Cushing’s triad is a combination of widened pulse pressure, bradycardia, and reduced respirations. It is a physiological response of the nervous system to acute increases in intracranial pressure (ICP). This response, known as the Cushing reflex, can cause the symptoms of Cushing’s triad. These symptoms include an increase in systolic blood pressure and a decrease in diastolic blood pressure, a slower heart rate, and irregular or reduced breathing. Additionally, raised ICP can also lead to other symptoms such as headache, papilloedema, and vomiting.

Further Reading:

Intracranial pressure (ICP) refers to the pressure within the craniospinal compartment, which includes neural tissue, blood, and cerebrospinal fluid (CSF). Normal ICP for a supine adult is 5-15 mmHg. The body maintains ICP within a narrow range through shifts in CSF production and absorption. If ICP rises, it can lead to decreased cerebral perfusion pressure, resulting in cerebral hypoperfusion, ischemia, and potentially brain herniation.

The cranium, which houses the brain, is a closed rigid box in adults and cannot expand. It is made up of 8 bones and contains three main components: brain tissue, cerebral blood, and CSF. Brain tissue accounts for about 80% of the intracranial volume, while CSF and blood each account for about 10%. The Monro-Kellie doctrine states that the sum of intracranial volumes is constant, so an increase in one component must be offset by a decrease in the others.

There are various causes of raised ICP, including hematomas, neoplasms, brain abscesses, edema, CSF circulation disorders, venous sinus obstruction, and accelerated hypertension. Symptoms of raised ICP include headache, vomiting, pupillary changes, reduced cognition and consciousness, neurological signs, abnormal fundoscopy, cranial nerve palsy, hemiparesis, bradycardia, high blood pressure, irregular breathing, focal neurological deficits, seizures, stupor, coma, and death.

Measuring ICP typically requires invasive procedures, such as inserting a sensor through the skull. Management of raised ICP involves a multi-faceted approach, including antipyretics to maintain normothermia, seizure control, positioning the patient with a 30º head up tilt, maintaining normal blood pressure, providing analgesia, using drugs to lower ICP (such as mannitol or saline), and inducing hypocapnoeic vasoconstriction through hyperventilation. If these measures are ineffective, second-line therapies like barbiturate coma, optimised hyperventilation, controlled hypothermia, or decompressive craniectomy may be considered.

Orthostatic hypotension is a condition where patients feel lightheaded and may experience tunnel vision when they stand up from a lying down position. These symptoms are often worse in the morning. The patient’s history of recurrent episodes after being in a supine position for a long time strongly suggests orthostatic hypotension. There are no signs of epilepsy, such as deja-vu or jambs vu prodrome, tongue biting, loss of bladder or bowel control, or postictal confusion. The normal ECG and consistent timing of symptoms make postural orthostatic tachycardia syndrome (PAF) less likely. There are no neurological deficits to suggest a transient ischemic attack (TIA). The prodromal symptoms, such as tunnel vision and lightheadedness, align more with orthostatic hypotension rather than vasovagal syncope, which typically occurs after long periods of standing and is characterized by feeling hot and sweaty. Although carotid sinus syndrome could be considered as a differential diagnosis, as the patient’s head turning on getting out of bed may trigger symptoms, it is not one of the options.

Further Reading:

Blackouts, also known as syncope, are defined as a spontaneous transient loss of consciousness with complete recovery. They are most commonly caused by transient inadequate cerebral blood flow, although epileptic seizures can also result in blackouts. There are several different causes of blackouts, including neurally-mediated reflex syncope (such as vasovagal syncope or fainting), orthostatic hypotension (a drop in blood pressure upon standing), cardiovascular abnormalities, and epilepsy.

When evaluating a patient with blackouts, several key investigations should be performed. These include an electrocardiogram (ECG), heart auscultation, neurological examination, vital signs assessment, lying and standing blood pressure measurements, and blood tests such as a full blood count and glucose level. Additional investigations may be necessary depending on the suspected cause, such as ultrasound or CT scans for aortic dissection or other abdominal and thoracic pathology, chest X-ray for heart failure or pneumothorax, and CT pulmonary angiography for pulmonary embolism.

During the assessment, it is important to screen for red flags and signs of any underlying serious life-threatening condition. Red flags for blackouts include ECG abnormalities, clinical signs of heart failure, a heart murmur, blackouts occurring during exertion, a family history of sudden cardiac death at a young age, an inherited cardiac condition, new or unexplained breathlessness, and blackouts in individuals over the age of 65 without a prodrome. These red flags indicate the need for urgent assessment by an appropriate specialist.

There are several serious conditions that may be suggested by certain features. For example, myocardial infarction or ischemia may be indicated by a history of coronary artery disease, preceding chest pain, and ECG signs such as ST elevation or arrhythmia. Pulmonary embolism may be suggested by dizziness, acute shortness of breath, pleuritic chest pain, and risk factors for venous thromboembolism. Aortic dissection may be indicated by chest and back pain, abnormal ECG findings, and signs of cardiac tamponade include low systolic blood pressure, elevated jugular venous pressure, and muffled heart sounds. Other conditions that may cause blackouts include severe hypoglycemia, Addisonian crisis, and electrolyte abnormalities.

Patients who experience post-tonsillectomy bleeding, even if it stops, should be closely monitored and assessed by an ear, nose, and throat specialist before being discharged. It is important to note that minor bleeding episodes may occur before a more severe hemorrhage. Therefore, patients with post-tonsillectomy bleeds, even if they seem to have resolved, should be admitted to the hospital under the care of an ENT specialist.

Further Reading:

Tonsillectomy is a common procedure performed by ENT surgeons in the UK, with over 50,000 surgeries performed each year. While it is considered routine, there are risks of serious complications, including post-tonsillectomy bleeding. Approximately 5% of patients experience bleeding after the procedure, with most cases being self-limiting. However, severe bleeding can lead to hypovolemia and airway obstruction from clots, which can be life-threatening.

Post-tonsillectomy bleeding can be classified as primary (reactive) or secondary (delayed). Primary bleeding occurs within 24 hours of the procedure, while secondary bleeding occurs more than 24 hours post-procedure. Secondary bleeding is often caused by factors such as sloughing of eschar, trauma from solid food ingestion, tonsil bed infection, postoperative NSAID usage, or unknown causes.

Patients may present with symptoms such as vomiting blood, coughing up blood, tasting blood in the throat, finding blood on pillows or bed sheets, or excessive swallowing (especially in children). It is important for clinicians to assess the severity of blood loss, although it can be challenging to accurately estimate in children.

The ABCDE approach should be used to assess patients, with a focus on airway compromise, hemodynamic instability, and evidence of bleeding. Clinicians may use a head torch to identify any bleeding points, which may be actively bleeding or appear as fresh red clots. It is important to note that the tonsillar fossa may appear white or yellow, which is a normal postoperative finding.

Investigations such as a full blood count, coagulation profile, group and save, and venous blood gas may be performed to assess the patient’s condition. Senior support from ENT or anesthesiology should be called if there is active bleeding.

Management of post-tonsillectomy bleeding includes positioning the patient upright and keeping them calm, establishing intravenous access, administering fluids and blood products as needed, and administering tranexamic acid to stop bleeding. Bleeding points may require gentle suction removal of fresh clots, and topical medications such as Co-phenylcaine spray or topical adrenaline may be applied to the oropharynx. All patients with post-tonsillectomy bleeding should be assessed by ENT and observed for a prolonged period, typically 12-24 hours.

If bleeding remains uncontrolled, the patient should be kept nil by mouth in preparation for surgery, and early intervention.

Cardiac tamponade is characterized by several classical signs, including distended neck veins, muffled heart sounds, and hypotension. When neck veins are distended, it suggests that the right ventricle is not filling properly. In cases of trauma, this is often caused by the compression of air (tension pneumothorax) or fluid (blood in the pericardial space). One important distinguishing feature is the deviation of the trachea.

Further Reading:

Cardiac tamponade, also known as pericardial tamponade, occurs when fluid accumulates in the pericardial sac and compresses the heart, leading to compromised blood flow. Classic clinical signs of cardiac tamponade include distended neck veins, hypotension, muffled heart sounds, and pulseless electrical activity (PEA). Diagnosis is typically done through a FAST scan or an echocardiogram.

