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

Chest X-rays are not typically recommended as a routine investigation for acute asthma. However, they may be necessary in specific situations. These situations include suspected pneumomediastinum or consolidation, as well as cases of life-threatening asthma. Additionally, if a patient fails to respond adequately to treatment or requires ventilation, a chest X-ray may be performed. It is important to note that these circumstances warrant the use of chest X-rays, but they are not routinely indicated for the investigation of acute asthma.

Ondansetron is a medication that works by blocking serotonin receptors in the body. It is commonly used as a first-line treatment for postoperative nausea and vomiting (PONV), which can occur after procedures done under sedation or anesthesia.

Further Reading:

postoperative nausea and vomiting (PONV) is a common occurrence following procedures performed under sedation or anesthesia. It can be highly distressing for patients. Several risk factors have been identified for PONV, including female gender, a history of PONV or motion sickness, non-smoking status, patient age, use of volatile anesthetics, longer duration of anesthesia, perioperative opioid use, use of nitrous oxide, and certain types of surgery such as abdominal and gynecological procedures.

To manage PONV, antiemetics are commonly used. These medications work by targeting different receptors in the body. Cyclizine and promethazine are histamine H1-receptor antagonists, which block the action of histamine and help reduce nausea and vomiting. Ondansetron is a serotonin 5-HT3 receptor antagonist, which blocks the action of serotonin and is effective in preventing and treating PONV. Prochlorperazine is a dopamine D2 receptor antagonist, which blocks the action of dopamine and helps alleviate symptoms of nausea and vomiting. Metoclopramide is also a dopamine D2 receptor antagonist and a 5-HT3 receptor antagonist, providing dual action against PONV. It is also a 5-HT4 receptor agonist, which helps improve gastric emptying and reduces the risk of PONV.

Assessment and management of PONV involves a comprehensive approach. Healthcare professionals need to assess the patient’s risk factors for PONV and take appropriate measures to prevent its occurrence. This may include selecting the appropriate anesthesia technique, using antiemetics prophylactically, and providing adequate pain control. In cases where PONV does occur, prompt treatment with antiemetics should be initiated to alleviate symptoms and provide relief to the patient. Close monitoring of the patient’s condition and response to treatment is essential to ensure effective management of PONV.

Penicillin is frequently responsible for drug-induced anaphylaxis, making it the primary cause. Following closely behind are NSAIDs, which are the second most common cause. Additionally, ACE inhibitors and aspirin are commonly associated with anaphylaxis.

Haloperidol, when administered during the third trimester of pregnancy, can lead to extrapyramidal symptoms in the newborn. These symptoms may include agitation, poor feeding, excessive sleepiness, and difficulty breathing. The severity of these side effects can vary, with some infants requiring intensive care and extended hospital stays. It is important to closely monitor exposed neonates for signs of extrapyramidal syndrome or withdrawal. Haloperidol should only be used during pregnancy if the benefits clearly outweigh the risks to the fetus.

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

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

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

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

Benzodiazepines (e.g. diazepam): When administered late in pregnancy, these drugs can cause respiratory depression and a neonatal withdrawal syndrome.

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

Carbamazepine: This drug can lead to hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol: Administration of chloramphenicol can cause gray baby syndrome in newborns.

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

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

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

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

The Civil Contingencies Act 2004 establishes a framework for civil protection in the United Kingdom. This legislation categorizes local responders to major incidents into two groups, each with their own set of responsibilities.

Category 1 responders consist of organizations that play a central role in responding to most emergencies, such as the emergency services, local authorities, and NHS bodies. These Category 1 responders are obligated to fulfill a comprehensive range of civil protection duties. These duties include assessing the likelihood of emergencies occurring and using this information to inform contingency planning. They must also develop emergency plans, establish business continuity management arrangements, and ensure that information regarding civil protection matters is readily available to the public. Additionally, Category 1 responders are responsible for maintaining systems to warn, inform, and advise the public in the event of an emergency. They are expected to share information with other local responders to enhance coordination and efficiency. Furthermore, local authorities within this category are required to provide guidance and support to businesses and voluntary organizations regarding business continuity management.

