Early assessment of the airway is a critical aspect of managing a patient who has suffered burns. Airway blockage can occur rapidly due to direct injury, such as inhalation injury, or as a result of swelling caused by the burn. If there is a history of trauma, the airway should be evaluated and treated while maintaining control of the cervical spine.

Signs of airway obstruction may not be immediately apparent, as swelling typically does not occur right away. Children with thermal burns are at a higher risk of airway obstruction compared to adults due to their smaller airway size, so they require careful observation.

There are several risk factors for airway obstruction in burned patients, including inhalation injury, the presence of soot in the mouth or nostrils, singed nasal hairs, burns to the head, face, or neck, burns inside the mouth, a large burn area with increasing depth, and associated trauma. A carboxyhemoglobin level above 10% is also suggestive of an inhalation injury.

Acute mastoiditis commonly occurs as a complication of acute otitis media (AOM). In this case, the patient exhibits symptoms indicative of acute mastoiditis. The infection typically spreads from the middle ear tympanic cavity (acute otitis media) to the mastoid antrum through a narrow canal within the petrous temporal bone.

Further Reading:

Mastoiditis is an infection of the mastoid air cells, which are located in the mastoid process of the skull. It is usually caused by the spread of infection from the middle ear. The most common organism responsible for mastoiditis is Streptococcus pneumoniae, but other bacteria and fungi can also be involved. The infection can spread to surrounding structures, such as the meninges, causing serious complications like meningitis or cerebral abscess.

Mastoiditis can be classified as acute or chronic. Acute mastoiditis is a rare complication of acute otitis media, which is inflammation of the middle ear. It is characterized by severe ear pain, fever, swelling and redness behind the ear, and conductive deafness. Chronic mastoiditis is usually associated with chronic suppurative otitis media or cholesteatoma and presents with recurrent episodes of ear pain, headache, and fever.

Mastoiditis is more common in children, particularly those between 6 and 13 months of age. Other risk factors include immunocompromised patients, those with intellectual impairment or communication difficulties, and individuals with cholesteatoma.

Diagnosis of mastoiditis involves a physical examination, blood tests, ear swab for culture and sensitivities, and imaging studies like contrast-enhanced CT or MRI. Treatment typically involves referral to an ear, nose, and throat specialist, broad-spectrum intravenous antibiotics, pain relief, and myringotomy (a procedure to drain fluid from the middle ear).

Complications of mastoiditis are rare but can be serious. They include intracranial abscess, meningitis, subperiosteal abscess, neck abscess, venous sinus thrombosis, cranial nerve palsies, hearing loss, labyrinthitis, extension to the zygoma, and carotid artery arteritis. However, most patients with mastoiditis have a good prognosis and do not experience long-term ear problems.

De Quervain’s tenosynovitis is a condition characterized by inflammation and thickening of the sheath that contains the tendons of the extensor pollicis brevis and abductor pollicis longus. This leads to pain on the radial side of the wrist. It is more commonly observed in women, particularly those aged between 30 and 50 years. The condition is often associated with repetitive activities that involve pinching and grasping.

During examination, swelling and tenderness along the tendon sheath may be observed. The tendon sheath itself may also appear thickened. The most pronounced tenderness is usually felt over the tip of the radial styloid. A positive Finkelstein’s test, which involves flexing the wrist and moving it towards the ulnar side while the thumb is flexed across the palm, can help confirm the diagnosis.

Treatment for De Quervain’s tenosynovitis involves avoiding movements that can trigger symptoms and using a thumb splint to immobilize the thumb. In cases where symptoms persist, a local corticosteroid injection or surgical decompression may be considered.

Broca’s area is situated in the frontal lobe of the dominant cerebral hemisphere. Specifically, it can be located in the posterior section of the inferior frontal gyrus, and it comprises of the pars opercularis and the pars triangularis.

Broca’s area is responsible for regulating the motor functions involved in speech production. It facilitates the creation of words through its connections with neighboring motor areas, which stimulate the muscles of the larynx, mouth, tongue, and soft palate.

If there is damage to Broca’s area, it will lead to speech paralysis and expressive aphasia, commonly referred to as Broca’s aphasia.

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

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

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

Calcium-channel blocker overdose is a serious condition that should always be taken seriously as it can be potentially life-threatening. The two most dangerous types of calcium channel blockers in overdose are verapamil and diltiazem. These medications work by binding to the alpha-1 subunit of L-type calcium channels, which prevents the entry of calcium into the cells. These channels play a crucial role in the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

Significant toxicity can occur with the ingestion of more than 10 tablets of verapamil (160 mg or 240 mg immediate or sustained-release capsules) or diltiazem (180 mg, 240 mg or 360 mg immediate or sustained-release capsules). In children, even 1-2 tablets of immediate or sustained-release verapamil or diltiazem can be harmful. Symptoms usually appear within 1-2 hours of taking standard preparations, but with slow-release versions, the onset of severe toxicity may be delayed by 12-16 hours, with peak effects occurring after 24 hours.

The main clinical manifestations of calcium-channel blocker overdose include nausea and vomiting, low blood pressure, slow heart rate and first-degree heart block, heart muscle ischemia and stroke, kidney failure, pulmonary edema, and high blood sugar levels.

When managing a patient with calcium-channel blocker overdose, certain bedside investigations are crucial. These include checking blood glucose levels, performing an electrocardiogram (ECG), and obtaining an arterial blood gas sample. Additional investigations that can provide helpful information include assessing urea and electrolyte levels, conducting a chest X-ray to check for pulmonary edema, and performing an echocardiography.

Faget sign is a unique occurrence where a fever and a relatively slow heart rate, known as bradycardia, are observed together. This phenomenon is sometimes called sphygmothermic dissociation. It can be observed in various infectious diseases, such as yellow fever, typhoid fever, tularaemia, brucellosis, Colorado tick fever, Legionella pneumonia, and Mycoplasma pneumonia. Normally, when a person has a fever, their heart rate increases, but in cases of Faget sign, the heart rate remains slow. Another term used to describe the combination of fever and increased heart rate is Leibermeister’s rule.

Auspitz’s sign is a characteristic feature seen in psoriasis. When the scales of psoriasis are scraped off, small bleeding spots, known as punctate bleeding spots, appear. This sign helps in the diagnosis of psoriasis.

Frank sign is a term used to describe a diagonal crease that appears on the earlobe. It has been hypothesized that this crease may be linked to cardiovascular disease and diabetes.

Levine’s sign refers to a specific response to chest pain caused by reduced blood flow to the heart, known as ischemic chest pain. In this sign, the person clenches their fist and holds it over their chest in an instinctive reaction to the pain.

Shingles is caused by the varicella-zoster virus (VZV), which primarily infects individuals during childhood as chickenpox. However, the initial infection can also be subclinical. After the primary infection, the virus remains dormant in the sensory nervous system, specifically in the geniculate, trigeminal, or dorsal root ganglia.

During the dormant phase, the virus is kept under control by the immune system for many years. However, it can later become active and cause a flare-up in a specific dermatomal segment. This reactivation occurs when the virus travels down the affected nerve over a period of 3 to 5 days, leading to inflammation within and around the nerve. The decline in cell-mediated immunity is believed to trigger the virus’s reactivation.

Several factors can trigger the reactivation of the varicella-zoster virus, including advancing age (with most patients being older than 50), immunosuppressive illnesses, physical trauma, and psychological stress. In immunocompetent patients, the most common site of reactivation is the thoracic nerves, followed by the ophthalmic division of the trigeminal nerve.

Diagnosing shingles can usually be done based on the patient’s history and clinical examination alone, as it has a distinct history and appearance. While various techniques can be used to detect the virus or antibodies, they are often unnecessary. Microscopy and culture tests using scrapings and smears typically yield negative results.

Verapamil is a type of calcium-channel blocker that is commonly used to treat irregular heart rhythms and chest pain. It is important to note that verapamil should not be taken at the same time as beta-blockers like atenolol. This is because when these medications are combined, they can have a negative impact on the heart’s ability to contract and its heart rate. This can lead to low blood pressure, slow heart rate, problems with the electrical signals in the heart, heart failure, and even a pause in the heart’s normal rhythm. However, the other medications mentioned in this question can be safely used together with beta-blockers.

Hypothermia can cause various changes in an electrocardiogram (ECG). These changes include a slower heart rate (bradycardia), the presence of Osborn Waves (also known as J waves), a prolonged PR interval, a widened QRS complex, and a prolonged QT interval. Additionally, the ECG may show artifacts caused by shivering, as well as the presence of ventricular ectopics. In severe cases, hypothermia can lead to cardiac arrest, which may manifest as ventricular tachycardia (VT), ventricular fibrillation (VF), or asystole.

Further Reading:

Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, the basal metabolic rate decreases and cell signaling between neurons decreases, leading to reduced tissue perfusion. This can result in decreased myocardial contractility, vasoconstriction, ventilation-perfusion mismatch, and increased blood viscosity. Symptoms of hypothermia progress as the core temperature drops, starting with compensatory increases in heart rate and shivering, and eventually leading to bradyarrhythmias, prolonged PR, QRS, and QT intervals, and cardiac arrest.

In the management of hypothermic cardiac arrest, ALS should be initiated with some modifications. The pulse check during CPR should be prolonged to 1 minute due to difficulty in obtaining a pulse. Rewarming the patient is important, and mechanical ventilation may be necessary due to stiffness of the chest wall. Drug metabolism is slowed in hypothermic patients, so dosing of drugs should be adjusted or withheld. Electrolyte disturbances are common in hypothermic patients and should be corrected.

Frostbite refers to a freezing injury to human tissue and occurs when tissue temperature drops below 0ºC. It can be classified as superficial or deep, with superficial frostbite affecting the skin and subcutaneous tissues, and deep frostbite affecting bones, joints, and tendons. Frostbite can be classified from 1st to 4th degree based on the severity of the injury. Risk factors for frostbite include environmental factors such as cold weather exposure and medical factors such as peripheral vascular disease and diabetes.

Signs and symptoms of frostbite include skin changes, cold sensation or firmness to the affected area, stinging, burning, or numbness, clumsiness of the affected extremity, and excessive sweating, hyperemia, and tissue gangrene. Frostbite is diagnosed clinically and imaging may be used in some cases to assess perfusion or visualize occluded vessels. Management involves moving the patient to a warm environment, removing wet clothing, and rapidly rewarming the affected tissue. Analgesia should be given as reperfusion is painful, and blisters should be de-roofed and aloe vera applied. Compartment syndrome is a risk and should be monitored for. Severe cases may require surgical debridement of amputation.

Spontaneous bacterial peritonitis (SBP) is a sudden bacterial infection of the fluid in the abdomen. It typically occurs in patients with high blood pressure in the portal vein, and about 70% of patients are classified as Child-Pugh class C. In any given year, around 30% of patients with ascites, a condition characterized by fluid buildup in the abdomen, will develop SBP.

SBP can present with a wide range of symptoms, so it’s important to be vigilant when caring for patients with ascites, especially if there is a sudden decline in their condition. Some patients may not show any symptoms at all.

Common clinical features of SBP include fever, chills, nausea, vomiting, abdominal pain, tenderness, worsening ascites, general malaise, and hepatic encephalopathy. Certain factors can increase the risk of developing SBP, such as severe liver disease, gastrointestinal bleeding, urinary tract infection, intestinal bacterial overgrowth, indwelling lines (e.g., central venous catheters or urinary catheters), previous episodes of SBP, and low levels of protein in the ascitic fluid.

To diagnose SBP, an abdominal paracentesis, also known as an ascitic tap, is performed. This involves locating the area of dullness on the flank, next to the rectus abdominis muscle, and performing the tap about 5 cm above and towards the midline from the anterior superior iliac spines.

Certain features on the analysis of the peritoneal fluid strongly suggest SBP, including a total white cell count in the ascitic fluid of more than 500 cells/µL, a total neutrophil count of more than 250 cells/µL, a lactate level in the ascitic fluid of more than 25 mg/dL, a pH of less than 7.35, and the presence of bacteria on Gram-stain.

Patients diagnosed with SBP should be admitted to the hospital and given broad-spectrum antibiotics. The preferred choice is an intravenous 3rd generation cephalosporin, such as ceftriaxone. If the patient is allergic to beta-lactam antibiotics, ciprofloxacin can be considered as an alternative. Administering intravenous albumin can help reduce the risk of kidney failure and mortality.

Gillick competence is a legal concept that determines whether a child under the age of 16 has the ability to give consent for their own medical treatment, even without parental consent or knowledge. This term originated in England and Wales and is commonly used in medical law. On the other hand, Fraser guidelines are specifically applied to situations involving advice and treatment related to a young person’s sexual health and contraception.

Further Reading:

Patients have the right to determine what happens to their own bodies, and for consent to be valid, certain criteria must be met. These criteria include the person being informed about the intervention, having the capacity to consent, and giving consent voluntarily and freely without any pressure or undue influence.

In order for a person to be deemed to have capacity to make a decision on a medical intervention, they must be able to understand the decision and the information provided, retain that information, weigh up the pros and cons, and communicate their decision.

Valid consent can only be provided by adults, either by the patient themselves, a person authorized under a Lasting Power of Attorney, or someone with the authority to make treatment decisions, such as a court-appointed deputy or a guardian with welfare powers.

In the UK, patients aged 16 and over are assumed to have the capacity to consent. If a patient is under 18 and appears to lack capacity, parental consent may be accepted. However, a young person of any age may consent to treatment if they are considered competent to make the decision, known as Gillick competence. Parental consent may also be given by those with parental responsibility.

The Fraser guidelines apply to the prescription of contraception to under 16’s without parental involvement. These guidelines allow doctors to provide contraceptive advice and treatment without parental consent if certain criteria are met, including the young person understanding the advice, being unable to be persuaded to inform their parents, and their best interests requiring them to receive contraceptive advice or treatment.

Competent adults have the right to refuse consent, even if it is deemed unwise or likely to result in harm. However, there are exceptions to this, such as compulsory treatment authorized by the mental health act or if the patient is under 18 and refusing treatment would put their health at serious risk.

In emergency situations where a patient is unable to give consent, treatment may be provided without consent if it is immediately necessary to save their life or prevent a serious deterioration of their condition. Any treatment decision made without consent must be in the patient’s best interests, and if a decision is time-critical and the patient is unlikely to regain capacity in time, a best interest decision should be made. The treatment provided should be the least restrictive on the patient’s future choices.

Toxic epidermal necrolysis is a severe and potentially life-threatening form of erythema multiforme. This condition leads to the detachment of the dermis from the lower layers of the skin. In some cases, it can result in death due to sepsis and failure of multiple organs.

Stevens-Johnson syndrome and toxic epidermal necrolysis are considered to be different stages of the same mucocutaneous disease, with toxic epidermal necrolysis being more severe. The degree of epidermal detachment is used to differentiate between the two conditions. In Stevens-Johnson syndrome, less than 10% of the body surface area is affected by epidermal detachment, while in toxic epidermal necrolysis, it is greater than 30%. An overlap syndrome occurs when the detachment is between 10-30% of the body surface area.

Certain medications can trigger Stevens-Johnson syndrome and toxic epidermal necrolysis. These include tetracyclines, penicillins, vancomycin, sulphonamides, NSAIDs, and barbiturates. It is important to be aware of these potential triggers and seek medical attention if any symptoms or signs of these conditions develop.

Q fever is a highly contagious infection caused by Coxiella burnetii, which can be transmitted from animals to humans. It is commonly observed as an occupational disease among individuals working in farming, slaughterhouses, and animal research. Approximately 50% of cases do not show any symptoms, while those who are affected often experience flu-like symptoms such as headache, fever, muscle pain, diarrhea, nausea, and vomiting.

In some cases, patients may develop an atypical pneumonia characterized by a dry cough and minimal chest signs. Q fever can also lead to hepatitis and enlargement of the liver (hepatomegaly), although jaundice is not commonly observed. Typical blood test results for Q fever include an elevated white cell count (30-40%), ALT/AST levels that are usually 2-3 times higher than normal, increased ALP levels (70%), reduced sodium levels (30%), and reactive thrombocytosis.

It is important to check patients for heart murmurs and signs of valve disease, as these conditions increase the risk of developing infective endocarditis. Treatment for Q fever typically involves a two-week course of doxycycline.

Between 60 and 80% of individuals who experience seizures will have their seizure stopped by a single dose of intravenous benzodiazepine. Benzodiazepines have a high solubility in lipids and can quickly pass through the blood-brain barrier. This is why they have a fast onset of action.

As the initial treatment, intravenous lorazepam should be administered. If intravenous lorazepam is not accessible, intravenous diazepam can be used instead. In cases where it is not possible to establish intravenous access promptly, buccal midazolam can be utilized.

Fluoroquinolones are a rare but acknowledged cause of tendinopathy and spontaneous tendon rupture. It is estimated that tendon disorders related to fluoroquinolones occur in approximately 15 to 20 out of every 100,000 patients. These issues are most commonly observed in individuals who are over the age of 60.

The Achilles tendon is the most frequently affected, although cases involving other tendons such as the quadriceps, peroneus brevis, extensor pollicis longus, the long head of biceps brachii, and rotator cuff tendons have also been reported. The exact underlying mechanism is not fully understood, but it is believed that fluoroquinolone drugs may hinder collagen function and/or disrupt blood supply to the tendon.

There are other risk factors associated with spontaneous tendon rupture, including corticosteroid therapy, hypercholesterolemia, gout, rheumatoid arthritis, long-term dialysis, and renal transplantation.

The Fraser guidelines pertain to the guidelines established by Lord Fraser during the Gillick case in 1985. These guidelines specifically address the provision of contraceptive advice to individuals under the age of 16. According to the Fraser guidelines, a doctor may proceed with providing advice and treatment if they are satisfied with the following criteria:

1. The individual (despite being under 16 years old) possesses a sufficient understanding of the advice being given.
2. The doctor is unable to convince the individual to inform their parents or allow the doctor to inform the parents about seeking contraceptive advice.
3. The individual is likely to engage in sexual intercourse, regardless of whether they receive contraceptive treatment.
4. Without contraceptive advice or treatment, the individual’s physical and/or mental health is likely to deteriorate.
5. The doctor deems it in the individual’s best interests to provide contraceptive advice, treatment, or both without parental consent.

In summary, the Fraser guidelines outline the conditions under which a doctor can offer contraceptive advice to individuals under 16 years old, ensuring their well-being and best interests are taken into account.

Transfusion-related lung injury (TRALI) is responsible for about one-third of all transfusion-related deaths, making it the leading cause. On the other hand, transfusion-associated circulatory overload (TACO) accounts for approximately 20% of these fatalities, making it the second leading cause. TACO occurs when a large volume of blood is rapidly infused, particularly in patients with limited cardiac reserve or chronic anemia. Elderly individuals, infants, and severely anemic patients are especially vulnerable to this reaction.

The typical signs of TACO include acute respiratory distress, rapid heart rate, high blood pressure, the appearance of acute or worsening pulmonary edema on a chest X-ray, and evidence of excessive fluid accumulation. In many cases, simply reducing the transfusion rate, positioning the patient upright, and administering diuretics will be sufficient to manage the condition. However, in more severe cases, it is necessary to halt the transfusion and consider non-invasive ventilation.

Transfusion-related acute lung injury (TRALI) is defined as new acute lung injury (ALI) that occurs during or within six hours of transfusion, not explained by another ALI risk factor. Transfusion of part of one unit of any blood product can cause TRALI.

Haemothorax often leads to reduced or absent air entry, a dull percussion sound, and decreased fremitus on the affected side. Commonly observed symptoms in patients with haemothorax include decreased or absent air entry, a dull percussion note when the affected side is tapped, reduced fremitus on the affected side, and in cases of massive haemothorax, tracheal deviation away from the affected side. Other signs that may be present include a rapid heart rate (tachycardia), rapid breathing (tachypnoea), low blood pressure (hypotension), and signs of shock.

Further Reading:

Haemothorax is the accumulation of blood in the pleural cavity of the chest, usually resulting from chest trauma. It can be difficult to differentiate from other causes of pleural effusion on a chest X-ray. Massive haemothorax refers to a large volume of blood in the pleural space, which can impair physiological function by causing blood loss, reducing lung volume for gas exchange, and compressing thoracic structures such as the heart and IVC.

The management of haemothorax involves replacing lost blood volume and decompressing the chest. This is done through supplemental oxygen, IV access and cross-matching blood, IV fluid therapy, and the insertion of a chest tube. The chest tube is connected to an underwater seal and helps drain the fluid, pus, air, or blood from the pleural space. In cases where there is prompt drainage of a large amount of blood, ongoing significant blood loss, or the need for blood transfusion, thoracotomy and ligation of bleeding thoracic vessels may be necessary. It is important to have two IV accesses prior to inserting the chest drain to prevent a drop in blood pressure.

In summary, haemothorax is the accumulation of blood in the pleural cavity due to chest trauma. Managing haemothorax involves replacing lost blood volume and decompressing the chest through various interventions, including the insertion of a chest tube. Prompt intervention may be required in cases of significant blood loss or ongoing need for blood transfusion.

Eclampsia is the most likely diagnosis in this case. It is characterized by the occurrence of one or more convulsions on top of pre-eclampsia. To control seizures in eclampsia, the recommended treatment is magnesium sulphate. The Collaborative Eclampsia Trial regimen should be followed for administering magnesium sulphate. Initially, a loading dose of 4 g should be given intravenously over 5 to 15 minutes. This should be followed by a continuous infusion of 1 g per hour for 24 hours. If the woman experiences another eclamptic seizure, the infusion should be continued for an additional 24 hours after the last seizure. In case of recurrent seizures, a further dose of 2-4 g should be administered intravenously over 5 to 15 minutes. It is important to note that the only cure for eclampsia is the delivery of the fetus and placenta. Once the patient is stabilized, she should be prepared for an emergency caesarean section.

