If a child who is experiencing convulsions reaches step 3 of the APLS algorithm and has already been given phenytoin as part of their ongoing treatment, it is recommended to initiate a phenobarbitone infusion. This infusion should be administered at a dosage of 20 mg/kg over a period of 30 to 60 minutes.

Whooping cough is a respiratory infection caused by the bacteria Bordetella pertussis. It is highly contagious and spreads to about 90% of close household contacts. Public Health England (PHE) has identified two priority groups for managing whooping cough contacts. Group 1 includes infants under one year who have received less than three doses of the pertussis vaccine and are at risk of severe infection. Group 2 includes pregnant women at 32 weeks or more, healthcare workers dealing with infants and pregnant women, individuals working with unvaccinated infants under 4 months old, and individuals living with unvaccinated infants under 4 months old.

According to current guidelines, antibiotic prophylaxis with a macrolide antibiotic like erythromycin should only be given to close contacts if the following criteria are met: the index case has had symptoms within the past 21 days and there is a close contact in one of the priority groups. If both criteria are met, all contacts, regardless of age and vaccination status, should be offered chemoprophylaxis. In this case, the mother falls into group 2, so the recommended action is to provide chemoprophylaxis to all household contacts, including the mother, father, and brother. Additionally, those who receive chemoprophylaxis should also consider immunization or a booster dose based on their current vaccination status.

Ascending cholangitis occurs when there is an infection in the common bile duct, often caused by a stone that has led to a blockage of bile flow. This condition is characterized by the presence of Charcot’s triad, which includes jaundice, fever with rigors, and pain in the right upper quadrant of the abdomen. It is a serious medical emergency that can be life-threatening, with some patients also experiencing altered mental status and low blood pressure due to septic shock, known as Reynold’s pentad. Urgent biliary drainage is the recommended treatment for ascending cholangitis.

In acute cholecystitis, Murphy’s sign is typically positive, indicating tenderness in the right upper quadrant when the gallbladder is palpated. However, it is negative in cases of biliary colic and ascending cholangitis. The white cell count and C-reactive protein (CRP) levels are usually elevated in ascending cholangitis, along with the presence of jaundice and significantly increased levels of alkaline phosphatase (ALP) and bilirubin.

To differentiate between biliary colic, acute cholecystitis, and ascending cholangitis, the following can be helpful:

Biliary colic:
– Pain duration: Less than 12 hours
– Fever: Absent
– Murphy’s sign: Negative
– WCC & CRP: Normal
– AST, ALT & ALP: Normal
– Bilirubin: Normal

Acute cholecystitis:
– Pain duration: More than 12 hours
– Fever: Present
– Murphy’s sign: Positive
– WCC & CRP: Elevated
– AST, ALT & ALP: Normal or mildly elevated
– Bilirubin: Normal or mildly elevated

Ascending cholangitis:
– Pain duration: Variable
– Fever: Present
– Murphy’s sign: Negative
– WCC & CRP: Elevated
– AST, ALT & ALP: Elevated
– Bilirubin: Elevated

The superior orbital fissure is a gap in the back wall of the orbit, created by the space between the greater and lesser wings of the sphenoid bone. Several structures pass through it to enter the orbit, starting from the top and going downwards. These include the lacrimal nerve (a branch of CN V1), the frontal nerve (another branch of CN V1), the superior ophthalmic vein, the trochlear nerve (CN IV), the superior division of the oculomotor nerve (CN III), the nasociliary nerve (a branch of CN V1), the inferior division of the oculomotor nerve (CN III), the abducens nerve (CN VI), and the inferior ophthalmic vein.

Adjacent to the superior orbital fissure, on the back wall of the orbit and towards the middle, is the optic canal. The optic nerve (CN II) exits the orbit through this canal, along with the ophthalmic artery.

Superior orbital fissure syndrome (SOFS) is a condition characterized by a combination of symptoms and signs that occur when cranial nerves III, IV, V1, and VI are compressed or injured as they pass through the superior orbital fissure. This condition also leads to swelling and protrusion of the eye due to impaired drainage and congestion. The main causes of SOFS are trauma, tumors, and inflammation. It is important to note that CN II is not affected by this syndrome, as it follows a separate path through the optic canal.

