Heat stroke is a condition characterized by a systemic inflammatory response, where the core body temperature exceeds 40.6°C. It is accompanied by changes in mental state and varying levels of organ dysfunction. Heat stroke occurs when the body’s ability to regulate temperature is overwhelmed by a combination of excessive environmental heat, excessive heat production from metabolic processes (usually due to exertion), and inadequate heat loss.

It is important to consider other clinical conditions that can cause an increased core temperature. Sepsis can present similarly and should be ruled out. Neuroleptic malignant syndrome should be excluded in patients taking phenothiazines or other antipsychotics. Serotonin syndrome should be considered and excluded in patients taking serotonergic medications such as SSRIs. Malignant hyperthermia should be considered in patients with a recent history of general anesthesia. Screening for recreational drug use, particularly cocaine, amphetamines, and ecstasy, is also recommended.

Antipyretics, such as paracetamol, aspirin, and NSAIDs, do not have a role in the treatment of heat stroke. They work by interrupting the change in the hypothalamic set point caused by pyrogens, which is not the case in heat stroke where the hypothalamus is overwhelmed but functioning properly. In fact, antipyretics may be harmful in patients who develop complications in the liver, blood, and kidneys, as they can worsen bleeding tendencies.

Benzodiazepines, like diazepam, can be beneficial in patients experiencing agitation and/or shivering. They help reduce excessive heat production and agitation. In severe cases of agitation, paralysis may be necessary.

There are various cooling techniques recommended for the treatment of heat stroke, but currently, there is limited conclusive evidence on the most effective approach. Some possible methods include simple measures like consuming cold drinks, using fans, applying ice water packs, and spraying tepid water. Cold water immersion therapy can be helpful, but it requires the patient to be stable and cooperative, making it impractical for very sick patients. Advanced cooling techniques, such as cold IV fluids, surface cooling devices (SCD), intravascular cooling devices (ICD), and extracorporeal circuits, may be used for sicker patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Classical symptoms of a urinary tract infection (UTI) typically include dysuria, suprapubic tenderness, urgency, haematuria, increased frequency of micturition, and polyuria. To effectively manage UTIs, SIGN has developed excellent guidelines. According to these guidelines, if a patient presents with mild symptoms of a UTI (experiencing two or fewer classical symptoms), it is recommended to use a dipstick test to aid in the diagnosis and treatment process.

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

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

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

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

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

Damage to the ulnar nerve at either the elbow or wrist leads to a characteristic claw hand appearance, characterized by hyperextension of the metacarpophalangeal joints and flexion of the distal and proximal interphalangeal joint of the little and ring fingers.

Heat stroke is a condition characterized by a core temperature higher than 40.6°C, accompanied by changes in mental state and varying levels of organ dysfunction. There are two forms of heat stroke: classic non-exertional heat stroke, which occurs during high environmental temperatures and typically affects elderly patients during heat waves, and exertional heat stroke, which occurs during strenuous physical exercise in hot conditions, such as endurance athletes competing in hot weather.

The main treatment for heat stroke involves supportive measures. It is important to rapidly reduce the core temperature to around 39.0°C. Patients with severe heat stroke should be managed in a critical care setting. The ABCDE approach should be followed, with a focus on cooling the patient. This includes obtaining a definitive airway if the patient is unresponsive, providing ventilation if necessary, using haemodynamic monitoring to guide fluid therapy, correcting electrolyte imbalances, managing blood glucose levels, removing clothes, eliminating the cause of hyperthermia, and monitoring core and skin temperatures.

There are various cooling techniques that can be used, although there is limited evidence on which approach is the most effective. Some possible methods include simple measures like cold drinks, fanning, ice water packs, and spraying tepid water. Cold water immersion therapy can be beneficial, but it requires the patient to be stable and cooperative, making it impractical for very sick patients. Advanced cooling techniques, such as cold IV fluids, surface cooling devices, intravascular cooling devices, and extracorporeal circuits, may be used for sicker patients.

