The BTS guidelines for acute asthma in children recommend administering oral steroids early in the treatment of asthma attacks. It is advised to give a dose of 20 mg prednisolone for children aged 2–5 years and a dose of 30–40 mg for children over 5 years old. If a child is already taking maintenance steroid tablets, they should receive 2 mg/kg prednisolone, up to a maximum dose of 60 mg. If a child vomits after taking the medication, the dose of prednisolone should be repeated. In cases where a child is unable to keep down orally ingested medication, intravenous steroids should be considered. Typically, treatment for up to three days is sufficient, but the duration of the course should be adjusted based on the time needed for recovery. Tapering off the medication is not necessary unless the steroid course exceeds 14 days. For more information, refer to the BTS/SIGN Guideline on the Management of Asthma.

Emotional incongruity, although not a primary symptom, is one of the negative symptoms that define chronic schizophrenia. These symptoms, as described by Kurt Schneider, are known as first-rank symptoms. They include auditory hallucinations such as hearing third-person voices discussing the patient, thought echo, and commentary on actions. Passivity phenomena, such as thought insertion, thought withdrawal, thought broadcast, and feelings of thoughts and actions being under external control, are also considered first-rank symptoms. Delusions, which can be primary or secondary, are another characteristic of schizophrenia.

Chronic schizophrenia is primarily characterized by negative symptoms. These symptoms include poor motivation and self-care, social withdrawal, depression, flat and blunted affect, emotional incongruity, decreased activity, poverty of thought and speech. On the other hand, symptoms like loss of inhibitions, pressure of speech, and grandiose delusions are more indicative of mania. Increased anxiety in social circumstances is often associated with social anxiety disorder.

In summary, emotional incongruity is a negative symptom of chronic schizophrenia, while the first-rank symptoms described by Kurt Schneider encompass auditory hallucinations, passivity phenomena, and delusions. It is important to differentiate these symptoms from those associated with mania or social anxiety disorder.

Leukaemic infiltrates in the gingiva are frequently observed in cases of acute myeloid leukaemia. This type of leukaemia primarily affects adults and is most commonly seen in individuals between the ages of 65 and 70. The typical presentation of acute myeloid leukaemia involves clinical symptoms that arise as a result of leukaemic infiltration in the bone marrow and other areas outside of the marrow. These symptoms may include anaemia (resulting in lethargy, pallor, and breathlessness), thrombocytopaenia (manifesting as petechiae, bruising, epistaxis, and bleeding), neutropenia (leading to increased susceptibility to infections), hepatosplenomegaly, and infiltration of the gingiva.

The monospot test is the preferred method for testing for infectious mononucleosis (glandular fever) when looking for heterophile antibodies. The timing and choice of investigations for glandular fever depend on factors such as the patient’s age, immune system status, and duration of symptoms. The monospot test is a latex agglutination test that uses equine erythrocytes as the primary substrate to detect specific heterophile antibodies produced by the human immune system in response to EBV infection. It is simpler and faster to use compared to the Paul Bunnell test, which uses sheep red cells. The monospot test is recommended by NICE due to its advantages. However, it has lower sensitivity and negative predictive value in young children, which is why EBV serology is preferred for those under 12 years old.

Further Reading:

Glandular fever, also known as infectious mononucleosis or mono, is a clinical syndrome characterized by symptoms such as sore throat, fever, and swollen lymph nodes. It is primarily caused by the Epstein-Barr virus (EBV), with other viruses and infections accounting for the remaining cases. Glandular fever is transmitted through infected saliva and primarily affects adolescents and young adults. The incubation period is 4-8 weeks.

The majority of EBV infections are asymptomatic, with over 95% of adults worldwide having evidence of prior infection. Clinical features of glandular fever include fever, sore throat, exudative tonsillitis, lymphadenopathy, and prodromal symptoms such as fatigue and headache. Splenomegaly (enlarged spleen) and hepatomegaly (enlarged liver) may also be present, and a non-pruritic macular rash can sometimes occur.

Glandular fever can lead to complications such as splenic rupture, which increases the risk of rupture in the spleen. Approximately 50% of splenic ruptures associated with glandular fever are spontaneous, while the other 50% follow trauma. Diagnosis of glandular fever involves various investigations, including viral serology for EBV, monospot test, and liver function tests. Additional serology tests may be conducted if EBV testing is negative.

Management of glandular fever involves supportive care and symptomatic relief with simple analgesia. Antiviral medication has not been shown to be beneficial. It is important to identify patients at risk of serious complications, such as airway obstruction, splenic rupture, and dehydration, and provide appropriate management. Patients can be advised to return to normal activities as soon as possible, avoiding heavy lifting and contact sports for the first month to reduce the risk of splenic rupture.

Rare but serious complications associated with glandular fever include hepatitis, upper airway obstruction, cardiac complications, renal complications, neurological complications, haematological complications, chronic fatigue, and an increased risk of lymphoproliferative cancers and multiple sclerosis.

