deflating the cuff is typically done after removing the inner tube and any additional devices like speaking valves or caps, and passing a suction catheter. If deflating the cuff does not have the desired effect, the next step would be to remove the tracheostomy tube. If this also proves ineffective, the clinician should consider ventilating the patient through the mouth or stoma.

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.

Functional murmurs, also referred to as physiological or flow murmurs, are frequently observed during pregnancy and other conditions associated with increased blood flow. These murmurs arise as a result of the heightened resting cardiac output and do not necessitate any additional examination.

When a complete quadriceps rupture occurs, it leads to the inability to actively extend the knee. Please refer to the following notes for more detailed information.

Further Reading:

A quadriceps tendon tear or rupture is a traumatic lower limb and joint injury that occurs when there is heavy loading on the leg, causing forced contraction of the quadriceps while the foot is planted and the knee is partially bent. These tears most commonly happen at the osteotendinous junction between the tendon and the superior pole of the patella. Quadriceps tendon ruptures are more common than patellar tendon ruptures.

When a quadriceps tendon tear occurs, the patient usually experiences a tearing sensation and immediate pain. They will then typically complain of pain around the knee and over the tendon. Clinically, there will often be a knee effusion and weakness or inability to actively extend the knee.

In cases of complete quadriceps tears, the patella will be displaced distally, resulting in a low lying patella or patella infera, also known as patella baja. Radiological measurements, such as the Insall-Salvati ratio, can be used to measure patella height. The Insall-Salvati ratio is calculated by dividing the patellar tendon length by the patellar length. A normal ratio is between 0.8 to 1.2, while a low lying patella (patella baja) is less than 0.8 and a high lying patella (patella alta) is greater than 1.2.

The risk of infection is highest with femoral central lines.

A central venous catheter (CVC) is a type of catheter that is inserted into a large vein in the body, typically in the neck, chest, or groin. It has several important uses, including CVP monitoring, pulmonary artery pressure monitoring, repeated blood sampling, IV access for large volumes of fluids or drugs, TPN administration, dialysis, pacing, and other procedures such as placement of IVC filters or venous stents.

When inserting a central line, it is ideal to use ultrasound guidance to ensure accurate placement. However, there are certain contraindications to central line insertion, including infection or injury to the planned access site, coagulopathy, thrombosis or stenosis of the intended vein, a combative patient, or raised intracranial pressure for jugular venous lines.

The most common approaches for central line insertion are the internal jugular, subclavian, femoral, and PICC (peripherally inserted central catheter) veins. The internal jugular vein is often chosen due to its proximity to the carotid artery, but variations in anatomy can occur. Ultrasound can be used to identify the vessels and guide catheter placement, with the IJV typically lying superficial and lateral to the carotid artery. Compression and Valsalva maneuvers can help distinguish between arterial and venous structures, and doppler color flow can highlight the direction of flow.

In terms of choosing a side for central line insertion, the right side is usually preferred to avoid the risk of injury to the thoracic duct and potential chylothorax. However, the left side can also be used depending on the clinical situation.

Femoral central lines are another option for central venous access, with the catheter being inserted into the femoral vein in the groin. Local anesthesia is typically used to establish a field block, with lidocaine being the most commonly used agent. Lidocaine works by blocking sodium channels and preventing the propagation of action potentials.

In summary, central venous catheters have various important uses and should ideally be inserted using ultrasound guidance. There are contraindications to their insertion, and different approaches can be used depending on the clinical situation. Local anesthesia is commonly used for central line insertion, with lidocaine being the preferred agent.

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.

If the distance between the canines is less than 3 cm, it indicates that the bite was likely caused by a child. On the other hand, if the distance is greater than 3 cm, it suggests that the bite was likely caused by an adult. In this particular case, the intercanine distance does not support the mother’s explanation of the injury, indicating that a child is not responsible. Therefore, measures should be taken to ensure the safety of the child, as the story provided by the mother does not align with the injury. In most hospitals, the child protection team is typically led by paediatricians. It is usually possible to differentiate between dog bites and human bites based on the shape of the arch, as well as the morphology of the incisors and canines.