Benzodiazepines, like diazepam, can be helpful in managing agitation and shivering in heat stroke patients. They not only reduce excessive heat production but also help to calm the patient. In severe cases of agitation, paralysis may be necessary. Dantrolene is commonly used, although there is currently limited high-level evidence to support its use. Neuroleptics, such as chlorpromazine, which were once commonly used, should be avoided due to their potential adverse effects, including lowering the seizure threshold, interfering with thermoregulation, causing anticholinergic side effects, hypotension, and hepatotoxicity.

The British Society of Gastroenterology (BSG) has developed guidelines for evaluating cases of acute lower intestinal bleeding in a hospital setting. These guidelines are useful in determining which patients should be referred for further assessment.

When patients present with lower gastrointestinal bleeding (LGIB), they should be categorized as either unstable or stable. Unstable is defined as having a shock index greater than 1, which is calculated by dividing the heart rate by the systolic blood pressure (HR/SBP). For example, if the heart rate is 80 and the systolic blood pressure is 120, the shock index would be 0.66.

For patients with stable bleeds, they should be further classified as either major (requiring hospitalization) or minor (suitable for outpatient management) based on a risk assessment tool. The BSG recommends using the Oakland risk score, which takes into account factors such as age, hemoglobin level, and findings from a digital rectal examination.

Patients with a minor self-terminating bleed (e.g., an Oakland score of less than 8 points) and no other indications for hospital admission can be discharged with urgent follow-up for outpatient investigation.

Patients with a major bleed should be admitted to the hospital for a colonoscopy, which will be scheduled based on availability.

If a patient is hemodynamically unstable or has a shock index greater than 1 after initial resuscitation, and/or active bleeding is suspected, CT angiography (CTA) should be considered, followed by endoscopic or radiological therapy.

If no bleeding source is identified by initial CTA and the patient is stable, an upper endoscopy should be performed immediately, as LGIB associated with hemodynamic instability may indicate an upper gastrointestinal bleeding source. Gastroscopy may be the first investigation if the patient stabilizes after initial resuscitation.

If indicated, catheter angiography with the possibility of embolization should be performed as soon as possible after a positive CTA to increase the chances of success. In centers with a 24/7 interventional radiology service, this procedure should be available within 60 minutes for hemodynamically unstable patients.

Emergency laparotomy should only be considered if all efforts to locate the bleeding source using radiological and/or endoscopic methods have been exhausted, except in exceptional circumstances.

Red blood cell transfusion may be necessary. It is recommended to use restrictive blood transfusion thresholds, such as a hemoglobin trigger of 7 g/d

Thiamine deficiency is frequently seen in individuals who are dependent on alcohol. This is primarily due to their inadequate diet, the presence of gastritis which affects thiamine absorption, and the fact that thiamine is involved in alcohol metabolism as a coenzyme. If left untreated, thiamine deficiency can lead to Wernicke’s encephalopathy, which can further progress to Korsakoff’s syndrome.

It is important to note that administering glucose-containing intravenous fluids without thiamine to a patient with chronic thiamine deficiency can trigger Wernicke’s encephalopathy. Therefore, individuals undergoing detoxification should receive parenteral high-potency B complex vitamins (Pabrinex) as a preventive treatment. However, it is crucial to have resuscitation facilities available during administration due to the risk of anaphylaxis. The risk of anaphylaxis is lower when the drug is given intramuscularly (IM). A daily dose of one pair of ampoules of Pabrinex, containing 250 mg of thiamine, should be administered IM or intravenously (IV) for a period of three to five days.

Once the 3-5 day course of Pabrinex is completed, the patient should transition to oral vitamin B Compound-strong and oral thiamine tablets for continued treatment.

For more information, please refer to the NICE pathway for acute alcohol withdrawal.

The connection between latex sensitivity and food allergy is commonly known as the latex-fruit syndrome. Foods that have been found to be allergenic in relation to latex are categorized into high, moderate, or low risk groups.

High risk foods include banana, avocado, chestnut, and kiwi fruit.

Moderate risk foods include apple, carrot, celery, melon, papaya, potato, and tomato.

Citrus fruits and pears are considered to have a low risk of causing allergic reactions in individuals with latex sensitivity.

