Carboxyhaemoglobin (COHb) blood levels are utilized for the identification of carbon monoxide poisoning. COHb is the substance produced when carbon monoxide attaches to haemoglobin. It is important to note that carbaminohemoglobin (also known as carbaminohaemoglobin, carboxyhemoglobin, and carbohemoglobin) is the compound formed when carbon dioxide binds to hemoglobin, and should not be mistaken for COHb.

Further Reading:

Carbon monoxide (CO) is a dangerous gas that is produced by the combustion of hydrocarbon fuels and can be found in certain chemicals. It is colorless and odorless, making it difficult to detect. In England and Wales, there are approximately 60 deaths each year due to accidental CO poisoning.

When inhaled, carbon monoxide binds to haemoglobin in the blood, forming carboxyhaemoglobin (COHb). It has a higher affinity for haemoglobin than oxygen, causing a left-shift in the oxygen dissociation curve and resulting in tissue hypoxia. This means that even though there may be a normal level of oxygen in the blood, it is less readily released to the tissues.

The clinical features of carbon monoxide toxicity can vary depending on the severity of the poisoning. Mild or chronic poisoning may present with symptoms such as headache, nausea, vomiting, vertigo, confusion, and weakness. More severe poisoning can lead to intoxication, personality changes, breathlessness, pink skin and mucosae, hyperpyrexia, arrhythmias, seizures, blurred vision or blindness, deafness, extrapyramidal features, coma, or even death.

To help diagnose domestic carbon monoxide poisoning, there are four key questions that can be asked using the COMA acronym. These questions include asking about co-habitees and co-occupants in the house, whether symptoms improve outside of the house, the maintenance of boilers and cooking appliances, and the presence of a functioning CO alarm.

Typical carboxyhaemoglobin levels can vary depending on whether the individual is a smoker or non-smoker. Non-smokers typically have levels below 3%, while smokers may have levels below 10%. Symptomatic individuals usually have levels between 10-30%, and severe toxicity is indicated by levels above 30%.

When managing carbon monoxide poisoning, the first step is to administer 100% oxygen. Hyperbaric oxygen therapy may be considered for individuals with a COHb concentration of over 20% and additional risk factors such as loss of consciousness, neurological signs, myocardial ischemia or arrhythmia, or pregnancy. Other management strategies may include fluid resuscitation, sodium bicarbonate for metabolic acidosis, and mannitol for cerebral edema.

Before starting BiPAP, it is important for patients with COPD to have already started maximum medical therapy. This includes receiving supplemental oxygen, using nebulizers with salbutamol and ipratropium, taking steroids and antibiotics if necessary, and potentially receiving IV bronchodilators. Additionally, patients should meet the blood gas requirements of having a pH level below 7.35 and a pCO2 level above 6 Kpa. Another criteria for initiating NIV is having a respiratory rate higher than 23.

Further Reading:

Mechanical ventilation is the use of artificial means to assist or replace spontaneous breathing. It can be invasive, involving instrumentation inside the trachea, or non-invasive, where there is no instrumentation of the trachea. Non-invasive mechanical ventilation (NIV) in the emergency department typically refers to the use of CPAP or BiPAP.

CPAP, or continuous positive airways pressure, involves delivering air or oxygen through a tight-fitting face mask to maintain a continuous positive pressure throughout the patient’s respiratory cycle. This helps maintain small airway patency, improves oxygenation, decreases airway resistance, and reduces the work of breathing. CPAP is mainly used for acute cardiogenic pulmonary edema.

BiPAP, or biphasic positive airways pressure, also provides positive airway pressure but with variations during the respiratory cycle. The pressure is higher during inspiration than expiration, generating a tidal volume that assists ventilation. BiPAP is mainly indicated for type 2 respiratory failure in patients with COPD who are already on maximal medical therapy.

The pressure settings for CPAP typically start at 5 cmH2O and can be increased to a maximum of 15 cmH2O. For BiPAP, the starting pressure for expiratory pressure (EPAP) or positive end-expiratory pressure (PEEP) is 3-5 cmH2O, while the starting pressure for inspiratory pressure (IPAP) is 10-15 cmH2O. These pressures can be titrated up if there is persisting hypoxia or acidosis.

In terms of lung protective ventilation, low tidal volumes of 5-8 ml/kg are used to prevent atelectasis and reduce the risk of lung injury. Inspiratory pressures (plateau pressure) should be kept below 30 cm of water, and permissible hypercapnia may be allowed. However, there are contraindications to lung protective ventilation, such as unacceptable levels of hypercapnia, acidosis, and hypoxemia.

Overall, mechanical ventilation, whether invasive or non-invasive, is used in various respiratory and non-respiratory conditions to support or replace spontaneous breathing and improve oxygenation and ventilation.

