Anti-D is an antibody of the IgG class that targets the Rhesus D (RhD) antigen. It is specifically administered to women who are RhD negative, meaning they do not have the RhD antigen on their red blood cells. When a RhD negative woman is exposed to the blood of a RhD positive fetus, she may develop antibodies against RhD that can cross the placenta and attack the red blood cells of the fetus, leading to a condition called hemolytic disease of the newborn. Anti-D is given to bind to the fetal red blood cells in the mother’s circulation and neutralize them before an immune response is triggered.

RhD should be administered in the event of a sensitizing event, which can include childbirth, antepartum hemorrhage, miscarriage, ectopic pregnancy, intrauterine death, amniocentesis, chorionic villus sampling, or abdominal trauma. It is important to administer Anti-D as soon as possible after a sensitizing event, but it can still provide some benefit even if given outside of the recommended 72-hour window, according to the British National Formulary (BNF).

For RhD negative women, routine antenatal prophylaxis with Anti-D is recommended at 28 and 34 weeks of pregnancy, regardless of whether they have already received Anti-D earlier in the same pregnancy due to a sensitizing event.

In cases of uncomplicated miscarriage before 12 weeks of gestation, confirmed by ultrasound, or mild and painless vaginal bleeding, prophylactic Anti-D is not necessary because the risk of feto-maternal hemorrhage is extremely low. However, in cases of therapeutic termination of pregnancy, whether through surgical or medical methods, confirmed RhD negative women who are not known to be sensitized to RhD should receive 250 IU of prophylactic Anti-D immunoglobulin.

Second degree frostbite is characterized by tissue necrosis that affects both the epidermis and a variable depth of the dermis. However, there is still some healthy dermis present, which allows for regeneration and recovery of the skin. This type of frostbite is often referred to as partial thickness. Clinically, it is observed as the formation of blisters filled with clear or milky fluid on the surface of the skin, accompanied by redness and swelling.

Further Reading:

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

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

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

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

Arterial blood gas (ABG) interpretation is essential for evaluating a patient’s respiratory gas exchange and acid-base balance. While the normal values on an ABG may slightly vary between analyzers, they generally fall within the following ranges:

pH: 7.35 – 7.45
pO2: 10 – 14 kPa
PCO2: 4.5 – 6 kPa
HCO3-: 22 – 26 mmol/l
Base excess: -2 – 2 mmol/l

In this particular case, the patient’s medical history raises concerns about a possible diagnosis of diabetic ketoacidosis (DKA). The relevant ABG findings are as follows:

Normal PO2
Low pH (acidaemia)
Low PCO2
Low bicarbonate
Raised lactate

The anion gap refers to the concentration of unmeasured anions in the plasma. It is calculated by subtracting the primary measured cations from the primary measured anions in the serum. The reference range for anion gap varies depending on the measurement methodology but typically falls between 8 to 16 mmol/L.

To calculate her anion gap, we can use the formula:

Anion gap = [Na+] – [Cl-] – [HCO3-]

Using the provided values, her anion gap can be calculated as:

Anion gap = [149] – [100] – [17]
Anion gap = 32

Therefore, it is evident that she has a raised anion gap metabolic acidosis.

It is likely that she is experiencing a type B lactic acidosis secondary to diabetic ketoacidosis. Some potential causes of type A and type B lactic acidosis are listed below:

Type A lactic acidosis:
– Shock (including septic shock)
– Left ventricular failure
– Severe anemia
– Asphyxia
– Cardiac arrest
– Carbon monoxide poisoning
– Respiratory failure
– Severe asthma and COPD
– Regional hypoperfusion

Type B lactic acidosis:
– Renal failure
– Liver failure
– Sepsis (non-hypoxic sepsis)
– Thiamine deficiency
– Alcoholic ketoacidosis
– Diabetic ketoacidosis
– Cyanide poisoning
– Methanol poisoning
– Biguanide poisoning

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

Further Reading:

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

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

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

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

This girl is displaying symptoms and signs that are consistent with a diagnosis of meningococcal septicaemia. It is crucial that she receives urgent antibiotic treatment. If a patient has a penicillin allergy, but not anaphylaxis, a third-generation cephalosporin like cefotaxime may be administered. However, in this particular case, the girl has a documented history of anaphylaxis to penicillin. It is important to note that up to 10% of patients who are allergic to penicillin may experience an adverse reaction to cephalosporins. In situations where there is a true anaphylactic reaction to penicillins, the British National Formulary (BNF) recommends the use of chloramphenicol as an alternative treatment option.

