Nitrous oxide should not be used in cases where there is trapped air, such as pneumothorax. This is because nitrous oxide can diffuse into the trapped air and increase the pressure, which can be harmful. This can be particularly dangerous in conditions like pneumothorax, where the trapped air can expand and affect breathing, or in cases of intracranial air after a head injury, trapped air after a recent underwater dive, or recent injection of gas into the eye.

Further Reading:

Entonox® is a mixture of 50% nitrous oxide and 50% oxygen that can be used for self-administration to reduce anxiety. It can also be used alongside other anesthesia agents. However, its mechanism of action for anxiety reduction is not fully understood. The Entonox bottles are typically identified by blue and white color-coded collars, but a new standard will replace these with dark blue shoulders in the future. It is important to note that Entonox alone cannot be used as the sole maintenance agent in anesthesia.

One of the effects of nitrous oxide is the second-gas effect, where it speeds up the absorption of other inhaled anesthesia agents. Nitrous oxide enters the alveoli and diffuses into the blood, displacing nitrogen. This displacement causes the remaining alveolar gases to become more concentrated, increasing the fractional content of inhaled anesthesia gases and accelerating the uptake of volatile agents into the blood.

However, when nitrous oxide administration is stopped, it can cause diffusion hypoxia. Nitrous oxide exits the blood and diffuses back into the alveoli, while nitrogen diffuses in the opposite direction. Nitrous oxide enters the alveoli much faster than nitrogen leaves, resulting in the dilution of oxygen within the alveoli. This can lead to diffusion hypoxia, where the oxygen concentration in the alveoli is diluted, potentially causing oxygen deprivation in patients breathing air.

There are certain contraindications for using nitrous oxide, as it can expand in air-filled spaces. It should be avoided in conditions such as head injuries with intracranial air, pneumothorax, recent intraocular gas injection, and entrapped air following a recent underwater dive.

Penicillin is frequently responsible for drug-induced anaphylaxis, making it the primary cause. Following closely behind are NSAIDs, which are the second most common cause. Additionally, ACE inhibitors and aspirin are commonly associated with anaphylaxis.

According to the current NICE guidelines on febrile illness in children under the age of 5, there are certain symptoms and signs that may indicate the presence of pneumonia. These include tachypnoea, which is a rapid breathing rate. For infants aged 0-5 months, a respiratory rate (RR) of over 60 breaths per minute is considered suggestive of pneumonia. For infants aged 6-12 months, an RR of over 50 breaths per minute is indicative, and for children older than 12 months, an RR of over 40 breaths per minute may suggest pneumonia.

Other signs that may point towards pneumonia include crackles in the chest, nasal flaring, chest indrawing, and cyanosis. Crackles are abnormal sounds heard during breathing, while nasal flaring refers to the widening of the nostrils during breathing. Chest indrawing is the inward movement of the chest wall during inhalation, and cyanosis is the bluish discoloration of the skin or mucous membranes due to inadequate oxygen supply.

Additionally, a low oxygen saturation level of less than 95% while breathing air is also considered suggestive of pneumonia. These guidelines can be found in more detail in the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

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

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

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

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

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

A pleural effusion refers to the accumulation of excess fluid in the pleural cavity, which is the fluid-filled space between the parietal and visceral pleura. Normally, this cavity contains about 5-10 ml of lubricating fluid that allows the pleurae to slide over each other and helps the lungs fill with air as the thorax expands. However, when there is too much fluid in the pleural cavity, it hinders breathing by limiting lung expansion.

Percutaneous pleural aspiration is commonly performed for two main reasons: to investigate pleural effusion and to provide relief from breathlessness caused by pleural effusion. According to the guidelines from the British Thoracic Society (BTS), pleural aspiration should be reserved for the investigation of unilateral exudative pleural effusions. It should not be done if unilateral or bilateral transudative effusion is suspected, unless there are atypical features or a lack of response to therapy. In urgent cases where respiratory distress is caused by pleural effusion, pleural aspiration can also be used to quickly decompress the pleural space.

During the procedure, the patient is typically seated upright with a pillow supporting their arms and head. It is important for the patient not to lean too far forward, as this increases the risk of injury to the liver and spleen. The conventional site for aspiration is in the mid-scapular line at the back (approximately 10 cm to the side of the spine), one or two spaces below the upper level of the fluid. To avoid damaging the intercostal nerves and vessels that run just below the rib, the needle should be inserted just above the upper border of the chosen rib.

