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

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

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

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

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

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

Activated charcoal is a useful treatment for many drug poisonings, but it is not effective against certain types of poisonings. To remember these exceptions, you can use the mnemonic PHAILS. This stands for Pesticides (specifically organophosphates), Hydrocarbons, Acids (strong), alkalis (strong), alcohols (such as ethanol, methanol, and ethylene glycol), Iron, Lithium, and Solvents.

Further Reading:

Poisoning in the emergency department is often caused by accidental or intentional overdose of prescribed drugs. Supportive treatment is the primary approach for managing most poisonings. This includes ensuring a clear airway, proper ventilation, maintaining normal fluid levels, temperature, and blood sugar levels, correcting any abnormal blood chemistry, controlling seizures, and assessing and treating any injuries.

In addition to supportive treatment, clinicians may need to consider strategies for decontamination, elimination, and administration of antidotes. Decontamination involves removing poisons from the skin or gastrointestinal tract. This can be done through rinsing the skin or using methods such as activated charcoal, gastric lavage, induced emesis, or whole bowel irrigation. However, induced emesis is no longer commonly used, while gastric lavage and whole bowel irrigation are rarely used.

Elimination methods include urinary alkalinization, hemodialysis, and hemoperfusion. These techniques help remove toxins from the body.

Activated charcoal is a commonly used method for decontamination. It works by binding toxins in the gastrointestinal tract, preventing their absorption. It is most effective if given within one hour of ingestion. However, it is contraindicated in patients with an insecure airway due to the risk of aspiration. Activated charcoal can be used for many drugs, but it is ineffective for certain poisonings, including pesticides (organophosphates), hydrocarbons, strong acids and alkalis, alcohols (ethanol, methanol, ethylene glycol), iron, lithium, and solvents.

Antidotes are specific treatments for poisoning caused by certain drugs or toxins. For example, cyanide poisoning can be treated with dicobalt edetate, hydroxocobalamin, or sodium nitrite and sodium thiosulphate. Benzodiazepine poisoning can be treated with flumazanil, while opiate poisoning can be treated with naloxone. Other examples include protamine for heparin poisoning, vitamin K or fresh frozen plasma for warfarin poisoning, fomepizole or ethanol for methanol poisoning, and methylene blue for methemoglobinemia caused by benzocaine or nitrates.

There are many other antidotes available for different types of poisoning, and resources such as TOXBASE and the National Poisons Information Service (NPIS) can provide valuable advice on managing poisonings.

One of the clinical features of mitral stenosis is malar flush, which refers to a reddening or flushing of the cheeks. Other clinical features include a mid-late diastolic murmur that is best heard during expiration, a loud S1 heart sound with an opening snap, a low volume pulse, atrial fibrillation, and signs of pulmonary edema such as crepitations or the presence of white or pink frothy sputum.

Further Reading:

Mitral Stenosis:
– Causes: Rheumatic fever, Mucopolysaccharidoses, Carcinoid, Endocardial fibroelastosis
– Features: Mid-late diastolic murmur, loud S1, opening snap, low volume pulse, malar flush, atrial fibrillation, signs of pulmonary edema, tapping apex beat
– Features of severe mitral stenosis: Length of murmur increases, opening snap becomes closer to S2
– Investigation findings: CXR may show left atrial enlargement, echocardiography may show reduced cross-sectional area of the mitral valve

Mitral Regurgitation:
– Causes: Mitral valve prolapse, Myxomatous degeneration, Ischemic heart disease, Rheumatic fever, Connective tissue disorders, Endocarditis, Dilated cardiomyopathy
– Features: pansystolic murmur radiating to left axilla, soft S1, S3, laterally displaced apex beat with heave
– Signs of acute MR: Decompensated congestive heart failure symptoms
– Signs of chronic MR: Leg edema, fatigue, arrhythmia (atrial fibrillation)
– Investigation findings: Doppler echocardiography to detect regurgitant flow and pulmonary hypertension, ECG may show signs of LA enlargement and LV hypertrophy, CXR may show LA and LV enlargement in chronic MR and pulmonary edema in acute MR.

Retinal detachment is a condition where the retina separates from the retinal pigment epithelium, resulting in a fluid-filled space between them. This case presents a classic description of retinal detachment. Several risk factors increase the likelihood of developing this condition, including myopia, being male, having a family history of retinal detachment, previous episodes of retinal detachment, blunt ocular trauma, previous cataract surgery, diabetes mellitus (especially if proliferative retinopathy is present), glaucoma, and cataracts.

The clinical features commonly associated with retinal detachment include flashes of light, particularly at the edges of vision (known as photopsia), a dense shadow in the peripheral vision that spreads towards the center, a sensation of a curtain drawing across the eye, and central visual loss. Fundoscopy, a procedure to examine the back of the eye, reveals a sheet of sensory retina billowing towards the center of the eye. Additionally, a positive Amsler grid test, where straight lines appear curved or wavy, may indicate retinal detachment.

Other possible causes of floaters include posterior vitreous detachment, retinal tears, vitreous hemorrhage, and migraine with aura. However, in this case, the retinal appearance described is consistent with retinal detachment.

It is crucial to arrange an urgent same-day ophthalmology referral for this patient. Fortunately, approximately 90% of retinal detachments can be successfully repaired with one operation, and an additional 6% can be salvaged with subsequent procedures. If the retina remains fixed six months after surgery, the likelihood of it becoming detached again is low.

The earliest and most frequent clinical indication of malignant hyperthermia is typically an increase in end tidal CO2. An unexplained elevation in end tidal CO2 is often the initial and most reliable sign of this condition.

Further Reading:

Malignant hyperthermia is a rare and life-threatening syndrome that can be triggered by certain medications in individuals who are genetically susceptible. The most common triggers are suxamethonium and inhalational anaesthetic agents. The syndrome is caused by the release of stored calcium ions from skeletal muscle cells, leading to uncontrolled muscle contraction and excessive heat production. This results in symptoms such as high fever, sweating, flushed skin, rapid heartbeat, and muscle rigidity. It can also lead to complications such as acute kidney injury, rhabdomyolysis, and metabolic acidosis. Treatment involves discontinuing the trigger medication, administering dantrolene to inhibit calcium release and promote muscle relaxation, and managing any associated complications such as hyperkalemia and acidosis. Referral to a malignant hyperthermia center for further investigation is also recommended.

Neisseria gonorrhoeae is a type of bacteria that causes the sexually transmitted infection known as gonorrhoea. It is a Gram-negative diplococcus, meaning it appears as pairs of bacteria under a microscope. This infection is most commonly seen in individuals between the ages of 15 and 35, and it is primarily transmitted through sexual contact. One important characteristic of Neisseria gonorrhoeae is its ability to undergo antigenic variation, which means that recovering from an infection does not provide immunity and reinfection is possible.

When Neisseria gonorrhoeae infects the body, it first attaches to the genitourinary epithelium using pili, which are hair-like structures on the surface of the bacteria. It then invades the epithelial layer and triggers a local acute inflammatory response. In men, the clinical features of gonorrhoea often include urethritis (inflammation of the urethra) in about 80% of cases, dysuria (painful urination) in around 50% of cases, and mucopurulent discharge. Rectal infection may also occur, usually without symptoms, but it can cause anal discharge. Pharyngitis, or inflammation of the throat, is usually asymptomatic in men.

In women, the clinical features of gonorrhoea commonly include vaginal discharge in about 50% of cases, lower abdominal pain in around 25% of cases, dysuria in 10-15% of cases, and pelvic/lower abdominal tenderness in less than 5% of cases. Endocervical discharge and/or bleeding may also be present. Similar to men, rectal infection is usually asymptomatic but can cause anal discharge, and pharyngitis is usually asymptomatic in women as well.

Complications of Neisseria gonorrhoeae infection can be serious and include pelvic inflammatory disease (PID) in women, epididymo-orchitis or prostatitis in men, arthritis, dermatitis, pericarditis and/or myocarditis, hepatitis, and meningitis.

To diagnose gonorrhoea, samples of pus from the urethra, cervix, rectum, or throat should be collected and promptly sent to the laboratory in specialized transport medium. Traditionally, diagnosis has been made using Gram-stain and culture techniques, but newer PCR testing methods are becoming more commonly used.

Toxocariasis is a rare infection caused by the parasitic roundworm Toxocara canis. The main way it spreads to humans is through contact with dog feces. However, practicing good hand hygiene can help prevent transmission. While most people who come into contact with Toxocara canis don’t show any symptoms, a small number may experience a mild flu-like illness.

The most common presentation of toxocariasis is in children, who may experience unilateral visual loss. This loss of vision is typically caused by conditions such as vitritis, macular edema, and tractional retinal detachment. It is believed that these lesions occur due to a toxic or immunoallergic reaction to the larval antigens.

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

The causes of AKI can be categorized into pre-renal, intrinsic renal, and post-renal factors. The majority of AKI cases in the community are due to pre-renal causes, accounting for 90% of cases. These are often associated with conditions such as hypotension from sepsis or fluid depletion. Medications, particularly ACE inhibitors and NSAIDs, are also frequently implicated in AKI.

The table below summarizes the most common causes of AKI:

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

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

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

Reported parental perception of a fever should be regarded as valid and taken seriously by healthcare professionals.

For infants under the age of 4 weeks, it is recommended to measure body temperature using an electronic thermometer in the axilla.

In children aged 4 weeks to 5 years, body temperature can be measured using one of the following methods: an electronic thermometer in the axilla, a chemical dot thermometer in the axilla, or an infra-red tympanic thermometer.

It is important to note that oral and rectal routes should not be utilized for temperature measurement in this age group. Additionally, forehead chemical thermometers are not reliable and should be avoided.

