The recommended daily oral dose for adults is 900 mg, which should be taken in 2-3 divided doses. For severe asthma or COPD, the initial intravenous dose is 5 mg/kg and should be administered over 10-20 minutes. This can be followed by a continuous infusion of 0.5 mg/kg/hour. In the case of a 60 kg patient, the appropriate infusion rate would be 30 mg/hour. It is important to note that the therapeutic range for aminophylline is narrow, ranging from 10-20 microgram/ml. Therefore, it is beneficial to estimate the plasma concentration of aminophylline during long-term treatment.

This patient is currently experiencing moderate shock, classified as class III. This level of shock corresponds to a loss of 30-40% of their circulatory volume, which is equivalent to a blood loss of 1500-2000 mL.

Hemorrhage can be categorized into four different classes based on physiological parameters and clinical signs. These classes are classified as class I, class II, class III, and class IV.

In class I hemorrhage, the blood loss is up to 750 mL or up to 15% of the blood volume. The pulse rate is less than 100 beats per minute, and the systolic blood pressure is normal. The pulse pressure may be normal or increased, and the respiratory rate is within the range of 14-20 breaths per minute. The urine output is greater than 30 mL per hour, and the patient’s CNS/mental status is slightly anxious.

In class II hemorrhage, the blood loss ranges from 750-1500 mL or 15-30% of the blood volume. The pulse rate is between 100-120 beats per minute, and the systolic blood pressure remains normal. The pulse pressure is decreased, and the respiratory rate increases to 20-30 breaths per minute. The urine output decreases to 20-30 mL per hour, and the patient may experience mild anxiety.

The patient in this case is in class III hemorrhage, with a blood loss of 1500-2000 mL or 30-40% of the blood volume. The pulse rate is elevated, ranging from 120-140 beats per minute, and the systolic blood pressure is decreased. The pulse pressure is also decreased, and the respiratory rate is elevated to 30-40 breaths per minute. The urine output decreases significantly to 5-15 mL per hour, and the patient may experience anxiety and confusion.

Class IV hemorrhage represents the most severe level of blood loss, with a loss of over 40% of the blood volume. The pulse rate is greater than 140 beats per minute, and the systolic blood pressure is significantly decreased. The pulse pressure is decreased, and the respiratory rate is over 40 breaths per minute. The urine output becomes negligible, and the patient may become confused and lethargic.

Theophylline, a medication commonly used to treat respiratory conditions, can be affected by certain drugs, either increasing or decreasing its plasma concentration and half-life. Drugs that can increase the plasma concentration of theophylline include calcium channel blockers like verapamil, cimetidine, fluconazole, macrolides such as erythromycin, methotrexate, and quinolones like ciprofloxacin. On the other hand, drugs like carbamazepine, phenobarbitol, phenytoin (and fosphenytoin), rifampicin, and St. John’s wort can decrease the plasma concentration of theophylline. It is important to be aware of these interactions when prescribing or taking theophylline to ensure its effectiveness and avoid potential side effects.

Anti-D is an antibody of the IgG class that targets the Rhesus D (RhD) antigen. It is specifically administered to women who are RhD negative, meaning they do not have the RhD antigen on their red blood cells. When a RhD negative woman is exposed to the blood of a RhD positive fetus, she may develop antibodies against RhD that can cross the placenta and attack the red blood cells of the fetus, leading to a condition called hemolytic disease of the newborn. Anti-D is given to bind to the fetal red blood cells in the mother’s circulation and neutralize them before an immune response is triggered.

RhD should be administered in the event of a sensitizing event, which can include childbirth, antepartum hemorrhage, miscarriage, ectopic pregnancy, intrauterine death, amniocentesis, chorionic villus sampling, or abdominal trauma. It is important to administer Anti-D as soon as possible after a sensitizing event, but it can still provide some benefit even if given outside of the recommended 72-hour window, according to the British National Formulary (BNF).

For RhD negative women, routine antenatal prophylaxis with Anti-D is recommended at 28 and 34 weeks of pregnancy, regardless of whether they have already received Anti-D earlier in the same pregnancy due to a sensitizing event.

In cases of uncomplicated miscarriage before 12 weeks of gestation, confirmed by ultrasound, or mild and painless vaginal bleeding, prophylactic Anti-D is not necessary because the risk of feto-maternal hemorrhage is extremely low. However, in cases of therapeutic termination of pregnancy, whether through surgical or medical methods, confirmed RhD negative women who are not known to be sensitized to RhD should receive 250 IU of prophylactic Anti-D immunoglobulin.

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.

The primary treatment for paracetamol overdose is acetylcysteine. Acetylcysteine is an extremely effective antidote, but its effectiveness decreases quickly if administered more than a few hours after a significant ingestion. Ingestions that exceed 75 mg/kg are considered to be significant.

For patients who decline treatment, methionine is a helpful alternative. It is taken orally in a dosage of 2.5 g every 4 hours, with a total dose of 10 g.

Diabetic amyotrophy, also referred to as proximal diabetic neuropathy, is the second most prevalent form of diabetic neuropathy. It typically manifests with pain in the buttocks, hips, or thighs and is often initially experienced on one side of the body. The pain may start off as mild and gradually progress or it can suddenly appear, as seen in this particular case. Subsequently, weakness and wasting of the proximal muscles in the lower limbs occur, potentially leading to the patient requiring assistance when transitioning from a seated to a standing position. Reflexes in the affected areas can also be impacted. Fortunately, diabetic amyotrophy can be reversed through effective management of blood sugar levels, physiotherapy, and adopting a healthy lifestyle.

Vestibular neuronitis is believed to occur when the vestibular nerve becomes inflamed, often following a viral infection like a cold. This condition causes a constant feeling of dizziness, which can worsen with head movements. On the other hand, BPPV (benign paroxysmal positional vertigo) is characterized by brief episodes of vertigo lasting around 10-20 seconds, triggered by specific head movements. To diagnose BPPV, the Dix-Hallpike test is performed, and a positive result is indicated by a specific type of eye movement called nystagmus. In contrast, vestibular neuritis typically presents with horizontal nystagmus that only occurs in one direction.

Further Reading:

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

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

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

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

The initial stage of SJS is characterized by a rash on the skin, specifically on the macular area. As the condition progresses, the rash transforms into blisters, known as bullae, which eventually detach from the skin.

Further Reading:

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe mucocutaneous immune reactions characterized by blistering skin rash and erosions/ulceration of mucous membranes. SJS has less than 10% total body surface area (TBSA) involvement, SJS/TEN overlap has 10% to 30% TBSA involvement, and TEN has more than 30% TBSA involvement. The exact cause of SJS and TEN is not well understood, but it is believed to be a T-cell–mediated cytotoxic reaction triggered by drugs, infections, or vaccinations. Drugs are responsible for 50% of SJS cases and up to 95% of TEN cases, with antibiotics and anticonvulsants being the most common culprits.

The clinical features of SJS and TEN include a prodrome of malaise, fever, headache, and cough, followed by the appearance of small pink-red macules with darker centers. These macules can coalesce and develop into larger blisters (bullae) that eventually break and cause the epidermis to slough off. Painful mucosal erosions can also occur, affecting various parts of the body and leading to complications such as renal failure, hepatitis, pneumonia, and urethritis. Nikolsky’s sign, which refers to the easy sloughing off of the epidermal layer with pressure, is a characteristic feature of SJS and TEN.

The diagnosis of SJS, SJS/TEN overlap, and TEN can be confirmed through a skin biopsy, which typically shows desquamation at the epidermal-papillary dermal junction and the presence of necrotic epithelium and lymphocytes. Management of SJS and TEN involves supportive care, withdrawal of the causative agent if drug-related, monitoring for metabolic derangement and infection, maintaining the airway, treating respiratory function and pneumonia, fluid resuscitation, wound care, analgesia, and nutritional support. Ophthalmology consultation is also recommended. Intravenous immunoglobulin, ciclosporin, corticosteroids, and plasmapheresis may be used in treatment, but there is limited evidence supporting their effectiveness.

The prognosis of SJS and TEN can be assessed using the SCORTEN score, which comprises of 7 clinical and biological parameters, with the predicted probability of mortality ranging from 3.2% to 90.0%.

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.

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.

Acute aortic dissection is characterized by the rapid formation of a false, blood-filled channel within the middle layer of the aorta. It is estimated to occur in 3 out of every 100,000 individuals per year.

Patients with aortic dissection typically experience intense chest pain that spreads to the area between the shoulder blades. The pain is often described as tearing or ripping and may also extend to the neck. Sweating, paleness, and rapid heartbeat are commonly observed at the time of presentation. Other possible symptoms include focal neurological deficits, weak pulses, fainting, and reduced blood flow to organs.

A significant difference in blood pressure between the arms, greater than 20 mmHg, is a highly sensitive indicator. If the dissection extends backward, it can involve the aortic valve, leading to the early diastolic murmur of aortic regurgitation.

Risk factors for aortic dissection include hypertension, atherosclerosis, aortic coarctation, the use of sympathomimetic drugs like cocaine, Marfan syndrome, Ehlers-Danlos syndrome, Turner’s syndrome, tertiary syphilis, and pre-existing aortic aneurysm.

Aortic dissection can be classified according to the Stanford classification system:
– Type A affects the ascending aorta and the arch, accounting for 60% of cases. These cases are typically managed surgically and may result in the blockage of coronary arteries and aortic regurgitation.
– Type B begins distal to the left subclavian artery and accounts for approximately 40% of cases. These cases are usually managed with medication to control blood pressure.

Patients who have a STEMI caused by a blockage in the left circumflex artery (LCX) will usually show ST elevation in leads I and AVL. These leads correspond to the high lateral area of the heart, which is supplied by the LCX artery.

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.

Legionella pneumophila, a Gram-negative bacterium, can be found in natural water supplies and soil. It is responsible for causing Legionnaires’ disease, a serious illness. Outbreaks of this disease have been associated with poorly maintained air conditioning systems, whirlpool spas, and hot tubs.

The pneumonic form of Legionnaires’ disease presents with specific clinical features. Initially, there may be a mild flu-like prodrome lasting for 1-3 days. A non-productive cough, occurring in approximately 90% of cases, is also common. Pleuritic chest pain, haemoptysis, headache, nausea, vomiting, diarrhoea, and anorexia are other symptoms that may be experienced.

Fortunately, Legionella pneumophila infections can be effectively treated with macrolide antibiotics like erythromycin, or quinolones such as ciprofloxacin. Tetracyclines, including doxycycline, can also be used as a treatment option.

While the majority of Legionnaires’ disease cases are caused by Legionella pneumophila, there are several other species of Legionella that have been identified. One such species is Legionella longbeachae, which is less commonly encountered. It is primarily found in soil and potting compost and has been associated with outbreaks of Pontiac fever, a milder variant of Legionnaires’ disease that does not primarily affect the respiratory system.

The patient is showing signs of confusion and restlessness. Upon examination, it is found that the patient has high blood pressure, a rapid pulse rate, increased respiration rate, and a high temperature. An ECG reveals rapid atrial fibrillation. Additionally, the patient exhibits crackling sounds in the lower parts of the lungs, pitting edema in both legs below the knee, and a mild yellowish tint in the sclera. The patient’s medical history is obtained from their GP office, which reveals that they have not renewed their prescription for carbimazole and bisoprolol on time. Based on these findings, the most probable diagnosis is a thyroid storm.

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.

Anterior uveitis refers to the inflammation of the iris and is characterized by a painful and red eye. It is often accompanied by symptoms such as sensitivity to light, excessive tearing, and a decrease in visual clarity. In less than 10% of cases, the inflammation may extend to the posterior chamber. The condition can also lead to the formation of adhesions between the iris and the lens or cornea, resulting in an irregularly shaped pupil known as synechia. In severe cases, pus may accumulate in the front part of the eye, specifically the anterior chamber, causing a condition called hypopyon.

There are various factors that can cause anterior uveitis, including idiopathic cases where no specific cause can be identified. Other causes include trauma, chronic joint diseases like spondyloarthropathies and juvenile chronic arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriasis, sarcoidosis, and infections such as Lyme disease, tuberculosis, leptospirosis, herpes simplex virus (HSV), and varicella-zoster virus (VZV). It is worth noting that approximately 50% of patients with anterior uveitis have a strong association with the HLA-B27 genotype.

Complications that can arise from uveitis include the development of cataracts, glaucoma, band keratopathy (a condition where calcium deposits form on the cornea), and even blindness.

Testicular torsion is the correct diagnosis in this case. When a patient presents with sudden, severe, and acute testicular pain, testicular torsion should be assumed until proven otherwise. There are several historical factors that support this diagnosis. These include the pain occurring suddenly, being accompanied by vomiting, happening during sleep (as half of torsions occur during sleep), a previous history of torsion in the other testis, previous episodes that have resolved recently, and a history of undescended testis.

On examination, there are certain findings that further suggest testicular torsion. The testis may be positioned high in the scrotum and too tender to touch. The opposite testis may lie horizontally (known as Angell’s sign). Pain is not relieved by elevating the testis (negative Prehn’s sign), and the cremasteric reflex may be absent.

It is important to recognize that testicular torsion is a surgical emergency that requires immediate assessment and intervention to restore blood flow. Irreversible damage can occur within six hours of onset, so prompt treatment is crucial in this patient.

