Blood transfusion is a crucial 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.

Delayed haemolytic transfusion reactions (DHTRs) typically occur 4-8 days after a blood transfusion, but can sometimes manifest up to a month later. The symptoms are similar to acute haemolytic transfusion reactions but are usually less severe. Patients may experience fever, inadequate rise in haemoglobin, jaundice, reticulocytosis, positive antibody screen, and positive Direct Antiglobulin Test (Coombs test). DHTRs are more common in patients with sickle cell disease who have received frequent transfusions.

These reactions are caused by the presence of a low titre antibody that is too weak to be detected during cross-match and unable to cause lysis at the time of transfusion. The severity of DHTRs depends on the immunogenicity or dose of the antigen. Blood group antibodies associated with DHTRs include those of the Kidd, Duffy, Kell, and MNS systems. Most DHTRs have a benign course and do not require treatment. However, severe haemolysis with anaemia and renal failure can occur, so monitoring of haemoglobin levels and renal function is necessary. If an antibody is detected, antigen-negative blood can be requested for future transfusions.

Here is a summary of the main transfusion reactions and complications:

1. Febrile transfusion reaction: Presents with a 1-degree rise in temperature from baseline, along with chills and malaise. It is the most common reaction and is usually caused by cytokines from leukocytes in transfused red cell or platelet components. Supportive treatment with paracetamol is helpful.

2. Acute haemolytic reaction: Symptoms include fever, chills, pain at the transfusion site, nausea, vomiting, and dark urine. It is the most serious type of reaction and often occurs due to ABO incompatibility from administration errors. The transfusion should be stopped, and IV fluids should be administered. Diuretics may be required.

3. Delayed haemolytic reaction: This reaction typically occurs 4-8 days after a blood transfusion and presents with fever, anaemia, jaundice and haemoglobuinuria. Direct antiglobulin (Coombs) test positive. Due to low titre antibody too weak to detect in cross-match and unable to cause lysis at time of transfusion. Most delayed haemolytic reactions have a benign course and require no treatment. Monitor anaemia and renal function and treat as required.

Most histamine receptors in the skin are of the H1 type. Therefore, when treating urticaria without airway compromise, it is appropriate to use an H1 blocking antihistamine such as chlorpheniramine, fexofenadine, or loratadine. However, if the case is mild and the trigger is easily identifiable and avoidable, NICE advises that no treatment may be necessary. In the given case, the trigger is not obvious. For more severe cases, an oral systemic steroid course like prednisolone 40 mg for 5 days may be used in addition to antihistamines. Topical steroids do not have a role in this treatment.

Further Reading:

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

Harmful drinking is when a person consumes at least 35 units of alcohol per week if they are a woman, or at least 50 units per week if they are a man. This level of drinking can lead to negative consequences for their mental and physical health.

Hazardous drinking, also known as increasing risk drinking, refers to a pattern of alcohol consumption that raises the likelihood of harm. For women, this means drinking more than 14 units but less than 35 units per week, while for men it means drinking more than 14 units but less than 50 units per week.

High-risk drinking, or harmful drinking, is a pattern of alcohol consumption that causes mental or physical damage. This occurs when a woman drinks 35 units or more per week, or when a man drinks 50 units or more per week.

Further Reading:

Alcoholic liver disease (ALD) is a spectrum of disease that ranges from fatty liver at one end to alcoholic cirrhosis at the other. Fatty liver is generally benign and reversible with alcohol abstinence, while alcoholic cirrhosis is a more advanced and irreversible form of the disease. Alcoholic hepatitis, which involves inflammation of the liver, can lead to the development of fibrotic tissue and cirrhosis.

Several factors can increase the risk of progression of ALD, including female sex, genetics, advanced age, induction of liver enzymes by drugs, and co-existent viral hepatitis, especially hepatitis C.

The development of ALD is multifactorial and involves the metabolism of alcohol in the liver. Alcohol is metabolized to acetaldehyde and then acetate, which can result in the production of damaging reactive oxygen species. Genetic polymorphisms and co-existing hepatitis C infection can enhance the pathological effects of alcohol metabolism.

Patients with ALD may be asymptomatic or present with non-specific symptoms such as abdominal discomfort, vomiting, or anxiety. Those with alcoholic hepatitis may have fever, anorexia, and deranged liver function tests. Advanced liver disease can manifest with signs of portal hypertension and cirrhosis, such as ascites, varices, jaundice, and encephalopathy.

