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.

Shingles, also known as herpes zoster, occurs when the varicella zoster virus becomes active again in a specific area of the skin. This results in a rash characterized by clusters of fluid-filled blisters or vesicles on a red base. Over time, these blisters will dry up and form crusts before eventually healing.

Further Reading:

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

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

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

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

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

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

The primary way hepatitis A is transmitted is through the ingestion of fecal matter containing the virus. On the other hand, all the other organisms mentioned in this question are typically transmitted through sexual contact.

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

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

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

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

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

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

During the first trimester of pregnancy, the use of warfarin can lead to a condition known as fetal warfarin syndrome. This condition is characterized by nasal hypoplasia, bone stippling, bilateral optic atrophy, and intellectual disability in the baby. However, if warfarin is taken during the second or third trimester, it can cause optic atrophy, cataracts, microcephaly, microphthalmia, intellectual disability, and both fetal and maternal hemorrhage.

There are several other drugs that can have adverse effects during pregnancy. For example, ACE inhibitors like ramipril can cause hypoperfusion, renal failure, and the oligohydramnios sequence if taken during the second and third trimesters. Aminoglycosides such as gentamicin can lead to ototoxicity and deafness in the baby. 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 of aspirin (e.g. 75 mg) do not pose significant risks.

Benzodiazepines like diazepam, when taken late in pregnancy, can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if taken during the first trimester, can cause phalangeal abnormalities, while their use in the second and third trimesters can lead to fetal growth retardation. Carbamazepine can result in hemorrhagic disease of the newborn and neural tube defects. Chloramphenicol can cause gray baby syndrome. Corticosteroids, if taken during the first trimester, may cause orofacial clefts.

Danazol, if taken during the first trimester, can cause masculinization of the female fetuses genitals. Finasteride should not be handled by pregnant women as crushed or broken tablets can be absorbed through the skin and affect male sex organ development. Haloperidol, if taken during the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the newborn.

Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the baby. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations and spontaneous abortion.

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.

One type of brainstem infarction is characterized by the presence of complete deafness on the same side as the affected area. This condition is unlikely to be caused by a transient ischemic attack (TIA) or stroke due to the patient’s age and absence of risk factors. Benign paroxysmal positional vertigo (BPPV) causes brief episodes of vertigo triggered by head movements. On the other hand, vestibular neuronitis (also known as vestibular neuritis) causes a persistent sensation of vertigo rather than intermittent episodes.

Further Reading:

Meniere’s disease is a disorder of the inner ear that is characterized by recurrent episodes of vertigo, tinnitus, and low frequency hearing loss. The exact cause of the disease is unknown, but it is believed to be related to excessive pressure and dilation of the endolymphatic system in the middle ear. Meniere’s disease is more common in middle-aged adults, but can occur at any age and affects both men and women equally.

The clinical features of Meniere’s disease include episodes of vertigo that can last from minutes to hours. These attacks often occur in clusters, with several episodes happening in a week. Vertigo is usually the most prominent symptom, but patients may also experience a sensation of aural fullness or pressure. Nystagmus and a positive Romberg test are common findings, and the Fukuda stepping test may also be positive. While symptoms are typically unilateral, bilateral symptoms may develop over time.

Rinne’s and Weber’s tests can be used to help diagnose Meniere’s disease. In Rinne’s test, air conduction should be better than bone conduction in both ears. In Weber’s test, the sound should be heard loudest in the unaffected (contralateral) side due to the sensorineural hearing loss.

The natural history of Meniere’s disease is that symptoms often resolve within 5-10 years, but most patients are left with some residual hearing loss. Psychological distress is common among patients with this condition.

The diagnostic criteria for Meniere’s disease include clinical features consistent with the disease, confirmed sensorineural hearing loss on audiometry, and exclusion of other possible causes.

Management of Meniere’s disease involves an ENT assessment to confirm the diagnosis and perform audiometry. Patients should be advised to inform the DVLA and may need to cease driving until their symptoms are under control. Acute attacks can be treated with buccal or intramuscular prochlorperazine, and hospital admission may be necessary in some cases. Betahistine may be beneficial for prevention of symptoms.

Epididymo-orchitis refers to the inflammation of the epididymis and/or testicle. It typically presents with sudden pain, swelling, and inflammation in the affected area. This condition can also occur chronically, which means that the pain and inflammation last for more than six months.

The causes of epididymo-orchitis vary depending on the age of the patient. In men under 35 years old, the infection is usually sexually transmitted and caused by Chlamydia trachomatis or Neisseria gonorrhoeae. In men over 35 years old, the infection is usually non-sexually transmitted and occurs as a result of enteric organisms that cause urinary tract infections, with Escherichia coli being the most common. However, there can be some overlap between these groups, so it is important to obtain a thorough sexual history in all age groups.

Mumps should also be considered as a potential cause of epididymo-orchitis in the 15 to 30 age group, as mumps orchitis occurs in around 40% of post-pubertal boys with mumps.

While most cases of epididymo-orchitis are infective, non-infectious causes can also occur. These include genito-urinary surgery, vasectomy, urinary catheterization, Behcet’s disease, sarcoidosis, and drug-induced cases such as those caused by amiodarone.

Patients with epididymo-orchitis typically present with unilateral scrotal pain and swelling that develops relatively quickly. The affected testis will be tender to touch, and there is usually a palpable swelling of the epididymis that starts at the lower pole of the testis and spreads towards the upper pole. The testis itself may also be involved, and there may be redness and/or swelling of the scrotum on the affected side. Patients may experience fever and urethral discharge as well.

The most important differential diagnosis to consider is testicular torsion, which requires immediate medical attention within 6 hours of onset to save the testicle. Testicular torsion is more likely in men under the age of 20, especially if the pain is very severe and sudden. It typically presents around four hours after onset. In this case, the patient’s age, longer history of symptoms, and the presence of fever are more indicative of epididymo-orchitis.

This woman is displaying symptoms and signs that are in line with a diagnosis of meningococcal septicaemia. In the United Kingdom, the majority of cases of meningococcal septicaemia are caused by Neisseria meningitidis group B.

The implementation of a vaccination program for Neisseria meningitidis group C has significantly reduced the prevalence of this particular type. However, a vaccine for group B disease is currently undergoing clinical trials and is not yet accessible for widespread use.

Addison’s disease, also known as adrenal insufficiency, is characterized by a gradual onset of symptoms over several weeks, although it can sometimes occur suddenly. The diagnosis of Addison’s disease can be challenging as its symptoms, such as fatigue, muscle pain, weight loss, and nausea, are non-specific. However, a key feature is low blood pressure. The disease is associated with changes in pigmentation, ranging from increased pigmentation due to elevated ACTH levels to the development of vitiligo caused by the autoimmune destruction of melanocytes.

Patients with Addison’s disease often exhibit hyponatremia (low sodium levels) and hyperkalemia (high potassium levels). If the patient is dehydrated, this may be reflected in elevated urea and creatinine levels. While hypercalcemia (high calcium levels) and hypoglycemia (low blood sugar levels) can occur in Addison’s disease, they are less common than hyponatremia and hyperkalemia.

In contrast, diabetes insipidus, characterized by normal or elevated sodium levels, does not cause pigmentation changes. Cushing’s syndrome, which results from excess steroid production, is almost the opposite of Addison’s disease, with hypertension (high blood pressure) and hypokalemia (low potassium levels) being typical symptoms. Phaeochromocytoma, on the other hand, is associated with episodes of high blood pressure and hyperglycemia (high blood sugar levels).

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.

This individual is diagnosed with an acquired cholesteatoma, which is an expanding growth of the stratified keratinising epithelium in the middle ear. It develops due to dysfunction of the Eustachian tube and chronic otitis media caused by the retraction of the squamous elements of the tympanic membrane into the middle ear space.

The most important method for assessing the presence of a cholesteatoma is otoscopy. A retraction pocket observed in the attic or posterosuperior quadrant of the tympanic membrane is a characteristic sign of an acquired cholesteatoma. This is often accompanied by the presence of granulation tissue and squamous debris. The presence of a granular polyp within the ear canal also strongly suggests a cholesteatoma.

If left untreated, a cholesteatoma can lead to various complications including conductive deafness, facial nerve palsy, brain abscess, meningitis, and labyrinthitis. Therefore, it is crucial to urgently refer this individual to an ear, nose, and throat (ENT) specialist for a CT scan and surgical removal of the lesion.

Diabetes Mellitus:
– Definition: a group of metabolic disorders characterized by persistent hyperglycemia caused by deficient insulin secretion, resistance to insulin, or both.
– Types: Type 1 diabetes (absolute insulin deficiency), Type 2 diabetes (insulin resistance and relative insulin deficiency), Gestational diabetes (develops during pregnancy), Other specific types (monogenic diabetes, diabetes secondary to pancreatic or endocrine disorders, diabetes secondary to drug treatment).
– Diagnosis: Type 1 diabetes diagnosed based on clinical grounds in adults presenting with hyperglycemia. Type 2 diabetes diagnosed in patients with persistent hyperglycemia and presence of symptoms or signs of diabetes.
– Risk factors for type 2 diabetes: obesity, inactivity, family history, ethnicity, history of gestational diabetes, certain drugs, polycystic ovary syndrome, metabolic syndrome, low birth weight.

Hypoglycemia:
– Definition: lower than normal blood glucose concentration.
– Diagnosis: defined by Whipple’s triad (signs and symptoms of low blood glucose, low blood plasma glucose concentration, relief of symptoms after correcting low blood glucose).
– Blood glucose level for hypoglycemia: NICE defines it as <3.5 mmol/L, but there is inconsistency across the literature.
– Signs and symptoms: adrenergic or autonomic symptoms (sweating, hunger, tremor), neuroglycopenic symptoms (confusion, coma, convulsions), non-specific symptoms (headache, nausea).
– Treatment options: oral carbohydrate, buccal glucose gel, glucagon, dextrose. Treatment should be followed by re-checking glucose levels.

Treatment of neonatal hypoglycemia:
– Treat with glucose IV infusion 10% given at a rate of 5 mL/kg/hour.
– Initial stat dose of 2 mL/kg over five minutes may be required for severe hypoglycemia.
– Mild asymptomatic persistent hypoglycemia may respond to a single dose of glucagon.
– If hypoglycemia is caused by an oral anti-diabetic drug, the patient should be admitted and ongoing glucose infusion or other therapies may be required.

Note: Patients who have a hypoglycemic episode with a loss of warning symptoms should not drive and should inform the DVLA.

The FeverPAIN score is a scoring system that is 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, different recommendations are given regarding the use of antibiotics.

If the score is 0-1, it is unlikely to be a streptococcal infection, with only a 13-18% chance of streptococcus isolation. Therefore, antibiotics are not recommended in this case. If the score is 2-3, there is a higher chance (34-40%) of streptococcus isolation, so delayed prescribing of antibiotics is considered, with a 3-day ‘back-up prescription’. If the score is 4 or higher, there is a 62-65% chance of streptococcus isolation, and immediate antibiotic use is recommended if the infection is severe. Otherwise, a 48-hour short back-up prescription is suggested.

The Fever PAIN score was developed from a study that included 1760 adults and children aged three and over. It was then tested in a trial that compared three different prescribing strategies: empirical delayed prescribing, using the score to guide prescribing, and combining the score with the use of a near-patient test (NPT) for streptococcus. The use of the score resulted in faster symptom resolution and a reduction in antibiotic prescribing, both by one third. However, the addition of the NPT did not provide any additional benefit.

Overall, the FeverPAIN score is a useful tool for assessing acute sore throats and guiding antibiotic prescribing decisions. It has been shown to be effective in reducing unnecessary antibiotic use and improving patient outcomes.

The guidelines from the European League Against Rheumatism (EULAR) regarding the diagnosis of gout state that if a joint becomes swollen, tender, and red, accompanied by acute pain that intensifies over a period of 6-12 hours, it is highly likely to be a crystal arthropathy. While pseudogout is also a possibility, it is much less probable, with gout being the most likely diagnosis in such cases.

In cases of acute gout, the joint most commonly affected is the first metatarsal-phalangeal joint, accounting for 50-75% of cases. The underlying cause of gout is hyperuricaemia, and the clinical diagnosis can be confirmed by the presence of negatively birefringent crystals in the synovial fluid aspirate.

For the treatment of acute gout attacks, the usual approach involves the use of either NSAIDs or colchicine.

Prussian blue is a substance that helps remove radioactive caesium from the body, a process known as decorporation. It is specifically effective for caesium exposure. When taken orally, Prussian blue binds to the radioactive caesium, forming a compound that can be excreted from the body, preventing further absorption. By using Prussian blue, the whole body radiation dose can be reduced by approximately two-thirds. Radioactive caesium is utilized in various medical, geological, and industrial applications, although incidents of environmental contamination are rare, they have been reported in Western Australia and Eastern Thailand during the first quarter of 2023.

Further Reading:

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

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

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

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

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

Slipped upper femoral epiphysis (SUFE), also referred to as slipped capital femoral epiphysis, is a rare but significant hip disorder that primarily affects children. It occurs when the growth plate slips at the epiphysis, causing the head of the femur to shift from its normal position on the femoral neck. Specifically, the femoral epiphysis remains in the acetabulum while the metaphysis moves forward and externally rotates.

SUFE typically presents later in boys, usually between the ages of 10 and 17, compared to girls who typically experience it between 8 and 15 years of age. Several risk factors contribute to its development, including being male, being overweight, having immature skeletal maturity, having a positive family history, being of Pacific Island or African origin, having hypothyroidism, growth hormone deficiency, or hypogonadism.

Patients with SUFE commonly experience hip pain and a limp. In severe cases, a leg length discrepancy may be noticeable. While the condition may not be immediately apparent on an anteroposterior (AP) film, it is usually detectable on a frog-leg lateral film. A diagnostic sign is the failure of a line drawn up the lateral edge of the femoral neck (known as the line of Klein) to intersect the epiphysis during the acute stage, also known as Trethowan’s sign.

Surgical pinning is the most common treatment for SUFE. In approximately 20% of cases, bilateral SUFE occurs, prompting some surgeons to recommend prophylactic pinning of the unaffected hip. If a significant deformity is present, osteotomies or even arthroplasty may be necessary.

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

One of the clinical features of mitral stenosis is malar flush, which refers to a reddening or flushing of the cheeks. Other clinical features include a mid-late diastolic murmur that is best heard during expiration, a loud S1 heart sound with an opening snap, a low volume pulse, atrial fibrillation, and signs of pulmonary edema such as crepitations or the presence of white or pink frothy sputum.

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.

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

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

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

High doses of aspirin can lead to 1st trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g. 75 mg) do not pose significant risks.

Benzodiazepines, including diazepam, when administered late in pregnancy, can result in respiratory depression and a neonatal withdrawal syndrome.

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

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

Chloramphenicol is associated with grey baby syndrome.

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

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

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

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

Heparin can lead to maternal bleeding and thrombocytopenia.

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

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

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

This question delves into the challenges of managing chronic illnesses and promoting patient self-care, while also considering concerns regarding confidentiality. The patient in question is mentally capable and already has caregivers at home. It is both the patient’s preference and the most clinically sensible decision to discharge them back home. It is important to address any family concerns, ensuring that the family members have the patient’s best interests at heart rather than personal or financial motives. It is not appropriate to delegate this conversation to a nurse, as it is your responsibility as the healthcare provider. It is crucial to communicate with the patient’s general practitioner, but it is important to involve the patient in any decision regarding a referral to a nursing home.

Hypercalcaemia, which is an elevated level of calcium in the blood, is most commonly caused by primary hyperparathyroidism and malignancy in the UK. However, there are other factors that can contribute to hypercalcaemia as well. These include an increase in dietary intake of calcium, excessive intake of vitamin D, tertiary hyperparathyroidism, overactive thyroid gland (hyperthyroidism), Addison’s disease, sarcoidosis, Paget’s disease, multiple myeloma, phaeochromocytoma, and milk-alkali syndrome. Additionally, certain medications such as lithium, thiazide diuretics, and theophyllines can also lead to hypercalcaemia. It is important to be aware of these various causes in order to properly diagnose and treat this condition.

This patient is displaying symptoms and signs that are consistent with a diagnosis of acute pyelonephritis. Additionally, they are showing signs of sepsis, which indicates a more serious illness or condition. Therefore, it would be advisable to admit the patient for inpatient treatment.

According to the recommendations from the National Institute for Health and Care Excellence (NICE), patients with pyelonephritis should be admitted if it is severe or if they exhibit any signs or symptoms that suggest a more serious condition, such as sepsis. Signs of sepsis include significant tachycardia, hypotension, or breathlessness, as well as marked signs of illness like impaired level of consciousness, profuse sweating, rigors, pallor, or significantly reduced mobility. A temperature greater than 38°C or less than 36°C is also indicative of sepsis.

NICE also advises considering referral or seeking specialist advice for individuals with acute pyelonephritis if they are significantly dehydrated or unable to take oral fluids and medicines, if they are pregnant, if they have a higher risk of developing complications due to known or suspected abnormalities of the genitourinary tract or underlying diseases like diabetes mellitus or immunosuppression, or if they have recurrent episodes of urinary tract infections (UTIs).

For non-pregnant women and men, the recommended choice of antibacterial therapy is as follows: oral first-line options include cefalexin, ciprofloxacin, or co-amoxiclav (taking into account local microbial resistance data), and trimethoprim if sensitivity is known. Intravenous first-line options are amikacin, ceftriaxone, cefuroxime, ciprofloxacin, or gentamicin if the patient is severely unwell or unable to take oral treatment. Co-amoxiclav may be used if given in combination or if sensitivity is known. Antibacterials may be combined if there are concerns about susceptibility or sepsis. For intravenous second-line options, it is recommended to consult a local microbiologist.

