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

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

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

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

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

Further Reading:

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

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

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

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

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

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

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

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

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In this case, the patient has already received two doses of benzodiazepine and is currently on a phenytoin infusion. However, despite these treatments, the seizures persist, and it has been 20 minutes since the infusion started. At this point, the preferred treatment option is to induce general anesthesia. The induction agents that can be considered include thiopental sodium, propofol, and midazolam. There is no need to administer intravenous thiamine in this situation.

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

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

2nd stage (0-30 minutes):
– Implement regular monitoring
– Consider the possibility of non-epileptic status
– Initiate emergency antiepileptic drug (AED) therapy
– Perform emergency investigations
– Administer glucose or intravenous thiamine if alcohol abuse or impaired nutrition is suspected
– Treat severe acidosis if present

3rd stage (0-60 minutes):
– Determine the underlying cause of status epilepticus
– Notify the anesthetist and intensive care unit (ITU)
– Identify and treat any medical complications
– Consider pressor therapy if necessary

4th stage (30-90 minutes):
– Transfer the patient to the intensive care unit
– Establish intensive care and EEG monitoring
– Initiate long-term maintenance AED therapy
– Perform further investigations as needed, such as brain imaging or lumbar puncture

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

Monitoring during the management of status epilepticus involves regular neurological observations and measurements of pulse, blood pressure, and temperature.

Croup is usually preceded by symptoms such as cough, runny nose, and nasal congestion. These symptoms typically occur 12 to 72 hours before the onset of a distinctive barking cough. The barking cough, which resembles the sound of a seal, is particularly severe at night. It is important to note that the cough may be preceded by prodromal upper respiratory tract symptoms, including cough, runny nose, and nasal congestion, within a timeframe of 12 to 72 hours.

Further Reading:

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

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

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

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

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

Addison’s disease occurs when the adrenal glands do not produce enough steroid hormones. This includes glucocorticoids, mineralocorticoids, and sex steroids. The most common cause is autoimmune adrenalitis, which accounts for about 70-80% of cases. It is more prevalent in women and typically occurs between the ages of 30 and 50.

The clinical symptoms of Addison’s disease include weakness, lethargy, low blood pressure (especially when standing up), nausea, vomiting, weight loss, reduced hair in the armpits and pubic area, depression, and hyperpigmentation (darkening of the skin in certain areas like the palms, mouth, and exposed skin).

Biochemically, Addison’s disease is characterized by increased levels of ACTH (a hormone that tries to stimulate the adrenal glands), low sodium levels, high potassium levels, high calcium levels, low blood sugar, and metabolic acidosis.

People with Addison’s disease have a higher risk of developing type 1 diabetes, Hashimoto’s thyroiditis, Grave’s disease, premature ovarian failure, pernicious anemia, vitiligo, and alopecia.

Management of Addison’s disease should be overseen by an Endocrinologist. Treatment typically involves taking hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also need thyroxine if there is hypothalamic-pituitary disease present. Treatment is lifelong, and patients should carry a steroid card and a MedicAlert bracelet in case of an Addisonian crisis.

Etomidate is a derivative of imidazole that is commonly used to induce anesthesia due to its short-acting nature. Its main mechanism of action is believed to involve the modulation of fast inhibitory synaptic transmission within the central nervous system by acting on GABA type A receptors.

This patient has been diagnosed with primary biliary cirrhosis (PBC). PBC is a liver disease caused by an autoimmune response, leading to the progressive destruction of the small bile ducts in the liver. The damage primarily affects the intralobular ducts. As a result, the patient experiences cholestatic jaundice, followed by liver fibrosis and cirrhosis. PBC is more common in females, with 90% of patients being women. It typically occurs between the ages of 30 and 65. Liver function tests show elevated levels of alkaline phosphatase (ALP), often before any symptoms appear. Antimitochondrial antibodies are positive in 95% of cases. Around 50% of patients have smooth muscle antibodies (SMA), and approximately 20% have antinuclear antibodies (ANA). IgM levels are raised in over 80% of cases.