Further Reading:

Bite wounds from animals and humans can cause significant injury and infection. It is important to properly assess and manage these wounds to prevent complications. In human bites, both the biter and the injured person are at risk of infection transmission, although the risk is generally low.

Bite wounds can take various forms, including lacerations, abrasions, puncture wounds, avulsions, and crush or degloving injuries. The most common mammalian bites are associated with dogs, cats, and humans.

When assessing a human bite, it is important to gather information about how and when the bite occurred, who was involved, whether the skin was broken or blood was involved, and the nature of the bite. The examination should include vital sign monitoring if the bite is particularly traumatic or sepsis is suspected. The location, size, and depth of the wound should be documented, along with any functional loss or signs of infection. It is also important to check for the presence of foreign bodies in the wound.

Factors that increase the risk of infection in bite wounds include the nature of the bite, high-risk sites of injury (such as the hands, feet, face, genitals, or areas of poor perfusion), wounds penetrating bone or joints, delayed presentation, immunocompromised patients, and extremes of age.

The management of bite wounds involves wound care, assessment and administration of prophylactic antibiotics if indicated, assessment and administration of tetanus prophylaxis if indicated, and assessment and administration of antiviral prophylaxis if indicated. For initial wound management, any foreign bodies should be removed, the wound should be encouraged to bleed if fresh, and thorough irrigation with warm, running water or normal saline should be performed. Debridement of necrotic tissue may be necessary. Bite wounds are usually not appropriate for primary closure.

Prophylactic antibiotics should be considered for human bites that have broken the skin and drawn blood, especially if they involve high-risk areas or the patient is immunocompromised. Co-amoxiclav is the first-line choice for prophylaxis, but alternative antibiotics may be used in penicillin-allergic patients. Antibiotics for wound infection should be based on wound swab culture and sensitivities.

Tetanus prophylaxis should be administered based on the cleanliness and risk level of the wound, as well as the patient’s vaccination status. Blood-borne virus risk should also be assessed, and testing for hepatitis B, hepatitis C, and HIV

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

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.

Lesions that occur in the optic nerve, specifically those that are located outside of the optic chiasm, result in visual loss in only one eye on the same side as the lesion. There are several factors that can cause these optic nerve lesions, including optic neuritis which is often associated with multiple sclerosis. Other causes include compression of the optic nerve due to tumors in the eye, toxicity from substances like ethambutol or methanol, and trauma to the optic nerve such as fractures in the orbital bone. The diagram provided below illustrates the different types of visual field defects that can occur depending on the location of the lesion along the visual pathway.

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.

Pemphigus, derived from the Greek word for bubble ‘pemphix’, refers to a group of autoimmune disorders that cause blistering of the skin and/or mucosal surfaces. The most common subset is pemphigus vulgaris (PV), which accounts for approximately 70% of cases worldwide. PV is characterized by an autoimmune response where autoantibodies target cell surface antigens on keratinocytes, specifically desmogleins 1 and 3. This leads to a loss of cell-to-cell adhesion and separation, resulting in blister formation.

On the other hand, bullous pemphigoid (BP) is a chronic autoimmune blistering skin disorder that affects the subepidermal layer. It occurs when the basement membrane of the epidermis is attacked by IgG and sometimes IgE immunoglobulins, as well as activated T lymphocytes. The binding of autoantibodies to proteins and the release of cytokines from T cells trigger complement activation, neutrophil recruitment, and the release of proteolytic enzymes. These enzymes destroy the hemidesmosomes, leading to the formation of subepidermal blisters.