The primary treatment option for hypertensive encephalopathy, a condition characterized by sudden confusion, severe headache, and coordination problems due to significantly elevated blood pressure, is labetalol.

Further Reading:

A hypertensive emergency is characterized by a significant increase in blood pressure accompanied by acute or progressive damage to organs. While there is no specific blood pressure value that defines a hypertensive emergency, systolic blood pressure is typically above 180 mmHg and/or diastolic blood pressure is above 120 mmHg. The most common presentations of hypertensive emergencies include cerebral infarction, pulmonary edema, encephalopathy, and congestive cardiac failure. Less common presentations include intracranial hemorrhage, aortic dissection, and pre-eclampsia/eclampsia.

The signs and symptoms of hypertensive emergencies can vary widely due to the potential dysfunction of every physiological system. Some common signs and symptoms include headache, nausea and/or vomiting, chest pain, arrhythmia, proteinuria, signs of acute kidney failure, epistaxis, dyspnea, dizziness, anxiety, confusion, paraesthesia or anesthesia, and blurred vision. Clinical assessment focuses on detecting acute or progressive damage to the cardiovascular, renal, and central nervous systems.

Investigations that are essential in evaluating hypertensive emergencies include U&Es (electrolyte levels), urinalysis, ECG, and CXR. Additional investigations may be considered depending on the suspected underlying cause, such as a CT head for encephalopathy or new onset confusion, CT thorax for suspected aortic dissection, and CT abdomen for suspected phaeochromocytoma. Plasma free metanephrines, urine total catecholamines, vanillylmandelic acid (VMA), and metanephrine may be tested if phaeochromocytoma is suspected. Urine screening for cocaine and/or amphetamines may be appropriate in certain cases, as well as an endocrine screen for Cushing’s syndrome.

The management of hypertensive emergencies involves cautious reduction of blood pressure to avoid precipitating renal, cerebral, or coronary ischemia. Staged blood pressure reduction is typically the goal, with an initial reduction in mean arterial pressure (MAP) by no more than 25% in the first hour. Further gradual reduction to a systolic blood pressure of 160 mmHg and diastolic blood pressure of 100 mmHg over the next 2 to 6 hours is recommended. Initial management involves treatment with intravenous antihypertensive agents in an intensive care setting with appropriate monitoring.

When a patient is semi-conscious, it is less likely for the nasopharyngeal airway adjuncts (NPA’s) to trigger the gag reflex compared to oropharyngeal airways. Therefore, NPA’s are typically the preferred option in these cases.

Further Reading:

Techniques to keep the airway open:

1. Suction: Used to remove obstructing material such as blood, vomit, secretions, and food debris from the oral cavity.

2. Chin lift manoeuvres: Involves lifting the head off the floor and lifting the chin to extend the head in relation to the neck. Improves alignment of the pharyngeal, laryngeal, and oral axes.

3. Jaw thrust: Used in trauma patients with cervical spine injury concerns. Fingers are placed under the mandible and gently pushed upward.

Airway adjuncts:

1. Oropharyngeal airway (OPA): Prevents the tongue from occluding the airway. Sized according to the patient by measuring from the incisor teeth to the angle of the mandible. Inserted with the tip facing backwards and rotated 180 degrees once it touches the back of the palate or oropharynx.

2. Nasopharyngeal airway (NPA): Useful when it is difficult to open the mouth or in semi-conscious patients. Sized by length (distance between nostril and tragus of the ear) and diameter (roughly that of the patient’s little finger). Contraindicated in basal skull and midface fractures.

Laryngeal mask airway (LMA):

– Supraglottic airway device used as a first line or rescue airway.
– Easy to insert, sized according to patient’s bodyweight.
– Advantages: Easy insertion, effective ventilation, some protection from aspiration.
– Disadvantages: Risk of hypoventilation, greater gastric inflation than endotracheal tube (ETT), risk of aspiration and laryngospasm.

Note: Proper training and assessment of the patient’s condition are essential for airway management.

C. difficile infection is often linked to the use of certain antibiotics such as clindamycin, cephalosporins (particularly third and fourth generation), fluoroquinolones, and broad-spectrum penicillins. To treat C. difficile diarrhea, metronidazole and vancomycin are commonly prescribed.

Further Reading:

Clostridium difficile (C.diff) is a gram positive rod commonly found in hospitals. Some strains of C.diff produce exotoxins that can cause intestinal damage, leading to pseudomembranous colitis. This infection can range from mild diarrhea to severe illness. Antibiotic-associated diarrhea is often caused by C.diff, with 20-30% of cases being attributed to this bacteria. Antibiotics such as clindamycin, cephalosporins, fluoroquinolones, and broad-spectrum penicillins are frequently associated with C.diff infection.

