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

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

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

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

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

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

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.

The most appropriate course of action would be to adhere to the Fraser guidelines. These guidelines consider whether a child under the age of 16 possesses the maturity and understanding to make a reasonable assessment of the benefits and drawbacks of the proposed treatment. They were established following the 1982 Gillick case, which dealt with the prescription of contraception for individuals under 16 years old.

It may also be important to gather more information about the patient’s partner, given her age. However, this is not as crucial as the aforementioned response. It is possible that she may require reassurance regarding the confidentiality of her medical information. However, if her partner is an adult or holds a position of authority, there are circumstances in which breaching confidentiality may be necessary in her best interests.

Requesting that a colleague see her is a potential option, but it does not involve taking on any responsibility yourself. A better approach would have been to discuss the case with a colleague while still being involved in the process.

Insisting that she inform a responsible adult would be a threat to breach her confidentiality, which could have serious implications for any future doctor-patient relationship. It would be wise to suggest that she discuss her situation with a responsible adult, but you cannot compel her to do so.

Refusing to prescribe would be the worst choice, as it neglects the patient’s treatment and fails to consider the potential consequences of her becoming pregnant against her wishes.

Neisseria gonorrhoeae is a type of bacteria that is shaped like two spheres and stains pink when tested. It is responsible for causing the sexually transmitted infection known as gonorrhoea. This infection is most commonly seen in individuals between the ages of 15 and 35, and it is primarily transmitted through sexual contact. One important thing to note is that the gonococcal pili, which are hair-like structures on the bacteria, can change their appearance. This means that even if someone has recovered from a previous infection, they can still be reinfected due to the bacteria’s ability to change.

In men, the clinical signs of gonorrhoea include inflammation of the urethra, which is seen in approximately 80% of cases. Around 50% of men experience pain or discomfort during urination, and a mucopurulent discharge may also be present. Rectal infection is possible, although it is usually asymptomatic. In some cases, it can cause anal discharge. Pharyngitis, or inflammation of the throat, is also possible but typically does not cause any noticeable symptoms.

Women with gonorrhoea may experience a vaginal discharge, which is seen in about 50% of cases. Lower abdominal pain is reported in approximately 25% of women, and dysuria, or painful urination, is seen in 10-15% of cases. Pelvic or lower abdominal tenderness is less common, occurring in less than 5% of women. Additionally, women may have an endocervical discharge and/or bleeding. Similar to men, rectal infection is usually asymptomatic but can cause anal discharge. Pharyngitis is also possible in women, but it is typically asymptomatic.

This presentation strongly indicates a diagnosis of whooping cough, also known as pertussis. Whooping cough is a respiratory infection caused by the bacteria Bordetella pertussis. It is transmitted through respiratory droplets and has an incubation period of about 7-21 days. The disease is highly contagious and can be transmitted to around 90% of close household contacts.

The clinical course of whooping cough can be divided into two stages. The first stage is called the catarrhal stage, which resembles a mild respiratory infection with low-grade fever and symptoms similar to a cold. A cough may be present, but it is usually mild and not as severe as in the second stage. The catarrhal stage typically lasts for about a week.

The second stage is known as the paroxysmal stage. During this stage, the characteristic paroxysmal cough develops as the symptoms from the catarrhal stage start to improve. The coughing occurs in spasms, often preceded by an inspiratory whoop sound, followed by a series of rapid coughs. Vomiting may occur, and patients may develop subconjunctival hemorrhages and petechiae. Patients generally feel well between coughing spasms, and there are usually no abnormal chest findings. This stage can last up to 3 months, with a gradual recovery over this period. The later stages of this stage are sometimes referred to as the convalescent stage.

Complications of whooping cough can include secondary pneumonia, rib fractures, pneumothorax, hernias, syncopal episodes, encephalopathy, and seizures. It is important to note that a history of vaccination does not guarantee immunity, as it only provides about 95% protection.

The presence of marked lymphocytosis in this case also supports a diagnosis of pertussis, as it is a common finding. A lymphocyte count greater than 20 x 109/l is highly suggestive of the disease.

Vestibular neuronitis is characterized by the sudden and prolonged onset of rotational vertigo. This vertigo can occur spontaneously, upon waking up, or gradually worsen throughout the day. It is particularly aggravated by changes in head position, although it remains constant even when the head is still. Unlike other conditions, vestibular neuronitis does not cause hearing loss, tinnitus, or focal neurological deficits. On the other hand, in BPPV, episodes of vertigo are usually brief, lasting less than 20 seconds, and only occur when there is a change in head position.

Further Reading:

Vestibular neuritis, also known as vestibular neuronitis, is a condition characterized by sudden and prolonged vertigo of peripheral origin. It is believed to be caused by inflammation of the vestibular nerve, often following a viral infection. It is important to note that vestibular neuritis and labyrinthitis are not the same condition, as labyrinthitis involves inflammation of the labyrinth. Vestibular neuritis typically affects individuals between the ages of 30 and 60, with a 1:1 ratio of males to females. The annual incidence is approximately 3.5 per 100,000 people, making it one of the most commonly diagnosed causes of vertigo.

Clinical features of vestibular neuritis include nystagmus, which is a rapid, involuntary eye movement, typically in a horizontal or horizontal-torsional direction away from the affected ear. The head impulse test may also be positive. Other symptoms include spontaneous onset of rotational vertigo, which is worsened by changes in head position, as well as nausea, vomiting, and unsteadiness. These severe symptoms usually last for 2-3 days, followed by a gradual recovery over a few weeks. It is important to note that hearing is not affected in vestibular neuritis, and symptoms such as tinnitus and focal neurological deficits are not present.

Differential diagnosis for vestibular neuritis includes benign paroxysmal positional vertigo (BPPV), labyrinthitis, Meniere’s disease, migraine, stroke, and cerebellar lesions. Management of vestibular neuritis involves drug treatment for nausea and vomiting associated with vertigo, typically through short courses of medication such as prochlorperazine or cyclizine. If symptoms are severe and fluids cannot be tolerated, admission and administration of IV fluids may be necessary. General advice should also be given, including avoiding driving while symptomatic, considering the suitability to work based on occupation and duties, and the increased risk of falls. Follow-up is required, and referral is necessary if there are atypical symptoms, symptoms do not improve after a week of treatment, or symptoms persist for more than 6 weeks.

The prognosis for vestibular neuritis is generally good, with the majority of individuals fully recovering within 6 weeks. Recurrence is thought to occur in 2-11% of cases, and approximately 10% of individuals may develop BPPV following an episode of vestibular neuritis. A very rare complication of vestibular neuritis is ph

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

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

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

Phenoxymethylpenicillin is the preferred antibiotic for treating streptococcal sore throat, especially in patients with a CENTOR score of 3/4 and a FeverPAIN score of 4/5. In such cases, antibiotics are necessary to effectively treat the infection.

Further Reading:

Pharyngitis and tonsillitis are common conditions that cause inflammation in the throat. Pharyngitis refers to inflammation of the oropharynx, which is located behind the soft palate, while tonsillitis refers to inflammation of the tonsils. These conditions can be caused by a variety of pathogens, including viruses and bacteria. The most common viral causes include rhinovirus, coronavirus, parainfluenza virus, influenza types A and B, adenovirus, herpes simplex virus type 1, and Epstein Barr virus. The most common bacterial cause is Streptococcus pyogenes, also known as Group A beta-hemolytic streptococcus (GABHS). Other bacterial causes include Group C and G beta-hemolytic streptococci and Fusobacterium necrophorum.

Group A beta-hemolytic streptococcus is the most concerning pathogen as it can lead to serious complications such as rheumatic fever and glomerulonephritis. These complications can occur due to an autoimmune reaction triggered by antigen/antibody complex formation or from cell damage caused by bacterial exotoxins.

When assessing a patient with a sore throat, the clinician should inquire about the duration and severity of the illness, as well as associated symptoms such as fever, malaise, headache, and joint pain. It is important to identify any red flags and determine if the patient is immunocompromised. Previous non-suppurative complications of Group A beta-hemolytic streptococcus infection should also be considered, as there is an increased risk of further complications with subsequent infections.

Red flags that may indicate a more serious condition include severe pain, neck stiffness, or difficulty swallowing. These symptoms may suggest epiglottitis or a retropharyngeal abscess, which require immediate attention.

To determine the likelihood of a streptococcal infection and the need for antibiotic treatment, two scoring systems can be used: CENTOR and FeverPAIN. The CENTOR criteria include tonsillar exudate, tender anterior cervical lymphadenopathy or lymphadenitis, history of fever, and absence of cough. The FeverPAIN criteria include fever, purulence, rapid onset of symptoms, severely inflamed tonsils, and absence of cough or coryza. Based on the scores from these criteria, the likelihood of a streptococcal infection can be estimated, and appropriate management can be undertaken.

The recommended dose of etomidate for rapid sequence intubation (RSI) is typically 0.3mg per kilogram of body weight. For example, a patient weighing 70 kilograms would receive a dose of 21mg (70 x 0.3 = 21mg). This dosage falls within the accepted range of 0.15-0.3 mg/kg as suggested by the British National Formulary (BNF). Therefore, the only option within this range is the fourth option.

Further Reading:

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

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

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

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

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

Congenital adrenal hyperplasia (CAH) is a group of inherited disorders that are caused by autosomal recessive genes. The majority of affected patients, over 90%, have a deficiency of the enzyme 21-hydroxylase. This enzyme is encoded by the 21-hydroxylase gene, which is located on chromosome 6p21 within the HLA histocompatibility complex. The second most common cause of CAH is a deficiency of the enzyme 11-beta-hydroxylase. The condition is rare, with an incidence of approximately 1 in 500 births in the UK. It is more prevalent in the offspring of consanguineous marriages.

The deficiency of 21-hydroxylase leads to a deficiency of cortisol and/or aldosterone, as well as an excess of precursor steroids. As a result, there is an increased secretion of ACTH from the anterior pituitary, leading to adrenocortical hyperplasia.

The severity of CAH varies depending on the degree of 21-hydroxylase deficiency. Female infants often exhibit ambiguous genitalia, such as clitoral hypertrophy and labial fusion. Male infants may have an enlarged scrotum and/or scrotal pigmentation. Hirsutism, or excessive hair growth, occurs in 10% of cases.

Boys with CAH often experience a salt-losing adrenal crisis at around 1-3 weeks of age. This crisis is characterized by symptoms such as vomiting, weight loss, floppiness, and circulatory collapse.

The diagnosis of CAH can be made by detecting markedly elevated levels of the metabolic precursor 17-hydroxyprogesterone. Neonatal screening is possible through the detection of persistently elevated 17-hydroxyprogesterone.

In infants presenting with a salt-losing crisis, the following biochemical abnormalities are typically observed: hyponatremia (low sodium levels), hyperkalemia (high potassium levels), metabolic acidosis, and hypoglycemia.

Boys experiencing a salt-losing crisis will require fluid resuscitation, intravenous dextrose, and intravenous hydrocortisone. Affected females may require corrective surgery for their external genitalia. However, they have an intact uterus and ovaries and are able to have children.

The long-term management of CAH involves lifelong replacement of hydrocortisone to suppress ACTH levels.

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

Pyloric stenosis is a condition that primarily affects infants and is often seen in those with a positive family history. It is more commonly observed in first-born children and those who were bottle-fed or delivered by c-section. Additionally, it is more prevalent in white and hispanic children compared to other races and ethnicities. Smoking during pregnancy and premature birth are also associated with an increased risk of developing pyloric stenosis.

Further Reading:

Pyloric stenosis is a condition that primarily affects infants, characterized by the thickening of the muscles in the pylorus, leading to obstruction of the gastric outlet. It typically presents between the 3rd and 12th weeks of life, with recurrent projectile vomiting being the main symptom. The condition is more common in males, with a positive family history and being first-born being additional risk factors. Bottle-fed children and those delivered by c-section are also more likely to develop pyloric stenosis.

Clinical features of pyloric stenosis include projectile vomiting, usually occurring about 30 minutes after a feed, as well as constipation and dehydration. A palpable mass in the upper abdomen, often described as like an olive, may also be present. The persistent vomiting can lead to electrolyte disturbances, such as hypochloremia, alkalosis, and mild hypokalemia.

Ultrasound is the preferred diagnostic tool for confirming pyloric stenosis. It can reveal specific criteria, including a pyloric muscle thickness greater than 3 mm, a pylorus longitudinal length greater than 15-17 mm, a pyloric volume greater than 1.5 cm3, and a pyloric transverse diameter greater than 13 mm.

The definitive treatment for pyloric stenosis is pyloromyotomy, a surgical procedure that involves making an incision in the thickened pyloric muscle to relieve the obstruction. Before surgery, it is important to correct any hypovolemia and electrolyte disturbances with intravenous fluids. Overall, pyloric stenosis is a relatively common condition in infants, but with prompt diagnosis and appropriate management, it can be effectively treated.

Febrile transfusion reactions, also known as non-haemolytic transfusion reactions, occur when there is an unexpected increase in body temperature (≥ 38ºC or ≥ 1ºC above the baseline, if the baseline is ≥ 37ºC) during or shortly after a blood transfusion. This temperature rise is usually the only symptom, although sometimes it may be accompanied by chills.

Febrile transfusion reactions are the most common type of transfusion reaction, happening in approximately 1 out of every 8 transfusions.

The main cause of febrile transfusion reactions is believed to be the accumulation of cytokines during the storage of blood components, particularly in platelet units. Cytokines are substances released by white blood cells, and the risk of symptoms can be reduced by removing these cells before storage.

In addition to cytokine accumulation, febrile transfusion reactions can also be triggered by recipient antibodies that have been produced as a result of previous transfusions or pregnancies. These antibodies react to specific antigens, such as human leukocyte antigen (HLA), found on the donor’s lymphocytes, granulocytes, or platelets.

Treatment for febrile transfusion reactions is mainly supportive. Other potential causes of fever should be ruled out, and antipyretic medications like paracetamol can be used to reduce the fever. If another cause is suspected, the transfusion should be temporarily stopped, but it can be resumed at a slower rate once other potential causes of fever have been ruled out.

Patients with mitral regurgitation can go for extended periods without experiencing any symptoms. They may have a normal exercise tolerance and show no signs of congestive cardiac failure. However, when cardiac failure does occur, patients often complain of breathlessness, especially during physical exertion. They may also experience fatigue, difficulty breathing while lying flat (orthopnoea), and sudden episodes of difficulty breathing at night (paroxysmal nocturnal dyspnoea).

In terms of clinical signs, mitral regurgitation can be identified through various indicators. These include a displaced and volume loaded apex beat, which can be felt during a physical examination. A palpable thrill may also be detected at the apex. Additionally, a pansystolic murmur, which is loudest at the apex and radiates to the axilla, can be heard. This murmur is typically most pronounced when the patient holds their breath during expiration. Furthermore, a soft first heart sound and signs of left ventricular failure may be present.

A threatened miscarriage is characterized by bleeding in the first trimester of pregnancy, but without the passing of any products of conception and with a closed cervical os. The main features of a threatened miscarriage include vaginal bleeding, often in the form of brown discharge or spotting, minimal abdominal pain, and a positive pregnancy test. It is important for stable patients who are more than 6 weeks pregnant and experiencing bleeding in early pregnancy, without any signs of an ectopic pregnancy, to seek follow-up care at an early pregnancy assessment unit (EPAU).

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.

Adrenal insufficiency, also known as Addison’s disease, is a condition that is more frequently observed in women and typically manifests in individuals aged 30-50 years. In the UK alone, nearly 9000 individuals have received a diagnosis for this disorder. While it can affect people of all ages, it predominantly occurs in women and those within the 30-50 age range.