To summarize the differences between pemphigus vulgaris and bullous pemphigoid, the following provides a comparison:

Pemphigus Vulgaris:
– Age: Middle-aged people (mean age 50)
– Oral involvement: Common
– Blister type: Large, flaccid, and painful
– Blister content: Fluid-filled, often haemorrhagic
– Areas commonly affected: Initially face and scalp, then spread to the chest and back
– Nikolsky sign: Usually positive
– Pruritus: Rare
– Skin biopsy: Intra-epidermal deposition of IgG between cells throughout the epidermis

Bullous Pemphigoid:
– Age: Elderly people (mean age 80)
– Oral involvement: Rare
– Blister type: Large and tense
– Blister content: Fluid-filled
– Areas commonly affected: Upper arms, thighs, and skin flexures
– Nikolsky sign: Usually negative
– Pruritus: Common
– Skin biopsy: A band of IgG and/or C3 at the dermo-epidermal junction

Thiopental sodium is a barbiturate with a very short duration of action. It is primarily used to induce anesthesia. Barbiturates are believed to primarily affect synapses by reducing the sensitivity of postsynaptic receptors to neurotransmitters and by interfering with the release of neurotransmitters from presynaptic neurons.

Thiopental sodium specifically binds to a unique site associated with a chloride ionophore at the GABAA receptor, which is responsible for the opening of chloride ion channels. This binding increases the length of time that the chloride ionophore remains open. As a result, the inhibitory effect of GABA on postsynaptic neurons in the thalamus is prolonged.

In summary, thiopental sodium acts as a short-acting barbiturate that is commonly used to induce anesthesia. It affects synapses by reducing postsynaptic receptor sensitivity and interfering with neurotransmitter release. By binding to a specific site at the GABAA receptor, thiopental sodium prolongs the inhibitory effect of GABA in the thalamus.

Plasmodium falciparum malaria is transmitted by female mosquitoes of the Anopheles genus. While it can be found worldwide, it is most prevalent in Africa. The incubation period for this type of malaria is typically between 7 to 14 days.

The parasite, known as sporozoites, invades hepatocytes (liver cells). Inside the hepatocyte, the parasite undergoes asexual reproduction, resulting in the production of merozoites. These merozoites are then released into the bloodstream and invade the red blood cells of the host.

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 different classes. Some of the 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.

In cases where artemisinin combination therapy is not available, oral quinine or atovaquone with proguanil hydrochloride can be used as alternatives. 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).

For severe or complicated cases of falciparum malaria, it is recommended to manage the patient in a high dependency unit or intensive care setting. Intravenous artesunate is indicated 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 once the patient has shown improvement and can tolerate oral treatment, a full course of artemisinin combination therapy should be administered.

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.

To perform rapid sequence induction in adults, it is recommended to administer a dose of sodium thiopentone ranging from 3 to 5 mg per kilogram of body weight.

Further Reading:

There are four commonly used induction agents in the UK: propofol, ketamine, thiopentone, and etomidate.

Propofol is a 1% solution that produces significant venodilation and myocardial depression. It can also reduce cerebral perfusion pressure. The typical dose for propofol is 1.5-2.5 mg/kg. However, it can cause side effects such as hypotension, respiratory depression, and pain at the site of injection.

Ketamine is another induction agent that produces a dissociative state. It does not display a dose-response continuum, meaning that the effects do not necessarily increase with higher doses. Ketamine can cause bronchodilation, which is useful in patients with asthma. The initial dose for ketamine is 0.5-2 mg/kg, with a typical IV dose of 1.5 mg/kg. Side effects of ketamine include tachycardia, hypertension, laryngospasm, unpleasant hallucinations, nausea and vomiting, hypersalivation, increased intracranial and intraocular pressure, nystagmus and diplopia, abnormal movements, and skin reactions.

Thiopentone is an ultra-short acting barbiturate that acts on the GABA receptor complex. It decreases cerebral metabolic oxygen and reduces cerebral blood flow and intracranial pressure. The adult dose for thiopentone is 3-5 mg/kg, while the child dose is 5-8 mg/kg. However, these doses should be halved in patients with hypovolemia. Side effects of thiopentone include venodilation, myocardial depression, and hypotension. It is contraindicated in patients with acute porphyrias and myotonic dystrophy.

Etomidate is the most haemodynamically stable induction agent and is useful in patients with hypovolemia, anaphylaxis, and asthma. It has similar cerebral effects to thiopentone. The dose for etomidate is 0.15-0.3 mg/kg. Side effects of etomidate include injection site pain, movement disorders, adrenal insufficiency, and apnoea. It is contraindicated in patients with sepsis due to adrenal suppression.

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.