Dementia with Lewy bodies (DLB), also known as Lewy body dementia (LBD), is a progressive neurodegenerative condition that is closely linked to Parkinson’s disease (PD). It is the third most common cause of dementia in older individuals, following Alzheimer’s disease and vascular dementia.

DLB is characterized by several clinical features, including the presence of Parkinsonism or co-existing PD, a gradual decline in cognitive function, fluctuations in cognition, alertness, and attention span, episodes of temporary loss of consciousness, recurrent falls, visual hallucinations, depression, and complex, systematized delusions. The level of cognitive impairment can vary from hour to hour and day to day.

Pathologically, DLB is marked by the formation of abnormal protein collections called Lewy bodies within the cytoplasm of neurons. These intracellular protein collections share similar structural characteristics with the classic Lewy bodies observed in Parkinson’s disease.

If a child who is experiencing convulsions reaches step 3 of the APLS algorithm and has already been given phenytoin as part of their ongoing treatment, it is recommended to initiate a phenobarbitone infusion. This infusion should be administered at a dosage of 20 mg/kg over a period of 30 to 60 minutes.

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

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

Hospitalization for croup is rare and typically reserved for children who are experiencing increasing respiratory distress or showing signs of drowsiness/agitation. The Westley croup score is a useful tool for assessing the child’s condition and making appropriate management decisions. Children with moderate (score 2-7) or severe croup (score >7) may require hospital admission. On the other hand, many children with mild croup (score 0-1) can be safely discharged and treated at home.

The Westley croup score is determined based on the following criteria: the presence of stridor at rest, the severity of retractions, air entry, SaO2 levels below 92% when agitated, and the conscious level of the child. In this particular case, the child’s Westley croup score is 8 points, indicating severe croup.

In the UK, the most prevalent cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. On a global scale, hypothyroidism is primarily caused by iodine deficiency. However, in areas where iodine levels are sufficient, such as the UK, hypothyroidism and subclinical hypothyroidism are most commonly attributed to autoimmune thyroiditis. This condition can manifest with or without a goitre, known as atrophic thyroiditis.

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.

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

Further Reading:

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

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

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

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

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

Neonatal jaundice is a complex subject, and it is crucial for candidates to have knowledge about the different causes, presentations, and management of conditions that lead to jaundice in newborns. Neonatal jaundice can be divided into two groups: unconjugated hyperbilirubinemia, which can be either physiological or pathological, and conjugated hyperbilirubinemia, which is always pathological.

The causes of neonatal jaundice can be categorized as follows:

Haemolytic unconjugated hyperbilirubinemia:
– Intrinsic causes of haemolysis include hereditary spherocytosis, G6PD deficiency, sickle-cell disease, and pyruvate kinase deficiency.
– Extrinsic causes of haemolysis include haemolytic disease of the newborn and Rhesus disease.

Non-haemolytic unconjugated hyperbilirubinemia:
– Breastmilk jaundice, cephalhaematoma, polycythemia, infection (particularly urinary tract infections), Gilbert syndrome.

Hepatic conjugated hyperbilirubinemia:
– Hepatitis A and B, TORCH infections, galactosaemia, alpha 1-antitrypsin deficiency, drugs.

Post-hepatic conjugated hyperbilirubinemia:
– Biliary atresia, bile duct obstruction, choledochal cysts.

By understanding these different categories and their respective examples, candidates will be better equipped to handle neonatal jaundice cases.

Dabigatran etexilate is a medication that directly inhibits thrombin, a protein involved in blood clotting. It is prescribed to prevent venous thromboembolism in adults who have undergone total hip or knee replacement surgery. It is also approved for the treatment of deep-vein thrombosis and pulmonary embolism, as well as the prevention of recurrent episodes in adults.

The duration of treatment with dabigatran etexilate should be determined by considering the benefits of the medication against the risk of bleeding. For individuals with temporary risk factors such as recent surgery, trauma, or immobilization, a shorter duration of treatment (at least three months) may be appropriate. On the other hand, individuals with permanent risk factors or those with idiopathic deep-vein thrombosis or pulmonary embolism may require a longer duration of treatment.

Dabigatran etexilate is also indicated for the prevention of stroke and systemic embolism in patients with non-valvular atrial fibrillation who have additional risk factors such as previous stroke or transient ischemic attack, symptomatic heart failure, age 75 years or older, diabetes mellitus, or hypertension.

One of the advantages of dabigatran etexilate is its rapid onset of action. Additionally, routine monitoring of anticoagulant activity is not necessary as traditional tests like INR may not accurately reflect its effects. However, it is important to monitor patients for signs of bleeding or anemia, as hemorrhage is the most common side effect. If severe bleeding occurs, treatment with dabigatran etexilate should be discontinued.

There are certain situations in which dabigatran etexilate should not be used. These include active bleeding, a significant risk of major bleeding (such as recent gastrointestinal ulcer, oesophageal varices, recent brain, spine, or ophthalmic surgery, recent intracranial hemorrhage, malignant neoplasms, or vascular aneurysm), and as an anticoagulant for prosthetic heart valves.

In the UK, idarucizumab is the first approved agent that can reverse the anticoagulant effect of dabigatran etexilate.

Based on the patient’s symptoms and medical history, the most likely organism responsible for this case of infective endocarditis is Streptococcus viridans. This is because the patient has a history of aortic stenosis, which is a risk factor for developing infective endocarditis. Additionally, the patient had a tooth extraction prior to the onset of symptoms, which can introduce bacteria into the bloodstream and increase the risk of infective endocarditis. Streptococcus viridans is a common cause of infective endocarditis, particularly in patients with underlying heart valve disease.

Further Reading:

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

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

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

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

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

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.

Fragility fractures occur when a person experiences a fracture from a force that would not typically cause a fracture, such as a fall from a standing height or less. The most common areas for fragility fractures are the vertebrae, hip, and wrist. Osteoporosis is diagnosed when a patient’s bone mineral density, measured by a T-score on a DEXA scan, is -2.5 standard deviations or below. This T-score compares the patient’s bone density to the peak bone density of a population. In women over 75 years old, osteoporosis can be assumed without a DEXA scan. Osteopenia is diagnosed when a patient’s T-score is between -1 and -2.5 standard deviations below peak bone density. Risk factors for fractures include a family history of hip fractures, excessive alcohol consumption, and rheumatoid arthritis. Low bone mineral density can be indicated by a BMI below 22 kg/m2, untreated menopause, and conditions causing prolonged immobility or certain medical conditions. Medications used to prevent osteoporotic fractures in postmenopausal women include alendronate, risedronate, etidronate, and strontium ranelate. Raloxifene is not used for primary prevention. Alendronate is typically the first-choice medication and is recommended for women over 70 years old with confirmed osteoporosis and either a risk factor for fracture or low bone mineral density. Women over 75 years old with two risk factors or two indicators of low bone mineral density may be assumed to have osteoporosis without a DEXA scan. Other pharmacological interventions can be tried if alendronate is not tolerated.

Acamprosate, also known as Campral, is a medication used in the treatment of alcohol dependence. It is believed to work by stabilizing a chemical pathway in the brain that is disrupted during alcohol withdrawal. For optimal results, Acamprosate should be used alongside psychosocial support, as it helps reduce alcohol consumption and promote abstinence.

When starting treatment with Acamprosate, it is important to begin as soon as possible after assisted withdrawal. The typical dosage is 1998 mg (666 mg three times a day), unless the patient weighs less than 60 kg, in which case a maximum of 1332 mg per day should be prescribed.

Generally, Acamprosate is prescribed for up to 6 months. However, for those who benefit from the medication and wish to continue, it can be taken for a longer duration. If drinking persists 4-6 weeks after starting the drug, it should be discontinued.

Patients who are prescribed Acamprosate should be closely monitored, with regular check-ins at least once a month for the first six months. If the medication is continued beyond six months, the frequency of check-ins can be reduced but should still occur at regular intervals.

While routine blood tests are not mandatory, they can be considered if there is a need to monitor liver function recovery or as a motivational tool to show patients their progress.

Tetralogy of Fallot (TOF) is the most prevalent cause of cyanotic congenital heart disease. It is characterized by four distinct features: pulmonary infundibular stenosis, overriding aorta, ventricular septal defect, and right ventricular hypertrophy. TOF is often associated with various congenital syndromes, including DiGeorge syndrome (22q11 microdeletion syndrome), Trisomy 21, Foetal alcohol syndrome, and Maternal phenylketonuria.

Nowadays, many cases of TOF are identified during antenatal screening or early postnatal assessment due to the presence of a heart murmur. Initially, severe cyanosis is uncommon shortly after birth because the patent ductus arteriosus provides additional blood flow to the lungs. However, once the ductus arteriosus closes, typically a few days after birth, cyanosis can develop.

In cases where TOF goes undetected, the clinical manifestations may include severe cyanosis, poor feeding, breathlessness, dyspnea on exertion (such as prolonged crying), hypercyanotic spells triggered by activity, agitation, developmental delay, and failure to thrive. A cardiac examination may reveal a loud, long ejection systolic murmur caused by pulmonary stenosis, a systolic thrill at the lower left sternal edge, an aortic ejection click, and digital clubbing. Radiologically, a characteristic finding in TOF is a ‘boot-shaped’ heart (Coeur en sabot).

Treatment for TOF often involves two stages. Initially, a palliative procedure is performed to alleviate symptoms, followed by a total repair at a later stage.

Cluster headaches are a type of headache that is commonly seen in young men in their 20s. The male to female ratio for this condition is 6:1. Smoking is also known to increase the risk of developing cluster headaches. These headaches occur in clusters, usually lasting for a few weeks every year or two. The pain experienced is severe and typically affects one side of the head, often around or behind the eye. It tends to occur at the same time each day and can cause the patient to become agitated, sometimes resorting to hitting their head against a wall or the floor in an attempt to distract from the pain.

