The upper part of the nose receives blood supply from the anterior and posterior ethmoidal arteries, which are derived from the internal carotid artery. On the other hand, the remaining parts of the nose and sinuses are nourished by the greater palatine, sphenopalatine, and superior labial arteries. These arteries are branches of the external carotid arteries.

In the front part of the nasal septum, there exists a network of blood vessels where the branches of the internal and external carotid artery connect. This network is known as Kiesselbach’s plexus, also referred to as Little’s area. It is worth noting that Kiesselbach’s plexus is the most common location for anterior bleeding.

Le Fort fractures are complex fractures of the midface that involve the maxillary bone and surrounding structures. These fractures can occur in a horizontal, pyramidal, or transverse direction. The distinguishing feature of Le Fort fractures is the traumatic separation of the pterygomaxillary region. They make up approximately 10% to 20% of all facial fractures and can have severe consequences, both in terms of potential life-threatening injuries and disfigurement.

The Le Fort classification system categorizes midface fractures into three groups based on the plane of injury. As the classification level increases, the location of the maxillary fracture moves from inferior to superior within the maxilla.

Le Fort I fractures are horizontal fractures that occur across the lower aspect of the maxilla. These fractures cause the teeth to separate from the upper face and extend through the lower nasal septum, the lateral wall of the maxillary sinus, and into the palatine bones and pterygoid plates. They are sometimes referred to as a floating palate because they often result in the mobility of the hard palate from the midface. Common accompanying symptoms include facial swelling, loose teeth, dental fractures, and misalignment of the teeth.

Le Fort II fractures are pyramidal-shaped fractures, with the base of the pyramid located at the level of the teeth and the apex at the nasofrontal suture. The fracture line extends from the nasal bridge and passes through the superior wall of the maxilla, the lacrimal bones, the inferior orbital floor and rim, and the anterior wall of the maxillary sinus. These fractures are sometimes called a floating maxilla because they typically result in the mobility of the maxilla from the midface. Common symptoms include facial swelling, nosebleeds, subconjunctival hemorrhage, cerebrospinal fluid leakage from the nose, and widening and flattening of the nasal bridge.

Le Fort III fractures are transverse fractures of the midface. The fracture line passes through the nasofrontal suture, the maxillo frontal suture, the orbital wall, and the zygomatic arch and zygomaticofrontal suture. These fractures cause separation of all facial bones from the cranial base, earning them the nickname craniofacial disjunction or floating face fractures. They are the rarest and most severe type of Le Fort fracture. Common symptoms include significant facial swelling, bruising around the eyes, facial flattening, and the entire face can be shifted.

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

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

Bodyweight: First 10 kg
Daily fluid requirement: 100 ml/kg
Hourly fluid requirement: 4 ml/kg

Bodyweight: Second 10 kg
Daily fluid requirement: 50 ml/kg
Hourly fluid requirement: 2 ml/kg

Bodyweight: Subsequent kg
Daily fluid requirement: 20 ml/kg
Hourly fluid requirement: 1 ml/kg

For a well and normal child weighing less than 10 kg, the hourly maintenance fluid requirement is 4 ml/kg. Therefore, for this child, the hourly maintenance fluid requirement would be:

9 x 4 ml/hour = 36 ml/hour

The presentation, in this instance, is consistent with retinal (ocular) migraine. As per the International Headache Society, the primary clinical features of retinal migraine include an expanding blind-spot in the center of vision, flickering or flashing lights, temporary loss of vision in one eye lasting less than an hour, headache lasting anywhere from 4 to 72 hours (often affecting only one side of the head), nausea and vomiting, sensitivity to light and sound, and a prodrome present in 50-60% of cases. Retinal migraine is relatively uncommon, affecting only 1 in 200 individuals with migraines, and is believed to occur due to the narrowing of blood vessels in the choroidal or retinal arteries. Factors that can trigger retinal migraine include recent intense exercise, changes in posture, and the use of oral contraceptives.

Acute optic neuritis typically presents with unilateral vision loss that worsens over a couple of weeks and then spontaneously improves within three weeks. This condition is more commonly seen in individuals under the age of 45 and is often accompanied by pain around the eyes that worsens with eye movement. A relative afferent pupillary defect and pallor of the optic disc, visible 4-6 weeks after the onset, are frequently observed. The most common cause of optic neuritis in this age group is acute demyelination.

Retinal hemorrhage leads to painless vision loss, while acute glaucoma and amaurosis fugax are unlikely to occur in individuals of this age group.

A central venous catheter (CVC) is a type of catheter that is inserted into a large vein in the body, typically in the neck, chest, or groin. It has several important uses, including CVP monitoring, pulmonary artery pressure monitoring, repeated blood sampling, IV access for large volumes of fluids or drugs, TPN administration, dialysis, pacing, and other procedures such as placement of IVC filters or venous stents.

When inserting a central line, it is ideal to use ultrasound guidance to ensure accurate placement. However, there are certain contraindications to central line insertion, including infection or injury to the planned access site, coagulopathy, thrombosis or stenosis of the intended vein, a combative patient, or raised intracranial pressure for jugular venous lines.

The most common approaches for central line insertion are the internal jugular, subclavian, femoral, and PICC (peripherally inserted central catheter) veins. The internal jugular vein is often chosen due to its proximity to the carotid artery, but variations in anatomy can occur. Ultrasound can be used to identify the vessels and guide catheter placement, with the IJV typically lying superficial and lateral to the carotid artery. Compression and Valsalva maneuvers can help distinguish between arterial and venous structures, and doppler color flow can highlight the direction of flow.

In terms of choosing a side for central line insertion, the right side is usually preferred to avoid the risk of injury to the thoracic duct and potential chylothorax. However, the left side can also be used depending on the clinical situation.

Femoral central lines are another option for central venous access, with the catheter being inserted into the femoral vein in the groin. Local anesthesia is typically used to establish a field block, with lidocaine being the most commonly used agent. Lidocaine works by blocking sodium channels and preventing the propagation of action potentials.

In summary, central venous catheters have various important uses and should ideally be inserted using ultrasound guidance. There are contraindications to their insertion, and different approaches can be used depending on the clinical situation. Local anesthesia is commonly used for central line insertion, with lidocaine being the preferred agent.

According to the Royal College of Emergency Medicine (RCEM), Prilocaine is the preferred choice for intravenous regional anesthesia. This is because Bupivacaine and lidocaine have a higher risk of causing harmful side effects.

