Intussusception occurs when a section of the bowel folds into another section, causing a blockage. This can be due to a specific underlying issue, like a Meckel’s diverticulum, or it can happen without any specific cause. The condition is most commonly seen in boys between the ages of 5 and 10 months. Symptoms include sudden vomiting and episodes of abdominal pain that come and go. The vomit quickly becomes greenish-yellow in color. Dance’s sign, which is the absence of bowel in the lower right part of the abdomen, may be observed. Redcurrant jelly-like stools are a late indication of the condition. It is believed that more than 90% of cases are caused by a non-specific underlying issue, often viral infections like rotavirus, adenovirus, and human herpesvirus 6.

It is crucial to be able to distinguish between the underlying causes of congenital cyanotic and acyanotic heart disease. Tricuspid atresia is one of the causes of congenital cyanotic heart disease. Other causes in this category include Ebstein’s anomaly, Hypoplastic left heart syndrome, Tetralogy of Fallot, and Transposition of the great vessels.

On the other hand, congenital acyanotic heart disease has different causes. These include Ventricular septal defect, Patent ductus arteriosus, Atrial septal defect, Atrioventricular septal defect, Pulmonary stenosis, Aortic stenosis, and Coarctation of the aorta.

By understanding the distinctions between these causes, healthcare professionals can provide appropriate diagnosis and treatment for patients with congenital heart disease.

The mortality rate associated with pulmonary edema as a result of acute heart failure secondary to cardiogenic shock during hospitalization is 50%.

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.

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.

Patients who have suffered burns should receive high-flow oxygen (15 L) through a reservoir bag while their breathing is being evaluated. If intubation is necessary, it is crucial to use an appropriately sized endotracheal tube (ETT). Using a tube that is too small can make it difficult or even impossible to ventilate the patient, clear secretions, or perform bronchoscopy.

According to the ATLS guidelines, adults should be intubated using an ETT with an internal diameter (ID) of at least 7.5 mm or larger. Children, on the other hand, should have an ETT with an ID of at least 4.5 mm. Once a patient has been intubated, it is important to continue administering 100% oxygen until their carboxyhemoglobin levels drop to less than 5%.

To protect the lungs, it is recommended to use lung protective ventilation techniques. This involves using low tidal volumes (4-8 mL/kg) and ensuring that peak inspiratory pressures do not exceed 30 cmH2O.

The principle of autonomy pertains to the right of capable individuals to make well-informed choices regarding their personal healthcare. Autonomy emphasizes the importance of respecting an individual’s ability to make decisions about their own health, based on their own values, beliefs, and preferences. It recognizes that individuals have the right to be informed about their healthcare options, to give informed consent, and to have their choices respected by healthcare providers. Autonomy is a fundamental principle in medical ethics that promotes patient-centered care and respects the individual’s right to self-determination.

Further Reading:

Principles of Medical Ethics:

1. Autonomy: Competent adults have the right to make informed decisions about their own medical care.
2. Beneficence: Healthcare professionals should take actions that serve the best interests of patients.
3. Non-maleficence: Healthcare professionals should not take actions that may injure or harm patients.
4. Justice: Healthcare professionals should take actions that are fair and equitable to both the individual and society as a whole.

Confidentiality:

1. Use minimum necessary personal information and consider anonymizing information if possible.
2. Manage and protect personal information to prevent improper access, disclosure, or loss.
3. Understand and adhere to information governance appropriate to your role.
4. Comply with the law when handling personal information.
5. Share relevant information for direct care unless the patient objects.
6. Obtain explicit consent to disclose identifiable information for purposes other than care or local clinical audit, unless required by law or justified in the public interest.
7. Inform patients about disclosures of personal information they would not reasonably expect, unless not practicable or undermines the purpose of the disclosure.
8. Support patients in accessing their information and respecting their legal rights.

Obtaining Patient’s Consent for Disclosure:

– Consent should be obtained for disclosing personal information for purposes other than direct care or local clinical audit, unless required by law or not appropriate or practicable.

Situations Where Patient Consent is Not Required for Disclosure:

– Adults at risk of or suffering abuse or neglect, as required by law.
– Adults lacking capacity, if neglect or harm is suspected, unless not overall beneficial to the patient.
– When required by law or approved through a statutory process.
– When justified in the public interest, such as for the prevention, detection, or prosecution of serious crime, patient’s fitness to drive, serious communicable disease, or posing a serious risk to others through being unfit for work.

Confidentiality Following a Patient’s Death:

– Respect the patient’s confidentiality even after their death.
– If the patient previously requested not to share personal information with those close to them, abide by their wishes.
– Be considerate, sensitive, and responsive to those close to the patient, providing as much information as possible.

The Law & Caldicott Guardians:

Data Protection Act:
– Sets rules and standards for the use and handling of personal data by organizations.
– Personal data must be used fairly, lawfully, transparently, and for specified purposes.
– Individuals have rights

The ratio of chest compressions to ventilations is 15:2. This ratio has not been proven through experiments, but it has been validated through mathematical studies. When performing chest compressions on a child, it is recommended to make them at least 1/3 of the depth of the child’s chest. Additionally, the optimal compression rate is between 100 and 120 compressions per minute.
To protect the airway of an unconscious child, the oropharyngeal (Guedel) airway is the best option. However, it should not be used on awake patients as there is a risk of vomiting and aspiration.
In children, asystole is the most common arrest rhythm. This occurs when the young heart responds to prolonged hypoxia and acidosis by progressively slowing down, eventually resulting in asystole.

The current recommendations by NICE and the BNF for non-typhoid salmonella enteritis suggest that ciprofloxacin should be used as the first-line treatment if necessary. Alternatively, cefotaxime can be considered as a suitable alternative. It is important to note that cases of salmonella enteritis often resolve on their own without treatment and are frequently self-limiting. Therefore, the BNF advises against treatment unless there is a risk of developing invasive infection. This includes individuals who are immunocompromised, have haemoglobinopathy, or are children under 6 months old. However, in the case of an elderly patient who is regularly taking corticosteroids, treatment would be recommended.

The current guidelines from NICE and the BNF suggest that if treatment is necessary for campylobacter enteritis, clarithromycin should be the first choice. Azithromycin and erythromycin can be used interchangeably, and ciprofloxacin is a suitable alternative. It is important to note that many cases of campylobacter enteritis resolve on their own without treatment. However, individuals with severe infections or those who are immunocompromised should receive treatment.

Calcium-channel blocker overdose is a serious condition that should always be taken seriously as it can be potentially life-threatening. The two most dangerous types of calcium channel blockers in overdose are verapamil and diltiazem. These medications work by binding to the alpha-1 subunit of L-type calcium channels, which prevents the entry of calcium into the cells. These channels play a crucial role in the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

Significant toxicity can occur with the ingestion of more than 10 tablets of verapamil (160 mg or 240 mg immediate or sustained-release capsules) or diltiazem (180 mg, 240 mg or 360 mg immediate or sustained-release capsules). In children, even 1-2 tablets of immediate or sustained-release verapamil or diltiazem can be harmful. Symptoms usually appear within 1-2 hours of taking standard preparations, but with slow-release versions, the onset of severe toxicity may be delayed by 12-16 hours, with peak effects occurring after 24 hours.

The main clinical manifestations of calcium-channel blocker overdose include nausea and vomiting, low blood pressure, slow heart rate and first-degree heart block, heart muscle ischemia and stroke, kidney failure, pulmonary edema, and high blood sugar levels.

When managing a patient with calcium-channel blocker overdose, certain bedside investigations are crucial. These include checking blood glucose levels, performing an electrocardiogram (ECG), and obtaining an arterial blood gas sample. Additional investigations that can provide helpful information include assessing urea and electrolyte levels, conducting a chest X-ray to check for pulmonary edema, and performing an echocardiography.

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.

Respiratory acidosis occurs when the respiratory system is unable to effectively remove carbon dioxide from the body, leading to an increase in acidity. This is often seen in cases of opioid overdose, where respiratory depression can occur. In respiratory acidosis, the bicarbonate levels may rise as the body’s metabolic system tries to compensate for the increased acidity.

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 collateral 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.

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.

The management of anaphylaxis involves several important steps. First and foremost, it is crucial to ensure proper airway management. Additionally, early administration of adrenaline is essential, preferably in the anterolateral aspect of the middle third of the thigh. Aggressive fluid resuscitation is also necessary. In severe cases, intubation may be required. However, it is important to note that the administration of chlorpheniramine and hydrocortisone should only be considered after early resuscitation has taken place.

Adrenaline is the most vital medication for treating anaphylactic reactions. It acts as an alpha-adrenergic receptor agonist, which helps reverse peripheral vasodilatation and reduce oedema. Furthermore, its beta-adrenergic effects aid in dilating the bronchial airways, increasing the force of myocardial contraction, and suppressing histamine and leukotriene release. Administering adrenaline as the first drug is crucial, and the intramuscular (IM) route is generally the most effective for most individuals.

The recommended doses of IM adrenaline for different age groups during anaphylaxis are as follows:

– Children under 6 years: 150 mcg (0.15 mL of 1:1000)
– Children aged 6-12 years: 300 mcg (0.3 mL of 1:1000)
– Children older than 12 years: 500 mcg (0.5 mL of 1:1000)
– Adults: 500 mcg (0.5 mL of 1:1000)

In patients with pre-existing hypovolaemia, the amount of sodium thiopentone administered should be reduced by half. This is because sodium thiopentone can cause venodilation and myocardial depression, which can result in significant hypovolaemia. Alternatively, an induction agent that does not cause hypotension, such as Etomidate, can be used instead. It is important to note that both propofol and thiopentone are known to cause hypotension.

Further Reading:

There are four commonly used induction agents in the UK: propofol, ketamine, thiopentone, and etomidate.

Propofol is a 1% solution that produces significant venodilation and myocardial depression. It can also reduce cerebral perfusion pressure. The typical dose for propofol is 1.5-2.5 mg/kg. However, it can cause side effects such as hypotension, respiratory depression, and pain at the site of injection.

