The guidelines from the British Thoracic Society (BTS) recommend conducting investigations for Legionella infection in the following cases: severe community-acquired pneumonia, patients with specific risk factors, and during outbreaks of community-acquired pneumonia. To confirm a case, the Public Health England (PHE) requires one of the following: isolation and culture of Legionella species from clinical specimens (typically sputum), seroconversion with a four-fold increase in titre of indirect immunofluorescent antibody test (IFAT) using a validated technique, or confirmation of Legionella pneumophila urinary antigen using validated reagents or kits. The gold standard for confirmation is the isolation and culture of Legionella species, while cases of Pontiac fever are usually culture-negative. The HPA considers a case presumptive if there is a clinical diagnosis of pneumonia with a single high titre of 128 using IFAT, or a single titre of 64 in an outbreak. A positive result by direct immunofluorescence on a clinical specimen using validated monoclonal antibodies is also considered a presumptive case.

Croup is usually preceded by symptoms such as cough, runny nose, and nasal congestion. These symptoms typically occur 12 to 72 hours before the onset of a distinctive barking cough. The barking cough, which resembles the sound of a seal, is particularly severe at night. It is important to note that the cough may be preceded by prodromal upper respiratory tract symptoms, including cough, runny nose, and nasal congestion, within a timeframe of 12 to 72 hours.

Further Reading:

Croup, also known as laryngotracheobronchitis, is a respiratory infection that primarily affects infants and toddlers. It is characterized by a barking cough and can cause stridor (a high-pitched sound during breathing) and respiratory distress due to swelling of the larynx and excessive secretions. The majority of cases are caused by parainfluenza viruses 1 and 3. Croup is most common in children between 6 months and 3 years of age and tends to occur more frequently in the autumn.

The clinical features of croup include a barking cough that is worse at night, preceded by symptoms of an upper respiratory tract infection such as cough, runny nose, and congestion. Stridor, respiratory distress, and fever may also be present. The severity of croup can be graded using the NICE system, which categorizes it as mild, moderate, severe, or impending respiratory failure based on the presence of symptoms such as cough, stridor, sternal/intercostal recession, agitation, lethargy, and decreased level of consciousness. The Westley croup score is another commonly used tool to assess the severity of croup based on the presence of stridor, retractions, air entry, oxygen saturation levels, and level of consciousness.

In cases of severe croup with significant airway obstruction and impending respiratory failure, symptoms may include a minimal barking cough, harder-to-hear stridor, chest wall recession, fatigue, pallor or cyanosis, decreased level of consciousness, and tachycardia. A respiratory rate over 70 breaths per minute is also indicative of severe respiratory distress.

Children with moderate or severe croup, as well as those with certain risk factors such as chronic lung disease, congenital heart disease, neuromuscular disorders, immunodeficiency, age under 3 months, inadequate fluid intake, concerns about care at home, or high fever or a toxic appearance, should be admitted to the hospital. The mainstay of treatment for croup is corticosteroids, which are typically given orally. If the child is too unwell to take oral medication, inhaled budesonide or intramuscular dexamethasone may be used as alternatives. Severe cases may require high-flow oxygen and nebulized adrenaline.

When considering the differential diagnosis for acute stridor and breathing difficulty, non-infective causes such as inhaled foreign bodies

Salicylate poisoning is a fairly common form of poisoning that can lead to organ damage and death if not treated promptly. The symptoms of salicylate poisoning include nausea, vomiting, ringing in the ears, hearing loss, excessive sweating, dehydration, rapid breathing, flushed skin, and high fever in children. In severe cases, convulsions, swelling of the brain, coma, kidney failure, fluid in the lungs, and unstable heart function can occur.

The treatment for salicylate poisoning involves stabilizing the patient’s airway, breathing, and circulation as needed, preventing further absorption of the poison, enhancing its elimination from the body, correcting any metabolic abnormalities, and providing supportive care. Unfortunately, there is no specific antidote available for salicylates. If a large amount of salicylate has been ingested within the past hour (more than 4.5 grams in adults or more than 2 grams in children), gastric lavage (stomach pumping) and administration of activated charcoal (50 grams) are recommended to reduce absorption and increase elimination.