Children with gastroenteritis who exhibit jittery movements, increased muscle tone, hyper-reflexia, or convulsions should be suspected of having hypernatraemic dehydration. This condition occurs when there is an excessive amount of sodium in the body. In this case, the patient’s history aligns with gastroenteritis, which puts them at risk for hypernatraemia. The presence of jittery movements, increased muscle tone, and hyper-reflexia further support this suspicion. To confirm the diagnosis, it is recommended to send a sample for urea and electrolyte testing to assess the patient’s sodium levels.

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 current school exclusion advice for certain infectious diseases with a rash is as follows:

– For chickenpox, children should be excluded for at least 5 days from the onset of the rash and until all blisters have crusted over.
– In the case of measles, children should be excluded for 4 days from the onset of the rash, provided they are well enough to attend.
– Mumps requires a 5-day exclusion after the onset of swelling.
– Rubella, also known as German measles, requires a 5-day exclusion from the onset of the rash.
– Scarlet fever necessitates exclusion until 24 hours after starting antibiotic treatment.

It is important to note that school exclusion advice has undergone changes in recent years, and the information provided above reflects the updated advice as of May 2022.

Further Reading:

Measles is a highly contagious viral infection caused by an RNA paramyxovirus. It is primarily spread through aerosol transmission, specifically through droplets in the air. The incubation period for measles is typically 10-14 days, during which patients are infectious from 4 days before the appearance of the rash to 4 days after.

Common complications of measles include pneumonia, otitis media (middle ear infection), and encephalopathy (brain inflammation). However, a rare but fatal complication called subacute sclerosing panencephalitis (SSPE) can also occur, typically presenting 5-10 years after the initial illness.

The onset of measles is characterized by a prodrome, which includes symptoms such as irritability, malaise, conjunctivitis, and fever. Before the appearance of the rash, white spots known as Koplik spots can be seen on the buccal mucosa. The rash itself starts behind the ears and then spreads to the entire body, presenting as a discrete maculopapular rash that becomes blotchy and confluent.

In terms of complications, encephalitis typically occurs 1-2 weeks after the onset of the illness. Febrile convulsions, giant cell pneumonia, keratoconjunctivitis, corneal ulceration, diarrhea, increased incidence of appendicitis, and myocarditis are also possible complications of measles.

When managing contacts of individuals with measles, it is important to offer the MMR vaccine to children who have not been immunized against measles. The vaccine-induced measles antibody develops more rapidly than that following natural infection, so it should be administered within 72 hours of contact.

Wernicke’s encephalopathy is a condition that is commonly associated with alcohol abuse and other causes of thiamine deficiency. It is characterized by a classic triad of symptoms, including acute confusion, ophthalmoplegia (paralysis or weakness of the eye muscles), and ataxia (loss of coordination). Additional possible features of this condition may include papilloedema (swelling of the optic disc), hearing loss, apathy, dysphagia (difficulty swallowing), memory impairment, and hypothermia. The majority of cases also experience peripheral neuropathy, which typically affects the legs.

The condition is marked by acute capillary haemorrhages, astrocytosis (increase in the number of astrocytes, a type of brain cell), and neuronal death in the upper brainstem and diencephalon. These abnormalities can be visualized using MRI scanning, while CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will go on to develop a Korsakoff psychosis. This condition is characterized by retrograde amnesia (loss of memory for events that occurred before the onset of amnesia), an inability to form new memories, disordered time perception, and confabulation (fabrication of false memories).

When Wernicke’s encephalopathy is suspected, it is crucial to administer parenteral thiamine (such as Pabrinex) for at least 5 days. Following the parenteral therapy, oral thiamine should be continued.

The Mallampati score is a measure that assesses the distance between the base of the tongue and the roof of the mouth. This score is used to classify the level of airway obstruction during certain medical procedures. Please refer to the notes below for the complete classification.

Further Reading:

A difficult airway refers to a situation where factors have been identified that make airway management more challenging. These factors can include body habitus, head and neck anatomy, mouth characteristics, jaw abnormalities, and neck mobility. The LEMON criteria can be used to predict difficult intubation by assessing these factors. The criteria include looking externally at these factors, evaluating the 3-3-2 rule which assesses the space in the mouth and neck, assessing the Mallampati score which measures the distance between the tongue base and roof of the mouth, and considering any upper airway obstructions or reduced neck mobility.

Direct laryngoscopy is a method used to visualize the larynx and assess the size of the tracheal opening. The Cormack-Lehane grading system can be used to classify the tracheal opening, with higher grades indicating more difficult access. In cases of a failed airway, where intubation attempts are unsuccessful and oxygenation cannot be maintained, the immediate priority is to oxygenate the patient and prevent hypoxic brain injury. This can be done through various measures such as using a bag-valve-mask ventilation, high flow oxygen, suctioning, and optimizing head positioning.