Ketamine is another induction agent that produces a dissociative state. It does not display a dose-response continuum, meaning that the effects do not necessarily increase with higher doses. Ketamine can cause bronchodilation, which is useful in patients with asthma. The initial dose for ketamine is 0.5-2 mg/kg, with a typical IV dose of 1.5 mg/kg. Side effects of ketamine include tachycardia, hypertension, laryngospasm, unpleasant hallucinations, nausea and vomiting, hypersalivation, increased intracranial and intraocular pressure, nystagmus and diplopia, abnormal movements, and skin reactions.

Thiopentone is an ultra-short acting barbiturate that acts on the GABA receptor complex. It decreases cerebral metabolic oxygen and reduces cerebral blood flow and intracranial pressure. The adult dose for thiopentone is 3-5 mg/kg, while the child dose is 5-8 mg/kg. However, these doses should be halved in patients with hypovolemia. Side effects of thiopentone include venodilation, myocardial depression, and hypotension. It is contraindicated in patients with acute porphyrias and myotonic dystrophy.

Etomidate is the most haemodynamically stable induction agent and is useful in patients with hypovolemia, anaphylaxis, and asthma. It has similar cerebral effects to thiopentone. The dose for etomidate is 0.15-0.3 mg/kg. Side effects of etomidate include injection site pain, movement disorders, adrenal insufficiency, and apnoea. It is contraindicated in patients with sepsis due to adrenal suppression.

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

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

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

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

Gout and pseudogout are both characterized by the presence of crystal deposits in the joints that are affected. Gout occurs when urate crystals are deposited, while pseudogout occurs when calcium pyrophosphate crystals are deposited. Under a microscope, these crystals can be distinguished by their appearance. Urate crystals are needle-shaped and negatively birefringent, while calcium pyrophosphate crystals are brick-shaped and positively birefringent.

Gout can affect any joint in the body, but it most commonly manifests in the hallux metatarsophalangeal joint, which is the joint at the base of the big toe. This joint is affected in approximately 50% of gout cases. On the other hand, pseudogout primarily affects the larger joints, such as the knee.

There are various specific remedies available for different types of poisons and overdoses. The following list provides an outline of some of these antidotes:

Poison: Benzodiazepines
Antidote: Flumazenil

Poison: Beta-blockers
Antidotes: Atropine, Glucagon, Insulin

Poison: Carbon monoxide
Antidote: Oxygen

Poison: Cyanide
Antidotes: Hydroxocobalamin, Sodium nitrite, Sodium thiosulphate

Poison: Ethylene glycol
Antidotes: Ethanol, Fomepizole

Poison: Heparin
Antidote: Protamine sulphate

Poison: Iron salts
Antidote: Desferrioxamine

Poison: Isoniazid
Antidote: Pyridoxine

Poison: Methanol
Antidotes: Ethanol, Fomepizole

Poison: Opioids
Antidote: Naloxone

Poison: Organophosphates
Antidotes: Atropine, Pralidoxime

Poison: Paracetamol
Antidotes: Acetylcysteine, Methionine

Poison: Sulphonylureas
Antidotes: Glucose, Octreotide

Poison: Thallium
Antidote: Prussian blue

Poison: Warfarin
Antidote: Vitamin K, Fresh frozen plasma (FFP)

By utilizing these specific antidotes, medical professionals can effectively counteract the harmful effects of various poisons and overdoses.

If a patient’s INR reading is above 5, it is necessary to take action. In this case, the patient’s INR is between 5 and 8, but there is no evidence of bleeding. According to the provided table, it is recommended to temporarily stop 1-2 doses of warfarin and closely monitor the INR. While it may be optional to switch antibiotics, it is not a crucial step in this situation.

Further Reading:

Management of High INR with Warfarin

Major Bleeding:
– Stop warfarin immediately.
– Administer intravenous vitamin K 5 mg.
– Administer 25-50 u/kg four-factor prothrombin complex concentrate.
– If prothrombin complex concentrate is not available, consider using fresh frozen plasma (FFP).
– Seek medical attention promptly.

INR > 8.0 with Minor Bleeding:
– Stop warfarin immediately.
– Administer intravenous vitamin K 1-3mg.
– Repeat vitamin K dose if INR remains high after 24 hours.
– Restart warfarin when INR is below 5.0.
– Seek medical advice if bleeding worsens or persists.

INR > 8.0 without Bleeding:
– Stop warfarin immediately.
– Administer oral vitamin K 1-5 mg using the intravenous preparation orally.
– Repeat vitamin K dose if INR remains high after 24 hours.
– Restart warfarin when INR is below 5.0.
– Seek medical advice if any symptoms or concerns arise.

INR 5.0-8.0 with Minor Bleeding:
– Stop warfarin immediately.
– Administer intravenous vitamin K 1-3mg.
– Restart warfarin when INR is below 5.0.
– Seek medical advice if bleeding worsens or persists.

INR 5.0-8.0 without Bleeding:
– Withhold 1 or 2 doses of warfarin.
– Reduce subsequent maintenance dose.
– Monitor INR closely and seek medical advice if any concerns arise.

Note: In cases of intracranial hemorrhage, prothrombin complex concentrate should be considered as it is faster acting than fresh frozen plasma (FFP).

The CENTOR score is a clinical prediction rule used to assess the likelihood of a patient having a streptococcal infection, which is commonly associated with sore throat. It is based on the presence or absence of four clinical criteria: fever, tonsillar exudate, tender anterior cervical lymphadenopathy, and absence of cough. Each criterion is assigned one point, and the total score ranges from 0 to 4. In this case, the patient has a fever, tonsillar exudate, tender anterior cervical lymphadenopathy, and no cough, resulting in a CENTOR score of 4. A higher score indicates a higher likelihood of a streptococcal infection, and further diagnostic testing or treatment may be warranted.

Further Reading:

Pharyngitis and tonsillitis are common conditions that cause inflammation in the throat. Pharyngitis refers to inflammation of the oropharynx, which is located behind the soft palate, while tonsillitis refers to inflammation of the tonsils. These conditions can be caused by a variety of pathogens, including viruses and bacteria. The most common viral causes include rhinovirus, coronavirus, parainfluenza virus, influenza types A and B, adenovirus, herpes simplex virus type 1, and Epstein Barr virus. The most common bacterial cause is Streptococcus pyogenes, also known as Group A beta-hemolytic streptococcus (GABHS). Other bacterial causes include Group C and G beta-hemolytic streptococci and Fusobacterium necrophorum.

Group A beta-hemolytic streptococcus is the most concerning pathogen as it can lead to serious complications such as rheumatic fever and glomerulonephritis. These complications can occur due to an autoimmune reaction triggered by antigen/antibody complex formation or from cell damage caused by bacterial exotoxins.

When assessing a patient with a sore throat, the clinician should inquire about the duration and severity of the illness, as well as associated symptoms such as fever, malaise, headache, and joint pain. It is important to identify any red flags and determine if the patient is immunocompromised. Previous non-suppurative complications of Group A beta-hemolytic streptococcus infection should also be considered, as there is an increased risk of further complications with subsequent infections.

Red flags that may indicate a more serious condition include severe pain, neck stiffness, or difficulty swallowing. These symptoms may suggest epiglottitis or a retropharyngeal abscess, which require immediate attention.

To determine the likelihood of a streptococcal infection and the need for antibiotic treatment, two scoring systems can be used: CENTOR and FeverPAIN. The CENTOR criteria include tonsillar exudate, tender anterior cervical lymphadenopathy or lymphadenitis, history of fever, and absence of cough. The FeverPAIN criteria include fever, purulence, rapid onset of symptoms, severely inflamed tonsils, and absence of cough or coryza. Based on the scores from these criteria, the likelihood of a streptococcal infection can be estimated, and appropriate management can be undertaken. can

To prevent diffusion hypoxia, it is recommended to administer supplemental oxygen to patients for about 5 minutes after discontinuing nitrous oxide. This is important because there is a risk of developing diffusion hypoxia after the termination of nitrous oxide.

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.

The management of anaphylaxis involves several important steps. First and foremost, it is crucial to ensure proper airway management. Additionally, early administration of adrenaline is essential, preferably in the anterolateral aspect of the middle third of the thigh. Aggressive fluid resuscitation is also necessary. In severe cases, intubation may be required. However, it is important to note that the administration of chlorpheniramine and hydrocortisone should only be considered after early resuscitation has taken place.

Adrenaline is the most vital medication for treating anaphylactic reactions. It acts as an alpha-adrenergic receptor agonist, which helps reverse peripheral vasodilatation and reduce oedema. Furthermore, its beta-adrenergic effects aid in dilating the bronchial airways, increasing the force of myocardial contraction, and suppressing histamine and leukotriene release. Administering adrenaline as the first drug is crucial, and the intramuscular (IM) route is generally the most effective for most individuals.

The recommended doses of IM adrenaline for different age groups during anaphylaxis are as follows:

– Children under 6 years: 150 mcg (0.15 mL of 1:1000)
– Children aged 6-12 years: 300 mcg (0.3 mL of 1:1000)
– Children older than 12 years: 500 mcg (0.5 mL of 1:1000)
– Adults: 500 mcg (0.5 mL of 1:1000)

Ipratropium bromide is a medication that falls under the category of antimuscarinic drugs. It is commonly used to manage acute asthma and chronic obstructive pulmonary disease (COPD). While it can provide short-term relief for chronic asthma, it is generally recommended to use short-acting β2 agonists as they act more quickly and are preferred.

According to the guidelines set by the British Thoracic Society (BTS), nebulized ipratropium bromide (0.5 mg every 4-6 hours) can be added to β2 agonist treatment for patients with acute severe or life-threatening asthma, or those who do not respond well to initial β2 agonist therapy.

