The most probable diagnosis in this case is anterior uveitis. Anterior uveitis refers to the inflammation of the iris and typically manifests as a painful and red eye. It is often accompanied by symptoms such as sensitivity to light, excessive tearing, and decreased visual clarity. In some instances, there may be the presence of pus in the front part of the eye known as hypopyon.

Anterior uveitis can have various causes, including idiopathic (no known cause), 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 also be associated with anterior uveitis.

A significant association has been observed 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 middle spine area and sacroiliitis. It is worth noting that around 30% of men with unilateral uveitis will be found to have ankylosing spondylitis.

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

Further Reading:

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

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

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

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

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

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

The current guidelines from NICE provide recommendations for managing low back pain. It is suggested to consider using oral non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, while taking into account the potential risks of gastrointestinal, liver, and cardio-renal toxicity, as well as the person’s individual risk factors and age. When prescribing oral NSAIDs, it is important to conduct appropriate clinical assessments, monitor risk factors regularly, and consider the use of gastroprotective treatment. It is advised to prescribe the lowest effective dose of oral NSAIDs for the shortest duration possible. In cases where NSAIDs are contraindicated, not tolerated, or ineffective, weak opioids (with or without paracetamol) may be considered for managing acute low back pain. However, NICE does not recommend the use of paracetamol alone, opioids for chronic low back pain, serotonin reuptake inhibitors, serotonin-noradrenaline reuptake inhibitors, tricyclic antidepressants for non-neuropathic pain, anticonvulsants, or benzodiazepines for muscle spasm associated with acute low back pain. For more information, you can refer to the NICE guidance on low back pain and sciatica in individuals over 16 years old, as well as the NICE Clinical Knowledge Summary on low back pain without radiculopathy.

Blood transfusion is a crucial medical treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion use, errors and adverse reactions still occur. One common adverse reaction is febrile transfusion reactions, which present as an unexpected rise in temperature during or after transfusion. This can be caused by cytokine accumulation or recipient antibodies reacting to donor antigens. Treatment for febrile transfusion reactions is supportive, and other potential causes should be ruled out.

Another serious complication is acute haemolytic reaction, which is often caused by ABO incompatibility due to administration errors. This reaction requires the transfusion to be stopped and IV fluids to be administered. Delayed haemolytic reactions can occur several days after a transfusion and may require monitoring and treatment for anaemia and renal function. Allergic reactions, TRALI (Transfusion Related Acute Lung Injury), TACO (Transfusion Associated Circulatory Overload), and GVHD (Graft-vs-Host Disease) are other potential complications that require specific management approaches.

In summary, blood transfusion carries risks and potential complications, but efforts have been made to improve safety procedures. It is important to be aware of these complications and to promptly address any adverse reactions that may occur during or after a transfusion.

When it comes to managing bacterial conjunctivitis, NICE provides some helpful guidance. It is important to inform the patient that most cases of bacterial conjunctivitis will resolve on their own within 5-7 days without any treatment. However, in severe cases or situations where a quick resolution is necessary, topical antibiotics may be necessary. In some cases, it may be appropriate to delay treatment and advise the patient to start using topical antibiotics if their symptoms have not improved within 3 days.

There are a few options for topical antibiotics that can be used. One option is Chloramphenicol 0.5% drops, which should be applied every 2 hours for 2 days and then 4 times daily for 5 days. Another option is Chloramphenicol 1% ointment, which should be applied four times daily for 2 days and then twice daily for 5 days. Fusidic acid 1% eye drops can also be used as a second-line treatment and should be applied twice daily for 7 days.

By following these guidelines, healthcare professionals can effectively manage bacterial conjunctivitis and provide appropriate treatment options for their patients.

The most probable diagnosis in this case is a subarachnoid haemorrhage (SAH).

When assessing patients who present with an SAH, there may be focal neurological signs that can indicate the potential location of the aneurysm. Common sites for aneurysms include the bifurcation of the middle cerebral artery, the junction of the anterior communicating cerebral artery, and the junction of the posterior communicating artery with the internal carotid artery. If there is complete or partial palsy of the oculomotor nerve, it suggests the rupture of a posterior communicating artery aneurysm.

While hypertension is a risk factor for SAH, a significant increase in blood pressure may occur as a reflex response following the haemorrhage.

The first-line investigation for SAH is a CT head scan, which can detect over 95% of cases if performed within the first 24 hours. The sensitivity of the scan increases to nearly 100% if done within 6 hours of symptom onset. If the CT head scan is negative and there are no contraindications, a lumbar puncture (LP) should be performed to diagnose SAH. It is recommended to perform the LP at least 12 hours after the onset of headache. It is important to note that approximately 3% of patients with a negative CT scan will be confirmed to have had an SAH after undergoing an LP.

Zygomaticomaxillary complex fractures, also known as quadramalar or tripod fractures, make up around 40% of all midface fractures and are the second most common facial bone fractures after nasal bone fractures.

These injuries typically occur when a direct blow is delivered to the malar eminence of the cheek. They consist of four components:

1. Widening of the zygomaticofrontal suture
2. Fracture of the zygomatic arch
3. Fracture of the inferior orbital rim and the walls of the anterior and posterior maxillary sinuses
4. Fracture of the lateral orbital rim.

Given the patient’s symptoms and physical findings, the most appropriate initial treatment would be to administer Furosemide 40 mg intravenously. Furosemide is a loop diuretic that helps remove excess fluid from the body, which can alleviate symptoms of fluid overload such as shortness of breath and edema. By reducing fluid volume, Furosemide can help improve the patient’s breathing and relieve the strain on the heart.

Further Reading:

Cardiac failure, also known as heart failure, is a clinical syndrome characterized by symptoms and signs resulting from abnormalities in the structure or function of the heart. This can lead to reduced cardiac output or high filling pressures at rest or with stress. Heart failure can be caused by various problems such as myocardial, valvular, pericardial, endocardial, or arrhythmic issues.

The most common causes of heart failure in the UK are coronary heart disease and hypertension. However, there are many other possible causes, including valvular heart disease, structural heart disease, cardiomyopathies, certain drugs or toxins, endocrine disorders, nutritional deficiencies, infiltrative diseases, infections, and arrhythmias. Conditions that increase peripheral demand on the heart, such as anemia, pregnancy, sepsis, hyperthyroidism, Paget’s disease of bone, arteriovenous malformations, and beriberi, can also lead to high-output cardiac failure.

Signs and symptoms of heart failure include edema, lung crepitations, tachycardia, tachypnea, hypotension, displaced apex beat, right ventricular heave, elevated jugular venous pressure, cyanosis, hepatomegaly, ascites, pleural effusions, breathlessness, fatigue, orthopnea, paroxysmal nocturnal dyspnea, nocturnal cough or wheeze, and Presyncope.

To diagnose heart failure, NICE recommends three key tests: N-terminal pro-B-type natriuretic peptide (NT‑proBNP), transthoracic echocardiography, and ECG. Additional tests may include chest X-ray, blood tests (U&Es, thyroid function, LFT’s, lipid profile, HbA1C, FBC), urinalysis, and peak flow or spirometry.

Management of cardiogenic pulmonary edema, a complication of heart failure, involves ensuring a patent airway, optimizing breathing with supplemental oxygen and non-invasive ventilation if necessary, and addressing circulation with loop diuretics to reduce preload, vasodilators to reduce preload and afterload, and inotropes if hypotension or signs of end organ hypoperfusion persist.

In summary, cardiac failure is a clinical syndrome resulting from abnormalities in cardiac function. It can have various causes and is characterized by specific signs and symptoms. Diagnosis involves specific tests, and management focuses on addressing

This patient presents with symptoms and signs that are consistent with an atypical pneumonia, most likely caused by an infection with Mycoplasma pneumoniae. The clinical features of Mycoplasma pneumoniae infection include a flu-like illness that precedes respiratory symptoms, along with fever, myalgia, headache, diarrhea, and cough (initially dry but often becoming productive). Focal chest signs typically develop later in the course of the illness.

Mycoplasma pneumoniae infection is commonly associated with the development of erythema multiforme, a rash characterized by multiple red lesions on the limbs that evolve into target lesions a few days after the rash appears. Additionally, this infection can also cause Steven-Johnson syndrome. It is worth noting that haemolytic anaemia with cold agglutinins can complicate Mycoplasma pneumoniae infections, providing further evidence for the diagnosis.

The recommended first-line antibiotic for treating this case would be a macrolide, such as clarithromycin. Doxycycline can also be used but is generally considered a second-line option.

Croup is identified by a cough that sounds like a seal barking, especially worse during the night. Before the barking cough, there may be initial symptoms of a cough, runny nose, and congestion for 12 to 72 hours. Other signs of croup include a high-pitched sound when breathing (stridor), difficulty breathing (respiratory distress), and fever.

Further Reading:

Croup, also known as laryngotracheobronchitis, is a respiratory infection that primarily affects infants and toddlers. It is characterized by a barking cough and can cause stridor (a high-pitched sound during breathing) and respiratory distress due to swelling of the larynx and excessive secretions. The majority of cases are caused by parainfluenza viruses 1 and 3. Croup is most common in children between 6 months and 3 years of age and tends to occur more frequently in the autumn.

The clinical features of croup include a barking cough that is worse at night, preceded by symptoms of an upper respiratory tract infection such as cough, runny nose, and congestion. Stridor, respiratory distress, and fever may also be present. The severity of croup can be graded using the NICE system, which categorizes it as mild, moderate, severe, or impending respiratory failure based on the presence of symptoms such as cough, stridor, sternal/intercostal recession, agitation, lethargy, and decreased level of consciousness. The Westley croup score is another commonly used tool to assess the severity of croup based on the presence of stridor, retractions, air entry, oxygen saturation levels, and level of consciousness.

In cases of severe croup with significant airway obstruction and impending respiratory failure, symptoms may include a minimal barking cough, harder-to-hear stridor, chest wall recession, fatigue, pallor or cyanosis, decreased level of consciousness, and tachycardia. A respiratory rate over 70 breaths per minute is also indicative of severe respiratory distress.

Children with moderate or severe croup, as well as those with certain risk factors such as chronic lung disease, congenital heart disease, neuromuscular disorders, immunodeficiency, age under 3 months, inadequate fluid intake, concerns about care at home, or high fever or a toxic appearance, should be admitted to the hospital. The mainstay of treatment for croup is corticosteroids, which are typically given orally. If the child is too unwell to take oral medication, inhaled budesonide or intramuscular dexamethasone may be used as alternatives. Severe cases may require high-flow oxygen and nebulized adrenaline.

When considering the differential diagnosis for acute stridor and breathing difficulty, non-infective causes such as inhaled foreign bodies

The median nerve originates from the lateral and medial cords of the brachial plexus and receives contributions from the ventral roots of C5-C7 (lateral cord) and C8 and T1 (medial cord). It serves both motor and sensory functions.

In terms of motor function, the median nerve innervates the flexor muscles in the anterior compartment of the forearm, excluding the flexor carpi ulnaris and a portion of the flexor digitorum profundus, which are instead innervated by the ulnar nerve. Additionally, it innervates the thenar muscles and the lateral two lumbricals.

Regarding sensory function, the median nerve gives rise to the palmar cutaneous branch, which provides innervation to the lateral part of the palm. It also gives rise to the digital cutaneous branch, which innervates the lateral three and a half fingers on the palmar surface of the hand.

Within the forearm, the median nerve branches into two major branches: the anterior interosseous nerve (AIN) and the palmar cutaneous branch. The AIN supplies the flexor pollicis longus, pronator quadratus, and the lateral half of the flexor digitorum profundus. On the other hand, the palmar cutaneous branch provides sensory innervation to the skin of the radial palm.

Differentiating between damage to the median nerve at the elbow and wrist can be done by considering these two branches. Injury at the elbow affects these branches, while injury at the wrist spares them. It is important to note that the palmar cutaneous branch remains functional in carpal tunnel syndrome as it travels superficial to the flexor retinaculum. However, it can be damaged by laceration at the wrist.

A comparison of median nerve lesions at the wrist and elbow is presented in the table below:

Median nerve at elbow:
– Motor loss: Weak wrist flexion and abduction, loss of thumb abduction and opposition, loss of flexion of index and middle fingers
– Sensory loss: Lateral 3 and ½ fingers and nail beds, lateral side of palm
– Hand deformity: Ulnar deviation of wrist, thenar wasting, papal benediction on flexing fingers

Median nerve at wrist:
– Motor loss: Loss of thumb abduction and opposition, wrist and finger flexion intact (due to intact AIN)
– Sensory loss: Lateral 3 and ½ fingers and nail beds, lateral side of palm (but can be preserved depending upon palmar cutaneous branch)
– Hand deformity: Thenar wasting, no ulnar deviation of wrist or papal benediction (due to intact AIN)

Theophylline is a medication used to treat severe asthma. It is a bronchodilator that comes in modified-release forms, which can maintain therapeutic levels in the blood for 12 hours. Theophylline works by inhibiting phosphodiesterase and blocking the breakdown of cyclic AMP. It also competes with adenosine on A1 and A2 receptors.

Achieving the right dose of theophylline can be challenging because there is a narrow range between therapeutic and toxic levels. The half-life of theophylline can be influenced by various factors, further complicating dosage adjustments. It is recommended to aim for serum levels of 10-20 mg/l six to eight hours after the last dose.

Unlike many other medications, the specific brand of theophylline can significantly impact its effects. Therefore, it is important to prescribe theophylline by both its brand name and generic name.

Several factors can increase the half-life of theophylline, including heart failure, cirrhosis, viral infections, and certain drugs. Conversely, smoking, heavy drinking, and certain medications can decrease the half-life of theophylline.

There are several drugs that can either increase or decrease the plasma concentration of theophylline. Calcium channel blockers, cimetidine, fluconazole, macrolides, methotrexate, and quinolones can increase the concentration. On the other hand, carbamazepine, phenobarbitol, phenytoin, rifampicin, and St. John’s wort can decrease the concentration.

The clinical symptoms of theophylline toxicity are more closely associated with acute overdose rather than chronic overexposure. Common symptoms include headache, dizziness, nausea, vomiting, abdominal pain, rapid heartbeat, dysrhythmias, seizures, mild metabolic acidosis, low potassium, low magnesium, low phosphates, abnormal calcium levels, and high blood sugar.

Seizures are more prevalent in acute overdose cases, while chronic overdose typically presents with minimal gastrointestinal symptoms. Cardiac dysrhythmias are more common in chronic overdose situations compared to acute overdose.

The GCS scoring system evaluates a patient’s level of consciousness based on three criteria: eye opening, verbal response, and motor response. Each criterion is assigned a score, and the total score determines the patient’s GCS score. For example, if a patient has a GCS score of 10 (E3 V2 M5), it means they scored 3 out of 4 in eye opening, 2 out of 5 in verbal response, and 5 out of 6 in motor response.

Further Reading:

A subdural hematoma (SDH) is a condition where there is a collection of blood between the dura mater and the arachnoid mater of the brain. It occurs when the cortical bridging veins tear and bleed into the subdural space. Risk factors for SDH include head trauma, cerebral atrophy, advancing age, alcohol misuse, and certain medications or bleeding disorders. SDH can be classified as acute, subacute, or chronic depending on its age or speed of onset. Acute SDH is typically the result of head trauma and can progress to become chronic if left untreated.

The clinical presentation of SDH can vary depending on the nature of the condition. In acute SDH, patients may initially feel well after a head injury but develop more serious neurological symptoms later on. Chronic SDH may be detected after a CT scan is ordered to investigate confusion or cognitive decline. Symptoms of SDH can include increasing confusion, progressive decline in neurological function, seizures, headache, loss of consciousness, and even death.

Management of SDH involves an ABCDE approach, seizure management, confirming the diagnosis with CT or MRI, checking clotting and correcting coagulation abnormalities, managing raised intracranial pressure, and seeking neurosurgical opinion. Some SDHs may be managed conservatively if they are small, chronic, the patient is not a good surgical candidate, and there are no neurological symptoms. Neurosurgical intervention typically involves a burr hole craniotomy to decompress the hematoma. In severe cases with high intracranial pressure and significant brain swelling, a craniectomy may be performed, where a larger section of the skull is removed and replaced in a separate cranioplasty procedure.

CT imaging can help differentiate between subdural hematoma and other conditions like extradural hematoma. SDH appears as a crescent-shaped lesion on CT scans.

Glucagon may be an option for individuals experiencing anaphylaxis while taking beta blockers. However, it should not be chosen over Adrenaline as the primary treatment. Glucagon stimulates the production of cyclic AMP, which helps to increase heart contractility and heart rate, both of which are necessary during anaphylaxis. It is important to note that rapid administration of glucagon may lead to adverse effects such as nausea and vomiting.

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 with head injuries who show any signs of basal skull fracture, such as haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, or Battle’s sign, should undergo urgent CT imaging. Additionally, the following indications also warrant a CT scan: 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, post-traumatic seizure, new focal neurological deficit, greater than 1 episode of vomiting, or the patient being on anticoagulation. If any of these signs are present, a CT scan should be performed within 1 hour, except for patients on anticoagulation who should have a CT scan within 8 hours if they do not have any other signs. However, if patients on anticoagulation do have 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.

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

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

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

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

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

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

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

According to the latest NICE guidance, it is recommended that women aged 55 and over with unexplained symptoms of vaginal discharge should undergo a direct access ultrasound scan to assess for endometrial cancer. This recommendation applies to women who are experiencing these symptoms for the first time or who have thrombocytosis, haematuria (blood in the urine), visible haematuria, low haemoglobin levels, or high blood glucose levels. For more information, please refer to the NICE referral guidelines on the recognition and referral of suspected cancer.

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

When it comes to decision making and utilizing the wider medical team, it is crucial to always consider the possibility of new medical issues, even if the symptoms have occurred multiple times before. In the case of chest pain in elderly individuals, it is important to conduct further investigations, even if the presentation is similar to previous instances.

In addition, this patient appears to be displaying signs of depression. The loss of a pet can intensify feelings of loneliness. To address this, it would be wise to send a discharge summary to the patient’s general practitioner, outlining the findings and suggesting the potential benefits of providing social support for the patient.

By rephrasing and organizing the information with paragraph spacing, the explanation becomes clearer and easier to read.

To remove contaminated material, it is recommended to remove and dispose of clothing. It is important to seal the clothing and treat it as hazardous waste. If wet decontamination is being utilized, patients should shower using warm water and detergent.

Further Reading:

Chemical incidents can occur as a result of leaks, spills, explosions, fires, terrorism, or the use of chemicals during wars. Industrial sites that use chemicals are required to conduct risk assessments and have accident plans in place for such incidents. Health services are responsible for decontamination, unless mass casualties are involved, and all acute health trusts must have major incident plans in place.

When responding to a chemical incident, hospitals prioritize containment of the incident and prevention of secondary contamination, triage with basic first aid, decontamination if not done at the scene, recognition and management of toxidromes (symptoms caused by exposure to specific toxins), appropriate supportive or antidotal treatment, transfer to definitive treatment, a safe end to the hospital response, and continuation of business after the event.

To obtain advice when dealing with chemical incidents, the two main bodies are Toxbase and the National Poisons Information Service. Signage on containers carrying chemicals and material safety data sheets (MSDS) accompanying chemicals also provide information on the chemical contents and their hazards.

Contamination in chemical incidents can occur in three phases: primary contamination from the initial incident, secondary contamination spread via contaminated people leaving the initial scene, and tertiary contamination spread to the environment, including becoming airborne and waterborne. The ideal personal protective equipment (PPE) for chemical incidents is an all-in-one chemical-resistant overall with integral head/visor and hands/feet worn with a mask, gloves, and boots.

Decontamination of contaminated individuals involves the removal and disposal of contaminated clothing, followed by either dry or wet decontamination. Dry decontamination is suitable for patients contaminated with non-caustic chemicals and involves blotting and rubbing exposed skin gently with dry absorbent material. Wet decontamination is suitable for patients contaminated with caustic chemicals and involves a warm water shower while cleaning the body with simple detergent.

After decontamination, the focus shifts to assessing the extent of any possible poisoning and managing it. The patient’s history should establish the chemical the patient was exposed to, the volume and concentration of the chemical, the route of exposure, any protective measures in place, and any treatment given. Most chemical poisonings require supportive care using standard resuscitation principles, while some chemicals have specific antidotes. Identifying toxidromes can be useful in guiding treatment, and specific antidotes may be administered accordingly.

Rhabdomyolysis leads to an increase in phosphate levels in the blood, which in turn causes a decrease in the levels of ionized calcium. On the other hand, conditions such as Addison’s disease, hyperthyroidism, the use of thiazide diuretics, and lithium can all contribute to an elevation in calcium levels. There are also other factors that can result in low calcium levels, including hypoparathyroidism, a deficiency of vitamin D, sepsis, fluoride poisoning, a lack of magnesium, renal failure, tumor lysis syndrome, pancreatitis, and the administration of EDTA infusions.

There is no indication for an independent psychiatric evaluation of this patient. However, it is important to clearly document in his medical records that you have assessed his mental capacity and determined that he is capable of making decisions. It would not be appropriate in this case to refer him to a specialist against his wishes or to breach confidentiality by discussing his illness with his family or next of kin. According to the guidelines set by the General Medical Council (GMC), it is necessary to document the fact that the patient has declined relevant information. It is also important to avoid pressuring the patient to change their mind in these circumstances.

For further information, please refer to the GMC guidelines on treatment and care towards the end of life: good practice in decision making.

The most likely diagnosis in this case is Goodpasture’s syndrome, which is a rare autoimmune vasculitic disorder. It is characterized by a triad of symptoms including pulmonary hemorrhage, glomerulonephritis, and the presence of anti-glomerular basement membrane (Anti-GBM) antibodies. Goodpasture’s syndrome is more commonly seen in men, particularly in smokers. There is also an association with certain HLA types, specifically HLA-B7 and HLA-DRw2.