In addition to the intense pain, cluster headaches are also associated with autonomic involvement. This can manifest as various symptoms on the same side as the headache, including conjunctival injection (redness of the eye), rhinorrhea (runny nose), lacrimation (tearing of the eye), miosis (constriction of the pupil), and ptosis (drooping of the eyelid).

On the other hand, migraine with typical aura presents with temporary visual disturbances, such as hemianopia (loss of vision in half of the visual field) or scintillating scotoma (a visual aura that appears as a shimmering or flashing area of distorted vision). Migraine without aura, on the other hand, needs to meet specific criteria set by the International Headache Society. These criteria include having at least five headache attacks lasting between 4 to 72 hours, with the headache having at least two of the following characteristics: unilateral location, pulsating quality, moderate to severe pain intensity, and aggravation by routine physical activity.

During a migraine headache, the patient may also experience symptoms such as nausea and/or vomiting, as well as sensitivity to light (photophobia) and sound (phonophobia). It is important to note that these symptoms should not be attributed to another underlying disorder.

If a patient over the age of 50 presents with a new-onset headache, it raises the possibility of giant cell arteritis (temporal arteritis). Other symptoms and signs that may be associated with this condition include jaw claudication (pain in the jaw when chewing), systemic upset, scalp tenderness, and an elevated erythrocyte sedimentation rate (ESR).

Medication overuse headache is a condition that is suspected when a patient is using multiple medications, often at low doses, without experiencing any relief from their headaches.

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

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

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

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

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

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

This patient is experiencing a condition called acute alveolar osteitis, commonly known as ‘dry socket’. It occurs when the blood clot covering the socket gets dislodged, leaving the bone and nerve exposed. This can result in infection and intense pain.

There are several risk factors associated with the development of a dry socket. These include smoking, inadequate dental hygiene, extraction of wisdom teeth, use of oral contraceptive pills, and a previous history of dry socket.

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

Further Reading:

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

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

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

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

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

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

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

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

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

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

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

To treat DKA, the girl is receiving intravenous fluids to rehydrate her. Additionally, insulin needs to be prescribed to help regulate her blood sugar levels.

The most suitable insulin regimen in this case would be an IV insulin infusion at 0.05 units/kg/hour. This means that the insulin will be administered through an intravenous line at a rate of 0.05 units per kilogram of the girl’s body weight per hour. This dosage is appropriate for managing DKA and will help to lower her blood sugar levels effectively.

Further Reading:

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

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

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

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

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

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

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

The clinical presentation of pericarditis often includes retrosternal chest pain that is pleuritic in nature. This pain is typically relieved by sitting forwards and worsened when lying flat. It may also radiate to the shoulders. Other symptoms may include shortness of breath, tachycardia, and the presence of a pericardial friction rub.

The pericardium receives sensory supply from the phrenic nerve, which also provides sensory innervation to the diaphragm, various mediastinal structures, and certain abdominal structures such as the superior peritoneum, liver, and gallbladder. Since the phrenic nerve originates from the 4th cervical nerve, which also provides cutaneous innervation to the front of the shoulder girdle, pain from pericarditis can also radiate to the shoulders.

Beta blockers are the primary treatment for long QT syndrome (LQTS). This patient probably has an undiagnosed congenital LQTS because there is no obvious cause. If there is a known cause of LQTS that can be removed, removing it may be the only necessary treatment. However, in all other cases, beta blockers are usually needed to prevent ventricular arrhythmias. Ventricular arrhythmias happen because of increased adrenergic activity. Beta blockers reduce the effects of adrenergic stimulation.

Further Reading:

Long QT syndrome (LQTS) is a condition characterized by a prolonged QT interval on an electrocardiogram (ECG), which represents abnormal repolarization of the heart. LQTS can be either acquired or congenital. Congenital LQTS is typically caused by gene abnormalities that affect ion channels responsible for potassium or sodium flow in the heart. There are 15 identified genes associated with congenital LQTS, with three genes accounting for the majority of cases. Acquired LQTS can be caused by various factors such as certain medications, electrolyte imbalances, hypothermia, hypothyroidism, and bradycardia from other causes.

The normal QTc values, which represent the corrected QT interval for heart rate, are typically less than 450 ms for men and less than 460ms for women. Prolonged QTc intervals are considered to be greater than these values. It is important to be aware of drugs that can cause QT prolongation, as this can lead to potentially fatal arrhythmias. Some commonly used drugs that can cause QT prolongation include antimicrobials, antiarrhythmics, antipsychotics, antidepressants, antiemetics, and others.

Management of long QT syndrome involves addressing any underlying causes and using beta blockers. In some cases, an implantable cardiac defibrillator (ICD) may be recommended for patients who have experienced recurrent arrhythmic syncope, documented torsades de pointes, previous ventricular tachyarrhythmias or torsades de pointes, previous cardiac arrest, or persistent syncope. Permanent pacing may be used in patients with bradycardia or atrioventricular nodal block and prolonged QT. Mexiletine is a treatment option for those with LQT3. Cervicothoracic sympathetic denervation may be considered in patients with recurrent syncope despite beta-blockade or in those who are not ideal candidates for an ICD. The specific treatment options for LQTS depend on the type and severity of the condition.

It is recommended to obtain an arterial blood gas (ABG) sample from all patients who have experienced submersion (drowning) as even individuals without symptoms may have a surprising level of hypoxia. Draining the lungs is not effective and not recommended. There is no strong evidence to support the routine use of antibiotics as a preventive measure. Steroids have not been proven to be effective in treating drowning. All drowning patients, except those with normal oxygen levels, normal saturations, and normal lung sounds, should receive supplemental oxygen as significant hypoxia can occur without causing difficulty in breathing.

Further Reading:

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

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

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

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

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

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

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

Registered medical practitioners in England and Wales are legally obligated to inform a designated official from the Local Authority if they suspect a patient has contracted specific infectious diseases. For more information on which diseases and their causative organisms require reporting, please refer to the following resource: Notifiable diseases and causative organisms: how to report.

Women who are 18 years or older and have a pelvic mass that is not clearly uterine fibroids should be promptly referred for assessment. In this case, an abdominal X-ray would not provide much useful information, and it is not advisable to take no action at this point. For more information, please refer to the NICE referral guidelines for suspected cancer.

Compartment syndrome can occur when there are circumferential burns on the arms or legs. This typically happens with full thickness burns, where the burnt skin becomes stiff and compresses the compartment, making it difficult for blood to flow out. To treat this condition, escharotomy and possibly fasciotomy may be necessary.

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.

When it comes to managing viral conjunctivitis, it’s important to reassure the patient that most cases are self-limiting and don’t require antimicrobial treatment. In fact, viral conjunctivitis usually resolves on its own within one to two weeks. However, there are some self-care measures that can help ease symptoms. These include cleaning the eyelids with cotton wool soaked in sterile saline or boiled and cooled water, applying cool compresses around the eye area, and using lubricating drops or artificial tears. It’s also important to avoid prescribing antibiotics if possible.

It’s crucial to inform the person that infective conjunctivitis is contagious and they should take steps to prevent spreading the infection to their other eye and other people. This includes washing hands frequently with soap and water, using separate towels and flannels, and avoiding close contact with others, especially if they are a healthcare professional or child-care provider. It’s worth noting that the infection can be contagious for up to 14 days from onset.

According to Public Health England, there is no recommended exclusion period from school, nursery, or childminders unless there is an outbreak or cluster of cases. It’s important to provide written information to the patient, explain the red flags for an urgent review, and advise them to seek further help if symptoms persist beyond 7 days. If the person returns with symptoms of conjunctivitis, it may be necessary to consider sending swabs for viral PCR and bacterial culture, as well as prescribing empirical topical antibiotics if they haven’t already been prescribed. If symptoms persist for more than 7-10 days after initiating treatment, it may be necessary to discuss with or refer to ophthalmology.

Enterotoxigenic E.coli is a strain that does not invade the body and does not lead to inflammation or bloody diarrhea. On the other hand, enterogenic strains result in excessive watery diarrhea and are typically not accompanied by abdominal cramping.

There are several infectious causes of bloody diarrhea, including Campylobacter spp., Shigella spp., Salmonella spp., Clostridium difficile, Enterohaemorrhagic Escherichia coli, Yersinia spp., Schistosomiasis, and Amoebiasis (Entamoeba histolytica).

NICE provides a list of reasons for admitting patients with acute alcohol withdrawal. These include individuals who are deemed to be at risk of experiencing withdrawal seizures or delirium tremens. Additionally, young people under the age of 16 who are going through acute alcohol withdrawal may also require admission. Furthermore, vulnerable individuals, such as those who are frail, have cognitive impairment or multiple comorbidities, lack social support, or have learning difficulties, may also benefit from being admitted for acute alcohol withdrawal. For more information, please refer to the NICE pathway for acute alcohol withdrawal.

Digoxin-specific antibody (DigiFab) is an antidote used to counteract digoxin overdose. It is a purified and sterile preparation of digoxin-immune ovine Fab immunoglobulin fragments. These fragments are derived from healthy sheep that have been immunized with a digoxin derivative called digoxin-dicarboxymethoxylamine (DDMA). DDMA is a digoxin analogue that contains the essential cyclopentanoperhydrophenanthrene: lactone ring moiety coupled to keyhole limpet hemocyanin (KLH).