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

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

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

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

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

Intracranial hemorrhages can be categorized based on their location into epidural, subdural, subarachnoid, or intracerebral hemorrhages. The patient in this case is experiencing a severe headache accompanied by signs of meningismus, which strongly suggests a diagnosis of subarachnoid hemorrhage. Additionally, there is no history of trauma, and most cases of subarachnoid hemorrhage are caused by the rupture of a berry aneurysm located in the circle of Willis. Hypertension is a significant risk factor for the rupture of an aneurysm.

During the patient’s hospital stay, they develop an ischemic stroke, which is confirmed by a CT scan. This is most likely a result of cerebral vasospasm secondary to the subarachnoid hemorrhage. To prevent this complication, patients are often treated with the cerebral selective calcium channel blocker Nimodipine.

Another potential complication of this condition is rebleeding, with the highest risk occurring in the first few days. Rebleeding can be potentially fatal, so it is crucial to repair the aneurysm as soon as possible. The presence of blood in the subarachnoid space can also disrupt the production and drainage of cerebrospinal fluid, leading to hydrocephalus.

Long-term complications of subarachnoid hemorrhage include epilepsy, with most patients experiencing their first seizure within a year after the hemorrhage. However, the risk of epilepsy decreases over time. Cognitive dysfunction is also a common long-term complication and can manifest as memory loss, difficulty concentrating, or challenges in performing regular tasks. Emotional problems, such as depression and anxiety, are frequently observed as well.

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

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

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

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

Patients with dental abscess should be evaluated for signs of spread into deep fascial planes. Infection of the sublingual space can lead to serious complications that can be life-threatening. Swelling in this area can cause the tongue to elevate, potentially obstructing the airway. Other complications include infections such as mediastinitis, necrotizing fasciitis, cavernous sinus thrombosis, sepsis, thoracic empyema, Lemierre’s syndrome, cerebral abscess, orbital abscess, and osteomyelitis.

There are certain indications that may require admission to the hospital for dental abscess. These include evidence of significant systemic disturbance, inability to control the infection with antibiotics, rapid spread of infection, stridor or compromised airway, swelling of the sublingual space or pharynx, difficulty swallowing or speaking, immunocompromised patients, abscess requiring drainage under general anesthesia.

Fever and pain are common symptoms of dental abscess but by themselves are not enough to warrant admission. Ideally, dental abscess should be managed through urgent dental review. However, if immediate dental review is not available, the patient may be treated with antibiotics as long as there are no signs of more severe infection.

Further Reading:

Dental abscess is a condition that usually occurs as a result of dental caries or following a dental procedure or trauma. Dental caries refers to the loss of enamel caused by acids produced by bacteria in the mouth. This allows bacteria to enter the pulp, root, and local tissues, leading to infection. The infection can then spread to surrounding tissues, causing conditions such as gingivitis or dental abscess. In severe cases, the infection can spread to deep fascial planes, resulting in conditions like retropharyngeal abscess or Ludwig’s angina.

A dental abscess is typically caused by a combination of gram-positive and gram-negative bacteria, such as Streptococcus, Staphylococcus, and Prevotella. When assessing a patient with a suspected dental abscess, a thorough history and inspection of the mouth, face, and neck are necessary. This helps confirm the diagnosis and assess the risk of serious complications, such as airway compromise or deep/spreading infection.

Some concerning features on history or examination include systemic upset (e.g., fever, vomiting), sublingual or pharyngeal swelling, stridor, dysphagia, dysphonia, dyspnea, and progression of illness despite current antibiotic treatment. It’s important to consider non-dental causes of mouth and jaw pain, such as trauma, referred sinus pain, cardiac pain radiating to the jaw, trigeminal neuralgia, otalgia radiating to the jaw, and parotid gland swelling.

Management of a dental abscess typically involves providing analgesia (NSAIDs and paracetamol) and facilitating early dental review. Antibiotics may be prescribed in certain cases, such as when the patient does not have immediate access to a dentist and is systemically unwell, shows signs of severe infection, or is a high-risk individual (e.g., immunocompromised or diabetic). The choice of antibiotics includes amoxicillin, phenoxymethylpenicillin, or clarithromycin (if penicillin allergic). In severe or spreading infections, metronidazole may be added. The typical course of antibiotics is 5 days.

This presentation strongly suggests a diagnosis of whooping cough, which is an infection of the upper respiratory tract caused by the bacteria Bordetella pertussis. The disease is highly contagious and is transmitted through respiratory droplets. The incubation period is typically 7-21 days, and it is estimated that about 90% of close household contacts will become infected.

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

The second stage, called the paroxysmal stage, is characterized by the development of a distinctive cough. The coughing occurs in spasms, often preceded by an inspiratory whoop sound. These spasms are followed by a series of rapid, hacking coughs. Patients may also experience vomiting and develop subconjunctival hemorrhages and petechiae. Between spasms, patients generally feel well 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 phase 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.

Public Health England (PHE) has specific recommendations for testing for whooping cough based on the age of the patient, the time since onset of illness, and the severity of the presentation.

For infants under 12 months of age, hospitalized patients should be tested using PCR testing. Non-hospitalized patients within two weeks of onset should be investigated with culture of a nasopharyngeal swab or aspirate. Non-hospitalized patients presenting over two weeks after onset should be tested using serology for anti-pertussis toxin IgG antibody levels.

For children over 12 months of age and adults, patients within two weeks of onset should be tested using culture of a nasopharyngeal swab or aspirate. Patients aged 5 to 16 who have not received the vaccine within the last year and present over two weeks after onset should have oral fluid testing for anti-pertussis toxin IgG antibody levels.

The co-epidemic of tuberculosis and HIV is a significant global health challenge at present. According to the WHO, there were 10 million new cases of tuberculosis in 2019, with approximately 11% of these cases being co-infected with HIV. Tuberculosis is the most common contagious infection in individuals with compromised immune systems due to HIV, often leading to death.

Tuberculosis is caused by an infection with the bacterium Mycobacterium tuberculosis. While it primarily affects the lungs, it can also impact various other parts of the body. The disease is spread through aerosol transmission, meaning it is transmitted through droplets in the air.

The primary symptoms of tuberculosis infection include a chronic cough, coughing up blood (haemoptysis), fever, night sweats, and weight loss. In individuals who have not been previously affected, tuberculosis can cause a primary lesion known as the Ghon focus. This lesion typically develops in the upper lobes of the lungs.

In 15-20% of cases, the infection spreads to extrapulmonary sites such as the pleura, central nervous system, lymphatics, bones, joints, and genitourinary system. Extrapulmonary tuberculosis that affects the spine is known as Pott’s disease, primarily affecting the lower thoracic and upper lumbar vertebrae. Cervical tuberculous lymphadenopathy, also known as scrofula, is characterized by cold abscesses without erythema or warmth.

Only a small percentage of patients, around 5-10%, go on to develop post-primary tuberculosis, also known as reactivation tuberculosis. This typically occurs a year or two after the primary infection and is more likely to happen in individuals with a weakened immune system. Reactivation tuberculosis often involves the lung apex.

The FeverPAIN score is a clinical scoring system that helps determine the likelihood of a streptococcal infection and whether antibiotic treatment is necessary. It consists of several criteria that are assessed to assign a score.

Firstly, if the patient has a fever higher than 38°C, they score 0 or 1 depending on the presence or absence of this symptom.

Secondly, the presence of purulence, such as pharyngeal or tonsillar exudate, results in a score of 1.

Thirdly, if the patient sought medical attention within 3 days or less, they score 1.

Fourthly, if the patient has severely inflamed tonsils, they score 1.

Lastly, if the patient does not have a cough or coryza (nasal congestion), they score 1.

By adding up the scores from each criterion, the FeverPAIN score can help healthcare professionals determine the likelihood of a streptococcal infection and guide the decision on whether antibiotic treatment is necessary. In this particular case, the patient has a score of 4.

Further Reading:

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

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

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

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

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

Moderate hypothermia is indicated by core temperatures ranging from 28-32ºC.

Further Reading:

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

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

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

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

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

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

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

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

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

A Focussed Assessment with Sonography for Trauma (FAST) scan is a point-of-care ultrasound examination conducted when a trauma patient arrives. Its primary purpose is to identify the presence of intra-abdominal free fluid, which is typically assumed to be haemoperitoneum in the context of trauma. This information is crucial for making decisions regarding further management of the patient.

The sensitivity of FAST scanning for detecting intraperitoneal fluid is approximately 90%, while its specificity is around 95%. However, its sensitivity for detecting solid organ injuries is much lower. As a result, FAST scanning has largely replaced diagnostic peritoneal lavage as the preferred initial method for assessing haemoperitoneum.

During a standard FAST scan, four regions are examined. The subxiphoid transverse view is used to assess for pericardial effusion and left lobe liver injuries. The longitudinal view of the right upper quadrant helps identify right liver injuries, right kidney injury, and fluid in the hepatorenal recess (Morison’s pouch). The longitudinal view of the left upper quadrant is used to assess for splenic injury and left kidney injury. Lastly, the transverse and longitudinal views of the suprapubic region are used to examine the bladder and fluid in the pouch of Douglas.

In addition to the standard FAST scan, an extended FAST or eFAST may be performed to assess the left and right thoracic regions. This helps determine the presence of pneumothorax and haemothorax.

The hepatorenal recess is the deepest part of the peritoneal cavity when the patient is lying flat. Consequently, it is the most likely area for fluid to accumulate.

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.

When the INR (International Normalized Ratio) is above 8 but there is no sign of bleeding, the usual approach is to stop administering warfarin and instead provide oral vitamin K. If the INR is below 8 and there is no evidence of bleeding, it is appropriate to discontinue warfarin. However, if there is evidence of bleeding or the INR exceeds 8, reversal agents are administered. In cases where the INR is greater than 8 without any bleeding, oral vitamin K is typically prescribed at a dosage of 1-5 mg.

Further Reading:

Management of High INR with Warfarin

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

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

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

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

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

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

Addison’s disease occurs when the adrenal glands do not produce enough steroid hormones. This includes glucocorticoids, mineralocorticoids, and sex steroids. The most common cause is autoimmune adrenalitis, which accounts for about 70-80% of cases. It is more prevalent in women and typically occurs between the ages of 30 and 50.

The clinical symptoms of Addison’s disease include weakness, lethargy, low blood pressure (especially when standing up), nausea, vomiting, weight loss, reduced hair in the armpits and pubic area, depression, and hyperpigmentation (darkening of the skin in certain areas like the palms, mouth, and exposed skin).

Biochemically, Addison’s disease is characterized by increased levels of ACTH (a hormone that tries to stimulate the adrenal glands), low sodium levels, high potassium levels, high calcium levels, low blood sugar, and metabolic acidosis.

People with Addison’s disease have a higher risk of developing type 1 diabetes, Hashimoto’s thyroiditis, Grave’s disease, premature ovarian failure, pernicious anemia, vitiligo, and alopecia.

Management of Addison’s disease should be overseen by an Endocrinologist. Treatment typically involves taking 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 in case of an Addisonian crisis.

Regular use of medications that decrease gastric acid secretion, such as proton pump inhibitors (esomeprazole, lansoprazole, omeprazole, pantoprazole, and rabeprazole) and H2 receptor antagonists like ranitidine, can increase the risk of developing clostridium difficile diarrhoea. However, it is important to note that antibiotics are the most common cause of this condition.

Further Reading:

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

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

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

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

Classical symptoms of a urinary tract infection (UTI) typically include dysuria, suprapubic tenderness, urgency, haematuria, increased frequency of micturition, and polyuria. The Scottish Intercollegiate Guidelines Network (SIGN) has developed comprehensive guidelines for the management of UTIs. According to these guidelines, if a patient presents with three or more classical UTI symptoms and is not pregnant, it is recommended to initiate empirical treatment with a three-day course of either trimethoprim or nitrofurantoin. For more detailed information, you can refer to the SIGN guidelines on the management of suspected bacterial urinary tract infection in adults.

Klumpke’s palsy, also known as Dejerine-Klumpke palsy, is a condition where the arm becomes paralyzed due to an injury to the lower roots of the brachial plexus. The most commonly affected root is C8, but T1 can also be involved. The main cause of Klumpke’s palsy is when the arm is pulled forcefully in an outward position during a difficult childbirth. It can also occur in adults with apical lung carcinoma (Pancoast’s syndrome).

Clinically, Klumpke’s palsy is characterized by a deformity known as ‘claw hand’, which is caused by the paralysis of the intrinsic hand muscles. There is also a loss of sensation along the ulnar side of the forearm and hand. In some cases where T1 is affected, a condition called Horner’s syndrome may also be present.

Klumpke’s palsy can be distinguished from Erb’s palsy, which affects the upper roots of the brachial plexus (C5 and sometimes C6). In Erb’s palsy, the arm hangs by the side with the elbow extended and the forearm turned inward (known as the ‘waiter’s tip sign’). Additionally, there is a loss of shoulder abduction, external rotation, and elbow flexion.

A subarachnoid haemorrhage (SAH) occurs when there is spontaneous bleeding into the subarachnoid space and is often a catastrophic event. The incidence of SAH is 9 cases per 100,000 people per year, and it typically affects individuals between the ages of 35 and 65.

The majority of SAH cases (80%) are caused by the rupture of berry (saccular) aneurysms, while 15% are caused by arteriovenous malformations (AVM). In less than 5% of cases, no specific cause can be found. Berry aneurysms are associated with polycystic kidneys, Ehlers-Danlos Syndrome, and coarctation of the aorta.

There are several risk factors for SAH, including smoking, hypertension, bleeding disorders, alcohol misuse, mycotic aneurysm, and a family history of the condition.