If a person shows symptoms after ingesting salicylate, their salicylate levels should be measured 2 hours after ingestion. However, if the person does not show any symptoms, the levels should be measured 4 hours after ingestion. It is important to note that if enteric coated preparations are taken, salicylate levels may continue to increase for up to 12 hours. Therefore, it is necessary to regularly check the levels every 2-3 hours until they start to decrease.

Further Reading:

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

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

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

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

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

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

The recommended target SpO2, which measures the percentage of oxygen saturation in the blood, following a cardiac arrest is 94-98%. This range ensures that the patient receives adequate oxygenation without the risk of hyperoxia, which is an excess of oxygen in the body.

Further Reading:

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

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

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

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

The British Thoracic Society (BTS) advises that chest drains should be inserted within the safe triangle to minimize the risk of harm to underlying structures and prevent damage to muscle and breast tissue, which can result in unsightly scarring. The safe triangle is defined by the base of the axilla, the lateral border of the latissimus dorsi, the lateral border of the pectoralis major, and the 5th intercostal space.

There are several potential complications associated with the insertion of small-bore chest drains. These include puncture of the intercostal artery, accidental perforation of organs due to over-introduction of the dilator into the chest cavity, hospital-acquired pleural infection caused by a non-aseptic technique, inadequate stay suture that may lead to the chest tube falling out, and tube blockage, which may occur more frequently compared to larger bore Argyle drains.

For more information on this topic, please refer to the British Thoracic Society pleural disease guidelines.

This is a classical history for a simple urinary tract infection. The other possible causes mentioned can also result in frank haematuria, but they would be less likely based on the given history.

Bladder cancer typically presents with additional symptoms such as an abdominal mass, weight loss, and fatigue. Nephritis is more likely to cause renal angle tenderness and some systemic upset. It is often preceded by another infection.

Tuberculosis may also have more systemic involvement, although it can present on its own. Renal stones commonly cause severe pain from the loin to the groin and renal angle tenderness.

Appendicitis is characterized by inflammation of the appendix. It is believed to occur when the appendix lumen becomes blocked, and in confirmed cases, about 75-80% of resected specimens contain faecoliths. This condition is most commonly seen in childhood and becomes less common after the age of 40. Mortality rates increase with age, with the highest rates observed in the elderly.

The classic presentation of appendicitis involves early, poorly localized pain around the belly button, which then moves to the lower right side of the abdomen (known as the right iliac fossa). Other common symptoms include loss of appetite, vomiting, and fever. The initial belly button pain is an example of visceral pain, which is pain that originates from the embryonic origin of the affected organ. The later pain in the right iliac fossa is known as parietal pain, which occurs when the inflamed appendix irritates the peritoneum (the lining of the abdominal cavity).

Approximately 20% of appendicitis cases occur in an extraperitoneal location, specifically in the retrocaecal position. In these cases, a digital rectal examination is crucial for making the diagnosis.

The administration of propofol can result in venodilation, leading to a significant drop in blood pressure. This effect is particularly significant in patients who are already experiencing unstable blood flow.

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.

A Meckel’s diverticulum is a leftover part of the vitellointestinal duct, which is no longer needed in the body. It is the most common abnormality in the gastrointestinal tract, found in about 2% of people. Interestingly, it is twice as likely to occur in men compared to women.

When a Meckel’s diverticulum is present, it is usually located in the lower part of the small intestine, specifically within 60-100 cm (2 feet) of the ileocaecal valve. These diverticula are typically 3-6 cm (approximately 2 inches) long and may have a larger opening than the ileum.

Meckel’s diverticula are often discovered incidentally, especially during an appendectomy. Most of the time, they do not cause any symptoms. However, they can lead to complications such as bleeding (25-50% of cases), intestinal blockage (10-40% of cases), diverticulitis, or perforation.

These diverticula run in the opposite direction of the intestine’s natural folds but receive their blood supply from the ileum mesentery. They can be identified by a specific blood vessel called the vitelline artery. Typically, they are lined with the same type of tissue as the ileum, but they often contain abnormal tissue, with gastric tissue being the most common (50%) and pancreatic tissue being the second most common (5%). In rare cases, colonic or jejunal tissue may be present.

To remember some key facts about Meckel’s diverticulum, the rule of 2s can be helpful:
– It is found in 2% of the population.
– It is more common in men, with a ratio of 2:1 compared to women.
– It is located 2 feet away from the ileocaecal valve.
– It is approximately 2 inches long.
– It often contains two types of abnormal tissue: gastric and pancreatic.
– The most common age for clinical presentation is 2 years old.