Enzyme-inducing anticonvulsants have been found to enhance the metabolism of ethinyl estradiol and progestogens. This increased breakdown diminishes the effectiveness of the oral contraceptive pill (OCP) in preventing pregnancy. Some examples of enzyme-inducing anticonvulsants include carbamazepine, phenytoin, phenobarbitol, and topiramate.

On the other hand, non-enzyme-inducing anticonvulsants are unlikely to have an impact on contraception. Some examples of these anticonvulsants are sodium valproate, clonazepam, gabapentin, levetiracetam, and piracetam.

It is important to note that lamotrigine, although classified as a non-enzyme-inducing anticonvulsant, requires special consideration. While there is no evidence suggesting that the OCP directly affects epilepsy, there is evidence indicating that it reduces the levels of lamotrigine in the bloodstream. This reduction in lamotrigine levels could potentially compromise seizure control and increase the likelihood of experiencing seizures.

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.

Section 136 of the Mental Health Act (MHA) grants authority to a police officer to relocate an individual who seems to be experiencing a mental health disorder to a secure location. This provision permits detention for a period of 72 hours, during which time the patient can undergo evaluation by a medical professional.

Heat stroke is a condition characterized by a core temperature higher than 40.6°C, accompanied by changes in mental state and varying levels of organ dysfunction. There are two forms of heat stroke: classic non-exertional heat stroke, which occurs during high environmental temperatures and typically affects elderly patients during heat waves, and exertional heat stroke, which occurs during strenuous physical exercise in hot conditions, such as endurance athletes competing in hot weather.

The typical clinical features of heat stroke include a core temperature greater than 40.6°C, extreme fatigue, headache, syncope, facial flushing, vomiting, and diarrhea. The skin is usually hot and dry, although sweating can occur in around 50% of cases of exertional heat stroke. The loss of the ability to sweat is a late and concerning sign. Hyperventilation is almost always present. Cardiovascular dysfunction, including arrhythmias, hypotension, and shock, as well as respiratory dysfunction, including acute respiratory distress syndrome (ARDS), can occur. Central nervous system dysfunction, such as seizures and coma, may also be observed. If the temperature rises above 41.5°C, multi-organ failure, coagulopathy, and rhabdomyolysis can occur.

In the management of heat stroke, benzodiazepines like diazepam can be helpful in patients with agitation and/or shivering. They help reduce excessive heat production and agitation. In severe cases, patients may require paralysis. Antipyretics like paracetamol, aspirin, and NSAIDs have no role in the treatment of heat stroke. They do not work because the hypothalamus, which regulates body temperature, is healthy but overloaded in heat stroke. Moreover, antipyretics may actually be harmful in patients who develop complications like liver, blood, and kidney problems as they can worsen bleeding tendencies.

Dantrolene is commonly used in the treatment of heat stroke, although there is currently no high-level evidence to support its use. Neuroleptics, such as chlorpromazine, which were once commonly used, should be avoided due to their potential adverse effects, including lowering the seizure threshold, interfering with thermoregulation, causing anticholinergic side effects, hypotension, and hepatotoxicity.

Public Health England (PHE) has a primary goal of promptly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is important, it is not the main focus. Since 1968, clinical suspicion of a notifiable infection has been sufficient for reporting.
Registered medical practitioners (RMPs) are legally obligated to notify the designated proper officer at their local council or local health protection team (HPT) if they suspect cases of certain infectious diseases.
The Health Protection (Notification) Regulations 2010 specify the diseases that RMPs must report to the proper officers at local authorities. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever. However, as of April 2010, ophthalmia neonatorum is no longer considered a notifiable disease in the UK.

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

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

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

Bier’s block is a regional intravenous anesthesia technique commonly used for minor surgical procedures of the forearm or for reducing distal radius fractures in the emergency department (ED). It is recommended by NICE as the preferred anesthesia block for adults requiring manipulation of distal forearm fractures in the ED.

Before performing the procedure, a pre-procedure checklist should be completed, including obtaining consent, recording the patient’s weight, ensuring the resuscitative equipment is available, and monitoring the patient’s vital signs throughout the procedure. The air cylinder should be checked if not using an electronic machine, and the cuff should be checked for leaks.