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.

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

Many individuals with vWD do not experience any symptoms and are diagnosed incidentally during a routine clotting profile check. However, if symptoms do occur, the most common ones include easy bruising, nosebleeds (epistaxis), and heavy menstrual bleeding (menorrhagia). In severe cases, more significant bleeding and joint bleeding (haemarthrosis) can occur.

For mild cases of von Willebrand disease, bleeding can be treated with desmopressin. This medication works by increasing the patient’s own levels of vWF, as it releases vWF stored in the Weibel-Palade bodies found in the endothelial cells. In more severe cases, replacement therapy is necessary, which involves cryoprecipitate infusions or Factor VIII concentrate. Replacement therapy is recommended for patients with severe von Willebrand’s disease who are undergoing moderate or major surgical procedures.

Congenital afibrinogenaemia is a rare coagulation disorder characterized by a deficiency or malfunction of fibrinogen. This condition leads to a prolongation of the prothrombin time, bleeding time, and APTT. However, it does not affect the platelet count.

Aspirin therapy works by inhibiting platelet cyclo-oxygenase, an essential enzyme in the generation of thromboxane A2 (TXA2). By inhibiting TXA2, aspirin reduces platelet activation and aggregation. Consequently, aspirin therapy prolongs the bleeding time but does not have an impact on the platelet count, prothrombin time, or APTT.

Warfarin, on the other hand, inhibits the synthesis of clotting factors II, VII, IX, and X, as well as protein C and protein S, which are all dependent on vitamin K.

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In such cases, it is important to address any low blood glucose levels urgently by administering intravenous glucose. While the patient may require additional antiepileptic drug (AED) therapy, the management of status epilepticus involves several general measures.

During the early stage of status epilepticus (0-10 minutes), the airway should be secured and resuscitation measures should be taken. Oxygen should be administered and the cardiorespiratory function should be assessed. It is also important to establish intravenous access. In the second stage (0-30 minutes), regular monitoring should be instituted and the possibility of non-epileptic status should be considered. Emergency AED therapy should be initiated and emergency investigations should be conducted. If there are indications of alcohol abuse or impaired nutrition, glucose and/or intravenous thiamine may be administered. Acidosis should be treated if severe.

In the third stage (0-60 minutes), the underlying cause of status epilepticus should be identified. The anaesthetist and intensive care unit (ITU) should be alerted. Any medical complications should be identified and treated, and pressor therapy may be considered if appropriate. In the fourth stage (30-90 minutes), the patient should be transferred to intensive care. Intensive care and EEG monitoring should be established, and intracranial pressure monitoring may be initiated if necessary. Initial long-term, maintenance AED therapy should also be initiated.

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

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

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.

Epiglottitis commonly occurs in children aged 2-6 years, while adults in their 40’s and 50’s are more prone to experiencing this condition.

Further Reading:

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

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

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

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

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

To ensure prompt response in case of an adverse reaction, it is important to have adrenaline, antihistamine, and steroid readily available when administering Zagreb antivenom.

Further Reading:

Snake bites in the UK are primarily caused by the adder, which is the only venomous snake species native to the country. While most adder bites result in minor symptoms such as pain, swelling, and inflammation, there have been cases of life-threatening illness and fatalities. Additionally, there are instances where venomous snakes that are kept legally or illegally also cause bites in the UK.

Adder bites typically occur from early spring to late autumn, with the hand being the most common site of the bite. Symptoms can be local or systemic, with local symptoms including sharp pain, tingling or numbness, and swelling that spreads proximally. Systemic symptoms may include spreading pain, tenderness, inflammation, regional lymph node enlargement, and bruising. In severe cases, anaphylaxis can occur, leading to symptoms such as nausea, vomiting, abdominal pain, diarrhea, and shock.

It is important for clinicians to be aware of the potential complications and complications associated with adder bites. These can include acute renal failure, pulmonary and cerebral edema, acute gastric dilatation, paralytic ileus, acute pancreatitis, and coma and seizures. Anaphylaxis symptoms can appear within minutes or be delayed for hours, and hypotension is a critical sign to monitor.

Initial investigations for adder bites include blood tests, ECG, and vital sign monitoring. Further investigations such as chest X-ray may be necessary based on clinical signs. Blood tests may reveal abnormalities such as leukocytosis, raised hematocrit, anemia, thrombocytopenia, and abnormal clotting profile. ECG changes may include tachyarrhythmias, bradyarrhythmias, atrial fibrillation, and ST segment changes.

First aid measures at the scene include immobilizing the patient and the bitten limb, avoiding aspirin and ibuprofen, and cleaning the wound site in the hospital. Tetanus prophylaxis should be considered. In cases of anaphylaxis, prompt administration of IM adrenaline is necessary. In the hospital, rapid assessment and appropriate resuscitation with intravenous fluids are required.

Antivenom may be indicated in cases of hypotension, systemic envenoming, ECG abnormalities, peripheral neutrophil leucocytosis, elevated serum creatine kinase or metabolic acidosis, and extensive or rapidly spreading local swelling. Zagreb antivenom is commonly used in the UK, with an initial dose of 8 mL.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This results in the accumulation of waste products and disturbances in fluid and electrolyte balance. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease. It is a relatively common condition, with approximately 15% of adults admitted to hospitals in the UK developing AKI.

The causes of AKI can be categorized into pre-renal, intrinsic renal, and post-renal factors. The majority of AKI cases in the community are due to pre-renal causes, accounting for 90% of cases. These are often associated with conditions such as hypotension from sepsis or fluid depletion. Medications, particularly ACE inhibitors and NSAIDs, are also frequently implicated in AKI.