Patients with SAH typically experience a sudden and severe occipital headache, often described as the worst headache of my life. This may be accompanied by vomiting, collapse, seizures, and coma. Clinical signs of SAH include neck stiffness, a positive Kernig’s sign, and focal neurological abnormalities. Fundoscopy may reveal subhyaloid retinal haemorrhages in approximately 25% of patients.

Re-bleeding occurs in 30-40% of patients who survive the initial episode, with the highest risk occurring between 7 and 14 days after the initial event.

Untreated SAH has a mortality rate of nearly 50% within the first eight weeks following presentation. Prolonged coma is associated with a 100% mortality rate.

The first-line investigation for SAH is a CT head scan, which can detect over 95% of cases if performed within the first 24 hours. The sensitivity of the CT scan increases to nearly 100% if performed within 6 hours of symptom onset. If the CT scan is negative and there are no contraindications, a lumbar puncture (LP) should be performed at least 12 hours after the onset of headache to diagnose SAH. Approximately 3% of patients with a negative CT scan will be confirmed to have had an SAH following an LP.

The interpretation of facial X-rays is often assisted by the use of McGrigor-Campbell lines and Dolan lines. These lines, along with accompanying notes and images, provide additional information for a more accurate analysis.

Further Reading:

Facial X-rays are commonly used to assess and diagnose facial fractures. Two standard views are typically performed: the Occipitomental view and the Occipitomental 30º view. The Occipitomental view provides a comprehensive look at the upper and middle thirds of the face, including the orbital margins, frontal sinuses, zygomatic arches, and maxillary antra. On the other hand, the Occipitomental 30º view uses a 30-degree caudal angulation to better visualize the zygomatic arches and walls of the maxillary antra, although it may compromise the clear view of the orbital margins.

To assist in the interpretation of facial X-rays, imaginary lines are often drawn across the images to highlight any asymmetry or disruption. Two commonly used sets of lines are the McGrigor-Campbell lines and Dolan’s lines. McGrigor-Campbell lines are used to aid in the interpretation of both the Occipitomental and Occipitomental 30º views. These lines include an upper line that passes through the zygomatico-frontal sutures and the upper edge of the orbits, a middle line that follows the zygomatic arch and crosses the zygomatic bone, and a lower line that passes through the condyle and coronoid process of the mandible and the walls of the maxillary antra.

Dolan’s lines, described by Dolan and Jacoby, are often used in conjunction with McGrigor-Campbell lines. These lines include the orbital line, which traces the inner margins of the orbital walls and the nasal arch, the zygomatic line, which traces the superior margin of the zygomatic arch and body, and the maxillary line, which traces the inferior margin of the zygomatic arch, body, and buttress, as well as the lateral wall of the maxillary sinus. Together, the zygomatic and maxillary lines resemble the profile of an elephant’s head and are referred to as Dolan’s elephant. These lines help provide additional information and aid in the interpretation of facial X-rays.

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.

Retinal detachment is a condition where the retina separates from the retinal pigment epithelium, resulting in a fluid-filled space between them. This case presents a classic description of retinal detachment. Several risk factors increase the likelihood of developing this condition, including myopia, being male, having a family history of retinal detachment, previous episodes of retinal detachment, blunt ocular trauma, previous cataract surgery, diabetes mellitus (especially if proliferative retinopathy is present), glaucoma, and cataracts.

The clinical features commonly associated with retinal detachment include flashes of light, particularly at the edges of vision (known as photopsia), a dense shadow in the peripheral vision that spreads towards the center, a sensation of a curtain drawing across the eye, and central visual loss. Fundoscopy, a procedure to examine the back of the eye, reveals a sheet of sensory retina billowing towards the center of the eye. Additionally, a positive Amsler grid test, where straight lines appear curved or wavy, may indicate retinal detachment.

Other possible causes of floaters include posterior vitreous detachment, retinal tears, vitreous hemorrhage, and migraine with aura. However, in this case, the retinal appearance described is consistent with retinal detachment.

It is crucial to arrange an urgent same-day ophthalmology referral for this patient. Fortunately, approximately 90% of retinal detachments can be successfully repaired with one operation, and an additional 6% can be salvaged with subsequent procedures. If the retina remains fixed six months after surgery, the likelihood of it becoming detached again is low.

When patients with diabetic ketoacidosis (DKA) are treated with insulin infusion, it is expected that their plasma bicarbonate levels will increase by at least 3 mmol/L per hour. Insulin therapy is aimed at correcting both hyperglycemia and ketoacidosis. However, if capillary ketones are not decreasing by at least 0.5 mmol/L per hour, venous bicarbonate is not rising by at least 3 mmol/L per hour, or plasma glucose is not decreasing by at least 3 mmol/L per hour, the insulin infusion rate should be reevaluated.

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.

St. John’s wort can reduce the effectiveness of warfarin, an anticoagulant medication. Therefore, it is important for patients who are taking warfarin to be aware that they should avoid using St. John’s wort as a supplement. For more information on this interaction, you can refer to the BNF section on warfarin interactions.

All individuals diagnosed with stage 5 chronic kidney disease should be given the option to choose between haemodialysis or peritoneal dialysis. Peritoneal dialysis should be prioritized as the preferred treatment for the following groups of patients: those who still have some remaining kidney function, adult patients without major additional health conditions, and children who are two years old or younger.

Small cell lung cancer (SCLC) that originates from neuroendocrine tissue can lead to the development of paraneoplastic endocrine syndromes, such as Cushing syndrome. This occurs due to the inappropriate secretion of ectopic adrenocorticotropic hormone (ACTH). In this case, it is highly likely that the patient has a neuroendocrine tumor within the lung that is secreting ACTH.

The signs and symptoms of Cushing syndrome may be minimal in cases of ectopic ACTH-secreting tumors, and the onset of symptoms may be sudden, especially in rapidly growing SCLCs. The typical biochemical profile observed in these cases includes elevated sodium levels, low potassium levels, and a metabolic alkalosis.

The tumors associated with the production of ectopic ACTH are as follows:
– Small cell lung cancer (SCLC) – 50%
– Bronchial carcinoid tumors – 10%
– Thymic carcinoma – 10%
– Pancreatic islet cell tumors – 5%
– Phaeochromocytoma – 5%
– Medullary thyroid carcinoma – 5%

The AUDIT screening tool is recommended by NICE for identifying patients who may be at risk of hazardous drinking.

Alcoholic liver disease (ALD) is a spectrum of disease that ranges from fatty liver at one end to alcoholic cirrhosis at the other. Fatty liver is generally benign and reversible with alcohol abstinence, while alcoholic cirrhosis is a more advanced and irreversible form of the disease. Alcoholic hepatitis, which involves inflammation of the liver, can lead to the development of fibrotic tissue and cirrhosis.

Several factors can increase the risk of progression of ALD, including female sex, genetics, advanced age, induction of liver enzymes by drugs, and co-existent viral hepatitis, especially hepatitis C.

The development of ALD is multifactorial and involves the metabolism of alcohol in the liver. Alcohol is metabolized to acetaldehyde and then acetate, which can result in the production of damaging reactive oxygen species. Genetic polymorphisms and co-existing hepatitis C infection can enhance the pathological effects of alcohol metabolism.

Patients with ALD may be asymptomatic or present with non-specific symptoms such as abdominal discomfort, vomiting, or anxiety. Those with alcoholic hepatitis may have fever, anorexia, and deranged liver function tests. Advanced liver disease can manifest with signs of portal hypertension and cirrhosis, such as ascites, varices, jaundice, and encephalopathy.

Screening tools such as the AUDIT questionnaire can be used to assess alcohol consumption and identify hazardous or harmful drinking patterns. Liver function tests, FBC, and imaging studies such as ultrasound or liver biopsy may be performed to evaluate liver damage.

Management of ALD involves providing advice on reducing alcohol intake, administering thiamine to prevent Wernicke’s encephalopathy, and addressing withdrawal symptoms with benzodiazepines. Complications of ALD, such as intoxication, encephalopathy, variceal bleeding, ascites, hypoglycemia, and coagulopathy, require specialized interventions.

Heavy alcohol use can also lead to thiamine deficiency and the development of Wernicke Korsakoff’s syndrome, characterized by confusion, ataxia, hypothermia, hypotension, nystagmus, and vomiting. Prompt treatment is necessary to prevent progression to Korsakoff’s psychosis.

In summary, alcoholic liver disease is a spectrum of disease that can range from benign fatty liver to irreversible cirrhosis. Risk factors for progression include female sex, genetics, advanced age, drug-induced liver enzyme induction, and co-existing liver conditions.

Spontaneous bacterial peritonitis (SBP) is a sudden bacterial infection of the fluid in the abdomen. It typically occurs in patients with high blood pressure in the portal vein, and about 70% of cases are seen in patients with severe liver disease. In any given year, around 30% of patients with fluid buildup in the abdomen will develop SBP.

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

Common clinical features of SBP include fever (80% of cases), abdominal pain (70% of cases), worsening or unexplained confusion due to liver dysfunction, diarrhea, nausea and vomiting, and bowel obstruction.

There are several factors that increase the risk of developing SBP, including severe liver disease (Child-Pugh class C), gastrointestinal bleeding, urinary tract infection, excessive growth of bacteria in the intestines, presence of indwelling lines such as central venous catheters or urinary catheters, previous episodes of SBP, and low levels of protein in the fluid buildup in the abdomen.

To diagnose SBP, a procedure called abdominal paracentesis is performed to collect fluid from the abdomen. The following findings on fluid analysis strongly suggest SBP: total white blood cell count in the fluid greater than 500 cells/µL, total neutrophil count in the fluid greater than 250 cells/µL, lactate level in the fluid higher than 25 mg/dL, pH of the fluid below 7.35, and presence of bacteria on Gram-stain.

Patients with SBP should be admitted to the hospital and treated with broad-spectrum antibiotics. The preferred antibiotic is an intravenous third-generation cephalosporin, such as Ceftriaxone. If the patient is allergic to beta-lactam antibiotics, ciprofloxacin can be considered as an alternative. Administration of intravenous albumin has been shown to reduce the risk of kidney failure and death.

The classic ECG features of atrial fibrillation include an irregularly irregular rhythm, the absence of p-waves, an irregular ventricular rate, and the presence of fibrillation waves. This irregular rhythm occurs because the atrial impulses are filtered out by the AV node.

In addition, Ashman beats may be observed in atrial fibrillation. These beats are characterized by wide complex QRS complexes, often with a morphology resembling right bundle branch block. They occur after a short R-R interval that is preceded by a prolonged R-R interval. Fortunately, Ashman beats are generally considered harmless.

The disorganized electrical activity in atrial fibrillation typically originates at the root of the pulmonary veins.

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.

Parental responsibility encompasses the legal rights, duties, powers, responsibilities, and authority that a parent holds for their child. This includes the ability to provide consent for medical treatment on behalf of the child. Any individual with parental responsibility has the authority to give consent for their child. If a father meets any of the aforementioned criteria, he is considered to have parental responsibility. On the other hand, a mother is automatically granted parental responsibility for her child from the moment of birth.

Further Reading:

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

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

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

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

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

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

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

The sepsis 6 pathway is a time-sensitive protocol that should be started promptly and all 6 initial steps should be completed within 1 hour. It is important not to confuse the sepsis 6 pathway with the 6 hour care bundle. Time is of the essence when managing septic patients, and initiating the sepsis 6 pathway immediately has been proven to enhance survival rates in sepsis patients.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

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.

The duration of the pause in chest compressions should be kept short, not exceeding 5 seconds. This applies to both pausing to assess the rhythm and pausing to administer a shock if the rhythm is deemed shockable. It is important to note that a pulse check lasting less than two seconds may fail to detect a palpable pulse, particularly in individuals with a slow heart rate (bradycardia).

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.

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

Respiratory acidosis is often associated with chronic obstructive pulmonary disease (COPD) or life-threatening asthma. Other causes include pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or certain medications.

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

Metabolic acidosis with a raised anion gap can be caused by conditions like lactic acidosis (which can result from hypoxemia, shock, sepsis, or infarction) or ketoacidosis (commonly seen in diabetes, starvation, or alcohol excess). Other causes include renal failure or poisoning (such as late stages of aspirin overdose, methanol, or ethylene glycol).

Metabolic acidosis with a normal anion gap can be attributed to conditions like renal tubular acidosis, diarrhea, ammonium chloride ingestion, or adrenal insufficiency.

The ECG shows the following findings:
– There is ST depression in leads V1-V4 and aVR.
– There is ST elevation in leads V5-V6, II, III, and aVF.
– There is a positive R wave in leads V1 and V2, which indicates a reverse Q wave.
These ECG changes indicate that there is an acute inferoposterior myocardial infarction.

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.

This patient has been diagnosed with severe hyperkalemia and is showing significant ECG changes. The top priority in this situation is to protect the heart. It is recommended to administer 10 ml of 10% calcium chloride immediately over a period of 2-5 minutes. Calcium helps counteract the harmful effects of hyperkalemia on the heart by stabilizing the cardiac cell membrane and preventing unwanted depolarization.

Hyperkalemia is a commonly encountered electrolyte disorder, affecting up to 10% of hospitalized patients. It is typically caused by an increase in potassium release from cells or impaired excretion by the kidneys. The main causes of hyperkalemia include renal failure, certain medications (such as ACE inhibitors, ARBs, potassium-sparing diuretics, and NSAIDs), tissue breakdown (as seen in conditions like tumor lysis, rhabdomyolysis, and hemolysis), metabolic acidosis (often associated with renal failure or diabetic ketoacidosis), and endocrine disorders like Addison’s disease.