The recommended diagnostic tests for Cushing’s syndrome include the 24-hour urinary free cortisol test, the 1 mg overnight dexamethasone suppression test, and the late-night salivary cortisol test. In this case, the patient exhibits symptoms of Cushing syndrome such as a moon face, abdominal striae, and hirsutism. These symptoms may be caused by Cushing’s disease, which is Cushing syndrome due to a pituitary adenoma. The patient also experiences headaches and visual disturbances, which could potentially be caused by high blood sugar levels. It is important to note that Cushing syndrome caused by an adrenal or pituitary tumor is more common in females, with a ratio of 5:1. The peak incidence of Cushing syndrome caused by an adrenal or pituitary adenoma occurs between the ages of 25 and 40 years.

Further Reading:

Cushing’s syndrome is a clinical syndrome caused by prolonged exposure to high levels of glucocorticoids. The severity of symptoms can vary depending on the level of steroid exposure. There are two main classifications of Cushing’s syndrome: ACTH-dependent disease and non-ACTH-dependent disease. ACTH-dependent disease is caused by excessive ACTH production from the pituitary gland or ACTH-secreting tumors, which stimulate excessive cortisol production. Non-ACTH-dependent disease is characterized by excess glucocorticoid production independent of ACTH stimulation.

The most common cause of Cushing’s syndrome is exogenous steroid use. Pituitary adenoma is the second most common cause and the most common endogenous cause. Cushing’s disease refers specifically to Cushing’s syndrome caused by an ACTH-producing pituitary tumor.

Clinical features of Cushing’s syndrome include truncal obesity, supraclavicular fat pads, buffalo hump, weight gain, moon facies, muscle wasting and weakness, diabetes or impaired glucose tolerance, gonadal dysfunction, hypertension, nephrolithiasis, skin changes (such as skin atrophy, striae, easy bruising, hirsutism, acne, and hyperpigmentation in ACTH-dependent causes), depression and emotional lability, osteopenia or osteoporosis, edema, irregular menstrual cycles or amenorrhea, polydipsia and polyuria, poor wound healing, and signs related to the underlying cause, such as headaches and visual problems.

Diagnostic tests for Cushing’s syndrome include 24-hour urinary free cortisol, 1 mg overnight dexamethasone suppression test, and late-night salivary cortisol. Other investigations aim to assess metabolic disturbances and identify the underlying cause, such as plasma ACTH, full blood count (raised white cell count), electrolytes, and arterial blood gas analysis. Imaging, such as CT or MRI of the abdomen, chest, and/or pituitary, may be required to assess suspected adrenal tumors, ectopic ACTH-secreting tumors, and pituitary tumors. The choice of imaging is guided by the ACTH result, with undetectable ACTH and elevated serum cortisol levels indicating ACTH-independent Cushing’s syndrome and raised ACTH suggesting an ACTH-secreting tumor.

The mortality rate associated with pulmonary edema as a result of acute heart failure secondary to cardiogenic shock during hospitalization is 50%.

Further Reading:

Cardiac failure, also known as heart failure, is a clinical syndrome characterized by symptoms and signs resulting from abnormalities in the structure or function of the heart. This can lead to reduced cardiac output or high filling pressures at rest or with stress. Heart failure can be caused by various problems such as myocardial, valvular, pericardial, endocardial, or arrhythmic issues.

The most common causes of heart failure in the UK are coronary heart disease and hypertension. However, there are many other possible causes, including valvular heart disease, structural heart disease, cardiomyopathies, certain drugs or toxins, endocrine disorders, nutritional deficiencies, infiltrative diseases, infections, and arrhythmias. Conditions that increase peripheral demand on the heart, such as anemia, pregnancy, sepsis, hyperthyroidism, Paget’s disease of bone, arteriovenous malformations, and beriberi, can also lead to high-output cardiac failure.

Signs and symptoms of heart failure include edema, lung crepitations, tachycardia, tachypnea, hypotension, displaced apex beat, right ventricular heave, elevated jugular venous pressure, cyanosis, hepatomegaly, ascites, pleural effusions, breathlessness, fatigue, orthopnea, paroxysmal nocturnal dyspnea, nocturnal cough or wheeze, and Presyncope.