Further Reading:

Addison’s disease, also known as primary adrenal insufficiency or hypoadrenalism, is a rare disorder caused by the destruction of the adrenal cortex. This leads to reduced production of glucocorticoids, mineralocorticoids, and adrenal androgens. The deficiency of cortisol results in increased production of adrenocorticotropic hormone (ACTH) due to reduced negative feedback to the pituitary gland. This condition can cause metabolic disturbances such as hyperkalemia, hyponatremia, hypercalcemia, and hypoglycemia.

The symptoms of Addison’s disease can vary but commonly include fatigue, weight loss, muscle weakness, and low blood pressure. It is more common in women and typically affects individuals between the ages of 30-50. The most common cause of primary hypoadrenalism in developed countries is autoimmune destruction of the adrenal glands. Other causes include tuberculosis, adrenal metastases, meningococcal septicaemia, HIV, and genetic disorders.

The diagnosis of Addison’s disease is often suspected based on low cortisol levels and electrolyte abnormalities. The adrenocorticotropic hormone stimulation test is commonly used for confirmation. Other investigations may include adrenal autoantibodies, imaging scans, and genetic screening.

Addisonian crisis is a potentially life-threatening condition that occurs when there is an acute deficiency of cortisol and aldosterone. It can be the first presentation of undiagnosed Addison’s disease. Precipitating factors of an Addisonian crisis include infection, dehydration, surgery, trauma, physiological stress, pregnancy, hypoglycemia, and acute withdrawal of long-term steroids. Symptoms of an Addisonian crisis include malaise, fatigue, nausea or vomiting, abdominal pain, fever, muscle pains, dehydration, confusion, and loss of consciousness.

There is no fixed consensus on diagnostic criteria for an Addisonian crisis, as symptoms are non-specific. Investigations may include blood tests, blood gas analysis, and septic screens if infection is suspected. Management involves administering hydrocortisone and fluids. Hydrocortisone is given parenterally, and the dosage varies depending on the age of the patient. Fluid resuscitation with saline is necessary to correct any electrolyte disturbances and maintain blood pressure. The underlying cause of the crisis should also be identified and treated. Close monitoring of sodium levels is important to prevent complications such as osmotic demyelination syndrome.

Early assessment of the airway is a critical aspect of managing a burned patient. Airway obstruction can occur rapidly due to direct injury or swelling from the burn. If there is a history of trauma, the airway should be evaluated while maintaining cervical spine control.

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

In cases where significant swelling is anticipated, it may be necessary to urgently secure the airway with an uncut endotracheal tube before the swelling becomes severe. Delaying recognition of impending airway obstruction can make intubation difficult, and a surgical airway may be required.

The American Burn Life Support (ABLS) guidelines recommend early intubation in certain situations. These include signs of airway obstruction, extensive burns, deep facial burns, burns inside the mouth, significant swelling or risk of swelling, difficulty swallowing, respiratory compromise, decreased level of consciousness, and anticipated transfer of a patient with a large burn and airway issues without qualified personnel to intubate during transport.

Circumferential burns of the neck can cause tissue swelling around the airway, making early intubation necessary in these cases as well.

The patient in this case has been diagnosed with type 1 autoimmune hepatitis, also known as classic type autoimmune hepatitis. This condition is characterized by inflammation of the liver due to reduced levels of regulatory T-cells (Treg cells), leading to the production of autoantibodies against hepatocyte surface antigens. It primarily affects women (70%) between the ages of 15 and 40.

Autoimmune hepatitis causes chronic and progressive hepatitis, which eventually progresses to cirrhosis. Patients typically experience non-specific symptoms of malaise, but in some cases, the disease may present in its later stages with jaundice and severe illness. During this stage, liver function tests often show significantly elevated transaminases (ALT and AST), usually more than ten times the normal levels, and a normal or slightly elevated alkaline phosphatase (ALP). Around 80% of cases show positive antinuclear antibodies (ANA), while approximately 70% show positive smooth muscle antibodies (SMA). Antimitochondrial antibodies are usually low or absent.

There are four recognized subtypes of autoimmune hepatitis:
1. Type 1 (Classic type): Positive ANA and SMA, and grossly elevated IgG
2. Type 2: Positive liver kidney microsomal antibodies (affects children)
3. Type 3: Positive soluble liver antigen antibodies
4. Type 4: Seronegative

Treatment for autoimmune hepatitis involves the use of corticosteroids and/or azathioprine. Remission can be achieved in approximately 70% of cases. In some cases where drug therapy is not effective, liver transplantation may be necessary.

Primary sclerosing cholangitis (PSC) is a condition that affects the bile ducts, causing progressive inflammation and obstruction. It is characterized by recurrent episodes of cholangitis and progressive scarring of the bile ducts. PSC can ultimately lead to liver cirrhosis, liver failure, and hepatocellular carcinoma. There is a known association between PSC and ulcerative colitis, with more than 80% of PSC patients also having ulcerative colitis.

Primary biliary cirrhosis (PBC) is an autoimmune disease that results in the progressive destruction of the small bile ducts in the liver, primarily affecting the intralobular ducts. This leads to cholestatic jaundice, liver fibrosis, and eventually cirrhosis. PBC is more common in females (90%)

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

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

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

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

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

The effects of adrenaline on alpha-adrenergic receptors result in the narrowing of blood vessels throughout the body, leading to increased pressure in the coronary and cerebral arteries. On the other hand, the effects of adrenaline on beta-adrenergic receptors enhance the strength of the heart’s contractions and increase the heart rate, which can potentially improve blood flow to the coronary and cerebral arteries. However, it is important to note that these positive effects may be counteracted by the simultaneous increase in oxygen consumption by the heart, the occurrence of abnormal heart rhythms, reduced oxygen levels due to abnormal blood flow patterns, impaired small blood vessel function, and worsened heart function following a cardiac arrest.

Registered medical practitioners in England and Wales are legally obligated to inform a designated official from the Local Authority if they suspect a patient has contracted specific infectious diseases. For more information on which diseases and their causative organisms require reporting, please refer to the following resource: Notifiable diseases and causative organisms: how to report.

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.

Bleeding in a confirmed early pregnancy, along with adnexal tenderness and cervical motion tenderness, is indicative of an ectopic pregnancy until proven otherwise. The amount of bleeding caused by an ectopic pregnancy can range from no bleeding or slight spotting to a level similar to a normal menstrual period. It is important to note that 90% of patients with an ectopic pregnancy experience abdominal pain. Other clinical features that may be present include shoulder tip pain, which is caused by irritation of the diaphragm, as well as adnexal tenderness, cervical motion tenderness, rebound tenderness, guarding, and adnexal masses in some cases. Additionally, hypotension and shock may occur.

The recommended dose of rectal diazepam for treating a child experiencing convulsions is 0.5 mg per kilogram of body weight.

A PaO2/FiO2 ratio ranging from 100 mmHg to 200 mmHg indicates the presence of moderate Acute Respiratory Distress Syndrome (ARDS).

Further Reading:

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

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

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

The first-line treatment for Addisonian (adrenal) crisis is hydrocortisone. This patient displays symptoms that indicate an Addisonian crisis, and the main components of their management involve administering hydrocortisone and providing intravenous fluids for resuscitation.

Further Reading:

Addison’s disease, also known as primary adrenal insufficiency or hypoadrenalism, is a rare disorder caused by the destruction of the adrenal cortex. This leads to reduced production of glucocorticoids, mineralocorticoids, and adrenal androgens. The deficiency of cortisol results in increased production of adrenocorticotropic hormone (ACTH) due to reduced negative feedback to the pituitary gland. This condition can cause metabolic disturbances such as hyperkalemia, hyponatremia, hypercalcemia, and hypoglycemia.

The symptoms of Addison’s disease can vary but commonly include fatigue, weight loss, muscle weakness, and low blood pressure. It is more common in women and typically affects individuals between the ages of 30-50. The most common cause of primary hypoadrenalism in developed countries is autoimmune destruction of the adrenal glands. Other causes include tuberculosis, adrenal metastases, meningococcal septicaemia, HIV, and genetic disorders.

The diagnosis of Addison’s disease is often suspected based on low cortisol levels and electrolyte abnormalities. The adrenocorticotropic hormone stimulation test is commonly used for confirmation. Other investigations may include adrenal autoantibodies, imaging scans, and genetic screening.

Addisonian crisis is a potentially life-threatening condition that occurs when there is an acute deficiency of cortisol and aldosterone. It can be the first presentation of undiagnosed Addison’s disease. Precipitating factors of an Addisonian crisis include infection, dehydration, surgery, trauma, physiological stress, pregnancy, hypoglycemia, and acute withdrawal of long-term steroids. Symptoms of an Addisonian crisis include malaise, fatigue, nausea or vomiting, abdominal pain, fever, muscle pains, dehydration, confusion, and loss of consciousness.

There is no fixed consensus on diagnostic criteria for an Addisonian crisis, as symptoms are non-specific. Investigations may include blood tests, blood gas analysis, and septic screens if infection is suspected. Management involves administering hydrocortisone and fluids. Hydrocortisone is given parenterally, and the dosage varies depending on the age of the patient. Fluid resuscitation with saline is necessary to correct any electrolyte disturbances and maintain blood pressure. The underlying cause of the crisis should also be identified and treated. Close monitoring of sodium levels is important to prevent complications such as osmotic demyelination syndrome.

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%)

The traffic light system is a useful tool for evaluating the potential risk of serious illness in children. This system categorizes clinical features into three groups based on severity: red (high-risk), amber (intermediate-risk), and green (low-risk).

Children displaying any of the following symptoms or signs fall into the high-risk group for serious illness: pale/mottled/ashen/blue skin, lips or tongue; lack of response to social cues; appearing unwell to a healthcare professional; inability to wake or stay awake when roused; weak, high-pitched, or continuous cry; grunting; respiratory rate exceeding 60 breaths per minute; moderate or severe chest indrawing; reduced skin turgor; and bulging fontanelle.

Children exhibiting any of the following symptoms or signs are considered at least intermediate-risk for serious illness: pallor of skin, lips or tongue reported by parent or caregiver; abnormal response to social cues; absence of a smile; waking only with prolonged stimulation; decreased activity; nasal flaring; dry mucous membranes; poor feeding in infants; reduced urine output; and rigors.

Children displaying any of the following symptoms or signs are classified as low-risk for serious illness: normal color of skin, lips, and tongue; normal response to social cues; contentment and smiles; staying awake or quickly awakening; strong normal cry or absence of crying; normal skin and eyes; and moist mucous membranes.

To summarize, children with fever and any symptoms or signs in the red column are considered high-risk, while those with fever and any symptoms or signs in the amber column (but none in the red column) are considered intermediate-risk. Children with symptoms and signs in the green column (and none in the amber or red columns) are classified as low-risk.

For more information, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

Croup is identified by a cough that sounds like a seal barking, especially worse during the night. Before the barking cough, there may be initial symptoms of a cough, runny nose, and congestion for 12 to 72 hours. Other signs of croup include a high-pitched sound when breathing (stridor), difficulty breathing (respiratory distress), and fever.

Further Reading:

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

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

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

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

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

A normal CD4 count ranges from 500-1000 cells/mm3. In individuals diagnosed with HIV, the CD4 count is typically monitored every 3-6 months. It is important to note that the CD4 count can fluctuate on a daily basis and can be influenced by the timing of the blood test as well as the presence of other infections or illnesses.

When the CD4 count falls below 350 cells/mm3, it is recommended to consider starting antiretroviral therapy. A CD4 count below 200 cells/mm3 is indicative of advanced HIV disease, also known as AIDS defining.

CAGE, AUDIT, and T-ACE are all tools used to screen for alcohol misuse. The CAGE tool is the most commonly used by clinicians and consists of four simple questions. It is easy to remember and effective in identifying potential alcohol-related issues. The CAGE questionnaire asks if the individual has ever felt the need to cut down on their drinking, if others have criticized their drinking, if they have felt guilty about their drinking, and if they have ever had a drink first thing in the morning to alleviate a hangover or calm their nerves. A score of 2 or 3 suggests a high likelihood of alcoholism, while a score of 4 is almost diagnostic.

T-ACE is specifically designed to screen for alcohol abuse in pregnant women. It helps identify potential issues and allows for appropriate intervention and support.

The AUDIT tool is a more comprehensive questionnaire consisting of 10 points. It is typically used after initial screening and provides a more detailed assessment of alcohol consumption and potential dependency. The AUDIT-C, a simplified version of the AUDIT tool, is often used in primary care settings. It consists of three questions and is a quick and effective way to assess alcohol-related concerns.

While asking patients about their alcohol intake can provide some insight into excessive drinking, the screening tools are specifically designed to assess alcohol dependence and hazardous drinking. They offer a more comprehensive evaluation and help healthcare professionals identify individuals who may require further intervention or support.

It is important to note that advising patients on the harmful effects of alcohol is a valuable component of brief interventions. However, it is not as effective as using screening tools to identify potential alcohol-related issues.

Severe aortic stenosis is characterized by several distinct features. These include a narrow pulse pressure, which refers to the difference between the systolic and diastolic blood pressure readings. Additionally, individuals with severe aortic stenosis may exhibit a slow rising pulse, meaning that the pulse wave takes longer to reach its peak. Another common feature is a delayed ejection systolic murmur, which is a heart sound that occurs during the ejection phase of the cardiac cycle. The second heart sound (S2) may also be soft or absent in individuals with severe aortic stenosis. Another potential finding is the presence of an S4 heart sound, which occurs during the filling phase of the cardiac cycle. A thrill, which is a palpable vibration, may also be felt in severe cases. The duration of the murmur, as well as the presence of left ventricular hypertrophy or failure, are additional features that may be observed in individuals with severe aortic stenosis.

Further Reading:

Valvular heart disease refers to conditions that affect the valves of the heart. In the case of aortic valve disease, there are two main conditions: aortic regurgitation and aortic stenosis.

Aortic regurgitation is characterized by an early diastolic murmur, a collapsing pulse (also known as a water hammer pulse), and a wide pulse pressure. In severe cases, there may be a mid-diastolic Austin-Flint murmur due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams. The first and second heart sounds (S1 and S2) may be soft, and S2 may even be absent. Additionally, there may be a hyperdynamic apical pulse. Causes of aortic regurgitation include rheumatic fever, infective endocarditis, connective tissue diseases like rheumatoid arthritis and systemic lupus erythematosus, and a bicuspid aortic valve. Aortic root diseases such as aortic dissection, spondyloarthropathies like ankylosing spondylitis, hypertension, syphilis, and genetic conditions like Marfan’s syndrome and Ehler-Danlos syndrome can also lead to aortic regurgitation.

Aortic stenosis, on the other hand, is characterized by a narrow pulse pressure, a slow rising pulse, and a delayed ESM (ejection systolic murmur). The second heart sound (S2) may be soft or absent, and there may be an S4 (atrial gallop) that occurs just before S1. A thrill may also be felt. The duration of the murmur is an important factor in determining the severity of aortic stenosis. Causes of aortic stenosis include degenerative calcification (most common in older patients), a bicuspid aortic valve (most common in younger patients), William’s syndrome (supravalvular aortic stenosis), post-rheumatic disease, and subvalvular conditions like hypertrophic obstructive cardiomyopathy (HOCM).

Management of aortic valve disease depends on the severity of symptoms. Asymptomatic patients are generally observed, while symptomatic patients may require valve replacement. Surgery may also be considered for asymptomatic patients with a valvular gradient greater than 40 mmHg and features such as left ventricular systolic dysfunction. Balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement.