The clinical features of Goodpasture’s syndrome include constitutional symptoms such as fever, fatigue, nausea, and weight loss. Patients may also experience haemoptysis or pulmonary hemorrhage, chest pain, breathlessness, and inspiratory crackles at the lung bases. Anemia due to intrapulmonary bleeding, arthralgia, rapidly progressive glomerulonephritis, haematuria, hypertension, and hepatosplenomegaly (rarely) may also be present.

Blood tests will reveal an iron deficiency anemia, elevated white cell count, and renal impairment. Elisa for Anti-GBM antibodies is highly sensitive and specific, but it is not widely available. Approximately 30% of patients may also have circulating antineutrophilic cytoplasmic antibodies (ANCAs), although these are not specific for Goodpasture’s syndrome and can be found in other conditions such as Wegener’s granulomatosis.

Diagnosis is typically confirmed through renal biopsy, which can detect the presence of anti-GBM antibodies. The management of Goodpasture’s syndrome involves a combination of plasmapheresis to remove circulating antibodies and the use of corticosteroids or cyclophosphamide.

It is important to note that this patient’s history is inconsistent with a diagnosis of pulmonary embolism, as renal impairment, haematuria, and the presence of ANCAs and anti-GBM antibodies would not be expected. While pulmonary hemorrhage and renal impairment can occur in systemic lupus erythematosus, these are uncommon presentations, and the presence of ANCAs and anti-GBM antibodies would also be inconsistent with this diagnosis.

Churg-Strauss syndrome can present with pulmonary hemorrhage, and c-ANCA may be present, but patients typically have a history of asthma, sinusitis, and eosinophilia. Wegener’s granulomatosis can present similarly to Goodpasture’s syndrome,

Conn’s syndrome, also known as primary hyperaldosteronism, is often characterized by hypertension along with hypokalaemia and hypernatraemia. On the other hand, Addison’s disease typically leads to hypotension, hyponatremia, and hyperkalaemia. Hyponatraemia is commonly associated with pituitary adenoma, while acute renal failure (ARF) is characterized by elevated levels of urea and creatinine, and hyperkalaemia is frequently observed in ARF.

Further Reading:

Hyperaldosteronism is a condition characterized by excessive production of aldosterone by the adrenal glands. It can be classified into primary and secondary hyperaldosteronism. Primary hyperaldosteronism, also known as Conn’s syndrome, is typically caused by adrenal hyperplasia or adrenal tumors. Secondary hyperaldosteronism, on the other hand, is a result of high renin levels in response to reduced blood flow across the juxtaglomerular apparatus.

Aldosterone is the main mineralocorticoid steroid hormone produced by the adrenal cortex. It acts on the distal renal tubule and collecting duct of the nephron, promoting the reabsorption of sodium ions and water while secreting potassium ions.

The causes of hyperaldosteronism vary depending on whether it is primary or secondary. Primary hyperaldosteronism can be caused by adrenal adenoma, adrenal hyperplasia, adrenal carcinoma, or familial hyperaldosteronism. Secondary hyperaldosteronism can be caused by renal artery stenosis, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, or cor pulmonale.

Clinical features of hyperaldosteronism include hypertension, hypokalemia, metabolic alkalosis, hypernatremia, polyuria, polydipsia, headaches, lethargy, muscle weakness and spasms, and numbness. It is estimated that hyperaldosteronism is present in 5-10% of patients with hypertension, and hypertension in primary hyperaldosteronism is often resistant to drug treatment.

Diagnosis of hyperaldosteronism involves various investigations, including U&Es to assess electrolyte disturbances, aldosterone-to-renin plasma ratio (ARR) as the gold standard diagnostic test, ECG to detect arrhythmia, CT/MRI scans to locate adenoma, fludrocortisone suppression test or oral salt testing to confirm primary hyperaldosteronism, genetic testing to identify familial hyperaldosteronism, and adrenal venous sampling to determine lateralization prior to surgery.

Treatment of primary hyperaldosteronism typically involves surgical adrenalectomy for patients with unilateral primary aldosteronism. Diet modification with sodium restriction and potassium supplementation may also be recommended.

The nerve agents, also known as nerve gases, are a group of highly toxic chemical warfare agents that were initially developed just before and during World War II.

The first compounds to be created are referred to as the G agents (with G representing German, as they were discovered and synthesized by German scientists). These include Tabun (GA), Sarin (GB), and Soman (GD).

In the 1950s, the V agents (with V standing for venomous) were synthesized, and they are approximately 10 times more poisonous than sarin. These include Venomous agent X (VX), Venomous agent E (VE), Venomous agent G (VG), and Venomous agent M (VM).

One of the most well-known incidents involving the use of a nerve agent was the March 1995 Tokyo subway sarin attack. During this attack, Sarin was released into the Tokyo subway system during rush hour. As a result, over 5,000 people sought medical attention. Among them, 984 were moderately poisoned, 54 were severely poisoned, and 12 lost their lives.

The nerve agents are organophosphorus esters that are chemically related to organophosphorus insecticides. They work by inhibiting acetylcholinesterase (AChE), an enzyme that breaks down the neurotransmitter acetylcholine (ACh). This leads to an accumulation of ACh at both muscarinic and nicotinic cholinergic receptors.

Nerve agents can be absorbed through any body surface. When dispersed as a spray or aerosol, they can be absorbed through the skin, eyes, and respiratory tract. When dispersed as a vapor, they are primarily absorbed through the respiratory tract and eyes. If a sufficient amount of agent is absorbed, local effects are followed by generalized systemic effects.

Acute pancreatitis is a frequently encountered and serious source of acute abdominal pain. It involves the sudden inflammation of the pancreas, leading to the release of enzymes that cause self-digestion of the organ.

The clinical manifestations of acute pancreatitis include severe epigastric pain, accompanied by feelings of nausea and vomiting. The pain may radiate to the T6-T10 dermatomes or even to the shoulder tip through the phrenic nerve if the diaphragm is irritated. Other symptoms may include fever or sepsis, tenderness in the epigastric region, jaundice, and the presence of Gray-Turner sign (bruising on the flank) or Cullen sign (bruising around the belly button).

The most common causes of acute pancreatitis are gallstones and alcohol consumption. Additionally, many cases are considered idiopathic, meaning the cause is unknown. To aid in remembering the various causes, the mnemonic ‘I GET SMASHED’ can be helpful. Each letter represents a potential cause: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion stings, Hyperlipidemia/hypercalcemia, ERCP (endoscopic retrograde cholangiopancreatography), and Drugs.

The first line of treatment for neuropathic pain includes options such as amitriptyline, duloxetine, gabapentin, or pregabalin. The dosage should be adjusted based on how the individual responds to the medication and their ability to tolerate it. If the initial treatment does not provide relief or is not well tolerated, one of the remaining three medications can be considered as an alternative option.

The ability to rotate the neck actively by 45 degrees to the left and right is a crucial distinction between the ‘no risk’ and ‘low risk’ categories when applying the Canadian C-spine rules. In this case, the patient does not exhibit any high-risk factors for cervical spine injury according to the Canadian C-spine rule. However, they do have a low-risk factor due to their involvement in a minor rear-end motor collision. If a patient with a low-risk factor is unable to actively rotate their neck by 45 degrees in either direction, they should undergo imaging. It is important to note that while the patient’s use of anticoagulation medication may affect the need for brain imaging, it typically does not impact the decision to perform a CT scan of the cervical spine.

Further Reading:

When assessing for cervical spine injury, it is recommended to use the Canadian C-spine rules. These rules help determine the risk level for a potential injury. High-risk factors include being over the age of 65, experiencing a dangerous mechanism of injury (such as a fall from a height or a high-speed motor vehicle collision), or having paraesthesia in the upper or lower limbs. Low-risk factors include being involved in a minor rear-end motor vehicle collision, being comfortable in a sitting position, being ambulatory since the injury, having no midline cervical spine tenderness, or experiencing a delayed onset of neck pain. If a person is unable to actively rotate their neck 45 degrees to the left and right, their risk level is considered low. If they have one of the low-risk factors and can actively rotate their neck, their risk level remains low.

If a high-risk factor is identified or if a low-risk factor is identified and the person is unable to actively rotate their neck, full in-line spinal immobilization should be maintained and imaging should be requested. Additionally, if a patient has risk factors for thoracic or lumbar spine injury, imaging should be requested. However, if a patient has low-risk factors for cervical spine injury, is pain-free, and can actively rotate their neck, full in-line spinal immobilization and imaging are not necessary.

NICE recommends CT as the primary imaging modality for cervical spine injury in adults aged 16 and older, while MRI is recommended as the primary imaging modality for children under 16.

Different mechanisms of spinal trauma can cause injury to the spine in predictable ways. The majority of cervical spine injuries are caused by flexion combined with rotation. Hyperflexion can result in compression of the anterior aspects of the vertebral bodies, stretching and tearing of the posterior ligament complex, chance fractures (also known as seatbelt fractures), flexion teardrop fractures, and odontoid peg fractures. Flexion and rotation can lead to disruption of the posterior ligament complex and posterior column, fractures of facet joints, lamina, transverse processes, and vertebral bodies, and avulsion of spinous processes. Hyperextension can cause injury to the anterior column, anterior fractures of the vertebral body, and potential retropulsion of bony fragments or discs into the spinal canal. Rotation can result in injury to the posterior ligament complex and facet joint dislocation.

Patients who are on beta-blockers may not respond effectively to adrenaline during anaphylaxis. Research conducted on animals and reported cases have indicated that glucagon can be utilized to counteract the effects of beta-blockade if initial adrenaline doses prove ineffective.

Although prednisolone and hydrocortisone can be beneficial later on, it typically takes 6-8 hours for them to take full effect. Therefore, they are unlikely to have any impact on the patient during the brief period it will take for the ambulance to arrive.

Suxamethonium, also called succinylcholine, is a type of drug used to block neuromuscular transmission. It acts as an agonist by binding to acetylcholine receptors at the neuromuscular junction. Unlike acetylcholine, suxamethonium is not broken down by acetylcholinesterase, which means it stays bound to the receptors for a longer time, leading to prolonged inhibition of neuromuscular transmission. Eventually, suxamethonium is metabolized by plasma cholinesterase.

Further Reading:

Rapid sequence induction (RSI) is a method used to place an endotracheal tube (ETT) in the trachea while minimizing the risk of aspiration. It involves inducing loss of consciousness while applying cricoid pressure, followed by intubation without face mask ventilation. The steps of RSI can be remembered using the 7 P’s: preparation, pre-oxygenation, pre-treatment, paralysis and induction, protection and positioning, placement with proof, and post-intubation management.

Preparation involves preparing the patient, equipment, team, and anticipating any difficulties that may arise during the procedure. Pre-oxygenation is important to ensure the patient has an adequate oxygen reserve and prolongs the time before desaturation. This is typically done by breathing 100% oxygen for 3 minutes. Pre-treatment involves administering drugs to counter expected side effects of the procedure and anesthesia agents used.

Paralysis and induction involve administering a rapid-acting induction agent followed by a neuromuscular blocking agent. Commonly used induction agents include propofol, ketamine, thiopentone, and etomidate. The neuromuscular blocking agents can be depolarizing (such as suxamethonium) or non-depolarizing (such as rocuronium). Depolarizing agents bind to acetylcholine receptors and generate an action potential, while non-depolarizing agents act as competitive antagonists.

Protection and positioning involve applying cricoid pressure to prevent regurgitation of gastric contents and positioning the patient’s neck appropriately. Tube placement is confirmed by visualizing the tube passing between the vocal cords, auscultation of the chest and stomach, end-tidal CO2 measurement, and visualizing misting of the tube. Post-intubation management includes standard care such as monitoring ECG, SpO2, NIBP, capnography, and maintaining sedation and neuromuscular blockade.

Overall, RSI is a technique used to quickly and safely secure the airway in patients who may be at risk of aspiration. It involves a series of steps to ensure proper preparation, oxygenation, drug administration, and tube placement. Monitoring and post-intubation care are also important aspects of RSI.

An HBA1C result between 42-47 mmol/mol indicates a pre-diabetic condition.

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.

The use of glucose infusion is not recommended due to its hypertonic nature, which can potentially increase the risk of extravasation injury.

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.

To determine the amount of oxygen needed for a transfer, you can use the formula: 2 x Minute Volume (MV) x FiO2 x transfer time in minutes. This formula calculates the volume of oxygen that should be taken on the transfer. The Minute Volume (MV) represents the expected oxygen consumption. It is recommended to double the expected consumption to account for any unforeseen delays or increased oxygen demand during the transfer. Therefore, the second equation is used to calculate the volume of oxygen that will be taken on the transfer.

Further Reading:

Transfer of critically ill patients in the emergency department is a common occurrence and can involve intra-hospital transfers or transfers to another hospital. However, there are several risks associated with these transfers that doctors need to be aware of and manage effectively.

Technical risks include equipment failure or inadequate equipment, unreliable power or oxygen supply, incompatible equipment, restricted positioning, and restricted monitoring equipment. These technical issues can hinder the ability to detect and treat problems with ventilation, blood pressure control, and arrhythmias during the transfer.

Non-technical risks involve limited personal and medical team during the transfer, isolation and lack of resources in the receiving hospital, and problems with communication and liaison between the origin and destination sites.

Organizational risks can be mitigated by having a dedicated consultant lead for transfers who is responsible for producing guidelines, training staff, standardizing protocols, equipment, and documentation, as well as capturing data and conducting audits.

To optimize the patient’s clinical condition before transfer, several key steps should be taken. These include ensuring a low threshold for intubation and anticipating airway and ventilation problems, securing the endotracheal tube (ETT) and verifying its position, calculating oxygen requirements and ensuring an adequate supply, monitoring for circulatory issues and inserting at least two IV accesses, providing ongoing analgesia and sedation, controlling seizures, and addressing any fractures or temperature changes.

It is also important to have the necessary equipment and personnel for the transfer. Standard monitoring equipment should include ECG, oxygen saturation, blood pressure, temperature, and capnographic monitoring for ventilated patients. Additional monitoring may be required depending on the level of care needed by the patient.

In terms of oxygen supply, it is standard practice to calculate the expected oxygen consumption during transfer and multiply it by two to ensure an additional supply in case of delays. The suggested oxygen supply for transfer can be calculated using the minute volume, fraction of inspired oxygen, and estimated transfer time.

Overall, managing the risks associated with patient transfers requires careful planning, communication, and coordination to ensure the safety and well-being of critically ill patients.

In order to gain a comprehensive understanding of AF management, it is crucial to familiarize oneself with the terminology used to describe its various subtypes. These terms help categorize different episodes of AF based on their characteristics and outcomes.

Acute AF refers to any episode that occurs within the previous 48 hours. It can manifest with or without symptoms and may or may not recur. On the other hand, paroxysmal AF describes episodes that spontaneously end within 7 days, typically within 48 hours. While these episodes are often recurrent, they can progress into a sustained form of AF.

Recurrent AF is defined as experiencing two or more episodes of AF. If the episodes self-terminate, they are classified as paroxysmal AF. However, if the episodes do not self-terminate, they are categorized as persistent AF. Persistent AF lasts longer than 7 days or has occurred after a previous cardioversion. To terminate persistent AF, electrical or pharmacological intervention is required. In some cases, persistent AF can progress into permanent AF.

Permanent AF, also known as Accepted AF, refers to episodes that cannot be successfully terminated, have relapsed after termination, or where cardioversion is not pursued. This subtype signifies a more chronic and ongoing form of AF.

By understanding and utilizing these terms, healthcare professionals can effectively communicate and manage the different subtypes of AF.

The guidelines from the British Thoracic Society (BTS) recommend conducting investigations for Legionella infection in the following cases: severe community-acquired pneumonia, patients with specific risk factors, and during outbreaks of community-acquired pneumonia. To confirm a case, the Public Health England (PHE) requires one of the following: isolation and culture of Legionella species from clinical specimens (typically sputum), seroconversion with a four-fold increase in titre of indirect immunofluorescent antibody test (IFAT) using a validated technique, or confirmation of Legionella pneumophila urinary antigen using validated reagents or kits. The gold standard for confirmation is the isolation and culture of Legionella species, while cases of Pontiac fever are usually culture-negative. The HPA considers a case presumptive if there is a clinical diagnosis of pneumonia with a single high titre of 128 using IFAT, or a single titre of 64 in an outbreak. A positive result by direct immunofluorescence on a clinical specimen using validated monoclonal antibodies is also considered a presumptive case.

Chest X-rays are not typically recommended as a routine investigation for acute asthma. However, they may be necessary in specific situations. These situations include suspected pneumomediastinum or consolidation, as well as cases of life-threatening asthma. Additionally, if a patient fails to respond adequately to treatment or requires ventilation, a chest X-ray may be performed. It is important to note that these circumstances warrant the use of chest X-rays, but they are not routinely indicated for the investigation of acute asthma.

Due to the potentially life-threatening nature of the disease, it is crucial to initiate treatment without waiting for laboratory confirmation. Immediate administration of antibiotics is necessary.

In a hospital setting, the preferred agents for treatment are IV ceftriaxone (2 g for adults; 80 mg/kg for children) or IV cefotaxime (2 g for adults; 80 mg/kg for children). In the prehospital setting, IM benzylpenicillin can be given as an alternative. If there is a history of anaphylaxis to cephalosporins, chloramphenicol is a suitable alternative.

It is important to prioritize prompt treatment due to the severity of the disease. The recommended antibiotics should be administered as soon as possible to ensure the best possible outcome for the patient.

The administration of IV drugs (adrenaline and amiodarone) should be delayed until the core body temperature of patients with severe hypothermia reaches above 30°C, as recommended by the resus council.

Further Reading:

Cardiopulmonary arrest is a serious event with low survival rates. In non-traumatic cardiac arrest, only about 20% of patients who arrest as an in-patient survive to hospital discharge, while the survival rate for out-of-hospital cardiac arrest is approximately 8%. The Resus Council BLS/AED Algorithm for 2015 recommends chest compressions at a rate of 100-120 per minute with a compression depth of 5-6 cm. The ratio of chest compressions to rescue breaths is 30:2.

After a cardiac arrest, the goal of patient care is to minimize the impact of post cardiac arrest syndrome, which includes brain injury, myocardial dysfunction, the ischaemic/reperfusion response, and the underlying pathology that caused the arrest. The ABCDE approach is used for clinical assessment and general management. Intubation may be necessary if the airway cannot be maintained by simple measures or if it is immediately threatened. Controlled ventilation is aimed at maintaining oxygen saturation levels between 94-98% and normocarbia. Fluid status may be difficult to judge, but a target mean arterial pressure (MAP) between 65 and 100 mmHg is recommended. Inotropes may be administered to maintain blood pressure. Sedation should be adequate to gain control of ventilation, and short-acting sedating agents like propofol are preferred. Blood glucose levels should be maintained below 8 mmol/l. Pyrexia should be avoided, and there is some evidence for controlled mild hypothermia but no consensus on this.

Post ROSC investigations may include a chest X-ray, ECG monitoring, serial potassium and lactate measurements, and other imaging modalities like ultrasonography, echocardiography, CTPA, and CT head, depending on availability and skills in the local department. Treatment should be directed towards the underlying cause, and PCI or thrombolysis may be considered for acute coronary syndrome or suspected pulmonary embolism, respectively.

Patients who are comatose after ROSC without significant pre-arrest comorbidities should be transferred to the ICU for supportive care. Neurological outcome at 72 hours is the best prognostic indicator of outcome.

Digoxin is a medication used to treat atrial fibrillation and flutter as well as congestive cardiac failure. It belongs to a class of drugs called cardiac glycosides. Digoxin works by inhibiting the Na/K ATPase pump in the cardiac myocytes, which are the cells of the heart. This inhibition leads to an increase in the concentration of sodium inside the cells and indirectly increases the availability of calcium through the Na/Ca exchange mechanism. The rise in intracellular calcium levels results in a positive inotropic effect, meaning it strengthens the force of the heart’s contractions, and a negative chronotropic effect, meaning it slows down the heart rate.

However, it’s important to note that digoxin can cause toxicity, which is characterized by high levels of potassium in the blood, known as hyperkalemia. Normally, the Na/K ATPase pump helps maintain the balance of sodium and potassium by allowing sodium to leave the cells and potassium to enter. When digoxin blocks this pump, it disrupts this balance and leads to higher levels of potassium in the bloodstream.

Interestingly, the risk of developing digoxin toxicity is higher in individuals with low levels of potassium, known as hypokalemia. This is because digoxin binds to the ATPase pump at the same site as potassium. When potassium levels are low, digoxin can more easily bind to the ATPase pump and exert its inhibitory effects.

In summary, digoxin is a cardiac glycoside that is used to treat certain heart conditions. It works by inhibiting the Na/K ATPase pump, leading to increased intracellular calcium levels and resulting in a positive inotropic effect and negative chronotropic effect. However, digoxin can also cause toxicity, leading to high levels of potassium in the blood. The risk of toxicity is higher in individuals with low potassium levels.

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.

In a clinical setting, the prioritization of patient safety and the safety of staff members is crucial. Violence against other patients and health professionals is not tolerated. However, it is important to consider that the patient in question may be intoxicated or experiencing delirium tremens, which could impair their insight into their own behavior.

To address this situation, it would be wise to call local security as a precautionary measure. This action can serve as a backup if additional assistance is required. However, involving the police at this stage may escalate the situation unnecessarily and potentially agitate the patient further.

Administering sedation to the patient without understanding their medical history or gathering more information would not be appropriate. It is essential to have a comprehensive understanding of the patient’s condition before considering any interventions.

Similarly, asking the patient to leave the department immediately could potentially worsen the situation. It is important to approach the situation with caution and consider alternative strategies to de-escalate the situation effectively.

The appropriate dose of adrenaline for treating anaphylaxis in children under 6 years old is 150 micrograms, which is equivalent to 0.15 ml of a 1 in 1,000 solution.

Further Reading:

Anaphylaxis is a severe and life-threatening allergic reaction that affects the entire body. It is characterized by a rapid onset and can lead to difficulty breathing, low blood pressure, and loss of consciousness. In paediatrics, anaphylaxis is often caused by food allergies, with nuts being the most common trigger. Other causes include drugs and insect venom, such as from a wasp sting.

