Neonatal jaundice is a complex subject, and it is crucial for candidates to have knowledge about the different causes, presentations, and management of conditions that lead to jaundice in newborns. Neonatal jaundice can be divided into two groups: unconjugated hyperbilirubinemia, which can be either physiological or pathological, and conjugated hyperbilirubinemia, which is always pathological.

The causes of neonatal jaundice can be categorized as follows:

Haemolytic unconjugated hyperbilirubinemia:
– Intrinsic causes of haemolysis include hereditary spherocytosis, G6PD deficiency, sickle-cell disease, and pyruvate kinase deficiency.
– Extrinsic causes of haemolysis include haemolytic disease of the newborn and Rhesus disease.

Non-haemolytic unconjugated hyperbilirubinemia:
– Breastmilk jaundice, cephalhaematoma, polycythemia, infection (particularly urinary tract infections), Gilbert syndrome.

Hepatic conjugated hyperbilirubinemia:
– Hepatitis A and B, TORCH infections, galactosaemia, alpha 1-antitrypsin deficiency, drugs.

Post-hepatic conjugated hyperbilirubinemia:
– Biliary atresia, bile duct obstruction, choledochal cysts.

By understanding these different categories and their respective examples, candidates will be better equipped to handle neonatal jaundice cases.

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

To diagnose neutropenic sepsis, doctors look for a neutrophil count of 0.5 x 109 per litre or lower in patients undergoing cancer treatment. Additionally, patients must have a temperature higher than 38°C or show other signs and symptoms of significant sepsis.

According to the current guidelines from the National Institute for Health and Care Excellence (NICE), the recommended initial antibiotic treatment for suspected neutropenic sepsis is monotherapy with piperacillin with tazobactam (Tazocin 4.5 g IV). It is important to note that aminoglycosides should not be used as monotherapy or in combination therapy unless there are specific patient-related or local microbiological reasons to do so.

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

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

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

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

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

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

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

The superior orbital fissure is a gap in the back wall of the orbit, created by the space between the greater and lesser wings of the sphenoid bone. Several structures pass through it to enter the orbit, starting from the top and going downwards. These include the lacrimal nerve (a branch of CN V1), the frontal nerve (another branch of CN V1), the superior ophthalmic vein, the trochlear nerve (CN IV), the superior division of the oculomotor nerve (CN III), the nasociliary nerve (a branch of CN V1), the inferior division of the oculomotor nerve (CN III), the abducens nerve (CN VI), and the inferior ophthalmic vein.

Adjacent to the superior orbital fissure, on the back wall of the orbit and towards the middle, is the optic canal. The optic nerve (CN II) exits the orbit through this canal, along with the ophthalmic artery.

Superior orbital fissure syndrome (SOFS) is a condition characterized by a combination of symptoms and signs that occur when cranial nerves III, IV, V1, and VI are compressed or injured as they pass through the superior orbital fissure. This condition also leads to swelling and protrusion of the eye due to impaired drainage and congestion. The main causes of SOFS are trauma, tumors, and inflammation. It is important to note that CN II is not affected by this syndrome, as it follows a separate path through the optic canal.

Amiodarone is a medication that is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) while chest compressions are being performed. The prescribed dose is 300 mg, given as an intravenous bolus that is diluted in 5% dextrose to a volume of 20 mL. It is important to note that amiodarone is not suitable for treating PEA or asystole.

In cases where VF/pVT persists after five defibrillation attempts, an additional dose of 150 mg of amiodarone should be given. However, if amiodarone is not available, lidocaine can be used as an alternative. The recommended dose of lidocaine is 1 mg/kg. It is crucial to avoid administering lidocaine if amiodarone has already been given.

Amiodarone is classified as a membrane-stabilizing antiarrhythmic drug. It works by prolonging the duration of the action potential and the refractory period in both the atrial and ventricular myocardium. This medication also slows down atrioventricular conduction and has a similar effect on accessory pathways.

Additionally, amiodarone has a mild negative inotropic action, meaning it weakens the force of heart contractions. It also causes peripheral vasodilation through non-competitive alpha-blocking effects.

It is important to note that while there is no evidence of long-term benefits from using amiodarone, it may improve short-term survival rates, which justifies its continued use.