Prussian blue is a substance that helps remove radioactive caesium from the body, a process known as decorporation. It is specifically effective for caesium exposure. When taken orally, Prussian blue binds to the radioactive caesium, forming a compound that can be excreted from the body, preventing further absorption. By using Prussian blue, the whole body radiation dose can be reduced by approximately two-thirds. Radioactive caesium is utilized in various medical, geological, and industrial applications, although incidents of environmental contamination are rare, they have been reported in Western Australia and Eastern Thailand during the first quarter of 2023.

Further Reading:

Radiation exposure refers to the emission or transmission of energy in the form of waves or particles through space or a material medium. There are two types of radiation: ionizing and non-ionizing. Non-ionizing radiation, such as radio waves and visible light, has enough energy to move atoms within a molecule but not enough to remove electrons from atoms. Ionizing radiation, on the other hand, has enough energy to ionize atoms or molecules by detaching electrons from them.

There are different types of ionizing radiation, including alpha particles, beta particles, gamma rays, and X-rays. Alpha particles are positively charged and consist of 2 protons and 2 neutrons from the atom’s nucleus. They are emitted from the decay of heavy radioactive elements and do not travel far from the source atom. Beta particles are small, fast-moving particles with a negative electrical charge that are emitted from an atom’s nucleus during radioactive decay. They are more penetrating than alpha particles but less damaging to living tissue. Gamma rays and X-rays are weightless packets of energy called photons. Gamma rays are often emitted along with alpha or beta particles during radioactive decay and can easily penetrate barriers. X-rays, on the other hand, are generally lower in energy and less penetrating than gamma rays.

Exposure to ionizing radiation can damage tissue cells by dislodging orbital electrons, leading to the generation of highly reactive ion pairs. This can result in DNA damage and an increased risk of future malignant change. The extent of cell damage depends on factors such as the type of radiation, time duration of exposure, distance from the source, and extent of shielding.

The absorbed dose of radiation is directly proportional to time, so it is important to minimize the amount of time spent in the vicinity of a radioactive source. A lethal dose of radiation without medical management is 4.5 sieverts (Sv) to kill 50% of the population at 60 days. With medical management, the lethal dose is 5-6 Sv. The immediate effects of ionizing radiation can range from radiation burns to radiation sickness, which is divided into three main syndromes: hematopoietic, gastrointestinal, and neurovascular. Long-term effects can include hematopoietic cancers and solid tumor formation.

In terms of management, support is mainly supportive and includes IV fluids, antiemetics, analgesia, nutritional support, antibiotics, blood component substitution, and reduction of brain edema.

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 supraspinatus tendon passes through a narrow space located between the underside of the acromion and acromioclavicular joint, as well as the head of the humerus. When the tendon becomes trapped in this space, it can cause pain and restrict movement, especially during overhead activities. This condition is known as subacromial impingement.

Impingement can occur due to various factors, such as thickening of the tendon caused by partial tears, inflammation, or degeneration. It can also be a result of the space narrowing due to osteoarthritis of the acromioclavicular joint or the presence of bone spurs. Some individuals may have a naturally downward sloping acromion, which makes them more susceptible to impingement.

Certain professions that involve a significant amount of overhead work, like plasterers, builders, and decorators, are particularly prone to developing subacromial impingement.

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

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

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

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

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

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.

Oral rehydration therapy (ORT) is a method used to prevent or treat dehydration by replacing fluids in the body. It is a less invasive approach compared to other methods and has been successful in reducing the mortality rate of diarrhea in developing nations.

ORT includes glucose, such as 90 mmol/L in Dioralyte, which helps improve the absorption of sodium and water in the intestines and prevents low blood sugar levels. It also contains essential mineral salts.

According to current guidelines from the National Institute for Health and Care Excellence (NICE), for mild dehydration, it is recommended to administer 50 mL/kg of ORT over a period of 4 hours.

Once a child has been rehydrated, they should continue their normal daily fluid intake and consume an additional 200 ml of ORT after each loose stool. For infants, ORT should be given at 1-1.5 times their regular feeding volume, while adults should consume 200-400 mL of ORT after each loose stool.

For more information, you can refer to the NICE guidelines on the diagnosis and management of diarrhea and vomiting caused by gastroenteritis in children under 5 years old.

The subtraction of serial 7s is included in the 30-point Folstein mini-mental state examination (MMSE), but it is not included in the AMTS. The AMTS consists of ten questions that assess various cognitive abilities. These questions include asking about age, the nearest hour, the current year, the name of the hospital or location, the ability to recognize two people, date of birth, knowledge of historical events, knowledge of the present monarch or prime minister, counting backwards from 20 to 1, and recalling an address given earlier in the test. The AMTS is referenced in the RCEM syllabus under the topic of memory loss.

