Meniere’s disease is characterized by recurring episodes of vertigo, tinnitus, and low frequency hearing loss that typically last for a few minutes to a few hours. A patient with Meniere’s disease would be expected to experience these symptoms. During the Weber test, the sound would be heard loudest in the unaffected (contralateral) side. The Romberg test would show a positive result, indicating impaired balance. Additionally, the Fukuda (also known as Unterberger) stepping test would also be positive, suggesting a tendency to veer or lean to one side while walking.

Further Reading:

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

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

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

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

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

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

Heat stroke is a condition characterized by a systemic inflammatory response, where the core body temperature rises above 40.6°C. It is accompanied by alterations in mental state and varying degrees of organ dysfunction.

There are two types of heat stroke. The first is classic non-exertional heat stroke, which occurs when individuals are exposed to high environmental temperatures. This form of heat stroke is commonly seen in elderly patients during heat waves.

The second type is exertional heat stroke, which occurs during intense physical activity in hot weather conditions. This form of heat stroke is often observed in endurance athletes who participate in strenuous exercise in high temperatures.

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

Further Reading:

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

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

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

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

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

This patient is exhibiting the psoas sign, which is a medical indication of irritation in the iliopsoas group of hip flexors located in the abdomen. In this particular case, it is highly likely that the patient has acute appendicitis.

The psoas sign can be observed by extending the patient’s thigh while they are lying on their side with their knees extended, or by asking the patient to actively flex their thigh at the hip. If these movements result in abdominal pain or if the patient resists due to pain, then the psoas sign is considered positive.

The pain occurs because the psoas muscle is adjacent to the peritoneal cavity. When the muscles are stretched or contracted, they rub against the inflamed tissues nearby, causing discomfort. This strongly suggests that the appendix is positioned retrocaecal.

Thiazide diuretics, like bendroflumethiazide and hydrochlorothiazide, have the potential to raise levels of uric acid in the blood, which can worsen gout symptoms in individuals who are susceptible to the condition.

Other medications, such as diuretics, beta-blockers, ACE inhibitors, and non-losartan ARBs, are also linked to an increased risk of gout.

On the other hand, calcium-channel blockers like amlodipine and verapamil, as well as losartan, have been found to lower uric acid levels and are associated with a reduced risk of gout.

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In this particular patient’s case, his history of chronic alcohol abuse, homelessness, and likely impaired nutrition necessitates the administration of intravenous thiamine in the form of Pabrinex. Additionally, a second dose of benzodiazepine should be given, and his blood glucose levels should be urgently checked.

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

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

2nd stage (0-30 minutes):
– Implement regular monitoring
– Consider the possibility of non-epileptic status
– Initiate emergency antiepileptic drug (AED) therapy
– Perform emergency investigations
– Administer glucose (50 ml of 50% solution) and/or intravenous thiamine as Pabrinex if there are indications of alcohol abuse or impaired nutrition
– Treat severe acidosis if present

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

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

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

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

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

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

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

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

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

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

SCUBA divers face the potential danger of developing pulmonary barotrauma, which can lead to conditions like arterial gas embolism (AGE) or pneumothorax. Based on the patient’s diving history and clinical symptoms, it is highly likely that they are experiencing a left-sided pneumothorax caused by barotrauma. To confirm the presence of pneumothorax, a chest X-ray is usually performed, unless the patient shows signs of tension pneumothorax. In such cases, immediate decompression is necessary, which can be achieved by inserting a chest tube.

Further Reading:

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

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

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

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

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

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

Cardiac enzymes do not increase in unstable angina. However, if cardiac markers do rise, it is classified as a non-ST elevation myocardial infarction (NSTEMI). Both unstable angina and NSTEMI can have a normal ECG. An extended ventricular activation time indicates damage to the heart muscle. This occurs because infarcting myocardium conducts electrical impulses at a slower pace, resulting in a prolonged interval between the start of the QRS complex and the apex of the R wave. A positive troponin test indicates the presence of necrosis in cardiac myocytes.

Summary:
Marker | Initial Rise | Peak | Normal at
Creatine kinase | 4-8 hours | 18 hours 2-3 days | CK-MB = main cardiac isoenzyme
Myoglobin | 1-4 hours | 6-7 hours | 24 hours | Low specificity due to skeletal muscle damage
Troponin I | 3-12 hours | 24 hours | 3-10 days | Appears to be the most sensitive and specific
HFABP | 1-2 hours | 5-10 hours | 24 hours | HFABP = heart fatty acid binding protein
LDH | 10 hours | 24-48 hours | 14 days | Cardiac muscle mainly contains LDH

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

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

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

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

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

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

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

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

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

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.

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

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

When a patient is semi-conscious, it is less likely for the nasopharyngeal airway adjuncts (NPA’s) to trigger the gag reflex compared to oropharyngeal airways. Therefore, NPA’s are typically the preferred option in these cases.

Further Reading:

Techniques to keep the airway open:

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

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

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

Airway adjuncts:

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

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

Laryngeal mask airway (LMA):

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

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

Intercostal artery laceration during the insertion of a chest drain is a potentially life-threatening complication. Although rare, it occurs more frequently than other complications mentioned. To minimize the risk of damage to underlying structures and unsightly scarring, the British Thoracic Society (BTS) recommends inserting chest drains within the safe triangle. This triangle is defined by the base of the axilla, the lateral border of the latissimus dorsi, the lateral border of the pectoralis major, and the 5th intercostal space.

Possible complications associated with the insertion of small-bore chest drains include puncture of the intercostal artery, organ perforation due to over-introduction of the dilator into the chest cavity, hospital-acquired pleural infection from non-aseptic techniques, inadequate stay suture leading to the chest tube falling out, and tube blockage, which may be more common with smaller bore Argyle drains.

When using an intercostal approach, it is important to place the chest drain closer to the superior border of the rib below in the intercostal space. This positioning helps avoid injury to the intercostal neurovascular bundle located under the costal groove of the rib above.