TBSA, or Total Body Surface Area, is a method commonly used to estimate the size of small burns and very large burns by including the area of unburnt skin. However, it is not considered a reliable method for medium-sized burns.

Further Reading:

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

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

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

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

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

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

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

The current guidelines from NICE provide recommendations for managing low back pain. It is suggested to consider using oral non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, while taking into account the potential risks of gastrointestinal, liver, and cardio-renal toxicity, as well as the person’s individual risk factors and age. When prescribing oral NSAIDs, it is important to conduct appropriate clinical assessments, monitor risk factors regularly, and consider the use of gastroprotective treatment. It is advised to prescribe the lowest effective dose of oral NSAIDs for the shortest duration possible. In cases where NSAIDs are contraindicated, not tolerated, or ineffective, weak opioids (with or without paracetamol) may be considered for managing acute low back pain. However, NICE does not recommend the use of paracetamol alone, opioids for chronic low back pain, serotonin reuptake inhibitors, serotonin-noradrenaline reuptake inhibitors, tricyclic antidepressants for non-neuropathic pain, anticonvulsants, or benzodiazepines for muscle spasm associated with acute low back pain. For more information, you can refer to the NICE guidance on low back pain and sciatica in individuals over 16 years old, as well as the NICE Clinical Knowledge Summary on low back pain without radiculopathy.

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.

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

Further Reading:

Cirrhosis is a condition where the liver undergoes structural changes, resulting in dysfunction of its normal functions. It can be classified as either compensated or decompensated. Compensated cirrhosis refers to a stage where the liver can still function effectively with minimal symptoms, while decompensated cirrhosis is when the liver damage is severe and clinical complications are present.

Cirrhosis develops over a period of several years due to repeated insults to the liver. Risk factors for cirrhosis include alcohol misuse, hepatitis B and C infection, obesity, type 2 diabetes, autoimmune liver disease, genetic conditions, certain medications, and other rare conditions.

The prognosis of cirrhosis can be assessed using the Child-Pugh score, which predicts mortality based on parameters such as bilirubin levels, albumin levels, INR, ascites, and encephalopathy. The score ranges from A to C, with higher scores indicating a poorer prognosis.

Complications of cirrhosis include portal hypertension, ascites, hepatic encephalopathy, variceal hemorrhage, increased infection risk, hepatocellular carcinoma, and cardiovascular complications.

Diagnosis of cirrhosis is typically done through liver function tests, blood tests, viral hepatitis screening, and imaging techniques such as transient elastography or acoustic radiation force impulse imaging. Liver biopsy may also be performed in some cases.

Management of cirrhosis involves treating the underlying cause, controlling risk factors, and monitoring for complications. Complications such as ascites, spontaneous bacterial peritonitis, oesophageal varices, and hepatic encephalopathy require specific management strategies.

Overall, cirrhosis is a progressive condition that requires ongoing monitoring and management to prevent further complications and improve outcomes for patients.

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

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

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

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

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

Femoral shaft fractures are quite common among children and have a significant impact on both the child and their family. It is important to carefully examine children with these fractures for any associated injuries, such as soft-tissue injury, head trauma, or additional fractures. In fact, up to 40% of children who experience a femoral shaft fracture due to high-energy trauma may have these associated injuries. Additionally, a thorough neurovascular examination should be conducted.

Rapidly immobilizing the limb is crucial for managing pain and limiting further blood loss from the fracture. For distal femoral shaft fractures, well-padded long leg splints with split plaster casts can be applied. However, for more proximal shaft fractures, long leg splints alone may not provide adequate control. In these cases, skin traction is a better option. Skin traction involves attaching a large foam pad to the patient’s lower leg using spray adhesive. A weight, approximately 10% of the child’s body weight, is then applied to the foam pad and allowed to hang over the foot of the bed. This constant longitudinal traction helps keep the bone fragments aligned.

When children experience severe pain, it is important to manage it aggressively yet safely. Immobilizing the fracture can provide significant relief. The Royal College of Emergency Medicine recommends other pain control measures for children, such as intranasal diamorphine (0.1 mg/kg in 0.2 ml sterile water), intravenous morphine (0.1-0.2 mg/kg), and oral analgesia (e.g., paracetamol 20 mg/kg, max 1 g, and ibuprofen 10 mg/kg, max 400 mg).

There is no indication for an independent psychiatric evaluation of this patient. However, it is important to clearly document in his medical records that you have assessed his mental capacity and determined that he is capable of making decisions. It would not be appropriate in this case to refer him to a specialist against his wishes or to breach confidentiality by discussing his illness with his family or next of kin. According to the guidelines set by the General Medical Council (GMC), it is necessary to document the fact that the patient has declined relevant information. It is also important to avoid pressuring the patient to change their mind in these circumstances.

For further information, please refer to the GMC guidelines on treatment and care towards the end of life: good practice in decision making.

After the fluid restriction period, the urine is checked to determine if it remains relatively dilute (less than 600 mOsm/kg). If it does, desmopressin is administered and the urine is rechecked to see if it responds and becomes more concentrated.

If the urine osmolality significantly increases after desmopressin, it indicates that the kidneys have responded appropriately to the medication and the urine has concentrated. This suggests that the patient is not producing ADH in response to water loss, indicating cranial DI.

It is important to note that some units may use a lower cut-off of greater than 600 mOsm/kg instead of 800 mOsm/kg.

Further Reading:

Diabetes insipidus (DI) is a condition characterized by either a decrease in the secretion of antidiuretic hormone (cranial DI) or insensitivity to antidiuretic hormone (nephrogenic DI). Antidiuretic hormone, also known as arginine vasopressin, is produced in the hypothalamus and released from the posterior pituitary. The typical biochemical disturbances seen in DI include elevated plasma osmolality, low urine osmolality, polyuria, and hypernatraemia.

Cranial DI can be caused by various factors such as head injury, CNS infections, pituitary tumors, and pituitary surgery. Nephrogenic DI, on the other hand, can be genetic or result from electrolyte disturbances or the use of certain drugs. Symptoms of DI include polyuria, polydipsia, nocturia, signs of dehydration, and in children, irritability, failure to thrive, and fatigue.

To diagnose DI, a 24-hour urine collection is done to confirm polyuria, and U&Es will typically show hypernatraemia. High plasma osmolality with low urine osmolality is also observed. Imaging studies such as MRI of the pituitary, hypothalamus, and surrounding tissues may be done, as well as a fluid deprivation test to evaluate the response to desmopressin.

Management of cranial DI involves supplementation with desmopressin, a synthetic form of arginine vasopressin. However, hyponatraemia is a common side effect that needs to be monitored. In nephrogenic DI, desmopressin supplementation is usually not effective, and management focuses on ensuring adequate fluid intake to offset water loss and monitoring electrolyte levels. Causative drugs need to be stopped, and there is a risk of developing complications such as hydroureteronephrosis and an overdistended bladder.

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.

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

The FeverPAIN score is a scoring system recommended by the current NICE guidelines for assessing acute sore throats. It consists of five items: fever in the last 24 hours, purulence, attendance within three days, inflamed tonsils, and no cough or coryza. Based on the score, recommendations for antibiotic use are as follows: a score of 0-1 indicates an unlikely streptococcal infection, with antibiotics not recommended; a score of 2-3 suggests a 34-40% chance of streptococcus, and delayed prescribing of antibiotics may be considered; a score of 4 or higher indicates a 62-65% chance of streptococcus, and immediate antibiotic use is recommended for severe cases, or a short back-up prescription may be given for 48 hours.

The Fever PAIN score was developed through a study involving 1760 adults and children aged three and over. It was tested in a trial comparing three prescribing strategies: empirical delayed prescribing, score-directed prescribing, and a combination of the score with a near-patient test (NPT) for streptococcus. The use of the score resulted in faster symptom resolution and reduced antibiotic prescribing by one third. The addition of the NPT did not provide any additional benefit.

According to the current NICE guidelines, if antibiotics are necessary, phenoxymethylpenicillin is recommended as the first-choice antibiotic. In cases of true penicillin allergy, clarithromycin can be used as an alternative. For pregnant women with a penicillin allergy, erythromycin is prescribed. It is important to note that the threshold for prescribing antibiotics should be lower for individuals at risk of rheumatic fever and vulnerable groups managed in primary care, such as infants, the elderly, and those who are immunosuppressed or immunocompromised. Antibiotics should not be withheld if the person has severe symptoms and there are concerns about their clinical condition.

If a polytrauma patient with a penetrating chest injury has an expanding cardiac tamponade that is left untreated, it can potentially lead to pulseless electrical activity.

Further Reading:

Cardiac tamponade, also known as pericardial tamponade, occurs when fluid accumulates in the pericardial sac and compresses the heart, leading to compromised blood flow. Classic clinical signs of cardiac tamponade include distended neck veins, hypotension, muffled heart sounds, and pulseless electrical activity (PEA). Diagnosis is typically done through a FAST scan or an echocardiogram.

Management of cardiac tamponade involves assessing for other injuries, administering IV fluids to reduce preload, performing pericardiocentesis (inserting a needle into the pericardial cavity to drain fluid), and potentially performing a thoracotomy. It is important to note that untreated expanding cardiac tamponade can progress to PEA cardiac arrest.

Pericardiocentesis can be done using the subxiphoid approach or by inserting a needle between the 5th and 6th intercostal spaces at the left sternal border. Echo guidance is the gold standard for pericardiocentesis, but it may not be available in a resuscitation situation. Complications of pericardiocentesis include ST elevation or ventricular ectopics, myocardial perforation, bleeding, pneumothorax, arrhythmia, acute pulmonary edema, and acute ventricular dilatation.

It is important to note that pericardiocentesis is typically used as a temporary measure until a thoracotomy can be performed. Recent articles published on the RCEM learning platform suggest that pericardiocentesis has a low success rate and may delay thoracotomy, so it is advised against unless there are no other options available.

Hypothyroidism often presents with various clinical features. These include weight gain, lethargy, intolerance to cold temperatures, non-pitting edema (such as swelling in the hands and face), dry skin, hair thinning and loss, loss of the outer part of the eyebrows, decreased appetite, constipation, decreased deep tendon reflexes, carpal tunnel syndrome, and menorrhagia.

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.

Tenecteplase is a medication known as a tissue plasminogen activator (tPA). Its main mechanism of action involves binding specifically to fibrin and converting plasminogen into plasmin. This process leads to the breakdown of the fibrin matrix and promotes reperfusion at the affected site. Among the options provided, Tenecteplase is the sole drug that primarily acts by facilitating reperfusion.

For patients suspected of having acute coronary syndromes (ACS), it is recommended that they receive 300 mg of aspirin and pain relief in the form of glyceryl trinitrate (GTN) with the option of intravenous opioids such as morphine. However, if the patient is pain-free after taking GTN, there is no need to administer morphine. The next steps in medical management or intervention will be determined once the diagnosis is confirmed.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

Congenital adrenal hyperplasia (CAH) is a group of inherited disorders that are caused by autosomal recessive genes. The majority of affected patients, over 90%, have a deficiency of the enzyme 21-hydroxylase. This enzyme is encoded by the 21-hydroxylase gene, which is located on chromosome 6p21 within the HLA histocompatibility complex. The second most common cause of CAH is a deficiency of the enzyme 11-beta-hydroxylase. The condition is rare, with an incidence of approximately 1 in 500 births in the UK. It is more prevalent in the offspring of consanguineous marriages.

The deficiency of 21-hydroxylase leads to a deficiency of cortisol and/or aldosterone, as well as an excess of precursor steroids. As a result, there is an increased secretion of ACTH from the anterior pituitary, leading to adrenocortical hyperplasia.

The severity of CAH varies depending on the degree of 21-hydroxylase deficiency. Female infants often exhibit ambiguous genitalia, such as clitoral hypertrophy and labial fusion. Male infants may have an enlarged scrotum and/or scrotal pigmentation. Hirsutism, or excessive hair growth, occurs in 10% of cases.

Boys with CAH often experience a salt-losing adrenal crisis at around 1-3 weeks of age. This crisis is characterized by symptoms such as vomiting, weight loss, floppiness, and circulatory collapse.

The diagnosis of CAH can be made by detecting markedly elevated levels of the metabolic precursor 17-hydroxyprogesterone. Neonatal screening is possible, primarily through the identification of persistently elevated 17-hydroxyprogesterone levels.

In infants presenting with a salt-losing crisis, the following biochemical abnormalities are observed: hyponatremia (low sodium levels), hyperkalemia (high potassium levels), metabolic acidosis, and hypoglycemia.

Boys experiencing a salt-losing crisis will require fluid resuscitation, intravenous dextrose, and intravenous hydrocortisone.

Affected females will require corrective surgery for their external genitalia. However, they have an intact uterus and ovaries and are capable of having children.

The long-term management of both sexes involves lifelong replacement of hydrocortisone (to suppress ACTH levels).

Due to the potentially life-threatening nature of the disease, it is crucial to initiate treatment without waiting for laboratory confirmation. Immediate administration of antibiotics is necessary.

In a hospital setting, the preferred agents for treatment are IV ceftriaxone (2 g for adults; 80 mg/kg for children) or IV cefotaxime (2 g for adults; 80 mg/kg for children). In the prehospital setting, IM benzylpenicillin can be given as an alternative. If there is a history of anaphylaxis to cephalosporins, chloramphenicol is a suitable alternative.

It is important to prioritize prompt treatment due to the severity of the disease. The recommended antibiotics should be administered as soon as possible to ensure the best possible outcome for the patient.

The therapeutic range for theophylline is quite limited, ranging from 10 to 20 micrograms per milliliter (10-20 mg/L). It is important to estimate the plasma concentration of aminophylline during long-term treatment as it can provide valuable information.

Neisseria gonorrhoeae is a type of bacteria that causes the sexually transmitted infection known as gonorrhoea. It is a Gram-negative diplococcus, meaning it appears as pairs of bacteria under a microscope. This infection is most commonly seen in individuals between the ages of 15 and 35, and it is primarily transmitted through sexual contact. One important characteristic of Neisseria gonorrhoeae is its ability to undergo antigenic variation, which means that recovering from an infection does not provide immunity and reinfection is possible.

When Neisseria gonorrhoeae infects the body, it first attaches to the genitourinary epithelium using pili, which are hair-like structures on the surface of the bacteria. It then invades the epithelial layer and triggers a local acute inflammatory response. In men, the clinical features of gonorrhoea often include urethritis (inflammation of the urethra) in about 80% of cases, dysuria (painful urination) in around 50% of cases, and mucopurulent discharge. Rectal infection may also occur, usually without symptoms, but it can cause anal discharge. Pharyngitis, or inflammation of the throat, is usually asymptomatic in men.

In women, the clinical features of gonorrhoea commonly include vaginal discharge in about 50% of cases, lower abdominal pain in around 25% of cases, dysuria in 10-15% of cases, and pelvic/lower abdominal tenderness in less than 5% of cases. Endocervical discharge and/or bleeding may also be present. Similar to men, rectal infection is usually asymptomatic but can cause anal discharge, and pharyngitis is usually asymptomatic in women as well.

Complications of Neisseria gonorrhoeae infection can be serious and include pelvic inflammatory disease (PID) in women, epididymo-orchitis or prostatitis in men, arthritis, dermatitis, pericarditis and/or myocarditis, hepatitis, and meningitis.

To diagnose gonorrhoea, samples of pus from the urethra, cervix, rectum, or throat should be collected and promptly sent to the laboratory in specialized transport medium. Traditionally, diagnosis has been made using Gram-stain and culture techniques, but newer PCR testing methods are becoming more commonly used.

