The therapeutic range for lithium typically falls between 0.4-0.8 mmol/l, although this range may differ depending on the laboratory. In general, the lower end of the range is the desired level for maintenance therapy and treatment in older individuals. Toxic effects are typically observed when levels exceed 1.5 mmol/l.

This patient has presented with an Addisonian crisis, which is a rare but potentially catastrophic condition if not diagnosed promptly. The most likely underlying rheumatological diagnosis in this case is polymyalgia rheumatica, and it is likely that the GP started the patient on prednisolone medication.

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

An Addisonian crisis is most commonly triggered by the deliberate or accidental withdrawal of steroid therapy in patients with Addison’s disease. Other factors that can precipitate a crisis include infection, trauma, myocardial infarction, cerebral infarction, asthma, hypothermia, and alcohol abuse.

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

Biochemically, Addison’s disease is characterized by increased ACTH levels (as a compensatory response to stimulate the adrenal glands), elevated serum renin levels, hyponatremia, hyperkalemia, hypercalcemia, hypoglycemia, and metabolic acidosis. Diagnostic investigations may include the Synacthen test, plasma ACTH level, plasma renin level, and adrenocortical antibodies.

Management of Addison’s disease should be overseen by an Endocrinologist. Typically, patients require 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, being aware of the possibility of an Addisonian crisis.

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

Further Reading:

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

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

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

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

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

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

The duration of the pause in chest compressions should be kept short, not exceeding 5 seconds. This applies to both pausing to assess the rhythm and pausing to administer a shock if the rhythm is deemed shockable. It is important to note that a pulse check lasting less than two seconds may fail to detect a palpable pulse, particularly in individuals with a slow heart rate (bradycardia).

Further Reading:

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

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

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

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

If a child who is experiencing convulsions reaches step 3 of the APLS algorithm, it is recommended to prepare a phenytoin infusion. This infusion should be administered at a dosage of 20 mg/kg over a period of 20 minutes.

Most nosebleeds, also known as epistaxis, occur at a specific area called Little’s area.

Epistaxis, or nosebleed, is a common condition that can occur in both children and older adults. It is classified as either anterior or posterior, depending on the location of the bleeding. Anterior epistaxis usually occurs in younger individuals and arises from the nostril, most commonly from an area called Little’s area. These bleeds are usually not severe and account for the majority of nosebleeds seen in hospitals. Posterior nosebleeds, on the other hand, occur in older patients with conditions such as hypertension and atherosclerosis. The bleeding in posterior nosebleeds is likely to come from both nostrils and originates from the superior or posterior parts of the nasal cavity or nasopharynx.

The management of epistaxis involves assessing the patient for signs of instability and implementing measures to control the bleeding. Initial measures include sitting the patient upright with their upper body tilted forward and their mouth open. Firmly pinching the cartilaginous part of the nose for 10-15 minutes without releasing the pressure can also help stop the bleeding. If these measures are successful, a cream called Naseptin or mupirocin nasal ointment can be prescribed for further treatment.

If bleeding persists after the initial measures, nasal cautery or nasal packing may be necessary. Nasal cautery involves using a silver nitrate stick to cauterize the bleeding point, while nasal packing involves inserting nasal tampons or inflatable nasal packs to stop the bleeding. In cases of posterior bleeding, posterior nasal packing or surgery to tie off the bleeding vessel may be considered.

Complications of epistaxis can include nasal bleeding, hypovolemia, anemia, aspiration, and even death. Complications specific to nasal packing include sinusitis, septal hematoma or abscess, pressure necrosis, toxic shock syndrome, and apneic episodes. Nasal cautery can lead to complications such as septal perforation and caustic injury to the surrounding skin.

In children under the age of 2 presenting with epistaxis, it is important to refer them for further investigation as an underlying cause is more likely in this age group.

SCUBA divers face the potential danger of developing pulmonary barotrauma, which can lead to conditions like arterial gas embolism (AGE) or pneumothorax. Based on the patient’s diving history and clinical symptoms, it is highly likely that they are experiencing a left-sided pneumothorax caused by barotrauma. To confirm the presence of pneumothorax, a chest X-ray is usually performed, unless the patient shows signs of tension pneumothorax. In such cases, immediate decompression is necessary, which can be achieved by inserting a chest tube.

Further Reading:

Decompression illness (DCI) is a term that encompasses both decompression sickness (DCS) and arterial gas embolism (AGE). When diving underwater, the increasing pressure causes gases to become more soluble and reduces the size of gas bubbles. As a diver ascends, nitrogen can come out of solution and form gas bubbles, leading to decompression sickness or the bends. Boyle’s and Henry’s gas laws help explain the changes in gases during changing pressure.

