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

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

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

This patient is clearly experiencing pyelonephritis with systemic involvement, which may indicate sepsis. According to NICE guidelines, it is recommended to admit individuals to the hospital if they exhibit any symptoms or signs that suggest a more serious illness or condition, such as sepsis. In cases of acute pyelonephritis, it is advisable to consider referring or seeking specialist advice for individuals who are significantly dehydrated or unable to consume oral fluids and medications, pregnant women, those at a higher risk of developing complications (e.g., individuals with known or suspected structural or functional abnormalities of the genitourinary tract or underlying diseases like diabetes mellitus or immunosuppression), and individuals who have recurrent episodes of urinary tract infections (e.g., two or more episodes within a 6-month period). Additionally, it is recommended to consider referral for men who have experienced a single episode without an obvious cause and women with recurrent pyelonephritis. For more information, please refer to the NICE Clinical Knowledge Summary on the management of acute pyelonephritis.

The intravascular volume of an infant is approximately 80 ml/kg. As children get older, their intravascular volume decreases to around 70 ml/kg. Dehydration itself does not lead to death, but it can cause shock. Shock can occur when there is a loss of 20 ml/kg from the intravascular space. Clinical dehydration, on the other hand, is only noticeable after total losses greater than 25 ml/kg.

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

Bodyweight:
– First 10 kg: Daily fluid requirement 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

For a well and normal child weighing less than 10 kg, their daily maintenance fluid requirement would be 800 ml/day.

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

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

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

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.

A phaeochromocytoma is a rare functional tumor that develops from chromaffin cells in the adrenal medulla. Extra-adrenal paragangliomas, also known as extra-adrenal pheochromocytomas, are similar tumors that originate in the ganglia of the sympathetic nervous system but are less common. These tumors secrete catecholamines and cause a range of symptoms and signs related to hyperactivity of the sympathetic nervous system.

The most common initial symptom is high blood pressure, which can be either sustained or sporadic. Symptoms tend to come and go, occurring multiple times a day or very infrequently. As the disease progresses, the symptoms usually become more severe and frequent.

Surgical removal is the preferred and definitive treatment option. If the tumor is completely removed without any spread to other parts of the body, it often leads to a cure for hypertension.

Before surgery, it is crucial to manage the condition medically to reduce the risk of hypertensive crises during the operation. This is typically done by using a combination of non-competitive alpha-blockers (such as phenoxybenzamine) and beta-blockers. Alpha-blockade should be started first, at least 7-10 days before the surgery, to allow for expansion of blood volume. Once this is achieved, beta-blockade can be initiated to help control rapid heart rate and certain irregular heart rhythms. Starting beta-blockade too early can trigger a hypertensive crisis.

Genetic counseling should also be provided, and any associated conditions should be identified and managed appropriately.

When furosemide and gentamicin are prescribed together, there is a higher chance of experiencing ototoxicity and deafness. It is recommended to avoid co-prescribing these medications. For more information, you can refer to the BNF section on furosemide interactions.

The risk of contracting meningococcal disease from a close contact is low. However, the risk is highest within the first seven days after the disease is diagnosed and decreases significantly afterwards.

Prophylaxis or vaccination for close contacts is typically organized by secondary care. It is recommended for the following individuals, regardless of their meningococcal vaccination status:

– People who have had prolonged close contact with the infected person in a household-type setting during the seven days prior to the onset of illness. This includes individuals living or sleeping in the same household, students in the same dormitory, partners, or university students sharing a kitchen in a hall of residence.

– People who have had brief close contact with the infected person, but only if they have been directly exposed to large particle droplets or secretions from the respiratory tract of the case around the time of admission to the hospital.

Antibiotic prophylaxis should be administered as soon as possible, ideally within 24 hours after the diagnosis of the index case.

Post-exposure prophylaxis is recommended for healthcare staff who have been exposed to direct nasopharyngeal secretions (without wearing a mask or personal protective equipment) from a known or highly probable case. This includes situations such as mouth-to-mouth resuscitation, airway management (suction/intubation), or prolonged close care within 1 meter of the patient who has been coughing or sneezing droplet secretions.

For more information, you can refer to the NICE Clinical Knowledge Summary on the management of close contacts of patients with meningococcal disease.

The Apgar score is a straightforward way to evaluate the well-being of a newborn baby right after birth. It consists of five criteria, each assigned a score ranging from zero to two. Typically, the assessment is conducted at one and five minutes after delivery, with the possibility of repeating it later if the score remains low. A score of 7 or higher is considered normal, while a score of 4-6 is considered fairly low, and a score of 3 or below is regarded as critically low. To remember the five criteria, you can use the acronym APGAR:

Appearance
Pulse rate
Grimace
Activity
Respiratory effort

The Apgar score criteria are as follows:

Score of 0:
Appearance (skin color): Blue or pale all over
Pulse rate: Absent
Reflex irritability (grimace): No response to stimulation
Activity: None
Respiratory effort: Absent

Score of 1:
Appearance (skin color): Blue at extremities (acrocyanosis)
Pulse rate: Less than 100 per minute
Reflex irritability (grimace): Grimace on suction or aggressive stimulation
Activity: Some flexion
Respiratory effort: Weak, irregular, gasping

Score of 2:
Appearance (skin color): No cyanosis, body and extremities pink
Pulse rate: More than 100 per minute
Reflex irritability (grimace): Cry on stimulation
Activity: Flexed arms and legs that resist extension
Respiratory effort: Strong, robust cry

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

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

The 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 50 kg individual, the appropriate infusion rate would be 25 mg/hour. It is important to note that the therapeutic range for aminophylline is narrow, ranging from 10-20 microgram/ml. Therefore, it is beneficial to estimate the plasma concentration of aminophylline during long-term treatment.

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.

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

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

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

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

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

The Parkinson-plus syndromes are a group of neurodegenerative disorders that share similar features with Parkinson’s disease but also have additional clinical characteristics that set them apart from idiopathic Parkinson’s disease (iPD). These syndromes include Multiple System Atrophy (MSA), Progressive Supranuclear Palsy (PSP), Corticobasal degeneration (CBD), and Dementia with Lewy Bodies (DLB).

Multiple System Atrophy (MSA) is a less common condition than iPD and PSP. It is characterized by the loss of cells in multiple areas of the nervous system. MSA progresses rapidly, often leading to wheelchair dependence within 3-4 years of diagnosis. Some distinguishing features of MSA include autonomic dysfunction, bladder control problems, erectile dysfunction, blood pressure changes, early-onset balance problems, neck or facial dystonia, and a high-pitched voice.

To summarize the distinguishing features of the Parkinson-plus syndromes compared to iPD, the following table provides a comparison:

iPD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Typically starts at rest on one side of the body
– Levodopa response: Excellent response
– Mental changes: Depression
– Balance/falls: Late in the disease
– Common eye abnormalities: Dry eyes, trouble focusing

MSA:
– Symptom onset: Both sides equally affected
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

PSP:
– Symptom onset: Both sides equally affected
– Tremor: Less common, if present affects both sides
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Personality changes, depression
– Balance/falls: Within 1 year
– Common eye abnormalities: Dry eyes, difficulty in looking downwards

CBD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

A patient with central vertigo would typically show a normal head impulse test result, indicating a normal vestibulo-ocular reflex. However, they would likely have an abnormal alternate cover test result, with a slight vertical correction, suggesting a central lesion like a stroke. A positive Romberg’s test can identify instability related to vertigo but cannot differentiate between peripheral and central causes. On the other hand, a positive Unterberger’s test indicates labyrinth dysfunction but does not indicate a central cause.

Further Reading:

Vertigo is a symptom characterized by a false sensation of movement, such as spinning or rotation, in the absence of any actual physical movement. It is not a diagnosis itself, but rather a description of the sensation experienced by the individual. Dizziness, on the other hand, refers to a perception of disturbed or impaired spatial orientation without a false sense of motion.

Vertigo can be classified as either peripheral or central. Peripheral vertigo is more common and is caused by problems in the inner ear that affect the labyrinth or vestibular nerve. Examples of peripheral vertigo include BPPV, vestibular neuritis, labyrinthitis, and Meniere’s disease. Central vertigo, on the other hand, is caused by pathology in the brain, such as in the brainstem or cerebellum. Examples of central vertigo include migraine, TIA and stroke, cerebellar tumor, acoustic neuroma, and multiple sclerosis.

There are certain features that can help differentiate between peripheral and central vertigo. Peripheral vertigo is often associated with severe nausea and vomiting, hearing loss or tinnitus, and a positive head impulse test. Central vertigo may be characterized by prolonged and severe vertigo, new-onset headache, recent trauma, cardiovascular risk factors, inability to stand or walk with eyes open, focal neurological deficit, and a negative head impulse test.

Nystagmus, an involuntary eye movement, can also provide clues about the underlying cause of vertigo. Central causes of vertigo often have nystagmus that is direction-changing on lateral gaze, purely vertical or torsional, not suppressed by visual fixation, non-fatigable, and commonly large amplitude. Peripheral causes of vertigo often have horizontal nystagmus with a torsional component that does not change direction with gaze, disappears with fixation of the gaze, and may have large amplitude early in the course of Meniere’s disease or vestibular neuritis.

There are various causes of vertigo, including viral labyrinthitis, vestibular neuritis, benign paroxysmal positional vertigo, Meniere’s disease, vertebrobasilar ischemia, and acoustic neuroma. Each of these disorders has its own unique characteristics and may be associated with other symptoms such as hearing loss, tinnitus, or neurological deficits.

When assessing a patient with vertigo, it is important to perform a cardiovascular and neurological examination, including assessing cranial nerves, cerebellar signs, eye movements, gait, coordination, and evidence of peripheral neuropathy.