The patient’s symptoms strongly suggest a diagnosis of acute cholecystitis. This condition occurs when a gallstone becomes stuck in the outlet of the gallbladder, causing irritation and inflammation of the gallbladder wall. As a result, the gallbladder fills with pus, which is initially sterile but can become infected with bacteria such as Escherichia coli and Klebsiella spp.

The clinical features of acute cholecystitis include severe pain in the upper right quadrant or epigastric, which can radiate to the back and lasts for more than 12 hours. Fevers and rigors are also commonly present, along with nausea and vomiting. Murphy’s sign, a physical examination finding, is highly sensitive and has a high positive predictive value for acute cholecystitis. However, its specificity is lower, as it can also be positive in biliary colic and ascending cholangitis.

In acute cholecystitis, the white cell count and C-reactive protein (CRP) levels are usually elevated. Liver function tests, such as AST, ALT, and ALP, may also be elevated but can often be within the normal range. Bilirubin levels may be mildly elevated, but they can also be normal. If there is a significant elevation in AST, ALT, ALP, or bilirubin, it may indicate other biliary tract conditions, such as ascending cholangitis or choledocholithiasis.

It is important to differentiate acute cholecystitis from other conditions with similar presentations. Renal colic, for example, presents with pain in the loin area and tenderness in the renal angle, which is different from the symptoms seen in acute cholecystitis. Cholangiocarcinoma, a rare type of cancer originating from the biliary epithelium, typically presents with painless jaundice and itching.

To help distinguish between biliary colic, acute cholecystitis, and ascending cholangitis, the following summarizes their key differences:

Biliary colic:
– Pain duration: Less than 12 hours
– Fever: Absent
– Murphy’s sign: Negative
– WCC & CRP: Normal
– AST, ALT & ALP: Normal
– Bilirubin: Normal

Acute cholecystitis:
– Pain duration: More than 12 hours
– Fever: Present
– Murphy’s sign: Positive
– WCC &

Hereditary angioedema is a condition caused by a lack of C1 esterase inhibitor, a protein that is part of the complement system. It is typically inherited in an autosomal dominant manner. Symptoms usually start in childhood and continue sporadically into adulthood. Attacks can be triggered by minor surgical procedures, dental work, and stress. The main clinical signs of hereditary angioedema include swelling of the skin and mucous membranes, with the face, tongue, and extremities being the most commonly affected areas. There is often a tingling sensation before an attack, sometimes accompanied by a non-itchy rash.

Angioedema and anaphylaxis resulting from C1 esterase inhibitor deficiency do not respond to adrenaline, steroids, or antihistamines. Treatment requires the use of C1 esterase inhibitor concentrate or fresh frozen plasma, both of which contain C1 esterase inhibitor. In situations that may trigger an attack, short-term prophylaxis can be achieved by administering C1 esterase inhibitor or fresh frozen plasma infusions prior to the event. For long-term prevention, androgenic steroids like stanozolol or antifibrinolytic drugs such as tranexamic acid can be used.

Acute pancreatitis is a frequently encountered and serious source of acute abdominal pain. It involves the sudden inflammation of the pancreas, leading to the release of enzymes that cause self-digestion of the organ.

The clinical manifestations of acute pancreatitis include severe epigastric pain, accompanied by feelings of nausea and vomiting. The pain may radiate to the T6-T10 dermatomes or even to the shoulder tip through the phrenic nerve if the diaphragm is irritated. Other symptoms may include fever or sepsis, tenderness in the epigastric region, jaundice, and the presence of Gray-Turner sign (bruising on the flank) or Cullen sign (bruising around the belly button).

The most common causes of acute pancreatitis are gallstones and alcohol consumption. Additionally, many cases are considered idiopathic, meaning the cause is unknown. To aid in remembering the various causes, the mnemonic ‘I GET SMASHED’ can be helpful. Each letter represents a potential cause: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion stings, Hyperlipidemia/hypercalcemia, ERCP (endoscopic retrograde cholangiopancreatography), and Drugs.

A phaeochromocytoma is a rare functional tumor that develops from chromaffin cells in the adrenal medulla. Extra-adrenal paragangliomas, also known as extra-adrenal pheochromocytomas, are similar tumors that originate in the ganglia of the sympathetic nervous system but are less common. These tumors secrete catecholamines and cause a range of symptoms and signs related to hyperactivity of the sympathetic nervous system.