If oxygenation cannot be maintained, it is important to call for help from senior medical professionals and obtain a difficult airway trolley if not already available. If basic airway management techniques do not improve oxygenation, further intubation attempts may be considered using different equipment or techniques. If oxygen saturations remain below 90%, a surgical airway such as a cricothyroidotomy may be necessary.

Post-intubation hypoxia can occur for various reasons, and the mnemonic DOPES can be used to identify and address potential problems. DOPES stands for displacement of the endotracheal tube, obstruction, pneumothorax, equipment failure, and stacked breaths. If intubation attempts fail, a maximum of three attempts should be made before moving to an alternative plan, such as using a laryngeal mask airway or considering a cricothyroidotomy.

Hypothermia occurs when the core body temperature drops below 35°C. It is categorized as mild (32-35°C), moderate (28-32°C), or severe (<28°C). Rescuers at the scene can use the Swiss staging system to describe the condition of victims. The stages range from clearly conscious and shivering to unconscious and not breathing, with death due to irreversible hypothermia being the most severe stage. There are several risk factors for hypothermia, including environmental exposure, unsatisfactory housing, poverty, lack of cold awareness, drugs, alcohol, acute confusion, hypothyroidism, and sepsis. The clinical features of hypothermia vary depending on the severity. At 32-35°C, symptoms may include apathy, amnesia, ataxia, and dysarthria. At 30-32°C, there may be a decreased level of consciousness, hypotension, arrhythmias, respiratory depression, and muscular rigidity. Below 30°C, ventricular fibrillation may occur, especially with excessive movement or invasive procedures. Diagnosing hypothermia involves checking the core temperature using an oesophageal, rectal, or tympanic probe with a low reading thermometer. Rectal and tympanic temperatures may lag behind core temperature and are unreliable in hypothermia. Various investigations should be carried out, including blood tests, blood glucose, amylase, blood cultures, arterial blood gas, ECG, chest X-ray, and CT head if there is suspicion of head injury or CVA. The management of hypothermia involves supporting the ABCs, treating the patient in a warm room, removing wet clothes and drying the skin, monitoring the ECG, providing warmed, humidified oxygen, correcting hypoglycemia with IV glucose, and handling the patient gently to avoid VF arrest. Rewarming methods include passive Rewarming with warm blankets or Bair hugger/polythene sheets, surface Rewarming with a water bath, core Rewarming with heated, humidified oxygen or peritoneal lavage, and extracorporeal Rewarming via cardiopulmonary bypass for severe hypothermia/cardiac arrest. In the case of hypothermic cardiac arrest, CPR should be performed with chest compressions and ventilations at standard rates.

Epididymo-orchitis refers to the inflammation of the epididymis and/or testicle. It typically presents with sudden pain, swelling, and inflammation in the affected area. This condition can also occur chronically, which means that the pain and inflammation last for more than six months.

The causes of epididymo-orchitis vary depending on the age of the patient. In men under 35 years old, the infection is usually sexually transmitted and caused by Chlamydia trachomatis or Neisseria gonorrhoeae. In men over 35 years old, the infection is usually non-sexually transmitted and occurs as a result of enteric organisms that cause urinary tract infections, with Escherichia coli being the most common. However, there can be some overlap between these groups, so it is important to obtain a thorough sexual history in all age groups.

Mumps should also be considered as a potential cause of epididymo-orchitis in the 15 to 30 age group, as mumps orchitis occurs in around 40% of post-pubertal boys with mumps.

While most cases of epididymo-orchitis are infective, non-infectious causes can also occur. These include genito-urinary surgery, vasectomy, urinary catheterization, Behcet’s disease, sarcoidosis, and drug-induced cases such as those caused by amiodarone.

Patients with epididymo-orchitis typically present with unilateral scrotal pain and swelling that develops relatively quickly. The affected testis will be tender to touch, and there is usually a palpable swelling of the epididymis that starts at the lower pole of the testis and spreads towards the upper pole. The testis itself may also be involved, and there may be redness and/or swelling of the scrotum on the affected side. Patients may experience fever and urethral discharge as well.

