Shingles is caused by the varicella-zoster virus (VZV), which primarily infects individuals during childhood as chickenpox. However, the initial infection can also be subclinical. After the primary infection, the virus remains dormant in the sensory nervous system, specifically in the geniculate, trigeminal, or dorsal root ganglia.

During the dormant phase, the virus is kept under control by the immune system for many years. However, it can later become active and cause a flare-up in a specific dermatomal segment. This reactivation occurs when the virus travels down the affected nerve over a period of 3 to 5 days, leading to inflammation within and around the nerve. The decline in cell-mediated immunity is believed to trigger the virus’s reactivation.

Several factors can trigger the reactivation of the varicella-zoster virus, including advancing age (with most patients being older than 50), immunosuppressive illnesses, physical trauma, and psychological stress. In immunocompetent patients, the most common site of reactivation is the thoracic nerves, followed by the ophthalmic division of the trigeminal nerve.

Diagnosing shingles can usually be done based on the patient’s history and clinical examination alone, as it has a distinct history and appearance. While various techniques can be used to detect the virus or antibodies, they are often unnecessary. Microscopy and culture tests using scrapings and smears typically yield negative results.

Peripheral and central vertigo can be differentiated based on certain characteristics. Peripheral vertigo typically has a sudden onset and is associated with more severe symptoms of vertigo. The vertigo symptoms may come and go intermittently. Individuals with peripheral vertigo often experience severe nausea and vomiting. Their vertigo is also affected by head movement, particularly in certain positions. Peripheral vertigo is usually not accompanied by any focal neurology. Nystagmus, which is an involuntary eye movement, tends to occur away from the side of the lesion. In some cases, hearing may also be impaired, as seen in conditions like Meniere’s disease and labyrinthitis.

On the other hand, central vertigo tends to have a gradual onset and milder symptoms of vertigo. The vertigo symptoms are constant and do not fluctuate. Nausea and vomiting may be present but are usually less severe compared to peripheral vertigo. Unlike peripheral vertigo, central vertigo is not influenced by head movement and is considered fixed. Individuals with central vertigo may experience new-onset headaches. Additionally, central vertigo is often accompanied by focal neurology, indicating involvement of specific areas of the brain. Nystagmus in central vertigo occurs towards the side of the lesion. Unlike peripheral vertigo, hearing is typically unaffected in central vertigo cases.

Auer rods are small, needle-shaped structures that can be found within the cytoplasm of blast cells. These structures have a distinct eosinophilic appearance. While they are most frequently observed in cases of acute myeloid leukemia, they can also be present in high-grade myelodysplastic syndromes and myeloproliferative disorders.

To remove contaminated material, it is recommended to remove and dispose of clothing. It is important to seal the clothing and treat it as hazardous waste. If wet decontamination is being utilized, patients should shower using warm water and detergent.

Further Reading:

Chemical incidents can occur as a result of leaks, spills, explosions, fires, terrorism, or the use of chemicals during wars. Industrial sites that use chemicals are required to conduct risk assessments and have accident plans in place for such incidents. Health services are responsible for decontamination, unless mass casualties are involved, and all acute health trusts must have major incident plans in place.

When responding to a chemical incident, hospitals prioritize containment of the incident and prevention of secondary contamination, triage with basic first aid, decontamination if not done at the scene, recognition and management of toxidromes (symptoms caused by exposure to specific toxins), appropriate supportive or antidotal treatment, transfer to definitive treatment, a safe end to the hospital response, and continuation of business after the event.

To obtain advice when dealing with chemical incidents, the two main bodies are Toxbase and the National Poisons Information Service. Signage on containers carrying chemicals and material safety data sheets (MSDS) accompanying chemicals also provide information on the chemical contents and their hazards.

Contamination in chemical incidents can occur in three phases: primary contamination from the initial incident, secondary contamination spread via contaminated people leaving the initial scene, and tertiary contamination spread to the environment, including becoming airborne and waterborne. The ideal personal protective equipment (PPE) for chemical incidents is an all-in-one chemical-resistant overall with integral head/visor and hands/feet worn with a mask, gloves, and boots.

Decontamination of contaminated individuals involves the removal and disposal of contaminated clothing, followed by either dry or wet decontamination. Dry decontamination is suitable for patients contaminated with non-caustic chemicals and involves blotting and rubbing exposed skin gently with dry absorbent material. Wet decontamination is suitable for patients contaminated with caustic chemicals and involves a warm water shower while cleaning the body with simple detergent.