For more information, refer to the British Thoracic Society pleural disease guidelines.

During pre-oxygenation, inspired Oxygen primarily works by removing Nitrogen and increasing the presence of Oxygen. Additionally, it helps to optimize the levels of oxygen in the alveolar, arterial, tissue, and venous areas.

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.

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

Further Reading:

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

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

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

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

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

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

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

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

The FeverPAIN score is a scoring system that is recommended by the current NICE guidelines for assessing acute sore throats. It consists of five items: fever in the last 24 hours, purulence, attendance within three days, inflamed tonsils, and no cough or coryza. Based on the score, different recommendations are given regarding the use of antibiotics.

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

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

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

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.

Harmful drinking is when a person consumes at least 35 units of alcohol per week if they are a woman, or at least 50 units per week if they are a man. This level of drinking can lead to negative consequences for their mental and physical health.

Hazardous drinking, also known as increasing risk drinking, refers to a pattern of alcohol consumption that raises the likelihood of harm. For women, this means drinking more than 14 units but less than 35 units per week, while for men it means drinking more than 14 units but less than 50 units per week.

High-risk drinking, or harmful drinking, is a pattern of alcohol consumption that causes mental or physical damage. This occurs when a woman drinks 35 units or more per week, or when a man drinks 50 units or more per week.

Further Reading:

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.

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.

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

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

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

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

Activated charcoal should be given to patients who have ingested paracetamol and meet two criteria: they must present within one hour of ingestion, and they must have taken a dose of paracetamol that is equal to or greater than 150 mg/kg. The recommended dose of activated charcoal is 50g, which is typically administered as 300ml. It is important to note that the dose criteria of 150 mg/kg is based on the amount of paracetamol reported by the patient, not on paracetamol levels, which should not be assessed until at least four hours after ingestion.

Further Reading:

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

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

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

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

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

Dexamethasone is the preferred medication for treating Acute Mountain Sickness (AMS) and High Altitude Cerebral Edema (HACE). In cases of mild AMS, simply halting the ascent and giving the body time to acclimatize may be sufficient. However, if mild AMS persists or worsens, or if the patient experiences moderate to severe AMS, descending to a lower altitude is the most effective treatment, preferably with the addition of supplemental oxygen. Dexamethasone is the recommended medication for managing both AMS and HACE.

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.

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

Further Reading:

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

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

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

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

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

This patient is experiencing an increased heart rate and respiratory rate, as well as a decrease in urine output. Additionally, they are feeling anxious and confused. These symptoms indicate that the patient has suffered a class III haemorrhage at this point in time.

Recognizing the extent of blood loss based on vital signs and mental status abnormalities is a crucial skill. The Advanced Trauma Life Support (ATLS) haemorrhagic shock classification connects the amount of blood loss to expected physiological responses in a healthy 70 kg patient. In a 70 kg male patient, the total circulating blood volume is approximately five liters, which accounts for about 7% of their total body weight.

The ATLS haemorrhagic shock classification is summarized as follows:

CLASS I:
– Blood loss: Up to 750 mL
– Blood loss (% blood volume): Up to 15%
– Pulse rate: Less than 100 bpm
– Systolic BP: 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 BP: 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 BP: 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 BP: Decreased
– Pulse pressure: Decreased
– Respiratory rate: More than 40 breaths per minute
– Urine output: Negligible
– CNS/mental status: Confused, leth

This patient is displaying symptoms consistent with a malabsorption syndrome, which is supported by the findings of subtotal villous atrophy in his small bowel biopsy. Based on this information, the possible causes can be narrowed down to tropical sprue, coeliac disease, and giardiasis.

Considering that the patient was previously healthy before his trip to Nepal, it is unlikely that he has coeliac disease. Additionally, tropical sprue is rare outside of the regions around the equator and is uncommon in Nepal. On the other hand, giardiasis is prevalent in Nepal and is the most probable cause of the patient’s symptoms.

Giardiasis is a chronic diarrheal illness caused by a parasite called Giardia lamblia. Infection occurs when individuals ingest cysts present in contaminated food or water. Common symptoms associated with giardiasis include chronic diarrhea, weakness, abdominal cramps, flatulence, smelly and greasy stools, nausea, vomiting, and weight loss.

Stool culture often yields negative results, so the preferred diagnostic test is a stool ova and parasite (O&P) examination. This test should be repeated three times for accuracy. Additionally, the small bowel biopsy should be re-evaluated to check for the presence of Giardia lamblia.

The standard treatment for giardiasis involves antibiotic therapy with a nitroimidazole antibiotic, such as metronidazole.

Common causes for different acid-base disorders.

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

Respiratory acidosis is often associated with chronic obstructive pulmonary disease (COPD) or life-threatening asthma. It can also occur due to pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or other respiratory conditions.

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

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

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

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 patient weighing 60 kg, the appropriate loading dose would be 300 mg. 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.

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.

Perthes’ disease is a hip disorder that occurs in childhood due to a disruption in the blood supply to the femoral head. This leads to a lack of blood flow, causing the bone to die. The condition typically affects children between the ages of 4 and 10, with boys being more commonly affected than girls. In about 10-15% of cases, there is a family history of the disease, and approximately 15% of patients have the condition in both hips.

The progression of Perthes’ disease can be seen through characteristic changes on X-rays, which can take between 2 and 4 years to fully heal. The earliest sign is an increased density of the epiphysis (the end of the bone) and widening of the medial joint space. As the disease progresses, the epiphysis may fragment and the head of the femur may flatten. Over time, the bone gradually heals, with the dense bone being reabsorbed and replaced by new bone. This process continues until growth stops, and the bone is remodeled.

Children with Perthes’ disease typically present with hip pain and a limp. The pain can vary in severity, and clinical signs may be minor, with only a slight restriction in hip joint movement.