Medical investigations for salicylate poisoning should include measuring the level of salicylate in the blood, analyzing arterial blood gases, performing an electrocardiogram (ECG), checking blood glucose levels, assessing kidney function and electrolyte levels, and evaluating blood clotting. ECG abnormalities that may be present include widening of the QRS complex, AV block, and ventricular arrhythmias.

The severity of salicylate poisoning is determined by the level of salicylate in the blood. Mild poisoning is defined as a salicylate level below 450 mg/L, moderate poisoning is between 450-700 mg/L, and severe poisoning is above 700 mg/L. In severe cases, aggressive intravenous fluid therapy is necessary to correct dehydration, and administration of 1.26% sodium bicarbonate can help eliminate the salicylate from the body. It is important to maintain a urine pH of greater than 7.5, ideally between 8.0-8.5. However, forced alkaline diuresis is no longer recommended. Life-threatening cases may require admission to the intensive care unit, intubation and ventilation, and possibly hemodialysis.

Blood transfusion is a potentially life-saving treatment that can provide great clinical benefits. However, it also carries several risks and potential problems. These include immunological complications, administration errors, infections, immune dilution, and transfusion errors. While there have been improvements in safety procedures and efforts to minimize the use of transfusion, errors and serious adverse reactions still occur and often go unreported.

One rare complication of blood transfusion is transfusion-associated graft-vs-host disease (TA-GVHD). This condition typically presents with fever, rash, and diarrhea 1-4 weeks after the transfusion. Laboratory findings may show pancytopenia and abnormalities in liver function. Unlike GVHD after marrow transplantation, TA-GVHD leads to severe marrow aplasia with a mortality rate exceeding 90%. Unfortunately, there are currently no effective treatments available for this condition, and survival is rare, with death usually occurring within 1-3 weeks of the first symptoms.

During a blood transfusion, viable T lymphocytes from the donor are transfused into the recipient’s body. In TA-GVHD, these lymphocytes engraft and react against the recipient’s tissues. However, the recipient is unable to reject the donor lymphocytes due to factors such as immunodeficiency, severe immunosuppression, or shared HLA antigens. Supportive management is the only option for TA-GVHD.

The following summarizes the main complications and reactions that can occur during a blood transfusion:

Complication Features Management
Febrile transfusion reaction
– Presents with a 1-degree rise in temperature from baseline, along with chills and malaise.
– Most common reaction, occurring in 1 out of 8 transfusions.
– Usually caused by cytokines from leukocytes in transfused red cell or platelet components.
– Supportive management, with the use of paracetamol for symptom relief.

Acute haemolytic reaction
– Symptoms include fever, chills, pain at the transfusion site, nausea, vomiting, and dark urine.
– Often accompanied by a feeling of ‘impending doom’.
– Most serious type of reaction, often due to ABO incompatibility caused by administration errors.
– Immediate action required: stop the transfusion, administer IV fluids, and consider diuretics if necessary.

Delayed haemolytic reaction
– Typically occurs 4-8 days after a blood transfusion.
– Symptoms include fever, anemia and/or hyperbilirubinemia

In cases where there are no contraindications, high-dose NSAIDs are the recommended initial treatment for acute gout. A commonly used and effective regimen is to administer a stat dose of Naproxen 750 mg, followed by 250 mg three times a day. It is important to note that Aspirin should not be used in gout as it hinders the urinary clearance of urate and interferes with the action of uricosuric agents. Instead, more appropriate choices include Naproxen, diclofenac, or indomethacin.

Allopurinol is typically used as a prophylactic measure to prevent future gout attacks by reducing serum uric acid levels. However, it should not be initiated during the acute phase of an attack as it can worsen the severity and duration of symptoms.

Colchicine works by binding to tubulin and preventing neutrophil migration into the joint. It is just as effective as NSAIDs in relieving acute gout attacks. Additionally, it has a role in prophylactic treatment if a patient cannot tolerate Allopurinol.

It is important to note that NSAIDs are contraindicated in patients with heart failure as they can lead to fluid retention and congestive cardiac failure. In such cases, Colchicine is the preferred treatment option for patients with heart failure or those who cannot tolerate NSAIDs.

SIADH is a medical condition that is not brought on by lithium toxicity. However, lithium toxicity does have its own distinct set of symptoms. These symptoms include nausea and vomiting, diarrhea, tremors, ataxia, confusion, increased muscle tone, clonus, nephrogenic diabetes insipidus, convulsions, coma, and renal failure. It is important to note that SIADH and lithium toxicity are separate conditions with their own unique characteristics.

