First-generation antipsychotics, also known as conventional or typical antipsychotics, are potent blockers of dopamine D2 receptors. However, these drugs also have varying effects on other receptors such as serotonin type 2 (5-HT2), alpha1, histaminic, and muscarinic receptors.

One of the major drawbacks of first-generation antipsychotics is their high incidence of extrapyramidal side effects. These include rigidity, bradykinesia, dystonias, tremor, akathisia, and tardive dyskinesia. Additionally, there is a rare but life-threatening reaction called neuroleptic malignant syndrome (NMS) that can occur with these medications. NMS is characterized by fever, muscle rigidity, altered mental status, and autonomic dysfunction. It typically occurs shortly after starting or increasing the dose of a neuroleptic medication.

In contrast, second-generation antipsychotics, also known as novel or atypical antipsychotics, have a lower risk of extrapyramidal side effects and NMS compared to their first-generation counterparts. However, they are associated with higher rates of metabolic effects and weight gain.

It is important to differentiate serotonin syndrome from NMS as they share similar features. Serotonin syndrome is most commonly caused by serotonin-specific reuptake inhibitors.

Here are some commonly encountered examples of first- and second-generation antipsychotics:

First-generation:
– Chlopromazine
– Haloperidol
– Fluphenazine
– Trifluoperazine

Second-generation:
– Clozapine
– Olanzapine
– Quetiapine
– Risperidone
– Aripiprazole

Ondansetron is a medication that works by blocking serotonin receptors in the body. It is commonly used as a first-line treatment for postoperative nausea and vomiting (PONV), which can occur after procedures done under sedation or anesthesia.

Further Reading:

postoperative nausea and vomiting (PONV) is a common occurrence following procedures performed under sedation or anesthesia. It can be highly distressing for patients. Several risk factors have been identified for PONV, including female gender, a history of PONV or motion sickness, non-smoking status, patient age, use of volatile anesthetics, longer duration of anesthesia, perioperative opioid use, use of nitrous oxide, and certain types of surgery such as abdominal and gynecological procedures.

To manage PONV, antiemetics are commonly used. These medications work by targeting different receptors in the body. Cyclizine and promethazine are histamine H1-receptor antagonists, which block the action of histamine and help reduce nausea and vomiting. Ondansetron is a serotonin 5-HT3 receptor antagonist, which blocks the action of serotonin and is effective in preventing and treating PONV. Prochlorperazine is a dopamine D2 receptor antagonist, which blocks the action of dopamine and helps alleviate symptoms of nausea and vomiting. Metoclopramide is also a dopamine D2 receptor antagonist and a 5-HT3 receptor antagonist, providing dual action against PONV. It is also a 5-HT4 receptor agonist, which helps improve gastric emptying and reduces the risk of PONV.

Assessment and management of PONV involves a comprehensive approach. Healthcare professionals need to assess the patient’s risk factors for PONV and take appropriate measures to prevent its occurrence. This may include selecting the appropriate anesthesia technique, using antiemetics prophylactically, and providing adequate pain control. In cases where PONV does occur, prompt treatment with antiemetics should be initiated to alleviate symptoms and provide relief to the patient. Close monitoring of the patient’s condition and response to treatment is essential to ensure effective management of PONV.

Klumpke’s palsy, also known as Dejerine-Klumpke palsy, is a condition where the arm becomes paralyzed due to an injury to the lower roots of the brachial plexus. The most commonly affected root is C8, but T1 can also be involved. The main cause of Klumpke’s palsy is when the arm is pulled forcefully in an outward position during a difficult childbirth. It can also occur in adults with apical lung carcinoma (Pancoast’s syndrome).

Clinically, Klumpke’s palsy is characterized by a deformity known as ‘claw hand’, which is caused by the paralysis of the intrinsic hand muscles. There is also a loss of sensation along the ulnar side of the forearm and hand. In some cases where T1 is affected, a condition called Horner’s syndrome may also be present.