The treatment of Perthes’ disease is a topic of debate. Around 50% of patients can achieve good results with conservative management alone, without the need for surgery. Surgical intervention, such as osteotomy (reshaping the bone), is usually reserved for cases where the disease progresses unfavorably or when conservative treatment fails. Potential complications of Perthes’ disease include permanent hip deformity and secondary arthritis.

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

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

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

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

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

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

The most probable causative organism in this case is Streptococcus pneumoniae. This bacterium is a common cause of acute otitis media, especially in young children. It is known to cause infection in the middle ear, leading to symptoms such as ear pain (otalgia), fever, and a red, bulging tympanic membrane. Other organisms such as Escherichia coli, Candida albicans, Pseudomonas aeruginosa, and Staphylococcus aureus can also cause ear infections, but Streptococcus pneumoniae is the most likely culprit in this particular case.

Further Reading:

Acute otitis media (AOM) is an inflammation in the middle ear accompanied by symptoms and signs of an ear infection. It is commonly seen in young children below 4 years of age, with the highest incidence occurring between 9 to 15 months of age. AOM can be caused by viral or bacterial pathogens, and co-infection with both is common. The most common viral pathogens include respiratory syncytial virus (RSV), rhinovirus, adenovirus, influenza virus, and parainfluenza virus. The most common bacterial pathogens include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pyogenes.

Clinical features of AOM include ear pain (otalgia), fever, a red or cloudy tympanic membrane, and a bulging tympanic membrane with loss of anatomical landmarks. In young children, symptoms may also include crying, grabbing or rubbing the affected ear, restlessness, and poor feeding.

Most children with AOM will recover within 3 days without treatment. Serious complications are rare but can include persistent otitis media with effusion, recurrence of infection, temporary hearing loss, tympanic membrane perforation, labyrinthitis, mastoiditis, meningitis, intracranial abscess, sinus thrombosis, and facial nerve paralysis.

Management of AOM involves determining whether admission to the hospital is necessary based on the severity of systemic infection or suspected acute complications. For patients who do not require admission, regular pain relief with paracetamol or ibuprofen is advised. Decongestants or antihistamines are not recommended. Antibiotics may be offered immediately for patients who are systemically unwell, have symptoms and signs of a more serious illness or condition, or have a high risk of complications. For other patients, a decision needs to be made on the antibiotic strategy, considering the rarity of acute complications and the possible adverse effects of antibiotics. Options include no antibiotic prescription with advice to seek medical help if symptoms worsen rapidly or significantly, a back-up antibiotic prescription to be used if symptoms do not improve within 3 days, or an immediate antibiotic prescription with advice to seek medical advice if symptoms worsen rapidly or significantly.

The first-line antibiotic choice for AOM is a 5-7 day course of amoxicillin. For individuals allergic to or intolerant of penicillin, clarithromycin or erythromycin a 5–7 day course of clarithromycin or erythromycin (erythromycin is preferred in pregnant women).

Aplastic anaemia is a rare and potentially life-threatening condition where the bone marrow fails to produce enough blood cells. This results in a decrease in the number of red blood cells, white blood cells, and platelets in the body, a condition known as pancytopenia. The main cause of aplastic anaemia is damage to the bone marrow and the stem cells that reside there. This damage can be caused by various factors such as autoimmune disorders, certain medications like sulphonamide antibiotics and phenytoin, viral infections like EBV and parvovirus, chemotherapy, radiotherapy, or inherited conditions like Fanconi anaemia. Patients with aplastic anaemia typically experience symptoms such as anaemia, recurrent infections due to a low white blood cell count, and an increased tendency to bleed due to low platelet levels.

Mycoplasma pneumoniae infection does not have a connection with infective endocarditis. However, it is associated with various extra-pulmonary complications. These include skin conditions such as erythema multiforme and Stevens-Johnson syndrome. In the central nervous system, it can lead to Guillain-Barre syndrome, meningitis, encephalitis, optic neuritis, cerebellar ataxia, and cranial nerve palsies. Gastrointestinal symptoms may include anorexia, nausea, diarrhea, hepatitis, and pancreatitis. Hematological complications can manifest as cold agglutinins, hemolytic anemia, thrombocytopenia, and disseminated intravascular coagulation. Mycoplasma pneumoniae infection can also cause pericarditis and myocarditis. Rheumatic symptoms such as arthralgia and arthritides may occur, and acute glomerulonephritis can affect the kidneys.

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

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

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

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

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

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

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.

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

According to NICE guidelines, it is recommended that adults and young people aged 16 years or older who receive emergency treatment for suspected anaphylaxis should be observed for a minimum of 6-12 hours from the time symptoms first appear. There are certain situations where a longer observation period of 12 hours is advised. These include cases where the allergen is still being absorbed slowly, the patient required more than 2 doses of adrenaline, there is severe asthma or respiratory compromise, or if the presentation occurs at night or there is difficulty in accessing emergency care.

Further Reading:

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

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

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

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

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

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

This patient’s physiological parameters are mostly within normal range, but there is an increased pulse pressure and slight anxiety, suggesting a class I haemorrhage. It is crucial to be able to identify the degree of blood loss based on vital signs and mental status changes. The Advanced Trauma Life Support (ATLS) classification for haemorrhagic shock correlates the amount of blood loss with expected physiological responses in a healthy 70 kg individual. In a 70 kg male patient, the total circulating blood volume is approximately five litres, which accounts for about 7% of their total body weight.

The ATLS haemorrhagic shock classification is as follows:

CLASS I:
– Blood loss: Up to 750 mL
– Blood loss (% blood volume): Up to 15%
– Pulse rate: Less than 100 bpm
– Systolic BP: 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 BP: 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 BP: 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: Greater than 140 bpm
– Systolic BP: Decreased
– Pulse pressure: Decreased
– Respiratory rate: More than 40 breaths per minute
– Urine output: Negligible
– CNS/mental status: Confused, lethargic

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

Further Reading:

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

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

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

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

Ipratropium bromide is a medication that falls under the category of antimuscarinic drugs. It is commonly used to manage acute asthma and chronic obstructive pulmonary disease (COPD). While it can provide short-term relief for chronic asthma, it is generally recommended to use short-acting β2 agonists as they act more quickly and are preferred.