For pregnant women, the recommended choice of antibacterial therapy is cefalexin for oral first-line treatment. If the patient is severely unwell or unable to take oral treatment, cefuroxime is the recommended intravenous first-line option.

The maximum safe dose of plain lidocaine is 3 mg per kilogram of body weight, with a maximum limit of 200 mg. However, when lidocaine is administered with adrenaline in a 1:200,000 ratio, the maximum safe dose increases to 7 mg per kilogram of body weight, with a maximum limit of 500 mg.

In this particular case, the patient weighs 50 kg, so the maximum safe dose of lidocaine hydrochloride would be 50 multiplied by 3 mg, resulting in a total of 150 mg.

For more detailed information on lidocaine hydrochloride, you can refer to the BNF section dedicated to this topic.

The clinical history and examination strongly suggest that the patient has a pulmonary embolism caused by a deep vein thrombosis in his right leg.

The typical symptoms of a pulmonary embolism include shortness of breath, chest pain that worsens with breathing, coughing, and/or coughing up blood. There may also be symptoms indicating the presence of a deep vein thrombosis. Other signs include rapid breathing and heart rate, fever, and in severe cases, signs of shock, an abnormal heart rhythm, and increased pressure in the jugular veins.

Given the patient’s high probability Wells score, it is recommended that an immediate CT pulmonary angiogram (CPTA) be performed. This test is considered the most reliable method for diagnosing a pulmonary embolism. A d-dimer test would not provide any additional benefit in this case. While a chest X-ray and ECG may provide useful information, they alone cannot confirm the diagnosis.

For patients who have an allergy to contrast media, renal impairment, or are at high risk from radiation exposure, a ventilation/perfusion single-photon emission computed tomography (V/Q SPECT) scan or a V/Q planar scan can be offered as an alternative to CTPA.

Tinea cruris, commonly known as ‘jock itch’, is a fungal infection that affects the groin area. It is primarily caused by Trichophyton rubrum and is more prevalent in young men, particularly athletes. The typical symptoms include a reddish or brownish rash that is accompanied by intense itching. Pustules and vesicles may also develop, and there is often a raised border with a clear center. Notably, the infection usually does not affect the penis and scrotum.

It is worth mentioning that patients with tinea cruris often have concurrent tinea pedis, also known as athlete’s foot, which may have served as the source of the infection. The infection can be transmitted through sharing towels or by using towels that have come into contact with infected feet, leading to the spread of the fungus to the groin area.

Fortunately, treatment for tinea cruris typically involves the use of topical imidazole creams, such as clotrimazole. This is usually sufficient to alleviate the symptoms and eradicate the infection. Alternatively, terbinafine cream can be used as an alternative treatment option.

Corneal microdeposits are found in almost all individuals (over 90%) who have been taking amiodarone for more than six months, particularly at doses higher than 400 mg/day. These deposits generally do not cause any symptoms, although approximately 10% of patients may experience a perception of a ‘bluish halo’ around objects they see.

Amiodarone can also have other effects on the eye, but these are much less common, occurring in only 1-2% of patients. These effects include optic neuropathy, nonarteritic anterior ischemic optic neuropathy (N-AION), optic disc swelling, and visual field defects.

Carvallo’s sign is a term used to describe the phenomenon where the systolic murmur of tricuspid regurgitation becomes louder when taking a deep breath in. Tricuspid regurgitation is characterized by a continuous murmur that starts in systole and continues throughout the entire cardiac cycle. This murmur is best heard at the lower left sternal edge and has a low frequency. In addition to Carvallo’s sign, other features of tricuspid regurgitation include the presence of an S3 heart sound, the possibility of atrial arrhythmias such as flutter or fibrillation, the presence of giant C-V waves in the jugular pulse, hepatomegaly (often with a pulsatile nature), and the development of edema, which may be accompanied by lung crepitations or pleural effusions.

Further Reading:

Tricuspid regurgitation (TR) is a condition where blood flows backwards through the tricuspid valve in the heart. It is classified as either primary or secondary, with primary TR being caused by abnormalities in the tricuspid valve itself and secondary TR being the result of other conditions outside of the valve. Mild TR is common, especially in young adults, and often does not cause symptoms. However, severe TR can lead to right-sided heart failure and the development of symptoms such as ascites, peripheral edema, and hepatomegaly.

The causes of TR can vary. Primary TR can be caused by conditions such as rheumatic heart disease, myxomatous valve disease, or Ebstein anomaly. Secondary TR is often the result of right ventricular dilatation due to left heart failure or pulmonary hypertension. Other causes include endocarditis, traumatic chest injury, left ventricular systolic dysfunction, chronic lung disease, pulmonary thromboembolism, myocardial disease, left to right shunts, and carcinoid heart disease. In some cases, TR can occur as a result of infective endocarditis in IV drug abusers.

Clinical features of TR can include a pansystolic murmur that is best heard at the lower left sternal edge, Carvallo’s sign (murmur increases with inspiration and decreases with expiration), an S3 heart sound, and the presence of atrial arrhythmias such as flutter or fibrillation. Other signs can include giant C-V waves in the jugular pulse, hepatomegaly (often pulsatile), and edema with lung crepitations or pleural effusions.

The management of TR depends on the underlying cause and the severity of the condition. In severe cases, valve repair or replacement surgery may be necessary. Treatment may also involve addressing the underlying conditions contributing to TR, such as managing left heart failure or pulmonary hypertension.

Based on the provided information, it is highly probable that this patient is suffering from chronic obstructive pulmonary disease (COPD). This conclusion is supported by several factors. Firstly, the patient has a history of chronic productive cough and wheezing, which are common symptoms of COPD. Additionally, the patient has a long-term smoking history, which is a major risk factor for developing this condition.

Furthermore, the patient’s raised packed cell volume (PCV) is likely a result of chronic hypoxemia, a common complication of COPD. This indicates that the patient’s body is trying to compensate for the low oxygen levels in their blood.

Moreover, the chest X-ray reveals evidence of hyperinflation, which is a characteristic finding in patients with COPD. This suggests that the patient’s lungs are overinflated and not functioning optimally.

Lastly, the arterial blood gas analysis shows hypoxemia, indicating that the patient has low levels of oxygen in their blood. This is another significant finding that aligns with a diagnosis of COPD.

In summary, based on the patient’s history, smoking habits, raised PCV, chest X-ray findings, and arterial blood gas results, it is highly likely that they have COPD.

Uterine rupture can occur in two forms: primary, which happens without any previous uterine surgery or trauma, and secondary, which occurs when there is scar dehiscence. In secondary rupture, the rupture can range from the peritoneum to the endometrium, or the peritoneum may remain intact while the underlying uterine tissue ruptures.

There are several risk factors associated with uterine rupture, including multiparity, a uterine scar from a previous Caesarean section, previous uterine surgery, dysfunctional labor, and augmented labor with medications like oxytocin or prostaglandins.

The clinical features of uterine rupture include abdominal pain and tenderness, abdominal guarding and rigidity, inability to feel the uterine fundus (in cases of fundal rupture), cessation of uterine contractions, chest pain or shoulder tip pain, vaginal bleeding, abnormal fetal lie (such as oblique or transverse), easy palpation of fetal parts outside the uterus, absent fetal heart sounds, and abnormal CTG findings like late decelerations and reduced variability. Maternal shock can also occur and may be severe.

Immediate resuscitation is crucial and should involve intravenous fluids and/or blood transfusion. This should be followed by a laparotomy. After the baby is delivered, the uterus should be repaired or a hysterectomy may be performed. The decision between these two management options depends on factors such as the site and extent of the rupture, as well as the mother’s condition, age, and parity.

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.

Gentamicin is an antibiotic belonging to the aminoglycoside class. It works by binding to the 30S subunit of the ribosome in bacteria, thereby preventing the binding of aminoacyl-tRNA and ultimately inhibiting the initiation of protein synthesis.

The two most significant side effects associated with gentamicin are hearing loss and reversible nephrotoxicity. These side effects are directly related to the dosage of the medication and are more commonly observed in elderly individuals.

Hearing loss occurs due to damage to the vestibular apparatus located in the inner ear. On the other hand, nephrotoxicity is caused by the inhibition of protein synthesis in renal cells. This inhibition leads to necrosis of the cells in the proximal convoluted tubule and results in a condition known as acute tubular necrosis.

In summary, gentamicin mechanism of action and side effects, such as hearing loss and reversible nephrotoxicity, are closely linked to its interaction with the bacterial ribosome and its impact on protein synthesis. These effects are particularly prevalent in the elderly population.

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

Dantrolene works by blocking the release of calcium ions from the sarcoplasmic reticulum in skeletal muscle cells. This reduces the amount of calcium available to bind to troponin on actin filaments, which in turn decreases the muscle’s ability to contract and reduces energy usage.

Further Reading:

Malignant hyperthermia is a rare and life-threatening syndrome that can be triggered by certain medications in individuals who are genetically susceptible. The most common triggers are suxamethonium and inhalational anaesthetic agents. The syndrome is caused by the release of stored calcium ions from skeletal muscle cells, leading to uncontrolled muscle contraction and excessive heat production. This results in symptoms such as high fever, sweating, flushed skin, rapid heartbeat, and muscle rigidity. It can also lead to complications such as acute kidney injury, rhabdomyolysis, and metabolic acidosis. Treatment involves discontinuing the trigger medication, administering dantrolene to inhibit calcium release and promote muscle relaxation, and managing any associated complications such as hyperkalemia and acidosis. Referral to a malignant hyperthermia center for further investigation is also recommended.

Rapid tranquillisation involves the administration of medication through injection when oral medication is not feasible or appropriate and immediate sedation is necessary. The current guidelines from NICE recommend two options for rapid tranquillisation in adults: intramuscular lorazepam alone or a combination of intramuscular haloperidol and intramuscular promethazine. The choice of medication depends on various factors such as advanced statements, potential intoxication, previous responses to these medications, interactions with other drugs, and existing physical health conditions or pregnancy.

If there is insufficient information to determine the appropriate medication or if the individual has not taken antipsychotic medication before, intramuscular lorazepam is recommended. However, if there is evidence of cardiovascular disease or a prolonged QT interval, or if an electrocardiogram has not been conducted, the combination of intramuscular haloperidol and intramuscular promethazine should be avoided, and intramuscular lorazepam should be used instead.

If there is a partial response to intramuscular lorazepam, a second dose should be considered. If there is no response to intramuscular lorazepam, then intramuscular haloperidol combined with intramuscular promethazine should be considered. If there is a partial response to this combination, a further dose should be considered.

If there is no response to intramuscular haloperidol combined with intramuscular promethazine and intramuscular lorazepam has not been used yet, it should be considered. However, if intramuscular lorazepam has already been administered, it is recommended to arrange an urgent team meeting to review the situation and seek a second opinion if necessary.

After rapid tranquillisation, the patient should be closely monitored for any side effects, and their vital signs should be regularly checked, including heart rate, blood pressure, respiratory rate, temperature, hydration level, and level of consciousness. These observations should be conducted at least hourly until there are no further concerns about the patient’s physical health.

For more information, refer to the NICE guidance on violence and aggression: short-term management in mental health, health, and community settings.

Sodium bicarbonate is used to treat severe TCA toxicity by reducing the risk of seizures and arrhythmia. The goal is to increase the serum pH to a range of 7.45 to 7.55 through alkalinisation.

Further Reading:

Tricyclic antidepressant (TCA) overdose is a common occurrence in emergency departments, with drugs like amitriptyline and dosulepin being particularly dangerous. TCAs work by inhibiting the reuptake of norepinephrine and serotonin in the central nervous system. In cases of toxicity, TCAs block various receptors, including alpha-adrenergic, histaminic, muscarinic, and serotonin receptors. This can lead to symptoms such as hypotension, altered mental state, signs of anticholinergic toxicity, and serotonin receptor effects.

TCAs primarily cause cardiac toxicity by blocking sodium and potassium channels. This can result in a slowing of the action potential, prolongation of the QRS complex, and bradycardia. However, the blockade of muscarinic receptors also leads to tachycardia in TCA overdose. QT prolongation and Torsades de Pointes can occur due to potassium channel blockade. TCAs can also have a toxic effect on the myocardium, causing decreased cardiac contractility and hypotension.

Early symptoms of TCA overdose are related to their anticholinergic properties and may include dry mouth, pyrexia, dilated pupils, agitation, sinus tachycardia, blurred vision, flushed skin, tremor, and confusion. Severe poisoning can lead to arrhythmias, seizures, metabolic acidosis, and coma. ECG changes commonly seen in TCA overdose include sinus tachycardia, widening of the QRS complex, prolongation of the QT interval, and an R/S ratio >0.7 in lead aVR.

Management of TCA overdose involves ensuring a patent airway, administering activated charcoal if ingestion occurred within 1 hour and the airway is intact, and considering gastric lavage for life-threatening cases within 1 hour of ingestion. Serial ECGs and blood gas analysis are important for monitoring. Intravenous fluids and correction of hypoxia are the first-line therapies. IV sodium bicarbonate is used to treat haemodynamic instability caused by TCA overdose, and benzodiazepines are the treatment of choice for seizure control. Other treatments that may be considered include glucagon, magnesium sulfate, and intravenous lipid emulsion.

There are certain things to avoid in TCA overdose, such as anti-arrhythmics like quinidine and flecainide, as they can prolonged depolarization.

The first step in decontaminating radioactive material from an individual is to remove their clothing carefully, without shaking it too much to avoid spreading radioactive dust. The clothing should then be placed in a plastic bag or sealable container. Next, the person should be washed down with warm water from a clean source and scrubbed with detergent using a rinse-wipe-rinse method.

Further Reading:

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

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

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

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

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

Moderate to severe cyanide poisoning typically leads to a condition called high anion gap metabolic acidosis, characterized by elevated levels of lactate (>10 mmol/L). Cyanide toxicity can occur from inhaling smoke produced by burning materials such as plastics, wools, silk, and other natural and synthetic polymers, which can release hydrogen cyanide (HCN). Symptoms of cyanide poisoning include headaches, nausea, decreased consciousness or loss of consciousness, and seizures. Measuring cyanide levels is not immediately helpful in managing a patient suspected of cyanide toxicity. Cyanide binds to the ferric (Fe3+) ion of cytochrome oxidase, causing a condition known as histotoxic hypoxia and resulting in lactic acidosis. The presence of a high lactate level (>10) and a classic high anion gap metabolic acidosis should raise suspicion of cyanide poisoning in a clinician.

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 term renal colic is commonly used to describe 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. However, a more accurate term is ureteric colic, as the pain usually arises from a blockage in the ureter itself.

Renal or ureteric colic typically presents with a sudden onset of severe abdominal pain on one side, starting in the lower back or flank and radiating to the genital area in women or to the groin or testicle in men.

The pain usually:
– Lasts for minutes to hours and comes in spasms, with periods of no pain or a dull ache
– Is often accompanied by nausea, vomiting, and blood in the urine
– Is often described as the most intense pain a person has ever experienced (many women describe it as worse than childbirth).

People with renal or ureteric colic:
– Are restless and unable to find relief by lying still (which helps distinguish it from peritonitis)
– May have a history of previous episodes
– May have a fever and sweating if there is a urinary tract infection present
– May complain of painful urination, frequent urination, and straining when the stone reaches the junction between the ureter and bladder (due to irritation of the bladder muscle).

If possible, a urine dipstick test should be done to support the diagnosis and check for signs of a urinary tract infection.

Checking for blood in the urine can also support the diagnosis of renal or ureteric colic. However, the absence of blood does not rule out the diagnosis and other causes of pain should be considered.

Checking for nitrite and leukocyte esterase in the urine can indicate an infection.

Pain management:
– Non-steroidal anti-inflammatory drugs (NSAIDs) are the first-line treatment for adults, children, and young people with suspected renal colic.
– Intravenous paracetamol can be given to adults, children, and young people if NSAIDs are not suitable or not providing enough pain relief.
– Opioids may be considered if both NSAIDs and intravenous paracetamol are not suitable or not providing enough pain relief.
– Antispasmodics should not be given to adults, children, and young people with suspected renal colic.

In a clinical setting, the prioritization of patient safety and the safety of staff members is crucial. Violence against other patients and health professionals is not tolerated. However, it is important to consider that the patient in question may be intoxicated or experiencing delirium tremens, which could impair their insight into their own behavior.

To address this situation, it would be wise to call local security as a precautionary measure. This action can serve as a backup if additional assistance is required. However, involving the police at this stage may escalate the situation unnecessarily and potentially agitate the patient further.

Administering sedation to the patient without understanding their medical history or gathering more information would not be appropriate. It is essential to have a comprehensive understanding of the patient’s condition before considering any interventions.

Similarly, asking the patient to leave the department immediately could potentially worsen the situation. It is important to approach the situation with caution and consider alternative strategies to de-escalate the situation effectively.

A recent audit conducted by the Royal College of Emergency Medicine (RCEM) in 2018 revealed a concerning decline in the standards of pain management for children with fractured limbs in Emergency Departments (EDs). The audit found that the majority of patients experienced longer waiting times for pain relief compared to previous years. Shockingly, more than 1 in 10 children who presented with significant pain due to a limb fracture did not receive any pain relief at all.

To address this issue, the Agency for Health Care Policy and Research (AHCPR) in the USA recommends following the ABCs of pain management for all patients, including children. This approach involves regularly asking about pain, systematically assessing it, believing the patient and their family in their reports of pain and what relieves it, choosing appropriate pain control options, delivering interventions in a timely and coordinated manner, and empowering patients and their families to have control over their pain management.

The RCEM has established standards that require a child’s pain to be assessed within 15 minutes of their arrival at the ED. This is considered a fundamental standard. Various rating scales are available for assessing pain in children, with the choice depending on the child’s age and ability to use the scale. These scales include the Wong-Baker Faces Pain Rating Scale, Numeric rating scale, and Behavioural scale.