Several studies have shown that elevating the head by 20-30 degrees is beneficial for increasing oxygen levels compared to lying flat on the back.

Further Reading:

Rapid sequence induction (RSI) is a method used to place an endotracheal tube (ETT) in the trachea while minimizing the risk of aspiration. It involves inducing loss of consciousness while applying cricoid pressure, followed by intubation without face mask ventilation. The steps of RSI can be remembered using the 7 P’s: preparation, pre-oxygenation, pre-treatment, paralysis and induction, protection and positioning, placement with proof, and post-intubation management.

Preparation involves preparing the patient, equipment, team, and anticipating any difficulties that may arise during the procedure. Pre-oxygenation is important to ensure the patient has an adequate oxygen reserve and prolongs the time before desaturation. This is typically done by breathing 100% oxygen for 3 minutes. Pre-treatment involves administering drugs to counter expected side effects of the procedure and anesthesia agents used.

Paralysis and induction involve administering a rapid-acting induction agent followed by a neuromuscular blocking agent. Commonly used induction agents include propofol, ketamine, thiopentone, and etomidate. The neuromuscular blocking agents can be depolarizing (such as suxamethonium) or non-depolarizing (such as rocuronium). Depolarizing agents bind to acetylcholine receptors and generate an action potential, while non-depolarizing agents act as competitive antagonists.

Protection and positioning involve applying cricoid pressure to prevent regurgitation of gastric contents and positioning the patient’s neck appropriately. Tube placement is confirmed by visualizing the tube passing between the vocal cords, auscultation of the chest and stomach, end-tidal CO2 measurement, and visualizing misting of the tube. Post-intubation management includes standard care such as monitoring ECG, SpO2, NIBP, capnography, and maintaining sedation and neuromuscular blockade.

Overall, RSI is a technique used to quickly and safely secure the airway in patients who may be at risk of aspiration. It involves a series of steps to ensure proper preparation, oxygenation, drug administration, and tube placement. Monitoring and post-intubation care are also important aspects of RSI.

This patient presents with a classic case of temporal arteritis, also known as giant cell arteritis (GCA). Temporal arteritis is a chronic condition characterized by inflammation in the walls of medium and large arteries, specifically granulomatous inflammation. It typically affects individuals who are over 50 years old.

The clinical features of temporal arteritis include headache, tenderness in the scalp, jaw claudication, and episodes of sudden blindness or amaurosis fugax (usually occurring in one eye). Some patients may also experience systemic symptoms such as fever, fatigue, loss of appetite, weight loss, and depression.

Temporal arteritis is often associated with polymyalgia rheumatica (PMR) in about 50% of cases. PMR is characterized by stiffness, aching, and tenderness in the upper arms (bilateral) and pain in the pelvic girdle.

Visual loss is an early and significant complication of temporal arteritis, and once it occurs, it rarely improves. Therefore, early treatment with high-dose corticosteroids is crucial to prevent further visual loss and other ischemic complications. If temporal arteritis is suspected, immediate initiation of high-dose glucocorticosteroid treatment (40 – 60 mg prednisolone daily) is necessary. It is also important to arrange an urgent referral for specialist evaluation, including a same-day ophthalmology assessment for those with visual symptoms, and a temporal artery biopsy.

The best single test to evaluate thyroid function is TSH. Goitres can be associated with either hypothyroidism or hyperthyroidism, although hypothyroidism is more common. According to NICE guidelines, when there is suspicion of hypothyroidism, it is recommended to first check the TSH level. If the TSH level is above the normal range, then the free thyroxine (FT4) should be checked on the same sample. Similarly, in cases of suspected hyperthyroidism, it is advised to first check the TSH level. If the TSH level is below the normal range, then the free thyroxine (FT4) and free triiodothyronine (FT3) should be checked on the same sample.

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.

Addison’s disease occurs when the adrenal cortex is destroyed. The anterior pituitary gland produces and releases adrenocorticotropic hormone (ACTH), not the posterior pituitary gland. The adrenal cortex is responsible for producing cortisol, not the adrenal medulla.

Further Reading:

Addison’s disease, also known as primary adrenal insufficiency or hypoadrenalism, is a rare disorder caused by the destruction of the adrenal cortex. This leads to reduced production of glucocorticoids, mineralocorticoids, and adrenal androgens. The deficiency of cortisol results in increased production of adrenocorticotropic hormone (ACTH) due to reduced negative feedback to the pituitary gland. This condition can cause metabolic disturbances such as hyperkalemia, hyponatremia, hypercalcemia, and hypoglycemia.

The symptoms of Addison’s disease can vary but commonly include fatigue, weight loss, muscle weakness, and low blood pressure. It is more common in women and typically affects individuals between the ages of 30-50. The most common cause of primary hypoadrenalism in developed countries is autoimmune destruction of the adrenal glands. Other causes include tuberculosis, adrenal metastases, meningococcal septicaemia, HIV, and genetic disorders.

The diagnosis of Addison’s disease is often suspected based on low cortisol levels and electrolyte abnormalities. The adrenocorticotropic hormone stimulation test is commonly used for confirmation. Other investigations may include adrenal autoantibodies, imaging scans, and genetic screening.

Addisonian crisis is a potentially life-threatening condition that occurs when there is an acute deficiency of cortisol and aldosterone. It can be the first presentation of undiagnosed Addison’s disease. Precipitating factors of an Addisonian crisis include infection, dehydration, surgery, trauma, physiological stress, pregnancy, hypoglycemia, and acute withdrawal of long-term steroids. Symptoms of an Addisonian crisis include malaise, fatigue, nausea or vomiting, abdominal pain, fever, muscle pains, dehydration, confusion, and loss of consciousness.

There is no fixed consensus on diagnostic criteria for an Addisonian crisis, as symptoms are non-specific. Investigations may include blood tests, blood gas analysis, and septic screens if infection is suspected. Management involves administering hydrocortisone and fluids. Hydrocortisone is given parenterally, and the dosage varies depending on the age of the patient. Fluid resuscitation with saline is necessary to correct any electrolyte disturbances and maintain blood pressure. The underlying cause of the crisis should also be identified and treated. Close monitoring of sodium levels is important to prevent complications such as osmotic demyelination syndrome.

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

The causes of neonatal jaundice can be categorized as follows:

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

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

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

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

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

Spondyloarthritis is a term that encompasses various inflammatory conditions affecting both the joints and the entheses, which are the attachment sites of ligaments and tendons to the bones. The primary cause of spondyloarthritis is ankylosing spondylitis, but it can also be triggered by reactive arthritis, psoriatic arthritis, and enteropathic arthropathies.

If individuals below the age of 45 experience four or more of the following symptoms, they should be referred for a potential diagnosis of spondyloarthritis:

– Presence of low back pain and being younger than 35 years old
– Waking up in the second half of the night due to pain
– Buttock pain
– Pain that improves with movement or within 48 hours of using nonsteroidal anti-inflammatory drugs (NSAIDs)
– Having a first-degree relative with spondyloarthritis
– History of current or past arthritis, psoriasis, or enthesitis.

Pyloric stenosis is characterized by recurring episodes of projectile vomiting and the presence of a mass in the upper abdomen, often described as an olive. This patient exhibits clinical features that align with pyloric stenosis and possesses several common risk factors, including being a male, being the firstborn son, being bottle-fed, and being delivered via C-section. It is important to note that intestinal atresia is typically diagnosed either during pregnancy or shortly after birth.

Further Reading:

Pyloric stenosis is a condition that primarily affects infants, characterized by the thickening of the muscles in the pylorus, leading to obstruction of the gastric outlet. It typically presents between the 3rd and 12th weeks of life, with recurrent projectile vomiting being the main symptom. The condition is more common in males, with a positive family history and being first-born being additional risk factors. Bottle-fed children and those delivered by c-section are also more likely to develop pyloric stenosis.

Clinical features of pyloric stenosis include projectile vomiting, usually occurring about 30 minutes after a feed, as well as constipation and dehydration. A palpable mass in the upper abdomen, often described as like an olive, may also be present. The persistent vomiting can lead to electrolyte disturbances, such as hypochloremia, alkalosis, and mild hypokalemia.

Ultrasound is the preferred diagnostic tool for confirming pyloric stenosis. It can reveal specific criteria, including a pyloric muscle thickness greater than 3 mm, a pylorus longitudinal length greater than 15-17 mm, a pyloric volume greater than 1.5 cm3, and a pyloric transverse diameter greater than 13 mm.

The definitive treatment for pyloric stenosis is pyloromyotomy, a surgical procedure that involves making an incision in the thickened pyloric muscle to relieve the obstruction. Before surgery, it is important to correct any hypovolemia and electrolyte disturbances with intravenous fluids. Overall, pyloric stenosis is a relatively common condition in infants, but with prompt diagnosis and appropriate management, it can be effectively treated.

To calculate the overall rate of fluid administration for a patient, we need to consider both the deficit and maintenance requirements. The deficit is determined by the weight of the patient, with a 1kg deficit equaling 1000ml. However, we also need to subtract the 200 ml bolus from the deficit calculation. So, the deficit is 1000 ml – 200 ml = 800 ml.

The deficit calculation is for the next 48 hours, while maintenance is calculated per day. For maintenance, we use the Holliday-Segar formula based on the patient’s weight. For this patient, the formula is as follows:

– 100 ml/kg/day for the first 10 kg of body weight = 10 x 100 = 1000 ml
– 50 ml/kg/day for the next 10 to 20 kg = 50 x 10 = 500 ml
– 20 ml/kg/day for each additional kilogram above 20 kg = 0 (as the patient only weighs 20kg)

So, the total maintenance requirement is 1500 ml per day (over 24 hours), which equals 62 ml/hour.

To determine the overall rate, we add the maintenance requirement (62 ml/hr) to the deficit requirement (17 ml/hr). Therefore, the overall rate of fluid administration for this patient is 79 ml/hr.

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.

NSAIDs have been found to have a relatively high occurrence of renal adverse drug reactions (ADRs). These ADRs primarily occur due to changes in renal haemodynamics caused by alterations in prostaglandin levels.

Normally, prostaglandins play a role in dilating the afferent arteriole of the glomerulus. This dilation helps maintain normal glomerular perfusion and glomerular filtration rate (GFR).

However, NSAIDs work by reducing prostaglandin levels. This reduction leads to unopposed vasoconstriction of the afferent arteriole, resulting in decreased renal plasma flow. Consequently, this decrease in renal plasma flow leads to a decrease in GFR. It is important to note that NSAIDs do not have any impact on the filtration fraction itself.

Cauda equina syndrome (CES) is a rare but serious complication that can occur when a disc ruptures. This happens when the material from the disc is pushed into the spinal canal and puts pressure on the bundle of nerves in the lower back and sacrum. As a result, individuals may experience loss of control over their bladder and bowel functions.

There are certain red flags that may indicate the presence of CES. These include experiencing sciatica on both sides of the body, having severe or worsening neurological issues in both legs (such as significant weakness in knee extension, ankle eversion, or foot dorsiflexion), difficulty starting urination or a decreased sensation of urinary flow, loss of sensation in the rectum, experiencing numbness or tingling in the perianal, perineal, or genital areas (also known as saddle anesthesia or paresthesia), and having a lax anal sphincter.

Conus medullaris syndrome (CMS) is a condition that affects the conus medullaris, which is located above the cauda equina at the T12-L2 level. Unlike CES, CMS primarily causes back pain and may have less noticeable nerve root pain. The main symptoms of CMS are urinary retention and constipation.

To confirm a diagnosis of CES and determine the level of compression and any underlying causes, an MRI scan is considered the gold-standard investigation. In cases where an MRI is not possible or contraindicated, a CT myelogram or standard CT scans can be helpful. However, plain radiographs have limited value and may only show significant degenerative or traumatic bone diseases.

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

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

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

Schistosomiasis, also known as bilharzia, is a tropical disease caused by parasitic trematodes (flukes) of the Schistosoma type. The transmission of this disease occurs when water becomes contaminated with faeces or urine containing eggs, and a specific freshwater snail serves as the intermediate host. Human contact with water inhabited by the intermediate host snail is necessary for transmission to occur.

There are five species of Schistosoma that can cause human disease: S. japonicum, S. mansoni, S. haematobium, S. intercalatum, and S. mekongi. Among these, S. japonicum and S. mansoni are the most significant causes of intestinal schistosomiasis, while S. haematobium is the primary cause of urogenital schistosomiasis.

Urogenital schistosomiasis occurs when adult worms migrate from their initial site in the liver to the vesical plexus. The presence of blood in the urine, known as haematuria, is a characteristic sign of urogenital schistosomiasis. In women, this condition may manifest with genital and vaginal lesions, as well as dyspareunia. pathology in the seminal vesicles and prostate. Advanced cases of urogenital schistosomiasis can result in fibrosis of the ureter and bladder, as well as kidney damage. Complications such as bladder cancer and infertility are also recognized in association with this disease.

Nasal cautery is a suitable option for patients who are experiencing epistaxis (nosebleeds) and have not responded to initial measures. It is particularly effective when a specific bleeding point in the anterior nasal septum (known as Little’s area) has been identified. This procedure is recommended for adult patients who have already undergone an appropriate period of nasal pressure application (10-15 minutes). It is important to note that naseptin or mupirocin should not be used to control active bleeding, but rather after the bleeding has been successfully managed. Nasal packing, on the other hand, is a more invasive procedure that requires hospital admission and is typically reserved for cases where the bleeding point cannot be visualized or when cautery has been unsuccessful.

Further Reading:

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

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

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

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

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

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

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

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

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

The primary cause for the majority of out-of-hospital cardiac arrests is cardiovascular disease. This refers to conditions that affect the heart and blood vessels, such as coronary artery disease, heart attacks, and arrhythmias. These conditions can lead to sudden 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.

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 lower back or flank and radiating to the groin or genital area 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.

People experiencing renal or ureteric colic are usually restless and unable to find relief by lying still, which helps to distinguish this condition from peritonitis. They may have a history of previous episodes and may also present with fever and sweating if there is an associated urinary infection. Some individuals 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.

In terms of pain management, the first-line treatment for adults, children, and young people with suspected renal colic is a non-steroidal anti-inflammatory drug (NSAID), which can be administered through various routes. If NSAIDs are contraindicated or not providing sufficient pain relief, intravenous paracetamol can be offered as an alternative. Opioids may be considered if both NSAIDs and intravenous paracetamol are contraindicated or not effective in relieving pain. Antispasmodics should not be given to individuals with suspected renal colic.

For more detailed information, you can refer to the NICE guidelines on the assessment and management of renal and ureteric stones.

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

An abdominal aortic aneurysm (AAA) is a condition where the abdominal aorta becomes enlarged, either in a specific area or throughout its length, reaching 1.5 times its normal size. Most AAAs are found between the diaphragm and the point where the aorta splits into two branches. They can be classified into three types based on their location: suprarenal, pararenal, and infrarenal. Suprarenal AAAs involve the origin of one or more visceral arteries, pararenal AAAs involve the origins of the renal arteries, and infrarenal AAAs start below the renal arteries. The majority of AAAs (approximately 85%) are infrarenal. In individuals over 50 years old, a normal infrarenal aortic diameter is 1.7 cm in men and 1.5 cm in women. An infrarenal aorta with a diameter greater than 3 cm is considered to be an aneurysm. While most AAAs do not cause symptoms, an expanding aneurysm can sometimes lead to abdominal pain or pulsatile sensations. Symptomatic AAAs have a high risk of rupture. In the UK, elective surgery for AAAs is typically recommended if the aneurysm is larger than 5.5 cm in diameter or if it is larger than 4.5 cm in diameter and has increased in size by more than 0.5 cm in the past six months.