Screening tools such as the AUDIT questionnaire can be used to assess alcohol consumption and identify hazardous or harmful drinking patterns. Liver function tests, FBC, and imaging studies such as ultrasound or liver biopsy may be performed to evaluate liver damage.

Management of ALD involves providing advice on reducing alcohol intake, administering thiamine to prevent Wernicke’s encephalopathy, and addressing withdrawal symptoms with benzodiazepines. Complications of ALD, such as intoxication, encephalopathy, variceal bleeding, ascites, hypoglycemia, and coagulopathy, require specialized interventions.

Heavy alcohol use can also lead to thiamine deficiency and the development of Wernicke Korsakoff’s syndrome, characterized by confusion, ataxia, hypothermia, hypotension, nystagmus, and vomiting. Prompt treatment is necessary to prevent progression to Korsakoff’s psychosis.

In summary, alcoholic liver disease is a spectrum of disease that can range from benign fatty liver to irreversible cirrhosis. Risk factors for progression include female sex, genetics, advanced age, drug-induced liver enzyme induction, and co-existing liver conditions.

Infantile hypertrophic pyloric stenosis is a condition characterized by the thickening and enlargement of the smooth muscle in the antrum of the stomach, leading to the narrowing of the pyloric canal. This narrowing can easily cause obstruction. It is a relatively common condition, occurring in about 1 in 500 live births, and is more frequently seen in males than females, with a ratio of 4 to 1. It is most commonly observed in first-born male children, although it can rarely occur in adults as well.

The main symptom of infantile hypertrophic pyloric stenosis is vomiting, which typically begins between 2 to 8 weeks of age. The vomit is usually non-bilious and forcefully expelled. It tends to occur around 30 to 60 minutes after feeding, leaving the baby hungry despite the vomiting. In some cases, there may be blood in the vomit. Other clinical features include persistent hunger, dehydration, weight loss, and constipation. An enlarged pylorus, often described as olive-shaped, can be felt in the right upper quadrant or epigastric in approximately 95% of cases. This is most noticeable at the beginning of a feed.

The typical acid-base disturbance seen in this condition is hypochloremic metabolic alkalosis. This occurs due to the loss of hydrogen and chloride ions in the vomit, as well as decreased secretion of pancreatic bicarbonate. The increased bicarbonate ions in the distal tubule of the kidney lead to the production of alkaline urine. Hyponatremia and hypokalemia are also commonly present.

Ultrasound scanning is the preferred diagnostic tool for infantile hypertrophic pyloric stenosis, as it is reliable and easy to perform. It has replaced barium studies as the investigation of choice.

Initial management involves fluid resuscitation, which should be tailored to the weight and degree of dehydration. Any electrolyte imbalances should also be corrected.

The definitive treatment for this condition is surgical intervention, with the Ramstedt pyloromyotomy being the procedure of choice. Laparoscopic pyloromyotomy is also an effective alternative if suitable facilities are available. The prognosis for infants with this condition is excellent, as long as there is no delay in diagnosis and treatment initiation.

The size of the cannula used for IV fluid infusion determines the maximum flow rate. For a 20g cannula, the maximum flow rate is around 60 ml per minute. As a result, the fastest infusion time through a 20g cannula is approximately 15 minutes for a maximum volume of 1000 ml.

Further Reading:

Peripheral venous cannulation is a procedure that should be performed following established guidelines to minimize the risk of infection, injury, extravasation, and early failure of the cannula. It is important to maintain good hand hygiene, use personal protective equipment, ensure sharps safety, and employ an aseptic non-touch technique during the procedure.

According to the National Institute for Health and Care Excellence (NICE), the skin should be disinfected with a solution of 2% chlorhexidine gluconate and 70% alcohol before inserting the catheter. It is crucial to allow the disinfectant to completely dry before inserting the cannula.

The flow rates of IV cannulas can vary depending on factors such as the gauge, color, type of fluid used, presence of a bio-connector, length of the cannula, and whether the fluid is drained under gravity or pumped under pressure. However, the following are typical flow rates for different gauge sizes: 14 gauge (orange) has a flow rate of 270 ml/minute, 16 gauge (grey) has a flow rate of 180 ml/minute, 18 gauge (green) has a flow rate of 90 ml/minute, 20 gauge (pink) has a flow rate of 60 ml/minute, and 22 gauge (blue) has a flow rate of 36 ml/minute. These flow rates are based on infusing 1000 ml of normal saline under ideal circumstances, but they may vary in practice.