Management of cardiac tamponade involves assessing for other injuries, administering IV fluids to reduce preload, performing pericardiocentesis (inserting a needle into the pericardial cavity to drain fluid), and potentially performing a thoracotomy. It is important to note that untreated expanding cardiac tamponade can progress to PEA cardiac arrest.

Pericardiocentesis can be done using the subxiphoid approach or by inserting a needle between the 5th and 6th intercostal spaces at the left sternal border. Echo guidance is the gold standard for pericardiocentesis, but it may not be available in a resuscitation situation. Complications of pericardiocentesis include ST elevation or ventricular ectopics, myocardial perforation, bleeding, pneumothorax, arrhythmia, acute pulmonary edema, and acute ventricular dilatation.

It is important to note that pericardiocentesis is typically used as a temporary measure until a thoracotomy can be performed. Recent articles published on the RCEM learning platform suggest that pericardiocentesis has a low success rate and may delay thoracotomy, so it is advised against unless there are no other options available.

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

Further Reading:

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

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

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

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

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

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

The clinical symptoms of mitral stenosis include shortness of breath, which tends to worsen during exercise and when lying flat. Tiredness, palpitations, ankle swelling, cough, and haemoptysis are also common symptoms. Chest discomfort is rarely reported.

The clinical signs of mitral stenosis can include a malar flush, an irregular pulse if atrial fibrillation is present, a tapping apex beat that can be felt as the first heart sound, and a left parasternal heave if there is pulmonary hypertension. The first heart sound is often loud, and a mid-diastolic murmur can be heard.

The mid-diastolic murmur of mitral stenosis is a rumbling sound that is best heard at the apex, in the left lateral position during expiration, using the bell of the stethoscope.

Mitral stenosis is typically caused by rheumatic heart disease, and it is more common in females, with about two-thirds of patients being female.

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%.

Warfarin has been found to heighten the likelihood of bleeding events when consumed alongside specific juices, such as cranberry juice and grapefruit juice. As a result, individuals who are taking warfarin should be cautioned against consuming these beverages. For more information on this topic, please refer to the BNF section on warfarin interactions and the interaction between warfarin and cranberry juice.

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.

Shenton’s line is a useful tool for identifying hip fractures on radiographs. It is a curved line that is drawn along the bottom edge of the upper pubic bone and the inner lower edge of the femur neck. This line should be smooth and uninterrupted. If there are any breaks or irregularities in the line, it could indicate a fracture, dysplasia, or dislocation.

Further Reading:

Fractured neck of femur is a common injury, especially in elderly patients who have experienced a low impact fall. Risk factors for this type of fracture include falls, osteoporosis, and other bone disorders such as metastatic cancers, hyperparathyroidism, and osteomalacia.

There are different classification systems for hip fractures, but the most important differentiation is between intracapsular and extracapsular fractures. The blood supply to the femoral neck and head is primarily from ascending cervical branches that arise from an arterial anastomosis between the medial and lateral circumflex branches of the femoral arteries. Fractures in the intracapsular region can damage the blood supply and lead to avascular necrosis (AVN), with the risk increasing with displacement. The Garden classification can be used to classify intracapsular neck of femur fractures and determine the risk of AVN. Those at highest risk will typically require hip replacement or arthroplasty.

Fractures below or distal to the capsule are termed extracapsular and can be further described as intertrochanteric or subtrochanteric depending on their location. The blood supply to the femoral neck and head is usually maintained with these fractures, making them amenable to surgery that preserves the femoral head and neck, such as dynamic hip screw fixation.

Diagnosing hip fractures can be done through radiographs, with Shenton’s line and assessing the trabecular pattern of the proximal femur being helpful techniques. X-rays should be obtained in both the AP and lateral views, and if an occult fracture is suspected, an MRI or CT scan may be necessary.

In terms of standards of care, it is important to assess the patient’s pain score within 15 minutes of arrival in the emergency department and provide appropriate analgesia within the recommended timeframes. Patients with moderate or severe pain should have their pain reassessed within 30 minutes of receiving analgesia. X-rays should be obtained within 120 minutes of arrival, and patients should be admitted within 4 hours of arrival.

In cases of myocarditis, levels of cardiac muscle enzymes (CK-MB, Troponin I, and Troponin T) and B-type natriuretic peptide (BNP) are usually elevated. It is important to note that CK-MB is a subtype of CK, so an increase in CK-MB will also result in an increase in total CK levels. This poses a challenge in differentiating myocarditis from coronary artery disease in the emergency department. Typically, a definitive diagnosis is not made until the patient undergoes additional tests such as angiography and possibly endomyocardial biopsy (EMB).

Further Reading:

Myocarditis is inflammation of the myocardium, the middle layer of the heart wall, that is not caused by a blockage in the coronary arteries. It can be caused by various factors, including infections (such as viruses, bacteria, parasites, and fungi), immune reactions, toxins, physical injury, and certain medications or vaccines. Coxsackie virus is the most common cause of myocarditis in Europe and the USA, while globally, Trypanosoma cruzi, which causes Chagas disease, is the most common cause.

The symptoms of myocarditis can vary widely and often resemble those of heart failure or coronary heart disease. Common symptoms include chest pain, palpitations, breathlessness, fatigue, and swelling. The clinical presentation can also be influenced by the underlying cause of the inflammation. Diagnosis of myocarditis is challenging as there is no specific clinical presentation, and the gold standard test, endomyocardial biopsy, is not readily available in emergency departments.

Various tests can be performed to aid in the diagnosis of myocarditis, including electrocardiogram (ECG), chest X-ray, cardiac enzymes (such as troponin or CK-MB), brain natriuretic peptide (BNP) levels, and echocardiogram. These tests may show non-specific abnormalities, such as ST-segment and T-wave abnormalities on ECG, bilateral pulmonary infiltrates on chest X-ray, elevated cardiac enzymes and BNP levels, and left ventricular motion abnormalities on echocardiogram.

Management of myocarditis is primarily supportive, focusing on treating cardiac failure and addressing the underlying cause. Supportive care and conventional heart failure therapy, such as ACE inhibitors or angiotensin II receptor blockers, vasodilators, beta-blockers, and diuretics, may be used to improve cardiac function and reduce symptoms. Treatment of the underlying cause, such as antiparasitic agents for Chagas disease or antibiotics for bacterial infections, may also be necessary. In severe cases leading to cardiogenic shock, more aggressive treatment with invasive monitoring, inotropes, vasopressors, and potentially heart transplantation may be required.

In summary, myocarditis is inflammation of the myocardium that can be caused by various factors. It presents with a wide range of symptoms and can be challenging to diagnose. Management involves supportive care, treatment of cardiac failure, and addressing the underlying cause. Severe cases may require more aggressive treatment and potentially heart transplantation.

This patient has been diagnosed with severe hyperkalemia and is showing significant ECG changes. The top priority in this situation is to protect the heart. It is recommended to administer 10 ml of 10% calcium chloride immediately over a period of 2-5 minutes. Calcium helps counteract the harmful effects of hyperkalemia on the heart by stabilizing the cardiac cell membrane and preventing unwanted depolarization.

Hyperkalemia is a commonly encountered electrolyte disorder, affecting up to 10% of hospitalized patients. It is typically caused by an increase in potassium release from cells or impaired excretion by the kidneys. The main causes of hyperkalemia include renal failure, certain medications (such as ACE inhibitors, ARBs, potassium-sparing diuretics, and NSAIDs), tissue breakdown (as seen in conditions like tumor lysis, rhabdomyolysis, and hemolysis), metabolic acidosis (often associated with renal failure or diabetic ketoacidosis), and endocrine disorders like Addison’s disease.

ECG changes that may be observed in hyperkalemia include a prolonged PR interval, peaked T-waves, widening of the QRS complex, reduced or absent P wave, sine wave pattern, AV dissociation, asystole, and bradycardia. It is important to note that the severity of ECG changes may not always correlate with the actual serum potassium levels in a patient.

The treatment approach for hyperkalemia depends on its severity. Mild hyperkalemia is defined as a potassium level of 5.5-5.9 mmol/L, moderate hyperkalemia as 6.0-6.4 mmol/L, and severe hyperkalemia as >6.5 mmol/L.

