The ATLS guidelines categorize chest injuries in trauma into two groups: life-threatening injuries that require immediate identification and treatment in the primary survey, and potentially life-threatening injuries that should be identified and treated in the secondary survey.

During the primary survey, the focus is on identifying and treating life-threatening thoracic injuries. These include airway obstruction, tracheobronchial tree injury, tension pneumothorax, open pneumothorax, massive haemothorax, and cardiac tamponade. Prompt recognition and intervention are crucial in order to prevent further deterioration and potential fatality.

In the secondary survey, attention is given to potentially life-threatening injuries that may not be immediately apparent. These include simple pneumothorax, haemothorax, flail chest, pulmonary contusion, blunt cardiac injury, traumatic aortic disruption, traumatic diaphragmatic injury, and blunt oesophageal rupture. These injuries may not pose an immediate threat to life, but they still require identification and appropriate management to prevent complications and ensure optimal patient outcomes.

By dividing chest injuries into these two categories and addressing them in a systematic manner, healthcare providers can effectively prioritize and manage trauma patients, ultimately improving their chances of survival and recovery.

Zygomaticomaxillary complex fractures, also known as quadramalar or tripod fractures, make up around 40% of all midface fractures and are the second most common facial bone fractures after nasal bone fractures.

These injuries typically occur when a direct blow is delivered to the malar eminence of the cheek. They consist of four components:

1. Widening of the zygomaticofrontal suture
2. Fracture of the zygomatic arch
3. Fracture of the inferior orbital rim and the walls of the anterior and posterior maxillary sinuses
4. Fracture of the lateral orbital rim.

Generally speaking, if a child shows clinical signs of dehydration but does not exhibit shock, it can be assumed that they are 5% dehydrated. On the other hand, if shock is also present, it can be assumed that the child is 10% dehydrated or more. When a child is 5% dehydrated, it means that their body has lost 5 grams of fluid per 100 grams of body weight, which is equivalent to 50 ml of fluid per kilogram. In the case of 10% dehydration, the body has lost 100 ml of fluid per kilogram.

For example, if a child is 10% dehydrated and weighs 30 kilograms, their estimated fluid loss would be 100 ml/kg x 30 kg = 3000 ml.

The clinical features of dehydration and shock are summarized below:

Dehydration (5%):
– The child appears unwell
– Their heart rate may be normal or increased (tachycardia)
– Their respiratory rate may be normal or increased (tachypnea)
– Peripheral pulses are normal
– Capillary refill time (CRT) is normal or slightly prolonged
– Blood pressure is normal
– Extremities feel warm
– Urine output is decreased
– Skin turgor is reduced
– Eyes may appear sunken
– The fontanelle (soft spot on the baby’s head) may be depressed
– Mucous membranes are dry

Clinical shock (10%):
– The child appears pale, lethargic, and mottled
– Heart rate is increased (tachycardia)
– Respiratory rate is increased (tachypnea)
– Peripheral pulses are weak
– Capillary refill time (CRT) is prolonged
– Blood pressure is low (hypotension)
– Extremities feel cold
– Urine output is decreased
– Level of consciousness is decreased

In order to gain a comprehensive understanding of AF management, it is crucial to familiarize oneself with the terminology used to describe its various subtypes. These terms help categorize different episodes of AF based on their characteristics and outcomes.

Acute AF refers to any episode that occurs within the previous 48 hours. It can manifest with or without symptoms and may or may not recur. On the other hand, paroxysmal AF describes episodes that spontaneously end within 7 days, typically within 48 hours. While these episodes are often recurrent, they can progress into a sustained form of AF.

Recurrent AF is defined as experiencing two or more episodes of AF. If the episodes self-terminate, they are classified as paroxysmal AF. However, if the episodes do not self-terminate, they are categorized as persistent AF. Persistent AF lasts longer than 7 days or has occurred after a previous cardioversion. To terminate persistent AF, electrical or pharmacological intervention is required. In some cases, persistent AF can progress into permanent AF.

Permanent AF, also known as Accepted AF, refers to episodes that cannot be successfully terminated, have relapsed after termination, or where cardioversion is not pursued. This subtype signifies a more chronic and ongoing form of AF.

By understanding and utilizing these terms, healthcare professionals can effectively communicate and manage the different subtypes of AF.

Iodine deficiency is a widespread issue globally and is the leading cause of hypothyroidism worldwide. It is particularly prevalent in numerous African countries, as well as in developed nations such as Norway, Germany, Russia, and Ukraine. In the UK, however, autoimmune thyroiditis is the most common cause of hypothyroidism.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

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

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

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

The symptoms of acute mountain sickness (AMS) typically appear within 6-12 hours of reaching an altitude above 2500 meters. On the other hand, the onset of high altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE) usually occurs after 2-4 days of being at high altitude.

Further Reading:

High Altitude Illnesses

Altitude & Hypoxia:
– As altitude increases, atmospheric pressure decreases and inspired oxygen pressure falls.
– Hypoxia occurs at altitude due to decreased inspired oxygen.
– At 5500m, inspired oxygen is approximately half that at sea level, and at 8900m, it is less than a third.

Acute Mountain Sickness (AMS):
– AMS is a clinical syndrome caused by hypoxia at altitude.
– Symptoms include headache, anorexia, sleep disturbance, nausea, dizziness, fatigue, malaise, and shortness of breath.
– Symptoms usually occur after 6-12 hours above 2500m.
– Risk factors for AMS include previous AMS, fast ascent, sleeping at altitude, and age <50 years old.
– The Lake Louise AMS score is used to assess the severity of AMS.
– Treatment involves stopping ascent, maintaining hydration, and using medication for symptom relief.
– Medications for moderate to severe symptoms include dexamethasone and acetazolamide.
– Gradual ascent, hydration, and avoiding alcohol can help prevent AMS.

High Altitude Pulmonary Edema (HAPE):
– HAPE is a progression of AMS but can occur without AMS symptoms.
– It is the leading cause of death related to altitude illness.
– Risk factors for HAPE include rate of ascent, intensity of exercise, absolute altitude, and individual susceptibility.
– Symptoms include dyspnea, cough, chest tightness, poor exercise tolerance, cyanosis, low oxygen saturations, tachycardia, tachypnea, crepitations, and orthopnea.
– Management involves immediate descent, supplemental oxygen, keeping warm, and medication such as nifedipine.

High Altitude Cerebral Edema (HACE):
– HACE is thought to result from vasogenic edema and increased vascular pressure.
– It occurs 2-4 days after ascent and is associated with moderate to severe AMS symptoms.
– Symptoms include headache, hallucinations, disorientation, confusion, ataxia, drowsiness, seizures, and manifestations of raised intracranial pressure.
– Immediate descent is crucial for management, and portable hyperbaric therapy may be used if descent is not possible.
– Medication for treatment includes dexamethasone and supplemental oxygen. Acetazolamide is typically used for prophylaxis.

Amiodarone is a medication that is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) while chest compressions are being performed. The prescribed dose is 300 mg, given as an intravenous bolus that is diluted in 5% dextrose to a volume of 20 mL. It is important to note that amiodarone is not suitable for treating PEA or asystole.

In cases where VF/pVT persists after five defibrillation attempts, an additional dose of 150 mg of amiodarone should be given. However, if amiodarone is not available, lidocaine can be used as an alternative. The recommended dose of lidocaine is 1 mg/kg. It is crucial to avoid administering lidocaine if amiodarone has already been given.

Amiodarone is classified as a membrane-stabilizing antiarrhythmic drug. It works by prolonging the duration of the action potential and the refractory period in both the atrial and ventricular myocardium. This medication also slows down atrioventricular conduction and has a similar effect on accessory pathways.

Additionally, amiodarone has a mild negative inotropic action, meaning it weakens the force of heart contractions. It also causes peripheral vasodilation through non-competitive alpha-blocking effects.

It is important to note that while there is no evidence of long-term benefits from using amiodarone, it may improve short-term survival rates, which justifies its continued use.

If a child with gastroenteritis shows signs of jittery movements, increased muscle tone, hyper-reflexia, or convulsions, hypernatraemic dehydration should be considered. Additional signs of hypernatraemic dehydration include drowsiness or coma.

Further Reading:

Gastroenteritis is a common condition in children, particularly those under the age of 5. It is characterized by the sudden onset of diarrhea, with or without vomiting. The most common cause of gastroenteritis in infants and young children is rotavirus, although other viruses, bacteria, and parasites can also be responsible. Prior to the introduction of the rotavirus vaccine in 2013, rotavirus was the leading cause of gastroenteritis in children under 5 in the UK. However, the vaccine has led to a significant decrease in cases, with a drop of over 70% in subsequent years.

Norovirus is the most common cause of gastroenteritis in adults, but it also accounts for a significant number of cases in children. In England & Wales, there are approximately 8,000 cases of norovirus each year, with 15-20% of these cases occurring in children under 9.

When assessing a child with gastroenteritis, it is important to consider whether there may be another more serious underlying cause for their symptoms. Dehydration assessment is also crucial, as some children may require intravenous fluids. The NICE traffic light system can be used to identify the risk of serious illness in children under 5.

In terms of investigations, stool microbiological testing may be indicated in certain cases, such as when the patient has been abroad, if diarrhea lasts for more than 7 days, or if there is uncertainty over the diagnosis. U&Es may be necessary if intravenous fluid therapy is required or if there are symptoms and/or signs suggestive of hypernatremia. Blood cultures may be indicated if sepsis is suspected or if antibiotic therapy is planned.

Fluid management is a key aspect of treating children with gastroenteritis. In children without clinical dehydration, normal oral fluid intake should be encouraged, and oral rehydration solution (ORS) supplements may be considered. For children with dehydration, ORS solution is the preferred method of rehydration, unless intravenous fluid therapy is necessary. Intravenous fluids may be required for children with shock or those who are unable to tolerate ORS solution.

Antibiotics are generally not required for gastroenteritis in children, as most cases are viral or self-limiting. However, there are some exceptions, such as suspected or confirmed sepsis, Extraintestinal spread of bacterial infection, or specific infections like Clostridium difficile-associated pseudomembranous enterocolitis or giardiasis.

The intravascular volume of an infant is approximately 80 ml/kg, while in older children it is around 70 ml/kg. Dehydration itself does not lead to death, but shock can occur when there is a loss of 20 ml/kg from the intravascular space. Clinical dehydration becomes evident only after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children: Bodyweight:

– First 10 kg: Daily fluid requirement of 100 ml/kg and hourly fluid requirement of 4 ml/kg.

– Second 10 kg: Daily fluid requirement of 50 ml/kg and hourly fluid requirement of 2 ml/kg.

– Subsequent kg: Daily fluid requirement of 20 ml/kg and hourly fluid requirement of 1 ml/kg.

Based on this information, the hourly maintenance fluid requirements for this child can be calculated as follows:

– First 10 kg: 4 ml/kg = 40 ml

– Second 10 kg: 2 ml/kg = 20 ml

– Subsequent kg: 1 ml/kg = 5 ml

Therefore, the total hourly maintenance fluid requirement for this child is 65 ml.

To relieve the patient’s respiratory distress, the most suitable initial intervention would be positive pressure ventilation. This involves providing mechanical assistance to the patient’s breathing by delivering air or oxygen under pressure through a mask or endotracheal tube. This helps to improve oxygenation and ventilation, ensuring that the patient’s lungs are adequately supplied with oxygen and carbon dioxide is effectively removed. Positive pressure ventilation can help stabilize the patient’s breathing and alleviate the respiratory distress caused by the flail segment.

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.

The most probable diagnosis in this case is idiopathic intracranial hypertension, also known as benign intracranial hypertension or pseudotumour cerebri. This condition typically affects overweight women in their 20s and 30s.

The clinical features of idiopathic intracranial hypertension include:
– Headache: The headache is usually worse in the morning and evenings, relieved by standing, and worsened when lying down. It can also be aggravated by coughing and sneezing. Some patients may experience pain around the shoulder girdle.
– Nausea and vomiting
– Visual field defects: These develop gradually over time.
– 6th nerve palsy and diplopia
– Bilateral papilloedema

To investigate this condition, the patient should undergo a CT scan and/or MRI of the brain, as well as a lumbar puncture to measure the opening pressure and analyze the cerebrospinal fluid (CSF).