On the other hand, Category 2 organizations, such as the Health and Safety Executive, transport companies, and utility companies, are considered co-operating bodies. While they may not be directly involved in the core planning work, they play a crucial role in incidents that impact their respective sectors. Category 2 responders have a more limited set of duties, primarily focused on cooperating and sharing relevant information with both Category 1 and Category 2 responders.

For more information on this topic, please refer to the Civil Contingencies Act 2004.

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In this case, the patient has already received two doses of benzodiazepine and is currently on a phenytoin infusion. However, despite these treatments, the seizures persist, and it has been 20 minutes since the infusion started. At this point, the preferred treatment option is to induce general anesthesia. The induction agents that can be considered include thiopental sodium, propofol, and midazolam. There is no need to administer intravenous thiamine in this situation.

The management of status epilepticus involves several general measures, which are outlined in the following table:

1st stage (Early status, 0-10 minutes):
– Secure the airway and provide resuscitation
– Administer oxygen
– Assess cardiorespiratory function
– Establish intravenous access

2nd stage (0-30 minutes):
– Implement regular monitoring
– Consider the possibility of non-epileptic status
– Initiate emergency antiepileptic drug (AED) therapy
– Perform emergency investigations
– Administer glucose or intravenous thiamine if alcohol abuse or impaired nutrition is suspected
– Treat severe acidosis if present

3rd stage (0-60 minutes):
– Determine the underlying cause of status epilepticus
– Notify the anesthetist and intensive care unit (ITU)
– Identify and treat any medical complications
– Consider pressor therapy if necessary

4th stage (30-90 minutes):
– Transfer the patient to the intensive care unit
– Establish intensive care and EEG monitoring
– Initiate long-term maintenance AED therapy
– Perform further investigations as needed, such as brain imaging or lumbar puncture

Emergency investigations include blood tests for gases, glucose, renal and liver function, calcium and magnesium levels, full blood count (including platelets), blood clotting, and AED drug levels. Serum and urine samples should be saved for future analysis, including toxicology if the cause of convulsive status epilepticus is uncertain. A chest radiograph may be done to evaluate the possibility of aspiration. Additional investigations depend on the clinical circumstances and may include brain imaging or lumbar puncture.

Monitoring during the management of status epilepticus involves regular neurological observations and measurements of pulse, blood pressure, and temperature.

Blood transfusion is a crucial medical treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion usage, errors and adverse reactions still occur.

One serious complication is acute haemolytic transfusion reactions, which happen when incompatible red cells are transfused and react with the patient’s own antibodies. This usually occurs due to human error, such as mislabelling sample tubes or request forms. Symptoms of this reaction include a feeling of impending doom, fever, chills, pain and warmth at the transfusion site, nausea, vomiting, and back, joint, and chest pain. Immediate action should be taken to stop the transfusion, replace the donor blood with normal saline or another suitable crystalloid, and check the blood to confirm the intended recipient. IV diuretics may be administered to increase renal blood flow, and urine output should be maintained.

Another common complication is febrile transfusion reaction, which presents with a 1-degree rise in temperature from baseline, along with chills and malaise. This reaction is usually caused by cytokines from leukocytes in the transfused blood components. Supportive treatment is typically sufficient, and paracetamol can be helpful.

Allergic reactions can also occur, usually due to foreign plasma proteins or anti-IgA. These reactions often present with urticaria, pruritus, and hives, and in severe cases, laryngeal edema or bronchospasm may occur. Symptomatic treatment with antihistamines is usually enough, and there is usually no need to stop the transfusion. However, if anaphylaxis occurs, the transfusion should be stopped, and the patient should be administered adrenaline and treated according to the ALS protocol.

Transfusion-related acute lung injury (TRALI) is a severe complication characterized by non-cardiogenic pulmonary edema within 6 hours of transfusion. It is associated with antibodies in the donor blood reacting with recipient leukocyte antigens. This is the most common cause of death related to transfusion reactions. Treatment involves stopping the transfusion, administering oxygen, and providing aggressive respiratory support in approximately 75% of patients. Diuretic usage should be avoided.