Ulcerative colitis is a condition that is less common among smokers, as around 70-80% of individuals affected by this disease are non-smokers. There are several recognized associations of ulcerative colitis, including aphthous ulcers, uveitis and episcleritis, seronegative spondyloarthropathies, sacroiliitis, erythema nodosum, pyoderma gangrenosum, finger clubbing, autoimmune hemolytic anemia, primary biliary cirrhosis, primary sclerosing cholangitis, and chronic active hepatitis. These conditions often coexist with ulcerative colitis and can provide additional insight into the disease.

Anaphylaxis is a type I hypersensitivity reaction, where the body’s response is triggered by the attachment of an antigen to a specific antibody. This attachment then leads to the release of histamine and other mediators, such as leukotrienes, tumor necrosis factor, and various cytokines, from mast cells and basophils. These substances are released when these cells are exposed to the antigen.

Patients who have acute otitis media (AOM) and are immunocompromised or systemically unwell should be given an immediate prescription for antibiotics. However, for most patients with AOM, antibiotics are not necessary or can be delayed. An immediate antibiotic prescription should be offered to patients who are systemically unwell but do not require hospitalization, patients at high risk of complications due to underlying health conditions, and patients whose symptoms have persisted for four days or more without improvement. The recommended first choice antibiotic for AOM is amoxicillin.

Further Reading:

Acute otitis media (AOM) is an inflammation in the middle ear accompanied by symptoms and signs of an ear infection. It is commonly seen in young children below 4 years of age, with the highest incidence occurring between 9 to 15 months of age. AOM can be caused by viral or bacterial pathogens, and co-infection with both is common. The most common viral pathogens include respiratory syncytial virus (RSV), rhinovirus, adenovirus, influenza virus, and parainfluenza virus. The most common bacterial pathogens include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pyogenes.

Clinical features of AOM include ear pain (otalgia), fever, a red or cloudy tympanic membrane, and a bulging tympanic membrane with loss of anatomical landmarks. In young children, symptoms may also include crying, grabbing or rubbing the affected ear, restlessness, and poor feeding.

Most children with AOM will recover within 3 days without treatment. Serious complications are rare but can include persistent otitis media with effusion, recurrence of infection, temporary hearing loss, tympanic membrane perforation, labyrinthitis, mastoiditis, meningitis, intracranial abscess, sinus thrombosis, and facial nerve paralysis.

Management of AOM involves determining whether admission to the hospital is necessary based on the severity of systemic infection or suspected acute complications. For patients who do not require admission, regular pain relief with paracetamol or ibuprofen is advised. Decongestants or antihistamines are not recommended. Antibiotics may be offered immediately for patients who are systemically unwell, have symptoms and signs of a more serious illness or condition, or have a high risk of complications. For other patients, a decision needs to be made on the antibiotic strategy, considering the rarity of acute complications and the possible adverse effects of antibiotics. Options include no antibiotic prescription with advice to seek medical help if symptoms worsen rapidly or significantly, a back-up antibiotic prescription to be used if symptoms do not improve within 3 days, or an immediate antibiotic prescription with advice to seek medical advice if symptoms worsen rapidly or significantly.

The first-line antibiotic choice for AOM is a 5-7 day course of amoxicillin. For individuals allergic to or intolerant of penicillin, clarithromycin or erythromycin a 5–7 day course of clarithromycin or erythromycin (erythromycin is preferred in pregnant women).

During the third trimester of pregnancy, the use of selective serotonin reuptake inhibitors (SSRIs) has been associated with a discontinuation syndrome and persistent pulmonary hypertension of the newborn. It is important to be aware of the adverse effects of various drugs during pregnancy. For example, ACE inhibitors like ramipril, if given in the second and third trimester, can cause hypoperfusion, renal failure, and the oligohydramnios sequence. Aminoglycosides such as gentamicin can lead to ototoxicity and deafness. High doses of aspirin can result in first-trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g., 75 mg) do not pose significant risks. Late administration of benzodiazepines like diazepam during pregnancy can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if given in the first trimester, may cause phalangeal abnormalities, while their use in the second and third trimester can lead to fetal growth retardation. Carbamazepine has been associated with hemorrhagic disease of the newborn and neural tube defects. Chloramphenicol can cause grey baby syndrome. Corticosteroids, if given in the first trimester, may cause orofacial clefts. Danazol, if administered in the first trimester, can result in masculinization of the female fetuses genitals. Pregnant women should avoid handling crushed or broken tablets of finasteride as it can be absorbed through the skin and affect male sex organ development. Haloperidol, if given in the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the neonate. Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability. The use of lithium in the first trimester increases the risk of fetal cardiac malformations, while its use in the second and third trimesters can result in hypotonia, lethargy, feeding problems, hypothyroidism, goiter, and nephrogenic diabetes insipidus.

COHb is a measure used to evaluate the presence of carbon monoxide poisoning in individuals who are in good health. hHb refers to deoxygenated 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%.

Moderate hypothermia is indicated by core temperatures ranging from 28-32ºC.

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 depressed 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.

Extradural hematoma is most frequently caused by injury to the middle meningeal artery. This artery is particularly susceptible to damage as it passes behind the pterion.

Further Reading:

Extradural haematoma (EDH) is a collection of blood that forms between the inner surface of the skull and the outer layer of the dura, the dura mater. It is typically caused by head trauma and is often associated with a skull fracture, with the pterion being the most common site of injury. The middle meningeal artery is the most common source of bleeding in EDH.

