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

Further Reading:

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

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

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

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

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

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

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

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

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

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

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

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

This patient is displaying symptoms that are characteristic of normal-pressure hydrocephalus (NPH). NPH is a type of communicating hydrocephalus where the pressure inside the skull, as measured through lumbar puncture, is either normal or occasionally elevated. It primarily affects elderly individuals, and the likelihood of developing NPH increases with age.

Around 50% of NPH cases are idiopathic, meaning that no clear cause can be identified. The remaining cases are secondary to various conditions such as head injury, meningitis, subarachnoid hemorrhage, central nervous system tumors, and radiotherapy.

The typical presentation of NPH includes a classic triad of symptoms: gait disturbance (often characterized by a broad-based and shuffling gait), sphincter disturbance leading to incontinence (usually urinary incontinence), and progressive dementia with memory loss, inattention, inertia, and bradyphrenia.

Diagnosing NPH primarily relies on identifying the classic clinical triad mentioned above. Additional investigations can provide supportive evidence and may involve CT and MRI scans, which reveal enlarged ventricles and periventricular lucency. Lumbar puncture can also be performed to assess cerebrospinal fluid (CSF) levels, which are typically normal or intermittently elevated. Intraventricular monitoring may show beta waves present for more than 5% of a 24-hour period.

NPH is one of the few reversible causes of dementia, making early recognition and treatment crucial. Medical treatment options include the use of carbonic anhydrase inhibitors (such as acetazolamide) and repeated lumbar punctures as temporary measures. However, the definitive treatment for NPH involves surgically inserting a cerebrospinal fluid (CSF) shunt. This procedure provides lasting clinical benefits for 70% to 90% of patients compared to their pre-operative state.

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

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

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

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

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

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

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

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

An Addisonian crisis can be triggered by the intentional or accidental withdrawal of steroid therapy, as well as factors such as infection, trauma, myocardial infarction, cerebral infarction, asthma, hypothermia, and alcohol abuse.

The clinical features of Addison’s disease include weakness, lethargy, hypotension (especially orthostatic hypotension), nausea, vomiting, weight loss, reduced axillary and pubic hair, depression, and hyperpigmentation in areas such as palmar creases, buccal mucosa, and exposed skin.

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

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

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

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

Further Reading:

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

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

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

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

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

An overdose of aspirin often leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the stimulation of the respiratory center causes hyperventilation and results in respiratory alkalosis. However, as the overdose progresses, the direct acidic effects of aspirin cause an increase in the anion gap and metabolic acidosis.

Here is a summary of common causes for different acid-base disorders:

Respiratory alkalosis can be caused by hyperventilation due to factors such as anxiety, pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, and the early stages of aspirin overdose.

Respiratory acidosis can occur in individuals with chronic obstructive pulmonary disease (COPD), life-threatening asthma, pulmonary edema, sedative drug overdose (such as opioids or benzodiazepines), neuromuscular diseases, and obesity.

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

Metabolic acidosis with a raised anion gap can result from conditions such as lactic acidosis (caused by factors like hypoxemia, shock, sepsis, or tissue infarction), ketoacidosis (associated with diabetes, starvation, or excessive alcohol consumption), renal failure, and poisoning (including the late stages of aspirin overdose, methanol or ethylene glycol ingestion).

Metabolic acidosis with a normal anion gap can be seen in renal tubular acidosis, diarrhea, ammonium chloride ingestion, and adrenal insufficiency.

Clostridium difficile is a type of bacteria that is Gram-positive, anaerobic, and capable of forming spores. It is found in the intestines of about 3% of healthy adults, according to estimates from the UK Health Protection Agency in 2012.

Clostridium difficile associated diarrhea (CDAD) often occurs after the use of broad-spectrum antibiotics, which disrupt the normal bacteria in the gut and allow Clostridium difficile to multiply. This leads to inflammation and bleeding in the lining of the large intestine, resulting in a distinct pseudomembranous appearance. The majority of Clostridium difficile infections are reported in individuals over the age of 65.

The main symptoms of CDAD include abdominal cramps, severe bloody and/or watery diarrhea, offensive-smelling diarrhea, and fever.

The gold standard for diagnosing Clostridium difficile colitis is a cytotoxin assay. However, this test can be challenging to perform and results may take up to 48 hours to obtain. The most commonly used laboratory test for diagnosing Clostridium difficile colitis is an enzyme-mediated immunoassay that detects toxins A and B. This test has a specificity of 93-100% and a sensitivity of 63-99%.

In some cases, patients may develop a condition called toxic megacolon, which can be life-threatening, especially in frail or elderly individuals.

The current recommended first-line treatment for CDAD is oral vancomycin. For more information, refer to the guidance provided by the National Institute for Health and Care Excellence (NICE) regarding the risk of Clostridium difficile infection associated with the use of broad-spectrum antibiotics.

Women who are 18 years or older and have a pelvic mass that is not clearly uterine fibroids should be promptly referred for assessment. In this case, an abdominal X-ray would not provide much useful information, and it is not advisable to take no action at this point. For more information, please refer to the NICE referral guidelines for suspected cancer.

For the treatment of men with lower urinary tract infection (UTI), it is recommended to offer an immediate prescription of antibiotics. However, certain factors should be taken into account. This includes considering previous urine culture and susceptibility results, as well as any history of antibiotic use that may have led to the development of resistant bacteria.

Before starting antibiotics, it is important to obtain a midstream urine sample from men and send it for culture and susceptibility testing. This will help determine the most appropriate choice of antibiotic.

Once the microbiological results are available, it is necessary to review the initial choice of antibiotic. If the bacteria are found to be resistant and symptoms are not improving, it is recommended to switch to a narrow-spectrum antibiotic whenever possible.

The first-choice antibiotics for men with lower UTI are trimethoprim 200 mg taken orally twice daily for 7 days, or nitrofurantoin 100 mg modified-release taken orally twice daily for 7 days if the estimated glomerular filtration rate (eGFR) is above 45 ml/minute.

If there is no improvement in lower UTI symptoms after at least 48 hours on the first-choice antibiotics, or if the first-choice is not suitable, it is important to consider alternative diagnoses and follow the recommendations in the NICE guidelines on pyelonephritis (acute): antimicrobial prescribing or prostatitis (acute): antimicrobial prescribing. The choice of antibiotic should be based on recent culture and susceptibility results.