When treating anaphylaxis, time is of the essence and there may not be enough time to look up medication doses. Adrenaline is the most important drug in managing anaphylaxis and should be administered as soon as possible. The recommended doses of adrenaline vary based on the age of the child. For children under 6 months, the dose is 150 micrograms, while for children between 6 months and 6 years, the dose remains the same. For children between 6 and 12 years, the dose is increased to 300 micrograms, and for adults and children over 12 years, the dose is 500 micrograms. Adrenaline can be repeated every 5 minutes if necessary.

The preferred site for administering adrenaline is the anterolateral aspect of the middle third of the thigh. This ensures quick absorption and effectiveness of the medication. It is important to follow the Resuscitation Council guidelines for anaphylaxis management, as they have recently been updated.

In some cases, 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. This can help confirm the diagnosis and guide further management.

Overall, prompt recognition and administration of adrenaline are crucial in managing anaphylaxis in paediatrics. Following the recommended doses and guidelines can help ensure the best outcomes for patients experiencing this severe allergic reaction.

Based on the assessment findings, the most likely diagnosis for the 45-year-old patient with increasing hearing loss in the right ear is an acoustic neuroma. This is suggested by the lateralization of Weber’s test to the left side, indicating that sound is being heard better in the left ear. Additionally, the positive Rinne’s test in both ears suggests that air conduction is better than bone conduction, which is consistent with an acoustic neuroma. Other possible diagnoses such as otosclerosis, otitis media, cerumen impaction, and tympanic membrane perforation are less likely based on the given information.

Further Reading:

Hearing loss is a common complaint that can be caused by various conditions affecting different parts of the ear and nervous system. The outer ear is the part of the ear outside the eardrum, while the middle ear is located between the eardrum and the cochlea. The inner ear is within the bony labyrinth and consists of the vestibule, semicircular canals, and cochlea. The vestibulocochlear nerve connects the inner ear to the brain.

Hearing loss can be classified based on severity, onset, and type. Severity is determined by the quietest sound that can be heard, measured in decibels. It can range from mild to profound deafness. Onset can be sudden, rapidly progressive, slowly progressive, or fluctuating. Type of hearing loss can be either conductive or sensorineural. Conductive hearing loss is caused by issues in the external ear, eardrum, or middle ear that disrupt sound transmission. Sensorineural hearing loss is caused by problems in the cochlea, auditory nerve, or higher auditory processing pathways.

To diagnose sensorineural and conductive deafness, a 512 Hz tuning fork is used to perform Rinne and Weber’s tests. These tests help determine the type of hearing loss based on the results. In Rinne’s test, air conduction (AC) and bone conduction (BC) are compared, while Weber’s test checks for sound lateralization.

Cholesteatoma is a condition characterized by the abnormal accumulation of skin cells in the middle ear or mastoid air cell spaces. It is believed to develop from a retraction pocket that traps squamous cells. Cholesteatoma can cause the accumulation of keratin and the destruction of adjacent bones and tissues due to the production of destructive enzymes. It can lead to mixed sensorineural and conductive deafness as it affects both the middle and inner ear.

An acoustic neuroma, also referred to as a vestibular schwannoma, is a slow-growing tumor that develops from the Schwann cells of the vestibulocochlear nerve (8th cranial nerve). These growths are typically found at the cerebellopontine angle or within the internal auditory canal.

The most commonly affected nerves are the vestibulocochlear and trigeminal nerves. Patients typically present with a gradual deterioration of hearing in one ear, along with numbness and tingling in the face, ringing in the ears, and episodes of dizziness. Additionally, some patients may have a history of headaches. In rare cases, the facial nerve, glossopharyngeal nerve, vagus nerve, or accessory nerve may also be affected.

It is important to note that the trochlear nerve, which passes through the superior orbital fissure, is not impacted by an acoustic neuroma.

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.

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

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

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

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

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

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

Nitrous oxide should not be used in cases where there is trapped air, such as pneumothorax. This is because nitrous oxide can diffuse into the trapped air and increase the pressure, which can be harmful. This can be particularly dangerous in conditions like pneumothorax, where the trapped air can expand and affect breathing, or in cases of intracranial air after a head injury, trapped air after a recent underwater dive, or recent injection of gas into the eye.

Further Reading:

Entonox® is a mixture of 50% nitrous oxide and 50% oxygen that can be used for self-administration to reduce anxiety. It can also be used alongside other anesthesia agents. However, its mechanism of action for anxiety reduction is not fully understood. The Entonox bottles are typically identified by blue and white color-coded collars, but a new standard will replace these with dark blue shoulders in the future. It is important to note that Entonox alone cannot be used as the sole maintenance agent in anesthesia.

One of the effects of nitrous oxide is the second-gas effect, where it speeds up the absorption of other inhaled anesthesia agents. Nitrous oxide enters the alveoli and diffuses into the blood, displacing nitrogen. This displacement causes the remaining alveolar gases to become more concentrated, increasing the fractional content of inhaled anesthesia gases and accelerating the uptake of volatile agents into the blood.

However, when nitrous oxide administration is stopped, it can cause diffusion hypoxia. Nitrous oxide exits the blood and diffuses back into the alveoli, while nitrogen diffuses in the opposite direction. Nitrous oxide enters the alveoli much faster than nitrogen leaves, resulting in the dilution of oxygen within the alveoli. This can lead to diffusion hypoxia, where the oxygen concentration in the alveoli is diluted, potentially causing oxygen deprivation in patients breathing air.

There are certain contraindications for using nitrous oxide, as it can expand in air-filled spaces. It should be avoided in conditions such as head injuries with intracranial air, pneumothorax, recent intraocular gas injection, and entrapped air following a recent underwater dive.

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

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

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

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

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

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

Patients experiencing an anaphylactic reaction should be observed for a minimum of 6 hours. However, according to the Royal College of Emergency Medicine (RCEM), certain situations require a 24-hour observation period. These situations include patients with a history of biphasic reactions or known asthma, cases where there is a possibility of ongoing absorption of the allergen, limited access to emergency care, presentation during the evening or night, and severe reactions with a slow onset caused by idiopathic anaphylaxis. It is important to note that the National Institute for Health and Care Excellence (NICE) recommends that patients under the age of 16 be admitted under the care of a pediatrician for observation.

Further Reading:

Anaphylaxis is a severe and life-threatening allergic reaction that affects the entire body. It is characterized by a rapid onset and can lead to difficulty breathing, low blood pressure, and loss of consciousness. In paediatrics, anaphylaxis is often caused by food allergies, with nuts being the most common trigger. Other causes include drugs and insect venom, such as from a wasp sting.

When treating anaphylaxis, time is of the essence and there may not be enough time to look up medication doses. Adrenaline is the most important drug in managing anaphylaxis and should be administered as soon as possible. The recommended doses of adrenaline vary based on the age of the child. For children under 6 months, the dose is 150 micrograms, while for children between 6 months and 6 years, the dose remains the same. For children between 6 and 12 years, the dose is increased to 300 micrograms, and for adults and children over 12 years, the dose is 500 micrograms. Adrenaline can be repeated every 5 minutes if necessary.

The preferred site for administering adrenaline is the anterolateral aspect of the middle third of the thigh. This ensures quick absorption and effectiveness of the medication. It is important to follow the Resuscitation Council guidelines for anaphylaxis management, as they have recently been updated.

In some cases, 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. This can help confirm the diagnosis and guide further management.

Overall, prompt recognition and administration of adrenaline are crucial in managing anaphylaxis in paediatrics. Following the recommended doses and guidelines can help ensure the best outcomes for patients experiencing this severe allergic reaction.

Bronchiolitis is primarily caused by the respiratory syncytial virus (RSV), while whooping cough is caused by pertussis.

Further Reading:

Croup, also known as laryngotracheobronchitis, is a respiratory infection that primarily affects infants and toddlers. It is characterized by a barking cough and can cause stridor (a high-pitched sound during breathing) and respiratory distress due to swelling of the larynx and excessive secretions. The majority of cases are caused by parainfluenza viruses 1 and 3. Croup is most common in children between 6 months and 3 years of age and tends to occur more frequently in the autumn.

The clinical features of croup include a barking cough that is worse at night, preceded by symptoms of an upper respiratory tract infection such as cough, runny nose, and congestion. Stridor, respiratory distress, and fever may also be present. The severity of croup can be graded using the NICE system, which categorizes it as mild, moderate, severe, or impending respiratory failure based on the presence of symptoms such as cough, stridor, sternal/intercostal recession, agitation, lethargy, and decreased level of consciousness. The Westley croup score is another commonly used tool to assess the severity of croup based on the presence of stridor, retractions, air entry, oxygen saturation levels, and level of consciousness.

In cases of severe croup with significant airway obstruction and impending respiratory failure, symptoms may include a minimal barking cough, harder-to-hear stridor, chest wall recession, fatigue, pallor or cyanosis, decreased level of consciousness, and tachycardia. A respiratory rate over 70 breaths per minute is also indicative of severe respiratory distress.

Children with moderate or severe croup, as well as those with certain risk factors such as chronic lung disease, congenital heart disease, neuromuscular disorders, immunodeficiency, age under 3 months, inadequate fluid intake, concerns about care at home, or high fever or a toxic appearance, should be admitted to the hospital. The mainstay of treatment for croup is corticosteroids, which are typically given orally. If the child is too unwell to take oral medication, inhaled budesonide or intramuscular dexamethasone may be used as alternatives. Severe cases may require high-flow oxygen and nebulized adrenaline.

When considering the differential diagnosis for acute stridor and breathing difficulty, non-infective causes such as inhaled foreign bodies

To treat DKA, the girl is receiving intravenous fluids to rehydrate her. Additionally, insulin needs to be prescribed to help regulate her blood sugar levels.

The most suitable insulin regimen in this case would be an IV insulin infusion at 0.05 units/kg/hour. This means that the insulin will be administered through an intravenous line at a rate of 0.05 units per kilogram of the girl’s body weight per hour. This dosage is appropriate for managing DKA and will help to lower her blood sugar levels effectively.

Further Reading:

Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

According to the 2021 resus council guidelines, when administering an IV fluid challenge to a child with anaphylaxis, the recommended dose is 10 ml/kg. It is important to note that prior to the update, the advised dose was 20 ml/kg. In an exam, if you are provided with the child’s weight, you may be required to calculate the volume requirement.

Further Reading:

Anaphylaxis is a severe and life-threatening allergic reaction that affects the entire body. It is characterized by a rapid onset and can lead to difficulty breathing, low blood pressure, and loss of consciousness. In paediatrics, anaphylaxis is often caused by food allergies, with nuts being the most common trigger. Other causes include drugs and insect venom, such as from a wasp sting.

When treating anaphylaxis, time is of the essence and there may not be enough time to look up medication doses. Adrenaline is the most important drug in managing anaphylaxis and should be administered as soon as possible. The recommended doses of adrenaline vary based on the age of the child. For children under 6 months, the dose is 150 micrograms, while for children between 6 months and 6 years, the dose remains the same. For children between 6 and 12 years, the dose is increased to 300 micrograms, and for adults and children over 12 years, the dose is 500 micrograms. Adrenaline can be repeated every 5 minutes if necessary.

The preferred site for administering adrenaline is the anterolateral aspect of the middle third of the thigh. This ensures quick absorption and effectiveness of the medication. It is important to follow the Resuscitation Council guidelines for anaphylaxis management, as they have recently been updated.

In some cases, 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. This can help confirm the diagnosis and guide further management.

Overall, prompt recognition and administration of adrenaline are crucial in managing anaphylaxis in paediatrics. Following the recommended doses and guidelines can help ensure the best outcomes for patients experiencing this severe allergic reaction.

In stable patients with SVT, it is recommended to first try vagal manoeuvres before resorting to drug treatment. This approach is particularly applicable to patients who do not exhibit any adverse features, as mentioned in the case above.

Further Reading:

Supraventricular tachycardia (SVT) is a type of tachyarrhythmia that originates from the atria or above the bundle of His in the heart. It includes all atrial and junctional tachycardias, although atrial fibrillation is often considered separately. SVT typically produces a narrow QRS complex tachycardia on an electrocardiogram (ECG), unless there is an underlying conduction abnormality below the atrioventricular (AV) node. Narrow complex tachycardias are considered SVTs, while some broad complex tachycardias can also be SVTs with co-existent conduction delays.

SVT can be classified into three main subtypes based on where it arises: re-entrant accessory circuits (the most common type), atrial tachycardias, and junctional tachycardias. The most common SVTs are AVNRT (AV nodal re-entry tachycardia) and AVRT (AV re-entry tachycardia), which arise from accessory circuits within the heart. AVNRT involves an accessory circuit within the AV node itself, while AVRT involves an accessory pathway between the atria and ventricles that allows additional electrical signals to trigger the AV node.

Atrial tachycardias originate from abnormal foci within the atria, except for the SA node, AV node, or accessory pathway. Junctional tachycardias arise in the AV junction. The ECG features of SVTs vary depending on the type. Atrial tachycardias may have abnormal P wave morphology, an isoelectric baseline between P waves (in atrial flutter), and inverted P waves in certain leads. AVNRT may show pseudo R waves in V1 or pseudo S waves in certain leads, with an RP interval shorter than the PR interval. AVRT (WPW) may exhibit a delta wave on a resting ECG and retrograde P waves in the ST segment, with an RP interval shorter than the PR interval. Junctional tachycardias may have retrograde P waves before, during, or after the QRS complex, with inverted P waves in certain leads and upright P waves in others.

Treatment of SVT follows the 2021 resuscitation council algorithm for tachycardia with a pulse. The algorithm provides guidelines for managing stable patients with SVT.

Rapid tranquillisation involves administering medication through injection (typically into the muscle) when oral medication is not feasible or appropriate and immediate sedation is necessary. The current guidelines from NICE regarding the short-term management of violent and aggressive patients recommend the use of intramuscular lorazepam for rapid tranquillisation in children and young individuals. The dosage should be adjusted based on their age and weight. If there is only a partial response to intramuscular lorazepam, the dosage should be assessed according to the child or young person’s age and weight, and an additional dose may be considered.

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

This woman is displaying symptoms and signs that are in line with a diagnosis of meningococcal septicaemia. In the United Kingdom, the majority of cases of meningococcal septicaemia are caused by Neisseria meningitidis group B.

The implementation of a vaccination program for Neisseria meningitidis group C has significantly reduced the prevalence of this particular type. However, a vaccine for group B disease is currently undergoing clinical trials and is not yet accessible for widespread use.

To calculate the overall rate of fluid administration for a patient, we need to consider both the deficit and maintenance requirements. The deficit is determined by the weight of the patient, with a 1kg deficit equaling 1000ml. However, we also need to subtract the 200 ml bolus from the deficit calculation. So, the deficit is 1000 ml – 200 ml = 800 ml.

The deficit calculation is for the next 48 hours, while maintenance is calculated per day. For maintenance, we use the Holliday-Segar formula based on the patient’s weight. For this patient, the formula is as follows:

– 100 ml/kg/day for the first 10 kg of body weight = 10 x 100 = 1000 ml
– 50 ml/kg/day for the next 10 to 20 kg = 50 x 10 = 500 ml
– 20 ml/kg/day for each additional kilogram above 20 kg = 0 (as the patient only weighs 20kg)

So, the total maintenance requirement is 1500 ml per day (over 24 hours), which equals 62 ml/hour.

To determine the overall rate, we add the maintenance requirement (62 ml/hr) to the deficit requirement (17 ml/hr). Therefore, the overall rate of fluid administration for this patient is 79 ml/hr.

Further Reading:

Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

The finger has a total of four digital nerves. Two of these nerves, known as the palmar digital nerves, run along the palm side of each finger. The other two nerves, called the dorsal digital nerves, are located on the back side of the finger. However, the dorsal nerve supply changes slightly at the level of the proximal IP joint. Beyond this point, the dorsal nerve supply comes from the dorsal branch of the palmar digital nerve.

Further Reading:

Digital nerve blocks are commonly used to numb the finger for various procedures such as foreign body removal, dislocation reduction, and suturing. Sensation to the finger is primarily provided by the proper digital nerves, which arise from the common digital nerve. Each common digital nerve divides into two proper digital nerves, which run along the palmar aspect of the finger. These proper digital nerves give off a dorsal branch that supplies the dorsal aspect of the finger.

The most common technique for digital nerve blocks is the digital (ring) block. The hand is cleaned and the injection sites are cleansed with an alcohol swab. A syringe containing 1% lidocaine is prepared, and the needle is inserted at the base of the finger from a dorsal approach. Lidocaine is infiltrated under the skin, and the needle is then advanced towards the palmar aspect of the finger to inject more lidocaine. This process is repeated on the opposite side of the finger.

It is important not to use lidocaine with adrenaline for this procedure, as it may cause constriction and ischemia of the digital artery. Lidocaine 1% is the preferred local anesthetic, and the maximum dose is 3 ml/kg up to 200 mg. Contraindications for digital nerve blocks include compromised circulation to the finger, infection at the planned injection site, contraindication to local anesthetic (e.g. allergy), and suspected compartment syndrome (which is rare in the finger).

Complications of digital nerve blocks can include vascular injury to the digital artery or vein, injury to the digital nerve, infection, pain, allergic reaction, intravascular injection (which can be avoided by aspirating prior to injection), and systemic local anesthetic toxicity (which is uncommon with typical doses of lidocaine).

Spondyloarthritis is a term that encompasses various inflammatory conditions affecting both the joints and the sites where ligaments and tendons attach to the bones, known as entheses. The primary cause of spondyloarthritis is ankylosing spondylitis, but it can also be caused by reactive arthritis, psoriatic arthritis, and enteropathic arthropathies.

If individuals under the age of 45 exhibit four or more of the following symptoms, they should be referred for a potential diagnosis of spondyloarthritis:
– Presence of low back pain and being younger than 35 years old
– Waking up in the second half of the night due to pain
– Experiencing buttock pain
– Pain that improves with movement or within 48 hours of using nonsteroidal anti-inflammatory drugs (NSAIDs)
– Having a first-degree relative with spondyloarthritis
– History of current or past arthritis, psoriasis, or enthesitis

It is important to note that a progressive neurological deficit would be an atypical presentation for spondyloarthritis and may instead indicate cauda equina syndrome (CES).

A tension pneumothorax occurs when there is an air leak from the lung or chest wall that acts like a one-way valve. This causes air to build up in the pleural space without any way to escape. As a result, pressure in the pleural space increases and pushes the mediastinum into the opposite hemithorax. If left untreated, this can lead to cardiovascular instability, shock, and cardiac arrest.

The clinical features of tension pneumothorax include respiratory distress and cardiovascular instability. Tracheal deviation away from the side of the injury, unilateral absence of breath sounds on the affected side, and a hyper-resonant percussion note are also characteristic. Other signs include distended neck veins and cyanosis, which is a late sign. It’s important to note that both tension pneumothorax and massive haemothorax can cause decreased breath sounds on auscultation. However, percussion can help differentiate between the two conditions. Hyper-resonance suggests tension pneumothorax, while dullness suggests a massive haemothorax.

Tension pneumothorax is a clinical diagnosis and should not be delayed for radiological confirmation. Requesting a chest X-ray in this situation can delay treatment and put the patient at risk. Immediate decompression through needle thoracocentesis is the recommended treatment. Traditionally, a large-bore needle or cannula is inserted into the 2nd intercostal space in the midclavicular line of the affected hemithorax. However, studies on cadavers have shown better success in reaching the thoracic cavity when the 4th or 5th intercostal space in the midaxillary line is used in adult patients. ATLS now recommends this location for needle decompression in adults. The site for needle thoracocentesis in children remains the same, using the 2nd intercostal space in the midclavicular line. It’s important to remember that needle thoracocentesis is a temporary measure, and the insertion of a chest drain is the definitive treatment.

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.

Public Health England (PHE) has a primary goal of promptly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is important, it is not the main focus. Since 1968, the clinical suspicion of a notifiable infection has been sufficient for reporting purposes.

Registered medical practitioners (RMPs) are legally obligated to notify the designated proper officer at their local council or local health protection team (HPT) when they suspect cases of certain infectious diseases.

The Health Protection (Notification) Regulations 2010 specify the diseases that RMPs must report to the proper officers. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

It is worth noting that leptospirosis is not considered a notifiable disease, making it the least likely option among the diseases listed above.

Fragility fractures occur when a person experiences a fracture from a force that would not typically cause a fracture, such as a fall from a standing height or less. The most common areas for fragility fractures are the vertebrae, hip, and wrist. Osteoporosis is diagnosed when a patient’s bone mineral density, measured by a T-score on a DEXA scan, is -2.5 standard deviations or below. This T-score compares the patient’s bone density to the peak bone density of a population. In women over 75 years old, osteoporosis can be assumed without a DEXA scan. Osteopenia is diagnosed when a patient’s T-score is between -1 and -2.5 standard deviations below peak bone density. Risk factors for fractures include a family history of hip fractures, excessive alcohol consumption, and rheumatoid arthritis. Low bone mineral density can be indicated by a BMI below 22 kg/m2, untreated menopause, and conditions causing prolonged immobility or certain medical conditions. Medications used to prevent osteoporotic fractures in postmenopausal women include alendronate, risedronate, etidronate, and strontium ranelate. Raloxifene is not used for primary prevention. Alendronate is typically the first-choice medication and is recommended for women over 70 years old with confirmed osteoporosis and either a risk factor for fracture or low bone mineral density. Women over 75 years old with two risk factors or two indicators of low bone mineral density may be assumed to have osteoporosis without a DEXA scan. Other pharmacological interventions can be tried if alendronate is not tolerated.

Subdural hematoma (SDH) occurs when the bridging veins in the cortex of the brain tear and cause bleeding in the space between the brain and the outermost protective layer. This is different from extradural hematoma (EDH), which is usually caused by a rupture in the middle meningeal artery.

Further Reading:

A subdural hematoma (SDH) is a condition where there is a collection of blood between the dura mater and the arachnoid mater of the brain. It occurs when the cortical bridging veins tear and bleed into the subdural space. Risk factors for SDH include head trauma, cerebral atrophy, advancing age, alcohol misuse, and certain medications or bleeding disorders. SDH can be classified as acute, subacute, or chronic depending on its age or speed of onset. Acute SDH is typically the result of head trauma and can progress to become chronic if left untreated.

The clinical presentation of SDH can vary depending on the nature of the condition. In acute SDH, patients may initially feel well after a head injury but develop more serious neurological symptoms later on. Chronic SDH may be detected after a CT scan is ordered to investigate confusion or cognitive decline. Symptoms of SDH can include increasing confusion, progressive decline in neurological function, seizures, headache, loss of consciousness, and even death.

Management of SDH involves an ABCDE approach, seizure management, confirming the diagnosis with CT or MRI, checking clotting and correcting coagulation abnormalities, managing raised intracranial pressure, and seeking neurosurgical opinion. Some SDHs may be managed conservatively if they are small, chronic, the patient is not a good surgical candidate, and there are no neurological symptoms. Neurosurgical intervention typically involves a burr hole craniotomy to decompress the hematoma. In severe cases with high intracranial pressure and significant brain swelling, a craniectomy may be performed, where a larger section of the skull is removed and replaced in a separate cranioplasty procedure.

CT imaging can help differentiate between subdural hematoma and other conditions like extradural hematoma. SDH appears as a crescent-shaped lesion on CT scans.

The symptoms and signs of strokes can vary depending on which blood vessel is affected. Here is a summary of the main symptoms based on the territory affected:

Anterior cerebral artery: This can cause weakness on the opposite side of the body, with the leg and shoulder being more affected than the arm, hand, and face. There may also be minimal loss of sensation on the opposite side of the body. Other symptoms can include difficulty speaking (dysarthria), language problems (aphasia), apraxia (difficulty with limb movements), urinary incontinence, and changes in behavior and personality.

Middle cerebral artery: This can lead to weakness on the opposite side of the body, with the face and arm being more affected than the leg. There may also be a loss of sensation on the opposite side of the body. Depending on the dominant hemisphere of the brain, there may be difficulties with expressive or receptive language (dysphasia). In the non-dominant hemisphere, there may be neglect of the opposite side of the body.

Posterior cerebral artery: This can cause a loss of vision on the opposite side of both eyes (homonymous hemianopia). There may also be defects in a specific quadrant of the visual field. In some cases, there may be a syndrome affecting the thalamus on the opposite side of the body.

It’s important to note that these are just general summaries and individual cases may vary. If you suspect a stroke, it’s crucial to seek immediate medical attention.

All patients who present with painless haematuria should undergo cystoscopy to rule out bladder cancer. This procedure is typically done in an outpatient setting as part of a haematuria clinic, using a flexible cystoscope and local anaesthetic.

In this case, the likelihood of prostate cancer is much lower due to the patient’s relatively normal prostate examination and mild symptoms of bladder outlet obstruction.

Bladder cancer is the seventh most common cancer in the UK, with men being three times more likely to develop it than women. The main risk factors for bladder cancer are increasing age and smoking. Approximately 50% of bladder cancers are caused by smoking, which is believed to be due to the presence of certain chemicals that are excreted through the kidneys. Smokers have a 2-6 times higher risk of developing bladder cancer compared to non-smokers.

Painless macroscopic haematuria is the most common symptom in 80-90% of bladder cancer cases. There are usually no abnormalities found during a standard physical examination.

According to current recommendations, the following patients should be urgently referred for a urological assessment:
– Adults over 45 years old with unexplained visible haematuria and no urinary tract infection.
– Adults over 45 years old with visible haematuria that persists or recurs after successful treatment of a urinary tract infection.
– Adults aged 60 and over with unexplained non-visible haematuria and either dysuria or an elevated white cell count on a blood test.

For those aged 60 and over with recurrent or persistent unexplained urinary tract infection, a non-urgent referral for bladder cancer is recommended.

Entonox®, also known as ‘gas and air’ or ‘laughing gas’, is a combination of nitrous oxide and oxygen in equal proportions. It offers a mild sedative effect and helps reduce anxiety.

Further Reading:

Procedural sedation is commonly used by emergency department (ED) doctors to minimize pain and discomfort during procedures that may be painful or distressing for patients. Effective procedural sedation requires the administration of analgesia, anxiolysis, sedation, and amnesia. This is typically achieved through the use of a combination of short-acting analgesics and sedatives.

There are different levels of sedation, ranging from minimal sedation (anxiolysis) to general anesthesia. It is important for clinicians to understand the level of sedation being used and to be able to manage any unintended deeper levels of sedation that may occur. Deeper levels of sedation are similar to general anesthesia and require the same level of care and monitoring.

Various drugs can be used for procedural sedation, including propofol, midazolam, ketamine, and fentanyl. Each of these drugs has its own mechanism of action and side effects. Propofol is commonly used for sedation, amnesia, and induction and maintenance of general anesthesia. Midazolam is a benzodiazepine that enhances the effect of GABA on the GABA A receptors. Ketamine is an NMDA receptor antagonist and is used for dissociative sedation. Fentanyl is a highly potent opioid used for analgesia and sedation.

The doses of these drugs for procedural sedation in the ED vary depending on the drug and the route of administration. It is important for clinicians to be familiar with the appropriate doses and onset and peak effect times for each drug.

Safe sedation requires certain requirements, including appropriate staffing levels, competencies of the sedating practitioner, location and facilities, and monitoring. The level of sedation being used determines the specific requirements for safe sedation.

After the procedure, patients should be monitored until they meet the criteria for safe discharge. This includes returning to their baseline level of consciousness, having vital signs within normal limits, and not experiencing compromised respiratory status. Pain and discomfort should also be addressed before discharge.

For patients with sepsis and hypotension, it is recommended to administer 30ml of crystalloid fluid per kilogram of body weight. However, if the patient does not have acute kidney injury, is not hypotensive, and has a lactate level below 2 mmol/l, a 500ml immediate dose may be given.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

In an elderly patient with a history of gradual decline accompanied by symptoms of hyperglycemia, excessive thirst, recent infection, and very high blood sugar levels, the most likely diagnosis is a hyperosmolar hyperglycemic state (HHS). This condition can be life-threatening, with a mortality rate of approximately 50%. Common symptoms include high blood sugar levels, dehydration, altered mental status, and electrolyte imbalances. About 50% of patients with HHS also experience hypernatremia, an elevated sodium level in the blood.

To calculate the serum osmolality, the following formula can be used: 2 (K+ + Na+) + urea + glucose. In this particular case, the calculation would be 2 (3.2 + 154) + 17.6 + 32 = 364 mmol/l. Patients with HHS typically have a serum osmolality greater than 350 mmol/l.

In order to manage HHS, it is important to address the underlying cause and gradually and safely achieve the following goals:
1. Normalize the osmolality
2. Replace fluid and electrolyte losses
3. Normalize blood glucose levels

Given the presence of 1+ ketones in the patient’s urine, which is likely due to vomiting and a mild acidosis, it is recommended to discontinue the use of metformin due to the risk of metformin-associated lactic acidosis (MALA). Additionally, an intravenous infusion of insulin should be initiated in this case.

If significant ketonaemia is present (3β-hydroxybutyrate is more than 1 mmol/L), it indicates a relative deficiency of insulin, and insulin treatment should be started immediately. However, if significant ketonaemia is not present, insulin should not be initiated.

Patients with HHS are at a high risk of developing thromboembolism, and therefore, routine administration of low molecular weight heparin is recommended. In cases where the serum osmolality exceeds 350 mmol/l, full heparinization should be considered.

Sialolithiasis is a condition in which a calcified stone (sialolith) forms inside a salivary gland. The submandibular gland (Wharton’s duct) is the most common site, accounting for about 90% of cases, while the parotid gland is the second most affected. In rare instances, sialoliths can also develop in the sublingual gland or minor salivary glands.

The presence of a sialolith obstructs the flow of saliva, leading to pain and swelling in the affected gland during eating. The pain is most intense when salivary flow is high, such as before and during meals, and gradually subsides within an hour after eating. By palpating the floor of the mouth with both hands, a stone may be detected, and sometimes it can even be seen at the opening of the duct. If there is an accompanying infection, pus may be expressed from the gland.

To assess salivary flow, acidic foods like lemon juice can be used as a simple test. X-rays of the mouth’s floor can reveal the presence of a stone. Patients should be referred to an ear, nose, and throat specialist (ENT) for the removal of the stone.

Sialadenitis refers to inflammation of the salivary glands and can be either acute or chronic. Acute sialadenitis is most commonly caused by a bacterial infection, usually ascending from Staphylococcus aureus or Streptococcus viridans. It can occur as a result of sialolithiasis or poor oral hygiene. Clinically, there will be a painful swelling in the affected gland area, with redness of the overlying skin and potential swelling of the cheek and nearby regions. Patients often experience general malaise, with a low-grade fever and elevated inflammatory markers.

Parotitis, on the other hand, refers to inflammation of one or both parotid glands. This inflammation can be caused by bacteria (particularly Staphylococcus aureus), viruses (such as mumps), or tuberculosis.

Sjögren’s syndrome is an autoimmune disorder characterized by dry eyes and dry mouth.

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 patients are classified as Child-Pugh class C. In any given year, around 30% of patients with ascites, a condition characterized by 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 ascites, 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, chills, nausea, vomiting, abdominal pain, tenderness, worsening ascites, general malaise, and hepatic encephalopathy. Certain factors can increase the risk of developing SBP, such as severe liver disease, gastrointestinal bleeding, urinary tract infection, intestinal bacterial overgrowth, indwelling lines (e.g., central venous catheters or urinary catheters), previous episodes of SBP, and low levels of protein in the ascitic fluid.

To diagnose SBP, an abdominal paracentesis, also known as an ascitic tap, is performed. This involves locating the area of dullness on the flank, next to the rectus abdominis muscle, and performing the tap about 5 cm above and towards the midline from the anterior superior iliac spines.

Certain features on the analysis of the peritoneal fluid strongly suggest SBP, including a total white cell count in the ascitic fluid of more than 500 cells/µL, a total neutrophil count of more than 250 cells/µL, a lactate level in the ascitic fluid of more than 25 mg/dL, a pH of less than 7.35, and the presence of bacteria on Gram-stain.

Patients diagnosed with SBP should be admitted to the hospital and given broad-spectrum antibiotics. The preferred choice is an intravenous 3rd generation cephalosporin, such as ceftriaxone. If the patient is allergic to beta-lactam antibiotics, ciprofloxacin can be considered as an alternative. Administering intravenous albumin can help reduce the risk of kidney failure and mortality.

This child is displaying a typical pattern of symptoms for type I diabetes mellitus. He has recently experienced increased urination, excessive thirst, weight loss, and fatigue. Blood tests have revealed metabolic acidosis, and the presence of ketones in his urine indicates the development of diabetic ketoacidosis.

Based on the clinical history and examination, it strongly indicates that the patient has developed a pulmonary embolism due to a deep vein thrombosis in his right leg.

The symptoms commonly associated with a pulmonary embolism include shortness of breath, pleuritic chest pain, coughing, and/or coughing up blood. These symptoms may also suggest the presence of a deep vein thrombosis. Other clinical features that may be observed are rapid breathing and heart rate, fever, and in severe cases, signs of systemic shock, a gallop heart rhythm, and increased jugular venous pressure.

Dantrolene works by blocking the release of calcium ions from the sarcoplasmic reticulum in skeletal muscle cells. This reduces the amount of calcium available to bind to troponin on actin filaments, which in turn decreases the muscle’s ability to contract and reduces energy usage.

Further Reading:

Malignant hyperthermia is a rare and life-threatening syndrome that can be triggered by certain medications in individuals who are genetically susceptible. The most common triggers are suxamethonium and inhalational anaesthetic agents. The syndrome is caused by the release of stored calcium ions from skeletal muscle cells, leading to uncontrolled muscle contraction and excessive heat production. This results in symptoms such as high fever, sweating, flushed skin, rapid heartbeat, and muscle rigidity. It can also lead to complications such as acute kidney injury, rhabdomyolysis, and metabolic acidosis. Treatment involves discontinuing the trigger medication, administering dantrolene to inhibit calcium release and promote muscle relaxation, and managing any associated complications such as hyperkalemia and acidosis. Referral to a malignant hyperthermia center for further investigation is also recommended.

Amiodarone is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) while performing chest compressions. The prescribed dose is 300 mg, which should be given as an intravenous bolus. To ensure proper administration, the medication should be diluted in 20 mL of 5% dextrose solution.

In cases where VF/pVT continues after five defibrillation attempts, an additional dose of 150 mg of Amiodarone should be administered. It is important to note that Amiodarone is not suitable for treating PEA or asystole, and its use is specifically indicated for shockable cardiac arrest situations.

Amiodarone is a medication that can have numerous harmful side effects, making it crucial to conduct a comprehensive clinical assessment before starting treatment with it. Some of the side effects associated with amiodarone include corneal microdeposits, photosensitivity, nausea, sleep disturbance, hyperthyroidism, hypothyroidism, acute hepatitis and jaundice, peripheral neuropathy, lung fibrosis, QT prolongation, and optic neuritis (although this is very rare). If optic neuritis occurs, immediate discontinuation of amiodarone is necessary to prevent the risk of blindness.

The majority of patients taking amiodarone experience corneal microdeposits, but these typically resolve after treatment is stopped and rarely affect vision. Amiodarone has a chemical structure similar to thyroxine and can bind to the nuclear thyroid receptor, leading to both hypothyroidism and hyperthyroidism. However, hypothyroidism is more commonly observed, affecting around 5-10% of patients.

Small cell lung cancer (SCLC) that originates from neuroendocrine tissue can lead to the development of paraneoplastic endocrine syndromes, such as Cushing syndrome. This occurs due to the inappropriate secretion of ectopic adrenocorticotropic hormone (ACTH). In this case, it is highly likely that the patient has a neuroendocrine tumor within the lung that is secreting ACTH.

The signs and symptoms of Cushing syndrome may be minimal in cases of ectopic ACTH-secreting tumors, and the onset of symptoms may be sudden, especially in rapidly growing SCLCs. The typical biochemical profile observed in these cases includes elevated sodium levels, low potassium levels, and a metabolic alkalosis.

The tumors associated with the production of ectopic ACTH are as follows:
– Small cell lung cancer (SCLC) – 50%
– Bronchial carcinoid tumors – 10%
– Thymic carcinoma – 10%
– Pancreatic islet cell tumors – 5%
– Phaeochromocytoma – 5%
– Medullary thyroid carcinoma – 5%

Meniere’s disease is a condition that affects the inner ear and its cause is still unknown. It is believed to occur due to increased pressure and gradual enlargement of the endolymphatic system in the middle ear, also known as the membranous labyrinth.

Further Reading:

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

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

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

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

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

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

Phenytoin is a potent anti-epileptic drug that is no longer recommended as the initial treatment for generalized or partial epilepsy due to its toxic effects. Users often experience common symptoms such as ataxia, nystagmus, diplopia, tremor, and dysarthria. Additionally, other side effects may include depression, decreased cognitive abilities, coarse facial features, acne, gum enlargement, polyneuropathy, and blood disorders.

Cannabinoid hyperemesis syndrome (CHS) is an extremely rare form of cannabinoid toxicity that occurs in chronic smokers. It is characterized by recurring episodes of severe nausea and vomiting. One distinctive feature of this syndrome is that individuals who suffer from it often find relief from their symptoms by taking hot baths or showers, and they may compulsively bathe during episodes of nausea and vomiting.

CHS typically develops in heavy, long-term cannabis users who consume the drug multiple times a day for many years. On average, symptoms appear after about 16 years of cannabis use, although some patients may experience symptoms after as little as three years.

In 2009, Sontineni and colleagues established criteria for diagnosing cannabinoid hyperemesis syndrome. These criteria include essential factors such as long-term cannabis use, major factors like severe nausea and vomiting that occur in a cyclic pattern over months, and resolution of symptoms after discontinuing cannabis use. Supportive criteria include compulsive hot baths with symptom relief, colicky abdominal pain, and no evidence of inflammation in the gallbladder or pancreas.

The exact cause of CHS is not fully understood, but there are two main theories. One theory suggests that the syndrome is a result of a build-up of cannabinoids in the body, which leads to toxicity. Another theory proposes that the functionality of cannabinoid receptors in the brain, particularly in the hypothalamus, is affected, resulting in CHS.

Most conventional anti-emetic drugs are effective in treating the vomiting phase of CHS. During acute episodes, it is important to monitor the patient’s hydration status as the combination of hot baths and prolonged vomiting can lead to cannabinoid hyperemesis acute renal failure (CHARF). This can be easily prevented and treated with intravenous fluids.

Once the acute episode of vomiting and dehydration has been addressed, the condition can be easily cured by discontinuing cannabis consumption.

Diabetic amyotrophy, also referred to as proximal diabetic neuropathy, is the second most prevalent form of diabetic neuropathy. It typically begins with discomfort in the buttocks, hips, or thighs and is often initially experienced on one side. The pain may start off as mild and gradually progress or it can suddenly manifest, as seen in this case. Subsequently, weakness and wasting of the proximal muscles in the lower limbs occur, making it difficult for the patient to transition from sitting to standing without assistance. Reflexes in the affected areas can also be impacted. Good control of blood sugar levels, physiotherapy, and lifestyle adjustments can reverse diabetic amyotrophy.

Peripheral neuropathy is the most common type of diabetic neuropathy and typically manifests as pain or loss of sensation in the feet or hands.

Autonomic neuropathy leads to changes in digestion, bowel and bladder function, sexual response, and perspiration. It can also affect the cardiovascular system, resulting in rapid heart rates and orthostatic hypotension.

Focal neuropathy causes sudden weakness in a single nerve or group of nerves, resulting in pain, sensory loss, or muscle weakness. Any nerve in the body can be affected.

Patients diagnosed with ulcerative colitis face a significantly heightened risk of developing colon cancer. It is crucial for these individuals, especially those with severe or extensive disease, to undergo regular monitoring to detect any potential signs of colon cancer. The risk of developing colon cancer increases as the duration of ulcerative colitis progresses. After 10 years, the risk stands at 1 in 50. After 20 years, the risk increases to 1 in 12. And after 30 years, the risk further rises to 1 in 6. While Crohn’s disease also carries a risk of colonic carcinoma, it is comparatively smaller than that associated with ulcerative colitis.

Recognizing the extent of blood loss based on vital sign and mental status abnormalities is a crucial skill. The Advanced Trauma Life Support (ATLS) classification for hemorrhagic shock correlates the amount of blood loss with expected physiological responses in a healthy individual weighing 70 kg. In terms of body weight, the total circulating blood volume accounts for approximately 7%, which is roughly equivalent to five liters in an average 70 kg male patient.

The ATLS classification for hemorrhagic shock is as follows:

CLASS I:
– Blood loss: Up to 750 mL
– Blood loss (% blood volume): Up to 15%
– Pulse rate: Less than 100 beats per minute (bpm)
– Systolic blood pressure: Normal
– Pulse pressure: Normal (or increased)
– Respiratory rate: 14-20 breaths per minute
– Urine output: Greater than 30 mL/hr
– CNS/mental status: Slightly anxious

CLASS II:
– Blood loss: 750-1500 mL
– Blood loss (% blood volume): 15-30%
– Pulse rate: 100-120 bpm
– Systolic blood pressure: Normal
– Pulse pressure: Decreased
– Respiratory rate: 20-30 breaths per minute
– Urine output: 20-30 mL/hr
– CNS/mental status: Mildly anxious

CLASS III:
– Blood loss: 1500-2000 mL
– Blood loss (% blood volume): 30-40%
– Pulse rate: 120-140 bpm
– Systolic blood pressure: Decreased
– Pulse pressure: Decreased
– Respiratory rate: 30-40 breaths per minute
– Urine output: 5-15 mL/hr
– CNS/mental status: Anxious, confused

CLASS IV:
– Blood loss: More than 2000 mL
– Blood loss (% blood volume): More than 40%
– Pulse rate: More than 140 bpm
– Systolic blood pressure: Decreased
– Pulse pressure: Decreased
– Respiratory rate: More than 40 breaths per minute
– Urine output: Negligible
– CNS/mental status: Confused, lethargic

This patient is likely to have pigeon fancier’s lung, which is a type of extrinsic allergic alveolitis (EAA) caused by chronic exposure to avian antigens found in bird droppings. This condition leads to hypersensitivity pneumonitis and the formation of granulomas in the lungs.

While his presentation could also be consistent with idiopathic pulmonary fibrosis, the fact that he keeps and races pigeons makes EAA more likely in this case.

EAA can manifest as either an acute or chronic condition. The acute form typically presents with flu-like symptoms such as fever, cough, chest tightness, and breathlessness occurring 4 to 6 hours after exposure.

The clinical features of chronic pigeon fancier’s lung include a productive cough, progressive breathlessness, weight loss, anorexia, fatigue, and malaise.

Other forms of EAA include farmer’s lung (caused by exposure to Saccharopolyspora rectivirgula from wet hay), malt-worker’s lung (caused by exposure to Aspergillus clavatus from moldy malt), cheese-worker’s lung (caused by exposure to Penicillium casei from moldy cheese), chemical worker’s lung (caused by exposure to trimetallic anhydride, diisocyanate, and methylene diisocyanate), mushroom worker’s lung (caused by exposure to thermophilic actinomycetes in mushroom compost), and hot tub lung (caused by exposure to Mycobacterium avium from poorly maintained hot tubs).

Sheehan’s syndrome is a condition where the pituitary gland becomes damaged due to insufficient blood flow and shock during and after childbirth, leading to hypopituitarism. The risk of developing this syndrome is higher in pregnancies with conditions that increase the chances of bleeding, such as placenta praevia and multiple pregnancies. However, Sheehan’s syndrome is quite rare, affecting only 1 in 10,000 pregnancies.

During pregnancy, the anterior pituitary gland undergoes hypertrophy, making it more vulnerable to ischaemia in the later stages. While the posterior pituitary gland is usually not affected due to its own direct blood supply, there have been rare cases where it is involved. In these instances, central diabetes insipidus, a form of posterior pituitary dysfunction, can occur as a complication of Sheehan’s syndrome.

The clinical features of Sheehan’s syndrome include the absence or infrequency of menstrual periods, the inability to produce milk and breastfeed (galactorrhoea), decreased libido, fatigue and tiredness, loss of pubic and axillary hair, and the potential development of secondary hypothyroidism and adrenal insufficiency. Serum prolactin levels are typically low (less than 5ng/ml). An MRI can be helpful in ruling out other pituitary issues, such as a pituitary tumor.

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

Narrow QRS complex tachycardia is a term used to describe a fast heart rhythm with a pulse rate over 100 bpm and a QRS duration shorter than 120 ms.

Further Reading:

Supraventricular tachycardia (SVT) is a type of tachyarrhythmia that originates from the atria or above the bundle of His in the heart. It includes all atrial and junctional tachycardias, although atrial fibrillation is often considered separately. SVT typically produces a narrow QRS complex tachycardia on an electrocardiogram (ECG), unless there is an underlying conduction abnormality below the atrioventricular (AV) node. Narrow complex tachycardias are considered SVTs, while some broad complex tachycardias can also be SVTs with co-existent conduction delays.

SVT can be classified into three main subtypes based on where it arises: re-entrant accessory circuits (the most common type), atrial tachycardias, and junctional tachycardias. The most common SVTs are AVNRT (AV nodal re-entry tachycardia) and AVRT (AV re-entry tachycardia), which arise from accessory circuits within the heart. AVNRT involves an accessory circuit within the AV node itself, while AVRT involves an accessory pathway between the atria and ventricles that allows additional electrical signals to trigger the AV node.

Atrial tachycardias originate from abnormal foci within the atria, except for the SA node, AV node, or accessory pathway. Junctional tachycardias arise in the AV junction. The ECG features of SVTs vary depending on the type. Atrial tachycardias may have abnormal P wave morphology, an isoelectric baseline between P waves (in atrial flutter), and inverted P waves in certain leads. AVNRT may show pseudo R waves in V1 or pseudo S waves in certain leads, with an RP interval shorter than the PR interval. AVRT (WPW) may exhibit a delta wave on a resting ECG and retrograde P waves in the ST segment, with an RP interval shorter than the PR interval. Junctional tachycardias may have retrograde P waves before, during, or after the QRS complex, with inverted P waves in certain leads and upright P waves in others.

Treatment of SVT follows the 2021 resuscitation council algorithm for tachycardia with a pulse. The algorithm provides guidelines for managing stable patients with SVT.

Urinary alkalinisation, which involves the intravenous administration of sodium bicarbonate, carries the risk of hypokalaemia. It is important to note that both alkalosis and acidosis can cause shifts in potassium levels. In the case of alkalinisation, potassium is shifted from the plasma into the cells. Therefore, it is crucial to closely monitor the patient for hypokalaemia by checking their potassium levels every 1-2 hours.

Further Reading:

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

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

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

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

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

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

Lown-Ganong-Levine (LGL) syndrome is a condition that affects the electrical conducting system of the heart. It is classified as a pre-excitation syndrome, similar to the more well-known Wolff-Parkinson-White (WPW) syndrome. However, unlike WPW syndrome, LGL syndrome does not involve an accessory pathway for conduction. Instead, it is believed that there may be accessory fibers present that bypass all or part of the atrioventricular node.

When looking at an electrocardiogram (ECG) of a patient with LGL syndrome in sinus rhythm, there are several characteristic features to observe. The PR interval, which represents the time it takes for the electrical signal to travel from the atria to the ventricles, is typically shortened and measures less than 120 milliseconds. The QRS duration, which represents the time it takes for the ventricles to contract, is normal. The P wave, which represents the electrical activity of the atria, may be normal or inverted. However, what distinguishes LGL syndrome from other pre-excitation syndromes is the absence of a delta wave, which is a slurring of the initial rise in the QRS complex.

It is important to note that LGL syndrome predisposes individuals to paroxysmal supraventricular tachycardia (SVT), a rapid heart rhythm that originates above the ventricles. However, it does not increase the risk of developing atrial fibrillation or flutter, which are other types of abnormal heart rhythms.

Early assessment of the airway is a critical aspect of managing a patient who has suffered burns. Airway blockage can occur rapidly due to direct injury, such as inhalation injury, or as a result of swelling caused by the burn. If there is a history of trauma, the airway should be evaluated and treated while maintaining control of the cervical spine.

Signs of airway obstruction may not be immediately apparent, as swelling typically does not occur right away. Children with thermal burns are at a higher risk of airway obstruction compared to adults due to their smaller airway size, so they require careful observation.

There are several risk factors for airway obstruction in burned patients, including inhalation injury, the presence of soot in the mouth or nostrils, singed nasal hairs, burns to the head, face, or neck, burns inside the mouth, a large burn area with increasing depth, and associated trauma. A carboxyhemoglobin level above 10% is also suggestive of an inhalation injury.

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

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

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

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

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

Most duodenal ulcers are caused by H. pylori infection, while peptic ulcers not associated with H. pylori are typically caused by the use of NSAIDs.

Further Reading:

Peptic ulcer disease (PUD) is a condition characterized by a break in the mucosal lining of the stomach or duodenum. It is caused by an imbalance between factors that promote mucosal damage, such as gastric acid, pepsin, Helicobacter pylori infection, and NSAID drug use, and factors that maintain mucosal integrity, such as prostaglandins, mucus lining, bicarbonate, and mucosal blood flow.

The most common causes of peptic ulcers are H. pylori infection and NSAID use. Other factors that can contribute to the development of ulcers include smoking, alcohol consumption, certain medications (such as steroids), stress, autoimmune conditions, and tumors.

Diagnosis of peptic ulcers involves screening for H. pylori infection through breath or stool antigen tests, as well as upper gastrointestinal endoscopy. Complications of PUD include bleeding, perforation, and obstruction. Acute massive hemorrhage has a case fatality rate of 5-10%, while perforation can lead to peritonitis with a mortality rate of up to 20%.

The symptoms of peptic ulcers vary depending on their location. Duodenal ulcers typically cause pain that is relieved by eating, occurs 2-3 hours after eating and at night, and may be accompanied by nausea and vomiting. Gastric ulcers, on the other hand, cause pain that occurs 30 minutes after eating and may be associated with nausea and vomiting.

Management of peptic ulcers depends on the underlying cause and presentation. Patients with active gastrointestinal bleeding require risk stratification, volume resuscitation, endoscopy, and proton pump inhibitor (PPI) therapy. Those with perforated ulcers require resuscitation, antibiotic treatment, analgesia, PPI therapy, and urgent surgical review.

For stable patients with peptic ulcers, lifestyle modifications such as weight loss, avoiding trigger foods, eating smaller meals, quitting smoking, reducing alcohol consumption, and managing stress and anxiety are recommended. Medication review should be done to stop causative drugs if possible. PPI therapy, with or without H. pylori eradication therapy, is also prescribed. H. pylori testing is typically done using a carbon-13 urea breath test or stool antigen test, and eradication therapy involves a 7-day triple therapy regimen of antibiotics and PPI.

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.

This patient is currently experiencing moderate shock, classified as class III. This level of shock corresponds to a loss of 30-40% of their circulatory volume, which is equivalent to a blood loss of 1500-2000 mL.

Hemorrhage can be categorized into four different classes based on physiological parameters and clinical signs. These classes are classified as class I, class II, class III, and class IV.

In class I hemorrhage, the blood loss is up to 750 mL or up to 15% of the blood volume. The pulse rate is less than 100 beats per minute, and the systolic blood pressure is normal. The pulse pressure may be normal or increased, and the respiratory rate is within the range of 14-20 breaths per minute. The urine output is greater than 30 mL per hour, and the patient’s CNS/mental status is slightly anxious.

In class II hemorrhage, the blood loss ranges from 750-1500 mL or 15-30% of the blood volume. The pulse rate is between 100-120 beats per minute, and the systolic blood pressure remains normal. The pulse pressure is decreased, and the respiratory rate increases to 20-30 breaths per minute. The urine output decreases to 20-30 mL per hour, and the patient may experience mild anxiety.

The patient in this case is in class III hemorrhage, with a blood loss of 1500-2000 mL or 30-40% of the blood volume. The pulse rate is elevated, ranging from 120-140 beats per minute, and the systolic blood pressure is decreased. The pulse pressure is also decreased, and the respiratory rate is elevated to 30-40 breaths per minute. The urine output decreases significantly to 5-15 mL per hour, and the patient may experience anxiety and confusion.

Class IV hemorrhage represents the most severe level of blood loss, with a loss of over 40% of the blood volume. The pulse rate is greater than 140 beats per minute, and the systolic blood pressure is significantly decreased. The pulse pressure is decreased, and the respiratory rate is over 40 breaths per minute. The urine output becomes negligible, and the patient may become confused and lethargic.

In patients with hypothermia, the pulse check during CPR should be extended to 1 minute. Additionally, several adjustments need to be made to the CPR protocol. Firstly, mechanical ventilation should be used due to the stiffness of the chest wall. Secondly, the dosing or omission of cardiac arrest drugs should be adjusted based on the patient’s temperature. The defibrillation pattern should also be modified, with 3 shocks attempted before re-attempting defibrillation only when the body temperature is above 30ºC. Certain electrolyte disturbances, such as mild hypokalemia, should not be treated as potassium levels typically rise with Rewarming. It is important to plan for prolonged resuscitation in these cases. Lastly, uncorrected ABG results should be used, without adjusting for temperature.

Further Reading:

Hypothermic cardiac arrest is a rare situation that requires a tailored approach. Resuscitation is typically prolonged, but the prognosis for young, previously healthy individuals can be good. Hypothermic cardiac arrest may be associated with drowning. Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, basal metabolic rate falls and cell signaling between neurons decreases, leading to reduced tissue perfusion. Signs and symptoms of hypothermia progress as the core temperature drops, initially presenting as compensatory increases in heart rate and shivering, but eventually ceasing as the temperature drops into moderate hypothermia territory.

ECG changes associated with hypothermia include bradyarrhythmias, Osborn waves, prolonged PR, QRS, and QT intervals, shivering artifact, ventricular ectopics, and cardiac arrest. When managing hypothermic cardiac arrest, ALS should be initiated as per the standard ALS algorithm, but with modifications. It is important to check for signs of life, re-warm the patient, consider mechanical ventilation due to chest wall stiffness, adjust dosing or withhold drugs due to slowed drug metabolism, and correct electrolyte disturbances. The resuscitation of hypothermic patients is often prolonged and may continue for a number of hours.

Pulse checks during CPR may be difficult due to low blood pressure, and the pulse check is prolonged to 1 minute for this reason. Drug metabolism is slowed in hypothermic patients, leading to a build-up of potentially toxic plasma concentrations of administered drugs. Current guidance advises withholding drugs if the core temperature is below 30ºC and doubling the drug interval at core temperatures between 30 and 35ºC. Electrolyte disturbances are common in hypothermic patients, and it is important to interpret results keeping the setting in mind. Hypoglycemia should be treated, hypokalemia will often correct as the patient re-warms, ABG analyzers may not reflect the reality of the hypothermic patient, and severe hyperkalemia is a poor prognostic indicator.

Different warming measures can be used to increase the core body temperature, including external passive measures such as removal of wet clothes and insulation with blankets, external active measures such as forced heated air or hot-water immersion, and internal active measures such as inhalation of warm air, warmed intravenous fluids, gastric, bladder, peritoneal and/or pleural lavage and high volume renal haemofilter.

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

Erythroderma is a condition characterized by widespread redness affecting more than 90% of the body surface. It is also known as exfoliative erythroderma due to the presence of skin exfoliation. Another term used to describe this condition is the red man syndrome.

The clinical features of exfoliative erythroderma include the rapid spread of redness to cover more than 90% of the body surface. Scaling of the skin occurs between days 2 and 6, leading to thickening of the skin. Despite the skin feeling hot, patients often experience a sensation of coldness. Keratoderma, which is the thickening of the skin on the palms and soles, may develop. Over time, erythema and scaling of the scalp can result in hair loss. The nails may become thickened, ridged, and even lost. Lymphadenopathy, or enlarged lymph nodes, is a common finding. In some cases, the patient’s overall health may be compromised.

Exfoliative erythroderma can be caused by various factors, including eczema (with atopic dermatitis being the most common underlying cause), psoriasis, lymphoma and leukemia (with cutaneous T-cell lymphoma and Hodgkin lymphoma being the most common malignant causes), certain drugs (more than 60 drugs have been implicated, with sulphonamides, isoniazid, penicillin, antimalarials, phenytoin, captopril, and cimetidine being the most commonly associated), idiopathic (unknown cause), and rare conditions such as pityriasis rubra pilaris and pemphigus foliaceus. Withdrawal of corticosteroids, underlying infections, hypocalcemia, and the use of strong coal tar preparations can also precipitate exfoliative erythroderma.

Potential complications of exfoliative erythroderma include dehydration, hypothermia, cardiac failure, overwhelming secondary infection, protein loss and edema, anemia (due to loss of iron, B12, and folate), and lymphadenopathy.

Management of exfoliative erythroderma should involve referring the patient to the medical on-call team and dermatology for admission. It is important to keep the patient warm and start intravenous fluids, such as warmed 0.9% saline. Applying generous amounts of emollients and wet dressings can help alleviate

Based on the clinical history and examination, it strongly indicates that the patient may have a pulmonary embolism caused by a deep vein thrombosis in his right leg. To confirm this, it is recommended that he undergoes a CT pulmonary angiogram and doppler ultrasound scan of his right leg.

The typical symptoms of a pulmonary embolism include shortness of breath, pleuritic chest pain, coughing, and/or coughing up blood. Additionally, there may be symptoms suggesting the presence of a deep vein thrombosis. Other signs to look out for are rapid breathing and heart rate, fever, and in severe cases, signs of systemic shock, a gallop heart rhythm, and increased jugular venous pressure.

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.

Cement contains lime, which is a powerful alkali, and this can cause a serious eye emergency that requires immediate treatment. Alkaline chemicals, such as oven cleaner, ammonia, household bleach, drain cleaner, oven cleaner, and plaster, can also cause damage to the eyes. They lead to colliquative necrosis, which is a type of tissue death that results in liquefaction. On the other hand, acids cause damage through coagulative necrosis. Common acids that can harm the eyes include toilet cleaners, certain household cleaning products, and battery fluid.

The initial management of a patient with cement or alkali exposure to the eyes should be as follows:

1. Irrigate the eye with a large amount of normal saline for 20-30 minutes.
2. Administer local anaesthetic drops every 5 minutes to help keep the eye open and alleviate pain.
3. Monitor the pH every 5 minutes until a neutral pH (7.0-7.5) is achieved. Briefly pause irrigation to test the fluid from the forniceal space using litmus paper.

After the initial management, a thorough examination should be conducted, which includes the following steps:

1. Examine the eye directly and with a slit lamp.
2. Remove any remaining cement debris from the surface of the eye.
3. Evert the eyelids to check for hidden cement debris.
4. Administer fluorescein drops and check for corneal abrasion.
5. Assess visual acuity, which may be reduced.
6. Perform fundoscopy to check for retinal necrosis if the alkali has penetrated the sclera.
7. Measure intraocular pressure through tonometry to detect secondary glaucoma.

Once the eye’s pH has returned to normal, irrigation can be stopped, and the patient should be promptly referred to an ophthalmology specialist for further evaluation.

Potential long-term complications of cement or alkali exposure to the eyes include closed-angle glaucoma, cataract formation, entropion, keratitis sicca, and permanent vision loss.

Toxocariasis is a rare infection caused by the parasitic roundworm Toxocara canis. The main way it spreads to humans is through contact with dog feces. However, practicing good hand hygiene can help prevent transmission. While most people who come into contact with Toxocara canis don’t show any symptoms, a small number may experience a mild flu-like illness.

The most common presentation of toxocariasis is in children, who may experience unilateral visual loss. This loss of vision is typically caused by conditions such as vitritis, macular edema, and tractional retinal detachment. It is believed that these lesions occur due to a toxic or immunoallergic reaction to the larval antigens.

Excessive intake of lithium is linked to the development of low anion gap acidosis. In cases of lithium overdose, a common outcome is the occurrence of low anion gap acidosis.

Further Reading:

Arterial blood gases (ABG) are an important diagnostic tool used to assess a patient’s acid-base status and respiratory function. When obtaining an ABG sample, it is crucial to prioritize safety measures to minimize the risk of infection and harm to the patient. This includes performing hand hygiene before and after the procedure, wearing gloves and protective equipment, disinfecting the puncture site with alcohol, using safety needles when available, and properly disposing of equipment in sharps bins and contaminated waste bins.

To reduce the risk of harm to the patient, it is important to test for co-lateral circulation using the modified Allen test for radial artery puncture. Additionally, it is essential to inquire about any occlusive vascular conditions or anticoagulation therapy that may affect the procedure. The puncture site should be checked for signs of infection, injury, or previous surgery. After the test, pressure should be applied to the puncture site or the patient should be advised to apply pressure for at least 5 minutes to prevent bleeding.

Interpreting ABG results requires a systematic approach. The core set of results obtained from a blood gas analyser includes the partial pressures of oxygen and carbon dioxide, pH, bicarbonate concentration, and base excess. These values are used to assess the patient’s acid-base status.

The pH value indicates whether the patient is in acidosis, alkalosis, or within the normal range. A pH less than 7.35 indicates acidosis, while a pH greater than 7.45 indicates alkalosis.

The respiratory system is assessed by looking at the partial pressure of carbon dioxide (pCO2). An elevated pCO2 contributes to acidosis, while a low pCO2 contributes to alkalosis.

The metabolic aspect is assessed by looking at the bicarbonate (HCO3-) level and the base excess. A high bicarbonate concentration and base excess indicate alkalosis, while a low bicarbonate concentration and base excess indicate acidosis.

Analyzing the pCO2 and base excess values can help determine the primary disturbance and whether compensation is occurring. For example, a respiratory acidosis (elevated pCO2) may be accompanied by metabolic alkalosis (elevated base excess) as a compensatory response.

The anion gap is another important parameter that can help determine the cause of acidosis. It is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium.

Of all the medications mentioned in this question, only pioglitazone is known to be a potential cause of hypoglycemia. Glucagon, on the other hand, is specifically used as a treatment for hypoglycemia. The remaining medications mentioned are antidiabetic drugs that do not typically lead to hypoglycemia when used alone.

Pernicious anaemia is a condition that affects the stomach and is characterized by the loss of gastric parietal cells and impaired secretion of intrinsic factor (IF). IF is crucial for the absorption of vitamin B12 in the ileum, and as a result, megaloblastic anaemia occurs. This condition is commonly seen in individuals who have undergone gastrectomy.

The clinical manifestations of pernicious anaemia include weight loss, loss of appetite, fatigue, diarrhoea, and a distinct lemon-yellow skin color, which is caused by a combination of haemolytic jaundice and the paleness associated with anaemia. Other symptoms may include glossitis (inflammation of the tongue) and oral ulceration. Neurological symptoms can also occur, such as subacute combined degeneration of the spinal cord and peripheral neuropathy. The earliest sign of central nervous system involvement is often the loss of position and vibratory sense in the extremities.

When investigating pernicious anaemia, certain findings may be observed. These include macrocytic anaemia, neutropaenia, thrombocytopaenia, anisocytosis and poikilocytosis on a blood film, low serum B12 levels, elevated serum bilirubin levels (indicating haemolysis), the presence of intrinsic factor antibodies, and a positive Schilling test.

The treatment for pernicious anaemia involves lifelong supplementation of vitamin B12, typically administered through intramuscular injections.

Auer rods are small, needle-shaped structures that can be found within the cytoplasm of blast cells. These structures have a distinct eosinophilic appearance. While they are most frequently observed in cases of acute myeloid leukemia, they can also be present in high-grade myelodysplastic syndromes and myeloproliferative disorders.

Klumpke’s palsy, also known as Dejerine-Klumpke palsy, is a condition where the arm becomes paralyzed due to an injury to the lower roots of the brachial plexus. The most commonly affected root is C8, but T1 can also be involved. The main cause of Klumpke’s palsy is when the arm is pulled forcefully in an outward position during a difficult childbirth. It can also occur in adults with apical lung carcinoma (Pancoast’s syndrome).

Clinically, Klumpke’s palsy is characterized by a deformity known as ‘claw hand’, which is caused by the paralysis of the intrinsic hand muscles. There is also a loss of sensation along the ulnar side of the forearm and hand. In some cases where T1 is affected, a condition called Horner’s syndrome may also be present.

Klumpke’s palsy can be distinguished from Erb’s palsy, which affects the upper roots of the brachial plexus (C5 and sometimes C6). In Erb’s palsy, the arm hangs by the side with the elbow extended and the forearm turned inward (known as the ‘waiter’s tip sign’). Additionally, there is a loss of shoulder abduction, external rotation, and elbow flexion.

From the moment a child is born, the mother is automatically granted parental responsibility. However, fathers must fulfill specific criteria in order to have the same rights. A father can provide consent on behalf of the child if he meets any of the following conditions: being married to the child’s mother, having been married to the child’s mother at the time of birth but subsequently divorced, being listed as the child’s father on the birth certificate, obtaining parental responsibility through a court order or a parental responsibility agreement with the mother, or legally adopting the child.

Further Reading:

Patients have the right to determine what happens to their own bodies, and for consent to be valid, certain criteria must be met. These criteria include the person being informed about the intervention, having the capacity to consent, and giving consent voluntarily and freely without any pressure or undue influence.

In order for a person to be deemed to have capacity to make a decision on a medical intervention, they must be able to understand the decision and the information provided, retain that information, weigh up the pros and cons, and communicate their decision.

Valid consent can only be provided by adults, either by the patient themselves, a person authorized under a Lasting Power of Attorney, or someone with the authority to make treatment decisions, such as a court-appointed deputy or a guardian with welfare powers.

In the UK, patients aged 16 and over are assumed to have the capacity to consent. If a patient is under 18 and appears to lack capacity, parental consent may be accepted. However, a young person of any age may consent to treatment if they are considered competent to make the decision, known as Gillick competence. Parental consent may also be given by those with parental responsibility.

