The Health Protection (Notification) Regulations currently require the reporting of certain diseases. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ Disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, SARS, scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

This patient is currently experiencing neuropathic pain due to spinal metastases from their lung malignancy.

The first line of treatment for neuropathic pain includes options such as amitriptyline, duloxetine, gabapentin, or pregabalin. If the initial treatment is not effective or well-tolerated, one of the remaining three drugs can be considered. If the second and third drugs tried also prove to be ineffective or not well-tolerated, it may be necessary to switch to a different medication. Tramadol should only be considered as a last resort for acute rescue therapy.

For more information on the pharmacological management of neuropathic pain in adults, please refer to the NICE guidance.

The most common symptom of infective endocarditis is fever, which occurs in the majority of cases and is consistently present throughout the course of the disease. Cardiac murmurs are also frequently detected, although they may only be present in one third of patients at the initial presentation. Individuals who use intravenous drugs often develop right-sided disease affecting the tricuspid and pulmonary valves, making it challenging to detect cardiac murmurs in these cases. Splinter hemorrhages and other symptoms may also be observed.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

The most commonly identified causative pathogen in patients with spontaneous bacterial peritonitis (SBP) is Escherichia coli. SBP is a serious infection that occurs in individuals with liver cirrhosis, where bacteria from the gut migrate into the peritoneal cavity, leading to infection and inflammation. E. coli is a gram-negative bacterium commonly found in the intestines and is known to be a frequent cause of SBP. It is important to promptly diagnose and treat SBP to prevent further complications and improve patient outcomes.

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.

Based on the patient’s symptoms and medical history, the most likely organism responsible for this case of infective endocarditis is Streptococcus viridans. This is because the patient has a history of aortic stenosis, which is a risk factor for developing infective endocarditis. Additionally, the patient had a tooth extraction prior to the onset of symptoms, which can introduce bacteria into the bloodstream and increase the risk of infective endocarditis. Streptococcus viridans is a common cause of infective endocarditis, particularly in patients with underlying heart valve disease.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

Eosinophilic oesophagitis (EoE), also known as allergic inflammatory condition of the oesophagus, is characterized by the presence of eosinophils. It was identified as a clinical condition about two decades ago but has gained recognition more recently. EoE is most commonly observed in middle-aged individuals, with an average age of diagnosis ranging from 30 to 50 years. It is more prevalent in men, with a male-to-female ratio of 3:1. Allergic conditions, particularly atopy, are often associated with EoE.

The clinical manifestations of EoE vary depending on the age of the patient. In adults, common symptoms include dysphagia, food bolus obstruction, heartburn, and chest pain. On the other hand, children with EoE may present with failure to thrive, food refusal, difficulty feeding, vomiting, and abdominal pain.

To diagnose EoE, it is crucial to consider the possibility of this condition in patients who have persistent heartburn and/or difficulty swallowing, especially if they have a history of allergies or atopic disease. Diagnosis is confirmed by identifying more than 15 eosinophils per high-power field on an oesophageal biopsy. Allergy testing is not effective as EoE is not mediated by IgE.

There are three main management options for EoE, all of which are considered first-line treatments. The first option is proton pump inhibitors (PPIs), which are effective in approximately one-third of patients. If an endoscopic biopsy confirms the presence of eosinophils, an 8-week trial of PPIs can be initiated. After the trial, a repeat endoscopy and biopsy should be performed to assess for persistent eosinophils. Patients who respond to PPIs are diagnosed with PPI responsive oesophageal eosinophilia, while those who do not respond are diagnosed with true eosinophilic oesophagitis.

The second management option is dietary manipulation, which can be effective in both children and adults. It can be used as an initial treatment or in combination with pharmacological therapy. The six most commonly implicated food groups in EoE are cow’s milk, wheat, egg, soy, peanut/tree nut, and fish/shellfish. There are four main approaches to dietary manipulation: elemental diet, six food elimination diet (SFED), four food elimination diet (FFED),

The PaO2/FiO2 ratio is a measurement used to determine the severity of Acute Respiratory Distress Syndrome (ARDS). It is calculated by dividing the arterial oxygen partial pressure (PaO2) by the fraction of inspired oxygen (FiO2). However, it is important to note that this calculation should only be done when the patient is receiving a minimum positive end-expiratory pressure (PEEP) of 5 cm water. The resulting ratio is then used to classify the severity of ARDS, with specific thresholds provided below.