Bacterial vaginosis (BV) is a common condition that affects up to a third of women during their childbearing years. It occurs when there is an overgrowth of bacteria, specifically Gardnerella vaginalis. This bacterium is anaerobic, meaning it thrives in environments without oxygen. As it multiplies, it disrupts the balance of bacteria in the vagina, leading to a rise in pH levels and a decrease in lactic acid-producing lactobacilli. It’s important to note that BV is not a sexually transmitted infection.

The main symptom of BV is a greyish discharge with a distinct fishy odor. However, it’s worth mentioning that around 50% of affected women may not experience any symptoms at all.

To diagnose BV, healthcare providers often use Amsel’s criteria. This involves looking for the presence of three out of four specific criteria: a vaginal pH greater than 4.5, a positive fishy smell test when potassium hydroxide is added, the presence of clue cells on microscopy, and a thin, white, homogeneous discharge.

The primary treatment for BV is oral metronidazole, typically taken for 5-7 days. This medication has an initial cure rate of about 75%. It’s crucial to provide special care to pregnant patients diagnosed with BV, as it has been linked to an increased risk of late miscarriage, early labor, and chorioamnionitis. Therefore, prompt treatment for these patients is of utmost importance.

To determine the amount of fluid that should be given to the 5-year-old child over the next 24 hours, we need to account for the following components of fluid therapy:

1. Deficit Replacement: The fluid lost due to dehydration.
2. Maintenance Fluid: The fluid needed for normal physiological needs.
3. Ongoing Losses: Any additional fluid loss (e.g., continued diarrhea or vomiting), which may need to be estimated and added if applicable.

Calculation Steps

1. Calculate the Fluid Deficit

The child is 10% dehydrated. This means that the child has lost 10% of their body weight in fluids.

• Body Weight: 20 kg
• Percentage Dehydration: 10%

Fluid Deficit=Body Weight×Percentage Dehydration

Fluid Deficit=20 kg×0.10=2 kg=2 liters=2000 ml

2. Calculate the Maintenance Fluid Requirement

Use the standard maintenance fluid calculation for children (the Holliday-Segar method):

• First 10 kg: 100 ml/kg/day
• Next 10 kg: 50 ml/kg/day

For a 20 kg child:

• First 10 kg: 10 kg×100 ml/kg/day=1000 ml/day
• Next 10 kg: 10 kg×50 ml/kg/day=500 ml/day

Total maintenance fluid requirement:

Maintenance Fluid=1000 ml+500 ml=1500 ml/day

3. Subtract the Initial Fluid Bolus

An initial fluid bolus of 20 ml/kg was given to treat shock:

• Fluid Bolus Given: 20 ml/kg×20 kg=400 ml

This amount should be subtracted from the deficit to avoid overhydration:

Remaining Deficit=2000 ml−400 ml=1600 ml

4. Total Fluid Requirement for 24 Hours

The total fluid requirement for the next 24 hours is the sum of the remaining deficit and the maintenance fluid:

Total Fluid for 24 hours=Remaining Deficit+Maintenance Fluid

Total Fluid for 24 hours=1600 ml+1500 ml=3100 ml

If you have missed one pill, which means it has been 48-72 hours since you took the last pill in your current packet or you started the first pill in a new packet 24-48 hours late, you need to take the missed pill as soon as you remember. Make sure to continue taking the remaining pills at your usual time. Emergency contraception is generally not necessary in this situation, but it may be worth considering if you have missed pills earlier in the packet or during the last week of the previous packet.

To diagnose diabetic ketoacidosis (DKA), all three of the following criteria must be present: ketonaemia (≥3 mmol/L) or ketonuria (> 2+ on urine dipstick), blood glucose > 11 mmol/L or known diabetes mellitus, and blood pH <7.3 or bicarbonate < 15 mmol/L. It is important to note that plasma osmolality and anion gap, although typically elevated in DKA, are not included in the diagnostic criteria. Further Reading: Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia. The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis. DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain. The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels. Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L. Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

The sepsis 6 pathway is a time-sensitive protocol that should be started promptly and all 6 initial steps should be completed within 1 hour. It is important not to confuse the sepsis 6 pathway with the 6 hour care bundle. Time is of the essence when managing septic patients, and initiating the sepsis 6 pathway immediately has been proven to enhance survival rates in sepsis patients.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