Lung protective ventilation involves several important elements, with low tidal volumes being a crucial component. Specifically, using tidal volumes of 5-8 ml/kg is recommended to minimize the risk of lung injury. Additionally, it is important to maintain inspiratory pressures, also known as plateau pressure, below 30 cm of water to further protect the lungs. Lastly, permissible hypercapnia, or allowing for higher levels of carbon dioxide in the blood, is another key aspect of lung protective ventilation.

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.

Maintaining adequate blood pressure is crucial in managing increased intracranial pressure (ICP). The recommended blood pressure targets may vary depending on the source. The Scottish Intercollegiate Guidelines Network (SIGN) suggests maintaining an adequate blood pressure, while the 4th edition of the Brain Trauma Foundation recommends maintaining a systolic blood pressure (SBP) above 100 mm Hg for individuals aged 50-69 years (or above 110 mm Hg for those aged 15-49 years) to reduce mortality and improve outcomes.

When managing a patient with increased ICP, the initial steps should include maintaining normal body temperature to prevent fever, positioning the patient with a 30º head-up tilt, and administering analgesia and sedation as needed. It is important to monitor and maintain blood pressure, using inotropes if necessary to achieve the target. Additionally, preparations should be made to use medications such as Mannitol or hypertonic saline to lower ICP if required. Hyperventilation may also be considered, although it carries the risk of inducing ischemia and requires monitoring of carbon dioxide levels.

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.

Type I hypersensitivity reactions are allergic reactions that occur when a person is exposed again to a particular antigen, known as an allergen. These reactions are triggered by IgE and typically happen within 15 to 30 minutes after exposure to the allergen.

A rapid onset of an urticarial rash, which occurs shortly after being exposed to an allergen (such as latex), is highly likely to be caused by a type I hypersensitivity reaction.

Amiodarone, a medication used to treat heart rhythm problems, can have effects on the thyroid gland. It can either cause hypothyroidism (low thyroid hormone levels) or hyperthyroidism (high thyroid hormone levels). Amiodarone is a highly fat-soluble drug that accumulates in various tissues, including the thyroid. Even after stopping the medication, its effects can still be seen due to its long elimination half-life of around 100 days.

The reason behind amiodarone impact on the thyroid is believed to be its high iodine content. In patients with sufficient iodine levels, amiodarone-induced hypothyroidism is more likely to occur. On the other hand, in populations with low iodine levels, amiodarone can lead to a condition called iodine-induced thyrotoxicosis, which is characterized by hyperthyroidism.

The mechanism of amiodarone-induced hypothyroidism involves the release of iodide from the drug, which blocks the uptake of further iodide by the thyroid gland and hampers the production of thyroid hormones. Additionally, amiodarone inhibits the conversion of the inactive thyroid hormone T4 to the active form T3.

Amiodarone-induced hyperthyroidism, on the other hand, is thought to occur in individuals with abnormal thyroid glands, such as those with nodular goiters, autonomous nodules, or latent Graves’ disease. In these cases, the excess iodine from amiodarone overwhelms the thyroid’s normal regulatory mechanisms, leading to hyperthyroidism.

Further Reading:

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

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

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

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

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

To treat DKA, the girl is receiving intravenous fluids to rehydrate her. Additionally, insulin needs to be prescribed to help regulate her blood sugar levels.

The most suitable insulin regimen in this case would be an IV insulin infusion at 0.05 units/kg/hour. This means that the insulin will be administered through an intravenous line at a rate of 0.05 units per kilogram of the girl’s body weight per hour. This dosage is appropriate for managing DKA and will help to lower her blood sugar levels effectively.

Further Reading:

Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

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

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

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

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

Chlamydia trachomatis is a type of bacteria that is accountable for causing the infection known as chlamydia. This bacterium is mainly transmitted through sexual contact.

There are various serological variants of C. trachomatis, and each variant is associated with different patterns of disease. Specifically, types D-K are responsible for causing genitourinary infections.

In the United Kingdom, chlamydia is the most commonly diagnosed sexually transmitted infection (STI). It is also the leading preventable cause of infertility worldwide. Interestingly, around 50% of men infected with chlamydia do not experience any symptoms, while at least 70% of infected women are asymptomatic.