Activated charcoal is a useful treatment for many drug poisonings, but it is not effective against certain types of poisonings. To remember these exceptions, you can use the mnemonic PHAILS. This stands for Pesticides (specifically organophosphates), Hydrocarbons, Acids (strong), alkalis (strong), alcohols (such as ethanol, methanol, and ethylene glycol), Iron, Lithium, and Solvents.

Further Reading:

Poisoning in the emergency department is often caused by accidental or intentional overdose of prescribed drugs. Supportive treatment is the primary approach for managing most poisonings. This includes ensuring a clear airway, proper ventilation, maintaining normal fluid levels, temperature, and blood sugar levels, correcting any abnormal blood chemistry, controlling seizures, and assessing and treating any injuries.

In addition to supportive treatment, clinicians may need to consider strategies for decontamination, elimination, and administration of antidotes. Decontamination involves removing poisons from the skin or gastrointestinal tract. This can be done through rinsing the skin or using methods such as activated charcoal, gastric lavage, induced emesis, or whole bowel irrigation. However, induced emesis is no longer commonly used, while gastric lavage and whole bowel irrigation are rarely used.

Elimination methods include urinary alkalinization, hemodialysis, and hemoperfusion. These techniques help remove toxins from the body.

Activated charcoal is a commonly used method for decontamination. It works by binding toxins in the gastrointestinal tract, preventing their absorption. It is most effective if given within one hour of ingestion. However, it is contraindicated in patients with an insecure airway due to the risk of aspiration. Activated charcoal can be used for many drugs, but it is ineffective for certain poisonings, including pesticides (organophosphates), hydrocarbons, strong acids and alkalis, alcohols (ethanol, methanol, ethylene glycol), iron, lithium, and solvents.

Antidotes are specific treatments for poisoning caused by certain drugs or toxins. For example, cyanide poisoning can be treated with dicobalt edetate, hydroxocobalamin, or sodium nitrite and sodium thiosulphate. Benzodiazepine poisoning can be treated with flumazanil, while opiate poisoning can be treated with naloxone. Other examples include protamine for heparin poisoning, vitamin K or fresh frozen plasma for warfarin poisoning, fomepizole or ethanol for methanol poisoning, and methylene blue for methemoglobinemia caused by benzocaine or nitrates.

There are many other antidotes available for different types of poisoning, and resources such as TOXBASE and the National Poisons Information Service (NPIS) can provide valuable advice on managing poisonings.

If an adult with a head injury experiences more than one episode of vomiting, it is recommended to undergo a CT scan of the head. There are several criteria for an urgent CT scan in individuals with a head injury, including a Glasgow Coma Scale (GCS) score of less than 13 on initial assessment in the emergency department (ED), a GCS score of less than 15 at 2 hours after the injury on assessment in the ED, suspected open or depressed skull fracture, any sign of basal skull fracture (such as haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, or Battle’s sign), post-traumatic seizure, new focal neurological deficit, and being on anticoagulation medication. If any of these signs are present, a CT scan should be performed within 1 hour, except for patients on anticoagulation medication who should undergo a CT scan within 8 hours if none of the other signs are present. However, if a patient on anticoagulation medication has any of the other signs, the CT scan should be performed within 1 hour.

Further Reading:

Indications for CT Scanning in Head Injuries (Adults):
– CT head scan should be performed within 1 hour if any of the following features are present:
– GCS < 13 on initial assessment in the ED
– GCS < 15 at 2 hours after the injury on assessment in the ED
– Suspected open or depressed skull fracture
– Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign)
– Post-traumatic seizure
– New focal neurological deficit
– > 1 episode of vomiting

Indications for CT Scanning in Head Injuries (Children):
– CT head scan should be performed within 1 hour if any of the features in List 1 are present:
– Suspicion of non-accidental injury
– Post-traumatic seizure but no history of epilepsy
– GCS < 14 on initial assessment in the ED for children more than 1 year of age
– Paediatric GCS < 15 on initial assessment in the ED for children under 1 year of age
– At 2 hours after the injury, GCS < 15
– Suspected open or depressed skull fracture or tense fontanelle
– Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign)
– New focal neurological deficit
– For children under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head

– CT head scan should be performed within 1 hour if none of the above features are present but two or more of the features in List 2 are present:
– Loss of consciousness lasting more than 5 minutes (witnessed)
– Abnormal drowsiness
– Three or more discrete episodes of vomiting
– Dangerous mechanism of injury (high-speed road traffic accident, fall from a height.