Klumpke’s palsy can be distinguished from Erb’s palsy, which affects the upper roots of the brachial plexus (C5 and sometimes C6). In Erb’s palsy, the arm hangs by the side with the elbow extended and the forearm turned inward (known as the ‘waiter’s tip sign’). Additionally, there is a loss of shoulder abduction, external rotation, and elbow flexion.

Hyperosmolar hyperglycaemic state (HHS) is a condition characterized by extremely high blood sugar levels, dehydration, and increased osmolality without significant ketosis. In this patient, the symptoms are consistent with HHS as they have high blood sugar levels without significant ketoacidosis (pH is above 7.3 and ketones are less than 3 mmol/L). Additionally, they show signs of dehydration with low blood pressure and a fast heart rate. The osmolality is calculated to be equal to or greater than 320 mosmol/kg, indicating increased concentration of solutes in the blood.

Further Reading:

Hyperosmolar hyperglycaemic state (HHS) is a syndrome that occurs in people with type 2 diabetes and is characterized by extremely high blood glucose levels, dehydration, and hyperosmolarity without significant ketosis. It can develop over days or weeks and has a mortality rate of 5-20%, which is higher than that of diabetic ketoacidosis (DKA). HHS is often precipitated by factors such as infection, inadequate diabetic treatment, physiological stress, or certain medications.

Clinical features of HHS include polyuria, polydipsia, nausea, signs of dehydration (hypotension, tachycardia, poor skin turgor), lethargy, confusion, and weakness. Initial investigations for HHS include measuring capillary blood glucose, venous blood gas, urinalysis, and an ECG to assess for any potential complications such as myocardial infarction. Osmolality should also be calculated to monitor the severity of the condition.

The management of HHS aims to correct dehydration, hyperglycaemia, hyperosmolarity, and electrolyte disturbances, as well as identify and treat any underlying causes. Intravenous 0.9% sodium chloride solution is the principal fluid used to restore circulating volume and reverse dehydration. If the osmolality does not decline despite adequate fluid balance, a switch to 0.45% sodium chloride solution may be considered. Care must be taken in correcting plasma sodium and osmolality to avoid complications such as cerebral edema and osmotic demyelination syndrome.

The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours, and the fall in blood glucose should be no more than 5 mmol/L per hour. Low-dose intravenous insulin may be initiated if the blood glucose is not falling with fluids alone or if there is significant ketonaemia. Potassium replacement should be guided by the potassium level, and the patient should be encouraged to drink as soon as it is safe to do so.

Complications of treatment, such as fluid overload, cerebral edema, or central pontine myelinolysis, should be assessed for, and underlying precipitating factors should be identified and treated. Prophylactic anticoagulation is required in most patients, and all patients should be assumed to be at high risk of foot ulceration, necessitating appropriate foot protection and daily foot checks.

In a child with a non-blanching rash, it is important to always consider the possibility of meningococcal septicaemia. This is especially true if the child appears unwell, has purpura (lesions larger than 2 mm in diameter), a capillary refill time of more than 3 seconds, or neck stiffness. In the UK, most cases of meningococcal septicaemia are caused by Neisseria meningitidis group B, although the vaccination program for Neisseria meningitidis group C has reduced the prevalence of this type. A vaccine for group B disease has now been introduced for children. It is also worth noting that Streptococcus pneumoniae can also cause meningitis.

In this particular case, the child is clearly very sick and showing signs of septic shock. It is crucial to administer a single dose of benzylpenicillin without delay and arrange for immediate transfer to the nearest Emergency Department via ambulance.

The recommended doses of benzylpenicillin based on age are as follows:
– Infants under 1 year of age: 300 mg of IM or IV benzylpenicillin
– Children aged 1 to 9 years: 600 mg of IM or IV benzylpenicillin
– Children and adults aged 10 years or older: 1.2 g of IM or IV benzylpenicillin.

When a person’s systolic blood pressure is less than 90 mmHg, it indicates low blood pressure. A pulse rate above 100 or below 60 beats per minute is considered abnormal. An anion gap above 16 is indicative of an imbalance in the body’s electrolytes.

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.