For mild cases of chronic obstructive pulmonary disease, aerosol inhalation of ipratropium can be used for short-term relief, as long as the patient is not already using a long-acting antimuscarinic drug like tiotropium. The maximum effect of ipratropium occurs within 30-60 minutes after use, and its bronchodilating effects can last for 3-6 hours. Typically, treatment with ipratropium is recommended three times a day to maintain bronchodilation.

The most common side effect of ipratropium bromide is dry mouth. Other potential side effects include constipation, cough, paroxysmal bronchospasm, headache, nausea, and palpitations. It is important to note that ipratropium can cause urinary retention in patients with prostatic hyperplasia and bladder outflow obstruction. Additionally, it can trigger acute closed-angle glaucoma in susceptible patients.

For more information on the management of asthma, it is recommended to refer to the BTS/SIGN Guideline on the Management of Asthma.

Adrenaline can be given in cases of life-threatening anaphylactic reactions, even if there are certain conditions that may make it less advisable. These conditions include coronary artery disease, uncontrolled hypertension, serious ventricular arrhythmias, and the second stage of labor. Despite these relative contraindications, adrenaline may still be administered to address the immediate danger posed by anaphylaxis.

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

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

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

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

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

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

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

COHb is a measure used to evaluate the presence of carbon monoxide poisoning in individuals who are in good health. hHb refers to deoxygenated haemoglobin.

Further Reading:

Methaemoglobinaemia is a condition where haemoglobin is oxidised from Fe2+ to Fe3+. This process is normally regulated by NADH methaemoglobin reductase, which transfers electrons from NADH to methaemoglobin, converting it back to haemoglobin. In healthy individuals, methaemoglobin levels are typically less than 1% of total haemoglobin. However, an increase in methaemoglobin can lead to tissue hypoxia as Fe3+ cannot bind oxygen effectively.

Methaemoglobinaemia can be congenital or acquired. Congenital causes include haemoglobin chain variants (HbM, HbH) and NADH methaemoglobin reductase deficiency. Acquired causes can be due to exposure to certain drugs or chemicals, such as sulphonamides, local anaesthetics (especially prilocaine), nitrates, chloroquine, dapsone, primaquine, and phenytoin. Aniline dyes are also known to cause methaemoglobinaemia.

Clinical features of methaemoglobinaemia include slate grey cyanosis (blue to grey skin coloration), chocolate blood or chocolate cyanosis (brown color of blood), dyspnoea, low SpO2 on pulse oximetry (which often does not improve with supplemental oxygen), and normal PaO2 on arterial blood gas (ABG) but low SaO2. Patients may tolerate hypoxia better than expected. Severe cases can present with acidosis, arrhythmias, seizures, and coma.

Diagnosis of methaemoglobinaemia is made by directly measuring the level of methaemoglobin using a co-oximeter, which is present in most modern blood gas analysers. Other investigations, such as a full blood count (FBC), electrocardiogram (ECG), chest X-ray (CXR), and beta-human chorionic gonadotropin (bHCG) levels (in pregnancy), may be done to assess the extent of the condition and rule out other contributing factors.

Active treatment is required if the methaemoglobin level is above 30% or if it is below 30% but the patient is symptomatic or shows evidence of tissue hypoxia. Treatment involves maintaining the airway and delivering high-flow oxygen, removing the causative agents, treating toxidromes and consider giving IV dextrose 5%.

Osgood-Schlatter disease is commonly observed in active teenagers and is characterized by pain and tenderness in the tibial tuberosity. Rest is typically recommended as part of the treatment plan, and the diagnosis is made based on clinical evaluation.

Chondromalacia patella is most prevalent in teenage girls and is often accompanied by knee pain while going up and downstairs. Discomfort tends to worsen after prolonged periods of sitting. Treatment options include pain relief medication and physiotherapy.

Prepatellar bursitis, also known as housemaid’s knee, is linked to excessive kneeling.

Pseudogout is an inflammatory arthritis caused by the accumulation of pyrophosphate crystals. While the knees are frequently affected, it is unlikely to occur in this age group.

Still’s disease accounts for approximately 10% of cases of juvenile chronic arthritis. It typically involves multiple systems in the body and is often characterized by fever, rash, swollen lymph nodes, and joint pain.

The current algorithm for treating a convulsing child, known as APLS, is as follows:

Step 1 (5 minutes after the start of convulsion):
If a child has been convulsing for 5 minutes or more, they should be given an initial dose of benzodiazepine. This can be administered intravenously (IV) or intraosseously (IO) if vascular access is available. Alternatively, buccal midazolam or rectal diazepam can be given if vascular access is not available.

Step 2 (10 minutes after the start of step 1):
If the convulsion continues for another 10 minutes, a second dose of benzodiazepine should be given. It is also important to seek senior help at this point.

Step 3 (10 minutes after the start of step 2):
At this stage, it is necessary to involve senior medical personnel to reassess the child and provide guidance on further management. The recommended approach is as follows:
– If the child is not already receiving phenytoin, a phenytoin infusion should be initiated. This involves administering 20 mg/kg of phenytoin intravenously over a period of 20 minutes.
– If the child is already taking phenytoin, phenobarbitone can be used instead. The recommended dosage is 20 mg/kg administered intravenously over 20 minutes.
– In the meantime, rectal paraldehyde can be considered at a dose of 0.8 ml/kg of the 50:50 mixture while preparing the infusion.

Step 4 (20 minutes after the start of step 3):
If the child is still experiencing convulsions at this stage, it is crucial to have an anaesthetist present. A rapid sequence induction with thiopental is recommended for further management.

In the case of this specific child who weighs 25 kg and has already received a dose of lorazepam, they should receive a second dose of 0.1 mg/kg, which amounts to 2.5 mg.

This patient has presented with an Addisonian crisis, which is a rare but potentially catastrophic condition if not diagnosed promptly. It is more commonly seen in women than men and typically occurs between the ages of 30 and 50.

Addison’s disease is caused by insufficient production of steroid hormones by the adrenal glands, affecting the production of glucocorticoids, mineralocorticoids, and sex steroids. The main causes of Addison’s disease include autoimmune adrenalitis (accounting for 80% of cases), bilateral adrenalectomy, Waterhouse-Friderichsen syndrome (hemorrhage into the adrenal glands), and tuberculosis.

The most common trigger for an Addisonian crisis in patients with Addison’s disease is the intentional or accidental withdrawal of steroid therapy. Other factors that can precipitate a crisis include infection, trauma, myocardial infarction, cerebral infarction, asthma, hypothermia, and alcohol abuse.

Clinical features of Addison’s disease include weakness, lethargy, hypotension (especially orthostatic hypotension), nausea, vomiting, weight loss, reduced axillary and pubic hair, depression, and hyperpigmentation (particularly in palmar creases, buccal mucosa, and exposed areas). In an Addisonian crisis, the main symptoms are usually hypoglycemia and shock, characterized by tachycardia, peripheral vasoconstriction, hypotension, altered consciousness, and even coma.

Biochemical markers of Addison’s disease typically include increased ACTH levels (as a compensatory response to stimulate the adrenal glands), elevated serum renin levels, hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, and metabolic acidosis. Confirmatory investigations may involve the Synacthen test, plasma ACTH level measurement, plasma renin level measurement, and testing for adrenocortical antibodies.

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

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.

Instances of local anaesthetic systemic toxicity (LAST) should be promptly reported to the National Patient Safety Agency (NPSA). Additionally, it is advisable to report any adverse drug reactions to the Medicines and Healthcare products Regulatory Agency (MHRA) through their yellow card scheme. Please refer to the follow-up section in the notes for further details.

Further Reading:

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

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

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

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

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

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.

The following provides a summary of common causes for different acid-base disorders.

Respiratory alkalosis can be caused by hyperventilation, such as during periods of anxiety. It can also be a result of conditions like pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, or the early stages of aspirin overdose.

Respiratory acidosis, on the other hand, is often associated with chronic obstructive pulmonary disease (COPD), life-threatening asthma, pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or other respiratory conditions.

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

Metabolic acidosis with a raised anion gap can be caused by lactic acidosis (such as in cases of hypoxemia, shock, sepsis, or infarction), ketoacidosis (such as in diabetes, starvation, or alcohol excess), renal failure, or poisoning (such as in late stages of aspirin overdose, methanol or ethylene glycol ingestion).

Lastly, metabolic acidosis with a normal anion gap can be a result of conditions like diarrhea, ammonium chloride ingestion, or adrenal insufficiency.

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 recommended dose of activated charcoal for adults and children aged 12 or over to prevent the absorption of poisons in the gastrointestinal tract is 50g.

Further Reading:

Paracetamol poisoning occurs when the liver is unable to metabolize paracetamol properly, leading to the production of a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI). Normally, NAPQI is conjugated by glutathione into a non-toxic form. However, during an overdose, the liver’s conjugation systems become overwhelmed, resulting in increased production of NAPQI and depletion of glutathione stores. This leads to the formation of covalent bonds between NAPQI and cell proteins, causing cell death in the liver and kidneys.

Symptoms of paracetamol poisoning may not appear for the first 24 hours or may include abdominal symptoms such as nausea and vomiting. After 24 hours, hepatic necrosis may develop, leading to elevated liver enzymes, right upper quadrant pain, and jaundice. Other complications can include encephalopathy, oliguria, hypoglycemia, renal failure, and lactic acidosis.

The management of paracetamol overdose depends on the timing and amount of ingestion. Activated charcoal may be given if the patient presents within 1 hour of ingesting a significant amount of paracetamol. N-acetylcysteine (NAC) is used to increase hepatic glutathione production and is given to patients who meet specific criteria. Blood tests are taken to assess paracetamol levels, liver function, and other parameters. Referral to a medical or liver unit may be necessary, and psychiatric follow-up should be considered for deliberate overdoses.

In cases of staggered ingestion, all patients should be treated with NAC without delay. Blood tests are also taken, and if certain criteria are met, NAC can be discontinued. Adverse reactions to NAC are common and may include anaphylactoid reactions, rash, hypotension, and nausea. Treatment for adverse reactions involves medications such as chlorpheniramine and salbutamol, and the infusion may be stopped if necessary.