The primary treatment goal for idiopathic intracranial hypertension is to prevent visual loss. This can be achieved through one of the following strategies:
– Repeated lumbar puncture to control intracranial pressure (ICP)
– Medical treatment with acetazolamide
– Surgical decompression of the optic nerve sheath

The most suitable approach for investigation in this case would be to send a blood test for Epstein-Barr virus (EBV) viral serology. Glandular fever, also known as infectious mononucleosis, is commonly caused by the Epstein-Barr virus. The symptoms described by the patient, including a sore throat, fever, and feeling unwell, are consistent with this condition. To confirm the diagnosis, a blood test for EBV viral serology can be performed. This test detects antibodies produced by the body in response to the virus. It is important to note that the Monospot test, which is another blood test for infectious mononucleosis, may not be as accurate in younger children. Therefore, the most appropriate option would be to send a blood test for EBV viral serology in 2-3 days time. This will allow for the detection of specific antibodies and provide a more accurate diagnosis.

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.

An inguinal hernia occurs when the contents of the abdominal cavity protrude through the inguinal canal. There are two main types of inguinal hernias: indirect and direct. Indirect hernias, which account for 75% of cases, originate lateral to the inferior epigastric artery and follow the path of the spermatic cord or round ligament through the internal inguinal ring and along the inguinal canal. On the other hand, direct hernias, which make up 25% of cases, originate medial to the inferior epigastric artery and protrude through the posterior wall of the inguinal canal.

Indirect inguinal hernias can be distinguished from direct hernias by several features. They have an elliptical shape, unlike the round shape of direct hernias. They are also less likely to be easily reducible and reduce spontaneously on reclining. Additionally, indirect hernias take longer to appear when standing compared to direct hernias, which appear immediately. They can be reduced superiorly then superolaterally, while direct hernias reduce superiorly and posteriorly. Pressure over the deep inguinal ring can control indirect hernias. However, they are more prone to strangulation due to the narrow neck of the deep inguinal ring and can extend into the scrotum.

In contrast, a femoral hernia occurs when the abdominal cavity contents protrude through the femoral canal. These hernias occur below and lateral to the pubic tubercle, whereas inguinal hernias occur above and medial to the pubic tubercle. Femoral hernias are more easily visible when the patient is lying supine.

A sports hernia, also known as athletic pubalgia, is characterized by chronic groin pain in athletes and the presence of a dilated superficial inguinal ring. However, there is no palpable hernia during examination.

It is important to note that the hernia described here is not located near any scars, making it unlikely to be an incisional hernia.

For patients with croup, the usual dose of oral dexamethasone is 0.15mg/kg. However, if the patient cannot take it orally, an alternative option is to administer intramuscular dexamethasone at a dose of 0.6 mg/kg as a single dose.

Further Reading:

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

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

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

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

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

Anhydrosis, or the inability to sweat, is frequently observed in individuals who experience heat stroke. This patient exhibits the main characteristics of heat stroke, including a core body temperature exceeding 40ºC and encephalopathy, which is evident through significant confusion. Additionally, the patient’s use of diuretics and advanced age are risk factors that increase the likelihood of developing severe heat-related illness. It is important to note that in the UK, most fatalities resulting from heat stroke occur in individuals aged 70 or older, typically within the initial days of a heat wave.

Further Reading:

Heat Stroke:
– Core temperature >40°C with central nervous system dysfunction
– Classified into classic/non-exertional heat stroke and exertional heat stroke
– Classic heat stroke due to passive exposure to severe environmental heat
– Exertional heat stroke due to strenuous physical activity in combination with excessive environmental heat
– Mechanisms to reduce core temperature overwhelmed, leading to tissue damage
– Symptoms include high body temperature, vascular endothelial surface damage, inflammation, dehydration, and renal failure
– Management includes cooling methods and supportive care
– Target core temperature for cooling is 38.5°C

Heat Exhaustion:
– Mild to moderate heat illness that can progress to heat stroke if untreated
– Core temperature elevated but <40°C
– Symptoms include nausea, vomiting, dizziness, and mild neurological symptoms
– Normal thermoregulation is disrupted
– Management includes moving patient to a cooler environment, rehydration, and rest

Other Heat-Related Illnesses:
– Heat oedema: transitory swelling of hands and feet, resolves spontaneously
– Heat syncope: results from volume depletion and peripheral vasodilatation, managed by moving patient to a cooler environment and rehydration
– Heat cramps: painful muscle contractions associated with exertion, managed with cooling, rest, analgesia, and rehydration

Risk Factors for Severe Heat-Related Illness:
– Old age, very young age, chronic disease and debility, mental illness, certain medications, housing issues, occupational factors

Management:
– Cooling methods include spraying with tepid water, fanning, administering cooled IV fluids, cold or ice water immersion, and ice packs
– Benzodiazepines may be used to control shivering
– Rapid cooling to achieve rapid normothermia should be avoided to prevent overcooling and hypothermia
– Supportive care includes intravenous fluid replacement, seizure treatment if required, and consideration of haemofiltration
– Some patients may require liver transplant due to significant liver damage
– Patients with heat stroke should ideally be managed in a HDU/ICU setting with CVP and urinary catheter output measurements

In an elderly patient with a history of gradual decline accompanied by high blood sugar levels, excessive thirst, and recent infection, the most likely diagnosis is hyperosmolar hyperglycemic state (HHS). This condition can be life-threatening, with a mortality rate of approximately 50%. Common symptoms include dehydration, elevated blood sugar levels, altered mental status, and electrolyte imbalances. About half of the patients with HHS also experience hypernatremia.

To calculate the serum osmolality, the formula is 2(K+ + Na+) + urea + glucose. In this case, the serum osmolality is 364 mmol/l, indicating a high level. It is important to discontinue the use of metformin in this patient due to the risk of metformin-associated lactic acidosis (MALA). Additionally, an intravenous infusion of insulin should be initiated.

The treatment goals for HHS are to address the underlying cause and gradually and safely:
– Normalize the osmolality
– Replace fluid and electrolyte losses
– Normalize blood glucose levels

If significant ketonaemia is present (3β-hydroxybutyrate is more than 1 mmol/L), it indicates a relative lack of insulin, and insulin should be administered immediately. However, if significant ketonaemia is not present, insulin should not be started.

Patients with HHS are at a high risk of thromboembolism, and it is recommended to routinely administer low molecular weight heparin. In cases where the serum osmolality exceeds 350 mmol/l, full heparinization should be considered.

To insert an IJV line, the patient should be positioned in the Trendelenburg position. This means that the patient should lie on their back with their head tilted down by at least 15 degrees. Additionally, the patient’s head should be turned away or laterally rotated from the side where the cannulation will take place. This positioning helps to distend the neck veins, making it easier to access them for the procedure.

Further Reading:

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

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

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

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

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

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

Epididymo-orchitis refers to the inflammation of the testis and epididymis caused by an infectious source. The most common way of infection is through local extension, often resulting from infections spreading from the urethra or bladder.

In individuals below the age of 35, sexually transmitted pathogens like Chlamydia trachomatis and Neisseria gonorrhoeae are the primary causes. On the other hand, in individuals over the age of 35, non-sexually transmitted infections caused by Gram-negative enteric organisms that lead to urinary tract infections are more common.

Typically, patients with epididymo-orchitis experience sudden onset of unilateral scrotal pain and swelling. The affected testis is tender to touch, and there is usually a noticeable swelling of the epididymis that starts at the lower pole of the testis and spreads towards the upper pole. The testis itself may also be affected, and there may be redness and/or swelling of the scrotum on the affected side. Patients may have a fever and may also have urethral discharge.

It is crucial to consider testicular torsion as the most important differential diagnosis. This should be taken into account for all patients with sudden testicular pain, as the testicle needs to be saved within 6 hours of onset. Torsion is more likely in men under the age of 20, especially if the pain is extremely acute and severe. Typically, torsion presents around four hours after onset. In this case, the patient’s age, longer history of symptoms, and the presence of fever are more indicative of epididymo-orchitis.

Digoxin is a medication used to treat atrial fibrillation and flutter, as well as congestive cardiac failure. It belongs to a class of drugs called cardiac glycosides. Its mechanism of action involves inhibiting the Na/K ATPase in cardiac myocytes, which leads to an increase in intracellular sodium concentration. This, in turn, indirectly increases the availability of intracellular calcium through Na/Ca exchange.

The rise in intracellular calcium levels caused by digoxin results in a positive inotropic effect, meaning it strengthens the force of heart contractions, and a negative chronotropic effect, meaning it slows down the heart rate.

Therapeutic plasma levels of digoxin typically range between 1.0-1.5 nmol/l. However, higher concentrations may be necessary, and the specific value can vary between different laboratories. It is important to note that the risk of toxicity significantly increases when digoxin levels exceed 2 nmol/l.

Signs and symptoms of digoxin toxicity include nausea, vomiting, diarrhea, abdominal pain, confusion, tachyarrhythmias or bradyarrhythmias, xanthopsia (yellow-green vision), and hyperkalemia (an early sign of significant toxicity).

Several factors can potentially contribute to digoxin toxicity. These include being elderly, having renal failure, experiencing myocardial ischemia, having hypokalemia, hypomagnesemia, hypercalcemia, hypernatremia, acidosis, or hypothyroidism.

Additionally, there are several drugs that can increase the risk of digoxin toxicity. These include spironolactone, amiodarone, quinidine, verapamil, diltiazem, and drugs that cause hypokalemia, such as thiazide and loop diuretics.

According to NICE guidelines, when it comes to imaging for cervical spine injury, CT is recommended as the primary modality for adults aged 16 and above, while MRI is recommended for children. This applies to patients who are either at high risk for cervical spine injury or are unable to actively rotate their neck 45 degrees to the left and right.

Further Reading:

When assessing for cervical spine injury, it is recommended to use the Canadian C-spine rules. These rules help determine the risk level for a potential injury. High-risk factors include being over the age of 65, experiencing a dangerous mechanism of injury (such as a fall from a height or a high-speed motor vehicle collision), or having paraesthesia in the upper or lower limbs. Low-risk factors include being involved in a minor rear-end motor vehicle collision, being comfortable in a sitting position, being ambulatory since the injury, having no midline cervical spine tenderness, or experiencing a delayed onset of neck pain. If a person is unable to actively rotate their neck 45 degrees to the left and right, their risk level is considered low. If they have one of the low-risk factors and can actively rotate their neck, their risk level remains low.

If a high-risk factor is identified or if a low-risk factor is identified and the person is unable to actively rotate their neck, full in-line spinal immobilization should be maintained and imaging should be requested. Additionally, if a patient has risk factors for thoracic or lumbar spine injury, imaging should be requested. However, if a patient has low-risk factors for cervical spine injury, is pain-free, and can actively rotate their neck, full in-line spinal immobilization and imaging are not necessary.

NICE recommends CT as the primary imaging modality for cervical spine injury in adults aged 16 and older, while MRI is recommended as the primary imaging modality for children under 16.

Different mechanisms of spinal trauma can cause injury to the spine in predictable ways. The majority of cervical spine injuries are caused by flexion combined with rotation. Hyperflexion can result in compression of the anterior aspects of the vertebral bodies, stretching and tearing of the posterior ligament complex, chance fractures (also known as seatbelt fractures), flexion teardrop fractures, and odontoid peg fractures. Flexion and rotation can lead to disruption of the posterior ligament complex and posterior column, fractures of facet joints, lamina, transverse processes, and vertebral bodies, and avulsion of spinous processes. Hyperextension can cause injury to the anterior column, anterior fractures of the vertebral body, and potential retropulsion of bony fragments or discs into the spinal canal. Rotation can result in injury to the posterior ligament complex and facet joint dislocation.

The primary location for aortic dissection, which is being considered in this case, is the ascending aorta.

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

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

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

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

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

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

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

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

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

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

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

There is a significant link between methotrexate and the development of pulmonary fibrosis. While there have been instances of pulmonary fibrosis occurring as a result of infliximab, this particular side effect is more commonly associated with methotrexate use.