Dressler’s syndrome is a form of pericarditis that occurs within 2 to 10 weeks following a heart attack or cardiac surgery. It is distinguished by intense chest pain that is usually alleviated by assuming an upright position. Additionally, individuals may experience a mild fever, a pericardial rub, pulsus paradoxus, and indications of right ventricular failure.

The UK chief medical officer and Department of Health recommend that both men and women should limit their alcohol consumption to no more than 14 units per week in order to minimize health risks. It is advised that individuals who consume up to 14 units per week should spread this amount over at least 3 days. Pregnant women are advised to completely avoid alcohol for the safest approach. Hazardous drinking refers to a pattern of alcohol consumption that increases the risk of harm. This includes consuming more than 14 units per week, but less than 35 units per week for women.

Further Reading:

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

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

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

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

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

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

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

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

Grey baby syndrome is a rare but serious side effect that can occur in neonates, especially premature babies, as a result of the build-up of the antibiotic chloramphenicol. This condition is characterized by several symptoms, including ashen grey skin color, poor feeding, vomiting, cyanosis, hypotension, hypothermia, hypotonia, cardiovascular collapse, abdominal distension, and respiratory difficulties.

During pregnancy, there are several drugs that can have adverse effects on the developing fetus. ACE inhibitors, such as ramipril, if given in the second and third trimesters, can lead to hypoperfusion, renal failure, and the oligohydramnios sequence. Aminoglycosides, like gentamicin, can cause ototoxicity and deafness. High doses of aspirin can result in first-trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses of aspirin (e.g., 75 mg) do not pose significant risks.

Benzodiazepines, such as diazepam, when administered late in pregnancy, can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if given in the first trimester, may lead to phalangeal abnormalities, while their use in the second and third trimesters can result in fetal growth retardation. Carbamazepine can cause hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol, as mentioned earlier, can cause grey baby syndrome. Corticosteroids, if given in the first trimester, may cause orofacial clefts. Danazol, if administered in the first trimester, can cause masculinization of the female fetuses genitals. Pregnant women should avoid handling crushed or broken tablets of finasteride, as it can be absorbed through the skin and affect male sex organ development.

Haloperidol, if given in the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the neonate. Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability

Rocuronium is a type of neuromuscular blocker that does not cause depolarization.

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.

When treating adults with bradycardia, it is recommended to administer a maximum of 6 doses of atropine 500 mcg. These doses can be repeated every 3-5 minutes. The total cumulative dose of atropine should not exceed 3 mg in adults.

Further Reading:

Causes of Bradycardia:
– Physiological: Athletes, sleeping
– Cardiac conduction dysfunction: Atrioventricular block, sinus node disease
– Vasovagal & autonomic mediated: Vasovagal episodes, carotid sinus hypersensitivity
– Hypothermia
– Metabolic & electrolyte disturbances: Hypothyroidism, hyperkalaemia, hypermagnesemia
– Drugs: Beta-blockers, calcium channel blockers, digoxin, amiodarone
– Head injury: Cushing’s response
– Infections: Endocarditis
– Other: Sarcoidosis, amyloidosis

Presenting symptoms of Bradycardia:
– Presyncope (dizziness, lightheadedness)
– Syncope
– Breathlessness
– Weakness
– Chest pain
– Nausea

Management of Bradycardia:
– Assess and monitor for adverse features (shock, syncope, myocardial ischaemia, heart failure)
– Treat reversible causes of bradycardia
– Pharmacological treatment: Atropine is first-line, adrenaline and isoprenaline are second-line
– Transcutaneous pacing if atropine is ineffective
– Other drugs that may be used: Aminophylline, dopamine, glucagon, glycopyrrolate

Bradycardia Algorithm:
– Follow the algorithm for management of bradycardia, which includes assessing and monitoring for adverse features, treating reversible causes, and using appropriate medications or pacing as needed.
https://acls-algorithms.com/wp-content/uploads/2020/12/Website-Bradycardia-Algorithm-Diagram.pdf

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

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

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

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

In order to achieve satisfactory bronchodilation, most individuals require a plasma theophylline concentration of 10-20 mg/litre (55-110 micromol/litre). However, it is possible for a lower concentration to still be effective. Adverse effects can occur within the range of 10-20 mg/litre, and their frequency and severity increase when concentrations exceed 20 mg/litre.