The Fraser guidelines apply to the prescription of contraception to under 16’s without parental involvement. These guidelines allow doctors to provide contraceptive advice and treatment without parental consent if certain criteria are met, including the young person understanding the advice, being unable to be persuaded to inform their parents, and their best interests requiring them to receive contraceptive advice or treatment.

Competent adults have the right to refuse consent, even if it is deemed unwise or likely to result in harm. However, there are exceptions to this, such as compulsory treatment authorized by the mental health act or if the patient is under 18 and refusing treatment would put their health at serious risk.

In emergency situations where a patient is unable to give consent, treatment may be provided without consent if it is immediately necessary to save their life or prevent a serious deterioration of their condition. Any treatment decision made without consent must be in the patient’s best interests, and if a decision is time-critical and the patient is unlikely to regain capacity in time, a best interest decision should be made. The treatment provided should be the least restrictive on the patient’s future choices.

A 512 Hz tuning fork is commonly used for both the Rinne’s and Weber’s tests. However, a lower-pitched fork, such as a 128 Hz tuning fork, is typically used to assess vibration sense during a peripheral nervous system examination. Although a 256 Hz tuning fork can be used for either test, it is considered less reliable for both.

To perform a Rinne’s test, the 512 Hz tuning fork is first made to vibrate and then placed on the mastoid process until the sound is no longer heard. The top of the tuning fork is then positioned 2 cm away from the external auditory meatus, and 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 is no longer appreciated on the mastoid. This is because air conduction should be greater than bone conduction.

In cases of conductive hearing loss, the patient will no longer hear the tuning fork once it is no longer appreciated on the mastoid. This suggests that their bone conduction is greater than their air conduction, indicating an obstruction in 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 yield a false negative result if the patient has a severe unilateral sensorineural deficit and senses 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 on both the mastoid and outside the external auditory canal is equally diminished compared to the opposite ear. Although the sound will still be heard outside the external auditory canal, it will disappear earlier on the mastoid process and outside the external auditory canal compared to the other ear.

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

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

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

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

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

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

Further Reading:

High Altitude Illnesses

Altitude & Hypoxia:
– As altitude increases, atmospheric pressure decreases and inspired oxygen pressure falls.
– Hypoxia occurs at altitude due to decreased inspired oxygen.
– At 5500m, inspired oxygen is approximately half that at sea level, and at 8900m, it is less than a third.

Acute Mountain Sickness (AMS):
– AMS is a clinical syndrome caused by hypoxia at altitude.
– Symptoms include headache, anorexia, sleep disturbance, nausea, dizziness, fatigue, malaise, and shortness of breath.
– Symptoms usually occur after 6-12 hours above 2500m.
– Risk factors for AMS include previous AMS, fast ascent, sleeping at altitude, and age <50 years old.
– The Lake Louise AMS score is used to assess the severity of AMS.
– Treatment involves stopping ascent, maintaining hydration, and using medication for symptom relief.
– Medications for moderate to severe symptoms include dexamethasone and acetazolamide.
– Gradual ascent, hydration, and avoiding alcohol can help prevent AMS.

High Altitude Pulmonary Edema (HAPE):
– HAPE is a progression of AMS but can occur without AMS symptoms.
– It is the leading cause of death related to altitude illness.
– Risk factors for HAPE include rate of ascent, intensity of exercise, absolute altitude, and individual susceptibility.
– Symptoms include dyspnea, cough, chest tightness, poor exercise tolerance, cyanosis, low oxygen saturations, tachycardia, tachypnea, crepitations, and orthopnea.
– Management involves immediate descent, supplemental oxygen, keeping warm, and medication such as nifedipine.

High Altitude Cerebral Edema (HACE):
– HACE is thought to result from vasogenic edema and increased vascular pressure.
– It occurs 2-4 days after ascent and is associated with moderate to severe AMS symptoms.
– Symptoms include headache, hallucinations, disorientation, confusion, ataxia, drowsiness, seizures, and manifestations of raised intracranial pressure.
– Immediate descent is crucial for management, and portable hyperbaric therapy may be used if descent is not possible.
– Medication for treatment includes dexamethasone and supplemental oxygen. Acetazolamide is typically used for prophylaxis.

The septum, which is a part of the heart, can be best identified by examining leads V1 and V2. The septum receives its blood supply from the proximal left anterior descending artery (LAD). The LAD is responsible for supplying blood to the anterior myocardium and also contributes to the blood supply of the lateral myocardium. If the LAD becomes blocked, it can result in ST elevation in all the chest leads.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

Statins, although generally safe and well-tolerated, can cause myopathy and myotoxicity. This range of muscle-related side effects can vary from mild muscle pain to the most severe case of rhabdomyolysis, which can lead to kidney failure, blood clotting issues, and even death.

The different levels of myotoxicity associated with statins are as follows:
– Myalgia: muscle symptoms without an increase in creatine kinase (CK) levels.
– Asymptomatic myopathy: elevated CK levels without muscle symptoms.
– Myositis: muscle symptoms with CK levels elevated less than 10 times the upper limit of normal.
– Rhabdomyolysis: muscle symptoms with CK levels elevated more than 10 times the upper limit of normal, potentially leading to myoglobinuria (presence of myoglobin in urine) and renal failure.

Most statins are broken down by the cytochrome P450 enzyme system. When taken with drugs that strongly inhibit this system, the concentration of statins in the blood can significantly increase. This, in turn, raises the risk of myopathy. A well-known example of this is the combination of statins with macrolide antibiotics like erythromycin and clarithromycin. Co-prescribing these drugs with statins has been linked to a higher risk of myopathy, hospitalization due to rhabdomyolysis, acute kidney injury, and increased mortality rates.

Multiple myeloma is a cancerous growth of plasma cells, a type of white blood cell responsible for producing antibodies. It is more prevalent in men and typically occurs in individuals over the age of 60.

When a patient over 60 presents with an elevated ESR, unexplained anemia, hypercalcemia, renal impairment, and bone pain, the initial diagnosis is usually multiple myeloma until proven otherwise.

The most common symptoms of multiple myeloma include:

1. Anemia: This is caused by the infiltration of the bone marrow and suppression of blood cell production. It is typically normocytic and normochromic, but can also be macrocytic.

2. Bone pain: Approximately 70% of patients experience bone pain, which commonly affects the spine and ribs. Localized pain and tenderness may indicate a pathological fracture, and vertebral fractures can lead to spinal cord compression.

3. Renal failure: Acute or chronic renal failure occurs in about one-third of patients. This is generally due to the effects of light chains on the tubules.

4. Neurological symptoms: Hypercalcemia can cause weakness, lethargy, and confusion, while hyperviscosity can result in headaches and retinopathy. Amyloid infiltration can lead to peripheral neuropathies, with carpal tunnel syndrome being the most common.

5. Infection: The most common infections seen in multiple myeloma patients are pyelonephritis and pneumonia.

In addition to the routine blood tests already conducted, a suspected diagnosis of multiple myeloma should prompt further investigations, including:

– Plasma viscosity measurement
– Urinary protein electrophoresis to detect Bence-Jones proteins
– Serum electrophoresis to identify the type of paraprotein
– Quantitative immunoglobulin level testing
– Skeletal survey to look for lytic lesions
– Bone marrow aspirate and possibly biopsy

A diagnosis of multiple myeloma is confirmed by the presence of a monoclonal protein in the serum or urine, lytic lesions on X-ray, and an increased number of plasma cells in the bone marrow.

Lithium is a medication used to stabilize mood and is approved for the treatment and prevention of mania, bipolar disorder, recurrent depression, and aggressive or self-harming behavior. During pregnancy and the postnatal period, it is important to monitor lithium levels more frequently. If taken during the first trimester, lithium is associated with an increased risk of fetal cardiac malformations, such as Ebstein’s anomaly. If taken during the second and third trimesters, there is a risk of various complications in the newborn, including hypotonia, lethargy, feeding problems, hypothyroidism, goiter, and nephrogenic diabetes insipidus.

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

Drug: ACE inhibitors (e.g. ramipril)
Adverse effects: If taken during the second and third trimesters, ACE inhibitors can cause hypoperfusion, renal failure, and the oligohydramnios sequence.

Drug: Aminoglycosides (e.g. gentamicin)
Adverse effects: Aminoglycosides can cause ototoxicity and deafness in the fetus.

Drug: Aspirin
Adverse effects: High doses of aspirin 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 a significant risk.

Drug: Benzodiazepines (e.g. diazepam)
Adverse effects: When taken late in pregnancy, benzodiazepines can cause respiratory depression and a neonatal withdrawal syndrome.

Drug: Calcium-channel blockers
Adverse effects: If taken during the first trimester, calcium-channel blockers can cause phalangeal abnormalities. If taken during the second and third trimesters, they can lead to fetal growth retardation.

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

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.

Anaphylaxis is a severe allergic reaction that is caused by the immune system overreaction to a specific allergen. This reaction is classified as a Type I hypersensitivity reaction, which means it is mediated by the IgE antibodies.

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

When there is suspicion of phaeochromocytoma, the first tests to be done are plasma and/or urinary metanephrines. This patient exhibits paroxysmal symptoms that are consistent with phaeochromocytoma, such as high blood pressure, headache, sweating, anxiety, and fear. The initial diagnostic tests aim to confirm any metabolic disturbances by measuring levels of plasma and/or urine metanephrines, catecholamines, and urine vanillylmandelic acid (VMA). If these levels are found to be elevated, further imaging tests will be needed to determine the location and structure of the phaeochromocytoma tumor.

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.

In this case, the most appropriate target parameter to guide oxygen therapy would be an SpO2 (oxygen saturation) level of greater than 94%.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

The arterial line needle is inserted into the skin at an angle between 30 and 45 degrees. For a more detailed demonstration, please refer to the video provided in the media links section.

Further Reading:

Arterial line insertion is a procedure used to monitor arterial blood pressure continuously and obtain frequent blood gas samples. It is typically done when non-invasive blood pressure monitoring is not possible or when there is an anticipation of hemodynamic instability. The most common site for arterial line insertion is the radial artery, although other sites such as the ulnar, brachial, axillary, posterior tibial, femoral, and dorsalis pedis arteries can also be used.

The radial artery is preferred for arterial line insertion due to its superficial location, ease of identification and access, and lower complication rate compared to other sites. Before inserting the arterial line, it is important to perform Allen’s test to check for collateral circulation to the hand.

The procedure begins by identifying the artery by palpating the pulse at the wrist and confirming its position with doppler ultrasound if necessary. The wrist is then positioned dorsiflexed, and the skin is prepared and aseptic technique is maintained throughout the procedure. Local anesthesia is infiltrated at the insertion site, and the catheter needle is inserted at an angle of 30-45 degrees to the skin. Once flashback of pulsatile blood is seen, the catheter angle is flattened and advanced a few millimeters into the artery. Alternatively, a guide wire can be used with an over the wire technique.

After the catheter is advanced, the needle is withdrawn, and the catheter is connected to the transducer system and secured in place with sutures. It is important to be aware of absolute and relative contraindications to arterial line placement, as well as potential complications such as infection, thrombosis, hemorrhage, emboli, pseudo-aneurysm formation, AV fistula formation, arterial dissection, and nerve injury/compression.

Overall, arterial line insertion is a valuable procedure for continuous arterial blood pressure monitoring and frequent blood gas sampling, and the radial artery is the most commonly used site due to its accessibility and lower complication rate.

The MASCC Risk Index Score, developed by the Multinational Association of Supportive Care in Cancer, is a tool that can be utilized to identify patients who are at low risk for experiencing serious complications of febrile neutropenia. This score takes into account various characteristics of the patient to determine their risk level. For example, patients who have a minimal burden of febrile neutropenia with no or mild symptoms, no hypotension (with a systolic blood pressure above 90 mmHg), and no chronic obstructive pulmonary disease are assigned higher scores. Additionally, patients with a solid tumor or hematological malignancy and no previous fungal infection, as well as those who do not require parental fluids for dehydration, are also given higher scores. On the other hand, patients with a moderate burden of febrile neutropenia symptoms, those in an outpatient setting at the onset of fever, and those under the age of 60 receive lower scores. It is important to note that the qSOFA Score, CURB-65 Score, SCAP Score, and qCSI Score are different tools used for assessing different conditions and are not specifically used in the context of febrile neutropenia.

According to NICE, the presence of certain clinical features in a child between three months and five years old may indicate a urinary tract infection (UTI). These features include vomiting, poor feeding, lethargy, irritability, abdominal pain or tenderness, and urinary frequency or dysuria. For more information on this topic, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

A peptic ulcer is a condition where there is a hole or defect in the lining of the stomach or duodenum that is larger than 5mm in diameter. If left untreated, there is a risk that the ulcer may perforate, meaning it can create a rupture or tear in the lining. It is important to note that if the defect is smaller than 5mm, it is classified as an erosion rather than an ulcer.

Further Reading:

Peptic ulcer disease (PUD) is a condition characterized by a break in the mucosal lining of the stomach or duodenum. It is caused by an imbalance between factors that promote mucosal damage, such as gastric acid, pepsin, Helicobacter pylori infection, and NSAID drug use, and factors that maintain mucosal integrity, such as prostaglandins, mucus lining, bicarbonate, and mucosal blood flow.

The most common causes of peptic ulcers are H. pylori infection and NSAID use. Other factors that can contribute to the development of ulcers include smoking, alcohol consumption, certain medications (such as steroids), stress, autoimmune conditions, and tumors.

Diagnosis of peptic ulcers involves screening for H. pylori infection through breath or stool antigen tests, as well as upper gastrointestinal endoscopy. Complications of PUD include bleeding, perforation, and obstruction. Acute massive hemorrhage has a case fatality rate of 5-10%, while perforation can lead to peritonitis with a mortality rate of up to 20%.

The symptoms of peptic ulcers vary depending on their location. Duodenal ulcers typically cause pain that is relieved by eating, occurs 2-3 hours after eating and at night, and may be accompanied by nausea and vomiting. Gastric ulcers, on the other hand, cause pain that occurs 30 minutes after eating and may be associated with nausea and vomiting.

Management of peptic ulcers depends on the underlying cause and presentation. Patients with active gastrointestinal bleeding require risk stratification, volume resuscitation, endoscopy, and proton pump inhibitor (PPI) therapy. Those with perforated ulcers require resuscitation, antibiotic treatment, analgesia, PPI therapy, and urgent surgical review.

For stable patients with peptic ulcers, lifestyle modifications such as weight loss, avoiding trigger foods, eating smaller meals, quitting smoking, reducing alcohol consumption, and managing stress and anxiety are recommended. Medication review should be done to stop causative drugs if possible. PPI therapy, with or without H. pylori eradication therapy, is also prescribed. H. pylori testing is typically done using a carbon-13 urea breath test or stool antigen test, and eradication therapy involves a 7-day triple therapy regimen of antibiotics and PPI.

Common side effects of bendroflumethiazide include postural hypotension, electrolyte disturbance (such as hypokalaemia, hyponatraemia, and hypercalcaemia), impaired glucose tolerance, gout, impotence, and fatigue. Rare side effects of bendroflumethiazide include thrombocytopenia, agranulocytosis, photosensitive rash, pancreatitis, and renal failure.

An anal fissure is a tear in the wall of the anal mucosa that exposes the circular muscle layer. The majority of these tears occur in the posterior midline. The most common cause is the passage of a large, hard stool after a period of constipation. If multiple fissures are present, it may indicate an underlying condition such as Crohn’s disease or tuberculosis.

Both men and women are equally affected by anal fissures, and they are most commonly seen in individuals in their thirties. The typical symptoms of an anal fissure include intense, sharp pain during bowel movements, which can last up to an hour after passing stool. Additionally, there may be spots of bright red blood on the toilet paper when wiping, and a history of constipation.

The initial management of an anal fissure involves non-operative measures such as using stool softeners and bulking agents. To alleviate the intense anal pain, analgesics and topical local anesthetics may be prescribed. According to a recent meta-analysis, first-line therapy should involve the use of topical GTN or diltiazem, with botulinum toxin being used as a rescue treatment if necessary (Modern perspectives in the treatment of chronic anal fissures. Ann R Coll Surg Engl. 2007 Jul;89(5):472-8.)

Sphincterotomy, a surgical procedure, should be reserved for fissures that do not heal and has a success rate of 90%. Anal dilatation, also known as Lord’s procedure, is rarely used nowadays due to the high risk of subsequent fecal incontinence.

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

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

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

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

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

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

Thiamine deficiency is frequently seen in individuals who are dependent on alcohol. This is primarily due to their inadequate diet, the presence of gastritis which affects thiamine absorption, and the fact that thiamine is involved in alcohol metabolism as a coenzyme. If left untreated, thiamine deficiency can lead to Wernicke’s encephalopathy, which can further progress to Korsakoff’s syndrome.

It is important to note that administering glucose-containing intravenous fluids without thiamine to a patient with chronic thiamine deficiency can trigger Wernicke’s encephalopathy. Therefore, individuals undergoing detoxification should receive parenteral high-potency B complex vitamins (Pabrinex) as a preventive treatment. However, it is crucial to have resuscitation facilities available during administration due to the risk of anaphylaxis. The risk of anaphylaxis is lower when the drug is given intramuscularly (IM). A daily dose of one pair of ampoules of Pabrinex, containing 250 mg of thiamine, should be administered IM or intravenously (IV) for a period of three to five days.

Once the 3-5 day course of Pabrinex is completed, the patient should transition to oral vitamin B Compound-strong and oral thiamine tablets for continued treatment.

For more information, please refer to the NICE pathway for acute alcohol withdrawal.

The OPG is the recommended first-line imaging test for diagnosing TMJ dislocation and mandibular fractures.

Further Reading:

Mandibular fractures are a common type of facial fracture that often present to the emergency department. The mandible, or lower jaw, is formed by the fusion of two hemimandibles and articulates with the temporomandibular joints. Fractures of the mandible are typically caused by direct lateral force and often involve multiple fracture sites, including the body, condylar head and neck, and ramus.

When assessing for mandibular fractures, clinicians should use a look, feel, move method similar to musculoskeletal examination. However, it is important to note that TMJ effusion, muscle spasm, and pain can make moving the mandible difficult. Key signs of mandibular fracture include malocclusion, trismus (limited mouth opening), pain with the mouth closed, broken teeth, step deformity, hematoma in the sublingual space, lacerations to the gum mucosa, and bleeding from the ear.

The Manchester Mandibular Fracture Decision Rule uses the absence of five exam findings (malocclusion, trismus, broken teeth, pain with closed mouth, and step deformity) to exclude mandibular fracture. This rule has been found to be 100% sensitive and 39% specific in detecting mandibular fractures. Imaging is an important tool in diagnosing mandibular fractures, with an OPG X-ray considered the best initial imaging for TMJ dislocation and mandibular fracture. CT may be used if the OPG is technically difficult or if a CT is being performed for other reasons, such as a head injury.

It is important to note that head injury often accompanies mandibular fractures, so a thorough head injury assessment should be performed. Additionally, about a quarter of patients with mandibular fractures will also have a fracture of at least one other facial bone.

When rescuing drowning patients, it is important to extricate them from the water in a horizontal position whenever possible. This is because the pressure of the water on the body when submerged increases the flow of blood back to the heart, which in turn increases cardiac output. However, when the patient is removed from the water, this pressure effect is lost, which can lead to a sudden drop in blood pressure and circulatory collapse due to the loss of peripheral resistance and pooling of blood in the veins. By extricating the patient in a horizontal position, we can help counteract this effect.

It is worth noting that the amount of water in the lungs after drowning is typically small, usually less than 4 milliliters per kilogram of body weight. Therefore, attempting to drain the water from the lungs is ineffective and not recommended.

In cases of fresh water drowning, pneumonia may occur due to unusual pathogens such as aeromonas spp, burkholderia pseudomallei, chromobacterium spp, pseudomonas species, and leptospirosis.

If the patient experiences bronchospasm, nebulized bronchodilators can be used as a treatment.

To prevent secondary brain injury, it is important to prevent hyperthermia. This can be achieved by maintaining the patient’s core body temperature below 36 degrees Celsius during the rewarming process.

Further Reading:

Drowning is the process of experiencing respiratory impairment from submersion or immersion in liquid. It can be classified as cold-water or warm-water drowning. Risk factors for drowning include young age and male sex. Drowning impairs lung function and gas exchange, leading to hypoxemia and acidosis. It also causes cardiovascular instability, which contributes to metabolic acidosis and cell death.

When someone is submerged or immersed, they will voluntarily hold their breath to prevent aspiration of water. However, continued breath holding causes progressive hypoxia and hypercapnia, leading to acidosis. Eventually, the respiratory center sends signals to the respiratory muscles, forcing the individual to take an involuntary breath and allowing water to be aspirated into the lungs. Water entering the lungs stimulates a reflex laryngospasm that prevents further penetration of water. Aspirated water can cause significant hypoxia and damage to the alveoli, leading to acute respiratory distress syndrome (ARDS).

Complications of drowning include cardiac ischemia and infarction, infection with waterborne pathogens, hypothermia, neurological damage, rhabdomyolysis, acute tubular necrosis, and disseminated intravascular coagulation (DIC).

In children, the diving reflex helps reduce hypoxic injury during submersion. It causes apnea, bradycardia, and peripheral vasoconstriction, reducing cardiac output and myocardial oxygen demand while maintaining perfusion of the brain and vital organs.

Associated injuries with drowning include head and cervical spine injuries in patients rescued from shallow water. Investigations for drowning include arterial blood gases, chest X-ray, ECG and cardiac monitoring, core temperature measurement, and blood and sputum cultures if secondary infection is suspected.

Management of drowning involves extricating the patient from water in a horizontal position with spinal precautions if possible. Cardiovascular considerations should be taken into account when removing patients from water to prevent hypotension and circulatory collapse. Airway management, supplemental oxygen, and ventilation strategies are important in maintaining oxygenation and preventing further lung injury. Correcting hypotension, electrolyte disturbances, and hypothermia is also necessary. Attempting to drain water from the lungs is ineffective.