Henry’s law states that the amount of gas that dissolves in a liquid is proportional to the partial pressure of the gas. Divers often use atmospheres (ATM) as a measure of pressure, with 1 ATM being the pressure at sea level. Boyle’s law states that the volume of gas is inversely proportional to the pressure. As pressure increases, volume decreases.

Decompression sickness occurs when nitrogen comes out of solution as a diver ascends. The evolved gas can physically damage tissue by stretching or tearing it as bubbles expand, or by provoking an inflammatory response. Joints and spinal nervous tissue are commonly affected. Symptoms of primary damage usually appear immediately or soon after a dive, while secondary damage may present hours or days later.

Arterial gas embolism occurs when nitrogen bubbles escape into the arterial circulation and cause distal ischemia. The consequences depend on where the embolism lodges, ranging from tissue ischemia to stroke if it lodges in the cerebral arterial circulation. Mechanisms for distal embolism include pulmonary barotrauma, right to left shunt, and pulmonary filter overload.

Clinical features of decompression illness vary, but symptoms often appear within six hours of a dive. These can include joint pain, neurological symptoms, chest pain or breathing difficulties, rash, vestibular problems, and constitutional symptoms. Factors that increase the risk of DCI include diving at greater depth, longer duration, multiple dives close together, problems with ascent, closed rebreather circuits, flying shortly after diving, exercise shortly after diving, dehydration, and alcohol use.

Diagnosis of DCI is clinical, and investigations depend on the presentation. All patients should receive high flow oxygen, and a low threshold for ordering a chest X-ray should be maintained. Hydration is important, and IV fluids may be necessary. Definitive treatment is recompression therapy in a hyperbaric oxygen chamber, which should be arranged as soon as possible. Entonox should not be given, as it will increase the pressure effect in air spaces.

Transient global amnesia (TGA) is a neurological condition where individuals experience a temporary loss of short-term memory. This disorder is commonly observed in individuals over the age of 50 and is often associated with migraines.

The onset of TGA is typically sudden and can occur after engaging in strenuous exercise, sexual activity, or exposure to cold temperatures. These episodes usually last for a few hours and almost always resolve within 24 hours. One distinctive characteristic of TGA is perseveration, where patients repetitively ask the same question. Interestingly, once the episode has passed, individuals are unable to recall it.

Unlike a transient ischemic attack, TGA does not result in any focal neurological deficits, and the patient’s physical examination will appear normal.

On the other hand, a fugue state also involves temporary memory loss but presents differently. It is characterized by a loss of personal identity, past memories, and personality traits. Individuals experiencing a fugue state may even adopt entirely new identities and often engage in unplanned travel away from familiar surroundings.

First-generation antipsychotics, also known as conventional or typical antipsychotics, are powerful blockers of the dopamine D2 receptor. However, each drug in this category has different effects on other receptors, such as serotonin type 2 (5-HT2), alpha1, histaminic, and muscarinic receptors.

These first-generation antipsychotics are known to have a high incidence of extrapyramidal side effects, which include rigidity, bradykinesia, dystonias, tremor, akathisia, tardive dyskinesia, and neuroleptic malignant syndrome (NMS). NMS is a rare and life-threatening reaction to neuroleptic medications, characterized by fever, muscle stiffness, changes in mental state, and dysfunction of the autonomic nervous system. NMS typically occurs shortly after starting or increasing the dose of neuroleptic treatment.

On the other hand, second-generation antipsychotics, also referred to as novel or atypical antipsychotics, are dopamine D2 antagonists, except for aripiprazole. These medications are associated with lower rates of extrapyramidal side effects and NMS compared to the first-generation antipsychotics. However, they have higher rates of metabolic side effects and weight gain.

It is important to note that serotonin syndrome shares similar features with NMS but can be distinguished by the causative agent, most commonly the serotonin-specific reuptake inhibitors.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This results in the accumulation of urea and other waste products in the body and disrupts the balance of fluids and electrolytes. 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 that develop outside of healthcare settings are due to pre-renal causes, accounting for 90% of cases. These causes typically involve low blood pressure associated with conditions like sepsis and fluid depletion. Medications, particularly ACE inhibitors and NSAIDs, are also frequently implicated.