If left untreated, chlamydia can lead to various complications. In women, these complications may include pelvic inflammatory disease (PID), ectopic pregnancy, and tubal infertility. Men, on the other hand, may experience complications such as proctitis, epididymitis, and epididymo-orchitis.

Methaemoglobinaemia is a condition that can occur when prilocaine is used, particularly when administered at doses higher than 16 mg/kg.

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.

Generally speaking, if a child shows clinical signs of dehydration but does not exhibit shock, it can be assumed that they are 5% dehydrated. On the other hand, if shock is also present, it can be assumed that the child is 10% dehydrated or more. When a child is 5% dehydrated, it means that their body has lost 5 grams of fluid per 100 grams of body weight, which is equivalent to 50 ml of fluid per kilogram. In the case of 10% dehydration, the body has lost 100 ml of fluid per kilogram.

For example, if a child is 10% dehydrated and weighs 30 kilograms, their estimated fluid loss would be 100 ml/kg x 30 kg = 3000 ml.

The clinical features of dehydration and shock are summarized below:

Dehydration (5%):
– The child appears unwell
– Their heart rate may be normal or increased (tachycardia)
– Their respiratory rate may be normal or increased (tachypnea)
– Peripheral pulses are normal
– Capillary refill time (CRT) is normal or slightly prolonged
– Blood pressure is normal
– Extremities feel warm
– Urine output is decreased
– Skin turgor is reduced
– Eyes may appear sunken
– The fontanelle (soft spot on the baby’s head) may be depressed
– Mucous membranes are dry

Clinical shock (10%):
– The child appears pale, lethargic, and mottled
– Heart rate is increased (tachycardia)
– Respiratory rate is increased (tachypnea)
– Peripheral pulses are weak
– Capillary refill time (CRT) is prolonged
– Blood pressure is low (hypotension)
– Extremities feel cold
– Urine output is decreased
– Level of consciousness is decreased

The recommended dose of ketamine for rapid sequence intubation (RSI) is typically 1.5 mg/kg administered intravenously. This dosage is commonly used in UK medical centers. According to the British National Formulary (BNF), intravenous induction doses of ketamine range from 0.5 to 2 mg/kg for longer procedures and 1 to 4.5 mg/kg for shorter procedures. Ketamine is known to cause an increase in blood pressure, making it a suitable option for individuals with hemodynamic compromise.

Further Reading:

There are four commonly used induction agents in the UK: propofol, ketamine, thiopentone, and etomidate.

Propofol is a 1% solution that produces significant venodilation and myocardial depression. It can also reduce cerebral perfusion pressure. The typical dose for propofol is 1.5-2.5 mg/kg. However, it can cause side effects such as hypotension, respiratory depression, and pain at the site of injection.

Ketamine is another induction agent that produces a dissociative state. It does not display a dose-response continuum, meaning that the effects do not necessarily increase with higher doses. Ketamine can cause bronchodilation, which is useful in patients with asthma. The initial dose for ketamine is 0.5-2 mg/kg, with a typical IV dose of 1.5 mg/kg. Side effects of ketamine include tachycardia, hypertension, laryngospasm, unpleasant hallucinations, nausea and vomiting, hypersalivation, increased intracranial and intraocular pressure, nystagmus and diplopia, abnormal movements, and skin reactions.

Thiopentone is an ultra-short acting barbiturate that acts on the GABA receptor complex. It decreases cerebral metabolic oxygen and reduces cerebral blood flow and intracranial pressure. The adult dose for thiopentone is 3-5 mg/kg, while the child dose is 5-8 mg/kg. However, these doses should be halved in patients with hypovolemia. Side effects of thiopentone include venodilation, myocardial depression, and hypotension. It is contraindicated in patients with acute porphyrias and myotonic dystrophy.

Etomidate is the most haemodynamically stable induction agent and is useful in patients with hypovolemia, anaphylaxis, and asthma. It has similar cerebral effects to thiopentone. The dose for etomidate is 0.15-0.3 mg/kg. Side effects of etomidate include injection site pain, movement disorders, adrenal insufficiency, and apnoea. It is contraindicated in patients with sepsis due to adrenal suppression.

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

Many systemic illnesses have distinct dermatological associations. Some of these are listed below:

Addison’s disease is characterized by pigmentation and vitiligo.

Cushing’s disease is associated with pigmentation, striae, hirsutism, and acne.