To ensure timely administration of analgesia to children in acute pain, the RCEM has set specific standards. These standards state that 100% of patients in severe pain should receive appropriate analgesia within 60 minutes of their arrival or triage, whichever comes first. Additionally, 75% should receive analgesia within 30 minutes, and 50% within 20 minutes.

Primary sclerosing cholangitis (PSC) is a condition that affects the bile ducts, causing inflammation and blockage over time. This leads to recurrent episodes of cholangitis and progressive scarring of the bile ducts. Ultimately, PSC can result in liver cirrhosis, liver failure, and even hepatocellular carcinoma. It is commonly associated with ulcerative colitis, with more than 80% of PSC patients also having ulcerative colitis. However, there is no association between PSC and Crohn’s disease.

On the other hand, Crohn’s disease has its own set of recognized associations. For instance, there is an increased incidence of Crohn’s disease among smokers, with approximately 50-60% of Crohn’s patients being smokers. Other associations include the presence of aphthous ulcers, uveitis and episcleritis (eye inflammation), seronegative spondyloarthropathies (inflammatory joint diseases), erythema nodosum (painful skin nodules), pyoderma gangrenosum (skin ulceration), finger clubbing, autoimmune hemolytic anemia, cholelithiasis (gallstones), and osteoporosis.

It is important to note the distinct associations and characteristics of these two conditions, as they have different implications for diagnosis, treatment, and management.

Traumatic aortic rupture is a relatively common cause of sudden death following major trauma, especially high-speed road traffic accidents (RTAs). It is estimated that 15-20% of deaths from RTAs are due to this injury. If the aortic rupture is promptly recognized and treated, patients who survive the initial injury can fully recover.

Surviving patients often have an incomplete laceration near the ligamentum arteriosum of the aorta. The continuity is maintained by either an intact adventitial layer or a contained mediastinal hematoma, which prevents immediate exsanguination and death.

Detecting traumatic aortic rupture can be challenging as many patients do not exhibit specific symptoms, and other injuries may also be present, making the diagnosis unclear.

Chest X-ray findings can aid in the diagnosis and include fractures of the 1st and 2nd ribs, a grossly widened mediastinum, a hazy left lung field, obliteration of the aortic knob, deviation of the trachea to the right, presence of a pleural cap, elevation and rightward shift of the right mainstem bronchus, depression of the left mainstem bronchus, obliteration of the space between the pulmonary artery and aorta, and deviation of the esophagus (or NG tube) to the right.

Helical contrast-enhanced CT scanning is highly sensitive and specific for detecting aortic rupture, but it should only be performed on hemodynamically stable patients.

Treatment options include primary repair or resection of the torn segment with replacement using an interposition graft. Endovascular repair is also now considered an acceptable alternative approach.

Infantile hypertrophic pyloric stenosis is a condition characterized by the thickening and enlargement of the smooth muscle in the antrum of the stomach, leading to the narrowing of the pyloric canal. This narrowing can easily cause obstruction. It is a relatively common condition, occurring in about 1 in 500 live births, and is more frequently seen in males than females, with a ratio of 4 to 1. It is most commonly observed in first-born male children, although it can rarely occur in adults as well.

The main symptom of infantile hypertrophic pyloric stenosis is vomiting, which typically begins between 2 to 8 weeks of age. The vomit is usually non-bilious and forcefully expelled. It tends to occur around 30 to 60 minutes after feeding, leaving the baby hungry despite the vomiting. In some cases, there may be blood in the vomit. Other clinical features include persistent hunger, dehydration, weight loss, and constipation. An enlarged pylorus, often described as olive-shaped, can be felt in the right upper quadrant or epigastric in approximately 95% of cases. This is most noticeable at the beginning of a feed.

The typical acid-base disturbance seen in this condition is hypochloremic metabolic alkalosis. This occurs due to the loss of hydrogen and chloride ions in the vomit, as well as decreased secretion of pancreatic bicarbonate. The increased bicarbonate ions in the distal tubule of the kidney lead to the production of alkaline urine. Hyponatremia and hypokalemia are also commonly present.

Ultrasound scanning is the preferred diagnostic tool for infantile hypertrophic pyloric stenosis, as it is reliable and easy to perform. It has replaced barium studies as the investigation of choice.

Initial management involves fluid resuscitation, which should be tailored to the weight and degree of dehydration. Any electrolyte imbalances should also be corrected.

The definitive treatment for this condition is surgical intervention, with the Ramstedt pyloromyotomy being the procedure of choice. Laparoscopic pyloromyotomy is also an effective alternative if suitable facilities are available. The prognosis for infants with this condition is excellent, as long as there is no delay in diagnosis and treatment initiation.

Appendicitis is characterized by inflammation of the appendix. It is believed to occur when the appendix lumen becomes blocked, and in confirmed cases, about 75-80% of resected specimens contain faecoliths. This condition is most commonly seen in childhood and becomes less common after the age of 40. Mortality rates increase with age, with the highest rates observed in the elderly.

The classic presentation of appendicitis involves early, poorly localized pain around the belly button, which then moves to the lower right side of the abdomen (known as the right iliac fossa). Other common symptoms include loss of appetite, vomiting, and fever. The initial belly button pain is an example of visceral pain, which is pain that originates from the embryonic origin of the affected organ. The later pain in the right iliac fossa is known as parietal pain, which occurs when the inflamed appendix irritates the peritoneum (the lining of the abdominal cavity).

Approximately 20% of appendicitis cases occur in an extraperitoneal location, specifically in the retrocaecal position. In these cases, a digital rectal examination is crucial for making the diagnosis.

A Meckel’s diverticulum is a leftover part of the vitellointestinal duct, which is no longer needed in the body. It is the most common abnormality in the gastrointestinal tract, found in about 2% of people. Interestingly, it is twice as likely to occur in men compared to women.

When a Meckel’s diverticulum is present, it is usually located in the lower part of the small intestine, specifically within 60-100 cm (2 feet) of the ileocaecal valve. These diverticula are typically 3-6 cm (approximately 2 inches) long and may have a larger opening than the ileum.

Meckel’s diverticula are often discovered incidentally, especially during an appendectomy. Most of the time, they do not cause any symptoms. However, they can lead to complications such as bleeding (25-50% of cases), intestinal blockage (10-40% of cases), diverticulitis, or perforation.

These diverticula run in the opposite direction of the intestine’s natural folds but receive their blood supply from the ileum mesentery. They can be identified by a specific blood vessel called the vitelline artery. Typically, they are lined with the same type of tissue as the ileum, but they often contain abnormal tissue, with gastric tissue being the most common (50%) and pancreatic tissue being the second most common (5%). In rare cases, colonic or jejunal tissue may be present.

To remember some key facts about Meckel’s diverticulum, the rule of 2s can be helpful:
– It is found in 2% of the population.
– It is more common in men, with a ratio of 2:1 compared to women.
– It is located 2 feet away from the ileocaecal valve.
– It is approximately 2 inches long.
– It often contains two types of abnormal tissue: gastric and pancreatic.
– The most common age for clinical presentation is 2 years old.

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

Further Reading:

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

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

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

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

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

This patient’s medical history and physical examination findings are indicative of a diagnosis of asbestosis. Additionally, the patient exhibits characteristics consistent with interstitial lung disease that has developed as a result of the asbestosis.

Exposure to asbestos was prevalent in various professions, particularly during the 1970s and earlier. Occupations commonly associated with asbestos exposure include shipyard workers, builders, miners, and pipefitters.

It is important to consider the possibility of mesothelioma in individuals who have been exposed to asbestos. This should be suspected if the patient presents with constitutional symptoms such as weight loss, fatigue, and loss of appetite, along with the presence of thickening of the pleura and/or accumulation of fluid in the pleural space.

Activated charcoal is a commonly used substance for decontamination in cases of poisoning. Its main function is to adsorb the molecules of the ingested toxin onto its surface.

Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. It is produced by subjecting carbonaceous matter to high temperatures, a process known as pyrolysis, and then concentrating it with a zinc chloride solution. This creates a network of pores within the charcoal, giving it a large absorptive area of approximately 3,000 m2/g. This porous structure helps prevent the absorption of the harmful toxin by up to 50%.

The usual dosage of activated charcoal is 50 grams for adults and 1 gram per kilogram of body weight for children. It can be administered orally or through a nasogastric tube. It is important to give the charcoal within one hour of ingestion, and it may be repeated after one hour if necessary.

However, there are certain situations where activated charcoal should not be used. If the patient is unconscious or in a coma, there is a risk of aspiration, so the charcoal should not be given. Similarly, if seizures are likely to occur, there is a risk of aspiration and the charcoal should be avoided. Additionally, if there is reduced gastrointestinal motility, there is a risk of obstruction, so activated charcoal should not be used in such cases.

Activated charcoal is effective in treating overdose with various drugs and toxins, including aspirin, paracetamol, barbiturates, tricyclic antidepressants, digoxin, amphetamines, morphine, cocaine, and phenothiazines. However, it is ineffective in treating overdose with substances such as iron, lithium, boric acid, cyanide, ethanol, ethylene glycol, methanol, malathion, DDT, carbamate, hydrocarbon, strong acids, or alkalis.

There are some potential adverse effects associated with activated charcoal. These include nausea and vomiting, diarrhea, constipation, bezoar formation (a mass of undigested material that can cause blockages), bowel obstruction, pulmonary aspiration (inhaling the charcoal into the lungs), and impaired absorption of oral medications or antidotes.

The typical range for lactate levels in the body is 0.5-2.2 mmol/L, according to most UK trusts. However, it is important to mention that the RCEM sepsis guides consider a lactate level above 2 mmol/L to be abnormal.

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.

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.

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.

This patient is displaying symptoms and signs that are consistent with an atypical pneumonia, most likely caused by an infection from Mycoplasma pneumoniae. The clinical features commonly associated with Mycoplasma pneumoniae infection include a flu-like illness that occurs before respiratory symptoms, fever, myalgia, headache, diarrhea, and cough (initially dry but often becoming productive). Focal chest signs typically develop later in the course of the illness. It is worth noting that Mycoplasma pneumoniae is frequently linked to the development of erythema multiforme and can also be a cause of Steven-Johnson syndrome. The rash associated with erythema multiforme is characterized by multiple red lesions on the limbs that develop into target lesions a few days after the rash first appears.

Cement contains lime, which is a powerful alkali, and this can cause a serious eye emergency that requires immediate treatment. Alkaline chemicals, such as oven cleaner, ammonia, household bleach, drain cleaner, oven cleaner, and plaster, can also cause damage to the eyes. They lead to colliquative necrosis, which is a type of tissue death that results in liquefaction. On the other hand, acids cause damage through coagulative necrosis. Common acids that can harm the eyes include toilet cleaners, certain household cleaning products, and battery fluid.

The initial management of a patient with cement or alkali exposure to the eyes should be as follows:

1. Irrigate the eye with a large amount of normal saline for 20-30 minutes.
2. Administer local anaesthetic drops every 5 minutes to help keep the eye open and alleviate pain.
3. Monitor the pH every 5 minutes until a neutral pH (7.0-7.5) is achieved. Briefly pause irrigation to test the fluid from the forniceal space using litmus paper.

After the initial management, a thorough examination should be conducted, which includes the following steps:

1. Examine the eye directly and with a slit lamp.
2. Remove any remaining cement debris from the surface of the eye.
3. Evert the eyelids to check for hidden cement debris.
4. Administer fluorescein drops and check for corneal abrasion.
5. Assess visual acuity, which may be reduced.
6. Perform fundoscopy to check for retinal necrosis if the alkali has penetrated the sclera.
7. Measure intraocular pressure through tonometry to detect secondary glaucoma.

Once the eye’s pH has returned to normal, irrigation can be stopped, and the patient should be promptly referred to an ophthalmology specialist for further evaluation.

Potential long-term complications of cement or alkali exposure to the eyes include closed-angle glaucoma, cataract formation, entropion, keratitis sicca, and permanent vision loss.

The age of the child can help determine the most probable diagnosis. Transient synovitis (irritable hip) is commonly observed in children aged 3 to 10. Septic arthritis is more prevalent in children under 4 years old, while Perthes disease is typically diagnosed between the ages of 4 and 8. SUFE is usually seen in girls around the age of 12 and boys around the age of 13.

Further Reading:

– Transient Synovitis (irritable hip):
– Most common hip problem in children
– Causes transient inflammation of the synovium
– Presents with thigh, groin, and/or hip pain with impaired weight bearing
– Mild to moderate restriction of hip internal rotation is common
– Symptoms usually resolve quickly with rest and anti-inflammatory treatment

– Slipped Upper Femoral Epiphysis (SUFE):
– Displacement of the femoral head epiphysis postero-inferiorly
– Usually affects adolescents
– Can present acutely following trauma or with chronic, persistent symptoms
– Associated with loss of internal rotation of the leg in flexion
– Treatment involves surgical fixation by pinning

– Perthes disease:
– Degenerative condition affecting the hip joints of children
– Avascular necrosis of the femoral head is the cause
– Presents with hip pain, limp, stiffness, and reduced range of hip movements
– X-ray changes include widening of joint space and decreased femoral head size/flattening
– Treatment can be conservative or operative, depending on the severity

– Important differentials:
– Septic arthritis: Acute hip pain associated with systemic upset and severe limitation of affected joint
– Non-accidental injury (NAI): Should be considered in younger children and toddlers presenting with a limp, even without a trauma history
– Malignancy: Rare, but osteosarcoma may present with hip pain or limp, especially in tall teenage boys
– Developmental dysplasia of the hip: Often picked up on newborn examination with positive Barlow and Ortolani tests
– Juvenile idiopathic arthritis (JIA): Joint pain and swelling, limp, positive ANA in some cases
– Coagulopathy: Haemophilia, HSP, and sickle cell disease can cause hip pain through different mechanisms

Fragility fractures occur when a person experiences a fracture from a force that would not typically cause a fracture, such as a fall from a standing height or less. The most common areas for fragility fractures are the vertebrae, hip, and wrist. Osteoporosis is diagnosed when a patient’s bone mineral density, measured by a T-score on a DEXA scan, is -2.5 standard deviations or below. This T-score compares the patient’s bone density to the peak bone density of a population. In women over 75 years old, osteoporosis can be assumed without a DEXA scan. Osteopenia is diagnosed when a patient’s T-score is between -1 and -2.5 standard deviations below peak bone density. Risk factors for fractures include a family history of hip fractures, excessive alcohol consumption, and rheumatoid arthritis. Low bone mineral density can be indicated by a BMI below 22 kg/m2, untreated menopause, and conditions causing prolonged immobility or certain medical conditions. Medications used to prevent osteoporotic fractures in postmenopausal women include alendronate, risedronate, etidronate, and strontium ranelate. Raloxifene is not used for primary prevention. Alendronate is typically the first-choice medication and is recommended for women over 70 years old with confirmed osteoporosis and either a risk factor for fracture or low bone mineral density. Women over 75 years old with two risk factors or two indicators of low bone mineral density may be assumed to have osteoporosis without a DEXA scan. Other pharmacological interventions can be tried if alendronate is not tolerated.

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

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

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

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

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

Cement contains lime, which is a powerful alkali, and this can cause a serious eye emergency that requires immediate treatment. Alkaline chemicals, such as oven cleaner, ammonia, household bleach, drain cleaner, oven cleaner, and plaster, can also cause damage to the eyes. They lead to colliquative necrosis, which is a type of tissue death that results in liquefaction. On the other hand, acids cause damage through coagulative necrosis. Common acids that can harm the eyes include toilet cleaners, certain household cleaning products, and battery fluid.

The initial management of a patient with cement or alkali exposure to the eyes should be as follows:

1. Irrigate the eye with a large amount of normal saline for 20-30 minutes.
2. Administer local anaesthetic drops every 5 minutes to help keep the eye open and alleviate pain.
3. Monitor the pH every 5 minutes until a neutral pH (7.0-7.5) is achieved. Briefly pause irrigation to test the fluid from the forniceal space using litmus paper.

After the initial management, a thorough examination should be conducted, which includes the following steps:

1. Examine the eye directly and with a slit lamp.
2. Remove any remaining cement debris from the surface of the eye.
3. Evert the eyelids to check for hidden cement debris.
4. Administer fluorescein drops and check for corneal abrasion.
5. Assess visual acuity, which may be reduced.
6. Perform fundoscopy to check for retinal necrosis if the alkali has penetrated the sclera.
7. Measure intraocular pressure through tonometry to detect secondary glaucoma.

Once the eye’s pH has returned to normal, irrigation can be stopped, and the patient should be promptly referred to an ophthalmology specialist for further evaluation.

Potential long-term complications of cement or alkali exposure to the eyes include closed-angle glaucoma, cataract formation, entropion, keratitis sicca, and permanent vision loss.

Central retinal artery occlusion (CRAO) is characterized by sudden and painless loss of vision in the affected eye. It can occur due to emboli from atheromatous carotid arteries, thrombosis caused by arteriosclerosis or hypertension, or vasospasm resulting from giant cell arteritis. The pupil on the affected side typically shows poor reactivity to light, but the consensual light reaction remains normal. The typical retinal findings in CRAO include a pale retina due to edema, narrowed blood vessels, segmentation of blood columns in arteries (resembling cattle-trucking), and a cherry red spot indicating sparing of the macular center supplied by the underlying choroid. Over several weeks, optic atrophy may develop. Immediate referral to an eye specialist is necessary as CRAO is an ophthalmological emergency.

On the other hand, central retinal vein occlusion (CRVO) leads to painless and unilateral visual loss. The retina in CRVO has a distinct appearance likened to a pizza thrown against a wall. Fundoscopic examination reveals engorged retinal veins, disc edema, multiple flame-shaped hemorrhages, and cotton wool spots.