The table below summarizes the most common causes of AKI:

Pre-renal:
– Volume depletion (e.g., hemorrhage, severe vomiting or diarrhea, burns)
– Oedematous states (e.g., cardiac failure, liver cirrhosis, nephrotic syndrome)
– Hypotension (e.g., cardiogenic shock, sepsis, anaphylaxis)
– Cardiovascular conditions (e.g., severe cardiac failure, arrhythmias)
– Renal hypoperfusion: NSAIDs, COX-2 inhibitors, ACE inhibitors or ARBs, Abdominal aortic aneurysm
– Renal artery stenosis
– Hepatorenal syndrome

Intrinsic renal:
– Glomerular disease (e.g., glomerulonephritis, thrombosis, hemolytic-uremic syndrome)
– Tubular injury: acute tubular necrosis (ATN) following prolonged ischemia
– Acute interstitial nephritis due to drugs (e.g., NSAIDs), infection, or autoimmune diseases
– Vascular disease (e.g., vasculitis, polyarteritis nodosa, thrombotic microangiopathy, cholesterol emboli, renal vein thrombosis, malignant hypertension)
– Eclampsia

Post-renal:
– Renal stones
– Blood clot
– Papillary necrosis
– Urethral stricture
– Prostatic hypertrophy or malignancy
– Bladder tumor
– Radiation fibrosis
– Pelvic malignancy
– Retroperitoneal fibrosis

Blood transfusion is a crucial treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there has been an improvement in safety procedures and a reduction in transfusion use, errors and serious adverse reactions still occur and often go unreported.

Mild allergic reactions during blood transfusion are relatively common and typically occur within a few minutes of starting the transfusion. These reactions happen when patients have antibodies that react with foreign plasma proteins in the transfused blood components. Symptoms of mild allergic reactions include urticaria, Pruritus, and hives.

Anaphylaxis, on the other hand, is much rarer and occurs when an individual has previously been sensitized to an allergen present in the blood. When re-exposed to the allergen, the body releases IgE or IgG antibodies, leading to severe symptoms such as bronchospasm, laryngospasm, abdominal pain, nausea, vomiting, hypotension, shock, and loss of consciousness. Anaphylaxis can be fatal.

Mild allergic reactions can be managed by slowing down the transfusion rate and administering antihistamines. If there is no progression after 30 minutes, the transfusion may continue. Patients who have experienced repeated allergic reactions to transfusion should be given pre-treatment with chlorpheniramine. In cases of anaphylaxis, the transfusion should be stopped immediately, and the patient should receive oxygen, adrenaline, corticosteroids, and antihistamines following the ALS protocol.

The table below summarizes the main transfusion reactions and complications, along with their features and management:

Complication | Features | Management
Febrile transfusion reaction | 1 degree rise in temperature, chills, malaise | Supportive care, paracetamol
Acute haemolytic reaction | Fever, chills, pain at transfusion site, nausea, vomiting, dark urine | STOP THE TRANSFUSION, administer IV fluids, diuretics if necessary
Delayed haemolytic reaction | Fever, anaemia, jaundice, haemoglobinuria | Monitor anaemia and renal function, treat as required
Allergic reaction | Urticaria, Pruritus, hives | Symptomatic treatment with ant

Myxoedema coma is a condition characterized by severe hypothyroidism, leading to a state of metabolic decompensation and changes in mental status. Patients with myxoedema coma often experience electrolyte disturbances such as hypoglycemia and hyponatremia. In addition, laboratory findings typically show elevated levels of TSH, as well as low levels of T4 and T3. Other expected findings include hypoxemia and hypercapnia.

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.

Blunt abdominal trauma often leads to injuries in certain organs. According to the latest edition of the ATLS manual, the spleen is the most frequently injured organ, with a prevalence of 40-55%. Following closely behind is the liver, which sustains injuries in about 35-45% of cases. The small bowel, although less commonly affected, still experiences injuries in approximately 5-10% of patients. It is worth noting that patients who undergo laparotomy for blunt trauma have a 15% incidence of retroperitoneal hematoma. These statistics highlight the significant impact of blunt abdominal trauma on organ health.

Confidentiality plays a crucial role in the doctor-patient relationship and is vital for maintaining trust in the medical profession. However, there are certain situations, such as cases involving gun and knife crimes that pose a potential risk to the public, where it may be necessary to breach this confidentiality and provide information to the police, even if the patient refuses.

It is important to make every effort to obtain the patient’s consent, while also explaining your legal obligation to report such incidents. When sharing information with the police, it is essential to disclose only the minimum amount of information required. Typically, this would include the patient’s basic details and the fact that they have sought medical attention for a non-self-inflicted deliberate knife wound.

In some cases, where it is evident that the injury was accidental or a result of deliberate self-harm due to a mental health condition, there may be no need to involve the police. However, regardless of the circumstances, the necessary medical treatment should still be provided for the wound, as long as the patient gives their consent.

For more information on this topic, you can refer to the GMC Guidance on Reporting Gunshot and Knife Wounds.

Urinary alkalinisation, which involves the intravenous administration of sodium bicarbonate, carries the risk of hypokalaemia. It is important to note that both alkalosis and acidosis can cause shifts in potassium levels. In the case of alkalinisation, potassium is shifted from the plasma into the cells. Therefore, it is crucial to closely monitor the patient for hypokalaemia by checking their potassium levels every 1-2 hours.

Further Reading:

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

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

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

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

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

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

The guidelines from the European League Against Rheumatism (EULAR) regarding the diagnosis of gout state that if a joint becomes swollen, tender, and red, and if acute pain develops in that joint over a period of 6-12 hours, it is highly likely to be a crystal arthropathy. Pseudogout is also a possibility, but it is much less likely. In this case, gout is the most probable diagnosis.

The joint that is most commonly affected in acute gout is the first metatarsal-phalangeal joint, which accounts for 50-75% of cases.

The main cause of gout is hyperuricaemia, and the clinical diagnosis can be confirmed by the presence of negatively birefringent crystals in the synovial fluid aspirate.

For the treatment of acute gout attacks, NSAIDs or colchicine are generally used.

According to NICE, the presence of certain clinical features in a child between three months and five years old may indicate a urinary tract infection (UTI). These features include vomiting, poor feeding, lethargy, irritability, abdominal pain or tenderness, and urinary frequency or dysuria. For more information on this topic, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

When someone takes too much paracetamol, it can harm their liver cells and the tubules in their kidneys. This is because paracetamol produces a harmful substance called NAPQI, which is normally combined with glutathione. However, when there is too much NAPQI, it can cause damage and death to liver and kidney cells.

Further Reading:

Paracetamol poisoning occurs when the liver is unable to metabolize paracetamol properly, leading to the production of a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI). Normally, NAPQI is conjugated by glutathione into a non-toxic form. However, during an overdose, the liver’s conjugation systems become overwhelmed, resulting in increased production of NAPQI and depletion of glutathione stores. This leads to the formation of covalent bonds between NAPQI and cell proteins, causing cell death in the liver and kidneys.