Diabetes mellitus can cause necrobiosis lipoidica, which presents as shiny, yellowish plaques on the shin. It can also lead to xanthoma, a condition characterized by yellowish lipid deposits in the skin, and granuloma annulare, which manifests as palpable ring lesions on the hands, face, or feet.

Hyperlipidemia is linked to xanthoma and xanthomata, which are yellowish plaques on the eyelids.

Crohn’s disease is associated with erythema nodosum.

Ulcerative colitis can cause pyoderma gangrenosum and erythema nodosum.

Liver disease often presents with pruritus, spider naevi, and erythema.

Malignancy can lead to mycosis fungoides, a type of lymphoma that affects the skin. It is also associated with acanthosis nigricans, which is often seen in gastrointestinal malignancies.

Hypothyroidism is linked to alopecia, while thyrotoxicosis can cause both alopecia and pretibial myxedema.

Intralipid is a lipid emulsion that is commonly used as a source of nutrition in parenteral nutrition. However, it has also been found to be effective in treating local anesthetic toxicity. When administered intravenously, Intralipid acts as a lipid sink, meaning it can bind to the local anesthetic agent and remove it from the affected tissues, thereby reversing the toxic effects.

In cases of cardiac arrest related to local anesthetic toxicity, Intralipid can be administered as a bolus followed by an infusion. The recommended dose is typically 1.5 mL/kg bolus over 1 minute, followed by an infusion of 0.25 mL/kg/minute for 10 minutes. This can be repeated if necessary.

It is important to note that while Intralipid has shown promising results in treating local anesthetic toxicity, it should not replace standard ALS protocols. Basic life support (BLS) measures, such as cardiopulmonary resuscitation (CPR), should still be initiated immediately, and advanced cardiac life support (ACLS) protocols should be followed.

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 diagnosis in this case is clearly gout. According to the guidelines from the European League Against Rheumatism (EULAR), the development of sudden joint pain accompanied by swelling, tenderness, and redness, which worsens over a period of 6-12 hours, strongly suggests crystal arthropathy.

Checking serum urate levels to confirm high levels of uric acid before starting treatment for acute gout attacks is not very beneficial and should not delay treatment. While these levels can be useful for monitoring treatment response, they often decrease during an acute attack and can even be normal. If levels are checked and found to be normal during an attack, they should be rechecked once the attack has resolved.

The first-line treatment for acute gout attacks is non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen. However, caution should be exercised when using NSAIDs in patients with a history of hypertension. Since this patient has had difficulty controlling their blood pressure and remains hypertensive, it would be wise to avoid NSAIDs in this case.

Colchicine is an effective alternative for treating gout, although it may take longer to take effect. It is often used in patients who cannot take NSAIDs due to contraindications, such as hypertension or a history of peptic ulcer disease. It’s important to note that colchicine can have effects on the bone marrow, leading to an increase in neutrophils and a decrease in platelets. Therefore, it should not be used in patients with blood disorders, as is the case with this patient.

Allopurinol should not be used during an acute gout attack as it can prolong the attack and even trigger another acute attack. If a patient is already taking allopurinol, it should be continued, and the acute attack should be treated with NSAIDs, colchicine, or corticosteroids as appropriate.

Corticosteroids are an effective alternative for managing acute gout in patients who cannot take NSAIDs or colchicine. They can be administered orally, intramuscularly, intravenously, or directly into the affected joint. In this patient’s case, using corticosteroids would be the safest and most reasonable treatment option.

Lithium is a medication used to stabilize mood and is approved for the treatment and prevention of mania, bipolar disorder, recurrent depression, and aggressive or self-harming behavior. During pregnancy and the postnatal period, it is important to monitor lithium levels more frequently. If taken during the first trimester, lithium is associated with an increased risk of fetal cardiac malformations, such as Ebstein’s anomaly. If taken during the second and third trimesters, there is a risk of various complications in the newborn, including hypotonia, lethargy, feeding problems, hypothyroidism, goiter, and nephrogenic diabetes insipidus.

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

Drug: ACE inhibitors (e.g. ramipril)
Adverse effects: If taken during the second and third trimesters, ACE inhibitors can cause hypoperfusion, renal failure, and the oligohydramnios sequence.

Drug: Aminoglycosides (e.g. gentamicin)
Adverse effects: Aminoglycosides can cause ototoxicity and deafness in the fetus.