The prognosis for paracetamol poisoning can be poor, especially in cases of severe liver injury. Fulminant liver failure may occur, and liver transplant may be necessary. Poor prognostic indicators include low arterial pH, prolonged prothrombin time, high plasma creatinine, and hepatic encephalopathy.

Renal colic, also known as ureteric colic, refers to a sudden and intense pain in the lower back caused by a blockage in the ureter, which is the tube that carries urine from the kidney to the bladder. This condition is commonly associated with the presence of a urinary tract stone.

The main symptoms of renal or ureteric colic include severe abdominal pain on one side, starting in the lower back or flank and radiating to the groin or genital area in men, or to the labia in women. The pain comes and goes in spasms, lasting for minutes to hours, with periods of no pain or a dull ache. Nausea, vomiting, and the presence of blood in the urine are often accompanying symptoms.

People experiencing renal or ureteric colic are usually restless and unable to find relief by lying still, which helps to distinguish this condition from peritonitis. They may have a history of previous episodes and may also present with fever and sweating if there is an associated urinary infection. Some individuals may complain of painful urination, frequent urination, and straining when the stone reaches the junction between the ureter and the bladder, as the stone irritates the detrusor muscle.

In terms of pain management, the first-line treatment for adults, children, and young people with suspected renal colic is a non-steroidal anti-inflammatory drug (NSAID), which can be administered through various routes. If NSAIDs are contraindicated or not providing sufficient pain relief, intravenous paracetamol can be offered as an alternative. Opioids may be considered if both NSAIDs and intravenous paracetamol are contraindicated or not effective in relieving pain. Antispasmodics should not be given to individuals with suspected renal colic.

For more detailed information, you can refer to the NICE guidelines on the assessment and management of renal and ureteric stones.

In cases of delirium with challenging behavior, short-term low-dose haloperidol is typically the preferred medication. This patient is likely experiencing delirium due to a urinary tract infection. If the patient’s behavior becomes aggressive or poses a risk to themselves or others, pharmacological intervention may be necessary if non-verbal and verbal de-escalation techniques are ineffective or inappropriate. It is important to note that antipsychotics should be avoided in patients with Parkinson’s disease. Low-dose haloperidol can be administered orally or through an intramuscular injection. However, if the patient refuses oral medication, alternative methods may need to be considered.

Further Reading:

Delirium is an acute syndrome that causes disturbances in consciousness, attention, cognition, and perception. It is also known as an acute confusional state. The DSM-IV criteria for diagnosing delirium include recent onset of fluctuating awareness, impairment of memory and attention, and disorganized thinking. Delirium typically develops over hours to days and may be accompanied by behavioral changes, personality changes, and psychotic features. It often occurs in individuals with predisposing factors, such as advanced age or multiple comorbidities, when exposed to new precipitating factors, such as medications or infection. Symptoms of delirium fluctuate throughout the day, with lucid intervals occurring during the day and worse disturbances at night. Falling and loss of appetite are often warning signs of delirium.

Delirium can be classified into three subtypes based on the person’s symptoms. Hyperactive delirium is characterized by inappropriate behavior, hallucinations, and agitation. Restlessness and wandering are common in this subtype. Hypoactive delirium is characterized by lethargy, reduced concentration, and appetite. The person may appear quiet or withdrawn. Mixed delirium presents with signs and symptoms of both hyperactive and hypoactive subtypes.

The exact pathophysiology of delirium is not fully understood, but it is believed to involve multiple mechanisms, including cholinergic deficiency, dopaminergic excess, and inflammation. The cause of delirium is usually multifactorial, with predisposing factors and precipitating factors playing a role. Predisposing factors include older age, cognitive impairment, frailty, significant injuries, and iatrogenic events. Precipitating factors include infection, metabolic or electrolyte disturbances, cardiovascular disorders, respiratory disorders, neurological disorders, endocrine disorders, urological disorders, gastrointestinal disorders, severe uncontrolled pain, alcohol intoxication or withdrawal, medication use, and psychosocial factors.

Delirium is highly prevalent in hospital settings, affecting up to 50% of inpatients aged over 65 and occurring in 30% of people aged over 65 presenting to the emergency department. Complications of delirium include increased risk of death, high in-hospital mortality rates, higher mortality rates following hospital discharge, increased length of stay in hospital, nosocomial infections, increased risk of admission to long-term care or re-admission to hospital, increased incidence of dementia, increased risk of falls and associated injuries, pressure sores.

Between 60 and 80% of individuals who experience seizures will have their seizure stopped by a single dose of intravenous benzodiazepine. Benzodiazepines have a high solubility in lipids and can quickly pass through the blood-brain barrier. This is why they have a fast onset of action.

As the initial treatment, intravenous lorazepam should be administered. If intravenous lorazepam is not accessible, intravenous diazepam can be used instead. In cases where it is not possible to establish intravenous access promptly, buccal midazolam can be utilized.

Peritonsillar abscess, also known as quinsy, is most commonly seen in adolescents and young adults between the ages of 20 and 40. Risk factors for developing quinsy include being male and smoking. It is a relatively common condition, with studies showing an incidence rate of 10 to 30 cases per 100,000 population. When treating quinsy, it is important to use a broader range of antibiotics compared to standard treatment for pharyngotonsillitis, as the causative organisms may not be limited to Group A Streptococcus. Common antibiotic choices include intravenous amoxicillin with clindamycin or metronidazole, although the specific antibiotic used may vary depending on local antimicrobial policies.

Further Reading:

A peritonsillar abscess, also known as quinsy, is a collection of pus that forms between the palatine tonsil and the pharyngeal muscles. It is often a complication of acute tonsillitis and is most commonly seen in adolescents and young adults. The exact cause of a peritonsillar abscess is not fully understood, but it is believed to occur when infection spreads beyond the tonsillar capsule or when small salivary glands in the supratonsillar space become blocked.

The most common causative organisms for a peritonsillar abscess include Streptococcus pyogenes, Staphylococcus aureus, Haemophilus influenzae, and anaerobic organisms. Risk factors for developing a peritonsillar abscess include smoking, periodontal disease, male sex, and a previous episode of the condition.

Clinical features of a peritonsillar abscess include severe throat pain, difficulty opening the mouth (trismus), fever, headache, drooling of saliva, bad breath, painful swallowing, altered voice, ear pain on the same side, neck stiffness, and swelling of the soft palate. Diagnosis is usually made based on clinical presentation, but imaging scans such as CT or ultrasound may be used to assess for complications or determine the best site for drainage.

Treatment for a peritonsillar abscess involves pain relief, intravenous antibiotics to cover for both aerobic and anaerobic organisms, intravenous fluids if swallowing is difficult, and drainage of the abscess either through needle aspiration or incision and drainage. Tonsillectomy may be recommended to prevent recurrence. Complications of a peritonsillar abscess can include sepsis, spread to deeper neck tissues leading to necrotizing fasciitis or retropharyngeal abscess, airway compromise, recurrence of the abscess, aspiration pneumonia, erosion into major blood vessels, and complications related to the causative organism. All patients with a peritonsillar abscess should be referred to an ear, nose, and throat specialist for further management.

Nifedipine is the preferred medication for treating high altitude pulmonary edema (HAPE). When a patient shows signs of HAPE, the best course of action is to immediately descend to a lower altitude while receiving supplemental oxygen. However, if descent is not possible, nifedipine can be used to alleviate symptoms and assist with descent. Nifedipine works by reducing the pressure in the pulmonary artery. On the other hand, dexamethasone is the preferred medication for treating acute mountain sickness and high altitude cerebral edema (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 risk of contracting meningococcal disease from a close contact is low. However, the risk is highest within the first seven days after the disease is diagnosed and decreases significantly afterwards.

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

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

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

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

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

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

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

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

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

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

This man is experiencing an acute episode of asthma. His initial peak flow measurement is 46% of his best, indicating a severe exacerbation. According to the BTS guidelines, acute asthma can be classified as moderate, acute severe, life-threatening, or near-fatal.

Moderate asthma is characterized by increasing symptoms and a peak expiratory flow rate (PEFR) between 50-75% of the individual’s best or predicted value. There are no signs of acute severe asthma in this case.

Acute severe asthma is identified by any one of the following criteria: a PEFR between 33-50% of the best or predicted value, a respiratory rate exceeding 25 breaths per minute, a heart rate over 110 beats per minute, or the inability to complete sentences in one breath.

Life-threatening asthma is indicated by any one of the following: a PEFR below 33% of the best or predicted value, oxygen saturation (SpO2) below 92%, arterial oxygen pressure (PaO2) below 8 kPa, normal arterial carbon dioxide pressure (PaCO2) between 4.6-6.0 kPa, a silent chest, cyanosis, poor respiratory effort, arrhythmia, exhaustion, altered conscious level, or hypotension.

Near-fatal asthma is characterized by elevated PaCO2 levels and/or the need for mechanical ventilation with increased inflation pressures.

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.

For the treatment of pregnant women with lower urinary tract infections (UTIs), it is recommended to provide them with an immediate prescription for antibiotics. It is important to consider their previous urine culture and susceptibility results, as well as any prior use of antibiotics that may have contributed to the development of resistant bacteria. Before starting antibiotics, it is advised to obtain a midstream urine sample from pregnant women and send it for culture and susceptibility testing.

Once the microbiological results are available, it is necessary to review the choice of antibiotic. If the bacteria are found to be resistant, it is recommended to switch to a narrow-spectrum antibiotic whenever possible. The choice of antibiotics for pregnant women aged 12 years and over is summarized below:

First-choice:
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days, if the estimated glomerular filtration rate (eGFR) is above 45 ml/minute.

Second-choice (if there is no improvement in lower UTI symptoms with the first-choice antibiotic for at least 48 hours, or if the first-choice is not suitable):
– Amoxicillin 500 mg taken orally three times daily for 7 days (only if culture results are available and show susceptibility).
– Cefalexin 500 mg taken twice daily for 7 days.