Further Reading:

ARDS is a severe form of lung injury that occurs in patients with a predisposing risk factor. It is characterized by the onset of respiratory symptoms within 7 days of a known clinical insult, bilateral opacities on chest X-ray, and respiratory failure that cannot be fully explained by cardiac failure or fluid overload. Hypoxemia is also present, as indicated by a specific threshold of the PaO2/FiO2 ratio measured with a minimum requirement of positive end-expiratory pressure (PEEP) ≥5 cm H2O. The severity of ARDS is classified based on the PaO2/FiO2 ratio, with mild, moderate, and severe categories.

Lung protective ventilation is a set of measures aimed at reducing lung damage that may occur as a result of mechanical ventilation. Mechanical ventilation can cause lung damage through various mechanisms, including high air pressure exerted on lung tissues (barotrauma), over distending the lung (volutrauma), repeated opening and closing of lung units (atelectrauma), and the release of inflammatory mediators that can induce lung injury (biotrauma). These mechanisms collectively contribute to ventilator-induced lung injury (VILI).

The key components of lung protective ventilation include using low tidal volumes (5-8 ml/kg), maintaining inspiratory pressures (plateau pressure) below 30 cm of water, and allowing for permissible hypercapnia. However, there are some contraindications to lung protective ventilation, such as an unacceptable level of hypercapnia, acidosis, and hypoxemia. These factors need to be carefully considered when implementing lung protective ventilation strategies in patients with ARDS.

St. John’s wort can reduce the effectiveness of warfarin, an anticoagulant medication. Therefore, it is important for patients who are taking warfarin to be aware that they should avoid using St. John’s wort as a supplement. For more information on this interaction, you can refer to the BNF section on warfarin interactions.

Meadow syndrome, formerly known as Munchausen syndrome by proxy, is the most likely diagnosis in this case. It involves a caregiver intentionally creating the appearance of health problems in another person, usually their own child. This can involve causing harm to the child or manipulating test results to make it seem like the child is sick or injured.

There are several features that support a diagnosis of Meadow syndrome. These include symptoms or signs that only appear when the parent or guardian is present, symptoms that are only observed by the parent or guardian, and symptoms that do not respond to treatment or medication. Additionally, there may be a history of unlikely illnesses, such as a significant amount of blood loss without any change in physiological data. The parent or guardian may also seek multiple clinical opinions despite already receiving a definitive opinion, and they may persistently disagree with the clinical opinion.

Another characteristic of Meadow syndrome is the significant impact it has on the child’s normal activities, such as frequent school absenteeism. The child may also use aids to daily living that are seemingly unnecessary, like a wheelchair. It is important to note that a principal risk factor for this condition is the parent having experienced a negative event or trauma during their own childhood, such as the death of a parent or being a victim of child abuse or neglect.

It is crucial not to confuse Meadow syndrome with Munchausen syndrome, where an individual pretends to be ill or deliberately produces symptoms in themselves. Hypochondriasis is another condition where a person excessively worries about having a serious illness. Somatic symptom disorder, previously known as somatisation disorder, is characterized by an intense focus on physical symptoms that causes significant emotional distress and impairs functioning. Lastly, Ganser syndrome is a rare dissociative disorder that involves giving nonsensical or incorrect answers to questions and experiencing other dissociative symptoms like fugue, amnesia, or conversion disorder, often accompanied by visual pseudohallucinations and a decreased state of consciousness.

Extrapyramidal side effects refer to drug-induced movements that encompass acute dyskinesias and dystonic reactions, tardive dyskinesia, Parkinsonism, akinesia, akathisia, and neuroleptic malignant syndrome. These side effects occur due to the blockade or depletion of dopamine in the basal ganglia, leading to a lack of dopamine that often resembles idiopathic disorders of the extrapyramidal system.