This patient is displaying symptoms and signs that are consistent with a diagnosis of acute pyelonephritis. Additionally, they are showing signs of sepsis, which indicates a more serious illness or condition. Therefore, it would be advisable to admit the patient for inpatient treatment.

According to the recommendations from the National Institute for Health and Care Excellence (NICE), patients with pyelonephritis should be admitted if it is severe or if they exhibit any signs or symptoms that suggest a more serious condition, such as sepsis. Signs of sepsis include significant tachycardia, hypotension, or breathlessness, as well as marked signs of illness like impaired level of consciousness, profuse sweating, rigors, pallor, or significantly reduced mobility. A temperature greater than 38°C or less than 36°C is also indicative of sepsis.

NICE also advises considering referral or seeking specialist advice for individuals with acute pyelonephritis if they are significantly dehydrated or unable to take oral fluids and medicines, if they are pregnant, if they have a higher risk of developing complications due to known or suspected abnormalities of the genitourinary tract or underlying diseases like diabetes mellitus or immunosuppression, or if they have recurrent episodes of urinary tract infections (UTIs).

For non-pregnant women and men, the recommended choice of antibacterial therapy is as follows: oral first-line options include cefalexin, ciprofloxacin, or co-amoxiclav (taking into account local microbial resistance data), and trimethoprim if sensitivity is known. Intravenous first-line options are amikacin, ceftriaxone, cefuroxime, ciprofloxacin, or gentamicin if the patient is severely unwell or unable to take oral treatment. Co-amoxiclav may be used if given in combination or if sensitivity is known. Antibacterials may be combined if there are concerns about susceptibility or sepsis. For intravenous second-line options, it is recommended to consult a local microbiologist.

For pregnant women, the recommended choice of antibacterial therapy is cefalexin for oral first-line treatment. If the patient is severely unwell or unable to take oral treatment, cefuroxime is the recommended intravenous first-line option.

This individual has a typical history for a transient ischaemic attack (TIA). According to the NICE recommendations, it is advised to offer aspirin (300 mg daily) to individuals who have experienced a suspected TIA, unless there are contraindications. This treatment should be started immediately. It is also important to refer individuals who have had a suspected TIA for specialist assessment and investigation, with the aim of being seen within 24 hours of symptom onset. Scoring systems, such as ABCD2, should not be used to assess the risk of subsequent stroke or determine the urgency of referral for individuals with a suspected or confirmed TIA. Secondary prevention measures, in addition to aspirin, should be offered as soon as possible after the diagnosis of TIA is confirmed.

In terms of imaging, it is not recommended to offer CT brain scanning to individuals with a suspected TIA, unless there is clinical suspicion of an alternative diagnosis that CT could detect. After a specialist assessment in the TIA clinic, MRI (including diffusion-weighted and blood-sensitive sequences) may be considered to determine the area of ischaemia, detect haemorrhage, or identify alternative pathologies. If an MRI is performed, it should ideally be done on the same day as the assessment. Carotid imaging is also important for everyone with a TIA who is considered a candidate for carotid endarterectomy, and this should be done urgently.

to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old: diagnosis and initial management.

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

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

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

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

This patient has presented with an Addisonian crisis, which is a rare but potentially catastrophic condition if not diagnosed promptly. The most likely underlying rheumatological diagnosis in this case is polymyalgia rheumatica, and it is likely that the GP started the patient on prednisolone medication.

Addison’s disease occurs when the adrenal glands underproduce steroid hormones, affecting the production of glucocorticoids, mineralocorticoids, and sex steroids. The main causes of Addison’s disease include autoimmune adrenalitis (accounting for 80% of cases), bilateral adrenalectomy, Waterhouse-Friderichsen syndrome (hemorrhage into the adrenal glands), and tuberculosis.

An Addisonian crisis is most commonly triggered by the deliberate or accidental withdrawal of steroid therapy in patients with Addison’s disease. Other factors that can precipitate a crisis include infection, trauma, myocardial infarction, cerebral infarction, asthma, hypothermia, and alcohol abuse.

The clinical features of Addison’s disease include weakness, lethargy, hypotension (especially orthostatic hypotension), nausea, vomiting, weight loss, reduced axillary and pubic hair, depression, and hyperpigmentation (particularly in palmar creases, buccal mucosa, and exposed areas). In an Addisonian crisis, the main features are usually hypoglycemia and shock, characterized by tachycardia, peripheral vasoconstriction, hypotension, altered consciousness, and coma.

Biochemically, Addison’s disease is characterized by increased ACTH levels (as a compensatory response to stimulate the adrenal glands), elevated serum renin levels, hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, and metabolic acidosis. Diagnostic investigations may include the Synacthen test, plasma ACTH level, plasma renin level, and adrenocortical antibodies.

Management of Addison’s disease should be overseen by an Endocrinologist. Typically, patients require hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also need thyroxine if there is hypothalamic-pituitary disease present. Treatment is lifelong, and patients should carry a steroid card and a MedicAlert bracelet, being aware of the possibility of an Addisonian crisis.

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

Further Reading:

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

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

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

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

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

The therapeutic range for lithium typically falls between 0.4-0.8 mmol/l, although this range may differ depending on the laboratory. In general, the lower end of the range is the desired level for maintenance therapy and treatment in older individuals. Toxic effects are typically observed when levels exceed 1.5 mmol/l.

Recognizing the extent of blood loss based on vital sign and mental status abnormalities is a crucial skill. The Advanced Trauma Life Support (ATLS) classification for hemorrhagic shock correlates the amount of blood loss with expected physiological responses in a healthy individual weighing 70 kg. In terms of body weight, the total circulating blood volume accounts for approximately 7%, which is roughly equivalent to five liters in an average 70 kg male patient.

The ATLS classification for hemorrhagic shock is as follows:

CLASS I:
– Blood loss: Up to 750 mL
– Blood loss (% blood volume): Up to 15%
– Pulse rate: Less than 100 beats per minute (bpm)
– Systolic blood pressure: Normal
– Pulse pressure: Normal (or increased)
– Respiratory rate: 14-20 breaths per minute
– Urine output: Greater than 30 mL/hr
– CNS/mental status: Slightly anxious

CLASS II:
– Blood loss: 750-1500 mL
– Blood loss (% blood volume): 15-30%
– Pulse rate: 100-120 bpm
– Systolic blood pressure: Normal
– Pulse pressure: Decreased
– Respiratory rate: 20-30 breaths per minute
– Urine output: 20-30 mL/hr
– CNS/mental status: Mildly anxious

CLASS III:
– Blood loss: 1500-2000 mL
– Blood loss (% blood volume): 30-40%
– Pulse rate: 120-140 bpm
– Systolic blood pressure: Decreased
– Pulse pressure: Decreased
– Respiratory rate: 30-40 breaths per minute
– Urine output: 5-15 mL/hr
– CNS/mental status: Anxious, confused

CLASS IV:
– Blood loss: More than 2000 mL
– Blood loss (% blood volume): More than 40%
– Pulse rate: More than 140 bpm
– Systolic blood pressure: Decreased
– Pulse pressure: Decreased
– Respiratory rate: More than 40 breaths per minute
– Urine output: Negligible
– CNS/mental status: Confused, lethargic

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

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

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

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

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

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

9 x 4 ml/hour = 36 ml/hour

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.

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

Grey baby syndrome is a rare but serious side effect that can occur in neonates, especially premature babies, as a result of the build-up of the antibiotic chloramphenicol. This condition is characterized by several symptoms, including ashen grey skin color, poor feeding, vomiting, cyanosis, hypotension, hypothermia, hypotonia, cardiovascular collapse, abdominal distension, and respiratory difficulties.

During pregnancy, there are several drugs that can have adverse effects on the developing fetus. ACE inhibitors, such as ramipril, if given in the second and third trimesters, can lead to hypoperfusion, renal failure, and the oligohydramnios sequence. Aminoglycosides, like gentamicin, can cause 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 of aspirin (e.g., 75 mg) do not pose significant risks.

Benzodiazepines, such as diazepam, when administered late in pregnancy, can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if given in the first trimester, may lead to phalangeal abnormalities, while their use in the second and third trimesters can result in fetal growth retardation. Carbamazepine can cause hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol, as mentioned earlier, can cause grey baby syndrome. Corticosteroids, if given in the first trimester, may cause orofacial clefts. Danazol, if administered in the first trimester, can cause 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

According to the latest NICE guidance, it is recommended that women aged 55 and over with unexplained symptoms of vaginal discharge should undergo a direct access ultrasound scan to assess for endometrial cancer. This recommendation applies to women who are experiencing these symptoms for the first time or who have thrombocytosis, haematuria (blood in the urine), visible haematuria, low haemoglobin levels, or high blood glucose levels. For more information, please refer to the NICE referral guidelines on the recognition and referral of suspected cancer.

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.

Chickenpox is a highly contagious illness caused by the varicella-zoster virus, a DNA virus from the Herpesviridae family. Most cases are mild to moderate, and the infection usually resolves on its own. Severe complications are rare but can occur, especially in individuals with weakened immune systems or underlying health conditions.

The incubation period for chickenpox is typically between 14 to 21 days. It is contagious from a few days before the rash appears until about a week after the first lesions show up.

The common clinical features of chickenpox include:

– Fever, which lasts for approximately 3-5 days.
– The initial rash starts as flat red spots and progresses into raised bumps.
– These bumps then turn into fluid-filled blisters and eventually form pustules surrounded by redness.
– The lesions are extremely itchy.
– The rash reaches its peak around 48 hours in individuals with a healthy immune system.
– The rash tends to be more concentrated on the face and trunk, with fewer lesions on the limbs.
– The blisters eventually dry up and form crusts, which can lead to scarring if scratched.
– Headache, fatigue, and abdominal pain may also occur.

Chickenpox tends to be more severe in teenagers and adults compared to children. Antiviral treatment should be considered for these individuals if they seek medical attention within 24 hours of rash onset. The recommended oral dose of aciclovir is 800 mg taken five times a day for seven days.

Immunocompromised patients and those at higher risk, such as individuals with severe cardiovascular or respiratory disease or chronic skin disorders, should receive antiviral treatment for ten days, with at least seven days of intravenous administration.

Although most cases are relatively mild, if serious complications like pneumonia, encephalitis, or dehydration are suspected, it is important to refer the patient for hospital admission.

For more information, you can refer to the NICE Clinical Knowledge Summary on Chickenpox.
https://cks.nice.org.uk/topics/chickenpox/

In the UK, the classification of pressure ulcers is done using the international NPUAP-EPUAP system. This particular description refers to a pressure ulcer of grade 2. Please refer to the notes below for more information on the classification of pressure ulcers.

Further Reading:

Pressure ulcers, also known as bedsores, are localized damage to the skin and underlying tissues caused by pressure or pressure combined with shear force. They most commonly occur over bony prominences but can develop on any part of the body. Pressure ulcers develop due to five main factors: pressure, shear, friction, moisture, and circulation and tissue perfusion. Pressure is the most important factor, with intensity and duration playing key roles in the development of pressure ulcers.

Assessment of pressure ulcers in adults should be done using a validated classification tool. The International NPUAP-EPUAP pressure ulcer classification system is preferred in the UK. This system categorizes pressure ulcers into four stages. Stage I is characterized by non-blanchable erythema, which is non-blanchable redness of the skin. Stage II involves partial thickness loss of the dermis, presenting as a shallow open ulcer with a red pink wound bed. Stage III is full thickness skin loss, with subcutaneous fat visible but no exposure of bone, tendon, or muscle. Stage IV is also full thickness tissue loss, but with exposed bone, tendon, or muscle. In addition, some pressure ulcers may be classified as suspected deep tissue injury or unstageable.

Management of pressure ulcers involves general measures such as pressure reducing aids, repositioning, hygiene, cleansing, dressings, analgesia, and dietary optimization. It is also important to optimize or treat underlying health conditions, such as diabetes. For grade 3 and 4 ulcers, additional measures to consider include antibiotics and surgical debridement with or without skin flap coverage.

Patients diagnosed with ulcerative colitis face a significantly heightened risk of developing colon cancer. It is crucial for these individuals, especially those with severe or extensive disease, to undergo regular monitoring to detect any potential signs of colon cancer. The risk of developing colon cancer increases as the duration of ulcerative colitis progresses. After 10 years, the risk stands at 1 in 50. After 20 years, the risk increases to 1 in 12. And after 30 years, the risk further rises to 1 in 6. While Crohn’s disease also carries a risk of colonic carcinoma, it is comparatively smaller than that associated with ulcerative colitis.

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

To calculate the serum osmolality, the following formula can be used: 2 (K+ + Na+) + urea + glucose. In this particular case, the calculation would be 2 (3.2 + 154) + 17.6 + 32 = 364 mmol/l. Patients with HHS typically have a serum osmolality greater than 350 mmol/l.

In order to manage HHS, it is important to address the underlying cause and gradually and safely achieve the following goals:
1. Normalize the osmolality
2. Replace fluid and electrolyte losses
3. Normalize blood glucose levels

Given the presence of 1+ ketones in the patient’s urine, which is likely due to vomiting and a mild acidosis, it is recommended to discontinue the use of metformin due to the risk of metformin-associated lactic acidosis (MALA). Additionally, an intravenous infusion of insulin should be initiated in this case.

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

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

The recommended dosage of buccal midazolam for treating a child experiencing seizures is 0.5 mg per kilogram of body weight.

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

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

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

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

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

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

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

The mast cell tryptase test, also known as the tryptase test, is a valuable tool for detecting mast cell activation and confirming the diagnosis of anaphylaxis in cases where there is uncertainty. Tryptase is the primary protein found in mast cells. During anaphylaxis, mast cells release their contents, leading to an increase in blood tryptase levels. Typically, these levels start to rise approximately 30 minutes after symptoms begin, reach their peak at 1-2 hours, and return to normal within 6-8 hours.

For optimal results, it is recommended to collect three timed samples. The first sample should be taken as soon as possible after resuscitation efforts have commenced. The second sample should be obtained 1-2 hours after the onset of symptoms. Lastly, a third sample should be collected at the 24-hour mark to establish a baseline level.

While skin allergy tests, like the patch test, and blood tests for specific IgE can help identify the trigger of an allergic reaction, they alone cannot confirm the occurrence of anaphylaxis. The mast cell tryptase test, on the other hand, provides valuable information in confirming the diagnosis.

Cholelithiasis is a common occurrence in individuals with Crohn’s disease. There are several other conditions that are known to be associated with Crohn’s disease. These include a higher prevalence in smokers, with approximately 50-60% of patients being smokers. Additionally, individuals with Crohn’s disease may experience aphthous ulcers, uveitis, episcleritis, seronegative spondyloarthropathies, erythema nodosum, pyoderma gangrenosum, finger clubbing, autoimmune hemolytic anemia, and osteoporosis. However, it is important to note that primary biliary cirrhosis, primary sclerosing cholangitis, and chronic active hepatitis are associations commonly seen in ulcerative colitis rather than Crohn’s disease. Lastly, dermatitis herpetiformis is a condition that is associated with coeliac disease.

Bladder cancer is the most likely diagnosis in this case, as patients with painless haematuria should undergo cystoscopy to rule out bladder cancer. This procedure is typically done in an outpatient setting as part of a haematuria clinic, using a flexible cystoscope and local anaesthetic.

Prostate cancer is less likely in this case, as the patient’s prostate examination was relatively normal and he only had mild symptoms of bladder outlet obstruction.

Bladder cancer is the seventh most common cancer in the UK, with men being three times more likely to develop it than women. The main risk factors for bladder cancer are increasing age and smoking. Smoking is responsible for about 50% of bladder cancers, as it is believed to be linked to the excretion of aromatic amines and polycyclic aromatic hydrocarbons through the kidneys. Smokers have a 2-6 times higher risk of developing bladder cancer compared to non-smokers.

Painless macroscopic haematuria is the most common symptom in 80-90% of bladder cancer patients. There are usually no abnormalities found during a standard physical examination.

Current recommendations state that the following patients should be urgently referred for a urological assessment: adults over 45 years old with unexplained visible haematuria not caused by a urinary tract infection, adults over 45 years old with visible haematuria that persists or recurs after successful treatment of a urinary tract infection, and adults aged 60 and over with unexplained non-visible haematuria and either dysuria or a raised white cell count on a blood test.

For those aged 60 and over with recurrent or persistent unexplained urinary tract infections, a non-urgent referral for bladder cancer is recommended.

In cases of anaphylaxis, it is important to administer non-sedating antihistamines after adrenaline administration and initial resuscitation. Previous guidelines recommended the use of chlorpheniramine and hydrocortisone as third line treatments, but the 2021 guidelines have removed this recommendation. Corticosteroids are no longer advised. Instead, it is now recommended to use non-sedating antihistamines such as cetirizine, loratadine, and fexofenadine, as alternatives to the sedating antihistamine chlorpheniramine. The top priority treatments for anaphylaxis are adrenaline, oxygen, and fluids. The Resuscitation Council advises that administration of non-sedating antihistamines should occur after the initial resuscitation.

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.

Individuals who have gastroenteritis should be instructed to refrain from going to work or participating in social activities until at least 48 hours have passed since their last episode of diarrhea or vomiting.

Further Reading:

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

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

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

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

Protamine sulphate is a potent base that forms a stable salt complex with heparin, an acidic substance. This complex renders heparin inactive, making protamine sulphate a useful tool for neutralizing the effects of heparin. Additionally, protamine sulphate can be used to reverse the effects of LMWHs, although it is not as effective, providing only about two-thirds of the relative effect.

It is important to note that protamine sulphate also possesses its own weak intrinsic anticoagulant effect. This effect is believed to stem from its ability to inhibit the formation and activity of thromboplastin.