DigiFab has a higher affinity for digoxin compared to the affinity of digoxin for its sodium pump receptor, which is believed to be the receptor responsible for its therapeutic and toxic effects. When administered to a patient who has overdosed on digoxin, DigiFab binds to digoxin molecules, reducing the levels of free digoxin in the body. This shift in equilibrium away from binding to the receptors helps to reduce the cardiotoxic effects of digoxin. The Fab-digoxin complexes are then eliminated from the body through the kidney and reticuloendothelial system.

The indications for using DigiFab in cases of acute and chronic digoxin toxicity are summarized below:

Acute digoxin toxicity:
– Cardiac arrest
– Life-threatening arrhythmia
– Potassium level >5 mmol/l
– Ingestion of >10 mg of digoxin (in adults)
– Ingestion of >4 mg of digoxin (in children)
– Digoxin level >12 ng/ml

Chronic digoxin toxicity:
– Cardiac arrest
– Life-threatening arrhythmia
– Significant gastrointestinal symptoms
– Symptoms of digoxin toxicity in the presence of renal failure

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

Further Reading:

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

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

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

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

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

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

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

This man is at high risk of contracting HIV due to his history of intravenous drug abuse and sharing needles. If a patient has a flu-like illness and a history of risk factors, it is important to suspect that they may be experiencing an HIV seroconversion illness.

Around 20-60% of individuals who contract HIV go through a seroconversion illness. This typically occurs within 1 to 6 weeks after exposure and presents with symptoms similar to the flu. Common clinical features include fever, malaise, myalgia, pharyngitis, diarrhea, headaches, maculopapular rash, lymphadenopathy, and neuralgia.

During this stage of the disease, antibody tests will show negative results. However, a diagnosis of HIV can still be made by conducting a P24 antigen test or measuring HIV RNA levels. CD4 and CD8 counts are usually within the normal range at this stage.

Mycoplasma pneumoniae infection does not have a connection with infective endocarditis. However, it is associated with various extra-pulmonary complications. These include skin conditions such as erythema multiforme and Stevens-Johnson syndrome. In the central nervous system, it can lead to Guillain-Barre syndrome, meningitis, encephalitis, optic neuritis, cerebellar ataxia, and cranial nerve palsies. Gastrointestinal symptoms may include anorexia, nausea, diarrhea, hepatitis, and pancreatitis. Hematological complications can manifest as cold agglutinins, hemolytic anemia, thrombocytopenia, and disseminated intravascular coagulation. Mycoplasma pneumoniae infection can also cause pericarditis and myocarditis. Rheumatic symptoms such as arthralgia and arthritides may occur, and acute glomerulonephritis can affect the kidneys.

Fifth disease, also known as ‘slapped cheek syndrome’, is a common childhood exanthem caused by parvovirus B19.

The clinical features of fifth disease include:

– A mild coryzal illness usually occurs as a prodrome.
– The classic ‘slapped cheek’ rash appears after 3-7 days, characterized by a red rash on the cheeks with pale skin around the mouth.
– A morbilliform rash develops on the extensor surfaces of the arms and legs 1-4 days after the facial rash appears.

This disease is generally harmless and resolves on its own in children. However, it can be dangerous for pregnant women who are exposed to the virus, as it can cause intrauterine infection and hydrops fetalis. Additionally, it can lead to transient aplastic crisis. Therefore, it is important to keep affected children away from pregnant women and individuals with weakened immune systems or blood disorders.

In a young patient who has been experiencing diarrhea and abdominal pain for more than 6 weeks, it is important to consider inflammatory bowel disease as a possible diagnosis. The challenge lies in distinguishing between ulcerative colitis and Crohn’s disease. In this case, a biopsy was performed and the results showed transmural inflammation with the presence of non-caseating granulomas, which strongly suggests a diagnosis of Crohn’s disease.

To differentiate between ulcerative colitis and Crohn’s disease, it is helpful to consider the following characteristics. Ulcerative colitis typically only affects the rectum and colon, although the terminal ileum may be affected in some cases known as backwash ileitis. On the other hand, Crohn’s disease can affect any part of the gastrointestinal tract from the mouth to the anus, and there may be areas of normal mucosa between the affected areas, known as skip lesions.

There are also differences in the associations and systemic manifestations of these two conditions. Ulcerative colitis has a decreased incidence in smokers and is associated with liver conditions such as primary biliary cirrhosis, chronic active hepatitis, and primary sclerosing cholangitis. Crohn’s disease, on the other hand, has an increased incidence in smokers and is more commonly associated with systemic manifestations such as erythema nodosum, pyoderma gangrenosum, iritis/uveitis, cholelithiasis, and joint pain/arthropathy.

Pathologically, ulcerative colitis primarily affects the mucosa and submucosa, with the presence of mucosal ulcers, inflammatory cell infiltrate, and crypt abscesses. In contrast, Crohn’s disease is characterized by transmural inflammation, lymphoid aggregates, and neutrophil infiltrates. Non-caseating granulomas are seen in approximately 30% of cases, which is a distinguishing feature of Crohn’s disease.

When it comes to clinical features, abdominal pain is less prominent in ulcerative colitis, while bloody diarrhea is present in 90% of cases. The passage of mucus is also common, and fever may be present. Symptoms such as urgency, tenesmus (a feeling of incomplete bowel movement), and pre-defecation pain that is relieved by passing stools are frequently reported. In Crohn’s disease, abdominal pain is more prominent, and diarrhea is common, with the possibility of it being bloody.

Blunt abdominal trauma often results in injury to the liver and spleen, which are the two organs most commonly affected. The liver, being the largest and located in a vulnerable position, is particularly prone to injury in such cases.

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.

In order to gain a comprehensive understanding of AF management, it is crucial to familiarize oneself with the terminology used to describe its various subtypes. These terms help categorize different episodes of AF based on their characteristics and outcomes.

Acute AF refers to any episode that occurs within the previous 48 hours. It can manifest with or without symptoms and may or may not recur. On the other hand, paroxysmal AF describes episodes that spontaneously end within 7 days, typically within 48 hours. While these episodes are often recurrent, they can progress into a sustained form of AF.

Recurrent AF is defined as experiencing two or more episodes of AF. If the episodes self-terminate, they are classified as paroxysmal AF. However, if the episodes do not self-terminate, they are categorized as persistent AF. Persistent AF lasts longer than 7 days or has occurred after a previous cardioversion. To terminate persistent AF, electrical or pharmacological intervention is required. In some cases, persistent AF can progress into permanent AF.

Permanent AF, also known as Accepted AF, refers to episodes that cannot be successfully terminated, have relapsed after termination, or where cardioversion is not pursued. This subtype signifies a more chronic and ongoing form of AF.

By understanding and utilizing these terms, healthcare professionals can effectively communicate and manage the different subtypes of AF.

As a person ascends to higher altitudes, their risk of developing high altitude pulmonary edema (HAPE) increases. This patient is displaying signs and symptoms of HAPE, including a dry cough that may progress to frothy sputum, possibly containing blood. Breathlessness, initially experienced during exertion, may progress to being present even at rest.

Further Reading:

High Altitude Illnesses

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

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

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

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

Thought insertion is one of the primary symptoms identified by Schneider in schizophrenia. This symptom refers to the patient’s belief that their thoughts are being controlled or influenced by external sources, such as other individuals or entities. In some cases, they may even experience auditory hallucinations, hearing distinct voices.

Spontaneous bacterial peritonitis (SBP) is a condition where bacteria infect the fluid in the abdomen, known as ascites. It is commonly seen in patients with ascites. Symptoms of SBP include fever, chills, nausea, vomiting, abdominal pain, and mental confusion. To diagnose SBP, a procedure called paracentesis is done to analyze the fluid in the abdomen. If the neutrophil count in the fluid is higher than 250 cells/mm³, it confirms the diagnosis of SBP, regardless of whether bacteria are found in the culture. The initial treatment for acute community-acquired SBP is usually a 3rd generation cephalosporin antibiotic like cefotaxime or ceftriaxone. However, hospital-acquired SBP may require different antibiotics based on local resistance patterns. Patients who have had SBP in the past are at a high risk of recurrence and may need long-term antibiotic prophylaxis.

Further Reading:

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

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

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

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

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

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

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

The most likely cause of the fainting episode in this 25-year-old third year medical student is vasovagal syncope. Vasovagal syncope is a common type of fainting that occurs in response to certain triggers, such as emotional stress, pain, or seeing blood. In this case, the prolonged delivery and emergency C-section likely triggered the patient’s vasovagal response.

The patient’s symptoms of feeling warm and sweaty before fainting are consistent with vasovagal syncope. During a vasovagal episode, there is a sudden drop in blood pressure and heart rate, leading to a temporary loss of consciousness. The absence of loss of bladder or bowel control and tongue biting further support this diagnosis.

The physical examination findings of no focal neurological deficits and a normal cardiovascular examination also align with vasovagal syncope. Additionally, the blood pressure measurements of 122/74 mmHg when lying down and 120/72 mmHg when standing suggest orthostatic hypotension, which is commonly seen in vasovagal syncope.

Further Reading:

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

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

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

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

The first-line treatment for Addisonian (adrenal) crisis is hydrocortisone. This patient displays symptoms that indicate an Addisonian crisis, and the main components of their management involve administering hydrocortisone and providing intravenous fluids for resuscitation.

Further Reading:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. It is produced by subjecting carbonaceous matter to high temperatures, a process known as pyrolysis, and then concentrating it with a zinc chloride solution. This creates a network of pores within the charcoal, giving it a large absorptive area of approximately 3,000 m2/g. This porous structure helps prevent the absorption of the harmful toxin by up to 50%.

The usual dosage of activated charcoal is 50 grams for adults and 1 gram per kilogram of body weight for children. It can be administered orally or through a nasogastric tube. It is important to give the charcoal within one hour of ingestion, and it may be repeated after one hour if necessary.