Patients with myxoedema coma often exhibit several common ECG abnormalities. These include bradycardia, a prolonged QT interval, and T wave flattening or inversion. Additionally, severe hypothyroidism (myxoedema) is associated with other ECG findings such as low QRS voltage, conduction blocks, and T wave inversions without ST deviation.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

Ketamine sedation in children should only be performed by a trained and competent clinician who is capable of managing complications, especially those related to the airway. The clinician should have completed the necessary training and have the appropriate skills for procedural sedation. It is important for the clinician to consider the length of the procedure before deciding to use ketamine sedation, as lengthy procedures may be more suitable for general anesthesia.

Examples of procedures where ketamine may be used in children include suturing, fracture reduction/manipulation, joint reduction, burn management, incision and drainage of abscess, tube thoracostomy placement, foreign body removal, and wound exploration/irrigation.

During the ketamine sedation procedure, a minimum of three staff members should be present: a doctor to manage the sedation and airway, a clinician to perform the procedure, and an experienced nurse to monitor and support the patient, family, and clinical staff. The child should be sedated and managed in a high dependency or resuscitation area with immediate access to resuscitation facilities. Monitoring should include sedation level, pain, ECG, blood pressure, respiration, pulse oximetry, and capnography, with observations taken and recorded every 5 minutes.

Prior to the procedure, consent should be obtained from the parent or guardian after discussing the proposed procedure and use of ketamine sedation. The risks and potential complications should be explained, including mild or moderate/severe agitation, rash, vomiting, transient clonic movements, and airway problems. The parent should also be informed that certain common side effects, such as nystagmus, random purposeless movements, muscle twitching, rash, and vocalizations, are of no clinical significance.

Topical anesthesia may be considered to reduce the pain of intravenous cannulation, but this step may not be advisable if the procedure is urgent. The clinician should also ensure that key resuscitation drugs are readily available and doses are calculated for the patient in case they are needed.

Before administering ketamine, the child should be prepared by encouraging the parents or guardians to talk to them about happy thoughts and topics to minimize unpleasant emergence phenomena. The dose of ketamine is typically 1.0 mg/kg by slow intravenous injection over at least one minute, with additional doses of 0.5 mg/kg administered as required after 5-10 minutes to achieve the desired dissociative state.

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.

Several studies have shown that elevating the head by 20-30 degrees is beneficial for increasing oxygen levels compared to lying flat on the back.

Further Reading:

Rapid sequence induction (RSI) is a method used to place an endotracheal tube (ETT) in the trachea while minimizing the risk of aspiration. It involves inducing loss of consciousness while applying cricoid pressure, followed by intubation without face mask ventilation. The steps of RSI can be remembered using the 7 P’s: preparation, pre-oxygenation, pre-treatment, paralysis and induction, protection and positioning, placement with proof, and post-intubation management.

Preparation involves preparing the patient, equipment, team, and anticipating any difficulties that may arise during the procedure. Pre-oxygenation is important to ensure the patient has an adequate oxygen reserve and prolongs the time before desaturation. This is typically done by breathing 100% oxygen for 3 minutes. Pre-treatment involves administering drugs to counter expected side effects of the procedure and anesthesia agents used.

Paralysis and induction involve administering a rapid-acting induction agent followed by a neuromuscular blocking agent. Commonly used induction agents include propofol, ketamine, thiopentone, and etomidate. The neuromuscular blocking agents can be depolarizing (such as suxamethonium) or non-depolarizing (such as rocuronium). Depolarizing agents bind to acetylcholine receptors and generate an action potential, while non-depolarizing agents act as competitive antagonists.

Protection and positioning involve applying cricoid pressure to prevent regurgitation of gastric contents and positioning the patient’s neck appropriately. Tube placement is confirmed by visualizing the tube passing between the vocal cords, auscultation of the chest and stomach, end-tidal CO2 measurement, and visualizing misting of the tube. Post-intubation management includes standard care such as monitoring ECG, SpO2, NIBP, capnography, and maintaining sedation and neuromuscular blockade.

Overall, RSI is a technique used to quickly and safely secure the airway in patients who may be at risk of aspiration. It involves a series of steps to ensure proper preparation, oxygenation, drug administration, and tube placement. Monitoring and post-intubation care are also important aspects of RSI.