Clinical features of EDH include a history of head injury with transient loss of consciousness, followed by a lucid interval and gradual loss of consciousness. Other symptoms may include severe headache, sixth cranial nerve palsies, nausea and vomiting, seizures, signs of raised intracranial pressure, and focal neurological deficits.

Imaging of EDH typically shows a biconvex shape and may cause mass effect with brain herniation. It can be differentiated from subdural haematoma by its appearance on imaging.

Management of EDH involves prompt referral to neurosurgery for evacuation of the haematoma. In some cases with a small EDH, conservative management may be considered. With prompt evacuation, the prognosis for EDH is generally good.

Hypothermia can lead to various abnormalities in the electrocardiogram (ECG). These abnormalities include bradyarrhythmias, the presence of a J wave (also known as an Osborn wave), and prolonged intervals such as PR, QRS, and QT. Additionally, shivering artefact and ventricular ectopics may be observed. In severe cases, hypothermia can even result in cardiac arrest, which can manifest as ventricular tachycardia (VT), ventricular fibrillation (VF), or asystole.

One distinctive feature of hypothermia on an ECG is the appearance of a small extra wave immediately following the QRS complex. This wave, known as a J wave or Osborn wave, was named after the individual who first described it. Interestingly, this wave tends to disappear as the body temperature is warmed. Despite its recognition, the exact mechanism behind the presence of the J wave in hypothermia remains unknown.

Before performing arterial blood gas sampling, it is necessary to disinfect the skin. This is typically done using alcohol, which should be applied and given enough time to dry completely before proceeding with the skin puncture. In the UK, it is common to use solutions that combine alcohol with Chlorhexidine, such as Chloraprep® (2).

Further Reading:

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

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

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

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

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

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

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

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

This woman is showing signs of obstructive jaundice along with a history of ulcerative colitis. The most probable diagnosis in this case is primary sclerosing cholangitis (PSC). PSC is a condition that causes inflammation and blockage of the bile ducts, leading to progressive damage. It is characterized by recurrent episodes of cholangitis and the development of scar tissue in the bile ducts. In severe cases, it can lead to liver cirrhosis, liver failure, and even liver cancer. PSC is commonly associated with ulcerative colitis, with more than 80% of PSC patients also having ulcerative colitis.

The underlying cause of PSC is believed to be autoimmune in nature. Around 80% of patients with PSC test positive for p-ANCA antibodies, which are associated with autoimmune diseases. Other antibodies such as antinuclear antibodies (ANA) and anti-smooth muscle antibodies may also be present, but they are only found in about one-third of PSC patients.

Autoimmune hepatitis, on the other hand, is a liver inflammation caused by a decrease in regulatory T-cells (Treg cells), leading to the production of autoantibodies against hepatocyte surface antigens. It primarily affects women (70%) between the ages of 15 and 40. The condition causes chronic and progressive hepatitis, often presenting in the later stages when the patient is severely unwell and jaundiced. Liver function tests typically show significantly elevated levels of transaminases (ALT and AST), often more than ten times the normal range. Alkaline phosphatase (ALP) levels may be normal or slightly elevated. Antinuclear antibodies (ANA) are positive in approximately 80% of cases, while smooth muscle antibodies (SMA) are positive in about 70% of cases. Antimitochondrial antibodies are usually low or absent.

Primary biliary cirrhosis is another autoimmune liver disease that leads to the progressive destruction of the small bile ducts in the liver, primarily affecting the intralobular ducts. This results in cholestatic jaundice, liver fibrosis, and eventually cirrhosis. The condition is more common in women (90%) and typically occurs between the ages of 30 and 65. Liver function tests show predominantly elevated levels of alkaline phosphatase (ALP), often before any symptoms or signs of the disease appear.

The maximum dose of adrenaline is 2 mg/kg, regardless of its concentration or addition. However, when calculating the volume requirements, the concentration of adrenaline becomes a factor.

Further Reading:

Local anaesthetics, such as lidocaine, bupivacaine, and prilocaine, are commonly used in the emergency department for topical or local infiltration to establish a field block. Lidocaine is often the first choice for field block prior to central line insertion. These anaesthetics work by blocking sodium channels, preventing the propagation of action potentials.

However, local anaesthetics can enter the systemic circulation and cause toxic side effects if administered in high doses. Clinicians must be aware of the signs and symptoms of local anaesthetic systemic toxicity (LAST) and know how to respond. Early signs of LAST include numbness around the mouth or tongue, metallic taste, dizziness, visual and auditory disturbances, disorientation, and drowsiness. If not addressed, LAST can progress to more severe symptoms such as seizures, coma, respiratory depression, and cardiovascular dysfunction.

The management of LAST is largely supportive. Immediate steps include stopping the administration of local anaesthetic, calling for help, providing 100% oxygen and securing the airway, establishing IV access, and controlling seizures with benzodiazepines or other medications. Cardiovascular status should be continuously assessed, and conventional therapies may be used to treat hypotension or arrhythmias. Intravenous lipid emulsion (intralipid) may also be considered as a treatment option.