After decontamination, the focus shifts to assessing the extent of any possible poisoning and managing it. The patient’s history should establish the chemical the patient was exposed to, the volume and concentration of the chemical, the route of exposure, any protective measures in place, and any treatment given. Most chemical poisonings require supportive care using standard resuscitation principles, while some chemicals have specific antidotes. Identifying toxidromes can be useful in guiding treatment, and specific antidotes may be administered accordingly.

There are two scoring systems that NICE recommends for assessing sore throat: the Centor Clinical Prediction Score and the FeverPAIN Score.

The Centor Clinical Prediction Score was initially developed as a tool to determine the likelihood of a group A beta-haemolytic Streptococcus (GABHS) infection in adults with a sore throat. It was created and tested in US Emergency Departments, specifically for adults.

The Centor score evaluates patients based on several criteria, with one point given for each positive criterion. These criteria include a history of fever (temperature above 38°C), the presence of exudate or swelling on the tonsils, tender or swollen anterior cervical lymph nodes, and the absence of cough.

According to the current NICE guidance, the Centor score can be used to guide management in the following way:
– A score of 0 to 2 indicates a 3-17% likelihood of streptococcus isolation, and antibiotics are not recommended.
– A score of 3 to 4 suggests a 32-56% likelihood of streptococcus isolation, and immediate treatment with empirical antibiotics or a ‘backup prescription’ should be considered.

Chronic lymphocytic leukaemia (CLL) is the most common type of leukaemia in adults. It occurs when mature lymphocytes multiply uncontrollably. About 95% of cases are of B-cell lineage.

CLL is typically a slow-growing form of leukaemia and is often discovered incidentally during routine blood tests. As the disease progresses, patients may experience swollen lymph nodes, enlarged liver and spleen, anemia, and increased susceptibility to infections.

This condition primarily affects adult men, with over 75% of CLL patients being men over the age of 50.

A blood test for CLL usually reveals an increased number of lymphocytes (typically more than 5 x 109/l, but it can be higher). Advanced stages of the disease may also show normochromic, normocytic anemia. A peripheral blood smear can confirm the presence of lymphocytosis, and smudge cells are often observed.

The Binet system is used to stage CLL, categorizing it as follows:
– Stage A: Hemoglobin (Hb) levels above 10 g/dl, platelet count above 100 x 109/l, involvement of fewer than 3 lymph node areas.
– Stage B: Hb levels above 10 g/dl, platelet count above 100 x 109/l, involvement of more than 3 lymph node areas.
– Stage C: Hb levels below 10 g/dl, platelet count below 100 x 109/l, or both.

Early stages of CLL (Binet stage A and B without active disease) do not require immediate treatment and can be monitored through regular follow-up and blood tests. Patients with more advanced disease have various treatment options available, including monoclonal antibodies (such as rituximab), purine analogues (like fludarabine), and alkylating agents (such as chlorambucil).

Spondyloarthritis is a term that encompasses various inflammatory conditions affecting both the joints and the sites where ligaments and tendons attach to the bones, known as entheses. The primary cause of spondyloarthritis is ankylosing spondylitis, but it can also be caused by reactive arthritis, psoriatic arthritis, and enteropathic arthropathies.

If individuals under the age of 45 exhibit four or more of the following symptoms, they should be referred for a potential diagnosis of spondyloarthritis:
– Presence of low back pain and being younger than 35 years old
– Waking up in the second half of the night due to pain
– Experiencing buttock pain
– Pain that improves with movement or within 48 hours of using nonsteroidal anti-inflammatory drugs (NSAIDs)
– Having a first-degree relative with spondyloarthritis
– History of current or past arthritis, psoriasis, or enthesitis

It is important to note that a progressive neurological deficit would be an atypical presentation for spondyloarthritis and may instead indicate cauda equina syndrome (CES).

Vomiting after a head injury should raise concerns about increased intracranial pressure (ICP). Signs of elevated ICP include vomiting, changes in pupil size or shape in one eye, decreased cognitive function or consciousness, abnormal findings during fundoscopy (such as blurry optic discs or bleeding in the retina), cranial nerve dysfunction (most commonly affecting CN III and VI), weakness on one side of the body (a late sign), bradycardia (slow heart rate), high blood pressure, and a wide pulse pressure. Irregular breathing that may progress to respiratory distress, focal neurological deficits, and seizures can also be indicative of elevated 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.