Infectious mononucleosis is typically a self-limiting infection that is primarily caused by the Epstein-Barr virus (EBV), a member of the human herpesvirus family. About 10% of cases are caused by cytomegalovirus (CMV) infection.

This clinical infection is most commonly observed in populations with a large number of young adults, such as university students and active-duty military personnel.

The main clinical features of infectious mononucleosis include a low-grade fever, fatigue, prolonged malaise, sore throat (often accompanied by tonsillar enlargement and exudate), a transient, fine, non-itchy rash, lymphadenopathy (most commonly in the cervical region), arthralgia and myalgia, mild enlargement of the liver and spleen, and jaundice (which is less common in young adults but more prevalent in the elderly).

To diagnose EBV infectious mononucleosis, a variety of unrelated non-EBV heterophile antibodies and specific EBV antibodies can be used.

1. Heterophile antibodies:
Around 70-90% of patients with EBV infectious mononucleosis produce heterophile antibodies, which are antibodies that react against antigens from other species. False positives can occur with hepatitis, malaria, toxoplasmosis, rubella, systemic lupus erythematosus (SLE), lymphoma, and leukemia. Two main screening tests can detect these antibodies and provide rapid results within a day:
– Paul-Bunnell test: Sheep red blood cells agglutinate in the presence of heterophile antibodies.
– Monospot test: Horse red blood cells agglutinate in the presence of heterophile antibodies.

2. EBV-specific antibodies:
Patients who remain heterophile-negative after six weeks are considered heterophile-negative and should be tested for EBV-specific antibodies. These antibodies are also useful in cases where a false positive heterophile antibody test is suspected.

Other useful investigations include a full blood count, which often shows a raised white cell count with lymphocytosis and atypical lymphocytes in more than 20% of cases, an elevated erythrocyte sedimentation rate (ESR) in most patients, liver function tests (LFTs) that may show mild elevation of serum transaminases, throat swabs to rule out group A streptococci pharyngitis as a differential diagnosis, and abdominal ultrasound if splenomegaly is present.

Confidentiality is a crucial aspect of the doctor-patient relationship and plays a vital role in upholding trust within the medical profession. However, there are certain situations, such as cases involving gun and knife crimes, where the safety of the wider public may be at risk. In such circumstances, it may be necessary to breach this relationship and provide the police with information, even if the patient refuses to consent.

It is important to make every effort to obtain the patient’s consent, while also explaining the 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 involve providing the patient’s demographic details and informing the police that they have sought medical attention for a non-self-inflicted deliberate knife wound.

However, there are instances where contacting the police may not be necessary. For example, if it is evident that the injury was sustained accidentally or as a result of deliberate self-harm due to a mental health condition, there may be no need to involve law enforcement. In such cases, the patient should still receive the necessary medical treatment for their wound, as long as they provide consent.

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

An overdose of aspirin often leads to a combination of respiratory alkalosis and metabolic acidosis. Initially, the stimulation of the respiratory center causes hyperventilation and results in respiratory alkalosis. However, as the overdose progresses, the direct acidic effects of aspirin cause an increase in the anion gap and metabolic acidosis.

Here is a summary of common causes for different acid-base disorders:

Respiratory alkalosis can be caused by hyperventilation due to factors such as anxiety, pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, and the early stages of aspirin overdose.

Respiratory acidosis can occur in individuals with chronic obstructive pulmonary disease (COPD), life-threatening asthma, pulmonary edema, sedative drug overdose (such as opioids or benzodiazepines), neuromuscular diseases, and obesity.

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

Metabolic acidosis with a raised anion gap can result from conditions such as lactic acidosis (caused by factors like hypoxemia, shock, sepsis, or tissue infarction), ketoacidosis (associated with diabetes, starvation, or excessive alcohol consumption), renal failure, and poisoning (including the late stages of aspirin overdose, methanol or ethylene glycol ingestion).

Metabolic acidosis with a normal anion gap can be seen in renal tubular acidosis, diarrhea, ammonium chloride ingestion, and adrenal insufficiency.

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

Guillain-Barré syndrome (GBS) affects approximately 1-2 individuals per 100,000 annually and is a condition that primarily affects the peripheral nervous system, including the autonomic system. The most common initial symptom is weakness in the hands or feet, often accompanied by pain and tingling sensations as the paralysis spreads. Miller Fisher syndrome, a variant of GBS, is characterized by a triad of symptoms: ataxia, areflexia, and ophthalmoplegia.

Due to the potential serious consequences of autonomic involvement, such as fluctuations in blood pressure and cardiac arrhythmias, patients with GBS are typically hospitalized. As the diaphragm becomes paralyzed and swallowing becomes difficult, patients may require ventilation and nasogastric feeding.