The most important differential diagnosis to consider is testicular torsion, which requires immediate medical attention within 6 hours of onset to save the testicle. Testicular torsion is more likely in men under the age of 20, especially if the pain is very severe and sudden. It typically presents around four hours after onset. In this case, the patient’s age, longer history of symptoms, and the presence of fever are more indicative of epididymo-orchitis.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by the presence of low sodium levels and low osmolality due to the inappropriate and continuous release or action of the hormone, despite normal or increased blood volume. This leads to a decreased ability to excrete water.
There are several factors that can cause SIADH, with carbamazepine being a well-known example. These causes can be grouped into different categories. One category is CNS damage, which includes conditions like meningitis and subarachnoid hemorrhage. Another category is malignancy, with small-cell lung cancer being a common cause. Certain drugs, such as carbamazepine, SSRIs, amitriptyline, and morphine, can also trigger SIADH. Infections, such as pneumonia, lung abscess, and brain abscess, are another potential cause. Lastly, endocrine disorders like hypothyroidism can contribute to the development of SIADH.

When assessing a patient with epistaxis (nosebleed), it is important to start with a standard ABC assessment, focusing on the airway and hemodynamic status. Even if the bleeding appears to have stopped, it is crucial to evaluate the patient’s condition. If active bleeding is still present and there are signs of hemodynamic compromise, immediate resuscitative and first aid measures should be initiated.

Epistaxis should be treated as a circulatory emergency, especially in elderly patients, those with clotting disorders or bleeding tendencies, and individuals taking anticoagulants. In these cases, it is necessary to establish intravenous access using at least an 18-gauge (green) cannula. Blood samples, including a full blood count, urea and electrolytes, clotting profile, and group and save (depending on the amount of blood loss), should be sent for analysis. Patients should be assigned to a majors or closely observed area, as dislodgement of a blood clot can lead to severe bleeding.

First aid measures to control bleeding include the following steps:
1. The patient should be seated upright with their body tilted forward and their mouth open. Lying down should be avoided, unless the patient feels faint or there is evidence of hemodynamic compromise. Leaning forward helps reduce the flow of blood into the nasopharynx.
2. The patient should be encouraged to spit out any blood that enters the throat and advised not to swallow it.
3. Firmly pinch the soft, cartilaginous part of the nose, compressing the nostrils for 10-15 minutes. Pressure should not be released, and the patient should breathe through their mouth.
4. If the patient is unable to comply, an alternative technique is to ask a relative, staff member, or use an external pressure device like a swimmer’s nose clip.
5. It is important to dispel the misconception that compressing the bones will help stop the bleeding. Applying ice to the neck or forehead does not influence nasal blood flow. However, sucking on an ice cube or applying an ice pack directly to the nose may reduce nasal blood flow.

If bleeding stops with first aid measures, it is recommended to apply a topical antiseptic preparation to reduce crusting and vestibulitis. Naseptin cream (containing chlorhexidine and neomycin) is commonly used and should be applied to the nostrils four times daily for 10 days.

Anaphylaxis caused by a lack of C1 esterase inhibitor is not effectively treated with adrenaline, steroids, or antihistamines. Instead, treatment requires the use of C1 esterase inhibitor concentrate or fresh frozen plasma.

Further Reading:

Anaphylaxis is a severe and life-threatening allergic reaction that affects the entire body. It is characterized by a rapid onset and can lead to difficulty breathing, low blood pressure, and loss of consciousness. In paediatrics, anaphylaxis is often caused by food allergies, with nuts being the most common trigger. Other causes include drugs and insect venom, such as from a wasp sting.

When treating anaphylaxis, time is of the essence and there may not be enough time to look up medication doses. Adrenaline is the most important drug in managing anaphylaxis and should be administered as soon as possible. The recommended doses of adrenaline vary based on the age of the child. For children under 6 months, the dose is 150 micrograms, while for children between 6 months and 6 years, the dose remains the same. For children between 6 and 12 years, the dose is increased to 300 micrograms, and for adults and children over 12 years, the dose is 500 micrograms. Adrenaline can be repeated every 5 minutes if necessary.

The preferred site for administering adrenaline is the anterolateral aspect of the middle third of the thigh. This ensures quick absorption and effectiveness of the medication. It is important to follow the Resuscitation Council guidelines for anaphylaxis management, as they have recently been updated.

In some cases, it can be challenging to determine if a patient had a true episode of anaphylaxis. In such cases, serum tryptase levels may be measured, as they remain elevated for up to 12 hours following an acute episode of anaphylaxis. This can help confirm the diagnosis and guide further management.