When assessing a patient with epistaxis (nosebleed), it is important to start with a standard ABC assessment, focusing on the airway and hemodynamic status. Even if the bleeding appears to have stopped, it is crucial to evaluate the patient’s condition. If active bleeding is still present and there are signs of hemodynamic compromise, immediate resuscitative and first aid measures should be initiated.

Epistaxis should be treated as a circulatory emergency, especially in elderly patients, those with clotting disorders or bleeding tendencies, and individuals taking anticoagulants. In these cases, it is necessary to establish intravenous access using at least an 18-gauge (green) cannula. Blood samples, including a full blood count, urea and electrolytes, clotting profile, and group and save (depending on the amount of blood loss), should be sent for analysis. Patients should be assigned to a majors or closely observed area, as dislodgement of a blood clot can lead to severe bleeding.

First aid measures to control bleeding include the following steps:
1. The patient should be seated upright with their body tilted forward and their mouth open. Lying down should be avoided, unless the patient feels faint or there is evidence of hemodynamic compromise. Leaning forward helps reduce the flow of blood into the nasopharynx.
2. The patient should be encouraged to spit out any blood that enters the throat and advised not to swallow it.
3. Firmly pinch the soft, cartilaginous part of the nose, compressing the nostrils for 10-15 minutes. Pressure should not be released, and the patient should breathe through their mouth.
4. If the patient is unable to comply, an alternative technique is to ask a relative, staff member, or use an external pressure device like a swimmer’s nose clip.
5. It is important to dispel the misconception that compressing the bones will help stop the bleeding. Applying ice to the neck or forehead does not influence nasal blood flow. However, sucking on an ice cube or applying an ice pack directly to the nose may reduce nasal blood flow.

If bleeding stops with first aid measures, it is recommended to apply a topical antiseptic preparation to reduce crusting and vestibulitis. Naseptin cream (containing chlorhexidine and neomycin) is commonly used and should be applied to the nostrils four times daily for 10 days.

This patient has presented with acute closed-angle glaucoma, which is a serious eye condition requiring immediate medical attention. It occurs when the iris pushes forward and blocks the fluid access to the trabecular meshwork, leading to increased pressure within the eye and damage to the optic nerve.

The main symptoms of acute closed-angle glaucoma include severe eye pain, decreased vision, redness around the cornea, swelling of the cornea, a fixed semi-dilated pupil, nausea, vomiting, and episodes of blurred vision or seeing haloes.

To confirm the diagnosis, tonometry is performed to measure the intraocular pressure. Normal pressure ranges from 10 to 21 mmHg, but in acute closed-angle glaucoma, it is often higher than 30 mmHg. Goldmann’s applanation tonometer is commonly used in hospitals for this purpose.

Management of acute closed-angle glaucoma involves providing pain relief, such as morphine, and antiemetics if the patient is experiencing vomiting. Intravenous acetazolamide is administered to reduce intraocular pressure. Additionally, a topical miotic medication like pilocarpine is started about an hour after initiating other treatments to help constrict the pupil, as it may initially be paralyzed and unresponsive.

Overall, acute closed-angle glaucoma is a medical emergency that requires prompt intervention to alleviate symptoms and prevent further damage to the eye.

According to the latest guidelines from NICE and the BNF, the recommended initial treatment for typhoid fever is cefotaxime. It is important to note that infections originating from the Middle-East, South Asia, and South-East Asia may have multiple antibiotic resistance, so it is advisable to test for sensitivity. In cases where the microorganism is found to be sensitive, ciprofloxacin can be considered as a suitable alternative.

For asymptomatic patients, it is recommended to measure salicylate levels 4 hours after ingestion. However, if the patient is experiencing symptoms, the initial levels should be taken 2 hours after ingestion. In this case, the levels should be monitored every 2-3 hours until a decrease is observed.

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.

Sialolithiasis is a medical condition characterized by the formation of a calcified stone, known as a sialolith, within one of the salivary glands. The submandibular gland, specifically Wharton’s duct, is the site of approximately 90% of these occurrences, while the parotid gland accounts for most of the remaining cases. In rare instances, sialoliths may also develop in the sublingual gland or minor salivary glands.

Renal colic, also known as ureteric colic, refers to a sudden and intense pain in the lower back caused by a blockage in the ureter, which is the tube that carries urine from the kidney to the bladder. This condition is commonly associated with the presence of a urinary tract stone.

The main symptoms of renal or ureteric colic include severe abdominal pain on one side, starting in the flank or loin area and radiating to the groin or testicle in men, or to the labia in women. The pain comes and goes in spasms, lasting for minutes to hours, with periods of no pain or a dull ache. Nausea, vomiting, and the presence of blood in the urine are often accompanying symptoms.

The pain experienced during renal or ureteric colic is often described as the most intense pain a person has ever felt, with many women comparing it to the pain of childbirth. Restlessness and an inability to find relief by lying still are common signs, which can help differentiate renal colic from peritonitis. Previous episodes of similar pain may also be reported by the individual. In cases where there is a concomitant urinary infection, fever and sweating may be present. Additionally, the person may complain of painful urination, frequent urination, and straining when the stone reaches the junction between the ureter and the bladder, as the stone irritates the detrusor muscle.

It is important to seek urgent medical attention if certain conditions are met. These include signs of systemic infection or sepsis, such as fever or sweating, or if the person is at a higher risk of acute kidney injury, such as having pre-existing chronic kidney disease, a solitary or transplanted kidney, or suspected bilateral obstructing stones. Hospital admission is also necessary if the person is dehydrated and unable to consume fluids orally due to nausea and/or vomiting. If there is uncertainty regarding the diagnosis, it is recommended to consult further resources, such as the NICE guidelines on the assessment and management of renal and ureteric stones.

Generalized anxiety disorder (GAD) is the most probable diagnosis in this case.

The primary distinction between GAD and panic disorder lies in their symptoms. GAD is primarily characterized by anxiety, whereas panic disorder is characterized by panic attacks. Individuals with GAD typically do not experience frequent panic attacks, although they may occasionally occur. In this patient’s case, while he did experience occasional panic attacks, they were not his main symptom, and his anxiety was not centered around these episodes.

GAD is associated with persistent physical symptoms such as muscle tension, aches, headaches, fatigue, trembling, twitching, irritability, difficulty swallowing, and the sensation of a lump in the throat.

On the other hand, panic disorder primarily revolves around the panic attacks themselves. A panic attack is a brief and intense episode characterized by overwhelming feelings of dread and fear, which may or may not be triggered by a specific situation. Common physical symptoms experienced during panic attacks include dizziness, sweating, chills, nausea, trembling, shaking, abdominal cramps, throat tightness, shortness of breath, numbness in the extremities, rapid heartbeat, palpitations, and chest pain.

NSAIDs are known to have a relaxing effect on the ureter, but a randomized controlled trial found no difference between NSAIDs and a placebo in terms of this effect. Currently, only two classes of drugs, calcium channel blockers and alpha-blockers, are considered effective as medical expulsive therapy (MET). Calcium channel blockers work by blocking the active calcium channel pump that the smooth muscle of the ureter uses to contract, resulting in relaxation of the muscle and improved stone passage. Alpha-blockers, on the other hand, are commonly used as the first-line treatment to enhance stone passage. They reduce the basal tone of the ureter smooth muscle, decrease the frequency of peristaltic waves, and lower ureteric contraction. This leads to a decrease in intraureteric pressure below the stone, increasing the chances of stone passage. Patients treated with calcium channel blockers or alpha-blockers have been shown to have a 65% higher likelihood of spontaneous stone passage compared to those not given these medications.

The cerebellum, also known as the ‘little brain’ in Latin, is a structure within the central nervous system. It is situated at the posterior part of the brain, beneath the occipital and temporal lobes of the cerebral cortex. Despite its relatively small size, the cerebellum houses more than half of the total number of neurons in the brain, accounting for about 10% of its volume.

The cerebellum serves several crucial functions. It is responsible for maintaining balance and posture, ensuring that we stay upright and steady. Additionally, it plays a vital role in coordinating voluntary movements, allowing us to perform tasks that require precise and synchronized actions. The cerebellum is also involved in motor learning, enabling us to acquire new skills and improve our motor abilities over time. Furthermore, it contributes to cognitive function, supporting various mental processes.

It is important to note that spontaneous facial expression is controlled by the frontal lobes and is unlikely to be impacted by a tumor located in the cerebellum.

Adrenaline is the most crucial drug in treating anaphylaxis. It is essential to be aware of the appropriate dosage and administration method for all age groups. Additionally, high flow oxygen should be administered, as mentioned in the question stem. While there are other drugs that should be given, they are considered less important than adrenaline. These include IV fluid challenge, slow administration of chlorpheniramine (either IM or IV), slow administration of hydrocortisone (particularly in individuals with asthma), and the consideration of nebulized salbutamol or ipratropium for wheezing individuals (especially those with known asthma).

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

The risk of primary spontaneous pneumothorax is associated with smoking tobacco and increases as the duration of exposure and daily consumption rise. The changes caused by smoking in the small airways may contribute to the development of local emphysema, leading to the formation of bullae. In this case, the patient does not have any clinical features or significant risk factors for the other conditions mentioned. Therefore, primary spontaneous pneumothorax is the most probable diagnosis.

The use of antibiotics can impact the effectiveness of warfarin and other coumarin anticoagulants. This can lead to changes in the International Normalized Ratio (INR) and, in severe cases, increase the risk of bleeding. Some antibiotics, such as chloramphenicol, ciprofloxacin, co-trimoxazole, doxycycline, erythromycin, macrolides (e.g., clarithromycin), metronidazole, ofloxacin, and sulphonamide, are known to enhance the anticoagulant effect of warfarin. However, cefalexin is considered relatively safe and is the most suitable option in this situation.

Migraine is a common neurological complaint, affecting approximately 16% of individuals throughout their lifetime. Vestibular migraine is characterized by the presence of migrainous symptoms along with recurring episodes of vertigo and/or unsteadiness. It is a leading cause of vertigo and the most frequent cause of spontaneous episodic vertigo. The disturbance in the vestibular system can manifest as part of the aura phase or occur independently. The duration of these episodes can range from a few seconds to several days, typically lasting for minutes to hours. Interestingly, they often occur without accompanying headaches. Diagnosing vestibular migraine is primarily based on ruling out other potential causes. For prolonged individual attacks, antivertiginous and antiemetic medications are commonly used. However, specific antimigraine drugs may not provide significant relief in rescue situations. The cornerstone of managing vestibular migraine lies in the use of prophylactic medication. In some cases, referral to a neurologist may be necessary, especially if the patient is experiencing acute symptoms for the first time.

The modified SAD PERSONS scoring system is a valuable tool used to evaluate a patient’s risk of suicide. This scoring system consists of ten yes/no questions, and points are assigned for each affirmative answer. The points are distributed as follows: 1 point for being male, 1 point for being younger than 19 or older than 45 years, 2 points for experiencing depression or hopelessness, 1 point for having a history of previous suicidal attempts or psychiatric care, 1 point for excessive alcohol or drug use, 2 points for exhibiting a loss of rational thinking due to psychotic or organic illness, 1 point for being single, widowed, or divorced, 2 points for an organized or serious suicide attempt, 1 point for lacking social support, and 2 points for expressing future intent to repeat or being ambivalent about suicide.

Based on the total score, the patient’s risk level can be determined. A score of 0-5 suggests that it may be safe to discharge the patient or provide outpatient management, depending on the circumstances. A score of 6-8 indicates that the patient probably requires psychiatric consultation. Finally, a score higher than 8 suggests that the patient likely requires hospital admission for further evaluation and care. This scoring system helps healthcare professionals make informed decisions regarding the appropriate level of intervention and support needed for patients at risk of suicide.

The presence of both fever and a murmur in an individual who engages in intravenous drug use (IVDU) should raise suspicion for infective endocarditis. IVDU is a significant risk factor for this condition. In this particular patient, the symptoms of fever and cardiac murmur are important indicators that may be emphasized in an exam scenario. It is important to note that infective endocarditis in IVDU patients typically affects the right side of the heart, with the tricuspid valve being the most commonly affected. Murmurs in this patient population can be subtle and challenging to detect during a clinical examination. Additionally, the presence of septic emboli can lead to the entry of infected material into the pulmonary circulation, potentially causing pneumonia and pulmonary vessel occlusion, which may manifest as a pulmonary embolism (PE).

Further Reading:

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

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

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

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

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

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

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

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

Pityriasis versicolor, also known as tinea versicolor, is a common skin condition caused by an infection with the yeasts Malassezia furfur and Malassezia globosa. It typically presents as multiple patches of altered pigmentation, primarily on the trunk. In individuals with fair skin, these patches are usually darker in color, while in those with darker skin or a tan, they may appear lighter (known as pityriasis versicolor alba). It is not uncommon for the rash to cause itching.

The recommended treatment for pityriasis versicolor involves the use of antifungal agents. One particularly effective option is ketoconazole shampoo, which is sold under the brand name Nizoral. To use this shampoo, it should be applied to the affected areas and left on for approximately five minutes before being rinsed off. This process should be repeated daily for a total of five days.

Le Fort III fractures can be distinguished from Le Fort II fractures by the presence of damage to the zygomatic arch.

Further Reading:

The Le Fort fracture classification describes three fracture patterns seen in midface fractures, all involving the maxilla and pterygoid plate disruption. As the classification grading increases, the anatomic level of the maxillary fracture ascends from inferior to superior.

Le Fort I fractures, also known as floating palate fractures, typically result from a downward blow struck above the upper dental row. Signs include swelling of the upper lip, bruising to the upper buccal sulcus, malocclusion, and mobile upper teeth.

Le Fort II fractures, also known as floating maxilla fractures, are typically the result of a forceful blow to the midaxillary area. Signs include a step deformity at the infraorbital margin, oedema over the middle third of the face, sensory disturbance of the cheek, and bilateral circumorbital ecchymosis.

Le Fort III fractures, also known as craniofacial dislocation or floating face fractures, are typically the result of high force blows to the nasal bridge or upper maxilla. These fractures involve the zygomatic arch and extend through various structures in the face. Signs include tenderness at the frontozygomatic suture, lengthening of the face, enophthalmos, and bilateral circumorbital ecchymosis.

Management of Le Fort fractures involves securing the airway as a priority, following the ABCDE approach, and identifying and managing other injuries, especially cervical spine injuries. Severe bleeding may occur and should be addressed appropriately. Surgery is almost always required, and patients should be referred to maxillofacial surgeons. Other specialties, such as neurosurgery and ophthalmology, may need to be involved depending on the specific case.

The symptoms and signs of strokes can vary depending on which blood vessel is affected. Here is a summary of the main symptoms based on the territory affected:

Anterior cerebral artery: This can cause weakness on the opposite side of the body, with the leg and shoulder being more affected than the arm, hand, and face. There may also be minimal loss of sensation on the opposite side of the body. Other symptoms can include difficulty speaking (dysarthria), language problems (aphasia), apraxia (difficulty with limb movements), urinary incontinence, and changes in behavior and personality.

Middle cerebral artery: This can lead to weakness on the opposite side of the body, with the face and arm being more affected than the leg. There may also be a loss of sensation on the opposite side of the body. Depending on the dominant hemisphere of the brain, there may be difficulties with expressive or receptive language (dysphasia). In the non-dominant hemisphere, there may be neglect of the opposite side of the body.

Posterior cerebral artery: This can cause a loss of vision on the opposite side of both eyes (homonymous hemianopia). There may also be defects in a specific quadrant of the visual field. In some cases, there may be a syndrome affecting the thalamus on the opposite side of the body.

It’s important to note that these are just general summaries and individual cases may vary. If you suspect a stroke, it’s crucial to seek immediate medical attention.

Blood transfusion is a crucial medical treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion use, errors and adverse reactions still occur. One common adverse reaction is febrile transfusion reactions, which present as an unexpected rise in temperature during or after transfusion. This can be caused by cytokine accumulation or recipient antibodies reacting to donor antigens. Treatment for febrile transfusion reactions is supportive, and other potential causes should be ruled out.

Another serious complication is acute haemolytic reaction, which is often caused by ABO incompatibility due to administration errors. This reaction requires the transfusion to be stopped and IV fluids to be administered. Delayed haemolytic reactions can occur several days after a transfusion and may require monitoring and treatment for anaemia and renal function. Allergic reactions, TRALI (Transfusion Related Acute Lung Injury), TACO (Transfusion Associated Circulatory Overload), and GVHD (Graft-vs-Host Disease) are other potential complications that require specific management approaches.

In summary, blood transfusion carries risks and potential complications, but efforts have been made to improve safety procedures. It is important to be aware of these complications and to promptly address any adverse reactions that may occur during or after a transfusion.

Von Willebrand disease (vWD) is a common hereditary coagulation disorder that affects approximately 1 in 100 individuals. It occurs due to a deficiency in Von Willebrand factor (vWF), which plays a crucial role in blood clotting. vWF not only binds to factor VIII to protect it from rapid breakdown, but it is also necessary for proper platelet adhesion. When vWF is lacking, both factor VIII levels and platelet function are affected, leading to prolonged APTT and bleeding time. However, the platelet count and thrombin time remain unaffected.

While some individuals with vWD may not experience any symptoms and are diagnosed incidentally during a clotting profile check, others may present with 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 managed with desmopressin. This medication works by stimulating the release of vWF stored in the Weibel-Palade bodies, which are storage granules found in the endothelial cells lining the blood vessels and heart. By increasing the patient’s own levels of vWF, desmopressin helps improve clotting. In more severe cases, replacement therapy is necessary. This involves infusing cryoprecipitate or Factor VIII concentrate to provide the missing vWF. Replacement therapy is particularly recommended for patients with severe von Willebrand’s disease who are undergoing moderate or major surgical procedures.

Thought insertion is one of the primary symptoms identified by Schneider in schizophrenia. This symptom refers to the patient’s belief that their thoughts are being controlled or influenced by external sources, such as other individuals or entities. In some cases, they may even experience auditory hallucinations, hearing distinct voices.

Hepatitis B vaccination is included in the routine childhood immunisation schedule to provide long-term protection against hepatitis for children under 1 year of age. For these children, the vaccination consists of a primary course that includes the diphtheria with tetanus, pertussis, hepatitis B, poliomyelitis, and Haemophilus influenza type B vaccine. This primary course is given at 4 weekly intervals.

The Hepatitis B vaccine is a conjugate vaccine that contains a surface antigen of the hepatitis virus (HBsAg) and is combined with an aluminium adjuvant to enhance its effectiveness. It is produced using a recombinant DNA technique.

When administering the vaccine to adults and older children, the preferred injection site is the deltoid muscle. However, in younger children, the anterolateral thigh is the preferred site. It is not recommended to inject the vaccine in the gluteal area as it has been found to have reduced efficacy.

The standard vaccination regime for Hepatitis B consists of three primary doses. The initial dose is followed by further doses at one and six months later. A booster dose is recommended at five years if the individual is still at risk.

In cases of post-exposure prophylaxis, an accelerated vaccination regime is used. This involves administering a vaccination at the time of exposure, followed by repeat doses at one and two months later.

In high-risk situations, Hepatitis B immunoglobulin can be given up to 7 days after exposure. Ideally, it should be administered within 12 hours, but according to the BNF, it can still be effective if given within 7 days after exposure.

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

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

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

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

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

When giving chest compressions to an adult, it is important to compress the sternum to a depth of 5-6 cm. The resuscitation council updated their guidance in 2015 and now recommends a ratio of 30 chest compressions to 2 rescue breaths. It is worth noting that according to the algorithm, checking for a pulse is no longer necessary in the latest BLS sequence. The chest compressions should be administered at a rate of 100-120 per minute, with a ratio of 30 compressions to 2 rescue breaths.

Further Reading:

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

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

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

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

postmenopausal bleeding should always be treated as a potential malignancy until proven otherwise. The first-line investigation for this condition is transvaginal ultrasound (TVUS). This method effectively assesses the risk of endometrial cancer by measuring the thickness of the endometrium.

In postmenopausal women, the average endometrial thickness is much thinner compared to premenopausal women. The likelihood of endometrial cancer increases as the endometrium becomes thicker. Currently, in the UK, an endometrial thickness of 5 mm is considered the threshold.

If the endometrial thickness is greater than 5 mm, there is a 7.3% chance of endometrial cancer. However, if a woman with postmenopausal bleeding has a uniform endometrial thickness of less than 5 mm, the likelihood of endometrial cancer is less than 1%.

In cases where there is a high clinical risk, hysteroscopy and endometrial biopsy should also be performed. The definitive diagnosis is made through histological examination. If the endometrial thickness is greater than 5 mm, an endometrial biopsy is recommended.

Salicylate poisoning often leads to a metabolic acidosis characterized by a high anion gap. The patient in question is experiencing this type of acid-base disturbance. This particular acid-base imbalance is typically seen in cases of poisoning with substances such as glycols (ethylene and propylene), salicylates (aspirin), paracetamol, methanol, isoniazid, and paraldehyde.