Mitral stenosis is a condition characterized by a narrowing of the mitral valve, which can lead to various symptoms. One common symptom is a mid-late diastolic murmur, which can be heard during a physical examination. This murmur may also be described as mid-diastolic, late-diastolic, or mid-late diastolic. Additionally, patients with chronic mitral stenosis may not experience any symptoms, and the murmur may only be detected incidentally.

A significant risk associated with mitral stenosis is the development of atrial fibrillation (AF). When AF occurs in patients with mitral stenosis, it can trigger acute pulmonary edema. This happens because the left atrium, which is responsible for pumping blood across the narrowed mitral valve into the left ventricle, needs to generate higher pressure. However, when AF occurs, the atrial contraction becomes inefficient, leading to impaired emptying of the left atrium. This, in turn, causes increased back pressure in the pulmonary circulation.

The elevated pressure in the left atrium and pulmonary circulation can result in the rupture of bronchial veins, leading to the production of pink frothy sputum. This symptom is often observed in patients with mitral stenosis who develop acute pulmonary edema.

Further Reading:

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

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

Congenital adrenal hyperplasia (CAH) is a group of inherited disorders that are caused by autosomal recessive genes. The majority of affected patients, over 90%, have a deficiency of the enzyme 21-hydroxylase. This enzyme is encoded by the 21-hydroxylase gene, which is located on chromosome 6p21 within the HLA histocompatibility complex. The second most common cause of CAH is a deficiency of the enzyme 11-beta-hydroxylase. The condition is rare, with an incidence of approximately 1 in 500 births in the UK. It is more prevalent in the offspring of consanguineous marriages.

The deficiency of 21-hydroxylase leads to a deficiency of cortisol and/or aldosterone, as well as an excess of precursor steroids. As a result, there is an increased secretion of ACTH from the anterior pituitary, leading to adrenocortical hyperplasia.

The severity of CAH varies depending on the degree of 21-hydroxylase deficiency. Female infants often exhibit ambiguous genitalia, such as clitoral hypertrophy and labial fusion. Male infants may have an enlarged scrotum and/or scrotal pigmentation. Hirsutism, or excessive hair growth, occurs in 10% of cases.

Boys with CAH often experience a salt-losing adrenal crisis at around 1-3 weeks of age. This crisis is characterized by symptoms such as vomiting, weight loss, floppiness, and circulatory collapse.

The diagnosis of CAH can be made by detecting markedly elevated levels of the metabolic precursor 17-hydroxyprogesterone. Neonatal screening is possible, primarily through the identification of persistently elevated 17-hydroxyprogesterone levels.

In infants presenting with a salt-losing crisis, the following biochemical abnormalities are observed: hyponatremia (low sodium levels), hyperkalemia (high potassium levels), metabolic acidosis, and hypoglycemia.

Boys experiencing a salt-losing crisis will require fluid resuscitation, intravenous dextrose, and intravenous hydrocortisone.

Affected females will require corrective surgery for their external genitalia. However, they have an intact uterus and ovaries and are capable of having children.

The long-term management of both sexes involves lifelong replacement of hydrocortisone (to suppress ACTH levels).

Acute epiglottitis is inflammation of the epiglottis, which can be life-threatening if not treated promptly. When the soft tissues surrounding the epiglottis are also affected, it is called acute supraglottitis. This condition is most commonly seen in children between the ages of 3 and 5, but it can occur at any age, with adults typically presenting in their 40s and 50s.

In the past, Haemophilus influenzae type B was the main cause of acute epiglottitis, but with the introduction of the Hib vaccination, it has become rare in children. Streptococcus spp. is now the most common causative organism. Other potential culprits include Staphylococcus aureus, Pseudomonas spp., Moraxella catarrhalis, Mycobacterium tuberculosis, and the herpes simplex virus. In immunocompromised patients, Candida spp. and Aspergillus spp. infections can occur.

The typical symptoms of acute epiglottitis include fever, sore throat, painful swallowing, difficulty swallowing secretions (especially in children who may drool), muffled voice, stridor, respiratory distress, rapid heartbeat, tenderness in the front of the neck over the hyoid bone, ear pain, and swollen lymph nodes in the neck. Some patients may also exhibit the tripod sign, where they lean forward on outstretched arms to relieve upper airway obstruction.

To diagnose acute epiglottitis, fibre-optic laryngoscopy is considered the gold standard investigation. However, this procedure should only be performed by an anaesthetist in a setting prepared for intubation or tracheostomy in case of airway obstruction. Other useful tests include a lateral neck X-ray to look for the thumbprint sign, throat swabs, blood cultures, and a CT scan of the neck if an abscess is suspected.

When dealing with a case of acute epiglottitis, it is crucial not to panic or distress the patient, especially in pediatric cases. Avoid attempting to examine the throat with a tongue depressor, as this can trigger spasm and worsen airway obstruction. Instead, keep the patient as calm as possible and immediately call a senior anaesthetist, a senior paediatrician, and an ENT surgeon. Nebulized adrenaline can be used as a temporary measure if there is critical airway obstruction.

Acute pancreatitis is a frequently encountered and serious source of acute abdominal pain. It involves the sudden inflammation of the pancreas, leading to the release of enzymes that cause self-digestion of the organ.

The clinical manifestations of acute pancreatitis include severe epigastric pain, accompanied by feelings of nausea and vomiting. The pain may radiate to the T6-T10 dermatomes or even to the shoulder tip through the phrenic nerve if the diaphragm is irritated. Other symptoms may include fever or sepsis, tenderness in the epigastric region, jaundice, and the presence of Gray-Turner sign (bruising on the flank) or Cullen sign (bruising around the belly button).

The most common causes of acute pancreatitis are gallstones and alcohol consumption. Additionally, many cases are considered idiopathic, meaning the cause is unknown. To aid in remembering the various causes, the mnemonic ‘I GET SMASHED’ can be helpful. Each letter represents a potential cause: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion stings, Hyperlipidemia/hypercalcemia, ERCP (endoscopic retrograde cholangiopancreatography), and Drugs.

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

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

Further Reading:

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

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

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

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

Cricoid pressure is applied during intubation to compress the oesophagus and prevent the backflow of stomach contents, reducing the risk of aspiration.

Further Reading:

Rapid sequence induction (RSI) is a method used to place an endotracheal tube (ETT) in the trachea while minimizing the risk of aspiration. It involves inducing loss of consciousness while applying cricoid pressure, followed by intubation without face mask ventilation. The steps of RSI can be remembered using the 7 P’s: preparation, pre-oxygenation, pre-treatment, paralysis and induction, protection and positioning, placement with proof, and post-intubation management.

Preparation involves preparing the patient, equipment, team, and anticipating any difficulties that may arise during the procedure. Pre-oxygenation is important to ensure the patient has an adequate oxygen reserve and prolongs the time before desaturation. This is typically done by breathing 100% oxygen for 3 minutes. Pre-treatment involves administering drugs to counter expected side effects of the procedure and anesthesia agents used.

Paralysis and induction involve administering a rapid-acting induction agent followed by a neuromuscular blocking agent. Commonly used induction agents include propofol, ketamine, thiopentone, and etomidate. The neuromuscular blocking agents can be depolarizing (such as suxamethonium) or non-depolarizing (such as rocuronium). Depolarizing agents bind to acetylcholine receptors and generate an action potential, while non-depolarizing agents act as competitive antagonists.

Protection and positioning involve applying cricoid pressure to prevent regurgitation of gastric contents and positioning the patient’s neck appropriately. Tube placement is confirmed by visualizing the tube passing between the vocal cords, auscultation of the chest and stomach, end-tidal CO2 measurement, and visualizing misting of the tube. Post-intubation management includes standard care such as monitoring ECG, SpO2, NIBP, capnography, and maintaining sedation and neuromuscular blockade.

Overall, RSI is a technique used to quickly and safely secure the airway in patients who may be at risk of aspiration. It involves a series of steps to ensure proper preparation, oxygenation, drug administration, and tube placement. Monitoring and post-intubation care are also important aspects of RSI.

Ketamine stands out among other anaesthetic agents due to its unique combination of analgesic, hypnotic, and amnesic properties. This makes it an incredibly valuable and adaptable drug when administered correctly.

The mechanism of action of ketamine involves non-competitive antagonism of the Ca2+ channel pore within the NMDA receptor. Additionally, it inhibits NMDA receptor activity by interacting with the binding site of phencyclidine.

In summary, ketamine’s multifaceted effects and its ability to target specific receptors make it an indispensable tool in the field of anaesthesia.

Parkinson’s disease is primarily characterized by the degeneration of cells in the substantia nigra, a region located in the midbrain. The most severely affected part is the pars compacta, which plays a crucial role in motor control. As a result, there is a significant decrease in the activity of cells that secrete dopamine.

The main symptoms of Parkinson’s disease include tremors that occur when the body is at rest, rigidity in the muscles, and bradykinesia, which refers to a slowness in movement. These symptoms can greatly impact a person’s ability to perform everyday tasks and can progressively worsen over time.

The Zika virus is a newly emerging virus that is transmitted by mosquitoes. It was first discovered in humans in Uganda in 1952. Recently, there has been a significant outbreak of the virus in South America.

When a person contracts the Zika virus, about 1 in 5 individuals will experience clinical illness, while the rest will show no symptoms at all. The most common symptoms of the virus include fever, rash, joint pain, and conjunctivitis. These symptoms typically last for no more than a week.

While not completely conclusive, the evidence from the recent outbreak strongly suggests a connection between Zika virus infection and microcephaly.

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.

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

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

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

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

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

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

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

Insect removal from the ear can be quite challenging due to the distress it causes the patient and the inevitable movement of the insect during the process.

To begin, it is important to make the patient comfortable by providing analgesia. In some cases, inhaled Entonox can be helpful, and if the patient is extremely distressed or experiencing significant discomfort, sedation may be necessary.

The first step in the removal process involves immobilizing or killing the insect to prevent further movement and potential damage within the ear. This can be achieved using options such as microscope immersion oil, mineral oil, or lidocaine solution.

Once the insect is confirmed to be dead, the actual removal can be performed using forceps or the highly effective Frazier suction technique. After inspecting the ear and ensuring the insect is no longer alive, connect the Frazier suction device to low continuous suction and slowly insert it into the patient’s external ear canal. By occluding the insufflation port, the contents of the ear canal can be suctioned out. Once no more liquid returns, withdraw the catheter and verify that the insect has been successfully removed.

Wernicke’s encephalopathy is a condition that is commonly associated with alcohol abuse and other causes of thiamine deficiency. It is characterized by a classic triad of symptoms, including acute confusion, ophthalmoplegia (paralysis or weakness of the eye muscles), and ataxia (loss of coordination). Additional possible features of this condition may include papilloedema (swelling of the optic disc), hearing loss, apathy, dysphagia (difficulty swallowing), memory impairment, and hypothermia. The majority of cases also experience peripheral neuropathy, which typically affects the legs.

The condition is marked by acute capillary haemorrhages, astrocytosis (increase in the number of astrocytes, a type of brain cell), and neuronal death in the upper brainstem and diencephalon. These abnormalities can be visualized using MRI scanning, while CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will go on to develop a Korsakoff psychosis. This condition is characterized by retrograde amnesia (loss of memory for events that occurred before the onset of amnesia), an inability to form new memories, disordered time perception, and confabulation (fabrication of false memories).

When Wernicke’s encephalopathy is suspected, it is crucial to administer parenteral thiamine (such as Pabrinex) for at least 5 days. Following the parenteral therapy, oral thiamine should be continued.

Based on the child’s medical history, it appears that they have multiple areas of infected eczema. In such cases, the NICE guidelines recommend starting treatment with flucloxacillin as the first-line option for bacterial infections. This is because staphylococcus and/or streptococcus bacteria are the most common causes of these infections. Swabs should only be taken if there is a likelihood of antibiotic resistance or if a different pathogen is suspected. In cases where the child is allergic to flucloxacillin, erythromycin can be used as an alternative. If the child cannot tolerate erythromycin, clarithromycin is the recommended option. For more information, you can refer to the NICE Clinical Knowledge Summary on the management of infected eczema.

TSH-secreting pituitary adenoma is an uncommon cause of hyperthyroidism in the United Kingdom, accounting for only a small number of cases.

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.

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.

Pelvic inflammatory disease (PID) is an infection that affects the upper female reproductive tract, including the uterus, fallopian tubes, and ovaries. It is typically caused by an ascending infection from the cervix. The most common culprits are sexually transmitted diseases like chlamydia and gonorrhea, with chlamydia being the most prevalent infection seen in UK genitourinary medicine clinics.

PID can often be asymptomatic, but when symptoms do occur, they may include lower abdominal pain and tenderness, fever, painful urination, painful intercourse, purulent vaginal discharge, abnormal vaginal bleeding, and tenderness in the cervix and adnexa. It’s important to note that symptoms of ectopic pregnancy can be mistaken for PID, so a pregnancy test should always be conducted in patients with suspicious symptoms.

To investigate a potential case of PID, endocervical swabs are taken to test for chlamydia and gonorrhea using nucleic acid amplification tests. It is recommended to start empirical antibiotic treatment as soon as a presumptive diagnosis of PID is made, without waiting for swab results.

Mild to moderate cases of PID can usually be managed in primary care or outpatient settings. However, patients with severe disease should be admitted to the hospital for intravenous antibiotics. Signs of severe disease include a fever above 38°C, signs of a tubo-ovarian abscess, signs of pelvic peritonitis, or concurrent pregnancy.

The current recommended treatment for outpatient cases of PID is a single intramuscular dose of ceftriaxone 500 mg, followed by oral doxycycline 100 mg twice daily and oral metronidazole 400 mg twice daily for 14 days. An alternative regimen is oral ofloxacin 400 mg twice daily and oral metronidazole 400 mg twice daily for 14 days.

For severely ill patients in the inpatient setting, initial treatment consists of intravenous doxycycline, a single-dose of intravenous ceftriaxone, and intravenous metronidazole. Afterward, the treatment is switched to oral doxycycline and metronidazole to complete a 14-day course.

If a patient fails to respond to treatment, laparoscopy is necessary to confirm the diagnosis or consider alternative diagnoses.

Traveller’s diarrhoea (TD) is a prevalent illness that affects travellers all around the world. It is estimated that up to 50% of Europeans who spend two or more weeks in developing regions experience TD. This condition is characterized by the passage of three or more loose stools within a 24-hour period. Typically, individuals with TD also experience abdominal cramps, nausea, and bloating.

In most cases of gastroenteritis, there is no need for stool microscopy and culture. However, it is advisable to arrange these tests if the patient has recently returned from overseas travel, is severely ill, has prolonged symptoms, comes from an institution, or works as a food handler.

Bacteria are responsible for approximately 80% of TD cases, while viruses and protozoa account for the remaining cases. The most common causative organism is Escherichia coli, with Enterohaemorrhagic Escherichia coli being the strain most likely to cause bloody diarrhoea.

Infective causes of bloody diarrhoea include Campylobacter jejuni, Shigella spp., Salmonella spp., Clostridium difficile, Yersinia spp., Schistosomiasis, and Amoebiasis (Entamoeba histolytica).

Vomiting after a head injury should raise concerns about increased intracranial pressure (ICP). Signs of elevated ICP include vomiting, changes in pupil size or shape in one eye, decreased cognitive function or consciousness, abnormal findings during fundoscopy (such as blurry optic discs or bleeding in the retina), cranial nerve dysfunction (most commonly affecting CN III and VI), weakness on one side of the body (a late sign), bradycardia (slow heart rate), high blood pressure, and a wide pulse pressure. Irregular breathing that may progress to respiratory distress, focal neurological deficits, and seizures can also be indicative of elevated ICP.

