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

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

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

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

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

Anaphylaxis is a severe allergic reaction that is caused by the immune system overreaction to a specific allergen. This reaction is classified as a Type I hypersensitivity reaction, which means it is mediated by the IgE antibodies.

Further Reading:

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

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

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

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

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

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.
https://www.resus.org.uk/sites/default/files/2021-05/Emergency%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf

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

In cases of acute glandular fever, certain antibiotics like ampicillin and amoxicillin can potentially cause severe rashes that affect the entire body and specifically the extremities. The exact cause of these rashes is still unknown. If there is uncertainty in the diagnosis and the clinician wants to cover the possibility of streptococcal tonsillitis, it is recommended to use phenoxymethylpenicillin (penicillin V) as the preferred treatment.

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.

The majority of dissections happen in individuals between the ages of 40 and 70, with the highest occurrence observed in the age group of 50 to 65.

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.

Bladder cancer is the most likely diagnosis considering the patient’s history of smoking and working in a rubber factory, as these are well-known risk factors for developing this condition. It affects approximately 1 in 5000 people and is more common in men, with a threefold higher incidence compared to women. Transitional cell carcinomas account for 90% of bladder cancer cases.

The risk factors for bladder cancer include smoking, which is responsible for 50% of male and 25% of female cases. Exposure to aromatic amine, such as working in rubber, leather, or textile factories, is also a known risk factor. Other factors include urinary stasis and schistosomiasis.

Bladder cancer can present with either visible or microscopic blood in the urine (haematuria). It may be painless or accompanied by pelvic or loin pain, as well as symptoms of recurrent urinary tract infections. A midstream urine sample (MSU) can be helpful in ruling out a urinary tract infection and detecting microscopic haematuria.

If bladder cancer is suspected, it is important to refer the patient urgently. Diagnosis is typically confirmed through biopsies taken during cystoscopy. At the time of diagnosis, 80% of tumours are confined to the mucosa or submucosa (stage T1). Treatment involves transurethral resection of the tumour (TURBT) with intravesical chemotherapy. The prognosis at this stage is excellent, with most patients dying from other causes.

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

Further Reading:

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

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

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

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

According to the GMC, if a doctor becomes aware that a patient is driving despite being unfit to do so, they should do everything they can to convince the patient to stop driving. If these efforts are unsuccessful and the patient continues to drive, the GMC advises promptly contacting the DVLA or DVA and sharing any pertinent medical information with the medical adviser, ensuring confidentiality.

Further Reading:

Blackouts are a common occurrence in the emergency department and can have serious consequences if they happen while a person is driving. It is crucial for doctors in the ED to be familiar with the guidelines set by the DVLA (Driver and Vehicle Licensing Agency) regarding driving restrictions for patients who have experienced a blackout.

The DVLA has specific rules for different types of conditions that may cause syncope (loss of consciousness). For group 1 license holders (car/motorcycle use), if a person has had a first unprovoked isolated seizure, they must refrain from driving for 6 months or 12 months if there is an underlying causative factor that may increase the risk. They must also notify the DVLA. For group 2 license holders (bus and heavy goods vehicles), the restrictions are more stringent, with a requirement of 12 months off driving for a first unprovoked isolated seizure and 5 years off driving if there is an underlying causative factor.

For epilepsy or multiple seizures, both group 1 and group 2 license holders must remain seizure-free for 12 months before their license can be considered. They must also notify the DVLA. In the case of a stroke or isolated transient ischemic attack (TIA), group 1 license holders need to refrain from driving for 1 month, while group 2 license holders must wait for 12 months before being re-licensed subject to medical evaluation. Multiple TIAs require 3 months off driving for both groups.

Isolated vasovagal syncope requires no driving restriction for group 1 license holders, but group 2 license holders must refrain from driving for 3 months. Both groups must notify the DVLA. If syncope is caused by a reversible and treated condition, group 1 license holders need 4 weeks off driving, while group 2 license holders require 3 months. In the case of an isolated syncopal episode with an unknown cause, group 1 license holders must refrain from driving for 6 months, while group 2 license holders will have their license refused or revoked for 12 months.

For patients who continue to drive against medical advice, the GMC (General Medical Council) has provided guidance on how doctors should manage the situation. Doctors should explain to the patient why they are not allowed to drive and inform them of their legal duty to notify the DVLA or DVA (Driver and Vehicle Agency in Northern Ireland). Doctors should also record the advice given to the patient in their medical record

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.

Rhabdomyolysis leads to an increase in phosphate levels in the blood, which in turn causes a decrease in the levels of ionized calcium. On the other hand, conditions such as Addison’s disease, hyperthyroidism, the use of thiazide diuretics, and lithium can all contribute to an elevation in calcium levels. There are also other factors that can result in low calcium levels, including hypoparathyroidism, a deficiency of vitamin D, sepsis, fluoride poisoning, a lack of magnesium, renal failure, tumor lysis syndrome, pancreatitis, and the administration of EDTA infusions.