For mild hyperkalemia, the focus should be on addressing the underlying cause and preventing further increase in serum potassium levels. This may involve adjusting medications or dietary changes. If treatment is necessary, potassium exchange resins like calcium resonium can be used to remove potassium from the body.

In cases of moderate hyperkalemia, the goal is to shift potassium from the extracellular space into the cells. This can be achieved by administering insulin and glucose intravenously. Monitoring blood glucose levels is crucial in this situation. Potassium exchange resins should also be considered, and dialysis may be necessary.

Severe hyperkalemia without ECG changes requires immediate medical attention.

Acamprosate, also known as Campral, is a medication used in the treatment of alcohol dependence. It is believed to work by stabilizing a chemical pathway in the brain that is disrupted during alcohol withdrawal. For optimal results, Acamprosate should be used alongside psychosocial support, as it helps reduce alcohol consumption and promote abstinence.

When starting treatment with Acamprosate, it is important to begin as soon as possible after assisted withdrawal. The typical dosage is 1998 mg (666 mg three times a day), unless the patient weighs less than 60 kg, in which case a maximum of 1332 mg per day should be prescribed.

Generally, Acamprosate is prescribed for up to 6 months. However, for those who benefit from the medication and wish to continue, it can be taken for a longer duration. If drinking persists 4-6 weeks after starting the drug, it should be discontinued.

Patients who are prescribed Acamprosate should be closely monitored, with regular check-ins at least once a month for the first six months. If the medication is continued beyond six months, the frequency of check-ins can be reduced but should still occur at regular intervals.

While routine blood tests are not mandatory, they can be considered if there is a need to monitor liver function recovery or as a motivational tool to show patients their progress.

Depression and dementia are both more prevalent in the elderly population and often coexist. Diagnosing these conditions can be challenging due to the overlapping symptoms they share.

Depression is characterized by a persistent low mood throughout the day, significant unintentional weight changes, sleep disturbances, fatigue, feelings of worthlessness or guilt, difficulty concentrating, loss of interest in activities, and recurrent thoughts of death. It may also manifest as agitation or slowed movements, which can be observed by others.

Dementia, on the other hand, refers to a group of symptoms resulting from a pathological process that leads to significant cognitive impairment. This impairment is more severe than what would be expected for a person’s age. Alzheimer’s disease is the most common form of dementia.

Symptoms of dementia include memory loss, particularly in the short-term, changes in mood that are usually reactive to situations and improve with support and stimulation, infrequent thoughts about death, alterations in personality, difficulty finding the right words, struggles with complex tasks, urinary incontinence, loss of appetite and weight in later stages, and agitation in unfamiliar environments.

By understanding the distinct features of depression and dementia, healthcare professionals can better identify and differentiate between these conditions in the elderly population.

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.

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

Further Reading:

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

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

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

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

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

Further Reading:

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

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

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

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

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

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

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

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

Hyperventilation leads to the constriction of blood vessels in the brain, which in turn reduces the flow and volume of blood in the brain, ultimately decreasing intracranial pressure (ICP). This is because hyperventilation lowers the levels of carbon dioxide (PaCO2) in the blood, resulting in an increase in pH and causing the arteries in the brain to constrict and reduce blood flow. As a result, cerebral blood volume and ICP decrease. The effects of hyperventilation are immediate, but they gradually diminish over a period of 6-24 hours as the brain adjusts its bicarbonate levels to normalize pH. However, caution must be exercised when discontinuing hyperventilation after a prolonged period, as the sudden increase in PaCO2 can lead to a rapid rise in cerebral blood flow and a detrimental increase in ICP.

Further Reading:

Intracranial pressure (ICP) refers to the pressure within the craniospinal compartment, which includes neural tissue, blood, and cerebrospinal fluid (CSF). Normal ICP for a supine adult is 5-15 mmHg. The body maintains ICP within a narrow range through shifts in CSF production and absorption. If ICP rises, it can lead to decreased cerebral perfusion pressure, resulting in cerebral hypoperfusion, ischemia, and potentially brain herniation.

The cranium, which houses the brain, is a closed rigid box in adults and cannot expand. It is made up of 8 bones and contains three main components: brain tissue, cerebral blood, and CSF. Brain tissue accounts for about 80% of the intracranial volume, while CSF and blood each account for about 10%. The Monro-Kellie doctrine states that the sum of intracranial volumes is constant, so an increase in one component must be offset by a decrease in the others.

There are various causes of raised ICP, including hematomas, neoplasms, brain abscesses, edema, CSF circulation disorders, venous sinus obstruction, and accelerated hypertension. Symptoms of raised ICP include headache, vomiting, pupillary changes, reduced cognition and consciousness, neurological signs, abnormal fundoscopy, cranial nerve palsy, hemiparesis, bradycardia, high blood pressure, irregular breathing, focal neurological deficits, seizures, stupor, coma, and death.

Measuring ICP typically requires invasive procedures, such as inserting a sensor through the skull. Management of raised ICP involves a multi-faceted approach, including antipyretics to maintain normothermia, seizure control, positioning the patient with a 30º head up tilt, maintaining normal blood pressure, providing analgesia, using drugs to lower ICP (such as mannitol or saline), and inducing hypocapnoeic vasoconstriction through hyperventilation. If these measures are ineffective, second-line therapies like barbiturate coma, optimised hyperventilation, controlled hypothermia, or decompressive craniectomy may be considered.

ATLS guidelines now suggest administering only 1 liter of crystalloid fluid during the initial assessment. If patients do not respond to the crystalloid, it is recommended to quickly transition to blood products. Studies have shown that infusing more than 1.5 liters of crystalloid fluid is associated with higher mortality rates in trauma cases. Therefore, it is advised to prioritize the early use of blood products and avoid large volumes of crystalloid fluid in trauma patients. In cases where it is necessary, massive transfusion should be considered, defined as the transfusion of more than 10 units of blood in 24 hours or more than 4 units of blood in one hour. For patients with evidence of Class III and IV hemorrhage, early resuscitation with blood and blood products in low ratios is recommended.

Based on the findings of significant trials, such as the CRASH-2 study, the use of tranexamic acid is now recommended within 3 hours. This involves administering a loading dose of 1 gram intravenously over 10 minutes, followed by an infusion of 1 gram over eight hours. In some regions, tranexamic acid is also being utilized in the prehospital setting.

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

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

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

If a patient with a zygoma fracture experiences visual disturbance, limited eye movements (especially upward gaze), or shows a teardrop sign on a facial X-ray, it is important to refer them urgently to ophthalmology or maxillofacial surgeons.

Further Reading:

Zygomatic injuries, also known as zygomatic complex fractures, involve fractures of the zygoma bone and often affect surrounding bones such as the maxilla and temporal bones. These fractures can be classified into four positions: the lateral and inferior orbital rim, the zygomaticomaxillary buttress, and the zygomatic arch. The full extent of these injuries may not be visible on plain X-rays and may require a CT scan for accurate diagnosis.

Zygomatic fractures can pose risks to various structures in the face. The temporalis muscle and coronoid process of the mandible may become trapped in depressed fractures of the zygomatic arch. The infraorbital nerve, which passes through the infraorbital foramen, can be injured in zygomaticomaxillary complex fractures. In orbital floor fractures, the inferior rectus muscle may herniate into the maxillary sinus.

Clinical assessment of zygomatic injuries involves observing facial asymmetry, depressed facial bones, contusion, and signs of eye injury. Visual acuity must be assessed, and any persistent bleeding from the nose or mouth should be noted. Nasal injuries, including septal hematoma, and intra-oral abnormalities should also be evaluated. Tenderness of facial bones and the temporomandibular joint should be assessed, along with any step deformities or crepitus. Eye and jaw movements must also be evaluated.

Imaging for zygomatic injuries typically includes facial X-rays, such as occipitomental views, and CT scans for a more detailed assessment. It is important to consider the possibility of intracranial hemorrhage and cervical spine injury in patients with facial fractures.