For alternative second-choice antibiotics, it is recommended to consult a local microbiologist and choose the appropriate antibiotics based on the culture and sensitivity results.

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

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

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

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

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

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

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

The most probable diagnosis in this case is septic arthritis, which occurs when an infectious agent invades a joint and causes pus formation. The clinical features of septic arthritis 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 overall feeling of being unwell.

The most common cause of septic arthritis is Staphylococcus aureus, but other bacteria can also be responsible. These 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 using specific antibiotics. Flucloxacillin is the first-line choice, but if a patient is allergic to penicillin, clindamycin can be used instead. If there is suspicion of MRSA (Methicillin-resistant Staphylococcus aureus), vancomycin is recommended. In cases where gonococcal arthritis or Gram-negative infection is suspected, cefotaxime is the preferred antibiotic.

The suggested duration of treatment for septic arthritis is 4-6 weeks, although it may be longer if the infection is complicated.

Whooping cough is a respiratory infection caused by the bacteria Bordetella pertussis. It is highly contagious and spreads to about 90% of close household contacts. Public Health England (PHE) has identified two priority groups for managing whooping cough contacts. Group 1 includes infants under one year who have received less than three doses of the pertussis vaccine and are at risk of severe infection. Group 2 includes pregnant women at 32 weeks or more, healthcare workers dealing with infants and pregnant women, individuals working with unvaccinated infants under 4 months old, and individuals living with unvaccinated infants under 4 months old.

According to current guidelines, antibiotic prophylaxis with a macrolide antibiotic like erythromycin should only be given to close contacts if the following criteria are met: the index case has had symptoms within the past 21 days and there is a close contact in one of the priority groups. If both criteria are met, all contacts, regardless of age and vaccination status, should be offered chemoprophylaxis. In this case, the mother falls into group 2, so the recommended action is to provide chemoprophylaxis to all household contacts, including the mother, father, and brother. Additionally, those who receive chemoprophylaxis should also consider immunization or a booster dose based on their current vaccination status.

The explanation states that the increased activity of the enzyme kininogenase is caused by hormonal factors, specifically oestrogen, as well as genetic factors.

Further Reading:

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

During the examination, the child is observed to be grunting and has had an episode of urinary incontinence. The question asks about the likely complication that has developed.

The most likely complication in this case is cerebral edema. Cerebral edema refers to the swelling of the brain due to an increase in fluid accumulation. It is a severe and potentially life-threatening complication of diabetic ketoacidosis, particularly in children. The symptoms observed, such as headaches, increasing drowsiness, grunting, and urinary incontinence, are indicative of cerebral edema.

Cerebral edema can occur due to various factors, including the rapid correction of hyperglycemia and dehydration, as well as the release of inflammatory mediators. It is crucial to recognize and manage cerebral edema promptly as it can lead to increased intracranial pressure and neurological deterioration.

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.

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.

There is an increased risk of neural tube defects in women with epilepsy who take carbamazepine during pregnancy, ranging from 2 to 10 times higher. Additionally, there is a risk of haemorrhagic disease of the newborn associated with this medication. It is crucial to have discussions about epilepsy treatments with women of childbearing age during the planning stages so that they can start early supplementation of folic acid.

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

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

Aminoglycosides (e.g. gentamicin): These drugs can lead to ototoxicity and deafness in the fetus.

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

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

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

Carbamazepine: This medication is associated with haemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol: Use of this drug can cause grey baby syndrome in newborns.

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

Danazol: When administered in the first trimester, danazol can cause masculinization of the female fetuses genitals.

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

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

Heparin: Use of heparin during pregnancy is associated with an acceptable bleeding rate and a low rate of thrombotic recurrence in the mother.

Aortic stenosis can be identified through various clinical signs. These signs include a slow rising and low-volume pulse, as well as a narrow pulse pressure. The ejection systolic murmur, which is loudest in the aortic area (2nd intercostal space, close to the sternum), is another indicator. Additionally, a sustained apex beat and a thrill in the aortic area can be felt when the patient is sitting forward at the end of expiration. In some cases, a 4th heart sound may also be present. It is important to note that in severe cases of aortic stenosis, there may be reverse splitting of the second heart sound. However, fixed splitting of the 2nd heart sound is typically associated with ASD and VSD. Lastly, the presence of an ejection click can help exclude supra- or subaortic stenosis, especially if the valve is pliable.

For children experiencing moderate pain, diclofenac (taken orally or rectally), oral codeine, or oral morphine are suitable options for providing relief. The patient has already been given the appropriate initial analgesia for mild pain. Therefore, it is now appropriate to administer analgesia for moderate pain, following the next step on the analgesic ladder. Considering diclofenac, codeine, or oral morphine would be appropriate in this case.

Further Reading:

Assessment and alleviation of pain should be a priority when treating ill and injured children, according to the RCEM QEC standards. These standards state that all children attending the Emergency Department should receive analgesia for moderate and severe pain within 20 minutes of arrival. The effectiveness of the analgesia should be re-evaluated within 60 minutes of receiving the first dose. Additionally, patients in moderate pain should be offered oral analgesia at triage or assessment.

Pain assessment in children should take into account their age. Visual analogue pain scales are commonly used, and the RCEM has developed its own version of this. Other indicators of pain, such as crying, limping, and holding or not-moving limbs, should also be observed and utilized in the pain assessment.

Managing pain in children involves a combination of psychological strategies, non-pharmacological adjuncts, and pharmacological methods. Psychological strategies include involving parents, providing cuddles, and utilizing child-friendly environments with toys. Explanation and reassurance are also important in building trust. Distraction with stories, toys, and activities can help divert the child’s attention from the pain.

Non-pharmacological adjuncts for pain relief in children include limb immobilization with slings, plasters, or splints, as well as dressings and other treatments such as reduction of dislocation or trephine subungual hematoma.

Pharmacological methods for pain relief in children include the use of anesthetics, analgesics, and sedation. Topical anesthetics, such as lidocaine with prilocaine cream, tetracaine gel, or ethyl chloride spray, should be considered for children who are likely to require venesection or placement of an intravenous cannula.

Procedural sedation in children often utilizes either ketamine or midazolam. When administering analgesia, the analgesic ladder should be followed as recommended by the RCEM.

Overall, effective pain management in children requires a comprehensive approach that addresses both the physical and psychological aspects of pain. By prioritizing pain assessment and providing appropriate pain relief, healthcare professionals can help alleviate the suffering of ill and injured children.

If a patient with a tracheostomy is experiencing difficulty breathing and it is not possible to pass a suction catheter, the next step is to deflate the cuff. Deflating the cuff can help determine if the tracheostomy tube is obstructed or displaced by allowing air to flow around the tube within the airway. The following steps are followed in order: 1) Remove the inner tube and any speaking cap/valve if present. 2) Attempt to pass the suction catheter. 3) If the suction catheter cannot be passed, deflate the cuff. 4) If the patient’s condition does not stabilize or improve, the tracheostomy tube may need to be removed. This process is summarized in the green algorithm.

Further Reading:

Patients with tracheostomies may experience emergencies such as tube displacement, tube obstruction, and bleeding. Tube displacement can occur due to accidental dislodgement, migration, or erosion into tissues. Tube obstruction can be caused by secretions, lodged foreign bodies, or malfunctioning humidification devices. Bleeding from a tracheostomy can be classified as early or late, with causes including direct injury, anticoagulation, mucosal or tracheal injury, and granulation tissue.

When assessing a patient with a tracheostomy, an ABCDE approach should be used, with attention to red flags indicating a tracheostomy or laryngectomy emergency. These red flags include audible air leaks or bubbles of saliva indicating gas escaping past the cuff, grunting, snoring, stridor, difficulty breathing, accessory muscle use, tachypnea, hypoxia, visibly displaced tracheostomy tube, blood or blood-stained secretions around the tube, increased discomfort or pain, increased air required to keep the cuff inflated, tachycardia, hypotension or hypertension, decreased level of consciousness, and anxiety, restlessness, agitation, and confusion.

Algorithms are available for managing tracheostomy emergencies, including obstruction or displaced tube. Oxygen should be delivered to the face and stoma or tracheostomy tube if there is uncertainty about whether the patient has had a laryngectomy. Tracheostomy bleeding can be classified as early or late, with causes including direct injury, anticoagulation, mucosal or tracheal injury, and granulation tissue. Tracheo-innominate fistula (TIF) is a rare but life-threatening complication that occurs when the tracheostomy tube erodes into the innominate artery. Urgent surgical intervention is required for TIF, and management includes general resuscitation measures and specific measures such as bronchoscopy and applying direct digital pressure to the innominate artery.

Calcium-channel blocker overdose is a serious matter and should always be treated as potentially life-threatening. The two most dangerous types of calcium channel blockers in overdose are verapamil and diltiazem. These medications work by binding to the alpha-1 subunit of L-type calcium channels, which prevents the entry of calcium into cells. These channels play a crucial role in the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

The toxic effects of calcium-channel blockers can be summarized as follows:

Cardiac effects:
– Excessive negative inotropy: causing myocardial depression
– Negative chronotropy: leading to sinus bradycardia
– Negative dromotropy: resulting in atrioventricular node blockade

Vascular smooth muscle tone effects:
– Decreased afterload: causing systemic hypotension
– Coronary vasodilation: leading to widened blood vessels in the heart

Metabolic effects:
– Hypoinsulinaemia: insulin release depends on calcium influx through L-type calcium channels in islet beta-cells
– Calcium channel blocker-induced insulin resistance: causing reduced responsiveness to insulin.

It is important to be aware of these effects and take appropriate action in cases of calcium-channel blocker overdose.

The primary route of ethanol oxidation in the liver is through the alcohol dehydrogenase (ADH) pathway. Additionally, the accessory pathways of cytochrome P450 2E1 (CYP2E1) and catalase also play a role in the oxidative metabolism of alcohol.