According to the guidelines set by the British Thoracic Society (BTS), nebulized ipratropium bromide (0.5 mg every 4-6 hours) can be added to β2 agonist treatment for patients with acute severe or life-threatening asthma, or those who do not respond well to initial β2 agonist therapy.

For mild cases of chronic obstructive pulmonary disease, aerosol inhalation of ipratropium can be used for short-term relief, as long as the patient is not already using a long-acting antimuscarinic drug like tiotropium. The maximum effect of ipratropium occurs within 30-60 minutes after use, and its bronchodilating effects can last for 3-6 hours. Typically, treatment with ipratropium is recommended three times a day to maintain bronchodilation.

The most common side effect of ipratropium bromide is dry mouth. Other potential side effects include constipation, cough, paroxysmal bronchospasm, headache, nausea, and palpitations. It is important to note that ipratropium can cause urinary retention in patients with prostatic hyperplasia and bladder outflow obstruction. Additionally, it can trigger acute closed-angle glaucoma in susceptible patients.

For more information on the management of asthma, it is recommended to refer to the BTS/SIGN Guideline on the Management of Asthma.

Carboxyhaemoglobin (COHb) blood levels are utilized for the identification of carbon monoxide poisoning. COHb is the substance produced when carbon monoxide attaches to haemoglobin. It is important to note that carbaminohemoglobin (also known as carbaminohaemoglobin, carboxyhemoglobin, and carbohemoglobin) is the compound formed when carbon dioxide binds to hemoglobin, and should not be mistaken for COHb.

Further Reading:

Carbon monoxide (CO) is a dangerous gas that is produced by the combustion of hydrocarbon fuels and can be found in certain chemicals. It is colorless and odorless, making it difficult to detect. In England and Wales, there are approximately 60 deaths each year due to accidental CO poisoning.

When inhaled, carbon monoxide binds to haemoglobin in the blood, forming carboxyhaemoglobin (COHb). It has a higher affinity for haemoglobin than oxygen, causing a left-shift in the oxygen dissociation curve and resulting in tissue hypoxia. This means that even though there may be a normal level of oxygen in the blood, it is less readily released to the tissues.

The clinical features of carbon monoxide toxicity can vary depending on the severity of the poisoning. Mild or chronic poisoning may present with symptoms such as headache, nausea, vomiting, vertigo, confusion, and weakness. More severe poisoning can lead to intoxication, personality changes, breathlessness, pink skin and mucosae, hyperpyrexia, arrhythmias, seizures, blurred vision or blindness, deafness, extrapyramidal features, coma, or even death.

To help diagnose domestic carbon monoxide poisoning, there are four key questions that can be asked using the COMA acronym. These questions include asking about co-habitees and co-occupants in the house, whether symptoms improve outside of the house, the maintenance of boilers and cooking appliances, and the presence of a functioning CO alarm.

Typical carboxyhaemoglobin levels can vary depending on whether the individual is a smoker or non-smoker. Non-smokers typically have levels below 3%, while smokers may have levels below 10%. Symptomatic individuals usually have levels between 10-30%, and severe toxicity is indicated by levels above 30%.

When managing carbon monoxide poisoning, the first step is to administer 100% oxygen. Hyperbaric oxygen therapy may be considered for individuals with a COHb concentration of over 20% and additional risk factors such as loss of consciousness, neurological signs, myocardial ischemia or arrhythmia, or pregnancy. Other management strategies may include fluid resuscitation, sodium bicarbonate for metabolic acidosis, and mannitol for cerebral edema.

The NICE recommendations for managing patients with suspected TIA are as follows:

– Offer aspirin (300 mg daily) to individuals who have experienced a suspected TIA, unless there are contraindications. This treatment should be started immediately.
– Immediately refer individuals who have had a suspected TIA for specialist assessment and investigation. They should be seen within 24 hours of the onset of symptoms.
– Avoid using scoring systems, such as ABCD2, to assess the risk of subsequent stroke or determine the urgency of referral for individuals with suspected or confirmed TIA.
– Provide secondary prevention measures, in addition to aspirin, as soon as possible after confirming the diagnosis of TIA.

The NICE recommendations for imaging in individuals with suspected TIA or acute non-disabling stroke are as follows:

– Do not offer CT brain scanning to individuals with suspected TIA, unless there is clinical suspicion of an alternative diagnosis that CT could detect.
– After a specialist assessment in the TIA clinic, consider performing an MRI (including diffusion-weighted and blood-sensitive sequences) to determine the area of ischemia, detect hemorrhage, or identify alternative pathologies. If an MRI is conducted, it should be done on the same day as the assessment.
– Carotid imaging is necessary for all individuals with TIA who, after specialist assessment, are considered candidates for carotid endarterectomy. This imaging should be done urgently.

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

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, and they are often caused by 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 for 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 approach for 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 cases where the fissure does not heal with conservative measures. It has a success rate of 90%.

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. 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 unaffected due to its direct arterial supply, there have been rare cases where it is also involved.

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, and loss of pubic and axillary hair. Additionally, secondary hypothyroidism and adrenal insufficiency may also occur.

Serum prolactin levels are typically low, measuring less than 5ng/ml. An MRI can be helpful in ruling out other pituitary issues, such as a pituitary tumor.

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

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.

If you are a woman under the age of 55 and experiencing postmenopausal bleeding, it is important to seek medical attention promptly. One possible cause of this symptom could be endometrial cancer. To ensure timely diagnosis and treatment, it is recommended to follow the suspected cancer pathway referral guidelines provided by NICE. These guidelines aim to facilitate recognition and referral of suspected cancer cases. By adhering to these guidelines, you can increase the likelihood of securing an appointment for further evaluation within two weeks. to the NICE referral guidelines on recognition and referral of suspected cancer.