The diagnosis in this case is non-alcoholic steatohepatitis (NASH), which is characterized by fatty infiltration of the liver and is commonly associated with obesity. It is the most frequent cause of persistently elevated ALT levels in patients without risk factors for chronic liver disease.

Risk factors for developing NASH include obesity, particularly truncal obesity, diabetes mellitus, and hypercholesterolemia.

The clinical features of NASH can vary, with many patients being completely asymptomatic. However, some may experience right upper quadrant pain, nausea and vomiting, and hepatomegaly (enlarged liver).

The typical biochemical profile seen in NASH includes elevated transaminases, with an AST:ALT ratio of less than 1. Often, there is an isolated elevation of ALT, and gamma-GT levels may be mildly elevated. In about one-third of patients, non-organ specific autoantibodies may be present. The presence of antinuclear antibodies (ANA) is associated with insulin resistance and indicates a higher risk of rapid progression to advanced liver disease.

If the AST level is significantly elevated or if the gamma-GT level is markedly elevated, further investigation for other potential causes should be considered. A markedly elevated gamma-GT level may suggest alcohol abuse, although it can also be elevated in NASH alone.

Diagnosis of NASH is confirmed through a liver biopsy, which will reveal increased fat deposition and a necro-inflammatory response within the hepatocytes.

Currently, there is no specific treatment for NASH. However, weight loss and medications that improve insulin resistance, such as metformin, may help slow down the progression of the disease.

Ascending cholangitis occurs when there is an infection in the common bile duct, often caused by a stone that has led to a blockage of bile flow. This condition is characterized by the presence of Charcot’s triad, which includes jaundice, fever with rigors, and pain in the right upper quadrant of the abdomen. It is a serious medical emergency that can be life-threatening, with some patients also experiencing altered mental status and low blood pressure due to septic shock, known as Reynold’s pentad. Urgent biliary drainage is the recommended treatment for ascending cholangitis.

In acute cholecystitis, Murphy’s sign is typically positive, indicating tenderness in the right upper quadrant when the gallbladder is palpated. However, it is negative in cases of biliary colic and ascending cholangitis. The white cell count and C-reactive protein (CRP) levels are usually elevated in ascending cholangitis, along with the presence of jaundice and significantly increased levels of alkaline phosphatase (ALP) and bilirubin.

To differentiate between biliary colic, acute cholecystitis, and ascending cholangitis, the following can be helpful:

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

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

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

The NICE guidelines for suspected DVT state that if a person scores two points or more on the DVT Wells score, they are likely to have DVT. On the other hand, if a person scores one point or less, it is unlikely that they have DVT.

For individuals who are likely to have DVT, it is recommended to offer a proximal leg vein ultrasound scan with the results available within 4 hours if possible. However, if the ultrasound scan cannot be done within 4 hours, the following steps should be taken: a D-dimer test should be offered, followed by interim therapeutic anticoagulation. It is preferable to choose an anticoagulant that can be continued if DVT is confirmed. Additionally, a proximal leg vein ultrasound scan should be conducted with the results available within 24 hours.

For individuals who are unlikely to have DVT, it is advised to offer a D-dimer test with the results available within 4 hours. If obtaining the results within 4 hours is not possible, interim therapeutic anticoagulation should be provided while awaiting the result. If feasible, an anticoagulant that can be continued if DVT is confirmed should be chosen.

For more information, you can refer to the NICE Clinical Knowledge Summary on deep vein thrombosis.

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

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

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

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

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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Further Reading:

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

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

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

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

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

During the later stages of pregnancy, the use of diazepam has been linked to respiratory depression in newborns and a withdrawal syndrome. There are several drugs that can have adverse effects during pregnancy, and the list below outlines the most commonly encountered ones.

ACE inhibitors, such as ramipril, can cause hypoperfusion, renal failure, and the oligohydramnios sequence if given in the second and third trimesters. Aminoglycosides, like gentamicin, can lead to ototoxicity and deafness. High doses of aspirin can result in first-trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g., 75 mg) do not pose significant risks.

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

Chloramphenicol is associated with grey baby syndrome. Corticosteroids, if given in the first trimester, may cause orofacial clefts. Danazol, when administered in the first trimester, can cause masculinization of the female fetuses genitals. Pregnant women should avoid handling crushed or broken tablets of finasteride as it can affect male sex organ development.

Haloperidol, if given in the first trimester, may cause limb malformations. In the third trimester, there is an increased risk of extrapyramidal symptoms in the neonate. Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability.

Lithium, if given in the first trimester, poses a risk of fetal cardiac malformations. In the second and third trimesters, it can result in hypotonia, lethargy, feeding problems, hypothyroidism, goiter, and nephrogenic diabetes insipidus in the neonate.

The primary location for aortic dissection, which is being considered in this case, is the ascending aorta.

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

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

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

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

The 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.

The zone of hyperaemia, located at the outermost part of the burn, experiences heightened tissue perfusion. Typically, this area will return to its normal tissue state.

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

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

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

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

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

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