If the patient goes into cardiac arrest, CPR should be initiated following ALS arrest algorithms, but lidocaine should not be used as an anti-arrhythmic therapy. Prolonged resuscitation may be necessary, and intravenous lipid emulsion should be administered. After the acute episode, the patient should be transferred to a clinical area with appropriate equipment and staff for further monitoring and care.

It is important to report cases of local anaesthetic toxicity to the appropriate authorities, such as the National Patient Safety Agency in the UK or the Irish Medicines Board in the Republic of Ireland. Additionally, regular clinical review should be conducted to exclude pancreatitis, as intravenous lipid emulsion can interfere with amylase or lipase assays.

The ulnar nerve provides innervation to several muscles in the hand. These include the palmar interossei, dorsal interossei, medial two lumbricals, and abductor digiti minimi. On the other hand, the median nerve innervates the opponens pollicis, lateral two lumbricals, and flexor pollicis brevis. Lastly, the radial nerve is responsible for innervating the extensor digitorum muscle.

An anal fissure is a tear in the wall of the anal mucosa that exposes the circular muscle layer. The majority of these tears occur in the posterior midline, and they are often caused by the passage of a large, hard stool after a period of constipation. If multiple fissures are present, it may indicate an underlying condition such as Crohn’s disease or tuberculosis.

Both men and women are equally affected by anal fissures, and they are most commonly seen in individuals in their thirties. The typical symptoms of an anal fissure include intense, sharp pain during bowel movements, which can last for up to an hour after passing stool. Additionally, there may be spots of bright red blood on the toilet paper when wiping, and a history of constipation.

The initial management approach for an anal fissure involves non-operative measures such as using stool softeners and bulking agents. To alleviate the intense anal pain, analgesics and topical local anesthetics may be prescribed. According to a recent meta-analysis, first-line therapy should involve the use of topical GTN or diltiazem, with botulinum toxin being used as a rescue treatment if necessary (Modern perspectives in the treatment of chronic anal fissures. Ann R Coll Surg Engl. 2007 Jul;89(5):472-8.)

Sphincterotomy, a surgical procedure, should be reserved for cases where the fissure does not heal with conservative measures. It has a success rate of 90%.

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)

Gynaecomastia, a condition characterized by the enlargement of breast tissue in males, can be caused by certain drugs. Some medications that have been associated with gynaecomastia include Cimetidine, Omeprazole, Spironolactone, Digoxin, Furosemide, Finasteride, and certain antipsychotics. Interestingly, Ranitidine, another medication commonly used for gastric issues, does not tend to cause gynaecomastia. In fact, studies have shown that gynaecomastia caused by Cimetidine can be resolved when it is substituted with Ranitidine.

The patient is experiencing acidosis, as indicated by the low pH. The low bicarb and base excess levels suggest that the metabolic system is contributing to or causing the acidosis. Additionally, the low pCO2 indicates that the respiratory system is attempting to compensate by driving alkalosis. However, the metabolic system is the primary factor in this case, leading to a diagnosis of metabolic acidosis with incomplete respiratory compensation.

Further Reading:

Salicylate poisoning, particularly from aspirin overdose, is a common cause of poisoning in the UK. One important concept to understand is that salicylate overdose leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the overdose stimulates the respiratory center, leading to hyperventilation and respiratory alkalosis. However, as the effects of salicylate on lactic acid production, breakdown into acidic metabolites, and acute renal injury occur, it can result in high anion gap metabolic acidosis.

The clinical features of salicylate poisoning include hyperventilation, tinnitus, lethargy, sweating, pyrexia (fever), nausea/vomiting, hyperglycemia and hypoglycemia, seizures, and coma.

When investigating salicylate poisoning, it is important to measure salicylate levels in the blood. The sample should be taken at least 2 hours after ingestion for symptomatic patients or 4 hours for asymptomatic patients. The measurement should be repeated every 2-3 hours until the levels start to decrease. Other investigations include arterial blood gas analysis, electrolyte levels (U&Es), complete blood count (FBC), coagulation studies (raised INR/PTR), urinary pH, and blood glucose levels.

To manage salicylate poisoning, an ABC approach should be followed to ensure a patent airway and adequate ventilation. Activated charcoal can be administered if the patient presents within 1 hour of ingestion. Oral or intravenous fluids should be given to optimize intravascular volume. Hypokalemia and hypoglycemia should be corrected. Urinary alkalinization with intravenous sodium bicarbonate can enhance the elimination of aspirin in the urine. In severe cases, hemodialysis may be necessary.

Urinary alkalinization involves targeting a urinary pH of 7.5-8.5 and checking it hourly. It is important to monitor for hypokalemia as alkalinization can cause potassium to shift from plasma into cells. Potassium levels should be checked every 1-2 hours.

In cases where the salicylate concentration is high (above 500 mg/L in adults or 350 mg/L in children), sodium bicarbonate can be administered intravenously. Hemodialysis is the treatment of choice for severe poisoning and may be indicated in cases of high salicylate levels, resistant metabolic acidosis, acute kidney injury, pulmonary edema, seizures and coma.