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

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

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

The main sensory supply to the back of the scalp comes from the C2 and C3 cervical nerves. The scalp receives innervation from branches of both the trigeminal nerve and the cervical nerves, as depicted in the illustration in the notes. The C2 and C3 cervical nerves are primarily responsible for supplying sensation to the posterior scalp.

Further Reading:

The scalp is the area of the head that is bordered by the face in the front and the neck on the sides and back. It consists of several layers, including the skin, connective tissue, aponeurosis, loose connective tissue, and periosteum of the skull. These layers provide protection and support to the underlying structures of the head.

The blood supply to the scalp primarily comes from branches of the external carotid artery and the ophthalmic artery, which is a branch of the internal carotid artery. These arteries provide oxygen and nutrients to the scalp tissues.

The scalp also has a complex venous drainage system, which is divided into superficial and deep networks. The superficial veins correspond to the arterial branches and are responsible for draining blood from the scalp. The deep venous network is drained by the pterygoid venous plexus.

In terms of innervation, the scalp receives sensory input from branches of the trigeminal nerve and the cervical nerves. These nerves transmit sensory information from the scalp to the brain, allowing us to perceive touch, pain, and temperature in this area.

Drug-induced acute dystonic reactions are frequently seen in the Emergency Department. These reactions occur in approximately 0.5% to 1% of patients who have been administered metoclopramide or prochlorperazine. Procyclidine, an anticholinergic medication, has proven to be effective in treating drug-induced parkinsonism, akathisia, and acute dystonia. In emergency situations, a dose of 10 mg IV of procyclidine can be administered to promptly treat acute drug-induced dystonic reactions.

According to NICE guidelines, when treating a campylobacter infection, clarithromycin is recommended as the first choice of antibiotic. Antibiotics are typically only prescribed for individuals with severe symptoms, such as a high fever, bloody or frequent diarrhea, or for those who have a weakened immune system, like this patient who has diabetes. NICE advises a dosage of clarithromycin 250-500 mg taken twice daily for a duration of 5-7 days. It is best to start treatment within 3 days of the onset of illness.

Further Reading:

Campylobacter jejuni is a common cause of gastrointestinal infections, particularly travellers diarrhoea. It is a gram-negative bacterium that appears as curved rods. The infection is transmitted through the feco-oral route, often through the ingestion of contaminated meat, especially poultry. The incubation period for Campylobacter jejuni is typically 1-7 days, and the illness usually lasts for about a week.

The main symptoms of Campylobacter jejuni infection include watery, and sometimes bloody, diarrhea accompanied by abdominal cramps, fever, malaise, and headache. In some cases, complications can arise from the infection. Guillain-Barre syndrome (GBS) is one such complication that is associated with Campylobacter jejuni. Approximately 30% of GBS cases are caused by this bacterium.

When managing Campylobacter jejuni infection, conservative measures are usually sufficient, with a focus on maintaining hydration. However, in cases where symptoms are severe, such as high fever, bloody diarrhea, or high-output diarrhea, or if the person is immunocompromised, antibiotics may be necessary. NICE recommends the use of clarithromycin, administered at a dose of 250-500 mg twice daily for 5-7 days, starting within 3 days of the onset of illness.

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

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

Acute aortic dissection is characterized by the rapid formation of a false, blood-filled channel within the middle layer of the aorta. It is estimated to occur in 3 out of every 100,000 individuals per year.

Patients with aortic dissection typically experience intense chest pain that spreads to the area between the shoulder blades. The pain is often described as tearing or ripping and may also extend to the neck. Sweating, paleness, and rapid heartbeat are commonly observed at the time of presentation. Other possible symptoms include focal neurological deficits, weak pulses, fainting, and reduced blood flow to organs.

A significant difference in blood pressure between the arms, greater than 20 mmHg, is a highly sensitive indicator. If the dissection extends backward, it can involve the aortic valve, leading to the early diastolic murmur of aortic regurgitation.

Risk factors for aortic dissection include hypertension, atherosclerosis, aortic coarctation, the use of sympathomimetic drugs like cocaine, Marfan syndrome, Ehlers-Danlos syndrome, Turner’s syndrome, tertiary syphilis, and pre-existing aortic aneurysm.

Aortic dissection can be classified according to the Stanford classification system:
– Type A affects the ascending aorta and the arch, accounting for 60% of cases. These cases are typically managed surgically and may result in the blockage of coronary arteries and aortic regurgitation.
– Type B begins distal to the left subclavian artery and accounts for approximately 40% of cases. These cases are usually managed with medication to control blood pressure.

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.

The percentage of patients who survive to hospital discharge after experiencing an out of hospital cardiac arrest.