This patient has presented with an Addisonian crisis, which is a rare but potentially catastrophic condition if not diagnosed promptly. The most likely underlying rheumatological diagnosis in this case is polymyalgia rheumatica, and it is likely that the GP started the patient on prednisolone medication.

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

An Addisonian crisis is most commonly triggered by the deliberate or accidental withdrawal of steroid therapy in patients with Addison’s disease. Other factors that can precipitate a crisis include infection, trauma, myocardial infarction, cerebral infarction, asthma, hypothermia, and alcohol abuse.

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

Biochemically, Addison’s disease is characterized by increased ACTH levels (as a compensatory response to stimulate the adrenal glands), elevated serum renin levels, hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, and metabolic acidosis. Diagnostic investigations may include the Synacthen test, plasma ACTH level, plasma renin level, and adrenocortical antibodies.

Management of Addison’s disease should be overseen by an Endocrinologist. Typically, patients require hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also need thyroxine if there is hypothalamic-pituitary disease present. Treatment is lifelong, and patients should carry a steroid card and a MedicAlert bracelet, being aware of the possibility of an Addisonian crisis.

The appendix is a slender and curved tube that is attached to the back and middle part of the caecum. It has a small triangular tissue called the mesoappendix that holds it in place from the tissue of the terminal ileum.

Although it contains a significant amount of lymphoid tissue, the appendix does not serve any important function in humans. The position of the free end of the appendix can vary greatly. There are five main locations where it can be found, with the most common being the retrocaecal and subcaecal positions.

The distribution of these positions is as follows:

– Ascending retrocaecal (64%)
– Subcaecal (32%)
– Transverse retrocaecal (2%)
– Ascending preileal (1%)
– Ascending retroileal (0.5%)

Hepatic encephalopathy is a condition caused by the accumulation of nitrogenous waste products in the body due to impaired liver function. These waste products cross the blood brain barrier and contribute to the production of glutamine, leading to changes in astrocyte osmotic pressure, brain edema, and neurotransmitter dysfunction.

To address hepatic encephalopathy, the first-line drugs used are Rifaximin and lactulose. Rifaximin is an oral antibiotic that helps reduce the presence of ammonia-producing bacteria in the intestines. Lactulose, on the other hand, converts soluble ammonia into insoluble ammonium and aids in relieving constipation.

It is important to note that Chlordiazepoxide, a benzodiazepine, may be used to treat alcohol withdrawal but should be avoided in cases of hepatic encephalopathy as it can worsen the condition.

Further Reading:

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

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

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

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

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

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

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

Methaemoglobinaemia is a condition characterized by high levels of haemoglobin with iron in the ferric (Fe3+) state. This occurs when haemoglobin is oxidized from Fe2+ to Fe3+. Normally, NADH methaemoglobin reductase, also known as Cytochrome b5 reductase, regulates this process by transferring electrons from NADH to methaemoglobin, converting it back to haemoglobin. However, if there is a congenital or acquired dysfunction in the NADH methaemoglobin reductase enzyme system, it can lead to elevated levels of haemoglobin with iron in the Fe3+ state. Unfortunately, Fe3+ is unable to bind to haemoglobin.

Further Reading:

Methaemoglobinaemia is a condition where haemoglobin is oxidised from Fe2+ to Fe3+. This process is normally regulated by NADH methaemoglobin reductase, which transfers electrons from NADH to methaemoglobin, converting it back to haemoglobin. In healthy individuals, methaemoglobin levels are typically less than 1% of total haemoglobin. However, an increase in methaemoglobin can lead to tissue hypoxia as Fe3+ cannot bind oxygen effectively.

Methaemoglobinaemia can be congenital or acquired. Congenital causes include haemoglobin chain variants (HbM, HbH) and NADH methaemoglobin reductase deficiency. Acquired causes can be due to exposure to certain drugs or chemicals, such as sulphonamides, local anaesthetics (especially prilocaine), nitrates, chloroquine, dapsone, primaquine, and phenytoin. Aniline dyes are also known to cause methaemoglobinaemia.

Clinical features of methaemoglobinaemia include slate grey cyanosis (blue to grey skin coloration), chocolate blood or chocolate cyanosis (brown color of blood), dyspnoea, low SpO2 on pulse oximetry (which often does not improve with supplemental oxygen), and normal PaO2 on arterial blood gas (ABG) but low SaO2. Patients may tolerate hypoxia better than expected. Severe cases can present with acidosis, arrhythmias, seizures, and coma.