Drug: Aspirin
Adverse effects: High doses of aspirin can lead to 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 a significant risk.

Drug: Benzodiazepines (e.g. diazepam)
Adverse effects: When taken late in pregnancy, benzodiazepines can cause respiratory depression and a neonatal withdrawal syndrome.

Drug: Calcium-channel blockers
Adverse effects: If taken during the first trimester, calcium-channel blockers can cause phalangeal abnormalities. If taken during the second and third trimesters, they can lead to fetal growth retardation.

The Royal College of Emergency Medicine (RCEM) recommends asking four important questions to individuals showing signs and symptoms of carbon monoxide poisoning. These questions can be easily remembered using the acronym COMA. The questions are as follows:
1. Is anyone else in the house, including pets, experiencing similar symptoms?
2. Do the symptoms improve when you are outside of the house?
3. Are the boilers and cooking appliances in your house properly maintained?
4. Do you have a functioning carbon monoxide alarm?

Further Reading:

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.

Gout and pseudogout are both characterized by the presence of crystal deposits in the joints that are affected. Gout occurs when urate crystals are deposited, while pseudogout occurs when calcium pyrophosphate crystals are deposited. Under a microscope, these crystals can be distinguished by their appearance. Urate crystals are needle-shaped and negatively birefringent, while calcium pyrophosphate crystals are brick-shaped and positively birefringent.

Gout can affect any joint in the body, but it most commonly manifests in the hallux metatarsophalangeal joint, which is the joint at the base of the big toe. This joint is affected in approximately 50% of gout cases. On the other hand, pseudogout primarily affects the larger joints, such as the knee.

The current recommendations from NICE for managing warfarin in the presence of bleeding or an abnormal INR are as follows:

In cases of major active bleeding, regardless of the INR level, the first step is to stop administering warfarin. Next, 5 mg of vitamin K (phytomenadione) should be given intravenously. Additionally, dried prothrombin complex concentrate, which contains factors II, VII, IX, and X, should be administered. If dried prothrombin complex is not available, fresh frozen plasma can be given at a dose of 15 ml/kg.

If the INR is greater than 8.0 and there is minor bleeding, warfarin should be stopped. Slow injection of 1-3 mg of vitamin K can be given, and this dose can be repeated after 24 hours if the INR remains high. Warfarin can be restarted once the INR is less than 5.0.

If the INR is greater than 8.0 with no bleeding, warfarin should be stopped. Oral administration of 1-5 mg of vitamin K can be given, and this dose can be repeated after 24 hours if the INR remains high. Warfarin can be restarted once the INR is less than 5.0.

If the INR is between 5.0-8.0 with minor bleeding, warfarin should be stopped. Slow injection of 1-3 mg of vitamin K can be given, and warfarin can be restarted once the INR is less than 5.0.

If the INR is between 5.0-8.0 with no bleeding, one or two doses of warfarin should be withheld, and the subsequent maintenance dose should be reduced.

For more information, please refer to the NICE Clinical Knowledge Summary on the management of warfarin therapy and the BNF guidance on the use of phytomenadione.

This situation is potentially complicated and involves another family member. The patient currently lives alone and based on the given history, it seems to be a mild episode of epistaxis. Without any additional information, it would be reasonable to assume that the patient can continue living in his current conditions.

It is crucial to listen to the family’s concerns. However, it is important to keep the patient as the main focus. Out of the options provided, the most sensible approach would be to have a conversation with the patient regarding his son’s concerns and understand his perspective on those concerns.

During Bier’s block, the cuff is inflated to a pressure that is 100 mmHg higher than the patient’s systolic blood pressure. For example, if the systolic blood pressure is 150 mmHg, the cuff would be inflated to 250 mmHg. It is important to note that Bier’s block should not be performed if the systolic blood pressure is greater than 200 mmHg, as this is considered a contraindication. Therefore, the maximum pressure ever used during Bier’s block is 300mmHg.

Further Reading:

Bier’s block is a regional intravenous anesthesia technique commonly used for minor surgical procedures of the forearm or for reducing distal radius fractures in the emergency department (ED). It is recommended by NICE as the preferred anesthesia block for adults requiring manipulation of distal forearm fractures in the ED.

Before performing the procedure, a pre-procedure checklist should be completed, including obtaining consent, recording the patient’s weight, ensuring the resuscitative equipment is available, and monitoring the patient’s vital signs throughout the procedure. The air cylinder should be checked if not using an electronic machine, and the cuff should be checked for leaks.