Management of most zygomatic fractures can be done on an outpatient basis with maxillofacial follow-up, assuming the patient is stable and there is no evidence of eye injury. However, orbital floor fractures should be referred immediately to ophthalmologists or maxillofacial surgeons. Zygomatic arch injuries that restrict mouth opening or closing due to entrapment of the temporalis muscle or mandibular condyle also require urgent referral. Nasal fractures, often seen in conjunction with other facial fractures, can be managed by outpatient ENT follow-up but should be referred urgently if there is uncontrolled epistaxis, CSF rhinorrhea, or septal hematoma.

Every year in the UK, 5,000 individuals lose their lives to suicide. Shockingly, only 25% of these individuals were known to receive specialized mental health services. The demographic with the highest suicide rates is men aged between 30 and 60, but there is a concerning increase in rates among teenagers aged 15 to 19.

It is crucial for doctors to be able to identify and provide support to patients who suffer from severe depression or other mental health issues, as they are at a higher risk of suicide. Certain factors significantly increase the risk of suicide, including a history of self-harm, previous mental illness, being male, experiencing severe depression, and substance abuse. It is important to note that combinations of these risk factors are more significant than individual factors alone.

Despite the belief that hospital admission provides a safe environment, the risk of suicide remains high for inpatients. Additionally, the risk remains elevated in the months following discharge from the hospital.

On the other hand, there are protective factors that decrease the likelihood of suicide. These include having dependent children, having family members who would be deeply affected by the loss, and having religious beliefs.

The Royal College of Emergency Medicine (RCEM) recognizes four antidotes that can be used to treat cyanide poisoning: Hydroxycobalamin, Sodium thiosulphate, Sodium nitrite, and Dicobalt edetate. When managing cyanide toxicity, it is important to provide supportive treatment using the ABCDE approach. This includes administering supplemental high flow oxygen, providing hemodynamic support (including the use of inotropes if necessary), and administering the appropriate antidotes. In the UK, these four antidotes should be readily available in Emergency Departments according to the RCEM/NPIS guideline on antidote availability. Hydroxocobalamin followed by sodium thiosulphate is generally the preferred treatment if both options are available. Healthcare workers should be aware that patients with cyanide poisoning may expel HCN through vomit and skin, so it is crucial to use appropriate personal protective equipment when caring for these patients.

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.

This patient has presented with acute closed-angle glaucoma, which is a medical emergency in the field of ophthalmology. It occurs when the iris bows forward and blocks the fluid access to the trabecular meshwork, which is located at the entrance to Schlemm’s canal. As a result, the intraocular pressure rises and leads to glaucomatous optic neuropathy.

The main clinical features of acute closed-angle glaucoma include severe eye pain, loss of vision or decreased visual acuity, congestion and redness around the cornea, corneal swelling, a fixed semi-dilated oval-shaped pupil, nausea and vomiting, and preceding episodes of blurred vision or seeing haloes.

The diagnosis can be confirmed by tonometry, which measures the pressure inside the eye. The normal range of intraocular pressure is 10-21 mmHg, but in acute closed-angle glaucoma, it is often higher than 30 mmHg. Goldmann’s applanation tonometer is commonly used in hospitals for this purpose.

Management of acute closed-angle glaucoma should include providing pain relief, such as morphine, and antiemetics if the patient is experiencing vomiting. Intravenous administration of acetazolamide 500 mg is recommended to reduce intraocular pressure. Treatment with a topical miotic, like pilocarpine 1% or 2%, should be initiated approximately one hour after starting other measures, as the pupil may initially be paralyzed and unresponsive.

On the other hand, chronic open-angle glaucoma is a more common presentation than acute closed-angle glaucoma. It affects approximately 1 in 50 people over the age of 40 and 1 in 10 people over the age of 75. In this condition, there is a partial blockage within the trabecular meshwork, which hinders the drainage of aqueous humor and gradually increases intraocular pressure, leading to optic neuropathy. Unlike acute closed-angle glaucoma, chronic open-angle glaucoma does not cause eye pain or redness. It presents gradually with a progressive loss of peripheral vision, while central vision is relatively preserved.

If a polytrauma patient with a penetrating chest injury has an expanding cardiac tamponade that is left untreated, it can potentially lead to pulseless electrical activity.

Further Reading:

Cardiac tamponade, also known as pericardial tamponade, occurs when fluid accumulates in the pericardial sac and compresses the heart, leading to compromised blood flow. Classic clinical signs of cardiac tamponade include distended neck veins, hypotension, muffled heart sounds, and pulseless electrical activity (PEA). Diagnosis is typically done through a FAST scan or an echocardiogram.

Management of cardiac tamponade involves assessing for other injuries, administering IV fluids to reduce preload, performing pericardiocentesis (inserting a needle into the pericardial cavity to drain fluid), and potentially performing a thoracotomy. It is important to note that untreated expanding cardiac tamponade can progress to PEA cardiac arrest.

Pericardiocentesis can be done using the subxiphoid approach or by inserting a needle between the 5th and 6th intercostal spaces at the left sternal border. Echo guidance is the gold standard for pericardiocentesis, but it may not be available in a resuscitation situation. Complications of pericardiocentesis include ST elevation or ventricular ectopics, myocardial perforation, bleeding, pneumothorax, arrhythmia, acute pulmonary edema, and acute ventricular dilatation.

It is important to note that pericardiocentesis is typically used as a temporary measure until a thoracotomy can be performed. Recent articles published on the RCEM learning platform suggest that pericardiocentesis has a low success rate and may delay thoracotomy, so it is advised against unless there are no other options available.

The guidelines from the European League Against Rheumatism (EULAR) regarding the diagnosis of gout state that if a joint becomes swollen, tender, and red, and if acute pain develops in that joint over a period of 6-12 hours, it is highly likely to be a crystal arthropathy. Pseudogout is also a possibility, but it is much less likely. In this case, gout is the most probable diagnosis.

The joint that is most commonly affected in acute gout is the first metatarsal-phalangeal joint, which accounts for 50-75% of cases.

The main cause of gout is hyperuricaemia, and the clinical diagnosis can be confirmed by the presence of negatively birefringent crystals in the synovial fluid aspirate.

For the treatment of acute gout attacks, NSAIDs or colchicine are generally used.

When patients with diabetic ketoacidosis (DKA) are treated with insulin infusion, it is expected that their plasma bicarbonate levels will increase by at least 3 mmol/L per hour. Insulin therapy is aimed at correcting both hyperglycemia and ketoacidosis. However, if capillary ketones are not decreasing by at least 0.5 mmol/L per hour, venous bicarbonate is not rising by at least 3 mmol/L per hour, or plasma glucose is not decreasing by at least 3 mmol/L per hour, the insulin infusion rate should be reevaluated.

Further Reading:

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

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

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

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

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

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

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

Adenosine is given through a rapid IV bolus, followed by a flush of saline solution. In adults, the starting dose is 6 mg, and if needed, an additional dose of 12 mg is given. If necessary, another dose of either 12 mg or 18 mg can be administered at intervals of 1-2 minutes until the desired effect is observed.

It is important to note that the latest ALS guidelines recommend an 18 mg dose for the third administration, while the BNF/NICE guidelines suggest a 12 mg dose.

However, patients who have undergone a heart transplant are particularly sensitive to the effects of adenosine. Therefore, their initial dose should be reduced to 3 mg, followed by 6 mg, and then 12 mg.

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

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

The second stage is known as the paroxysmal stage. During this stage, the characteristic paroxysmal cough develops as the symptoms from the catarrhal stage start to improve. The coughing occurs in spasms, often preceded by an inspiratory whoop sound, followed by a series of rapid coughs. Vomiting may occur, and patients may develop subconjunctival hemorrhages and petechiae. Patients generally feel well between coughing spasms, and there are usually no abnormal chest findings. This stage can last up to 3 months, with a gradual recovery over this period. The later stages of this stage 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. It is important to note that a history of vaccination does not guarantee immunity, as it only provides about 95% protection.

The presence of marked lymphocytosis in this case also supports a diagnosis of pertussis, as it is a common finding. A lymphocyte count greater than 20 x 109/l is highly suggestive of the disease.