However, there are certain situations where activated charcoal should not be used. If the patient is unconscious or in a coma, there is a risk of aspiration, so the charcoal should not be given. Similarly, if seizures are likely to occur, there is a risk of aspiration and the charcoal should be avoided. Additionally, if there is reduced gastrointestinal motility, there is a risk of obstruction, so activated charcoal should not be used in such cases.

Activated charcoal is effective in treating overdose with various drugs and toxins, including aspirin, paracetamol, barbiturates, tricyclic antidepressants, digoxin, amphetamines, morphine, cocaine, and phenothiazines. However, it is ineffective in treating overdose with substances such as iron, lithium, boric acid, cyanide, ethanol, ethylene glycol, methanol, malathion, DDT, carbamate, hydrocarbon, strong acids, or alkalis.

There are some potential adverse effects associated with activated charcoal. These include nausea and vomiting, diarrhea, constipation, bezoar formation (a mass of undigested material that can cause blockages), bowel obstruction, pulmonary aspiration (inhaling the charcoal into the lungs), and impaired absorption of oral medications or antidotes.

Haemolytic disease of the newborn is a condition that occurs in the fetus when IgG antibodies from the mother pass through the placenta. This is classified as a type II hypersensitivity reaction, also known as cytotoxic hypersensitivity. In this type of reaction, antibodies produced by the immune response attach to antigens on the patient’s own cell surfaces.

The rhesus gene is composed of three parts, which can be C or c, D or d, and E or e. Approximately 15% of the population consists of rhesus negative women who are homozygous for d. When rhesus-positive fetal cells enter the bloodstream of a rhesus-negative mother, maternal anti-D IgG antibodies may be produced. This commonly occurs during delivery, but can also happen after fetal-maternal hemorrhage and certain medical procedures.

Some other examples of type II hypersensitivity reactions include autoimmune hemolytic anemia, ANCA-associated vasculitides, Goodpasture’s syndrome, myasthenia gravis, and rhesus incompatibility.

In the blood tests, certain findings can support a diagnosis of glandular fever. One of these findings is lymphocytosis, which refers to an increased number of lymphocytes in the blood. Lymphocytes are a type of white blood cell that plays a crucial role in the immune response. In glandular fever, the Epstein-Barr virus (EBV) is the most common cause, and it primarily infects and activates lymphocytes, leading to their increased numbers in the blood.

On the other hand, neutropenia (a decreased number of neutrophils) and neutrophilia (an increased number of neutrophils) are not typically associated with glandular fever. Neutrophils are another type of white blood cell that helps fight off bacterial infections. In glandular fever, the primary involvement is with lymphocytes rather than neutrophils.

Monocytosis, which refers to an increased number of monocytes, can also be seen in glandular fever. Monocytes are another type of white blood cell that plays a role in the immune response. Their increased numbers can be a result of the immune system’s response to the Epstein-Barr virus.

Eosinophilia, an increased number of eosinophils, is not commonly associated with glandular fever. Eosinophils are white blood cells involved in allergic reactions and parasitic infections, and their elevation is more commonly seen in those conditions.

In summary, the presence of lymphocytosis and possibly monocytosis in the blood tests would support a diagnosis of glandular fever, while neutropenia, neutrophilia, and eosinophilia are less likely to be associated with this condition.

Further Reading:

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

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

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

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

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

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

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

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

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

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

The typical clinical characteristics of acne fulminans are as follows:

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

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

Adrenaline acts on all types of adrenergic receptors without preference. It is administered in doses of 1 mg every 3-5 minutes during cardiac arrest. On the other hand, Amiodarone functions by blocking voltage-gated potassium channels and is typically administered after the third shock.

Further Reading:

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

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

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

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

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

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

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

Hypothermic cardiac arrest is a rare situation that requires a tailored approach. Resuscitation is typically prolonged, but the prognosis for young, previously healthy individuals can be good. Hypothermic cardiac arrest may be associated with drowning. Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, basal metabolic rate falls and cell signaling between neurons decreases, leading to reduced tissue perfusion. Signs and symptoms of hypothermia progress as the core temperature drops, initially presenting as compensatory increases in heart rate and shivering, but eventually ceasing as the temperature drops into moderate hypothermia territory.

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

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

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

The human papillomavirus (HPV) is a viral infection that is primarily responsible for the development of genital warts. This virus is predominantly transmitted through sexual contact.

Abducens nerve palsy is often linked to extradural hematoma. When there is a mass effect, downward brain herniation can occur, leading to the involvement of the 6th cranial nerve (abducens nerve, CN VI). This nerve controls the lateral rectus muscle, which is responsible for eye abduction. When the abducens nerve is affected, the lateral rectus muscle is unable to function properly, resulting in an inward turning of the affected eye towards the nose (esotropia).

Further Reading:

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

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

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

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

The presence of both fever and a murmur in an individual who engages in intravenous drug use (IVDU) should raise suspicion for infective endocarditis. IVDU is a significant risk factor for this condition. In this particular patient, the symptoms of fever and cardiac murmur are important indicators that may be emphasized in an exam scenario. It is important to note that infective endocarditis in IVDU patients typically affects the right side of the heart, with the tricuspid valve being the most commonly affected. Murmurs in this patient population can be subtle and challenging to detect during a clinical examination. Additionally, the presence of septic emboli can lead to the entry of infected material into the pulmonary circulation, potentially causing pneumonia and pulmonary vessel occlusion, which may manifest as a pulmonary embolism (PE).

Further Reading:

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

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

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

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

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

The guidelines from the British Thoracic Society (BTS) recommend conducting investigations for Legionella infection in the following cases: severe community-acquired pneumonia, patients with specific risk factors, and during outbreaks of community-acquired pneumonia. To confirm a case, the Public Health England (PHE) requires one of the following: isolation and culture of Legionella species from clinical specimens (typically sputum), seroconversion with a four-fold increase in titre of indirect immunofluorescent antibody test (IFAT) using a validated technique, or confirmation of Legionella pneumophila urinary antigen using validated reagents or kits. The gold standard for confirmation is the isolation and culture of Legionella species, while cases of Pontiac fever are usually culture-negative. The HPA considers a case presumptive if there is a clinical diagnosis of pneumonia with a single high titre of 128 using IFAT, or a single titre of 64 in an outbreak. A positive result by direct immunofluorescence on a clinical specimen using validated monoclonal antibodies is also considered a presumptive case.

To manage aortic dissection, it is important to lower the systolic blood pressure to a range of 100-120 mmHg. This helps decrease the strain on the damaged artery and minimizes the chances of the dissection spreading further. In this patient, symptoms such as tearing chest pain and a widened mediastinum on the chest X-ray are consistent with aortic dissection.

Further Reading:

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

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

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

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

Managing a difficult situation that involves teamwork and patient safety can be challenging. The first priority is to ensure the patient’s safety from a clinical standpoint. It is important to promptly inform the consultant on duty about the incident and gather all relevant information.

In the meantime, it is crucial to gather information from the patient, nursing staff, and written notes to fully understand the situation. A thorough investigation will be necessary, including a discussion with the doctor involved. Complaints of this nature must be taken seriously, and it may be necessary to send the doctor home while the investigation takes place.

Additionally, it is important to escalate the matter to the hospital hierarchy to ensure appropriate action is taken. The doctor should also be directed to support services as this process is likely to be stressful for them.

For further guidance on this matter, it is recommended to refer to the GMC Guidance on Intimate Examinations and Chaperones.

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 term renal colic is commonly used to describe a sudden and intense pain in the lower back caused by a blockage in the ureter, which is the tube that carries urine from the kidney to the bladder. However, a more accurate term is ureteric colic, as the pain usually arises from a blockage in the ureter itself.

Renal or ureteric colic typically presents with a sudden onset of severe abdominal pain on one side, starting in the lower back or flank and radiating to the genital area in women or to the groin or testicle in men.

The pain usually:
– Lasts for minutes to hours and comes in spasms, with periods of no pain or a dull ache
– Is often accompanied by nausea, vomiting, and blood in the urine
– Is often described as the most intense pain a person has ever experienced (many women describe it as worse than childbirth).

People with renal or ureteric colic:
– Are restless and unable to find relief by lying still (which helps distinguish it from peritonitis)
– May have a history of previous episodes
– May have a fever and sweating if there is a urinary tract infection present
– May complain of painful urination, frequent urination, and straining when the stone reaches the junction between the ureter and bladder (due to irritation of the bladder muscle).

If possible, a urine dipstick test should be done to support the diagnosis and check for signs of a urinary tract infection.

Checking for blood in the urine can also support the diagnosis of renal or ureteric colic. However, the absence of blood does not rule out the diagnosis and other causes of pain should be considered.

Checking for nitrite and leukocyte esterase in the urine can indicate an infection.

Pain management:
– Non-steroidal anti-inflammatory drugs (NSAIDs) are the first-line treatment for adults, children, and young people with suspected renal colic.
– Intravenous paracetamol can be given to adults, children, and young people if NSAIDs are not suitable or not providing enough pain relief.
– Opioids may be considered if both NSAIDs and intravenous paracetamol are not suitable or not providing enough pain relief.
– Antispasmodics should not be given to adults, children, and young people with suspected renal colic.

For children experiencing moderate pain, diclofenac (taken orally or rectally), oral codeine, or oral morphine are suitable options for providing relief. The patient has already been given the appropriate initial analgesia for mild pain. Therefore, it is now appropriate to administer analgesia for moderate pain, following the next step on the analgesic ladder. Considering diclofenac, codeine, or oral morphine would be appropriate in this case.