Lipohaemathrosis is commonly seen in the suprapatellar pouch in individuals who have tibial plateau fractures. Notable X-ray characteristics of tibial plateau fractures include a visible fracture of the tibial plateau and the presence of lipohaemathrosis in the suprapatellar pouch.

Further Reading:

Tibial plateau fractures are a type of traumatic lower limb and joint injury that can involve the medial or lateral tibial plateau, or both. These fractures are classified using the Schatzker classification, with higher grades indicating a worse prognosis. X-ray imaging can show visible fractures of the tibial plateau and the presence of lipohaemathrosis in the suprapatellar pouch. However, X-rays often underestimate the severity of these fractures, so CT scans are typically used for a more accurate assessment.

Tibial spine fractures, on the other hand, are separate from tibial plateau fractures. They occur when the tibial spine is avulsed by the anterior cruciate ligament (ACL). This can happen due to forced knee hyperextension or a direct blow to the femur when the knee is flexed. These fractures are most common in children aged 8-14.

Tibial tuberosity avulsion fractures primarily affect adolescent boys and are often caused by jumping or landing from a jump. These fractures can be associated with Osgood-Schlatter disease. The treatment for these fractures depends on their grading. Low-grade fractures may be managed with immobilization for 4-6 weeks, while more significant avulsions are best treated with surgical fixation.

Whooping cough, also known as pertussis, 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. This 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 symptoms like low-grade fever and a runny nose. A cough may be present, but it is usually mild compared to the second stage. The catarrhal stage typically lasts for about a week.

The second stage is known as the paroxysmal stage. During this phase, the cough becomes more severe as the catarrhal symptoms start to subside. 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 time. The later stages of this phase 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.

Public Health England (PHE) provides recommendations for testing whooping cough based on the patient’s age, time since onset of illness, and severity of symptoms. For infants under 12 months of age who are hospitalized, PCR testing is recommended. Non-hospitalized infants within two weeks of symptom onset should undergo culture testing of a nasopharyngeal swab or aspirate. Non-hospitalized infants presenting over two weeks after symptom onset should be tested for anti-pertussis toxin IgG antibody levels using serology.

For children over 12 months of age and adults, culture testing of a nasopharyngeal swab or aspirate is recommended within two weeks of symptom onset. Children aged 5 to 16 who have not received the vaccine within the last year and present over two weeks after symptom onset should undergo oral fluid testing for anti-pertussis toxin IgG antibody levels. Children under 5 or adults over

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.

This patient’s medical history suggests a diagnosis of Guillain-Barré syndrome (GBS). GBS typically presents with initial symptoms of sensory changes or pain, accompanied by muscle weakness in the hands and/or feet. This weakness often spreads to the arms and upper body, affecting both sides. During the acute phase, GBS can be life-threatening, with around 15% of patients experiencing respiratory muscle weakness and requiring mechanical ventilation.

The exact cause of GBS is unknown, but it is believed to involve an autoimmune response where the body’s immune system attacks the myelin sheath surrounding the peripheral nerves. In about 75% of cases, there is a preceding infection, commonly affecting the gastrointestinal or respiratory tracts.

In this particular case, the most likely underlying cause is Campylobacter jejuni, a gastrointestinal pathogen. This is supported by the recent history of a severe diarrheal illness.

Amiodarone functions by inhibiting voltage-gated potassium channels, leading to an extended repolarization period and decreased excitability of the heart muscle.

Further Reading:

In the management of respiratory and cardiac arrest, several drugs are commonly used to help restore normal function and improve outcomes. Adrenaline is a non-selective agonist of adrenergic receptors and is administered intravenously at a dose of 1 mg every 3-5 minutes. It works by causing vasoconstriction, increasing systemic vascular resistance (SVR), and improving cardiac output by increasing the force of heart contraction. Adrenaline also has bronchodilatory effects.

Amiodarone is another drug used in cardiac arrest situations. It blocks voltage-gated potassium channels, which prolongs repolarization and reduces myocardial excitability. The initial dose of amiodarone is 300 mg intravenously after 3 shocks, followed by a dose of 150 mg after 5 shocks.