Autoimmune hepatitis is liver inflammation caused by a decrease in regulatory T-cells (Treg cells), leading to the production of autoantibodies against hepatocyte surface antigens. It mainly affects women (70%) between the ages of 15 and 40. The condition causes chronic, progressive hepatitis, which eventually progresses to cirrhosis. Patients typically present with non-specific symptoms of malaise, although in some cases, the disease may be more advanced, resulting in jaundice and severe illness. In later stages, liver function tests show significantly elevated levels of transaminases (ALT and AST), often exceeding ten times the normal range. Alkaline phosphatase (ALP) levels are usually normal or slightly elevated. Antinuclear antibodies (ANA) are positive in approximately 80% of cases, while smooth muscle antibodies (SMA) are positive in around 70% of cases. Antimitochondrial antibodies are typically low or absent.

Primary sclerosing cholangitis (PSC) is a condition that causes progressive inflammation and obstruction of the bile ducts. It is characterized by recurrent episodes of cholangitis and the gradual scarring of the bile ducts. PSC can eventually lead to liver cirrhosis, liver failure, and hepatocellular carcinoma. There is a known association between PSC and ulcerative colitis, with over 80% of PSC patients also having ulcerative colitis.

Hepatic damage caused by hydroxychloroquine is extremely rare.

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

To perform the Weber’s test, the 512 Hz tuning fork should be set in motion and then placed on the center of the patient’s forehead. The patient should be asked if they perceive the sound in the middle of their forehead or if it is heard more on one side.

If the sound is heard more on one side, it may indicate either ipsilateral conductive hearing loss or contralateral sensorineural hearing loss.

Desmopressin, a common treatment for cranial diabetes insipidus (DI) following pituitary surgery, can often lead to hyponatremia as a side effect. Therefore, it is important for patients to have their electrolyte levels regularly monitored. Symptoms of hyponatremia may include nausea, vomiting, headache, confusion, lethargy, fatigue, restlessness, irritability, muscle weakness or spasms, seizures, and drowsiness (which can progress to coma in severe cases).

Further Reading:

Diabetes insipidus (DI) is a condition characterized by either a decrease in the secretion of antidiuretic hormone (cranial DI) or insensitivity to antidiuretic hormone (nephrogenic DI). Antidiuretic hormone, also known as arginine vasopressin, is produced in the hypothalamus and released from the posterior pituitary. The typical biochemical disturbances seen in DI include elevated plasma osmolality, low urine osmolality, polyuria, and hypernatraemia.

Cranial DI can be caused by various factors such as head injury, CNS infections, pituitary tumors, and pituitary surgery. Nephrogenic DI, on the other hand, can be genetic or result from electrolyte disturbances or the use of certain drugs. Symptoms of DI include polyuria, polydipsia, nocturia, signs of dehydration, and in children, irritability, failure to thrive, and fatigue.

To diagnose DI, a 24-hour urine collection is done to confirm polyuria, and U&Es will typically show hypernatraemia. High plasma osmolality with low urine osmolality is also observed. Imaging studies such as MRI of the pituitary, hypothalamus, and surrounding tissues may be done, as well as a fluid deprivation test to evaluate the response to desmopressin.

Management of cranial DI involves supplementation with desmopressin, a synthetic form of arginine vasopressin. However, hyponatraemia is a common side effect that needs to be monitored. In nephrogenic DI, desmopressin supplementation is usually not effective, and management focuses on ensuring adequate fluid intake to offset water loss and monitoring electrolyte levels. Causative drugs need to be stopped, and there is a risk of developing complications such as hydroureteronephrosis and an overdistended bladder.

The Insall-Salvati ratio is determined by dividing the length of the patellar tendon (TL) by the length of the patella (PL). This ratio is used to compare the relative lengths of these two structures. A normal ratio is typically 1:1.

Further Reading:

A quadriceps tendon tear or rupture is a traumatic lower limb and joint injury that occurs when there is heavy loading on the leg, causing forced contraction of the quadriceps while the foot is planted and the knee is partially bent. These tears most commonly happen at the osteotendinous junction between the tendon and the superior pole of the patella. Quadriceps tendon ruptures are more common than patellar tendon ruptures.

When a quadriceps tendon tear occurs, the patient usually experiences a tearing sensation and immediate pain. They will then typically complain of pain around the knee and over the tendon. Clinically, there will often be a knee effusion and weakness or inability to actively extend the knee.