During the procedure, a double cuff tourniquet is placed on the upper arm, and the arm is elevated to exsanguinate the limb. The proximal cuff is inflated to a pressure 100 mmHg above the systolic blood pressure, up to a maximum of 300 mmHg. The time of inflation and pressure should be recorded, and the absence of the radial pulse should be confirmed. 0.5% plain prilocaine is then injected slowly, and the time of injection is recorded. The patient should be warned about the potential cold/hot sensation and mottled appearance of the arm. After injection, the cannula is removed and pressure is applied to the venipuncture site to prevent bleeding. After approximately 10 minutes, the patient should have anesthesia and should not feel pain during manipulation. If anesthesia is successful, the manipulation can be performed, and a plaster can be applied by a second staff member. A check x-ray should be obtained with the arm lowered onto a pillow. The tourniquet should be monitored at all times, and the cuff should be inflated for a minimum of 20 minutes and a maximum of 45 minutes. If rotation of the cuff is required, it should be done after the manipulation and plaster application. After the post-reduction x-ray is satisfactory, the cuff can be deflated while observing the patient and monitors. Limb circulation should be checked prior to discharge, and appropriate follow-up and analgesia should be arranged.

There are several contraindications to performing Bier’s block, including allergy to local anesthetic, hypertension over 200 mm Hg, infection in the limb, lymphedema, methemoglobinemia, morbid obesity, peripheral vascular disease, procedures needed in both arms, Raynaud’s phenomenon, scleroderma, severe hypertension and sickle cell disease.

In patients with hypothermia, it is important to use a low reading thermometer such as an oesophageal temperature probe or vascular temperature probe. Skin surface thermometers are not effective in hypothermia cases, and rectal and tympanic thermometers may not provide accurate readings. Therefore, it is recommended to use oesophageal temperature or vascular temperature probes. However, it is worth noting that oesophageal probes may not be accurate if the patient is receiving warmed inhaled air.

Further Reading:

Hypothermic cardiac arrest is a rare situation that requires a tailored approach. Resuscitation is typically prolonged, but the prognosis for young, previously healthy individuals can be good. Hypothermic cardiac arrest may be associated with drowning. 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, basal metabolic rate falls and cell signaling between neurons decreases, leading to reduced tissue perfusion. Signs and symptoms of hypothermia progress as the core temperature drops, initially presenting as compensatory increases in heart rate and shivering, but eventually ceasing as the temperature drops into moderate hypothermia territory.

ECG changes associated with hypothermia include bradyarrhythmias, Osborn waves, prolonged PR, QRS, and QT intervals, shivering artifact, ventricular ectopics, and cardiac arrest. When managing hypothermic cardiac arrest, ALS should be initiated as per the standard ALS algorithm, but with modifications. It is important to check for signs of life, re-warm the patient, consider mechanical ventilation due to chest wall stiffness, adjust dosing or withhold drugs due to slowed drug metabolism, and correct electrolyte disturbances. The resuscitation of hypothermic patients is often prolonged and may continue for a number of hours.

Pulse checks during CPR may be difficult due to low blood pressure, and the pulse check is prolonged to 1 minute for this reason. Drug metabolism is slowed in hypothermic patients, leading to a build-up of potentially toxic plasma concentrations of administered drugs. Current guidance advises withholding drugs if the core temperature is below 30ºC and doubling the drug interval at core temperatures between 30 and 35ºC. Electrolyte disturbances are common in hypothermic patients, and it is important to interpret results keeping the setting in mind. Hypoglycemia should be treated, hypokalemia will often correct as the patient re-warms, ABG analyzers may not reflect the reality of the hypothermic patient, and severe hyperkalemia is a poor prognostic indicator.

Different warming measures can be used to increase the core body temperature, including external passive measures such as removal of wet clothes and insulation with blankets, external active measures such as forced heated air or hot-water immersion, and internal active measures such as inhalation of warm air, warmed intravenous fluids, gastric, bladder, peritoneal and/or pleural lavage and high volume renal haemofilter.