Flumazenil is a specific antagonist for benzodiazepines that can be beneficial in certain situations. It acts quickly, taking less than 1 minute to take effect, but its effects are short-lived and only last for less than 1 hour. The recommended dosage is 200 μg every 1-2 minutes, with a maximum dose of 3mg per hour.

It is important to avoid using Flumazenil if the patient is dependent on benzodiazepines or is taking tricyclic antidepressants. This is because it can trigger a withdrawal syndrome in these individuals, potentially leading to seizures or cardiac arrest.

In the UK, the most commonly used treatment for acute exacerbations of hereditary angioedema (HAE) in emergency departments is C1-Esterase inhibitor. However, there are alternative options available. Icatibant acetate, sold under the brand name Firazyr®, is a bradykinin receptor antagonist that is licensed in the UK and Europe and can be used as an alternative treatment. Another alternative is the transfusion of fresh frozen plasma.

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.

Triage is a crucial process that involves determining the priority of patients’ treatment based on the severity of their condition and their chances of recovery. Its purpose is to ensure that limited resources are used efficiently, maximizing the number of lives saved. During a major incident, primary triage takes place in the bronze area, which is located within the inner cordon.

In the context of a major incident, priorities are assigned numbers from 1 to 3, with 1 being the highest priority. These priorities are also color-coded for easy identification:
– P1: Immediate priority. This category includes patients who require immediate life-saving intervention to prevent death. They are color-coded red.
– P2: Intermediate priority. Patients in this group also require significant interventions, but their treatment can be delayed for a few hours. They are color-coded yellow.
– P3: Delayed priority. Patients in this category require medical treatment, but it can be safely delayed. This category also includes walking wounded individuals. The classification as P3 is based on the motor score of the Glasgow Coma Scale, which predicts a favorable outcome. They are color-coded green.

The fourth classification is for deceased individuals. It is important to identify and classify them to prevent the unnecessary use of limited resources on those who cannot be helped. Dead bodies should be left in their current location, both to avoid wasting resources and because the area may be considered a crime scene. Deceased individuals are color-coded black.

Lactulose and the oral antibiotic Rifaximin are commonly prescribed to patients with hepatic encephalopathy. The main goal of treatment for this condition is to identify and address any factors that may have triggered it. Lactulose is administered to relieve constipation, which can potentially lead to hepatic encephalopathy. On the other hand, Rifaximin is used to decrease the presence of enteric bacteria that produce ammonia.

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.

Croup, also known as laryngo-tracheo-bronchitis, is typically caused by the parainfluenza virus. Other viruses such as rhinovirus, influenza, and respiratory syncytial viruses can also be responsible. Before the onset of stridor, there is often a mild cold-like illness that lasts for 1-2 days. Symptoms usually reach their peak within 1-3 days, with the cough often being more troublesome at night. A milder cough may persist for another 7-10 days.

Since croup is caused by a viral infection, antibiotics are not effective unless there is a suspicion of a secondary bacterial infection. It is important to note that sedation should not be used in a child experiencing respiratory distress. To reduce airway swelling, dexamethasone and prednisolone are commonly prescribed, although they do not shorten the duration of the illness. In severe cases, nebulized adrenaline can be administered.

A barking cough is a characteristic symptom of croup, but it does not necessarily indicate the severity of the condition. Hospitalization for croup is rare and typically reserved for children who show worsening respiratory distress or signs of drowsiness/agitation.

The prolonged use of nitrous oxide (Entonox) in patients with sepsis may have a negative impact on DNA synthesis, and it is not recommended to use it in this situation. However, sepsis itself does not prevent the use of nitrous oxide.

There are several conditions that make the use of nitrous oxide inappropriate. These include a reduced level of consciousness, diving injuries, pneumothorax, middle ear disease, sinus disease, bowel obstruction, a documented allergy to nitrous oxide, hypoxia, and violent or disabled psychiatric patients.

It is important to note that the use of nitrous oxide should be avoided in patients with sepsis due to its potential effects on DNA synthesis. However, there are other contraindications to its use that should be considered in different clinical scenarios.

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

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

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

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

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

After the third shock is administered to patients with a shockable rhythm, it is recommended to administer two drugs: adrenaline and amiodarone. Adrenaline should be given at a dose of 1 mg intravenously (or intraosseously) for adult patients in cardiac arrest with a shockable rhythm. For adult patients in cardiac arrest who are in ventricular fibrillation or pulseless ventricular tachycardia, amiodarone should be given at a dose of 300 mg intravenously (or intraosseously) after three shocks have been administered. In cases where amiodarone is unavailable, lidocaine may be used as an alternative.

Further Reading:

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

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

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

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

The intravascular volume of an infant is approximately 80 ml/kg, while in older children it is around 70 ml/kg. Dehydration itself does not lead to death, but shock can occur when there is a loss of 20 ml/kg from the intravascular space. Clinical dehydration becomes evident only after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children:

Bodyweight:
– First 10 kg: Daily fluid requirement of 100 ml/kg and hourly fluid requirement of 4 ml/kg.
– Second 10 kg: Daily fluid requirement of 50 ml/kg and hourly fluid requirement of 2 ml/kg.
– Subsequent kg: Daily fluid requirement of 20 ml/kg and hourly fluid requirement of 1 ml/kg.