ECG changes that may be observed in hyperkalemia include a prolonged PR interval, peaked T-waves, widening of the QRS complex, reduced or absent P wave, sine wave pattern, AV dissociation, asystole, and bradycardia. It is important to note that the severity of ECG changes may not always correlate with the actual serum potassium levels in a patient.

The treatment approach for hyperkalemia depends on its severity. Mild hyperkalemia is defined as a potassium level of 5.5-5.9 mmol/L, moderate hyperkalemia as 6.0-6.4 mmol/L, and severe hyperkalemia as >6.5 mmol/L.

For mild hyperkalemia, the focus should be on addressing the underlying cause and preventing further increase in serum potassium levels. This may involve adjusting medications or dietary changes. If treatment is necessary, potassium exchange resins like calcium resonium can be used to remove potassium from the body.

In cases of moderate hyperkalemia, the goal is to shift potassium from the extracellular space into the cells. This can be achieved by administering insulin and glucose intravenously. Monitoring blood glucose levels is crucial in this situation. Potassium exchange resins should also be considered, and dialysis may be necessary.

Severe hyperkalemia without ECG changes requires immediate medical attention.

Acute adrenal insufficiency, also known as Addisonian crisis, is a rare condition that can have catastrophic consequences if not diagnosed in a timely manner. It is more prevalent in women and typically occurs between the ages of 30 and 50.

Addison’s disease is caused by a deficiency in the production of steroid hormones by the adrenal glands, affecting glucocorticoid, mineralocorticoid, and sex steroid production. The main causes of Addison’s disease include autoimmune adrenalitis, bilateral adrenalectomy, Waterhouse-Friderichsen syndrome, tuberculosis, and congenital adrenal hyperplasia.

An Addisonian crisis can be triggered by the intentional or accidental withdrawal of steroid therapy, as well as factors such as 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 in areas such as palmar creases, buccal mucosa, and exposed skin.

During an Addisonian crisis, the main symptoms are usually hypoglycemia and shock, characterized by tachycardia, peripheral vasoconstriction, hypotension, altered consciousness, and even coma.

Biochemical features that can confirm the diagnosis of Addison’s disease include increased ACTH levels, hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, and metabolic acidosis. Diagnostic investigations may involve the Synacthen test, plasma ACTH level measurement, plasma renin level measurement, and adrenocortical antibody testing.

Management of Addison’s disease should be overseen by an Endocrinologist. Treatment typically involves the administration of hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also require thyroxine if there is hypothalamic-pituitary disease present. Treatment is lifelong, and patients should carry a steroid card and MedicAlert bracelet to alert healthcare professionals of their condition and the potential for an Addisonian crisis.

When administering treatment to patients with hepatic impairment, it is crucial to consider that midazolam is metabolized in the liver.

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 CENTOR score is a tool used to assess the likelihood of a patient having a streptococcal infection, which is a common cause of sore throat. It is based on four clinical criteria: presence of tonsillar exudates, tender anterior cervical lymphadenopathy, absence of cough, and history of fever. Each criterion is assigned one point, with a maximum score of four.

In this case, the patient has a sore throat without cough or runny nose, and her temperature is slightly elevated at 37.7°C. The examination reveals redness in the oropharynx and tonsils, but no tender neck or palpable masses. Based on this information, the patient would score one point on the CENTOR score.

Further Reading:

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

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

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

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

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

The mortality rate linked to sepsis can vary depending on various factors such as the patient’s age, overall health, and the severity of the infection. However, on average, the mortality rate for sepsis is estimated to be around 30%.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

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

Public Health England (PHE) has the primary goal of promptly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is not the main focus, clinical suspicion of a notifiable infection has been sufficient since 1968.

Registered medical practitioners (RMPs) are legally obligated to inform the designated proper officer at their local council or local health protection team (HPT) about suspected cases of specific infectious diseases.

The Health Protection (Notification) Regulations 2010 outline 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.

Urinary tract stones form when the concentration of salt and minerals in the urine becomes too high. These stones can be classified into five types based on their mineral composition and how they develop.

The most common type of stone is the calcium stone, which can be further divided into calcium oxalate and calcium phosphate stones. These account for 60-80% of all urinary tract stones.

Another type is the struvite or magnesium ammonium phosphate stone, making up about 10-15% of cases. Uric acid stones, also known as urate stones, occur in 3-10% of cases.

Cystine stones are less common, accounting for less than 2% of urinary tract stones. Finally, there are drug-induced stones, which are caused by certain medications such as triamterene, protease inhibitors like indinavir sulphate, and sulfa drugs. These account for approximately 1% of cases.

By understanding the different types of urinary tract stones, healthcare professionals can better diagnose and treat patients with this condition.

Methaemoglobinaemia is a condition characterized by various symptoms such as headache, anxiety, acidosis, arrhythmia, seizure activity, reduced consciousness or coma. One notable feature is the presence of brown or chocolate coloured blood. It is important to note that the patient is taking chloroquine, which is a known trigger for methaemoglobinaemia. Additionally, despite the condition, the patient’s arterial blood gas analysis shows a normal partial pressure of oxygen.

Further Reading:

Methaemoglobinaemia is a condition where haemoglobin is oxidised from Fe2+ to Fe3+. This process is normally regulated by NADH methaemoglobin reductase, which transfers electrons from NADH to methaemoglobin, converting it back to haemoglobin. In healthy individuals, methaemoglobin levels are typically less than 1% of total haemoglobin. However, an increase in methaemoglobin can lead to tissue hypoxia as Fe3+ cannot bind oxygen effectively.

Methaemoglobinaemia can be congenital or acquired. Congenital causes include haemoglobin chain variants (HbM, HbH) and NADH methaemoglobin reductase deficiency. Acquired causes can be due to exposure to certain drugs or chemicals, such as sulphonamides, local anaesthetics (especially prilocaine), nitrates, chloroquine, dapsone, primaquine, and phenytoin. Aniline dyes are also known to cause methaemoglobinaemia.

Clinical features of methaemoglobinaemia include slate grey cyanosis (blue to grey skin coloration), chocolate blood or chocolate cyanosis (brown color of blood), dyspnoea, low SpO2 on pulse oximetry (which often does not improve with supplemental oxygen), and normal PaO2 on arterial blood gas (ABG) but low SaO2. Patients may tolerate hypoxia better than expected. Severe cases can present with acidosis, arrhythmias, seizures, and coma.

Diagnosis of methaemoglobinaemia is made by directly measuring the level of methaemoglobin using a co-oximeter, which is present in most modern blood gas analysers. Other investigations, such as a full blood count (FBC), electrocardiogram (ECG), chest X-ray (CXR), and beta-human chorionic gonadotropin (bHCG) levels (in pregnancy), may be done to assess the extent of the condition and rule out other contributing factors.

Active treatment is required if the methaemoglobin level is above 30% or if it is below 30% but the patient is symptomatic or shows evidence of tissue hypoxia. Treatment involves maintaining the airway and delivering high-flow oxygen, removing the causative agents, treating toxidromes and consider giving IV dextrose 5%.

When the paramedian branches of the basilar artery are blocked, it leads to a condition known as medial pontine syndrome. This syndrome is characterized by several symptoms. Firstly, there is contralateral hemiplegia, which refers to paralysis on the opposite side of the body due to damage to the pyramidal tracts. Additionally, there is contralateral loss of joint position sense, vibratory sense, and discriminatory touch, which occurs as a result of damage to the medial lemniscus. Lastly, individuals with medial pontine syndrome may experience double vision caused by paralysis of the lateral rectus muscle, which is due to damage to the sixth cranial nerve.

Assessing the depth of a burn is crucial for determining the severity of the injury and planning appropriate wound care. Burns are typically classified as first-, second-, or third-degree, depending on how deeply they penetrate the skin’s surface.

First-degree burns, also known as superficial burns, only affect the outer layer of skin called the epidermis. These burns are characterized by redness and pain, with dry skin and no blistering. An example of a first-degree burn is mild sunburn. They usually do not require intravenous fluid replacement and are not included in the assessment of the burn’s extent. Long-term tissue damage is rare with these burns.

Second-degree burns, also called partial-thickness burns, involve both the epidermis and part of the dermis layer of skin. They can be further categorized as superficial partial-thickness or deep partial-thickness burns. Superficial partial-thickness burns are moist, hypersensitive, potentially blistered, uniformly pink, and blanch when touched. Deep partial-thickness burns are drier, less painful, potentially blistered, red or mottled in appearance, and do not blanch when touched.

Third-degree burns, also known as full-thickness burns, destroy both the epidermis and dermis layers of skin and extend into the subcutaneous tissue. These burns may also damage underlying bones, muscles, and tendons. The burn site appears translucent or waxy white, or it can be charred. Once the epidermis is removed, the underlying dermis may initially appear red but does not blanch under pressure. This dermis is typically dry and does not produce any fluid. Since the nerve endings are destroyed, there is no sensation in the affected area.

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

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

Cannabinoid hyperemesis syndrome (CHS) is an extremely rare form of cannabinoid toxicity that occurs in chronic smokers. It is characterized by recurring episodes of severe nausea and vomiting. One distinctive feature of this syndrome is that individuals who suffer from it often find relief from their symptoms by taking hot baths or showers, and they may compulsively bathe during episodes of nausea and vomiting.

CHS typically develops in heavy, long-term cannabis users who consume the drug multiple times a day for many years. On average, symptoms appear after about 16 years of cannabis use, although some patients may experience symptoms after as little as three years.

In 2009, Sontineni and colleagues established criteria for diagnosing cannabinoid hyperemesis syndrome. These criteria include essential factors such as long-term cannabis use, major factors like severe nausea and vomiting that occur in a cyclic pattern over months, and resolution of symptoms after discontinuing cannabis use. Supportive criteria include compulsive hot baths with symptom relief, colicky abdominal pain, and no evidence of inflammation in the gallbladder or pancreas.

The exact cause of CHS is not fully understood, but there are two main theories. One theory suggests that the syndrome is a result of a build-up of cannabinoids in the body, which leads to toxicity. Another theory proposes that the functionality of cannabinoid receptors in the brain, particularly in the hypothalamus, is affected, resulting in CHS.

Most conventional anti-emetic drugs are effective in treating the vomiting phase of CHS. During acute episodes, it is important to monitor the patient’s hydration status as the combination of hot baths and prolonged vomiting can lead to cannabinoid hyperemesis acute renal failure (CHARF). This can be easily prevented and treated with intravenous fluids.

Once the acute episode of vomiting and dehydration has been addressed, the condition can be easily cured by discontinuing cannabis consumption.

Testicular cancer is the most common form of cancer that affects men between the ages of 20 and 34. In recent times, there have been campaigns aimed at raising awareness about the importance of self-examination for early detection. Some risk factors for this type of cancer include having undescended testes, especially if it affects both testicles, which increases the risk by ten times. Additionally, individuals who have had testicular cancer in the past have a 4% chance of developing a second cancer.

The typical presentation of testicular cancer is a painless swelling in the testicles. When examined, the swelling feels hard and is located within the testis. It cannot be illuminated when light is shone through it. Approximately 60% of cases are seminomas, which are slow-growing and usually confined to the testis at the time of diagnosis. If seminomas are diagnosed at stage 1 (confined to the testis only), the 5-year survival rate is 98%. The remaining 40% of cases are teratomas, which can grow at a faster rate and often coexist with seminomas. In cases where the tumors are of mixed type, they are treated as teratomas due to their more aggressive nature. The main treatment for testicular cancer is surgery, with the possibility of additional chemotherapy and radiotherapy.

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.

Sheehan’s syndrome is a condition where the pituitary gland becomes damaged due to insufficient blood flow and shock during and after childbirth, leading to hypopituitarism. The risk of developing this syndrome is higher in pregnancies with conditions that increase the chances of bleeding, such as placenta praevia and multiple pregnancies. However, Sheehan’s syndrome is quite rare, affecting only 1 in 10,000 pregnancies.

During pregnancy, the anterior pituitary gland undergoes hypertrophy, making it more vulnerable to ischaemia in the later stages. While the posterior pituitary gland is usually not affected due to its own direct blood supply, there have been rare cases where it is involved. In these instances, central diabetes insipidus, a form of posterior pituitary dysfunction, can occur as a complication of Sheehan’s syndrome.

The clinical features of Sheehan’s syndrome include the absence or infrequency of menstrual periods, the inability to produce milk and breastfeed (galactorrhoea), decreased libido, fatigue and tiredness, loss of pubic and axillary hair, and the potential development of secondary hypothyroidism and adrenal insufficiency. Serum prolactin levels are typically low (less than 5ng/ml). An MRI can be helpful in ruling out other pituitary issues, such as a pituitary tumor.

Treatment for Sheehan’s syndrome involves hormone replacement therapy. With appropriate management, the prognosis for this condition is excellent.

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.

When assessing a patient with epistaxis (nosebleed), it is important to start with a standard ABC assessment, focusing on the airway and hemodynamic status. Even if the bleeding appears to have stopped, it is crucial to evaluate the patient’s airway and circulation.

If active bleeding is still present and there are signs of hemodynamic compromise, immediate resuscitative and first aid measures should be initiated. Epistaxis should be treated as a circulatory emergency, especially in elderly patients, those with clotting disorders or bleeding tendencies, and individuals taking anticoagulants. In these cases, it is necessary to establish intravenous access using at least an 18-gauge (green) cannula and collect blood samples for tests such as full blood count, urea and electrolytes, clotting studies, and blood typing and crossmatching (depending on the amount of blood loss). These patients should be closely monitored in a majors area or a designated observation area, as dislodgement of a blood clot can lead to severe bleeding.