Addison’s disease is characterized by several classical biochemical features. One of these features is an increase in ACTH levels, which is a hormone that stimulates the production of cortisol. Additionally, individuals with Addison’s disease often have elevated serum renin levels, which is an enzyme involved in regulating blood pressure. Another common biochemical feature is hyponatremia, which refers to low levels of sodium in the blood. Hyperkalemia, or high levels of potassium, is also frequently observed in individuals with Addison’s disease. Furthermore, hypercalcemia, an excess of calcium in the blood, may be present. Hypoglycemia, or low blood sugar levels, is another characteristic feature. Lastly, metabolic acidosis, a condition where the body produces too much acid or cannot eliminate it properly, is often seen in individuals with Addison’s disease.

A central venous catheter (CVC) is a type of catheter that is inserted into a large vein in the body, typically in the neck, chest, or groin. It has several important uses, including CVP monitoring, pulmonary artery pressure monitoring, repeated blood sampling, IV access for large volumes of fluids or drugs, TPN administration, dialysis, pacing, and other procedures such as placement of IVC filters or venous stents.

When inserting a central line, it is ideal to use ultrasound guidance to ensure accurate placement. However, there are certain contraindications to central line insertion, including infection or injury to the planned access site, coagulopathy, thrombosis or stenosis of the intended vein, a combative patient, or raised intracranial pressure for jugular venous lines.

The most common approaches for central line insertion are the internal jugular, subclavian, femoral, and PICC (peripherally inserted central catheter) veins. The internal jugular vein is often chosen due to its proximity to the carotid artery, but variations in anatomy can occur. Ultrasound can be used to identify the vessels and guide catheter placement, with the IJV typically lying superficial and lateral to the carotid artery. Compression and Valsalva maneuvers can help distinguish between arterial and venous structures, and doppler color flow can highlight the direction of flow.

In terms of choosing a side for central line insertion, the right side is usually preferred to avoid the risk of injury to the thoracic duct and potential chylothorax. However, the left side can also be used depending on the clinical situation.

Femoral central lines are another option for central venous access, with the catheter being inserted into the femoral vein in the groin. Local anesthesia is typically used to establish a field block, with lidocaine being the most commonly used agent. Lidocaine works by blocking sodium channels and preventing the propagation of action potentials.

In summary, central venous catheters have various important uses and should ideally be inserted using ultrasound guidance. There are contraindications to their insertion, and different approaches can be used depending on the clinical situation. Local anesthesia is commonly used for central line insertion, with lidocaine being the preferred agent.

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

Treatment for Mycoplasma pneumoniae infection can involve the use of macrolides, such as clarithromycin, or tetracyclines, such as doxycycline. The recommended minimum treatment period is 10-14 days, making clarithromycin a preferable option over doxycycline in this particular case.

CT scan is considered the most reliable imaging technique for diagnosing intra-abdominal conditions. It is also considered the gold standard for evaluating organ damage. However, it is crucial to carefully consider the specific circumstances before using CT scan, as it may not be suitable for unstable patients or those who clearly require immediate surgical intervention. In such cases, other methods like FAST can be used to detect fluid in the abdominal cavity, although it is not as accurate in assessing injuries to solid organs or hollow structures within the abdomen.

Further Reading:

Abdominal trauma can be classified into two categories: blunt trauma and penetrating trauma. Blunt trauma occurs when compressive or deceleration forces are applied to the abdomen, often resulting from road traffic accidents or direct blows during sports. The spleen and liver are the organs most commonly injured in blunt abdominal trauma. On the other hand, penetrating trauma involves injuries that pierce the skin and enter the abdominal cavity, such as stabbings, gunshot wounds, or industrial accidents. The bowel and liver are the organs most commonly affected in penetrating injuries.

When it comes to imaging in blunt abdominal trauma, there are three main modalities that are commonly used: focused assessment with sonography in trauma (FAST), diagnostic peritoneal lavage (DPL), and computed tomography (CT). FAST is a non-invasive and quick method used to detect free intraperitoneal fluid, aiding in the decision on whether a laparotomy is needed. DPL is also used to detect intraperitoneal blood and can be used in both unstable blunt abdominal trauma and penetrating abdominal trauma. However, it is more invasive and time-consuming compared to FAST and has largely been replaced by it. CT, on the other hand, is the gold standard for diagnosing intra-abdominal pathology and is used in stable abdominal trauma patients. It offers high sensitivity and specificity but requires a stable and cooperative patient. It also involves radiation and may have delays in availability.

In the case of penetrating trauma, it is important to assess these injuries with the help of a surgical team. Penetrating objects should not be removed in the emergency department as they may be tamponading underlying vessels. Ideally, these injuries should be explored in the operating theater.

In summary, abdominal trauma can be classified into blunt trauma and penetrating trauma. Blunt trauma is caused by compressive or deceleration forces and commonly affects the spleen and liver. Penetrating trauma involves injuries that pierce the skin and commonly affect the bowel and liver. Imaging modalities such as FAST, DPL, and CT are used to assess and diagnose abdominal trauma, with CT being the gold standard. Penetrating injuries should be assessed by a surgical team and should ideally be explored in the operating theater.

The typical range for the normal angle of Gissane is between 120 and 145 degrees. An increase in this angle suggests that the posterior facet of the subtalar joint is depressed, which may indicate a calcaneal fracture. Similarly, the normal range for Bohler’s angle is between 20 and 40 degrees. For more detailed information and visual representations of these angles, please refer to the accompanying notes.

Further Reading:

calcaneus fractures are a common type of lower limb and joint injury. The calcaneus, or heel bone, is the most frequently fractured tarsal bone. These fractures are often intra-articular, meaning they involve the joint. The most common cause of calcaneus fractures is a fall or jump from a height.

When assessing calcaneus fractures, X-rays are used to visualize the fracture lines. Two angles are commonly assessed to determine the severity of the fracture. Böhler’s angle, which measures the angle between two tangent lines drawn across the anterior and posterior borders of the calcaneus, should be between 20-40 degrees. If it is less than 20 degrees, it indicates a calcaneal fracture with flattening. The angle of Gissane, which measures the depression of the posterior facet of the subtalar joint, should be between 120-145 degrees. An increased angle of Gissane suggests a calcaneal fracture.

In the emergency department, the management of a fractured calcaneus involves identifying the injury and any associated injuries, providing pain relief, elevating the affected limb(s), and referring the patient to an orthopedic specialist. It is important to be aware that calcaneus fractures are often accompanied by other injuries, such as bilateral fractures of vertebral fractures.

The definitive management of a fractured calcaneus can be done conservatively or through surgery, specifically open reduction internal fixation (ORIF). The orthopedic team will typically order a CT or MRI scan to classify the fracture and determine the most appropriate treatment. However, a recent UK heel fracture trial suggests that in most cases, ORIF does not improve fracture outcomes.

The primary cause of upper gastrointestinal bleeding in adults is peptic ulcer disease. Peptic ulcers are open sores that develop on the lining of the stomach or the upper part of the small intestine. These ulcers can be caused by factors such as infection with Helicobacter pylori bacteria, long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs), or excessive alcohol consumption. When a peptic ulcer bleeds, it can result in the vomiting of blood, which may appear as coffee ground vomit or have speckles of fresh red blood. Other symptoms that may accompany an upper gastrointestinal bleed include abdominal pain, nausea, and a feeling of fullness.

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.

CAGE, AUDIT, and T-ACE are all tools used to screen for alcohol misuse. The CAGE tool is the most commonly used by clinicians and consists of four simple questions. It is easy to remember and effective in identifying potential alcohol-related issues. The CAGE questionnaire asks if the individual has ever felt the need to cut down on their drinking, if others have criticized their drinking, if they have felt guilty about their drinking, and if they have ever had a drink first thing in the morning to alleviate a hangover or calm their nerves. A score of 2 or 3 suggests a high likelihood of alcoholism, while a score of 4 is almost diagnostic.

T-ACE is specifically designed to screen for alcohol abuse in pregnant women. It helps identify potential issues and allows for appropriate intervention and support.

The AUDIT tool is a more comprehensive questionnaire consisting of 10 points. It is typically used after initial screening and provides a more detailed assessment of alcohol consumption and potential dependency. The AUDIT-C, a simplified version of the AUDIT tool, is often used in primary care settings. It consists of three questions and is a quick and effective way to assess alcohol-related concerns.