Further Reading:

Alcoholic liver disease (ALD) is a spectrum of disease that ranges from fatty liver at one end to alcoholic cirrhosis at the other. Fatty liver is generally benign and reversible with alcohol abstinence, while alcoholic cirrhosis is a more advanced and irreversible form of the disease. Alcoholic hepatitis, which involves inflammation of the liver, can lead to the development of fibrotic tissue and cirrhosis.

Several factors can increase the risk of progression of ALD, including female sex, genetics, advanced age, induction of liver enzymes by drugs, and co-existent viral hepatitis, especially hepatitis C.

The development of ALD is multifactorial and involves the metabolism of alcohol in the liver. Alcohol is metabolized to acetaldehyde and then acetate, which can result in the production of damaging reactive oxygen species. Genetic polymorphisms and co-existing hepatitis C infection can enhance the pathological effects of alcohol metabolism.

Patients with ALD may be asymptomatic or present with non-specific symptoms such as abdominal discomfort, vomiting, or anxiety. Those with alcoholic hepatitis may have fever, anorexia, and deranged liver function tests. Advanced liver disease can manifest with signs of portal hypertension and cirrhosis, such as ascites, varices, jaundice, and encephalopathy.

Screening tools such as the AUDIT questionnaire can be used to assess alcohol consumption and identify hazardous or harmful drinking patterns. Liver function tests, FBC, and imaging studies such as ultrasound or liver biopsy may be performed to evaluate liver damage.

Management of ALD involves providing advice on reducing alcohol intake, administering thiamine to prevent Wernicke’s encephalopathy, and addressing withdrawal symptoms with benzodiazepines. Complications of ALD, such as intoxication, encephalopathy, variceal bleeding, ascites, hypoglycemia, and coagulopathy, require specialized interventions.

Heavy alcohol use can also lead to thiamine deficiency and the development of Wernicke Korsakoff’s syndrome, characterized by confusion, ataxia, hypothermia, hypotension, nystagmus, and vomiting. Prompt treatment is necessary to prevent progression to Korsakoff’s psychosis.

In summary, alcoholic liver disease is a spectrum of disease that can range from benign fatty liver to irreversible cirrhosis. Risk factors for progression include female sex, genetics, advanced age, drug-induced liver enzyme induction, and co-existing liver conditions.

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.

When administering treatment to patients with hepatic impairment, it is crucial to consider that midazolam is metabolized in the liver.

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.

Peptic ulcer disease is most commonly caused by NSAIDs, making them the leading drug cause. However, h.pylori infection is the primary cause of peptic ulcers, with NSAIDs being the second most common cause.

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.

Salivary gland stones often cause intermittent swelling that tends to worsen during meal times. This pattern of symptoms is indicative of Sialolithiasis, which refers to the presence of stones in the salivary glands. In cases of acute sialadenitis, the affected gland or duct would typically be enlarged and tender to touch, accompanied by signs of infection such as redness or fever. While mucoepidermoid carcinoma is the most common type of salivary gland cancer, malignant salivary gland tumors are rare. On the other hand, pleomorphic adenoma is the most common benign neoplasm of the salivary glands, with an incidence rate of approximately 2-3.5 cases per 100,000 population. However, it is important to note that salivary gland stones are much more common than tumors, with an annual incidence rate that is 10 times higher.

Further Reading:

Salivary gland disease refers to various conditions that affect the salivary glands, which are responsible for producing saliva. Humans have three pairs of major salivary glands, including the parotid, submandibular, and sublingual glands, as well as numerous minor salivary glands. These glands produce around 1 to 1.5 liters of saliva each day, which serves several functions such as moistening and lubricating the mouth, dissolving food, aiding in swallowing, and protecting the mucosal lining.

There are several causes of salivary gland dysfunction, including infections (such as bacterial or viral infections like mumps), the presence of stones in the salivary ducts, benign or malignant tumors, dry mouth (xerostomia) due to medication, dehydration, or certain medical conditions like Sjögren’s syndrome, granulomatous diseases like sarcoidosis, and rare conditions like HIV-related lymphocytic infiltration. Mucoceles can also affect the minor salivary glands.

Salivary gland stones, known as sialolithiasis, are the most common salivary gland disorder. They typically occur in adults between the ages of 30 and 60, with a higher incidence in males. These stones can develop within the salivary glands or their ducts, leading to obstruction and swelling of the affected gland. Risk factors for stones include certain medications, dehydration, gout, smoking, chronic periodontal disease, and hyperparathyroidism. Diagnosis of salivary gland stones can be made through imaging techniques such as X-ray, ultrasound, sialography, CT, or MRI. Management options include conservative measures like pain relief, antibiotics if there is evidence of infection, hydration, warm compresses, and gland massage. Invasive options may be considered if conservative management fails.

Salivary gland infection, known as sialadenitis, can be caused by bacterial or viral pathogens. Decreased salivary flow, often due to factors like dehydration, malnutrition, immunosuppression, or certain medications, can contribute to the development of sialadenitis. Risk factors for sialadenitis include age over 40, recent dental procedures, Sjögren’s syndrome, immunosuppression, and conditions that decrease salivary flow. Staphylococcus aureus is the most common bacterial cause, while mumps is the most common viral cause. Ac

One of the clinical features of a tension pneumothorax is the deviation of the trachea away from the side where the pneumothorax is located. This particular feature is typically observed in cases of right-sided tension pneumothorax.

Further Reading:

A pneumothorax is an abnormal collection of air in the pleural cavity of the lung. It can be classified by cause as primary spontaneous, secondary spontaneous, or traumatic. Primary spontaneous pneumothorax occurs without any obvious cause in the absence of underlying lung disease, while secondary spontaneous pneumothorax occurs in patients with significant underlying lung diseases. Traumatic pneumothorax is caused by trauma to the lung, often from blunt or penetrating chest wall injuries.

Tension pneumothorax is a life-threatening condition where the collection of air in the pleural cavity expands and compresses normal lung tissue and mediastinal structures. It can be caused by any of the aforementioned types of pneumothorax. Immediate management of tension pneumothorax involves the ABCDE approach, which includes ensuring a patent airway, controlling the C-spine, providing supplemental oxygen, establishing IV access for fluid resuscitation, and assessing and managing other injuries.

Treatment of tension pneumothorax involves needle thoracocentesis as a temporary measure to provide immediate decompression, followed by tube thoracostomy as definitive management. Needle thoracocentesis involves inserting a 14g cannula into the pleural space, typically via the 4th or 5th intercostal space midaxillary line. If the patient is peri-arrest, immediate thoracostomy is advised.

The pathophysiology of tension pneumothorax involves disruption to the visceral or parietal pleura, allowing air to flow into the pleural space. This can occur through an injury to the lung parenchyma and visceral pleura, or through an entry wound to the external chest wall in the case of a sucking pneumothorax. Injured tissue forms a one-way valve, allowing air to enter the pleural space with inhalation but prohibiting air outflow. This leads to a progressive increase in the volume of non-absorbable intrapleural air with each inspiration, causing pleural volume and pressure to rise within the affected hemithorax.

Hyperglycemia is a common occurrence in patients with phaeochromocytoma. This is primarily due to the excessive release of catecholamines, which suppress insulin secretion from the pancreas and promote glycogenolysis. Calcium levels in phaeochromocytoma patients can vary, with hypercalcemia being most frequently observed in cases where hyperparathyroidism coexists, particularly in MEN II. However, some phaeochromocytomas may secrete calcitonin and/or adrenomedullin, which can lower plasma calcium levels and lead to hypocalcemia. While not typical, potassium disturbances may occur in patients experiencing severe vomiting or acute kidney injury. On the other hand, anemia is not commonly associated with phaeochromocytoma, although there are rare cases where the tumor secretes erythropoietin, resulting in elevated hemoglobin levels and hematocrit.

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.

Pick’s disease is a rare neurodegenerative disorder that leads to a gradual decline in cognitive function known as frontotemporal dementia. One of the key features of this condition is the accumulation of tau proteins in neurons, forming silver-staining, spherical aggregations called Pick bodies.

Typically, Pick’s disease manifests between the ages of 40 and 60. Initially, individuals may experience changes in their personality, such as disinhibition, tactlessness, and vulgarity. They may also exhibit alterations in their moral values and attempt to distance themselves from their family. Concentration problems, over-activity, pacing, and wandering are also common symptoms during this stage.

What sets Pick’s disease apart from Alzheimer’s disease is that the personality changes occur before memory loss. As the disease progresses, patients will experience deficits in intellect, memory, and language.

On the other hand, Lewy body dementia (LBD) is characterized by the presence of Lewy bodies, which are different from the Pick bodies seen in Pick’s disease.

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

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

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

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

Several studies have shown that elevating the head by 20-30 degrees is beneficial for increasing oxygen levels compared to lying flat on the back.

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.

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

Further Reading:

Paracetamol poisoning occurs when the liver is unable to metabolize paracetamol properly, leading to the production of a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI). Normally, NAPQI is conjugated by glutathione into a non-toxic form. However, during an overdose, the liver’s conjugation systems become overwhelmed, resulting in increased production of NAPQI and depletion of glutathione stores. This leads to the formation of covalent bonds between NAPQI and cell proteins, causing cell death in the liver and kidneys.

Symptoms of paracetamol poisoning may not appear for the first 24 hours or may include abdominal symptoms such as nausea and vomiting. After 24 hours, hepatic necrosis may develop, leading to elevated liver enzymes, right upper quadrant pain, and jaundice. Other complications can include encephalopathy, oliguria, hypoglycemia, renal failure, and lactic acidosis.

The management of paracetamol overdose depends on the timing and amount of ingestion. Activated charcoal may be given if the patient presents within 1 hour of ingesting a significant amount of paracetamol. N-acetylcysteine (NAC) is used to increase hepatic glutathione production and is given to patients who meet specific criteria. Blood tests are taken to assess paracetamol levels, liver function, and other parameters. Referral to a medical or liver unit may be necessary, and psychiatric follow-up should be considered for deliberate overdoses.