Symptoms of paracetamol poisoning may not appear for the first 24 hours or may include abdominal symptoms such as nausea and vomiting. After 24 hours, hepatic necrosis may develop, leading to elevated liver enzymes, right upper quadrant pain, and jaundice. Other complications can include encephalopathy, oliguria, hypoglycemia, renal failure, and lactic acidosis.

The management of paracetamol overdose depends on the timing and amount of ingestion. Activated charcoal may be given if the patient presents within 1 hour of ingesting a significant amount of paracetamol. N-acetylcysteine (NAC) is used to increase hepatic glutathione production and is given to patients who meet specific criteria. Blood tests are taken to assess paracetamol levels, liver function, and other parameters. Referral to a medical or liver unit may be necessary, and psychiatric follow-up should be considered for deliberate overdoses.

In cases of staggered ingestion, all patients should be treated with NAC without delay. Blood tests are also taken, and if certain criteria are met, NAC can be discontinued. Adverse reactions to NAC are common and may include anaphylactoid reactions, rash, hypotension, and nausea. Treatment for adverse reactions involves medications such as chlorpheniramine and salbutamol, and the infusion may be stopped if necessary.

The prognosis for paracetamol poisoning can be poor, especially in cases of severe liver injury. Fulminant liver failure may occur, and liver transplant may be necessary. Poor prognostic indicators include low arterial pH, prolonged prothrombin time, high plasma creatinine, and hepatic encephalopathy.

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

The causes of neonatal jaundice can be categorized as follows:

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

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

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

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

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

Norovirus is the leading cause of gastroenteritis in adults in the UK. Viruses are responsible for the majority of cases of infectious diarrhea, with norovirus being the most common culprit in adults. Among young children, rotavirus is the primary pathogen, although its prevalence has decreased since the introduction of a rotavirus vaccine. As of 2023, rotavirus remains the most common cause of viral gastroenteritis in children.

Further Reading:

Gastroenteritis is a transient disorder characterized by the sudden onset of diarrhea, with or without vomiting. It is caused by enteric infections with viruses, bacteria, or parasites. The most common viral causes of gastroenteritis in adults include norovirus, rotavirus, and adenovirus. Bacterial pathogens such as Campylobacter jejuni and coli, Escherichia coli, Clostridium perfringens, Bacillus cereus, Staphylococcus aureus, Salmonella typhi and paratyphi, and Shigella dysenteriae, flexneri, boydii, and sonnei can also cause gastroenteritis. Parasites such as Cryptosporidium, Entamoeba histolytica, and Giardia intestinalis or Giardia lamblia can also lead to diarrhea.

Diagnosis of gastroenteritis is usually based on clinical symptoms, and investigations are not required in many cases. However, stool culture may be indicated in certain situations, such as when the patient is systemically unwell or immunocompromised, has acute painful diarrhea or blood in the stool suggesting dysentery, has recently taken antibiotics or acid-suppressing medications, or has not resolved diarrhea by day 7 or has recurrent diarrhea.

Management of gastroenteritis in adults typically involves advice on oral rehydration. Intravenous rehydration and more intensive treatment may be necessary for patients who are systemically unwell, exhibit severe dehydration, or have intractable vomiting or high-output diarrhea. Antibiotics are not routinely required unless a specific organism is identified that requires treatment. Antidiarrheal drugs, antiemetics, and probiotics are not routinely recommended.

Complications of gastroenteritis can occur, particularly in young children, the elderly, pregnant women, and immunocompromised individuals. These complications include dehydration, electrolyte disturbance, acute kidney injury, haemorrhagic colitis, haemolytic uraemic syndrome, reactive arthritis, Reiter’s syndrome, aortitis, osteomyelitis, sepsis, toxic megacolon, pancreatitis, sclerosing cholangitis, liver cirrhosis, weight loss, chronic diarrhea, irritable bowel syndrome, inflammatory bowel disease, acquired lactose intolerance, Guillain-Barré syndrome, meningitis, invasive entamoeba infection, and liver abscesses.

Acute bacterial prostatitis is a sudden inflammation of the prostate gland, which can be either focal or diffuse and is characterized by the presence of pus. The most common organisms that cause this condition include Escherichia coli, Streptococcus faecalis, Staphylococcus aureus, and Neisseria gonorrhoea. The infection usually reaches the prostate through direct extension from the posterior urethra or urinary bladder, but it can also spread through the blood or lymphatics. In some cases, the infection may originate from the rectum.

According to the National Institute for Health and Care Excellence (NICE), acute prostatitis should be suspected in men who present with a sudden onset of feverish illness, which may be accompanied by rigors, arthralgia, or myalgia. Irritative urinary symptoms like dysuria, frequency, urgency, or acute urinary retention are also common. Perineal or suprapubic pain, as well as penile pain, low back pain, pain during ejaculation, and pain during bowel movements, can occur. A rectal examination may reveal an exquisitely tender prostate. A urine dipstick test showing white blood cells and a urine culture confirming urinary infection are also indicative of acute prostatitis.

The current recommendations by NICE and the British National Formulary (BNF) for the treatment of acute prostatitis involve prescribing an oral antibiotic for a duration of 14 days, taking into consideration local antimicrobial resistance data. The first-line antibiotics recommended are Ciprofloxacin 500 mg twice daily or Ofloxacin 200 mg twice daily. If these are not suitable, Trimethoprim 200 mg twice daily can be used. Second-line options include Levofloxacin 500 mg once daily or Co-trimoxazole 960 mg twice daily, but only when there is bacteriological evidence of sensitivity and valid reasons to prefer this combination over a single antibiotic.

For more information, you can refer to the NICE Clinical Knowledge Summary on acute prostatitis.

Potentially, there can be a serious condition called hypokalaemia, which is characterized by low levels of potassium in the body. This condition should be taken seriously, especially in cases of severe asthma, as it can be made worse by certain medications like theophyllines (such as aminophylline and Uniphyllin Continus), corticosteroids, and low oxygen levels. Additionally, the use of thiazide and loop diuretics can also worsen hypokalaemia. Therefore, it is important to regularly monitor the levels of potassium in the blood of individuals with severe asthma.

It is worth noting that spironolactone, a type of diuretic, is known as a potassium-sparing medication. This means that it does not typically contribute to hypokalaemia.

One of the diagnostic criteria for ARDS is the presence of hypoxemia. Other criteria include the onset of symptoms within 7 days of a clinical insult or new/worsening respiratory symptoms, bilateral opacities on chest X-ray that cannot be fully explained by other conditions, and respiratory failure that cannot be fully attributed to cardiac failure or fluid overload.