Further Reading:

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

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

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

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

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

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

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

This woman is showing signs of obstructive jaundice along with a history of ulcerative colitis. The most probable diagnosis in this case is primary sclerosing cholangitis (PSC). PSC is a condition that causes inflammation and blockage of the bile ducts, leading to progressive damage. It is characterized by recurrent episodes of cholangitis and the development of scar tissue in the bile ducts. In severe cases, it can lead to liver cirrhosis, liver failure, and even liver cancer. PSC is commonly associated with ulcerative colitis, with more than 80% of PSC patients also having ulcerative colitis.

The underlying cause of PSC is believed to be autoimmune in nature. Around 80% of patients with PSC test positive for p-ANCA antibodies, which are associated with autoimmune diseases. Other antibodies such as antinuclear antibodies (ANA) and anti-smooth muscle antibodies may also be present, but they are only found in about one-third of PSC patients.

Autoimmune hepatitis, on the other hand, is a liver inflammation caused by a decrease in regulatory T-cells (Treg cells), leading to the production of autoantibodies against hepatocyte surface antigens. It primarily affects women (70%) between the ages of 15 and 40. The condition causes chronic and progressive hepatitis, often presenting in the later stages when the patient is severely unwell and jaundiced. Liver function tests typically show significantly elevated levels of transaminases (ALT and AST), often more than ten times the normal range. Alkaline phosphatase (ALP) levels may be normal or slightly elevated. Antinuclear antibodies (ANA) are positive in approximately 80% of cases, while smooth muscle antibodies (SMA) are positive in about 70% of cases. Antimitochondrial antibodies are usually low or absent.

Primary biliary cirrhosis is another autoimmune liver disease that leads to the progressive destruction of the small bile ducts in the liver, primarily affecting the intralobular ducts. This results in cholestatic jaundice, liver fibrosis, and eventually cirrhosis. The condition is more common in women (90%) and typically occurs between the ages of 30 and 65. Liver function tests show predominantly elevated levels of alkaline phosphatase (ALP), often before any symptoms or signs of the disease appear.

Salicylate poisoning is a fairly common form of poisoning that can lead to organ damage and death if not treated promptly. The symptoms of salicylate poisoning include nausea, vomiting, ringing in the ears, hearing loss, excessive sweating, dehydration, rapid breathing, flushed skin, and high fever in children. In severe cases, convulsions, swelling of the brain, coma, kidney failure, fluid in the lungs, and unstable heart function can occur.

The treatment for salicylate poisoning involves stabilizing the patient’s airway, breathing, and circulation as needed, preventing further absorption of the poison, enhancing its elimination from the body, correcting any metabolic abnormalities, and providing supportive care. Unfortunately, there is no specific antidote available for salicylates. If a large amount of salicylate has been ingested within the past hour (more than 4.5 grams in adults or more than 2 grams in children), gastric lavage (stomach pumping) and administration of activated charcoal (50 grams) are recommended to reduce absorption and increase elimination.

Medical investigations for salicylate poisoning should include measuring the level of salicylate in the blood, analyzing arterial blood gases, performing an electrocardiogram (ECG), checking blood glucose levels, assessing kidney function and electrolyte levels, and evaluating blood clotting. ECG abnormalities that may be present include widening of the QRS complex, AV block, and ventricular arrhythmias.

The severity of salicylate poisoning is determined by the level of salicylate in the blood. Mild poisoning is defined as a salicylate level below 450 mg/L, moderate poisoning is between 450-700 mg/L, and severe poisoning is above 700 mg/L. In severe cases, aggressive intravenous fluid therapy is necessary to correct dehydration, and administration of 1.26% sodium bicarbonate can help eliminate the salicylate from the body. It is important to maintain a urine pH of greater than 7.5, ideally between 8.0-8.5. However, forced alkaline diuresis is no longer recommended. Life-threatening cases may require admission to the intensive care unit, intubation and ventilation, and possibly hemodialysis.

This patient has presented with an Addisonian crisis, which is a rare but potentially catastrophic condition if not diagnosed promptly. It is more commonly seen in women than men and typically occurs between the ages of 30 and 50.

Addison’s disease is caused by insufficient production of steroid hormones by the adrenal glands, affecting the production of glucocorticoids, mineralocorticoids, and sex steroids. The main causes of Addison’s disease include autoimmune adrenalitis (accounting for 80% of cases), bilateral adrenalectomy, Waterhouse-Friderichsen syndrome (hemorrhage into the adrenal glands), and tuberculosis.

The most common trigger for an Addisonian crisis in patients with Addison’s disease is the intentional or accidental withdrawal of steroid therapy. Other factors that can precipitate a crisis include infection, trauma, myocardial infarction, cerebral infarction, asthma, hypothermia, and alcohol abuse.

Clinical features of Addison’s disease include weakness, lethargy, hypotension (especially orthostatic hypotension), nausea, vomiting, weight loss, reduced axillary and pubic hair, depression, and hyperpigmentation (particularly in palmar creases, buccal mucosa, and exposed areas). In an Addisonian crisis, the main symptoms are usually hypoglycemia and shock, characterized by tachycardia, peripheral vasoconstriction, hypotension, altered consciousness, and even coma.

Biochemical markers of Addison’s disease typically include increased ACTH levels (as a compensatory response to stimulate the adrenal glands), elevated serum renin levels, hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, and metabolic acidosis. Confirmatory investigations may involve the Synacthen test, plasma ACTH level measurement, plasma renin level measurement, and testing for adrenocortical antibodies.

Management of Addison’s disease should be overseen by an Endocrinologist. Treatment usually involves the administration of hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also require thyroxine if there is concurrent hypothalamic-pituitary disease. Treatment is lifelong, and patients should carry a steroid card and MedicAlert bracelet to alert healthcare professionals about their condition and the potential for an Addisonian crisis.

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

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

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

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

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

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

The management of anaphylaxis involves several important steps. First and foremost, it is crucial to ensure proper airway management. Additionally, early administration of adrenaline is essential, preferably in the anterolateral aspect of the middle third of the thigh. Aggressive fluid resuscitation is also necessary. In severe cases, intubation may be required. However, it is important to note that the administration of chlorpheniramine and hydrocortisone should only be considered after early resuscitation has taken place.

Adrenaline is the most vital medication for treating anaphylactic reactions. It acts as an alpha-adrenergic receptor agonist, which helps reverse peripheral vasodilatation and reduce oedema. Furthermore, its beta-adrenergic effects aid in dilating the bronchial airways, increasing the force of myocardial contraction, and suppressing histamine and leukotriene release. Administering adrenaline as the first drug is crucial, and the intramuscular (IM) route is generally the most effective for most individuals.

The recommended doses of IM adrenaline for different age groups during anaphylaxis are as follows:

– Children under 6 years: 150 mcg (0.15 mL of 1:1000)
– Children aged 6-12 years: 300 mcg (0.3 mL of 1:1000)
– Children older than 12 years: 500 mcg (0.5 mL of 1:1000)
– Adults: 500 mcg (0.5 mL of 1:1000)

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

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

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

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

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

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.

Chickenpox in children is usually managed conservatively. In this case, the patient has chickenpox but does not show any signs of serious illness. The parents should be given advice on keeping the child out of school, ensuring they stay hydrated, and providing relief for their symptoms. It is important to provide appropriate safety measures in case the child’s condition worsens. Admission to the hospital is not recommended for uncomplicated chickenpox as it could spread the infection to other children, especially those who may have a weakened immune system. Aciclovir should not be used for uncomplicated chickenpox in children. VZIG is given as a preventive measure for infection, mainly for pregnant women without immunity, and is not a treatment for those already infected. There is no need to check both parents’ IgG levels unless the mother is pregnant and has no history of chickenpox or shingles, in which case testing may be appropriate.

Further Reading:

Chickenpox is caused by the varicella zoster virus (VZV) and is highly infectious. It is spread through droplets in the air, primarily through respiratory routes. It can also be caught from someone with shingles. The infectivity period lasts from 4 days before the rash appears until 5 days after the rash first appeared. The incubation period is typically 10-21 days.

Clinical features of chickenpox include mild symptoms that are self-limiting. However, older children and adults may experience more severe symptoms. The infection usually starts with a fever and is followed by an itchy rash that begins on the head and trunk before spreading. The rash starts as macular, then becomes papular, and finally vesicular. Systemic upset is usually mild.

Management of chickenpox is typically supportive. Measures such as keeping cool and trimming nails can help alleviate symptoms. Calamine lotion can be used to soothe the rash. People with chickenpox should avoid contact with others for at least 5 days from the onset of the rash until all blisters have crusted over. Immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG). If chickenpox develops, IV aciclovir should be considered. Aciclovir may be prescribed for immunocompetent, non-pregnant adults or adolescents with severe chickenpox or those at increased risk of complications. However, it is not recommended for otherwise healthy children with uncomplicated chickenpox.

Complications of chickenpox can include secondary bacterial infection of the lesions, pneumonia, encephalitis, disseminated haemorrhagic chickenpox, and rare conditions such as arthritis, nephritis, and pancreatitis.

Shingles is the reactivation of the varicella zoster virus that remains dormant in the nervous system after primary infection with chickenpox. It typically presents with signs of nerve irritation before the eruption of a rash within the dermatomal distribution of the affected nerve. Patients may feel unwell with malaise, myalgia, headache, and fever prior to the rash appearing. The rash appears as erythema with small vesicles that may keep forming for up to 7 days. It usually takes 2-3 weeks for the rash to resolve.

Management of shingles involves keeping the vesicles covered and dry to prevent secondary bacterial infection.

There are several factors that are known to increase the risk of violence from patients. These include being male, being young (under 40 years old), having poor levels of self-care, exhibiting coercive behavior, having a history of prior violent episodes, making multiple attendances to the hospital, being intoxicated with alcohol, and experiencing organic psychosis.