Further Reading:

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

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

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

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

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

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

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

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

This patient has a history of worsening breathlessness and lung function tests that show a pattern of restrictive lung disease. In restrictive lung disease, the ratio of FEV1 to FVC is usually normal, around 70% predicted, but the FVC is reduced to less than 80% predicted. Both the FVC and FEV1 can be reduced in this condition. The ratio can also be higher if the FVC is reduced to a greater extent. Out of the options provided, only idiopathic pulmonary fibrosis can cause a restrictive lung disease pattern. Smoking is a risk factor for developing idiopathic pulmonary fibrosis, especially if the person has smoked more than 20 packs of cigarettes per year.

The secretion of aldosterone occurs in the zona glomerulosa of the adrenal cortex.

Further Reading:

Hyperaldosteronism is a condition characterized by excessive production of aldosterone by the adrenal glands. It can be classified into primary and secondary hyperaldosteronism. Primary hyperaldosteronism, also known as Conn’s syndrome, is typically caused by adrenal hyperplasia or adrenal tumors. Secondary hyperaldosteronism, on the other hand, is a result of high renin levels in response to reduced blood flow across the juxtaglomerular apparatus.

Aldosterone is the main mineralocorticoid steroid hormone produced by the adrenal cortex. It acts on the distal renal tubule and collecting duct of the nephron, promoting the reabsorption of sodium ions and water while secreting potassium ions.

The causes of hyperaldosteronism vary depending on whether it is primary or secondary. Primary hyperaldosteronism can be caused by adrenal adenoma, adrenal hyperplasia, adrenal carcinoma, or familial hyperaldosteronism. Secondary hyperaldosteronism can be caused by renal artery stenosis, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, or cor pulmonale.

Clinical features of hyperaldosteronism include hypertension, hypokalemia, metabolic alkalosis, hypernatremia, polyuria, polydipsia, headaches, lethargy, muscle weakness and spasms, and numbness. It is estimated that hyperaldosteronism is present in 5-10% of patients with hypertension, and hypertension in primary hyperaldosteronism is often resistant to drug treatment.

Diagnosis of hyperaldosteronism involves various investigations, including U&Es to assess electrolyte disturbances, aldosterone-to-renin plasma ratio (ARR) as the gold standard diagnostic test, ECG to detect arrhythmia, CT/MRI scans to locate adenoma, fludrocortisone suppression test or oral salt testing to confirm primary hyperaldosteronism, genetic testing to identify familial hyperaldosteronism, and adrenal venous sampling to determine lateralization prior to surgery.

Treatment of primary hyperaldosteronism typically involves surgical adrenalectomy for patients with unilateral primary aldosteronism. Diet modification with sodium restriction and potassium supplementation may also be recommended.

Epiglottitis symptoms typically appear suddenly, usually within a day. This patient’s symptoms align with those of epiglottitis and his vaccination status puts him at a higher risk. Common clinical features of epiglottitis include a rapid onset of symptoms, high fever, a sore throat, a change in voice (often described as a muffled or hot potato voice), painful swallowing, a specific positioning called tripod positioning, excessive drooling, and stridor.

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.

The patient presents with a medical history and physical examination findings that are consistent with a diagnosis of Löfgren’s syndrome, which is a specific subtype of sarcoidosis. This syndrome is most commonly observed in women in their 30s and 40s, and it is more prevalent among individuals of Nordic and Irish descent.

Löfgren’s syndrome is typically characterized by a triad of clinical features, including bilateral hilar lymphadenopathy seen on chest X-ray, erythema nodosum, and arthralgia, with a particular emphasis on ankle involvement. Additionally, other symptoms commonly associated with sarcoidosis may also be present, such as a dry cough, breathlessness, fever, night sweats, malaise, weight loss, Achilles tendonitis, and uveitis.

In order to further evaluate this patient’s condition, it is recommended to refer them to a respiratory specialist for additional investigations. These investigations may include measuring the serum calcium level, as it may be elevated, and assessing the serum angiotensin-converting enzyme (ACE) level, which may also be elevated. A high-resolution CT scan can be performed to assess the extent of involvement and identify specific lymph nodes for potential biopsy. If there are any atypical features, a lymph node biopsy may be necessary. Lung function tests can be conducted to evaluate the patient’s vital capacity, and an MRI scan of the ankles may also be considered.

Fortunately, the prognosis for Löfgren’s syndrome is generally very good, and it is considered a self-limiting and benign condition. The patient can expect to recover within a timeframe of six months to two years.

Benign paroxysmal positional vertigo (BPPV) occurs when there is dysfunction in the inner ear. This dysfunction causes the otoliths, which are located in the utricle, to become dislodged from their normal position and migrate into one of the semicircular canals over time. As a result, these detached otoliths continue to move even after head movement has stopped, leading to vertigo due to the conflicting sensation of ongoing movement with other sensory inputs.

While the majority of BPPV cases have no identifiable cause (idiopathic), approximately 40% of cases can be attributed to factors such as head injury, spontaneous labyrinthine degeneration, post-viral illness, middle ear surgery, or chronic middle ear disease.

The main clinical features of BPPV include symptoms that are provoked by head movement, rolling over, and upward gaze. These episodes are typically brief, lasting less than 5 minutes, and are often worse in the mornings. Unlike other inner ear disorders, BPPV does not cause hearing loss or tinnitus. Nausea is a common symptom, while vomiting is rare. The Dix-Hallpike test can be used to confirm the diagnosis of BPPV.

It is important to note that vestibular suppressant medications have not been proven to be beneficial in managing BPPV. These medications do not improve symptoms or reduce the duration of the disease.

The treatment of choice for BPPV is the Epley manoeuvre. This maneuver aims to reposition the dislodged otoliths back into the utricles from the semicircular canals. A 2014 Cochrane review concluded that the Epley manoeuvre is a safe and effective treatment for BPPV, with a number needed to treat of 2-4.

Referral to an ENT specialist is recommended for patients with BPPV in the following situations: if the treating clinician is unable to perform or access the Epley manoeuvre, if the Epley manoeuvre has not been beneficial after repeated attempts (minimum two), if the patient has been symptomatic for more than 4 weeks, or if the patient has experienced more than 3 episodes of BPPV.

Cauda equina syndrome (CES) is a rare but serious complication that can occur when a disc in the spine ruptures. This happens when the material from the disc is pushed into the spinal canal and puts pressure on a bundle of nerves in the lower back and sacrum. When this happens, it can lead to problems with controlling the bladder and bowels.

There are certain signs that may indicate the presence of CES, which are known as red flags. These include experiencing sciatica on both sides of the body, having a severe or worsening neurological deficit in both legs, such as significant weakness in the muscles that extend the knee, turn the ankle outward, or lift the foot upward. Other red flags include difficulty starting to urinate or a decreased sensation of the flow of urine, a loss of feeling when the rectum is full, a loss of sensation in the perianal, perineal, or genital areas (also known as saddle anesthesia or paresthesia), and a looseness in the anal sphincter muscle.

Activated charcoal is a useful treatment for many drug poisonings, but it is not effective against certain types of poisonings. To remember these exceptions, you can use the mnemonic PHAILS. This stands for Pesticides (specifically organophosphates), Hydrocarbons, Acids (strong), alkalis (strong), alcohols (such as ethanol, methanol, and ethylene glycol), Iron, Lithium, and Solvents.

Further Reading:

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

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

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

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

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

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

Subclinical hypothyroidism is a condition where the thyroid-stimulating hormone (TSH) levels are higher than normal, but the levels of free thyroxine (T4) are still within the normal range. On the other hand, subclinical hyperthyroidism is a condition where the TSH levels are lower than normal, but the levels of free triiodothyronine (T3) and free thyroxine (T4) are still within the normal range.

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.

The mortality rate associated with pulmonary edema as a result of acute heart failure secondary to cardiogenic shock during hospitalization is 50%.

Further Reading:

Cardiac failure, also known as heart failure, is a clinical syndrome characterized by symptoms and signs resulting from abnormalities in the structure or function of the heart. This can lead to reduced cardiac output or high filling pressures at rest or with stress. Heart failure can be caused by various problems such as myocardial, valvular, pericardial, endocardial, or arrhythmic issues.

The most common causes of heart failure in the UK are coronary heart disease and hypertension. However, there are many other possible causes, including valvular heart disease, structural heart disease, cardiomyopathies, certain drugs or toxins, endocrine disorders, nutritional deficiencies, infiltrative diseases, infections, and arrhythmias. Conditions that increase peripheral demand on the heart, such as anemia, pregnancy, sepsis, hyperthyroidism, Paget’s disease of bone, arteriovenous malformations, and beriberi, can also lead to high-output cardiac failure.

Signs and symptoms of heart failure include edema, lung crepitations, tachycardia, tachypnea, hypotension, displaced apex beat, right ventricular heave, elevated jugular venous pressure, cyanosis, hepatomegaly, ascites, pleural effusions, breathlessness, fatigue, orthopnea, paroxysmal nocturnal dyspnea, nocturnal cough or wheeze, and Presyncope.

To diagnose heart failure, NICE recommends three key tests: N-terminal pro-B-type natriuretic peptide (NT‑proBNP), transthoracic echocardiography, and ECG. Additional tests may include chest X-ray, blood tests (U&Es, thyroid function, LFT’s, lipid profile, HbA1C, FBC), urinalysis, and peak flow or spirometry.

Management of cardiogenic pulmonary edema, a complication of heart failure, involves ensuring a patent airway, optimizing breathing with supplemental oxygen and non-invasive ventilation if necessary, and addressing circulation with loop diuretics to reduce preload, vasodilators to reduce preload and afterload, and inotropes if hypotension or signs of end organ hypoperfusion persist.

When adjusting the dosage of oral morphine, if the initial dose does not provide relief, it is recommended to increase the dose by 50%. The goal of dosage titration is to identify the minimum amount of morphine required to effectively manage pain. Additionally, it is important to consider the use of supplementary analgesics like NSAIDs and paracetamol.

A pilonidal sinus is a small cyst found near the crease between the buttocks. It contains a clump of hairs and is most commonly seen in young males with thick, dark hair. This condition is rare in individuals over the age of 40. Several factors increase the risk of developing a pilonidal sinus, including being male, having excessive hair growth, having a job that involves prolonged sitting, being overweight, and having a family history of the condition.

This patient is experiencing a condition called right-sided abducens nerve palsy, which means that their sixth cranial nerve is paralyzed. As a result, the lateral rectus muscle, which is responsible for moving the eye outward, is also paralyzed. This means that the patient’s right eye is unable to turn outward. This can lead to a condition called convergent strabismus, where the eyes are not aligned properly, and diplopia, which is double vision. To compensate for the double vision, patients often tilt their head towards the side of the paralyzed muscle.

The first-line treatment for C.diff infection is typically oral vancomycin. When managing moderate cases, it is important to stop the antibiotics that caused the infection, ensure proper hydration, and provide guidance on hygiene measures. The recommended treatment is to prescribe oral vancomycin 125 mg four times a day for 10 days. Alternatively, fidaxomicin 200 mg twice a day for 10 days can be used as a second-line treatment. In severe cases, oral vancomycin may be combined with intravenous metronidazole, but it is advisable to consult with a local microbiologist or infectious disease specialist before proceeding.

Further Reading:

Clostridium difficile (C.diff) is a gram positive rod commonly found in hospitals. Some strains of C.diff produce exotoxins that can cause intestinal damage, leading to pseudomembranous colitis. This infection can range from mild diarrhea to severe illness. Antibiotic-associated diarrhea is often caused by C.diff, with 20-30% of cases being attributed to this bacteria. Antibiotics such as clindamycin, cephalosporins, fluoroquinolones, and broad-spectrum penicillins are frequently associated with C.diff infection.

Clinical features of C.diff infection include diarrhea, distinctive smell, abdominal pain, raised white blood cell count, and in severe cases, toxic megacolon. In some severe cases, diarrhea may be absent due to the infection causing paralytic ileus. Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool. There are two types of exotoxins produced by C.diff, toxin A and toxin B, which cause mucosal damage and the formation of a pseudomembrane in the colon.

Risk factors for developing C.diff infection include age over 65, antibiotic treatment, previous C.diff infection, exposure to infected individuals, proton pump inhibitor or H2 receptor antagonist use, prolonged hospitalization or residence in a nursing home, and chronic disease or immunosuppression. Complications of C.diff infection can include toxic megacolon, colon perforation, sepsis, and even death, especially in frail elderly individuals.

Management of C.diff infection involves stopping the causative antibiotic if possible, optimizing hydration with IV fluids if necessary, and assessing the severity of the infection. Treatment options vary based on severity, ranging from no antibiotics for mild cases to vancomycin or fidaxomicin for moderate cases, and hospital protocol antibiotics (such as oral vancomycin with IV metronidazole) for severe or life-threatening cases. Severe cases may require admission under gastroenterology or GI surgeons.

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.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This results in the accumulation of urea and other waste products in the body and disrupts the balance of fluids and electrolytes. 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 that develop outside of healthcare settings are due to pre-renal causes, accounting for 90% of cases. These causes typically involve low blood pressure associated with conditions like sepsis and fluid depletion. Medications, particularly ACE inhibitors and NSAIDs, are also frequently implicated.

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

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

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

When there is suspicion of phaeochromocytoma, the first tests to be done are plasma and/or urinary metanephrines. This patient exhibits paroxysmal symptoms that are consistent with phaeochromocytoma, such as high blood pressure, headache, sweating, anxiety, and fear. The initial diagnostic tests aim to confirm any metabolic disturbances by measuring levels of plasma and/or urine metanephrines, catecholamines, and urine vanillylmandelic acid (VMA). If these levels are found to be elevated, further imaging tests will be needed to determine the location and structure of the phaeochromocytoma tumor.

Further Reading:

Phaeochromocytoma is a rare neuroendocrine tumor that secretes catecholamines. It typically arises from chromaffin tissue in the adrenal medulla, but can also occur in extra-adrenal chromaffin tissue. The majority of cases are spontaneous and occur in individuals aged 40-50 years. However, up to 30% of cases are hereditary and associated with genetic mutations. About 10% of phaeochromocytomas are metastatic, with extra-adrenal tumors more likely to be metastatic.

The clinical features of phaeochromocytoma are a result of excessive catecholamine production. Symptoms are typically paroxysmal and include hypertension, headaches, palpitations, sweating, anxiety, tremor, abdominal and flank pain, and nausea. Catecholamines have various metabolic effects, including glycogenolysis, mobilization of free fatty acids, increased serum lactate, increased metabolic rate, increased myocardial force and rate of contraction, and decreased systemic vascular resistance.

Diagnosis of phaeochromocytoma involves measuring plasma and urine levels of metanephrines, catecholamines, and urine vanillylmandelic acid. Imaging studies such as abdominal CT or MRI are used to determine the location of the tumor. If these fail to find the site, a scan with metaiodobenzylguanidine (MIBG) labeled with radioactive iodine is performed. The highest sensitivity and specificity for diagnosis is achieved with plasma metanephrine assay.

The definitive treatment for phaeochromocytoma is surgery. However, before surgery, the patient must be stabilized with medical management. This typically involves alpha-blockade with medications such as phenoxybenzamine or phentolamine, followed by beta-blockade with medications like propranolol. Alpha blockade is started before beta blockade to allow for expansion of blood volume and to prevent a hypertensive crisis.

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

Intussusception occurs when a section of the bowel folds into another section, causing a blockage. This can be due to a specific underlying issue, like a Meckel’s diverticulum, or it can happen without any specific cause. The condition is most commonly seen in boys between the ages of 5 and 10 months. Symptoms include sudden vomiting and episodes of abdominal pain that come and go. The vomit quickly becomes greenish-yellow in color. Dance’s sign, which is the absence of bowel in the lower right part of the abdomen, may be observed. Redcurrant jelly-like stools are a late indication of the condition. It is believed that more than 90% of cases are caused by a non-specific underlying issue, often viral infections like rotavirus, adenovirus, and human herpesvirus 6.

Tryptase levels can be a valuable tool in diagnosing anaphylaxis. During an anaphylactic reaction, mast cell tryptase is released and can be measured in the blood. Research suggests that tryptase levels reach their highest point in the blood within 1 minute to 6 hours after the reaction begins, typically peaking around 1-2 hours after the onset of symptoms. This information is crucial for diagnosing and treating anaphylaxis, especially in cases where the diagnosis is uncertain. It’s important to note that tryptase levels may return to normal within 6 hours, so the timing of blood samples is crucial. The current recommendation is to take three tryptase level measurements: one as soon as resuscitation begins, another 1-2 hours after symptoms start, and a third 24 hours later or during the recovery period. It’s worth mentioning that some individuals may have elevated baseline tryptase levels, which should be taken into consideration during the diagnosis process.

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.

Lithium toxicity presents with various symptoms, including nausea and vomiting, diarrhea, tremor, ataxia, confusion, increased muscle tone, clonus, nephrogenic diabetes insipidus, convulsions, coma, and renal failure. One notable symptom associated with digoxin toxicity is xanthopsia.

The ROME IV criteria are utilized in secondary care to diagnose IBS, as recommended by NICE. The DSM-5 criteria are employed in diagnosing various mental health disorders. Coeliac disease diagnosis involves the use of modified marsh typing. Gastro-oesophageal reflux disease diagnosis relies on the Lyon Consensus.

Further Reading:

Irritable bowel syndrome (IBS) is a chronic disorder that affects the interaction between the gut and the brain. The exact cause of IBS is not fully understood, but factors such as genetics, drug use, enteric infections, diet, and psychosocial factors are believed to play a role. The main symptoms of IBS include abdominal pain, changes in stool form and/or frequency, and bloating. IBS can be classified into subtypes based on the predominant stool type, including diarrhea-predominant, constipation-predominant, mixed, and unclassified.

Diagnosing IBS involves using the Rome IV criteria, which includes recurrent abdominal pain associated with changes in stool frequency and form. It is important to rule out other more serious conditions that may mimic IBS through a thorough history, physical examination, and appropriate investigations. Treatment for IBS primarily involves diet and lifestyle modifications. Patients are advised to eat regular meals with a healthy, balanced diet and adjust their fiber intake based on symptoms. A low FODMAP diet may be trialed, and a dietician may be consulted for guidance. Regular physical activity and weight management are also recommended.

Psychosocial factors, such as stress, anxiety, and depression, should be addressed and managed appropriately. If constipation is a predominant symptom, soluble fiber supplements or foods high in soluble fiber may be recommended. Laxatives can be considered if constipation persists, and linaclotide may be tried if optimal doses of previous laxatives have not been effective. Antimotility drugs like loperamide can be used for diarrhea, and antispasmodic drugs or low-dose tricyclic antidepressants may be prescribed for abdominal pain. If symptoms persist or are refractory to treatment, alternative diagnoses should be considered, and referral to a specialist may be necessary.

Overall, the management of IBS should be individualized based on the patient’s symptoms and psychosocial situation. Clear explanation of the condition and providing resources for patient education, such as the NHS patient information leaflet and support from organizations like The IBS Network, can also be beneficial.

In an elderly patient with a history of gradual decline accompanied by high blood sugar levels, excessive thirst, and recent infection, the most likely diagnosis is hyperosmolar hyperglycemic state (HHS). This condition can be life-threatening, with a mortality rate of approximately 50%. Common symptoms include dehydration, elevated blood sugar levels, altered mental status, and electrolyte imbalances. About half of the patients with HHS also experience hypernatremia.

To calculate the serum osmolality, the formula is 2(K+ + Na+) + urea + glucose. In this case, the serum osmolality is 364 mmol/l, indicating a high level. It is important to discontinue the use of metformin in this patient due to the risk of metformin-associated lactic acidosis (MALA). Additionally, an intravenous infusion of insulin should be initiated.

The treatment goals for HHS are to address the underlying cause and gradually and safely:
– Normalize the osmolality
– Replace fluid and electrolyte losses
– Normalize blood glucose levels

If significant ketonaemia is present (3β-hydroxybutyrate is more than 1 mmol/L), it indicates a relative lack of insulin, and insulin should be administered immediately. However, if significant ketonaemia is not present, insulin should not be started.

Patients with HHS are at a high risk of thromboembolism, and it is recommended to routinely administer low molecular weight heparin. In cases where the serum osmolality exceeds 350 mmol/l, full heparinization should be considered.

For mild cases of otitis externa, using ear drops or spray as the initial treatment is a reasonable option. The insertion of a medicated wick, known as a Pope wick, is typically reserved for patients with severely narrowed external auditory canals. Microsuction, on the other hand, is helpful for patients with excessive debris in their ear canal but is not necessary for this particular patient. In general, microsuction is usually only used for severe cases of otitis externa that require referral to an ear, nose, and throat specialist for further management.

Further Reading:

Otitis externa is inflammation of the skin and subdermis of the external ear canal. It can be acute, lasting less than 6 weeks, or chronic, lasting more than 3 months. Malignant otitis externa, also known as necrotising otitis externa, is a severe and potentially life-threatening infection that can spread to the bones and surrounding structures of the ear. It is most commonly caused by Pseudomonas aeruginosa.

Symptoms of malignant otitis externa include severe and persistent ear pain, headache, discharge from the ear, fever, malaise, vertigo, and profound hearing loss. It can also lead to facial nerve palsy and other cranial nerve palsies. In severe cases, the infection can spread to the central nervous system, causing meningitis, brain abscess, and sepsis.

Acute otitis externa is typically caused by Pseudomonas aeruginosa or Staphylococcus aureus, while chronic otitis externa can be caused by fungal infections such as Aspergillus or Candida albicans. Risk factors for otitis externa include eczema, psoriasis, dermatitis, acute otitis media, trauma to the ear canal, foreign bodies in the ear, water exposure, ear canal obstruction, and long-term antibiotic or steroid use.