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

Further Reading:

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

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

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

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

The current guidelines from NICE recommend that the first-line treatment for confirmed deep-vein thrombosis (DVT) or pulmonary embolus (PE) should be either apixaban or rivaroxaban, which are direct oral anticoagulants.

If neither of these options is suitable, the following alternatives should be considered:

1. LMWH (low molecular weight heparin) should be administered for at least 5 days, followed by dabigatran or edoxaban.

2. LMWH should be combined with a vitamin K antagonist (VKA), such as warfarin, for at least 5 days or until the international normalized ratio (INR) reaches at least 2.0 on 2 consecutive readings. Afterward, the VKA can be continued alone.

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

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

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

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

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

Verapamil is a type of calcium-channel blocker that is commonly used to treat irregular heart rhythms and chest pain. It is important to note that verapamil should not be taken at the same time as beta-blockers like atenolol. This is because when these medications are combined, they can have a negative impact on the heart’s ability to contract and its heart rate. This can lead to low blood pressure, slow heart rate, problems with the electrical signals in the heart, heart failure, and even a pause in the heart’s normal rhythm. However, the other medications mentioned in this question can be safely used together with beta-blockers.

Oral bisphosphonates are the primary choice for treating osteoporotic fragility fractures in individuals who have already experienced such fractures. After a fragility fracture, it is advised to start taking a bisphosphonate, typically alendronic acid, and consider supplementing with calcium and vitamin D.

There are other treatment options available for preventing fragility fractures after an initial occurrence. These include raloxifene, teriparatide, and denosumab.

The primary treatment for paracetamol overdose is acetylcysteine. Acetylcysteine is an extremely effective antidote, but its effectiveness decreases quickly if administered more than a few hours after a significant ingestion. Ingestions that exceed 75 mg/kg are considered to be significant.

For patients who decline treatment, methionine is a helpful alternative. It is taken orally in a dosage of 2.5 g every 4 hours, with a total dose of 10 g.

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

The rash in measles typically begins as a maculopapular rash on the face and behind the ears. Within 24-36 hours, it spreads to the trunk and limbs. The rash may merge together, especially on the face, creating a confluent appearance. Usually, the rash appears along with a high fever. Before the rash appears, there are usually symptoms of a cold for 2-3 days. Koplik spots, which are blue-white spots on the inside of the cheeks (usually seen opposite the molars), can be observed 1-2 days before the rash appears and can be detected during a mouth examination.

It is important to note that the rash in rubella infection is similar to that of measles. However, there are two key differences: the presence of Koplik spots and a high fever (>38.3ºC) are characteristic of measles. Erythema infectiosum, on the other hand, causes a rash that resembles a slapped cheek.

Further Reading:

Measles is a highly contagious viral infection caused by an RNA paramyxovirus. It is primarily spread through aerosol transmission, specifically through droplets in the air. The incubation period for measles is typically 10-14 days, during which patients are infectious from 4 days before the appearance of the rash to 4 days after.

Common complications of measles include pneumonia, otitis media (middle ear infection), and encephalopathy (brain inflammation). However, a rare but fatal complication called subacute sclerosing panencephalitis (SSPE) can also occur, typically presenting 5-10 years after the initial illness.

The onset of measles is characterized by a prodrome, which includes symptoms such as irritability, malaise, conjunctivitis, and fever. Before the appearance of the rash, white spots known as Koplik spots can be seen on the buccal mucosa. The rash itself starts behind the ears and then spreads to the entire body, presenting as a discrete maculopapular rash that becomes blotchy and confluent.

In terms of complications, encephalitis typically occurs 1-2 weeks after the onset of the illness. Febrile convulsions, giant cell pneumonia, keratoconjunctivitis, corneal ulceration, diarrhea, increased incidence of appendicitis, and myocarditis are also possible complications of measles.

When managing contacts of individuals with measles, it is important to offer the MMR vaccine to children who have not been immunized against measles. The vaccine-induced measles antibody develops more rapidly than that following natural infection, so it should be administered within 72 hours of contact.

The Lake Louise score is widely accepted as the standard method for evaluating the seriousness of Acute Mountain Sickness (AMS). The scoring system, outlined below, is used to determine the severity of AMS. A score of 3 or higher is indicative of AMS.

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.

Brugada syndrome is a genetic disorder that is passed down from one generation to another in an autosomal dominant manner. It is characterized by abnormal findings on an electrocardiogram (ECG) and can lead to sudden cardiac death. The cause of death in individuals with Brugada syndrome is typically ventricular fibrillation, which occurs as a result of specific defects in ion channels that are determined by our genes. Interestingly, this syndrome is more commonly observed in South East Asia and is actually the leading cause of sudden unexplained cardiac death in Thailand.

One of the key features seen on an ECG that is consistent with Type 1 Brugada syndrome is a pattern known as right bundle branch block. Additionally, there is a distinct downward sloping coved ST elevation observed in leads V1-V3. These specific ECG findings help to identify individuals who may be at risk for developing Brugada syndrome and experiencing its potentially fatal consequences.