Lidocaine is an alternative to amiodarone in cardiac arrest situations. It works by blocking sodium channels and decreasing heart rate. The recommended dose is 1 mg/kg by slow intravenous injection, with a repeat half of the initial dose after 5 minutes. The maximum total dose of lidocaine is 3 mg/kg.

Magnesium sulfate is used to reverse myocardial hyperexcitability associated with hypomagnesemia. It is administered intravenously at a dose of 2 g over 10-15 minutes. An additional dose may be given if necessary, but the maximum total dose should not exceed 3 g.

Atropine is an antagonist of muscarinic acetylcholine receptors and is used to counteract the slowing of heart rate caused by the parasympathetic nervous system. It is administered intravenously at a dose of 500 mcg every 3-5 minutes, with a maximum dose of 3 mg.

Naloxone is a competitive antagonist for opioid receptors and is used in cases of respiratory arrest caused by opioid overdose. It has a short duration of action, so careful monitoring is necessary. The initial dose of naloxone is 400 micrograms, followed by 800 mcg after 1 minute. The dose can be gradually escalated up to 2 mg per dose if there is no response to the preceding dose.

It is important for healthcare professionals to have knowledge of the pharmacology and dosing schedules of these drugs in order to effectively manage respiratory and cardiac arrest situations.

In the treatment of diabetic ketoacidosis (DKA), it is important to continue the infusion of insulin until certain criteria are met. These criteria include ketone levels being less than 0.3 mmol/L and the pH of the blood being above 7.3 or the bicarbonate levels being above 18 mmol/L. Additionally, the patient should feel comfortable enough to eat at this point. It is crucial not to stop the intravenous insulin infusion until at least 30 minutes after administering subcutaneous short-acting insulin.

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.

Pericardial friction rub is a common finding in pericarditis and is often described as a sound similar to squeaking leather. This patient exhibits symptoms that are consistent with acute pericarditis, including flu-like illness with muscle pain and fatigue, chest pain that worsens when lying down and improves when sitting up or leaning forward, and the presence of a pleural rub. The gradual onset of symptoms rules out conditions like pulmonary embolism or acute myocardial ischemia. It is important to note that while the pericardial rub is often considered part of the classic triad of clinical features, it is only present in about one-third of patients. Additionally, the rub may come and go, so repeated examinations may increase the chances of detecting this sign.

Further Reading:

Pericarditis is an inflammation of the pericardium, which is the protective sac around the heart. It can be acute, lasting less than 6 weeks, and may present with chest pain, cough, dyspnea, flu-like symptoms, and a pericardial rub. The most common causes of pericarditis include viral infections, tuberculosis, bacterial infections, uremia, trauma, and autoimmune diseases. However, in many cases, the cause remains unknown. Diagnosis is based on clinical features, such as chest pain, pericardial friction rub, and electrocardiographic changes. Treatment involves symptom relief with nonsteroidal anti-inflammatory drugs (NSAIDs), and patients should avoid strenuous activity until symptoms improve. Complicated cases may require treatment for the underlying cause, and large pericardial effusions may need urgent drainage. In cases of purulent effusions, antibiotic therapy is necessary, and steroid therapy may be considered for pericarditis related to autoimmune disorders or if NSAIDs alone are ineffective.

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

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

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

Anaphylaxis, also known as anaphylactic shock, is characterized by certain symptoms similar to other types of shock. These symptoms include low blood pressure (hypotension), rapid heart rate (tachycardia), irregular heart rhythm (arrhythmia), changes in the electrocardiogram (ECG) indicating reduced blood flow to the heart (myocardial ischemia), such as ST elevation, and in severe cases, cardiac arrest.

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

According to the latest guidelines from NICE, it is recommended that adult patients who are undergoing treatment for acute leukaemia, stem cell transplants, or solid tumours and are expected to experience significant neutropenia as a result of chemotherapy, should be offered prophylaxis with a fluoroquinolone such as ciprofloxacin (500 mg taken orally twice daily) during the period when neutropenia is expected. This is to help prevent the occurrence of neutropenic sepsis, a serious infection that can occur in cancer patients with low levels of neutrophils.