Clinical features of otitis externa include itching of the ear canal, ear pain, tenderness of the tragus and/or pinna, ear discharge, hearing loss if the ear canal is completely blocked, redness and swelling of the ear canal, debris in the ear canal, and cellulitis of the pinna and adjacent skin. Tender regional lymphadenitis is uncommon.

Management of acute otitis externa involves general ear care measures, optimizing any underlying medical or skin conditions that are risk factors, avoiding the use of hearing aids or ear plugs if there is a suspected contact allergy, and avoiding the use of ear drops if there is a suspected allergy to any of its ingredients. Treatment options include over-the-counter acetic acid 2% ear drops or spray, aural toileting via dry swabbing, irrigation, or microsuction, and prescribing topical antibiotics with or without a topical corticosteroid. Oral antibiotics may be prescribed in severe cases or for immunocompromised individuals.

Follow-up is advised if symptoms do not improve within 48-72 hours of starting treatment, if symptoms have not fully resolved

Nelson’s syndrome is a rare condition that occurs many years after a bilateral adrenalectomy for Cushing’s syndrome. It is believed to develop due to the loss of the normal negative feedback control that suppresses high cortisol levels. As a result, the hypothalamus starts producing CRH again, which stimulates the growth of a pituitary adenoma that produces adrenocorticotropic hormone (ACTH).

Only 15-20% of patients who undergo bilateral adrenalectomy will develop this condition, and it is now rarely seen as the procedure is no longer commonly performed.

The symptoms and signs of Nelson’s syndrome are related to the growth of the pituitary adenoma and the increased production of ACTH and melanocyte-stimulating hormone (MSH) from the adenoma. These may include headaches, visual field defects (up to 50% of cases), increased skin pigmentation, and the possibility of hypopituitarism.

ACTH levels will be significantly elevated (usually >500 ng/L). Thyroxine, TSH, gonadotrophin, and sex hormone levels may be low. Prolactin levels may be high, but not as high as with a prolactin-producing tumor. MRI or CT scanning can be helpful in identifying the presence of an expanding pituitary mass.

The treatment of choice for Nelson’s syndrome is trans-sphenoidal surgery.

Stevens-Johnson syndrome is a severe and potentially deadly form of erythema multiforme. It can be triggered by anything that causes erythema multiforme, but it is most commonly seen as a reaction to medication within 1-3 weeks of starting treatment. Initially, there may be symptoms like fever, fatigue, joint pain, and digestive issues, followed by the development of severe mucocutaneous lesions that are blistering and ulcerating.

Stevens-Johnson syndrome and toxic epidermal necrolysis are considered to be different stages of the same mucocutaneous disease, with toxic epidermal necrolysis being more severe. The extent of epidermal detachment is used to differentiate between the two. In Stevens-Johnson syndrome, less than 10% of the body surface area is affected by epidermal detachment, while in toxic epidermal necrolysis, it is greater than 30%. An overlap syndrome occurs when detachment affects between 10-30% of the body surface area.

Several drugs can potentially cause Stevens-Johnson syndrome and toxic epidermal necrolysis, including tetracyclines, penicillins, vancomycin, sulphonamides, NSAIDs, and barbiturates.

Gentamicin has the potential to cause a severe form of hearing loss known as sensorineural hearing loss. In cases of severe sensorineural hearing loss, the Weber’s test will show a lateralization towards the side of the unaffected ear. Additionally, the Rinne’s test may yield a false negative result, with the patient perceiving the sound in the unaffected ear.

To perform the Rinne’s test, a 512 Hz tuning fork is vibrated and then placed on the mastoid process until the sound is no longer audible. The top of the tuning fork is then positioned 2 cm away from the external auditory meatus, and the patient is asked to indicate where they hear the sound loudest.

In individuals with normal hearing, the tuning fork should still be audible outside the external auditory canal even after it can no longer be heard on the mastoid. This is because air conduction should be more effective than bone conduction.

In cases of conductive hearing loss, the patient will no longer be able to hear the tuning fork once it is no longer audible on the mastoid. This indicates that their bone conduction is greater than their air conduction, suggesting an obstruction in the passage of sound waves through the ear canal and into the cochlea. This is considered a true negative result.

However, a Rinne’s test may yield a false negative result if the patient has a severe unilateral sensorineural deficit and perceives the sound in the unaffected ear through the transmission of sound waves through the base of the skull.

In sensorineural hearing loss, the ability to perceive the tuning fork both on the mastoid and outside the external auditory canal is equally diminished compared to the opposite ear. While they will still hear the tuning fork outside the external auditory canal, the sound will disappear earlier on the mastoid process and outside the external auditory canal compared to the other ear.

To perform the Weber’s test, a 512 Hz tuning fork is vibrated and placed on the center of the patient’s forehead. The patient is then asked if they perceive the sound in the middle of the forehead or if it lateralizes to one side or the other.

If the sound lateralizes to one side, it can indicate either ipsilateral conductive hearing loss or contralateral sensorineural hearing loss.

Severe hypertension, defined as blood pressure greater than 180/120 mmHg, is a condition that prevents the use of thrombolysis. In order to proceed with thrombolysis, it is necessary to lower the patient’s blood pressure to below this level within the designated time frame. Oral medications are unlikely to work quickly enough, so an intravenous antihypertensive agent is required.

One commonly used agent in these situations is labetalol, which is administered intravenously at a dose of 10 mg over 1-2 minutes. This dose can be repeated if necessary, or an infusion can be set up to deliver a continuous dose of 2-8 mg per minute. Once the blood pressure is reduced to less than 180/105 mmHg, thrombolysis can be safely performed.

Alternatively, a nitrate infusion, such as Isoket, can be used in patients who cannot tolerate beta-blockers due to contraindications like asthma, heart block, or cardiac failure. This provides an alternative option for lowering blood pressure in these individuals.

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.

The majority of treatments provided to individuals with sickle cell disease are supportive measures that have limited impact on the underlying pathophysiology of the condition.

Currently, the only approved therapy that can modify the disease is Hydroxyurea. This medication is believed to function by increasing the levels of fetal hemoglobin, which in turn decreases the concentration of HbS within the cells and reduces the abnormal hemoglobin tendency to form polymers.

Hydroxyurea is currently authorized for use in adult patients who experience recurrent moderate-to-severe painful crises (at least three in the past 12 months). Its approval is specifically for reducing the frequency of these painful episodes and the need for blood transfusions.

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.

The initial symptoms of ARS usually include feelings of nausea and the urge to vomit. During the prodromal stage, individuals may also experience a loss of appetite and, in some cases, diarrhea, which can vary depending on the amount of exposure. These symptoms can manifest within minutes to days after being exposed to ARS.

Further Reading:

Radiation exposure refers to the emission or transmission of energy in the form of waves or particles through space or a material medium. There are two types of radiation: ionizing and non-ionizing. Non-ionizing radiation, such as radio waves and visible light, has enough energy to move atoms within a molecule but not enough to remove electrons from atoms. Ionizing radiation, on the other hand, has enough energy to ionize atoms or molecules by detaching electrons from them.

There are different types of ionizing radiation, including alpha particles, beta particles, gamma rays, and X-rays. Alpha particles are positively charged and consist of 2 protons and 2 neutrons from the atom’s nucleus. They are emitted from the decay of heavy radioactive elements and do not travel far from the source atom. Beta particles are small, fast-moving particles with a negative electrical charge that are emitted from an atom’s nucleus during radioactive decay. They are more penetrating than alpha particles but less damaging to living tissue. Gamma rays and X-rays are weightless packets of energy called photons. Gamma rays are often emitted along with alpha or beta particles during radioactive decay and can easily penetrate barriers. X-rays, on the other hand, are generally lower in energy and less penetrating than gamma rays.

Exposure to ionizing radiation can damage tissue cells by dislodging orbital electrons, leading to the generation of highly reactive ion pairs. This can result in DNA damage and an increased risk of future malignant change. The extent of cell damage depends on factors such as the type of radiation, time duration of exposure, distance from the source, and extent of shielding.

The absorbed dose of radiation is directly proportional to time, so it is important to minimize the amount of time spent in the vicinity of a radioactive source. A lethal dose of radiation without medical management is 4.5 sieverts (Sv) to kill 50% of the population at 60 days. With medical management, the lethal dose is 5-6 Sv. The immediate effects of ionizing radiation can range from radiation burns to radiation sickness, which is divided into three main syndromes: hematopoietic, gastrointestinal, and neurovascular. Long-term effects can include hematopoietic cancers and solid tumor formation.

In terms of management, support is mainly supportive and includes IV fluids, antiemetics, analgesia, nutritional support, antibiotics, blood component substitution, and reduction of brain edema.

The current guidelines from NICE and the BNF suggest that if treatment is necessary for campylobacter enteritis, clarithromycin should be the first choice. Azithromycin and erythromycin can be used interchangeably, and ciprofloxacin is a suitable alternative. It is important to note that many cases of campylobacter enteritis resolve on their own without treatment. However, individuals with severe infections or those who are immunocompromised should receive treatment.

Anaemia can be categorized based on the size of red blood cells. Microcytic anaemia, characterized by a mean corpuscular volume (MCV) of less than 80 fl, can be caused by various factors such as iron deficiency, thalassaemia, anaemia of chronic disease (which can also be normocytic), sideroblastic anaemia (which can also be normocytic), lead poisoning, and aluminium toxicity (although this is now rare and mainly affects haemodialysis patients).

On the other hand, normocytic anaemia, with an MCV ranging from 80 to 100 fl, can be attributed to conditions like haemolysis, acute haemorrhage, bone marrow failure, anaemia of chronic disease (which can also be microcytic), mixed iron and folate deficiency, pregnancy, chronic renal failure, and sickle-cell disease.

Lastly, macrocytic anaemia, characterized by an MCV greater than 100 fl, can be caused by factors such as B12 deficiency, folate deficiency, hypothyroidism, reticulocytosis, liver disease, alcohol abuse, myeloproliferative disease, myelodysplastic disease, and certain drugs like methotrexate, hydroxyurea, and azathioprine.

It is important to understand the different causes of anaemia based on red cell size as this knowledge can aid in the diagnosis and management of this condition.

Varicella can have serious consequences for pregnant women. If a woman contracts varicella during the first 28 weeks of pregnancy, there is a 1% chance that the fetus will be affected and develop foetal varicella syndrome (FVS). FVS is characterized by eye defects, limb underdevelopment, skin scarring, and neurological abnormalities.

Pregnant women who have not had chickenpox or who test negative for VZV IgG should be advised to minimize contact with individuals who have chickenpox or shingles. If they are exposed, they should seek immediate medical help.

If a pregnant woman is exposed to varicella, the first step is to perform a blood test to check for VZV immunity. If she is not immune and the exposure is significant, she should be given VZV immunoglobulin as soon as possible. This treatment is effective within 10 days of exposure.

If a pregnant woman develops chickenpox, she should urgently seek medical assistance. There is an increased risk of pneumonia, encephalitis, and hepatitis for the mother, as well as a 1% risk of the fetus developing FVS.

Acyclovir should be used cautiously before 20 weeks of gestation but is recommended after 20 weeks if the woman seeks medical help within 24 hours of the rash appearing.

If a woman develops any complications of varicella, she must be referred to a hospital. Additionally, she should be referred to a specialized center five weeks after the infection for a detailed ultrasound scan to determine if FVS has occurred.

For more information, refer to the Royal College of Obstetricians and Gynaecologists green-top guidelines for the management of VZV exposure and infection in pregnancy.

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.

ATLS guidelines now suggest administering only 1 liter of crystalloid fluid during the initial assessment. If patients do not respond to the crystalloid, it is recommended to quickly transition to blood products. Studies have shown that infusing more than 1.5 liters of crystalloid fluid is associated with higher mortality rates in trauma cases. Therefore, it is advised to prioritize the early use of blood products and avoid large volumes of crystalloid fluid in trauma patients. In cases where it is necessary, massive transfusion should be considered, defined as the transfusion of more than 10 units of blood in 24 hours or more than 4 units of blood in one hour. For patients with evidence of Class III and IV hemorrhage, early resuscitation with blood and blood products in low ratios is recommended.

Based on the findings of significant trials, such as the CRASH-2 study, the use of tranexamic acid is now recommended within 3 hours. This involves administering a loading dose of 1 gram intravenously over 10 minutes, followed by an infusion of 1 gram over eight hours. In some regions, tranexamic acid is also being utilized in the prehospital setting.

Hypokalaemia, or low potassium levels, can be caused by various factors. One common cause is inadequate dietary intake, where a person does not consume enough potassium-rich foods. Gastrointestinal loss, such as through diarrhoea, can also lead to hypokalaemia as the body loses potassium through the digestive system. Certain drugs, like diuretics and insulin, can affect potassium levels and contribute to hypokalaemia.

Alkalosis, a condition characterized by an imbalance in the body’s pH levels, can also cause hypokalaemia. Hypomagnesaemia, or low magnesium levels, is another potential cause. Renal artery stenosis, a narrowing of the arteries that supply blood to the kidneys, can lead to hypokalaemia as well.

Renal tubular acidosis, specifically types 1 and 2, can cause hypokalaemia. These conditions affect the kidneys’ ability to regulate acid-base balance, resulting in low potassium levels. Conn’s syndrome, Bartter’s syndrome, and Gitelman’s syndrome are all rare inherited defects that can cause hypokalaemia. Bartter’s syndrome affects the ascending limb of the loop of Henle, while Gitelman’s syndrome affects the distal convoluted tubule of the kidney.

Hypokalaemic periodic paralysis is another condition that can cause low potassium levels. Excessive ingestion of liquorice, a sweet treat made from the root of the liquorice plant, can result in hypokalaemia due to its impact on mineralocorticoid levels.

It is important to note that while type 1 and 2 renal tubular acidosis cause hypokalaemia, type 4 renal tubular acidosis actually causes hyperkalaemia, or high potassium levels.

As a person ascends to higher altitudes, their risk of developing high altitude pulmonary edema (HAPE) increases. This patient is displaying signs and symptoms of HAPE, including a dry cough that may progress to frothy sputum, possibly containing blood. Breathlessness, initially experienced during exertion, may progress to being present even at rest.

Further Reading:

High Altitude Illnesses

Altitude & Hypoxia:
– As altitude increases, atmospheric pressure decreases and inspired oxygen pressure falls.
– Hypoxia occurs at altitude due to decreased inspired oxygen.
– At 5500m, inspired oxygen is approximately half that at sea level, and at 8900m, it is less than a third.

Acute Mountain Sickness (AMS):
– AMS is a clinical syndrome caused by hypoxia at altitude.
– Symptoms include headache, anorexia, sleep disturbance, nausea, dizziness, fatigue, malaise, and shortness of breath.
– Symptoms usually occur after 6-12 hours above 2500m.
– Risk factors for AMS include previous AMS, fast ascent, sleeping at altitude, and age <50 years old.
– The Lake Louise AMS score is used to assess the severity of AMS.
– Treatment involves stopping ascent, maintaining hydration, and using medication for symptom relief.
– Medications for moderate to severe symptoms include dexamethasone and acetazolamide.
– Gradual ascent, hydration, and avoiding alcohol can help prevent AMS.

High Altitude Pulmonary Edema (HAPE):
– HAPE is a progression of AMS but can occur without AMS symptoms.
– It is the leading cause of death related to altitude illness.
– Risk factors for HAPE include rate of ascent, intensity of exercise, absolute altitude, and individual susceptibility.
– Symptoms include dyspnea, cough, chest tightness, poor exercise tolerance, cyanosis, low oxygen saturations, tachycardia, tachypnea, crepitations, and orthopnea.
– Management involves immediate descent, supplemental oxygen, keeping warm, and medication such as nifedipine.

High Altitude Cerebral Edema (HACE):
– HACE is thought to result from vasogenic edema and increased vascular pressure.
– It occurs 2-4 days after ascent and is associated with moderate to severe AMS symptoms.
– Symptoms include headache, hallucinations, disorientation, confusion, ataxia, drowsiness, seizures, and manifestations of raised intracranial pressure.
– Immediate descent is crucial for management, and portable hyperbaric therapy may be used if descent is not possible.
– Medication for treatment includes dexamethasone and supplemental oxygen. Acetazolamide is typically used for prophylaxis.

The most probable diagnosis in this case is anterior uveitis. Anterior uveitis refers to the inflammation of the iris and typically manifests as a painful and red eye. It is often accompanied by symptoms such as sensitivity to light, excessive tearing, and decreased visual clarity. In some instances, there may be the presence of pus in the front part of the eye known as hypopyon.

Anterior uveitis can have various causes, including idiopathic (no known cause), trauma, chronic joint diseases like spondyloarthropathies and juvenile chronic arthritis, inflammatory bowel disease, psoriasis, sarcoidosis, and infections such as Lyme disease, tuberculosis, leptospirosis, herpes simplex virus (HSV), and varicella-zoster virus (VZV). Additionally, certain malignancies like non-Hodgkin lymphoma, ocular melanoma, and retinoblastoma can also be associated with anterior uveitis.

A significant association has been observed between the HLA-B27 genotype and anterior uveitis, with approximately 50% of patients having this genetic marker. In this particular case, the likely underlying diagnosis is ankylosing spondylitis, a condition characterized by chronic pain and stiffness in the middle spine area and sacroiliitis. It is worth noting that around 30% of men with unilateral uveitis will be found to have ankylosing spondylitis.

A 7-year-old girl is brought to the emergency department after being bitten by a bee. She is experiencing swelling in her arm and difficulty breathing, which are signs of anaphylaxis. To treat this condition, the most suitable dose of adrenaline to administer to the patient is 300 micrograms (0.3ml 1 in 1,000) by intramuscular injection.

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.

The most appropriate initial treatment for this patient would be intravenous labetalol. Labetalol is a non-selective beta blocker with alpha-blocking properties. It is the preferred initial treatment for aortic dissection because it helps to reduce blood pressure and heart rate, which can help to decrease the shear forces acting on the aortic wall and prevent further dissection. Intravenous administration of labetalol allows for rapid and effective control of blood pressure.

Other treatment options, such as intravenous magnesium sulphate, intravenous verapamil, GTN sublingual spray, and oral nifedipine, are not appropriate for the management of aortic dissection. Magnesium sulphate is used for the treatment of certain arrhythmias and pre-eclampsia, but it does not address the underlying issue of aortic dissection. Verapamil and nifedipine are calcium channel blockers that can lower blood pressure, but they can also cause reflex tachycardia, which can worsen the condition. GTN sublingual spray is used for the treatment of angina, but it does not address the underlying issue of aortic dissection.

Further Reading:

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

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

The causes of Le Fort fractures vary depending on the type of fracture. Common mechanisms include motor vehicle accidents, sports injuries, assaults, and falls from significant heights. Patients with Le Fort fractures often have concurrent head and cervical spine injuries. Additionally, they frequently experience other facial fractures, as well as neuromuscular injuries and dental avulsions.

The specific type of fracture sustained is determined by the direction of the force applied to the face. Le Fort type I fractures typically occur when a force is directed downward against the upper teeth. Le Fort type II fractures are usually the result of a force applied to the lower or mid maxilla. Lastly, Le Fort type III fractures are typically caused by a force applied to the nasal bridge and upper part of the maxilla.

To prevent diffusion hypoxia, it is recommended to administer supplemental oxygen to patients for about 5 minutes after discontinuing nitrous oxide. This is important because there is a risk of developing diffusion hypoxia after the termination of nitrous oxide.

Further Reading:

Entonox® is a mixture of 50% nitrous oxide and 50% oxygen that can be used for self-administration to reduce anxiety. It can also be used alongside other anesthesia agents. However, its mechanism of action for anxiety reduction is not fully understood. The Entonox bottles are typically identified by blue and white color-coded collars, but a new standard will replace these with dark blue shoulders in the future. It is important to note that Entonox alone cannot be used as the sole maintenance agent in anesthesia.

One of the effects of nitrous oxide is the second-gas effect, where it speeds up the absorption of other inhaled anesthesia agents. Nitrous oxide enters the alveoli and diffuses into the blood, displacing nitrogen. This displacement causes the remaining alveolar gases to become more concentrated, increasing the fractional content of inhaled anesthesia gases and accelerating the uptake of volatile agents into the blood.

However, when nitrous oxide administration is stopped, it can cause diffusion hypoxia. Nitrous oxide exits the blood and diffuses back into the alveoli, while nitrogen diffuses in the opposite direction. Nitrous oxide enters the alveoli much faster than nitrogen leaves, resulting in the dilution of oxygen within the alveoli. This can lead to diffusion hypoxia, where the oxygen concentration in the alveoli is diluted, potentially causing oxygen deprivation in patients breathing air.

There are certain contraindications for using nitrous oxide, as it can expand in air-filled spaces. It should be avoided in conditions such as head injuries with intracranial air, pneumothorax, recent intraocular gas injection, and entrapped air following a recent underwater dive.

Clostridium difficile is a type of bacteria that is Gram-positive, anaerobic, and capable of forming spores. When individuals take broad-spectrum antibiotics, it can disrupt the normal bacteria in their intestines, allowing C. difficile to multiply and cause C. difficile associated diarrhea (CDAD). This condition leads to inflammation and bleeding of the large intestine, resulting in a distinct pseudomembranous appearance. The main symptoms include abdominal cramps, bloody and/or watery diarrhea, and fever. It is worth noting that the majority of C. difficile infections occur in individuals aged 65 and above.