To diagnose heart failure, NICE recommends three key tests: N-terminal pro-B-type natriuretic peptide (NT‑proBNP), transthoracic echocardiography, and ECG. Additional tests may include chest X-ray, blood tests (U&Es, thyroid function, LFT’s, lipid profile, HbA1C, FBC), urinalysis, and peak flow or spirometry.

Management of cardiogenic pulmonary edema, a complication of heart failure, involves ensuring a patent airway, optimizing breathing with supplemental oxygen and non-invasive ventilation if necessary, and addressing circulation with loop diuretics to reduce preload, vasodilators to reduce preload and afterload, and inotropes if hypotension or signs of end organ hypoperfusion persist.

This patient is showing significant signs of distress, including a highly elevated heart rate and respiratory rate, as well as very little urine output. Additionally, they are experiencing drowsiness, lethargy, and confusion. These symptoms indicate that the patient has suffered a class IV haemorrhage at this stage.

Recognizing the extent of blood loss based on vital signs and mental status abnormalities is a crucial skill. The Advanced Trauma Life Support (ATLS) classification for haemorrhagic shock correlates the amount of blood loss with expected physiological responses in a healthy 70 kg patient. In a 70 kg male patient, the total circulating blood volume is approximately five litres, accounting for around 7% of their total body weight.

The ATLS haemorrhagic shock classification is summarized as follows:

CLASS I
Blood loss (mL): Up to 750
Blood loss (% blood volume): Up to 15%
Pulse rate (bpm): <100
Systolic BP: Normal
Pulse pressure: Normal (or increased)
Respiratory rate: 14-20
Urine output (ml/hr): >30
CNS/mental status: Slightly anxious

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

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

CLASS IV
Blood loss (mL): >2000
Blood loss (% blood volume): >40%
Pulse rate (bpm): >140
Systolic BP: Decreased
Pulse pressure: Decreased
Respiratory rate: >40
Urine output (ml/hr): Negligible
CNS/mental status: Confused, lethargic

Intracranial hemorrhages can be categorized based on their location into epidural, subdural, subarachnoid, or intracerebral hemorrhages. The patient in this case is experiencing a severe headache accompanied by signs of meningismus, which strongly suggests a diagnosis of subarachnoid hemorrhage. Additionally, there is no history of trauma, and most cases of subarachnoid hemorrhage are caused by the rupture of a berry aneurysm located in the circle of Willis. Hypertension is a significant risk factor for the rupture of an aneurysm.

During the patient’s hospital stay, they develop an ischemic stroke, which is confirmed by a CT scan. This is most likely a result of cerebral vasospasm secondary to the subarachnoid hemorrhage. To prevent this complication, patients are often treated with the cerebral selective calcium channel blocker Nimodipine.

Another potential complication of this condition is rebleeding, with the highest risk occurring in the first few days. Rebleeding can be potentially fatal, so it is crucial to repair the aneurysm as soon as possible. The presence of blood in the subarachnoid space can also disrupt the production and drainage of cerebrospinal fluid, leading to hydrocephalus.

Long-term complications of subarachnoid hemorrhage include epilepsy, with most patients experiencing their first seizure within a year after the hemorrhage. However, the risk of epilepsy decreases over time. Cognitive dysfunction is also a common long-term complication and can manifest as memory loss, difficulty concentrating, or challenges in performing regular tasks. Emotional problems, such as depression and anxiety, are frequently observed as well.

When administering treatment to patients with hepatic impairment, it is crucial to consider that midazolam is metabolized in the liver.

Further Reading:

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

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

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

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

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

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

The ulnar nerve originates from the medial cord of the brachial plexus, specifically from the C8-T1 nerve roots. It may also carry fibers from C7 on occasion. This nerve has both motor and sensory functions.

In terms of motor function, the ulnar nerve innervates the muscles of the hand, excluding the thenar muscles and the lateral two lumbricals (which are supplied by the median nerve). It also innervates two muscles in the anterior forearm: the flexor carpi ulnaris and the medial half of the flexor digitorum profundus.