Reference:
NICE guidance: ‘Neutropenic sepsis: prevention and management of neutropenic sepsis in cancer patients’

Altitude sickness is usually experienced at altitudes above 2,500 meters (8,000 ft), although some individuals may be affected at lower altitudes. It is important to note that climbers in the UK, where the highest peak is Ben Nevis at 1,345 meters, do not need to worry about altitude sickness.

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.

The top priority when dealing with suspected epiglottitis is to assess and secure the airway. This is especially important in patients who have not been vaccinated against Haemophilus influenzae type b (HiB), as they are at risk for complications from this infection. Classic signs of epiglottitis include tripod positioning, drooling, stridor, and a muffled voice. It is crucial to avoid agitating patients, particularly children, during examination or procedures, as this can trigger laryngospasm and potentially lead to airway obstruction. In such cases, it is recommended to call in senior ENT and anaesthetic support to perform laryngoscopy and be prepared for intubation or tracheostomy if necessary to address any airway compromise. If the patient is in a critical condition, securing the airway through intubation becomes the top priority.

Further Reading:

Epiglottitis is a rare but serious condition characterized by inflammation and swelling of the epiglottis, which can lead to a complete blockage of the airway. It is more commonly seen in children between the ages of 2-6, but can also occur in adults, particularly those in their 40s and 50s. Streptococcus infections are now the most common cause of epiglottitis in the UK, although other bacterial agents, viruses, fungi, and iatrogenic causes can also be responsible.

The clinical features of epiglottitis include a rapid onset of symptoms, high fever, sore throat, painful swallowing, muffled voice, stridor and difficulty breathing, drooling of saliva, irritability, and a characteristic tripod positioning with the arms forming the front two legs of the tripod. It is important for healthcare professionals to avoid examining the throat or performing any potentially upsetting procedures until the airway has been assessed and secured.

Diagnosis of epiglottitis is typically made through fibre-optic laryngoscopy, which is considered the gold standard investigation. Lateral neck X-rays may also show a characteristic thumb sign, indicating an enlarged and swollen epiglottis. Throat swabs and blood cultures may be taken once the airway is secured to identify the causative organism.

Management of epiglottitis involves assessing and securing the airway as the top priority. Intravenous or oral antibiotics are typically prescribed, and supplemental oxygen may be given if intubation or tracheostomy is planned. In severe cases where the airway is significantly compromised, intubation or tracheostomy may be necessary. Steroids may also be used, although the evidence for their benefit is limited.

Overall, epiglottitis is a potentially life-threatening condition that requires urgent medical attention. Prompt diagnosis, appropriate management, and securing the airway are crucial in ensuring a positive outcome for patients with this condition.

Epididymo-orchitis refers to the inflammation of the epididymis and/or testicle. It typically presents with sudden pain, swelling, and inflammation in the affected area. This condition can also occur chronically, which means that the pain and inflammation last for more than six months.

The causes of epididymo-orchitis vary depending on the age of the patient. In men under 35 years old, the infection is usually sexually transmitted and caused by Chlamydia trachomatis or Neisseria gonorrhoeae. In men over 35 years old, the infection is usually non-sexually transmitted and occurs as a result of enteric organisms that cause urinary tract infections, with Escherichia coli being the most common. However, there can be some overlap between these groups, so it is important to obtain a thorough sexual history in all age groups.

Mumps should also be considered as a potential cause of epididymo-orchitis in the 15 to 30 age group, as mumps orchitis occurs in around 40% of post-pubertal boys with mumps.

While most cases of epididymo-orchitis are infective, non-infectious causes can also occur. These include genito-urinary surgery, vasectomy, urinary catheterization, Behcet’s disease, sarcoidosis, and drug-induced cases such as those caused by amiodarone.

Patients with epididymo-orchitis typically present with unilateral scrotal pain and swelling that develops relatively quickly. The affected testis will be tender to touch, and there is usually a palpable swelling of the epididymis that starts at the lower pole of the testis and spreads towards the upper pole. The testis itself may also be involved, and there may be redness and/or swelling of the scrotum on the affected side. Patients may experience fever and urethral discharge as well.

The most important differential diagnosis to consider is testicular torsion, which requires immediate medical attention within 6 hours of onset to save the testicle. Testicular torsion is more likely in men under the age of 20, especially if the pain is very severe and sudden. It typically presents around four hours after onset. In this case, the patient’s age, longer history of symptoms, and the presence of fever are more indicative of epididymo-orchitis.