To prevent the spread of C. difficile, it is crucial to practice proper hand hygiene. This involves washing hands with water and plain or antibacterial soap for 15 to 30 seconds after using the bathroom and before eating. Paying attention to areas such as the fingernails, between the fingers, and the wrists is essential. Thoroughly rinsing hands and drying them with a single-use towel is also recommended. Additionally, patients and their family members should remind healthcare providers to wash their hands regularly.

While alcohol-based hand rubs can be effective against many bacteria, they may be less effective against C. difficile. Therefore, during an outbreak of C. difficile infection, it is advisable to use soap and running water instead.

Taking precautions such as wearing an apron and gloves and isolating patients in separate rooms are important measures to prevent contact transmission. However, it is crucial to remember that these precautions will be ineffective if proper hand washing is neglected. Hand hygiene remains the primary and most crucial step in preventing the spread of C. difficile.

When it comes to treatment, oral vancomycin is the recommended first-line option for C. difficile associated diarrhea. However, it is important to note that this treatment does not limit the spread of the bacteria from one patient to another.

If a child with gastroenteritis shows signs of jittery movements, increased muscle tone, hyper-reflexia, or convulsions, hypernatraemic dehydration should be considered. Additional signs of hypernatraemic dehydration include drowsiness or coma.

Further Reading:

Gastroenteritis is a common condition in children, particularly those under the age of 5. It is characterized by the sudden onset of diarrhea, with or without vomiting. The most common cause of gastroenteritis in infants and young children is rotavirus, although other viruses, bacteria, and parasites can also be responsible. Prior to the introduction of the rotavirus vaccine in 2013, rotavirus was the leading cause of gastroenteritis in children under 5 in the UK. However, the vaccine has led to a significant decrease in cases, with a drop of over 70% in subsequent years.

Norovirus is the most common cause of gastroenteritis in adults, but it also accounts for a significant number of cases in children. In England & Wales, there are approximately 8,000 cases of norovirus each year, with 15-20% of these cases occurring in children under 9.

When assessing a child with gastroenteritis, it is important to consider whether there may be another more serious underlying cause for their symptoms. Dehydration assessment is also crucial, as some children may require intravenous fluids. The NICE traffic light system can be used to identify the risk of serious illness in children under 5.

In terms of investigations, stool microbiological testing may be indicated in certain cases, such as when the patient has been abroad, if diarrhea lasts for more than 7 days, or if there is uncertainty over the diagnosis. U&Es may be necessary if intravenous fluid therapy is required or if there are symptoms and/or signs suggestive of hypernatremia. Blood cultures may be indicated if sepsis is suspected or if antibiotic therapy is planned.

Fluid management is a key aspect of treating children with gastroenteritis. In children without clinical dehydration, normal oral fluid intake should be encouraged, and oral rehydration solution (ORS) supplements may be considered. For children with dehydration, ORS solution is the preferred method of rehydration, unless intravenous fluid therapy is necessary. Intravenous fluids may be required for children with shock or those who are unable to tolerate ORS solution.

Antibiotics are generally not required for gastroenteritis in children, as most cases are viral or self-limiting. However, there are some exceptions, such as suspected or confirmed sepsis, Extraintestinal spread of bacterial infection, or specific infections like Clostridium difficile-associated pseudomembranous enterocolitis or giardiasis.

Infectious causes of bloody diarrhea include Campylobacter spp., Shigella spp., Salmonella spp., Clostridium difficile, Enterohaemorrhagic Escherichia coli, Yersinia spp., Schistosomiasis, and Amoebiasis (Entamoeba histolytica). Enterotoxigenic E.coli is a non-invasive strain that does not cause inflammation or bloody diarrhea. Instead, it typically presents with profuse watery diarrhea and is not usually associated with abdominal cramping. The other organisms mentioned in this question are associated with watery diarrhea, but not bloody diarrhea.

A surgical cricothyroidotomy is a procedure performed in emergency situations to secure the airway by making an incision in the cricothyroid membrane. It is also known as an emergency surgical airway (ESA) and is typically done when intubation and oxygenation are not possible.

There are certain conditions in which a surgical cricothyroidotomy should not be performed. These include patients who are under 12 years old, those with laryngeal fractures or pre-existing or acute laryngeal pathology, individuals with tracheal transection and retraction of the trachea into the mediastinum, and cases where the anatomical landmarks are obscured due to trauma.

The procedure is carried out in the following steps:
1. Gathering and preparing the necessary equipment.
2. Positioning the patient on their back with the neck in a neutral position.
3. Sterilizing the patient’s neck using antiseptic swabs.
4. Administering local anesthesia, if time permits.
5. Locating the cricothyroid membrane, which is situated between the thyroid and cricoid cartilage.
6. Stabilizing the trachea with the left hand until it can be intubated.
7. Making a transverse incision through the cricothyroid membrane.
8. Inserting the scalpel handle into the incision and rotating it 90°. Alternatively, a haemostat can be used to open the airway.
9. Placing a properly-sized, cuffed endotracheal tube (usually a size 5 or 6) into the incision, directing it into the trachea.
10. Inflating the cuff and providing ventilation.
11. Monitoring for chest rise and auscultating the chest to ensure adequate ventilation.
12. Securing the airway to prevent displacement.

Potential complications of a surgical cricothyroidotomy include aspiration of blood, creation of a false passage into the tissues, subglottic stenosis or edema, laryngeal stenosis, hemorrhage or hematoma formation, laceration of the esophagus or trachea, mediastinal emphysema, and vocal cord paralysis or hoarseness.

The superior orbital fissure is a gap in the back wall of the orbit, created by the space between the greater and lesser wings of the sphenoid bone. Several structures pass through it to enter the orbit, starting from the top and going downwards. These include the lacrimal nerve (a branch of CN V1), the frontal nerve (another branch of CN V1), the superior ophthalmic vein, the trochlear nerve (CN IV), the superior division of the oculomotor nerve (CN III), the nasociliary nerve (a branch of CN V1), the inferior division of the oculomotor nerve (CN III), the abducens nerve (CN VI), and the inferior ophthalmic vein.

Adjacent to the superior orbital fissure, on the back wall of the orbit and towards the middle, is the optic canal. The optic nerve (CN II) exits the orbit through this canal, along with the ophthalmic artery.

Superior orbital fissure syndrome (SOFS) is a condition characterized by a combination of symptoms and signs that occur when cranial nerves III, IV, V1, and VI are compressed or injured as they pass through the superior orbital fissure. This condition also leads to swelling and protrusion of the eye due to impaired drainage and congestion. The main causes of SOFS are trauma, tumors, and inflammation. It is important to note that CN II is not affected by this syndrome, as it follows a separate path through the optic canal.

Nelson’s syndrome is a rare condition that occurs many years after a bilateral adrenalectomy for Cushing’s syndrome. It is believed to develop due to the loss of the normal negative feedback control that suppresses high cortisol levels. As a result, the hypothalamus starts producing CRH again, which stimulates the growth of a pituitary adenoma that produces adrenocorticotropic hormone (ACTH).

Only 15-20% of patients who undergo bilateral adrenalectomy will develop this condition, and it is now rarely seen as the procedure is no longer commonly performed.

The symptoms and signs of Nelson’s syndrome are related to the growth of the pituitary adenoma and the increased production of ACTH and melanocyte-stimulating hormone (MSH) from the adenoma. These may include headaches, visual field defects (up to 50% of cases), increased skin pigmentation, and the possibility of hypopituitarism.

ACTH levels will be significantly elevated (usually >500 ng/L). Thyroxine, TSH, gonadotrophin, and sex hormone levels may be low. Prolactin levels may be high, but not as high as with a prolactin-producing tumor. MRI or CT scanning can be helpful in identifying the presence of an expanding pituitary mass.

The treatment of choice for Nelson’s syndrome is trans-sphenoidal surgery.

Section 136 of the Mental Health Act (MHA) grants authority to a police officer to relocate an individual who seems to be experiencing a mental health disorder to a secure location. This provision permits detention for a period of 72 hours, during which time the patient can undergo evaluation by a medical professional.

This patient is highly likely to have developed a tubo-ovarian abscess (TOA), which is a complication of pelvic inflammatory disease. TOA occurs when a pocket of pus forms in the fallopian tube and/or ovary. If the abscess ruptures, it can lead to sepsis and become life-threatening.

The initial imaging modality of choice is transabdominal and endovaginal ultrasound. This imaging technique often reveals multilocular complex retro-uterine/adnexal masses with debris, septations, and irregular thick walls. These masses can be present on both sides.

Urgent hospital admission is necessary, and the usual management involves draining the abscess and administering intravenous antibiotics. The abscess drainage can be guided by ultrasound or CT scanning.

In some cases, laparotomy or laparoscopy may be required to drain the abscess.

Pick’s disease is a rare neurodegenerative disorder that leads to a gradual decline in cognitive function known as frontotemporal dementia. One of the key features of this condition is the accumulation of tau proteins in neurons, forming silver-staining, spherical aggregations called ‘Pick bodies.’

Typically, Pick’s disease manifests between the ages of 40 and 60. Initially, individuals may experience changes in their personality, such as disinhibition, tactlessness, and vulgarity. They may also exhibit alterations in their moral values and attempt to distance themselves from their family. Difficulties with concentration, increased activity levels, pacing, and wandering are also common during this stage.

What sets Pick’s disease apart from Alzheimer’s disease is that the changes in personality occur before memory loss becomes apparent. As the disease progresses, patients will experience deficits in intellect, memory, and language.

Thiazide diuretics, a commonly prescribed medication, can lead to two main electrolyte imbalances in patients. One of these is hyponatremia, which occurs in around 13.7% of individuals taking thiazide diuretics. The other is hypokalemia, which is observed in approximately 8.5% of patients on this medication. These electrolyte disturbances are frequently encountered in primary care settings. For more information on this topic, please refer to the article titled Thiazide diuretic prescription and electrolyte abnormalities in primary care.

Diabetic ketoacidosis (DKA) is a life-threatening condition that occurs when there is a lack of insulin, leading to an inability to process glucose. This results in high blood sugar levels and excessive thirst. As the body tries to eliminate the excess glucose through urine, dehydration becomes inevitable. Without insulin, the body starts using fat as its main energy source, which leads to the production of ketones and a buildup of acid in the blood.

The main characteristics of DKA are high blood sugar levels (above 11 mmol/l), the presence of ketones in the blood or urine, and acidosis (low bicarbonate levels and/or low venous pH). Symptoms of DKA include nausea, vomiting, excessive thirst, frequent urination, abdominal pain, signs of dehydration, a distinct smell of ketones on the breath, rapid and deep breathing, confusion or reduced consciousness, and cardiovascular symptoms like rapid heartbeat, low blood pressure, and shock.

To diagnose DKA, various tests should be performed, including blood glucose measurement, urine dipstick test (which shows high levels of glucose and ketones), blood ketone assay (more accurate than urine dipstick), complete blood count, and electrolyte levels. Arterial or venous blood gas analysis can confirm the presence of metabolic acidosis.

The management of DKA involves careful fluid administration and insulin replacement. Fluid boluses should only be given if there are signs of shock and should be administered slowly in 10 ml/kg increments. Once shock is resolved, rehydration should be done over 48 hours. The first 20 ml/kg of fluid given for resuscitation should not be subtracted from the total fluid volume calculated for the 48-hour replacement. In cases of hypotensive shock, consultation with a pediatric intensive care specialist may be necessary.

Insulin replacement should begin 1-2 hours after starting intravenous fluid therapy. A soluble insulin infusion should be used at a dosage of 0.05-0.1 units/kg/hour. The goal is to bring blood glucose levels close to normal. Regular monitoring of electrolytes and blood glucose levels is important to prevent imbalances and rapid changes in serum osmolarity. Identifying and treating the underlying cause of DKA is also crucial.

When calculating fluid requirements for children and young people with DKA, assume a 5% fluid deficit for mild-to-moderate cases (blood pH of 7.1 or above) and a 10% fluid deficit in severe DKA (indicated by a blood pH below 7.1). The total replacement fluid to be given over 48 hours is calculated as follows: Hourly rate = (deficit/48 hours) + maintenance per hour.

For the treatment of women with lower urinary tract infections (UTIs) who are not pregnant, it is recommended to consider either a back-up antibiotic prescription or an immediate antibiotic prescription. This decision should take into account the severity of symptoms and the risk of developing complications, which is higher in individuals with known or suspected abnormalities of the genitourinary tract or weakened immune systems. The evidence for back-up antibiotic prescriptions is limited to non-pregnant women with lower UTIs where immediate antibiotic treatment is not deemed necessary. It is also important to consider previous urine culture and susceptibility results, as well as any history of antibiotic use that may have led to the development of resistant bacteria. Ultimately, the preferences of the woman regarding antibiotic use should be taken into account.

If a urine sample has been sent for culture and susceptibility testing and an antibiotic prescription has been given, it is crucial to review the choice of antibiotic once the microbiological results are available. If the bacteria are found to be resistant and symptoms are not improving, it is recommended to switch to a narrow-spectrum antibiotic whenever possible.

The following antibiotics are recommended for non-pregnant women aged 16 years and older:

First-choice:
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days (if eGFR >45 ml/minute)
– Trimethoprim 200 mg taken orally twice daily for 3 days (if low risk of resistance*)

Second-choice (if there is no improvement in lower UTI symptoms on first-choice treatment for at least 48 hours, or if first-choice treatment is not suitable):
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days (if eGFR >45 ml/minute)
– Pivmecillinam 400 mg initial dose taken orally, followed by 200 mg taken orally three times daily for 3 days
– Fosfomycin 3 g single sachet dose

*The risk of resistance may be lower if the antibiotic has not been used in the past 3 months, previous urine culture suggests susceptibility (although this was not used), and in younger individuals in areas where local epidemiology data indicate low resistance rates. Conversely, the risk of resistance may be higher with recent antibiotic use and in older individuals in residential facilities.

In a young patient who has been experiencing diarrhea and abdominal pain for more than 6 weeks, it is important to consider inflammatory bowel disease as a possible diagnosis. The challenge lies in distinguishing between ulcerative colitis and Crohn’s disease. In this case, a biopsy was performed and the results showed transmural inflammation with the presence of non-caseating granulomas, which strongly suggests a diagnosis of Crohn’s disease.

To differentiate between ulcerative colitis and Crohn’s disease, it is helpful to consider the following characteristics. Ulcerative colitis typically only affects the rectum and colon, although the terminal ileum may be affected in some cases known as backwash ileitis. On the other hand, Crohn’s disease can affect any part of the gastrointestinal tract from the mouth to the anus, and there may be areas of normal mucosa between the affected areas, known as skip lesions.

There are also differences in the associations and systemic manifestations of these two conditions. Ulcerative colitis has a decreased incidence in smokers and is associated with liver conditions such as primary biliary cirrhosis, chronic active hepatitis, and primary sclerosing cholangitis. Crohn’s disease, on the other hand, has an increased incidence in smokers and is more commonly associated with systemic manifestations such as erythema nodosum, pyoderma gangrenosum, iritis/uveitis, cholelithiasis, and joint pain/arthropathy.

Pathologically, ulcerative colitis primarily affects the mucosa and submucosa, with the presence of mucosal ulcers, inflammatory cell infiltrate, and crypt abscesses. In contrast, Crohn’s disease is characterized by transmural inflammation, lymphoid aggregates, and neutrophil infiltrates. Non-caseating granulomas are seen in approximately 30% of cases, which is a distinguishing feature of Crohn’s disease.

When it comes to clinical features, abdominal pain is less prominent in ulcerative colitis, while bloody diarrhea is present in 90% of cases. The passage of mucus is also common, and fever may be present. Symptoms such as urgency, tenesmus (a feeling of incomplete bowel movement), and pre-defecation pain that is relieved by passing stools are frequently reported. In Crohn’s disease, abdominal pain is more prominent, and diarrhea is common, with the possibility of it being bloody.

This patient has developed a non-ST elevation myocardial infarction (NSTEMI). The electrocardiogram (ECG) reveals widespread ST depression, indicating widespread subendocardial ischemia. Additionally, the troponin test results are positive, indicating myocyte necrosis.

The acute coronary syndromes consist of unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI).

Unstable angina is characterized by one or more of the following: angina of effort occurring over a few days with increasing frequency, angina episodes occurring recurrently and predictably without specific provocation, or an unprovoked and prolonged episode of cardiac chest pain. The ECG may show T-wave/ST-segment changes, similar to this case. Cardiac enzymes are typically normal, and the troponin test is negative in unstable angina.

Non-ST elevation myocardial infarction (NSTEMI) typically presents with sustained cardiac chest pain lasting more than 20 minutes. The ECG often shows abnormalities in T-waves or ST-segments. Cardiac enzymes are elevated, and the troponin test is positive.

ST-elevation myocardial infarction (STEMI) usually presents with typical cardiac chest pain suggestive of an acute myocardial infarction. The ECG reveals ST-segment elevation and the development of Q waves. Cardiac enzymes are elevated, and the troponin test is positive.

Phaeochromocytoma is characterized by certain clinical features, including paroxysmal hypertension, palpitations, headache, tremor, and profuse sweating. This patient exhibits paroxysmal symptoms that align with phaeochromocytoma, such as high blood pressure (systolic readings exceeding 220 mmHg are common), headache, sweating, and feelings of anxiety and fear. It is important to note that individuals with conditions like congenital adrenal hyperplasia, diabetes insipidus, and Addisonian crisis typically experience low blood pressure.

Further Reading:

Phaeochromocytoma is a rare neuroendocrine tumor that secretes catecholamines. It typically arises from chromaffin tissue in the adrenal medulla, but can also occur in extra-adrenal chromaffin tissue. The majority of cases are spontaneous and occur in individuals aged 40-50 years. However, up to 30% of cases are hereditary and associated with genetic mutations. About 10% of phaeochromocytomas are metastatic, with extra-adrenal tumors more likely to be metastatic.

The clinical features of phaeochromocytoma are a result of excessive catecholamine production. Symptoms are typically paroxysmal and include hypertension, headaches, palpitations, sweating, anxiety, tremor, abdominal and flank pain, and nausea. Catecholamines have various metabolic effects, including glycogenolysis, mobilization of free fatty acids, increased serum lactate, increased metabolic rate, increased myocardial force and rate of contraction, and decreased systemic vascular resistance.

Diagnosis of phaeochromocytoma involves measuring plasma and urine levels of metanephrines, catecholamines, and urine vanillylmandelic acid. Imaging studies such as abdominal CT or MRI are used to determine the location of the tumor. If these fail to find the site, a scan with metaiodobenzylguanidine (MIBG) labeled with radioactive iodine is performed. The highest sensitivity and specificity for diagnosis is achieved with plasma metanephrine assay.

The definitive treatment for phaeochromocytoma is surgery. However, before surgery, the patient must be stabilized with medical management. This typically involves alpha-blockade with medications such as phenoxybenzamine or phentolamine, followed by beta-blockade with medications like propranolol. Alpha blockade is started before beta blockade to allow for expansion of blood volume and to prevent a hypertensive crisis.

According to the GMC, if a doctor becomes aware that a patient is driving despite being unfit to do so, they should do everything they can to convince the patient to stop driving. If these efforts are unsuccessful and the patient continues to drive, the GMC advises promptly contacting the DVLA or DVA and sharing any pertinent medical information with the medical adviser, ensuring confidentiality.

Further Reading:

Blackouts are a common occurrence in the emergency department and can have serious consequences if they happen while a person is driving. It is crucial for doctors in the ED to be familiar with the guidelines set by the DVLA (Driver and Vehicle Licensing Agency) regarding driving restrictions for patients who have experienced a blackout.

The DVLA has specific rules for different types of conditions that may cause syncope (loss of consciousness). For group 1 license holders (car/motorcycle use), if a person has had a first unprovoked isolated seizure, they must refrain from driving for 6 months or 12 months if there is an underlying causative factor that may increase the risk. They must also notify the DVLA. For group 2 license holders (bus and heavy goods vehicles), the restrictions are more stringent, with a requirement of 12 months off driving for a first unprovoked isolated seizure and 5 years off driving if there is an underlying causative factor.

For epilepsy or multiple seizures, both group 1 and group 2 license holders must remain seizure-free for 12 months before their license can be considered. They must also notify the DVLA. In the case of a stroke or isolated transient ischemic attack (TIA), group 1 license holders need to refrain from driving for 1 month, while group 2 license holders must wait for 12 months before being re-licensed subject to medical evaluation. Multiple TIAs require 3 months off driving for both groups.

Isolated vasovagal syncope requires no driving restriction for group 1 license holders, but group 2 license holders must refrain from driving for 3 months. Both groups must notify the DVLA. If syncope is caused by a reversible and treated condition, group 1 license holders need 4 weeks off driving, while group 2 license holders require 3 months. In the case of an isolated syncopal episode with an unknown cause, group 1 license holders must refrain from driving for 6 months, while group 2 license holders will have their license refused or revoked for 12 months.

For patients who continue to drive against medical advice, the GMC (General Medical Council) has provided guidance on how doctors should manage the situation. Doctors should explain to the patient why they are not allowed to drive and inform them of their legal duty to notify the DVLA or DVA (Driver and Vehicle Agency in Northern Ireland). Doctors should also record the advice given to the patient in their medical record

Addison’s disease is characterized by several classical biochemical features. One of these features is an elevated level of ACTH, which is the body’s attempt to stimulate the adrenal glands. Additionally, individuals with Addison’s disease often experience hyponatremia, which is a decrease in the level of sodium in the blood. Another common feature is hyperkalemia, which refers to an excessive amount of potassium in the blood. Furthermore, individuals with Addison’s disease may also experience hypercalcemia, which is an elevated level of calcium in the blood. Hypoglycemia, which is low blood sugar, is another characteristic feature of this disease. Lastly, metabolic acidosis, which refers to an imbalance in the body’s acid-base levels, is also commonly observed in individuals with Addison’s disease.