Methotrexate can also cause other side effects such as nausea and vomiting, abdominal pain, gastrointestinal bleeding, dizziness, stomatitis, hepatotoxicity, neutropenia, and pneumonitis.

The typical range for lactate levels in the body is 0.5-2.2 mmol/L, according to most UK trusts. However, it is important to mention that the RCEM sepsis guides consider a lactate level above 2 mmol/L to be abnormal.

Further Reading:

Arterial blood gases (ABG) are an important diagnostic tool used to assess a patient’s acid-base status and respiratory function. When obtaining an ABG sample, it is crucial to prioritize safety measures to minimize the risk of infection and harm to the patient. This includes performing hand hygiene before and after the procedure, wearing gloves and protective equipment, disinfecting the puncture site with alcohol, using safety needles when available, and properly disposing of equipment in sharps bins and contaminated waste bins.

To reduce the risk of harm to the patient, it is important to test for collateral circulation using the modified Allen test for radial artery puncture. Additionally, it is essential to inquire about any occlusive vascular conditions or anticoagulation therapy that may affect the procedure. The puncture site should be checked for signs of infection, injury, or previous surgery. After the test, pressure should be applied to the puncture site or the patient should be advised to apply pressure for at least 5 minutes to prevent bleeding.

Interpreting ABG results requires a systematic approach. The core set of results obtained from a blood gas analyser includes the partial pressures of oxygen and carbon dioxide, pH, bicarbonate concentration, and base excess. These values are used to assess the patient’s acid-base status.

The pH value indicates whether the patient is in acidosis, alkalosis, or within the normal range. A pH less than 7.35 indicates acidosis, while a pH greater than 7.45 indicates alkalosis.

The respiratory system is assessed by looking at the partial pressure of carbon dioxide (pCO2). An elevated pCO2 contributes to acidosis, while a low pCO2 contributes to alkalosis.

The metabolic aspect is assessed by looking at the bicarbonate (HCO3-) level and the base excess. A high bicarbonate concentration and base excess indicate alkalosis, while a low bicarbonate concentration and base excess indicate acidosis.

Analyzing the pCO2 and base excess values can help determine the primary disturbance and whether compensation is occurring. For example, a respiratory acidosis (elevated pCO2) may be accompanied by metabolic alkalosis (elevated base excess) as a compensatory response.

The anion gap is another important parameter that can help determine the cause of acidosis. It is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium.

Diabetes insipidus (DI) is characterized by specific biochemical markers. One of these markers is a low urine osmolality, meaning that the concentration of solutes in the urine is lower than normal. In contrast, the serum osmolality, which measures the concentration of solutes in the blood, is high in individuals with DI. This combination of low urine osmolality and high serum osmolality is indicative of DI. Other common biochemical disturbances associated with DI include elevated plasma osmolality, polyuria (excessive urine production), and hypernatremia (high sodium levels in the blood). However, it is important to note that sodium levels can sometimes be within the normal range in individuals with DI. It is worth mentioning that conditions such as Addison’s disease, syndrome of inappropriate antidiuretic hormone secretion (SIADH), and primary polydipsia are associated with low serum osmolality and hyponatremia. Additionally, the use of selective serotonin reuptake inhibitors (SSRIs) can also lead to hyponatremia as a side effect.

Further Reading:

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

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

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

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

Chronic lymphocytic leukaemia (CLL) is the most common type of leukaemia in adults. It occurs when mature lymphocytes multiply uncontrollably. About 95% of cases are of B-cell lineage.

CLL is typically a slow-growing form of leukaemia and is often discovered incidentally during routine blood tests. As the disease progresses, patients may experience swollen lymph nodes, enlarged liver and spleen, anemia, and increased susceptibility to infections.

This condition primarily affects adult men, with over 75% of CLL patients being men over the age of 50.

A blood test for CLL usually reveals an increased number of lymphocytes (typically more than 5 x 109/l, but it can be higher). Advanced stages of the disease may also show normochromic, normocytic anemia. A peripheral blood smear can confirm the presence of lymphocytosis, and smudge cells are often observed.

The Binet system is used to stage CLL, categorizing it as follows:
– Stage A: Hemoglobin (Hb) levels above 10 g/dl, platelet count above 100 x 109/l, involvement of fewer than 3 lymph node areas.
– Stage B: Hb levels above 10 g/dl, platelet count above 100 x 109/l, involvement of more than 3 lymph node areas.
– Stage C: Hb levels below 10 g/dl, platelet count below 100 x 109/l, or both.

Early stages of CLL (Binet stage A and B without active disease) do not require immediate treatment and can be monitored through regular follow-up and blood tests. Patients with more advanced disease have various treatment options available, including monoclonal antibodies (such as rituximab), purine analogues (like fludarabine), and alkylating agents (such as chlorambucil).

Public Health England advises that children with impetigo should not attend school, nursery, or be under the care of childminders until the sores have formed a crust or until 48 hours after starting antibiotic treatment. Antibiotics help accelerate the healing process and decrease the period of contagiousness.

For more information, please refer to the Guidance on Infection Control in Schools and other Childcare Settings.
https://www.publichealth.hscni.net/sites/default/files/Guidance_on_infection_control_in%20schools_poster.pdf

In patients with hypothermia, the pulse check during CPR should be extended to 1 minute. Additionally, several adjustments need to be made to the CPR protocol. Firstly, mechanical ventilation should be used due to the stiffness of the chest wall. Secondly, the dosing or omission of cardiac arrest drugs should be adjusted based on the patient’s temperature. The defibrillation pattern should also be modified, with 3 shocks attempted before re-attempting defibrillation only when the body temperature is above 30ºC. Certain electrolyte disturbances, such as mild hypokalemia, should not be treated as potassium levels typically rise with Rewarming. It is important to plan for prolonged resuscitation in these cases. Lastly, uncorrected ABG results should be used, without adjusting for temperature.

Further Reading:

Hypothermic cardiac arrest is a rare situation that requires a tailored approach. Resuscitation is typically prolonged, but the prognosis for young, previously healthy individuals can be good. Hypothermic cardiac arrest may be associated with drowning. Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, basal metabolic rate falls and cell signaling between neurons decreases, leading to reduced tissue perfusion. Signs and symptoms of hypothermia progress as the core temperature drops, initially presenting as compensatory increases in heart rate and shivering, but eventually ceasing as the temperature drops into moderate hypothermia territory.

ECG changes associated with hypothermia include bradyarrhythmias, Osborn waves, prolonged PR, QRS, and QT intervals, shivering artifact, ventricular ectopics, and cardiac arrest. When managing hypothermic cardiac arrest, ALS should be initiated as per the standard ALS algorithm, but with modifications. It is important to check for signs of life, re-warm the patient, consider mechanical ventilation due to chest wall stiffness, adjust dosing or withhold drugs due to slowed drug metabolism, and correct electrolyte disturbances. The resuscitation of hypothermic patients is often prolonged and may continue for a number of hours.

Pulse checks during CPR may be difficult due to low blood pressure, and the pulse check is prolonged to 1 minute for this reason. Drug metabolism is slowed in hypothermic patients, leading to a build-up of potentially toxic plasma concentrations of administered drugs. Current guidance advises withholding drugs if the core temperature is below 30ºC and doubling the drug interval at core temperatures between 30 and 35ºC. Electrolyte disturbances are common in hypothermic patients, and it is important to interpret results keeping the setting in mind. Hypoglycemia should be treated, hypokalemia will often correct as the patient re-warms, ABG analyzers may not reflect the reality of the hypothermic patient, and severe hyperkalemia is a poor prognostic indicator.

Different warming measures can be used to increase the core body temperature, including external passive measures such as removal of wet clothes and insulation with blankets, external active measures such as forced heated air or hot-water immersion, and internal active measures such as inhalation of warm air, warmed intravenous fluids, gastric, bladder, peritoneal and/or pleural lavage and high volume renal haemofilter.

Methicillin-resistant Staphylococcus aureus (MRSA) has become a significant issue in hospitals and other healthcare facilities in recent years. MRSA refers to any strain of Staphylococcus aureus that has developed resistance to beta-lactam antibiotics, such as penicillins and cephalosporins. This resistance is caused by the presence of the mecA gene, which produces a penicillin-binding protein with low affinity. Fortunately, MRSA is typically susceptible to teicoplanin, vancomycin, daptomycin, and linezolid. On the other hand, imipenem is an intravenous beta-lactam antibiotic that belongs to the carbapenem subgroup.

Flumazenil is a specific antagonist for benzodiazepines that can be beneficial in certain situations. It acts quickly, taking less than 1 minute to take effect, but its effects are short-lived and only last for less than 1 hour. The recommended dosage is 200 μg every 1-2 minutes, with a maximum dose of 3mg per hour.

It is important to avoid using Flumazenil if the patient is dependent on benzodiazepines or is taking tricyclic antidepressants. This is because it can trigger a withdrawal syndrome in these individuals, potentially leading to seizures or cardiac arrest.

Gout is a form of arthritis that causes a swollen, tender, red, and hot joint. Initially, it was believed to primarily affect wealthy individuals due to dietary connections, but it is now becoming more prevalent and is estimated to impact around 1-2% of the Western population. This increase may be attributed to longer lifespans and changes in our eating habits. Additionally, there is a positive correlation between the rising rates of metabolic disease and gout.

While gout commonly affects the metatarsal-phalangeal joint of the big toe (approximately 50% of cases), it can also impact other joints such as the fingers, wrists, knees, and ankles. The pain experienced during an episode is often excruciating, and these episodes typically last about a week. Approximately half of the patients experience a recurrence within a year.

Hyperuricemia is the underlying cause of gout. Uric acid, a byproduct of purine metabolism, is typically eliminated through the kidneys. However, in about 90% of cases, hyperuricemia occurs due to the under-excretion of urate, while the remaining 10% is caused by overproduction. Elevated urate levels increase the likelihood of crystal formation. Measuring uric acid levels in the blood can be misleading, as some individuals with high levels do not develop gout, and levels can be normal during an attack. The crystallization process is complex and more likely to occur in cooler temperatures (which is why the feet are often affected, and symptoms worsen at night), during acidosis, and when there are rapid fluctuations in uric acid levels.

Diagnosing gout is primarily based on clinical evaluation. If there is a rapid onset of severe pain, swelling, and tenderness that reaches its peak within 6-12 hours, accompanied by redness, it strongly suggests crystal inflammation. The presence of monosodium urate crystals in synovial fluid or tophi confirms the diagnosis. When these crystals are examined under polarized light, they exhibit negative birefringence. Since gout symptoms can be mistaken for septic arthritis, if there is uncertainty in the diagnosis and the joint has been aspirated, it should also be sent for gram-staining.

Tophi are painless, hard lumps that develop when hyperuricemia persists for an extended period. They often appear on the elbows and ears.

Calcium-channel blocker overdose is a serious matter and should be regarded as potentially life-threatening. Verapamil and diltiazem are the two most dangerous types of calcium channel blockers when taken in excess. They work by attaching to the alpha-1 subunit of L-type calcium channels, which stops calcium from entering the cells. These channels play a crucial role in the functioning of cardiac myocytes, vascular smooth muscle cells, and islet beta-cells.

The occurrence of schizophrenia is consistent across all social classes. It affects individuals from all walks of life without discrimination. The likelihood of developing schizophrenia over one’s lifetime is 1%, and this probability remains the same for both men and women. However, it is worth noting that men tend to experience the onset of symptoms at a younger age compared to women, with the average age of onset falling between 15 and 45 years.

There is a recognized genetic predisposition for schizophrenia, meaning that certain individuals may have a higher likelihood of developing the condition due to their genetic makeup. The risk of schizophrenia affecting first-degree relatives, such as siblings or parents, is approximately 10%. Furthermore, the risk of children being affected by schizophrenia increases to 40%.

When considering the impact of genetics on schizophrenia, it is interesting to note that monozygotic twins, who share identical genetic material, have a concordance rate of around 50%. This suggests that genetic factors play a significant role in the development of the condition.

Tragically, approximately 10% of individuals suffering from schizophrenia ultimately die by suicide, particularly during the early stages of the illness. This highlights the importance of providing appropriate support and intervention to individuals with schizophrenia to prevent such devastating outcomes.

Septic arthritis occurs when an infectious agent invades a joint, causing it to become purulent. The main symptoms of septic arthritis include pain in the affected joint, redness, warmth, and swelling of the joint, and difficulty moving the joint. Patients may also experience fever and systemic upset. The most common cause of septic arthritis is Staphylococcus aureus, but other bacteria such as Streptococcus spp., Haemophilus influenzae, Neisseria gonorrhoea, and Escherichia coli can also be responsible.

According to the current recommendations by NICE and the BNF, the initial treatment for septic arthritis is flucloxacillin. However, if a patient is allergic to penicillin, clindamycin can be used instead. If there is a suspicion of MRSA infection, vancomycin is the recommended choice. In cases where gonococcal arthritis or a Gram-negative infection is suspected, cefotaxime is the preferred treatment. The suggested duration of treatment is typically 4-6 weeks, although it may be longer if the infection is complicated.

Psittacosis is a type of infection that can be transmitted from animals to humans, caused by a bacterium called Chlamydia psittaci. It is most commonly seen in people who own domestic birds, as well as those who work in pet shops or zoos. The typical symptoms of psittacosis include pneumonia that is acquired within the community, along with flu-like symptoms. Many patients also experience severe headaches and sensitivity to light. Enlargement of the spleen is a common finding in about two-thirds of individuals with this infection.

Infected individuals often develop a rash on their face, known as Horder’s spots, which appear as reddish macules. In some cases, erythema nodosum and erythema multiforme may also occur. The recommended treatment for psittacosis is a course of tetracycline or doxycycline for a period of 2-3 weeks.

On the other hand, rose spots are typically observed in cases of typhoid fever. These spots have a similar appearance to Horder’s spots but are usually found on the trunk rather than the face. Erythema marginatum is a pale red rash seen in rheumatic fever, while malar flush, also known as ‘mitral facies’, refers to the reddish discoloration of the cheeks commonly seen in individuals with mitral stenosis. Lastly, erythema chronicum migrans is the distinctive rash seen in Lyme disease, characterized by a circular rash with a central ‘bulls-eye’ appearance that spreads outward from the site of a tick bite.

Neisseria gonorrhoeae is a type of bacteria that is shaped like two spheres and stains pink when tested. It is responsible for causing the sexually transmitted infection known as gonorrhoea. This infection is most commonly seen in individuals between the ages of 15 and 35, and it is primarily transmitted through sexual contact. One important thing to note is that the gonococcal pili, which are hair-like structures on the bacteria, can change their appearance. This means that even if someone has recovered from a previous infection, they can still be reinfected due to the bacteria’s ability to alter its antigens.

In men, the most common symptoms of gonorrhoea include inflammation of the urethra, which is the tube that carries urine out of the body. This is seen in approximately 80% of cases. Other symptoms may include painful urination, as well as the presence of a discharge that is a combination of mucus and pus. In some cases, the infection can also affect the rectum, leading to anal discharge. It is worth noting that pharyngitis, which is inflammation of the throat, is usually asymptomatic in men.

On the other hand, women with gonorrhoea often experience a vaginal discharge as the main symptom, which is seen in about 50% of cases. Lower abdominal pain is another common symptom, occurring in approximately 25% of cases. Dysuria, or painful urination, is seen in about 10-15% of women with the infection. Some women may also experience tenderness in the pelvic or lower abdominal area. Additionally, there may be a discharge or bleeding from the endocervix, which is the opening of the cervix. Similar to men, rectal infection is usually asymptomatic in women, but it can cause anal discharge. Pharyngitis, or inflammation of the throat, is typically not accompanied by any noticeable symptoms in women.

Overall, it is important to be aware of the various clinical features of gonorrhoea in both men and women in order to recognize and seek appropriate treatment for this sexually transmitted infection.

Transfusion transmitted bacterial infection is a rare complication that can occur during blood transfusion. It is more commonly associated with platelet transfusion, as platelets are stored at room temperature. Additionally, previously frozen components that are thawed using a water bath and red cell components stored for several weeks are also at a higher risk for bacterial infection.

Both Gram-positive and Gram-negative bacteria have been implicated in transfusion-transmitted bacterial infection, but Gram-negative bacteria are known to cause more severe illness and have higher rates of morbidity and mortality. Among the bacterial organisms, Yersinia enterocolitica is the most commonly associated with this type of infection. This particular organism is able to multiply at low temperatures and utilizes iron as a nutrient, making it well-suited for proliferation in blood stores.

The clinical features of transfusion-transmitted bacterial infection typically manifest shortly after the transfusion begins. These features include a high fever, chills and rigors, nausea and vomiting, tachycardia, hypotension, and even circulatory collapse.

If there is suspicion of a transfusion-transmitted bacterial infection, it is crucial to immediately stop the transfusion. Blood cultures and a Gram-stain should be requested to identify the specific bacteria causing the infection. Broad-spectrum antibiotics should be initiated promptly. Furthermore, the blood pack should be returned to the blood bank urgently for culture and Gram-stain analysis.

Ketamine stands out among other anaesthetic agents due to its unique combination of analgesic, hypnotic, and amnesic properties. This makes it an incredibly valuable and adaptable drug when administered correctly.

The mechanism of action of ketamine involves non-competitive antagonism of the Ca2+ channel pore within the NMDA receptor. Additionally, it inhibits NMDA receptor activity by interacting with the binding site of phencyclidine.

In summary, ketamine’s multifaceted effects and its ability to target specific receptors make it an indispensable tool in the field of anaesthesia.

This patient has returned from West Africa exhibiting symptoms and signs consistent with a viral haemorrhagic fever, which strongly suggests a diagnosis of Ebola. Ebola, also known as Ebola haemorrhagic fever, is caused by RNA viruses belonging to the Ebola Virus genus. The virus is zoonotic, meaning it can be transmitted from animals to humans, with fruit bats believed to be the natural reservoir. It spreads through direct contact with bodily fluids and may also be transmitted through sexual intercourse. The incubation period typically ranges from 4 to 10 days, but it can extend up to 3 weeks.

The initial manifestations of the disease usually resemble those of a flu-like illness, characterized by fever, muscle pain, and headaches. However, the condition rapidly deteriorates, leading to worsening fever, vomiting, diarrhea, and abdominal pain. In a significant proportion of cases (30-50%), patients develop internal and external bleeding, presenting with petechiae, purpura, epistaxis, gastrointestinal bleeding, and bleeding from the urinary tract. Therefore, immediate isolation of suspected Ebola cases is crucial, followed by prompt transportation to a High-Level Isolation Unit. Contacting the Health Protection Team and initiating comprehensive public health measures is essential.

Healthcare staff involved in the management of suspected Ebola cases must adhere to strict personal protection protocols. This includes practicing thorough hand hygiene, wearing double gloves, utilizing fluid repellent disposable coveralls or gowns, donning full-length plastic aprons over the coveralls or gowns, wearing head covers such as surgical caps, using fluid repellent footwear like surgical boots, and wearing full face shields or goggles along with fluid repellent FFP3 respirators.

The management of Ebola primarily focuses on providing supportive care, often requiring intensive care treatment if available. The mortality rate of Ebola varies across different outbreaks, ranging from 50% to 90%. Death frequently occurs as a result of hypovolemic shock.

Vascular dementia is not as common as Alzheimer’s disease, accounting for about 20% of dementia cases compared to 50% for Alzheimer’s. Most individuals with vascular dementia have a history of atherosclerotic cardiovascular disease and/or hypertension.

There are notable differences in how these two diseases present themselves. Vascular dementia often has a sudden onset, while Alzheimer’s disease has a slower onset. The progression of vascular dementia tends to be stepwise, with periods of stability followed by sudden declines, whereas Alzheimer’s disease has a more gradual decline. The course of vascular dementia can also fluctuate, while Alzheimer’s disease shows a steady decline over time.

In terms of personality and insight, individuals with vascular dementia tend to have relatively preserved personality and insight in the early stages, whereas those with Alzheimer’s disease may experience early changes and loss in these areas. Gait is also affected differently, with individuals with vascular dementia taking small steps (known as marche a petit pas), while those with Alzheimer’s disease have a normal gait.

Sleep disturbance is less common in vascular dementia compared to Alzheimer’s disease, which commonly presents with sleep disturbances. Focal neurological signs, such as sensory and motor deficits and pseudobulbar palsy, are more common in vascular dementia, while they are uncommon in Alzheimer’s disease.

To differentiate between Alzheimer’s disease and vascular dementia, the modified Hachinski ischemia scale can be used. This scale assigns scores based on various features, such as abrupt onset, stepwise deterioration, fluctuating course, nocturnal confusion, preservation of personality, depression, somatic complaints, emotional incontinence, history of hypertension, history of strokes, evidence of associated atherosclerosis, focal neurological symptoms, and focal neurological signs. A score of 2 or greater suggests vascular dementia.

Overall, understanding the differences in presentation and using tools like the modified Hachinski ischemia scale can help in distinguishing between Alzheimer’s disease and vascular dementia.

Hypothyroidism is a condition characterized by an underactive thyroid gland, which leads to a decrease in the production of thyroid hormones. This can result in various clinical features. Some common symptoms include fatigue, lethargy, and cold intolerance. Patients may also experience bradycardia (a slow heart rate) and diastolic hypertension (high blood pressure). Hair loss and weight gain are also commonly seen in individuals with hypothyroidism. Other possible symptoms include constipation, poor appetite, and carpal tunnel syndrome. Skin pigmentation changes, particularly yellow discoloration, may occur due to carotene deposition in the dermis, most notably on the palms and soles.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

Dementia with Lewy bodies (DLB) is characterized by several key features, including spontaneous fluctuations in cognitive abilities, visual hallucinations, and Parkinsonism. Visual hallucinations are particularly prevalent in DLB and Parkinson’s disease dementia, which are considered to be part of the same spectrum. While visual hallucinations can occur in other forms of dementia, they are less frequently observed.

Further Reading:

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

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

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

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

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

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

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

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

Standard pain relievers are generally not effective in treating cluster headaches. They take too long to work, and by the time they start to relieve the pain, the headache has usually already gone away. It is not recommended to use opioids for cluster headaches as they may actually make the headaches worse, and using them for a long time can lead to dependency.

However, there are other options that can be effective in treating cluster headaches. One option is to use subcutaneous sumatriptan, which is a medication that works by stimulating a specific receptor in the brain. This can help reduce the inflammation in the blood vessels that is associated with migraines and cluster headaches. Most people find that subcutaneous sumatriptan starts to work within 10-15 minutes of being administered.

Another option is to use zolmitriptan nasal spray, which is also a medication that works in a similar way to sumatriptan. However, it may take a bit longer for the nasal spray to start working compared to the subcutaneous injection.

In addition to medication, high-flow oxygen can also be used as an alternative therapy for cluster headaches. This involves breathing in oxygen at a high flow rate, which can help relieve the pain and other symptoms of a cluster headache.

Lastly, octreotide can be administered subcutaneously and has been shown to be more effective than a placebo in treating acute cluster headache attacks.

The earliest and most frequent clinical indication of malignant hyperthermia is typically an increase in end tidal CO2. An unexplained elevation in end tidal CO2 is often the initial and most reliable sign of this condition.

Further Reading:

Malignant hyperthermia is a rare and life-threatening syndrome that can be triggered by certain medications in individuals who are genetically susceptible. The most common triggers are suxamethonium and inhalational anaesthetic agents. The syndrome is caused by the release of stored calcium ions from skeletal muscle cells, leading to uncontrolled muscle contraction and excessive heat production. This results in symptoms such as high fever, sweating, flushed skin, rapid heartbeat, and muscle rigidity. It can also lead to complications such as acute kidney injury, rhabdomyolysis, and metabolic acidosis. Treatment involves discontinuing the trigger medication, administering dantrolene to inhibit calcium release and promote muscle relaxation, and managing any associated complications such as hyperkalemia and acidosis. Referral to a malignant hyperthermia center for further investigation is also recommended.

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

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

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

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

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

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.
https://www.resus.org.uk/sites/default/files/2021-05/Emergency%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf

The presence of certain clinical features can indicate the possibility of acute severe asthma in children over the age of 5. These features include oxygen saturations below 92%, peak flow measurements below 50% of what is expected, a heart rate exceeding 120 beats per minute, a respiratory rate exceeding 30 breaths per minute, and the use of accessory muscles.