Diagnosis of methaemoglobinaemia is made by directly measuring the level of methaemoglobin using a co-oximeter, which is present in most modern blood gas analysers. Other investigations, such as a full blood count (FBC), electrocardiogram (ECG), chest X-ray (CXR), and beta-human chorionic gonadotropin (bHCG) levels (in pregnancy), may be done to assess the extent of the condition and rule out other contributing factors.

Active treatment is required if the methaemoglobin level is above 30% or if it is below 30% but the patient is symptomatic or shows evidence of tissue hypoxia. Treatment involves maintaining the airway and delivering high-flow oxygen, removing the causative agents, treating toxidromes and consider giving IV dextrose 5%.

The symptoms and signs of strokes can vary depending on which blood vessel is affected. Here is a summary of the main symptoms based on the territory affected:

Anterior cerebral artery: This can cause weakness on the opposite side of the body, with the leg and shoulder being more affected than the arm, hand, and face. There may also be minimal loss of sensation on the opposite side of the body. Other symptoms can include difficulty speaking (dysarthria), language problems (aphasia), apraxia (difficulty with limb movements), urinary incontinence, and changes in behavior and personality.

Middle cerebral artery: This can lead to weakness on the opposite side of the body, with the face and arm being more affected than the leg. There may also be a loss of sensation on the opposite side of the body. Depending on the dominant hemisphere of the brain, there may be difficulties with expressive or receptive language (dysphasia). In the non-dominant hemisphere, there may be neglect of the opposite side of the body.

Posterior cerebral artery: This can cause a loss of vision on the opposite side of both eyes (homonymous hemianopia). There may also be defects in a specific quadrant of the visual field. In some cases, there may be a syndrome affecting the thalamus on the opposite side of the body.

It’s important to note that these are just general summaries and individual cases may vary. If you suspect a stroke, it’s crucial to seek immediate medical attention.

Addison’s disease occurs when the adrenal cortex is destroyed. The anterior pituitary gland produces and releases adrenocorticotropic hormone (ACTH), not the posterior pituitary gland. The adrenal cortex is responsible for producing cortisol, not the adrenal medulla.

Further Reading:

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

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

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

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

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

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

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

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

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

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

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

A 512 Hz tuning fork is recommended for conducting both the Rinne’s and Weber’s tests. However, a lower-pitched 128 Hz tuning fork is commonly used to assess vibration sense during a peripheral nervous system examination. Although a 256 Hz tuning fork can be used for both tests, it is considered less reliable.

To perform the Weber’s test, the 512 Hz tuning fork should be set in motion and then placed on the center of the patient’s forehead. The patient should be asked if they perceive the sound in the middle of their forehead or if it is heard more on one side.

If the sound is heard more on one side, it may indicate either ipsilateral conductive hearing loss or contralateral sensorineural hearing loss.

ACE inhibitors work by inhibiting the conversion of angiotensin I to angiotensin II. As a result, the effects of angiotensin II are reduced, leading to the dilation of vascular smooth muscle and the efferent arteriole of the glomerulus. This, in turn, has several effects on renal measurements. Firstly, it causes an increase in renal plasma flow. Secondly, it leads to a decrease in filtration fraction. Lastly, it results in a decrease in glomerular filtration rate.

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.

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

Heat stroke happens when the body’s ability to regulate temperature is overwhelmed by a combination of excessive environmental heat, excessive production of heat from exertion, and inadequate heat loss. Several risk factors increase the likelihood of developing heat stroke, including hot and humid environmental conditions, age (particularly the elderly and infants), physical factors like obesity and excessive exertion, medical conditions like anorexia and cardiovascular disease, and certain medications such as alcohol, amphetamines, and diuretics.

The typical clinical features of heat stroke include a core temperature above 40.6°C, early symptoms like extreme fatigue, headache, syncope, facial flushing, vomiting, and diarrhea. The skin is usually hot and dry, although sweating may occur in around 50% of cases of exertional heat stroke. The loss of the ability to sweat is a late and concerning sign. Hyperventilation is almost always present. Heat stroke can also lead to cardiovascular dysfunction, respiratory dysfunction, central nervous system dysfunction, and potentially multi-organ failure, coagulopathy, and rhabdomyolysis if the temperature rises above 41.5°C.