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

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

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.

When an adult patient is choking and unable to clear the obstruction by coughing, the next step is to deliver either 5 back blows or abdominal thrusts. The appropriate action depends on the severity of the airway obstruction. If the choking is mild and not causing significant difficulty in breathing, it is recommended to encourage the patient to cough and closely monitor for any worsening symptoms. However, if the choking is severe and causing a complete blockage of the airway, it is necessary to administer either back blows or abdominal thrusts to dislodge the obstruction. In the event that the patient loses consciousness, immediate CPR should be initiated.

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.

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

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

The sigmoid colon is the last segment of the colon and is primarily situated in the left iliac fossa.

Altitude sickness is usually experienced at altitudes above 2,500 meters (8,000 ft), although some individuals may be affected at lower altitudes. It is important to note that climbers in the UK, where the highest peak is Ben Nevis at 1,345 meters, do not need to worry about altitude sickness.

Further Reading:

High Altitude Illnesses

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

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

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

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

Cushing’s triad is a combination of widened pulse pressure, bradycardia, and reduced respirations. It is a physiological response of the nervous system to acute increases in intracranial pressure (ICP). This response, known as the Cushing reflex, can cause the symptoms of Cushing’s triad. These symptoms include an increase in systolic blood pressure and a decrease in diastolic blood pressure, a slower heart rate, and irregular or reduced breathing. Additionally, raised ICP can also lead to other symptoms such as headache, papilloedema, and vomiting.

Further Reading:

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

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

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

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

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.

Hypothermic cardiac arrest is a rare situation that requires a tailored approach. Resuscitation is typically prolonged, but the prognosis for young, previously healthy individuals can be good. Hypothermic cardiac arrest may be associated with drowning. Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, basal metabolic rate falls and cell signaling between neurons decreases, leading to reduced tissue perfusion. Signs and symptoms of hypothermia progress as the core temperature drops, initially presenting as compensatory increases in heart rate and shivering, but eventually ceasing as the temperature drops into moderate hypothermia territory.

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

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

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

In order to gain a comprehensive understanding of AF management, it is crucial to familiarize oneself with the terminology used to describe its various subtypes. These terms help categorize different episodes of AF based on their characteristics and outcomes.

Acute AF refers to any episode that occurs within the previous 48 hours. It can manifest with or without symptoms and may or may not recur. On the other hand, paroxysmal AF describes episodes that spontaneously end within 7 days, typically within 48 hours. While these episodes are often recurrent, they can progress into a sustained form of AF.

Recurrent AF is defined as experiencing two or more episodes of AF. If the episodes self-terminate, they are classified as paroxysmal AF. However, if the episodes do not self-terminate, they are categorized as persistent AF. Persistent AF lasts longer than 7 days or has occurred after a previous cardioversion. To terminate persistent AF, electrical or pharmacological intervention is required. In some cases, persistent AF can progress into permanent AF.

Permanent AF, also known as Accepted AF, refers to episodes that cannot be successfully terminated, have relapsed after termination, or where cardioversion is not pursued. This subtype signifies a more chronic and ongoing form of AF.

By understanding and utilizing these terms, healthcare professionals can effectively communicate and manage the different subtypes of AF.

During the first trimester of pregnancy, the use of trimethoprim is linked to an increased risk of neural tube defects because it antagonizes folate. If it is not possible to use an alternative antibiotic, it is recommended that pregnant women taking trimethoprim also take high-dose folic acid. However, the use of trimethoprim in the second and third trimesters of pregnancy is considered safe.

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

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

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

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

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

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

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

Chloramphenicol: It can cause grey baby syndrome.

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

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

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

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

Heparin: It can cause maternal bleeding and thrombocytopenia.

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

The majority of dissections happen in individuals between the ages of 40 and 70, with the highest occurrence observed in the age group of 50 to 65.

Further Reading:

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

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

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

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

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

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

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

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

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

The most probable causative organism in a case of peritonsillar abscess is Streptococcus pyogenes.

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.

This question evaluates your ability to effectively communicate while promoting patient self-care and understanding of managing long-term conditions.

The most appropriate answer would be to initially talk to the patient himself. This approach allows for an assessment of the patient’s capacity to make decisions on his own. It is a gentle approach that respects his ability to make safe and sensible decisions.

In some cases, it can be helpful to include other close family members or friends when explaining a situation to a patient. However, it is important to avoid being coercive. While this option may be a good choice, it is not the best first step to take.

If all reasonable means have been tried and the patient continues to drive, there may come a time when it is necessary to contact the DVLA. However, this should be expressed in a less confrontational manner.

Suggesting to the patient’s wife to sell the car is not appropriate as it is not your place to make such a suggestion. Additionally, his wife may still need to use the car even if he cannot drive. This is not a suggestion that should be made by you.

It is not necessary to inform the DVLA immediately, as this could negatively impact the doctor-patient relationship in the future.

For more information, you can refer to the DVLA guidance on medical conditions affecting driving.

Two scoring systems are suggested by NICE to aid in the evaluation of sore throat: The Centor Clinical Prediction Score and The FeverPAIN Score.

The FeverPAIN score was developed from a study involving 1760 adults and children aged three and above. The score was tested in a trial that compared three prescribing strategies: empirical delayed prescribing, using the score to guide prescribing, or a combination of the score with the use of a near-patient test (NPT) for streptococcus. Utilizing the score resulted in faster symptom resolution and a reduction in the prescription of antibiotics (both reduced by one third). The inclusion of the NPT did not provide any additional benefit.

The score comprises of five factors, each of which is assigned one point: Fever (Temp >38°C) in the last 24 hours, Purulence, Attended rapidly in under three days, Inflamed tonsils, and No cough or coryza.

Based on the score, the recommendations are as follows:
– Score 0-1 = 13-18% likelihood of streptococcus infection, antibiotics are not recommended.
– Score 2-3 = 34-40% likelihood of streptococcus infection, consider delayed prescribing of antibiotics (3-5 day ‘backup prescription’).
– Score 4-5 = 62-65% likelihood of streptococcus infection, use immediate antibiotics if severe, or a 48-hour short ‘backup prescription.’

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

Further Reading:

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

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

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

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

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

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.

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

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.

Tietze’s syndrome is an uncommon condition that leads to localized pain and tenderness in one or more of the upper four ribs, with the second and third ribs being the most commonly affected. The exact cause of this syndrome is still unknown, although it has been suggested that it may be linked to repeated small injuries to the chest wall.

The pain experienced in Tietze’s syndrome is typically aggravated by movement, sneezing, and coughing, and it can also extend to the neck or shoulder on the affected side. In some cases, a firm swelling can be felt over the cartilage of the affected rib. While the pain usually diminishes after a few weeks or months, the swelling may persist.

Treatment for Tietze’s syndrome involves the use of pain-relieving medications, such as NSAIDs. In more severe or persistent cases, local steroid injections may be beneficial.

The most probable diagnosis in this situation is Goodpasture’s syndrome, a rare autoimmune vasculitic disorder characterized by three main symptoms: pulmonary hemorrhage, glomerulonephritis, and the presence of anti-glomerular basement membrane (Anti-GBM) antibodies. Goodpasture’s syndrome is more prevalent in men, particularly in smokers. It is also associated with HLA-B7 and HLA-DRw2.

The clinical manifestations of Goodpasture’s syndrome include constitutional symptoms like fever, fatigue, nausea, and weight loss. Patients may also experience hemoptysis or pulmonary hemorrhage, chest pain, breathlessness, and inspiratory crackles at the lung bases. Anemia due to bleeding within the lungs, arthralgia, rapidly progressive glomerulonephritis, hematuria, hypertension, and rarely hepatosplenomegaly may also be present.

Blood tests will reveal iron deficiency anemia, an elevated white cell count, and renal impairment. Elisa for Anti-GBM antibodies is highly sensitive and specific, but it is not widely available. Approximately 30% of patients may also have circulating antineutrophilic cytoplasmic antibodies (ANCAs), although these are not specific for Goodpasture’s syndrome and can be found in other conditions such as Wegener’s granulomatosis, which also cause renal impairment and pulmonary hemorrhage.

Diagnosis is typically confirmed through a renal biopsy, which can detect the presence of anti-GBM antibodies. This would be the most appropriate investigation to confirm the diagnosis in this case.

The management of Goodpasture’s syndrome involves a combination of plasmapheresis to remove circulating antibodies and the use of corticosteroids or cyclophosphamide.

An anal fissure is a tear in the wall of the anal mucosa that exposes the circular muscle layer. The majority of these tears occur in the posterior midline. The most common cause is the passage of a large, hard stool after a period of constipation. If multiple fissures are present, it may indicate an underlying condition such as Crohn’s disease or tuberculosis.

Both men and women are equally affected by anal fissures, and they are most commonly seen in individuals in their thirties. The typical symptoms of an anal fissure include intense, sharp pain during bowel movements, which can last up to an hour after passing stool. Additionally, there may be spots of bright red blood on the toilet paper when wiping, and a history of constipation.

The initial management of an anal fissure involves non-operative measures such as using stool softeners and bulking agents. To alleviate the intense anal pain, analgesics and topical local anesthetics may be prescribed. According to a recent meta-analysis, first-line therapy should involve the use of topical GTN or diltiazem, with botulinum toxin being used as a rescue treatment if necessary (Modern perspectives in the treatment of chronic anal fissures. Ann R Coll Surg Engl. 2007 Jul;89(5):472-8.)

Sphincterotomy, a surgical procedure, should be reserved for fissures that do not heal and has a success rate of 90%. Anal dilatation, also known as Lord’s procedure, is rarely used nowadays due to the high risk of subsequent fecal incontinence.

The most probable diagnosis in this case is septic arthritis, which occurs when an infectious agent invades a joint and causes pus formation. The patient’s recent travel to Bangkok, presence of a vesicular rash on the trunk, and the identification of Gram-negative diplococci support this diagnosis.

Septic arthritis is characterized by several clinical features. These include pain in the affected joint, redness, warmth, and swelling of the joint, and difficulty in moving the joint. Patients may also experience fever and systemic symptoms.

The most common cause of septic arthritis is Staphylococcus aureus. Other bacteria that can lead to this condition include Streptococcus spp., Haemophilus influenzae, Neisseria gonorrhoea (typically seen in sexually active young adults with macules or vesicles on the trunk), and Escherichia coli (common in intravenous drug users, the elderly, and seriously ill individuals).

According to the current recommendations by NICE (National Institute for Health and Care Excellence) and the BNF (British National Formulary), the treatment for septic arthritis involves the following approaches. Flucloxacillin is the first-line antibiotic. In cases of penicillin allergy, clindamycin is recommended. If there is suspicion of MRSA infection, vancomycin should be used. For gonococcal arthritis or Gram-negative infection, cefotaxime is the preferred choice. The suggested duration of treatment is 4-6 weeks, although it may be longer if the infection is complicated.

The FeverPAIN score is a clinical scoring system that helps determine the probability of streptococcal infection and the necessity of antibiotic treatment. NICE recommends using either the CENTOR or FeverPAIN clinical scoring systems to assess the likelihood of streptococcal infection and the need for antibiotics. The RSI score is utilized to evaluate laryngopharyngeal reflux, while the CSMCPI is employed to predict clinical outcomes in patients with upper gastrointestinal bleeding. Lastly, the Mallampati score is used to assess the oropharyngeal space and predict the difficulty of endotracheal intubation.

Further Reading:

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

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

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

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

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

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 presence of serum HBsAg for more than 6 months indicates chronic HBV infection. HBeAg can be detected in the serum during the early stages of acute infection and some chronic infections. Higher levels of virus replication are usually associated with the presence of HBeAg, making individuals with chronic HBV more infectious. If HBeAg is cleared, anti-HBe is typically detected, indicating lower infectivity. The presence of anti-HBe, along with a decline in HBV-DNA, suggests control of viral replication and the likelihood of resolving acute hepatitis B. The presence of anti-HBc indicates current or past HBV infection, appearing at the onset of symptoms in acute infection and persisting for life. However, it may be absent in the early stages of acute infection. Anti-HBc IgM indicates recent HBV infection within the last six months and can help differentiate between acute and chronic infection. Over time, it is gradually replaced by IgG anti-HBc. IgG anti-HBc generally persists for life and indicates past infection. Anti-HBs indicates recovery from and immunity to HBV. If anti-HBs is present without anti-HBc, it suggests immunization. The quantification of anti-HBs is used to measure the response to vaccination.

Further Reading:

Hepatitis B is a viral infection that is transmitted through exposure to infected blood or body fluids. It can also be passed from mother to child during childbirth. The incubation period for hepatitis B is typically 6-20 weeks. Common symptoms of hepatitis B include fever, jaundice, and elevated liver transaminases.

Complications of hepatitis B infection can include chronic hepatitis, which occurs in 5-10% of cases, fulminant liver failure, hepatocellular carcinoma, glomerulonephritis, polyarteritis nodosa, and cryoglobulinemia.

Immunization against hepatitis B is recommended for various at-risk groups, including healthcare workers, intravenous drug users, sex workers, close family contacts of infected individuals, and those with chronic liver disease or kidney disease. The vaccine contains HBsAg adsorbed onto an aluminum hydroxide adjuvant and is prepared using recombinant DNA technology. Most vaccination schedules involve three doses of the vaccine, with a booster recommended after 5 years.