Regarding sensory function, the ulnar nerve provides innervation to the anterior and posterior surfaces of the medial one and a half fingers, as well as the associated palm and dorsal hand area. There are three sensory branches responsible for the cutaneous innervation of the ulnar nerve. Two of these branches arise in the forearm and travel into the hand: the palmar cutaneous branch, which innervates the skin of the medial half of the palm, and the dorsal cutaneous branch, which innervates the dorsal skin of the medial one and a half fingers and the associated dorsal hand. The third branch arises in the hand and is called the superficial branch, which innervates the palmar surface of the medial one and a half fingers.

When the ulnar nerve is damaged at the elbow, the flexor carpi ulnaris and the medial half of the flexor digitorum profundus muscles in the anterior forearm will be spared. However, if the ulnar nerve is injured at the wrist, these muscles will be affected. Additionally, when the ulnar nerve is damaged at the elbow, flexion of the wrist can still occur due to the intact median nerve, but it will be accompanied by abduction as the flexor carpi ulnaris adducts the hand. On the other hand, wrist flexion will be unaffected when the ulnar nerve is damaged at the wrist.

The sensory function also differs depending on the site of damage. When the ulnar nerve is damaged at the elbow, all three cutaneous branches will be affected, resulting in complete sensory loss in the areas innervated by the ulnar nerve. However, if the damage occurs at the wrist, the two branches that arise in the forearm may be spared.

Damage to the ulnar nerve at either the elbow or wrist leads to a characteristic claw hand appearance.

When an adult patient is choking and unable to clear the obstruction by coughing, the next step is to deliver either 5 back blows or abdominal thrusts. The appropriate action depends on the severity of the airway obstruction. If the choking is mild and not causing significant difficulty in breathing, it is recommended to encourage the patient to cough and closely monitor for any worsening symptoms. However, if the choking is severe and causing a complete blockage of the airway, it is necessary to administer either back blows or abdominal thrusts to dislodge the obstruction. In the event that the patient loses consciousness, immediate CPR should be initiated.

Further Reading:

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

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

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

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

The 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.

Nelson’s syndrome is a rare condition that occurs many years after a bilateral adrenalectomy for Cushing’s syndrome. It is believed to develop due to the loss of the normal negative feedback control that suppresses high cortisol levels. As a result, the hypothalamus starts producing CRH again, which stimulates the growth of a pituitary adenoma that produces adrenocorticotropic hormone (ACTH).

Only 15-20% of patients who undergo bilateral adrenalectomy will develop this condition, and it is now rarely seen as the procedure is no longer commonly performed.

The symptoms and signs of Nelson’s syndrome are related to the growth of the pituitary adenoma and the increased production of ACTH and melanocyte-stimulating hormone (MSH) from the adenoma. These may include headaches, visual field defects (up to 50% of cases), increased skin pigmentation, and the possibility of hypopituitarism.

ACTH levels will be significantly elevated (usually >500 ng/L). Thyroxine, TSH, gonadotrophin, and sex hormone levels may be low. Prolactin levels may be high, but not as high as with a prolactin-producing tumor. MRI or CT scanning can be helpful in identifying the presence of an expanding pituitary mass.

The treatment of choice for Nelson’s syndrome is trans-sphenoidal surgery.

Patients who have a STEMI caused by a blockage in the left circumflex artery (LCX) will usually show ST elevation in leads I and AVL. These leads correspond to the high lateral area of the heart, which is supplied by the LCX artery.

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.

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 drug doses for adult acute asthma are as follows:

– Salbutamol: Administer 5 mg using an oxygen-driven nebulizer.
– Ipratropium bromide: Deliver 500 mcg via an oxygen-driven nebulizer.
– Prednisolone: Take orally at a dose of 40-50 mg.
– Hydrocortisone: Administer 100 mg intravenously.
– Magnesium sulphate: Infuse 1.2-2 g intravenously over a period of 20 minutes.

Terbutaline can be used as an alternative to salbutamol, with a dose of 10 mg via an oxygen-driven nebulizer. Intravenous salbutamol may be considered (250 mcg IV slowly) only when inhaled therapy is not possible, such as when a patient is receiving bag-mask ventilation.