Overall, prompt recognition and administration of adrenaline are crucial in managing anaphylaxis in paediatrics. Following the recommended doses and guidelines can help ensure the best outcomes for patients experiencing this severe allergic reaction.

Peptic ulcer disease is a fairly common condition that can affect either the stomach or the duodenum. However, the duodenum is more commonly affected, and in these cases, it is caused by a break in the mucosal lining of the duodenum.

This condition is more prevalent in men and is most commonly seen in individuals between the ages of 20 and 60. In fact, over 95% of patients with duodenal ulcers are found to be infected with H. pylori. Additionally, chronic usage of nonsteroidal anti-inflammatory drugs (NSAIDs) is often associated with the development of duodenal ulcers.

When it comes to the location of duodenal ulcers, they are most likely to occur in the superior (first) part of the duodenum, which is positioned in front of the body of the L1 vertebra.

The typical clinical features of duodenal ulcers include experiencing epigastric pain that radiates to the back, with the pain often worsening at night. This pain typically occurs 2-3 hours after eating and is relieved by consuming food and drinking milk. It can also be triggered by skipping meals or experiencing stress.

Possible complications that can arise from duodenal ulcers include perforation, which can lead to peritonitis, as well as gastrointestinal hemorrhage. Gastrointestinal hemorrhage can manifest as haematemesis (vomiting blood), melaena (black, tarry stools), or occult bleeding. Strictures causing obstruction can also occur as a result of duodenal ulcers.

In cases where gastrointestinal hemorrhage occurs as a result of duodenal ulceration, it is usually due to erosion of the gastroduodenal artery.

Plasmodium falciparum malaria is transmitted by female mosquitoes of the Anopheles genus. While it can be found worldwide, it is most prevalent in Africa. The incubation period for this type of malaria is typically between 7 to 14 days.

The parasite, known as sporozoites, invades hepatocytes (liver cells). Inside the hepatocyte, the parasite undergoes asexual reproduction, resulting in the production of merozoites. These merozoites are then released into the bloodstream and invade the red blood cells of the host.

Currently, the recommended treatment for P. falciparum malaria is artemisinin-based combination therapy (ACT). This involves combining fast-acting artemisinin-based compounds with drugs from different classes. Some of the companion drugs used in ACT include lumefantrine, mefloquine, amodiaquine, sulfadoxine/pyrimethamine, piperaquine, and chlorproguanil/dapsone. Artemisinin derivatives such as dihydroartemisinin, artesunate, and artemether are also used.

In cases where artemisinin combination therapy is not available, oral quinine or atovaquone with proguanil hydrochloride can be used as alternatives. However, quinine is not well-tolerated for prolonged treatment and should be combined with another drug, typically oral doxycycline (or clindamycin for pregnant women and young children).

For severe or complicated cases of falciparum malaria, it is recommended to manage the patient in a high dependency unit or intensive care setting. Intravenous artesunate is indicated for all patients with severe or complicated falciparum malaria, as well as those at high risk of developing severe disease (e.g., if more than 2% of red blood cells are parasitized) or if the patient is unable to take oral treatment. After a minimum of 24 hours of intravenous artesunate treatment and once the patient has shown improvement and can tolerate oral treatment, a full course of artemisinin combination therapy should be administered.

When treating diabetic foot ulcers that are infected, the severity of the ulcer is used to determine the appropriate antimicrobial therapy. In the case of a mild foot infection (PEDIS 2 grade), the first-line treatment is typically flucloxacillin. Based on the information provided, there is no indication that pseudomonas or MRSA should be suspected. For mild infections, it is reasonable to prescribe flucloxacillin at a dosage of 500 mg-1g four times a day for a duration of 7 days. It is important to reassess the patient at the end of the treatment course.

Further Reading:

Diabetic foot is a complication that can occur in individuals with diabetes due to long-standing high blood sugar levels. This leads to a process called glycation or glycosylation, where glucose binds to proteins and lipids in the body. Abnormal protein glycation can cause cellular dysfunction and various complications.

One of the main problems in diabetic foot is peripheral vascular disease and peripheral neuropathy. These conditions can result in significant foot issues, as trauma to the feet may go unnoticed and untreated. Vascular disease also impairs wound healing and increases the risk of developing ulcers.