Chickenpox in children is usually managed conservatively. In this case, the patient has chickenpox but does not show any signs of serious illness. The parents should be given advice on keeping the child out of school, ensuring they stay hydrated, and providing relief for their symptoms. It is important to provide appropriate safety measures in case the child’s condition worsens. Admission to the hospital is not recommended for uncomplicated chickenpox as it could spread the infection to other children, especially those who may have a weakened immune system. Aciclovir should not be used for uncomplicated chickenpox in children. VZIG is given as a preventive measure for infection, mainly for pregnant women without immunity, and is not a treatment for those already infected. There is no need to check both parents’ IgG levels unless the mother is pregnant and has no history of chickenpox or shingles, in which case testing may be appropriate.

Further Reading:

Chickenpox is caused by the varicella zoster virus (VZV) and is highly infectious. It is spread through droplets in the air, primarily through respiratory routes. It can also be caught from someone with shingles. The infectivity period lasts from 4 days before the rash appears until 5 days after the rash first appeared. The incubation period is typically 10-21 days.

Clinical features of chickenpox include mild symptoms that are self-limiting. However, older children and adults may experience more severe symptoms. The infection usually starts with a fever and is followed by an itchy rash that begins on the head and trunk before spreading. The rash starts as macular, then becomes papular, and finally vesicular. Systemic upset is usually mild.

Management of chickenpox is typically supportive. Measures such as keeping cool and trimming nails can help alleviate symptoms. Calamine lotion can be used to soothe the rash. People with chickenpox should avoid contact with others for at least 5 days from the onset of the rash until all blisters have crusted over. Immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG). If chickenpox develops, IV aciclovir should be considered. Aciclovir may be prescribed for immunocompetent, non-pregnant adults or adolescents with severe chickenpox or those at increased risk of complications. However, it is not recommended for otherwise healthy children with uncomplicated chickenpox.

Complications of chickenpox can include secondary bacterial infection of the lesions, pneumonia, encephalitis, disseminated haemorrhagic chickenpox, and rare conditions such as arthritis, nephritis, and pancreatitis.

Shingles is the reactivation of the varicella zoster virus that remains dormant in the nervous system after primary infection with chickenpox. It typically presents with signs of nerve irritation before the eruption of a rash within the dermatomal distribution of the affected nerve. Patients may feel unwell with malaise, myalgia, headache, and fever prior to the rash appearing. The rash appears as erythema with small vesicles that may keep forming for up to 7 days. It usually takes 2-3 weeks for the rash to resolve.

Management of shingles involves keeping the vesicles covered and dry to prevent secondary bacterial infection.

To relieve the patient’s respiratory distress, the most suitable initial intervention would be positive pressure ventilation. This involves providing mechanical assistance to the patient’s breathing by delivering air or oxygen under pressure through a mask or endotracheal tube. This helps to improve oxygenation and ventilation, ensuring that the patient’s lungs are adequately supplied with oxygen and carbon dioxide is effectively removed. Positive pressure ventilation can help stabilize the patient’s breathing and alleviate the respiratory distress caused by the flail segment.

Further Reading:

Flail chest is a serious condition that occurs when multiple ribs are fractured in two or more places, causing a segment of the ribcage to no longer expand properly. This condition is typically caused by high-impact thoracic blunt trauma and is often accompanied by other significant injuries to the chest.

The main symptom of flail chest is a chest deformity, where the affected area moves in a paradoxical manner compared to the rest of the ribcage. This can cause chest pain and difficulty breathing, known as dyspnea. X-rays may also show evidence of lung contusion, indicating further damage to the chest.

In terms of management, conservative treatment is usually the first approach. This involves providing adequate pain relief and respiratory support to the patient. However, if there are associated injuries such as a pneumothorax or hemothorax, specific interventions like thoracostomy or surgery may be necessary.

Positive pressure ventilation can be used to provide internal splinting of the airways, helping to prevent atelectasis, a condition where the lungs collapse. Overall, prompt and appropriate management is crucial in order to prevent further complications and improve the patient’s outcome.

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.

A distinctive feature of croup is a barking cough, but it does not indicate the severity of the condition. To reduce airway swelling, dexamethasone and prednisolone are commonly prescribed. If a child is experiencing vomiting, nebulized budesonide can be used as an alternative. However, it is important to note that steroids do not shorten the duration of the illness. In severe cases, nebulized adrenaline can be administered.

Hospitalization for croup is uncommon and typically reserved for children who are experiencing worsening respiratory distress or showing signs of drowsiness or agitation.