According to the current ALS guidelines, IV aminophylline may be considered in severe or life-threatening asthma, following senior advice. If used, a loading dose of 5 mg/kg should be given over 20 minutes, followed by an infusion of 500-700 mcg/kg/hour. It is important to maintain serum theophylline levels below 20 mcg/ml to prevent toxicity.

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

The clinical history and examination strongly suggest that the patient has a pulmonary embolism caused by a deep vein thrombosis in his right leg.

The typical symptoms of a pulmonary embolism include shortness of breath, chest pain that worsens with breathing, coughing, and/or coughing up blood. There may also be symptoms indicating the presence of a deep vein thrombosis. Other signs include rapid breathing and heart rate, fever, and in severe cases, signs of shock, an abnormal heart rhythm, and increased pressure in the jugular veins.

Given the patient’s high probability Wells score, it is recommended that an immediate CT pulmonary angiogram (CPTA) be performed. This test is considered the most reliable method for diagnosing a pulmonary embolism. A d-dimer test would not provide any additional benefit in this case. While a chest X-ray and ECG may provide useful information, they alone cannot confirm the diagnosis.

For patients who have an allergy to contrast media, renal impairment, or are at high risk from radiation exposure, a ventilation/perfusion single-photon emission computed tomography (V/Q SPECT) scan or a V/Q planar scan can be offered as an alternative to CTPA.

This question delves into the challenges of managing chronic illnesses and promoting patient self-care, while also considering concerns regarding confidentiality. The patient in question is mentally capable and already has caregivers at home. It is both the patient’s preference and the most clinically sensible decision to discharge them back home. It is important to address any family concerns, ensuring that the family members have the patient’s best interests at heart rather than personal or financial motives. It is not appropriate to delegate this conversation to a nurse, as it is your responsibility as the healthcare provider. It is crucial to communicate with the patient’s general practitioner, but it is important to involve the patient in any decision regarding a referral to a nursing home.

This individual, who has been smoking for a long time, is likely to have squamous cell carcinoma of the lung located at the right apex. This particular type of cancer is causing Pancoast’s syndrome. Pancoast’s syndrome typically presents with rib erosion, leading to severe shoulder pain, as well as Horner’s syndrome due to the infiltration of the lower part of the brachial plexus. Additionally, there may be hoarseness of the voice and a ‘bovine cough’ due to a concurrent recurrent laryngeal nerve palsy.

The classic description of Horner’s syndrome includes the following clinical features on the same side as the tumor: miosis (constricted pupil), ptosis (drooping eyelid), anhidrosis (lack of sweating), and enophthalmos (sunken appearance of the eye). A chest X-ray would be able to detect the presence of the apical tumor and confirm the diagnosis.

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.

Grey baby syndrome is a rare but serious side effect that can occur in neonates, especially premature babies, as a result of the build-up of the antibiotic chloramphenicol. This condition is characterized by several symptoms, including ashen grey skin color, poor feeding, vomiting, cyanosis, hypotension, hypothermia, hypotonia, cardiovascular collapse, abdominal distension, and respiratory difficulties.

During pregnancy, there are several drugs that can have adverse effects on the developing fetus. ACE inhibitors, such as ramipril, if given in the second and third trimesters, can lead to hypoperfusion, renal failure, and the oligohydramnios sequence. Aminoglycosides, like gentamicin, can cause ototoxicity and deafness. High doses of aspirin can result in first-trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses of aspirin (e.g., 75 mg) do not pose significant risks.

Benzodiazepines, such as diazepam, when administered late in pregnancy, can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if given in the first trimester, may lead to phalangeal abnormalities, while their use in the second and third trimesters can result in fetal growth retardation. Carbamazepine can cause hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol, as mentioned earlier, can cause grey baby syndrome. Corticosteroids, if given in the first trimester, may cause orofacial clefts. Danazol, if administered in the first trimester, can cause masculinization of the female fetuses genitals. Pregnant women should avoid handling crushed or broken tablets of finasteride, as it can be absorbed through the skin and affect male sex organ development.

Haloperidol, if given in the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the neonate. Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability.