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.

This patient is exhibiting the psoas sign, which is a medical indication of irritation in the iliopsoas group of hip flexors located in the abdomen. In this particular case, it is highly likely that the patient has acute appendicitis.

The psoas sign can be observed by extending the patient’s thigh while they are lying on their side with their knees extended, or by asking the patient to actively flex their thigh at the hip. If these movements result in abdominal pain or if the patient resists due to pain, then the psoas sign is considered positive.

The pain occurs because the psoas muscle is adjacent to the peritoneal cavity. When the muscles are stretched or contracted, they rub against the inflamed tissues nearby, causing discomfort. This strongly suggests that the appendix is positioned retrocaecal.

The Manchester Mandibular Fracture Decision Rule consists of five signs that indicate a possible mandibular fracture: malocclusion, trismus, pain with mouth closed, broken teeth, and step deformity. If none of these signs are present, it is unlikely that a mandibular fracture has occurred. However, if one or more of these signs are present, it is recommended to obtain an X-ray for further evaluation. It is important to note that gum lacerations, although commonly seen in mandibular fractures, are not included in the Manchester Mandibular Fracture Decision Rule.

Further Reading:

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

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

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

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

This is a classical history for a simple urinary tract infection. The other possible causes mentioned can also result in frank haematuria, but they would be less likely based on the given history.

Bladder cancer typically presents with additional symptoms such as an abdominal mass, weight loss, and fatigue. Nephritis is more likely to cause renal angle tenderness and some systemic upset. It is often preceded by another infection.

Tuberculosis may also have more systemic involvement, although it can present on its own. Renal stones commonly cause severe pain from the loin to the groin and renal angle tenderness.

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

When assessing patients who present with an SAH, they may exhibit focal neurological signs, which can indicate the potential location of the aneurysm. Common areas where aneurysms occur include the bifurcation of the middle cerebral artery, the junction of the anterior communicating cerebral artery, and the junction of the posterior communicating artery with the internal carotid artery. If there is complete or partial paralysis of the oculomotor nerve, it suggests the rupture of a posterior communicating artery aneurysm.

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

This patient is experiencing a blockage in one nostril, hearing loss in one ear, and a newly developed hearing impairment. Additionally, there is a noticeable swollen lymph node in the upper jugular chain on the affected side. These symptoms strongly suggest the possibility of nasopharyngeal carcinoma.
Nasopharyngeal carcinoma is not very common in the U.K., but it has a higher occurrence in individuals from Southeast Asia. In this region, the disease is often linked to the Epstein-Barr virus (EBV). It typically affects individuals between the ages of 40 and 70.
The most common signs of nasopharyngeal carcinoma include a lump in the neck (present in approximately 80% of cases), one-sided nasal blockage (present in approximately 60% of cases), one-sided deafness (present in approximately 50% of cases), and post-nasal discharge (present in approximately 50% of cases). Lymph nodes in the upper jugular chain are often detectable.
It is crucial to refer this patient urgently using a suspected cancer referral pathway to ensure an appointment within two weeks.
For more information, please refer to the NICE guidelines on the recognition and referral of suspected cancer.

A summary of the vessels involved in different types of myocardial infarction, along with the corresponding ECG leads and the location of the infarction.

For instance, an anteroseptal infarction involving the left anterior descending artery is indicated by ECG leads V1-V3. Similarly, an anterior infarction involving the left anterior descending artery is indicated by leads V3-V4.

In cases of anterolateral infarctions, both the left anterior descending artery and the left circumflex artery are involved, and this is reflected in ECG leads V5-V6. An extensive anterior infarction involving the left anterior descending artery is indicated by leads V1-V6.

Lateral infarcts involving the left circumflex artery are indicated by leads I, II, aVL, and V6. Inferior infarctions, on the other hand, involve either the right coronary artery (in 80% of cases) or the left circumflex artery (in 20% of cases), and this is shown by leads II, III, and aVF.

In the case of a right ventricular infarction, the right coronary artery is involved, and this is indicated by leads V1 and V4R. Lastly, a posterior infarction involving the right coronary artery is shown by leads V7-V9.

When it comes to managing seizures in cases of TCA overdose, benzodiazepines are considered the most effective treatment. Diazepam or lorazepam are commonly administered for this purpose. However, it’s important to note that lamotrigine and carbamazepine are typically used for preventing seizures rather than for immediate seizure control.

Further Reading:

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

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

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

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

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

Thought echo is a phenomenon where a patient perceives their own thoughts as if they are being spoken out loud. When there is a slight delay in this perception, it is referred to as echo de la pensée. On the other hand, when the thoughts are heard simultaneously, it is known as Gedankenlautwerden.

This presentation strongly suggests a diagnosis of whooping cough, which is an infection of the upper respiratory tract caused by the bacteria Bordetella pertussis. The disease is highly contagious and is transmitted through respiratory droplets. The incubation period is typically 7-21 days, and it is estimated that about 90% of close household contacts will become infected.

The clinical course of whooping cough can be divided into two stages. The first stage, known as the catarrhal stage, is similar to a mild respiratory infection with symptoms such as low-grade fever and a runny nose. A cough may be present, but it is usually not as severe as in the second stage. This phase typically lasts about a week.

The second stage, called the paroxysmal stage, is characterized by the development of a distinctive cough. The coughing occurs in spasms, often preceded by an inspiratory whoop sound. These spasms are followed by a series of rapid, hacking coughs. Patients may also experience vomiting and develop subconjunctival hemorrhages and petechiae. Between spasms, patients generally feel well and there are usually no abnormal chest findings. This stage can last up to 3 months, with a gradual recovery over this period. The later stages of this phase are sometimes referred to as the convalescent stage.

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

Public Health England (PHE) has specific recommendations for testing for whooping cough based on the age of the patient, the time since onset of illness, and the severity of the presentation.

For infants under 12 months of age, hospitalized patients should be tested using PCR testing. Non-hospitalized patients within two weeks of onset should be investigated with culture of a nasopharyngeal swab or aspirate. Non-hospitalized patients presenting over two weeks after onset should be tested using serology for anti-pertussis toxin IgG antibody levels.

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

Neisseria gonorrhoeae is a type of bacteria that causes the sexually transmitted infection known as gonorrhoea. It is a Gram-negative diplococcus, meaning it appears as pairs of bacteria under a microscope. This infection is most commonly seen in individuals between the ages of 15 and 35, and it is primarily transmitted through sexual contact. One important characteristic of Neisseria gonorrhoeae is its ability to undergo antigenic variation, which means that recovering from an infection does not provide immunity and reinfection is possible.

When Neisseria gonorrhoeae infects the body, it first attaches to the genitourinary epithelium using pili, which are hair-like structures on the surface of the bacteria. It then invades the epithelial layer and triggers a local acute inflammatory response. In men, the clinical features of gonorrhoea often include urethritis (inflammation of the urethra) in about 80% of cases, dysuria (painful urination) in around 50% of cases, and mucopurulent discharge. Rectal infection may also occur, usually without symptoms, but it can cause anal discharge. Pharyngitis, or inflammation of the throat, is usually asymptomatic in men.

In women, the clinical features of gonorrhoea commonly include vaginal discharge in about 50% of cases, lower abdominal pain in around 25% of cases, dysuria in 10-15% of cases, and pelvic/lower abdominal tenderness in less than 5% of cases. Endocervical discharge and/or bleeding may also be present. Similar to men, rectal infection is usually asymptomatic but can cause anal discharge, and pharyngitis is usually asymptomatic in women as well.

Complications of Neisseria gonorrhoeae infection can be serious and include pelvic inflammatory disease (PID) in women, epididymo-orchitis or prostatitis in men, arthritis, dermatitis, pericarditis and/or myocarditis, hepatitis, and meningitis.

To diagnose gonorrhoea, samples of pus from the urethra, cervix, rectum, or throat should be collected and promptly sent to the laboratory in specialized transport medium. Traditionally, diagnosis has been made using Gram-stain and culture techniques, but newer PCR testing methods are becoming more commonly used.

In the UK, not all dementia cases are suitable for treatment with acetylcholinesterase inhibitors and memantine. Specifically, patients with frontotemporal dementia should not be prescribed these medications. If a patient experiences visual hallucinations, it may indicate that they have dementia with Lewy bodies.

Further Reading:

Dementia is a progressive and irreversible clinical syndrome characterized by cognitive and behavioral symptoms. These symptoms include memory loss, impaired reasoning and communication, personality changes, and reduced ability to carry out daily activities. The decline in cognition affects multiple domains of intellectual functioning and is not solely due to normal aging.

To diagnose dementia, a person must have impairment in at least two cognitive domains that significantly impact their daily activities. This impairment cannot be explained by delirium or other major psychiatric disorders. Early-onset dementia refers to dementia that develops before the age of 65.

The most common cause of dementia is Alzheimer’s disease, accounting for 50-75% of cases. Other causes include vascular dementia, dementia with Lewy bodies, and frontotemporal dementia. Less common causes include Parkinson’s disease dementia, Huntington’s disease, prion disease, and metabolic and endocrine disorders.

There are several risk factors for dementia, including age, mild cognitive impairment, genetic predisposition, excess alcohol intake, head injury, depression, learning difficulties, diabetes, obesity, hypertension, smoking, Parkinson’s disease, low social engagement, low physical activity, low educational attainment, hearing impairment, and air pollution.

Assessment of dementia involves taking a history from the patient and ideally a family member or close friend. The person’s current level of cognition and functional capabilities should be compared to their baseline level. Physical examination, blood tests, and cognitive assessment tools can also aid in the diagnosis.

Differential diagnosis for dementia includes normal age-related memory changes, mild cognitive impairment, depression, delirium, vitamin deficiencies, hypothyroidism, adverse drug effects, normal pressure hydrocephalus, and sensory deficits.

Management of dementia involves a multi-disciplinary approach that includes non-pharmacological and pharmacological measures. Non-pharmacological interventions may include driving assessment, modifiable risk factor management, and non-pharmacological therapies to promote cognition and independence. Drug treatments for dementia should be initiated by specialists and may include acetylcholinesterase inhibitors, memantine, and antipsychotics in certain cases.

In summary, dementia is a progressive and irreversible syndrome characterized by cognitive and behavioral symptoms. It has various causes and risk factors, and its management involves a multi-disciplinary approach.

The initial symptoms of ARS usually include feelings of nausea and the urge to vomit. During the prodromal stage, individuals may also experience a loss of appetite and, in some cases, diarrhea, which can vary depending on the amount of exposure. These symptoms can manifest within minutes to days after being exposed to ARS.

Further Reading:

Radiation exposure refers to the emission or transmission of energy in the form of waves or particles through space or a material medium. There are two types of radiation: ionizing and non-ionizing. Non-ionizing radiation, such as radio waves and visible light, has enough energy to move atoms within a molecule but not enough to remove electrons from atoms. Ionizing radiation, on the other hand, has enough energy to ionize atoms or molecules by detaching electrons from them.

There are different types of ionizing radiation, including alpha particles, beta particles, gamma rays, and X-rays. Alpha particles are positively charged and consist of 2 protons and 2 neutrons from the atom’s nucleus. They are emitted from the decay of heavy radioactive elements and do not travel far from the source atom. Beta particles are small, fast-moving particles with a negative electrical charge that are emitted from an atom’s nucleus during radioactive decay. They are more penetrating than alpha particles but less damaging to living tissue. Gamma rays and X-rays are weightless packets of energy called photons. Gamma rays are often emitted along with alpha or beta particles during radioactive decay and can easily penetrate barriers. X-rays, on the other hand, are generally lower in energy and less penetrating than gamma rays.

Exposure to ionizing radiation can damage tissue cells by dislodging orbital electrons, leading to the generation of highly reactive ion pairs. This can result in DNA damage and an increased risk of future malignant change. The extent of cell damage depends on factors such as the type of radiation, time duration of exposure, distance from the source, and extent of shielding.

The absorbed dose of radiation is directly proportional to time, so it is important to minimize the amount of time spent in the vicinity of a radioactive source. A lethal dose of radiation without medical management is 4.5 sieverts (Sv) to kill 50% of the population at 60 days. With medical management, the lethal dose is 5-6 Sv. The immediate effects of ionizing radiation can range from radiation burns to radiation sickness, which is divided into three main syndromes: hematopoietic, gastrointestinal, and neurovascular. Long-term effects can include hematopoietic cancers and solid tumor formation.

In terms of management, support is mainly supportive and includes IV fluids, antiemetics, analgesia, nutritional support, antibiotics, blood component substitution, and reduction of brain edema.

Cauda equina syndrome (CES) is a rare but serious complication that can occur when a disc ruptures. This happens when the material from the disc is pushed into the spinal canal and puts pressure on the bundle of nerves in the lower back and sacrum. As a result, individuals may experience loss of control over their bladder and bowel functions.

There are certain red flags that may indicate the presence of CES. These include experiencing sciatica on both sides of the body, having severe or worsening neurological issues in both legs (such as significant weakness in knee extension, ankle eversion, or foot dorsiflexion), difficulty starting urination or a decreased sensation of urinary flow, loss of sensation in the rectum, experiencing numbness or tingling in the perianal, perineal, or genital areas (also known as saddle anesthesia or paresthesia), and having a lax anal sphincter.

Conus medullaris syndrome (CMS) is a condition that affects the conus medullaris, which is located above the cauda equina at the T12-L2 level. Unlike CES, CMS primarily causes back pain and may have less noticeable nerve root pain. The main symptoms of CMS are urinary retention and constipation.

To confirm a diagnosis of CES and determine the level of compression and any underlying causes, an MRI scan is considered the gold-standard investigation. In cases where an MRI is not possible or contraindicated, a CT myelogram or standard CT scans can be helpful. However, plain radiographs have limited value and may only show significant degenerative or traumatic bone diseases.

Homonymous quadrantanopias occur when there are lesions in the optic radiation. The optic tract passes through the posterolateral angle of the optic chiasm, running alongside the cerebral peduncle and inside the uncus of the temporal lobe. Eventually, it reaches the lateral geniculate body (LGN) in the thalamus. Acting as a relay center, the LGN sends axons through the optic radiation to the primary visual cortex in the occipital lobe. The upper optic radiation carries fibers from the superior retinal quadrants (which corresponds to the lower half of the visual field) and travels through the parietal lobe. On the other hand, the lower optic radiation carries fibers from the inferior retinal quadrants (which corresponds to the upper half of the visual field) and travels through the temporal lobe. Consequently, lesions in the temporal lobe can lead to superior homonymous quadrantanopias, while lesions in the parietal lobe can cause inferior homonymous quadrantanopias. The diagram below provides a summary of the different visual field defects resulting from lesions at various points in the visual pathway.

The Royal College of Emergency Medicine (RCEM) recommends asking four important questions to individuals showing signs and symptoms of carbon monoxide poisoning. These questions can be easily remembered using the acronym COMA. The questions are as follows:
1. Is anyone else in the house, including pets, experiencing similar symptoms?
2. Do the symptoms improve when you are outside of the house?
3. Are the boilers and cooking appliances in your house properly maintained?
4. Do you have a functioning carbon monoxide alarm?

Further Reading:

Carbon monoxide (CO) is a dangerous gas that is produced by the combustion of hydrocarbon fuels and can be found in certain chemicals. It is colorless and odorless, making it difficult to detect. In England and Wales, there are approximately 60 deaths each year due to accidental CO poisoning.

When inhaled, carbon monoxide binds to haemoglobin in the blood, forming carboxyhaemoglobin (COHb). It has a higher affinity for haemoglobin than oxygen, causing a left-shift in the oxygen dissociation curve and resulting in tissue hypoxia. This means that even though there may be a normal level of oxygen in the blood, it is less readily released to the tissues.

The clinical features of carbon monoxide toxicity can vary depending on the severity of the poisoning. Mild or chronic poisoning may present with symptoms such as headache, nausea, vomiting, vertigo, confusion, and weakness. More severe poisoning can lead to intoxication, personality changes, breathlessness, pink skin and mucosae, hyperpyrexia, arrhythmias, seizures, blurred vision or blindness, deafness, extrapyramidal features, coma, or even death.

To help diagnose domestic carbon monoxide poisoning, there are four key questions that can be asked using the COMA acronym. These questions include asking about co-habitees and co-occupants in the house, whether symptoms improve outside of the house, the maintenance of boilers and cooking appliances, and the presence of a functioning CO alarm.

Typical carboxyhaemoglobin levels can vary depending on whether the individual is a smoker or non-smoker. Non-smokers typically have levels below 3%, while smokers may have levels below 10%. Symptomatic individuals usually have levels between 10-30%, and severe toxicity is indicated by levels above 30%.

When managing carbon monoxide poisoning, the first step is to administer 100% oxygen. Hyperbaric oxygen therapy may be considered for individuals with a COHb concentration of over 20% and additional risk factors such as loss of consciousness, neurological signs, myocardial ischemia or arrhythmia, or pregnancy. Other management strategies may include fluid resuscitation, sodium bicarbonate for metabolic acidosis, and mannitol for cerebral edema.

