N-acetylcysteine (NAC) enhances the production of glutathione, a substance that helps in the detoxification process. Specifically, NAC aids in the conjugation of NAPQI, a harmful metabolite of paracetamol, with glutathione, thereby neutralizing its toxicity.

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.

Aortic dissection is a condition that occurs when the middle layer of the aorta, known as the tunica media, becomes weakened. This weakening leads to the development of cases of aortic dissection.

Further Reading:

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

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

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

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

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.

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

Further Reading:

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

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

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

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

A significant proportion of the population experiences a difference of 10 mmHg or more in blood pressure between their upper limbs. Pericarditis can be identified by the presence of saddle-shaped ST elevation and pain in the trapezius ridge. Aortic dissection is characterized by a diastolic murmur with a decrescendo pattern, which indicates aortic incompetence.

Further Reading:

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

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

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

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

presbycusis is a type of hearing loss that occurs gradually as a person ages. It affects both ears and is characterized by a decrease in hearing ability, particularly at higher frequencies. This type of hearing loss worsens over time. When a person has bilateral sensorineural hearing loss, a central Weber’s test and bilaterally diminished Rinne’s tests would be expected.

To perform a Rinne’s test, a 512 Hertz tuning fork is vibrated and placed on the mastoid process until the sound can no longer be heard. Then, the top of the tuning fork is placed 2 centimeters from the external auditory meatus. The patient is asked to indicate where they hear the sound loudest.

In individuals with normal hearing, the tuning fork should still be audible outside the external auditory canal even after it can no longer be heard on the mastoid. This is because air conduction should be better than bone conduction.

In cases of conductive hearing loss, the patient will no longer be able to hear the tuning fork immediately after it can no longer be heard on the mastoid. This indicates that their bone conduction is better than their air conduction, and something is obstructing the passage of sound waves through the ear canal into the cochlea. This is considered a true negative result.

However, a Rinne’s test may produce a false negative result if the patient has a severe unilateral sensorineural deficit and can sense the sound in the unaffected ear through the transmission of sound waves through the base of the skull.

In sensorineural hearing loss, the ability to perceive the tuning fork both on the mastoid and outside the external auditory canal is equally diminished compared to the opposite ear. The sound will still be heard outside the external auditory canal, but it will disappear earlier on the mastoid process and outside the external auditory canal compared to the other ear.

To perform Weber’s test, a 512 Hz tuning fork is vibrated and placed on the center of the patient’s forehead. The patient is then asked if they perceive the sound in the middle of the forehead or if it seems to be more on one side or the other.

If the sound seems to be more on one side, it can indicate either ipsilateral conductive hearing loss or contralateral sensorineural hearing loss.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This leads to the accumulation of urea and other waste products in the body, as well as disturbances in fluid balance and electrolyte levels. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease. It is a relatively common condition, affecting approximately 15% of adults admitted to hospitals in the UK.

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

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

The most severe stage, stage 3 AKI, is identified by a creatinine rise of 200% or more from the baseline within 7 days. It can also be diagnosed if the creatinine level reaches 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours, or a rise of 50% or more within 7 days. Additionally, a urine output of less than 0.3 mL/kg/hour for 24 hours or anuria (no urine production) for 12 hours is indicative of stage 3 AKI.

Lipid emulsion is known to cause pancreatitis as a common side effect. According to the AAGBI guidelines, patients who are given lipid emulsion should be closely monitored with regular clinical evaluations. This includes conducting amylase or lipase tests daily for two days after receiving the emulsion.

Further Reading:

Local anaesthetics, such as lidocaine, bupivacaine, and prilocaine, are commonly used in the emergency department for topical or local infiltration to establish a field block. Lidocaine is often the first choice for field block prior to central line insertion. These anaesthetics work by blocking sodium channels, preventing the propagation of action potentials.

However, local anaesthetics can enter the systemic circulation and cause toxic side effects if administered in high doses. Clinicians must be aware of the signs and symptoms of local anaesthetic systemic toxicity (LAST) and know how to respond. Early signs of LAST include numbness around the mouth or tongue, metallic taste, dizziness, visual and auditory disturbances, disorientation, and drowsiness. If not addressed, LAST can progress to more severe symptoms such as seizures, coma, respiratory depression, and cardiovascular dysfunction.

The management of LAST is largely supportive. Immediate steps include stopping the administration of local anaesthetic, calling for help, providing 100% oxygen and securing the airway, establishing IV access, and controlling seizures with benzodiazepines or other medications. Cardiovascular status should be continuously assessed, and conventional therapies may be used to treat hypotension or arrhythmias. Intravenous lipid emulsion (intralipid) may also be considered as a treatment option.