Clinical features of C.diff infection include diarrhea, distinctive smell, abdominal pain, raised white blood cell count, and in severe cases, toxic megacolon. In some severe cases, diarrhea may be absent due to the infection causing paralytic ileus. Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool. There are two types of exotoxins produced by C.diff, toxin A and toxin B, which cause mucosal damage and the formation of a pseudomembrane in the colon.

Risk factors for developing C.diff infection include age over 65, antibiotic treatment, previous C.diff infection, exposure to infected individuals, proton pump inhibitor or H2 receptor antagonist use, prolonged hospitalization or residence in a nursing home, and chronic disease or immunosuppression. Complications of C.diff infection can include toxic megacolon, colon perforation, sepsis, and even death, especially in frail elderly individuals.

Management of C.diff infection involves stopping the causative antibiotic if possible, optimizing hydration with IV fluids if necessary, and assessing the severity of the infection. Treatment options vary based on severity, ranging from no antibiotics for mild cases to vancomycin or fidaxomicin for moderate cases, and hospital protocol antibiotics (such as oral vancomycin with IV metronidazole) for severe or life-threatening cases. Severe cases may require admission under gastroenterology or GI surgeons.

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

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

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

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

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

Further Reading:

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

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

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

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

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

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.

For individuals with traumatic cardiac tamponade, thoracotomy is the recommended treatment. In the case of a trauma patient with a significant buildup of fluid around the heart and the potential for tamponade, it is advised to transfer stable patients to the operating room for thoracotomy instead of performing pericardiocentesis. Pericardiocentesis, when done correctly, is likely to be unsuccessful due to the presence of clotted blood in the pericardium. Additionally, performing pericardiocentesis would cause a delay in the thoracotomy procedure. If access to the operating room is not possible, pericardiocentesis may be considered as a temporary solution.

Further Reading:

Cardiac tamponade, also known as pericardial tamponade, occurs when fluid accumulates in the pericardial sac and compresses the heart, leading to compromised blood flow. Classic clinical signs of cardiac tamponade include distended neck veins, hypotension, muffled heart sounds, and pulseless electrical activity (PEA). Diagnosis is typically done through a FAST scan or an echocardiogram.

Management of cardiac tamponade involves assessing for other injuries, administering IV fluids to reduce preload, performing pericardiocentesis (inserting a needle into the pericardial cavity to drain fluid), and potentially performing a thoracotomy. It is important to note that untreated expanding cardiac tamponade can progress to PEA cardiac arrest.

Pericardiocentesis can be done using the subxiphoid approach or by inserting a needle between the 5th and 6th intercostal spaces at the left sternal border. Echo guidance is the gold standard for pericardiocentesis, but it may not be available in a resuscitation situation. Complications of pericardiocentesis include ST elevation or ventricular ectopics, myocardial perforation, bleeding, pneumothorax, arrhythmia, acute pulmonary edema, and acute ventricular dilatation.

It is important to note that pericardiocentesis is typically used as a temporary measure until a thoracotomy can be performed. Recent articles published on the RCEM learning platform suggest that pericardiocentesis has a low success rate and may delay thoracotomy, so it is advised against unless there are no other options available.

Pyloric stenosis, a condition characterized by narrowing of the pylorus (the opening between the stomach and small intestine), often leads to an electrolyte imbalance. This imbalance typically presents as hypochloremia (low chloride levels), hypokalemia (low potassium levels), and metabolic alkalosis (an increase in blood pH). To confirm the diagnosis, it is recommended to perform U&Es (tests to measure electrolyte levels) and a venous blood gas analysis. The electrolyte abnormalities observed in pyloric stenosis are primarily caused by the loss of hydrogen and chloride ions through vomiting. While urine is usually alkaline in this condition, severe dehydration can lead to paradoxical aciduria, where hydrogen ions are preferentially secreted instead of potassium ions to prevent further decrease in potassium levels.

Further Reading:

Pyloric stenosis is a condition that primarily affects infants, characterized by the thickening of the muscles in the pylorus, leading to obstruction of the gastric outlet. It typically presents between the 3rd and 12th weeks of life, with recurrent projectile vomiting being the main symptom. The condition is more common in males, with a positive family history and being first-born being additional risk factors. Bottle-fed children and those delivered by c-section are also more likely to develop pyloric stenosis.

Clinical features of pyloric stenosis include projectile vomiting, usually occurring about 30 minutes after a feed, as well as constipation and dehydration. A palpable mass in the upper abdomen, often described as like an olive, may also be present. The persistent vomiting can lead to electrolyte disturbances, such as hypochloremia, alkalosis, and mild hypokalemia.

Ultrasound is the preferred diagnostic tool for confirming pyloric stenosis. It can reveal specific criteria, including a pyloric muscle thickness greater than 3 mm, a pylorus longitudinal length greater than 15-17 mm, a pyloric volume greater than 1.5 cm3, and a pyloric transverse diameter greater than 13 mm.