To measure plasma theophylline concentration, a blood sample should be taken five days after starting oral treatment and at least three days after any dose adjustment. For modified-release preparations, the blood sample should typically be taken 4-6 hours after an oral dose (specific sampling times may vary, so it is advisable to consult local guidelines). If aminophylline is administered intravenously, a blood sample should be taken 4-6 hours after initiating treatment.

In a patient with severe otitis externa on the left side, it is expected that they will experience conductive deafness on the left side. This means that their ability to hear sound will be impaired due to a problem in the ear canal or middle ear. When conducting a Rinne’s test, a vibrating 512 Hz tuning fork is placed on the mastoid process until the patient can no longer hear the sound. Then, the top of the tuning fork is positioned 2 cm from the external auditory meatus, and the patient is asked where they hear the sound loudest.

In individuals with normal hearing, the sound from the tuning fork should still be audible outside the external auditory canal even after it can no longer be heard on the mastoid. This is because air conduction should be better than bone conduction. However, in cases of conductive hearing loss, the patient will no longer be able to hear the tuning fork once it is removed from the mastoid. This indicates that their bone conduction is greater than their air conduction, suggesting an obstruction in the ear canal that prevents sound waves from reaching the cochlea. This is referred to as a true negative result.

It is important to note that a Rinne’s test may yield a false negative result if the patient has a severe unilateral sensorineural deficit. In this case, they may still sense the sound in the unaffected ear due to the transmission of sound through the base of the skull. In contrast, individuals with sensorineural hearing loss will have diminished ability to hear the tuning fork both on the mastoid and outside the external auditory canal compared to the opposite ear. The sound will disappear earlier on the mastoid and outside the external auditory canal in the affected ear.

When performing Weber’s test, a vibrating 512 Hz tuning fork is placed on the center of the patient’s forehead. The patient is then asked if they perceive the sound in the middle of the forehead or if it lateralizes to one side. If the sound lateralizes to one side, it can indicate either ipsilateral conductive hearing loss or contralateral sensorineural hearing loss.

Orthostatic hypotension is diagnosed using lying and standing blood pressure measurements. This condition is often seen in older individuals who are taking multiple medications for hypertension and depression. The patient exhibits symptoms such as light-headedness, dizziness, weakness, and tunnel vision when standing up. These symptoms do not occur when lying down and worsen upon standing, but can be relieved by sitting or lying down. They are typically more pronounced in the morning, in hot environments, after meals, after standing still, and after exercise. No other signs suggest an alternative diagnosis.

Further Reading:

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

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

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

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

Otoliths are commonly found in the inferior semicircular canal of patients, while their presence in the anterior semicircular canal is extremely uncommon.

Further Reading:

Benign paroxysmal positional vertigo (BPPV) is a common cause of vertigo, characterized by sudden dizziness and vertigo triggered by changes in head position. It typically affects individuals over the age of 55 and is less common in younger patients. BPPV is caused by dysfunction in the inner ear, specifically the detachment of otoliths (calcium carbonate particles) from the utricular otolithic membrane. These loose otoliths move through the semicircular canals, triggering a sensation of movement and resulting in conflicting sensory inputs that cause vertigo.

The majority of BPPV cases involve otoliths in the posterior semicircular canal, followed by the inferior semicircular canal. BPPV in the anterior semicircular canals is rare. Clinical features of BPPV include vertigo triggered by head position changes, such as rolling over in bed or looking upwards, accompanied by nausea. Episodes of vertigo typically last 10-20 seconds and can be diagnosed through positional nystagmus, which is a specific eye movement, observed during diagnostic maneuvers like the Dix-Hallpike maneuver.

Hearing loss and tinnitus are not associated with BPPV. The prognosis for BPPV is generally good, with spontaneous resolution occurring within a few weeks to months. Symptomatic relief can be achieved through the Epley maneuver, which is successful in around 80% of cases, or patient home exercises like the Brandt-Daroff exercises. Medications like Betahistine may be prescribed but have limited effectiveness in treating BPPV.