Femoral shaft fractures are quite common among children and have a significant impact on both the child and their family. It is important to carefully examine children with these fractures for any associated injuries, such as soft-tissue injury, head trauma, or additional fractures. In fact, up to 40% of children who experience a femoral shaft fracture due to high-energy trauma may have these associated injuries. Additionally, a thorough neurovascular examination should be conducted.

Rapidly immobilizing the limb is crucial for managing pain and limiting further blood loss from the fracture. For distal femoral shaft fractures, well-padded long leg splints with split plaster casts can be applied. However, for more proximal shaft fractures, long leg splints alone may not provide adequate control. In these cases, skin traction is a better option. Skin traction involves attaching a large foam pad to the patient’s lower leg using spray adhesive. A weight, approximately 10% of the child’s body weight, is then applied to the foam pad and allowed to hang over the foot of the bed. This constant longitudinal traction helps keep the bone fragments aligned.

When children experience severe pain, it is important to manage it aggressively yet safely. Immobilizing the fracture can provide significant relief. The Royal College of Emergency Medicine recommends other pain control measures for children, such as intranasal diamorphine (0.1 mg/kg in 0.2 ml sterile water), intravenous morphine (0.1-0.2 mg/kg), and oral analgesia (e.g., paracetamol 20 mg/kg, max 1 g, and ibuprofen 10 mg/kg, max 400 mg).

Acne conglobata is an extremely severe form of acne where acne nodules come together and create sinuses. Acne fulminans, on the other hand, is a rare and severe complication of acne conglobata that is accompanied by systemic symptoms. It is linked to elevated levels of androgenic hormones, specific autoimmune conditions, and a genetic predisposition.

The typical clinical characteristics of acne fulminans are as follows:

– Sudden and abrupt onset
– Inflammatory and ulcerated nodular acne primarily found on the chest and back
– Often painful lesions
– Ulcers on the upper trunk covered with bleeding crusts
– Severe acne scarring
– Fluctuating fever
– Painful joints and arthropathy
– General feeling of illness (malaise)
– Loss of appetite and weight loss
– Enlarged liver and spleen (hepatosplenomegaly)

It is crucial to refer patients immediately for a specialist evaluation and hospital admission. Treatment options for acne fulminans include systemic corticosteroids, dapsone, ciclosporin, and high-dose intravenous antibiotics.

Blood transfusion is a crucial medical treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion usage, errors and adverse reactions still occur.

One serious complication is acute haemolytic transfusion reactions, which happen when incompatible red cells are transfused and react with the patient’s own antibodies. This usually occurs due to human error, such as mislabelling sample tubes or request forms. Symptoms of this reaction include a feeling of impending doom, fever, chills, pain and warmth at the transfusion site, nausea, vomiting, and back, joint, and chest pain. Immediate action should be taken to stop the transfusion, replace the donor blood with normal saline or another suitable crystalloid, and check the blood to confirm the intended recipient. IV diuretics may be administered to increase renal blood flow, and urine output should be maintained.

Another common complication is febrile transfusion reaction, which presents with a 1-degree rise in temperature from baseline, along with chills and malaise. This reaction is usually caused by cytokines from leukocytes in the transfused blood components. Supportive treatment is typically sufficient, and paracetamol can be helpful.

Allergic reactions can also occur, usually due to foreign plasma proteins or anti-IgA. These reactions often present with urticaria, pruritus, and hives, and in severe cases, laryngeal edema or bronchospasm may occur. Symptomatic treatment with antihistamines is usually enough, and there is usually no need to stop the transfusion. However, if anaphylaxis occurs, the transfusion should be stopped, and the patient should be administered adrenaline and treated according to the ALS protocol.

Transfusion-related acute lung injury (TRALI) is a severe complication characterized by non-cardiogenic pulmonary edema within 6 hours of transfusion. It is associated with antibodies in the donor blood reacting with recipient leukocyte antigens. This is the most common cause of death related to transfusion reactions. Treatment involves stopping the transfusion, administering oxygen, and providing aggressive respiratory support in approximately 75% of patients. Diuretic usage should be avoided.

The connection between latex sensitivity and food allergy is commonly known as the latex-fruit syndrome. Foods that have been found to be allergenic in relation to latex are categorized into high, moderate, or low risk groups.

High risk foods include banana, avocado, chestnut, and kiwi fruit.

Moderate risk foods include apple, carrot, celery, melon, papaya, potato, and tomato.

Citrus fruits and pears are considered to have a low risk of causing allergic reactions in individuals with latex sensitivity.

Septic arthritis in adults is most commonly caused by Staphylococcus aureus. However, Streptococcus spp. is the most common group of bacteria responsible for this condition. In the past, Haemophilus influenzae used to be a significant cause of septic arthritis, but with the introduction of vaccination programs, its occurrence has significantly decreased. Other bacteria that can lead to septic arthritis include E. Coli, Salmonella, Neisseria gonorrhoea, and Mycobacterium.

It is important to note that viruses can also be a cause of septic arthritis. Examples of such viruses include hepatitis A, B, and C, coxsackie, adenovirus, and parvovirus. Additionally, fungi can also be responsible for septic arthritis, with Histoplasmosa and Blastomyces being notable examples.

When administering adrenaline to a pediatric patient experiencing cardiac arrest, the dosage given through the intraosseous (IO) route is identical to that given through the intravenous (IV) route. Both routes require a dosage of 10 mcg/kg. For instance, if the child weighs 30 kg, the appropriate dosage would be 300 mcg (0.3 mg).

Legionella pneumophila, a Gram-negative bacterium, can be found in natural water supplies and soil. It is responsible for causing Legionnaires’ disease, a serious illness. Outbreaks of this disease have been associated with poorly maintained air conditioning systems, whirlpool spas, and hot tubs.

The pneumonic form of Legionnaires’ disease presents with specific clinical features. Initially, there may be a mild flu-like prodrome lasting for 1-3 days. A non-productive cough, occurring in approximately 90% of cases, is also common. Pleuritic chest pain, haemoptysis, headache, nausea, vomiting, diarrhoea, and anorexia are other symptoms that may be experienced.

Fortunately, Legionella pneumophila infections can be effectively treated with macrolide antibiotics like erythromycin, or quinolones such as ciprofloxacin. Tetracyclines, including doxycycline, can also be used as a treatment option.

While the majority of Legionnaires’ disease cases are caused by Legionella pneumophila, there are several other species of Legionella that have been identified. One such species is Legionella longbeachae, which is less commonly encountered. It is primarily found in soil and potting compost and has been associated with outbreaks of Pontiac fever, a milder variant of Legionnaires’ disease that does not primarily affect the respiratory system.

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

Naloxone is a specific antidote for opioid overdose. It effectively reverses respiratory depression and coma when given in sufficient dosage. The initial dose is administered intravenously at 400 micrograms, followed by 800 micrograms for up to 2 doses at 1-minute intervals if there is no response to the preceding dose. If there is still no response, the dosage is increased to 2 mg for one dose. In seriously poisoned patients, a 4 mg dose may be required. If the intravenous route is not feasible, naloxone can also be given by intramuscular injection.

Due to its shorter duration of action compared to most opioids, close monitoring and repeated injections are necessary. The frequency of doses should be based on the respiratory rate and depth of coma, with the dose generally repeated every 2-3 minutes up to a maximum of 10 mg. In cases where repeated doses are needed, naloxone can be administered through a continuous infusion, which should be adjusted according to the vital signs. Initially, the infusion rate can be set at 60% of the initial resuscitative IV dose per hour.

It is important to note that in opioid addicts, the administration of naloxone may trigger a withdrawal syndrome characterized by symptoms such as abdominal cramps, nausea, and diarrhea. However, these symptoms typically subside within 2 hours.

Fluoxetine is the preferred antidepressant for children and young individuals, as it is the only medication approved for this purpose. Limited research exists regarding the effectiveness of other antidepressants in this specific age group.

Thought insertion is one of the primary symptoms identified by Schneider in schizophrenia. This symptom refers to the patient’s belief that their thoughts are being controlled or influenced by external sources, such as other individuals or entities. In some cases, they may even experience auditory hallucinations, hearing distinct voices.

Recurrent or chronic tonsillitis is a clear indication for tonsillectomy, which is the surgical removal of the palatine tonsils. One common complication of this procedure is bleeding, which occurs in approximately 0.5-2% of cases. The bleeding that occurs after tonsillectomy is typically venous in nature and most frequently originates from the external palatine vein. This vein drains the lateral tonsillar region and ultimately empties into the facial vein. Additionally, bleeding can also arise from the tonsillar branch of the facial artery, which supplies the inferior pole of the palatine tonsil.

The recommended daily oral dose for adults is 900 mg, which should be taken in 2-3 divided doses. For severe asthma or COPD, the initial intravenous dose is 5 mg/kg and should be administered over 10-20 minutes. This can be followed by a continuous infusion of 0.5 mg/kg/hour. In the case of a patient weighing 60 kg, the appropriate loading dose would be 300 mg. It is important to note that the therapeutic range for aminophylline is narrow, ranging from 10-20 microgram/ml. Therefore, it is beneficial to estimate the plasma concentration of aminophylline during long-term treatment.

The suggested amount of Prilocaine for Bier’s block is 3mg per kilogram of body weight. It is important to note that there is no available formulation of prilocaine combined with adrenaline, unlike other local anesthetics.

Further Reading:

Bier’s block is a regional intravenous anesthesia technique commonly used for minor surgical procedures of the forearm or for reducing distal radius fractures in the emergency department (ED). It is recommended by NICE as the preferred anesthesia block for adults requiring manipulation of distal forearm fractures in the ED.

Before performing the procedure, a pre-procedure checklist should be completed, including obtaining consent, recording the patient’s weight, ensuring the resuscitative equipment is available, and monitoring the patient’s vital signs throughout the procedure. The air cylinder should be checked if not using an electronic machine, and the cuff should be checked for leaks.

During the procedure, a double cuff tourniquet is placed on the upper arm, and the arm is elevated to exsanguinate the limb. The proximal cuff is inflated to a pressure 100 mmHg above the systolic blood pressure, up to a maximum of 300 mmHg. The time of inflation and pressure should be recorded, and the absence of the radial pulse should be confirmed. 0.5% plain prilocaine is then injected slowly, and the time of injection is recorded. The patient should be warned about the potential cold/hot sensation and mottled appearance of the arm. After injection, the cannula is removed and pressure is applied to the venipuncture site to prevent bleeding. After approximately 10 minutes, the patient should have anesthesia and should not feel pain during manipulation. If anesthesia is successful, the manipulation can be performed, and a plaster can be applied by a second staff member. A check x-ray should be obtained with the arm lowered onto a pillow. The tourniquet should be monitored at all times, and the cuff should be inflated for a minimum of 20 minutes and a maximum of 45 minutes. If rotation of the cuff is required, it should be done after the manipulation and plaster application. After the post-reduction x-ray is satisfactory, the cuff can be deflated while observing the patient and monitors. Limb circulation should be checked prior to discharge, and appropriate follow-up and analgesia should be arranged.

There are several contraindications to performing Bier’s block, including allergy to local anesthetic, hypertension over 200 mm Hg, infection in the limb, lymphedema, methemoglobinemia, morbid obesity, peripheral vascular disease, procedures needed in both arms, Raynaud’s phenomenon, scleroderma, severe hypertension and sickle cell disease.

Corneal microdeposits are found in almost all individuals (over 90%) who have been taking amiodarone for more than six months, particularly at doses higher than 400 mg/day. These deposits generally do not cause any symptoms, although approximately 10% of patients may experience a perception of a ‘bluish halo’ around objects they see.

Amiodarone can also have other effects on the eye, but these are much less common, occurring in only 1-2% of patients. These effects include optic neuropathy, nonarteritic anterior ischemic optic neuropathy (N-AION), optic disc swelling, and visual field defects.

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

Further Reading:

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

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

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

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

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

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

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

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

SIADH is a medical condition that is not brought on by lithium toxicity. However, lithium toxicity does have its own distinct set of symptoms. These symptoms include nausea and vomiting, diarrhea, tremors, ataxia, confusion, increased muscle tone, clonus, nephrogenic diabetes insipidus, convulsions, coma, and renal failure. It is important to note that SIADH and lithium toxicity are separate conditions with their own unique characteristics.