Whispering pectoriloquy is a phenomenon that occurs when there is lung consolidation. It is characterized by an amplified and clearer sound of whispering that can be heard when using a stethoscope to listen to the affected areas of the lungs. To conduct the test, patients are usually instructed to whisper the phrase ninety-nine.

Paracetamol overdose is the most common overdose in the U.K. and is also the leading cause of acute liver failure. The liver damage occurs due to a metabolite of paracetamol called N-acetyl-p-benzoquinoneimine (NAPQI), which depletes the liver’s glutathione stores and directly harms liver cells. Severe liver damage and even death can result from an overdose of more than 12 g or > 150 mg/kg body weight.

The clinical manifestations of paracetamol overdose can be divided into four stages:

Stage 1 (0-24 hours): Patients may not show any symptoms, but common signs include nausea, vomiting, and abdominal discomfort.

Stage 2 (24-48 hours): Right upper quadrant pain and tenderness develop, along with the possibility of hypoglycemia and reduced consciousness.

Stage 3 (48-96 hours): Hepatic failure begins, characterized by jaundice, coagulopathy, and encephalopathy. Loin pain, haematuria, and proteinuria may indicate early renal failure.

Stage 4 (> 96 hours): Hepatic failure worsens progressively, leading to cerebral edema, disseminated intravascular coagulation (DIC), and ultimately death.

The earliest and most sensitive indicator of liver damage is a prolonged INR, which starts to rise approximately 24 hours after the overdose. Liver function tests (LFTs) typically remain normal until 18 hours after the overdose. However, AST and ALT levels then sharply increase and can exceed 10,000 units/L by 72-96 hours. Bilirubin levels rise more slowly and peak around 5 days.

The primary treatment for paracetamol overdose is acetylcysteine. Acetylcysteine is a highly effective antidote, but its efficacy diminishes rapidly if administered more than 8 hours after a significant ingestion. Ingestions exceeding 75 mg/kg are considered significant.

Acetylcysteine should be given based on a 4-hour level or administered empirically if the presentation occurs more than 8 hours after a significant overdose. If the overdose is staggered or the timing is uncertain, empirical treatment is also recommended. The treatment regimen is as follows:

– First dose: 150 mg/kg in 200 mL 5% glucose over 1 hour
– Second dose 50 mg/kg in 500 mL 5% glucose over 4 hours
– Third dose 100 mg/kg in 1000 mL 5% glucose over 16 hours

According to NICE guidelines, it is recommended that adults and young people aged 16 years or older who receive emergency treatment for suspected anaphylaxis should be observed for a minimum of 6-12 hours from the time symptoms first appear. There are certain situations where a longer observation period of 12 hours is advised. These include cases where the allergen is still being absorbed slowly, the patient required more than 2 doses of adrenaline, there is severe asthma or respiratory compromise, or if the presentation occurs at night or there is difficulty in accessing emergency care.

Further Reading:

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

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

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

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

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

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

The Health Protection (Notification) Regulations currently require the reporting of certain diseases. 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, SARS, scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

Hepatitis B surface antigen (HBsAg) is a protein found on the surface of the hepatitis B virus. It can be detected in high levels in the blood during both acute and chronic hepatitis B virus infections. The presence of HBsAg indicates that the person is capable of spreading the infection to others. Normally, the body produces antibodies to HBsAg as part of the immune response to the infection. HBsAg is also used to create the hepatitis B vaccine.

Hepatitis B surface antibody (anti-HBs) indicates that a person has recovered from the hepatitis B virus infection and is now immune to it. This antibody can also develop in individuals who have been successfully vaccinated against hepatitis B.

Total hepatitis B core antibody (anti-HBc) appears when symptoms of acute hepatitis B begin and remains present for life. The presence of anti-HBc indicates that a person has either had a previous or ongoing infection with the hepatitis B virus, although the exact time frame cannot be determined. This antibody is not present in individuals who have received the hepatitis B vaccine.

IgM antibody to hepatitis B core antigen (IgM anti-HBc) indicates a recent infection or acute hepatitis B. If this antibody is present, it suggests that the infection occurred within the past six months.