Around 10-15% of adults may not respond adequately to the vaccine. Risk factors for poor response include age over 40, obesity, smoking, alcohol excess, and immunosuppression. Testing for anti-HBs levels is recommended for healthcare workers and patients with chronic kidney disease. Interpretation of anti-HBs levels can help determine the need for further vaccination or testing for infection.

In terms of serology, the presence of HBsAg indicates acute disease if present for 1-6 months, and chronic disease if present for more than 6 months. Anti-HBs indicates immunity, either through exposure or immunization. Anti-HBc indicates previous or current infection, with IgM anti-HBc appearing during acute or recent infection and IgG anti-HBc persisting. HbeAg is a marker of infectivity.

Management of hepatitis B involves notifying the Health Protection Unit for surveillance and contact tracing. Patients should be advised to avoid alcohol and take precautions to minimize transmission to partners and contacts. Referral to a gastroenterologist or hepatologist is recommended for all patients. Symptoms such as pain, nausea, and itch can be managed with appropriate drug treatment. Pegylated interferon-alpha and other antiviral medications like tenofovir and entecavir may be used to suppress viral replication in chronic carriers.

When a 35-year-old female comes to the emergency department after a motor vehicle collision, it is important to assess the potential for cervical spine injury. To do this, the Canadian C-spine rules should be utilized. These rules provide a systematic approach to determine whether imaging, such as X-rays, is necessary to evaluate the cervical spine. The Canadian C-spine rules take into account various factors such as the patient’s age, mechanism of injury, and presence of certain symptoms or physical findings. By following these rules, healthcare professionals can effectively evaluate the potential for cervical spine injury and determine the appropriate course of action for further assessment and management.

Further Reading:

When assessing for cervical spine injury, it is recommended to use the Canadian C-spine rules. These rules help determine the risk level for a potential injury. High-risk factors include being over the age of 65, experiencing a dangerous mechanism of injury (such as a fall from a height or a high-speed motor vehicle collision), or having paraesthesia in the upper or lower limbs. Low-risk factors include being involved in a minor rear-end motor vehicle collision, being comfortable in a sitting position, being ambulatory since the injury, having no midline cervical spine tenderness, or experiencing a delayed onset of neck pain. If a person is unable to actively rotate their neck 45 degrees to the left and right, their risk level is considered low. If they have one of the low-risk factors and can actively rotate their neck, their risk level remains low.

If a high-risk factor is identified or if a low-risk factor is identified and the person is unable to actively rotate their neck, full in-line spinal immobilization should be maintained and imaging should be requested. Additionally, if a patient has risk factors for thoracic or lumbar spine injury, imaging should be requested. However, if a patient has low-risk factors for cervical spine injury, is pain-free, and can actively rotate their neck, full in-line spinal immobilization and imaging are not necessary.

NICE recommends CT as the primary imaging modality for cervical spine injury in adults aged 16 and older, while MRI is recommended as the primary imaging modality for children under 16.

Different mechanisms of spinal trauma can cause injury to the spine in predictable ways. The majority of cervical spine injuries are caused by flexion combined with rotation. Hyperflexion can result in compression of the anterior aspects of the vertebral bodies, stretching and tearing of the posterior ligament complex, chance fractures (also known as seatbelt fractures), flexion teardrop fractures, and odontoid peg fractures. Flexion and rotation can lead to disruption of the posterior ligament complex and posterior column, fractures of facet joints, lamina, transverse processes, and vertebral bodies, and avulsion of spinous processes. Hyperextension can cause injury to the anterior column, anterior fractures of the vertebral body, and potential retropulsion of bony fragments or discs into the spinal canal. Rotation can result in injury to the posterior ligament complex and facet joint dislocation.

To minimize the risk of infection and promote proper healing, the best approach for preparing the skin would be to clean it for 30 seconds with 2% chlorhexidine gluconate in 70% alcohol. This solution has been shown to effectively kill bacteria and reduce the risk of infection. Other options such as povidone-iodine, 90% isopropyl alcohol, and 30% isopropyl alcohol may also have some antimicrobial properties, but they are not as effective as chlorhexidine gluconate.

Further Reading:

Peripheral venous cannulation is a procedure that should be performed following established guidelines to minimize the risk of infection, injury, extravasation, and early failure of the cannula. It is important to maintain good hand hygiene, use personal protective equipment, ensure sharps safety, and employ an aseptic non-touch technique during the procedure.

According to the National Institute for Health and Care Excellence (NICE), the skin should be disinfected with a solution of 2% chlorhexidine gluconate and 70% alcohol before inserting the catheter. It is crucial to allow the disinfectant to completely dry before inserting the cannula.

The flow rates of IV cannulas can vary depending on factors such as the gauge, color, type of fluid used, presence of a bio-connector, length of the cannula, and whether the fluid is drained under gravity or pumped under pressure. However, the following are typical flow rates for different gauge sizes: 14 gauge (orange) has a flow rate of 270 ml/minute, 16 gauge (grey) has a flow rate of 180 ml/minute, 18 gauge (green) has a flow rate of 90 ml/minute, 20 gauge (pink) has a flow rate of 60 ml/minute, and 22 gauge (blue) has a flow rate of 36 ml/minute. These flow rates are based on infusing 1000 ml of normal saline under ideal circumstances, but they may vary in practice.

In this scenario, it is crucial to evaluate whether the patient possesses the ability to make decisions regarding his medical care. The question indicates that he has the capacity to do so, making him competent in making these decisions. Therefore, it would be prudent to inform him about the potential management options if he chooses to stay, as well as the potential consequences if he decides to self-discharge. Since he is competent and capable of weighing the risks, the next step would be to have him sign a self-discharge form.

It is important to note that taking his bloods without his consent could be considered battery, and the patient would have every right to file a serious complaint against you. Additionally, arranging an ultrasound scan may not provide any further valuable information at this moment.

Asking a nurse to keep an eye on the patient may not be practical, as the nurse could be extremely busy, and finding your consultant quickly may not be feasible. Furthermore, telling the patient that he must stay would not allow him the opportunity to make an informed decision on his own. It is important to emphasize that in this case, the patient is deemed to have the capacity to make decisions, and therefore, the medical team cannot act in his best interests without his consent.

Bullous pemphigoid (BP) is a chronic autoimmune disorder that affects the skin, causing blistering. It occurs when the immune system mistakenly attacks the basement membrane of the epidermis. This attack is carried out by immunoglobulins (IgG and sometimes IgE) and activated T lymphocytes. The autoantibodies bind to proteins and release cytokines, leading to complement activation, neutrophil recruitment, and the release of enzymes that destroy the hemidesmosomes. As a result, subepidermal blisters form.

Pemphigus, on the other hand, is a group of autoimmune disorders characterized by blistering of the skin and mucosal surfaces. The most common type, pemphigus vulgaris (PV), accounts for about 70% of cases worldwide. PV is also autoimmune in nature, with autoantibodies targeting cell surface antigens on keratinocytes (desmogleins 1 and 3). This leads to a loss of adhesion between cells and their separation.

Here is a comparison of the key differences between pemphigus vulgaris and bullous pemphigoid:

Pemphigus vulgaris:
– Age: Middle-aged people (average age 50)
– Oral involvement: Common
– Blister type: Large, flaccid, and painful
– Blister content: Fluid-filled, often haemorrhagic
– Areas commonly affected: Initially face and scalp, then spread to the chest and back
– Nikolsky sign: Usually positive
– Pruritus: Rare
– Skin biopsy: Intra-epidermal deposition of IgG between cells throughout the epidermis

Bullous pemphigoid:
– Age: Elderly people (average age 80)
– Oral involvement: Rare
– Blister type: Large and tense
– Blister content: Fluid-filled
– Areas commonly affected: Upper arms, thighs, and skin flexures
– Nikolsky sign: Usually negative
– Pruritus: Common
– Skin biopsy: A band of IgG and/or C3 at the dermo-epidermal junction

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.

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

Further Reading:

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

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

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

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

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

Triage is a crucial process that involves determining the priority of patients’ treatment based on the severity of their condition and their chances of recovery. Its purpose is to ensure that limited resources are used efficiently, maximizing the number of lives saved. During a major incident, primary triage takes place in the bronze area, which is located within the inner cordon.

In the context of a major incident, priorities are assigned numbers from 1 to 3, with 1 being the highest priority. These priorities are also color-coded for easy identification:
– P1: Immediate priority. This category includes patients who require immediate life-saving intervention to prevent death. They are color-coded red.
– P2: Intermediate priority. Patients in this group also require significant interventions, but their treatment can be delayed for a few hours. They are color-coded yellow.
– P3: Delayed priority. Patients in this category require medical treatment, but it can be safely delayed. This category also includes walking wounded individuals. The classification as P3 is based on the motor score of the Glasgow Coma Scale, which predicts a favorable outcome. They are color-coded green.

The fourth classification is for deceased individuals. It is important to identify and classify them to prevent the unnecessary use of limited resources on those who cannot be helped. Dead bodies should be left in their current location, both to avoid wasting resources and because the area may be considered a crime scene. Deceased individuals are color-coded black.

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

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

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

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

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

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

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

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

Further Reading:

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

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

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

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

This individual is experiencing early symptoms such as tiredness, swollen tonsils with discharge, enlarged lymph nodes, and an enlarged liver. Additionally, they fall within the typical age group for developing glandular fever (infectious mononucleosis). Epstein-Barr virus (EBV) is responsible for the majority of glandular fever cases.

Further Reading:

Glandular fever, also known as infectious mononucleosis or mono, is a clinical syndrome characterized by symptoms such as sore throat, fever, and swollen lymph nodes. It is primarily caused by the Epstein-Barr virus (EBV), with other viruses and infections accounting for the remaining cases. Glandular fever is transmitted through infected saliva and primarily affects adolescents and young adults. The incubation period is 4-8 weeks.

The majority of EBV infections are asymptomatic, with over 95% of adults worldwide having evidence of prior infection. Clinical features of glandular fever include fever, sore throat, exudative tonsillitis, lymphadenopathy, and prodromal symptoms such as fatigue and headache. Splenomegaly (enlarged spleen) and hepatomegaly (enlarged liver) may also be present, and a non-pruritic macular rash can sometimes occur.

Glandular fever can lead to complications such as splenic rupture, which increases the risk of rupture in the spleen. Approximately 50% of splenic ruptures associated with glandular fever are spontaneous, while the other 50% follow trauma. Diagnosis of glandular fever involves various investigations, including viral serology for EBV, monospot test, and liver function tests. Additional serology tests may be conducted if EBV testing is negative.

Management of glandular fever involves supportive care and symptomatic relief with simple analgesia. Antiviral medication has not been shown to be beneficial. It is important to identify patients at risk of serious complications, such as airway obstruction, splenic rupture, and dehydration, and provide appropriate management. Patients can be advised to return to normal activities as soon as possible, avoiding heavy lifting and contact sports for the first month to reduce the risk of splenic rupture.

Rare but serious complications associated with glandular fever include hepatitis, upper airway obstruction, cardiac complications, renal complications, neurological complications, haematological complications, chronic fatigue, and an increased risk of lymphoproliferative cancers and multiple sclerosis.

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

This patient presents with clinical features that are indicative of a right middle/lower lobe pneumonia. Considering her past medical history of a stroke and the specific location of the chest signs, it is highly probable that she is suffering from aspiration pneumonia.

A tension pneumothorax occurs when there is an air leak from the lung or chest wall that acts like a one-way valve. This causes air to build up in the pleural space without any way to escape. As a result, the pressure in the pleural space increases and pushes the mediastinum into the opposite side of the chest. If left untreated, this can lead to cardiovascular instability and even cardiac arrest.

The clinical features that are typically seen in tension pneumothorax include respiratory distress and cardiovascular instability. Tracheal deviation away from the side of injury, unilateral absence of breath sounds on the affected side, and a hyper-resonant percussion note are also characteristic. Other signs may include distended neck veins and cyanosis, although cyanosis is usually a late sign.

Both tension pneumothorax and massive haemothorax can cause decreased breath sounds on auscultation. However, they can be differentiated by percussion. Hyper-resonance suggests tension pneumothorax, while dullness indicates a massive haemothorax.

It is important to note that tension pneumothorax is a clinical diagnosis and treatment should not be delayed for radiological confirmation. Immediate decompression through needle thoracocentesis is the recommended treatment. Traditionally, a large-bore needle or cannula is inserted into the 2nd intercostal space in the midclavicular line of the affected side. However, studies have shown that using the 4th or 5th intercostal space in the midaxillary line has better success in reaching the thoracic cavity in adult patients. ATLS now recommends this location for needle decompression in adults. The location for children remains the same, and the 2nd intercostal space in the midclavicular line should still be used. It is important to remember that needle thoracocentesis is a temporary measure and definitive treatment involves the insertion of a chest drain.

For patients with sepsis and hypotension, it is recommended to administer 30ml of crystalloid fluid per kilogram of body weight. However, if the patient does not have acute kidney injury, is not hypotensive, and has a lactate level below 2 mmol/l, a 500ml immediate dose may be given.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

This child is displaying a typical pattern of symptoms for type I diabetes mellitus. He has recently experienced increased urination, excessive thirst, weight loss, and fatigue. Blood tests have revealed metabolic acidosis, and the presence of ketones in his urine indicates the development of diabetic ketoacidosis.

Central retinal artery occlusion (CRAO) is characterized by sudden, painless, and unilateral loss of vision. The appearance of the retina in CRAO is distinct from that of CRVO. It shows a pale retina with narrowed blood vessels. A notable feature is the presence of a ‘cherry-red spot’ at the center of the macula, which is supplied by the underlying choroid. Additionally, examination often reveals an afferent pupillary defect.