While asking patients about their alcohol intake can provide some insight into excessive drinking, the screening tools are specifically designed to assess alcohol dependence and hazardous drinking. They offer a more comprehensive evaluation and help healthcare professionals identify individuals who may require further intervention or support.

It is important to note that advising patients on the harmful effects of alcohol is a valuable component of brief interventions. However, it is not as effective as using screening tools to identify potential alcohol-related issues.

The fascia iliaca compartment is a space within the body that has specific boundaries. It is located at the front of the hip and is surrounded by various muscles and structures. The anterior limit of this compartment is formed by the posterior surface of the fascia iliaca, which covers the iliacus muscle. Additionally, the medial reflection of this fascia covers every surface of the psoas major muscle. On the posterior side, the limit is formed by the anterior surface of the iliacus muscle and the psoas major muscle. The medial boundary is the vertebral column, while the cranially lateral boundary is the inner lip of the iliac crest. This compartment is also continuous with the space between the quadratus lumborum muscle and its fascia in a cranio-medial direction.

The fascia iliaca compartment is important because it allows for the deposition of local anesthetic in sufficient volumes. This can be achieved through a straightforward injection, which targets the femoral and lateral femoral cutaneous nerves. These nerves supply sensation to the medial, anterior, and lateral thigh. Occasionally, the obturator nerve is also blocked, although this can vary from person to person.

To perform a fascia iliaca compartment block (FICB), specific landmarks need to be identified. An imaginary line is drawn between the anterior superior iliac spine (ASIS) and the pubic tubercle. This line is then divided into thirds. The injection entry point is marked 1 cm caudal (inferior) from the junction of the lateral and middle third.

However, there are certain contraindications to performing a FICB. These include patient refusal, anticoagulation or bleeding disorders, allergy to local anesthetics, previous femoral bypass surgery, and infection or inflammation over the injection site.

As with any medical procedure, there are potential complications associated with a FICB. These can include intravascular injection, local anesthetic toxicity, allergy to the local anesthetic, temporary or permanent nerve damage, infection, and block failure. It is important for healthcare professionals to be aware of these risks and take appropriate precautions when performing a FICB.

Propofol often leads to hypotension as a common side effect. Other common side effects of Propofol include apnoea, arrhythmias, headache, and nausea with vomiting.

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.

Infective endocarditis is a condition that can be identified by certain signs, although none of them are definitive proof of the disease. The most reliable indicators are the presence of a heart murmur and a fever. However, there are other signs that are commonly associated with infective endocarditis, including splinter hemorrhages, Osler’s nodes, Janeway lesions, and Roth spots. It is important to note that these signs can also appear in other conditions, and they are not always present in patients with infective endocarditis. In fact, each of these signs is typically found in less than a third of patients diagnosed with the disease.

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.

The CHA2DS2-VASc score is a tool used to predict the likelihood of future stroke in individuals with atrial fibrillation (AF). It is scored on a scale of 0-9, with higher scores indicating a higher risk of stroke. If a male has a score of 1 or more, or if a female has a score of 2 or more, it is recommended to start anticoagulation therapy to prevent future strokes. However, it is important to assess the risk of bleeding before initiating anticoagulation using the HAS-BLED score. The HAS-BLED score does not evaluate the risk of stroke, but rather the risk of bleeding. QRISK3, on the other hand, is a tool used to estimate the risk of cardiovascular disease over a 10-year period and is primarily used to determine the benefits of starting lipid lowering drugs. It is the preferred tool recommended by NICE over the Framingham risk score.

Further Reading:

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting around 5% of patients over the age of 70-75 years and 10% of patients aged 80-85 years. While AF can cause palpitations and inefficient cardiac function, the most important aspect of managing patients with AF is reducing the increased risk of stroke.

AF can be classified as first detected episode, paroxysmal, persistent, or permanent. First detected episode refers to the initial occurrence of AF, regardless of symptoms or duration. Paroxysmal AF occurs when a patient has 2 or more self-terminating episodes lasting less than 7 days. Persistent AF refers to episodes lasting more than 7 days that do not self-terminate. Permanent AF is continuous atrial fibrillation that cannot be cardioverted or if attempts to do so are deemed inappropriate. The treatment goals for permanent AF are rate control and anticoagulation if appropriate.

Symptoms of AF include palpitations, dyspnea, and chest pain. The most common sign is an irregularly irregular pulse. An electrocardiogram (ECG) is essential for diagnosing AF, as other conditions can also cause an irregular pulse.

Managing patients with AF involves two key parts: rate/rhythm control and reducing stroke risk. Rate control involves slowing down the irregular pulse to avoid negative effects on cardiac function. This is typically achieved using beta-blockers or rate-limiting calcium channel blockers. If one drug is not effective, combination therapy may be used. Rhythm control aims to restore and maintain normal sinus rhythm through pharmacological or electrical cardioversion. However, the majority of patients are managed with a rate control strategy.

Reducing stroke risk in patients with AF is crucial. Risk stratifying tools, such as the CHA2DS2-VASc score, are used to determine the most appropriate anticoagulation strategy. Anticoagulation is recommended for patients with a score of 2 or more. Clinicians can choose between warfarin and novel oral anticoagulants (NOACs) for anticoagulation.

Before starting anticoagulation, the patient’s bleeding risk should be assessed using tools like the HAS-BLED score or the ORBIT tool. These tools evaluate factors such as hypertension, abnormal renal or liver function, history of bleeding, age, and use of drugs that predispose to bleeding.

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

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

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

The primary concern regarding this patient is airway obstruction. The patient’s complaint of progressive lip swelling, along with her previous diagnosis of hereditary angioedema (HAE), suggests that she may be experiencing an allergic reaction. Angioedema can cause swelling in various parts of the body, including the lips, tongue, and throat. If the swelling progresses and affects the airway, it can lead to difficulty breathing and potentially block the airway completely. This can be a life-threatening emergency and requires immediate intervention to ensure the patient’s airway remains open and they can breathe properly.

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.

Discitis is an infection that affects the space between the intervertebral discs in the spine. This condition can have serious consequences, including the formation of abscesses and sepsis. The most common cause of discitis is usually Staphylococcus aureus, but other organisms like Streptococcus viridans and Pseudomonas aeruginosa may be responsible in intravenous drug users and those with weakened immune systems. Gram-negative organisms such as Escherichia coli and Mycobacterium tuberculosis can also cause discitis.

There are several risk factors that increase the likelihood of developing discitis. These include having undergone spinal surgery (which occurs in 1-2% of cases post-operatively), having an immunodeficiency, being an intravenous drug user, being under the age of eight, having diabetes mellitus, or having a malignancy.

The typical symptoms of discitis include back or neck pain (which occurs in over 90% of cases), pain that often wakes the patient from sleep, fever (present in 60-70% of cases), and neurological deficits (which can occur in up to 50% of cases). In children, refusal to walk may also be a symptom.

When diagnosing discitis, MRI is the preferred imaging modality due to its high sensitivity and specificity. It is important to image the entire spine, as discitis often affects multiple levels. Plain radiographs are not very sensitive to the early changes of discitis and may appear normal for 2-4 weeks. CT scanning is also not very sensitive in detecting discitis.

Treatment for discitis involves admission to the hospital for intravenous antibiotics. Before starting the antibiotics, it is important to send three sets of blood cultures and a full set of blood tests, including a CRP, to the lab. The choice of antibiotics depends on the specific situation. A typical antibiotic regimen for discitis may include IV flucloxacillin as the first-line treatment if there is no penicillin allergy, IV vancomycin if the infection was acquired in the hospital or there is a high risk of MRSA, and possibly IV gentamicin if there is a possibility of a Gram-negative infection. In cases where there is acute kidney injury and Gram-negative cover is required, IV piperacillin-tazobactam alone may be used.

In the latest guideline published in 2021 by RCEM and NPIS regarding antidote availability for emergency departments, it is emphasized that immediate access to sodium bicarbonate is essential for treating TCA overdose. It is worth noting that previous versions of the guideline included glucagon as a recommended treatment for TCA overdose, but this reference has been omitted in the latest edition.