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.

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

The use of trimethoprim during the first trimester of pregnancy is linked to a higher risk of neural tube defects due to its interference with folate. If it is not possible to use an alternative antibiotic, it is recommended that pregnant women taking trimethoprim also take high-dose folic acid. However, the use of trimethoprim during the second and third trimesters of pregnancy is considered safe.

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

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

Aminoglycosides (e.g. gentamicin): They can cause ototoxicity and deafness.

Aspirin: High doses 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 significant risks.

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

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

Carbamazepine: It can cause haemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol: It can cause grey baby syndrome.

Corticosteroids: If given in the first trimester, they may cause orofacial clefts.

Danazol: If given in the first trimester, it can cause masculinization of the female fetuses genitals.

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

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

Heparin: It can cause maternal bleeding and thrombocytopenia.

Isoniazid: It can lead to maternal liver damage and neuropathy and seizures in the neonate.

Hepatitis B surface antigen (HBsAg) is a protein found on the surface of the hepatitis B virus. It can be detected in high levels in the blood during both acute and chronic hepatitis B virus infections. The presence of HBsAg indicates that the person is capable of spreading the infection to others. Normally, the body produces antibodies to HBsAg as part of the immune response to the infection. HBsAg is also used to create the hepatitis B vaccine.

Hepatitis B surface antibody (anti-HBs) indicates that a person has recovered from the hepatitis B virus infection and is now immune to it. This antibody can also develop in individuals who have been successfully vaccinated against hepatitis B.

Total hepatitis B core antibody (anti-HBc) appears when symptoms of acute hepatitis B begin and remains present for life. The presence of anti-HBc indicates that a person has either had a previous or ongoing infection with the hepatitis B virus, although the exact time frame cannot be determined. This antibody is not present in individuals who have received the hepatitis B vaccine.

IgM antibody to hepatitis B core antigen (IgM anti-HBc) indicates a recent infection or acute hepatitis B. If this antibody is present, it suggests that the infection occurred within the past six months.

This patient is displaying symptoms and signs that are consistent with community-acquired pneumonia (CAP). The most common cause of CAP in an adult patient who is otherwise in good health is Streptococcus pneumoniae.

When it comes to treating community-acquired pneumonia, the first-line antibiotic of choice is amoxicillin. According to the NICE guidelines, patients who are allergic to penicillin should be prescribed a macrolide (such as clarithromycin) or a tetracycline (such as doxycycline).

For more information, you can refer to the NICE guidelines on the diagnosis and management of pneumonia in adults.

Kiesselbach’s plexus, also known as Little’s area, is formed by the connection of four or five arteries. These arteries include the greater palatine artery, anterior ethmoidal artery, superior labial artery, and sphenopalatine artery. Some sources also include the posterior ethmoidal artery as part of the plexus. The greater palatine artery is a branch of the maxillary artery, while the anterior ethmoidal artery is a branch of the internal carotid artery. The superior labial artery and sphenopalatine artery are both branches of the external carotid artery. The posterior ethmoidal artery, if included, is a branch of the ophthalmic artery.

Further Reading:

Epistaxis, or nosebleed, is a common condition that can occur in both children and older adults. It is classified as either anterior or posterior, depending on the location of the bleeding. Anterior epistaxis usually occurs in younger individuals and arises from the nostril, most commonly from an area called Little’s area. These bleeds are usually not severe and account for the majority of nosebleeds seen in hospitals. Posterior nosebleeds, on the other hand, occur in older patients with conditions such as hypertension and atherosclerosis. The bleeding in posterior nosebleeds is likely to come from both nostrils and originates from the superior or posterior parts of the nasal cavity or nasopharynx.

The management of epistaxis involves assessing the patient for signs of instability and implementing measures to control the bleeding. Initial measures include sitting the patient upright with their upper body tilted forward and their mouth open. Firmly pinching the cartilaginous part of the nose for 10-15 minutes without releasing the pressure can also help stop the bleeding. If these measures are successful, a cream called Naseptin or mupirocin nasal ointment can be prescribed for further treatment.

If bleeding persists after the initial measures, nasal cautery or nasal packing may be necessary. Nasal cautery involves using a silver nitrate stick to cauterize the bleeding point, while nasal packing involves inserting nasal tampons or inflatable nasal packs to stop the bleeding. In cases of posterior bleeding, posterior nasal packing or surgery to tie off the bleeding vessel may be considered.

Complications of epistaxis can include nasal bleeding, hypovolemia, anemia, aspiration, and even death. Complications specific to nasal packing include sinusitis, septal hematoma or abscess, pressure necrosis, toxic shock syndrome, and apneic episodes. Nasal cautery can lead to complications such as septal perforation and caustic injury to the surrounding skin.

In children under the age of 2 presenting with epistaxis, it is important to refer them for further investigation as an underlying cause is more likely in this age group.

The Dix-Hallpike manoeuvre is the primary diagnostic test used for patients suspected of having benign paroxysmal positional vertigo (BPPV). If a patient exhibits nystagmus and vertigo during the test, it is considered a positive result for BPPV. Other special clinical tests that may be used to assess vertigo include Romberg’s test, which helps identify instability of either peripheral or central origin but is not very effective in differentiating between the two. The head impulse test is used to detect unilateral hypofunction of the peripheral vestibular system and can help distinguish between cerebellar infarction and vestibular neuronitis. Unterberger’s test is used to identify dysfunction in one of the labyrinths. Lastly, the alternate cover test can indicate an increased likelihood of stroke in individuals with acute vestibular syndrome if the result is abnormal.

Further Reading:

Benign paroxysmal positional vertigo (BPPV) is a common cause of vertigo, characterized by sudden dizziness and vertigo triggered by changes in head position. It typically affects individuals over the age of 55 and is less common in younger patients. BPPV is caused by dysfunction in the inner ear, specifically the detachment of otoliths (calcium carbonate particles) from the utricular otolithic membrane. These loose otoliths move through the semicircular canals, triggering a sensation of movement and resulting in conflicting sensory inputs that cause vertigo.

The majority of BPPV cases involve otoliths in the posterior semicircular canal, followed by the inferior semicircular canal. BPPV in the anterior semicircular canals is rare. Clinical features of BPPV include vertigo triggered by head position changes, such as rolling over in bed or looking upwards, accompanied by nausea. Episodes of vertigo typically last 10-20 seconds and can be diagnosed through positional nystagmus, which is a specific eye movement, observed during diagnostic maneuvers like the Dix-Hallpike maneuver.