On the other hand, branch retinal artery occlusion (BRAO) typically affects only one quadrant of the retina, leading to visual field deficits in that specific area rather than complete loss of vision.

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.

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.

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.

NICE has emphasized that there are particular symptoms and signs that may indicate specific diseases as the underlying cause of a fever. For instance, bacterial meningitis may be suggested if the following symptoms and signs are present: neck stiffness, bulging fontanelle, decreased level of consciousness, and convulsive status epilepticus. For more information, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

Antihistamines do not help in treating the life-threatening aspects of anaphylaxis and should not be used instead of adrenaline. However, they can be used to relieve symptoms such as skin reactions and itching once the patient’s condition has stabilized. The appropriate dose of cetirizine for children between the ages of 2 and 6 is 2.5-5 mg. It is important to note that chlorpheniramine is no longer recommended. The recommended doses of oral cetirizine for different age groups are as follows: less than 2 years – 250 micrograms/kg, 2-6 years – 2.5-5 mg, 6-11 years – 5-10 mg, 12 years and older – 10-20 mg.

Further Reading:

Anaphylaxis is a severe and life-threatening allergic reaction that affects the entire body. It is characterized by a rapid onset and can lead to difficulty breathing, low blood pressure, and loss of consciousness. In paediatrics, anaphylaxis is often caused by food allergies, with nuts being the most common trigger. Other causes include drugs and insect venom, such as from a wasp sting.

When treating anaphylaxis, time is of the essence and there may not be enough time to look up medication doses. Adrenaline is the most important drug in managing anaphylaxis and should be administered as soon as possible. The recommended doses of adrenaline vary based on the age of the child. For children under 6 months, the dose is 150 micrograms, while for children between 6 months and 6 years, the dose remains the same. For children between 6 and 12 years, the dose is increased to 300 micrograms, and for adults and children over 12 years, the dose is 500 micrograms. Adrenaline can be repeated every 5 minutes if necessary.

The preferred site for administering adrenaline is the anterolateral aspect of the middle third of the thigh. This ensures quick absorption and effectiveness of the medication. It is important to follow the Resuscitation Council guidelines for anaphylaxis management, as they have recently been updated.

In some cases, 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. This can help confirm the diagnosis and guide further management.

Overall, prompt recognition and administration of adrenaline are crucial in managing anaphylaxis in paediatrics. Following the recommended doses and guidelines can help ensure the best outcomes for patients experiencing this severe allergic reaction.

Bacillus cereus is a type of bacterium that is Gram-positive, rod-shaped, and beta-haemolytic. It is responsible for causing a condition known as ‘fried rice syndrome’.

The bacterium forms hardy spores that can withstand boiling temperatures and remain viable even when rice is left at room temperature for extended periods before being fried. When these spores germinate, they can lead to the development of the syndrome.

There are two types of strains associated with Bacillus cereus. The first type produces an emetic enterotoxin, which results in symptoms such as nausea and vomiting. These symptoms typically occur within 1 to 6 hours after consuming contaminated food and can be quite severe, lasting for about 6 to 24 hours.

The second type of strain produces a diarrheagenic enterotoxin. This strain is commonly associated with the ingestion of meat, vegetables, and dairy products. Symptoms of this type of infection include abdominal pain and vomiting, which usually begin 8 to 12 hours after ingestion and resolve within 12 to 24 hours.

Orthostatic hypotension is diagnosed using lying and standing blood pressure measurements. This condition is often seen in older individuals who are taking multiple medications for hypertension and depression. The patient exhibits symptoms such as light-headedness, dizziness, weakness, and tunnel vision when standing up. These symptoms do not occur when lying down and worsen upon standing, but can be relieved by sitting or lying down. They are typically more pronounced in the morning, in hot environments, after meals, after standing still, and after exercise. No other signs suggest an alternative diagnosis.

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.

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

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

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 due to 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 up to 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 when potassium hydroxide is added (known as the whiff test), 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 important to note that pregnant patients with BV require special attention, as the condition is associated with an increased risk of late miscarriage, early labor, and chorioamnionitis (inflammation of the fetal membranes). Therefore, prompt treatment is crucial for these patients.

Massive haemothorax is characterized by the presence of more than 1.5 litres of blood in the pleural space. The patient’s history and examination findings are indicative of haemothorax. When blood loss exceeds 1500ml, it is classified as grade 3 hypovolemic shock, which is considered severe. Symptoms such as a pulse rate over 120, respiration rate over 30, and low blood pressure align with grade 3 shock and are consistent with massive haemothorax. In the case of pneumothorax, percussion reveals a resonant or hyper-resonant sound. Chylothorax, on the other hand, is a rare condition that typically occurs due to injury to the thoracic duct.

Further Reading:

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

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

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

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

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

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

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.

Typhoid fever is a bacterial infection caused by Salmonella typhi. Paratyphoid fever, on the other hand, is a similar illness caused by Salmonella paratyphi. Together, these two conditions are collectively known as the enteric fevers.

Typhoid fever is prevalent in India and many other parts of Asia, Africa, Central America, and South America. It is primarily transmitted through the consumption of contaminated food or water that has been infected by the feces of an acutely infected or recovering person, or a chronic carrier. About 1-6% of individuals infected with S. typhi become chronic carriers. The incubation period for this illness ranges from 7 to 21 days.

During the first week of the illness, patients experience weakness and lethargy, accompanied by a gradually increasing fever. The onset of the illness is usually subtle, and constipation is more common than diarrhea in the early stages. Other early symptoms include headaches, abdominal pain, and nosebleeds. In cases of typhoid fever, the fever can occur with a relatively slow heart rate, known as Faget’s sign.

As the illness progresses into the second week, patients often become too fatigued to get out of bed. Diarrhea becomes more prominent, the fever intensifies, and patients may become agitated and delirious. The abdomen may become tender and swollen, and approximately 75% of patients develop an enlarged spleen. In up to a third of patients, red macules known as Rose spots may appear.

In the third week, the illness can lead to various complications. Intestinal bleeding may occur due to bleeding in congested Peyer’s patches. Other potential complications include intestinal perforation, secondary pneumonia, encephalitis, myocarditis, metastatic abscesses, and septic shock.

After the third week, surviving patients begin to show signs of improvement, with the fever and symptoms gradually subsiding over the course of 7-14 days. Untreated patients have a mortality rate of 15-30%. Traditionally, drugs like ampicillin and trimethoprim have been used for treatment. However, due to the emergence of multidrug resistant cases, azithromycin or fluoroquinolones are now the primary treatment options.

Ophthalmia neonatorum refers to any cause of conjunctivitis during the newborn period, regardless of the specific organism responsible.

Conjunctivitis is the most frequent occurrence of Chlamydia trachomatis infection in newborns. Chlamydia is now the leading cause, accounting for up to 40% of cases. Neisseria gonorrhoea, on the other hand, only accounts for less than 1% of reported cases. The remaining cases are caused by non-sexually transmitted bacteria like Staphylococcus, Streptococcus, Haemophilus species, and viruses.

Gonorrhoeal ophthalmia neonatorum typically presents within 1 to 5 days after birth. It is characterized by intense redness and swelling of the conjunctiva, eyelid swelling, and a severe discharge of pus. Corneal ulceration and perforation may also be present.

Chlamydial ophthalmia neonatorum, on the other hand, usually appears between 5 to 14 days after birth. It is characterized by a gradually increasing watery discharge that eventually becomes purulent. The inflammation in the eyes is usually less severe compared to gonococcal infection, and there is a lower risk of corneal ulceration and perforation.

The second most common manifestation of Chlamydia trachomatis infection in newborns is pneumonia. Approximately 5-30% of infected neonates will develop pneumonia. About half of these infants will also have a history of ophthalmia neonatorum.

This question revolves around the challenge of delivering difficult news. The family involved in this situation have good intentions as they aim to shield their loved one from the distress of understanding the true nature of their underlying condition.

However, if the patient possesses the mental capacity to comprehend, it is important to disclose the details of their condition if they express a desire to know. Engage in an open and sensitive conversation with the patient, allowing them to determine the extent of information they wish to receive about their condition.

For further information, refer to the GMC Guidance on the topic of utilizing and divulging patient information for direct care.
https://www.gmc-uk.org/ethical-guidance/ethical-guidance-for-doctors/confidentiality/using-and-disclosing-patient-information-for-direct-care

The Gold-Silver-bronze Hierarchy is utilized to establish the chain of command at the site of a significant incident in the United Kingdom.

Gold (Strategic):
The Gold Commander assumes overall control of their organization’s resources at the incident. They are situated at a remote location known as the Gold Command. Ideally, the Gold Commanders for each organization should be co-located, but if that is not feasible, they must maintain constant communication with each other.

Silver (Tactical):
The Silver Commander for each organization is the highest-ranking member of each service present at the scene of the major incident. Their responsibility is to manage the available resources at the scene in order to achieve the strategic objectives set by the Gold Commander. They work closely with the Silver Commanders of other organizations and are not directly involved in dealing with the incident itself.

Bronze (Operational):
The Bronze Commander directly oversees their organization’s resources at the incident. They collaborate with their staff on the scene of the incident. In cases where the incident is geographically widespread, multiple Bronze commanders may assume responsibility for different areas. In complex incidents, Bronze commanders may share tasks or responsibilities.

At the scene of the major incident, the Police and Fire Service establish a cordon to restrict access, requiring permission from the appropriate officer to enter. The Silver and Bronze areas are designated within the scene.

The Silver area is situated within an outer cordon that surrounds the inner cordon. It houses the Casualty Clearing Station (CCS), Ambulance Parking Point, and the service incident commanders for each organization. Medical personnel are only allowed to enter the Silver area if instructed to do so by the MIO (Medical Incident Officer) and if authorized by the service responsible for safety at the scene, typically the Fire Service. Primary triage, evacuation of casualties, and treatment of trapped casualties take place in this area.

The Bronze area is located within an inner cordon that surrounds the scene of the incident. All medical activities within the Bronze area are directed by the MIO and AIO (Ambulance Incident Officer), who work together. Doctors operate under the command of the MIO, while ambulance personnel are under the command of the AIO.

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

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

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

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

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

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

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

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

Acute limb ischaemia refers to a sudden reduction in blood flow to a limb, which puts the limb at risk of tissue death. This condition is most commonly caused by either a sudden blockage of a previously partially blocked artery by a blood clot or by an embolus that travels from another part of the body. Acute limb ischaemia is considered a medical emergency, and if not promptly treated with surgery to restore blood flow, it can lead to extensive tissue damage within six hours.

The classic signs of acute limb ischaemia are often described using the 6 Ps:
– Pain that is constant and persistent
– Absence of pulses in the ankle
– Pallor, cyanosis, or mottling of the skin
– Loss of power or paralysis in the affected limb
– Paraesthesia or reduced sensation, leading to numbness
– Feeling cold in the affected limb

It is important to be able to distinguish between ischaemia caused by a blood clot and ischaemia caused by an embolus. The following highlights the main differences:
Embolus Thrombus
– Onset is sudden, occurring within seconds to minutes – Onset is gradual, taking hours to days
– Ischaemia is usually severe due to the lack of collateral circulation – Ischaemia is less severe due to the presence of collateral circulation
– There is typically no history of claudication, and pulses may still be present in the other leg – There is often a history of claudication, and pulses may also be absent in the other leg
– Skin changes, such as marbling, may be visible in the feet. This can appear as a fine reticular blanching or mottling in the early stages, progressing to coarse, fixed mottling
– Skin changes are usually absent in cases of thrombus-induced ischaemia.

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 60 kg, so the maximum safe dose of lidocaine hydrochloride would be 60 multiplied by 7 mg, resulting in a total of 420 mg.

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

If a child who is experiencing convulsions reaches step 3 of the APLS algorithm and has already been given phenytoin as part of their ongoing treatment, it is recommended to initiate a phenobarbitone infusion. This infusion should be administered at a dosage of 20 mg/kg over a period of 30 to 60 minutes.

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

Further Reading:

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

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

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

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

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

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

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

The standard drug regimen for tuberculosis is generally safe to use during pregnancy, with the exception of streptomycin which should be avoided. However, the use of isoniazid during pregnancy has been associated with potential risks such as liver damage in the mother and the possibility of neuropathy and seizures in the newborn.

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

ACE inhibitors (e.g. ramipril): If taken during the second and third trimesters, these medications can lead to reduced blood flow, kidney failure, and a condition called oligohydramnios.

Aminoglycosides (e.g. gentamicin): These drugs can cause ototoxicity, resulting in hearing loss in the baby.

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

Benzodiazepines (e.g. diazepam): When taken late in pregnancy, these medications can cause respiratory depression in the baby and lead to a withdrawal syndrome.

Calcium-channel blockers: If taken during the first trimester, these drugs can cause abnormalities in the fingers and toes. If taken during the second and third trimesters, they may result in fetal growth retardation.

Carbamazepine: This medication can increase the risk of hemorrhagic disease in the newborn and neural tube defects.

Chloramphenicol: Use of this drug in newborns can lead to a condition known as grey baby syndrome.

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

Danazol: When taken during the first trimester, this medication can cause masculinization of the female fetuses genitals.

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

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

Heparin: Use of heparin during pregnancy is associated with an acceptable bleeding rate and a low rate of thrombotic recurrence in the mother.

The meninges refer to the protective tissue layers that surround the brain and spinal cord. These layers, along with the cerebrospinal fluid (CSF), work together to safeguard the central nervous system structures from physical harm and provide support for the blood vessels in the brain and skull.