In cases of complete quadriceps tears, the patella will be displaced distally, resulting in a low lying patella or patella infera, also known as patella baja. Radiological measurements, such as the Insall-Salvati ratio, can be used to measure patella height. The Insall-Salvati ratio is calculated by dividing the patellar tendon length by the patellar length. A normal ratio is between 0.8 to 1.2, while a low lying patella (patella baja) is less than 0.8 and a high lying patella (patella alta) is greater than 1.2.

Malignant otitis externa (MOE), also known as necrotizing otitis externa, is a rare form of ear canal infection that primarily affects elderly diabetic patients, particularly those with poorly controlled diabetes.

MOE initially infects the ear canal and gradually spreads to the surrounding bony structures and soft tissues. In 98% of cases, the responsible pathogen is Pseudomonas aeruginosa.

Typically, MOE presents with severe and unrelenting ear pain, which tends to worsen at night. Even after the swelling of the ear canal subsides with topical antibiotics, the pain may persist. Other symptoms may include pus drainage from the ear and temporal headaches. Approximately 50% of patients also experience facial nerve paralysis, and cranial nerves IX to XII may be affected as well.

To confirm the diagnosis, technetium scanning and contrast-enhanced CT scanning are usually performed to detect any extension of the infection into the surrounding bony structures.

If left untreated, MOE can be life-threatening and may lead to serious complications such as skull base osteomyelitis, subdural empyema, and cerebral abscess.

Treatment typically involves long-term administration of intravenous antibiotics. While surgical intervention is not effective for MOE, exploratory surgery may be necessary to obtain cultures of unusual organisms that are not responding adequately to intravenous antibiotics.

Anticholinergic drugs work by blocking the effects of acetylcholine, a neurotransmitter, in both the central and peripheral nervous systems. These drugs are commonly used in clinical practice and include antihistamines, typical and atypical antipsychotics, anticonvulsants, antidepressants, antispasmodics, antiemetics, antiparkinsonian agents, antimuscarinics, and certain plants. When someone ingests an anticholinergic drug, they may experience a toxidrome, which is characterized by an agitated delirium and various signs of acetylcholine receptor blockade in the central and peripheral systems.

The central effects of anticholinergic drugs result in an agitated delirium, which is marked by fluctuating mental status, confusion, restlessness, visual hallucinations, picking at objects in the air, mumbling, slurred speech, disruptive behavior, tremor, myoclonus, and in rare cases, coma or seizures. On the other hand, the peripheral effects can vary and may include dilated pupils, sinus tachycardia, dry mouth, hot and flushed skin, increased body temperature, urinary retention, and ileus.

The BTS guidelines for managing acute asthma in adults provide the following recommendations:

Oxygen:
– It is important to give supplementary oxygen to all patients with acute severe asthma who have low levels of oxygen in their blood (hypoxemia). The goal is to maintain a blood oxygen saturation level (SpO2) between 94-98%. Even if pulse oximetry is not available, oxygen should still be administered.

β2 agonists therapy:
– High-dose inhaled β2 agonists should be used as the first-line treatment for patients with acute asthma. It is important to administer these medications as early as possible.
– Intravenous β2 agonists should be reserved for patients who cannot reliably use inhaled therapy.
– For patients with life-threatening asthma symptoms, nebulized β2 agonists driven by oxygen are recommended.
– In cases of severe asthma that does not respond well to an initial dose of β2 agonist, continuous nebulization with an appropriate nebulizer may be considered.

Ipratropium bromide:
– Nebulized ipratropium bromide (0.5 mg every 4-6 hours) should be added to β2 agonist treatment for patients with acute severe or life-threatening asthma, or those who do not respond well to initial β2 agonist therapy.

Steroid therapy:
– Steroids should be given in adequate doses for all cases of acute asthma attacks.
– Prednisolone should be continued at a dose of 40-50 mg daily for at least five days or until the patient recovers.

Other therapies:
– Nebulized magnesium is not recommended for the treatment of acute asthma in adults.
– A single dose of intravenous magnesium sulfate may be considered for patients with acute severe asthma (peak expiratory flow rate <50% of the best or predicted value) who do not respond well to inhaled bronchodilator therapy. However, this should only be done after consulting with senior medical staff.
– Routine prescription of antibiotics is not necessary for patients with acute asthma.