The most commonly identified causative pathogen in patients with spontaneous bacterial peritonitis (SBP) is Escherichia coli. SBP is a serious infection that occurs in individuals with liver cirrhosis, where bacteria from the gut migrate into the peritoneal cavity, leading to infection and inflammation. E. coli is a gram-negative bacterium commonly found in the intestines and is known to be a frequent cause of SBP. It is important to promptly diagnose and treat SBP to prevent further complications and improve patient outcomes.

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.

Diagnosing spontaneous bacterial peritonitis (SBP) requires an abdominal paracentesis of ascitic tap. Other reasons for performing a diagnostic tap include determining the cause of ascites, distinguishing between transudate and exudate, and detecting cancerous cells. Additionally, a therapeutic paracentesis can be done to alleviate respiratory distress or abdominal pain caused by the ascites.

However, there are certain contraindications to consider. These include having an uncooperative patient, a skin infection at the proposed puncture site, being pregnant, or experiencing severe bowel distension. Relative contraindications involve having severe thrombocytopenia (platelet count less than 20 x 103/μL) or coagulopathy (INR greater than 2.0).

For patients with an INR greater than 2.0, it is recommended to administer fresh frozen plasma (FFP) before the procedure. One approach is to infuse one unit of fresh frozen plasma prior to the procedure and then proceed with the paracentesis while the second unit is being infused.

In the case of patients with a platelet count lower than 20 x 103/μL, it is advisable to provide a platelet infusion before the procedure.

In cases where there are no reasons to avoid them, high-dose NSAIDs are the first choice for treating acute gout. A commonly used and effective regimen is to take Naproxen 750 mg as a single dose, followed by 250 mg three times a day. Aspirin should not be used for gout because it reduces the clearance of urate in the urine and interferes with the action of uricosuric agents. Instead, Naproxen, diclofenac, or indomethacin are more suitable options.

Allopurinol is used as a preventive measure to reduce future gout attacks by lowering the levels of uric acid in the blood. However, it should not be started during an acute gout episode as it can worsen the severity and duration of symptoms. Colchicine works by affecting neutrophils, binding to tubulin to prevent their migration into the affected joint. It is equally effective as NSAIDs in relieving acute gout attacks and can also be used for prophylactic treatment if a patient cannot tolerate allopurinol.

NSAIDs should not be used in patients with heart failure as they can lead to fluid retention and congestive cardiac failure. In such cases, colchicine is the preferred treatment option. Colchicine is also recommended for patients who cannot tolerate NSAIDs. Febuxostat (Uloric) is an alternative to allopurinol and is used for managing chronic gout.

Corticosteroids are an effective alternative for managing acute gout in patients who cannot take NSAIDs or colchicine. They can be administered orally, intramuscularly, intravenously, or directly into the affected joint.

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

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

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

In some cases, the signs of skin or mucosal involvement may be difficult to detect or may not be present at all. The Royal College of Emergency Medicine (RCEM) states that anaphylaxis is likely when three specific criteria are met: the illness has a sudden and rapid onset, there are noticeable changes in the skin or mucosal areas such as flushing, hives, or swelling, and there are severe problems with the airway, breathing, or circulation that pose a life-threatening risk.

Further Reading:

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

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

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

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

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

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

Patients who experience a seizure(s) should be informed about their ability to drive. There are two important instructions to follow in this regard. Firstly, they must refrain from driving for a period of 6 months. Secondly, they must notify the appropriate authority, such as the DVLA or DVA in Northern Ireland. In the case of a single seizure, driving should be suspended for 6 months from the date of the seizure. However, if an underlying cause that increases the risk of seizures is identified, driving should be halted for 12 months. In the case of multiple seizures or epilepsy, driving should be ceased for 12 months from the most recent seizure.

Further Reading:

Blackouts are a common occurrence in the emergency department and can have serious consequences if they happen while a person is driving. It is crucial for doctors in the ED to be familiar with the guidelines set by the DVLA (Driver and Vehicle Licensing Agency) regarding driving restrictions for patients who have experienced a blackout.