The most common initial symptom is high blood pressure, which can be either sustained or sporadic. Symptoms tend to come and go, occurring multiple times a day or very infrequently. As the disease progresses, the symptoms usually become more severe and frequent.

Surgical removal is the preferred and definitive treatment option. If the tumor is completely removed without any spread to other parts of the body, it often leads to a cure for hypertension.

Before surgery, it is crucial to manage the condition medically to reduce the risk of hypertensive crises during the operation. This is typically done by using a combination of non-competitive alpha-blockers (such as phenoxybenzamine) and beta-blockers. Alpha-blockade should be started first, at least 7-10 days before the surgery, to allow for expansion of blood volume. Once this is achieved, beta-blockade can be initiated to help control rapid heart rate and certain irregular heart rhythms. Starting beta-blockade too early can trigger a hypertensive crisis.

Genetic counseling should also be provided, and any associated conditions should be identified and managed appropriately.

Given the patient’s symptoms and physical findings, the most appropriate initial treatment would be to administer Furosemide 40 mg intravenously. Furosemide is a loop diuretic that helps remove excess fluid from the body, which can alleviate symptoms of fluid overload such as shortness of breath and edema. By reducing fluid volume, Furosemide can help improve the patient’s breathing and relieve the strain on the heart.

Further Reading:

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

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

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

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

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

In summary, cardiac failure is a clinical syndrome resulting from abnormalities in cardiac function. It can have various causes and is characterized by specific signs and symptoms. Diagnosis involves specific tests, and management focuses on addressing

The diagnostic criteria for hypertrophic pyloric stenosis (HPS) on ultrasound are as follows: the thickness of the pyloric muscle should be greater than 3 mm, the longitudinal length of the pylorus should be greater than 15-17 mm, the volume of the pylorus should be greater than 1.5 cm3, and the transverse diameter of the pylorus should be greater than 13 mm.

Further Reading:

Pyloric stenosis is a condition that primarily affects infants, characterized by the thickening of the muscles in the pylorus, leading to obstruction of the gastric outlet. It typically presents between the 3rd and 12th weeks of life, with recurrent projectile vomiting being the main symptom. The condition is more common in males, with a positive family history and being first-born being additional risk factors. Bottle-fed children and those delivered by c-section are also more likely to develop pyloric stenosis.

Clinical features of pyloric stenosis include projectile vomiting, usually occurring about 30 minutes after a feed, as well as constipation and dehydration. A palpable mass in the upper abdomen, often described as like an olive, may also be present. The persistent vomiting can lead to electrolyte disturbances, such as hypochloremia, alkalosis, and mild hypokalemia.

Ultrasound is the preferred diagnostic tool for confirming pyloric stenosis. It can reveal specific criteria, including a pyloric muscle thickness greater than 3 mm, a pylorus longitudinal length greater than 15-17 mm, a pyloric volume greater than 1.5 cm3, and a pyloric transverse diameter greater than 13 mm.

The definitive treatment for pyloric stenosis is pyloromyotomy, a surgical procedure that involves making an incision in the thickened pyloric muscle to relieve the obstruction. Before surgery, it is important to correct any hypovolemia and electrolyte disturbances with intravenous fluids. Overall, pyloric stenosis is a relatively common condition in infants, but with prompt diagnosis and appropriate management, it can be effectively treated.

Distinguishing between unstable angina and other acute coronary syndromes can be done by looking at normal troponin results. If serial troponin tests come back negative, it can rule out a diagnosis of myocardial infarction. Unstable angina is characterized by myocardial ischemia occurring at rest or with minimal exertion, without any acute damage or death of heart muscle cells. The patient in question shows ECG and biochemical features that align with this definition. Vincent’s angina, on the other hand, refers to an infection in the throat accompanied by ulcerative gingivitis.

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.

Patients who are on beta-blockers may not respond effectively to adrenaline during anaphylaxis. Research conducted on animals and reported cases have indicated that glucagon can be utilized to counteract the effects of beta-blockade if initial adrenaline doses prove ineffective.

Although prednisolone and hydrocortisone can be beneficial later on, it typically takes 6-8 hours for them to take full effect. Therefore, they are unlikely to have any impact on the patient during the brief period it will take for the ambulance to arrive.