Based on this information, the hourly maintenance fluid requirements for this child can be calculated as follows:

– First 10 kg: 4 ml/kg = 40 ml
– Second 10 kg: 2 ml/kg = 20 ml
– Subsequent kg: 1 ml/kg = 5 ml

Therefore, the total hourly maintenance fluid requirement for this child is 65 ml.

When treating adults with bradycardia, a maximum of 6 doses of atropine 500 mcg can be administered. Each dose is given intravenously every 3-5 minutes. The total dose should not exceed 3mg.

Further Reading:

Causes of Bradycardia:
– Physiological: Athletes, sleeping
– Cardiac conduction dysfunction: Atrioventricular block, sinus node disease
– Vasovagal & autonomic mediated: Vasovagal episodes, carotid sinus hypersensitivity
– Hypothermia
– Metabolic & electrolyte disturbances: Hypothyroidism, hyperkalaemia, hypermagnesemia
– Drugs: Beta-blockers, calcium channel blockers, digoxin, amiodarone
– Head injury: Cushing’s response
– Infections: Endocarditis
– Other: Sarcoidosis, amyloidosis

Presenting symptoms of Bradycardia:
– Presyncope (dizziness, lightheadedness)
– Syncope
– Breathlessness
– Weakness
– Chest pain
– Nausea

Management of Bradycardia:
– Assess and monitor for adverse features (shock, syncope, myocardial ischaemia, heart failure)
– Treat reversible causes of bradycardia
– Pharmacological treatment: Atropine is first-line, adrenaline and isoprenaline are second-line
– Transcutaneous pacing if atropine is ineffective
– Other drugs that may be used: Aminophylline, dopamine, glucagon, glycopyrrolate

Bradycardia Algorithm:
– Follow the algorithm for management of bradycardia, which includes assessing and monitoring for adverse features, treating reversible causes, and using appropriate medications or pacing as needed.
https://acls-algorithms.com/wp-content/uploads/2020/12/Website-Bradycardia-Algorithm-Diagram.pdf

Meniere’s disease is a condition that affects the inner ear due to changes in fluid volume within the vestibular labyrinth. This leads to the progressive distension of the labyrinth, known as endolymphatic hydrops, which causes damage to the vestibular system and the cochlea. The classic symptoms associated with Meniere’s disease are vertigo, hearing loss, and tinnitus.

The main clinical features of Meniere’s disease include episodes of vertigo that typically last for 2-3 hours. These episodes are usually shorter than 24 hours in duration. Hearing loss, which is often gradual and affects only one ear, is also a common symptom. Tinnitus, a ringing or buzzing sound in the ears, is frequently associated with Meniere’s disease. Other symptoms may include a sensation of fullness or pressure in the ears, as well as nausea and vomiting. Nystagmus, an involuntary eye movement, may occur away from the side of the lesion. Meniere’s disease is more prevalent in individuals who suffer from migraines.

The management of Meniere’s disease aims to alleviate acute attacks, reduce their severity and frequency, and improve hearing while minimizing the impact of tinnitus. If Meniere’s disease is suspected, patients should be referred to an ear, nose, and throat specialist.

During acute attacks, medications such as prochlorperazine, cinnarizine, and cyclizine can help reduce nausea and vertigo symptoms. If vomiting is present, buccal or intramuscular administration of these medications may be necessary. In severe cases, hospital admission may be required to prevent dehydration.

For long-term prevention, lifestyle measures can be beneficial. Avoiding caffeine, chocolate, alcohol, and tobacco is recommended. Excessive fatigue should also be avoided. Following a low-salt diet may be helpful. Betahistine, a medication that initially starts at a dose of 16 mg three times a day, can be used for prophylaxis to reduce the frequency and severity of attacks. Diuretics may also be beneficial, but they are typically not recommended for primary care use.

Overall, the management of Meniere’s disease involves a combination of lifestyle changes and medication to control symptoms and improve the patient’s quality of life.

Subfalcine herniation occurs when a mass in one side of the brain causes the cingulate gyrus to be pushed under the falx cerebri. This condition often leads to specific neurological symptoms. These symptoms include a motor deficit in the lower limb on the opposite side of the body, bladder incontinence, motor and sensory deficits on the same side of the body as the herniation, and difficulty with speech (dysarthria).

Further Reading:

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

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

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

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

Moderate to severe cyanide poisoning typically leads to a condition called high anion gap metabolic acidosis, characterized by elevated levels of lactate (>10 mmol/L). Cyanide toxicity can occur from inhaling smoke produced by burning materials such as plastics, wools, silk, and other natural and synthetic polymers, which can release hydrogen cyanide (HCN). Symptoms of cyanide poisoning include headaches, nausea, decreased consciousness or loss of consciousness, and seizures. Measuring cyanide levels is not immediately helpful in managing a patient suspected of cyanide toxicity. Cyanide binds to the ferric (Fe3+) ion of cytochrome oxidase, causing a condition known as histotoxic hypoxia and resulting in lactic acidosis. The presence of a high lactate level (>10) and a classic high anion gap metabolic acidosis should raise suspicion of cyanide poisoning in a clinician.