If the patient goes into cardiac arrest, CPR should be initiated following ALS arrest algorithms, but lidocaine should not be used as an anti-arrhythmic therapy. Prolonged resuscitation may be necessary, and intravenous lipid emulsion should be administered. After the acute episode, the patient should be transferred to a clinical area with appropriate equipment and staff for further monitoring and care.

It is important to report cases of local anaesthetic toxicity to the appropriate authorities, such as the National Patient Safety Agency in the UK or the Irish Medicines Board in the Republic of Ireland. Additionally, regular clinical review should be conducted to exclude pancreatitis, as intravenous lipid emulsion can interfere with amylase or lipase assays.

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.

Scleroderma disorders are a group of connective tissue disorders that affect multiple systems in the body. These disorders are characterized by damage to endothelial cells, oxidative stress, inflammation around blood vessels, and the activation of fibroblasts leading to fibrosis. Autoantibodies also play a significant role in the development of these conditions.

Scleroderma, which refers to thickened skin, can also involve internal organs, resulting in a condition called systemic sclerosis. Systemic sclerosis can be further classified into two types: limited cutaneous involvement and diffuse involvement.

The cardinal features of limited cutaneous involvement, such as in CREST syndrome, include subcutaneous calcifications (calcinosis), Raynaud’s phenomenon leading to ischemia in the fingers or organs, difficulty swallowing (dysphagia) or painful swallowing (odynophagia) due to oesophageal dysmotility, localized thickening and tightness of the skin in the fingers and toes (sclerodactyly), and abnormal dilatation of small blood vessels (telangiectasia).

In the case of the patient mentioned in this question, they present with progressive dysphagia and Raynaud’s phenomenon. Physical examination reveals sclerodactyly and telangiectasia. These findings strongly suggest a diagnosis of systemic sclerosis with limited cutaneous involvement. The most specific autoantibody associated with this condition is anti-centromere.

It is important to note that anti-dsDNA and anti-Smith antibodies are typically seen in systemic lupus erythematosus, while anti-Jo1 is associated with polymyositis and dermatomyositis. Anti-SS-B (also known as anti-La antibody) is commonly found in Sjogren’s syndrome.

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

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

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

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

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

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

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

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

Chloramphenicol: It can cause grey baby syndrome.

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

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

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

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

Heparin: It can cause maternal bleeding and thrombocytopenia.

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

This patient is displaying symptoms and signs that are consistent with community-acquired pneumonia (CAP). The most common cause of CAP in an adult patient who is otherwise in good health is Streptococcus pneumoniae.

When it comes to treating community-acquired pneumonia, the first-line antibiotic of choice is amoxicillin. According to the NICE guidelines, patients who are allergic to penicillin should be prescribed a macrolide (such as clarithromycin) or a tetracycline (such as doxycycline).

For more information, you can refer to the NICE guidelines on the diagnosis and management of pneumonia in adults.

Hyperkalaemia can be identified by certain signs, such as muscle weakness, cramps, and delayed deep tendon reflexes. Additionally, there are neurological signs that may be present, including flaccid paralysis, twitching, peripheral paresthesia, weakness, and hypo-reflexia.

Further Reading:

Vasoactive drugs can be classified into three categories: inotropes, vasopressors, and unclassified. Inotropes are drugs that alter the force of muscular contraction, particularly in the heart. They primarily stimulate adrenergic receptors and increase myocardial contractility. Commonly used inotropes include adrenaline, dobutamine, dopamine, isoprenaline, and ephedrine.

Vasopressors, on the other hand, increase systemic vascular resistance (SVR) by stimulating alpha-1 receptors, causing vasoconstriction. This leads to an increase in blood pressure. Commonly used vasopressors include norepinephrine, metaraminol, phenylephrine, and vasopressin.

Electrolytes, such as potassium, are essential for proper bodily function. Solutions containing potassium are often given to patients to prevent or treat hypokalemia (low potassium levels). However, administering too much potassium can lead to hyperkalemia (high potassium levels), which can cause dangerous arrhythmias. It is important to monitor potassium levels and administer it at a controlled rate to avoid complications.

Hyperkalemia can be caused by various factors, including excessive potassium intake, decreased renal excretion, endocrine disorders, certain medications, metabolic acidosis, tissue destruction, and massive blood transfusion. It can present with cardiovascular, respiratory, gastrointestinal, and neuromuscular symptoms. ECG changes, such as tall tented T-waves, prolonged PR interval, flat P-waves, widened QRS complex, and sine wave, are also characteristic of hyperkalemia.