Hearing loss and tinnitus are not associated with BPPV. The prognosis for BPPV is generally good, with spontaneous resolution occurring within a few weeks to months. Symptomatic relief can be achieved through the Epley maneuver, which is successful in around 80% of cases, or patient home exercises like the Brandt-Daroff exercises. Medications like Betahistine may be prescribed but have limited effectiveness in treating BPPV.

The symptoms observed in the casualties of this CBRN event strongly indicate exposure to a nerve agent. Among the options provided, VX gas is the only nerve agent listed, making it the most likely culprit.

Nerve agents, also known as nerve gases, are a highly toxic group of chemical warfare agents that were developed just before and during World War II. The initial compounds in this category, known as the G agents, were discovered and synthesized by German scientists. They include Tabun (GA), Sarin (GB), and Soman (GD). In the 1950s, the V agents, which are approximately 10 times more poisonous than Sarin, were synthesized. These include Venomous agent X (VX), Venomous agent E (VE), Venomous agent G (VG), and Venomous agent M (VM).

One of the most well-known incidents involving a nerve agent was the Tokyo subway sarin attack in March 1995. During this attack, Sarin was released into the Tokyo subway system during rush hour, resulting in over 5,000 people seeking medical attention. Among them, 984 were moderately poisoned, 54 were severely poisoned, and 12 lost their lives.

Nerve agents are organophosphorus esters that are chemically related to organophosphorus insecticides. They work by inhibiting acetylcholinesterase (AChE), an enzyme responsible for breaking down the neurotransmitter acetylcholine (ACh). This inhibition leads to an accumulation of ACh at both muscarinic and nicotinic cholinergic receptors.

Nerve agents can be absorbed through any body surface. When dispersed as a spray or aerosol, they can enter the body through the skin, eyes, and respiratory tract. In vapor form, they are primarily absorbed through the respiratory tract and eyes. If a sufficient amount of the agent is absorbed, it can cause local effects followed by systemic effects throughout the body.

The clinical symptoms observed after exposure to nerve agents are a result of the combined effects on the muscarinic, nicotinic, and central nervous systems. Muscarinic effects, often remembered using the acronym DUMBBELS, include diarrhea, urination, miosis (constriction of the pupils), bronchorrhea (excessive mucus production in the airways), bronchospasm (narrowing of the airways), emesis (vomiting), lacrimation (excessive tearing), and salivation.

In some cases, the signs of skin or mucosal involvement may be difficult to detect or may not be present at all. The Royal College of Emergency Medicine (RCEM) states that anaphylaxis is likely when three specific criteria are met: the illness has a sudden and rapid onset, there are noticeable changes in the skin or mucosal areas such as flushing, hives, or swelling, and there are severe problems with the airway, breathing, or circulation that pose a life-threatening risk.

Further Reading:

Anaphylaxis is a severe and life-threatening hypersensitivity reaction that can have sudden onset and progression. It is characterized by skin or mucosal changes and can lead to life-threatening airway, breathing, or circulatory problems. Anaphylaxis can be allergic or non-allergic in nature.

In allergic anaphylaxis, there is an immediate hypersensitivity reaction where an antigen stimulates the production of IgE antibodies. These antibodies bind to mast cells and basophils. Upon re-exposure to the antigen, the IgE-covered cells release histamine and other inflammatory mediators, causing smooth muscle contraction and vasodilation.

Non-allergic anaphylaxis occurs when mast cells degrade due to a non-immune mediator. The clinical outcome is the same as in allergic anaphylaxis.

The management of anaphylaxis is the same regardless of the cause. Adrenaline is the most important drug and should be administered as soon as possible. The recommended doses for adrenaline vary based on age. Other treatments include high flow oxygen and an IV fluid challenge. Corticosteroids and chlorpheniramine are no longer recommended, while non-sedating antihistamines may be considered as third-line treatment after initial stabilization of airway, breathing, and circulation.

Common causes of anaphylaxis include food (such as nuts, which is the most common cause in children), drugs, and venom (such as wasp stings). Sometimes it can be challenging to determine if a patient had a true episode of anaphylaxis. In such cases, serum tryptase levels may be measured, as they remain elevated for up to 12 hours following an acute episode of anaphylaxis.

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.
https://www.resus.org.uk/sites/default/files/2021-05/Emergency%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf

Testicular torsion is a condition where the spermatic cord twists, leading to a lack of blood flow to the testis. It is a surgical emergency and prompt action is necessary to save the testis. It is most commonly seen in individuals aged 15-30 years.

Varicocele refers to the presence of varicose veins in the pampiniform plexus of the cord and scrotum. It is more frequently observed in the left testis and may be associated with infertility. This is believed to be due to the increased temperature caused by the varicose veins. Symptoms include a dull ache in the testis, which is often worse after exercise or at the end of the day. Standing examination can reveal the presence of Varicocele. Treatment is usually conservative, with surgery reserved for severe cases.

Hydrocoele can occur at any age and is characterized by the accumulation of fluid in the tunica vaginalis. It presents as scrotal swelling, which can be palpated above. The surface of the hydrocoele is smooth and it can be transilluminated. The testis is contained within the swelling and cannot be felt separately. Primary or secondary causes can lead to hydrocoele, and in adults, an ultrasound is performed to rule out underlying pathology such as tumors. Conservative management is often sufficient unless the hydrocoele is large.

Testicular cancer is the most common cancer in men aged 20-34 years. Awareness campaigns have emphasized the importance of self-examination for early detection. Risk factors include undescended testes, which increase the risk by 10-fold if bilateral. A previous history of testicular cancer carries a 4% risk of developing a second cancer. The usual presentation is a painless lump in the testis, which can also manifest as a secondary hydrocoele. Seminomas account for 60% of cases and are slow-growing, usually confined to the testis upon diagnosis. Stage 1 seminomas have a 98% 5-year survival rate. Teratomas, which can grow faster, make up 40% of cases and can occur within seminomas. Mixed type tumors are treated as teratomas due to their more aggressive nature. Surgical treatment, with or without chemotherapy and radiotherapy, is the primary approach.

Epididymo-orchitis is inflammation of the testis and epididymis caused by infection.