During the procedure, a double cuff tourniquet is placed on the upper arm, and the arm is elevated to exsanguinate the limb. The proximal cuff is inflated to a pressure 100 mmHg above the systolic blood pressure, up to a maximum of 300 mmHg. The time of inflation and pressure should be recorded, and the absence of the radial pulse should be confirmed. 0.5% plain prilocaine is then injected slowly, and the time of injection is recorded. The patient should be warned about the potential cold/hot sensation and mottled appearance of the arm. After injection, the cannula is removed and pressure is applied to the venipuncture site to prevent bleeding. After approximately 10 minutes, the patient should have anesthesia and should not feel pain during manipulation. If anesthesia is successful, the manipulation can be performed, and a plaster can be applied by a second staff member. A check x-ray should be obtained with the arm lowered onto a pillow. The tourniquet should be monitored at all times, and the cuff should be inflated for a minimum of 20 minutes and a maximum of 45 minutes. If rotation of the cuff is required, it should be done after the manipulation and plaster application. After the post-reduction x-ray is satisfactory, the cuff can be deflated while observing the patient and monitors. Limb circulation should be checked prior to discharge, and appropriate follow-up and analgesia should be arranged.

There are several contraindications to performing Bier’s block, including allergy to local anesthetic, hypertension over 200 mm Hg, infection in the limb, lymphedema, methemoglobinemia, morbid obesity, peripheral vascular disease, procedures needed in both arms, Raynaud’s phenomenon, scleroderma, severe hypertension and sickle cell disease.

Emotional incongruity, although not a primary symptom, is one of the negative symptoms that define chronic schizophrenia. These symptoms, as described by Kurt Schneider, are known as first-rank symptoms. They include auditory hallucinations such as hearing third-person voices discussing the patient, thought echo, and commentary on actions. Passivity phenomena, such as thought insertion, thought withdrawal, thought broadcast, and feelings of thoughts and actions being under external control, are also considered first-rank symptoms. Delusions, which can be primary or secondary, are another characteristic of schizophrenia.

Chronic schizophrenia is primarily characterized by negative symptoms. These symptoms include poor motivation and self-care, social withdrawal, depression, flat and blunted affect, emotional incongruity, decreased activity, poverty of thought and speech. On the other hand, symptoms like loss of inhibitions, pressure of speech, and grandiose delusions are more indicative of mania. Increased anxiety in social circumstances is often associated with social anxiety disorder.

In summary, emotional incongruity is a negative symptom of chronic schizophrenia, while the first-rank symptoms described by Kurt Schneider encompass auditory hallucinations, passivity phenomena, and delusions. It is important to differentiate these symptoms from those associated with mania or social anxiety disorder.

The Arthus reaction is a response that occurs when antigen/antibody complexes are formed in the skin after an antigen is injected. Although rare, these reactions can happen after receiving vaccines that contain tetanus toxoid or diphtheria toxoid. They are classified as a type III hypersensitivity reaction.

Arthus reactions are characterized by pain, swelling, induration, hemorrhage, and sometimes necrosis. Typically, these symptoms appear 4-12 hours after vaccination.

Type III hypersensitivity reactions occur when insoluble antigen-antibody complexes accumulate in different tissues and are not effectively cleared by the body’s innate immune cells. This leads to an inflammatory response in the affected tissues.

Some other examples of type III hypersensitivity reactions include immune complex glomerulonephritis, rheumatoid arthritis, systemic lupus erythematosus, serum sickness, and extrinsic allergic alveolitis.

In cases of myocarditis, levels of cardiac muscle enzymes (CK-MB, Troponin I, and Troponin T) and B-type natriuretic peptide (BNP) are usually elevated. It is important to note that CK-MB is a subtype of CK, so an increase in CK-MB will also result in an increase in total CK levels. This poses a challenge in differentiating myocarditis from coronary artery disease in the emergency department. Typically, a definitive diagnosis is not made until the patient undergoes additional tests such as angiography and possibly endomyocardial biopsy (EMB).