Clinical features of diabetic foot include reduced sensation, especially to vibration, non-dermatomal sensory loss, foot deformities such as pes cavus and claw toes, and weak or absent foot pulses. It is important for diabetic patients to have their feet assessed regularly, at least annually, to identify any potential problems. Additional foot assessments should also be conducted during hospital admissions.

During a diabetic foot assessment, the healthcare provider should remove shoes, socks, and any bandages or dressings to examine both feet. They should assess for neuropathy using a 10 g monofilament to test foot sensation and check for limb ischemia by examining pulses and performing ankle brachial pressure index (ABPI) measurements. Any abnormal tissue, such as ulcers, calluses, infections, inflammation, deformities, or gangrene, should be documented. The risk of Charcot arthropathy should also be assessed.

The severity of foot ulcers in diabetic patients can be documented using standardized systems such as SINBAD or the University of Texas classification. The presence and severity of diabetic foot infection can be determined based on criteria such as local swelling, induration, erythema, tenderness, pain, warmth, and purulent discharge.

Management of foot ulcers involves offloading, control of foot infection, control of ischemia, wound debridement, and appropriate wound dressings. Antibiotics may be necessary depending on the severity of the infection. Diabetic patients with foot ulcers should undergo initial investigations including blood tests, wound swabs, and imaging to assess for possible osteomyelitis.

Charcot foot is a serious complication of diabetic peripheral neuropathy that results in progressive destructive arthropathy and foot deformity. Signs of Charcot foot include redness, swelling, warm skin, pain, and deformity. The hallmark deformity is midfoot collapse, known as the rocker-bottom foot.

Benzodiazepines are helpful in reducing shivering and improving the effectiveness of active cooling techniques. They are particularly useful in controlling seizures and making cooling more tolerable for patients. By administering small doses of intravenous benzodiazepines like diazepam or midazolam, shivering can be reduced, which in turn prevents heat gain and enhances the cooling process. On the other hand, dantrolene does not currently have any role in managing heat stroke. Additionally, antipyretics are not effective in reducing high body temperature caused by excessive heat. They only work when the core body temperature is elevated due to pyrogens.

Further Reading:

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

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

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

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

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

Spondyloarthritis is a term that encompasses various inflammatory conditions affecting both the joints and the entheses, which are the attachment sites of ligaments and tendons to the bones. The primary cause of spondyloarthritis is ankylosing spondylitis, but it can also be triggered by reactive arthritis, psoriatic arthritis, and enteropathic arthropathies.

If individuals below the age of 45 experience four or more of the following symptoms, they should be referred for a potential diagnosis of spondyloarthritis:

– Presence of low back pain and being younger than 35 years old
– Waking up in the second half of the night due to pain
– Buttock pain
– Pain that improves with movement or within 48 hours of using nonsteroidal anti-inflammatory drugs (NSAIDs)
– Having a first-degree relative with spondyloarthritis
– History of current or past arthritis, psoriasis, or enthesitis.

Heat stroke is a condition characterized by a core temperature higher than 40.6°C, accompanied by changes in mental state and varying levels of organ dysfunction. There are two forms of heat stroke: classic non-exertional heat stroke, which occurs during high environmental temperatures and typically affects elderly patients during heat waves, and exertional heat stroke, which occurs during strenuous physical exercise in hot conditions, such as endurance athletes competing in hot weather.

The typical clinical features of heat stroke include a core temperature greater than 40.6°C, extreme fatigue, headache, syncope, facial flushing, vomiting, and diarrhea. The skin is usually hot and dry, although sweating can occur in around 50% of cases of exertional heat stroke. The loss of the ability to sweat is a late and concerning sign. Hyperventilation is almost always present. Cardiovascular dysfunction, including arrhythmias, hypotension, and shock, as well as respiratory dysfunction, including acute respiratory distress syndrome (ARDS), can occur. Central nervous system dysfunction, such as seizures and coma, may also be observed. If the temperature rises above 41.5°C, multi-organ failure, coagulopathy, and rhabdomyolysis can occur.

In the management of heat stroke, benzodiazepines like diazepam can be helpful in patients with agitation and/or shivering. They help reduce excessive heat production and agitation. In severe cases, patients may require paralysis. Antipyretics like paracetamol, aspirin, and NSAIDs have no role in the treatment of heat stroke. They do not work because the hypothalamus, which regulates body temperature, is healthy but overloaded in heat stroke. Moreover, antipyretics may actually be harmful in patients who develop complications like liver, blood, and kidney problems as they can worsen bleeding tendencies.