Acute diverticulitis occurs when a diverticulum becomes inflamed or perforated. This inflammation can either stay localized, forming a pericolic abscess, or spread and cause peritonitis. The typical symptoms of acute diverticulitis include abdominal pain (most commonly felt in the lower left quadrant), fever/sepsis, tenderness in the left iliac fossa, the presence of a mass in the left iliac fossa, and rectal bleeding. About 90% of cases involve the sigmoid colon, which is why left iliac fossa pain and tenderness are commonly seen.

To diagnose acute diverticulitis, various investigations should be conducted. These include blood tests such as a full blood count, urea and electrolytes, C-reactive protein, and blood cultures. Imaging studies like abdominal X-ray, erect chest X-ray, and possibly an abdominal CT scan may also be necessary.

Complications that can arise from acute diverticulitis include perforation leading to abscess formation or peritonitis, intestinal obstruction, massive rectal bleeding, fistulae, and strictures.

In the emergency department, the treatment for diverticulitis should involve providing suitable pain relief, administering intravenous fluids, prescribing broad-spectrum antibiotics (such as intravenous co-amoxiclav), and advising the patient to refrain from eating or drinking. It is also important to refer the patient to the on-call surgical team for further management.

For more information on diverticular disease, you can refer to the NICE Clinical Knowledge Summary.

The prolonged use of nitrous oxide (Entonox) in patients with sepsis may have a negative impact on DNA synthesis, and it is not recommended to use it in this situation. However, sepsis itself does not prevent the use of nitrous oxide.

There are several conditions that make the use of nitrous oxide inappropriate. These include a reduced level of consciousness, diving injuries, pneumothorax, middle ear disease, sinus disease, bowel obstruction, a documented allergy to nitrous oxide, hypoxia, and violent or disabled psychiatric patients.

It is important to note that the use of nitrous oxide should be avoided in patients with sepsis due to its potential effects on DNA synthesis. However, there are other contraindications to its use that should be considered in different clinical scenarios.

Bladder cancer is the most likely diagnosis considering the patient’s history of smoking and working in a rubber factory, as these are well-known risk factors for developing this condition. It affects approximately 1 in 5000 people and is more common in men, with a threefold higher incidence compared to women. Transitional cell carcinomas account for 90% of bladder cancer cases.

The risk factors for bladder cancer include smoking, which is responsible for 50% of male and 25% of female cases. Exposure to aromatic amine, such as working in rubber, leather, or textile factories, is also a known risk factor. Other factors include urinary stasis and schistosomiasis.

Bladder cancer can present with either visible or microscopic blood in the urine (haematuria). It may be painless or accompanied by pelvic or loin pain, as well as symptoms of recurrent urinary tract infections. A midstream urine sample (MSU) can be helpful in ruling out a urinary tract infection and detecting microscopic haematuria.

If bladder cancer is suspected, it is important to refer the patient urgently. Diagnosis is typically confirmed through biopsies taken during cystoscopy. At the time of diagnosis, 80% of tumours are confined to the mucosa or submucosa (stage T1). Treatment involves transurethral resection of the tumour (TURBT) with intravesical chemotherapy. The prognosis at this stage is excellent, with most patients dying from other causes.

The recommended diagnostic tests for Cushing’s syndrome include the 24-hour urinary free cortisol test, the 1 mg overnight dexamethasone suppression test, and the late-night salivary cortisol test. In this case, the patient exhibits symptoms of Cushing syndrome such as a moon face, abdominal striae, and hirsutism. These symptoms may be caused by Cushing’s disease, which is Cushing syndrome due to a pituitary adenoma. The patient also experiences headaches and visual disturbances, which could potentially be caused by high blood sugar levels. It is important to note that Cushing syndrome caused by an adrenal or pituitary tumor is more common in females, with a ratio of 5:1. The peak incidence of Cushing syndrome caused by an adrenal or pituitary adenoma occurs between the ages of 25 and 40 years.

Further Reading:

Cushing’s syndrome is a clinical syndrome caused by prolonged exposure to high levels of glucocorticoids. The severity of symptoms can vary depending on the level of steroid exposure. There are two main classifications of Cushing’s syndrome: ACTH-dependent disease and non-ACTH-dependent disease. ACTH-dependent disease is caused by excessive ACTH production from the pituitary gland or ACTH-secreting tumors, which stimulate excessive cortisol production. Non-ACTH-dependent disease is characterized by excess glucocorticoid production independent of ACTH stimulation.

The most common cause of Cushing’s syndrome is exogenous steroid use. Pituitary adenoma is the second most common cause and the most common endogenous cause. Cushing’s disease refers specifically to Cushing’s syndrome caused by an ACTH-producing pituitary tumor.

Clinical features of Cushing’s syndrome include truncal obesity, supraclavicular fat pads, buffalo hump, weight gain, moon facies, muscle wasting and weakness, diabetes or impaired glucose tolerance, gonadal dysfunction, hypertension, nephrolithiasis, skin changes (such as skin atrophy, striae, easy bruising, hirsutism, acne, and hyperpigmentation in ACTH-dependent causes), depression and emotional lability, osteopenia or osteoporosis, edema, irregular menstrual cycles or amenorrhea, polydipsia and polyuria, poor wound healing, and signs related to the underlying cause, such as headaches and visual problems.

Diagnostic tests for Cushing’s syndrome include 24-hour urinary free cortisol, 1 mg overnight dexamethasone suppression test, and late-night salivary cortisol. Other investigations aim to assess metabolic disturbances and identify the underlying cause, such as plasma ACTH, full blood count (raised white cell count), electrolytes, and arterial blood gas analysis. Imaging, such as CT or MRI of the abdomen, chest, and/or pituitary, may be required to assess suspected adrenal tumors, ectopic ACTH-secreting tumors, and pituitary tumors. The choice of imaging is guided by the ACTH result, with undetectable ACTH and elevated serum cortisol levels indicating ACTH-independent Cushing’s syndrome and raised ACTH suggesting an ACTH-secreting tumor.