The DVLA has specific rules for different types of conditions that may cause syncope (loss of consciousness). For group 1 license holders (car/motorcycle use), if a person has had a first unprovoked isolated seizure, they must refrain from driving for 6 months or 12 months if there is an underlying causative factor that may increase the risk. They must also notify the DVLA. For group 2 license holders (bus and heavy goods vehicles), the restrictions are more stringent, with a requirement of 12 months off driving for a first unprovoked isolated seizure and 5 years off driving if there is an underlying causative factor.

For epilepsy or multiple seizures, both group 1 and group 2 license holders must remain seizure-free for 12 months before their license can be considered. They must also notify the DVLA. In the case of a stroke or isolated transient ischemic attack (TIA), group 1 license holders need to refrain from driving for 1 month, while group 2 license holders must wait for 12 months before being re-licensed subject to medical evaluation. Multiple TIAs require 3 months off driving for both groups.

Isolated vasovagal syncope requires no driving restriction for group 1 license holders, but group 2 license holders must refrain from driving for 3 months. Both groups must notify the DVLA. If syncope is caused by a reversible and treated condition, group 1 license holders need 4 weeks off driving, while group 2 license holders require 3 months. In the case of an isolated syncopal episode with an unknown cause, group 1 license holders must refrain from driving for 6 months, while group 2 license holders will have their license refused or revoked for 12 months.

For patients who continue to drive against medical advice, the GMC (General Medical Council) has provided guidance on how doctors should manage the situation. Doctors should explain to the patient why they are not allowed to drive and inform them of their legal duty to notify the DVLA or DVA (Driver and Vehicle Agency in Northern Ireland). Doctors should also record the advice given to the patient in their medical record

This patient has experienced otic barotrauma, which is most commonly seen during aircraft descent but can also occur in divers. Otic barotrauma occurs when the eustachian tube fails to equalize the pressure between the middle ear and the atmosphere, resulting in a pressure difference. This is more likely to happen in patients with eustachian tube dysfunction, such as those with acute otitis media or glue ear.

Patients with otic barotrauma often complain of severe ear pain, conductive hearing loss, ringing in the ears (tinnitus), and dizziness (vertigo). Upon examination, fluid can be observed behind the eardrum, and in more severe cases, the eardrum may even rupture.

In most instances, the symptoms of otic barotrauma resolve within a few days without any treatment. However, in more severe cases, it may take 2-3 weeks for the symptoms to subside. Nasal decongestants can be beneficial before and during a flight, but their effectiveness is limited once symptoms have already developed. Nasal steroids have no role in the management of otic barotrauma, and antibiotics should only be used if an infection develops.

The most appropriate course of action in this case would be to provide the patient with an explanation of what has occurred and reassure them that their symptoms should improve soon.

The presence of borborygmi in the epigastrium can indicate that the endotracheal tube (ETT) is incorrectly placed in the esophagus. There are several ways to verify the correct placement of the endotracheal tube (ETT).

One method is through direct visualization, where the ETT is observed passing through the vocal cords. Another method is by checking for fogging in the ETT, which can indicate proper placement. Auscultation of bilateral equal breath sounds is also a reliable way to confirm correct ETT placement.

Additionally, the absence of borborygmi in the epigastrium is a positive sign that the ETT is in the correct position. Capnography or using a CO2 detector can provide further confirmation of proper ETT placement. Finally, chest radiography can be used to visually assess the placement of the endotracheal tube.

Flumazenil is a specific antagonist for benzodiazepines that can be beneficial in certain situations. It acts quickly, taking less than 1 minute to take effect, but its effects are short-lived and only last for less than 1 hour. The recommended dosage is 200 μg every 1-2 minutes, with a maximum dose of 3mg per hour.

It is important to avoid using Flumazenil if the patient is dependent on benzodiazepines or is taking tricyclic antidepressants. This is because it can trigger a withdrawal syndrome in these individuals, potentially leading to seizures or cardiac arrest.