The definitive treatment for pyloric stenosis is pyloromyotomy, a surgical procedure that involves making an incision in the thickened pyloric muscle to relieve the obstruction. Before surgery, it is important to correct any hypovolemia and electrolyte disturbances with intravenous fluids. Overall, pyloric stenosis is a relatively common condition in infants, but with prompt diagnosis and appropriate management, it can be effectively treated.

There is no indication for an independent psychiatric evaluation of this patient. However, it is important to clearly document in his medical records that you have assessed his mental capacity and determined that he is capable of making decisions. It would not be appropriate in this case to refer him to a specialist against his wishes or to breach confidentiality by discussing his illness with his family or next of kin. According to the guidelines set by the General Medical Council (GMC), it is necessary to document the fact that the patient has declined relevant information. It is also important to avoid pressuring the patient to change their mind in these circumstances.

For further information, please refer to the GMC guidelines on treatment and care towards the end of life: good practice in decision making.

A pilonidal sinus is a small cyst found near the crease between the buttocks. It contains a clump of hairs and is most commonly seen in young males with thick, dark hair. This condition is rare in individuals over the age of 40. Several factors increase the risk of developing a pilonidal sinus, including being male, having excessive hair growth, having a job that involves prolonged sitting, being overweight, and having a family history of the condition.

Defibrillation is a procedure used to treat two specific cardiac rhythms, ventricular fibrillation and pulseless ventricular tachycardia. It involves delivering an electrical shock randomly during the cardiac cycle to restore a normal heart rhythm. It is important to note that defibrillation is different from cardioversion, which involves delivering energy synchronized to the QRS complex.

Further Reading:

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

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

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

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

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

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

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

This individual has a typical history for a transient ischaemic attack (TIA). According to the NICE recommendations, it is advised to offer aspirin (300 mg daily) to individuals who have experienced a suspected TIA, unless there are contraindications. This treatment should be started immediately. It is also important to refer individuals who have had a suspected TIA for specialist assessment and investigation, with the aim of being seen within 24 hours of symptom onset. Scoring systems, such as ABCD2, should not be used to assess the risk of subsequent stroke or determine the urgency of referral for individuals with a suspected or confirmed TIA. Secondary prevention measures, in addition to aspirin, should be offered as soon as possible after the diagnosis of TIA is confirmed.

In terms of imaging, it is not recommended to offer CT brain scanning to individuals with a suspected TIA, unless there is clinical suspicion of an alternative diagnosis that CT could detect. After a specialist assessment in the TIA clinic, MRI (including diffusion-weighted and blood-sensitive sequences) may be considered to determine the area of ischaemia, detect haemorrhage, or identify alternative pathologies. If an MRI is performed, it should ideally be done on the same day as the assessment. Carotid imaging is also important for everyone with a TIA who is considered a candidate for carotid endarterectomy, and this should be done urgently.

to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old: diagnosis and initial management.

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.

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

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

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

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

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

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.

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

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

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

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

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

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

The cardiotoxic effects of TCAs occur when they block sodium channels, leading to broadening of the QRS complex, and potassium channels, resulting in prolongation of the QT interval. The severity of adverse events is directly related to the degree of QRS broadening. If the QRS complex is greater than 100 ms, it is likely that seizures may occur. If the QRS complex exceeds 160 ms, ventricular arrhythmias may be predicted. In cases of TCA overdose, certain changes can be observed on an ECG. These include sinus tachycardia, which is very common, prolongation of the PR interval, broadening of the QRS complex, prolongation of the QT interval, and in severe cases, ventricular arrhythmias.

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.

Aortic regurgitation is a condition where the aortic valve fails to close tightly, resulting in the backflow of blood from the aorta into the left ventricle during ventricular diastole. This valvular lesion presents with various clinical symptoms and signs.

The clinical symptoms of aortic regurgitation include exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. These symptoms are experienced by patients during physical activity, while lying flat, and during episodes of sudden nighttime breathlessness, respectively.

On the other hand, the clinical signs of aortic regurgitation can be observed during physical examination. These signs include a collapsing pulse, widened pulse pressure, hyperkinetic laterally displaced apex beat, and a thrill in the aortic area. Additionally, an early diastolic murmur can be heard, which is loudest at the lower left sternal edge when the patient is sitting forward and exhaling.

Aortic regurgitation is also associated with several eponymous signs, which are named after the physicians who first described them. These signs include Corrigan’s sign, which is characterized by visible and forceful neck pulsation. De Musset’s sign refers to head nodding in time with the heartbeat. Quincke’s sign is the observation of visible nail bed capillary pulsation. Duroziez’s sign is the presence of a diastolic murmur heard proximal to femoral artery compression. Traube’s sign is the perception of a pistol shot sound over the femoral arteries. The Lighthouse sign is the blanching and flushing of the forehead. Becker’s sign is the pulsation seen in retinal vessels. Rosenbach’s sign is the presence of a pulsatile liver. Lastly, Muller’s sign refers to pulsations of the uvula.