Further Reading:

Burn injuries can be classified based on their type (degree, partial thickness or full thickness), extent as a percentage of total body surface area (TBSA), and severity (minor, moderate, major/severe). Severe burns are defined as a >10% TBSA in a child and >15% TBSA in an adult.

When assessing a burn, it is important to consider airway injury, carbon monoxide poisoning, type of burn, extent of burn, special considerations, and fluid status. Special considerations may include head and neck burns, circumferential burns, thorax burns, electrical burns, hand burns, and burns to the genitalia.

Airway management is a priority in burn injuries. Inhalation of hot particles can cause damage to the respiratory epithelium and lead to airway compromise. Signs of inhalation injury include visible burns or erythema to the face, soot around the nostrils and mouth, burnt/singed nasal hairs, hoarse voice, wheeze or stridor, swollen tissues in the mouth or nostrils, and tachypnea and tachycardia. Supplemental oxygen should be provided, and endotracheal intubation may be necessary if there is airway obstruction or impending obstruction.

The initial management of a patient with burn injuries involves conserving body heat, covering burns with clean or sterile coverings, establishing IV access, providing pain relief, initiating fluid resuscitation, measuring urinary output with a catheter, maintaining nil by mouth status, closely monitoring vital signs and urine output, monitoring the airway, preparing for surgery if necessary, and administering medications.

Burns can be classified based on the depth of injury, ranging from simple erythema to full thickness burns that penetrate into subcutaneous tissue. The extent of a burn can be estimated using methods such as the rule of nines or the Lund and Browder chart, which takes into account age-specific body proportions.

Fluid management is crucial in burn injuries due to significant fluid losses. Evaporative fluid loss from burnt skin and increased permeability of blood vessels can lead to reduced intravascular volume and tissue perfusion. Fluid resuscitation should be aggressive in severe burns, while burns <15% in adults and <10% in children may not require immediate fluid resuscitation. The Parkland formula can be used to calculate the intravenous fluid requirements for someone with a significant burn injury.

This child has a past medical history consistent with acute purulent otitis media on the left side. The sudden improvement and discharge of pus from the ear strongly suggest a perforated tympanic membrane. It is not uncommon to be unable to see the tympanic membrane in these situations.

Initially, it is best to adopt a watchful waiting approach to tympanic membrane perforation. Spontaneous healing occurs in over 90% of patients, so only persistent cases should be referred for myringoplasty. There is no need for an urgent same-day referral in this case.

The use of topical corticosteroids and gentamicin is not recommended when there is a tympanic membrane perforation.

Legionella pneumophila is a type of Gram-negative bacterium that can be found in natural water supplies and soil. It is responsible for causing Legionnaires’ disease, a serious illness. Outbreaks of this disease have been associated with poorly maintained air conditioning systems, whirlpool spas, and hot tubs. In the past, there have been instances of Legionnaires’ disease outbreaks on cruise ships due to inadequate maintenance of air conditioning and shower units.

The pneumonic form of Legionnaires’ disease presents with certain clinical features. Initially, there may be a mild flu-like prodrome lasting for 1-3 days. A persistent cough, which is usually non-productive and occurs in approximately 90% of cases, is also common. Other symptoms include pleuritic chest pain, haemoptysis, headache, nausea, vomiting, diarrhoea, and anorexia. Additionally, some individuals may experience a condition called syndrome of inappropriate antidiuretic hormone secretion (SIADH), which can lead to hyponatraemia.

It is important to note that infections caused by Legionella pneumophila are resistant to amoxicillin. However, they can be effectively treated with macrolide antibiotics like erythromycin or quinolones such as ciprofloxacin. Tetracyclines, including doxycycline, can also be used for treatment.

Sickle-cell disease is a blood disorder that is inherited in an autosomal recessive manner. It is characterized by the production of abnormal red blood cells that have a sickle shape. These abnormal cells are triggered by various factors such as low oxygen levels, dehydration, stress, and infection. The disease is caused by a specific mutation in the beta-globin chain of hemoglobin, resulting in the substitution of glutamic acid with valine at the sixth position. The gene responsible for this mutation is located on chromosome 11.

On the other hand, sickle-cell trait refers to the carrier state of the disease. Individuals with sickle-cell trait have one normal allele and one abnormal allele. Both alleles are co-dominant, meaning that both normal and abnormal hemoglobin are produced. As a result, individuals with sickle-cell trait do not experience the same severity of symptoms as those with sickle-cell disease.

When both parents are carriers of the sickle-cell trait, there is a 50% chance that their child will also be an unaffected carrier, a 25% chance that the child will be unaffected, and a 25% chance that the child will develop sickle-cell disease. This is because the inheritance of the disease follows the principles of autosomal recessive inheritance.

An elevated pH (normal range 7.34-7.45) suggests alkalosis. A low pCO2 (normal range 4.4-6.0 Kpa) indicates that the respiratory system is causing the alkalosis. The metabolic system, on the other hand, is not contributing to either alkalosis or acidosis as both the bicarbonate and base excess levels are within the normal ranges.