In some cases, the signs of skin or mucosal involvement may be difficult to detect or may not be present at all. The Royal College of Emergency Medicine (RCEM) states that anaphylaxis is likely when three specific criteria are met: the illness has a sudden and rapid onset, there are noticeable changes in the skin or mucosal areas such as flushing, hives, or swelling, and there are severe problems with the airway, breathing, or circulation that pose a life-threatening risk.

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 primary treatment for malignant hyperthermia is dantrolene. Dantrolene works by blocking the release of calcium through calcium channels, resulting in the relaxation of skeletal muscles.

Further Reading:

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

Public Health England (PHE) has a primary goal of swiftly 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.
It is worth noting that roseola infantum is not considered a notifiable disease, making it the least likely option among the diseases listed above.

According to the 2011 recommendations from the World Health Organization (WHO), the following criteria are used to diagnose diabetes mellitus:

– A random venous plasma glucose concentration that exceeds 11.1 mmol/l.
– A fasting plasma glucose concentration that is higher than 7.0 mmol/l.
– A two-hour plasma glucose concentration that exceeds 11.1 mmol/l, measured two hours after consuming 75g of anhydrous glucose during an oral glucose tolerance test (OGTT).
– An HbA1c level that is greater than 48 mmol/mol (equivalent to 6.5%).

These guidelines provide specific thresholds for diagnosing diabetes mellitus based on various glucose measurements and HbA1c levels. It is important for healthcare professionals to consider these criteria when evaluating individuals for diabetes mellitus.

Grade 2 shock is characterized by a pulse rate of 100 to 120 beats per minute and a respiratory rate of 20 to 30 breaths per minute. These clinical features align with the symptoms of grade 2 hypovolemic shock, as indicated in the below notes.

Further Reading:

Shock is a condition characterized by inadequate tissue perfusion due to circulatory insufficiency. It can be caused by fluid loss or redistribution, as well as impaired cardiac output. The main causes of shock include haemorrhage, diarrhoea and vomiting, burns, diuresis, sepsis, neurogenic shock, anaphylaxis, massive pulmonary embolism, tension pneumothorax, cardiac tamponade, myocardial infarction, and myocarditis.

One common cause of shock is haemorrhage, which is frequently encountered in the emergency department. Haemorrhagic shock can be classified into different types based on the amount of blood loss. Type 1 haemorrhagic shock involves a blood loss of 15% or less, with less than 750 ml of blood loss. Patients with type 1 shock may have normal blood pressure and heart rate, with a respiratory rate of 12 to 20 breaths per minute.

Type 2 haemorrhagic shock involves a blood loss of 15 to 30%, with 750 to 1500 ml of blood loss. Patients with type 2 shock may have a pulse rate of 100 to 120 beats per minute and a respiratory rate of 20 to 30 breaths per minute. Blood pressure is typically normal in type 2 shock.

Type 3 haemorrhagic shock involves a blood loss of 30 to 40%, with 1.5 to 2 litres of blood loss. Patients with type 3 shock may have a pulse rate of 120 to 140 beats per minute and a respiratory rate of more than 30 breaths per minute. Urine output is decreased to 5-15 mls per hour.

Type 4 haemorrhagic shock involves a blood loss of more than 40%, with more than 2 litres of blood loss. Patients with type 4 shock may have a pulse rate of more than 140 beats per minute and a respiratory rate of more than 35 breaths per minute. They may also be drowsy, confused, and possibly experience loss of consciousness. Urine output may be minimal or absent.

In summary, shock is a condition characterized by inadequate tissue perfusion. Haemorrhage is a common cause of shock, and it can be classified into different types based on the amount of blood loss. Prompt recognition and management of shock are crucial in order to prevent further complications and improve patient outcomes

Hereditary angioedema is a condition caused by a lack of C1 esterase inhibitor, a protein that is part of the complement system. It is typically inherited in an autosomal dominant manner. Symptoms usually start in childhood and continue sporadically into adulthood. Attacks can be triggered by minor surgical procedures, dental work, and stress. The main clinical signs of hereditary angioedema include swelling of the skin and mucous membranes, with the face, tongue, and extremities being the most commonly affected areas. There is often a tingling sensation before an attack, sometimes accompanied by a non-itchy rash.