Psittacosis is a type of infection that can be transmitted from animals to humans, caused by a bacterium called Chlamydia psittaci. It is most commonly seen in people who own domestic birds, as well as those who work in pet shops or zoos. The typical symptoms of psittacosis include pneumonia that is acquired within the community, along with flu-like symptoms. Many patients also experience severe headaches and sensitivity to light. Enlargement of the spleen is a common finding in about two-thirds of individuals with this infection.

Infected individuals often develop a rash on their face, known as Horder’s spots, which appear as reddish macules. In some cases, erythema nodosum and erythema multiforme may also occur. The recommended treatment for psittacosis is a course of tetracycline or doxycycline for a period of 2-3 weeks.

On the other hand, rose spots are typically observed in cases of typhoid fever. These spots have a similar appearance to Horder’s spots but are usually found on the trunk rather than the face. Erythema marginatum is a pale red rash seen in rheumatic fever, while malar flush, also known as ‘mitral facies’, refers to the reddish discoloration of the cheeks commonly seen in individuals with mitral stenosis. Lastly, erythema chronicum migrans is the distinctive rash seen in Lyme disease, characterized by a circular rash with a central ‘bulls-eye’ appearance that spreads outward from the site of a tick bite.

The presence of borborygmi in the epigastrium can indicate that the endotracheal tube (ETT) is incorrectly placed in the esophagus. There are several ways to verify the correct placement of the endotracheal tube (ETT).

One method is through direct visualization, where the ETT is observed passing through the vocal cords. Another method is by checking for fogging in the ETT, which can indicate proper placement. Auscultation of bilateral equal breath sounds is also a reliable way to confirm correct ETT placement.

Additionally, the absence of borborygmi in the epigastrium is a positive sign that the ETT is in the correct position. Capnography or using a CO2 detector can provide further confirmation of proper ETT placement. Finally, chest radiography can be used to visually assess the placement of the endotracheal tube.

The therapeutic range for lithium typically falls between 0.4-0.8 mmol/l, although this range may differ depending on the laboratory. In general, the lower end of the range is the desired level for maintenance therapy and treatment in older individuals. Toxic effects are typically observed when levels exceed 1.5 mmol/l.

Nephrogenic diabetes insipidus may develop in a certain percentage of individuals who take lithium.

Further Reading:

Diabetes insipidus (DI) is a condition characterized by either a decrease in the secretion of antidiuretic hormone (cranial DI) or insensitivity to antidiuretic hormone (nephrogenic DI). Antidiuretic hormone, also known as arginine vasopressin, is produced in the hypothalamus and released from the posterior pituitary. The typical biochemical disturbances seen in DI include elevated plasma osmolality, low urine osmolality, polyuria, and hypernatraemia.

Cranial DI can be caused by various factors such as head injury, CNS infections, pituitary tumors, and pituitary surgery. Nephrogenic DI, on the other hand, can be genetic or result from electrolyte disturbances or the use of certain drugs. Symptoms of DI include polyuria, polydipsia, nocturia, signs of dehydration, and in children, irritability, failure to thrive, and fatigue.

To diagnose DI, a 24-hour urine collection is done to confirm polyuria, and U&Es will typically show hypernatraemia. High plasma osmolality with low urine osmolality is also observed. Imaging studies such as MRI of the pituitary, hypothalamus, and surrounding tissues may be done, as well as a fluid deprivation test to evaluate the response to desmopressin.

Management of cranial DI involves supplementation with desmopressin, a synthetic form of arginine vasopressin. However, hyponatraemia is a common side effect that needs to be monitored. In nephrogenic DI, desmopressin supplementation is usually not effective, and management focuses on ensuring adequate fluid intake to offset water loss and monitoring electrolyte levels. Causative drugs need to be stopped, and there is a risk of developing complications such as hydroureteronephrosis and an overdistended bladder.

Neonatal jaundice is a complex subject, and it is crucial for candidates to have knowledge about the different causes, presentations, and management of conditions that lead to jaundice in newborns. Neonatal jaundice can be divided into two groups: unconjugated hyperbilirubinemia, which can be either physiological or pathological, and conjugated hyperbilirubinemia, which is always pathological.