In summary, vasoactive drugs can be categorized as inotropes, vasopressors, or unclassified. Inotropes increase myocardial contractility, while vasopressors increase systemic vascular resistance. Electrolytes, particularly potassium, are important for bodily function, but administering too much can lead to hyperkalemia. Monitoring potassium levels and ECG changes is crucial in managing hyperkalemia.

Erb’s palsy, also known as Erb-Duchenne palsy, is a condition where the arm becomes paralyzed due to an injury to the upper roots of the brachial plexus. The primary root affected is usually C5, although C6 may also be involved in some cases. The main cause of Erb’s palsy is when the arm experiences excessive force during a difficult childbirth, but it can also occur in adults as a result of shoulder trauma.

Clinically, the affected arm will hang by the side with the elbow extended and the forearm turned inward (known as the waiter’s tip sign). Upon examination, there will be a loss of certain movements:

– Shoulder abduction (involving the deltoid and supraspinatus muscles)
– Shoulder external rotation (infraspinatus muscle)
– Elbow flexion (biceps and brachialis muscles)

It is important to differentiate Erb’s palsy from Klumpke’s palsy, which affects the lower roots of the brachial plexus (C8 and T1). Klumpke’s palsy presents with a claw hand due to paralysis of the intrinsic hand muscles, along with sensory loss along the ulnar side of the forearm and hand. If T1 is affected, there may also be the presence of Horner’s syndrome.

Anaemia of chronic disease is a type of anaemia that can occur in various chronic conditions, such as rheumatoid arthritis, systemic lupus erythematosus, tuberculosis, malignancy, malnutrition, hypothyroidism, hypopituitarism, chronic kidney disease, and chronic liver disease. The underlying mechanisms of this type of anaemia are complex and not fully understood, with multiple contributing factors involved. One important mediator in inflammatory diseases like rheumatoid arthritis is interleukin-6 (IL-6). Increased levels of IL-6 lead to the production of hepcidin, a hormone that regulates iron balance. Hepcidin prevents the release of iron from the reticulo-endothelial system and affects other aspects of iron metabolism.

Anaemia of chronic disease typically presents as a normochromic, normocytic anaemia, although it can also be microcytic. It is characterized by reduced serum iron, reduced transferrin saturation, and reduced total iron-binding capacity (TIBC). However, the serum ferritin levels are usually normal or increased. Distinguishing anaemia of chronic disease from iron-deficiency anaemia can be challenging, but in iron-deficiency anaemia, the TIBC is typically elevated, and serum ferritin is usually low.

This patient is displaying symptoms and signs that are consistent with a vestibular schwannoma, which is also known as an acoustic neuroma. A vestibular schwannoma typically affects the 5th and 8th cranial nerves and is characterized by the following classic presentations: gradual deterioration of hearing in one ear, facial numbness and tingling, tinnitus, and vertigo. It is also possible for the patient to have a history of headaches, and in rare cases, the 7th, 9th, and 10th cranial nerves may be affected. It is recommended that this patient be referred to either an ENT specialist or a neurosurgeon for further assessment, including an MRI of the internal auditory meatus. The main treatment options for vestibular schwannoma include surgery, radiotherapy, and stereotactic radiosurgery.

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

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

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

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

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

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

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

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

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

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

Intubation is rarely necessary for asthmatic patients, with only about 2% of asthma attacks requiring it. Most severe cases can be managed using non-invasive ventilation techniques. However, intubation can be a life-saving measure for asthmatic patients in critical condition. The indications for intubation include severe hypoxia, altered mental state, failure to respond to medications or non-invasive ventilation, and respiratory or cardiac arrest.

Before intubation, it is important to preoxygenate the patient and administer intravenous fluids. Nasal oxygen during intubation can provide additional time. Intravenous fluids are crucial because patients with acute asthma exacerbations can experience significant fluid loss, which can lead to severe hypotension during intubation and positive pressure ventilation.

There is no perfect combination of drugs for rapid sequence induction (RSI), but ketamine is often the preferred choice. Ketamine has bronchodilatory properties and does not cause hypotension as a side effect. Propofol can also be used, but it carries a risk of hypotension. In some cases, a subdissociative dose of ketamine can be helpful to facilitate the use of non-invasive ventilation in a hypoxic or combative patient.

Rocuronium and suxamethonium are commonly used as paralytic agents. Rocuronium has the advantage of providing a longer period of paralysis, which helps avoid ventilator asynchrony in the early stages of management.