Blood transfusion is a crucial treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there has been an improvement in safety procedures and a reduction in transfusion use, errors and serious adverse reactions still occur and often go unreported.

Mild allergic reactions during blood transfusion are relatively common and typically occur within a few minutes of starting the transfusion. These reactions happen when patients have antibodies that react with foreign plasma proteins in the transfused blood components. Symptoms of mild allergic reactions include urticaria, Pruritus, and hives.

Anaphylaxis, on the other hand, is much rarer and occurs when an individual has previously been sensitized to an allergen present in the blood. When re-exposed to the allergen, the body releases IgE or IgG antibodies, leading to severe symptoms such as bronchospasm, laryngospasm, abdominal pain, nausea, vomiting, hypotension, shock, and loss of consciousness. Anaphylaxis can be fatal.

Mild allergic reactions can be managed by slowing down the transfusion rate and administering antihistamines. If there is no progression after 30 minutes, the transfusion may continue. Patients who have experienced repeated allergic reactions to transfusion should be given pre-treatment with chlorpheniramine. In cases of anaphylaxis, the transfusion should be stopped immediately, and the patient should receive oxygen, adrenaline, corticosteroids, and antihistamines following the ALS protocol.

The table below summarizes the main transfusion reactions and complications, along with their features and management:

Complication | Features | Management
Febrile transfusion reaction | 1 degree rise in temperature, chills, malaise | Supportive care, paracetamol
Acute haemolytic reaction | Fever, chills, pain at transfusion site, nausea, vomiting, dark urine | STOP THE TRANSFUSION, administer IV fluids, diuretics if necessary
Delayed haemolytic reaction | Fever, anaemia, jaundice, haemoglobinuria | Monitor anaemia and renal function, treat as required
Allergic reaction | Urticaria, Pruritus, hives | Symptomatic treatment with ant

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

Further Reading:

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

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

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

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

Henry’s law describes the correlation between the quantity of dissolved gas in a liquid and its partial pressure above the liquid. According to Henry’s law, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas above the liquid. In the case of nitrogen narcosis, as the patient descends deeper into the water, the pressure increases, causing more nitrogen to dissolve in the bloodstream. As the patient ascends, the pressure decreases, leading to a decrease in the amount of dissolved nitrogen and improvement in symptoms.

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.

If you have missed one pill, which means it has been 48-72 hours since you took the last pill in your current packet or you started the first pill in a new packet 24-48 hours late, you need to take the missed pill as soon as you remember. Make sure to continue taking the remaining pills at your usual time. Emergency contraception is generally not necessary in this situation, but it may be worth considering if you have missed pills earlier in the packet or during the last week of the previous packet.

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 patients are exposed to the inhalation of combustion byproducts, they face the danger of being poisoned by carbon monoxide and cyanide. In situations where hydrocarbons and substances containing carbon and nitrogen are incompletely burned, the formation of both carbon monoxide and cyanide gas can occur. Individuals who inhale smoke are particularly vulnerable to this type of poisoning.

Further Reading:

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

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

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

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

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

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

The recommended dosage of intravenous lorazepam for treating a child experiencing seizures is 0.1 mg per kilogram of body weight.

In the UK, the most prevalent cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. On a global scale, hypothyroidism is primarily caused by iodine deficiency. However, in areas where iodine levels are sufficient, such as the UK, hypothyroidism and subclinical hypothyroidism are most commonly attributed to autoimmune thyroiditis. This condition can manifest with or without a goitre, known as atrophic thyroiditis.

Further Reading:

The thyroid gland is an endocrine organ located in the anterior neck. It consists of two lobes connected by an isthmus. The gland produces hormones called thyroxine (T4) and triiodothyronine (T3), which regulate energy use, protein synthesis, and the body’s sensitivity to other hormones. The production of T4 and T3 is stimulated by thyroid-stimulating hormone (TSH) secreted by the pituitary gland, which is in turn stimulated by thyrotropin-releasing hormone (TRH) from the hypothalamus.

Thyroid disorders can occur when there is an imbalance in the production or regulation of thyroid hormones. Hypothyroidism is characterized by a deficiency of thyroid hormones, while hyperthyroidism is characterized by an excess. The most common cause of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. It is more common in women and is often associated with goiter. Other causes include subacute thyroiditis, atrophic thyroiditis, and iodine deficiency. On the other hand, the most common cause of hyperthyroidism is Graves’ disease, which is also an autoimmune disorder. Other causes include toxic multinodular goiter and subacute thyroiditis.

The symptoms and signs of thyroid disorders can vary depending on whether the thyroid gland is underactive or overactive. In hypothyroidism, common symptoms include weight gain, lethargy, cold intolerance, and dry skin. In hyperthyroidism, common symptoms include weight loss, restlessness, heat intolerance, and increased sweating. Both hypothyroidism and hyperthyroidism can also affect other systems in the body, such as the cardiovascular, gastrointestinal, and neurological systems.

Complications of thyroid disorders can include dyslipidemia, metabolic syndrome, coronary heart disease, heart failure, subfertility and infertility, impaired special senses, and myxedema coma in severe cases of hypothyroidism. In hyperthyroidism, complications can include Graves’ orbitopathy, compression of the esophagus or trachea by goiter, thyrotoxic periodic paralysis, arrhythmias, osteoporosis, mood disorders, and increased obstetric complications.

Myxedema coma is a rare and life-threatening complication of severe hypothyroidism. It can be triggered by factors such as infection or physiological insult and presents with lethargy, bradycardia, hypothermia, hypotension, hypoventilation, altered mental state, seizures and/or coma.

The most likely diagnosis in this case is Goodpasture’s syndrome, which is a rare autoimmune vasculitic disorder. It is characterized by a triad of symptoms including pulmonary hemorrhage, glomerulonephritis, and the presence of anti-glomerular basement membrane (Anti-GBM) antibodies. Goodpasture’s syndrome is more commonly seen in men, particularly in smokers. There is also an association with certain HLA types, specifically HLA-B7 and HLA-DRw2.

The clinical features of Goodpasture’s syndrome include constitutional symptoms such as fever, fatigue, nausea, and weight loss. Patients may also experience haemoptysis or pulmonary hemorrhage, chest pain, breathlessness, and inspiratory crackles at the lung bases. Anemia due to intrapulmonary bleeding, arthralgia, rapidly progressive glomerulonephritis, haematuria, hypertension, and hepatosplenomegaly (rarely) may also be present.

Blood tests will reveal an iron deficiency anemia, elevated white cell count, and renal impairment. Elisa for Anti-GBM antibodies is highly sensitive and specific, but it is not widely available. Approximately 30% of patients may also have circulating antineutrophilic cytoplasmic antibodies (ANCAs), although these are not specific for Goodpasture’s syndrome and can be found in other conditions such as Wegener’s granulomatosis.

Diagnosis is typically confirmed through renal biopsy, which can detect the presence of anti-GBM antibodies. The management of Goodpasture’s syndrome involves a combination of plasmapheresis to remove circulating antibodies and the use of corticosteroids or cyclophosphamide.

It is important to note that this patient’s history is inconsistent with a diagnosis of pulmonary embolism, as renal impairment, haematuria, and the presence of ANCAs and anti-GBM antibodies would not be expected. While pulmonary hemorrhage and renal impairment can occur in systemic lupus erythematosus, these are uncommon presentations, and the presence of ANCAs and anti-GBM antibodies would also be inconsistent with this diagnosis.

Churg-Strauss syndrome can present with pulmonary hemorrhage, and c-ANCA may be present, but patients typically have a history of asthma, sinusitis, and eosinophilia. Wegener’s granulomatosis can present similarly to Goodpasture’s syndrome,

Children with severe croup require high flow oxygen and nebulized adrenaline as part of their treatment. If a child is agitated or lethargic, it is a sign that the disease is severe. In addition to standard steroid treatment, high flow oxygen and nebulized adrenaline are necessary for treating severe croup. It is important to note that beta 2 agonists are not effective for children under 2 years old.

Further Reading:

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

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

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

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

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

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

AKI is categorized into three stages based on specific criteria. In stage 1, there is a rise in creatinine levels of 26 micromol/L or more within 48 hours, or a rise of 50-99% from baseline within 7 days (1.5-1.99 times the baseline). Additionally, a urine output of less than 0.5 mL/kg/hour for more than 6 hours is indicative of stage 1 AKI.

Stage 2 AKI is characterized by a creatinine rise of 100-199% from baseline within 7 days (2.0-2.99 times the baseline), or a urine output of less than 0.5 mL/kg/hour for more than 12 hours.

In stage 3 AKI, there is a creatinine rise of 200% or more from baseline within 7 days (3.0 or more times the baseline). Alternatively, a creatinine rise to 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours, or a rise of 50% or more within 7 days, is indicative of stage 3 AKI. Additionally, a urine output of less than 0.3 mL/kg/hour for 24 hours or anuria (no urine output) for 12 hours also falls under stage 3 AKI.

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.

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

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

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

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

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

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

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

Statins, although generally safe and well-tolerated, can cause myopathy and myotoxicity. This range of muscle-related side effects can vary from mild muscle pain to the most severe case of rhabdomyolysis, which can lead to kidney failure, blood clotting issues, and even death.

The different levels of myotoxicity associated with statins are as follows:
– Myalgia: muscle symptoms without an increase in creatine kinase (CK) levels.
– Asymptomatic myopathy: elevated CK levels without muscle symptoms.
– Myositis: muscle symptoms with CK levels elevated less than 10 times the upper limit of normal.
– Rhabdomyolysis: muscle symptoms with CK levels elevated more than 10 times the upper limit of normal, potentially leading to myoglobinuria (presence of myoglobin in urine) and renal failure.

Most statins are broken down by the cytochrome P450 enzyme system. When taken with drugs that strongly inhibit this system, the concentration of statins in the blood can significantly increase. This, in turn, raises the risk of myopathy. A well-known example of this is the combination of statins with macrolide antibiotics like erythromycin and clarithromycin. Co-prescribing these drugs with statins has been linked to a higher risk of myopathy, hospitalization due to rhabdomyolysis, acute kidney injury, and increased mortality rates.

The risk of infection is highest with femoral central lines.

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

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

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

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

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

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

There are various specific remedies available for different types of poisons and overdoses. The following list provides an outline of some of these antidotes:

Poison: Benzodiazepines
Antidote: Flumazenil

Poison: Beta-blockers
Antidotes: Atropine, Glucagon, Insulin

Poison: Carbon monoxide
Antidote: Oxygen

Poison: Cyanide
Antidotes: Hydroxocobalamin, Sodium nitrite, Sodium thiosulphate

Poison: Ethylene glycol
Antidotes: Ethanol, Fomepizole

Poison: Heparin
Antidote: Protamine sulphate

Poison: Iron salts
Antidote: Desferrioxamine

Poison: Isoniazid
Antidote: Pyridoxine

Poison: Methanol
Antidotes: Ethanol, Fomepizole

Poison: Opioids
Antidote: Naloxone

Poison: Organophosphates
Antidotes: Atropine, Pralidoxime

Poison: Paracetamol
Antidotes: Acetylcysteine, Methionine

Poison: Sulphonylureas
Antidotes: Glucose, Octreotide

Poison: Thallium
Antidote: Prussian blue

Poison: Warfarin
Antidote: Vitamin K, Fresh frozen plasma (FFP)

By utilizing these specific antidotes, medical professionals can effectively counteract the harmful effects of various poisons and overdoses.

Bronchiolitis is primarily caused by the respiratory syncytial virus (RSV), while whooping cough is caused by pertussis.

Further Reading:

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

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

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

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

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

Bronchiolitis is a short-term infection of the lower respiratory tract that primarily affects infants aged 2 to 6 months. It is commonly caused by a viral infection, with respiratory syncytial virus (RSV) being the most prevalent culprit. RSV infections are most prevalent during the winter months, typically occurring between November and March. In the UK, bronchiolitis is the leading cause of hospitalization among infants.