When administering protamine sulphate, it is typically done through slow intravenous injection. The dosage should be adjusted based on the amount of heparin that needs to be neutralized, the time that has passed since heparin administration, and the aPTT (activated partial thromboplastin time). As a general guideline, 1 mg of protamine can neutralize 100 IU of heparin. However, it is crucial to adhere to a maximum adult dose of 50 mg within a 10-minute period.

It is worth mentioning that protamine sulphate can have some adverse effects. It acts as a myocardial depressant, potentially leading to bradycardia (slow heart rate) and hypotension (low blood pressure). These effects may arise due to complement activation and leukotriene release.

Dementia is a collection of symptoms caused by a pathological process that leads to significant cognitive impairment, surpassing what is typically expected for a person’s age. The most prevalent form of dementia is Alzheimer’s disease.

The symptoms of dementia are diverse and encompass various aspects. These include memory loss, particularly in the short-term. Additionally, individuals with dementia may experience fluctuations in mood, which are typically responsive to external stimuli and support. It is important to note that thoughts about death are infrequent in individuals with dementia.

Furthermore, changes in personality may occur as a result of dementia. Individuals may struggle to find the right words when communicating and face difficulties in completing complex tasks. In later stages, urinary incontinence may become a concern, along with a loss of appetite and subsequent weight loss. Additionally, individuals with dementia may exhibit agitation when placed in unfamiliar settings.

Overall, dementia is characterized by a range of symptoms that significantly impact cognitive functioning.

Orthostatic hypotension is a condition where patients feel lightheaded and may experience tunnel vision when they stand up from a lying down position. These symptoms are often worse in the morning. The patient’s history of recurrent episodes after being in a supine position for a long time strongly suggests orthostatic hypotension. There are no signs of epilepsy, such as deja-vu or jambs vu prodrome, tongue biting, loss of bladder or bowel control, or postictal confusion. The normal ECG and consistent timing of symptoms make postural orthostatic tachycardia syndrome (PAF) less likely. There are no neurological deficits to suggest a transient ischemic attack (TIA). The prodromal symptoms, such as tunnel vision and lightheadedness, align more with orthostatic hypotension rather than vasovagal syncope, which typically occurs after long periods of standing and is characterized by feeling hot and sweaty. Although carotid sinus syndrome could be considered as a differential diagnosis, as the patient’s head turning on getting out of bed may trigger symptoms, it is not one of the options.

Further Reading:

Blackouts, also known as syncope, are defined as a spontaneous transient loss of consciousness with complete recovery. They are most commonly caused by transient inadequate cerebral blood flow, although epileptic seizures can also result in blackouts. There are several different causes of blackouts, including neurally-mediated reflex syncope (such as vasovagal syncope or fainting), orthostatic hypotension (a drop in blood pressure upon standing), cardiovascular abnormalities, and epilepsy.

When evaluating a patient with blackouts, several key investigations should be performed. These include an electrocardiogram (ECG), heart auscultation, neurological examination, vital signs assessment, lying and standing blood pressure measurements, and blood tests such as a full blood count and glucose level. Additional investigations may be necessary depending on the suspected cause, such as ultrasound or CT scans for aortic dissection or other abdominal and thoracic pathology, chest X-ray for heart failure or pneumothorax, and CT pulmonary angiography for pulmonary embolism.

During the assessment, it is important to screen for red flags and signs of any underlying serious life-threatening condition. Red flags for blackouts include ECG abnormalities, clinical signs of heart failure, a heart murmur, blackouts occurring during exertion, a family history of sudden cardiac death at a young age, an inherited cardiac condition, new or unexplained breathlessness, and blackouts in individuals over the age of 65 without a prodrome. These red flags indicate the need for urgent assessment by an appropriate specialist.

There are several serious conditions that may be suggested by certain features. For example, myocardial infarction or ischemia may be indicated by a history of coronary artery disease, preceding chest pain, and ECG signs such as ST elevation or arrhythmia. Pulmonary embolism may be suggested by dizziness, acute shortness of breath, pleuritic chest pain, and risk factors for venous thromboembolism. Aortic dissection may be indicated by chest and back pain, abnormal ECG findings, and signs of cardiac tamponade include low systolic blood pressure, elevated jugular venous pressure, and muffled heart sounds. Other conditions that may cause blackouts include severe hypoglycemia, Addisonian crisis, and electrolyte abnormalities.

This patient’s medical history suggests a diagnosis of Guillain-Barré syndrome (GBS). GBS typically presents with initial symptoms of sensory changes or pain, accompanied by muscle weakness in the hands and/or feet. This weakness often spreads to the arms and upper body, affecting both sides. During the acute phase, GBS can be life-threatening, with around 15% of patients experiencing respiratory muscle weakness and requiring mechanical ventilation.

The exact cause of GBS is unknown, but it is believed to involve an autoimmune response where the body’s immune system attacks the myelin sheath surrounding the peripheral nerves. In about 75% of cases, there is a preceding infection, commonly affecting the gastrointestinal or respiratory tracts.

In this particular case, the most likely underlying cause is Campylobacter jejuni, a gastrointestinal pathogen. This is supported by the recent history of a severe diarrheal illness.

Chlamydia trachomatis is a type of Gram-negative bacteria that is responsible for causing the sexually transmitted infection known as chlamydia. This bacterium is typically either coccoid or rod-shaped in its appearance.

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

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

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

Epididymo-orchitis refers to the inflammation of the epididymis and/or testicle. It typically presents with sudden pain, swelling, and inflammation in the affected area. This condition can also occur chronically, which means that the pain and inflammation last for more than six months.

The causes of epididymo-orchitis vary depending on the age of the patient. In men under 35 years old, the infection is usually sexually transmitted and caused by Chlamydia trachomatis or Neisseria gonorrhoeae. In men over 35 years old, the infection is usually non-sexually transmitted and occurs as a result of enteric organisms that cause urinary tract infections, with Escherichia coli being the most common. However, there can be some overlap between these groups, so it is important to obtain a thorough sexual history in all age groups.

Mumps should also be considered as a potential cause of epididymo-orchitis in the 15 to 30 age group, as mumps orchitis occurs in around 40% of post-pubertal boys with mumps.

While most cases of epididymo-orchitis are infective, non-infectious causes can also occur. These include genito-urinary surgery, vasectomy, urinary catheterization, Behcet’s disease, sarcoidosis, and drug-induced cases such as those caused by amiodarone.

Patients with epididymo-orchitis typically present with unilateral scrotal pain and swelling that develops relatively quickly. The affected testis will be tender to touch, and there is usually a palpable swelling of the epididymis that starts at the lower pole of the testis and spreads towards the upper pole. The testis itself may also be involved, and there may be redness and/or swelling of the scrotum on the affected side. Patients may experience fever and urethral discharge as well.

The most important differential diagnosis to consider is testicular torsion, which requires immediate medical attention within 6 hours of onset to save the testicle. Testicular torsion is more likely in men under the age of 20, especially if the pain is very severe and sudden. It typically presents around four hours after onset. In this case, the patient’s age, longer history of symptoms, and the presence of fever are more indicative of epididymo-orchitis.

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.

Tranexamic acid is the best choice for this patient because her periods are heavy, but not very painful, and her fibroids are small. Additionally, she wants to start a family soon, so contraceptive options are not as suitable. For more information, you can refer to the NICE guidelines on the assessment and management of heavy menstrual bleeding.

A word salad refers to a jumbled or incomprehensible combination of seemingly arbitrary words and phrases. This phenomenon is frequently observed in individuals with schizophrenia and dementia.

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

Further Reading:

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

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

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

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

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

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

Peritonsillar abscess, also known as quinsy, is most commonly seen in adolescents and young adults between the ages of 20 and 40. Risk factors for developing quinsy include being male and smoking. It is a relatively common condition, with studies showing an incidence rate of 10 to 30 cases per 100,000 population. When treating quinsy, it is important to use a broader range of antibiotics compared to standard treatment for pharyngotonsillitis, as the causative organisms may not be limited to Group A Streptococcus. Common antibiotic choices include intravenous amoxicillin with clindamycin or metronidazole, although the specific antibiotic used may vary depending on local antimicrobial policies.

Further Reading:

A peritonsillar abscess, also known as quinsy, is a collection of pus that forms between the palatine tonsil and the pharyngeal muscles. It is often a complication of acute tonsillitis and is most commonly seen in adolescents and young adults. The exact cause of a peritonsillar abscess is not fully understood, but it is believed to occur when infection spreads beyond the tonsillar capsule or when small salivary glands in the supratonsillar space become blocked.

The most common causative organisms for a peritonsillar abscess include Streptococcus pyogenes, Staphylococcus aureus, Haemophilus influenzae, and anaerobic organisms. Risk factors for developing a peritonsillar abscess include smoking, periodontal disease, male sex, and a previous episode of the condition.

Clinical features of a peritonsillar abscess include severe throat pain, difficulty opening the mouth (trismus), fever, headache, drooling of saliva, bad breath, painful swallowing, altered voice, ear pain on the same side, neck stiffness, and swelling of the soft palate. Diagnosis is usually made based on clinical presentation, but imaging scans such as CT or ultrasound may be used to assess for complications or determine the best site for drainage.

Treatment for a peritonsillar abscess involves pain relief, intravenous antibiotics to cover for both aerobic and anaerobic organisms, intravenous fluids if swallowing is difficult, and drainage of the abscess either through needle aspiration or incision and drainage. Tonsillectomy may be recommended to prevent recurrence. Complications of a peritonsillar abscess can include sepsis, spread to deeper neck tissues leading to necrotizing fasciitis or retropharyngeal abscess, airway compromise, recurrence of the abscess, aspiration pneumonia, erosion into major blood vessels, and complications related to the causative organism. All patients with a peritonsillar abscess should be referred to an ear, nose, and throat specialist for further management.

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.

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

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

When performing Weber’s test, if the sound lateralizes to the unaffected side, it suggests sensorineural hearing loss. If the sound lateralizes to the right, it could mean that there is sensorineural hearing loss in the left ear or conductive hearing loss in the right ear. A positive Rinne test result indicates that air conduction is greater than bone conduction, which is normal or seen in sensorineural hearing loss. On the other hand, a negative Rinne test result suggests that bone conduction is greater than air conduction, which is typically seen in conductive hearing loss. Therefore, if there is conductive hearing loss in the left ear, a negative Rinne test result would indicate sensorineural loss on the left side.

Further Reading:

Hearing loss is a common complaint that can be caused by various conditions affecting different parts of the ear and nervous system. The outer ear is the part of the ear outside the eardrum, while the middle ear is located between the eardrum and the cochlea. The inner ear is within the bony labyrinth and consists of the vestibule, semicircular canals, and cochlea. The vestibulocochlear nerve connects the inner ear to the brain.

Hearing loss can be classified based on severity, onset, and type. Severity is determined by the quietest sound that can be heard, measured in decibels. It can range from mild to profound deafness. Onset can be sudden, rapidly progressive, slowly progressive, or fluctuating. Type of hearing loss can be either conductive or sensorineural. Conductive hearing loss is caused by issues in the external ear, eardrum, or middle ear that disrupt sound transmission. Sensorineural hearing loss is caused by problems in the cochlea, auditory nerve, or higher auditory processing pathways.

To diagnose sensorineural and conductive deafness, a 512 Hz tuning fork is used to perform Rinne and Weber’s tests. These tests help determine the type of hearing loss based on the results. In Rinne’s test, air conduction (AC) and bone conduction (BC) are compared, while Weber’s test checks for sound lateralization.

Cholesteatoma is a condition characterized by the abnormal accumulation of skin cells in the middle ear or mastoid air cell spaces. It is believed to develop from a retraction pocket that traps squamous cells. Cholesteatoma can cause the accumulation of keratin and the destruction of adjacent bones and tissues due to the production of destructive enzymes. It can lead to mixed sensorineural and conductive deafness as it affects both the middle and inner ear.

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.

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

Heat stroke happens when the body’s ability to regulate temperature is overwhelmed by a combination of excessive environmental heat, excessive production of heat from exertion, and inadequate heat loss. Several risk factors increase the likelihood of developing heat stroke, including hot and humid environmental conditions, age (particularly the elderly and infants), physical factors like obesity and excessive exertion, medical conditions like anorexia and cardiovascular disease, and certain medications such as alcohol, amphetamines, and diuretics.

The typical clinical features of heat stroke include a core temperature above 40.6°C, early symptoms like extreme fatigue, headache, syncope, facial flushing, vomiting, and diarrhea. The skin is usually hot and dry, although sweating may occur in around 50% of cases of exertional heat stroke. The loss of the ability to sweat is a late and concerning sign. Hyperventilation is almost always present. Heat stroke can also lead to cardiovascular dysfunction, respiratory dysfunction, central nervous system dysfunction, and potentially multi-organ failure, coagulopathy, and rhabdomyolysis if the temperature rises above 41.5°C.

Heat cramps, on the other hand, are characterized by intense thirst and muscle cramps. Body temperature is often elevated but typically remains below 40°C. Sweating, heat dissipation mechanisms, and cognition are preserved, and there is no neurological impairment. Heat exhaustion usually precedes heat stroke and if left untreated, can progress to heat stroke. Heat dissipation is still functioning, and the body temperature is usually below 41°C. Symptoms of heat exhaustion include nausea, oliguria, weakness, headache, thirst, and sinus tachycardia. Central nervous system functioning is usually largely preserved, and patients may complain of feeling hot and appear flushed and sweaty.

It is important to note that malignant hyperthermia and neuroleptic malignant syndrome are highly unlikely in this scenario as the patient has no recent history of a general anesthetic or taking phenothiazines or other antipsychotics, respectively.

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

The key components of first aid for snake bites in the UK involve immobilizing the patient and the affected limb, as well as administering paracetamol for pain relief. When it comes to venomous snake bites, it is important to immobilize the limb using a splint or sling, but not to use a tourniquet or pressure bandage for adder bites. In certain areas, such as NSW, Australia, where venomous snakes can cause rapidly progressing and life-threatening paralysis, pressure bandage immobilization is recommended. However, this is not the case in the UK. Anti-venom is not always necessary for adder bites, and its administration should be based on a thorough assessment of the patient’s condition and the presence of appropriate indications. Paracetamol is the preferred choice for pain relief in UK snake bites, as aspirin and ibuprofen can worsen bleeding tendencies that may result from adder bites. Similarly, heparin should be avoided for the same reason.

Further Reading:

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

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

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

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

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

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

The current school exclusion advice for certain infectious diseases with a rash is as follows:

– For chickenpox, children should be excluded for at least 5 days from the onset of the rash and until all blisters have crusted over.
– In the case of measles, children should be excluded for 4 days from the onset of the rash, provided they are well enough to attend.
– Mumps requires a 5-day exclusion after the onset of swelling.
– Rubella, also known as German measles, requires a 5-day exclusion from the onset of the rash.
– Scarlet fever necessitates exclusion until 24 hours after starting antibiotic treatment.

It is important to note that school exclusion advice has undergone changes in recent years, and the information provided above reflects the updated advice as of May 2022.

Further Reading:

Measles is a highly contagious viral infection caused by an RNA paramyxovirus. It is primarily spread through aerosol transmission, specifically through droplets in the air. The incubation period for measles is typically 10-14 days, during which patients are infectious from 4 days before the appearance of the rash to 4 days after.

Common complications of measles include pneumonia, otitis media (middle ear infection), and encephalopathy (brain inflammation). However, a rare but fatal complication called subacute sclerosing panencephalitis (SSPE) can also occur, typically presenting 5-10 years after the initial illness.

The onset of measles is characterized by a prodrome, which includes symptoms such as irritability, malaise, conjunctivitis, and fever. Before the appearance of the rash, white spots known as Koplik spots can be seen on the buccal mucosa. The rash itself starts behind the ears and then spreads to the entire body, presenting as a discrete maculopapular rash that becomes blotchy and confluent.

In terms of complications, encephalitis typically occurs 1-2 weeks after the onset of the illness. Febrile convulsions, giant cell pneumonia, keratoconjunctivitis, corneal ulceration, diarrhea, increased incidence of appendicitis, and myocarditis are also possible complications of measles.

When managing contacts of individuals with measles, it is important to offer the MMR vaccine to children who have not been immunized against measles. The vaccine-induced measles antibody develops more rapidly than that following natural infection, so it should be administered within 72 hours of contact.

When managing newly diagnosed atrial fibrillation, a rate control strategy is often used. In this approach, beta blockers are typically the first line of treatment. However, sotalol is not recommended, and instead, other beta blockers like atenolol, acebutolol, metoprolol, nadolol, oxprenolol, and propranolol are preferred. Among these options, atenolol is commonly chosen in NHS trusts due to its cost-effectiveness.

For patients with signs of hemodynamic instability or adverse features, rhythm control (cardioversion) may be considered if they present within 48 hours of likely onset. However, in the case of this patient, their symptoms started a week ago, and there are no indications of hemodynamic instability or adverse features.

Digoxin monotherapy is typically reserved for individuals who have limited physical activity or are unable to take other first-line rate control medications due to other health conditions or contraindications.

Further Reading:

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting around 5% of patients over the age of 70-75 years and 10% of patients aged 80-85 years. While AF can cause palpitations and inefficient cardiac function, the most important aspect of managing patients with AF is reducing the increased risk of stroke.

AF can be classified as first detected episode, paroxysmal, persistent, or permanent. First detected episode refers to the initial occurrence of AF, regardless of symptoms or duration. Paroxysmal AF occurs when a patient has 2 or more self-terminating episodes lasting less than 7 days. Persistent AF refers to episodes lasting more than 7 days that do not self-terminate. Permanent AF is continuous atrial fibrillation that cannot be cardioverted or if attempts to do so are deemed inappropriate. The treatment goals for permanent AF are rate control and anticoagulation if appropriate.

Symptoms of AF include palpitations, dyspnea, and chest pain. The most common sign is an irregularly irregular pulse. An electrocardiogram (ECG) is essential for diagnosing AF, as other conditions can also cause an irregular pulse.