Heat cramps, on the other hand, are characterized by intense thirst and muscle cramps. Body temperature is often elevated but typically remains below 40°C. Sweating, heat dissipation mechanisms, and cognition are preserved, and there is no neurological impairment. Heat exhaustion usually precedes heat stroke and if left untreated, can progress to heat stroke. Heat dissipation is still functioning, and the body temperature is usually below 41°C. Symptoms of heat exhaustion include nausea, oliguria, weakness, headache, thirst, and sinus tachycardia. Central nervous system functioning is usually largely preserved, and patients may complain of feeling hot and appear flushed and sweaty.

It is important to note that malignant hyperthermia and neuroleptic malignant syndrome are highly unlikely in this scenario as the patient has no recent history of a general anesthetic or taking phenothiazines or other antipsychotics, respectively.

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

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

The ATLS guidelines categorize chest injuries in trauma into two groups: life-threatening injuries that require immediate identification and treatment in the primary survey, and potentially life-threatening injuries that should be identified and treated in the secondary survey.

During the primary survey, the focus is on identifying and treating life-threatening thoracic injuries. These include airway obstruction, tracheobronchial tree injury, tension pneumothorax, open pneumothorax, massive haemothorax, and cardiac tamponade. Prompt recognition and intervention are crucial in order to prevent further deterioration and potential fatality.

In the secondary survey, attention is given to potentially life-threatening injuries that may not be immediately apparent. These include simple pneumothorax, haemothorax, flail chest, pulmonary contusion, blunt cardiac injury, traumatic aortic disruption, traumatic diaphragmatic injury, and blunt oesophageal rupture. These injuries may not pose an immediate threat to life, but they still require identification and appropriate management to prevent complications and ensure optimal patient outcomes.

By dividing chest injuries into these two categories and addressing them in a systematic manner, healthcare providers can effectively prioritize and manage trauma patients, ultimately improving their chances of survival and recovery.

This patient is currently experiencing a secondary haemorrhage after undergoing a dental extraction. There are three different types of haemorrhage that can occur following a dental extraction. The first type is immediate haemorrhage, which happens during the extraction itself. The second type is reactionary haemorrhage, which typically occurs 2-3 hours after the extraction when the vasoconstrictor effects of the local anaesthetic wear off. Lastly, there is secondary haemorrhage, which usually happens at around 48-72 hours after the extraction and is a result of the clot becoming infected.

The GMC provides guidance on confidentiality that highlights the importance of assessing whether adults have the ability to give consent for the disclosure of their medical information. If the patient is capable, meaning they can comprehend relevant information, retain it, evaluate it, and communicate their decision, then their preferences should be honored, even if you believe their decision is unwise or puts them at risk of serious harm.

In the event that the patient has the capacity but you believe it would be beneficial to involve social services, you can encourage them to allow you to contact them. However, it is crucial to respect their decision if they decline. On the other hand, if the patient lacks capacity, the doctor should make a decision based on what is in their best interests, which may include raising a concern for their protection.

Tricuspid regurgitation leads to a pansystolic murmur that is most pronounced in the tricuspid area during inhalation. The primary cause of tricuspid regurgitation is right ventricular failure.

Other clinical signs that may be present in tricuspid regurgitation include a raised jugular venous pressure (JVP) and giant C-V waves. Additionally, features of increased right atrial pressure, such as ascites and dependent edema, may be observed. Pulsatile hepatomegaly and a thrill at the left sternal edge are also possible indicators. Reverse splitting of the second heart sound, due to early closure of the pulmonary valve, and a third heart sound, caused by rapid right ventricular filling, may be heard as well.

Aortic regurgitation, on the other hand, produces an early diastolic murmur that is most audible at the lower left sternal edge when the patient is sitting forward and exhaling.

In the case of mitral stenosis, a rumbling mid-diastolic murmur is best heard at the apex while the patient is in the left lateral position and exhaling, using the bell of the stethoscope.

Atrial myxomas are benign tumors that can develop in the heart. Most commonly found on the left side, they may obstruct the mitral valve, resulting in a mid-diastolic murmur similar to that of mitral stenosis.

Lastly, left anterior descending artery stenosis can cause an early diastolic murmur, also known as Dock’s murmur. This murmur is similar to that of aortic regurgitation and is best heard at the left 2nd or 3rd intercostal space.