In cases of staggered ingestion, all patients should be treated with NAC without delay. Blood tests are also taken, and if certain criteria are met, NAC can be discontinued. Adverse reactions to NAC are common and may include anaphylactoid reactions, rash, hypotension, and nausea. Treatment for adverse reactions involves medications such as chlorpheniramine and salbutamol, and the infusion may be stopped if necessary.

The prognosis for paracetamol poisoning can be poor, especially in cases of severe liver injury. Fulminant liver failure may occur, and liver transplant may be necessary. Poor prognostic indicators include low arterial pH, prolonged prothrombin time, high plasma creatinine, and hepatic encephalopathy.

Corticosteroids can be beneficial in preventing or reducing prolonged reactions. According to the current APLS guidelines, the recommended doses of hydrocortisone for different age groups are as follows:

– Children under 6 months: 25 mg administered slowly via intramuscular (IM) or intravenous (IV) route.
– Children aged 6 months to 6 years: 50 mg administered slowly via IM or IV route.
– Children aged 6 to 12 years: 100 mg administered slowly via IM or IV route.
– Children over 12 years: 200 mg administered slowly via IM or IV route.
– Adults: 200 mg administered slowly via IM or IV route.

It is important to note that the most recent ALS guidelines do not recommend the routine use of corticosteroids for treating anaphylaxis in adults. However, the current APLS guidelines still advocate for the use of corticosteroids in children to manage anaphylaxis.

According to the latest guidelines from NICE and the BNF, the recommended initial treatment for typhoid fever is cefotaxime. It is important to note that infections originating from the Middle-East, South Asia, and South-East Asia may have multiple antibiotic resistance, so it is advisable to test for sensitivity. In cases where the microorganism is found to be sensitive, ciprofloxacin can be considered as a suitable alternative.

Thiazide diuretics, like bendroflumethiazide and hydrochlorothiazide, have the potential to raise levels of uric acid in the blood, which can worsen gout symptoms in individuals who are susceptible to the condition.

Other medications, such as diuretics, beta-blockers, ACE inhibitors, and non-losartan ARBs, are also linked to an increased risk of gout.

On the other hand, calcium-channel blockers like amlodipine and verapamil, as well as losartan, have been found to lower uric acid levels and are associated with a reduced risk of gout.

An abnormal QTc, which is the measurement of the time it takes for the heart to recharge between beats, is generally considered to be greater than 450 ms in males. However, some sources may use a cutoff of greater than 440 ms as abnormal in males. To further categorize the QTc, a measurement of 430ms or less is considered normal, 431-450 ms is borderline, and 450 ms or more is considered abnormal in males. Females typically have a longer QTc, so the categories for them are often quoted as less than 450 ms being normal, 451-470 ms being borderline, and greater than 470ms being abnormal.

Further Reading:

Long QT syndrome (LQTS) is a condition characterized by a prolonged QT interval on an electrocardiogram (ECG), which represents abnormal repolarization of the heart. LQTS can be either acquired or congenital. Congenital LQTS is typically caused by gene abnormalities that affect ion channels responsible for potassium or sodium flow in the heart. There are 15 identified genes associated with congenital LQTS, with three genes accounting for the majority of cases. Acquired LQTS can be caused by various factors such as certain medications, electrolyte imbalances, hypothermia, hypothyroidism, and bradycardia from other causes.

The normal QTc values, which represent the corrected QT interval for heart rate, are typically less than 450 ms for men and less than 460ms for women. Prolonged QTc intervals are considered to be greater than these values. It is important to be aware of drugs that can cause QT prolongation, as this can lead to potentially fatal arrhythmias. Some commonly used drugs that can cause QT prolongation include antimicrobials, antiarrhythmics, antipsychotics, antidepressants, antiemetics, and others.

Management of long QT syndrome involves addressing any underlying causes and using beta blockers. In some cases, an implantable cardiac defibrillator (ICD) may be recommended for patients who have experienced recurrent arrhythmic syncope, documented torsades de pointes, previous ventricular tachyarrhythmias or torsades de pointes, previous cardiac arrest, or persistent syncope. Permanent pacing may be used in patients with bradycardia or atrioventricular nodal block and prolonged QT. Mexiletine is a treatment option for those with LQT3. Cervicothoracic sympathetic denervation may be considered in patients with recurrent syncope despite beta-blockade or in those who are not ideal candidates for an ICD. The specific treatment options for LQTS depend on the type and severity of the condition.

In patients with COPD and type 2 respiratory failure, the desired range for oxygen saturation while receiving BiPAP is typically 88-92%.

Maintaining oxygen saturation within this range is crucial for individuals with COPD as it helps strike a balance between providing enough oxygen to meet the body’s needs and avoiding the risk of oxygen toxicity. Oxygen saturation levels below 88% may indicate inadequate oxygenation, while levels above 92% may lead to oxygen toxicity and other complications.

Further Reading:

Mechanical ventilation is the use of artificial means to assist or replace spontaneous breathing. It can be invasive, involving instrumentation inside the trachea, or non-invasive, where there is no instrumentation of the trachea. Non-invasive mechanical ventilation (NIV) in the emergency department typically refers to the use of CPAP or BiPAP.

CPAP, or continuous positive airways pressure, involves delivering air or oxygen through a tight-fitting face mask to maintain a continuous positive pressure throughout the patient’s respiratory cycle. This helps maintain small airway patency, improves oxygenation, decreases airway resistance, and reduces the work of breathing. CPAP is mainly used for acute cardiogenic pulmonary edema.

BiPAP, or biphasic positive airways pressure, also provides positive airway pressure but with variations during the respiratory cycle. The pressure is higher during inspiration than expiration, generating a tidal volume that assists ventilation. BiPAP is mainly indicated for type 2 respiratory failure in patients with COPD who are already on maximal medical therapy.

The pressure settings for CPAP typically start at 5 cmH2O and can be increased to a maximum of 15 cmH2O. For BiPAP, the starting pressure for expiratory pressure (EPAP) or positive end-expiratory pressure (PEEP) is 3-5 cmH2O, while the starting pressure for inspiratory pressure (IPAP) is 10-15 cmH2O. These pressures can be titrated up if there is persisting hypoxia or acidosis.

In terms of lung protective ventilation, low tidal volumes of 5-8 ml/kg are used to prevent atelectasis and reduce the risk of lung injury. Inspiratory pressures (plateau pressure) should be kept below 30 cm of water, and permissible hypercapnia may be allowed. However, there are contraindications to lung protective ventilation, such as unacceptable levels of hypercapnia, acidosis, and hypoxemia.

Overall, mechanical ventilation, whether invasive or non-invasive, is used in various respiratory and non-respiratory conditions to support or replace spontaneous breathing and improve oxygenation and ventilation.

Neutropenic sepsis is a serious condition that can occur when a person has low levels of neutrophils, which are a type of white blood cell. This condition can be life-threatening and is often caused by factors such as chemotherapy, immunosuppressive drugs, infections, and bone marrow disorders. Mortality rates can be as high as 20% in adults.

To diagnose neutropenic sepsis, doctors look for a neutrophil count of 0.5 x 109 per litre or lower in patients undergoing cancer treatment. Additionally, if a patient has a temperature higher than 38°C or other signs of significant sepsis, they may be diagnosed with neutropenic sepsis.

Cancer treatments, particularly chemotherapy, can weaken the bone marrow ability to fight off infections, making patients more susceptible to neutropenic sepsis. This risk can also be present with radiotherapy.

According to the current guidelines from the National Institute for Health and Care Excellence (NICE), adult patients with acute leukemia, stem cell transplants, or solid tumors should be offered prophylaxis with a fluoroquinolone antibiotic during periods of expected neutropenia.

When managing neutropenic sepsis, it is important to follow the UK Sepsis Trust Sepsis Six bundle, which includes specific actions to be taken within the first hour of recognizing sepsis.

For initial empiric antibiotic therapy in suspected cases of neutropenic sepsis, the NICE guidelines recommend using piperacillin with tazobactam as monotherapy. Aminoglycosides should not be used unless there are specific patient or local microbiological indications.

Reference:
NICE guidance: ‘Neutropenic sepsis: prevention and management of neutropenic sepsis in cancer patients’

Allopurinol should not be started during an acute gout attack as it can make the attack last longer and even trigger another one. However, if a patient is already taking allopurinol, they should continue taking it and treat the acute attack with NSAIDs or colchicine as usual.

The first choice for treating acute gout attacks is non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen. Colchicine can be used if NSAIDs are not suitable, for example, in patients with high blood pressure or a history of peptic ulcer disease. In this case, the patient has no reason to avoid NSAIDs, so naproxen would still be the preferred option.

Once the acute attack has subsided, it would be reasonable to gradually increase the dose of allopurinol, aiming for urate levels in the blood of less than 6 mg/dl (<360 µmol/l). Febuxostat (Uloric) is an alternative to allopurinol that can be used for long-term management of gout.

Heat stroke is a condition characterized by a core temperature higher 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 hot conditions, such as endurance athletes competing in hot weather.

The main treatment for heat stroke involves supportive measures. It is important to rapidly reduce the core temperature to around 39.0°C. Patients with severe heat stroke should be managed in a critical care setting. The ABCDE approach should be followed, with a focus on cooling the patient. This includes obtaining a definitive airway if the patient is unresponsive, providing ventilation if necessary, using haemodynamic monitoring to guide fluid therapy, correcting electrolyte imbalances, managing blood glucose levels, removing clothes, eliminating the cause of hyperthermia, and monitoring core and skin temperatures.

There are various cooling techniques that can be used, although there is limited evidence on which approach is the most effective. Some possible methods include simple measures like cold drinks, fanning, ice water packs, and spraying tepid water. Cold water immersion therapy can be beneficial, but it requires the patient to be stable and cooperative, making it impractical for very sick patients. Advanced cooling techniques, such as cold IV fluids, surface cooling devices, intravascular cooling devices, and extracorporeal circuits, may be used for sicker patients.