GBS is an autoimmune disease that usually develops within three weeks of an infection. The leading cause is Campylobacter jejuni, followed by Epstein-Barr virus, cytomegalovirus, and Mycoplasma pneumoniae. While the patient’s immune response effectively targets the initial infection, it also mistakenly attacks the host tissue.

Symptoms of GBS typically peak around four weeks and then gradually improve. Diagnosis is based on clinical examination, which confirms the presence of areflexia and progressive weakness in the legs (and sometimes arms). Nerve conduction studies and lumbar puncture can also aid in diagnosis, with the latter often showing elevated protein levels and few white blood cells.

Treatment for GBS is primarily supportive, with the use of immunoglobulins to shorten the duration of the illness being common. Plasma exchange may also be utilized, although it has become less common since the introduction of immunoglobulin therapy.

Approximately 80% of patients with GBS make a full recovery, although this often requires a lengthy hospital stay. The mortality rate is around 5%, depending on the availability of necessary facilities such as ventilatory support during the acute phase. Additionally, about 15% of patients may experience some permanent disability, such as weakness or pain.

Pityriasis versicolor, also known as tinea versicolor, is a common skin condition caused by an infection with the yeasts Malassezia furfur and Malassezia globosa. It typically presents as multiple patches of altered pigmentation, primarily on the trunk. In individuals with fair skin, these patches are usually darker in color, while in those with darker skin or a tan, they may appear lighter (known as pityriasis versicolor alba). It is not uncommon for the rash to cause itching.

The recommended treatment for pityriasis versicolor involves the use of antifungal agents. One particularly effective option is ketoconazole shampoo, which is sold under the brand name Nizoral. To use this shampoo, it should be applied to the affected areas and left on for approximately five minutes before being rinsed off. This process should be repeated daily for a total of five days.

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

Severe aortic stenosis is characterized by several distinct features. These include a narrow pulse pressure, which refers to the difference between the systolic and diastolic blood pressure readings. Additionally, individuals with severe aortic stenosis may exhibit a slow rising pulse, meaning that the pulse wave takes longer to reach its peak. Another common feature is a delayed ejection systolic murmur, which is a heart sound that occurs during the ejection phase of the cardiac cycle. The second heart sound (S2) may also be soft or absent in individuals with severe aortic stenosis. Another potential finding is the presence of an S4 heart sound, which occurs during the filling phase of the cardiac cycle. A thrill, which is a palpable vibration, may also be felt in severe cases. The duration of the murmur, as well as the presence of left ventricular hypertrophy or failure, are additional features that may be observed in individuals with severe aortic stenosis.

Further Reading:

Valvular heart disease refers to conditions that affect the valves of the heart. In the case of aortic valve disease, there are two main conditions: aortic regurgitation and aortic stenosis.

Aortic regurgitation is characterized by an early diastolic murmur, a collapsing pulse (also known as a water hammer pulse), and a wide pulse pressure. In severe cases, there may be a mid-diastolic Austin-Flint murmur due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams. The first and second heart sounds (S1 and S2) may be soft, and S2 may even be absent. Additionally, there may be a hyperdynamic apical pulse. Causes of aortic regurgitation include rheumatic fever, infective endocarditis, connective tissue diseases like rheumatoid arthritis and systemic lupus erythematosus, and a bicuspid aortic valve. Aortic root diseases such as aortic dissection, spondyloarthropathies like ankylosing spondylitis, hypertension, syphilis, and genetic conditions like Marfan’s syndrome and Ehler-Danlos syndrome can also lead to aortic regurgitation.

Aortic stenosis, on the other hand, is characterized by a narrow pulse pressure, a slow rising pulse, and a delayed ESM (ejection systolic murmur). The second heart sound (S2) may be soft or absent, and there may be an S4 (atrial gallop) that occurs just before S1. A thrill may also be felt. The duration of the murmur is an important factor in determining the severity of aortic stenosis. Causes of aortic stenosis include degenerative calcification (most common in older patients), a bicuspid aortic valve (most common in younger patients), William’s syndrome (supravalvular aortic stenosis), post-rheumatic disease, and subvalvular conditions like hypertrophic obstructive cardiomyopathy (HOCM).

Management of aortic valve disease depends on the severity of symptoms. Asymptomatic patients are generally observed, while symptomatic patients may require valve replacement. Surgery may also be considered for asymptomatic patients with a valvular gradient greater than 40 mmHg and features such as left ventricular systolic dysfunction. Balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement.

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.

The desired core body temperature when cooling a patient with heat stroke is

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

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

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