The primary culprits behind extrapyramidal side effects are the first-generation antipsychotics, which act as potent antagonists of the dopamine D2 receptor. Among these antipsychotics, haloperidol and fluphenazine are the two drugs most commonly associated with extrapyramidal side effects. On the other hand, second-generation antipsychotics like olanzapine have lower rates of adverse effects on the extrapyramidal system compared to their first-generation counterparts.

While less frequently, other medications can also contribute to extrapyramidal symptoms. These include certain antidepressants, lithium, various anticonvulsants, antiemetics, and, in rare cases, oral contraceptive agents.

Patients with decompression illness should avoid taking analgesics as they can potentially harm the patient. Instead, oxygen is the preferred method of analgesia and has been shown to improve prognosis. Symptoms of decompression illness can often be resolved by simply breathing oxygen from a cylinder. It is important to note that Entonox should never be administered to patients with suspected decompression illness as the additional inert gas load from the nitrous oxide can worsen symptoms. NSAIDs should also be avoided as they can exacerbate micro-hemorrhages caused by decompression illness. In cases of decompression illness, patients will typically be treated with recompression in a hyperbaric oxygen chamber. However, it is important to be cautious with the use of oxygen as it can cause pulmonary and neurological toxicity at certain pressures. Therefore, there is a risk of oxygen toxicity developing in patients undergoing recompression, and opioids should be avoided as they are believed to increase this risk.

Further Reading:

Decompression illness (DCI) is a term that encompasses both decompression sickness (DCS) and arterial gas embolism (AGE). When diving underwater, the increasing pressure causes gases to become more soluble and reduces the size of gas bubbles. As a diver ascends, nitrogen can come out of solution and form gas bubbles, leading to decompression sickness or the bends. Boyle’s and Henry’s gas laws help explain the changes in gases during changing pressure.

Henry’s law states that the amount of gas that dissolves in a liquid is proportional to the partial pressure of the gas. Divers often use atmospheres (ATM) as a measure of pressure, with 1 ATM being the pressure at sea level. Boyle’s law states that the volume of gas is inversely proportional to the pressure. As pressure increases, volume decreases.

Decompression sickness occurs when nitrogen comes out of solution as a diver ascends. The evolved gas can physically damage tissue by stretching or tearing it as bubbles expand, or by provoking an inflammatory response. Joints and spinal nervous tissue are commonly affected. Symptoms of primary damage usually appear immediately or soon after a dive, while secondary damage may present hours or days later.

Arterial gas embolism occurs when nitrogen bubbles escape into the arterial circulation and cause distal ischemia. The consequences depend on where the embolism lodges, ranging from tissue ischemia to stroke if it lodges in the cerebral arterial circulation. Mechanisms for distal embolism include pulmonary barotrauma, right to left shunt, and pulmonary filter overload.

Clinical features of decompression illness vary, but symptoms often appear within six hours of a dive. These can include joint pain, neurological symptoms, chest pain or breathing difficulties, rash, vestibular problems, and constitutional symptoms. Factors that increase the risk of DCI include diving at greater depth, longer duration, multiple dives close together, problems with ascent, closed rebreather circuits, flying shortly after diving, exercise shortly after diving, dehydration, and alcohol use.

Diagnosis of DCI is clinical, and investigations depend on the presentation. All patients should receive high flow oxygen, and a low threshold for ordering a chest X-ray should be maintained. Hydration is important, and IV fluids may be necessary. Definitive treatment is recompression therapy in a hyperbaric oxygen chamber, which should be arranged as soon as possible. Entonox should not be given, as it will increase the pressure effect in air spaces.

Cushing’s disease is a specific cause of Cushing’s syndrome and should be distinguished from it. It is characterized by an adenoma of the pituitary gland that produces excessive amounts of ACTH, leading to elevated cortisol levels. To confirm the presence of Cushing’s syndrome, a 24-hour urinary free cortisol collection can be done. However, to confirm Cushing’s disease and the presence of a pituitary adenoma, imaging of the pituitary gland using MRI or CT is necessary. Typically, ACTH levels are elevated in Cushing’s disease. The compression of the optic chiasm by the pituitary adenoma may result in bitemporal hemianopia. Cortisol levels in the body fluctuate throughout the day, with the highest levels occurring at 0900 hrs and the lowest during sleep at 2400 hrs. In Cushing’s disease, there is a loss of the normal diurnal variation in cortisol levels, and levels remain elevated throughout the entire 24-hour period. While cortisol levels may be within the normal range in the morning, they are often high at midnight when they are typically suppressed.