Benzodiazepines, like diazepam, can be helpful in managing agitation and shivering in heat stroke patients. They not only reduce excessive heat production but also help to calm the patient. In severe cases of agitation, paralysis may be necessary. Dantrolene is commonly used, although there is currently limited high-level evidence to support its use. Neuroleptics, such as chlorpromazine, which were once commonly used, should be avoided due to their potential adverse effects, including lowering the seizure threshold, interfering with thermoregulation, causing anticholinergic side effects, hypotension, and hepatotoxicity.

People with chronic mitral regurgitation often experience atrial fibrillation.

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

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

The patient presents with a medical history and physical examination findings that are consistent with a diagnosis of Löfgren’s syndrome, which is a specific subtype of sarcoidosis. This syndrome is most commonly observed in women in their 30s and 40s, and it is more prevalent among individuals of Nordic and Irish descent.

Löfgren’s syndrome is typically characterized by a triad of clinical features, including bilateral hilar lymphadenopathy seen on chest X-ray, erythema nodosum, and arthralgia, with a particular emphasis on ankle involvement. Additionally, other symptoms commonly associated with sarcoidosis may also be present, such as a dry cough, breathlessness, fever, night sweats, malaise, weight loss, Achilles tendonitis, and uveitis.

In order to further evaluate this patient’s condition, it is recommended to refer them to a respiratory specialist for additional investigations. These investigations may include measuring the serum calcium level, as it may be elevated, and assessing the serum angiotensin-converting enzyme (ACE) level, which may also be elevated. A high-resolution CT scan can be performed to assess the extent of involvement and identify specific lymph nodes for potential biopsy. If there are any atypical features, a lymph node biopsy may be necessary. Lung function tests can be conducted to evaluate the patient’s vital capacity, and an MRI scan of the ankles may also be considered.

Fortunately, the prognosis for Löfgren’s syndrome is generally very good, and it is considered a self-limiting and benign condition. The patient can expect to recover within a timeframe of six months to two years.

The recommended drug doses for adult acute asthma are as follows:

– Salbutamol: Administer 5 mg using an oxygen-driven nebulizer.
– Ipratropium bromide: Deliver 500 mcg via an oxygen-driven nebulizer.
– Prednisolone: Take orally at a dose of 40-50 mg.
– Hydrocortisone: Administer 100 mg intravenously.
– Magnesium sulphate: Infuse 1.2-2 g intravenously over a period of 20 minutes.

Terbutaline can be used as an alternative to salbutamol, with a dose of 10 mg via an oxygen-driven nebulizer. Intravenous salbutamol may be considered (250 mcg IV slowly) only when inhaled therapy is not possible, such as when a patient is receiving bag-mask ventilation.

According to the current ALS guidelines, IV aminophylline may be considered in severe or life-threatening asthma, following senior advice. If used, a loading dose of 5 mg/kg should be given over 20 minutes, followed by an infusion of 500-700 mcg/kg/hour. It is important to maintain serum theophylline levels below 20 mcg/ml to prevent toxicity.

For more information, please refer to the BTS/SIGN Guideline on the Management of Asthma.

Bladder cancer is the most likely diagnosis in this case, as patients 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.

Prostate cancer is less likely in this case, as the patient’s prostate examination was relatively normal and he only had 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. Smoking is responsible for about 50% of bladder cancers, as it is believed to be linked to the excretion of aromatic amines and polycyclic aromatic hydrocarbons 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 patients. There are usually no abnormalities found during a standard physical examination.

Current recommendations state that the following patients should be urgently referred for a urological assessment: adults over 45 years old with unexplained visible haematuria not caused by a urinary tract infection, adults over 45 years old with visible haematuria that persists or recurs after successful treatment of a urinary tract infection, and adults aged 60 and over with unexplained non-visible haematuria and either dysuria or a raised white cell count on a blood test.

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

The subtraction of serial 7s is included in the 30-point Folstein mini-mental state examination (MMSE), but it is not included in the AMTS. The AMTS consists of ten questions that assess various cognitive abilities. These questions include asking about age, the nearest hour, the current year, the name of the hospital or location, the ability to recognize two people, date of birth, knowledge of historical events, knowledge of the present monarch or prime minister, counting backwards from 20 to 1, and recalling an address given earlier in the test. The AMTS is referenced in the RCEM syllabus under the topic of memory loss.

Staphylococcus aureus is the primary organism responsible for infective endocarditis in individuals who use intravenous drugs (IVDUs). In fact, it is not only the most common cause of infective endocarditis overall, but also specifically in IVDUs. Please refer to the additional notes for more detailed information.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

Patients who have a STEMI caused by a blockage in the left circumflex artery (LCX) will usually show ST elevation in leads I and AVL. These leads correspond to the high lateral area of the heart, which is supplied by the LCX artery.

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.

This patient is displaying symptoms consistent with hyperthyroidism, including palpitations or a fast heart rate, anxiety, clubbing, tremors, and heat intolerance. Other common symptoms of hyperthyroidism include eye signs such as proptosis and lid retraction, weight loss, pretibial myxoedema, diarrhea, increased appetite, and irregular menstrual periods. It is important to note that while some of these symptoms can also occur in phaeochromocytoma, this condition is rare and typically accompanied by high blood pressure.

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. hypotension, hypoventilation, altered mental state, seizures and/or coma.

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

Further Reading:

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

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

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

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

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

In cases of conductive hearing loss, the Rinne test result is negative on the affected side, meaning that bone conduction is greater than air conduction. Additionally, the Weber test result will lateralize to the affected side. If the Weber test lateralizes to the right, it indicates either sensorineural hearing loss in the left ear (opposite side) or conductive hearing loss in the right ear (same side). A positive Rinne test result, where air conduction is greater than bone conduction, is typically seen in individuals with normal hearing or sensorineural hearing loss. In the case of conductive hearing loss in the right ear, a negative Rinne test result would be expected on the right side, indicating that bone conduction is greater than air conduction.

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.

For the treatment of women with lower urinary tract infections (UTIs) who are not pregnant, it is recommended to consider either a back-up antibiotic prescription or an immediate antibiotic prescription. This decision should take into account the severity of symptoms and the risk of developing complications, which is higher in individuals with known or suspected abnormalities of the genitourinary tract or weakened immune systems. The evidence for back-up antibiotic prescriptions is limited to non-pregnant women with lower UTIs where immediate antibiotic treatment is not deemed necessary. It is also important to consider previous urine culture and susceptibility results, as well as any history of antibiotic use that may have led to the development of resistant bacteria. Ultimately, the preferences of the woman regarding antibiotic use should be taken into account.

If a urine sample has been sent for culture and susceptibility testing and an antibiotic prescription has been given, it is crucial to review the choice of antibiotic once the microbiological results are available. If the bacteria are found to be resistant and symptoms are not improving, it is recommended to switch to a narrow-spectrum antibiotic whenever possible.

The following antibiotics are recommended for non-pregnant women aged 16 years and older:

First-choice:
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days (if eGFR >45 ml/minute)
– Trimethoprim 200 mg taken orally twice daily for 3 days (if low risk of resistance*)

Second-choice (if there is no improvement in lower UTI symptoms on first-choice treatment for at least 48 hours, or if first-choice treatment is not suitable):
– Nitrofurantoin 100 mg modified-release taken orally twice daily for 3 days (if eGFR >45 ml/minute)
– Pivmecillinam 400 mg initial dose taken orally, followed by 200 mg taken orally three times daily for 3 days
– Fosfomycin 3 g single sachet dose

*The risk of resistance may be lower if the antibiotic has not been used in the past 3 months, previous urine culture suggests susceptibility (although this was not used), and in younger individuals in areas where local epidemiology data indicate low resistance rates. Conversely, the risk of resistance may be higher with recent antibiotic use and in older individuals in residential facilities.

Pabrinex is a supplement that includes a combination of essential vitamins. These vitamins are Thiamine (also known as vitamin B1), Riboflavin (commonly referred to as vitamin B2), Nicotinamide (which encompasses Vitamin B3, niacin, and nicotinic acid), Pyridoxine (known as vitamin B6), and Ascorbic acid (which is vitamin C). Each of these vitamins plays a crucial role in maintaining our overall health and well-being. By incorporating Pabrinex into our daily routine, we can ensure that our bodies receive the necessary nutrients to support various bodily functions.

Ulnar nerve lesions can be assessed using Froment’s sign. To perform this test, a piece of paper is placed between the patient’s thumb and index finger. The examiner then tries to pull the paper out of the patient’s pinched grip. If the patient has an ulnar nerve palsy, they will struggle to maintain the grip and may compensate by flexing the flexor pollicis longus muscle of the thumb to maintain pressure. This compensation is evident when the patient’s interphalangeal joint of the thumb flexes. Froment’s sign is a useful indicator of ulnar nerve dysfunction.

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.

Wolff-Parkinson-White (WPW) syndrome is a condition that affects the electrical system of the heart. It occurs when there is an abnormal pathway, known as the bundle of Kent, between the atria and the ventricles. This pathway can cause premature contractions of the ventricles, leading to a type of rapid heartbeat called atrioventricular re-entrant tachycardia (AVRT).

In a normal heart rhythm, the electrical signals travel through the bundle of Kent and stimulate the ventricles. However, in WPW syndrome, these signals can cause the ventricles to contract prematurely. This can be seen on an electrocardiogram (ECG) as a shortened PR interval, a slurring of the initial rise in the QRS complex (known as a delta wave), and a widening of the QRS complex.

There are two distinct types of WPW syndrome that can be identified on an ECG. Type A is characterized by predominantly positive delta waves and QRS complexes in the praecordial leads, with a dominant R wave in V1. This can sometimes be mistaken for right bundle branch block (RBBB). Type B, on the other hand, shows predominantly negative delta waves and QRS complexes in leads V1 and V2, and positive in the other praecordial leads, resembling left bundle branch block (LBBB).

Overall, WPW syndrome is a condition that affects the electrical conduction system of the heart, leading to abnormal heart rhythms. It can be identified on an ECG by specific features such as shortened PR interval, delta waves, and widened QRS complex.