For individuals who have been in contact with patients diagnosed with Neisseria meningitidis meningitis, the recommended medication to prevent the infection is rifampicin 600 mg taken orally twice a day for two days. Alternatively, a single oral dose of ciprofloxacin 500 mg can also be administered. However, it is important to note that both rifampicin and ciprofloxacin should not be used during pregnancy and are contraindicated in such cases. Therefore, in situations involving pregnant individuals, the preferred option is a single 250 mg dose of ceftriaxone given intramuscularly.

This patient is displaying symptoms and signs that are consistent with a diagnosis of acute pyelonephritis. Additionally, she is showing signs of sepsis and is pregnant, which makes it necessary to admit her for inpatient treatment.

According to 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 illness or 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 recommends 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 structural or functional 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 intravenous first-line options (if severely unwell or unable to take oral treatment) include amikacin, ceftriaxone, cefuroxime, ciprofloxacin, or gentamicin. 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 as follows: oral first-line option is cefalexin, and intravenous first-line option (if severely unwell or unable to take oral treatment) is cefuroxime. Intravenous second-line options or combining antibacterials should be considered if there are concerns about susceptibility or sepsis, and consultation with a local microbiologist is recommended.

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

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

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

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

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

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

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

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.

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

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

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

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

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

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

Acute mastoiditis commonly occurs as a complication of acute otitis media (AOM). In this case, the patient exhibits symptoms indicative of acute mastoiditis. The infection typically spreads from the middle ear tympanic cavity (acute otitis media) to the mastoid antrum through a narrow canal within the petrous temporal bone.

Further Reading:

Mastoiditis is an infection of the mastoid air cells, which are located in the mastoid process of the skull. It is usually caused by the spread of infection from the middle ear. The most common organism responsible for mastoiditis is Streptococcus pneumoniae, but other bacteria and fungi can also be involved. The infection can spread to surrounding structures, such as the meninges, causing serious complications like meningitis or cerebral abscess.

Mastoiditis can be classified as acute or chronic. Acute mastoiditis is a rare complication of acute otitis media, which is inflammation of the middle ear. It is characterized by severe ear pain, fever, swelling and redness behind the ear, and conductive deafness. Chronic mastoiditis is usually associated with chronic suppurative otitis media or cholesteatoma and presents with recurrent episodes of ear pain, headache, and fever.

Mastoiditis is more common in children, particularly those between 6 and 13 months of age. Other risk factors include immunocompromised patients, those with intellectual impairment or communication difficulties, and individuals with cholesteatoma.

Diagnosis of mastoiditis involves a physical examination, blood tests, ear swab for culture and sensitivities, and imaging studies like contrast-enhanced CT or MRI. Treatment typically involves referral to an ear, nose, and throat specialist, broad-spectrum intravenous antibiotics, pain relief, and myringotomy (a procedure to drain fluid from the middle ear).

Complications of mastoiditis are rare but can be serious. They include intracranial abscess, meningitis, subperiosteal abscess, neck abscess, venous sinus thrombosis, cranial nerve palsies, hearing loss, labyrinthitis, extension to the zygoma, and carotid artery arteritis. However, most patients with mastoiditis have a good prognosis and do not experience long-term ear problems.

When assessing a patient with epistaxis (nosebleed), it is important to start with a standard ABC assessment, focusing on the airway and hemodynamic status. Even if the bleeding appears to have stopped, it is crucial to evaluate the patient’s condition. If active bleeding is still present and there are signs of hemodynamic compromise, immediate resuscitative and first aid measures should be initiated.

Epistaxis should be treated as a circulatory emergency, especially in elderly patients, those with clotting disorders or bleeding tendencies, and individuals taking anticoagulants. In these cases, it is necessary to establish intravenous access using at least an 18-gauge (green) cannula. Blood samples, including a full blood count, urea and electrolytes, clotting profile, and group and save (depending on the amount of blood loss), should be sent for analysis. Patients should be assigned to a majors or closely observed area, as dislodgement of a blood clot can lead to severe bleeding.

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

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

Patients who have acute otitis media (AOM) and are immunocompromised or systemically unwell should be given an immediate prescription for antibiotics. However, for most patients with AOM, antibiotics are not necessary or can be delayed. An immediate antibiotic prescription should be offered to patients who are systemically unwell but do not require hospitalization, patients at high risk of complications due to underlying health conditions, and patients whose symptoms have persisted for four days or more without improvement. The recommended first choice antibiotic for AOM is amoxicillin.