In summary, aortic regurgitation is a valvular lesion that leads to the incomplete closure of the aortic valve. It manifests with various clinical symptoms, signs, and eponymous findings, which can be identified through careful examination and observation.

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

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

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

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

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

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

To treat DKA, the girl is receiving intravenous fluids to rehydrate her. Additionally, insulin needs to be prescribed to help regulate her blood sugar levels.

The most suitable insulin regimen in this case would be an IV insulin infusion at 0.05 units/kg/hour. This means that the insulin will be administered through an intravenous line at a rate of 0.05 units per kilogram of the girl’s body weight per hour. This dosage is appropriate for managing DKA and will help to lower her blood sugar levels effectively.

Further Reading:

Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.

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

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

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

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

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

This patient presents with symptoms and signs that are consistent with an atypical pneumonia, most likely caused by an infection with Mycoplasma pneumoniae. The clinical features of Mycoplasma pneumoniae infection include a flu-like illness that precedes respiratory symptoms, along with fever, myalgia, headache, diarrhea, and cough (initially dry but often becoming productive). Focal chest signs typically develop later in the course of the illness.

Mycoplasma pneumoniae infection is commonly associated with the development of erythema multiforme, a rash characterized by multiple red lesions on the limbs that evolve into target lesions a few days after the rash appears. Additionally, this infection can also cause Steven-Johnson syndrome. It is worth noting that haemolytic anaemia with cold agglutinins can complicate Mycoplasma pneumoniae infections, providing further evidence for the diagnosis.

The recommended first-line antibiotic for treating this case would be a macrolide, such as clarithromycin. Doxycycline can also be used but is generally considered a second-line option.

This patient is currently experiencing moderate shock, classified as class III. This level of shock corresponds to a loss of 30-40% of their circulatory volume, which is equivalent to a blood loss of 1500-2000 mL.

Hemorrhage can be categorized into four classes based on physiological parameters and clinical signs. These classes are classified as class I, class II, class III, and class IV.

In class I hemorrhage, the blood loss is up to 750 mL or up to 15% of the blood volume. The pulse rate is less than 100 beats per minute, and the systolic blood pressure is normal. The pulse pressure may be normal or increased, and the respiratory rate is within the range of 14-20 breaths per minute. The urine output is greater than 30 mL per hour, and the patient’s CNS/mental status is slightly anxious.

In class II hemorrhage, the blood loss ranges from 750-1500 mL or 15-30% of the blood volume. The pulse rate is between 100-120 beats per minute, and the systolic blood pressure is still normal. The pulse pressure is decreased, and the respiratory rate increases to 20-30 breaths per minute. The urine output decreases to 20-30 mL per hour, and the patient may experience mild anxiety.

In class III hemorrhage, like the case of this patient, the blood loss is between 1500-2000 mL or 30-40% of the blood volume. The pulse rate further increases to 120-140 beats per minute, and the systolic blood pressure decreases. The pulse pressure continues to decrease, and the respiratory rate rises to 30-40 breaths per minute. The urine output significantly decreases to 5-15 mL per hour, and the patient becomes anxious and confused.

In class IV hemorrhage, the blood loss exceeds 2000 mL or more than 40% of the blood volume. The pulse rate is greater than 140 beats per minute, and the systolic blood pressure is significantly decreased. The pulse pressure is further decreased, and the respiratory rate exceeds 40 breaths per minute. The urine output becomes negligible, and the patient’s CNS/mental status deteriorates to a state of confusion and lethargy.

Due to the potentially life-threatening nature of the disease, it is crucial to initiate treatment without waiting for laboratory confirmation. Immediate administration of antibiotics is necessary.

In a hospital setting, the preferred agents for treatment are IV ceftriaxone (2 g for adults; 80 mg/kg for children) or IV cefotaxime (2 g for adults; 80 mg/kg for children). In the prehospital setting, IM benzylpenicillin can be given as an alternative. If there is a history of anaphylaxis to cephalosporins, chloramphenicol is a suitable alternative.

It is important to prioritize prompt treatment due to the severity of the disease. The recommended antibiotics should be administered as soon as possible to ensure the best possible outcome for the patient.

According to the latest guidelines from NICE and the BNF, the recommended initial treatment for typhoid fever is cefotaxime. It is important to note that infections originating from the Middle-East, South Asia, and South-East Asia may have multiple antibiotic resistance, so it is advisable to test for sensitivity. In cases where the microorganism is found to be sensitive, ciprofloxacin can be considered as a suitable alternative.