Hyperkalemia is a condition where the level of potassium in the blood is higher than normal, specifically greater than 5.5 mmol/l. It can be categorized as mild, moderate, or severe depending on the potassium level. Mild hyperkalemia is when the potassium level is between 5.5-5.9 mmol/l, moderate hyperkalemia is between 6.0-6.4 mmol/l, and severe hyperkalemia is above 6.5 mmol/l. The most common cause of hyperkalemia is renal failure, which can be acute or chronic. Other causes include acidosis, adrenal insufficiency, cell lysis, and excessive potassium intake.

In the treatment of hyperkalemia, calcium plays a crucial role. It works by counteracting the harmful effects of high potassium levels on the heart by stabilizing the cardiac cell membrane. Calcium acts quickly, with its effects seen within 15 minutes, but its effects are relatively short-lived. It is considered a first-line treatment for arrhythmias and significant ECG abnormalities caused by hyperkalemia. However, it is rare to see arrhythmias occur at potassium levels below 7.5 mmol/l.

It’s important to note that calcium does not lower the serum level of potassium. Therefore, when administering calcium, other therapies that actually help lower potassium levels, such as insulin and salbutamol, should also be used. Insulin and salbutamol are effective in reducing serum potassium levels.

When choosing between calcium chloride and calcium gluconate, calcium chloride is preferred when hyperkalemia is accompanied by hemodynamic compromise. This is because calcium chloride contains three times more elemental calcium than an equal volume of calcium gluconate.

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.

Conjunctivitis is the most frequent occurrence of Chlamydia trachomatis infection in newborns. Ophthalmia neonatorum refers to any cause of conjunctivitis during the newborn period, regardless of the specific organism responsible. Chlamydia is now the leading cause, accounting for up to 40% of cases. Neisseria gonorrhoea, on the other hand, only accounts for less than 1% of reported cases. The remaining cases are caused by non-sexually transmitted bacteria like Staphylococcus, Streptococcus, Haemophilus species, and viruses.

Gonorrhoeal ophthalmia neonatorum typically presents within 1 to 5 days after birth. It is characterized by intense redness and swelling of the conjunctiva, eyelid swelling, and a severe discharge of pus. Corneal ulceration and perforation may also be present.

Chlamydial ophthalmia neonatorum, on the other hand, usually appears between 5 to 14 days after birth. It is characterized by a gradually increasing watery discharge that eventually becomes purulent. The inflammation in the eyes is usually less severe compared to gonococcal infection, and there is a lower risk of corneal ulceration and perforation.

The second most common manifestation of Chlamydia trachomatis infection in newborns is pneumonia. Approximately 5-30% of infected neonates will develop pneumonia. About half of these infants will also have a history of ophthalmia neonatorum.

The primary symptom typically associated with carbon monoxide poisoning is a headache.

Carbon monoxide (CO) is a dangerous gas that is produced by the combustion of hydrocarbon fuels and can be found in certain chemicals. It is colorless and odorless, making it difficult to detect. In England and Wales, there are approximately 60 deaths each year due to accidental CO poisoning.

When inhaled, carbon monoxide binds to haemoglobin in the blood, forming carboxyhaemoglobin (COHb). It has a higher affinity for haemoglobin than oxygen, causing a left-shift in the oxygen dissociation curve and resulting in tissue hypoxia. This means that even though there may be a normal level of oxygen in the blood, it is less readily released to the tissues.

The clinical features of carbon monoxide toxicity can vary depending on the severity of the poisoning. Mild or chronic poisoning may present with symptoms such as headache, nausea, vomiting, vertigo, confusion, and weakness. More severe poisoning can lead to intoxication, personality changes, breathlessness, pink skin and mucosae, hyperpyrexia, arrhythmias, seizures, blurred vision or blindness, deafness, extrapyramidal features, coma, or even death.