Proper mechanical ventilation is essential, and it involves allowing the patient enough time to fully exhale the delivered breath and prevent hyperinflation. Therefore, permissive hypercapnia is typically used, and the ventilator settings should be adjusted accordingly. The recommended settings are a respiratory rate of 6-8 breaths per minute and a tidal volume of 6 ml per kilogram of body weight.

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 hypertension, which can be either sustained or paroxysmal. Other symptoms tend to be intermittent and can occur frequently or infrequently. As the disease progresses, these symptoms usually become more severe and frequent.

In addition to hypertension, patients with phaeochromocytoma may experience the following clinical features: headache, profuse sweating, palpitations or rapid heartbeat, tremors, fever, nausea and vomiting, anxiety and panic attacks, a sense of impending doom, epigastric or flank pain, constipation, hypertensive retinopathy, postural hypotension due to volume contraction, cardiomyopathy, and café au lait spots.

To confirm a suspected diagnosis of phaeochromocytoma, elevated levels of metanephrines (catecholamine metabolites) can be measured in the blood or urine. This can be done through methods such as a 24-hour urine collection for free catecholamines, vanillylmandelic acid (VMA), and metanephrines, high-performance liquid chromatography for catecholamines in plasma and/or urine, or radioimmunoassay (RIA) for urinary/plasma metanephrines.

Once the diagnosis of phaeochromocytoma is biochemically confirmed, imaging methods can be used to locate the tumor. The first imaging modality to be used is a CT scan, which has an overall sensitivity of 89%. An MRI scan is the most sensitive modality for identifying the tumor, especially in cases of extra-adrenal tumors or metastatic disease, with an overall sensitivity of 98%. In cases where CT or MRI does not show a tumor, a nuclear medicine scan such as MIBG scintigraphy can be useful.

Spontaneous bacterial peritonitis (SBP) is a serious infection that can occur in individuals with ascites, which is the accumulation of fluid in the abdominal cavity. In this case, the patient is a 42-year-old male intravenous drug user with a history of hepatitis C who has not received treatment. He presents to the emergency department with worsening abdominal distension, fever, and confusion.

To evaluate the patient, an abdominal paracentesis is performed, which involves removing a sample of the ascitic fluid for analysis. The findings from the ascitic fluid analysis can provide important information about the underlying cause of the patient’s symptoms.

In the given options, the finding that is indicative of spontaneous bacterial peritonitis (SBP) is an ascitic fluid absolute neutrophil count >250 cells/mm³. Neutrophils are a type of white blood cell that are typically elevated in the presence of infection. In SBP, there is an infection of the ascitic fluid, leading to an increase in neutrophils.

The other options provided do not specifically indicate SBP. An ascitic fluid absolute lymphocyte count >150 cells/mm³ may suggest a different type of infection or inflammation. An ascitic fluid absolute erythrocyte count >200 cells/mm³ may indicate bleeding into the ascitic fluid. An ascitic fluid albumin concentration of > 2.0 g/dL (20 g/L) and an ascitic fluid protein concentration of > 3.0 g/dL (30 g/L) may suggest liver disease or other causes of ascites, but they do not specifically indicate SBP.

Therefore, in this case, the presence of an ascitic fluid absolute neutrophil count >250 cells/mm³ is the finding that is indicative of spontaneous bacterial peritonitis (SBP).

Further Reading:

Cirrhosis is a condition where the liver undergoes structural changes, resulting in dysfunction of its normal functions. It can be classified as either compensated or decompensated. Compensated cirrhosis refers to a stage where the liver can still function effectively with minimal symptoms, while decompensated cirrhosis is when the liver damage is severe and clinical complications are present.

Cirrhosis develops over a period of several years due to repeated insults to the liver. Risk factors for cirrhosis include alcohol misuse, hepatitis B and C infection, obesity, type 2 diabetes, autoimmune liver disease, genetic conditions, certain medications, and other rare conditions.

The prognosis of cirrhosis can be assessed using the Child-Pugh score, which predicts mortality based on parameters such as bilirubin levels, albumin levels, INR, ascites, and encephalopathy. The score ranges from A to C, with higher scores indicating a poorer prognosis.

Complications of cirrhosis include portal hypertension, ascites, hepatic encephalopathy, variceal hemorrhage, increased infection risk, hepatocellular carcinoma, and cardiovascular complications.

Diagnosis of cirrhosis is typically done through liver function tests, blood tests, viral hepatitis screening, and imaging techniques such as transient elastography or acoustic radiation force impulse imaging. Liver biopsy may also be performed in some cases.