A normal venous lactate level is less than 2.5 mmol/l and arterial lactate less than 2.0 mmol/l. However, it is important to mention that sepsis guides consider a lactate level above 2 mmol/L to be abnormal.

Further Reading:

Arterial blood gases (ABG) are an important diagnostic tool used to assess a patient’s acid-base status and respiratory function. When obtaining an ABG sample, it is crucial to prioritize safety measures to minimize the risk of infection and harm to the patient. This includes performing hand hygiene before and after the procedure, wearing gloves and protective equipment, disinfecting the puncture site with alcohol, using safety needles when available, and properly disposing of equipment in sharps bins and contaminated waste bins.

To reduce the risk of harm to the patient, it is important to test for collateral circulation using the modified Allen test for radial artery puncture. Additionally, it is essential to inquire about any occlusive vascular conditions or anticoagulation therapy that may affect the procedure. The puncture site should be checked for signs of infection, injury, or previous surgery. After the test, pressure should be applied to the puncture site or the patient should be advised to apply pressure for at least 5 minutes to prevent bleeding.

Interpreting ABG results requires a systematic approach. The core set of results obtained from a blood gas analyser includes the partial pressures of oxygen and carbon dioxide, pH, bicarbonate concentration, and base excess. These values are used to assess the patient’s acid-base status.

The pH value indicates whether the patient is in acidosis, alkalosis, or within the normal range. A pH less than 7.35 indicates acidosis, while a pH greater than 7.45 indicates alkalosis.

The respiratory system is assessed by looking at the partial pressure of carbon dioxide (pCO2). An elevated pCO2 contributes to acidosis, while a low pCO2 contributes to alkalosis.

The metabolic aspect is assessed by looking at the bicarbonate (HCO3-) level and the base excess. A high bicarbonate concentration and base excess indicate alkalosis, while a low bicarbonate concentration and base excess indicate acidosis.

Analyzing the pCO2 and base excess values can help determine the primary disturbance and whether compensation is occurring. For example, a respiratory acidosis (elevated pCO2) may be accompanied by metabolic alkalosis (elevated base excess) as a compensatory response.

The anion gap is another important parameter that can help determine the cause of acidosis. It is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium.

This particular patient has a high risk of experiencing an acute coronary syndrome. Therefore, it is recommended to administer aspirin at a dosage of 300 mg and clopidogrel at a dosage ranging from 300-600 mg.

Further Reading:

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

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

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

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

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

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

High Altitude Cerebral Edema (HACE) is a condition that develops from acute mountain sickness (AMS). Ataxia, which refers to a lack of coordination, is the primary early indication of HACE. The mentioned symptoms are typical characteristics 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.

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.

Bartter’s syndrome is a rare genetic defect that affects the ascending limb of the loop of Henle. This condition is characterized by low blood pressure and a hypokalemic alkalosis, which means there is a decrease in potassium levels in the blood.

Hyperkalemia, on the other hand, is defined as having a plasma potassium level greater than 5.5 mmol/L. There are various non-drug factors that can cause hyperkalemia, such as renal failure, excessive potassium supplementation, Addison’s disease (adrenal insufficiency), congenital adrenal hyperplasia, renal tubular acidosis (type 4), rhabdomyolysis, burns and trauma, and tumor lysis syndrome. Additionally, acidosis can also contribute to the development of hyperkalemia.

In addition to these non-drug causes, certain medications can also lead to hyperkalemia. These include ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium. It is important to be aware of these potential causes and to monitor potassium levels in order to prevent and manage hyperkalemia effectively.

Blood transfusion is a potentially life-saving treatment that can provide great clinical benefits. However, it also carries several risks and potential problems. These include immunological complications, administration errors, infections, immune dilution, and transfusion errors. While there have been improvements in safety procedures and efforts to minimize the use of transfusion, errors and serious adverse reactions still occur and often go unreported.

One rare complication of blood transfusion is transfusion-associated graft-vs-host disease (TA-GVHD). This condition typically presents with fever, rash, and diarrhea 1-4 weeks after the transfusion. Laboratory findings may show pancytopenia and abnormalities in liver function. Unlike GVHD after marrow transplantation, TA-GVHD leads to severe marrow aplasia with a mortality rate exceeding 90%. Unfortunately, there are currently no effective treatments available for this condition, and survival is rare, with death usually occurring within 1-3 weeks of the first symptoms.