Extrapyramidal side effects are most commonly seen with the piperazine phenothiazines (fluphenazine, prochlorperazine, and trifluoperazine) and butyrophenones (benperidol and haloperidol). Among these, haloperidol is the most frequently implicated antipsychotic drug.

Tardive dyskinesia, which involves involuntary rhythmic movements of the tongue, face, and jaw, typically occurs after prolonged treatment or high doses. It is the most severe manifestation of extrapyramidal symptoms, as it may become irreversible even after discontinuing the causative medication, and treatment options are generally ineffective.

Dystonia, characterized by abnormal movements of the face and body, is more commonly observed in children and young adults and tends to appear after only a few doses. Acute dystonia can be managed with intravenous administration of procyclidine (5 mg) or benzatropine (2 mg) as a bolus.

Akathisia refers to an unpleasant sensation of restlessness, while akinesia refers to an inability to initiate movement.

In individuals with renal impairment, there is an increased sensitivity of the brain to antipsychotic drugs, necessitating the use of reduced doses.

Elderly patients with dementia-related psychosis who are treated with haloperidol face an elevated risk of mortality. This is believed to be due to an increased likelihood of cardiovascular events and infections such as pneumonia.

Contraindications for the use of antipsychotic drugs include reduced consciousness or coma, central nervous system depression, and the presence of phaeochromocytoma.

The CURB criteria, also referred to as the CURB-65 criteria, is a clinical prediction rule that has been scientifically proven to predict mortality in cases of community-acquired pneumonia. These criteria consist of five factors: confusion of new onset (AMTS <8), urea level greater than 7 mmol/l, respiratory rate exceeding 30 per minute, blood pressure below 90 mmHg systolic or 60 mmHg diastolic, and age over 65 years. Based on the score obtained from these criteria, the risk level can be determined. A score of 0-1 indicates a low-risk situation, where outpatient treatment is recommended. A score of 2-3 suggests a moderate risk, and either inpatient treatment or an ambulatory care pathway is recommended. A score of 4-5 indicates a high risk, requiring hospitalization and potentially critical care involvement.

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

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

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

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

Ciprofloxacin is known to inhibit the activity of cytochrome P450 enzymes, which can lead to increased levels of theophylline in the blood. Therefore, it is recommended to avoid prescribing ciprofloxacin and theophylline together. For more information on the interactions between these two medications, you can refer to the relevant section on theophylline interactions in the British National Formulary (BNF).

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

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

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

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

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

Écho de la pensée, also known as thought echo, is a psychiatric symptom characterized by the perception of a voice in one’s mind that appears to vocalize thoughts immediately after they are generated.

Thought withdrawal, on the other hand, is a delusional belief where individuals feel that their thoughts have been removed from their own consciousness without their control or consent.

In contrast, thought insertion is a delusional conviction that someone else is influencing or manipulating their thoughts, causing difficulty in distinguishing between their own thoughts and those that have been inserted by another person.

Folie à deux, also referred to as induced psychosis, is a specific type of delusional disorder that is shared by two or more individuals who have a close emotional relationship.

Lastly, echophonia refers to the replication of the voice that can sometimes be heard when listening to the chest during auscultation.

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

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

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

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

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

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

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

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

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

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

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

Bronchiolitis is a short-term infection of the lower respiratory tract that primarily affects infants aged 2 to 6 months. It is commonly caused by a viral infection, with respiratory syncytial virus (RSV) being the most prevalent culprit. RSV infections are most prevalent during the winter months, typically occurring between November and March. In the UK, bronchiolitis is the leading cause of hospitalization among infants.

The typical symptoms of bronchiolitis include fever, difficulty breathing, coughing, poor feeding, irritability, apnoeas (more common in very young infants), and wheezing or fine inspiratory crackles. To confirm the diagnosis, a nasopharyngeal aspirate can be taken for RSV rapid testing. This test is useful in preventing unnecessary further testing and facilitating the isolation of the affected infant.

Most infants with acute bronchiolitis experience a mild, self-limiting illness that does not require hospitalization. Treatment primarily focuses on supportive measures, such as ensuring adequate fluid and nutritional intake and controlling the infant’s temperature. The illness typically lasts for 7 to 10 days.

However, hospital referral and admission are recommended in certain cases, including poor feeding (less than 50% of usual intake over the past 24 hours), lethargy, a history of apnoea, a respiratory rate exceeding 70 breaths per minute, nasal flaring or grunting, severe chest wall recession, cyanosis, oxygen saturations below 90% for children aged 6 weeks and over, and oxygen saturations below 92% for babies under 6 weeks or those with underlying health conditions.

If hospitalization is necessary, treatment involves supportive measures, supplemental oxygen, and nasogastric feeding as needed. There is limited or no evidence supporting the use of antibiotics, antivirals, bronchodilators, corticosteroids, hypertonic saline, or adrenaline nebulizers in the management of bronchiolitis.

QFracture is a highly regarded tool used to predict the risk of osteoporotic fractures and determine if a DXA bone assessment is necessary. It is considered the preferred and gold standard tool by NICE and SIGN. FRAX is another fracture risk assessment tool that is also used to determine the need for a DXA bone assessment. The Rockwood score and electronic frailty Index (eFI) are both frailty scores. The informant questionnaire on cognitive decline in the elderly is a tool used to assess cognitive decline in older individuals.

Further Reading:

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

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

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

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

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

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

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

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.

Carpal tunnel syndrome is a condition where the median nerve becomes trapped, resulting in nerve damage. This can lead to weakness and abnormal sensations in the areas supplied by the median nerve. To remember the muscles that are innervated by the median nerve, you can use the acronym ‘LOAF’: L for the lateral two lumbricals, O for the Opponens pollicis, A for the Abductor pollicis, and F for the Flexor pollicis brevis. It’s important to note that the abductor digiti minimi is not affected by carpal tunnel syndrome as it is innervated by the deep branch of the ulnar nerve.

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.