Digoxin is a medication used to treat atrial fibrillation and flutter as well as congestive cardiac failure. It belongs to a class of drugs called cardiac glycosides. Digoxin works by inhibiting the Na/K ATPase pump in the cardiac myocytes, which are the cells of the heart. This inhibition leads to an increase in the concentration of sodium inside the cells and indirectly increases the availability of calcium through the Na/Ca exchange mechanism. The rise in intracellular calcium levels results in a positive inotropic effect, meaning it strengthens the force of the heart’s contractions, and a negative chronotropic effect, meaning it slows down the heart rate.

However, it’s important to note that digoxin can cause toxicity, which is characterized by high levels of potassium in the blood, known as hyperkalemia. Normally, the Na/K ATPase pump helps maintain the balance of sodium and potassium by allowing sodium to leave the cells and potassium to enter. When digoxin blocks this pump, it disrupts this balance and leads to higher levels of potassium in the bloodstream.

Interestingly, the risk of developing digoxin toxicity is higher in individuals with low levels of potassium, known as hypokalemia. This is because digoxin binds to the ATPase pump at the same site as potassium. When potassium levels are low, digoxin can more easily bind to the ATPase pump and exert its inhibitory effects.

In summary, digoxin is a cardiac glycoside that is used to treat certain heart conditions. It works by inhibiting the Na/K ATPase pump, leading to increased intracellular calcium levels and resulting in a positive inotropic effect and negative chronotropic effect. However, digoxin can also cause toxicity, leading to high levels of potassium in the blood. The risk of toxicity is higher in individuals with low potassium levels.

Adrenaline and isoprenaline are considered as second-line medications for the treatment of bradycardia. If atropine fails to improve the condition, transcutaneous pacing is recommended. However, if pacing is not available, the administration of second-line drugs becomes necessary. Adrenaline is typically given intravenously at a dosage of 2-10 mcg/minute, while isoprenaline is given at a dosage of 5 mcg/minute. It is important to note that glucagon is not mentioned as a treatment option for this patient’s bradycardia, as the cause of the condition is not specified as a beta-blocker overdose.

Further Reading:

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

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

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

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

Severe hypothermia is defined as having a core body temperature below 28ºC. The Royal College of Emergency Medicine (RCEM) also uses the term profound hypothermia to describe individuals with a core temperature below 20ºC.

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.

Schistosomiasis, also known as bilharzia, is a tropical disease caused by parasitic trematodes (flukes) of the Schistosoma type. It is transmitted through contaminated water that has been contaminated with faeces or urine containing eggs. The disease requires a specific freshwater snail as an intermediate host and human contact with water inhabited by the snail. There are five species of Schistosoma that cause human disease: S. japonicum, S. mansoni, S. haematobium, S. intercalatum, and S. mekongi. Schistosomiasis is a significant public health issue, second only to malaria, with over 200 million people infected worldwide. It is prevalent in the Middle East, Africa, and parts of South America and the Caribbean. Infection can manifest as acute or chronic.

Acute schistosomiasis is characterized by the early clinical sign of swimmers itch, which causes blisters and an urticarial response in the area where the parasite enters the skin. Most acute infections are asymptomatic, but some patients may develop an acute syndrome. The most common acute syndrome is known as Katayama fever, which typically occurs in individuals with no previous exposure. It is caused by an allergic reaction to the sudden release of highly antigenic eggs and usually presents a few weeks after initial exposure to S. japonicum. Symptoms of Katayama fever include fever, flu-like illness, arthralgia, myalgia, abdominal pain, diarrhea, and cough. Patients may also experience right upper quadrant tenderness and hepatosplenomegaly. An extremely high eosinophil count is commonly observed.

Chronic schistosomiasis can manifest as intestinal or urogenital forms. Intestinal schistosomiasis occurs when adult worms migrate from the liver to the mesenteric venules, where female worms continuously lay eggs. Common symptoms include abdominal pain and bloody diarrhea. Advanced cases may present with hepatosplenomegaly and portal hypertension. Schistosomiasis is the second most common cause of oesophageal varices worldwide. Urogenital schistosomiasis occurs when adult worms migrate to the vesical plexus. The hallmark sign is haematuria. In women, it may cause genital and vaginal lesions, as well as dyspareunia.

The Parkinson-plus syndromes are a group of neurodegenerative disorders that share similar features with Parkinson’s disease but also have additional clinical characteristics that set them apart from idiopathic Parkinson’s disease (iPD). These syndromes include Multiple System Atrophy (MSA), Progressive Supranuclear Palsy (PSP), Corticobasal degeneration (CBD), and Dementia with Lewy Bodies (DLB).

Multiple System Atrophy (MSA) is a less common condition than iPD and PSP. It is characterized by the loss of cells in multiple areas of the nervous system. MSA progresses rapidly, often leading to wheelchair dependence within 3-4 years of diagnosis. Some distinguishing features of MSA include autonomic dysfunction, bladder control problems, erectile dysfunction, blood pressure changes, early-onset balance problems, neck or facial dystonia, and a high-pitched voice.

To summarize the distinguishing features of the Parkinson-plus syndromes compared to iPD, the following table provides a comparison:

iPD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Typically starts at rest on one side of the body
– Levodopa response: Excellent response
– Mental changes: Depression
– Balance/falls: Late in the disease
– Common eye abnormalities: Dry eyes, trouble focusing

MSA:
– Symptom onset: Both sides equally affected
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

PSP:
– Symptom onset: Both sides equally affected
– Tremor: Less common, if present affects both sides
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Personality changes, depression
– Balance/falls: Within 1 year
– Common eye abnormalities: Dry eyes, difficulty in looking downwards

CBD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

BPPV is a condition where dizziness and vertigo occur suddenly when the position of the head is changed. This is a common symptom of benign paroxysmal positional vertigo, which is characterized by episodes of vertigo triggered by head movements.

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.

Respiratory acidosis occurs when the respiratory system is unable to effectively remove carbon dioxide from the body, leading to an increase in acidity. This is often seen in cases of opioid overdose, where respiratory depression can occur. In respiratory acidosis, the bicarbonate levels may rise as the body’s metabolic system tries to compensate for the increased acidity.

Further Reading:

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

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

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

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

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

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

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

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

Oral rehydration therapy (ORT) is a method used to prevent or treat dehydration by replacing fluids in the body. It is a less invasive approach compared to other methods and has been successful in reducing the mortality rate of diarrhea in developing nations.

ORT includes glucose, such as 90 mmol/L in Dioralyte, which helps improve the absorption of sodium and water in the intestines and prevents low blood sugar levels. It also contains essential mineral salts.

According to current guidelines from the National Institute for Health and Care Excellence (NICE), for mild dehydration, it is recommended to administer 50 mL/kg of ORT over a period of 4 hours.

Once a child has been rehydrated, they should continue their normal daily fluid intake and consume an additional 200 ml of ORT after each loose stool. For infants, ORT should be given at 1-1.5 times their regular feeding volume, while adults should consume 200-400 mL of ORT after each loose stool.

For more information, you can refer to the NICE guidelines on the diagnosis and management of diarrhea and vomiting caused by gastroenteritis in children under 5 years old.

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.

Haloperidol should not be used in patients with Parkinson’s, Lewy body dementia, or prolonged QT syndrome. It is the first choice for controlling aggressive behavior in most patients with delirium, but lorazepam is preferred for patients with Parkinson’s, Lewy body dementia, prolonged QT syndrome, extrapyramidal side effects, or delirium due to alcohol withdrawal. Haloperidol can reduce the effectiveness of levodopa in Parkinson’s disease by blocking dopamine receptors in the corpus striatum, which can lead to worsened motor function, psychosis, or a combination of both.

Further Reading:

Delirium is an acute syndrome that causes disturbances in consciousness, attention, cognition, and perception. It is also known as an acute confusional state. The DSM-IV criteria for diagnosing delirium include recent onset of fluctuating awareness, impairment of memory and attention, and disorganized thinking. Delirium typically develops over hours to days and may be accompanied by behavioral changes, personality changes, and psychotic features. It often occurs in individuals with predisposing factors, such as advanced age or multiple comorbidities, when exposed to new precipitating factors, such as medications or infection. Symptoms of delirium fluctuate throughout the day, with lucid intervals occurring during the day and worse disturbances at night. Falling and loss of appetite are often warning signs of delirium.

Delirium can be classified into three subtypes based on the person’s symptoms. Hyperactive delirium is characterized by inappropriate behavior, hallucinations, and agitation. Restlessness and wandering are common in this subtype. Hypoactive delirium is characterized by lethargy, reduced concentration, and appetite. The person may appear quiet or withdrawn. Mixed delirium presents with signs and symptoms of both hyperactive and hypoactive subtypes.

The exact pathophysiology of delirium is not fully understood, but it is believed to involve multiple mechanisms, including cholinergic deficiency, dopaminergic excess, and inflammation. The cause of delirium is usually multifactorial, with predisposing factors and precipitating factors playing a role. Predisposing factors include older age, cognitive impairment, frailty, significant injuries, and iatrogenic events. Precipitating factors include infection, metabolic or electrolyte disturbances, cardiovascular disorders, respiratory disorders, neurological disorders, endocrine disorders, urological disorders, gastrointestinal disorders, severe uncontrolled pain, alcohol intoxication or withdrawal, medication use, and psychosocial factors.

Delirium is highly prevalent in hospital settings, affecting up to 50% of inpatients aged over 65 and occurring in 30% of people aged over 65 presenting to the emergency department. Complications of delirium include increased risk of death, high in-hospital mortality rates, higher mortality rates following hospital discharge, increased length of stay in hospital, nosocomial infections, increased risk of admission to long-term care or re-admission to hospital, increased incidence of dementia, increased risk of falls and associated injuries and pressure sores.

Homonymous quadrantanopias occur when there are lesions in the optic radiation. The optic tract passes through the posterolateral angle of the optic chiasm, running alongside the cerebral peduncle and inside the uncus of the temporal lobe. Eventually, it reaches the lateral geniculate body (LGN) in the thalamus. Acting as a relay center, the LGN sends axons through the optic radiation to the primary visual cortex in the occipital lobe. The upper optic radiation carries fibers from the superior retinal quadrants (which corresponds to the lower half of the visual field) and travels through the parietal lobe. On the other hand, the lower optic radiation carries fibers from the inferior retinal quadrants (which corresponds to the upper half of the visual field) and travels through the temporal lobe. Consequently, lesions in the temporal lobe can lead to superior homonymous quadrantanopias, while lesions in the parietal lobe can cause inferior homonymous quadrantanopias. The diagram below provides a summary of the different visual field defects resulting from lesions at various points in the visual pathway.

The appendix is a slender and curved tube that is attached to the back and middle part of the caecum. It has a small triangular tissue called the mesoappendix that holds it in place from the tissue of the terminal ileum.

Although it contains a significant amount of lymphoid tissue, the appendix does not serve any important function in humans. The position of the free end of the appendix can vary greatly. There are five main locations where it can be found, with the most common being the retrocaecal and subcaecal positions.

The distribution of these positions is as follows:

– Ascending retrocaecal (64%)
– Subcaecal (32%)
– Transverse retrocaecal (2%)
– Ascending preileal (1%)
– Ascending retroileal (0.5%)

One way to assess for digoxin toxicity is by examining the patient’s electrocardiogram (ECG) for specific characteristics. In the case of digoxin toxicity, ECG findings may include downsloping ST depression, prolonged QT interval, tall tented T-waves, and possibly delta waves. However, a short PR interval (< 120ms) is not typically associated with digoxin toxicity. Further Reading: Digoxin is a medication used for rate control in atrial fibrillation and for improving symptoms in heart failure. It works by decreasing conduction through the atrioventricular node and increasing the force of cardiac muscle contraction. However, digoxin toxicity can occur, and plasma concentration alone does not determine if a patient has developed toxicity. Symptoms of digoxin toxicity include feeling generally unwell, lethargy, nausea and vomiting, anorexia, confusion, yellow-green vision, arrhythmias, and gynaecomastia. ECG changes seen in digoxin toxicity include downsloping ST depression with a characteristic Salvador Dali sagging appearance, flattened, inverted, or biphasic T waves, shortened QT interval, mild PR interval prolongation, and prominent U waves. There are several precipitating factors for digoxin toxicity, including hypokalaemia, increasing age, renal failure, myocardial ischaemia, electrolyte imbalances, hypoalbuminaemia, hypothermia, hypothyroidism, and certain medications such as amiodarone, quinidine, verapamil, and diltiazem. Management of digoxin toxicity involves the use of digoxin specific antibody fragments, also known as Digibind or digifab. Arrhythmias should be treated, and electrolyte disturbances should be corrected with close monitoring of potassium levels. It is important to note that digoxin toxicity can be precipitated by hypokalaemia, and toxicity can then lead to hyperkalaemia.

Ascending cholangitis occurs when there is an infection in the common bile duct, usually caused by a stone that has led to a blockage of bile flow. This condition is known as choledocholithiasis. The typical symptoms of ascending cholangitis are jaundice, fever (often accompanied by chills), and pain in the upper right quadrant of the abdomen. It is important to note that ascending cholangitis is a serious medical emergency that can be life-threatening, as patients often develop sepsis. Approximately 10-20% of patients may also experience altered mental status and low blood pressure due to septic shock. When these additional symptoms are present along with the classic triad of symptoms (Charcot’s triad), it is referred to as Reynold’s pentad. Urgent biliary drainage is the recommended treatment for ascending cholangitis. While a high white blood cell count is commonly seen in this condition, it is not considered part of Reynold’s pentad.

Thiamine deficiency is linked to episodes of acute confusion, but it is not typically associated with depression. On the other hand, depression is commonly seen in individuals with hypercalcemia. Chronic diseases like Parkinson’s disease and COPD are strongly correlated with depression. Additionally, both psychosis and depression can be associated with the use of steroids.

The primary cause of upper gastrointestinal bleeding in adults is peptic ulcer disease. Peptic ulcers are open sores that develop on the lining of the stomach or the upper part of the small intestine. These ulcers can be caused by factors such as infection with Helicobacter pylori bacteria, long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs), or excessive alcohol consumption. When a peptic ulcer bleeds, it can result in the vomiting of blood, which may appear as coffee ground vomit or have speckles of fresh red blood. Other symptoms that may accompany an upper gastrointestinal bleed include abdominal pain, nausea, and a feeling of fullness.

Further Reading:

Peptic ulcer disease (PUD) is a condition characterized by a break in the mucosal lining of the stomach or duodenum. It is caused by an imbalance between factors that promote mucosal damage, such as gastric acid, pepsin, Helicobacter pylori infection, and NSAID drug use, and factors that maintain mucosal integrity, such as prostaglandins, mucus lining, bicarbonate, and mucosal blood flow.

The most common causes of peptic ulcers are H. pylori infection and NSAID use. Other factors that can contribute to the development of ulcers include smoking, alcohol consumption, certain medications (such as steroids), stress, autoimmune conditions, and tumors.

Diagnosis of peptic ulcers involves screening for H. pylori infection through breath or stool antigen tests, as well as upper gastrointestinal endoscopy. Complications of PUD include bleeding, perforation, and obstruction. Acute massive hemorrhage has a case fatality rate of 5-10%, while perforation can lead to peritonitis with a mortality rate of up to 20%.

The symptoms of peptic ulcers vary depending on their location. Duodenal ulcers typically cause pain that is relieved by eating, occurs 2-3 hours after eating and at night, and may be accompanied by nausea and vomiting. Gastric ulcers, on the other hand, cause pain that occurs 30 minutes after eating and may be associated with nausea and vomiting.

Management of peptic ulcers depends on the underlying cause and presentation. Patients with active gastrointestinal bleeding require risk stratification, volume resuscitation, endoscopy, and proton pump inhibitor (PPI) therapy. Those with perforated ulcers require resuscitation, antibiotic treatment, analgesia, PPI therapy, and urgent surgical review.

For stable patients with peptic ulcers, lifestyle modifications such as weight loss, avoiding trigger foods, eating smaller meals, quitting smoking, reducing alcohol consumption, and managing stress and anxiety are recommended. Medication review should be done to stop causative drugs if possible. PPI therapy, with or without H. pylori eradication therapy, is also prescribed. H. pylori testing is typically done using a carbon-13 urea breath test or stool antigen test, and eradication therapy involves a 7-day triple therapy regimen of antibiotics and PPI.

Acute closed-angle glaucoma is a serious eye condition that requires immediate medical attention. It occurs when the iris pushes forward and blocks the fluid from reaching the trabecular meshwork, which is responsible for draining the eye. This blockage leads to increased pressure inside the eye and can cause damage to the optic nerve.

The main symptoms of acute closed-angle glaucoma include severe eye pain, vision loss or decreased visual acuity, redness and congestion around the cornea, swelling of the cornea, a fixed semi-dilated pupil, and nausea and vomiting. Some individuals may also experience episodes of blurred vision or seeing haloes before the onset of these symptoms.

On the other hand, chronic open-angle glaucoma is a more common form of the condition. It affects about 1 in 50 people over the age of 40 and 1 in 10 people over the age of 75. In this type of glaucoma, there is a partial blockage in the trabecular meshwork, which gradually restricts the drainage of fluid from the eye. As a result, the pressure inside the eye gradually increases, leading to optic nerve damage. Unlike acute closed-angle glaucoma, chronic open-angle glaucoma does not cause eye pain or redness. Instead, it presents slowly with a gradual loss of peripheral vision, while central vision is relatively preserved.

It is important to seek medical attention if you experience any symptoms of glaucoma, as early diagnosis and treatment can help prevent further vision loss.

The most commonly observed change in the electrocardiogram (ECG) during a tricyclic antidepressant (TCA) overdose is sinus tachycardia. Additionally, other ECG changes that can be seen in TCA overdose include prolongation of the PR interval, broadening of the QRS complex, prolongation of the QT interval, and the occurrence of ventricular arrhythmias in cases of severe toxicity. The cardiotoxic effects of TCAs are caused by the blocking of sodium channels, which leads to broadening of the QRS complex, and the blocking of potassium channels, which results in prolongation of the QT interval. The severity of the QRS broadening is associated with adverse events: a QRS duration greater than 100 ms is predictive of seizures, while a QRS duration greater than 160 ms is predictive of ventricular arrhythmias.

Heat stroke is a condition characterized by a core temperature greater than 40.6°C, accompanied by changes in mental state and varying levels of organ dysfunction. There are two forms of heat stroke: classic non-exertional heat stroke, which occurs during high environmental temperatures and typically affects elderly patients during heat waves, and exertional heat stroke, which occurs during strenuous physical exercise in high environmental temperatures, such as endurance athletes competing in hot conditions. Heat stroke happens when the body’s thermoregulation is overwhelmed by excessive environmental heat, excessive metabolic heat production, and insufficient heat loss.

Several risk factors increase the likelihood of developing heat stroke. These include hot and humid environmental conditions, age (with the elderly and infants being particularly vulnerable), physical factors like obesity, excessive exertion, and dehydration, as well as medical comorbidities such as anorexia, cardiovascular disease, skin conditions, poorly controlled diabetes, Parkinson’s disease, and thyrotoxicosis. Certain drugs, including alcohol, amphetamines, anticholinergics, beta-blockers, cocaine, diuretics, phenothiazines, SSRIs, and sympathomimetics, can also increase the risk of heat stroke.

The typical clinical features of heat stroke include a core temperature greater than 40.6°C. Early signs may include extreme fatigue, headache, syncope, facial flushing, vomiting, and diarrhea. The skin is usually hot and dry, although sweating can occur in around 50% of cases of exertional heat stroke. The loss of the ability to sweat is a late and concerning sign. Hyperventilation is almost always present. Heat stroke can also lead to cardiovascular dysfunction, such as arrhythmias, hypotension, and shock, respiratory dysfunction including acute respiratory distress syndrome (ARDS), and central nervous system dysfunction, including seizures and coma. If the temperature rises above 41.5°C, multi-organ failure, coagulopathy, and rhabdomyolysis can occur.

Heat cramps, on the other hand, typically present with intense thirst and muscle cramps. Body temperature is often elevated but usually remains below 40°C. Sweating, heat dissipation mechanisms, and cognition are preserved, and there is no neurological impairment.

Heat exhaustion usually precedes heat stroke and, if left untreated, can progress to heat stroke. Heat dissipation is still functioning, and the body temperature is usually below 41°C.

Neutropenic sepsis is a serious condition that can occur when a person has low levels of neutrophils, which are a type of white blood cell. This condition can be life-threatening and is often caused by factors such as chemotherapy, immunosuppressive drugs, infections, bone marrow disorders, and nutritional deficiencies.

To diagnose neutropenic sepsis, doctors look for a neutrophil count of 0.5 x 109 per litre or lower in patients undergoing cancer treatment. Additionally, patients must have a temperature higher than 38°C or show other signs and symptoms of significant sepsis.