The meninges consist of three distinct layers: the outermost layer called the dura mater, the middle layer known as the arachnoid mater, and the innermost layer called the pia mater.

There are three types of hemorrhage that involve the meninges. The first is extradural (or epidural) hemorrhage, which occurs when blood accumulates between the dura mater and the skull. The second is subdural hemorrhage, where blood gathers between the dura mater and the arachnoid mater. Lastly, subarachnoid hemorrhage happens when blood collects in the subarachnoid space, which is the area between the arachnoid mater and the pia mater.

Pyloric stenosis, a condition characterized by narrowing of the pylorus (the opening between the stomach and small intestine), often leads to an electrolyte imbalance. This imbalance typically presents as hypochloremia (low chloride levels), hypokalemia (low potassium levels), and metabolic alkalosis (an increase in blood pH). To confirm the diagnosis, it is recommended to perform U&Es (tests to measure electrolyte levels) and a venous blood gas analysis. The electrolyte abnormalities observed in pyloric stenosis are primarily caused by the loss of hydrogen and chloride ions through vomiting. While urine is usually alkaline in this condition, severe dehydration can lead to paradoxical aciduria, where hydrogen ions are preferentially secreted instead of potassium ions to prevent further decrease in potassium levels.

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.

Mandibular fractures are quite common, especially among young men. The most common cause of these fractures is assault, but they can also occur due to sporting injuries, motor vehicle accidents, and falls. The mandible and skull together form a complete bony ring, with the only interruption being the temporomandibular joints (TMJs). While it is expected that mandibular fractures would occur in two places, sometimes they only occur in one location. The most frequently affected areas are the angle of the mandible (27%), mandibular symphysis (21%), mandibular condylar and subcondylar (18%), body of the mandible (15%), ramus of the mandible (5%), coronoid process (1-3%), and alveolar ridge (2%).

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

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

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

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

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

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

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

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

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

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)

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

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

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

The post-cardiac arrest syndrome consists of four components. The first component is post-cardiac arrest brain injury, which refers to any damage or impairment to the brain that occurs after a cardiac arrest. The second component is post-cardiac arrest myocardial dysfunction, which is a condition where the heart muscle does not function properly after a 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.

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.

An Addisonian crisis is characterized by several distinct features. These include experiencing pain in the legs and abdomen, as well as symptoms of vomiting and dehydration. Hypotension, or low blood pressure, is also commonly observed during an Addisonian crisis. Confusion and psychosis may also occur, along with the presence of a fever. In some cases, convulsions may be present as well. Additionally, individuals experiencing an Addisonian crisis may also exhibit hypoglycemia, hyponatremia, hyperkalemia, hypercalcemia, eosinophilia, and metabolic acidosis.

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

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

Further Reading:

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

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

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

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

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

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.

Thiopental sodium is a barbiturate with a very short duration of action. It is primarily used to induce anesthesia. Barbiturates are believed to primarily affect synapses by reducing the sensitivity of postsynaptic receptors to neurotransmitters and by interfering with the release of neurotransmitters from presynaptic neurons.

Thiopental sodium specifically binds to a unique site associated with a chloride ionophore at the GABAA receptor, which is responsible for the opening of chloride ion channels. This binding increases the length of time that the chloride ionophore remains open. As a result, the inhibitory effect of GABA on postsynaptic neurons in the thalamus is prolonged.

In summary, thiopental sodium acts as a short-acting barbiturate that is commonly used to induce anesthesia. It affects synapses by reducing postsynaptic receptor sensitivity and interfering with neurotransmitter release. By binding to a specific site at the GABAA receptor, thiopental sodium prolongs the inhibitory effect of GABA in the thalamus.

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

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

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

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

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

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

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

The most frequent cause of atraumatic TMJ dislocation is yawning. Individuals with connective tissue disorders like Marfan’s and Ehlers-Danlos syndromes have a higher susceptibility to atraumatic dislocation.

Further Reading:

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

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

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

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

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

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

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

Lown-Ganong-Levine (LGL) syndrome is a condition that affects the electrical conducting system of the heart. It is classified as a pre-excitation syndrome, similar to the more well-known Wolff-Parkinson-White (WPW) syndrome. However, unlike WPW syndrome, LGL syndrome does not involve an accessory pathway for conduction. Instead, it is believed that there may be accessory fibers present that bypass all or part of the atrioventricular node.

When looking at an electrocardiogram (ECG) of a patient with LGL syndrome in sinus rhythm, there are several characteristic features to observe. The PR interval, which represents the time it takes for the electrical signal to travel from the atria to the ventricles, is typically shortened and measures less than 120 milliseconds. The QRS duration, which represents the time it takes for the ventricles to contract, is normal. The P wave, which represents the electrical activity of the atria, may be normal or inverted. However, what distinguishes LGL syndrome from other pre-excitation syndromes is the absence of a delta wave, which is a slurring of the initial rise in the QRS complex.

It is important to note that LGL syndrome predisposes individuals to paroxysmal supraventricular tachycardia (SVT), a rapid heart rhythm that originates above the ventricles. However, it does not increase the risk of developing atrial fibrillation or flutter, which are other types of abnormal heart rhythms.

NICE has emphasized that there are particular symptoms and indications that may indicate specific diseases as the underlying cause of a fever. In the case of herpes simplex encephalitis, the following symptoms and signs may suggest its presence: the presence of a focal neurological sign, focal seizures, and a decreased level of consciousness. For more information on this topic, you may refer to the NICE guidelines on the assessment and initial management of fever in children under the age of 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

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.

The patient is showing signs of pancytopenia along with a fever, indicating a likely case of neutropenic sepsis. Their blood test results reveal microcytic anemia, leucopenia (with significant neutropenia), and thrombocytopenia. Neutropenic sepsis is a serious condition that can be life-threatening, characterized by a low neutrophil count. There are several potential causes of neutropenia, including cytotoxic chemotherapy, immunosuppressive drugs, stem cell transplantation, infections, bone marrow disorders like aplastic anemia and myelodysplastic syndromes, and nutritional deficiencies.

To diagnose neutropenic sepsis in patients undergoing anticancer treatment, their neutrophil count should be 0.5 x 109 per liter or lower, and they should have either a temperature above 38°C or other signs and symptoms indicative of clinically significant sepsis. According to the current NICE guidelines, initial empiric antibiotic therapy for suspected neutropenic sepsis should involve monotherapy with piperacillin with tazobactam (Tazocin 4.5 g IV). It is not recommended to use an aminoglycoside, either alone or in combination therapy, unless there are specific patient-related or local microbiological reasons to do so.

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

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

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

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

This patient has come in with worsening breathlessness and coughing, along with coughing up blood, all of which are occurring on top of their existing lung cancer. The diagnosis in this case is superior vena cava obstruction, which is being caused by the primary bronchial neoplasm.

The typical clinical presentation of superior vena cava obstruction includes breathlessness and coughing, chest pain, swelling in the neck, face, and arms, dilated veins and telangiectasia on the arms, neck, and chest wall, facial flushing, stridor due to laryngeal edema, and cyanosis.

Given the urgency of the situation, this man will require immediate treatment. Upon initial presentation, it is important to elevate his head and provide supplemental oxygen to alleviate symptoms. Additionally, corticosteroids and diuretics may be administered. Further investigation will be necessary through CT scanning, and radiotherapy may be recommended as a potential course of action.

In the UK, peptic ulcer disease is the leading cause of upper gastrointestinal bleeding. It surpasses all other listed causes combined in terms of prevalence.

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 most probable diagnosis in this case is anterior uveitis, which refers to inflammation of the iris. It typically presents with symptoms such as a painful and red eye, sensitivity to light, excessive tearing, and decreased visual clarity. The photo above shows a possible indication of this condition, with the presence of pus in the front chamber of the eye, known as hypopyon.

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

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

The ‘B’ symptoms associated with Hodgkin’s lymphoma include fever, night sweats, and weight loss. Fever is defined as a body temperature exceeding 38 degrees Celsius. Night sweats refer to excessive sweating during sleep. Weight loss is considered significant if it amounts to more than 10% of a person’s body weight over a period of six months. It is important to note that pain after consuming alcohol is a distinctive sign of Hodgkin’s lymphoma, but it is not classified as a ‘B’ symptom. This symptom is relatively rare, occurring in only 2-3% of individuals diagnosed with Hodgkin’s lymphoma.

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

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

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

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

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

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

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

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

Further Reading:

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

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

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

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

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

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

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.

This patient has developed Wernicke’s encephalopathy, a condition that is associated with alcohol abuse and other causes of thiamine deficiency. It is important to note that the infusion of glucose-containing intravenous fluids without thiamine in a patient with chronic thiamine deficiency can trigger Wernicke’s encephalopathy. In this particular case, it seems that this is what has occurred.

Wernicke’s encephalopathy is typically characterized by a triad of symptoms, which include acute confusion, ophthalmoplegia, and ataxia. Additionally, other possible features of this condition may include papilloedema, hearing loss, apathy, dysphagia, memory impairment, and hypothermia. It is also common for peripheral neuropathy, primarily affecting the legs, to occur in the majority of cases.

This condition is characterized by the presence of acute capillary haemorrhages, astrocytosis, and neuronal death in the upper brainstem and diencephalon. These abnormalities can be visualized through MRI scanning, although CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will go on to develop a Korsakoff psychosis. This condition is characterized by retrograde amnesia, an inability to form new memories, disordered time perception, and confabulation.

Patients who are suspected to have Wernicke’s encephalopathy should be promptly treated with parenteral thiamine (such as Pabrinex) for a minimum of 5 days. Following the parenteral therapy, oral thiamine should be administered.

Metastatic spinal cord compression (MSCC) occurs when a tumor mass compresses the thecal sac and its components, leading to a spinal emergency. If the pressure on the spinal cord is not relieved promptly, it can result in irreversible loss of neurological function. The most crucial factor for predicting functional outcomes is the patient’s neurological function before treatment. Therefore, delayed treatment can lead to permanent disability and a decrease in quality of life.

The most common cancers that cause MSCC include prostate, lung, breast, and myeloma. In approximately 10 to 20% of cancer patients, MSCC is the first noticeable symptom. It is important to consider MSCC in any patient with a history of cancer if they experience any of the following symptoms: severe or worsening lower back pain, nocturnal pain that disrupts sleep, localized spinal tenderness, radicular pain, or neurological symptoms.

Thoracic pain can also be an indicator of MSCC or an aortic aneurysm. In patients aged 60 or older with persistent back pain, myeloma should be considered. For patients aged 60 or older with accompanying weight loss, pancreatic cancer should be taken into consideration.

Iodine deficiency is a widespread issue globally and is the leading cause of hypothyroidism worldwide. It is particularly prevalent in numerous African countries, as well as in developed nations such as Norway, Germany, Russia, and Ukraine. In the UK, however, autoimmune thyroiditis is the most common cause of hypothyroidism.

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.

Fluid deficit in children and young people with severe diabetic ketoacidosis (DKA) is determined by measuring their blood pH and bicarbonate levels. If the blood pH is below 7.1 and/or the bicarbonate level is below 5, it indicates a fluid deficit. This simplified explanation uses a cutoff value of 5 to determine the severity of the fluid deficit in DKA.

Further Reading:

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

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

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

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

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

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

The clinical frailty score is a tool used to evaluate frailty and determine the level of safety for a patient’s discharge from the hospital. A higher CFS score indicates a greater likelihood of an extended hospital stay, increased need for support after discharge, and higher risk of mortality. In the case of this patient with terminal cancer and a life expectancy of less than 6 months, they would be classified as having the highest possible frailty score.

Further Reading:

Falls are a common occurrence in the elderly population, with a significant number of individuals over the age of 65 experiencing at least one fall per year. These falls are often the result of various risk factors, including impaired balance, muscle weakness, visual impairment, cognitive impairment, depression, alcohol misuse, polypharmacy, and environmental hazards. The more risk factors a person has, the higher their risk of falling.

Falls can have serious complications, particularly in older individuals. They are a leading cause of injury, injury-related disability, and death in this population. Approximately 50% of falls in the elderly result in major lacerations, traumatic brain injuries, or fractures. About 5% of falls in older people living in the community lead to hospitalization or fractures. Hip fractures, in particular, are commonly caused by falls and have a high mortality rate within one year.

Complications of falls include fractures, soft tissue injuries, fragility fractures, distress, pain, loss of self-confidence, reduced quality of life, loss of independence, fear of falls and activity avoidance, social isolation, increasing frailty, functional decline, depression, and institutionalization. Additionally, individuals who remain on the floor for more than one hour after a fall are at risk of dehydration, pressure sores, pneumonia, hypothermia, and rhabdomyolysis.

Assessing falls requires a comprehensive history, including the course of events leading up to the fall, any pre-fall symptoms, and details about the fall itself. A thorough examination is also necessary, including an assessment of injuries, neurological and cardiovascular function, tests for underlying causes, vision assessment, and medication review. Home hazard assessments and frailty assessments are also important components of the assessment process.

Determining the frailty of older patients is crucial in deciding if they can be safely discharged and what level of care they require. The clinical Frailty Scale (CFS or Rockwood score) is commonly used for this purpose. It helps healthcare professionals evaluate the overall frailty of a patient and make appropriate care decisions.

In summary, falls are a significant concern in the elderly population, with multiple risk factors contributing to their occurrence. These falls can lead to serious complications and have a negative impact on an individual’s quality of life. Assessing falls requires a comprehensive approach, including a thorough history, examination, and consideration of frailty.