Further Reading:

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

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

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

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

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

Further Reading:

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

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

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

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

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

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.

An X-ray of the foot is recommended when there is pain in the base of the fifth metatarsal or the navicular bone, as well as an inability to bear weight immediately after an injury or in the emergency department. The Ottawa ankle rules can also be used to determine if an X-ray is necessary for ankle injuries. These rules focus on two specific areas (the malleolar and midfoot zones) to determine if an X-ray of the ankle or foot is needed. More information on these rules can be found in the notes below.

Further Reading:

Ankle fractures are traumatic lower limb and joint injuries that involve the articulation between the tibia, fibula, and talus bones. The ankle joint allows for plantar and dorsiflexion of the foot. The key bony prominences of the ankle are called malleoli, with the medial and posterior malleolus being prominences of the distal tibia and the lateral malleolus being a prominence of the distal fibula. The distal fibula and tibia are joined together by the distal tibiofibular joint or syndesmosis, which is comprised of three key ligaments. An ankle X-ray series is often used to guide clinical decision making in patients with ankle injuries, using the Ottawa ankle rules to determine if an X-ray is necessary. Ankle fractures are commonly described by the anatomical fracture pattern seen on X-ray relative to the malleoli involved, such as isolated malleolus fractures, bimalleolar fractures, and trimalleolar fractures. The Weber classification is a commonly used system for distal fibula fractures, categorizing them as Weber A, B, or C based on the level and extent of the fracture.

The mini-mental state examination (MMSE) is a tool consisting of 11 questions that is utilized to evaluate cognitive function. With a maximum score of 30, a score below 24 generally indicates impaired cognitive function. This assessment can be employed to categorize the severity of cognitive impairment in dementia. Mild dementia is typically associated with an MMSE score ranging from 20 to 24, while moderate dementia falls within the MMSE score range of 13 to 20. Severe dementia is characterized by an MMSE score below 12. For more information on testing and assessment for dementia, you can visit the Alzheimer’s Association website. Additionally, the RCEM syllabus references EIP9 for memory loss and EIC4 for dementia and cognitive impairment.

Aortic dissection is a condition that occurs when the middle layer of the aorta, known as the tunica media, becomes weakened. This weakening leads to the development of cases 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.

The ATLS guidelines categorize chest injuries in trauma into two groups: life-threatening injuries that require immediate identification and treatment in the primary survey, and potentially life-threatening injuries that should be identified and treated in the secondary survey.

During the primary survey, the focus is on identifying and treating life-threatening thoracic injuries. These include airway obstruction, tracheobronchial tree injury, tension pneumothorax, open pneumothorax, massive haemothorax, and cardiac tamponade. Prompt recognition and intervention are crucial in order to prevent further deterioration and potential fatality.

In the secondary survey, attention is given to potentially life-threatening injuries that may not be immediately apparent. These include simple pneumothorax, haemothorax, flail chest, pulmonary contusion, blunt cardiac injury, traumatic aortic disruption, traumatic diaphragmatic injury, and blunt oesophageal rupture. These injuries may not pose an immediate threat to life, but they still require identification and appropriate management to prevent complications and ensure optimal patient outcomes.

By dividing chest injuries into these two categories and addressing them in a systematic manner, healthcare providers can effectively prioritize and manage trauma patients, ultimately improving their chances of survival and recovery.

Patients with Parkinson’s disease (PD) typically exhibit the following clinical features:

– Hypokinesia (reduced movement)
– Bradykinesia (slow movement)
– Rest tremor (usually occurring at a rate of 4-6 cycles per second)
– Rigidity (increased muscle tone and ‘cogwheel rigidity’)

Other commonly observed clinical features include:

– Gait disturbance (characterized by a shuffling gait and loss of arm swing)
– Loss of facial expression
– Monotonous, slurred speech
– Micrographia (small, cramped handwriting)
– Increased salivation and dribbling
– Difficulty with fine movements

Initially, these signs are typically seen on one side of the body at the time of diagnosis, but they progressively worsen and may eventually affect both sides. In later stages of the disease, additional clinical features may become evident, including:

– Postural instability
– Cognitive impairment
– Orthostatic hypotension

Although PD primarily affects movement, patients often experience psychiatric issues such as depression and dementia. Autonomic disturbances and pain can also occur, leading to significant disability and reduced quality of life for the affected individual. Additionally, family members and caregivers may also be indirectly affected by the disease.

There are various specific remedies available for different types of poisons and overdoses. The following list provides an outline of some of these antidotes:

Poison: Benzodiazepines
Antidote: Flumazenil

Poison: Beta-blockers
Antidotes: Atropine, Glucagon, Insulin

Poison: Carbon monoxide
Antidote: Oxygen

Poison: Cyanide
Antidotes: Hydroxocobalamin, Sodium nitrite, Sodium thiosulphate

Poison: Ethylene glycol
Antidotes: Ethanol, Fomepizole

Poison: Heparin
Antidote: Protamine sulphate

Poison: Iron salts
Antidote: Desferrioxamine

Poison: Isoniazid
Antidote: Pyridoxine

Poison: Methanol
Antidotes: Ethanol, Fomepizole

Poison: Opioids
Antidote: Naloxone

Poison: Organophosphates
Antidotes: Atropine, Pralidoxime

Poison: Paracetamol
Antidotes: Acetylcysteine, Methionine

Poison: Sulphonylureas
Antidotes: Glucose, Octreotide

Poison: Thallium
Antidote: Prussian blue

Poison: Warfarin
Antidote: Vitamin K, Fresh frozen plasma (FFP)

By utilizing these specific antidotes, medical professionals can effectively counteract the harmful effects of various poisons and overdoses.

According to the current NICE guidelines on febrile illness in children under the age of 5, there are certain symptoms and signs that may indicate the presence of pneumonia. These include tachypnoea, which is a rapid breathing rate. For infants aged 0-5 months, a respiratory rate (RR) of over 60 breaths per minute is considered suggestive of pneumonia. For infants aged 6-12 months, an RR of over 50 breaths per minute is indicative, and for children older than 12 months, an RR of over 40 breaths per minute may suggest pneumonia.

Other signs that may point towards pneumonia include crackles in the chest, nasal flaring, chest indrawing, and cyanosis. Crackles are abnormal sounds heard during breathing, while nasal flaring refers to the widening of the nostrils during breathing. Chest indrawing is the inward movement of the chest wall during inhalation, and cyanosis is the bluish discoloration of the skin or mucous membranes due to inadequate oxygen supply.

Additionally, a low oxygen saturation level of less than 95% while breathing air is also considered suggestive of pneumonia. These guidelines can be found in more detail in the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

The use of a laryngeal mask airway (LMA) carries a higher risk of inducing laryngospasm compared to endotracheal intubation. However, LMAs are still considered excellent alternatives to bag masks as they reduce the risk of gastric inflation and aspiration. While they do decrease the risk of aspiration, they are not as protective as endotracheal tubes. Complications associated with LMA use include laryngospasm, nausea and vomiting, and a low risk of aspiration. LMAs have advantages over bag-mask ventilation, such as more effective ventilation, less gastric inflation, and a lower risk of aspiration. However, they also have disadvantages, including the risk of hypoventilation due to air leak around the cuff, greater gastric inflation compared to endotracheal intubation, and a very low risk of aspiration.

Further Reading:

Techniques to keep the airway open:

1. Suction: Used to remove obstructing material such as blood, vomit, secretions, and food debris from the oral cavity.

2. Chin lift manoeuvres: Involves lifting the head off the floor and lifting the chin to extend the head in relation to the neck. Improves alignment of the pharyngeal, laryngeal, and oral axes.

3. Jaw thrust: Used in trauma patients with cervical spine injury concerns. Fingers are placed under the mandible and gently pushed upward.

Airway adjuncts:

1. Oropharyngeal airway (OPA): Prevents the tongue from occluding the airway. Sized according to the patient by measuring from the incisor teeth to the angle of the mandible. Inserted with the tip facing backwards and rotated 180 degrees once it touches the back of the palate or oropharynx.

2. Nasopharyngeal airway (NPA): Useful when it is difficult to open the mouth or in semi-conscious patients. Sized by length (distance between nostril and tragus of the ear) and diameter (roughly that of the patient’s little finger). Contraindicated in basal skull and midface fractures.

Laryngeal mask airway (LMA):

– Supraglottic airway device used as a first line or rescue airway.
– Easy to insert, sized according to patient’s bodyweight.
– Advantages: Easy insertion, effective ventilation, some protection from aspiration.
– Disadvantages: Risk of hypoventilation, greater gastric inflation than endotracheal tube (ETT), risk of aspiration and laryngospasm.

Note: Proper training and assessment of the patient’s condition are essential for airway management.

There are various specific remedies available for different types of poisons and overdoses. The following list provides an outline of some of these antidotes:

Poison: Benzodiazepines
Antidote: Flumazenil

Poison: Beta-blockers
Antidotes: Atropine, Glucagon, Insulin

Poison: Carbon monoxide
Antidote: Oxygen

Poison: Cyanide
Antidotes: Hydroxocobalamin, Sodium nitrite, Sodium thiosulphate

Poison: Ethylene glycol
Antidotes: Ethanol, Fomepizole

Poison: Heparin
Antidote: Protamine sulphate

Poison: Iron salts
Antidote: Desferrioxamine

Poison: Isoniazid
Antidote: Pyridoxine

Poison: Methanol
Antidotes: Ethanol, Fomepizole

Poison: Opioids
Antidote: Naloxone

Poison: Organophosphates
Antidotes: Atropine, Pralidoxime

Poison: Paracetamol
Antidotes: Acetylcysteine, Methionine

Poison: Sulphonylureas
Antidotes: Glucose, Octreotide

Poison: Thallium
Antidote: Prussian blue

Poison: Warfarin
Antidote: Vitamin K, Fresh frozen plasma (FFP)

By utilizing these specific antidotes, medical professionals can effectively counteract the harmful effects of various poisons and overdoses.

Pernicious anaemia is a condition that affects the stomach and is characterized by the loss of gastric parietal cells and impaired secretion of intrinsic factor (IF). IF is crucial for the absorption of vitamin B12 in the ileum, and as a result, megaloblastic anaemia occurs. This condition is commonly seen in individuals who have undergone gastrectomy.

The clinical manifestations of pernicious anaemia include weight loss, loss of appetite, fatigue, diarrhoea, and a distinct lemon-yellow skin color, which is caused by a combination of haemolytic jaundice and the paleness associated with anaemia. Other symptoms may include glossitis (inflammation of the tongue) and oral ulceration. Neurological symptoms can also occur, such as subacute combined degeneration of the spinal cord and peripheral neuropathy. The earliest sign of central nervous system involvement is often the loss of position and vibratory sense in the extremities.

When investigating pernicious anaemia, certain findings may be observed. These include macrocytic anaemia, neutropaenia, thrombocytopaenia, anisocytosis and poikilocytosis on a blood film, low serum B12 levels, elevated serum bilirubin levels (indicating haemolysis), the presence of intrinsic factor antibodies, and a positive Schilling test.

The treatment for pernicious anaemia involves lifelong supplementation of vitamin B12, typically administered through intramuscular injections.

The use of tetracyclines is not recommended during pregnancy as it can have harmful effects on the developing fetus. When taken during the second half of pregnancy, tetracyclines may lead to permanent yellow-grey discoloration of the teeth and enamel hypoplasia. Children affected by this may also be more prone to cavities. Additionally, tetracyclines have been associated with congenital defects, problems with bone growth, and liver toxicity in pregnant women.

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

ACE inhibitors (e.g. ramipril): If taken in the second and third trimesters, ACE inhibitors can cause reduced blood flow, kidney failure, and a condition called oligohydramnios.

Aminoglycosides (e.g. gentamicin): Aminoglycosides can cause ototoxicity, leading to hearing loss in the fetus.

Aspirin: High doses of aspirin can result in first trimester abortions, delayed labor, premature closure of the fetal ductus arteriosus, and a condition called fetal kernicterus. However, low doses (e.g. 75 mg) do not pose significant risks.

Benzodiazepines (e.g. diazepam): When taken late in pregnancy, benzodiazepines can cause respiratory depression in the newborn and a withdrawal syndrome.

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

Carbamazepine: Carbamazepine has been associated with a condition called hemorrhagic disease of the newborn and an increased risk of neural tube defects.

Chloramphenicol: Chloramphenicol can cause a condition known as grey baby syndrome in newborns.

Corticosteroids: If taken in the first trimester, corticosteroids may increase the risk of orofacial clefts in the fetus.

Danazol: When taken in the first trimester, danazol can cause masculinization of the female fetuses genitals.

Finasteride: Pregnant women should avoid handling finasteride tablets as the drug can be absorbed through the skin and affect the development of male sex organs in the fetus.

Haloperidol: If taken during the first trimester, this medication may increase the risk of limb malformations. If taken during the third trimester, it can lead to an increased risk of extrapyramidal symptoms in the newborn.

The British Society of Gastroenterology (BSG) has developed guidelines for healthcare professionals who are assessing cases of acute lower intestinal bleeding in a hospital setting. These guidelines are particularly useful when determining which patients should be referred for further evaluation.

When patients present with lower gastrointestinal bleeding (LGIB), they should be categorized as either unstable or stable. Unstable patients are defined as those with a shock index greater than 1, which is calculated by dividing the heart rate by the systolic blood pressure (HR/SBP).

For stable patients, the next step is to determine whether their bleed is major (requiring hospitalization) or minor (suitable for outpatient management). This can be determined using a risk assessment tool called the Oakland risk score, which takes into account factors such as age, hemoglobin level, and findings from a digital rectal examination.

Patients with a minor self-limiting bleed (e.g., an Oakland score of less than 8 points) and no other indications for hospital admission can be discharged with urgent follow-up for further investigation as an outpatient.

Patients with a major bleed should be admitted to the hospital and scheduled for a colonoscopy as soon as possible.

If a patient is hemodynamically unstable or has a shock index greater than 1 even after initial resuscitation, and there is suspicion of active bleeding, a CT angiography (CTA) should be considered. This can be followed by endoscopic or radiological therapy.

If no bleeding source is identified by the initial CTA and the patient remains stable after resuscitation, an upper endoscopy should be performed immediately, as LGIB associated with hemodynamic instability may indicate an upper gastrointestinal bleeding source. Gastroscopy may be the first investigation if the patient stabilizes after initial resuscitation.

If indicated, catheter angiography with the possibility of embolization should be performed as soon as possible after a positive CTA to increase the chances of success. In centers with a 24/7 interventional radiology service, this procedure should be available within 60 minutes for hemodynamically unstable patients.

Emergency laparotomy should only be considered if all efforts to locate the bleeding using radiological and/or endoscopic methods have been exhausted, except in exceptional circumstances.

In some cases, red blood cell transfusion may be necessary. It is recommended to use restrictive blood transfusion thresholds, such as a hemoglobin trigger of 7 g/dL and a target of 7-9 g/d

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

Further Reading:

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

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

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

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

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

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

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

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

When attempting to ventilate a patient with a tracheostomy, the first approach is usually through the mouth. If this is not successful, ventilation through the tracheostomy stoma is appropriate. After removing the tracheostomy, the doctor should begin ventilating the patient through the mouth by performing standard oral manoeuvres and covering the stoma with a hand or swab. If these measures fail, the clinician should then proceed to ventilate through the tracheostomy stoma using a bag valve mask and appropriate adjuncts such as oral or nasal adjuncts or an LMA.