Further Reading:

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

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

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

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

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

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

Patients typically initiate dialysis when their glomerular filtration rate (GFR) drops to 10 ml/min. However, if the patient has diabetes, dialysis may be recommended when their GFR reaches 15 ml/min. The GFR is a measure of kidney function and indicates how well the kidneys are able to filter waste products from the blood. Dialysis is a medical procedure that helps perform the function of the kidneys by removing waste and excess fluid from the body.

Renal disease is not commonly seen as a presenting sign or symptom, but approximately a certain percentage of individuals may develop it. In the case of meningococcal septicaemia, patients usually experience acute illness along with abnormal observations and confusion. Immune thrombocytopenia (ITP) is known to cause easy bruising and nosebleeds, but it does not have the same distribution pattern as HSP and does not come with abdominal pain or joint pain. On the other hand, viral urticaria and roseola typically result in a rash that blanches.

Further Reading:

Henoch-Schonlein purpura (HSP) is a small vessel vasculitis that is mediated by IgA. It is commonly seen in children following an infection, with 90% of cases occurring in children under 10 years of age. The condition is characterized by a palpable purpuric rash, abdominal pain, gastrointestinal upset, and polyarthritis. Renal involvement occurs in approximately 50% of cases, with renal impairment typically occurring within 1 day to 1 month after the onset of other symptoms. However, renal impairment is usually mild and self-limiting, although 10% of cases may have serious renal impairment at presentation and 1% may progress to end-stage kidney failure long term. Treatment for HSP involves analgesia for arthralgia, and treatment for nephropathy is generally supportive. The prognosis for HSP is usually excellent, with the condition typically resolving fully within 4 weeks, especially in children without renal involvement. However, around 1/3rd of patients may experience relapses, which can occur for several months.

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

If individuals below the age of 45 experience four or more of the following symptoms, they should be referred for a potential diagnosis of spondyloarthritis:

– Presence of low back pain and being younger than 35 years old
– Waking up in the second half of the night due to pain
– Buttock pain
– Pain that improves with movement or within 48 hours of using nonsteroidal anti-inflammatory drugs (NSAIDs)
– Having a first-degree relative with spondyloarthritis
– History of current or past arthritis, psoriasis, or enthesitis.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This results in the accumulation of waste products and disturbances in fluid and electrolyte balance. 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, with approximately 15% of adults admitted to hospitals in the UK developing AKI.

The causes of AKI can be categorized into pre-renal, intrinsic renal, and post-renal factors. The majority of AKI cases in the community are due to pre-renal causes, accounting for 90% of cases. These are often associated with conditions such as hypotension from sepsis or fluid depletion. Medications, particularly ACE inhibitors and NSAIDs, are also frequently implicated in AKI.

The table below summarizes the most common causes of AKI:

Pre-renal:
– Volume depletion (e.g., hemorrhage, severe vomiting or diarrhea, burns)
– Oedematous states (e.g., cardiac failure, liver cirrhosis, nephrotic syndrome)
– Hypotension (e.g., cardiogenic shock, sepsis, anaphylaxis)
– Cardiovascular conditions (e.g., severe cardiac failure, arrhythmias)
– Renal hypoperfusion: NSAIDs, COX-2 inhibitors, ACE inhibitors or ARBs, Abdominal aortic aneurysm
– Renal artery stenosis
– Hepatorenal syndrome

Intrinsic renal:
– Glomerular disease (e.g., glomerulonephritis, thrombosis, hemolytic-uremic syndrome)
– Tubular injury: acute tubular necrosis (ATN) following prolonged ischemia
– Acute interstitial nephritis due to drugs (e.g., NSAIDs), infection, or autoimmune diseases
– Vascular disease (e.g., vasculitis, polyarteritis nodosa, thrombotic microangiopathy, cholesterol emboli, renal vein thrombosis, malignant hypertension)
– Eclampsia

Post-renal:
– Renal stones
– Blood clot
– Papillary necrosis
– Urethral stricture
– Prostatic hypertrophy or malignancy
– Bladder tumor
– Radiation fibrosis
– Pelvic malignancy
– Retroperitoneal fibrosis

Women who are 18 years or older and have a pelvic mass that is not clearly uterine fibroids should be promptly referred for assessment. In this case, an abdominal X-ray would not provide much useful information, and it is not advisable to take no action at this point. For more information, please refer to the NICE referral guidelines for suspected cancer.

Rapid tranquillisation involves the administration of medication through injection when oral medication is not feasible or appropriate and immediate sedation is necessary. The current guidelines from NICE recommend two options for rapid tranquillisation in adults: intramuscular lorazepam alone or a combination of intramuscular haloperidol and intramuscular promethazine. The choice of medication depends on various factors such as advanced statements, potential intoxication, previous responses to these medications, interactions with other drugs, and existing physical health conditions or pregnancy.

If there is insufficient information to determine the appropriate medication or if the individual has not taken antipsychotic medication before, intramuscular lorazepam is recommended. However, if there is evidence of cardiovascular disease or a prolonged QT interval, or if an electrocardiogram has not been conducted, the combination of intramuscular haloperidol and intramuscular promethazine should be avoided, and intramuscular lorazepam should be used instead.

If there is a partial response to intramuscular lorazepam, a second dose should be considered. If there is no response to intramuscular lorazepam, then intramuscular haloperidol combined with intramuscular promethazine should be considered. If there is a partial response to this combination, a further dose should be considered.

If there is no response to intramuscular haloperidol combined with intramuscular promethazine and intramuscular lorazepam has not been used yet, it should be considered. However, if intramuscular lorazepam has already been administered, it is recommended to arrange an urgent team meeting to review the situation and seek a second opinion if necessary.

After rapid tranquillisation, the patient should be closely monitored for any side effects, and their vital signs should be regularly checked, including heart rate, blood pressure, respiratory rate, temperature, hydration level, and level of consciousness. These observations should be conducted at least hourly until there are no further concerns about the patient’s physical health.

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

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

Further Reading:

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

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

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

In some cases, it can be challenging to determine if a patient had a true episode of anaphylaxis. In such cases, serum tryptase levels may be measured, as they remain elevated for up to 12 hours following an acute episode of anaphylaxis. This can help confirm the diagnosis and guide further management.

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

Loop diuretics, like furosemide, commonly result in several electrolyte imbalances. These imbalances include hyponatremia, which is a decrease in sodium levels in the blood. Another common imbalance is hypokalemia, which refers to low levels of potassium. Additionally, loop diuretics can cause hypocalcemia, a condition characterized by low levels of calcium in the blood. Another electrolyte affected by loop diuretics is magnesium, as they can lead to hypomagnesemia, which is a deficiency of magnesium. Lastly, loop diuretics can cause hypochloremic alkalosis, which is a condition characterized by low levels of chloride in the blood and an increase in blood pH.

Cauda equina syndrome (CES) is a rare but serious complication that can occur when a disc in the spine ruptures. This happens when the material from the disc is pushed into the spinal canal and puts pressure on a bundle of nerves in the lower back and sacrum. When this happens, it can lead to problems with controlling the bladder and bowels.

There are certain signs that may indicate the presence of CES, which are known as red flags. These include experiencing sciatica on both sides of the body, having a severe or worsening neurological deficit in both legs, such as significant weakness in the muscles that extend the knee, turn the ankle outward, or lift the foot upward. Other red flags include difficulty starting to urinate or a decreased sensation of the flow of urine, a loss of feeling when the rectum is full, a loss of sensation in the perianal, perineal, or genital areas (also known as saddle anesthesia or paresthesia), and a looseness in the anal sphincter muscle.

The Parkinson-plus syndromes are a group of neurodegenerative disorders that share similar features with Parkinson’s disease but also have additional clinical characteristics that set them apart from idiopathic Parkinson’s disease (iPD). These syndromes include Multiple System Atrophy (MSA), Progressive Supranuclear Palsy (PSP), Corticobasal degeneration (CBD), and Dementia with Lewy Bodies (DLB).

Multiple System Atrophy (MSA) is a less common condition than iPD and PSP. It is characterized by the loss of cells in multiple areas of the nervous system. MSA progresses rapidly, often leading to wheelchair dependence within 3-4 years of diagnosis. Some distinguishing features of MSA include autonomic dysfunction, bladder control problems, erectile dysfunction, blood pressure changes, early-onset balance problems, neck or facial dystonia, and a high-pitched voice.