Further Reading:

Salicylate poisoning, particularly from aspirin overdose, is a common cause of poisoning in the UK. One important concept to understand is that salicylate overdose leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the overdose stimulates the respiratory center, leading to hyperventilation and respiratory alkalosis. However, as the effects of salicylate on lactic acid production, breakdown into acidic metabolites, and acute renal injury occur, it can result in high anion gap metabolic acidosis.

The clinical features of salicylate poisoning include hyperventilation, tinnitus, lethargy, sweating, pyrexia (fever), nausea/vomiting, hyperglycemia and hypoglycemia, seizures, and coma.

When investigating salicylate poisoning, it is important to measure salicylate levels in the blood. The sample should be taken at least 2 hours after ingestion for symptomatic patients or 4 hours for asymptomatic patients. The measurement should be repeated every 2-3 hours until the levels start to decrease. Other investigations include arterial blood gas analysis, electrolyte levels (U&Es), complete blood count (FBC), coagulation studies (raised INR/PTR), urinary pH, and blood glucose levels.

To manage salicylate poisoning, an ABC approach should be followed to ensure a patent airway and adequate ventilation. Activated charcoal can be administered if the patient presents within 1 hour of ingestion. Oral or intravenous fluids should be given to optimize intravascular volume. Hypokalemia and hypoglycemia should be corrected. Urinary alkalinization with intravenous sodium bicarbonate can enhance the elimination of aspirin in the urine. In severe cases, hemodialysis may be necessary.

Urinary alkalinization involves targeting a urinary pH of 7.5-8.5 and checking it hourly. It is important to monitor for hypokalemia as alkalinization can cause potassium to shift from plasma into cells. Potassium levels should be checked every 1-2 hours.

In cases where the salicylate concentration is high (above 500 mg/L in adults or 350 mg/L in children), sodium bicarbonate can be administered intravenously. Hemodialysis is the treatment of choice for severe poisoning and may be indicated in cases of high salicylate levels, resistant metabolic acidosis, acute kidney injury, pulmonary edema, seizures and coma.

Conservative management of ureteric stones may involve the use of medical expulsive therapy (MET), which can be achieved through the administration of either an alpha-blocker or a calcium-channel blocker. This treatment aims to facilitate the natural passage of the stone during the observation period.

Research has shown that in adults, both alpha-blockers and calcium channel blockers have been effective in improving the passage of distal ureteric stones that are less than 10 mm in size, when compared to no treatment. Additionally, alpha-blockers have shown to be more effective than placebo in promoting stone passage. Alpha-blockers have also demonstrated more benefits than calcium channel blockers in terms of stone passage, as well as some advantages in terms of hospital stay and pain management. However, there was no significant difference in the time it took for the stone to pass or the overall quality of life.

Currently, the National Institute for Health and Care Excellence (NICE) recommends alpha-blockers as the preferred choice for medical expulsive therapy. For more detailed information, you can refer to the NICE guidelines on the assessment and management of renal and ureteric stones.

Activated charcoal prevents the absorption of poisons by absorbing them onto its surface through weak electrostatic forces.

Further Reading:

Poisoning in the emergency department is often caused by accidental or intentional overdose of prescribed drugs. Supportive treatment is the primary approach for managing most poisonings. This includes ensuring a clear airway, proper ventilation, maintaining normal fluid levels, temperature, and blood sugar levels, correcting any abnormal blood chemistry, controlling seizures, and assessing and treating any injuries.

In addition to supportive treatment, clinicians may need to consider strategies for decontamination, elimination, and administration of antidotes. Decontamination involves removing poisons from the skin or gastrointestinal tract. This can be done through rinsing the skin or using methods such as activated charcoal, gastric lavage, induced emesis, or whole bowel irrigation. However, induced emesis is no longer commonly used, while gastric lavage and whole bowel irrigation are rarely used.

Elimination methods include urinary alkalinization, hemodialysis, and hemoperfusion. These techniques help remove toxins from the body.

Activated charcoal is a commonly used method for decontamination. It works by binding toxins in the gastrointestinal tract, preventing their absorption. It is most effective if given within one hour of ingestion. However, it is contraindicated in patients with an insecure airway due to the risk of aspiration. Activated charcoal can be used for many drugs, but it is ineffective for certain poisonings, including pesticides (organophosphates), hydrocarbons, strong acids and alkalis, alcohols (ethanol, methanol, ethylene glycol), iron, lithium, and solvents.

Antidotes are specific treatments for poisoning caused by certain drugs or toxins. For example, cyanide poisoning can be treated with dicobalt edetate, hydroxocobalamin, or sodium nitrite and sodium thiosulphate. Benzodiazepine poisoning can be treated with flumazanil, while opiate poisoning can be treated with naloxone. Other examples include protamine for heparin poisoning, vitamin K or fresh frozen plasma for warfarin poisoning, fomepizole or ethanol for methanol poisoning, and methylene blue for methemoglobinemia caused by benzocaine or nitrates.

There are many other antidotes available for different types of poisoning, and resources such as TOXBASE and the National Poisons Information Service (NPIS) can provide valuable advice on managing poisonings.

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