The timing of the initial rise, peak, and return to normality of various cardiac enzymes can serve as a helpful guide. Creatine kinase, the main cardiac isoenzyme, typically experiences an initial rise within 4-8 hours, reaches its peak at 18 hours, and returns to normal within 2-3 days. Myoglobin, which lacks specificity due to its association with skeletal muscle damage, shows an initial rise within 1-4 hours, peaks at 6-7 hours, and returns to normal within 24 hours. Troponin I, known for its sensitivity and specificity, exhibits an initial rise within 3-12 hours, reaches its peak at 24 hours, and returns to normal within 3-10 days. HFABP, or heart fatty acid binding protein, experiences an initial rise within 1.5 hours, peaks at 5-10 hours, and returns to normal within 24 hours. Lastly, LDH, predominantly found in cardiac muscle, shows an initial rise at 10 hours, peaks at 24-48 hours, and returns to normal within 14 days.

Paracetamol levels should be measured 4 hours after ingestion. If the patient arrives at the emergency department more than 4 hours after ingestion, the levels can be taken immediately. However, if the patient has not reached the 4-hour mark yet, the measurement should be postponed until they reach that time.

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.

Slipped upper femoral epiphysis (SUFE), also referred to as slipped capital femoral epiphysis, is a rare but significant hip disorder that primarily affects children. It occurs when the growth plate slips at the epiphysis, causing the head of the femur to shift from its normal position on the femoral neck. Specifically, the femoral epiphysis remains in the acetabulum while the metaphysis moves forward and externally rotates.

SUFE typically presents later in boys, usually between the ages of 10 and 17, compared to girls who typically experience it between 8 and 15 years of age. Several risk factors contribute to its development, including being male, being overweight, having immature skeletal maturity, having a positive family history, being of Pacific Island or African origin, having hypothyroidism, growth hormone deficiency, or hypogonadism.

Patients with SUFE commonly experience hip pain and a limp. In severe cases, a leg length discrepancy may be noticeable. While the condition may not be immediately apparent on an anteroposterior (AP) film, it is usually detectable on a frog-leg lateral film. A diagnostic sign is the failure of a line drawn up the lateral edge of the femoral neck (known as the line of Klein) to intersect the epiphysis during the acute stage, also known as Trethowan’s sign.

Surgical pinning is the most common treatment for SUFE. In approximately 20% of cases, bilateral SUFE occurs, prompting some surgeons to recommend prophylactic pinning of the unaffected hip. If a significant deformity is present, osteotomies or even arthroplasty may be necessary.

Mandibular fractures are quite common, especially among young men. The most common cause of these fractures is assault, but they can also occur due to sporting injuries, motor vehicle accidents, and falls. The mandible and skull together form a complete bony ring, with the only interruption being the temporomandibular joints (TMJs). While it is expected that mandibular fractures would occur in two places, sometimes they only occur in one location. The most frequently affected areas are the angle of the mandible (27%), mandibular symphysis (21%), mandibular condylar and subcondylar (18%), body of the mandible (15%), ramus of the mandible (5%), coronoid process (1-3%), and alveolar ridge (2%).

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.

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

Further Reading:

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

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

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

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

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

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

If IV methylene blue is obtained, it is typically used to treat a specific cause. However, if there is no response to methylene blue, alternative treatments such as hyperbaric oxygen or exchange transfusion may be considered. In cases where the cause is NADH-methaemoglobinaemia reductase deficiency, ascorbic acid can be used as a potential treatment.

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%.

Fifth disease, also known as ‘slapped cheek syndrome’, is a common childhood exanthem caused by parvovirus B19.

The clinical features of fifth disease include:

– A mild coryzal illness usually occurs as a prodrome.
– The classic ‘slapped cheek’ rash appears after 3-7 days, characterized by a red rash on the cheeks with pale skin around the mouth.
– A morbilliform rash develops on the extensor surfaces of the arms and legs 1-4 days after the facial rash appears.

This disease is generally harmless and resolves on its own in children. However, it can be dangerous for pregnant women who are exposed to the virus, as it can cause intrauterine infection and hydrops fetalis. Additionally, it can lead to transient aplastic crisis. Therefore, it is important to keep affected children away from pregnant women and individuals with weakened immune systems or blood disorders.