Angioedema and anaphylaxis resulting from C1 esterase inhibitor deficiency do not respond to adrenaline, steroids, or antihistamines. Treatment requires the use of C1 esterase inhibitor concentrate or fresh frozen plasma, both of which contain C1 esterase inhibitor. In situations that may trigger an attack, short-term prophylaxis can be achieved by administering C1 esterase inhibitor or fresh frozen plasma infusions prior to the event. For long-term prevention, androgenic steroids like stanozolol or antifibrinolytic drugs such as tranexamic acid can be used.

Uveitis is the most prevalent eye complication that arises in individuals with ankylosing spondylitis (AS). Approximately one out of every three patients with AS will experience uveitis at some stage. The symptoms of uveitis include a red and painful eye, along with photophobia and blurred vision. Additionally, patients may notice the presence of floaters. The primary treatment for uveitis involves the use of corticosteroids, and it is crucial for patients to seek immediate attention from an ophthalmologist.

The recommended first line analgesics for mild pain are oral or rectal paracetamol and oral ibuprofen. When it comes to treating mild pain in children, it is best to consider either giving a loading dose of oral/rectal paracetamol at a rate of 20 mg/kg, followed by a maintenance dose of 15 mg/kg every 4-6 hours. Alternatively, oral ibuprofen can be administered at a rate of 10 mg/kg every 6-8 hours.

Further Reading:

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

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

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

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

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

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

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

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

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

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

Diabetic amyotrophy, also referred to as proximal diabetic neuropathy, is the second most prevalent form of diabetic neuropathy. It typically begins with discomfort in the buttocks, hips, or thighs and is often initially experienced on one side. The pain may start off as mild and gradually progress or it can suddenly manifest, as seen in this case. Subsequently, weakness and wasting of the proximal muscles in the lower limbs occur, making it difficult for the patient to transition from sitting to standing without assistance. Reflexes in the affected areas can also be impacted. Good control of blood sugar levels, physiotherapy, and lifestyle adjustments can reverse diabetic amyotrophy.

Peripheral neuropathy is the most common type of diabetic neuropathy and typically manifests as pain or loss of sensation in the feet or hands.

Autonomic neuropathy leads to changes in digestion, bowel and bladder function, sexual response, and perspiration. It can also affect the cardiovascular system, resulting in rapid heart rates and orthostatic hypotension.

Focal neuropathy causes sudden weakness in a single nerve or group of nerves, resulting in pain, sensory loss, or muscle weakness. Any nerve in the body can be affected.

Normal pressure hydrocephalus is a condition characterized by the classic triad of symptoms: gait instability, urinary incontinence, and dementia. Gait apraxia, which is a common feature, presents as a slow and cautious gait, difficulty initiating movement, unsteadiness, a widened standing base, reduced stride length, shuffling gait, falls, and freezing. The onset of symptoms typically occurs over a period of 3-6 months. This condition is a form of communicating hydrocephalus, where there is a gradual buildup of cerebrospinal fluid (CSF) due to impaired CSF absorption. As a result, the ventricles in the brain enlarge and intracranial pressure increases, leading to compression of brain tissue and neurological complications. Normal pressure hydrocephalus is more commonly seen in individuals over the age of 65, and a CT head or MRI is usually the initial diagnostic test.

Further Reading:

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

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

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

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

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

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

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

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

This presentation strongly indicates a diagnosis of whooping cough, also known as pertussis. Whooping cough is a respiratory infection caused by the bacteria Bordetella pertussis. It is transmitted through respiratory droplets and has an incubation period of about 7-21 days. The disease is highly contagious and can be transmitted to around 90% of close household contacts.

The clinical course of whooping cough can be divided into two stages. The first stage is called the catarrhal stage, which resembles a mild respiratory infection with low-grade fever and symptoms similar to a cold. A cough may be present, but it is usually mild and not as severe as in the second stage. The catarrhal stage typically lasts for about a week.

The second stage is known as the paroxysmal stage. During this stage, the characteristic paroxysmal cough develops as the symptoms from the catarrhal stage start to improve. The coughing occurs in spasms, often preceded by an inspiratory whoop sound, followed by a series of rapid coughs. Vomiting may occur, and patients may develop subconjunctival hemorrhages and petechiae. Patients generally feel well between coughing spasms, and there are usually no abnormal chest findings. This stage can last up to 3 months, with a gradual recovery over this period. The later stages of this stage are sometimes referred to as the convalescent stage.