Further Reading:

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

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

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

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

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

Methicillin-resistant Staphylococcus aureus (MRSA) has become a significant issue in hospitals and other healthcare facilities in recent years. MRSA refers to any strain of Staphylococcus aureus that has developed resistance to beta-lactam antibiotics, such as penicillins and cephalosporins. This resistance is caused by the presence of the mecA gene, which produces a penicillin-binding protein with low affinity. Fortunately, MRSA is typically susceptible to teicoplanin, vancomycin, daptomycin, and linezolid. On the other hand, imipenem is an intravenous beta-lactam antibiotic that belongs to the carbapenem subgroup.

Hypothermia occurs when the core body temperature drops below 35°C. It is categorized as mild (32-35°C), moderate (28-32°C), or severe (<28°C). Rescuers at the scene can use the Swiss staging system to describe the condition of victims. The stages range from clearly conscious and shivering to unconscious and not breathing, with death due to irreversible hypothermia being the most severe stage. There are several risk factors for hypothermia, including environmental exposure, unsatisfactory housing, poverty, lack of cold awareness, drugs, alcohol, acute confusion, hypothyroidism, and sepsis. The clinical features of hypothermia vary depending on the severity. At 32-35°C, symptoms may include apathy, amnesia, ataxia, and dysarthria. At 30-32°C, there may be a decreased level of consciousness, hypotension, arrhythmias, respiratory depression, and muscular rigidity. Below 30°C, ventricular fibrillation may occur, especially with excessive movement or invasive procedures. Diagnosing hypothermia involves checking the core temperature using an oesophageal, rectal, or tympanic probe with a low reading thermometer. Rectal and tympanic temperatures may lag behind core temperature and are unreliable in hypothermia. Various investigations should be carried out, including blood tests, blood glucose, amylase, blood cultures, arterial blood gas, ECG, chest X-ray, and CT head if there is suspicion of head injury or CVA. The management of hypothermia involves supporting the ABCs, treating the patient in a warm room, removing wet clothes and drying the skin, monitoring the ECG, providing warmed, humidified oxygen, correcting hypoglycemia with IV glucose, and handling the patient gently to avoid VF arrest. Rewarming methods include passive Rewarming with warm blankets or Bair hugger/polythene sheets, surface Rewarming with a water bath, core Rewarming with heated, humidified oxygen or peritoneal lavage, and extracorporeal Rewarming via cardiopulmonary bypass for severe hypothermia/cardiac arrest. In the case of hypothermic cardiac arrest, CPR should be performed with chest compressions and ventilations at standard rates.

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

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

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

Mitral regurgitation is characterized by a continuous murmur throughout systole that is often heard loudest at the apex and can be heard radiating to the left axilla.

Further Reading:

Mitral Stenosis:
– Causes: Rheumatic fever, Mucopolysaccharidoses, Carcinoid, Endocardial fibroelastosis
– Features: Mid-late diastolic murmur, loud S1, opening snap, low volume pulse, malar flush, atrial fibrillation, signs of pulmonary edema, tapping apex beat
– Features of severe mitral stenosis: Length of murmur increases, opening snap becomes closer to S2
– Investigation findings: CXR may show left atrial enlargement, echocardiography may show reduced cross-sectional area of the mitral valve

Mitral Regurgitation:
– Causes: Mitral valve prolapse, Myxomatous degeneration, Ischemic heart disease, Rheumatic fever, Connective tissue disorders, Endocarditis, Dilated cardiomyopathy
– Features: pansystolic murmur radiating to left axilla, soft S1, S3, laterally displaced apex beat with heave
– Signs of acute MR: Decompensated congestive heart failure symptoms
– Signs of chronic MR: Leg edema, fatigue, arrhythmia (atrial fibrillation)
– Investigation findings: Doppler echocardiography to detect regurgitant flow and pulmonary hypertension, ECG may show signs of LA enlargement and LV hypertrophy, CXR may show LA and LV enlargement in chronic MR and pulmonary edema in acute MR.