The symptoms and signs of strokes can vary depending on which blood vessel is affected. Here is a summary of the main symptoms based on the territory affected:

Anterior cerebral artery: This can cause weakness on the opposite side of the body, with the leg and shoulder being more affected than the arm, hand, and face. There may also be minimal loss of sensation on the opposite side of the body. Other symptoms can include difficulty speaking (dysarthria), language problems (aphasia), apraxia (difficulty with limb movements), urinary incontinence, and changes in behavior and personality.

Middle cerebral artery: This can lead to weakness on the opposite side of the body, with the face and arm being more affected than the leg. There may also be a loss of sensation on the opposite side of the body. Depending on the dominant hemisphere of the brain, there may be difficulties with expressive or receptive language (dysphasia). In the non-dominant hemisphere, there may be neglect of the opposite side of the body.

Posterior cerebral artery: This can cause a loss of vision on the opposite side of both eyes (homonymous hemianopia). There may also be defects in a specific quadrant of the visual field. In some cases, there may be a syndrome affecting the thalamus on the opposite side of the body.

It’s important to note that these are just general summaries and individual cases may vary. If you suspect a stroke, it’s crucial to seek immediate medical attention.

Managing a difficult situation that involves teamwork and patient safety can be challenging. The first priority is to ensure the patient’s safety from a clinical standpoint. It is important to promptly inform the consultant on duty about the incident and gather all relevant information.

In the meantime, it is crucial to gather information from the patient, nursing staff, and written notes to fully understand the situation. A thorough investigation will be necessary, including a discussion with the doctor involved. Complaints of this nature must be taken seriously, and it may be necessary to send the doctor home while the investigation takes place.

Additionally, it is important to escalate the matter to the hospital hierarchy to ensure appropriate action is taken. The doctor should also be directed to support services as this process is likely to be stressful for them.

For further guidance on this matter, it is recommended to refer to the GMC Guidance on Intimate Examinations and Chaperones.

Ipratropium bromide is a medication that falls under the category of antimuscarinic drugs. It is commonly used to manage acute asthma and chronic obstructive pulmonary disease (COPD). While it can provide short-term relief for chronic asthma, it is generally recommended to use short-acting β2 agonists as they act more quickly and are preferred.

According to the guidelines set by the British Thoracic Society (BTS), nebulized ipratropium bromide (0.5 mg every 4-6 hours) can be added to β2 agonist treatment for patients with acute severe or life-threatening asthma, or those who do not respond well to initial β2 agonist therapy.

For mild cases of chronic obstructive pulmonary disease, aerosol inhalation of ipratropium can be used for short-term relief, as long as the patient is not already using a long-acting antimuscarinic drug like tiotropium. The maximum effect of ipratropium occurs within 30-60 minutes after use, and its bronchodilating effects can last for 3-6 hours. Typically, treatment with ipratropium is recommended three times a day to maintain bronchodilation.

The most common side effect of ipratropium bromide is dry mouth. Other potential side effects include constipation, cough, paroxysmal bronchospasm, headache, nausea, and palpitations. It is important to note that ipratropium can cause urinary retention in patients with prostatic hyperplasia and bladder outflow obstruction. Additionally, it can trigger acute closed-angle glaucoma in susceptible patients.

For more information on the management of asthma, it is recommended to refer to the BTS/SIGN Guideline on the Management of Asthma.

All individuals diagnosed with chronic lymphocytic leukaemia (CLL) experience some level of weakened immune system, although for many, it is not severe enough to have a significant impact on their health. Infections are the leading cause of death for 25-50% of CLL patients, with respiratory tract, skin, and urinary tract bacterial infections being the most prevalent. The primary factor contributing to the weakened immune system in CLL patients is hypogammaglobulinaemia, which is present in approximately 85% of all individuals with this condition.

The patient in this case has been diagnosed with type 1 autoimmune hepatitis, also known as classic type autoimmune hepatitis. This condition is characterized by inflammation of the liver due to reduced levels of regulatory T-cells (Treg cells), leading to the production of autoantibodies against hepatocyte surface antigens. It primarily affects women (70%) between the ages of 15 and 40.

Autoimmune hepatitis causes chronic and progressive hepatitis, which eventually progresses to cirrhosis. Patients typically experience non-specific symptoms of malaise, but in some cases, the disease may present in its later stages with jaundice and severe illness. During this stage, liver function tests often show significantly elevated transaminases (ALT and AST), usually more than ten times the normal levels, and a normal or slightly elevated alkaline phosphatase (ALP). Around 80% of cases show positive antinuclear antibodies (ANA), while approximately 70% show positive smooth muscle antibodies (SMA). Antimitochondrial antibodies are usually low or absent.