According to the current guidelines from the National Institute for Health and Care Excellence (NICE), the recommended initial antibiotic treatment for suspected neutropenic sepsis is monotherapy with piperacillin with tazobactam (Tazocin 4.5 g IV). It is important to note that aminoglycosides should not be used as monotherapy or in combination therapy unless there are specific patient-related or local microbiological reasons to do so.

Osteoporosis and fragility fractures are more likely to occur in individuals with low levels of estrogen. Menopause, which causes a decrease in estrogen, can lead to estrogen deficiency. Estrogen plays a role in preventing bone breakdown by inhibiting osteoclast activity. After menopause, there is an increase in osteoclast activity, resulting in a rapid decline in bone mineral density. Osteoporosis is also associated with the long-term use of corticosteroids.

Further Reading:

Fragility fractures are fractures that occur following a fall from standing height or less, and may be atraumatic. They often occur in the presence of osteoporosis, a disease characterized by low bone mass and structural deterioration of bone tissue. Fragility fractures commonly affect the wrist, spine, hip, and arm.

Osteoporosis is defined as a bone mineral density (BMD) of 2.5 standard deviations below the mean peak mass, as measured by dual-energy X-ray absorptiometry (DXA). Osteopenia, on the other hand, refers to low bone mass between normal bone mass and osteoporosis, with a T-score between -1 to -2.5.

The pathophysiology of osteoporosis involves increased osteoclast activity relative to bone production by osteoblasts. The prevalence of osteoporosis increases with age, from approximately 2% at 50 years to almost 50% at 80 years.

There are various risk factors for fragility fractures, including endocrine diseases, GI causes of malabsorption, chronic kidney and liver diseases, menopause, immobility, low body mass index, advancing age, oral corticosteroids, smoking, alcohol consumption, previous fragility fractures, rheumatological conditions, parental history of hip fracture, certain medications, visual impairment, neuromuscular weakness, cognitive impairment, and unsafe home environment.

Assessment of a patient with a possible fragility fracture should include evaluating the risk of further falls, the risk of osteoporosis, excluding secondary causes of osteoporosis, and ruling out non-osteoporotic causes for fragility fractures such as metastatic bone disease, multiple myeloma, osteomalacia, and Paget’s disease.

Management of fragility fractures involves initial management by the emergency clinician, while treatment of low bone density is often delegated to the medical team or general practitioner. Management considerations include determining who needs formal risk assessment, who needs a DXA scan to measure BMD, providing lifestyle advice, and deciding who requires drug treatment.

Medication for osteoporosis typically includes vitamin D, calcium, and bisphosphonates. Vitamin D and calcium supplementation should be considered based on individual needs, while bisphosphonates are advised for postmenopausal women and men over 50 years with confirmed osteoporosis or those taking high doses of oral corticosteroids.

For the treatment of pregnant women with lower urinary tract infections (UTIs), it is recommended to provide them with an immediate prescription for antibiotics. It is important to consider their previous urine culture and susceptibility results, as well as any prior use of antibiotics that may have contributed to the development of resistant bacteria. Before starting antibiotics, it is advised to obtain a midstream urine sample from pregnant women and send it for culture and susceptibility testing.

Once the microbiological results are available, it is necessary to review the choice of antibiotic. If the bacteria are found to be resistant, it is recommended to switch to a narrow-spectrum antibiotic whenever possible. The choice of antibiotics for pregnant women aged 12 years and over is summarized below:

First-choice:
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days, if the estimated glomerular filtration rate (eGFR) is above 45 ml/minute.

Second-choice (if there is no improvement in lower UTI symptoms with the first-choice antibiotic for at least 48 hours, or if the first-choice is not suitable):
– Amoxicillin 500 mg taken orally three times daily for 7 days (only if culture results are available and show susceptibility).
– Cefalexin 500 mg taken twice daily for 7 days.

For alternative second-choice antibiotics, it is recommended to consult a local microbiologist and choose the appropriate antibiotics based on the culture and sensitivity results.

The Seidel test is a method used to assess ocular trauma. The procedure involves applying a 10% fluorescein strip to the affected area and examining it using a cobalt blue filter. If there is a corneal laceration with leakage of aqueous fluid, the dye will be diluted by the fluid, resulting in a visible stream.

In addition to the Seidel test, there are several other important steps to be taken during an eye examination for trauma. These include inspecting the overall appearance of the eye, examining the lids and peri-orbital bones, assessing visual acuity in both eyes, testing visual fields by confrontation, evaluating eye movements, measuring pupil size and response to light and accommodation, checking for foreign bodies using a slit lamp, performing fundoscopy and assessing the red reflex.

The Amsler grid test is a useful tool for detecting central visual field defects and aiding in the diagnosis of age-related macular degeneration. A positive Amsler test is indicated by the appearance of curved or wavy lines on the grid.

Tonometry is a technique used to measure intraocular pressure (IOP), which is helpful in diagnosing glaucoma.

Retinal photography is a sophisticated imaging process that involves using a digital camera to capture detailed pictures of the retina. It is primarily used to document the health of various structures in the eye, such as the optic nerve, posterior pole, macula, retina, and its blood vessels. However, it is not typically used as part of the initial evaluation for trauma.

Eye pH measurement is a valuable tool in evaluating chemical eye injuries.

Bacterial vaginosis (BV) is a common condition that affects up to a third of women during their childbearing years. It occurs when there is an overgrowth of bacteria, specifically Gardnerella vaginalis. This bacterium is anaerobic, meaning it thrives in environments without oxygen. As it multiplies, it disrupts the balance of bacteria in the vagina, leading to a rise in pH levels and a decrease in lactic acid-producing lactobacilli. It’s important to note that BV is not a sexually transmitted infection.

The main symptom of BV is a greyish discharge with a distinct fishy odor. However, it’s worth mentioning that around 50% of affected women may not experience any symptoms at all.

To diagnose BV, healthcare providers often use Amsel’s criteria. This involves looking for the presence of three out of four specific criteria: a vaginal pH greater than 4.5, a positive fishy smell test when potassium hydroxide is added, the presence of clue cells on microscopy, and a thin, white, homogeneous discharge.

The primary treatment for BV is oral metronidazole, typically taken for 5-7 days. This medication has an initial cure rate of about 75%. It’s crucial to provide special care to pregnant patients diagnosed with BV, as it has been linked to an increased risk of late miscarriage, early labor, and chorioamnionitis. Therefore, prompt treatment for these patients is of utmost importance.

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.

The median nerve originates from the lateral and medial cords of the brachial plexus and receives contributions from the ventral roots of C5-C7 (lateral cord) and C8 and T1 (medial cord). It serves both motor and sensory functions.

In terms of motor function, the median nerve innervates the flexor muscles in the anterior compartment of the forearm, excluding the flexor carpi ulnaris and a portion of the flexor digitorum profundus, which are instead innervated by the ulnar nerve. Additionally, it innervates the thenar muscles and the lateral two lumbricals.

Regarding sensory function, the median nerve gives rise to the palmar cutaneous branch, which provides innervation to the lateral part of the palm. It also gives rise to the digital cutaneous branch, which innervates the lateral three and a half fingers on the palmar surface of the hand.

Within the forearm, the median nerve branches into two major branches. The first is the anterior interosseous nerve (AIN), which supplies the flexor pollicis longus, pronator quadratus, and the lateral half of the flexor digitorum profundus. The second is the palmar cutaneous branch, which provides sensory innervation to the skin of the radial palm.

Differentiating between damage to the median nerve at the elbow and wrist can be done by considering these two branches. Injury at the elbow affects these branches, while injury at the wrist spares them. It is important to note that the palmar cutaneous branch travels superficially to the flexor retinaculum and therefore remains functional in carpal tunnel syndrome. However, it can be damaged by laceration at the wrist.

A comparison of median nerve lesions at the wrist and elbow is presented below:

Median nerve at elbow:
– Motor loss: Weak wrist flexion and abduction, loss of thumb abduction and opposition, loss of flexion of index and middle fingers
– Sensory loss: Lateral 3 and ½ fingers and nail beds, lateral side of palm
– Hand deformity: Ulnar deviation of wrist, thenar wasting, papal benediction on flexing fingers

Median nerve at wrist:
– Motor loss: Loss of thumb abduction and opposition, wrist and finger flexion intact (due to intact AIN)
– Sensory loss: Lateral 3 and ½ fingers and nail beds, lateral side of palm (but can be preserved depending upon palmar cutaneous branch)
– Hand deformity: Thenar wasting, no ulnar deviation of wrist or papal benediction (due to intact AIN)

Fibre-optic laryngoscopy is considered the most reliable method for diagnosing epiglottitis. In this case, the patient’s symptoms align with those typically seen in epiglottitis. It is crucial to prioritize the assessment of the airway before conducting any invasive procedures, such as using a tongue depressor to examine the oral cavity or performing needle aspiration of the tonsils.

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.

Ulnar nerve lesions can be assessed using Froment’s sign. To perform this test, a piece of paper is placed between the patient’s thumb and index finger. The examiner then tries to pull the paper out of the patient’s pinched grip. If the patient has an ulnar nerve palsy, they will struggle to maintain the grip and may compensate by flexing the flexor pollicis longus muscle of the thumb to maintain pressure. This compensation is evident when the patient’s interphalangeal joint of the thumb flexes. Froment’s sign is a useful indicator of ulnar nerve dysfunction.

Public Health England (PHE) has a primary goal of swiftly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is important, it takes a backseat to the speed of detection. Since 1968, the clinical suspicion of a notifiable infection has been sufficient for reporting purposes.

Registered medical practitioners (RMPs) are legally obligated to notify the designated proper officer at their local council or local health protection team (HPT) when they suspect cases of certain infectious diseases.

The Health Protection (Notification) Regulations 2010 specify the diseases that RMPs must report to the proper officers. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

It is worth noting that influenza is not considered a notifiable disease, making it the least likely option among the diseases listed above.

When starting treatment with strong opioids for pain relief in palliative care, it is recommended to offer patients regular oral sustained-release or oral immediate-release morphine, depending on their preference. In addition, provide rescue doses of oral immediate-release morphine for breakthrough pain. For patients without renal or hepatic comorbidities, a typical total daily starting dose schedule of 20-30 mg of oral morphine is suggested, along with 5 mg of oral immediate-release morphine for rescue doses during the titration phase. It is important to adjust the dose until a good balance is achieved between pain control and side effects. If this balance is not reached after a few dose adjustments, it is advisable to seek specialist advice. Patients should be reviewed frequently, especially during the titration phase. For patients with moderate to severe renal or hepatic impairment, it is recommended to consult a specialist before prescribing strong opioids.

For maintenance therapy, oral sustained-release morphine is recommended as the first-line treatment for patients with advanced and progressive disease who require strong opioids. Transdermal patch formulations should not be routinely offered as first-line maintenance treatment unless oral opioids are not suitable. If pain remains inadequately controlled despite optimizing first-line maintenance treatment, it is important to review the analgesic strategy and consider seeking specialist advice.

When it comes to breakthrough pain, oral immediate-release morphine should be offered as the first-line rescue medication for patients on maintenance oral morphine treatment. Fast-acting fentanyl should not be offered as the first-line rescue medication. If pain continues to be inadequately controlled despite optimizing treatment, it may be necessary to seek specialist advice.

In cases where oral opioids are not suitable and analgesic requirements are stable, transdermal patches with the lowest acquisition cost can be considered. However, it is important to consult a specialist for guidance if needed. Similarly, for patients in whom oral opioids are not suitable and analgesic requirements are unstable, subcutaneous opioids with the lowest acquisition cost can be considered, with specialist advice if necessary.

For more information, please refer to the NICE Clinical Knowledge Summary: Opioids for pain relief in palliative care. https://www.nice.org.uk/guidance/cg140

Aminoglycosides have the ability to pass through the placenta and can lead to damage to the 8th cranial nerve in the fetus, resulting in permanent bilateral deafness.

ACE inhibitors, such as ramipril, can cause hypoperfusion, renal failure, and the oligohydramnios sequence if given in the 2nd and 3rd trimesters.

Aminoglycosides, like gentamicin, can cause ototoxicity and deafness in the fetus.

High doses of aspirin can lead to 1st 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, including diazepam, when administered late in pregnancy, can result in respiratory depression and a neonatal withdrawal syndrome.

Calcium-channel blockers, if given in the 1st trimester, can cause phalangeal abnormalities. If given in the 2nd and 3rd trimesters, they can lead to fetal growth retardation.

Carbamazepine can cause hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol is associated with grey baby syndrome.

Corticosteroids, if given in the 1st trimester, may cause orofacial clefts.

Danazol, if given in the 1st trimester, can cause masculinization of the female fetuses genitals.

Finasteride should not be handled by pregnant women as crushed or broken tablets can be absorbed through the skin and affect male sex organ development.

Haloperidol, if given in the 1st trimester, may cause limb malformations. If given in the 3rd trimester, there is an increased risk of extrapyramidal symptoms in the neonate.

Heparin can lead to maternal bleeding and thrombocytopenia.

Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate.

Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability.

Lithium, if given in the 1st trimester, poses a risk of fetal cardiac malformations.

Patients with active cancer and a confirmed deep-vein thrombosis (DVT) should be considered for treatment with a direct oral anticoagulant (DOAC) such as apixaban. If a DOAC is not suitable for the patient, alternative options should be offered. One option is the use of low-molecular-weight heparin (LMWH) alone. Another option is the combination of LMWH and a vitamin K antagonist (VKA) like warfarin, which should be given for at least 5 days or until the international normalized ratio (INR) reaches at least 2.0 on 2 consecutive readings. After achieving the desired INR, the patient can continue with a VKA alone. It is important to note that anticoagulation treatment should be offered for a period of 3-6 months. to the NICE guidance on the diagnosis and management of venous thromboembolism.

The term Apparent Life-Threatening Event (ALTE) has traditionally been used to describe a specific type of event. However, in 2016, the American Academy of Paediatrics (AAP) recommended replacing this term with a new one called Brief Resolved Unexplained Event (BRUE).

An ALTE is defined as an episode that is frightening to the observer and is characterized by a combination of symptoms such as apnoea (central or occasionally obstructive), color change (usually cyanotic or pallid but occasionally erythematous or plethoric), significant change in muscle tone (usually marked limpness), choking, or gagging. In some cases, the observer may even fear that the infant has died.

On the other hand, BRUE has stricter criteria and is only applicable to episodes that occur in infants under 12 months old. A BRUE is considered brief, typically lasting 2-30 seconds but no longer than 1 minute. It must also have resolved, meaning the infant has returned to their baseline state. Additionally, it should not be explained by any identifiable medical condition and must be characterized by at least one of the following: cyanosis or pallor, absent, decreased, or irregular breathing, marked change in muscle tone (hyper- or hypotonia), or altered level of responsiveness.

To diagnose a BRUE, a full history and physical examination of the infant must be conducted, and if no explanation for the event is found, it can be classified as a BRUE. Once a BRUE is diagnosed, it can be risk-stratified to guide further management.

A BRUE is considered low risk if the infant has fully recovered, there are no concerning history or physical examination findings, and the following criteria are met: the infant is over 60 days old, born after 32 weeks gestation with a corrected gestational age over 45 weeks, no CPR was performed by a trained healthcare professional, and this was the first event that lasted less than 1 minute.

Low-risk infants can be safely discharged with early outpatient follow-up within 24 hours. However, it is important to involve the parents/caregivers in the decision-making process. They should be informed that a low-risk BRUE is unlikely to indicate a severe underlying disorder and that the event is unlikely to happen again.

Before discharge, it may be advisable to perform an ECG, observe the infant for a brief period, and conduct a pertussis swab

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

According to NICE, one of the recommended treatments for mild-to-moderate Alzheimer’s disease is the use of acetylcholinesterase (AChE) inhibitors. These inhibitors include Donepezil (Aricept), Galantamine, and Rivastigmine. They work by inhibiting the enzyme that breaks down acetylcholine, a neurotransmitter involved in memory and cognitive function.

On the other hand, Memantine is a different type of medication that acts by blocking NMDA-type glutamate receptors. It is recommended for patients with moderate Alzheimer’s disease who cannot tolerate or have a contraindication to AChE inhibitors, or for those with severe Alzheimer’s disease.

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, and immune dilution. While there has been an increased awareness of these risks and improved reporting systems, transfusion errors and serious adverse reactions still occur and may go unreported.

One specific transfusion reaction is transfusion-associated circulatory overload (TACO), which occurs when a large volume of blood is rapidly infused. It is the second leading cause of transfusion-related deaths, accounting for about 20% of fatalities. TACO is more likely to occur in patients with diminished cardiac reserve or chronic anemia, particularly in the elderly, infants, and severely anemic patients.

The typical clinical features of TACO include acute respiratory distress, tachycardia, hypertension, acute or worsening pulmonary edema on chest X-ray, and evidence of positive fluid balance. The B-type natriuretic peptide (BNP) can be a useful diagnostic tool for TACO, with levels usually elevated to at least 1.5 times the pre-transfusion baseline.

In many cases, simply slowing the transfusion rate, placing the patient in an upright position, and administering diuretics can be sufficient for managing TACO. In more severe cases, the transfusion should be stopped, and non-invasive ventilation may be considered.

Anaemia can be categorized based on the size of red blood cells. Microcytic anaemia, characterized by a mean corpuscular volume (MCV) of less than 80 fl, can be caused by various factors such as iron deficiency, thalassaemia, anaemia of chronic disease (which can also be normocytic), sideroblastic anaemia (which can also be normocytic), lead poisoning, and aluminium toxicity (although this is now rare and mainly affects haemodialysis patients).

On the other hand, normocytic anaemia, with an MCV ranging from 80 to 100 fl, can be attributed to conditions like haemolysis, acute haemorrhage, bone marrow failure, anaemia of chronic disease (which can also be microcytic), mixed iron and folate deficiency, pregnancy, chronic renal failure, and sickle-cell disease.

Lastly, macrocytic anaemia, characterized by an MCV greater than 100 fl, can be caused by factors such as B12 deficiency, folate deficiency, hypothyroidism, reticulocytosis, liver disease, alcohol abuse, myeloproliferative disease, myelodysplastic disease, and certain drugs like methotrexate, hydroxyurea, and azathioprine.

It is important to understand the different causes of anaemia based on red cell size as this knowledge can aid in the diagnosis and management of this condition.

Alzheimer’s disease is the most prevalent type of dementia, making up around 55-60% of all cases. In the UK, the occurrence of Alzheimer’s disease is approximately 5 per 1000 person-years, and the likelihood of developing it increases with age.

Chagas disease, also known as American Trypanosomiasis, is a tropical illness caused by the protozoan Trypanosoma cruzi. It is transmitted by Triatomine insects, commonly known as kissing bugs, which belong to the Reduviidae family. This zoonotic disease is prevalent in Central and South America, with an estimated 8 million people infected in the region. In Brazil alone, there are approximately 120,000 new cases reported each year.

The disease progresses through two stages: the acute stage and the chronic stage. During the acute stage, many patients may not experience any symptoms, and the infection can go unnoticed. However, some individuals may exhibit symptoms such as fever, malaise, muscle pain, loss of appetite, and occasionally vomiting and diarrhea. Clinical signs may include swollen lymph nodes and enlargement of the liver and spleen. At the site of the insect bite, an inflammatory response called a chagoma can occur. This is characterized by a swollen, violet-colored nodule that can last up to 8 weeks. Another distinctive sign of acute Chagas disease is Romaña’s sign, which is eyelid swelling caused by accidentally rubbing bug feces into the eyes.

Following the acute stage, an estimated 10-30% of individuals progress to the chronic stage of Chagas disease. There is typically a latent phase between the acute and chronic phases, which can last for as long as 20-30 years. The chronic phase is associated with various complications, including cardiovascular problems such as dilated cardiomyopathy, heart failure, and arrhythmias. Gastrointestinal issues like megacolon, megaesophagus, and secondary achalasia can also arise. Neurological complications, such as neuritis, sensory and motor deficits, and encephalopathy, may occur. Additionally, psychiatric symptoms, including dementia, can manifest in some cases.

This patient presents with elevated transaminases and gamma GT, along with mildly elevated ALP and hyperbilirubinemia. These findings strongly indicate a diagnosis of alcohol-induced hepatitis. Additionally, the patient’s history and examination features strongly suggest a history of chronic alcohol abuse and withdrawal, further supporting this diagnosis.

An open pneumothorax, also known as a sucking chest wound, occurs when air enters the pleural space due to an open chest wound or physical defect. This can lead to ineffective ventilation, causing hypoxia and hypercarbia. Air can enter the pleural cavity passively or be sucked in during inspiration, leading to lung collapse on that side. Sucking wounds can be heard audibly as air passes through the chest defect, and entry wounds are usually visible.

To manage an open pneumothorax, respiratory compromise can be alleviated by covering the wound with a dressing or using a chest seal device. It is important to ensure that one side of the dressing is not occluded, allowing the dressing to function as a flutter valve and prevent significant air ingress during inspiration while allowing air to escape the pleural cavity. If tension pneumothorax is suspected after applying a dressing, the dressing may need to be temporarily removed for decompression.

Intubation and intermittent positive pressure ventilation (IPPV) can be used to ventilate the patient and alleviate respiratory distress. Definitive management involves either inserting a chest drain or surgically repairing the defect. Surgical repair is typically preferred, especially for large wounds.

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.

The tricuspid valve is the most commonly affected valve in cases of infective endocarditis among intravenous drug users. This means that when IV drug users develop infective endocarditis, it is most likely to affect the tricuspid valve. On the other hand, in cases of native valve endocarditis and prosthetic valve endocarditis, the mitral valve is the valve that is most commonly affected.