Management of cirrhosis involves treating the underlying cause, controlling risk factors, and monitoring for complications. Complications such as ascites, spontaneous bacterial peritonitis, oesophageal varices, and hepatic encephalopathy require specific management strategies.

Overall, cirrhosis is a progressive condition that requires ongoing monitoring and management to prevent further complications and improve outcomes for patients.

Whooping cough, also known as pertussis, is a respiratory infection caused by the bacteria Bordetella pertussis. It is transmitted through respiratory droplets and has an incubation period of about 7-21 days. This disease is highly contagious and can be transmitted to around 90% of close household contacts.

The clinical course of whooping cough can be divided into two stages. The first stage is called the catarrhal stage, which resembles a mild respiratory infection with symptoms like low-grade fever and a runny nose. A cough may be present, but it is usually mild compared to the second stage. The catarrhal stage typically lasts for about a week.

The second stage is known as the paroxysmal stage. During this phase, the cough becomes more severe as the catarrhal symptoms start to subside. The coughing occurs in spasms, often preceded by an inspiratory whoop sound, followed by a series of rapid coughs. Vomiting may occur, and patients may develop subconjunctival hemorrhages and petechiae. Patients generally feel well between coughing spasms, and there are usually no abnormal chest findings. This stage can last up to 3 months, with a gradual recovery over time. The later stages of this phase are sometimes referred to as the convalescent stage.

Complications of whooping cough can include secondary pneumonia, rib fractures, pneumothorax, hernias, syncopal episodes, encephalopathy, and seizures.

Public Health England (PHE) provides recommendations for testing whooping cough based on the patient’s age, time since onset of illness, and severity of symptoms. For infants under 12 months of age who are hospitalized, PCR testing is recommended. Non-hospitalized infants within two weeks of symptom onset should undergo culture testing of a nasopharyngeal swab or aspirate. Non-hospitalized infants presenting over two weeks after symptom onset should be tested for anti-pertussis toxin IgG antibody levels using serology.

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

Epistaxis, or nosebleed, is a common condition that can occur in both children and older adults. It is classified as either anterior or posterior, depending on the location of the bleeding. Anterior epistaxis usually occurs in younger individuals and arises from the nostril, most commonly from an area called Little’s area. These bleeds are usually not severe and account for the majority of nosebleeds seen in hospitals. Posterior nosebleeds, on the other hand, occur in older patients with conditions such as hypertension and atherosclerosis. The bleeding in posterior nosebleeds is likely to come from both nostrils and originates from the superior or posterior parts of the nasal cavity or nasopharynx.

The management of epistaxis involves assessing the patient for signs of instability and implementing measures to control the bleeding. Initial measures include sitting the patient upright with their upper body tilted forward and their mouth open. Firmly pinching the cartilaginous part of the nose for 10-15 minutes without releasing the pressure can also help stop the bleeding. If these measures are successful, a cream called Naseptin or mupirocin nasal ointment can be prescribed for further treatment.

If bleeding persists after the initial measures, nasal cautery or nasal packing may be necessary. Nasal cautery involves using a silver nitrate stick to cauterize the bleeding point, while nasal packing involves inserting nasal tampons or inflatable nasal packs to stop the bleeding. In cases of posterior bleeding, posterior nasal packing or surgery to tie off the bleeding vessel may be considered.

Complications of epistaxis can include nasal bleeding, hypovolemia, anemia, aspiration, and even death. Complications specific to nasal packing include sinusitis, septal hematoma or abscess, pressure necrosis, toxic shock syndrome, and apneic episodes. Nasal cautery can lead to complications such as septal perforation and caustic injury to the surrounding skin.

In children under the age of 2 presenting with epistaxis, it is important to refer them for further investigation as an underlying cause is more likely in this age group.

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

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

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

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

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

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

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

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

The 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.

Wernicke’s area is situated in the dominant cerebral hemisphere temporal lobe. Specifically, it can be found in the posterior section of the superior temporal gyrus.

This area is responsible for comprehending both written and spoken language. It allows individuals to read a sentence, understand its meaning, and articulate it verbally.

When Wernicke’s area is damaged, patients may be able to string words together fluently, but the resulting phrases lack coherence and meaning. This condition is known as receptive aphasia or Wernicke’s aphasia.

Benzodiazepines are commonly prescribed in the UK to help manage symptoms of alcohol withdrawal. Currently, only diazepam and chlordiazepoxide have been approved for this purpose. If you would like to learn more about the NICE pathway for acute alcohol withdrawal or the RCEM syllabus reference, please refer to the provided links. Additionally, information on alcohol and substance misuse can be found in the MHC1 section.

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

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

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

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

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

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

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

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

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

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

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