The blood gas measurement of pO2 should be equal to or greater than 18 kilopascals (kPa) at a level of 10.

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.

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

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

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

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

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

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

Parkinson’s disease (PD) is a progressive neurodegenerative condition that occurs when the dopamine-containing cells in the substantia nigra die. It is estimated that PD affects around 100-180 individuals per 100,000 of the population, which translates to approximately 6-11 people per 6,000 individuals in the general population of the UK. The annual incidence of PD is between 4-20 cases per 100,000 people. The prevalence of PD increases with age, with approximately 0.5% of individuals aged 65 to 74 being affected and 1-2% of individuals aged 75 and older. Additionally, PD is more prevalent and has a higher incidence in males.

The classic clinical features of Parkinson’s disease include hypokinesia, which refers to a poverty of movement, and bradykinesia, which is characterized by slowness of movement. Rest tremor, typically occurring at a rate of 4-6 cycles per second, is also commonly observed in PD patients. Another clinical feature is rigidity, which is characterized by increased muscle tone and a phenomenon known as cogwheel rigidity.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by the presence of low sodium levels and low osmolality due to the inappropriate and continuous release or action of the hormone, despite normal or increased blood volume. This leads to a decreased ability to excrete water.
There are several factors that can cause SIADH, with carbamazepine being a well-known example. These causes can be grouped into different categories. One category is CNS damage, which includes conditions like meningitis and subarachnoid hemorrhage. Another category is malignancy, with small-cell lung cancer being a common cause. Certain drugs, such as carbamazepine, SSRIs, amitriptyline, and morphine, can also trigger SIADH. Infections, such as pneumonia, lung abscess, and brain abscess, are another potential cause. Lastly, endocrine disorders like hypothyroidism can contribute to the development of SIADH.

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

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

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

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

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

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

Based on his symptoms, the most likely diagnosis is benign paroxysmal positional vertigo. The most suitable initial treatment option for this condition would be the Epley maneuver.

Further Reading:

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

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

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

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.

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

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

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

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

Acute limb ischaemia refers to a sudden reduction in blood flow to a limb, which puts the limb’s viability at risk. This condition is most commonly caused by either a sudden blockage of a previously partially blocked artery due to a blood clot or by an embolus that travels from a distant site. It is considered a surgical emergency, as without prompt surgical intervention, complete acute ischaemia can lead to extensive tissue death within six hours.

The leading cause of acute limb ischaemia is the sudden blockage of a narrowed arterial segment due to a blood clot, accounting for 60% of cases. The second most common cause is an embolism, which makes up 30% of cases. Emboli can originate from various sources, such as a blood clot in the left atrium of patients with atrial fibrillation (which accounts for 80% of peripheral emboli), a clot formed on the heart’s wall following a heart attack, or from prosthetic heart valves. It is crucial to differentiate between these two conditions, as their treatment and prognosis differ.

To properly investigate acute limb ischaemia, several important tests should be arranged. These include a hand-held Doppler ultrasound scan, which can help determine if there is any remaining arterial flow. Blood tests, such as a full blood count, erythrocyte sedimentation rate, blood glucose level, and thrombophilia screen, are also necessary. If there is uncertainty regarding the diagnosis, urgent arteriography should be performed.

In cases where an embolus is suspected as the cause, additional investigations are needed to identify its source. These may include an electrocardiogram to detect atrial fibrillation, an echocardiogram to assess the heart’s function, an ultrasound of the aorta, and ultrasounds of the popliteal and femoral arteries.

By rewriting the explanation and using paragraph spacing, the information is presented in a clearer and more organized manner.

The diagnosis in this case is clearly gout. According to the guidelines from the European League Against Rheumatism (EULAR), the symptoms of acute pain, joint swelling, tenderness, and redness that worsen over a 6-12 hour period strongly suggest crystal arthropathy.

Checking serum urate levels to confirm hyperuricemia before starting treatment for acute gout attacks has little benefit and should not delay treatment. While these levels can be useful for monitoring treatment response, they often decrease during an acute attack and can even be normal. If levels are checked and found to be normal during the attack, they should be rechecked once the attack has resolved.

The first-line treatment for acute gout attacks is non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen. However, caution should be exercised when using NSAIDs in patients with a history of hypertension. Since this patient has had difficulty controlling their blood pressure and remains hypertensive, it would be wise to avoid NSAIDs in this case.

Colchicine is an effective alternative for treating gout, although it may take longer to take effect. It is often used in patients who cannot take NSAIDs due to contraindications such as hypertension or a history of peptic ulcer disease. Therefore, it is the most suitable choice for this patient.

During an acute gout attack, allopurinol should not be used as it can prolong the attack and even trigger another acute episode. However, in patients already taking allopurinol, it should be continued, and the acute attack should be treated with NSAIDs or colchicine as appropriate.

Febuxostat (Uloric) is another option for managing chronic gout, but like allopurinol, it should not be used for acute episodes.

Digoxin-specific antibody fragments, known as Digibind or Digifab, are utilized for the treatment of digoxin toxicity. These antibody fragments should be readily available in all hospital pharmacies across the UK and accessible within a maximum of one hour.

Further Reading:

Digoxin is a medication used for rate control in atrial fibrillation and for improving symptoms in heart failure. It works by decreasing conduction through the atrioventricular node and increasing the force of cardiac muscle contraction. However, digoxin toxicity can occur, and plasma concentration alone does not determine if a patient has developed toxicity. Symptoms of digoxin toxicity include feeling generally unwell, lethargy, nausea and vomiting, anorexia, confusion, yellow-green vision, arrhythmias, and gynaecomastia.

ECG changes seen in digoxin toxicity include downsloping ST depression with a characteristic Salvador Dali sagging appearance, flattened, inverted, or biphasic T waves, shortened QT interval, mild PR interval prolongation, and prominent U waves. There are several precipitating factors for digoxin toxicity, including hypokalaemia, increasing age, renal failure, myocardial ischaemia, electrolyte imbalances, hypoalbuminaemia, hypothermia, hypothyroidism, and certain medications such as amiodarone, quinidine, verapamil, and diltiazem.