Patients without associated physical injury who are asymptomatic and have no evidence of respiratory compromise after six hours can be safely discharged home. Ventilation strategies aim to maintain oxygenation while minimizing ventilator-associated lung injury.

Kiesselbach’s plexus, also known as Little’s area, is formed by the connection of four or five arteries. These arteries include the greater palatine artery, anterior ethmoidal artery, superior labial artery, and sphenopalatine artery. Some sources also include the posterior ethmoidal artery as part of the plexus. The greater palatine artery is a branch of the maxillary artery, while the anterior ethmoidal artery is a branch of the internal carotid artery. The superior labial artery and sphenopalatine artery are both branches of the external carotid artery. The posterior ethmoidal artery, if included, is a branch of the ophthalmic artery.

Further Reading:

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.

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

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

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

When patients are exposed to the inhalation of combustion byproducts, they face the danger of being poisoned by carbon monoxide and cyanide. In situations where hydrocarbons and substances containing carbon and nitrogen are incompletely burned, the formation of both carbon monoxide and cyanide gas can occur. Individuals who inhale smoke are particularly vulnerable to this type of poisoning.

Further Reading:

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

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

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

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

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

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

Spironolactone is a medication used to treat conditions such as congestive cardiac failure, hypertension, hepatic cirrhosis with ascites and edema, and Conn’s syndrome. It functions as a competitive aldosterone receptor antagonist, primarily working in the distal convoluted tubule. In this area, it hinders the reabsorption of sodium ions and enhances the reabsorption of potassium ions. Spironolactone is commonly known as a potassium-sparing diuretic.

The main side effect of spironolactone is hyperkalemia, particularly when renal impairment is present. In severe cases, hyperkalemia can be life-threatening. Additionally, there is a notable occurrence of gastrointestinal disturbances, with nausea and vomiting being the most common. Women may experience menstrual disturbances, while men may develop gynecomastia, both of which are attributed to the antiandrogenic effects of spironolactone.

The most probable diagnosis in this case is septic arthritis, which occurs when an infectious agent invades a joint and causes pus formation. The patient’s recent travel to Bangkok, presence of a vesicular rash on the trunk, and the identification of Gram-negative diplococci support this diagnosis.

Septic arthritis is characterized by several clinical features. These include pain in the affected joint, redness, warmth, and swelling of the joint, and difficulty in moving the joint. Patients may also experience fever and systemic upset.

The most common cause of septic arthritis is Staphylococcus aureus. Other bacteria that can lead to this condition include Streptococcus spp., Haemophilus influenzae, Neisseria gonorrhoea (typically seen in sexually active young adults with macules or vesicles on the trunk), and Escherichia coli (common in intravenous drug users, the elderly, and seriously ill individuals).

According to the current recommendations by NICE (National Institute for Health and Care Excellence) and the BNF (British National Formulary), the treatment for septic arthritis involves the following approaches. Flucloxacillin is the first-line antibiotic. In cases of penicillin allergy, clindamycin is recommended. If there is suspicion of MRSA (methicillin-resistant Staphylococcus aureus), vancomycin should be used. For suspected gonococcal arthritis or Gram-negative infection, cefotaxime is the preferred choice. The suggested duration of treatment is 4-6 weeks, although it may be longer if the infection is complicated.

Conservative management of ureteric stones may involve the use of medical expulsive therapy (MET), which can be achieved through the administration of either an alpha-blocker or a calcium-channel blocker. This treatment aims to facilitate the natural passage of the stone during the observation period.

Research has shown that in adults, both alpha-blockers and calcium channel blockers have been effective in improving the passage of distal ureteric stones that are less than 10 mm in size, when compared to no treatment. Additionally, alpha-blockers have shown to be more effective than placebo in promoting stone passage. Alpha-blockers have also demonstrated more benefits than calcium channel blockers in terms of stone passage, as well as some advantages in terms of hospital stay and pain management. However, there was no significant difference in the time it took for the stone to pass or the overall quality of life.

Currently, the National Institute for Health and Care Excellence (NICE) recommends alpha-blockers as the preferred choice for medical expulsive therapy. For more detailed information, you can refer to the NICE guidelines on the assessment and management of renal and ureteric stones.

Intracranial hemorrhages can be categorized based on their location into epidural, subdural, subarachnoid, or intracerebral hemorrhages. The patient in this case is experiencing a severe headache accompanied by signs of meningismus, which strongly suggests a diagnosis of subarachnoid hemorrhage. Additionally, there is no history of trauma, and most cases of subarachnoid hemorrhage are caused by the rupture of a berry aneurysm located in the circle of Willis. Hypertension is a significant risk factor for the rupture of an aneurysm.

During the patient’s hospital stay, they develop an ischemic stroke, which is confirmed by a CT scan. This is most likely a result of cerebral vasospasm secondary to the subarachnoid hemorrhage. To prevent this complication, patients are often treated with the cerebral selective calcium channel blocker Nimodipine.

Another potential complication of this condition is rebleeding, with the highest risk occurring in the first few days. Rebleeding can be potentially fatal, so it is crucial to repair the aneurysm as soon as possible. The presence of blood in the subarachnoid space can also disrupt the production and drainage of cerebrospinal fluid, leading to hydrocephalus.

Long-term complications of subarachnoid hemorrhage include epilepsy, with most patients experiencing their first seizure within a year after the hemorrhage. However, the risk of epilepsy decreases over time. Cognitive dysfunction is also a common long-term complication and can manifest as memory loss, difficulty concentrating, or challenges in performing regular tasks. Emotional problems, such as depression and anxiety, are frequently observed as well.

Digoxin-specific antibody (DigiFab) is an antidote used to counteract digoxin overdose. It is a purified and sterile preparation of digoxin-immune ovine Fab immunoglobulin fragments. These fragments are derived from healthy sheep that have been immunized with a digoxin derivative called digoxin-dicarboxymethoxylamine (DDMA). DDMA is a digoxin analogue that contains the essential cyclopentanoperhydrophenanthrene: lactone ring moiety coupled to keyhole limpet hemocyanin (KLH).

DigiFab has a higher affinity for digoxin compared to the affinity of digoxin for its sodium pump receptor, which is believed to be the receptor responsible for its therapeutic and toxic effects. When administered to a patient who has overdosed on digoxin, DigiFab binds to digoxin molecules, reducing the levels of free digoxin in the body. This shift in equilibrium away from binding to the receptors helps to reduce the cardiotoxic effects of digoxin. The Fab-digoxin complexes are then eliminated from the body through the kidney and reticuloendothelial system.

The indications for using DigiFab in cases of acute and chronic digoxin toxicity are summarized below:

Acute digoxin toxicity:
– Cardiac arrest
– Life-threatening arrhythmia
– Potassium level >5 mmol/l
– Ingestion of >10 mg of digoxin (in adults)
– Ingestion of >4 mg of digoxin (in children)
– Digoxin level >12 ng/ml

Chronic digoxin toxicity:
– Cardiac arrest
– Life-threatening arrhythmia
– Significant gastrointestinal symptoms
– Symptoms of digoxin toxicity in the presence of renal failure

Glanzmann’s thrombasthenia is an uncommon condition affecting platelets, where they have a deficiency or abnormality in glycoprotein IIb/IIIa. This disorder leads to platelet dysfunction and can result in various complications.

TCA toxicity can be identified through specific changes seen on an electrocardiogram (ECG). Sinus tachycardia, which is a faster than normal heart rate, and widening of the QRS complex are key features of TCA toxicity. These ECG changes occur due to the blocking of sodium channels and muscarinic receptors (M1) by the medication. In the case of an amitriptyline overdose, additional ECG changes may include prolongation of the QT interval, an R/S ratio greater than 0.7 in lead aVR, and the presence of ventricular arrhythmias such as torsades de pointes. The severity of the QRS prolongation on the ECG is associated with the likelihood of adverse events. A QRS duration greater than 100 ms is predictive of seizures, while a QRS duration greater than 160 ms is predictive of ventricular arrhythmias like ventricular tachycardia or torsades de pointes.

Further Reading:

Tricyclic antidepressant (TCA) overdose is a common occurrence in emergency departments, with drugs like amitriptyline and dosulepin being particularly dangerous. TCAs work by inhibiting the reuptake of norepinephrine and serotonin in the central nervous system. In cases of toxicity, TCAs block various receptors, including alpha-adrenergic, histaminic, muscarinic, and serotonin receptors. This can lead to symptoms such as hypotension, altered mental state, signs of anticholinergic toxicity, and serotonin receptor effects.

TCAs primarily cause cardiac toxicity by blocking sodium and potassium channels. This can result in a slowing of the action potential, prolongation of the QRS complex, and bradycardia. However, the blockade of muscarinic receptors also leads to tachycardia in TCA overdose. QT prolongation and Torsades de Pointes can occur due to potassium channel blockade. TCAs can also have a toxic effect on the myocardium, causing decreased cardiac contractility and hypotension.

Early symptoms of TCA overdose are related to their anticholinergic properties and may include dry mouth, pyrexia, dilated pupils, agitation, sinus tachycardia, blurred vision, flushed skin, tremor, and confusion. Severe poisoning can lead to arrhythmias, seizures, metabolic acidosis, and coma. ECG changes commonly seen in TCA overdose include sinus tachycardia, widening of the QRS complex, prolongation of the QT interval, and an R/S ratio >0.7 in lead aVR.

Management of TCA overdose involves ensuring a patent airway, administering activated charcoal if ingestion occurred within 1 hour and the airway is intact, and considering gastric lavage for life-threatening cases within 1 hour of ingestion. Serial ECGs and blood gas analysis are important for monitoring. Intravenous fluids and correction of hypoxia are the first-line therapies. IV sodium bicarbonate is used to treat haemodynamic instability caused by TCA overdose, and benzodiazepines are the treatment of choice for seizure control. Other treatments that may be considered include glucagon, magnesium sulfate, and intravenous lipid emulsion.

There are certain things to avoid in TCA overdose, such as anti-arrhythmics like quinidine and flecainide, as they can prolonged depolarization. Amiodarone should

Ketamine induces a distinct type of sedation known as dissociative sedation. This sedation state is unlike any other and is characterized by a trance-like, cataleptic condition. It provides deep pain relief and memory loss while still maintaining important protective reflexes for the airway, spontaneous breathing, and overall stability of the heart and lungs. Dissociative sedation with ketamine does not fit into the conventional categories of sedation.

Further Reading:

Procedural sedation is commonly used by emergency department (ED) doctors to minimize pain and discomfort during procedures that may be painful or distressing for patients. Effective procedural sedation requires the administration of analgesia, anxiolysis, sedation, and amnesia. This is typically achieved through the use of a combination of short-acting analgesics and sedatives.

There are different levels of sedation, ranging from minimal sedation (anxiolysis) to general anesthesia. It is important for clinicians to understand the level of sedation being used and to be able to manage any unintended deeper levels of sedation that may occur. Deeper levels of sedation are similar to general anesthesia and require the same level of care and monitoring.

Various drugs can be used for procedural sedation, including propofol, midazolam, ketamine, and fentanyl. Each of these drugs has its own mechanism of action and side effects. Propofol is commonly used for sedation, amnesia, and induction and maintenance of general anesthesia. Midazolam is a benzodiazepine that enhances the effect of GABA on the GABA A receptors. Ketamine is an NMDA receptor antagonist and is used for dissociative sedation. Fentanyl is a highly potent opioid used for analgesia and sedation.

The doses of these drugs for procedural sedation in the ED vary depending on the drug and the route of administration. It is important for clinicians to be familiar with the appropriate doses and onset and peak effect times for each drug.

Safe sedation requires certain requirements, including appropriate staffing levels, competencies of the sedating practitioner, location and facilities, and monitoring. The level of sedation being used determines the specific requirements for safe sedation.

After the procedure, patients should be monitored until they meet the criteria for safe discharge. This includes returning to their baseline level of consciousness, having vital signs within normal limits, and not experiencing compromised respiratory status. Pain and discomfort should also be addressed before discharge.

SIADH is a medical condition that is not brought on by lithium toxicity. However, lithium toxicity does have its own distinct set of symptoms. These symptoms include nausea and vomiting, diarrhea, tremors, ataxia, confusion, increased muscle tone, clonus, nephrogenic diabetes insipidus, convulsions, coma, and renal failure. It is important to note that SIADH and lithium toxicity are separate conditions with their own unique characteristics.

The initial noticeable abnormality in sensory testing for diabetic neuropathy is often the loss of vibration sense. Reduced sensation, particularly in vibration sense, is typically the first symptom to be observed in diabetic neuropathy.

Further Reading:

Diabetic foot is a complication that can occur in individuals with diabetes due to long-standing high blood sugar levels. This leads to a process called glycation or glycosylation, where glucose binds to proteins and lipids in the body. Abnormal protein glycation can cause cellular dysfunction and various complications.

One of the main problems in diabetic foot is peripheral vascular disease and peripheral neuropathy. These conditions can result in significant foot issues, as trauma to the feet may go unnoticed and untreated. Vascular disease also impairs wound healing and increases the risk of developing ulcers.

Clinical features of diabetic foot include reduced sensation, especially to vibration, non-dermatomal sensory loss, foot deformities such as pes cavus and claw toes, and weak or absent foot pulses. It is important for diabetic patients to have their feet assessed regularly, at least annually, to identify any potential problems. Additional foot assessments should also be conducted during hospital admissions.

During a diabetic foot assessment, the healthcare provider should remove shoes, socks, and any bandages or dressings to examine both feet. They should assess for neuropathy using a 10 g monofilament to test foot sensation and check for limb ischemia by examining pulses and performing ankle brachial pressure index (ABPI) measurements. Any abnormal tissue, such as ulcers, calluses, infections, inflammation, deformities, or gangrene, should be documented. The risk of Charcot arthropathy should also be assessed.

The severity of foot ulcers in diabetic patients can be documented using standardized systems such as SINBAD or the University of Texas classification. The presence and severity of diabetic foot infection can be determined based on criteria such as local swelling, induration, erythema, tenderness, pain, warmth, and purulent discharge.

Management of foot ulcers involves offloading, control of foot infection, control of ischemia, wound debridement, and appropriate wound dressings. Antibiotics may be necessary depending on the severity of the infection. Diabetic patients with foot ulcers should undergo initial investigations including blood tests, wound swabs, and imaging to assess for possible osteomyelitis.

Charcot foot is a serious complication of diabetic peripheral neuropathy that results in progressive destructive arthropathy and foot deformity. Signs of Charcot foot include redness, swelling, warm skin, pain, and deformity. The hallmark deformity is midfoot collapse, known as the rocker-bottom foot.

This particular patient has a high risk of experiencing an acute coronary syndrome. Therefore, it is recommended to administer aspirin at a dosage of 300 mg and clopidogrel at a dosage ranging from 300-600 mg.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

When starting treatment with strong opioids for pain relief in palliative care, it is recommended to offer patients regular oral sustained-release or oral immediate-release morphine, depending on their preference. In addition, provide rescue doses of oral immediate-release morphine for breakthrough pain. For patients without renal or hepatic comorbidities, a typical total daily starting dose schedule of 20-30 mg of oral morphine is suggested, along with 5 mg of oral immediate-release morphine for rescue doses during the titration phase. It is important to adjust the dose until a good balance is achieved between pain control and side effects. If this balance is not reached after a few dose adjustments, it is advisable to seek specialist advice. Patients should be reviewed frequently, especially during the titration phase. For patients with moderate to severe renal or hepatic impairment, it is recommended to consult a specialist before prescribing strong opioids.

For maintenance therapy, oral sustained-release morphine is recommended as the first-line treatment for patients with advanced and progressive disease who require strong opioids. Transdermal patch formulations should not be routinely offered as first-line maintenance treatment unless oral opioids are not suitable. If pain remains inadequately controlled despite optimizing first-line maintenance treatment, it is important to review the analgesic strategy and consider seeking specialist advice.

When it comes to breakthrough pain, oral immediate-release morphine should be offered as the first-line rescue medication for patients on maintenance oral morphine treatment. Fast-acting fentanyl should not be offered as the first-line rescue medication. If pain continues to be inadequately controlled despite optimizing treatment, it may be necessary to seek specialist advice.

In cases where oral opioids are not suitable and analgesic requirements are stable, transdermal patches with the lowest acquisition cost can be considered. However, it is important to consult a specialist for guidance if needed. Similarly, for patients in whom oral opioids are not suitable and analgesic requirements are unstable, subcutaneous opioids with the lowest acquisition cost can be considered, with specialist advice if necessary.

For more information, please refer to the NICE Clinical Knowledge Summary: Opioids for pain relief in palliative care. https://www.nice.org.uk/guidance/cg140

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 peak within 1-3 days, with the cough being more severe at night. A milder cough may persist for another 7-10 days.

A barking cough is a characteristic symptom of croup, but it does not indicate the severity of the condition. To reduce airway swelling, dexamethasone and prednisolone are commonly used. Nebulized budesonide can be an alternative if the child is experiencing vomiting. However, it’s 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 rare and typically reserved for children who are experiencing increasing respiratory distress or showing signs of drowsiness/agitation. The Westley croup score is a useful tool for assessing the child’s condition and making appropriate management decisions. Children with moderate (score 2-7) or severe croup (score >7) may require hospital admission. On the other hand, many children with mild croup (score 0-1) can be safely discharged and treated at home.

The Westley croup score is determined based on the following criteria: the presence of stridor at rest, the severity of retractions, air entry, SaO2 levels below 92% when agitated, and the conscious level of the child. In this particular case, the child’s Westley croup score is 8 points, indicating severe croup.

Instances where confidentiality may be breached include situations where there is a legal obligation, such as informing the Health Protection Agency (HPA) about a notifiable disease. Another example is in legal cases where a judge requests information. Additionally, confidentiality may be breached when there is a risk to the public, such as potential terrorism or serious criminal activity. It may also be breached when there is a risk to others, such as when a patient expresses homicidal intent towards a specific individual. Furthermore, confidentiality may be breached in cases relevant to statutory regulatory bodies, such as informing the Driver and Vehicle Licensing Agency (DVLA) about a patient who continues to drive despite a restriction.

However, it is important to note that there are examples where confidentiality should not be breached. It is inappropriate to disclose a patient’s diagnosis to third parties without their consent, including the police. The police should only be informed about what occurs within a consultation if there is a serious threat to the public or an individual.

If there is a consideration to breach patient confidentiality, it is crucial to seek the patient’s consent first. If consent is refused, it is advisable to seek guidance from your local trust and your medical defence union.

For more information, you can refer to the General Medical Council (GMC) guidance on patient confidentiality.

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

The leads V3 and V4 represent the anterior myocardial area.

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

The ROME IV criteria are utilized in secondary care to diagnose IBS, as recommended by NICE. The DSM-5 criteria are employed in diagnosing various mental health disorders. Coeliac disease diagnosis involves the use of modified marsh typing. Gastro-oesophageal reflux disease diagnosis relies on the Lyon Consensus.

Further Reading:

Irritable bowel syndrome (IBS) is a chronic disorder that affects the interaction between the gut and the brain. The exact cause of IBS is not fully understood, but factors such as genetics, drug use, enteric infections, diet, and psychosocial factors are believed to play a role. The main symptoms of IBS include abdominal pain, changes in stool form and/or frequency, and bloating. IBS can be classified into subtypes based on the predominant stool type, including diarrhea-predominant, constipation-predominant, mixed, and unclassified.

Diagnosing IBS involves using the Rome IV criteria, which includes recurrent abdominal pain associated with changes in stool frequency and form. It is important to rule out other more serious conditions that may mimic IBS through a thorough history, physical examination, and appropriate investigations. Treatment for IBS primarily involves diet and lifestyle modifications. Patients are advised to eat regular meals with a healthy, balanced diet and adjust their fiber intake based on symptoms. A low FODMAP diet may be trialed, and a dietician may be consulted for guidance. Regular physical activity and weight management are also recommended.

Psychosocial factors, such as stress, anxiety, and depression, should be addressed and managed appropriately. If constipation is a predominant symptom, soluble fiber supplements or foods high in soluble fiber may be recommended. Laxatives can be considered if constipation persists, and linaclotide may be tried if optimal doses of previous laxatives have not been effective. Antimotility drugs like loperamide can be used for diarrhea, and antispasmodic drugs or low-dose tricyclic antidepressants may be prescribed for abdominal pain. If symptoms persist or are refractory to treatment, alternative diagnoses should be considered, and referral to a specialist may be necessary.

Overall, the management of IBS should be individualized based on the patient’s symptoms and psychosocial situation. Clear explanation of the condition and providing resources for patient education, such as the NHS patient information leaflet and support from organizations like The IBS Network, can also be beneficial.

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

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

Nelson’s syndrome is a rare condition that occurs many years after a bilateral adrenalectomy for Cushing’s syndrome. It is believed to develop due to the loss of the normal negative feedback control that suppresses high cortisol levels. As a result, the hypothalamus starts producing CRH again, which stimulates the growth of a pituitary adenoma that produces adrenocorticotropic hormone (ACTH).

Only 15-20% of patients who undergo bilateral adrenalectomy will develop this condition, and it is now rarely seen as the procedure is no longer commonly performed.

The symptoms and signs of Nelson’s syndrome are related to the growth of the pituitary adenoma and the increased production of ACTH and melanocyte-stimulating hormone (MSH) from the adenoma. These may include headaches, visual field defects (up to 50% of cases), increased skin pigmentation, and the possibility of hypopituitarism.

ACTH levels will be significantly elevated (usually >500 ng/L). Thyroxine, TSH, gonadotrophin, and sex hormone levels may be low. Prolactin levels may be high, but not as high as with a prolactin-producing tumor. MRI or CT scanning can be helpful in identifying the presence of an expanding pituitary mass.

The treatment of choice for Nelson’s syndrome is trans-sphenoidal surgery.

Colonoscopy with histology is a useful tool in determining the extent and severity of ulcerative colitis. Chronic bloody diarrhea, lasting for more than four weeks, can be caused by various conditions. In this age group, the top differentials include inflammatory bowel disease (IBD) and infective causes such as C.diff and giardia. Other potential causes include drug use (such as laxatives and alcohol), hyperthyroidism (usually accompanied by other signs), coeliac disease (although blood in the stool is not a common symptom), and malabsorption syndromes like pancreatic insufficiency.