The patient in this scenario is exhibiting a clinical sign known as paradoxical breathing. This is characterized by an abnormal movement of the chest wall during respiration. Normally, the chest expands during inhalation and contracts during exhalation. However, in paradoxical breathing, the opposite occurs. The chest wall moves inward during inhalation and outward during exhalation. This can be seen in cases of chest trauma or injury, where there is a disruption in the normal mechanics of breathing.

Further Reading:

Flail chest is a serious condition that occurs when multiple ribs are fractured in two or more places, causing a segment of the ribcage to no longer expand properly. This condition is typically caused by high-impact thoracic blunt trauma and is often accompanied by other significant injuries to the chest.

The main symptom of flail chest is a chest deformity, where the affected area moves in a paradoxical manner compared to the rest of the ribcage. This can cause chest pain and difficulty breathing, known as dyspnea. X-rays may also show evidence of lung contusion, indicating further damage to the chest.

In terms of management, conservative treatment is usually the first approach. This involves providing adequate pain relief and respiratory support to the patient. However, if there are associated injuries such as a pneumothorax or hemothorax, specific interventions like thoracostomy or surgery may be necessary.

Positive pressure ventilation can be used to provide internal splinting of the airways, helping to prevent atelectasis, a condition where the lungs collapse. Overall, prompt and appropriate management is crucial in order to prevent further complications and improve the patient’s outcome.

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

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

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

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

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

All individuals diagnosed with stage 5 chronic kidney disease should be given the option to choose between haemodialysis or peritoneal dialysis. Peritoneal dialysis should be prioritized as the preferred treatment for the following groups of patients: those who still have some remaining kidney function, adult patients without major additional health conditions, and children who are two years old or younger.

Ketamine should not be used in individuals who have pulmonary hypertension, as it can worsen their condition. Additionally, it is contraindicated in children under 12 months old, as they are at a higher risk of experiencing laryngospasm and airway complications. Other contraindications include a high risk of laryngospasm (such as having an active respiratory infection or asthma), unstable or abnormal airway (due to tracheal surgery or stenosis), active upper or lower respiratory tract infection, proposed procedure within the mouth or pharynx, severe psychological problems, significant cardiac disease, intracranial hypertension with cerebrospinal fluid obstruction, intraocular pathology, previous psychotic illness, uncontrolled epilepsy, hyperthyroidism or taking thyroid medication, porphyria, prior adverse reaction to ketamine, altered conscious level due to acute illness or injury, and drug or alcohol intoxication.

Further Reading:

Ketamine sedation in children should only be performed by a trained and competent clinician who is capable of managing complications, especially those related to the airway. The clinician should have completed the necessary training and have the appropriate skills for procedural sedation. It is important for the clinician to consider the length of the procedure before deciding to use ketamine sedation, as lengthy procedures may be more suitable for general anesthesia.

Examples of procedures where ketamine may be used in children include suturing, fracture reduction/manipulation, joint reduction, burn management, incision and drainage of abscess, tube thoracostomy placement, foreign body removal, and wound exploration/irrigation.

During the ketamine sedation procedure, a minimum of three staff members should be present: a doctor to manage the sedation and airway, a clinician to perform the procedure, and an experienced nurse to monitor and support the patient, family, and clinical staff. The child should be sedated and managed in a high dependency or resuscitation area with immediate access to resuscitation facilities. Monitoring should include sedation level, pain, ECG, blood pressure, respiration, pulse oximetry, and capnography, with observations taken and recorded every 5 minutes.

Prior to the procedure, consent should be obtained from the parent or guardian after discussing the proposed procedure and use of ketamine sedation. The risks and potential complications should be explained, including mild or moderate/severe agitation, rash, vomiting, transient clonic movements, and airway problems. The parent should also be informed that certain common side effects, such as nystagmus, random purposeless movements, muscle twitching, rash, and vocalizations, are of no clinical significance.

Topical anesthesia may be considered to reduce the pain of intravenous cannulation, but this step may not be advisable if the procedure is urgent. The clinician should also ensure that key resuscitation drugs are readily available and doses are calculated for the patient in case they are needed.

Before administering ketamine, the child should be prepared by encouraging the parents or guardians to talk to them about happy thoughts and topics to minimize unpleasant emergence phenomena. The dose of ketamine is typically 1.0 mg/kg by slow intravenous injection over at least one minute, with additional doses of 0.5 mg/kg administered as required after 5-10 minutes to achieve the desired dissociative state.

For patients with sepsis and hypotension, it is recommended to administer 30ml of crystalloid fluid per kilogram of body weight. However, if the patient does not have acute kidney injury, is not hypotensive, and has a lactate level below 2 mmol/l, a 500ml immediate dose may be given.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

When starting treatment with strong opioids for pain relief in palliative care, it is recommended to offer patients regular oral sustained-release or oral immediate-release morphine, depending on their preference. In addition, provide rescue doses of oral immediate-release morphine for breakthrough pain. For patients without renal or hepatic comorbidities, a typical total daily starting dose schedule of 20-30 mg of oral morphine is suggested, along with 5 mg of oral immediate-release morphine for rescue doses during the titration phase. It is important to adjust the dose until a good balance is achieved between pain control and side effects. If this balance is not reached after a few dose adjustments, it is advisable to seek specialist advice. Patients should be reviewed frequently, especially during the titration phase. For patients with moderate to severe renal or hepatic impairment, it is recommended to consult a specialist before prescribing strong opioids.

For maintenance therapy, oral sustained-release morphine is recommended as the first-line treatment for patients with advanced and progressive disease who require strong opioids. Transdermal patch formulations should not be routinely offered as first-line maintenance treatment unless oral opioids are not suitable. If pain remains inadequately controlled despite optimizing first-line maintenance treatment, it is important to review the analgesic strategy and consider seeking specialist advice.

When it comes to breakthrough pain, oral immediate-release morphine should be offered as the first-line rescue medication for patients on maintenance oral morphine treatment. Fast-acting fentanyl should not be offered as the first-line rescue medication. If pain continues to be inadequately controlled despite optimizing treatment, it may be necessary to seek specialist advice.

In cases where oral opioids are not suitable and analgesic requirements are stable, transdermal patches with the lowest acquisition cost can be considered. However, it is important to consult a specialist for guidance if needed. Similarly, for patients in whom oral opioids are not suitable and analgesic requirements are unstable, subcutaneous opioids with the lowest acquisition cost can be considered, with specialist advice if necessary.

For more information, please refer to the NICE Clinical Knowledge Summary: Opioids for pain relief in palliative care. https://www.nice.org.uk/guidance/cg140

Discitis is an infection that affects the space between the intervertebral discs in the spine. This condition can have serious consequences, including the formation of abscesses and sepsis. The most common cause of discitis is usually Staphylococcus aureus, but other organisms like Streptococcus viridans and Pseudomonas aeruginosa may be responsible in certain cases, especially in immunocompromised individuals and intravenous drug users. Gram-negative organisms like Escherichia coli and Mycobacterium tuberculosis can also cause discitis, particularly in cases of Pott’s disease.

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

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

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

Treatment for discitis involves hospital admission for intravenous antibiotics. Before starting the antibiotics, it is recommended to send three sets of blood cultures and a full set of blood tests, including a C-reactive protein (CRP) test, to the laboratory.

A typical antibiotic regimen for discitis would include intravenous flucloxacillin 2 g every 6 hours as the first-line treatment if there is no penicillin allergy. Intravenous vancomycin may be used if the infection was acquired in the hospital, if there is a high risk of methicillin-resistant Staphylococcus aureus (MRSA) infection, or if there is a documented penicillin allergy.

Vomiting is a common occurrence during the early stages of pregnancy, typically happening between 7 and 12 weeks. However, there is a more severe condition called hyperemesis gravidarum, which involves uncontrollable and intense nausea and vomiting. This condition can lead to imbalances in fluids and electrolytes, significant ketonuria, malnutrition, and weight loss. It is relatively rare, affecting less than 1% of pregnancies.