Further Reading:

Patients with tracheostomies may experience emergencies such as tube displacement, tube obstruction, and bleeding. Tube displacement can occur due to accidental dislodgement, migration, or erosion into tissues. Tube obstruction can be caused by secretions, lodged foreign bodies, or malfunctioning humidification devices. Bleeding from a tracheostomy can be classified as early or late, with causes including direct injury, anticoagulation, mucosal or tracheal injury, and granulation tissue.

When assessing a patient with a tracheostomy, an ABCDE approach should be used, with attention to red flags indicating a tracheostomy or laryngectomy emergency. These red flags include audible air leaks or bubbles of saliva indicating gas escaping past the cuff, grunting, snoring, stridor, difficulty breathing, accessory muscle use, tachypnea, hypoxia, visibly displaced tracheostomy tube, blood or blood-stained secretions around the tube, increased discomfort or pain, increased air required to keep the cuff inflated, tachycardia, hypotension or hypertension, decreased level of consciousness, and anxiety, restlessness, agitation, and confusion.

Algorithms are available for managing tracheostomy emergencies, including obstruction or displaced tube. Oxygen should be delivered to the face and stoma or tracheostomy tube if there is uncertainty about whether the patient has had a laryngectomy. Tracheostomy bleeding can be classified as early or late, with causes including direct injury, anticoagulation, mucosal or tracheal injury, and granulation tissue. Tracheo-innominate fistula (TIF) is a rare but life-threatening complication that occurs when the tracheostomy tube erodes into the innominate artery. Urgent surgical intervention is required for TIF, and management includes general resuscitation measures and specific measures such as bronchoscopy and applying direct digital pressure to the innominate artery.

When administering adrenaline to a pediatric patient experiencing cardiac arrest, the dosage given through the intraosseous (IO) route is identical to that given through the intravenous (IV) route. Both routes require a dosage of 10 mcg/kg. For instance, if the child weighs 30 kg, the appropriate dosage would be 300 mcg (0.3 mg).

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

Further Reading:

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

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

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

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

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

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

The therapeutic range for carbamazepine is between 4 and 10 mg/L. This range indicates the optimal concentration of the medication in the bloodstream for it to be effective in treating certain conditions. It is important for healthcare professionals to monitor the levels of carbamazepine in a patient’s blood to ensure they are within this range. If the levels are too low, the medication may not be effective, while levels that are too high can lead to potential side effects. By maintaining carbamazepine levels within the therapeutic range, healthcare providers can maximize the benefits of the medication while minimizing any potential risks.

During the examination, the child is observed to be grunting and has had an episode of urinary incontinence. The question asks about the likely complication that has developed.

The most likely complication in this case is cerebral edema. Cerebral edema refers to the swelling of the brain due to an increase in fluid accumulation. It is a severe and potentially life-threatening complication of diabetic ketoacidosis, particularly in children. The symptoms observed, such as headaches, increasing drowsiness, grunting, and urinary incontinence, are indicative of cerebral edema.

Cerebral edema can occur due to various factors, including the rapid correction of hyperglycemia and dehydration, as well as the release of inflammatory mediators. It is crucial to recognize and manage cerebral edema promptly as it can lead to increased intracranial pressure and neurological deterioration.

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.

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

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

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

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

Congenital adrenal hyperplasia (CAH) is a group of inherited disorders that are caused by autosomal recessive genes. The majority of affected patients, over 90%, have a deficiency of the enzyme 21-hydroxylase. This enzyme is encoded by the 21-hydroxylase gene, which is located on chromosome 6p21 within the HLA histocompatibility complex. The second most common cause of CAH is a deficiency of the enzyme 11-beta-hydroxylase. The condition is rare, with an incidence of approximately 1 in 500 births in the UK. It is more prevalent in the offspring of consanguineous marriages.

The deficiency of 21-hydroxylase leads to a deficiency of cortisol and/or aldosterone, as well as an excess of precursor steroids. As a result, there is an increased secretion of ACTH from the anterior pituitary, leading to adrenocortical hyperplasia.

The severity of CAH varies depending on the degree of 21-hydroxylase deficiency. Female infants often exhibit ambiguous genitalia, such as clitoral hypertrophy and labial fusion. Male infants may have an enlarged scrotum and/or scrotal pigmentation. Hirsutism, or excessive hair growth, occurs in 10% of cases.

Boys with CAH often experience a salt-losing adrenal crisis at around 1-3 weeks of age. This crisis is characterized by symptoms such as vomiting, weight loss, floppiness, and circulatory collapse.

The diagnosis of CAH can be made by detecting markedly elevated levels of the metabolic precursor 17-hydroxyprogesterone. Neonatal screening is possible, primarily through the identification of persistently elevated 17-hydroxyprogesterone levels.

In infants presenting with a salt-losing crisis, the following biochemical abnormalities are observed: hyponatremia (low sodium levels), hyperkalemia (high potassium levels), metabolic acidosis, and hypoglycemia.

Boys experiencing a salt-losing crisis will require fluid resuscitation, intravenous dextrose, and intravenous hydrocortisone.

Affected females will require corrective surgery for their external genitalia. However, they have an intact uterus and ovaries and are capable of having children.

The long-term management of both sexes involves lifelong replacement of hydrocortisone (to suppress ACTH levels).

This patient is displaying symptoms and signs that are consistent with a diagnosis of phaeochromocytoma. Phaeochromocytoma is a rare functional tumor that originates from chromaffin cells in the adrenal medulla. There are also less common tumors called extra-adrenal paragangliomas, which develop in the ganglia of the sympathetic nervous system. Both types of tumors secrete catecholamines, leading to symptoms and signs associated with hyperactivity of the sympathetic nervous system.

The most common initial symptom is high blood pressure, which can either be sustained or occur in sudden episodes. The symptoms tend to be intermittent and can happen multiple times a day or very infrequently. However, as the disease progresses, the symptoms become more severe and occur more frequently.

Along with hypertension, the patient may experience the following clinical features:

– Headaches
– Excessive sweating
– Palpitations or rapid heartbeat
– Tremors
– Fever
– Nausea and vomiting
– Anxiety and panic attacks
– A feeling of impending doom
– Pain in the upper abdomen or flank
– Constipation
– Hypertensive retinopathy
– Low blood pressure upon standing (due to decreased blood volume)
– Cardiomyopathy
– Café au lait spots

It is important to note that these symptoms and signs can vary from person to person, and not all individuals with phaeochromocytoma will experience all of them.

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

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

The table below summarizes the most common causes of AKI:

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

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

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

According to NICE guidelines, when evaluating patients with acute upper GI bleeding, it is recommended to use the Blatchford score during the initial assessment and the full Rockall score after endoscopy. The Rockall score is specifically designed to assess the risk of re-bleeding or death in these patients. If a patient’s post-endoscopic Rockall score is less than 3, they are considered to have a low risk of re-bleeding or death and may be eligible for early discharge.

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.

Lipid emulsion is known to cause pancreatitis as a common side effect. According to the AAGBI guidelines, patients who are given lipid emulsion should be closely monitored with regular clinical evaluations. This includes conducting amylase or lipase tests daily for two days after receiving the emulsion.

Further Reading:

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

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

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

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

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

Arterial blood gas (ABG) interpretation is essential for evaluating a patient’s respiratory gas exchange and acid-base balance. The normal values on an ABG may slightly vary between analyzers, but generally, they fall within the following ranges:

pH: 7.35 – 7.45
pO2: 10 – 14 kPa
PCO2: 4.5 – 6 kPa
HCO3-: 22 – 26 mmol/l
Base excess: -2 – 2 mmol/l

In this particular case, the patient’s history indicates an overdose. However, there is no immediate need for intubation as her Glasgow Coma Scale (GCS) score is 11/15, and she can speak, albeit with slurred speech, indicating that she can maintain her own airway.

The relevant ABG findings are as follows:

– Mild hypoxia
– Decreased pH (acidaemia)
– Low PCO2
– Normal bicarbonate
– Elevated lactate

The anion gap is a measure of the concentration of unmeasured anions in the plasma. It is calculated by subtracting the primary measured cations from the primary measured anions in the serum. The reference range for anion gap varies depending on the methodology used, but it is typically between 8 to 16 mmol/L.

In this case, the patient’s anion gap can be calculated using the formula:

Anion gap = [Na+] – [Cl-] – [HCO3-]

Using the given values:

Anion gap = [143] – [99] – [22]
Anion gap = 22

Therefore, it is evident that she has a raised anion gap metabolic acidosis. It is likely a type A lactic acidosis resulting from tissue hypoxia and hypoperfusion. Some potential causes of type A and type B lactic acidosis include:

Type A lactic acidosis:
– Shock (including septic shock)
– Left ventricular failure
– Severe anemia
– Asphyxia
– Cardiac arrest
– Carbon monoxide poisoning
– Respiratory failure
– Severe asthma and COPD
– Regional hypoperfusion

Type B lactic acidosis:
– Renal failure
– Liver failure
– Sepsis (non-hypoxic sepsis)
– Thiamine deficiency
– Al

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

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

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

The supraspinatus muscle is a small muscle located in the upper back. It extends from the supraspinatus fossa of the scapula to the greater tubercle of the humerus. This muscle is part of the rotator cuff, along with three other muscles. The supraspinatus muscle is innervated by the suprascapular nerve, which also innervates the infraspinatus muscle. The suprascapular nerve originates from the upper trunk of the brachial plexus.

The main function of the supraspinatus muscle is to assist the deltoid muscle in abducting the arm at the shoulder joint. Specifically, it is responsible for the initial 15 degrees of arm abduction. Beyond this range, the deltoid muscle takes over as the primary abductor.

In addition to its role in arm movement, the supraspinatus muscle works together with the other rotator cuff muscles to stabilize the shoulder joint. It helps keep the humeral head in the glenoid fossa and counteracts the downward gravitational forces exerted on the shoulder joint by the weight of the arm.

One common test used to assess the supraspinatus muscle is called the empty can test. During this test, the patient is positioned either standing or sitting, with their arms raised parallel to the ground in the scapular plane. The arm is then internally rotated fully, with the thumb facing downward. The clinician applies downward pressure on either the wrists or the elbow, while the patient resists this pressure. If the patient experiences weakness, pain, or both during this resistance, it indicates a possible tear in the supraspinatus tendon or muscle, or a suprascapular nerve neuropathy.

The most effective treatment for pyloric stenosis is pyloromyotomy, a surgical procedure. Before undergoing surgery, the patient should be rehydrated and any electrolyte imbalances should be corrected.

Further Reading:

Pyloric stenosis is a condition that primarily affects infants, characterized by the thickening of the muscles in the pylorus, leading to obstruction of the gastric outlet. It typically presents between the 3rd and 12th weeks of life, with recurrent projectile vomiting being the main symptom. The condition is more common in males, with a positive family history and being first-born being additional risk factors. Bottle-fed children and those delivered by c-section are also more likely to develop pyloric stenosis.

Clinical features of pyloric stenosis include projectile vomiting, usually occurring about 30 minutes after a feed, as well as constipation and dehydration. A palpable mass in the upper abdomen, often described as like an olive, may also be present. The persistent vomiting can lead to electrolyte disturbances, such as hypochloremia, alkalosis, and mild hypokalemia.

Ultrasound is the preferred diagnostic tool for confirming pyloric stenosis. It can reveal specific criteria, including a pyloric muscle thickness greater than 3 mm, a pylorus longitudinal length greater than 15-17 mm, a pyloric volume greater than 1.5 cm3, and a pyloric transverse diameter greater than 13 mm.

The definitive treatment for pyloric stenosis is pyloromyotomy, a surgical procedure that involves making an incision in the thickened pyloric muscle to relieve the obstruction. Before surgery, it is important to correct any hypovolemia and electrolyte disturbances with intravenous fluids. Overall, pyloric stenosis is a relatively common condition in infants, but with prompt diagnosis and appropriate management, it can be effectively treated.

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 the bowel and allow C. difficile to multiply. This can lead to inflammation and bleeding in the mucosa of the large intestine, resulting in a distinct appearance known as pseudomembranous. The main symptoms of C. difficile infection (CDI) include abdominal cramps, bloody and/or watery diarrhea, and fever. It is worth noting that the majority of CDI cases occur in individuals over the age of 65.

CDI is considered to be the most severe consequence of antibiotic treatment and is now a significant cause of illness and death. While CDI can occur after treatment with any antibiotic, the risk is particularly high with prolonged use of broad-spectrum antibiotics. Recently, two research groups conducted a meta-analysis to assess the risk associated with different classes of antibiotics.

Their findings revealed that the risk of CDI increased nearly sevenfold after antibiotic treatment (odds ratio, 6.91). Among the various antibiotic classes, clindamycin posed the greatest risk (odds ratio, 20.43), followed by fluoroquinolones (odds ratio, 5.65), cephalosporins (odds ratio, 4.47), penicillins (odds ratio, 3.25), macrolides (odds ratio, 2.55), and trimethoprim/sulfonamides (odds ratio, 1.84). Tetracyclines, on the other hand, were not found to be associated with an increased risk of CDI (odds ratio, 0.91).

For more information on this topic, you may consider reading the article Antibiotic Classes and Risk for Clostridium difficile Infection.

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 clinical manifestations of theophylline toxicity are more closely associated with acute poisoning rather than chronic overexposure. The primary clinical features of theophylline toxicity include headache, dizziness, nausea and vomiting, abdominal pain, tachycardia and dysrhythmias, seizures, mild metabolic acidosis, hypokalaemia, hypomagnesaemia, hypophosphataemia, hypo- or hypercalcaemia, and hyperglycaemia. Seizures are more prevalent in cases of acute overdose compared to chronic overexposure. In contrast, chronic theophylline overdose typically presents with minimal gastrointestinal symptoms. Cardiac dysrhythmias are more frequently observed in individuals who have experienced chronic overdose rather than acute overdose.

The top priority when dealing with suspected epiglottitis is to assess and secure the airway. This is especially important in patients who have not been vaccinated against Haemophilus influenzae type b (HiB), as they are at risk for complications from this infection. Classic signs of epiglottitis include tripod positioning, drooling, stridor, and a muffled voice. It is crucial to avoid agitating patients, particularly children, during examination or procedures, as this can trigger laryngospasm and potentially lead to airway obstruction. In such cases, it is recommended to call in senior ENT and anaesthetic support to perform laryngoscopy and be prepared for intubation or tracheostomy if necessary to address any airway compromise. If the patient is in a critical condition, securing the airway through intubation becomes the top priority.

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.

According to the latest guidelines from NICE, it is recommended that adult patients who are undergoing treatment for acute leukaemia, stem cell transplants, or solid tumours and are expected to experience significant neutropenia as a result of chemotherapy, should be offered prophylaxis with a fluoroquinolone such as ciprofloxacin (500 mg taken orally twice daily) during the period when neutropenia is expected. This is to help prevent the occurrence of neutropenic sepsis, a serious infection that can occur in cancer patients with low levels of neutrophils.

Reference:
NICE guidance: ‘Neutropenic sepsis: prevention and management of neutropenic sepsis in cancer patients’

Typically, children with viral gastroenteritis experience diarrhoea for a duration of 5-7 days. Vomiting, on the other hand, usually subsides within 1-2 days.

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.

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.

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.

Cephalexin is a type of cephalosporin medication that is eliminated from the body through the kidneys. Cephalosporin drugs have been linked to direct harm to the kidneys and can build up in individuals with kidney problems.