There are four recognized subtypes of autoimmune hepatitis:
1. Type 1 (Classic type): Positive ANA and SMA, and grossly elevated IgG
2. Type 2: Positive liver kidney microsomal antibodies (affects children)
3. Type 3: Positive soluble liver antigen antibodies
4. Type 4: Seronegative

Treatment for autoimmune hepatitis involves the use of corticosteroids and/or azathioprine. Remission can be achieved in approximately 70% of cases. In some cases where drug therapy is not effective, liver transplantation may be necessary.

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

Primary biliary cirrhosis (PBC) is an autoimmune disease that results in the progressive destruction of the small bile ducts in the liver, primarily affecting the intralobular ducts. This leads to cholestatic jaundice, liver fibrosis, and eventually cirrhosis. PBC is more common in females (90%)

Prolongation of the QT interval can lead to a dangerous ventricular arrhythmia called torsades de pointes, which can result in sudden cardiac death. There are several commonly used medications that are known to cause QT prolongation.

Low levels of potassium (hypokalaemia) and magnesium (hypomagnesaemia) can increase the risk of QT prolongation. For example, diuretics can interact with QT-prolonging drugs by causing hypokalaemia.

The QT interval varies with heart rate, and formulas are used to correct the QT interval for heart rate. Once corrected, it is referred to as the QTc interval. The QTc interval is typically reported on the ECG printout. A normal QTc interval is less than 440 ms.

If the QTc interval is greater than 440 ms but less than 500 ms, it is considered borderline. Although there may be some variation in the literature, a QTc interval within these values is generally considered borderline prolonged. In such cases, it is important to consider reducing the dose of QT-prolonging drugs or switching to an alternative medication that does not prolong the QT interval.

A prolonged QTc interval exceeding 500 ms is clinically significant and is likely to increase the risk of arrhythmia. Any medications that prolong the QT interval should be reviewed immediately.

Here are some commonly encountered drugs that are known to prolong the QT interval:

Antimicrobials:
– Erythromycin
– Clarithromycin
– Moxifloxacin
– Fluconazole
– Ketoconazole

Antiarrhythmics:
– Dronedarone
– Sotalol
– Quinidine
– Amiodarone
– Flecainide

Antipsychotics:
– Risperidone
– Fluphenazine
– Haloperidol
– Pimozide
– Chlorpromazine
– Quetiapine
– Clozapine

Antidepressants:
– Citalopram/escitalopram
– Amitriptyline
– Clomipramine
– Dosulepin
– Doxepin
– Imipramine
– Lofepramine

Antiemetics:
– Domperidone
– Droperidol
– Ondansetron/Granisetron

Others:
– Methadone
– Protein kinase inhibitors (e.g. sunitinib)

Retinal detachment is a condition where the retina separates from the retinal pigment epithelium, resulting in a fluid-filled space between them. This case presents a classic description of retinal detachment. Several risk factors increase the likelihood of developing this condition, including myopia, being male, having a family history of retinal detachment, previous episodes of retinal detachment, blunt ocular trauma, previous cataract surgery, diabetes mellitus (especially if proliferative retinopathy is present), glaucoma, and cataracts.

The clinical features commonly associated with retinal detachment include flashes of light, particularly at the edges of vision (known as photopsia), a dense shadow in the peripheral vision that spreads towards the center, a sensation of a curtain drawing across the eye, and central visual loss. Fundoscopy, a procedure to examine the back of the eye, reveals a sheet of sensory retina billowing towards the center of the eye. Additionally, a positive Amsler grid test, where straight lines appear curved or wavy, may indicate retinal detachment.

Other possible causes of floaters include posterior vitreous detachment, retinal tears, vitreous hemorrhage, and migraine with aura. However, in this case, the retinal appearance described is consistent with retinal detachment.

It is crucial to arrange an urgent same-day ophthalmology referral for this patient. Fortunately, approximately 90% of retinal detachments can be successfully repaired with one operation, and an additional 6% can be salvaged with subsequent procedures. If the retina remains fixed six months after surgery, the likelihood of it becoming detached again is low.

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

Urticaria is a common condition that causes a red, raised, itchy rash on the skin and mucous membranes. It can be localized or spread out. Approximately 15% of people will experience urticaria at some point in their lives. There are two forms of urticaria: acute and chronic, with acute being more common.

According to the current guidelines from the National Institute for Health and Care Excellence (NICE), individuals seeking treatment for urticaria should be offered a non-sedating antihistamine from the second-generation category. Examples of second-generation antihistamines include cetirizine, loratadine, fexofenadine, desloratadine, and levocetirizine.

It is no longer recommended to use conventional first-generation antihistamines like promethazine and chlorpheniramine for urticaria. These medications have short-lasting effects and can cause sedation and anticholinergic side effects. They may also interfere with sleep, learning, and performance, as well as interact negatively with alcohol and other medications. In some cases, lethal overdoses have been reported. Terfenadine and astemizole should also be avoided as they can be harmful to the heart when combined with certain drugs like erythromycin and ketoconazole.