During a blood transfusion, viable T lymphocytes from the donor are transfused into the recipient’s body. In TA-GVHD, these lymphocytes engraft and react against the recipient’s tissues. However, the recipient is unable to reject the donor lymphocytes due to factors such as immunodeficiency, severe immunosuppression, or shared HLA antigens. Supportive management is the only option for TA-GVHD.

The following summarizes the main complications and reactions that can occur during a blood transfusion:

Complication Features Management
Febrile transfusion reaction
– Presents with a 1-degree rise in temperature from baseline, along with chills and malaise.
– Most common reaction, occurring in 1 out of 8 transfusions.
– Usually caused by cytokines from leukocytes in transfused red cell or platelet components.
– Supportive management, with the use of paracetamol for symptom relief.

Acute haemolytic reaction
– Symptoms include fever, chills, pain at the transfusion site, nausea, vomiting, and dark urine.
– Often accompanied by a feeling of ‘impending doom’.
– Most serious type of reaction, often due to ABO incompatibility caused by administration errors.
– Immediate action required: stop the transfusion, administer IV fluids, and consider diuretics if necessary.

Delayed haemolytic reaction
– Typically occurs 4-8 days after a blood transfusion.
– Symptoms include fever, anemia and/or hyperbilirubinemia

Terlipressin, a vasopressin analogue, has been found to significantly enhance survival rates in cases of acute upper gastrointestinal variceal haemorrhage when compared to a placebo. Alternatively, somatostatin and its analogue octreotide have also demonstrated similar benefits and can be used as alternatives. It is not recommended to administer proton pump inhibitors (PPIs) before endoscopy in cases of acute upper GI bleeds, but they are advised after endoscopy for non-variceal upper GI bleeds. There is no consensus on whether PPIs improve outcomes in variceal bleeding. Recombinant factor Vlla should only be considered if other blood products have failed to correct coagulopathy. Studies indicate that tranexamic acid does not reduce mortality from upper GI bleeding and may actually increase the risk of thromboembolic events.

Further Reading:

Upper gastrointestinal bleeding (UGIB) refers to the loss of blood from the gastrointestinal tract, occurring in the upper part of the digestive system. It can present as haematemesis (vomiting blood), coffee-ground emesis, bright red blood in the nasogastric tube, or melaena (black, tarry stools). UGIB can lead to significant hemodynamic compromise and is a major health burden.

The causes of UGIB vary, with peptic ulcer disease being the most common cause, followed by gastritis/erosions, esophagitis, and other less common causes such as varices, Mallory Weiss tears, and malignancy. Swift assessment, hemodynamic resuscitation, and appropriate interventions are essential for the management of UGIB.

Assessment of patients with UGIB should follow an ABCDE approach, and scoring systems such as the Glasgow-Blatchford bleeding score (GBS) and the Rockall score are recommended to risk stratify patients and determine the urgency of endoscopy. Transfusion may be necessary for patients with massive hemorrhage, and platelet transfusion, fresh frozen plasma (FFP), and prothrombin complex concentrate may be offered based on specific criteria.

Endoscopy plays a crucial role in the management of UGIB. Unstable patients with severe acute UGIB should undergo endoscopy immediately after resuscitation, while all other patients should undergo endoscopy within 24 hours of admission. Endoscopic treatment of non-variceal bleeding may involve mechanical methods of hemostasis, thermal coagulation, or the use of fibrin or thrombin with adrenaline. Proton pump inhibitors should only be used after endoscopy.

Variceal bleeding requires specific management, including the use of terlipressin and prophylactic antibiotics. Oesophageal varices can be treated with band ligation or transjugular intrahepatic portosystemic shunts (TIPS), while gastric varices may be treated with endoscopic injection of N-butyl-2-cyanoacrylate or TIPS if bleeding is not controlled.

For patients taking NSAIDs, aspirin, or clopidogrel, low-dose aspirin can be continued once hemostasis is achieved, NSAIDs should be stopped in patients presenting with UGIB

Prilocaine is the preferred choice for intravenous regional anesthesia. This is because Bupivacaine and lidocaine have a higher risk of causing harmful side effects.

Further Reading:

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.