Managing patients with AF involves two key parts: rate/rhythm control and reducing stroke risk. Rate control involves slowing down the irregular pulse to avoid negative effects on cardiac function. This is typically achieved using beta-blockers or rate-limiting calcium channel blockers. If one drug is not effective, combination therapy may be used. Rhythm control aims to restore and maintain normal sinus rhythm through pharmacological or electrical cardioversion. However, the majority of patients are managed with a rate control strategy.

Reducing stroke risk in patients with AF is crucial. Risk stratifying tools, such as the CHA2DS2-VASc score, are used to determine the most appropriate anticoagulation strategy. Anticoagulation is recommended for patients with a score of 2 or more. Clinicians can choose between warfarin and novel oral anticoagulants (NOACs) for anticoagulation.

Before starting anticoagulation, the patient’s bleeding risk should be assessed using tools like the HAS-BLED score or the ORBIT tool. These tools evaluate factors such as hypertension, abnormal renal or liver function, history of bleeding, age, and use of drugs that predispose to bleeding.

Cardiac arrest during pregnancy is a rare occurrence, happening in approximately 16 out of every 100,000 live births. It is crucial to consider both the mother and the fetus when dealing with cardiac arrest in pregnancy, as the best way to ensure a positive outcome for the fetus is by effectively resuscitating the mother.

The main causes of cardiac arrest during pregnancy include pre-existing cardiac disease, pulmonary embolism, hemorrhage, ectopic pregnancy, hypertensive disorders of pregnancy, amniotic fluid embolism, and suicide. Many cardiovascular problems associated with pregnancy are caused by compression of the inferior vena cava.

To prevent decompensation or potential cardiac arrest during pregnancy, it is important to follow these steps when dealing with a distressed or compromised pregnant patient:

– Place the patient in the left lateral position or manually displace the uterus to the left.
– Administer high-flow oxygen, guided by pulse oximetry.
– Give a fluid bolus if there is low blood pressure or signs of hypovolemia.
– Re-evaluate the need for any medications currently being administered.
– Seek expert help and involve obstetric and neonatal specialists early.
– Identify and treat the underlying cause.

In the event of cardiac arrest during pregnancy, in addition to following the standard guidelines for basic and advanced life support, the following modifications should be made:

– Immediately call for expert help, including an obstetrician, anesthetist, and neonatologist.
– Start CPR according to the standard ALS guidelines, but adjust the hand position slightly higher on the sternum.
– Ideally establish IV or IO access above the diaphragm to account for potential compression of the inferior vena cava.
– Manually displace the uterus to the left to relieve caval compression.
– Tilt the table to the left side (around 15-30 degrees of tilt).
– Perform early tracheal intubation to reduce the risk of aspiration (seek assistance from an expert anesthetist).
– Begin preparations for an emergency Caesarean section.

A perimortem Caesarean section should be performed within 5 minutes of the onset of cardiac arrest. This delivery will alleviate caval compression and increase the chances of successful resuscitation by improving venous return during CPR. It will also maximize the chances of the infant’s survival, as the best survival rate occurs when delivery is achieved within 5 minutes of the mother’s cardiac arrest.

Digoxin-specific antibody (DigiFab) is an antidote used to counteract digoxin overdose. It is a purified and sterile preparation of digoxin-immune ovine Fab immunoglobulin fragments. These fragments are derived from healthy sheep that have been immunized with a digoxin derivative called digoxin-dicarboxymethoxylamine (DDMA). DDMA is a digoxin analogue that contains the essential cyclopentanoperhydrophenanthrene: lactone ring moiety coupled to keyhole limpet hemocyanin (KLH).

DigiFab has a higher affinity for digoxin compared to the affinity of digoxin for its sodium pump receptor, which is believed to be the receptor responsible for its therapeutic and toxic effects. When administered to a patient who has overdosed on digoxin, DigiFab binds to digoxin molecules, reducing the levels of free digoxin in the body. This shift in equilibrium away from binding to the receptors helps to reduce the cardiotoxic effects of digoxin. The Fab-digoxin complexes are then eliminated from the body through the kidney and reticuloendothelial system.

The indications for using DigiFab in cases of acute and chronic digoxin toxicity are summarized below:

Acute digoxin toxicity:
– Cardiac arrest
– Life-threatening arrhythmia
– Potassium level >5 mmol/l
– Ingestion of >10 mg of digoxin (in adults)
– Ingestion of >4 mg of digoxin (in children)
– Digoxin level >12 ng/ml

Chronic digoxin toxicity:
– Cardiac arrest
– Life-threatening arrhythmia
– Significant gastrointestinal symptoms
– Symptoms of digoxin toxicity in the presence of renal failure

The healthcare provider should also assess the insulin infusion rate. It is important to note that the recommended minimum rate is 0.05 units per kilogram per hour. In this case, the patient weighs 60 kilograms and is currently receiving 3 units of Actrapid® insulin per hour, which is equivalent to 0.05 units per kilogram per hour. Therefore, the patient is already on the lowest possible dose. However, if the patient was on a higher dose of 0.1 units per kilogram per hour, it can be reduced once the glucose level falls below 14 mmol/l.

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.

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

Further Reading:

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

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

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

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

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.

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.

Acute epiglottitis is a condition characterized by inflammation of the epiglottis. It can be life-threatening as it can completely block the airway, especially if not diagnosed promptly. In the past, the most common cause was Haemophilus influenzae type b (Hib), but with the widespread use of the Hib vaccine, it has become rare in children and is now more commonly seen in adults caused by Streptococcus spp like Streptococcus pyogenes and Streptococcus pneumonia. Other bacterial causes include Staphylococcus aureus, Pseudomonas spp, Moraxella catarrhalis, and Mycobacterium tuberculosis.

The typical symptoms of acute epiglottitis include fever, sore throat (initially resembling a viral sore throat), painful swallowing, difficulty swallowing secretions (seen as drooling in children), muffled voice (referred to as ‘hot potato’ voice), rapid heartbeat, tenderness in the front of the neck over the hyoid bone, cervical lymph node enlargement, and rapid deterioration in children.

To diagnose acute epiglottitis, the gold standard investigation is fibre-optic laryngoscopy, which allows direct visualization of the epiglottis. However, laryngoscopy should only be performed in settings prepared for intubation or tracheostomy in case upper airway obstruction occurs. If laryngoscopy is not possible, a lateral neck X-ray may be helpful, as it can show the characteristic ‘thumbprint sign’.

Management of acute epiglottitis usually involves conservative measures such as intravenous or oral antibiotics. However, in some cases, intubation may be necessary.

Ketamine primarily works by blocking NMDA receptors, although its complete mechanism of action is not yet fully comprehended. Ongoing research is exploring its impact on various other receptors.

Further Reading:

Procedural sedation is commonly used by emergency department (ED) doctors to minimize pain and discomfort during procedures that may be painful or distressing for patients. Effective procedural sedation requires the administration of analgesia, anxiolysis, sedation, and amnesia. This is typically achieved through the use of a combination of short-acting analgesics and sedatives.

There are different levels of sedation, ranging from minimal sedation (anxiolysis) to general anesthesia. It is important for clinicians to understand the level of sedation being used and to be able to manage any unintended deeper levels of sedation that may occur. Deeper levels of sedation are similar to general anesthesia and require the same level of care and monitoring.

Various drugs can be used for procedural sedation, including propofol, midazolam, ketamine, and fentanyl. Each of these drugs has its own mechanism of action and side effects. Propofol is commonly used for sedation, amnesia, and induction and maintenance of general anesthesia. Midazolam is a benzodiazepine that enhances the effect of GABA on the GABA A receptors. Ketamine is an NMDA receptor antagonist and is used for dissociative sedation. Fentanyl is a highly potent opioid used for analgesia and sedation.

The doses of these drugs for procedural sedation in the ED vary depending on the drug and the route of administration. It is important for clinicians to be familiar with the appropriate doses and onset and peak effect times for each drug.

Safe sedation requires certain requirements, including appropriate staffing levels, competencies of the sedating practitioner, location and facilities, and monitoring. The level of sedation being used determines the specific requirements for safe sedation.

After the procedure, patients should be monitored until they meet the criteria for safe discharge. This includes returning to their baseline level of consciousness, having vital signs within normal limits, and not experiencing compromised respiratory status. Pain and discomfort should also be addressed before discharge.

The levels of thyroid stimulating hormone (TSH) and thyroxine (T4) are both below the normal range.

Further Reading:

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

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

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

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

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

Haemolytic disease of the newborn is a condition that occurs in the fetus when IgG antibodies from the mother pass through the placenta. This is classified as a type II hypersensitivity reaction, also known as cytotoxic hypersensitivity. In this type of reaction, antibodies produced by the immune response attach to antigens on the patient’s own cell surfaces.

The rhesus gene is composed of three parts, which can be C or c, D or d, and E or e. Approximately 15% of the population consists of rhesus negative women who are homozygous for d. When rhesus-positive fetal cells enter the bloodstream of a rhesus-negative mother, maternal anti-D IgG antibodies may be produced. This commonly occurs during delivery, but can also happen after fetal-maternal hemorrhage and certain medical procedures.

Some other examples of type II hypersensitivity reactions include autoimmune hemolytic anemia, ANCA-associated vasculitides, Goodpasture’s syndrome, myasthenia gravis, and rhesus incompatibility.

After administering any treatment for hypoglycemia, it is important to re-check glucose levels within 10-15 minutes. This allows for a reassessment of the effectiveness of the treatment and the possibility of administering additional treatment if needed. Obesity is a significant risk factor for developing type 2 diabetes, while most individuals with type 1 diabetes have a body mass index (BMI) below 25 kg/m2. It is crucial to provide carbohydrates promptly after treating hypoglycemia. The correct dose of glucagon for treating hypoglycemia in adults is 1 mg, and the same dose can be used for children aged 9 and above who weigh more than 25kg. HbA1c results between 42 and 47 indicate pre-diabetes.

Further Reading:

Diabetes Mellitus:
– Definition: a group of metabolic disorders characterized by persistent hyperglycemia caused by deficient insulin secretion, resistance to insulin, or both.
– Types: Type 1 diabetes (absolute insulin deficiency), Type 2 diabetes (insulin resistance and relative insulin deficiency), Gestational diabetes (develops during pregnancy), Other specific types (monogenic diabetes, diabetes secondary to pancreatic or endocrine disorders, diabetes secondary to drug treatment).
– Diagnosis: Type 1 diabetes diagnosed based on clinical grounds in adults presenting with hyperglycemia. Type 2 diabetes diagnosed in patients with persistent hyperglycemia and presence of symptoms or signs of diabetes.
– Risk factors for type 2 diabetes: obesity, inactivity, family history, ethnicity, history of gestational diabetes, certain drugs, polycystic ovary syndrome, metabolic syndrome, low birth weight.

Hypoglycemia:
– Definition: lower than normal blood glucose concentration.
– Diagnosis: defined by Whipple’s triad (signs and symptoms of low blood glucose, low blood plasma glucose concentration, relief of symptoms after correcting low blood glucose).
– Blood glucose level for hypoglycemia: NICE defines it as <3.5 mmol/L, but there is inconsistency across the literature.
– Signs and symptoms: adrenergic or autonomic symptoms (sweating, hunger, tremor), neuroglycopenic symptoms (confusion, coma, convulsions), non-specific symptoms (headache, nausea).
– Treatment options: oral carbohydrate, buccal glucose gel, glucagon, dextrose. Treatment should be followed by re-checking glucose levels.

Treatment of neonatal hypoglycemia:
– Treat with glucose IV infusion 10% given at a rate of 5 mL/kg/hour.
– Initial stat dose of 2 mL/kg over five minutes may be required for severe hypoglycemia.
– Mild asymptomatic persistent hypoglycemia may respond to a single dose of glucagon.
– If hypoglycemia is caused by an oral anti-diabetic drug, the patient should be admitted and ongoing glucose infusion or other therapies may be required.

Note: Patients who have a hypoglycemic episode with a loss of warning symptoms should not drive and should inform the DVLA.

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

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

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

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

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

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

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

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 particular patient’s case, his history of chronic alcohol abuse, homelessness, and likely impaired nutrition necessitates the administration of intravenous thiamine in the form of Pabrinex. Additionally, a second dose of benzodiazepine should be given, and his blood glucose levels should be urgently checked.

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 (50 ml of 50% solution) and/or intravenous thiamine as Pabrinex if there are indications of alcohol abuse or impaired nutrition
– Treat severe acidosis if present

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

4th stage (30-90 minutes):
– Transfer the patient to the intensive care unit
– Establish intensive care and EEG monitoring
– Initiate intracranial pressure monitoring if necessary
– Start initial long-term, maintenance AED therapy

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 performed to evaluate the possibility of aspiration. Additional investigations, such as brain imaging or lumbar puncture, depend on the clinical circumstances.

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

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

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

Occlusion of branches of the anterior spinal artery leads to the development of the medial medullary syndrome. This condition is characterized by several distinct symptoms. Firstly, there is contralateral hemiplegia, which occurs due to damage to the pyramidal tracts. Additionally, there is contralateral loss of joint position sense, vibratory sense, and discriminatory touch, resulting from damage to the medial lemniscus. Lastly, there is ipsilateral deviation and paralysis of the tongue, which is caused by damage to the hypoglossal nucleus.

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.

Based on the patient’s symptoms of suprapubic pain, increased urinary frequency, and foul-smelling urine, along with the presence of nitrites, leukocytes, and blood in the urine dipstick test, the most likely cause of her symptoms is a urinary tract infection (UTI). The most probable causative organism for UTIs is Escherichia coli.

Further Reading:

A urinary tract infection (UTI) is an infection that occurs in any part of the urinary system, from the kidneys to the bladder. It is characterized by symptoms such as dysuria, nocturia, polyuria, urgency, incontinence, and changes in urine appearance and odor. UTIs can be classified as lower UTIs, which affect the bladder, or upper UTIs, which involve the kidneys. Recurrent UTIs can be due to relapse or re-infection, and the number of recurrences considered significant depends on age and sex. Uncomplicated UTIs occur in individuals with a normal urinary tract and kidney function, while complicated UTIs are caused by anatomical, functional, or pharmacological factors that make the infection persistent, recurrent, or resistant to treatment.

The most common cause of UTIs is Escherichia coli, accounting for 70-95% of cases. Other causative organisms include Staphylococcus saprophyticus, Proteus mirabilis, and Klebsiella species. UTIs are typically caused by bacteria from the gastrointestinal tract entering the urinary tract through the urethra. Other less common mechanisms of entry include direct spread via the bloodstream or instrumentation of the urinary tract, such as catheter insertion.

Diagnosis of UTIs involves urine dipstick testing and urine culture. A urine culture should be sent in certain circumstances, such as in male patients, pregnant patients, women aged 65 years or older, patients with persistent or unresolved symptoms, recurrent UTIs, patients with urinary catheters, and those with risk factors for resistance or complicated UTIs. Further investigations, such as cystoscopy and imaging, may be required in cases of recurrent UTIs or suspected underlying causes.

Management of UTIs includes simple analgesia, advice on adequate fluid intake, and the prescription of appropriate antibiotics. The choice of antibiotic depends on the patient’s gender and risk factors. For women, first-line antibiotics include nitrofurantoin or trimethoprim, while second-line options include nitrofurantoin (if not used as first-line), pivmecillinam, or fosfomycin. For men, trimethoprim or nitrofurantoin are the recommended antibiotics. In cases of suspected acute prostatitis, fluoroquinolone antibiotics such as ciprofloxacin or ofloxacin may be prescribed for a 4-week course.

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

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

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

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

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

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

Public Health England (PHE) has a primary goal of swiftly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is important, it is not the main focus. Since 1968, clinical suspicion of a notifiable infection has been sufficient for reporting.
Registered medical practitioners (RMPs) are legally obligated to notify the designated proper officer at their local council or local health protection team (HPT) if they suspect cases of certain infectious diseases.
The Health Protection (Notification) Regulations 2010 specify the diseases that RMPs must report to the proper officers at local authorities. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.
It is worth noting that roseola infantum is not considered a notifiable disease, making it the least likely option among the diseases listed above.

Appendicitis is a condition characterized by the acute inflammation of the appendix. It is a common cause of the acute abdomen, particularly affecting children and young adults in their 20s and 30s. The typical presentation of appendicitis involves experiencing poorly localized periumbilical pain, which is pain originating from the visceral peritoneum. Within a day or two, this pain tends to localize to a specific point known as McBurney’s point, which is associated with pain from the parietal peritoneum. Alongside the pain, individuals with appendicitis often experience symptoms such as fever, loss of appetite, and nausea.

McBurney’s point is defined as the point that lies one-third of the distance from the anterior superior iliac spine to the umbilicus. This point roughly corresponds to the most common position where the base of the appendix attaches to the caecum.

This child’s medical history and chest X-ray findings are indicative of an inhaled foreign object. Upon careful examination, it is evident that the left lung appears more transparent than the right lung, and the foreign body is lodged in the left tracheobronchial tree.

Airway foreign bodies in children can be life-threatening, and it is important to consider this diagnosis when young children experience unexplained difficulty breathing and wheezing. Unfortunately, there is often a delay in diagnosing this condition.

Foreign objects typically get stuck in the right tracheobronchial tree because the right main bronchus is wider, shorter, and more vertically positioned compared to the left main bronchus. However, they can become lodged anywhere in the tracheobronchial tree.

While there is often a history of choking prior to the symptoms, this is not always the case. Any history of running with objects in the mouth or being in close proximity to small objects that can be placed in the mouth can provide important clues. In the absence of a choking history, clinical features may include paroxysmal coughing, unexplained difficulty breathing, changes in voice, poor appetite, irritability, decreased breath sounds on one side, and localized wheezing.