Complications of whooping cough can include secondary pneumonia, rib fractures, pneumothorax, hernias, syncopal episodes, encephalopathy, and seizures. It is important to note that a history of vaccination does not guarantee immunity, as it only provides about 95% protection.

The presence of marked lymphocytosis in this case also supports a diagnosis of pertussis, as it is a common finding. A lymphocyte count greater than 20 x 109/l is highly suggestive of the disease.

The ratio of chest compressions to ventilations is 15:2. This ratio has not been proven through experiments, but it has been validated through mathematical studies. When performing chest compressions on a child, it is recommended to make them at least 1/3 of the depth of the child’s chest. Additionally, the optimal compression rate is between 100 and 120 compressions per minute.
To protect the airway of an unconscious child, the oropharyngeal (Guedel) airway is the best option. However, it should not be used on awake patients as there is a risk of vomiting and aspiration.
In children, asystole is the most common arrest rhythm. This occurs when the young heart responds to prolonged hypoxia and acidosis by progressively slowing down, eventually resulting in asystole.

HAPE is a form of noncardiogenic pulmonary edema that occurs secondary to hypoxia. It is a clinical diagnosis characterized by fatigue, dyspnea, and dry cough with exertion. If left untreated, it can progress to dyspnea at rest, rales, cyanosis, and a mortality rate of up to 50%.

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.

Amiodarone is a medication that can have numerous harmful side effects, making it crucial to conduct a comprehensive clinical assessment before starting treatment with it. Some of the side effects associated with amiodarone include corneal microdeposits, photosensitivity, nausea, sleep disturbance, hyperthyroidism, hypothyroidism, acute hepatitis and jaundice, peripheral neuropathy, lung fibrosis, QT prolongation, and optic neuritis (although this is very rare). If optic neuritis occurs, immediate discontinuation of amiodarone is necessary to prevent the risk of blindness.

The majority of patients taking amiodarone experience corneal microdeposits, but these typically resolve after treatment is stopped and rarely affect vision. Amiodarone has a chemical structure similar to thyroxine and can bind to the nuclear thyroid receptor, leading to both hypothyroidism and hyperthyroidism. However, hypothyroidism is more commonly observed, affecting around 5-10% of patients.

Anaemia of chronic disease is a type of anaemia that can occur in various chronic conditions, such as rheumatoid arthritis, systemic lupus erythematosus, tuberculosis, malignancy, malnutrition, hypothyroidism, hypopituitarism, chronic kidney disease, and chronic liver disease. The underlying mechanisms of this type of anaemia are complex and not fully understood, with multiple contributing factors involved. One important mediator in inflammatory diseases like rheumatoid arthritis is interleukin-6 (IL-6). Increased levels of IL-6 lead to the production of hepcidin, a hormone that regulates iron balance. Hepcidin prevents the release of iron from the reticulo-endothelial system and affects other aspects of iron metabolism.

Anaemia of chronic disease typically presents as a normochromic, normocytic anaemia, although it can also be microcytic. It is characterized by reduced serum iron, reduced transferrin saturation, and reduced total iron-binding capacity (TIBC). However, the serum ferritin levels are usually normal or increased. Distinguishing anaemia of chronic disease from iron-deficiency anaemia can be challenging, but in iron-deficiency anaemia, the TIBC is typically elevated, and serum ferritin is usually low.

Klumpke’s palsy, also known as Dejerine-Klumpke palsy, is a condition where the arm becomes paralyzed due to an injury to the lower roots of the brachial plexus. The most commonly affected root is C8, but T1 can also be involved. The main cause of Klumpke’s palsy is when the arm is pulled forcefully in an outward position during a difficult childbirth. It can also occur in adults with apical lung carcinoma (Pancoast’s syndrome).

Clinically, Klumpke’s palsy is characterized by a deformity known as ‘claw hand’, which is caused by the paralysis of the intrinsic hand muscles. There is also a loss of sensation along the ulnar side of the forearm and hand. In some cases where T1 is affected, a condition called Horner’s syndrome may also be present.

Klumpke’s palsy can be distinguished from Erb’s palsy, which affects the upper roots of the brachial plexus (C5 and sometimes C6). In Erb’s palsy, the arm hangs by the side with the elbow extended and the forearm turned inward (known as the ‘waiter’s tip sign’). Additionally, there is a loss of shoulder abduction, external rotation, and elbow flexion.