Further Reading:

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

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

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

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

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

Early on in the overdose, arterial blood gas analysis typically reveals a respiratory alkalosis due to overstimulation of the respiratory center. As the overdose progresses, especially in moderate to severe cases, a metabolic acidosis with an increased anion gap may develop as a result of elevated levels of protons in the blood.

Electrocardiogram (ECG) abnormalities that may be observed include widening of the QRS complex, atrioventricular (AV) block, and ventricular arrhythmias.

An overdose of Amitriptyline, a tricyclic antidepressant, leads to a toxic effect known as anticholinergic toxidrome. This occurs when the muscarinic acetylcholine receptors are blocked, causing the characteristic signs and symptoms associated with this condition.

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.

This man is experiencing an acute asthma episode. His initial peak flow is 55% of his best, indicating a moderate exacerbation according to the BTS guidelines. Acute asthma can be classified as moderate, acute severe, life-threatening, or near-fatal.

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

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

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

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

Prophylactic VZIG is recommended for individuals at high risk who have had a significant exposure to varicella-zoster but have no known immunity (meaning they have not had chickenpox before). High-risk groups include neonates, pregnant women, the immunocompromised, and those on high dose steroids. For children on more than 2 mg/kg/day for more than 14 days, or adults on 40 mg/day for more than a week, it is important to temporarily increase their steroid dose during times of infection or stress. Stopping or reducing the dose of prednisolone would not be appropriate in this case. This patient is at high risk of adrenal insufficiency. Severe varicella infection can occur, leading to complications such as pneumonia, hepatitis, and DIC. It is important to note that varicella infection may not present with the typical rash and can have atypical or insidious symptoms. If a patient on high dose steroids develops varicella infection, they should be admitted for specialist review and receive intravenous aciclovir.

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

In the blood tests, certain findings can support a diagnosis of glandular fever. One of these findings is lymphocytosis, which refers to an increased number of lymphocytes in the blood. Lymphocytes are a type of white blood cell that plays a crucial role in the immune response. In glandular fever, the Epstein-Barr virus (EBV) is the most common cause, and it primarily infects and activates lymphocytes, leading to their increased numbers in the blood.

On the other hand, neutropenia (a decreased number of neutrophils) and neutrophilia (an increased number of neutrophils) are not typically associated with glandular fever. Neutrophils are another type of white blood cell that helps fight off bacterial infections. In glandular fever, the primary involvement is with lymphocytes rather than neutrophils.

Monocytosis, which refers to an increased number of monocytes, can also be seen in glandular fever. Monocytes are another type of white blood cell that plays a role in the immune response. Their increased numbers can be a result of the immune system’s response to the Epstein-Barr virus.

Eosinophilia, an increased number of eosinophils, is not commonly associated with glandular fever. Eosinophils are white blood cells involved in allergic reactions and parasitic infections, and their elevation is more commonly seen in those conditions.

In summary, the presence of lymphocytosis and possibly monocytosis in the blood tests would support a diagnosis of glandular fever, while neutropenia, neutrophilia, and eosinophilia are less likely to be associated with this condition.

Further Reading:

Glandular fever, also known as infectious mononucleosis or mono, is a clinical syndrome characterized by symptoms such as sore throat, fever, and swollen lymph nodes. It is primarily caused by the Epstein-Barr virus (EBV), with other viruses and infections accounting for the remaining cases. Glandular fever is transmitted through infected saliva and primarily affects adolescents and young adults. The incubation period is 4-8 weeks.

The majority of EBV infections are asymptomatic, with over 95% of adults worldwide having evidence of prior infection. Clinical features of glandular fever include fever, sore throat, exudative tonsillitis, lymphadenopathy, and prodromal symptoms such as fatigue and headache. Splenomegaly (enlarged spleen) and hepatomegaly (enlarged liver) may also be present, and a non-pruritic macular rash can sometimes occur.

Glandular fever can lead to complications such as splenic rupture, which increases the risk of rupture in the spleen. Approximately 50% of splenic ruptures associated with glandular fever are spontaneous, while the other 50% follow trauma. Diagnosis of glandular fever involves various investigations, including viral serology for EBV, monospot test, and liver function tests. Additional serology tests may be conducted if EBV testing is negative.

Management of glandular fever involves supportive care and symptomatic relief with simple analgesia. Antiviral medication has not been shown to be beneficial. It is important to identify patients at risk of serious complications, such as airway obstruction, splenic rupture, and dehydration, and provide appropriate management. Patients can be advised to return to normal activities as soon as possible, avoiding heavy lifting and contact sports for the first month to reduce the risk of splenic rupture.