For mild cases of nausea and vomiting in early pregnancy, dietary adjustments and non-pharmacological measures like consuming ginger or using P6 wrist acupressure can often provide relief.

In severe cases where heavy ketonuria and severe dehydration are present, hospital admission is usually necessary for intravenous fluid rehydration. The NICE Clinical Knowledge Summary (CKS) on nausea and vomiting in pregnancy recommends using oral promethazine, oral cyclizine, or oral prochlorperazine as the first-line treatment if an antiemetic is needed. After 24 hours, the situation should be reassessed to determine if the initial treatment is effective. If not, a second-line drug like metoclopramide or ondansetron should be considered.

It’s important to note that metoclopramide should not be used in patients under the age of 20 due to the increased risk of extrapyramidal side effects. Additionally, proton pump inhibitors (e.g., omeprazole) and histamine H2-receptor antagonists (e.g., ranitidine) can be beneficial for women experiencing significant dyspepsia alongside their nausea and vomiting.

For more information, you can refer to the NICE CKS on nausea and vomiting in pregnancy.

Korsakoff syndrome is a form of dementia that occurs due to a lack of thiamine (vitamin B1) in the body. This condition is most commonly observed in individuals who have a long history of alcoholism. The main features of Korsakoff syndrome include anterograde amnesia, patchy retrograde amnesia, and confabulation. Additionally, many patients also experience difficulties with language (aphasia), movement (apraxia), recognition (agnosia), or executive functioning. It is important to note that Korsakoff syndrome often coexists with Wernicke’s encephalopathy, which is characterized by a triad of symptoms including ophthalmoplegia, altered mental state, and gait disturbance (ataxia). When both conditions are present, it is referred to as Wernicke-Korsakoff syndrome (WKS).

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.

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

Further Reading:

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

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

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

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

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

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

Infectious factors that can lead to back pain consist of discitis, vertebral osteomyelitis, and spinal epidural abscess. There are certain warning signs, known as red flags, that indicate the presence of an infectious cause for back pain. These red flags include experiencing a fever, having tuberculosis, being diabetic, having recently had a bacterial infection such as a urinary tract infection, engaging in intravenous drug use, and having a weakened immune system due to conditions like HIV or the use of immunosuppressant drugs.

Thiamine deficiency is frequently seen in individuals who are dependent on alcohol. This is primarily due to their inadequate diet, the presence of gastritis which affects thiamine absorption, and the fact that thiamine is involved in alcohol metabolism as a coenzyme. If left untreated, thiamine deficiency can lead to Wernicke’s encephalopathy, which can further progress to Korsakoff’s syndrome.

It is important to note that administering glucose-containing intravenous fluids without thiamine to a patient with chronic thiamine deficiency can trigger Wernicke’s encephalopathy. Therefore, individuals undergoing detoxification should receive parenteral high-potency B complex vitamins (Pabrinex) as a preventive treatment. However, it is crucial to have resuscitation facilities available during administration due to the risk of anaphylaxis. The risk of anaphylaxis is lower when the drug is given intramuscularly (IM). A daily dose of one pair of ampoules of Pabrinex, containing 250 mg of thiamine, should be administered IM or intravenously (IV) for a period of three to five days.

Once the 3-5 day course of Pabrinex is completed, the patient should transition to oral vitamin B Compound-strong and oral thiamine tablets for continued treatment.

For more information, please refer to the NICE pathway for acute alcohol withdrawal.

According to NICE, one of the recommended treatments for mild-to-moderate Alzheimer’s disease is the use of acetylcholinesterase (AChE) inhibitors. These inhibitors include Donepezil (Aricept), Galantamine, and Rivastigmine. They work by inhibiting the enzyme that breaks down acetylcholine, a neurotransmitter involved in memory and cognitive function.

On the other hand, Memantine is a different type of medication that acts by blocking NMDA-type glutamate receptors. It is recommended for patients with moderate Alzheimer’s disease who cannot tolerate or have a contraindication to AChE inhibitors, or for those with severe Alzheimer’s disease.