The typical dosage for cephalexin is 250 mg taken four times a day. For more severe infections or infections caused by organisms that are less susceptible to the medication, the dosage may be doubled. The manufacturer recommends reducing the frequency of dosing in individuals with kidney impairment. In cases where the glomerular filtration rate (GFR) is less than 10 ml/minute, the recommended dosage is 250-500 mg taken once or twice a day, depending on the severity of the infection.

Acute cholecystitis occurs when a stone becomes stuck in the outlet of the gallbladder, causing irritation of the wall and resulting in chemical cholecystitis. This leads to the accumulation of pus within the gallbladder, which is typically sterile at first. However, there is a possibility of secondary infection with enteric organisms like Escherichia coli and Klebsiella spp.

The clinical features of acute cholecystitis include severe pain in the right upper quadrant or epigastrium, which can radiate to the back and lasts for more than 12 hours. Fevers and rigors are often present, along with common symptoms like nausea and vomiting. Murphy’s sign is a useful diagnostic tool, as it has a high sensitivity and positive predictive value for acute cholecystitis. However, its specificity is lower, as it can also be positive in biliary colic and ascending cholangitis.

In cases of acute cholecystitis, the white cell count and C-reactive protein (CRP) levels are usually elevated. AST, ALT, and ALP may also show elevation, but they can often be within the normal range. Bilirubin levels may be mildly elevated, but they can also be normal. If there is a significant increase in AST, ALT, ALP, and/or bilirubin, it may indicate the presence of other biliary tract conditions such as ascending cholangitis or choledocholithiasis.

It is important to note that there is some overlap in the presentation of biliary colic, acute cholecystitis, and ascending cholangitis. To differentiate between these diagnoses, the following list can be helpful:

Biliary colic:
– Pain duration: Less than 12 hours
– Fever: Absent
– Murphy’s sign: Negative
– WCC & CRP: Normal
– AST, ALT & ALP: Normal
– Bilirubin: Normal

Acute cholecystitis:
– Pain duration: More than 12 hours
– Fever: Present
– Murphy’s sign: Positive
– WCC & CRP: Elevated
– AST, ALT & ALP: Normal or mildly elevated
– Bilirubin: Normal or mildly elevated

Ascending cholangitis:
– Pain duration: Variable
– Fever: Present
– Murphy’s sign: Negative
– WCC & CRP: Elevated
– AST, ALT & ALP: Elevated

The septum, which is a part of the heart, can be best identified by examining leads V1 and V2. The septum receives its blood supply from the proximal left anterior descending artery (LAD). The LAD is responsible for supplying blood to the anterior myocardium and also contributes to the blood supply of the lateral myocardium. If the LAD becomes blocked, it can result in ST elevation in all the chest leads.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

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.

This patient is showing the psoas sign, which is a medical indication of irritation in the iliopsoas group of hip flexors located in the abdomen. In this case, it is most likely due to acute appendicitis.

To elicit the psoas sign, the thigh of a patient lying on their side with extended knees can be passively extended, or the patient can be asked to actively flex the thigh at the hip. If these movements result in abdominal pain or if the patient resists due to pain, then the psoas sign is considered positive.

The pain occurs because the psoas muscle is adjacent to the peritoneal cavity. When the muscles are stretched or contracted, they cause friction against the nearby inflamed tissues. This strongly suggests that the appendix is retrocaecal in position.

There are other clinical signs that support a diagnosis of appendicitis. These include Rovsing’s sign, which is pain in the right lower quadrant when the left lower quadrant is palpated. The obturator sign is pain experienced during internal rotation of the right thigh, indicating a pelvic appendix. Dunphy’s sign is increased pain with coughing, and Markle sign is pain in the right lower quadrant when dropping from standing on the toes to the heels with a jarring landing.

A positive Murphy’s sign is observed in cases of acute cholecystitis.

If a patient’s INR reading is above 5, it is necessary to take action. In this case, the patient’s INR is between 5 and 8, but there is no evidence of bleeding. According to the provided table, it is recommended to temporarily stop 1-2 doses of warfarin and closely monitor the INR. While it may be optional to switch antibiotics, it is not a crucial step in this situation.

Further Reading:

Management of High INR with Warfarin

Major Bleeding:
– Stop warfarin immediately.
– Administer intravenous vitamin K 5 mg.
– Administer 25-50 u/kg four-factor prothrombin complex concentrate.
– If prothrombin complex concentrate is not available, consider using fresh frozen plasma (FFP).
– Seek medical attention promptly.

INR > 8.0 with Minor Bleeding:
– Stop warfarin immediately.
– Administer intravenous vitamin K 1-3mg.
– Repeat vitamin K dose if INR remains high after 24 hours.
– Restart warfarin when INR is below 5.0.
– Seek medical advice if bleeding worsens or persists.

INR > 8.0 without Bleeding:
– Stop warfarin immediately.
– Administer oral vitamin K 1-5 mg using the intravenous preparation orally.
– Repeat vitamin K dose if INR remains high after 24 hours.
– Restart warfarin when INR is below 5.0.
– Seek medical advice if any symptoms or concerns arise.

INR 5.0-8.0 with Minor Bleeding:
– Stop warfarin immediately.
– Administer intravenous vitamin K 1-3mg.
– Restart warfarin when INR is below 5.0.
– Seek medical advice if bleeding worsens or persists.

INR 5.0-8.0 without Bleeding:
– Withhold 1 or 2 doses of warfarin.
– Reduce subsequent maintenance dose.
– Monitor INR closely and seek medical advice if any concerns arise.

Note: In cases of intracranial hemorrhage, prothrombin complex concentrate should be considered as it is faster acting than fresh frozen plasma (FFP).

Erb’s palsy, also known as Erb-Duchenne palsy, is a condition where the arm becomes paralyzed due to an injury to the upper roots of the brachial plexus. The primary root affected is usually C5, although C6 may also be involved in some cases. The main cause of Erb’s palsy is when the arm experiences excessive force during a difficult childbirth, but it can also occur in adults as a result of shoulder trauma.

Clinically, the affected arm will hang by the side with the elbow extended and the forearm turned inward (known as the waiter’s tip sign). Upon examination, there will be a loss of certain movements:

– Shoulder abduction (involving the deltoid and supraspinatus muscles)
– Shoulder external rotation (infraspinatus muscle)
– Elbow flexion (biceps and brachialis muscles)

It is important to differentiate Erb’s palsy from Klumpke’s palsy, which affects the lower roots of the brachial plexus (C8 and T1). Klumpke’s palsy presents with a claw hand due to paralysis of the intrinsic hand muscles, along with sensory loss along the ulnar side of the forearm and hand. If T1 is affected, there may also be the presence of Horner’s syndrome.

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

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In this case, the patient has already received two doses of benzodiazepine and is currently on a phenytoin infusion. However, despite these treatments, the seizures persist, and it has been 20 minutes since the infusion started. At this point, the preferred treatment option is to induce general anesthesia. The induction agents that can be considered include thiopental sodium, propofol, and midazolam. There is no need to administer intravenous thiamine in this situation.

The management of status epilepticus involves several general measures, which are outlined in the following table:

1st stage (Early status, 0-10 minutes):
– Secure the airway and provide resuscitation
– Administer oxygen
– Assess cardiorespiratory function
– Establish intravenous access

2nd stage (0-30 minutes):
– Implement regular monitoring
– Consider the possibility of non-epileptic status
– Initiate emergency antiepileptic drug (AED) therapy
– Perform emergency investigations
– Administer glucose or intravenous thiamine if alcohol abuse or impaired nutrition is suspected
– Treat severe acidosis if present

3rd stage (0-60 minutes):
– Determine the underlying cause of status epilepticus
– Notify the anesthetist and intensive care unit (ITU)
– Identify and treat any medical complications
– Consider pressor therapy if necessary

4th stage (30-90 minutes):
– Transfer the patient to the intensive care unit
– Establish intensive care and EEG monitoring
– Initiate long-term maintenance AED therapy
– Perform further investigations as needed, such as brain imaging or lumbar puncture

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

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

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

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

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

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

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

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

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.

According to NICE, hyoscine butylbromide is recommended as the initial medication for managing nausea and vomiting in individuals with obstructive bowel disorders who are in the last days of life. NICE provides guidance on how to handle these symptoms in the final days of life, which includes assessing the potential causes of nausea and vomiting in the dying person. This may involve considering factors such as certain medications, recent chemotherapy or radiotherapy, psychological causes, biochemical causes like hypercalcemia, raised intracranial pressure, gastrointestinal motility disorder, ileus, or bowel obstruction.

It is important to discuss the available options for treating nausea and vomiting with the dying person and their loved ones. Non-pharmacological methods should also be considered when managing these symptoms in someone in the last days of life. When selecting medications for nausea and vomiting, factors such as the likely cause and reversibility of the symptoms, potential side effects (including sedation), other symptoms the person may be experiencing, and the desired balancing of effects when managing other symptoms should be taken into account. Additionally, compatibility and potential drug interactions with other medications the person is taking should be considered.

For individuals in the last days of life with obstructive bowel disorders who have nausea or vomiting, hyoscine butylbromide is recommended as the first-line pharmacological treatment. If the symptoms do not improve within 24 hours of starting treatment with hyoscine butylbromide, octreotide may be considered as an alternative option.

For more information, refer to the NICE guidance on the care of dying adults in the last days of life. https://www.nice.org.uk/guidance/ng31

A summary of the vessels involved in different types of myocardial infarction, along with the corresponding ECG leads and the location of the infarction.

For instance, an anteroseptal infarction involving the left anterior descending artery is indicated by ECG leads V1-V3. Similarly, an anterior infarction involving the left anterior descending artery is indicated by leads V3-V4.

In cases of anterolateral infarctions, both the left anterior descending artery and the left circumflex artery are involved, and this is reflected in ECG leads V5-V6. An extensive anterior infarction involving the left anterior descending artery is indicated by leads V1-V6.

Lateral infarcts involving the left circumflex artery are indicated by leads I, II, aVL, and V6. Inferior infarctions, on the other hand, involve either the right coronary artery (in 80% of cases) or the left circumflex artery (in 20% of cases), and this is shown by leads II, III, and aVF.

In the case of a right ventricular infarction, the right coronary artery is involved, and this is indicated by leads V1 and V4R. Lastly, a posterior infarction involving the right coronary artery is shown by leads V7-V9.

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

Further Reading:

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

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

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

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

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

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

An anterolateral thoracotomy is a surgical procedure performed on the front part of the chest wall. It is commonly used in Emergency Department thoracotomy, with a preference for a left-sided approach in patients with traumatic arrest or left-sided chest injuries. However, in patients with right-sided chest injuries and profound hypotension but have not arrested, a right-sided approach is recommended.

The procedure is carried out in the following steps:
– An incision is made along the 4th or 5th intercostal space, starting from the sternum at the front and extending to the posterior axillary line.
– The incision should be deep enough to partially cut through the latissimus dorsi muscle.
– The skin, subcutaneous fat, and superficial portions of the pectoralis and serratus muscles are divided.
– The parietal pleura is divided, allowing entry into the pleural cavity.
– The intercostal muscles are completely cut, and a rib spreader is placed and opened to provide visualization of the thoracic cavity.
– The anterolateral approach allows access to important anatomical structures during resuscitation, including the pulmonary hilum, heart, and aorta.

In cases where there is suspicion of a right-sided heart injury, an additional incision can be made on the right side, extending across the entire chest. This is known as a bilateral anterolateral thoracotomy or a clamshell thoracotomy.

Oral bisphosphonates are the primary choice for treating osteoporotic fragility fractures in individuals who have already experienced such fractures. After a fragility fracture, it is advised to start taking a bisphosphonate, typically alendronic acid, and consider supplementing with calcium and vitamin D.

There are other treatment options available for preventing fragility fractures after an initial occurrence. These include raloxifene, teriparatide, and denosumab.

Epididymal cysts are commonly observed in men who are over the age of 40. They often appear in multiple numbers and can be found on both sides. These cysts are typically well-defined, soft to the touch, and can be illuminated when light is passed through them. Since they develop in the epididymis, they can be felt as separate from the testis, which helps to differentiate them from hydroceles. In most cases, these cysts cause no significant issues and do not require any treatment. However, larger cysts can become bothersome and may need to be drained or surgically removed.

In the latest guideline published in 2021 by RCEM and NPIS regarding antidote availability for emergency departments, it is emphasized that immediate access to sodium bicarbonate is essential for treating TCA overdose. It is worth noting that previous versions of the guideline included glucagon as a recommended treatment for TCA overdose, but this reference has been omitted in the latest edition.

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.

For adults, it is recommended to perform chest compressions at a rate of 100-120 compressions per minute. The depth of the compressions should be at least 5-6 cm.

Further Reading:

In the event of an adult experiencing cardiorespiratory arrest, it is crucial for doctors to be familiar with the Advanced Life Support (ALS) algorithm. They should also be knowledgeable about the proper technique for chest compressions, the appropriate rhythms for defibrillation, the reversible causes of arrest, and the drugs used in advanced life support.

During chest compressions, the rate should be between 100-120 compressions per minute, with a depth of compression of 5-6 cm. The ratio of chest compressions to rescue breaths should be 30:2. It is important to change the person giving compressions regularly to prevent fatigue.

There are two shockable ECG rhythms that doctors should be aware of: ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT). These rhythms require defibrillation.

There are four reversible causes of cardiorespiratory arrest, known as the 4 H’s and 4 T’s. The 4 H’s include hypoxia, hypovolemia, hypo or hyperkalemia or metabolic abnormalities, and hypothermia. The 4 T’s include thrombosis (coronary or pulmonary), tension pneumothorax, tamponade, and toxins. Identifying and treating these reversible causes is crucial for successful resuscitation.

When it comes to resus drugs, they are considered of secondary importance during CPR due to the lack of high-quality evidence for their efficacy. However, adrenaline (epinephrine) and amiodarone are the two drugs included in the ALS algorithm. Doctors should be familiar with the dosing, route, and timing of administration for both drugs.

Adrenaline should be administered intravenously at a concentration of 1 in 10,000 (100 micrograms/mL). It should be repeated every 3-5 minutes. Amiodarone is initially given at a dose of 300 mg, either from a pre-filled syringe or diluted in 20 mL of Glucose 5%. If required, an additional dose of 150 mg can be given by intravenous injection. This is followed by an intravenous infusion of 900 mg over 24 hours. The first dose of amiodarone is given after 3 shocks.

Hypothyroidism is a condition characterized by an underactive thyroid gland, which leads to a decrease in the production of thyroid hormones. This can result in various clinical features. Some common symptoms include fatigue, lethargy, and cold intolerance. Patients may also experience bradycardia (a slow heart rate) and diastolic hypertension (high blood pressure). Hair loss and weight gain are also commonly seen in individuals with hypothyroidism. Other possible symptoms include constipation, poor appetite, and carpal tunnel syndrome. Skin pigmentation changes, particularly yellow discoloration, may occur due to carotene deposition in the dermis, most notably on the palms and soles.

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.

According to the 2011 recommendations from the World Health Organization (WHO), the following criteria are used to diagnose diabetes mellitus:

– A random venous plasma glucose concentration that exceeds 11.1 mmol/l.
– A fasting plasma glucose concentration that is higher than 7.0 mmol/l.
– A two-hour plasma glucose concentration that exceeds 11.1 mmol/l, measured two hours after consuming 75g of anhydrous glucose during an oral glucose tolerance test (OGTT).
– An HbA1c level that is greater than 48 mmol/mol (equivalent to 6.5%).

These guidelines provide specific thresholds for diagnosing diabetes mellitus based on various glucose measurements and HbA1c levels. It is important for healthcare professionals to consider these criteria when evaluating individuals for diabetes mellitus.

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.