Vestibular neuronitis is characterized by the sudden and prolonged onset of rotational vertigo. This vertigo can occur spontaneously, upon waking up, or gradually worsen throughout the day. It is particularly aggravated by changes in head position, although it remains constant even when the head is still. Unlike other conditions, vestibular neuronitis does not cause hearing loss, tinnitus, or focal neurological deficits. On the other hand, in BPPV, episodes of vertigo are usually brief, lasting less than 20 seconds, and only occur when there is a change in head position.

Further Reading:

Vestibular neuritis, also known as vestibular neuronitis, is a condition characterized by sudden and prolonged vertigo of peripheral origin. It is believed to be caused by inflammation of the vestibular nerve, often following a viral infection. It is important to note that vestibular neuritis and labyrinthitis are not the same condition, as labyrinthitis involves inflammation of the labyrinth. Vestibular neuritis typically affects individuals between the ages of 30 and 60, with a 1:1 ratio of males to females. The annual incidence is approximately 3.5 per 100,000 people, making it one of the most commonly diagnosed causes of vertigo.

Clinical features of vestibular neuritis include nystagmus, which is a rapid, involuntary eye movement, typically in a horizontal or horizontal-torsional direction away from the affected ear. The head impulse test may also be positive. Other symptoms include spontaneous onset of rotational vertigo, which is worsened by changes in head position, as well as nausea, vomiting, and unsteadiness. These severe symptoms usually last for 2-3 days, followed by a gradual recovery over a few weeks. It is important to note that hearing is not affected in vestibular neuritis, and symptoms such as tinnitus and focal neurological deficits are not present.

Differential diagnosis for vestibular neuritis includes benign paroxysmal positional vertigo (BPPV), labyrinthitis, Meniere’s disease, migraine, stroke, and cerebellar lesions. Management of vestibular neuritis involves drug treatment for nausea and vomiting associated with vertigo, typically through short courses of medication such as prochlorperazine or cyclizine. If symptoms are severe and fluids cannot be tolerated, admission and administration of IV fluids may be necessary. General advice should also be given, including avoiding driving while symptomatic, considering the suitability to work based on occupation and duties, and the increased risk of falls. Follow-up is required, and referral is necessary if there are atypical symptoms, symptoms do not improve after a week of treatment, or symptoms persist for more than 6 weeks.

The prognosis for vestibular neuritis is generally good, with the majority of individuals fully recovering within 6 weeks. Recurrence is thought to occur in 2-11% of cases, and approximately 10% of individuals may develop BPPV following an episode of vestibular neuritis. A very rare complication of vestibular neuritis is ph

Transfusion-associated circulatory overload (TACO) is a reaction that occurs when a large volume of blood is infused rapidly. It is the second leading cause of deaths related to transfusions, accounting for about 20% of all fatalities.

TACO typically happens in patients with limited cardiac reserve or chronic anemia who receive a fast blood transfusion. Elderly individuals, infants, and severely anemic patients are particularly vulnerable.

The common signs of TACO include acute respiratory distress, rapid heartbeat, high blood pressure, the appearance of acute or worsening fluid accumulation in the lungs on a chest X-ray, and evidence of excessive fluid retention.

The B-type natriuretic peptide (BNP) can be a helpful diagnostic tool for TACO. Usually, the BNP level is elevated to at least 1.5 times the baseline before the transfusion.

In many cases, simply slowing down the rate of transfusion, positioning the patient upright, and administering diuretics will be sufficient. In more severe cases, the transfusion should be stopped, and non-invasive ventilation may be considered.

Corticosteroids can be beneficial in preventing or reducing prolonged reactions. According to the current APLS guidelines, the recommended doses of hydrocortisone for different age groups are as follows:

– Children under 6 months: 25 mg administered slowly via intramuscular (IM) or intravenous (IV) route.
– Children aged 6 months to 6 years: 50 mg administered slowly via IM or IV route.
– Children aged 6 to 12 years: 100 mg administered slowly via IM or IV route.
– Children over 12 years: 200 mg administered slowly via IM or IV route.
– Adults: 200 mg administered slowly via IM or IV route.

It is important to note that the most recent ALS guidelines do not recommend the routine use of corticosteroids for treating anaphylaxis in adults. However, the current APLS guidelines still advocate for the use of corticosteroids in children to manage anaphylaxis.