Indirect inguinal hernias have an elliptical shape, unlike direct hernias which are round. They are not easily reducible and do not reduce spontaneously when reclining. Unlike direct hernias that appear immediately, indirect hernias take longer to appear when standing. They are reduced superiorly and then superolaterally, while direct hernias reduce superiorly and posteriorly. Pressure over the deep inguinal ring helps control indirect hernias. However, they are more prone to strangulation due to the narrow neck of the deep inguinal ring.

Acute epiglottitis is inflammation of the epiglottis, which can be life-threatening if not treated promptly. When the soft tissues surrounding the epiglottis are also affected, it is called acute supraglottitis. This condition is most commonly seen in children between the ages of 3 and 5, but it can occur at any age, with adults typically presenting in their 40s and 50s.

In the past, Haemophilus influenzae type B was the main cause of acute epiglottitis, but with the introduction of the Hib vaccination, it has become rare in children. Streptococcus spp. is now the most common causative organism. Other potential culprits include Staphylococcus aureus, Pseudomonas spp., Moraxella catarrhalis, Mycobacterium tuberculosis, and the herpes simplex virus. In immunocompromised patients, Candida spp. and Aspergillus spp. infections can occur.

The typical symptoms of acute epiglottitis include fever, sore throat, painful swallowing, difficulty swallowing secretions (especially in children who may drool), muffled voice, stridor, respiratory distress, rapid heartbeat, tenderness in the front of the neck over the hyoid bone, ear pain, and swollen lymph nodes in the neck. Some patients may also exhibit the tripod sign, where they lean forward on outstretched arms to relieve upper airway obstruction.

To diagnose acute epiglottitis, fibre-optic laryngoscopy is considered the gold standard investigation. However, this procedure should only be performed by an anaesthetist in a setting prepared for intubation or tracheostomy in case of airway obstruction. Other useful tests include a lateral neck X-ray to look for the thumbprint sign, throat swabs, blood cultures, and a CT scan of the neck if an abscess is suspected.

When dealing with a case of acute epiglottitis, it is crucial not to panic or distress the patient, especially in pediatric cases. Avoid attempting to examine the throat with a tongue depressor, as this can trigger spasm and worsen airway obstruction. Instead, keep the patient as calm as possible and immediately call a senior anaesthetist, a senior paediatrician, and an ENT surgeon. Nebulized adrenaline can be used as a temporary measure if there is critical airway obstruction.

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

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

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

Calcium-channel blocker overdose is a serious condition that can be life-threatening. The 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 are important for the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

When managing a patient with calcium-channel blocker overdose, it is crucial to follow the standard ABC approach for resuscitation. If there is a risk of life-threatening toxicity, early intubation and ventilation should be considered. Invasive blood pressure monitoring is also necessary if hypotension and shock are developing.

The specific treatments for calcium-channel blocker overdose primarily focus on supporting the cardiovascular system. These treatments include:

1. Fluid resuscitation: Administer up to 20 mL/kg of crystalloid solution.

2. Calcium administration: This can temporarily increase blood pressure and heart rate. Options include 10% calcium gluconate (60 mL IV) or 10% calcium chloride (20 mL IV) via central venous access. Repeat boluses can be given up to three times, and a calcium infusion may be necessary to maintain serum calcium levels above 2.0 mEq/L.

3. Atropine: Consider administering 0.6 mg every 2 minutes, up to a total of 1.8 mg. However, atropine is often ineffective in these cases.

4. High dose insulin – euglycemic therapy (HIET): The use of HIET in managing cardiovascular toxicity has evolved. It used to be a last-resort measure, but early administration is now increasingly recommended. This involves giving a bolus of short-acting insulin (1 U/kg) and 50 mL of 50% glucose IV (unless there is marked hyperglycemia). Therapy should be continued with a short-acting insulin/dextrose infusion. Glucose levels should be monitored frequently, and potassium should be replaced if levels drop below 2.5 mmol/L.

5. Vasoactive infusions: Catecholamines such as dopamine, adrenaline, and/or noradrenaline can be titrated to achieve the desired inotropic and chronotropic effects.

6. Sodium bicarbonate: Consider using sodium bicarbonate in cases where a severe metabolic acidosis develops.

Based on the Lund and Browder chart, the total percentage of burns is calculated as 3 since it affects one side of both hands.

Further Reading:

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

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

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

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

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

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

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

Further Reading:

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

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

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

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