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

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

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

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

Sphincterotomy, a surgical procedure, should be reserved for cases where the fissure does not heal with conservative measures. It has a success rate of 90%.

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.

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

Further Reading:

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

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

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

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

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

For adults, it is recommended to perform chest compressions at a rate of 100-120 compressions per minute. The depth of the compressions should be at least 5-6 cm.

Further Reading:

In the event of an adult experiencing cardiorespiratory arrest, it is crucial for doctors to be familiar with the Advanced Life Support (ALS) algorithm. They should also be knowledgeable about the proper technique for chest compressions, the appropriate rhythms for defibrillation, the reversible causes of arrest, and the drugs used in advanced life support.

During chest compressions, the rate should be between 100-120 compressions per minute, with a depth of compression of 5-6 cm. The ratio of chest compressions to rescue breaths should be 30:2. It is important to change the person giving compressions regularly to prevent fatigue.

There are two shockable ECG rhythms that doctors should be aware of: ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT). These rhythms require defibrillation.

There are four reversible causes of cardiorespiratory arrest, known as the 4 H’s and 4 T’s. The 4 H’s include hypoxia, hypovolemia, hypo or hyperkalemia or metabolic abnormalities, and hypothermia. The 4 T’s include thrombosis (coronary or pulmonary), tension pneumothorax, tamponade, and toxins. Identifying and treating these reversible causes is crucial for successful resuscitation.

When it comes to resus drugs, they are considered of secondary importance during CPR due to the lack of high-quality evidence for their efficacy. However, adrenaline (epinephrine) and amiodarone are the two drugs included in the ALS algorithm. Doctors should be familiar with the dosing, route, and timing of administration for both drugs.

Adrenaline should be administered intravenously at a concentration of 1 in 10,000 (100 micrograms/mL). It should be repeated every 3-5 minutes. Amiodarone is initially given at a dose of 300 mg, either from a pre-filled syringe or diluted in 20 mL of Glucose 5%. If required, an additional dose of 150 mg can be given by intravenous injection. This is followed by an intravenous infusion of 900 mg over 24 hours. The first dose of amiodarone is given after 3 shocks.

The most recent guidelines from the National Institute for Health and Care Excellence (NICE) recommend using a LNG-IUS, such as Mirena IUS, as the initial treatment for heavy menstrual bleeding (HMB) in women who have no identified pathology, fibroids smaller than 3 cm without uterine cavity distortion, or suspected/diagnosed adenomyosis. If a woman declines or cannot use an LNG-IUS, alternative pharmacological treatments can be considered. These include non-hormonal options like Tranexamic acid or NSAIDs, as well as hormonal options like combined hormonal contraception or cyclical oral progestogens. to the NICE guidelines on the assessment and management of heavy menstrual bleeding.

This individual, who has been smoking for a long time, is likely to have squamous cell carcinoma of the lung located at the right apex. This particular type of cancer is causing Pancoast’s syndrome. Pancoast’s syndrome typically presents with rib erosion, leading to severe shoulder pain, as well as Horner’s syndrome due to the infiltration of the lower part of the brachial plexus. Additionally, there may be hoarseness of the voice and a ‘bovine cough’ due to a concurrent recurrent laryngeal nerve palsy.

The classic description of Horner’s syndrome includes the following clinical features on the same side as the tumor: miosis (constricted pupil), ptosis (drooping eyelid), anhidrosis (lack of sweating), and enophthalmos (sunken appearance of the eye). A chest X-ray would be able to detect the presence of the apical tumor and confirm the diagnosis.

Subfalcine herniation occurs when a mass in one side of the brain causes the cingulate gyrus to be pushed under the falx cerebri. This condition often leads to specific neurological symptoms. These symptoms include a motor deficit in the lower limb on the opposite side of the body, bladder incontinence, motor and sensory deficits on the same side of the body as the herniation, and difficulty with speech (dysarthria).

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.

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

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

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

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

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

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

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

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

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

Balanitis is the inflammation of the glans, which is the end of the penis. It often occurs alongside inflammation of the foreskin. Balanitis is a common condition that can affect individuals of any age. However, it is most commonly seen in boys under the age of four who have not undergone circumcision. The main symptoms include redness, irritation, and soreness of the glans. In some cases, it may be difficult to retract the foreskin, and there may be discomfort during urination.