Ulnar neuritis is characterized by hand clumsiness and can progress to muscle weakness and wasting in the ulnar nerve-supplied muscles. It may also cause numbness or tingling in the little finger and medial half of the ring finger. This condition is caused by the narrowing of the ulnar groove at the elbow and is associated with risk factors such as osteoarthritis, trauma, and rheumatoid arthritis. Nerve conduction studies and surgical decompression may be necessary for diagnosis and treatment.

De Quervain’s tenosynovitis occurs when there is inflammation of the thumb extensor and abductor tendon sheaths. This leads to pain over the radial styloid, which worsens with forced adduction and flexion of the thumb. Treatment options include anti-inflammatory medications, thumb splints, and steroid injections.

Dupuytren’s contracture occurs when the palmar fascia contracts, preventing finger extension. It commonly affects the fifth finger on the right hand and is more prevalent in men over the age of 65. Risk factors for this condition include male sex, family history, alcohol use, diabetes, smoking, trauma, and manual labor. Surgical release is necessary if the contracture affects daily activities or work.

Trigger finger occurs when a nodule becomes stuck in the tendon sheath, causing the affected finger to remain in a fixed flexed position. The ring and middle fingers are most commonly affected, and risk factors include rheumatoid arthritis and diabetes. Steroid injections or surgical removal can be used to treat this condition.

Carpal tunnel syndrome occurs when the median nerve is compressed under the flexor retinaculum, resulting in numbness, pain, and wasting of the thenar eminence in the lateral three and a half digits. Symptoms are often worse at night. While most cases are idiopathic, risk factors include obesity, oral contraceptive use, hypothyroidism, rheumatoid arthritis, pregnancy, diabetes, amyloidosis, acromegaly, tumors compressing the carpal tunnel, and previous wrist fractures. Tinel’s test and Phalen’s test can help diagnose carpal tunnel syndrome, and nerve conduction studies may be requested for further evaluation. Treatment options include splints, steroid injections, and surgical release if symptoms persist.

The first step in managing hypertension in patients with phaeochromocytoma is to use alpha blockade, usually with a medication called phenoxybenzamine. This is followed by beta blockade. Before undergoing surgery to remove the phaeochromocytoma, patients need to be on both alpha and beta blockers. Alpha blockade is typically achieved by giving phenoxybenzamine intravenously at a dose of 10-40 mg over one hour, and then switching to an oral form (10-60 mg/day in divided doses). It is important to start alpha blockade at least 7 to 10 days before surgery to allow for an increase in blood volume. Beta blockade is only considered once alpha blockade has been achieved, as starting beta blockers too soon can lead to a dangerous increase in blood pressure.

Further Reading:

Phaeochromocytoma is a rare neuroendocrine tumor that secretes catecholamines. It typically arises from chromaffin tissue in the adrenal medulla, but can also occur in extra-adrenal chromaffin tissue. The majority of cases are spontaneous and occur in individuals aged 40-50 years. However, up to 30% of cases are hereditary and associated with genetic mutations. About 10% of phaeochromocytomas are metastatic, with extra-adrenal tumors more likely to be metastatic.

The clinical features of phaeochromocytoma are a result of excessive catecholamine production. Symptoms are typically paroxysmal and include hypertension, headaches, palpitations, sweating, anxiety, tremor, abdominal and flank pain, and nausea. Catecholamines have various metabolic effects, including glycogenolysis, mobilization of free fatty acids, increased serum lactate, increased metabolic rate, increased myocardial force and rate of contraction, and decreased systemic vascular resistance.

Diagnosis of phaeochromocytoma involves measuring plasma and urine levels of metanephrines, catecholamines, and urine vanillylmandelic acid. Imaging studies such as abdominal CT or MRI are used to determine the location of the tumor. If these fail to find the site, a scan with metaiodobenzylguanidine (MIBG) labeled with radioactive iodine is performed. The highest sensitivity and specificity for diagnosis is achieved with plasma metanephrine assay.

The definitive treatment for phaeochromocytoma is surgery. However, before surgery, the patient must be stabilized with medical management. This typically involves alpha-blockade with medications such as phenoxybenzamine or phentolamine, followed by beta-blockade with medications like propranolol. Alpha blockade is started before beta blockade to allow for expansion of blood volume and to prevent a hypertensive crisis.