The beta thalassaemias are a group of blood disorders that occur when there is an abnormality in the production of the globin chains. These disorders are inherited in an autosomal recessive manner. In individuals with beta thalassaemia trait, there is a slight decrease in the production of beta-globin chains. This condition is most commonly found in people of Mediterranean and Asian descent.

The presentation of beta thalassaemia trait is characterized by a mild form of microcytic hypochromic anaemia. This type of anaemia can be challenging to differentiate from iron deficiency anaemia. However, it can be distinguished from iron deficiency anaemia by the presence of normal iron levels. Another useful marker for diagnosing beta thalassaemia trait is an elevated HbA2 level. A value greater than 3.5% is considered diagnostic for this condition.

Chickenpox is a highly contagious illness caused by the varicella-zoster virus, a DNA virus from the Herpesviridae family. Most cases are mild to moderate, and the infection usually resolves on its own. Severe complications are rare but can occur, especially in individuals with weakened immune systems or underlying health conditions.

The incubation period for chickenpox is typically between 14 to 21 days. It is contagious from a few days before the rash appears until about a week after the first lesions show up.

The common clinical features of chickenpox include:

– Fever, which lasts for approximately 3-5 days.
– The initial rash starts as flat red spots and progresses into raised bumps.
– These bumps then turn into fluid-filled blisters and eventually form pustules surrounded by redness.
– The lesions are extremely itchy.
– The rash reaches its peak around 48 hours in individuals with a healthy immune system.
– The rash tends to be more concentrated on the face and trunk, with fewer lesions on the limbs.
– The blisters eventually dry up and form crusts, which can lead to scarring if scratched.
– Headache, fatigue, and abdominal pain may also occur.

Chickenpox tends to be more severe in teenagers and adults compared to children. Antiviral treatment should be considered for these individuals if they seek medical attention within 24 hours of rash onset. The recommended oral dose of aciclovir is 800 mg taken five times a day for seven days.

Immunocompromised patients and those at higher risk, such as individuals with severe cardiovascular or respiratory disease or chronic skin disorders, should receive antiviral treatment for ten days, with at least seven days of intravenous administration.

Although most cases are relatively mild, if serious complications like pneumonia, encephalitis, or dehydration are suspected, it is important to refer the patient for hospital admission.

For more information, you can refer to the NICE Clinical Knowledge Summary on Chickenpox.
https://cks.nice.org.uk/topics/chickenpox/

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

If someone with IBS experiences unintentional weight loss or rectal bleeding, it is important to investigate further as these symptoms are not typical of IBS and may indicate a more serious underlying condition. Other alarm symptoms to watch out for include positive faecal immunochemical test (FIT), change in bowel habit after the age of 60, elevated faecal calprotectin levels, iron deficiency anaemia, persistent or frequent bloating in females (especially if over 50), the presence of an abdominal or rectal mass, or a family history of bowel cancer, ovarian cancer, coeliac disease, or inflammatory bowel disease.

Further Reading:

Irritable bowel syndrome (IBS) is a chronic disorder that affects the interaction between the gut and the brain. The exact cause of IBS is not fully understood, but factors such as genetics, drug use, enteric infections, diet, and psychosocial factors are believed to play a role. The main symptoms of IBS include abdominal pain, changes in stool form and/or frequency, and bloating. IBS can be classified into subtypes based on the predominant stool type, including diarrhea-predominant, constipation-predominant, mixed, and unclassified.

Diagnosing IBS involves using the Rome IV criteria, which includes recurrent abdominal pain associated with changes in stool frequency and form. It is important to rule out other more serious conditions that may mimic IBS through a thorough history, physical examination, and appropriate investigations. Treatment for IBS primarily involves diet and lifestyle modifications. Patients are advised to eat regular meals with a healthy, balanced diet and adjust their fiber intake based on symptoms. A low FODMAP diet may be trialed, and a dietician may be consulted for guidance. Regular physical activity and weight management are also recommended.

Psychosocial factors, such as stress, anxiety, and depression, should be addressed and managed appropriately. If constipation is a predominant symptom, soluble fiber supplements or foods high in soluble fiber may be recommended. Laxatives can be considered if constipation persists, and linaclotide may be tried if optimal doses of previous laxatives have not been effective. Antimotility drugs like loperamide can be used for diarrhea, and antispasmodic drugs or low-dose tricyclic antidepressants may be prescribed for abdominal pain. If symptoms persist or are refractory to treatment, alternative diagnoses should be considered, and referral to a specialist may be necessary.

Overall, the management of IBS should be individualized based on the patient’s symptoms and psychosocial situation. Clear explanation of the condition and providing resources for patient education, such as the NHS patient information leaflet and support from organizations like The IBS Network, can also be beneficial.

Ipratropium bromide commonly leads to dry mouth as a side effect. Additionally, it may result in constipation, cough, sudden bronchospasm, headache, nausea, and palpitations. In patients with prostatic hyperplasia and bladder outflow obstruction, it can cause urinary retention. Furthermore, susceptible individuals may experience acute closed-angle glaucoma as a result of using this medication.

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

Further Reading:

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

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

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

When adjusting the dosage of oral morphine, if the initial dose does not provide relief, it is recommended to increase the dose by 50%. The goal of dosage titration is to identify the minimum amount of morphine required to effectively manage pain. Additionally, it is important to consider the use of supplementary analgesics like NSAIDs and paracetamol.

A tension pneumothorax occurs when there is an air leak from the lung or chest wall that acts like a one-way valve. This causes air to build up in the pleural space without any way to escape. As a result, the pressure in the pleural space increases and pushes the mediastinum into the opposite side of the chest. If left untreated, this can lead to cardiovascular instability and even cardiac arrest.

The clinical features that are typically seen in tension pneumothorax include respiratory distress and cardiovascular instability. Tracheal deviation away from the side of injury, unilateral absence of breath sounds on the affected side, and a hyper-resonant percussion note are also characteristic. Other signs may include distended neck veins and cyanosis, although cyanosis is usually a late sign.

Both tension pneumothorax and massive haemothorax can cause decreased breath sounds on auscultation. However, they can be differentiated by percussion. Hyper-resonance suggests tension pneumothorax, while dullness indicates a massive haemothorax.

It is important to note that tension pneumothorax is a clinical diagnosis and treatment should not be delayed for radiological confirmation. Immediate decompression through needle thoracocentesis is the recommended treatment. Traditionally, a large-bore needle or cannula is inserted into the 2nd intercostal space in the midclavicular line of the affected side. However, studies have shown that using the 4th or 5th intercostal space in the midaxillary line has better success in reaching the thoracic cavity in adult patients. ATLS now recommends this location for needle decompression in adults. The location for children remains the same, and the 2nd intercostal space in the midclavicular line should still be used. It is important to remember that needle thoracocentesis is a temporary measure and definitive treatment involves the insertion of a chest drain.

NICE has emphasized that there are particular symptoms and indications that may indicate specific diseases as the underlying cause of a fever. In the case of herpes simplex encephalitis, the following symptoms and signs may suggest its presence: the presence of a focal neurological sign, focal seizures, and a decreased level of consciousness. For more information on this topic, you may refer to the NICE guidelines on the assessment and initial management of fever in children under the age of 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

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

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

Further Reading:

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

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

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

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

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

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

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

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

When assessing a patient with epistaxis (nosebleed), it is important to start with a standard ABC assessment, focusing on the airway and hemodynamic status. Even if the bleeding appears to have stopped, it is crucial to evaluate the patient’s condition. If active bleeding is still present and there are signs of hemodynamic compromise, immediate resuscitative and first aid measures should be initiated.

Epistaxis should be treated as a circulatory emergency, especially in elderly patients, those with clotting disorders or bleeding tendencies, and individuals taking anticoagulants. In these cases, it is necessary to establish intravenous access using at least an 18-gauge (green) cannula. Blood samples, including a full blood count, urea and electrolytes, clotting profile, and group and save (depending on the amount of blood loss), should be sent for analysis. Patients should be assigned to a majors or closely observed area, as dislodgement of a blood clot can lead to severe bleeding.

First aid measures to control bleeding include the following steps:
1. The patient should be seated upright with their body tilted forward and their mouth open. Lying down should be avoided, unless the patient feels faint or there is evidence of hemodynamic compromise. Leaning forward helps reduce the flow of blood into the nasopharynx.
2. The patient should be encouraged to spit out any blood that enters the throat and advised not to swallow it.
3. Firmly pinch the soft, cartilaginous part of the nose, compressing the nostrils for 10-15 minutes. Pressure should not be released, and the patient should breathe through their mouth.
4. If the patient is unable to comply, an alternative technique is to ask a relative, staff member, or use an external pressure device like a swimmer’s nose clip.
5. It is important to dispel the misconception that compressing the bones will help stop the bleeding. Applying ice to the neck or forehead does not influence nasal blood flow. However, sucking on an ice cube or applying an ice pack directly to the nose may reduce nasal blood flow.

If bleeding stops with first aid measures, it is recommended to apply a topical antiseptic preparation to reduce crusting and vestibulitis. Naseptin cream (containing chlorhexidine and neomycin) is commonly used and should be applied to the nostrils four times daily for 10 days.

The airway is deemed at risk when the Glasgow Coma Scale (GCS) falls below 8. There are various factors that can lead to airway obstruction, including the presence of blood or vomit in the airway, a foreign object such as a tooth or food blocking the passage, direct injury to the face or throat, inflammation of the epiglottis (epiglottitis), involuntary closure of the larynx (laryngospasm), constriction of the bronchial tubes (bronchospasm), swelling in the pharynx due to infection or fluid accumulation (oedema), excessive bronchial secretions, and blockage of a tracheostomy tube.