To aid in diagnosis, a chest X-ray should be taken during expiration as it can accentuate any differences between the two lungs. The following findings may be observed: the normal lung may appear smaller and denser than the affected lung, the affected lung may appear excessively transparent and overinflated, and a radio-opaque foreign object may be visible. However, it is important to note that approximately 35% of patients may have a normal chest X-ray.

Bronchoscopy is considered the gold-standard test for diagnosing tracheobronchial foreign bodies. This procedure not only confirms the presence of a foreign object but also allows for potential retrieval.

Possible complications of this condition include pneumonia, atelectasis (collapsed lung), bronchospasm (constriction of the airways), pneumothorax (collapsed lung due to air leakage), broncho-oesophageal fistula (abnormal connection between the bronchial tubes and the esophagus), and bronchiectasis (permanent dilation of the bronchial tubes).

Rapid tranquillisation involves the administration of medication through injection when oral medication is not feasible or appropriate and immediate sedation is necessary. The current guidelines from NICE recommend two options for rapid tranquillisation in adults: intramuscular lorazepam alone or a combination of intramuscular haloperidol and intramuscular promethazine. The choice of medication depends on various factors such as advanced statements, potential intoxication, previous responses to these medications, interactions with other drugs, and existing physical health conditions or pregnancy.

If there is insufficient information to determine the appropriate medication or if the individual has not taken antipsychotic medication before, intramuscular lorazepam is recommended. However, if there is evidence of cardiovascular disease or a prolonged QT interval, or if an electrocardiogram has not been conducted, the combination of intramuscular haloperidol and intramuscular promethazine should be avoided, and intramuscular lorazepam should be used instead.

If there is a partial response to intramuscular lorazepam, a second dose should be considered. If there is no response to intramuscular lorazepam, then intramuscular haloperidol combined with intramuscular promethazine should be considered. If there is a partial response to this combination, a further dose should be considered.

If there is no response to intramuscular haloperidol combined with intramuscular promethazine and intramuscular lorazepam has not been used yet, it should be considered. However, if intramuscular lorazepam has already been administered, it is recommended to arrange an urgent team meeting to review the situation and seek a second opinion if necessary.

After rapid tranquillisation, the patient should be closely monitored for any side effects, and their vital signs should be regularly checked, including heart rate, blood pressure, respiratory rate, temperature, hydration level, and level of consciousness. These observations should be conducted at least hourly until there are no further concerns about the patient’s physical health.

For more information, refer to the NICE guidance on violence and aggression: short-term management in mental health, health, and community settings.

For individuals with traumatic cardiac tamponade, thoracotomy is the recommended treatment. In the case of a trauma patient with a significant buildup of fluid around the heart and the potential for tamponade, it is advised to transfer stable patients to the operating room for thoracotomy instead of performing pericardiocentesis. Pericardiocentesis, when done correctly, is likely to be unsuccessful due to the presence of clotted blood in the pericardium. Additionally, performing pericardiocentesis would cause a delay in the thoracotomy procedure. If access to the operating room is not possible, pericardiocentesis may be considered as a temporary solution.

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.

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

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

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

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

The recommended dose of adrenaline is 7 mg per kilogram of body weight, with a maximum limit of 500 mg.

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.

During pregnancy, genital warts have the potential to grow larger in size and increase in number. This is because pregnancy causes a state of immunosuppression, which means that the patient’s immune system is unable to effectively suppress the latent HPV virus. Additionally, there are other factors that can contribute to the growth of genital warts. These include areas of moist skin, non-hair bearing skin, poor hygiene, and the presence of vaginal discharge.

The management of anaphylaxis involves several important steps. First and foremost, it is crucial to ensure proper airway management. Additionally, early administration of adrenaline is essential, preferably in the anterolateral aspect of the middle third of the thigh. Aggressive fluid resuscitation is also necessary. In severe cases, intubation may be required. However, it is important to note that the administration of chlorpheniramine and hydrocortisone should only be considered after early resuscitation has taken place.

Adrenaline is the most vital medication for treating anaphylactic reactions. It acts as an alpha-adrenergic receptor agonist, which helps reverse peripheral vasodilatation and reduce oedema. Furthermore, its beta-adrenergic effects aid in dilating the bronchial airways, increasing the force of myocardial contraction, and suppressing histamine and leukotriene release. Administering adrenaline as the first drug is crucial, and the intramuscular (IM) route is generally the most effective for most individuals.

The recommended doses of IM adrenaline for different age groups during anaphylaxis are as follows:

– Children under 6 years: 150 mcg (0.15 mL of 1:1000)
– Children aged 6-12 years: 300 mcg (0.3 mL of 1:1000)
– Children older than 12 years: 500 mcg (0.5 mL of 1:1000)
– Adults: 500 mcg (0.5 mL of 1:1000)

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

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

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

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

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

Klebsiella pneumoniae is commonly observed in individuals who are dependent on alcohol. It is more prevalent in men compared to women and typically manifests after the age of 40.

The clinical manifestations of this condition include fevers and rigors, pleuritic chest pain, purulent sputum, and haemoptysis, which occurs more frequently than with other bacterial pneumonias. Klebsiella pneumoniae tends to affect the upper lobes of the lungs and often leads to the formation of cavitating lesions.

While Staphylococcus aureus can also cause cavitation, it usually affects multiple lobes and is not limited to the upper lobes. Other potential causes of cavitating pneumonia include Pseudomonas aeruginosa, Mycobacterium tuberculosis, and, although rare, Legionella pneumophila.

Peptic ulcer disease is a fairly common condition that can affect either the stomach or the duodenum. However, the duodenum is more commonly affected, and in these cases, it is caused by a break in the mucosal lining of the duodenum.

This condition is more prevalent in men and is most commonly seen in individuals between the ages of 20 and 60. In fact, over 95% of patients with duodenal ulcers are found to be infected with H. pylori. Additionally, chronic usage of nonsteroidal anti-inflammatory drugs (NSAIDs) is often associated with the development of duodenal ulcers.

When it comes to the location of duodenal ulcers, they are most likely to occur in the superior (first) part of the duodenum, which is positioned in front of the body of the L1 vertebra.

The typical clinical features of duodenal ulcers include experiencing epigastric pain that radiates to the back, with the pain often worsening at night. This pain typically occurs 2-3 hours after eating and is relieved by consuming food and drinking milk. It can also be triggered by skipping meals or experiencing stress.

Possible complications that can arise from duodenal ulcers include perforation, which can lead to peritonitis, as well as gastrointestinal hemorrhage. Gastrointestinal hemorrhage can manifest as haematemesis (vomiting blood), melaena (black, tarry stools), or occult bleeding. Strictures causing obstruction can also occur as a result of duodenal ulcers.

In cases where gastrointestinal hemorrhage occurs as a result of duodenal ulceration, it is usually due to erosion of the gastroduodenal artery.

The Arthus reaction is a response that occurs when antigen/antibody complexes are formed in the skin after an antigen is injected. Although rare, these reactions can happen after receiving vaccines that contain tetanus toxoid or diphtheria toxoid. They are classified as a type III hypersensitivity reaction.

Arthus reactions are characterized by pain, swelling, induration, hemorrhage, and sometimes necrosis. Typically, these symptoms appear 4-12 hours after vaccination.

Type III hypersensitivity reactions occur when insoluble antigen-antibody complexes accumulate in different tissues and are not effectively cleared by the body’s innate immune cells. This leads to an inflammatory response in the affected tissues.

Some other examples of type III hypersensitivity reactions include immune complex glomerulonephritis, rheumatoid arthritis, systemic lupus erythematosus, serum sickness, and extrinsic allergic alveolitis.

A Meckel’s diverticulum is a leftover part of the vitellointestinal duct, which is no longer needed in the body. It is the most common abnormality in the gastrointestinal tract, found in about 2% of people. Interestingly, it is twice as likely to occur in men compared to women.

When a Meckel’s diverticulum is present, it is usually located in the lower part of the small intestine, specifically within 60-100 cm (2 feet) of the ileocaecal valve. These diverticula are typically 3-6 cm (approximately 2 inches) long and may have a larger opening than the ileum.

Meckel’s diverticula are often discovered incidentally, especially during an appendectomy. Most of the time, they do not cause any symptoms. However, they can lead to complications such as bleeding (25-50% of cases), intestinal blockage (10-40% of cases), diverticulitis, or perforation.

These diverticula run in the opposite direction of the intestine’s natural folds but receive their blood supply from the ileum mesentery. They can be identified by a specific blood vessel called the vitelline artery. Typically, they are lined with the same type of tissue as the ileum, but they often contain abnormal tissue, with gastric tissue being the most common (50%) and pancreatic tissue being the second most common (5%). In rare cases, colonic or jejunal tissue may be present.

To remember some key facts about Meckel’s diverticulum, the rule of 2s can be helpful:
– It is found in 2% of the population.
– It is more common in men, with a ratio of 2:1 compared to women.
– It is located 2 feet away from the ileocaecal valve.
– It is approximately 2 inches long.
– It often contains two types of abnormal tissue: gastric and pancreatic.
– The most common age for clinical presentation is 2 years old.

The primary goal of performing a FAST scan in cases of blunt abdominal trauma is to identify the existence of intraperitoneal fluid. According to the Royal College of Emergency Medicine (RCEM), the purpose of using ultrasound in the initial evaluation of abdominal trauma is specifically to confirm the presence of fluid within the peritoneal cavity, with the assumption that it is blood. However, it is important to note that ultrasound is not reliable for diagnosing injuries to solid organs or hollow viscus.

Further Reading:

Abdominal trauma can be classified into two categories: blunt trauma and penetrating trauma. Blunt trauma occurs when compressive or deceleration forces are applied to the abdomen, often resulting from road traffic accidents or direct blows during sports. The spleen and liver are the organs most commonly injured in blunt abdominal trauma. On the other hand, penetrating trauma involves injuries that pierce the skin and enter the abdominal cavity, such as stabbings, gunshot wounds, or industrial accidents. The bowel and liver are the organs most commonly affected in penetrating injuries.

When it comes to imaging in blunt abdominal trauma, there are three main modalities that are commonly used: focused assessment with sonography in trauma (FAST), diagnostic peritoneal lavage (DPL), and computed tomography (CT). FAST is a non-invasive and quick method used to detect free intraperitoneal fluid, aiding in the decision on whether a laparotomy is needed. DPL is also used to detect intraperitoneal blood and can be used in both unstable blunt abdominal trauma and penetrating abdominal trauma. However, it is more invasive and time-consuming compared to FAST and has largely been replaced by it. CT, on the other hand, is the gold standard for diagnosing intra-abdominal pathology and is used in stable abdominal trauma patients. It offers high sensitivity and specificity but requires a stable and cooperative patient. It also involves radiation and may have delays in availability.

In the case of penetrating trauma, it is important to assess these injuries with the help of a surgical team. Penetrating objects should not be removed in the emergency department as they may be tamponading underlying vessels. Ideally, these injuries should be explored in the operating theater.

In summary, abdominal trauma can be classified into blunt trauma and penetrating trauma. Blunt trauma is caused by compressive or deceleration forces and commonly affects the spleen and liver. Penetrating trauma involves injuries that pierce the skin and commonly affect the bowel and liver. Imaging modalities such as FAST, DPL, and CT are used to assess and diagnose abdominal trauma, with CT being the gold standard. Penetrating injuries should be assessed by a surgical team and should ideally be explored in the operating theater.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This leads to the accumulation of urea and other waste products in the body, as well as disturbances in fluid balance and electrolyte levels. 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.

AKI is categorized into three stages based on specific criteria. In stage 1, there is a rise in creatinine levels of 26 micromol/L or more within 48 hours, or a rise of 50-99% from baseline within 7 days (1.5-1.99 times the baseline). Additionally, a urine output of less than 0.5 mL/kg/hour for more than 6 hours is indicative of stage 1 AKI.

Stage 2 AKI is characterized by a creatinine rise of 100-199% from baseline within 7 days (2.0-2.99 times the baseline), or a urine output of less than 0.5 mL/kg/hour for more than 12 hours.

In stage 3 AKI, there is a creatinine rise of 200% or more from baseline within 7 days (3.0 or more times the baseline). Alternatively, a creatinine rise to 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours, or a rise of 50% or more within 7 days, is indicative of stage 3 AKI. Additionally, a urine output of less than 0.3 mL/kg/hour for 24 hours or anuria (no urine output) for 12 hours also falls under stage 3 AKI.

An acoustic neuroma, also referred to as a vestibular schwannoma, is a slow-growing tumor that develops from the Schwann cells of the vestibulocochlear nerve (8th cranial nerve). These growths are typically found at the cerebellopontine angle or within the internal auditory canal.

The most commonly affected nerves are the vestibulocochlear and trigeminal nerves. Patients typically present with a gradual deterioration of hearing in one ear, along with numbness and tingling in the face, ringing in the ears, and episodes of dizziness. Additionally, some patients may have a history of headaches. In rare cases, the facial nerve, glossopharyngeal nerve, vagus nerve, or accessory nerve may also be affected.

It is important to note that the trochlear nerve, which passes through the superior orbital fissure, is not impacted by an acoustic neuroma.

When treating men for uncomplicated urinary tract infections (UTIs), a 7-day course of antibiotics is typically recommended. Unlike women, men are advised to take a longer course of antibiotics, with a preference for 7 days instead of 3. The National Institute for Health and Care Excellence (NICE) suggests the following as the first-line treatment, although local microbiology departments may make adjustments based on antibiotic resistance patterns: Trimethoprim 200 mg taken twice daily for 7 days, or Nitrofurantoin 100 mg (modified-release) taken twice daily for 7 days. If prostatitis is suspected, a quinolone antibiotic like ciprofloxacin may be used, and treatment duration is usually 2-4 weeks.

Further Reading:

A urinary tract infection (UTI) is an infection that occurs in any part of the urinary system, from the kidneys to the bladder. It is characterized by symptoms such as dysuria, nocturia, polyuria, urgency, incontinence, and changes in urine appearance and odor. UTIs can be classified as lower UTIs, which affect the bladder, or upper UTIs, which involve the kidneys. Recurrent UTIs can be due to relapse or re-infection, and the number of recurrences considered significant depends on age and sex. Uncomplicated UTIs occur in individuals with a normal urinary tract and kidney function, while complicated UTIs are caused by anatomical, functional, or pharmacological factors that make the infection persistent, recurrent, or resistant to treatment.

The most common cause of UTIs is Escherichia coli, accounting for 70-95% of cases. Other causative organisms include Staphylococcus saprophyticus, Proteus mirabilis, and Klebsiella species. UTIs are typically caused by bacteria from the gastrointestinal tract entering the urinary tract through the urethra. Other less common mechanisms of entry include direct spread via the bloodstream or instrumentation of the urinary tract, such as catheter insertion.

Diagnosis of UTIs involves urine dipstick testing and urine culture. A urine culture should be sent in certain circumstances, such as in male patients, pregnant patients, women aged 65 years or older, patients with persistent or unresolved symptoms, recurrent UTIs, patients with urinary catheters, and those with risk factors for resistance or complicated UTIs. Further investigations, such as cystoscopy and imaging, may be required in cases of recurrent UTIs or suspected underlying causes.

Management of UTIs includes simple analgesia, advice on adequate fluid intake, and the prescription of appropriate antibiotics. The choice of antibiotic depends on the patient’s gender and risk factors. For women, first-line antibiotics include nitrofurantoin or trimethoprim, while second-line options include nitrofurantoin (if not used as first-line), pivmecillinam, or fosfomycin. For men, trimethoprim or nitrofurantoin are the recommended antibiotics. In cases of suspected acute prostatitis, fluoroquinolone antibiotics such as ciprofloxacin or ofloxacin may be prescribed for a 4-week course.

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.

The electrolyte imbalances that are commonly observed in individuals with Addison’s disease are decreased sodium levels, increased potassium levels, increased calcium levels, and decreased glucose levels. In cases of Addisonian crisis, which is a severe form of Addison’s disease, patients may also experience hyponatremia (low sodium levels), hyperkalemia (high potassium levels), hypercalcemia (high calcium levels), and hypoglycemia (low glucose levels). Additionally, these patients may often develop acidosis.

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.

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

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

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

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

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

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

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.

Since croup is caused by a viral infection, antibiotics are not effective unless there is a suspicion of a secondary bacterial infection. It is important to note that sedation should not be used in a child experiencing respiratory distress. To reduce airway swelling, dexamethasone and prednisolone are commonly prescribed, although they do not shorten the duration of the illness. In severe cases, nebulized adrenaline can be administered.

A barking cough is a characteristic symptom of croup, but it does not necessarily indicate the severity of the condition. Hospitalization for croup is rare and typically reserved for children who show worsening respiratory distress or signs of drowsiness/agitation.

The orbicularis oculi muscle encircles the eye socket and extends into the eyelid. It is composed of two parts: the orbital part, which forcefully closes the eye, and the palpebral part, which gently closes the eye. The innervation of the orbicularis oculi muscle is provided by the facial nerve. In the event of facial nerve damage, the orbicularis oculi muscle loses its functionality. As the sole muscle responsible for closing the eyelids, this can have significant clinical implications. The inability to shut the eye can lead to dryness of the cornea and the development of exposure keratitis. While mild cases can be managed with regular use of eye drops, severe cases may require surgical closure of the eye.

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

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

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

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

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

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

The leads V3 and V4 represent the anterior myocardial area.

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.

Loss of reactivity, in contrast to heightened reactivity, is a common trait seen in individuals with depression. The clinical manifestations of depression encompass various symptoms. These include experiencing a persistent low mood, which may fluctuate throughout the day. Another prominent feature is anhedonia, which refers to a diminished ability to experience pleasure. Additionally, individuals with depression often exhibit antipathy, displaying a lack of interest or enthusiasm towards activities or people. Their speech may become slow and have a reduced volume. They may also struggle with maintaining attention and concentration. Furthermore, depression can lead to a decrease in self-esteem, accompanied by thoughts of guilt and worthlessness. Insomnia, particularly early morning waking, is a classic symptom of depression. Other common signs include a decrease in libido, low energy levels, increased fatigue, and a poor appetite resulting in weight loss.