The typical symptoms of bronchiolitis include fever, difficulty breathing, coughing, poor feeding, irritability, apnoeas (more common in very young infants), and wheezing or fine inspiratory crackles. To confirm the diagnosis, a nasopharyngeal aspirate can be taken for RSV rapid testing. This test is useful in preventing unnecessary further testing and facilitating the isolation of the affected infant.

Most infants with acute bronchiolitis experience a mild, self-limiting illness that does not require hospitalization. Treatment primarily focuses on supportive measures, such as ensuring adequate fluid and nutritional intake and controlling the infant’s temperature. The illness typically lasts for 7 to 10 days.

However, hospital referral and admission are recommended in certain cases, including poor feeding (less than 50% of usual intake over the past 24 hours), lethargy, a history of apnoea, a respiratory rate exceeding 70 breaths per minute, nasal flaring or grunting, severe chest wall recession, cyanosis, oxygen saturations below 90% for children aged 6 weeks and over, and oxygen saturations below 92% for babies under 6 weeks or those with underlying health conditions.

If hospitalization is necessary, treatment involves supportive measures, supplemental oxygen, and nasogastric feeding as needed. There is limited or no evidence supporting the use of antibiotics, antivirals, bronchodilators, corticosteroids, hypertonic saline, or adrenaline nebulizers in the management of bronchiolitis.

This patient has been experiencing absence seizures, which are a form of primary generalized epilepsy that is frequently observed in children.

The defining characteristic of absence seizures is a sudden and immediate loss of consciousness, causing a disruption in ongoing activities. During these episodes, individuals may exhibit a vacant stare and occasionally a brief upward movement of the eyes.

While an EEG cannot definitively confirm or rule out an epilepsy diagnosis, it does provide valuable information in the diagnostic process. In the case of absence seizures, EEG results typically reveal generalized spike-and-slow wave complexes occurring at a frequency of 3-4 Hz.

The current guidelines from NICE recommend that the first-line treatment for confirmed deep-vein thrombosis (DVT) or pulmonary embolism (PE) should be either apixaban or rivaroxaban, which are direct oral anticoagulants.

If neither of these options is suitable, the following alternatives should be considered:

1. LMWH (low molecular weight heparin) should be administered for at least 5 days, followed by dabigatran or edoxaban.

2. LMWH should be combined with a vitamin K antagonist (VKA), such as warfarin, for at least 5 days or until the international normalized ratio (INR) reaches at least 2.0 on 2 consecutive readings. Afterward, the VKA can be continued alone.

The MASCC Risk Index Score, developed by the Multinational Association of Supportive Care in Cancer, is a tool that can be utilized to identify patients who are at low risk for experiencing serious complications of febrile neutropenia. This score takes into account various characteristics of the patient to determine their risk level. For example, patients who have a minimal burden of febrile neutropenia with no or mild symptoms, no hypotension (with a systolic blood pressure above 90 mmHg), and no chronic obstructive pulmonary disease are assigned higher scores. Additionally, patients with a solid tumor or hematological malignancy and no previous fungal infection, as well as those who do not require parental fluids for dehydration, are also given higher scores. On the other hand, patients with a moderate burden of febrile neutropenia symptoms, those in an outpatient setting at the onset of fever, and those under the age of 60 receive lower scores. It is important to note that the qSOFA Score, CURB-65 Score, SCAP Score, and qCSI Score are different tools used for assessing different conditions and are not specifically used in the context of febrile neutropenia.

Hyperkalaemia is a condition where the level of potassium in the blood is higher than normal, specifically greater than 5.5 mmol/l. It can be categorized as mild, moderate, or severe depending on the specific potassium levels. Mild hyperkalaemia is when the potassium level is between 5.5-5.9 mmol/l, moderate hyperkalaemia is between 6.0-6.4 mmol/l, and severe hyperkalaemia is when the potassium level exceeds 6.5 mmol/l. The most common cause of hyperkalaemia in renal failure, which can be either acute or chronic. Other causes include acidosis, adrenal insufficiency, cell lysis, and excessive potassium intake.

If the patient’s life is not immediately at risk due to an arrhythmia, the initial treatment for hyperkalaemia should involve the use of a beta-2 agonist, such as salbutamol (2.5-10 mg). Salbutamol activates cAMP, which stimulates the Na+/K+ ATPase pump. This action helps shift potassium into the intracellular compartment. The effects of salbutamol are rapid, typically occurring within 30 minutes. With the recommended dose, a decrease in the serum potassium level of approximately 1 mmol can be expected.

In stable patients with SVT, it is recommended to first try vagal manoeuvres before resorting to drug treatment. This approach is particularly applicable to patients who do not exhibit any adverse features, as mentioned in the case above.

Further Reading:

Supraventricular tachycardia (SVT) is a type of tachyarrhythmia that originates from the atria or above the bundle of His in the heart. It includes all atrial and junctional tachycardias, although atrial fibrillation is often considered separately. SVT typically produces a narrow QRS complex tachycardia on an electrocardiogram (ECG), unless there is an underlying conduction abnormality below the atrioventricular (AV) node. Narrow complex tachycardias are considered SVTs, while some broad complex tachycardias can also be SVTs with co-existent conduction delays.

SVT can be classified into three main subtypes based on where it arises: re-entrant accessory circuits (the most common type), atrial tachycardias, and junctional tachycardias. The most common SVTs are AVNRT (AV nodal re-entry tachycardia) and AVRT (AV re-entry tachycardia), which arise from accessory circuits within the heart. AVNRT involves an accessory circuit within the AV node itself, while AVRT involves an accessory pathway between the atria and ventricles that allows additional electrical signals to trigger the AV node.

Atrial tachycardias originate from abnormal foci within the atria, except for the SA node, AV node, or accessory pathway. Junctional tachycardias arise in the AV junction. The ECG features of SVTs vary depending on the type. Atrial tachycardias may have abnormal P wave morphology, an isoelectric baseline between P waves (in atrial flutter), and inverted P waves in certain leads. AVNRT may show pseudo R waves in V1 or pseudo S waves in certain leads, with an RP interval shorter than the PR interval. AVRT (WPW) may exhibit a delta wave on a resting ECG and retrograde P waves in the ST segment, with an RP interval shorter than the PR interval. Junctional tachycardias may have retrograde P waves before, during, or after the QRS complex, with inverted P waves in certain leads and upright P waves in others.

Treatment of SVT follows the 2021 resuscitation council algorithm for tachycardia with a pulse. The algorithm provides guidelines for managing stable patients with SVT.

Diabetic ketoacidosis (DKA) is a life-threatening condition that occurs when there is a lack of insulin, leading to an inability to process glucose. This results in high blood sugar levels and excessive thirst. As the body tries to eliminate the excess glucose through urine, dehydration becomes inevitable. Without insulin, the body starts using fat as its main energy source, which leads to the production of ketones and a buildup of acid in the blood.

The main characteristics of DKA are high blood sugar levels (above 11 mmol/l), the presence of ketones in the blood or urine, and acidosis (low bicarbonate levels and/or low venous pH). Symptoms of DKA include nausea, vomiting, excessive thirst, frequent urination, abdominal pain, signs of dehydration, a distinct smell of ketones on the breath, rapid and deep breathing, confusion or reduced consciousness, and cardiovascular symptoms like rapid heartbeat, low blood pressure, and shock.

To diagnose DKA, various tests should be performed, including blood glucose measurement, urine dipstick test (which shows high levels of glucose and ketones), blood ketone assay (more accurate than urine dipstick), complete blood count, and electrolyte levels. Arterial or venous blood gas analysis can confirm the presence of metabolic acidosis.

The management of DKA involves careful fluid administration and insulin replacement. Fluid boluses should only be given if there are signs of shock and should be administered slowly in 10 ml/kg increments. Once shock is resolved, rehydration should be done over 48 hours. The first 20 ml/kg of fluid given for resuscitation should not be subtracted from the total fluid volume calculated for the 48-hour replacement. In cases of hypotensive shock, consultation with a pediatric intensive care specialist may be necessary.

Insulin replacement should begin 1-2 hours after starting intravenous fluid therapy. A soluble insulin infusion should be used at a dosage of 0.05-0.1 units/kg/hour. The goal is to bring blood glucose levels close to normal. Regular monitoring of electrolytes and blood glucose levels is important to prevent imbalances and rapid changes in serum osmolarity. Identifying and treating the underlying cause of DKA is also crucial.

When calculating fluid requirements for children and young people with DKA, assume a 5% fluid deficit for mild-to-moderate cases (blood pH of 7.1 or above) and a 10% fluid deficit in severe DKA (indicated by a blood pH below 7.1). The total replacement fluid to be given over 48 hours is calculated as follows: Hourly rate = (deficit/48 hours) + maintenance per hour.

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.

The median nerve originates from the lateral and medial cords of the brachial plexus and receives contributions from the ventral roots of C5-C7 (lateral cord) and C8 and T1 (medial cord). It serves both motor and sensory functions.

In terms of motor function, the median nerve innervates the flexor muscles in the anterior compartment of the forearm, excluding the flexor carpi ulnaris and a portion of the flexor digitorum profundus, which are instead innervated by the ulnar nerve. Additionally, it innervates the thenar muscles and the lateral two lumbricals.

Regarding sensory function, the median nerve gives rise to the palmar cutaneous branch, which provides innervation to the lateral part of the palm. It also gives rise to the digital cutaneous branch, which innervates the lateral three and a half fingers on the palmar surface of the hand.

Within the forearm, the median nerve branches into two major branches: the anterior interosseous nerve (AIN) and the palmar cutaneous branch. The AIN supplies the flexor pollicis longus, pronator quadratus, and the lateral half of the flexor digitorum profundus. On the other hand, the palmar cutaneous branch provides sensory innervation to the skin of the radial palm.

Differentiating between damage to the median nerve at the elbow and wrist can be done by considering these two branches. Injury at the elbow affects these branches, while injury at the wrist spares them. It is important to note that the palmar cutaneous branch remains functional in carpal tunnel syndrome as it travels superficial to the flexor retinaculum. However, it can be damaged by laceration at the wrist.

A comparison of median nerve lesions at the wrist and elbow is presented in the table below:

Median nerve at elbow:
– Motor loss: Weak wrist flexion and abduction, loss of thumb abduction and opposition, loss of flexion of index and middle fingers
– Sensory loss: Lateral 3 and ½ fingers and nail beds, lateral side of palm
– Hand deformity: Ulnar deviation of wrist, thenar wasting, papal benediction on flexing fingers

Median nerve at wrist:
– Motor loss: Loss of thumb abduction and opposition, wrist and finger flexion intact (due to intact AIN)
– Sensory loss: Lateral 3 and ½ fingers and nail beds, lateral side of palm (but can be preserved depending upon palmar cutaneous branch)
– Hand deformity: Thenar wasting, no ulnar deviation of wrist or papal benediction (due to intact AIN)

To perform rapid sequence induction in adults, it is recommended to administer a dose of sodium thiopentone ranging from 3 to 5 mg per kilogram of body weight.

Further Reading:

There are four commonly used induction agents in the UK: propofol, ketamine, thiopentone, and etomidate.

Propofol is a 1% solution that produces significant venodilation and myocardial depression. It can also reduce cerebral perfusion pressure. The typical dose for propofol is 1.5-2.5 mg/kg. However, it can cause side effects such as hypotension, respiratory depression, and pain at the site of injection.

Ketamine is another induction agent that produces a dissociative state. It does not display a dose-response continuum, meaning that the effects do not necessarily increase with higher doses. Ketamine can cause bronchodilation, which is useful in patients with asthma. The initial dose for ketamine is 0.5-2 mg/kg, with a typical IV dose of 1.5 mg/kg. Side effects of ketamine include tachycardia, hypertension, laryngospasm, unpleasant hallucinations, nausea and vomiting, hypersalivation, increased intracranial and intraocular pressure, nystagmus and diplopia, abnormal movements, and skin reactions.

Thiopentone is an ultra-short acting barbiturate that acts on the GABA receptor complex. It decreases cerebral metabolic oxygen and reduces cerebral blood flow and intracranial pressure. The adult dose for thiopentone is 3-5 mg/kg, while the child dose is 5-8 mg/kg. However, these doses should be halved in patients with hypovolemia. Side effects of thiopentone include venodilation, myocardial depression, and hypotension. It is contraindicated in patients with acute porphyrias and myotonic dystrophy.