Rare but serious complications associated with glandular fever include hepatitis, upper airway obstruction, cardiac complications, renal complications, neurological complications, haematological complications, chronic fatigue, and an increased risk of lymphoproliferative cancers and multiple sclerosis.

Parkinson’s disease (PD) is a progressive neurodegenerative condition that occurs when the dopamine-containing cells in the substantia nigra die. It is estimated that PD affects around 100-180 individuals per 100,000 of the population, which translates to approximately 6-11 people per 6,000 individuals in the general population of the UK. The annual incidence of PD is between 4-20 cases per 100,000 people. The prevalence of PD increases with age, with approximately 0.5% of individuals aged 65 to 74 being affected and 1-2% of individuals aged 75 and older. Additionally, PD is more prevalent and has a higher incidence in males.

The classic clinical features of Parkinson’s disease include hypokinesia, which refers to a poverty of movement, and bradykinesia, which is characterized by slowness of movement. Rest tremor, typically occurring at a rate of 4-6 cycles per second, is also commonly observed in PD patients. Another clinical feature is rigidity, which is characterized by increased muscle tone and a phenomenon known as cogwheel rigidity.

Uveitis is the most prevalent eye complication that arises in individuals with ankylosing spondylitis (AS). Approximately one out of every three patients with AS will experience uveitis at some stage. The symptoms of uveitis include a red and painful eye, along with photophobia and blurred vision. Additionally, patients may notice the presence of floaters. The primary treatment for uveitis involves the use of corticosteroids, and it is crucial for patients to seek immediate attention from an ophthalmologist.

Benzodiazepines are commonly used in the UK to manage symptoms of alcohol withdrawal. Currently, only diazepam and chlordiazepoxide have been authorized for this purpose. Other benzodiazepines like alprazolam, clobazam, and lorazepam do not currently have authorization for treating alcohol withdrawal symptoms in the UK.

Carbamazepine is also used in the UK to manage alcohol-related withdrawal symptoms, but it does not have official authorization for this use.

Clomethiazole, on the other hand, does have UK marketing authorization for treating alcohol withdrawal symptoms, but it is only recommended for use in a hospital setting with close supervision. The product information for clomethiazole advises caution when prescribing it to individuals with a history of addiction or outpatient alcoholics. It is also not recommended for patients who continue to drink or abuse alcohol. Combining alcohol with clomethiazole, especially in alcoholics with cirrhosis, can lead to fatal respiratory depression even with short-term use. Therefore, clomethiazole should only be used in a hospital under close supervision or, in rare cases, by specialist units on an outpatient basis with careful monitoring of the daily dosage.

The superior pancreaticoduodenal artery is a branch of the gastroduodenal artery. It typically originates from the common hepatic artery of the coeliac trunk. Its main function is to supply blood to the duodenum and pancreas.

On the other hand, the inferior pancreaticoduodenal artery branches either directly from the superior mesenteric artery or from its first intestinal branch. This occurs opposite the upper border of the inferior part of the duodenum. Its primary role is to supply blood to the head of the pancreas and the descending and inferior parts of the duodenum.

Both the superior and inferior pancreaticoduodenal arteries have anastomoses with each other. This allows for multiple channels through which blood can perfuse the pancreas and duodenum.

In the provided image from Gray’s Anatomy, the anastomosis between the superior and inferior pancreaticoduodenal arteries can be observed at the bottom center.

Fluid deficit in children and young people with severe diabetic ketoacidosis (DKA) is determined by measuring their blood pH and bicarbonate levels. If the blood pH is below 7.1 and/or the bicarbonate level is below 5, it indicates a fluid deficit. This simplified explanation uses a cutoff value of 5 to determine the severity of the fluid deficit in DKA.

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.

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

Further Reading:

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

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

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

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

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

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

Respiratory acidosis is often associated with chronic obstructive pulmonary disease (COPD) or life-threatening asthma. Other causes include pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or certain medications.

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

Metabolic acidosis with a raised anion gap can be caused by conditions like lactic acidosis (which can result from hypoxemia, shock, sepsis, or infarction) or ketoacidosis (commonly seen in diabetes, starvation, or alcohol excess). Other causes include renal failure or poisoning (such as late stages of aspirin overdose, methanol, or ethylene glycol).

Metabolic acidosis with a normal anion gap can be attributed to conditions like renal tubular acidosis, diarrhea, ammonium chloride ingestion, or adrenal insufficiency.