There are various factors that can cause balanitis. These include poor hygiene, a non-retractile foreskin condition called phimosis, dermatological conditions like psoriasis, infections such as candidal infection, and allergies. In most cases, balanitis can be diagnosed based on clinical examination. However, if there is uncertainty, a swab may be taken for further investigation.

Treatment for balanitis involves practicing good hygiene and gently cleaning the affected area. If a candidal infection is suspected, clotrimazole may be used. Additionally, a mild steroid cream is often prescribed to reduce inflammation. In cases where recurrent balanitis is caused by phimosis, circumcision may be considered as a potential treatment option.

Adrenaline is known to cause vasoconstriction, which is the narrowing of blood vessels. As a result, it is not recommended to use adrenaline in areas such as the peripheries, end arteries, and flap lacerations because it can increase the risk of ischemia, which is a lack of blood supply to tissues. Additionally, there are certain contraindications to using adrenaline locally, including conditions like pheochromocytoma, hypertension, and arteriosclerosis. It is important to be cautious of these factors as adrenaline’s vasoconstrictive effects can also lead to an elevation in blood pressure.

Further Reading:

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

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

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

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

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

This individual has presented with an episode of acute asthma. Upon assessment, his initial peak flow is measured at 55% of his personal best, indicating a moderate exacerbation. In such cases, it is recommended to administer steroids, with a suggested dose of prednisolone 40-50 mg taken orally as the initial management step.

Currently, the use of nebulized magnesium sulfate is not recommended for the treatment of acute asthma in adults. However, according to the current ALS guidelines, in severe or life-threatening asthma cases, IV aminophylline can be considered after seeking senior advice. If used, a loading dose of 5 mg/kg should be given over 20 minutes, followed by an infusion of 500-700 mcg/kg/hour. It is important to maintain serum theophylline levels below 20 mcg/ml to prevent toxicity.

In situations where inhaled therapy is not possible, such as when a patient is receiving bag-mask ventilation, IV salbutamol can be considered at a slow dose of 250 mcg. However, it should be noted that there is currently no evidence supporting the use of leukotriene receptor antagonists, like montelukast, in the management of acute asthma.

The BTS guidelines classify acute asthma into four categories: moderate, acute severe, life-threatening, and near-fatal. Moderate asthma is characterized by increasing symptoms and a peak expiratory flow rate (PEFR) between 50-75% of the individual’s best or predicted value, with no features of acute severe asthma. Acute severe asthma is identified by a PEFR of 33-50% of the best or predicted value, along with respiratory rate >25/min, heart rate >110/min, or the inability to complete sentences in one breath.

Life-threatening asthma is indicated by a PEFR <33% of the best or predicted value, SpO2 <92%, PaO2 <8 kPa, normal PaCO2 (4.6-6.0 kPa), and additional symptoms such as silent chest, cyanosis, poor respiratory effort, arrhythmia, exhaustion, altered conscious level, or hypotension. Near-fatal asthma is characterized by raised PaCO2 and/or the need for mechanical ventilation with raised inflation pressures.

Tryptase levels can be a valuable tool in diagnosing anaphylaxis. During an anaphylactic reaction, mast cell tryptase is released and can be measured in the blood. Research suggests that tryptase levels reach their highest point in the blood within 1 minute to 6 hours after the reaction begins, typically peaking around 1-2 hours after the onset of symptoms. This information is crucial for diagnosing and treating anaphylaxis, especially in cases where the diagnosis is uncertain. It’s important to note that tryptase levels may return to normal within 6 hours, so the timing of blood samples is crucial. The current recommendation is to take three tryptase level measurements: one as soon as resuscitation begins, another 1-2 hours after symptoms start, and a third 24 hours later or during the recovery period. It’s worth mentioning that some individuals may have elevated baseline tryptase levels, which should be taken into consideration during the diagnosis process.

Further Reading:

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

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

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

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

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

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.

Sodium bicarbonate is recommended as a treatment for TCA overdose according to the latest guidelines from RCEM and NPIS in 2021. Previous editions also suggested using glucagon if IV fluids and sodium bicarbonate were ineffective in treating the overdose.