It is advisable to avoid antihistamines during pregnancy if possible. There is a lack of systematic studies on their safety during pregnancy. However, if an antihistamine is necessary, chlorpheniramine is the recommended choice. For breastfeeding women, loratadine or cetirizine are preferred options.

This patient is showing signs and symptoms that align with a C.diff infection. They also have several risk factors that increase their likelihood of developing this infection, including being over the age of 65, residing in a nursing home or being hospitalized for an extended period, recent use of antibiotics, and regular use of PPI medication.

Further Reading:

Clostridium difficile (C.diff) is a gram positive rod commonly found in hospitals. Some strains of C.diff produce exotoxins that can cause intestinal damage, leading to pseudomembranous colitis. This infection can range from mild diarrhea to severe illness. Antibiotic-associated diarrhea is often caused by C.diff, with 20-30% of cases being attributed to this bacteria. Antibiotics such as clindamycin, cephalosporins, fluoroquinolones, and broad-spectrum penicillins are frequently associated with C.diff infection.

Clinical features of C.diff infection include diarrhea, distinctive smell, abdominal pain, raised white blood cell count, and in severe cases, toxic megacolon. In some severe cases, diarrhea may be absent due to the infection causing paralytic ileus. Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool. There are two types of exotoxins produced by C.diff, toxin A and toxin B, which cause mucosal damage and the formation of a pseudomembrane in the colon.

Risk factors for developing C.diff infection include age over 65, antibiotic treatment, previous C.diff infection, exposure to infected individuals, proton pump inhibitor or H2 receptor antagonist use, prolonged hospitalization or residence in a nursing home, and chronic disease or immunosuppression. Complications of C.diff infection can include toxic megacolon, colon perforation, sepsis, and even death, especially in frail elderly individuals.

Management of C.diff infection involves stopping the causative antibiotic if possible, optimizing hydration with IV fluids if necessary, and assessing the severity of the infection. Treatment options vary based on severity, ranging from no antibiotics for mild cases to vancomycin or fidaxomicin for moderate cases, and hospital protocol antibiotics (such as oral vancomycin with IV metronidazole) for severe or life-threatening cases. Severe cases may require admission under gastroenterology or GI surgeons.

It is recommended to administer sodium chloride solution gradually over a period of 10-15 minutes. If the systolic does not respond adequately, the bolus dose may need to be repeated. It is important to note that patients with DKA often have a fluid deficit of more than 5 liters, which should be taken into consideration.

Further Reading:

Diabetic ketoacidosis (DKA) is a serious complication of diabetes that occurs due to a lack of insulin in the body. It is most commonly seen in individuals with type 1 diabetes but can also occur in type 2 diabetes. DKA is characterized by hyperglycemia, acidosis, and ketonaemia.

The pathophysiology of DKA involves insulin deficiency, which leads to increased glucose production and decreased glucose uptake by cells. This results in hyperglycemia and osmotic diuresis, leading to dehydration. Insulin deficiency also leads to increased lipolysis and the production of ketone bodies, which are acidic. The body attempts to buffer the pH change through metabolic and respiratory compensation, resulting in metabolic acidosis.

DKA can be precipitated by factors such as infection, physiological stress, non-compliance with insulin therapy, acute medical conditions, and certain medications. The clinical features of DKA include polydipsia, polyuria, signs of dehydration, ketotic breath smell, tachypnea, confusion, headache, nausea, vomiting, lethargy, and abdominal pain.

The diagnosis of DKA is based on the presence of ketonaemia or ketonuria, blood glucose levels above 11 mmol/L or known diabetes mellitus, and a blood pH below 7.3 or bicarbonate levels below 15 mmol/L. Initial investigations include blood gas analysis, urine dipstick for glucose and ketones, blood glucose measurement, and electrolyte levels.

Management of DKA involves fluid replacement, electrolyte correction, insulin therapy, and treatment of any underlying cause. Fluid replacement is typically done with isotonic saline, and potassium may need to be added depending on the patient’s levels. Insulin therapy is initiated with an intravenous infusion, and the rate is adjusted based on blood glucose levels. Monitoring of blood glucose, ketones, bicarbonate, and electrolytes is essential, and the insulin infusion is discontinued once ketones are below 0.3 mmol/L, pH is above 7.3, and bicarbonate is above 18 mmol/L.

Complications of DKA and its treatment include gastric stasis, thromboembolism, electrolyte disturbances, cerebral edema, hypoglycemia, acute respiratory distress syndrome, and acute kidney injury. Prompt medical intervention is crucial in managing DKA to prevent potentially fatal outcomes.