Tricuspid regurgitation is commonly caused by right ventricular dilatation, often as a result of heart failure. Other factors that can contribute to this condition include right ventricular infarction and cor pulmonale. The clinical signs of right-sided heart failure are frequently observed, such as an elevated jugular venous pressure, peripheral edema, hepatomegaly, and ascites.

The murmur associated with tricuspid regurgitation is a pansystolic murmur that is most audible at the tricuspid area during inspiration. A thrill may also be felt at the left sternal edge. Reverse splitting of the second heart sound can occur due to the early closure of the pulmonary valve. Additionally, a third heart sound may be present due to rapid filling of the right ventricle.

The supraspinatus tendon passes through a narrow space located between the underside of the acromion and acromioclavicular joint, as well as the head of the humerus. When the tendon becomes trapped in this space, it can cause pain and restrict movement, especially during overhead activities. This condition is known as subacromial impingement.

Impingement can occur due to various factors, such as thickening of the tendon caused by partial tears, inflammation, or degeneration. It can also be a result of the space narrowing due to osteoarthritis of the acromioclavicular joint or the presence of bone spurs. Some individuals may have a naturally downward sloping acromion, which makes them more susceptible to impingement.

Certain professions that involve a significant amount of overhead work, like plasterers, builders, and decorators, are particularly prone to developing subacromial impingement.

Ulnar neuritis is characterized by hand clumsiness and can progress to muscle weakness and wasting in the ulnar nerve-supplied muscles. It may also cause numbness or tingling in the little finger and medial half of the ring finger. This condition is caused by the narrowing of the ulnar groove at the elbow and is associated with risk factors such as osteoarthritis, trauma, and rheumatoid arthritis. Nerve conduction studies and surgical decompression may be necessary for diagnosis and treatment.

De Quervain’s tenosynovitis occurs when there is inflammation of the thumb extensor and abductor tendon sheaths. This leads to pain over the radial styloid, which worsens with forced adduction and flexion of the thumb. Treatment options include anti-inflammatory medications, thumb splints, and steroid injections.

Dupuytren’s contracture occurs when the palmar fascia contracts, preventing finger extension. It commonly affects the fifth finger on the right hand and is more prevalent in men over the age of 65. Risk factors for this condition include male sex, family history, alcohol use, diabetes, smoking, trauma, and manual labor. Surgical release is necessary if the contracture affects daily activities or work.

Trigger finger occurs when a nodule becomes stuck in the tendon sheath, causing the affected finger to remain in a fixed flexed position. The ring and middle fingers are most commonly affected, and risk factors include rheumatoid arthritis and diabetes. Steroid injections or surgical removal can be used to treat this condition.

Carpal tunnel syndrome occurs when the median nerve is compressed under the flexor retinaculum, resulting in numbness, pain, and wasting of the thenar eminence in the lateral three and a half digits. Symptoms are often worse at night. While most cases are idiopathic, risk factors include obesity, oral contraceptive use, hypothyroidism, rheumatoid arthritis, pregnancy, diabetes, amyloidosis, acromegaly, tumors compressing the carpal tunnel, and previous wrist fractures. Tinel’s test and Phalen’s test can help diagnose carpal tunnel syndrome, and nerve conduction studies may be requested for further evaluation. Treatment options include splints, steroid injections, and surgical release if symptoms persist.

Women have three options when requesting emergency contraception. The first option is Levonelle 1.5 mg, which contains levonorgestrel and can be used up to 72 hours after unprotected sexual intercourse (UPSI). If vomiting occurs within 2 hours of taking the tablet, another one should be given. Levonelle mainly works by preventing ovulation.

The second option is ulipristal acetate, the newest treatment available. It can be used up to 120 hours after UPSI. If vomiting occurs within 3 hours of ingestion, another tablet should be given. Ulipristal acetate also works by inhibiting ovulation. However, it should be avoided in patients taking enzyme-inducing drugs, those with severe hepatic impairment, or those with severe asthma requiring oral steroids.

The third option is the copper IUD, which can be fitted up to 5 days after UPSI or ovulation, whichever is longer. The failure rate of the copper IUD is less than 1 in 1000, making it 10-20 times more effective than oral emergency contraceptive options. It is important to note that Levonelle and ulipristal may be less effective in women with higher BMIs.

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.

The doses of commonly used drugs in paediatric cardiac arrest are summarized in the following table:

Drug: Adrenaline (epinephrine) IV/IO
Dose: 10 mcg/kg

Drug: Adrenaline (epinephrine) ET bolus
Dose: 100 mcg/kg

Drug: Amiodarone IV infusion
Dose: 5 mg/kg over 3 minutes (maximum 300 mg)

Drug: Calcium gluconate 10%
Dose: 0.3-0.5 ml/kg

Drug: Lidocaine IV/IO
Dose: 1 mg/kg (maximum 100 mg)

Drug: Magnesium sulphate IV
Dose: 25-50 mg/kg

Drug: Sodium bicarbonate IV
Dose: 1 ml/kg 8.4%

This patient has presented with a history consistent with retinal detachment preceded by posterior vitreous detachment.

Posterior vitreous detachment occurs when the vitreous membrane separates from the retina. There are several risk factors for posterior vitreous detachment, including myopia, recent cataract surgery, diabetes mellitus, increasing age, and eye trauma.

The main clinical features of posterior vitreous detachment include flashes of light (photopsia), increased numbers of floaters, a ring of floaters to the temporal side of central vision, and a feeling of heaviness in the eye. Another characteristic is Weiss’ ring, which is an irregular ring of translucent floating material in the vitreous.

It is important to note that there is a small associated risk of retinal detachment in the 6-12 weeks following a posterior vitreous detachment. Retinal detachment can be distinguished from posterior vitreous detachment by the presence of a dense shadow in the periphery that spreads centrally, a curtain drawing across the eye, straight lines suddenly appearing curved (positive Amsler grid test), and central visual loss with decreased visual acuity.

Given the patient’s presentation, an urgent referral to ophthalmology is necessary. In most cases of retinal detachment, surgical repair will be required.

Public Health England advises that children with impetigo should not attend school, nursery, or be under the care of childminders until the sores have formed a crust or until 48 hours after starting antibiotic treatment. Antibiotics help accelerate the healing process and decrease the period of contagiousness.

For more information, please refer to the Guidance on Infection Control in Schools and other Childcare Settings.
https://www.publichealth.hscni.net/sites/default/files/Guidance_on_infection_control_in%20schools_poster.pdf

Lidocaine functions by inhibiting the activity of voltage-gated sodium channels, preventing the flow of sodium ions through these channels.