To help diagnose domestic carbon monoxide poisoning, there are four key questions that can be asked using the COMA acronym. These questions include asking about co-habitees and co-occupants in the house, whether symptoms improve outside of the house, the maintenance of boilers and cooking appliances, and the presence of a functioning CO alarm.

Typical carboxyhaemoglobin levels can vary depending on whether the individual is a smoker or non-smoker. Non-smokers typically have levels below 3%, while smokers may have levels below 10%. Symptomatic individuals usually have levels between 10-30%, and severe toxicity is indicated by levels above 30%.

When managing carbon monoxide poisoning, the first step is to administer 100% oxygen. Hyperbaric oxygen therapy may be considered for individuals with a COHb concentration of over 20% and additional risk factors such as loss of consciousness, neurological signs, myocardial ischemia or arrhythmia, or pregnancy. Other management strategies may include fluid resuscitation, sodium bicarbonate for metabolic acidosis, and mannitol for cerebral edema.

Von Willebrand disease (vWD) is a common hereditary coagulation disorder that affects about 1 in 100 people. It occurs due to a deficiency in Von Willebrand factor (vWF), which is responsible for protecting factor VIII from breaking down too quickly in the blood. Additionally, vWF is necessary for proper platelet adhesion, so a lack of it can lead to abnormal platelet function. As a result, both the APTT and bleeding time are prolonged, while the platelet count and thrombin time remain unaffected.

In many cases, vWD goes unnoticed as patients do not experience any symptoms. It is often diagnosed incidentally during a routine clotting profile check. However, if symptoms do occur, the most common ones are easy bruising, nosebleeds, and heavy menstrual bleeding. In severe cases, more serious bleeding and joint bleeds can occur.

For mild cases of von Willebrand disease, bleeding can be treated with desmopressin. This medication helps increase the patient’s own levels of vWF by releasing stored vWF from the Weibel-Palade bodies in the endothelial cells. These bodies are storage granules found in the inner lining of blood vessels and the heart. In more severe cases, replacement therapy is necessary, which involves infusing cryoprecipitate or Factor VIII concentrate. Replacement therapy is recommended for patients with severe von Willebrand’s disease who are undergoing moderate or major surgical procedures.

Infective endocarditis is a condition that can be identified by certain signs, although none of them are definitive proof of the disease. The most reliable indicators are the presence of a heart murmur and a fever. However, there are other signs that are commonly associated with infective endocarditis, including splinter hemorrhages, Osler’s nodes, Janeway lesions, and Roth spots. It is important to note that these signs can also appear in other conditions, and they are not always present in patients with infective endocarditis. In fact, each of these signs is typically found in less than a third of patients diagnosed with the disease.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

The risk of contracting meningococcal disease from a close contact is low. However, the risk is highest within the first seven days after the disease is diagnosed and decreases significantly afterwards.

Prophylaxis or vaccination for close contacts is typically organized by secondary care. It is recommended for the following individuals, regardless of their meningococcal vaccination status:

– People who have had prolonged close contact with the infected person in a household-type setting during the seven days prior to the onset of illness. This includes individuals living or sleeping in the same household, students in the same dormitory, partners, or university students sharing a kitchen in a hall of residence.

– People who have had brief close contact with the infected person, but only if they have been directly exposed to large particle droplets or secretions from the respiratory tract of the case around the time of admission to the hospital.

Antibiotic prophylaxis should be administered as soon as possible, ideally within 24 hours after the diagnosis of the index case.

Post-exposure prophylaxis is recommended for healthcare staff who have been exposed to direct nasopharyngeal secretions (without wearing a mask or personal protective equipment) from a known or highly probable case. This includes situations such as mouth-to-mouth resuscitation, airway management (suction/intubation), or prolonged close care within 1 meter of the patient who has been coughing or sneezing droplet secretions.

For more information, you can refer to the NICE Clinical Knowledge Summary on the management of close contacts of patients with meningococcal disease.

This man is experiencing an acute asthma episode. His initial peak flow is 55% of his best, indicating a moderate exacerbation. In such cases, it is recommended to administer steroids, specifically a dose of prednisolone 40-50 mg orally.

Chest X-rays are not routinely performed to investigate acute asthma. However, they should be considered in certain situations, including suspected pneumomediastinum, consolidation, life-threatening asthma, inadequate response to treatment, and the need for ventilation.