For the exam, it is important to be familiar with the statistics regarding the outcomes of outpatient and inpatient cardiac arrest in the UK.

Further Reading:

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

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

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

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

The primary approach to managing nerve gas exposure through medication involves the repeated administration of antidotes. The two antidotes utilized for this purpose are atropine and pralidoxime.

Atropine is the standard anticholinergic medication employed to address the symptoms associated with nerve agent poisoning. It functions as an antagonist for muscarinic acetylcholine receptors, effectively blocking the effects caused by excessive acetylcholine. Initially, a 1.2 mg intravenous bolus of atropine is administered. This dosage is then repeated and doubled every 2-3 minutes until excessive bronchial secretion ceases and miosis (excessive constriction of the pupil) resolves. In some cases, as much as 100 mg of atropine may be necessary.

Pralidoxime (2-PAMCl) is the standard oxime used in the treatment of nerve agent poisoning. Its mechanism of action involves reactivating acetylcholinesterase by scavenging the phosphoryl group attached to the functional hydroxyl group of the enzyme, thereby counteracting the effects of the nerve agent itself. For patients who are moderately or severely poisoned, pralidoxime should be administered intravenously at a dosage of 30 mg/kg of body weight (or 2 g in the case of an adult) over a period of four minutes.

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

Blood transfusion is a crucial medical treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion use, errors and adverse reactions still occur. One common adverse reaction is febrile transfusion reactions, which present as an unexpected rise in temperature during or after transfusion. This can be caused by cytokine accumulation or recipient antibodies reacting to donor antigens. Treatment for febrile transfusion reactions is supportive, and other potential causes should be ruled out.

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

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

The CENTOR score is a clinical prediction rule used to assess the likelihood of a patient having a streptococcal infection, which is commonly associated with sore throat. It is based on the presence or absence of four clinical criteria: fever, tonsillar exudate, tender anterior cervical lymphadenopathy, and absence of cough. Each criterion is assigned one point, and the total score ranges from 0 to 4. In this case, the patient has a fever, tonsillar exudate, tender anterior cervical lymphadenopathy, and no cough, resulting in a CENTOR score of 4. A higher score indicates a higher likelihood of a streptococcal infection, and further diagnostic testing or treatment may be warranted.

Further Reading:

Pharyngitis and tonsillitis are common conditions that cause inflammation in the throat. Pharyngitis refers to inflammation of the oropharynx, which is located behind the soft palate, while tonsillitis refers to inflammation of the tonsils. These conditions can be caused by a variety of pathogens, including viruses and bacteria. The most common viral causes include rhinovirus, coronavirus, parainfluenza virus, influenza types A and B, adenovirus, herpes simplex virus type 1, and Epstein Barr virus. The most common bacterial cause is Streptococcus pyogenes, also known as Group A beta-hemolytic streptococcus (GABHS). Other bacterial causes include Group C and G beta-hemolytic streptococci and Fusobacterium necrophorum.

Group A beta-hemolytic streptococcus is the most concerning pathogen as it can lead to serious complications such as rheumatic fever and glomerulonephritis. These complications can occur due to an autoimmune reaction triggered by antigen/antibody complex formation or from cell damage caused by bacterial exotoxins.

When assessing a patient with a sore throat, the clinician should inquire about the duration and severity of the illness, as well as associated symptoms such as fever, malaise, headache, and joint pain. It is important to identify any red flags and determine if the patient is immunocompromised. Previous non-suppurative complications of Group A beta-hemolytic streptococcus infection should also be considered, as there is an increased risk of further complications with subsequent infections.

Red flags that may indicate a more serious condition include severe pain, neck stiffness, or difficulty swallowing. These symptoms may suggest epiglottitis or a retropharyngeal abscess, which require immediate attention.

To determine the likelihood of a streptococcal infection and the need for antibiotic treatment, two scoring systems can be used: CENTOR and FeverPAIN. The CENTOR criteria include tonsillar exudate, tender anterior cervical lymphadenopathy or lymphadenitis, history of fever, and absence of cough. The FeverPAIN criteria include fever, purulence, rapid onset of symptoms, severely inflamed tonsils, and absence of cough or coryza. Based on the scores from these criteria, the likelihood of a streptococcal infection can be estimated, and appropriate management can be undertaken. can

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

Further Reading:

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

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

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

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