When IBD is suspected, fecal calprotectin is often tested and typically found to be elevated. This test is usually performed before colonoscopy and biopsy in individuals under 40 years old. However, in those over 40, a colonoscopy is often the initial investigation to assess for possible underlying malignancy. It is important to note that calprotectin is not specific to IBD and can also be elevated in other conditions such as infectious enteritis and colorectal neoplasia, which limits its diagnostic value. NICE guidelines advise against using calprotectin in individuals with bloody diarrhea.

Initial investigations for chronic bloody diarrhea should include thyroid function testing, coeliac screening, and stool analysis for microscopy and culture. It is worth noting that different hospitals may vary in the specific tests included in stool microscopy and culture, but most labs will typically test for ova, cysts, and parasites. Stool antigen tests are commonly used to detect H.pylori. Vitamin B12 testing may also be appropriate, although deficiency in this vitamin usually leads to a macrocytic anemia and is therefore unlikely to contribute significantly to the diagnosis.

Further Reading:

Inflammatory bowel disease (IBD) is a chronic condition characterized by inflammation of the intestinal tract and an imbalance of the intestinal microbiota. The two main forms of IBD are Crohn’s disease and ulcerative colitis (UC). In some cases, it is not possible to differentiate between Crohn’s disease and UC, and the term inflammatory bowel disease type-unclassified may be used.

Crohn’s disease is a chronic, relapsing-remitting inflammatory disease that can affect any part of the gastrointestinal tract, from the mouth to the anus. It most commonly involves the ileum and colon. The inflammation in Crohn’s disease affects all layers of the intestinal wall, leading to complications such as strictures, fistulas, and adhesions. Risk factors for developing Crohn’s disease include a family history, smoking, infectious gastroenteritis, appendicectomy, and the use of NSAIDs and oral contraceptive drugs. Symptoms of Crohn’s disease can vary but often include diarrhea, abdominal pain, weight loss, and perianal disease. Extraintestinal features, such as arthritis, erythema nodosum, and uveitis, can also occur.

Ulcerative colitis is a chronic, relapsing-remitting inflammatory disease that primarily affects the large bowel. The inflammation in UC is limited to the intestinal mucosa and does not involve skip lesions like in Crohn’s disease. Risk factors for developing UC include a family history, not smoking, and no appendix. Symptoms of UC include bloody diarrhea, urgency, tenesmus, and abdominal pain. Extraintestinal features, such as arthritis and uveitis, can also occur. Complications of UC include toxic megacolon, bowel obstruction, bowel perforation, strictures, fistula formation, anemia, malnutrition, and colorectal cancer.

Diagnosing IBD involves various investigations, including blood tests, stool microscopy and culture, fecal calprotectin testing, endoscopy with biopsy, and imaging modalities such as CT and MR enterography. The management of Crohn’s disease and UC is complex and may involve corticosteroids, immunosuppressive drugs, biologic therapy, surgery, and nutritional support. Patients with IBD should also be monitored for nutritional deficiencies, colorectal cancer, and osteoporosis.

Kaposi’s sarcoma (KS) is a type of cancer that affects the connective tissues. It is caused by a virus called human herpesvirus 8 (HHV-8). This cancer is more likely to occur in individuals with weakened immune systems, such as those with HIV or those who have undergone organ transplants.

The main symptom of KS is the development of skin lesions. These lesions initially appear as red-purple spots and quickly progress to become raised bumps and nodules. They can appear on any part of the body, but are most commonly found on the lower limbs, back, face, mouth, and genital area.

Multiple sclerosis is a condition characterized by the demyelination of nerve cells in the brain and spinal cord. It is an autoimmune disease caused by recurring inflammation, primarily affecting individuals in early adulthood. The condition is more prevalent in females, with a ratio of 3:2 compared to males.

There are several risk factors associated with multiple sclerosis. These include being of Caucasian race, living at a greater distance from the equator (as the risk tends to increase further away), having a family history of the disease (with approximately 20% of patients having an affected relative), and smoking. Interestingly, the rates of relapse tend to decrease during pregnancy.

Multiple sclerosis can present in three main patterns. The most common is relapsing and remitting MS, where individuals experience periods without symptoms followed by relapses. This accounts for 80% of cases at the time of diagnosis. Another pattern is primary progressive MS, where symptoms develop and worsen from the beginning with few remissions. This is seen in approximately 10-15% of cases at diagnosis. Lastly, there is secondary progressive MS, which occurs after a relapsing/remitting phase. In this pattern, symptoms worsen with fewer remissions, and it affects around 50% of individuals with relapsing/remitting MS within 10 years of diagnosis.

Certain factors can indicate a more favorable prognosis for individuals with multiple sclerosis. These include having a relapsing/remitting course of the disease, being female, experiencing sensory symptoms, and having an early age at onset.

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In such cases, the next step in managing the patient would be to administer a second dose of benzodiazepine. Since the patient already has an intravenous line in place, this would be the most appropriate route to choose.

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

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

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

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

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

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

Monitoring during the management of status epilepticus involves regular neurological observations and measurements of pulse, blood pressure, and temperature. ECG, biochemistry, blood gases, clotting, and blood count should also be monitored.

Two types of tapeworms, Taenia solium and Taenia saginata, can infest humans. Infestation occurs when people consume meat from intermediate hosts that contain the parasite’s tissue stages. Tapeworms compete for nutrients and infestation is often without symptoms. However, in more severe cases, individuals may experience epigastric pain, diarrhea, and vomiting. Diagnosis involves identifying characteristic eggs in the patient’s stool.

Taenia solium infestation can also lead to a condition called cysticercosis. This occurs when larval cysts infiltrate and spread throughout the lung, liver, eye, or brain. Cysticercosis presents with neurological symptoms, seizures, and impaired vision. Confirmation of cysticercosis involves the presence of antibodies and imaging tests such as chest X-rays and CT brain scans.

The treatment for tapeworm infestation is highly effective and involves the use of medications like niclosamide or praziquantel. However, it is important to seek specialist advice when managing Taenia infections in the central nervous system, as severe inflammatory reactions can occur.

This question discusses the prioritization of patient care, specifically focusing on the initial management of acutely unwell patients. The sequence followed in such cases is known as ‘ABCDE’, which stands for airway, breathing, circulation, disability, and exposure. It is crucial to call for help as soon as possible, as the patient’s condition may deteriorate rapidly. If a patient’s consciousness level is dropping, urgent assistance is required, and it is unlikely that you will be able to handle the situation independently.

While waiting for the resuscitation team to arrive, you will be occupied with managing the patient. Therefore, it is not appropriate to make a phone call to the Emergency Department consultant for advice. Although the Emergency Department nurses may be helpful, it is essential to call the resuscitation team first. Continuing to handle the situation alone, regardless of the patient’s clinical condition, indicates a failure to recognize the need for assistance in this scenario.

According to the 2011 recommendations from the World Health Organization (WHO), HbA1c can now be used as a diagnostic test for diabetes. However, this is only applicable if stringent quality assurance tests are in place and the assays are standardized to criteria aligned with international reference values. Additionally, accurate measurement of HbA1c is only possible if there are no conditions present that could hinder its accuracy.

To diagnose diabetes using HbA1c, a value of 48 mmol/mol (6.5%) is recommended as the cut-off point. It’s important to note that a value lower than 48 mmol/mol (6.5%) does not exclude the possibility of diabetes, as glucose tests are still necessary for a definitive diagnosis.

When using glucose tests, the following criteria are considered diagnostic for diabetes mellitus:
– A random venous plasma glucose concentration greater than 11.1 mmol/l
– A fasting plasma glucose concentration greater than 7.0 mmol/l
– A two-hour plasma glucose concentration greater than 11.1 mmol/l, two hours after consuming 75g of anhydrous glucose in an oral glucose tolerance test (OGTT)

However, there are certain circumstances where HbA1c is not appropriate for diagnosing diabetes mellitus. These include:
– ALL children and young people
– Patients of any age suspected of having Type 1 diabetes
– Patients with symptoms of diabetes for less than two months
– Patients at high risk of diabetes who are acutely ill, such as those requiring hospital admission
– Patients taking medication that may cause a rapid rise in glucose levels, such as steroids or antipsychotics
– Patients with acute pancreatic damage, including those who have undergone pancreatic surgery
– Pregnant individuals
– Presence of genetic, hematologic, and illness-related factors that can influence HbA1c and its measurement.

The current recommendations from NICE for managing warfarin in the presence of bleeding or an abnormal INR are as follows:

In cases of major active bleeding, regardless of the INR level, the first step is to stop administering warfarin. Next, 5 mg of vitamin K (phytomenadione) should be given intravenously. Additionally, dried prothrombin complex concentrate, which contains factors II, VII, IX, and X, should be administered. If dried prothrombin complex is not available, fresh frozen plasma can be given at a dose of 15 ml/kg.

If the INR is greater than 8.0 and there is minor bleeding, warfarin should be stopped. Slow injection of 1-3 mg of vitamin K can be given, and this dose can be repeated after 24 hours if the INR remains high. Warfarin can be restarted once the INR is less than 5.0.

If the INR is greater than 8.0 with no bleeding, warfarin should be stopped. Oral administration of 1-5 mg of vitamin K can be given, and this dose can be repeated after 24 hours if the INR remains high. Warfarin can be restarted once the INR is less than 5.0.

If the INR is between 5.0-8.0 with minor bleeding, warfarin should be stopped. Slow injection of 1-3 mg of vitamin K can be given, and warfarin can be restarted once the INR is less than 5.0.

If the INR is between 5.0-8.0 with no bleeding, one or two doses of warfarin should be withheld, and the subsequent maintenance dose should be reduced.

For more information, please refer to the NICE Clinical Knowledge Summary on the management of warfarin therapy and the BNF guidance on the use of phytomenadione.

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

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

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

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

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

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

Vestibular neuronitis is believed to occur when the vestibular nerve becomes inflamed, often following a viral infection like a cold. This condition causes a constant feeling of dizziness, which can worsen with head movements. On the other hand, BPPV (benign paroxysmal positional vertigo) is characterized by brief episodes of vertigo lasting around 10-20 seconds, triggered by specific head movements. To diagnose BPPV, the Dix-Hallpike test is performed, and a positive result is indicated by a specific type of eye movement called nystagmus. In contrast, vestibular neuritis typically presents with horizontal nystagmus that only occurs in one direction.

Further Reading:

Vestibular neuritis, also known as vestibular neuronitis, is a condition characterized by sudden and prolonged vertigo of peripheral origin. It is believed to be caused by inflammation of the vestibular nerve, often following a viral infection. It is important to note that vestibular neuritis and labyrinthitis are not the same condition, as labyrinthitis involves inflammation of the labyrinth. Vestibular neuritis typically affects individuals between the ages of 30 and 60, with a 1:1 ratio of males to females. The annual incidence is approximately 3.5 per 100,000 people, making it one of the most commonly diagnosed causes of vertigo.

Clinical features of vestibular neuritis include nystagmus, which is a rapid, involuntary eye movement, typically in a horizontal or horizontal-torsional direction away from the affected ear. The head impulse test may also be positive. Other symptoms include spontaneous onset of rotational vertigo, which is worsened by changes in head position, as well as nausea, vomiting, and unsteadiness. These severe symptoms usually last for 2-3 days, followed by a gradual recovery over a few weeks. It is important to note that hearing is not affected in vestibular neuritis, and symptoms such as tinnitus and focal neurological deficits are not present.

Differential diagnosis for vestibular neuritis includes benign paroxysmal positional vertigo (BPPV), labyrinthitis, Meniere’s disease, migraine, stroke, and cerebellar lesions. Management of vestibular neuritis involves drug treatment for nausea and vomiting associated with vertigo, typically through short courses of medication such as prochlorperazine or cyclizine. If symptoms are severe and fluids cannot be tolerated, admission and administration of IV fluids may be necessary. General advice should also be given, including avoiding driving while symptomatic, considering the suitability to work based on occupation and duties, and the increased risk of falls. Follow-up is required, and referral is necessary if there are atypical symptoms, symptoms do not improve after a week of treatment, or symptoms persist for more than 6 weeks.

The prognosis for vestibular neuritis is generally good, with the majority of individuals fully recovering within 6 weeks. Recurrence is thought to occur in 2-11% of cases, and approximately 10% of individuals may develop BPPV following an episode of vestibular neuritis. A very rare complication of vestibular neuritis is ph

If a person has symptoms or signs that indicate diabetes, a random venous plasma glucose concentration of 11.1 mmol/l or higher is considered to be indicative of diabetes mellitus. However, it is important to note that a diagnosis should not be made based solely on one test. A second test should be conducted to confirm the diagnosis. It is also worth mentioning that temporary high blood sugar levels may occur in individuals who are experiencing acute infection, trauma, circulatory issues, or other forms of stress that are not related to 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.

Salicylate poisoning is a fairly common form of poisoning that can lead to organ damage and death if not treated promptly. The symptoms of salicylate poisoning include nausea, vomiting, ringing in the ears, hearing loss, excessive sweating, dehydration, rapid breathing, flushed skin, and high fever in children. In severe cases, convulsions, swelling of the brain, coma, kidney failure, fluid in the lungs, and unstable heart function can occur.

The treatment for salicylate poisoning involves stabilizing the patient’s airway, breathing, and circulation as needed, preventing further absorption of the poison, enhancing its elimination from the body, correcting any metabolic abnormalities, and providing supportive care. Unfortunately, there is no specific antidote available for salicylates. If a large amount of salicylate has been ingested within the past hour (more than 4.5 grams in adults or more than 2 grams in children), gastric lavage (stomach pumping) and administration of activated charcoal (50 grams) are recommended to reduce absorption and increase elimination.

Medical investigations for salicylate poisoning should include measuring the level of salicylate in the blood, analyzing arterial blood gases, performing an electrocardiogram (ECG), checking blood glucose levels, assessing kidney function and electrolyte levels, and evaluating blood clotting. ECG abnormalities that may be present include widening of the QRS complex, AV block, and ventricular arrhythmias.

The severity of salicylate poisoning is determined by the level of salicylate in the blood. Mild poisoning is defined as a salicylate level below 450 mg/L, moderate poisoning is between 450-700 mg/L, and severe poisoning is above 700 mg/L. In severe cases, aggressive intravenous fluid therapy is necessary to correct dehydration, and administration of 1.26% sodium bicarbonate can help eliminate the salicylate from the body. It is important to maintain a urine pH of greater than 7.5, ideally between 8.0-8.5. However, forced alkaline diuresis is no longer recommended. Life-threatening cases may require admission to the intensive care unit, intubation and ventilation, and possibly hemodialysis.

Thyroid storm, also known as thyrotoxic crisis, is a rare and potentially life-threatening complication of hyperthyroidism. The most common cause of thyroid storm is infection. Please refer to the yellow box at the bottom of the notes for additional information on thyroid storm.

Further Reading:

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

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

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

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

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

In most cases, TMJ dislocation occurs in an anterior and bilateral manner.

TMJ dislocation occurs when the mandibular condyle is displaced from its normal position in the mandibular fossa of the temporal bone. The most common type of dislocation is bilateral anterior dislocation. This occurs when the mandible is dislocated forward and the masseter and pterygoid muscles spasm, locking the condyle in place.

The temporomandibular joint is unique because it has an articular disc that separates the joint into upper and lower compartments. Dislocation can be caused by trauma, such as a direct blow to the open mouth, or by traumatic events like excessive mouth opening during yawning, laughing, shouting, or eating. It can also occur during dental work.

Signs and symptoms of TMJ dislocation include difficulty fully opening or closing the mouth, pain or tenderness in the TMJ region, jaw pain, ear pain, difficulty chewing, and facial pain. Connective tissue disorders like Marfan’s and Ehlers-Danlos syndrome can increase the likelihood of dislocation.

If TMJ dislocation is suspected, X-rays may be done to confirm the diagnosis. The best initial imaging technique is an orthopantomogram (OPG) or a standard mandibular series.

Management of anterior dislocations involves reducing the dislocated mandible, which is usually done in the emergency department. Dislocations to the posterior, medial, or lateral side are usually associated with a mandibular fracture and should be referred to a maxillofacial surgeon.

Reduction of an anterior dislocation involves applying distraction forces to the mandible. This can be done by gripping the mandible externally or intra-orally. In some cases, procedural sedation or local anesthesia may be used, and in rare cases, reduction may be done under general anesthesia.

After reduction, a post-reduction X-ray is done to confirm adequate reduction and rule out any fractures caused by the procedure. Discharge advice includes following a soft diet for at least 48 hours, avoiding wide mouth opening for at least 2 weeks, and supporting the mouth with the hand during yawning or laughing. A Barton bandage may be used to support the mandible if the patient is unable to comply with the discharge advice. Referral to a maxillofacial surgeon as an outpatient is also recommended.

To achieve sedation in children, it is recommended to administer an initial dose of ketamine at a rate of 1.0 mg/kg through a slow intravenous injection lasting at least one minute. It is important to note that administering the medication too quickly can lead to respiratory depression. In some cases, an additional dose of 0.5 mg/kg may be necessary to maintain the desired level of sedation.

Further Reading:

Ketamine sedation in children should only be performed by a trained and competent clinician who is capable of managing complications, especially those related to the airway. The clinician should have completed the necessary training and have the appropriate skills for procedural sedation. It is important for the clinician to consider the length of the procedure before deciding to use ketamine sedation, as lengthy procedures may be more suitable for general anesthesia.

Examples of procedures where ketamine may be used in children include suturing, fracture reduction/manipulation, joint reduction, burn management, incision and drainage of abscess, tube thoracostomy placement, foreign body removal, and wound exploration/irrigation.

During the ketamine sedation procedure, a minimum of three staff members should be present: a doctor to manage the sedation and airway, a clinician to perform the procedure, and an experienced nurse to monitor and support the patient, family, and clinical staff. The child should be sedated and managed in a high dependency or resuscitation area with immediate access to resuscitation facilities. Monitoring should include sedation level, pain, ECG, blood pressure, respiration, pulse oximetry, and capnography, with observations taken and recorded every 5 minutes.

Prior to the procedure, consent should be obtained from the parent or guardian after discussing the proposed procedure and use of ketamine sedation. The risks and potential complications should be explained, including mild or moderate/severe agitation, rash, vomiting, transient clonic movements, and airway problems. The parent should also be informed that certain common side effects, such as nystagmus, random purposeless movements, muscle twitching, rash, and vocalizations, are of no clinical significance.

Topical anesthesia may be considered to reduce the pain of intravenous cannulation, but this step may not be advisable if the procedure is urgent. The clinician should also ensure that key resuscitation drugs are readily available and doses are calculated for the patient in case they are needed.

Before administering ketamine, the child should be prepared by encouraging the parents or guardians to talk to them about happy thoughts and topics to minimize unpleasant emergence phenomena. The dose of ketamine is typically 1.0 mg/kg by slow intravenous injection over at least one minute, with additional doses of 0.5 mg/kg administered as required after 5-10 minutes to achieve the desired dissociative state.

Conjunctivitis is the most frequent occurrence of Chlamydia trachomatis infection in newborns. Ophthalmia neonatorum refers to any cause of conjunctivitis during the newborn period, regardless of the specific organism responsible. Chlamydia is now the leading cause, accounting for up to 40% of cases. Neisseria gonorrhoea, on the other hand, only accounts for less than 1% of reported cases. The remaining cases are caused by non-sexually transmitted bacteria like Staphylococcus, Streptococcus, Haemophilus species, and viruses.

Gonorrhoeal ophthalmia neonatorum typically presents within 1 to 5 days after birth. It is characterized by intense redness and swelling of the conjunctiva, eyelid swelling, and a severe discharge of pus. Corneal ulceration and perforation may also be present.

Chlamydial ophthalmia neonatorum, on the other hand, usually appears between 5 to 14 days after birth. It is characterized by a gradually increasing watery discharge that eventually becomes purulent. The inflammation in the eyes is usually less severe compared to gonococcal infection, and there is a lower risk of corneal ulceration and perforation.

The second most common manifestation of Chlamydia trachomatis infection in newborns is pneumonia. Approximately 5-30% of infected neonates will develop pneumonia. About half of these infants will also have a history of ophthalmia neonatorum.

This patient exhibits signs of potentially life-threatening asthma. In adults, acute severe asthma is characterized by a peak expiratory flow (PEF) of 33-50% of the best or predicted value, a respiratory rate exceeding 25 breaths per minute, a heart rate over 110 beats per minute, and an inability to complete sentences in one breath. On the other hand, life-threatening asthma is indicated by a PEF below 33% of the best or predicted value, a blood oxygen saturation (SpO2) below 92%, a partial pressure of oxygen (PaO2) below 8 kPA, a normal partial pressure of carbon dioxide (PaCO2) within the range of 4.6-6.0 kPa, a silent chest, cyanosis, poor respiratory effort, exhaustion, altered consciousness, and hypotension.

To address acute asthma in adults, the recommended drug doses include administering 5 mg of salbutamol through an oxygen-driven nebulizer, delivering 500 mcg of ipratropium bromide via an oxygen-driven nebulizer, providing 40-50 mg of prednisolone orally, administering 100 mg of hydrocortisone intravenously, and infusing 1.2-2 g of magnesium sulfate intravenously over a period of 20 minutes.

According to the current Advanced Life Support (ALS) guidelines, it is advisable to seek senior advice before considering the use of intravenous aminophylline in cases of severe or life-threatening asthma. If used, a loading dose of 5 mg/kg should be given over 20 minutes, followed by a continuous infusion of 500-700 mcg/kg/hour. To prevent toxicity, it is important to maintain serum theophylline levels below 20 mcg/ml.

In situations where inhaled therapy is not feasible, intravenous salbutamol can be considered, with a slow administration of 250 mcg. However, it should only be used when a patient is receiving bag-mask ventilation.

It is worth noting that there is currently no evidence supporting the use of leukotriene receptor antagonists, such as montelukast, or Heliox in the management of acute severe or life-threatening asthma.