Further Reading:

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

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

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

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

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

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

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

Tinnitus is often seen as an early indication of salicylate toxicity, which occurs when there is an excessive use of salicylate. Another common symptom is feeling nauseous and/or vomiting. In the initial stages of a salicylate overdose, individuals may experience respiratory alkalosis, which is caused by the direct stimulation of the respiratory centers in the medulla by salicylate. This leads to hyperventilation and the elimination of carbon dioxide, resulting in alkalosis. As the body metabolizes salicylate, a metabolic acidosis may develop.

Further Reading:

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

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

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

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

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

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

The recommended first-line diagnostic test for TMJ dislocation is an OPG. The Royal College of Emergency Medicine suggests that an OPG is the most effective initial imaging technique for diagnosing TMJ dislocation. However, mandibular series X-ray views and CT scans can also be used as alternative imaging methods.

Further Reading:

TMJ dislocation occurs when the mandibular condyle is displaced from its normal position in the mandibular fossa of the temporal bone. The most common type of dislocation is bilateral anterior dislocation. This occurs when the mandible is dislocated forward and the masseter and pterygoid muscles spasm, locking the condyle in place.

The temporomandibular joint is unique because it has an articular disc that separates the joint into upper and lower compartments. Dislocation can be caused by trauma, such as a direct blow to the open mouth, or by traumatic events like excessive mouth opening during yawning, laughing, shouting, or eating. It can also occur during dental work.

Signs and symptoms of TMJ dislocation include difficulty fully opening or closing the mouth, pain or tenderness in the TMJ region, jaw pain, ear pain, difficulty chewing, and facial pain. Connective tissue disorders like Marfan’s and Ehlers-Danlos syndrome can increase the likelihood of dislocation.

If TMJ dislocation is suspected, X-rays may be done to confirm the diagnosis. The best initial imaging technique is an orthopantomogram (OPG) or a standard mandibular series.

Management of anterior dislocations involves reducing the dislocated mandible, which is usually done in the emergency department. Dislocations to the posterior, medial, or lateral side are usually associated with a mandibular fracture and should be referred to a maxillofacial surgeon.

Reduction of an anterior dislocation involves applying distraction forces to the mandible. This can be done by gripping the mandible externally or intra-orally. In some cases, procedural sedation or local anesthesia may be used, and in rare cases, reduction may be done under general anesthesia.

After reduction, a post-reduction X-ray is done to confirm adequate reduction and rule out any fractures caused by the procedure. Discharge advice includes following a soft diet for at least 48 hours, avoiding wide mouth opening for at least 2 weeks, and supporting the mouth with the hand during yawning or laughing. A Barton bandage may be used to support the mandible if the patient is unable to comply with the discharge advice. Referral to a maxillofacial surgeon as an outpatient is also recommended.

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

Myelodysplastic syndromes are a group of disorders affecting the haemopoietic stem cell, leading to ineffective production of myeloid blood cells. These conditions typically manifest between the ages of 60 and 75 and are more prevalent in men than women.

The clinical features of myelodysplastic syndromes include tiredness due to anaemia (the most common presentation), easy bruising, and a tendency to bleed. Laboratory findings often reveal anaemia (usually macrocytic or normocytic), neutropenia, thrombocytopenia, and abnormal cell morphology with oddly shaped macrocytes.

Chronic lymphocytic leukaemia (CLL) is the most common form of adult leukaemia, primarily affecting B-lymphocytes. It often presents asymptomatically in patients who undergo routine blood tests revealing elevated white cell counts and lymphocytosis. Men over the age of 50 account for over 75% of CLL cases. Blood films typically show a predominance of mature-looking lymphocytes and smear cells.

Iron deficiency anaemia is characterized by hypochromic microcytic anaemia and a reduced red blood cell count. Peripheral blood smears in iron deficiency anaemia may exhibit poikilocytosis (varying shapes) and anisocytosis (varying sizes). Pencil cells are also observed in this condition.

Vitamin B12 and folate deficiency can also cause macrocytic anaemia. However, the severity of anaemia and macrocytosis would generally need to be much more pronounced to result in neutropenia and thrombocytopenia. Therefore, a myelodysplastic syndrome is more likely in such cases.

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

Further Reading:

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

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

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

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

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

Children with severe croup require high flow oxygen and nebulized adrenaline as part of their treatment. If a child is agitated or lethargic, it is a sign that the disease is severe. In addition to standard steroid treatment, high flow oxygen and nebulized adrenaline are necessary for treating severe croup. It is important to note that beta 2 agonists are not effective for children under 2 years old.

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

This patient is likely experiencing an acute coronary syndrome, possibly a non-ST-elevation myocardial infarction (NSTEMI) or unstable angina. The troponin test will help confirm the diagnosis. The patient’s ECG showed ST depression in the inferior leads, but this normalized after treatment with GTN and morphine, ruling out a ST-elevation myocardial infarction (STEMI).

Immediate pain relief should be provided. GTN (sublingual or buccal) can be used, but intravenous opioids like morphine should be considered, especially if a heart attack is suspected.

Aspirin should be given to all patients with unstable angina or NSTEMI as soon as possible and continued indefinitely, unless there are contraindications like bleeding risk or aspirin hypersensitivity. A loading dose of 300 mg should be administered right after presentation.

Fondaparinux should be given to patients without a high bleeding risk, unless coronary angiography is planned within 24 hours of admission. Unfractionated heparin can be an alternative to fondaparinux for patients who will undergo coronary angiography within 24 hours. For patients with significant renal impairment, unfractionated heparin can also be considered, with dose adjustment based on clotting function monitoring.

Routine administration of oxygen is no longer recommended, but oxygen saturation should be monitored using pulse oximetry as soon as possible, preferably before hospital admission. Supplemental oxygen should only be offered to individuals with oxygen saturation (SpO2) below 94% who are not at risk of hypercapnic respiratory failure, aiming for a SpO2 of 94-98%. For individuals with chronic obstructive pulmonary disease at risk of hypercapnic respiratory failure, a target SpO2 of 88-92% should be achieved until blood gas analysis is available.

Bivalirudin, a specific and reversible direct thrombin inhibitor (DTI), is recommended by NICE as a possible treatment for adults with STEMI undergoing percutaneous coronary intervention.

For more information, refer to the NICE guidelines on the assessment and diagnosis of chest pain of recent onset.