Nephrogenic diabetes insipidus may develop in a certain percentage of individuals who take lithium.

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.

If a patient with a zygoma fracture experiences visual disturbance, limited eye movements (especially upward gaze), or shows a teardrop sign on a facial X-ray, it is important to refer them urgently to ophthalmology or maxillofacial surgeons.

Further Reading:

Zygomatic injuries, also known as zygomatic complex fractures, involve fractures of the zygoma bone and often affect surrounding bones such as the maxilla and temporal bones. These fractures can be classified into four positions: the lateral and inferior orbital rim, the zygomaticomaxillary buttress, and the zygomatic arch. The full extent of these injuries may not be visible on plain X-rays and may require a CT scan for accurate diagnosis.

Zygomatic fractures can pose risks to various structures in the face. The temporalis muscle and coronoid process of the mandible may become trapped in depressed fractures of the zygomatic arch. The infraorbital nerve, which passes through the infraorbital foramen, can be injured in zygomaticomaxillary complex fractures. In orbital floor fractures, the inferior rectus muscle may herniate into the maxillary sinus.

Clinical assessment of zygomatic injuries involves observing facial asymmetry, depressed facial bones, contusion, and signs of eye injury. Visual acuity must be assessed, and any persistent bleeding from the nose or mouth should be noted. Nasal injuries, including septal hematoma, and intra-oral abnormalities should also be evaluated. Tenderness of facial bones and the temporomandibular joint should be assessed, along with any step deformities or crepitus. Eye and jaw movements must also be evaluated.

Imaging for zygomatic injuries typically includes facial X-rays, such as occipitomental views, and CT scans for a more detailed assessment. It is important to consider the possibility of intracranial hemorrhage and cervical spine injury in patients with facial fractures.

Management of most zygomatic fractures can be done on an outpatient basis with maxillofacial follow-up, assuming the patient is stable and there is no evidence of eye injury. However, orbital floor fractures should be referred immediately to ophthalmologists or maxillofacial surgeons. Zygomatic arch injuries that restrict mouth opening or closing due to entrapment of the temporalis muscle or mandibular condyle also require urgent referral. Nasal fractures, often seen in conjunction with other facial fractures, can be managed by outpatient ENT follow-up but should be referred urgently if there is uncontrolled epistaxis, CSF rhinorrhea, or septal hematoma.

A recent audit conducted by the Royal College of Emergency Medicine (RCEM) in 2018 revealed a concerning decline in the standards of pain management for children with fractured limbs in Emergency Departments (EDs). The audit found that the majority of patients experienced longer waiting times for pain relief compared to previous years. Shockingly, more than 1 in 10 children who presented with significant pain due to a limb fracture did not receive any pain relief at all.

To address this issue, the Agency for Health Care Policy and Research (AHCPR) in the USA recommends following the ABCs of pain management for all patients, including children. This approach involves regularly asking about pain, systematically assessing it, believing the patient and their family in their reports of pain and what relieves it, choosing appropriate pain control options, delivering interventions in a timely and coordinated manner, and empowering patients and their families to have control over their pain management.

The RCEM has established standards that require a child’s pain to be assessed within 15 minutes of their arrival at the ED. This is considered a fundamental standard. Various rating scales are available for assessing pain in children, with the choice depending on the child’s age and ability to use the scale. These scales include the Wong-Baker Faces Pain Rating Scale, Numeric rating scale, and Behavioural scale.

To ensure timely administration of analgesia to children in acute pain, the RCEM has set specific standards. These standards state that 100% of patients in severe pain should receive appropriate analgesia within 60 minutes of their arrival or triage, whichever comes first. Additionally, 75% should receive analgesia within 30 minutes, and 50% within 20 minutes.

FAST scans consist of four standard views that are obtained to assess different areas of the body. These views include the right upper quadrant (RUQ), left upper quadrant (LUQ), pericardial sac, and the pelvis.

In the RUQ view, the focus is on the right flank or peri-hepatic area, which includes Morison’s pouch and the right costophrenic pleural recess.

The LUQ view examines the left flank or peri-splenic area, which includes the spleen-renal recess and the left costophrenic pleural space.

The pericardial sac is also assessed to evaluate any abnormalities in this area.

Lastly, the pelvis is examined in two planes to ensure a comprehensive evaluation.

In addition to these four standard views, an anterior pleural view is often performed alongside the others. This view used to be part of the extended FAST (eFAST) scan but is now commonly included routinely.

Further Reading:

Abdominal trauma can be classified into two categories: blunt trauma and penetrating trauma. Blunt trauma occurs when compressive or deceleration forces are applied to the abdomen, often resulting from road traffic accidents or direct blows during sports. The spleen and liver are the organs most commonly injured in blunt abdominal trauma. On the other hand, penetrating trauma involves injuries that pierce the skin and enter the abdominal cavity, such as stabbings, gunshot wounds, or industrial accidents. The bowel and liver are the organs most commonly affected in penetrating injuries.

When it comes to imaging in blunt abdominal trauma, there are three main modalities that are commonly used: focused assessment with sonography in trauma (FAST), diagnostic peritoneal lavage (DPL), and computed tomography (CT). FAST is a non-invasive and quick method used to detect free intraperitoneal fluid, aiding in the decision on whether a laparotomy is needed. DPL is also used to detect intraperitoneal blood and can be used in both unstable blunt abdominal trauma and penetrating abdominal trauma. However, it is more invasive and time-consuming compared to FAST and has largely been replaced by it. CT, on the other hand, is the gold standard for diagnosing intra-abdominal pathology and is used in stable abdominal trauma patients. It offers high sensitivity and specificity but requires a stable and cooperative patient. It also involves radiation and may have delays in availability.

In the case of penetrating trauma, it is important to assess these injuries with the help of a surgical team. Penetrating objects should not be removed in the emergency department as they may be tamponading underlying vessels. Ideally, these injuries should be explored in the operating theater.

In summary, abdominal trauma can be classified into blunt trauma and penetrating trauma. Blunt trauma is caused by compressive or deceleration forces and commonly affects the spleen and liver. Penetrating trauma involves injuries that pierce the skin and commonly affect the bowel and liver. Imaging modalities such as FAST, DPL, and CT are used to assess and diagnose abdominal trauma, with CT being the gold standard. Penetrating injuries should be assessed by a surgical team and should ideally be explored in the operating theater.

This explanation describes the observation of a patient with psoriasis, the most common associated condition in adults. The observations suggest that the patient may be experiencing dehydration, which is a complication of this condition.

Further Reading:

Erythroderma is a rare inflammatory skin condition that affects the majority of a person’s skin surface area. It is characterized by widespread redness, intense itching, and peeling of the skin. The condition can occur in people of all ages and races, but it is more common in males. Erythroderma is considered a dermatological emergency due to the potential for life-threatening complications.

The most common causes of erythroderma are exacerbations of pre-existing skin conditions, such as atopic dermatitis, psoriasis, and lichen planus. However, approximately one-third of cases are idiopathic, meaning the cause is unknown. Other less common skin conditions and systemic illnesses, including certain types of lymphoma and leukemia, can also lead to erythroderma.

Clinical features of erythroderma include generalized redness and swelling of at least 90% of the skin surface area. This is often preceded by a rash or dermatitis. The intense itching associated with the condition can lead to scratching and thickening of the skin. Skin scaling or peeling typically occurs a few days after the onset of redness. Other symptoms may include hair loss, yellowing of the palms and soles, nail abnormalities, and swollen lymph nodes. Patients may also feel generally unwell.

Erythroderma can lead to significant complications, including dehydration, electrolyte imbalances, hypothermia, heart failure, and secondary skin infections. Diagnosis is typically made based on clinical presentation, but further investigations may be done to assess the patient’s overall condition and identify any underlying causes.

Treatment of erythroderma involves addressing the underlying cause, if known. Trigger medications should be discontinued, and supportive measures such as fluid resuscitation, correction of electrolyte imbalances, and treatment of secondary infections should be implemented. Medications for symptom relief, such as painkillers and antihistamines, may also be prescribed. Emollients are often recommended to soothe the skin. In some cases, steroids and immunosuppressants may be used, depending on the underlying cause of the erythroderma.

According to the current guidelines from NICE, alteplase is recommended as a thrombolysis treatment for acute ischaemic stroke. For more information, you can refer to the NICE guidelines on stroke and transient ischaemic attack in individuals over the age of 16.

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

Further Reading:

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

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

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

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

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

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

Bell’s palsy is a condition characterized by a facial paralysis that affects the lower motor neurons. It can be distinguished from an upper motor neuron lesion by the inability to raise the eyebrow and the involvement of the upper facial muscles.

One distinctive feature of Bell’s palsy is the occurrence of Bell’s phenomenon, which refers to the upward and outward rolling of the eye on the affected side when attempting to close the eye and bare the teeth.

Approximately 80% of sudden onset lower motor neuron facial palsies are attributed to Bell’s palsy. It is believed that this condition is caused by swelling of the facial nerve within the petrous temporal bone, which is secondary to a latent herpesvirus, specifically HSV-1 and HZV.

Unlike some other conditions, Bell’s palsy does not lead to sensorineural deafness and tinnitus.

Treatment options for Bell’s palsy include the use of steroids and acyclovir.

Intraosseous access is recommended in trauma, burns, or resuscitation situations when other attempts at venous access fail or would take longer than one minute. It is particularly recommended for circulatory access in pediatric cardiac arrest cases. This technique can also be used when urgent blood sampling or intravenous access is needed and traditional cannulation is difficult and time-consuming. It serves as a temporary measure to stabilize the patient and facilitate long-term intravenous access.

Potential complications of intraosseous access include compartment syndrome, infection, and fracture. Therefore, it is contraindicated to use this method on the side of definitively fractured bones or limbs with possible proximal fractures. It should also not be used at sites of previous attempts or in patients with conditions such as osteogenesis imperfecta or osteopetrosis.

There are several possible sites for intraosseous access insertion. These include the proximal humerus, approximately 1 cm above the surgical neck; the proximal tibia, on the anterior surface, 2-3 cm below the tibial tuberosity; the distal tibia, 3 cm proximal to the most prominent aspect of the medial malleolus; the femoral region, on the anterolateral surface, 3 cm above the lateral condyle; the iliac crest; and the sternum.

Motor Neuron Disease (MND) is a group of degenerative diseases that primarily involve the loss of specific neurons in the motor cortex, cranial nerve nuclei, and anterior horn cells. Both upper and lower motor neurons are affected in this condition. It is important to note that MND does not cause any sensory or sphincter disturbances, and it does not affect eye movements.

MND is relatively uncommon, with a prevalence of approximately 5-7 cases per 100,000 individuals. The median age of onset in the United Kingdom is 60 years, and unfortunately, it often leads to fatality within 2 to 4 years of diagnosis. The treatment for MND mainly focuses on providing supportive care through a multidisciplinary approach.

There are four distinct clinical patterns observed in MND. The first pattern, known as Amyotrophic Lateral Sclerosis (ALS), accounts for up to 50% of MND cases. It involves the loss of motor neurons in both the motor cortex and the anterior horn of the spinal cord. Clinically, individuals with ALS experience weakness and exhibit signs of both upper and lower motor neuron involvement.

The second pattern, called Progressive Bulbar Palsy, occurs in up to 10% of MND cases. This condition specifically affects cranial nerves IX-XII, resulting in Bulbar and pseudobulbar palsy.

Progressive Muscular Atrophy is the third pattern, also seen in up to 10% of MND cases. It primarily affects the anterior horn cells, leading to the presence of only lower motor neuron signs.

Lastly, Primary Lateral Sclerosis involves the loss of Betz cells in the motor cortex. Clinically, individuals with this pattern exhibit upper motor neuron signs, including marked spastic leg weakness and pseudobulbar palsy.

Hypothermia can lead to various abnormalities in the electrocardiogram (ECG). These abnormalities include bradyarrhythmias, the presence of a J wave (also known as an Osborn wave), and prolonged intervals such as PR, QRS, and QT. Additionally, shivering artefact and ventricular ectopics may be observed. In severe cases, hypothermia can even result in cardiac arrest, which can manifest as ventricular tachycardia (VT), ventricular fibrillation (VF), or asystole.

One distinctive feature of hypothermia on an ECG is the appearance of a small extra wave immediately following the QRS complex. This wave, known as a J wave or Osborn wave, was named after the individual who first described it. Interestingly, this wave tends to disappear as the body temperature is warmed. Despite its recognition, the exact mechanism behind the presence of the J wave in hypothermia remains unknown.

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

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

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

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

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

This patient has been experiencing absence seizures, which are a form of primary generalized epilepsy that is frequently observed in children.

The defining characteristic of absence seizures is a sudden and immediate loss of consciousness, causing a disruption in ongoing activities. During these episodes, individuals may exhibit a vacant stare and occasionally a brief upward movement of the eyes.

While an EEG cannot definitively confirm or rule out an epilepsy diagnosis, it does provide valuable information in the diagnostic process. In the case of absence seizures, EEG results typically reveal generalized spike-and-slow wave complexes occurring at a frequency of 3-4 Hz.

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

Further Reading:

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

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

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

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

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

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.

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

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

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

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

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

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

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.

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.

Pelvic inflammatory disease (PID) is a pelvic 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 and is commonly associated with sexually transmitted diseases like chlamydia and gonorrhea. In the UK, genital Chlamydia trachomatis infection is the most common cause of PID seen in genitourinary medicine clinics.

PID can often be asymptomatic, but when symptoms are present, 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 is important to note that symptoms of ectopic pregnancy can be similar to those of PID, so a pregnancy test should be conducted for all patients with suspicious symptoms.

To investigate a possible case of PID, endocervical swabs should be taken to test for C. trachomatis and N. gonorrhoeae using nucleic acid amplification tests if available. Mild to moderate cases of PID can usually be managed in primary care or outpatient settings, while 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.

Empirical antibiotic treatment should be initiated as soon as a presumptive diagnosis of PID is made clinically, without waiting for swab results. The current recommended outpatient treatment for 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 includes intravenous doxycycline, a single-dose of intravenous ceftriaxone, and intravenous metronidazole. This is then followed by a switch to oral doxycycline and metronidazole to complete a 14-day treatment course. If a patient fails to respond to treatment, laparoscopy is necessary to confirm the diagnosis or consider alternative diagnoses.

Unstable angina is characterized by the presence of one or more of the following symptoms: angina of effort occurring over a few days with increasing frequency, episodes of angina occurring recurrently and predictably without specific provocation, or an unprovoked and prolonged episode of cardiac chest pain. The electrocardiogram (ECG) may appear normal or show T-wave/ST-segment changes, and cardiac enzymes are typically within normal range.

On the other hand, stable angina is defined by central chest pain that is triggered by activities such as exercise and emotional stress. This pain may radiate to the jaw or left arm and is relieved by resting for a few minutes. It is usually brought on by a predictable amount of exertion.

Prinzmetal angina, although rare, is a variant of angina that primarily occurs at rest between midnight and early morning. The attacks can be severe and tend to happen in clusters. This type of angina is caused by coronary artery spasm, and patients may have normal coronary arteries.

Decubitus angina, on the other hand, is angina that occurs when lying down. It often develops as a result of cardiac failure due to an increased volume of blood within the blood vessels, which places additional strain on the heart.

Lastly, Ludwig’s angina is an extremely serious and potentially life-threatening cellulitis that affects the submandibular area. It most commonly arises from an infection in the floor of the mouth, which then spreads to the submandibular space.

Instances where confidentiality may be breached include situations where there is a legal obligation, such as informing the Health Protection Agency (HPA) about a notifiable disease. Another example is in legal cases where a judge requests information. Additionally, confidentiality may be breached when there is a risk to the public, such as potential terrorism or serious criminal activity. It may also be breached when there is a risk to others, such as when a patient expresses homicidal intent towards a specific individual. Cases relevant to statutory regulatory bodies, like informing the Driver and Vehicle Licensing Agency (DVLA) about a patient who continues to drive despite a restriction, may also require breaching confidentiality.

However, it is important to note that there are examples where confidentiality should not be breached. It is inappropriate to disclose a patient’s diagnosis to third parties without their consent, including the police, unless there is a serious threat to the public or an individual.

If you are considering breaching patient confidentiality, it is crucial to seek the patient’s consent first. If consent is refused, it is advisable to seek guidance from your local trust and your medical defense union.

For more information, you can refer to the General Medical Council (GMC) guidance on patient confidentiality.

Extradural hematoma is most frequently caused by injury to the middle meningeal artery. This artery is particularly susceptible to damage as it passes behind the pterion.

Further Reading:

Extradural haematoma (EDH) is a collection of blood that forms between the inner surface of the skull and the outer layer of the dura, the dura mater. It is typically caused by head trauma and is often associated with a skull fracture, with the pterion being the most common site of injury. The middle meningeal artery is the most common source of bleeding in EDH.

Clinical features of EDH include a history of head injury with transient loss of consciousness, followed by a lucid interval and gradual loss of consciousness. Other symptoms may include severe headache, sixth cranial nerve palsies, nausea and vomiting, seizures, signs of raised intracranial pressure, and focal neurological deficits.

Imaging of EDH typically shows a biconvex shape and may cause mass effect with brain herniation. It can be differentiated from subdural haematoma by its appearance on imaging.

Management of EDH involves prompt referral to neurosurgery for evacuation of the haematoma. In some cases with a small EDH, conservative management may be considered. With prompt evacuation, the prognosis for EDH is generally good.