Further Reading:

Myocarditis is inflammation of the myocardium, the middle layer of the heart wall, that is not caused by a blockage in the coronary arteries. It can be caused by various factors, including infections (such as viruses, bacteria, parasites, and fungi), immune reactions, toxins, physical injury, and certain medications or vaccines. Coxsackie virus is the most common cause of myocarditis in Europe and the USA, while globally, Trypanosoma cruzi, which causes Chagas disease, is the most common cause.

The symptoms of myocarditis can vary widely and often resemble those of heart failure or coronary heart disease. Common symptoms include chest pain, palpitations, breathlessness, fatigue, and swelling. The clinical presentation can also be influenced by the underlying cause of the inflammation. Diagnosis of myocarditis is challenging as there is no specific clinical presentation, and the gold standard test, endomyocardial biopsy, is not readily available in emergency departments.

Various tests can be performed to aid in the diagnosis of myocarditis, including electrocardiogram (ECG), chest X-ray, cardiac enzymes (such as troponin or CK-MB), brain natriuretic peptide (BNP) levels, and echocardiogram. These tests may show non-specific abnormalities, such as ST-segment and T-wave abnormalities on ECG, bilateral pulmonary infiltrates on chest X-ray, elevated cardiac enzymes and BNP levels, and left ventricular motion abnormalities on echocardiogram.

Management of myocarditis is primarily supportive, focusing on treating cardiac failure and addressing the underlying cause. Supportive care and conventional heart failure therapy, such as ACE inhibitors or angiotensin II receptor blockers, vasodilators, beta-blockers, and diuretics, may be used to improve cardiac function and reduce symptoms. Treatment of the underlying cause, such as antiparasitic agents for Chagas disease or antibiotics for bacterial infections, may also be necessary. In severe cases leading to cardiogenic shock, more aggressive treatment with invasive monitoring, inotropes, vasopressors, and potentially heart transplantation may be required.

In summary, myocarditis is inflammation of the myocardium that can be caused by various factors. It presents with a wide range of symptoms and can be challenging to diagnose. Management involves supportive care, treatment of cardiac failure, and addressing the underlying cause. Severe cases may require more aggressive treatment and potentially heart transplantation.

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.

Thyroid storm is a rare condition that affects only 1-2% of patients with hyperthyroidism. However, it is crucial to diagnose it promptly because it has a high mortality rate of approximately 10%. Thyroid storm is often triggered by a physiological stressor, such as stopping antithyroid therapy prematurely, recent surgery or radio-iodine treatment, infections (especially chest infections), trauma, diabetic ketoacidosis or hyperosmolar diabetic crisis, thyroid hormone overdose, pre-eclampsia. It typically occurs in patients with Graves’ disease or toxic multinodular goitre and presents with sudden and severe hyperthyroidism. Symptoms include high fever (over 41°C), dehydration, rapid heart rate (greater than 140 beats per minute) with or without irregular heart rhythms, low blood pressure, congestive heart failure, nausea, jaundice, vomiting, diarrhea, abdominal pain, confusion, agitation, delirium, psychosis, seizures, or coma.

To diagnose thyroid storm, various blood tests should be conducted, including a full blood count, urea and electrolytes, blood glucose, coagulation screen, CRP, and thyroid profile (T4/T3 and TSH). A bone profile/calcium test should also be done as 10% of patients develop hypocalcemia. Blood cultures should be taken as well. Other important investigations include a urine dipstick/MC&S, chest X-ray, and ECG.

The management of thyroid storm involves several steps. Intravenous fluids, such as 1-2 liters of 0.9% saline, should be administered. Airway support and management should be provided as necessary. A nasogastric tube should be inserted if the patient is vomiting. Urgent referral for inpatient management is essential. Paracetamol (1 g PO/IV) can be given to reduce fever. Benzodiazepines, such as diazepam (5-20 mg PO/IV), can be used for sedation. Steroids, like hydrocortisone (100 mg IV), may be necessary if there is co-existing adrenal suppression. Antibiotics should be prescribed if there is an intercurrent infection. Beta-blockers, such as propranolol (80 mg PO), can help control heart rate. High-dose carbimazole (45-60 mg/day) is recommended.