Nebulised ipratropium bromide is only added to treatment with nebulised salbutamol in patients with acute severe or life-threatening asthma, or those who do not respond well to salbutamol therapy. Therefore, it is not necessary in this particular case.

While it may be reasonable to prescribe an antihistamine for a patient with a history of worsening hay fever, it should not be prioritized over treatment with steroids.

Hypothermia occurs when the core body temperature drops below 35°C. It is categorized as mild (32-35°C), moderate (28-32°C), or severe (<28°C). Rescuers at the scene can use the Swiss staging system to describe the condition of victims. The stages range from clearly conscious and shivering to unconscious and not breathing, with death due to irreversible hypothermia being the most severe stage. There are several risk factors for hypothermia, including environmental exposure, unsatisfactory housing, poverty, lack of cold awareness, drugs, alcohol, acute confusion, hypothyroidism, and sepsis. The clinical features of hypothermia vary depending on the severity. At 32-35°C, symptoms may include apathy, amnesia, ataxia, and dysarthria. At 30-32°C, there may be a decreased level of consciousness, hypotension, arrhythmias, respiratory depression, and muscular rigidity. Below 30°C, ventricular fibrillation may occur, especially with excessive movement or invasive procedures. Diagnosing hypothermia involves checking the core temperature using an oesophageal, rectal, or tympanic probe with a low reading thermometer. Rectal and tympanic temperatures may lag behind core temperature and are unreliable in hypothermia. Various investigations should be carried out, including blood tests, blood glucose, amylase, blood cultures, arterial blood gas, ECG, chest X-ray, and CT head if there is suspicion of head injury or CVA. The management of hypothermia involves supporting the ABCs, treating the patient in a warm room, removing wet clothes and drying the skin, monitoring the ECG, providing warmed, humidified oxygen, correcting hypoglycemia with IV glucose, and handling the patient gently to avoid VF arrest. Re-warming methods include passive re-warming with warm blankets or Bair hugger/polythene sheets, surface re-warming with a water bath, core re-warming with heated, humidified oxygen or peritoneal lavage, and extracorporeal re-warming via cardiopulmonary bypass for severe hypothermia/cardiac arrest. In the case of hypothermic cardiac arrest, CPR should be performed with chest compressions and ventilations at standard rates.

Metastatic spinal cord compression (MSCC) occurs when a tumor mass compresses the thecal sac and its components, leading to a spinal emergency. If the pressure on the spinal cord is not relieved promptly, it can result in irreversible loss of neurological function. The most crucial factor for predicting functional outcomes is the patient’s neurological function before treatment. Therefore, delayed treatment can lead to permanent disability and a decrease in quality of life.

The most common cancers that cause MSCC include prostate, lung, breast, and myeloma. In approximately 10 to 20% of cancer patients, MSCC is the first noticeable symptom. It is important to consider MSCC in any patient with a history of cancer if they experience any of the following symptoms: severe or worsening lower back pain, nocturnal pain that disrupts sleep, localized spinal tenderness, radicular pain, or neurological symptoms.

Thoracic pain can also be an indicator of MSCC or an aortic aneurysm. In patients aged 60 or older with persistent back pain, myeloma should be considered. For patients aged 60 or older with accompanying weight loss, pancreatic cancer should be taken into consideration.

Metformin is a type of biguanide medication that, when taken alone, does not lead to low blood sugar levels (hypoglycemia). However, it can potentially worsen hypoglycemia when used in combination with other drugs like sulphonylureas.

Gliclazide, on the other hand, is a sulphonylurea medication known to cause hypoglycemia. Pioglitazone, a thiazolidinedione drug, is also recognized as a cause of hypoglycemia.

It’s important to note that Actrapid and Novomix are both forms of insulin, which can also result in hypoglycemia.

The duration of submersion is the most crucial factor in predicting the outcome of drowning incidents. If the submersion time is less than 10 minutes, it is considered a positive indicator for prognosis, while if it exceeds 25 minutes, it is considered a negative indicator. There are other factors that are associated with higher rates of illness and death, such as a low Glasgow Coma Score, absence of pupillary response, pH imbalance (acidosis), and low blood pressure (hypotension). However, it is important to note that these prognostic factors have not been consistently validated in studies and cannot reliably predict the outcome of drowning incidents.