To summarize the distinguishing features of the Parkinson-plus syndromes compared to iPD, the following table provides a comparison:

iPD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Typically starts at rest on one side of the body
– Levodopa response: Excellent response
– Mental changes: Depression
– Balance/falls: Late in the disease
– Common eye abnormalities: Dry eyes, trouble focusing

MSA:
– Symptom onset: Both sides equally affected
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

PSP:
– Symptom onset: Both sides equally affected
– Tremor: Less common, if present affects both sides
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Personality changes, depression
– Balance/falls: Within 1 year
– Common eye abnormalities: Dry eyes, difficulty in looking downwards

CBD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

Activated charcoal is a commonly used substance for decontamination in cases of poisoning. Its main function is to adsorb the molecules of the ingested toxin onto its surface.

Activated charcoal is a chemically inert form of carbon. It is a fine black powder that has no odor or taste. It is produced by subjecting carbonaceous matter to high heat, a process known as pyrolysis, and then treating it with a zinc chloride solution to increase its concentration. This process creates a network of pores within the charcoal, giving it a large absorptive area of approximately 3,000 m2/g. This allows it to effectively inhibit the absorption of toxins by up to 50%.

The usual dose of activated charcoal is 50 grams for adults and 1 gram per kilogram of body weight for children. It can be administered orally or through a nasogastric tube. It is important to administer it within one hour of ingestion, and it may be repeated after one hour if necessary.

However, there are certain situations where activated charcoal should not be used. These include cases where the patient is unconscious or in a coma, as there is a risk of aspiration. It should also be avoided if seizures are imminent, as there is a risk of aspiration. Additionally, if there is reduced gastrointestinal motility, activated charcoal should not be used to prevent the risk of obstruction.

Activated charcoal is effective in treating overdose with certain drugs and toxins, such as aspirin, paracetamol, barbiturates, tricyclic antidepressants, digoxin, amphetamines, morphine, cocaine, and phenothiazines. However, it is ineffective in cases of overdose with iron, lithium, boric acid, cyanide, ethanol, ethylene glycol, methanol, malathion, DDT, carbamate, hydrocarbon, strong acids, or alkalis.

There are potential adverse effects associated with the use of activated charcoal. These include nausea and vomiting, diarrhea, constipation, bezoar formation (a mass of undigested material that can cause blockages), bowel obstruction, pulmonary aspiration (inhalation of charcoal into the lungs), and impaired absorption of oral medications or antidotes.

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

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

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

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

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

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

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

The risk of infection is highest with femoral central lines.

A central venous catheter (CVC) is a type of catheter that is inserted into a large vein in the body, typically in the neck, chest, or groin. It has several important uses, including CVP monitoring, pulmonary artery pressure monitoring, repeated blood sampling, IV access for large volumes of fluids or drugs, TPN administration, dialysis, pacing, and other procedures such as placement of IVC filters or venous stents.

When inserting a central line, it is ideal to use ultrasound guidance to ensure accurate placement. However, there are certain contraindications to central line insertion, including infection or injury to the planned access site, coagulopathy, thrombosis or stenosis of the intended vein, a combative patient, or raised intracranial pressure for jugular venous lines.

The most common approaches for central line insertion are the internal jugular, subclavian, femoral, and PICC (peripherally inserted central catheter) veins. The internal jugular vein is often chosen due to its proximity to the carotid artery, but variations in anatomy can occur. Ultrasound can be used to identify the vessels and guide catheter placement, with the IJV typically lying superficial and lateral to the carotid artery. Compression and Valsalva maneuvers can help distinguish between arterial and venous structures, and doppler color flow can highlight the direction of flow.

In terms of choosing a side for central line insertion, the right side is usually preferred to avoid the risk of injury to the thoracic duct and potential chylothorax. However, the left side can also be used depending on the clinical situation.

Femoral central lines are another option for central venous access, with the catheter being inserted into the femoral vein in the groin. Local anesthesia is typically used to establish a field block, with lidocaine being the most commonly used agent. Lidocaine works by blocking sodium channels and preventing the propagation of action potentials.

In summary, central venous catheters have various important uses and should ideally be inserted using ultrasound guidance. There are contraindications to their insertion, and different approaches can be used depending on the clinical situation. Local anesthesia is commonly used for central line insertion, with lidocaine being the preferred agent.

Paracetamol overdose is the most common overdose in the U.K. and is also the leading cause of acute liver failure. The liver damage occurs due to a metabolite of paracetamol called N-acetyl-p-benzoquinoneimine (NAPQI), which depletes the liver’s glutathione stores and directly harms liver cells. Severe liver damage and even death can result from an overdose of more than 12 g or > 150 mg/kg body weight.

The clinical manifestations of paracetamol overdose can be divided into four stages:

Stage 1 (0-24 hours): Patients may not show any symptoms, but common signs include nausea, vomiting, and abdominal discomfort.

Stage 2 (24-48 hours): Right upper quadrant pain and tenderness develop, along with the possibility of hypoglycemia and reduced consciousness.

Stage 3 (48-96 hours): Hepatic failure begins, characterized by jaundice, coagulopathy, and encephalopathy. Loin pain, haematuria, and proteinuria may indicate early renal failure.

Stage 4 (> 96 hours): Hepatic failure worsens progressively, leading to cerebral edema, disseminated intravascular coagulation (DIC), and ultimately death.

The earliest and most sensitive indicator of liver damage is a prolonged INR, which starts to rise approximately 24 hours after the overdose. Liver function tests (LFTs) typically remain normal until 18 hours after the overdose. However, AST and ALT levels then sharply increase and can exceed 10,000 units/L by 72-96 hours. Bilirubin levels rise more slowly and peak around 5 days.

The primary treatment for paracetamol overdose is acetylcysteine. Acetylcysteine is a highly effective antidote, but its efficacy diminishes rapidly if administered more than 8 hours after a significant ingestion. Ingestions exceeding 75 mg/kg are considered significant.

Acetylcysteine should be given based on a 4-hour level or administered empirically if the presentation occurs more than 8 hours after a significant overdose. If the overdose is staggered or the timing is uncertain, empirical treatment is also recommended. The treatment regimen is as follows:

– First dose: 150 mg/kg in 200 mL 5% glucose over 1 hour
– Second dose 50 mg/kg in 500 mL 5% glucose over 4 hours
– Third dose 100 mg/kg in 1000 mL 5% glucose over 16 hours

Chancroid is a sexually transmitted infection caused by the bacteria Haemophilus ducreyi. It is not very common in the UK but is prevalent in Africa, Asia, and South America. HIV is often associated with chancroid, particularly in Africa where there is a 60% correlation.

The main symptom of chancroid is the development of painful ulcers on the genitalia. In women, these ulcers typically appear on the labia majora. Sometimes, kissing ulcers can form when ulcers are located on opposing surfaces of the labia. Painful swelling of the lymph nodes occurs in 30-60% of patients, and in some cases, these swollen nodes can turn into abscesses known as buboes.

The CDC recommends treating chancroid with a single oral dose of 1 gram of azithromycin or a single intramuscular dose of ceftriaxone. Alternatively, a 7-day course of oral erythromycin can be used. It’s important to note that Haemophilus ducreyi is resistant to several antibiotics, including penicillins, tetracyclines, trimethoprim, ciprofloxacin, aminoglycosides, and sulfonamides.

Possible complications of chancroid include extensive swelling of the lymph nodes, large abscesses and sinuses in the groin area, phimosis (a condition where the foreskin cannot be retracted), and superinfection with Fusarium spp. or Bacteroides spp.

Syphilis, caused by Treponema pallidum, presents with a painless ulcer called a chancre during its primary stage. This is different from chancroid, which causes painful ulcers. Chlamydia trachomatis can lead to lymphogranuloma venereum, where a painless genital ulcer may develop initially and go unnoticed. Granuloma inguinale, caused by Klebsiella granulomatis, causes painless nodules and ulcers on the genitals that eventually burst and create open, oozing lesions. Neisseria gonorrhoeae, on the other hand, typically causes vaginal or urethral discharge and is often asymptomatic, rather than causing genital ulceration.