Management of digoxin toxicity involves the use of digoxin specific antibody fragments, also known as Digibind or digifab. Arrhythmias should be treated, and electrolyte disturbances should be corrected with close monitoring of potassium levels. It is important to note that digoxin toxicity can be precipitated by hypokalaemia, and toxicity can then lead to hyperkalaemia.

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

Further Reading:

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

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

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

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

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

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

While some individuals with vWD may not experience any symptoms and are diagnosed incidentally during a clotting profile check, others may present with easy bruising, nosebleeds (epistaxis), and heavy menstrual bleeding (menorrhagia). In severe cases, more significant bleeding and joint bleeding (haemarthrosis) can occur.

For mild cases of von Willebrand disease, bleeding can be managed with desmopressin. This medication works by stimulating the release of vWF stored in the Weibel-Palade bodies, which are storage granules found in the endothelial cells lining the blood vessels and heart. By increasing the patient’s own levels of vWF, desmopressin helps improve clotting. In more severe cases, replacement therapy is necessary. This involves infusing cryoprecipitate or Factor VIII concentrate to provide the missing vWF. Replacement therapy is particularly recommended for patients with severe von Willebrand’s disease who are undergoing moderate or major surgical procedures.

The count of lymphocytes, a type of white blood cell, can serve as an early indication of the level of radiation exposure. The severity of the exposure can be determined by observing the decrease in lymphocyte count, which is directly related to the amount of radiation absorbed by the body. Ideally, the count is measured 12 hours after exposure and then repeated every 4 hours initially to track the rate of decrease.

Further Reading:

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

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

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

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

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

Neutropenic sepsis is a serious condition that can occur when a person has low levels of neutrophils, which are a type of white blood cell. This condition can be life-threatening and is often caused by factors such as chemotherapy, immunosuppressive drugs, infections, and bone marrow disorders. Mortality rates can be as high as 20% in adults.

To diagnose neutropenic sepsis, doctors look for a neutrophil count of 0.5 x 109 per litre or lower in patients undergoing cancer treatment. Additionally, if a patient has a temperature higher than 38°C or other signs of significant sepsis, they may be diagnosed with neutropenic sepsis.

Cancer treatments, particularly chemotherapy, can weaken the bone marrow ability to fight off infections, making patients more susceptible to neutropenic sepsis. This risk can also be present with radiotherapy.

According to the current guidelines from the National Institute for Health and Care Excellence (NICE), adult patients with acute leukemia, stem cell transplants, or solid tumors should be offered prophylaxis with a fluoroquinolone antibiotic during periods of expected neutropenia.

When managing neutropenic sepsis, it is important to follow the UK Sepsis Trust Sepsis Six bundle, which includes specific actions to be taken within the first hour of recognizing sepsis.

For initial empiric antibiotic therapy in suspected cases of neutropenic sepsis, the NICE guidelines recommend using piperacillin with tazobactam as monotherapy. Aminoglycosides should not be used unless there are specific patient or local microbiological indications.

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

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

Thought echo is a phenomenon where a patient perceives their own thoughts as if they are being spoken out loud. When there is a slight delay in this perception, it is referred to as echo de la pensée. On the other hand, when the thoughts are heard simultaneously, it is known as Gedankenlautwerden.

This patient’s ECG shows signs consistent with hyperkalemia, including broad QRS complexes, tall-peaked T waves, and bizarre p waves. It is estimated that around 10% of patients with SLE have hyperkalemia, which is believed to be caused by hyporeninemic hypoaldosteronism. Additionally, the patient has been taking a high dose of ibuprofen, which can also contribute to the development of hyperkalemia. NSAIDs are thought to induce hyperkalemia by reducing renin secretion, leading to decreased potassium excretion.

Vascular dementia is not as common as Alzheimer’s disease, accounting for about 20% of dementia cases compared to 50% for Alzheimer’s. Most individuals with vascular dementia have a history of atherosclerotic cardiovascular disease and/or hypertension.

There are notable differences in how these two diseases present themselves. Vascular dementia often has a sudden onset, while Alzheimer’s disease has a slower onset. The progression of vascular dementia tends to be stepwise, with periods of stability followed by sudden declines, whereas Alzheimer’s disease has a more gradual decline. The course of vascular dementia can also fluctuate, while Alzheimer’s disease shows a steady decline over time.

In terms of personality and insight, individuals with vascular dementia tend to have relatively preserved personality and insight in the early stages, whereas those with Alzheimer’s disease may experience early changes and loss in these areas. Gait is also affected differently, with individuals with vascular dementia taking small steps (known as marche a petit pas), while those with Alzheimer’s disease have a normal gait.

Sleep disturbance is less common in vascular dementia compared to Alzheimer’s disease, which commonly presents with sleep disturbances. Focal neurological signs, such as sensory and motor deficits and pseudobulbar palsy, are more common in vascular dementia, while they are uncommon in Alzheimer’s disease.

To differentiate between Alzheimer’s disease and vascular dementia, the modified Hachinski ischemia scale can be used. This scale assigns scores based on various features, such as abrupt onset, stepwise deterioration, fluctuating course, nocturnal confusion, preservation of personality, depression, somatic complaints, emotional incontinence, history of hypertension, history of strokes, evidence of associated atherosclerosis, focal neurological symptoms, and focal neurological signs. A score of 2 or greater suggests vascular dementia.

Overall, understanding the differences in presentation and using tools like the modified Hachinski ischemia scale can help in distinguishing between Alzheimer’s disease and vascular dementia.

Subfalcine herniation occurs when a mass in one side of the brain causes the cingulate gyrus to be pushed under the falx cerebri. This condition often leads to specific neurological symptoms. These symptoms include a motor deficit in the lower limb on the opposite side of the body, bladder incontinence, motor and sensory deficits on the same side of the body as the herniation, and difficulty with speech (dysarthria).

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.