Further Reading:

Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid. It can be classified as cold-water or warm-water drowning. Risk factors for drowning include young age and male sex. Drowning impairs lung function and gas exchange, leading to hypoxemia and acidosis. It also causes cardiovascular instability, which contributes to metabolic acidosis and cell death.

When someone is submerged or immersed, they will voluntarily hold their breath to prevent aspiration of water. However, continued breath holding causes progressive hypoxia and hypercapnia, leading to acidosis. Eventually, the respiratory center sends signals to the respiratory muscles, forcing the individual to take an involuntary breath and allowing water to be aspirated into the lungs. Water entering the lungs stimulates a reflex laryngospasm that prevents further penetration of water. Aspirated water can cause significant hypoxia and damage to the alveoli, leading to acute respiratory distress syndrome (ARDS).

Complications of drowning include cardiac ischemia and infarction, infection with waterborne pathogens, hypothermia, neurological damage, rhabdomyolysis, acute tubular necrosis, and disseminated intravascular coagulation (DIC).

In children, the diving reflex helps reduce hypoxic injury during submersion. It causes apnea, bradycardia, and peripheral vasoconstriction, reducing cardiac output and myocardial oxygen demand while maintaining perfusion of the brain and vital organs.

Associated injuries with drowning include head and cervical spine injuries in patients rescued from shallow water. Investigations for drowning include arterial blood gases, chest X-ray, ECG and cardiac monitoring, core temperature measurement, and blood and sputum cultures if secondary infection is suspected.

Management of drowning involves extricating the patient from water in a horizontal position with spinal precautions if possible. Cardiovascular considerations should be taken into account when removing patients from water to prevent hypotension and circulatory collapse. Airway management, supplemental oxygen, and ventilation strategies are important in maintaining oxygenation and preventing further lung injury. Correcting hypotension, electrolyte disturbances, and hypothermia is also necessary. Attempting to drain water from the lungs is ineffective.

Patients without associated physical injury who are asymptomatic and have no evidence of respiratory compromise after six hours can be safely discharged home. Ventilation strategies aim to maintain oxygenation while minimizing ventilator-associated lung injury.

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

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

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

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

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

Mitral regurgitation is characterized by several clinical features. One of the main signs is a pansystolic murmur that can be heard throughout the entire systolic phase of the cardiac cycle. This murmur often radiates to the left axilla. Another notable feature is a soft S1 heart sound, which is the first heart sound heard during the cardiac cycle. Additionally, a 3rd heart sound, also known as an added sound, can be detected in patients with mitral regurgitation. As the condition progresses to moderate to severe levels, signs such as a laterally displaced apex beat with a heave may become apparent.

Further Reading:

Mitral Stenosis:
– Causes: Rheumatic fever, Mucopolysaccharidoses, Carcinoid, Endocardial fibroelastosis
– Features: Mid-late diastolic murmur, loud S1, opening snap, low volume pulse, malar flush, atrial fibrillation, signs of pulmonary edema, tapping apex beat
– Features of severe mitral stenosis: Length of murmur increases, opening snap becomes closer to S2
– Investigation findings: CXR may show left atrial enlargement, echocardiography may show reduced cross-sectional area of the mitral valve

Mitral Regurgitation:
– Causes: Mitral valve prolapse, Myxomatous degeneration, Ischemic heart disease, Rheumatic fever, Connective tissue disorders, Endocarditis, Dilated cardiomyopathy
– Features: pansystolic murmur radiating to left axilla, soft S1, S3, laterally displaced apex beat with heave
– Signs of acute MR: Decompensated congestive heart failure symptoms
– Signs of chronic MR: Leg edema, fatigue, arrhythmia (atrial fibrillation)
– Investigation findings: Doppler echocardiography to detect regurgitant flow and pulmonary hypertension, ECG may show signs of LA enlargement and LV hypertrophy, CXR may show LA and LV enlargement in chronic MR and pulmonary edema in acute MR.

Currently, there are three beta-blockers that have been approved for the treatment of chronic heart failure. These medications include bisoprolol, carvedilol, and nebivolol.