The causes of neonatal jaundice can be categorized as follows:

Haemolytic unconjugated hyperbilirubinemia:
– Intrinsic causes of haemolysis include hereditary spherocytosis, G6PD deficiency, sickle-cell disease, and pyruvate kinase deficiency.
– Extrinsic causes of haemolysis include haemolytic disease of the newborn and Rhesus disease.

Non-haemolytic unconjugated hyperbilirubinemia:
– Breastmilk jaundice, cephalhaematoma, polycythemia, infection (particularly urinary tract infections), Gilbert syndrome.

Hepatic conjugated hyperbilirubinemia:
– Hepatitis A and B, TORCH infections, galactosaemia, alpha 1-antitrypsin deficiency, drugs.

Post-hepatic conjugated hyperbilirubinemia:
– Biliary atresia, bile duct obstruction, choledochal cysts.

By understanding these different categories and their respective examples, candidates will be better equipped to handle neonatal jaundice cases.

The management of anaphylaxis involves several important steps. First and foremost, it is crucial to ensure proper airway management. Additionally, early administration of adrenaline is essential, preferably in the anterolateral aspect of the middle third of the thigh. Aggressive fluid resuscitation is also necessary. In severe cases, intubation may be required. However, it is important to note that the administration of chlorpheniramine and hydrocortisone should only be considered after early resuscitation has taken place.

Adrenaline is the most vital medication for treating anaphylactic reactions. It acts as an alpha-adrenergic receptor agonist, which helps reverse peripheral vasodilatation and reduce oedema. Furthermore, its beta-adrenergic effects aid in dilating the bronchial airways, increasing the force of myocardial contraction, and suppressing histamine and leukotriene release. Administering adrenaline as the first drug is crucial, and the intramuscular (IM) route is generally the most effective for most individuals.

The recommended doses of IM adrenaline for different age groups during anaphylaxis are as follows:

– Children under 6 years: 150 mcg (0.15 mL of 1:1000)
– Children aged 6-12 years: 300 mcg (0.3 mL of 1:1000)
– Children older than 12 years: 500 mcg (0.5 mL of 1:1000)
– Adults: 500 mcg (0.5 mL of 1:1000)

An advanced decision is a legally binding document that allows individuals to express their preferences for end-of-life care in advance. It serves as a means of communication between patients, healthcare professionals, and family members, ensuring that the patient’s wishes are understood and respected. In situations where a patient becomes unable to make informed decisions about their care due to the progression of their illness, an advanced directive can help prevent any confusion or disagreements.

According to the General Medical Council (GMC), if there is a significant difference of opinion within the healthcare team or between the team and the patient’s loved ones regarding the patient’s care, it is advisable to seek advice or a second opinion from a colleague who has relevant expertise. In this particular case, it would be wise to consult a palliative care specialist to help resolve the disagreement between yourself and the patient’s wife.

For more information, you can refer to the GMC guidelines on treatment and care towards the end of life, which provide guidance on good practice in decision making.

Diagnosing spontaneous bacterial peritonitis (SBP) requires an abdominal paracentesis of ascitic tap. Other reasons for performing a diagnostic tap include determining the cause of ascites, distinguishing between transudate and exudate, and detecting cancerous cells. Additionally, a therapeutic paracentesis can be done to alleviate respiratory distress or abdominal pain caused by the ascites.

However, there are certain contraindications to consider. These include having an uncooperative patient, a skin infection at the proposed puncture site, being pregnant, or experiencing severe bowel distension. Relative contraindications involve having severe thrombocytopenia (platelet count less than 20 x 103/μL) or coagulopathy (INR greater than 2.0).

For patients with an INR greater than 2.0, it is recommended to administer fresh frozen plasma (FFP) before the procedure. One approach is to infuse one unit of fresh frozen plasma prior to the procedure and then proceed with the paracentesis while the second unit is being infused.

In the case of patients with a platelet count lower than 20 x 103/μL, it is advisable to provide a platelet infusion before the procedure.

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

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

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

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

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