Etomidate is the most haemodynamically stable induction agent and is useful in patients with hypovolemia, anaphylaxis, and asthma. It has similar cerebral effects to thiopentone. The dose for etomidate is 0.15-0.3 mg/kg. Side effects of etomidate include injection site pain, movement disorders, adrenal insufficiency, and apnoea. It is contraindicated in patients with sepsis due to adrenal suppression.

The most appropriate initial treatment for this patient would be intravenous labetalol. Labetalol is a non-selective beta blocker with alpha-blocking properties. It is the preferred initial treatment for aortic dissection because it helps to reduce blood pressure and heart rate, which can help to decrease the shear forces acting on the aortic wall and prevent further dissection. Intravenous administration of labetalol allows for rapid and effective control of blood pressure.

Other treatment options, such as intravenous magnesium sulphate, intravenous verapamil, GTN sublingual spray, and oral nifedipine, are not appropriate for the management of aortic dissection. Magnesium sulphate is used for the treatment of certain arrhythmias and pre-eclampsia, but it does not address the underlying issue of aortic dissection. Verapamil and nifedipine are calcium channel blockers that can lower blood pressure, but they can also cause reflex tachycardia, which can worsen the condition. GTN sublingual spray is used for the treatment of angina, but it does not address the underlying issue of aortic dissection.

Further Reading:

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

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

Further Reading:

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

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

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

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

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

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

The Act establishes five principles that aim to govern decisions made under the legislation:

1. Capacity is presumed unless proven otherwise: It is assumed that a person has the ability to make decisions unless it is proven that they lack capacity.

2. Assistance must be provided before determining incapacity: A person should not be considered unable to make a decision until all reasonable efforts have been made to support them in doing so.

3. Unwise decisions do not indicate incapacity: Making a decision that others may consider unwise does not automatically mean that a person lacks capacity.

4. Best interests must guide decision-making: All decisions made on behalf of an incapacitated person must be in their best interests.

5. Least restrictive approach should be taken: Decisions should be made in a way that minimizes any restrictions on the individual’s fundamental rights and freedoms.

If a decision significantly conflicts with these principles, it is unlikely to be lawful.

A person is deemed to lack capacity if they are unable to:

– Understand the relevant information related to the decision.
– Retain the information in their memory.
– Use or evaluate the information to make a decision.
– Communicate their decision effectively, using any means necessary.

When assessing capacity, it is important to consider the input of those close to the individual, if appropriate. Close friends and family may provide valuable insights, although their opinions should not unduly influence the assessment.

In urgent situations where a potentially life-saving decision needs to be made, an IMCA (Independent Mental Capacity Advocate) does not need to be involved.

Occlusion of branches of the anterior spinal artery leads to the development of the medial medullary syndrome. This condition is characterized by several distinct symptoms. Firstly, there is contralateral hemiplegia, which occurs due to damage to the pyramidal tracts. Additionally, there is contralateral loss of joint position sense, vibratory sense, and discriminatory touch, resulting from damage to the medial lemniscus. Lastly, there is ipsilateral deviation and paralysis of the tongue, which is caused by damage to the hypoglossal nucleus.

Confidentiality plays a crucial role in the doctor-patient relationship and is vital for maintaining trust in the medical profession. However, there are certain situations, such as cases involving gun and knife crimes that pose a potential risk to the public, where it may be necessary to breach this confidentiality and provide information to the police, even if the patient refuses.

It is important to make every effort to obtain the patient’s consent, while also explaining your legal obligation to report such incidents. When sharing information with the police, it is essential to disclose only the minimum amount of information required. Typically, this would include the patient’s basic details and the fact that they have sought medical attention for a non-self-inflicted deliberate knife wound.

In some cases, where it is evident that the injury was accidental or a result of deliberate self-harm due to a mental health condition, there may be no need to involve the police. However, regardless of the circumstances, the necessary medical treatment should still be provided for the wound, as long as the patient gives their consent.

For more information on this topic, you can refer to the GMC Guidance on Reporting Gunshot and Knife Wounds.

Chronic myeloid leukaemia (CML) is a type of blood disorder that arises from an abnormal pluripotent haemopoietic stem cell. The majority of CML cases, more than 80%, are caused by a cytogenetic abnormality called the Philadelphia chromosome. This abnormality occurs when there is a reciprocal translocation between the long arms of chromosomes 9 and 22.

CML typically develops slowly over a period of several years, known as the chronic stage. During this stage, patients usually do not experience any symptoms, and it is often discovered incidentally through routine blood tests. Around 90% of CML cases are diagnosed during this stage. In the bone marrow, less than 10% of the white cells are immature blasts.

Symptoms start to appear when the CML cells begin to expand, which is known as the accelerated stage. Approximately 10% of cases are diagnosed during this stage. Between 10 and 30% of the blood cells in the bone marrow are blasts at this point. Common clinical features during this stage include tiredness, fatigue, fever, night sweats, abdominal distension, left upper quadrant pain (splenic infarction), splenomegaly (enlarged spleen), hepatomegaly (enlarged liver), easy bruising, gout (due to rapid cell turnover), and hyperviscosity (which can lead to complications like stroke, priapism, etc.).

In some cases, a small number of patients may present with a blast crisis, also known as the blast stage. During this stage, more than 30% of the blood cells in the bone marrow are immature blast cells. Patients in this stage are generally very ill, experiencing severe constitutional symptoms such as fever, weight loss, and bone pain, as well as infections and bleeding tendencies.

Laboratory findings in CML include a significantly elevated white cell count (often greater than 100 x 109/l), a left shift with an increased number of immature leukocytes, mild to moderate normochromic, normocytic anaemia, variable platelet counts (low, normal, or elevated), presence of the Philadelphia chromosome in more than 80% of cases, and elevated levels of serum uric acid and alkaline phosphatase.

Vomiting is a common occurrence during the early stages of pregnancy, typically happening between 7 and 12 weeks. However, there is a more severe form called hyperemesis gravidarum, which affects less than 1% of pregnancies. This condition is characterized by uncontrollable and intense nausea and vomiting, leading to imbalances in fluids and electrolytes, significant ketonuria, nutritional deficiencies, and weight loss.

Hyperemesis gravidarum can result in electrolyte imbalances, particularly hyponatremia and hypokalemia. However, it does not cause hyperkalemia. This persistent vomiting can also lead to other complications such as dehydration, acidosis, deficiencies in vitamins B1, B12, and B6, Mallory-Weiss tears, retinal hemorrhages, pneumothorax, prematurity, and small-for-gestational age babies.

Pemphigus, derived from the Greek word for bubble ‘pemphix’, refers to a group of autoimmune disorders that cause blistering of the skin and/or mucosal surfaces. The most common subset is pemphigus vulgaris (PV), which accounts for approximately 70% of cases worldwide. PV is characterized by an autoimmune response where autoantibodies target cell surface antigens on keratinocytes, specifically desmogleins 1 and 3. This leads to a loss of cell-to-cell adhesion and separation, resulting in blister formation.

On the other hand, bullous pemphigoid (BP) is a chronic autoimmune blistering skin disorder that affects the subepidermal layer. It occurs when the basement membrane of the epidermis is attacked by IgG and sometimes IgE immunoglobulins, as well as activated T lymphocytes. The binding of autoantibodies to proteins and the release of cytokines from T cells trigger complement activation, neutrophil recruitment, and the release of proteolytic enzymes. These enzymes destroy the hemidesmosomes, leading to the formation of subepidermal blisters.

To summarize the differences between pemphigus vulgaris and bullous pemphigoid, the following provides a comparison:

Pemphigus Vulgaris:
– Age: Middle-aged people (mean age 50)
– Oral involvement: Common
– Blister type: Large, flaccid, and painful
– Blister content: Fluid-filled, often haemorrhagic
– Areas commonly affected: Initially face and scalp, then spread to the chest and back
– Nikolsky sign: Usually positive
– Pruritus: Rare
– Skin biopsy: Intra-epidermal deposition of IgG between cells throughout the epidermis

Bullous Pemphigoid:
– Age: Elderly people (mean age 80)
– Oral involvement: Rare
– Blister type: Large and tense
– Blister content: Fluid-filled
– Areas commonly affected: Upper arms, thighs, and skin flexures
– Nikolsky sign: Usually negative
– Pruritus: Common
– Skin biopsy: A band of IgG and/or C3 at the dermo-epidermal junction

The Alcohol Use Disorder Identification Test (AUDIT) has been developed by the World Health Organization as a straightforward screening tool to detect early signs of hazardous and harmful drinking, as well as mild dependence. This assessment is more comprehensive than the CAGE questionnaire and is currently recommended by NICE for identifying alcohol misuse.

NICE, the National Institute for Health and Care Excellence, suggests the use of specific assessment tools to evaluate the nature and severity of alcohol misuse. These tools include AUDIT for identification and as a routine outcome measure, SADQ or LDQ for assessing the severity of dependence, CIWA-Ar for evaluating the severity of withdrawal symptoms, and APQ for understanding the nature and extent of problems resulting from alcohol misuse.

For more information on this topic, you can refer to the NICE guidance titled Alcohol-use disorders: diagnosis, assessment and management of harmful drinking and alcohol dependence.

Benzodiazepines are medications that are utilized to address emergence phenomena, which are characterized by restlessness and distressing hallucinations experienced upon awakening from ketamine sedation or induction. These phenomena are more frequently observed in older children and adults, affecting approximately one out of every three adults. To manage emergence phenomena, benzodiazepines may be administered. It is important to note that the RCEM does not recommend preventive treatment and suggests addressing emergence phenomena as they arise.

Further Reading:

There are four commonly used induction agents in the UK: propofol, ketamine, thiopentone, and etomidate.

Propofol is a 1% solution that produces significant venodilation and myocardial depression. It can also reduce cerebral perfusion pressure. The typical dose for propofol is 1.5-2.5 mg/kg. However, it can cause side effects such as hypotension, respiratory depression, and pain at the site of injection.

Ketamine is another induction agent that produces a dissociative state. It does not display a dose-response continuum, meaning that the effects do not necessarily increase with higher doses. Ketamine can cause bronchodilation, which is useful in patients with asthma. The initial dose for ketamine is 0.5-2 mg/kg, with a typical IV dose of 1.5 mg/kg. Side effects of ketamine include tachycardia, hypertension, laryngospasm, unpleasant hallucinations, nausea and vomiting, hypersalivation, increased intracranial and intraocular pressure, nystagmus and diplopia, abnormal movements, and skin reactions.

Thiopentone is an ultra-short acting barbiturate that acts on the GABA receptor complex. It decreases cerebral metabolic oxygen and reduces cerebral blood flow and intracranial pressure. The adult dose for thiopentone is 3-5 mg/kg, while the child dose is 5-8 mg/kg. However, these doses should be halved in patients with hypovolemia. Side effects of thiopentone include venodilation, myocardial depression, and hypotension. It is contraindicated in patients with acute porphyrias and myotonic dystrophy.

Etomidate is the most haemodynamically stable induction agent and is useful in patients with hypovolemia, anaphylaxis, and asthma. It has similar cerebral effects to thiopentone. The dose for etomidate is 0.15-0.3 mg/kg. Side effects of etomidate include injection site pain, movement disorders, adrenal insufficiency, and apnoea. It is contraindicated in patients with sepsis due to adrenal suppression.

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.

The GMC provides guidance on confidentiality that highlights the importance of assessing whether adults have the ability to give consent for the disclosure of their medical information. If the patient is capable, meaning they can comprehend relevant information, retain it, evaluate it, and communicate their decision, then their preferences should be honored, even if you believe their decision is unwise or puts them at risk of serious harm.

In the event that the patient has the capacity but you believe it would be beneficial to involve social services, you can encourage them to allow you to contact them. However, it is crucial to respect their decision if they decline. On the other hand, if the patient lacks capacity, the doctor should make a decision based on what is in their best interests, which may include raising a concern for their protection.

In managing patients with carbon monoxide poisoning, the primary intervention is providing 100% oxygen. This is because carbon monoxide has a higher affinity for hemoglobin than oxyge