Chronic HF is a common clinical syndrome resulting from coronary artery disease (CAD), HTN, valvular heart disease, and/or primary cardiomyopathy. There is now conclusive evidence that β-blockers, when added to ACE inhibitors, substantially reduce mortality, decrease sudden death, and improve symptoms in patients with HF. Despite the overwhelming evidence and guidelines that mandate the use of β-blockers in all HF patients without contraindications, many patients do not receive this treatment.

Psittacosis is a type of infection that can be transmitted from animals to humans, known as a zoonotic infection. It is caused by a bacterium called Chlamydia psittaci. This infection is most commonly seen in people who own domestic birds, but it can also affect those who work in pet shops or zoos.

The typical presentation of psittacosis includes symptoms similar to those of pneumonia that is acquired within the community. People may experience flu-like symptoms along with severe headaches and sensitivity to light. In about two-thirds of patients, an enlargement of the spleen, known as splenomegaly, can be observed.

Infected individuals often develop a reddish rash with flat spots on their face, known as Horder’s spots. Additionally, they may experience skin conditions such as erythema nodosum or erythema multiforme.

The recommended treatment for psittacosis is a course of tetracycline or doxycycline, which should be taken for a period of 2-3 weeks.

The posterior interosseous nerve (PIN) is a motor branch of the radial nerve that is located deep within the body. It emerges above the elbow, between the brachioradialis and brachialis muscles, and then divides into two branches: the superficial radial nerve and the PIN. This division occurs at the lateral epicondyle level. As it travels through the forearm, the PIN passes through the supinator muscle, moving from the front to the back surface. In about 30% of individuals, it also passes through a fibrotendinous structure called the arcade of Frohse, which is located below the supinator muscle. The PIN is responsible for supplying all of the extrinsic wrist extensors, with the exception of the extensor carpi radialis longus muscle.

There are several potential causes of damage to the PIN. Fractures, such as a Monteggia fracture, can lead to injury. Inflammation of the radiocapitellar joint, known as radiocapitellar joint synovitis, can also be a contributing factor. Tumors, such as lipomas, may cause damage as well. Additionally, entrapment of the PIN within the arcade of Frohse can result in a condition known as PIN syndrome.

It is important to note that injury to the PIN can be easily distinguished from injury to the radial nerve in other areas of the arm, such as the spiral groove. This is because there will be no sensory involvement and no wrist drop, as the extensor carpi radialis longus muscle remains unaffected.

The anterior interosseous nerve (AIN) is a branch of the median nerve. It primarily functions as a motor nerve, supplying the flexor pollicis longus muscle, the lateral half of the flexor digitorum profundus muscle, and the pronator quadratus muscle. Damage to the AIN can result in weakness and difficulty moving the index and middle fingers.

When it comes to managing viral conjunctivitis, it’s important to reassure the patient that most cases are self-limiting and don’t require antimicrobial treatment. In fact, viral conjunctivitis usually resolves on its own within one to two weeks. However, there are some self-care measures that can help ease symptoms. These include cleaning the eyelids with cotton wool soaked in sterile saline or boiled and cooled water, applying cool compresses around the eye area, and using lubricating drops or artificial tears. It’s also important to avoid prescribing antibiotics if possible.

It’s crucial to inform the person that infective conjunctivitis is contagious and they should take steps to prevent spreading the infection to their other eye and other people. This includes washing hands frequently with soap and water, using separate towels and flannels, and avoiding close contact with others, especially if they are a healthcare professional or child-care provider. It’s worth noting that the infection can be contagious for up to 14 days from onset.

According to Public Health England, there is no recommended exclusion period from school, nursery, or childminders unless there is an outbreak or cluster of cases. It’s important to provide written information to the patient, explain the red flags for an urgent review, and advise them to seek further help if symptoms persist beyond 7 days. If the person returns with symptoms of conjunctivitis, it may be necessary to consider sending swabs for viral PCR and bacterial culture, as well as prescribing empirical topical antibiotics if they haven’t already been prescribed. If symptoms persist for more than 7-10 days after initiating treatment, it may be necessary to discuss with or refer to ophthalmology.