Further Reading:

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

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

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

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

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

Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, the basal metabolic rate decreases and cell signaling between neurons decreases, leading to reduced tissue perfusion. This can result in depressed myocardial contractility, vasoconstriction, ventilation-perfusion mismatch, and increased blood viscosity. Symptoms of hypothermia progress as the core temperature drops, starting with compensatory increases in heart rate and shivering, and eventually leading to bradyarrhythmias, prolonged PR, QRS, and QT intervals, and cardiac arrest.

In the management of hypothermic cardiac arrest, ALS should be initiated with some modifications. The pulse check during CPR should be prolonged to 1 minute due to difficulty in obtaining a pulse. Rewarming the patient is important, and mechanical ventilation may be necessary due to stiffness of the chest wall. Drug metabolism is slowed in hypothermic patients, so dosing of drugs should be adjusted or withheld. Electrolyte disturbances are common in hypothermic patients and should be corrected.

Frostbite refers to a freezing injury to human tissue and occurs when tissue temperature drops below 0ºC. It can be classified as superficial or deep, with superficial frostbite affecting the skin and subcutaneous tissues, and deep frostbite affecting bones, joints, and tendons. Frostbite can be classified from 1st to 4th degree based on the severity of the injury. Risk factors for frostbite include environmental factors such as cold weather exposure and medical factors such as peripheral vascular disease and diabetes.

Signs and symptoms of frostbite include skin changes, cold sensation or firmness to the affected area, stinging, burning, or numbness, clumsiness of the affected extremity, and excessive sweating, hyperemia, and tissue gangrene. Frostbite is diagnosed clinically and imaging may be used in some cases to assess perfusion or visualize occluded vessels. Management involves moving the patient to a warm environment, removing wet clothing, and rapidly rewarming the affected tissue. Analgesia should be given as reperfusion is painful, and blisters should be de-roofed and aloe vera applied. Compartment syndrome is a risk and should be monitored for. Severe cases may require surgical debridement of amputation.

The top priority when dealing with suspected epiglottitis is to assess and secure the airway. This is especially important in patients who have not been vaccinated against Haemophilus influenzae type b (HiB), as they are at risk for complications from this infection. Classic signs of epiglottitis include tripod positioning, drooling, stridor, and a muffled voice. It is crucial to avoid agitating patients, particularly children, during examination or procedures, as this can trigger laryngospasm and potentially lead to airway obstruction. In such cases, it is recommended to call in senior ENT and anaesthetic support to perform laryngoscopy and be prepared for intubation or tracheostomy if necessary to address any airway compromise. If the patient is in a critical condition, securing the airway through intubation becomes the top priority.

Further Reading:

Epiglottitis is a rare but serious condition characterized by inflammation and swelling of the epiglottis, which can lead to a complete blockage of the airway. It is more commonly seen in children between the ages of 2-6, but can also occur in adults, particularly those in their 40s and 50s. Streptococcus infections are now the most common cause of epiglottitis in the UK, although other bacterial agents, viruses, fungi, and iatrogenic causes can also be responsible.

The clinical features of epiglottitis include a rapid onset of symptoms, high fever, sore throat, painful swallowing, muffled voice, stridor and difficulty breathing, drooling of saliva, irritability, and a characteristic tripod positioning with the arms forming the front two legs of the tripod. It is important for healthcare professionals to avoid examining the throat or performing any potentially upsetting procedures until the airway has been assessed and secured.

Diagnosis of epiglottitis is typically made through fibre-optic laryngoscopy, which is considered the gold standard investigation. Lateral neck X-rays may also show a characteristic thumb sign, indicating an enlarged and swollen epiglottis. Throat swabs and blood cultures may be taken once the airway is secured to identify the causative organism.

Management of epiglottitis involves assessing and securing the airway as the top priority. Intravenous or oral antibiotics are typically prescribed, and supplemental oxygen may be given if intubation or tracheostomy is planned. In severe cases where the airway is significantly compromised, intubation or tracheostomy may be necessary. Steroids may also be used, although the evidence for their benefit is limited.

Overall, epiglottitis is a potentially life-threatening condition that requires urgent medical attention. Prompt diagnosis, appropriate management, and securing the airway are crucial in ensuring a positive outcome for patients with this condition.