Myelodysplastic syndromes are a group of disorders affecting the haemopoietic stem cell, leading to ineffective production of myeloid blood cells. These conditions typically manifest between the ages of 60 and 75 and are more prevalent in men than women.

The clinical features of myelodysplastic syndromes include tiredness due to anaemia (the most common presentation), easy bruising, and a tendency to bleed. Laboratory findings often reveal anaemia (usually macrocytic or normocytic), neutropenia, thrombocytopenia, and abnormal cell morphology with oddly shaped macrocytes.

Chronic lymphocytic leukaemia (CLL) is the most common form of adult leukaemia, primarily affecting B-lymphocytes. It often presents asymptomatically in patients who undergo routine blood tests revealing elevated white cell counts and lymphocytosis. Men over the age of 50 account for over 75% of CLL cases. Blood films typically show a predominance of mature-looking lymphocytes and smear cells.

Iron deficiency anaemia is characterized by hypochromic microcytic anaemia and a reduced red blood cell count. Peripheral blood smears in iron deficiency anaemia may exhibit poikilocytosis (varying shapes) and anisocytosis (varying sizes). Pencil cells are also observed in this condition.

Vitamin B12 and folate deficiency can also cause macrocytic anaemia. However, the severity of anaemia and macrocytosis would generally need to be much more pronounced to result in neutropenia and thrombocytopenia. Therefore, a myelodysplastic syndrome is more likely in such cases.

Haloperidol, when administered during the third trimester of pregnancy, can lead to extrapyramidal symptoms in the newborn. These symptoms may include agitation, poor feeding, excessive sleepiness, and difficulty breathing. The severity of these side effects can vary, with some infants requiring intensive care and extended hospital stays. It is important to closely monitor exposed neonates for signs of extrapyramidal syndrome or withdrawal. Haloperidol should only be used during pregnancy if the benefits clearly outweigh the risks to the fetus.

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

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

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

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

Benzodiazepines (e.g. diazepam): When administered late in pregnancy, these drugs can cause respiratory depression and a neonatal withdrawal syndrome.

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

Carbamazepine: This drug can lead to hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol: Administration of chloramphenicol can cause gray baby syndrome in newborns.

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

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

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

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

In stable patients with SVT, it is recommended to first try vagal manoeuvres before resorting to drug treatment. This approach is particularly applicable to patients who do not exhibit any adverse features, as mentioned in the case above.

Further Reading:

Supraventricular tachycardia (SVT) is a type of tachyarrhythmia that originates from the atria or above the bundle of His in the heart. It includes all atrial and junctional tachycardias, although atrial fibrillation is often considered separately. SVT typically produces a narrow QRS complex tachycardia on an electrocardiogram (ECG), unless there is an underlying conduction abnormality below the atrioventricular (AV) node. Narrow complex tachycardias are considered SVTs, while some broad complex tachycardias can also be SVTs with co-existent conduction delays.

SVT can be classified into three main subtypes based on where it arises: re-entrant accessory circuits (the most common type), atrial tachycardias, and junctional tachycardias. The most common SVTs are AVNRT (AV nodal re-entry tachycardia) and AVRT (AV re-entry tachycardia), which arise from accessory circuits within the heart. AVNRT involves an accessory circuit within the AV node itself, while AVRT involves an accessory pathway between the atria and ventricles that allows additional electrical signals to trigger the AV node.

Atrial tachycardias originate from abnormal foci within the atria, except for the SA node, AV node, or accessory pathway. Junctional tachycardias arise in the AV junction. The ECG features of SVTs vary depending on the type. Atrial tachycardias may have abnormal P wave morphology, an isoelectric baseline between P waves (in atrial flutter), and inverted P waves in certain leads. AVNRT may show pseudo R waves in V1 or pseudo S waves in certain leads, with an RP interval shorter than the PR interval. AVRT (WPW) may exhibit a delta wave on a resting ECG and retrograde P waves in the ST segment, with an RP interval shorter than the PR interval. Junctional tachycardias may have retrograde P waves before, during, or after the QRS complex, with inverted P waves in certain leads and upright P waves in others.

Treatment of SVT follows the 2021 resuscitation council algorithm for tachycardia with a pulse. The algorithm provides guidelines for managing stable patients with SVT.

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

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

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

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

Acute epiglottitis is a condition characterized by inflammation of the epiglottis. It can be life-threatening as it can completely block the airway, especially if not diagnosed promptly. In the past, the most common cause was Haemophilus influenzae type b (Hib), but with the widespread use of the Hib vaccine, it has become rare in children and is now more commonly seen in adults caused by Streptococcus spp like Streptococcus pyogenes and Streptococcus pneumonia. Other bacterial causes include Staphylococcus aureus, Pseudomonas spp, Moraxella catarrhalis, and Mycobacterium tuberculosis.

The typical symptoms of acute epiglottitis include fever, sore throat (initially resembling a viral sore throat), painful swallowing, difficulty swallowing secretions (seen as drooling in children), muffled voice (referred to as ‘hot potato’ voice), rapid heartbeat, tenderness in the front of the neck over the hyoid bone, cervical lymph node enlargement, and rapid deterioration in children.

To diagnose acute epiglottitis, the gold standard investigation is fibre-optic laryngoscopy, which allows direct visualization of the epiglottis. However, laryngoscopy should only be performed in settings prepared for intubation or tracheostomy in case upper airway obstruction occurs. If laryngoscopy is not possible, a lateral neck X-ray may be helpful, as it can show the characteristic ‘thumbprint sign’.

Management of acute epiglottitis usually involves conservative measures such as intravenous or oral antibiotics. However, in some cases, intubation may be necessary.

The intravascular volume of an infant is approximately 80 ml/kg, while in older children it is around 70 ml/kg. Dehydration itself does not lead to death, but shock can occur when there is a loss of 20 ml/kg from the intravascular space. Clinical dehydration becomes evident only after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children:

Bodyweight:
– First 10 kg: Daily fluid requirement of 100 ml/kg and hourly fluid requirement of 4 ml/kg.
– Second 10 kg: Daily fluid requirement of 50 ml/kg and hourly fluid requirement of 2 ml/kg.
– Subsequent kg: Daily fluid requirement of 20 ml/kg and hourly fluid requirement of 1 ml/kg.

Based on this information, the hourly maintenance fluid requirements for this child can be calculated as follows:

– First 10 kg: 4 ml/kg = 40 ml
– Second 10 kg: 2 ml/kg = 20 ml
– Subsequent kg: 1 ml/kg = 5 ml

Therefore, the total hourly maintenance fluid requirement for this child is 65 ml.

The subclavian approach for central lines carries the highest risk of pneumothorax. However, it does have advantages such as being accessible during airway control and having easily identifiable landmarks for insertion, even in obese patients. It is important to note that the carotid is not used for CVC’s.

Further Reading:

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.

Patients who are 16 years old and above are presumed to have the ability to make decisions about their treatment.

Further Reading:

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

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

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

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

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

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

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

Before starting BiPAP, it is important for patients with COPD to have already started maximum medical therapy. This includes receiving supplemental oxygen, using nebulizers with salbutamol and ipratropium, taking steroids and antibiotics if necessary, and potentially receiving IV bronchodilators. Additionally, patients should meet the blood gas requirements of having a pH level below 7.35 and a pCO2 level above 6 Kpa. Another criteria for initiating NIV is having a respiratory rate higher than 23.

Further Reading:

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

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

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

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

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

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

Tinea cruris, commonly known as ‘jock itch’, is a fungal infection that affects the groin area. It is primarily caused by Trichophyton rubrum and is more prevalent in young men, particularly athletes. The typical symptoms include a reddish or brownish rash that is accompanied by intense itching. Pustules and vesicles may also develop, and there is often a raised border with a clear center. Notably, the infection usually does not affect the penis and scrotum.

It is worth mentioning that patients with tinea cruris often have concurrent tinea pedis, also known as athlete’s foot, which may have served as the source of the infection. The infection can be transmitted through sharing towels or by using towels that have come into contact with infected feet, leading to the spread of the fungus to the groin area.

Fortunately, treatment for tinea cruris typically involves the use of topical imidazole creams, such as clotrimazole. This is usually sufficient to alleviate the symptoms and eradicate the infection. Alternatively, terbinafine cream can be used as an alternative treatment option.

Orthostatic hypotension is diagnosed using lying and standing blood pressure measurements. This condition is often seen in older individuals who are taking multiple medications for hypertension and depression. The patient exhibits symptoms such as light-headedness, dizziness, weakness, and tunnel vision when standing up. These symptoms do not occur when lying down and worsen upon standing, but can be relieved by sitting or lying down. They are typically more pronounced in the morning, in hot environments, after meals, after standing still, and after exercise. No other signs suggest an alternative diagnosis.

Further Reading:

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

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

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

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

The intravascular volume of an infant is approximately 80 ml/kg, while in older children it is around 70 ml/kg. Dehydration itself does not lead to death, but shock can occur when there is a loss of 20 ml/kg from the intravascular space. Clinical dehydration becomes evident only after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children: Bodyweight:

– First 10 kg: Daily fluid requirement of 100 ml/kg and hourly fluid requirement of 4 ml/kg.

– Second 10 kg: Daily fluid requirement of 50 ml/kg and hourly fluid requirement of 2 ml/kg.

– Subsequent kg: Daily fluid requirement of 20 ml/kg and hourly fluid requirement of 1 ml/kg.

Based on this information, the hourly maintenance fluid requirements for this child can be calculated as follows:

– First 10 kg: 4 ml/kg = 40 ml

– Second 10 kg: 2 ml/kg = 20 ml

– Subsequent kg: 1 ml/kg = 5 ml

Therefore, the total hourly maintenance fluid requirement for this child is 65 ml.