Further Reading:

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

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

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

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

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

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 most recent guidelines from the National Institute for Health and Care Excellence (NICE) recommend using a LNG-IUS, such as Mirena IUS, as the initial treatment for heavy menstrual bleeding (HMB) in women who have no identified pathology, fibroids smaller than 3 cm without uterine cavity distortion, or suspected/diagnosed adenomyosis. If a woman declines or cannot use an LNG-IUS, alternative pharmacological treatments can be considered. These include non-hormonal options like Tranexamic acid or NSAIDs, as well as hormonal options like combined hormonal contraception or cyclical oral progestogens. to the NICE guidelines on the assessment and management of heavy menstrual bleeding.

Osteoporosis is a condition characterized by weak and brittle bones, making them more prone to fractures. In this case, the patient’s sudden onset of central back pain and the X-ray findings of anterior wedging of the L2 vertebra suggest the possibility of undiagnosed osteoporosis.

One correct statement about osteoporosis is that it is defined as a T-score of less than -2.5. The T-score is a measure of bone density and is used to diagnose osteoporosis. A T-score of -2.5 or lower indicates a significant decrease in bone density and an increased risk of fractures.

Skeletal scintigraphy is not used to diagnose osteoporosis. Instead, it is commonly used to evaluate for other conditions such as bone infections or tumors.

The pubic rami is not the most common site for osteoporotic fractures. Osteoporotic fractures commonly occur in the spine (vertebral fractures), hip, and wrist.

Osteoporosis is not characterized by increased bone turnover in focal areas of the axial skeleton with a lytic phase followed by a rapid increase in bone formation by osteoblasts in the sclerotic phase. This description is more consistent with a condition called Paget’s disease of bone.

The prevalence of osteoporosis is not approximately 10% at 50 years of age. The prevalence of osteoporosis increases with age, and it is estimated that around 50% of women and 25% of men over the age of 50 will experience an osteoporotic fracture in their lifetime.

Further Reading:

Fragility fractures are fractures that occur following a fall from standing height or less, and may be atraumatic. They often occur in the presence of osteoporosis, a disease characterized by low bone mass and structural deterioration of bone tissue. Fragility fractures commonly affect the wrist, spine, hip, and arm.

Osteoporosis is defined as a bone mineral density (BMD) of 2.5 standard deviations below the mean peak mass, as measured by dual-energy X-ray absorptiometry (DXA). Osteopenia, on the other hand, refers to low bone mass between normal bone mass and osteoporosis, with a T-score between -1 to -2.5.

The pathophysiology of osteoporosis involves increased osteoclast activity relative to bone production by osteoblasts. The prevalence of osteoporosis increases with age, from approximately 2% at 50 years to almost 50% at 80 years.

There are various risk factors for fragility fractures, including endocrine diseases, GI causes of malabsorption, chronic kidney and liver diseases, menopause, immobility, low body mass index, advancing age, oral corticosteroids, smoking, alcohol consumption, previous fragility fractures, rheumatological conditions, parental history of hip fracture, certain medications, visual impairment, neuromuscular weakness, cognitive impairment, and unsafe home environment.

Assessment of a patient with a possible fragility fracture should include evaluating the risk of further falls, the risk of osteoporosis, excluding secondary causes of osteoporosis, and ruling out non-osteoporotic causes for fragility fractures such as metastatic bone disease, multiple myeloma, osteomalacia, and Paget’s disease.

Management of fragility fractures involves initial management by the emergency clinician, while treatment of low bone density is often delegated to the medical team or general practitioner. Management considerations include determining who needs formal risk assessment, who needs a DXA scan to measure BMD, providing lifestyle advice, and deciding who requires drug treatment.

Medication for osteoporosis typically includes vitamin D, calcium, and bisphosphonates. Vitamin D and calcium supplementation should be considered based on individual needs, while bisphosphonates are advised for postmenopausal women and men over 50 years with confirmed osteoporosis or those taking high doses of oral corticosteroids.

The nerve agents, also known as nerve gases, are a group of highly toxic chemical warfare agents that were initially developed just before and during World War II.

The first compounds to be created are referred to as the G agents (with G representing German, as they were discovered and synthesized by German scientists). These include Tabun (GA), Sarin (GB), and Soman (GD).

In the 1950s, the V agents (with V standing for venomous) were synthesized, and they are approximately 10 times more poisonous than sarin. 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 the use of a nerve agent was the March 1995 Tokyo subway sarin attack. During this attack, Sarin was released into the Tokyo subway system during rush hour. As a result, over 5,000 people sought medical attention. Among them, 984 were moderately poisoned, 54 were severely poisoned, and 12 lost their lives.

The nerve agents are organophosphorus esters that are chemically related to organophosphorus insecticides. They work by inhibiting acetylcholinesterase (AChE), an enzyme that breaks down the neurotransmitter acetylcholine (ACh). This 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 be absorbed through the skin, eyes, and respiratory tract. When dispersed as a vapor, they are primarily absorbed through the respiratory tract and eyes. If a sufficient amount of agent is absorbed, local effects are followed by generalized systemic effects.

The primary approach to managing nerve gas exposure through medication involves the repeated administration of antidotes. The two antidotes utilized for this purpose are atropine and pralidoxime.

Atropine is the standard anticholinergic medication employed to address the symptoms associated with nerve agent poisoning. It functions as an antagonist for muscarinic acetylcholine receptors, effectively blocking the effects caused by excessive acetylcholine. Initially, a 1.2 mg intravenous bolus of atropine is administered. This dosage is then repeated and doubled every 2-3 minutes until excessive bronchial secretion ceases and miosis (excessive constriction of the pupil) resolves. In some cases, as much as 100 mg of atropine may be necessary.

Pralidoxime (2-PAMCl) is the standard oxime used in the treatment of nerve agent poisoning. Its mechanism of action involves reactivating acetylcholinesterase by scavenging the phosphoryl group attached to the functional hydroxyl group of the enzyme, thereby counteracting the effects of the nerve agent itself. For patients who are moderately or severely poisoned, pralidoxime should be administered intravenously at a dosage of 30 mg/kg of body weight (or 2 g in the case of an adult) over a period of four minutes.

This patient is displaying symptoms of life-threatening asthma, and the only available option for treatment with the correct dosage is an aminophylline loading dose.

The signs of acute severe asthma in adults include a peak expiratory flow (PEF) of 33-50% of the best or predicted value, a respiratory rate of over 25 breaths per minute, a heart rate of over 110 beats per minute, and an inability to complete sentences in one breath.

On the other hand, life-threatening asthma is characterized by a PEF of less than 33% of the best or predicted value, a blood oxygen saturation level (SpO2) below 92%, a partial pressure of oxygen (PaO2) below 8 kPA, a normal partial pressure of carbon dioxide (PaCO2) within the range of 4.6-6.0 kPa, a silent chest, cyanosis, poor respiratory effort, exhaustion, altered consciousness, and hypotension.

The recommended drug doses for adult acute asthma are as follows: 5 mg of salbutamol delivered through an oxygen-driven nebulizer, 500 mcg of ipratropium bromide via an oxygen-driven nebulizer, 40-50 mg of prednisolone taken orally, 100 mg of hydrocortisone administered intravenously, and 1.2-2 g of magnesium sulfate given intravenously over a period of 20 minutes. Intravenous salbutamol may be considered (250 mcg administered slowly) only when inhaled therapy is not possible, such as in a patient receiving bag-mask ventilation.

According to the current ALS guidelines, IV aminophylline can be considered in cases of severe or life-threatening asthma, following consultation with a senior medical professional. If used, a loading dose of 5 mg/kg should be administered over 20 minutes, followed by a continuous infusion of 500-700 mcg/kg/hour. It is important to maintain serum theophylline levels below 20 mcg/ml to prevent toxicity.

For more information, please refer to the BTS/SIGN Guideline on the Management of Asthma.

Torsades de pointes is a condition that is linked to low levels of potassium (hypokalaemia) and magnesium (hypomagnesaemia). When potassium and magnesium levels are low, it can cause the QT interval to become prolonged, which increases the risk of developing Torsades de pointes.

Further Reading:

Torsades de pointes is an irregular broad-complex tachycardia that can be life-threatening. It is a polymorphic ventricular tachycardia that can lead to sudden cardiac death. It is characterized by distinct features on the electrocardiogram (ECG).

The causes of irregular broad-complex tachycardia include atrial fibrillation with bundle branch block, atrial fibrillation with ventricular pre-excitation (in patients with Wolff-Parkinson-White syndrome), and polymorphic ventricular tachycardia such as torsades de pointes. However, sustained polymorphic ventricular tachycardia is unlikely to be present without adverse features, so it is important to seek expert help for the assessment and treatment of this condition.

Torsades de pointes can be caused by drug-induced QT prolongation, diarrhea, hypomagnesemia, hypokalemia, and congenital long QT syndrome. It may also be seen in malnourished individuals due to low potassium and/or low magnesium levels. Additionally, it can occur in individuals taking drugs that prolong the QT interval or inhibit their metabolism.

The management of torsades de pointes involves immediate action. All drugs known to prolong the QT interval should be stopped. Amiodarone should not be given for definite torsades de pointes. Electrolyte abnormalities, especially hypokalemia, should be corrected. Magnesium sulfate should be administered intravenously. If adverse features are present, immediate synchronized cardioversion should be arranged. sought, as other treatments such as overdrive pacing may be necessary to prevent relapse once the arrhythmia has been corrected. If the patient becomes pulseless, defibrillation should be attempted immediately.

In summary, torsades de pointes is a dangerous arrhythmia that requires prompt management. It is important to identify and address the underlying causes, correct electrolyte abnormalities, and seek expert help for appropriate treatment.

Most duodenal ulcers are caused by H. pylori infection, while peptic ulcers not associated with H. pylori are typically caused by the use of NSAIDs.

Further Reading:

Peptic ulcer disease (PUD) is a condition characterized by a break in the mucosal lining of the stomach or duodenum. It is caused by an imbalance between factors that promote mucosal damage, such as gastric acid, pepsin, Helicobacter pylori infection, and NSAID drug use, and factors that maintain mucosal integrity, such as prostaglandins, mucus lining, bicarbonate, and mucosal blood flow.

The most common causes of peptic ulcers are H. pylori infection and NSAID use. Other factors that can contribute to the development of ulcers include smoking, alcohol consumption, certain medications (such as steroids), stress, autoimmune conditions, and tumors.

Diagnosis of peptic ulcers involves screening for H. pylori infection through breath or stool antigen tests, as well as upper gastrointestinal endoscopy. Complications of PUD include bleeding, perforation, and obstruction. Acute massive hemorrhage has a case fatality rate of 5-10%, while perforation can lead to peritonitis with a mortality rate of up to 20%.

The symptoms of peptic ulcers vary depending on their location. Duodenal ulcers typically cause pain that is relieved by eating, occurs 2-3 hours after eating and at night, and may be accompanied by nausea and vomiting. Gastric ulcers, on the other hand, cause pain that occurs 30 minutes after eating and may be associated with nausea and vomiting.

Management of peptic ulcers depends on the underlying cause and presentation. Patients with active gastrointestinal bleeding require risk stratification, volume resuscitation, endoscopy, and proton pump inhibitor (PPI) therapy. Those with perforated ulcers require resuscitation, antibiotic treatment, analgesia, PPI therapy, and urgent surgical review.

For stable patients with peptic ulcers, lifestyle modifications such as weight loss, avoiding trigger foods, eating smaller meals, quitting smoking, reducing alcohol consumption, and managing stress and anxiety are recommended. Medication review should be done to stop causative drugs if possible. PPI therapy, with or without H. pylori eradication therapy, is also prescribed. H. pylori testing is typically done using a carbon-13 urea breath test or stool antigen test, and eradication therapy involves a 7-day triple therapy regimen of antibiotics and PPI.

Discitis is an infection that affects the space between the intervertebral discs in the spine. This condition can have serious consequences, including the formation of abscesses and sepsis. The most common cause of discitis is usually Staphylococcus aureus, but other organisms like Streptococcus viridans and Pseudomonas aeruginosa may be responsible in intravenous drug users and those with weakened immune systems. Gram-negative organisms such as Escherichia coli and Mycobacterium tuberculosis can also cause discitis.

There are several risk factors that increase the likelihood of developing discitis. These include having undergone spinal surgery (which occurs in 1-2% of cases post-operatively), having an immunodeficiency, being an intravenous drug user, being under the age of eight, having diabetes mellitus, or having a malignancy.

The typical symptoms of discitis include back or neck pain (which occurs in over 90% of cases), pain that often wakes the patient from sleep, fever (present in 60-70% of cases), and neurological deficits (which can occur in up to 50% of cases). In children, refusal to walk may also be a symptom.

When diagnosing discitis, MRI is the preferred imaging modality due to its high sensitivity and specificity. It is important to image the entire spine, as discitis often affects multiple levels. Plain radiographs are not very sensitive to the early changes of discitis and may appear normal for 2-4 weeks. CT scanning is also not very sensitive in detecting discitis.

Treatment for discitis involves admission to the hospital for intravenous antibiotics. Before starting the antibiotics, it is important to send three sets of blood cultures and a full set of blood tests, including a CRP, to the lab. The choice of antibiotics depends on the specific situation. A typical antibiotic regimen for discitis may include IV flucloxacillin as the first-line treatment if there is no penicillin allergy, IV vancomycin if the infection was acquired in the hospital or there is a high risk of MRSA, and possibly IV gentamicin if there is a possibility of a Gram-negative infection. In cases where there is acute kidney injury and Gram-negative cover is required, IV piperacillin-tazobactam alone may be used.

During CPR of a hypothermic patient, it is important to follow specific guidelines. If the patient’s core temperature is below 30ºC, resuscitation drugs, such as adrenaline, should be withheld. Once the core temperature rises above 30ºC, cardiac arrest drugs can be administered. However, if the patient’s temperature is between 30-35ºC, the interval for administering cardiac arrest drugs should be doubled. For example, adrenaline should be given every 6-10 minutes instead of the usual 3-5 minutes for a normothermic patient.

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.

The following provides a summary of common causes for different acid-base disorders.

Respiratory alkalosis can be caused by hyperventilation, such as during periods of anxiety. It can also be a result of conditions like pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, or the early stages of aspirin overdose.

Respiratory acidosis, on the other hand, is often associated with chronic obstructive pulmonary disease (COPD), life-threatening asthma, pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or other respiratory conditions.

Metabolic alkalosis can occur due to vomiting, potassium depletion (often caused by diuretic usage), Cushing’s syndrome, or Conn’s syndrome.

Metabolic acidosis with a raised anion gap can be caused by lactic acidosis (such as in cases of hypoxemia, shock, sepsis, or infarction), ketoacidosis (such as in diabetes, starvation, or alcohol excess), renal failure, or poisoning (such as in late stages of aspirin overdose, methanol or ethylene glycol ingestion).

Lastly, metabolic acidosis with a normal anion gap can be a result of conditions like diarrhea, ammonium chloride ingestion, or adrenal insufficiency.

The primary concern regarding this patient is airway obstruction. The patient’s complaint of progressive lip swelling, along with her previous diagnosis of hereditary angioedema (HAE), suggests that she may be experiencing an allergic reaction. Angioedema can cause swelling in various parts of the body, including the lips, tongue, and throat. If the swelling progresses and affects the airway, it can lead to difficulty breathing and potentially block the airway completely. This can be a life-threatening emergency and requires immediate intervention to ensure the patient’s airway remains open and they can breathe properly.

Further Reading:

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

Adrenaline is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) once chest compressions have been resumed. The recommended dose is 1 mg, which can be administered as either 10 mL of a 1:10,000 solution or 1 mL of a 1:1000 solution.

Subsequently, adrenaline should be given every 3-5 minutes, alternating with chest compressions. It is important to administer adrenaline without interrupting chest compressions to ensure continuous circulation and maximize the chances of successful resuscitation.

After a cardiac arrest, it is recommended to maintain a mild hypothermia state with a target temperature range of 32-36ºC for at least 24 hours. It is important to avoid fever for a period of 72 hours following the cardiac arrest.

Further Reading:

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

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

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

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

Addison’s disease is characterized by several classical biochemical features. One of these features is an increase in ACTH levels, which is a hormone that stimulates the production of cortisol. Additionally, individuals with Addison’s disease often have elevated serum renin levels, which is an enzyme involved in regulating blood pressure. Another common biochemical feature is hyponatremia, which refers to low levels of sodium in the blood. Hyperkalemia, or high levels of potassium, is also frequently observed in individuals with Addison’s disease. Furthermore, hypercalcemia, an excess of calcium in the blood, may be present. Hypoglycemia, or low blood sugar levels, is another characteristic feature. Lastly, metabolic acidosis, a condition where the body produces too much acid or cannot eliminate it properly, is often seen in individuals with Addison’s disease.

There are several factors that are known to increase the risk of violence from patients. These include being male, being young (under 40 years old), having poor levels of self-care, exhibiting coercive behavior, having a history of prior violent episodes, making multiple attendances to the hospital, being intoxicated with alcohol, and experiencing organic psychosis.

The current algorithm for treating a convulsing child, known as APLS, is as follows:

Step 1 (5 minutes after the start of convulsion):
If a child has been convulsing for 5 minutes or more, they should be given an initial dose of benzodiazepine. This can be administered intravenously (IV) or intraosseously (IO) if vascular access is available. Alternatively, buccal midazolam or rectal diazepam can be given if vascular access is not available.

Step 2 (10 minutes after the start of step 1):
If the convulsion continues for another 10 minutes, a second dose of benzodiazepine should be given. It is also important to seek senior help at this point.

Step 3 (10 minutes after the start of step 2):
At this stage, it is necessary to involve senior medical personnel to reassess the child and provide guidance on further management. The recommended approach is as follows:
– If the child is not already receiving phenytoin, a phenytoin infusion should be initiated. This involves administering 20 mg/kg of phenytoin intravenously over a period of 20 minutes.
– If the child is already taking phenytoin, phenobarbitone can be used instead. The recommended dosage is 20 mg/kg administered intravenously over 20 minutes.
– In the meantime, rectal paraldehyde can be considered at a dose of 0.8 ml/kg of the 50:50 mixture while preparing the infusion.

Step 4 (20 minutes after the start of step 3):
If the child is still experiencing convulsions at this stage, it is crucial to have an anaesthetist present. A rapid sequence induction with thiopental is recommended for further management.

In the case of this specific child who weighs 25 kg and has already received a dose of lorazepam, they should receive a second dose of 0.1 mg/kg, which amounts to 2.5 mg.

Logorrhoea is a form of communication disorder characterized by an excessive use of words and repetitive speech patterns. This condition can result in challenges when it comes to effective communication and may lead to incoherent conversations. Logorrhoea is commonly observed in individuals with frontal lobe disorders and thalamic lesions.

Terlipressin, a vasopressin analogue, has been found to significantly enhance survival rates in cases of acute upper gastrointestinal variceal haemorrhage when compared to a placebo. Alternatively, somatostatin and its analogue octreotide have also demonstrated similar benefits and can be used as alternatives. It is not recommended to administer proton pump inhibitors (PPIs) before endoscopy in cases of acute upper GI bleeds, but they are advised after endoscopy for non-variceal upper GI bleeds. There is no consensus on whether PPIs improve outcomes in variceal bleeding. Recombinant factor Vlla should only be considered if other blood products have failed to correct coagulopathy. Studies indicate that tranexamic acid does not reduce mortality from upper GI bleeding and may actually increase the risk of thromboembolic events.

Further Reading:

Upper gastrointestinal bleeding (UGIB) refers to the loss of blood from the gastrointestinal tract, occurring in the upper part of the digestive system. It can present as haematemesis (vomiting blood), coffee-ground emesis, bright red blood in the nasogastric tube, or melaena (black, tarry stools). UGIB can lead to significant hemodynamic compromise and is a major health burden, accounting for approximately 70,000 hospital admissions each year in the UK with a mortality rate of 10%.

The causes of UGIB vary, with peptic ulcer disease being the most common cause, followed by gastritis/erosions, esophagitis, and other less common causes such as varices, Mallory Weiss tears, and malignancy. Swift assessment, hemodynamic resuscitation, and appropriate interventions are essential for the management of UGIB.

Assessment of patients with UGIB should follow an ABCDE approach, and scoring systems such as the Glasgow-Blatchford bleeding score (GBS) and the Rockall score are recommended to risk stratify patients and determine the urgency of endoscopy. Transfusion may be necessary for patients with massive hemorrhage, and platelet transfusion, fresh frozen plasma (FFP), and prothrombin complex concentrate may be offered based on specific criteria.

Endoscopy plays a crucial role in the management of UGIB. Unstable patients with severe acute UGIB should undergo endoscopy immediately after resuscitation, while all other patients should undergo endoscopy within 24 hours of admission. Endoscopic treatment of non-variceal bleeding may involve mechanical methods of hemostasis, thermal coagulation, or the use of fibrin or thrombin with adrenaline. Proton pump inhibitors should only be used after endoscopy.

Variceal bleeding requires specific management, including the use of terlipressin and prophylactic antibiotics. Oesophageal varices can be treated with band ligation or transjugular intrahepatic portosystemic shunts (TIPS), while gastric varices may be treated with endoscopic injection of N-butyl-2-cyanoacrylate or TIPS if bleeding is not controlled.

For patients taking NSAIDs, aspirin, or clopidogrel, low-dose aspirin can be continued once hemostasis is achieved, NSAIDs should be stopped in patients presenting with UGIB