Dantrolene is commonly used in the treatment of heat stroke, although there is currently no high-level evidence to support its use. Neuroleptics, such as chlorpromazine, which were once commonly used, should be avoided due to their potential adverse effects, including lowering the seizure threshold, interfering with thermoregulation, causing anticholinergic side effects, hypotension, and hepatotoxicity.

Acute pancreatitis is a common and serious cause of acute abdominal pain. It occurs when the pancreas becomes inflamed, leading to the release of enzymes that cause self-digestion of the organ.

The most common causes of acute pancreatitis are gallstones and alcohol consumption. Many cases are also of unknown origin. To remember the various causes, the mnemonic ‘I GET SMASHED’ can be helpful:

– I: Idiopathic
– G: Gallstones
– E: Ethanol
– T: Trauma
– S: Steroids
– M: Mumps
– A: Autoimmune
– S: Scorpion stings
– H: Hyperlipidemia/hypercalcemia
– E: ERCP
– D: Drugs

The clinical features of acute pancreatitis include severe epigastric pain, nausea and vomiting, referral of pain to specific dermatomes (or shoulder tip via the phrenic nerve), fever/sepsis, epigastric tenderness, jaundice, and signs such as Gray-Turner sign (ecchymosis of the flank) and Cullen sign (ecchymosis of the peri-umbilical area).

The stimulation of the thoracic splanchnic nerves is responsible for the referred pain to the T6-10 dermatomes that is sometimes observed in pancreatitis and other pancreatic disorders.

When investigating acute pancreatitis in the emergency department, it is important to perform blood glucose testing, a full blood count (which often shows an elevated white cell count), urea and electrolyte testing, calcium testing, liver function tests, coagulation screening, serum amylase testing (which should be more than 5 times the normal limit), an ECG, arterial blood gas analysis, and an abdominal X-ray.

Treatment for acute pancreatitis involves providing the patient with oxygen, adequate pain relief (including antiemetics), and fluid resuscitation. A nasogastric tube and urinary catheter should be inserted, and fluid balance should be carefully monitored. Most patients require management in a high dependency unit (HDU) or intensive care unit (ICU) setting.

Acute pancreatitis has a significant mortality rate, and complications are common. Early complications may include severe sepsis and circulatory shock, acute renal failure, disseminated intravascular coagulation, hypocalcemia, acute respiratory distress syndrome and pancreatic encephalopathy.

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

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

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

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

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

Vascular dementia is the second most common form of dementia, accounting for approximately 25% of all cases. It occurs when the brain is damaged due to various factors, such as major strokes, multiple smaller strokes that go unnoticed (known as multi-infarct), or chronic changes in smaller blood vessels (referred to as subcortical dementia). The term vascular cognitive impairment (VCI) is increasingly used to encompass this range of diseases.

Unlike Alzheimer’s disease, which has a gradual and subtle onset, vascular dementia can occur suddenly and typically shows a series of stepwise increases in symptom severity. The presentation and progression of the disease can vary significantly.

There are certain features that suggest a vascular cause of dementia. These include a history of transient ischemic attacks (TIAs) or cardiovascular disease, the presence of focal neurological abnormalities, prominent memory impairment in the early stages of the disease, early onset of gait disturbance and unsteadiness, frequent unprovoked falls in the early stages, bladder symptoms (such as incontinence) without any identifiable urological condition in the early stages, and seizures.

Urinary tract stones form when the concentration of salt and minerals in the urine becomes too high. These stones can be classified into five types based on their mineral composition and how they develop.

The most common type of stone is the calcium stone, which can be further divided into calcium oxalate and calcium phosphate stones. These account for 60-80% of all urinary tract stones.

Another type is the struvite or magnesium ammonium phosphate stone, making up about 10-15% of cases. Uric acid stones, also known as urate stones, occur in 3-10% of cases.

Cystine stones are less common, accounting for less than 2% of urinary tract stones. Finally, there are drug-induced stones, which are caused by certain medications such as triamterene, protease inhibitors like indinavir sulphate, and sulfa drugs. These account for approximately 1% of cases.

By understanding the different types of urinary tract stones, healthcare professionals can better diagnose and treat patients with this condition.

Public Health England (PHE) has a primary goal of swiftly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is important, it is not the main focus. Since 1968, clinical suspicion of a notifiable infection has been sufficient for reporting.
Registered medical practitioners (RMPs) are legally obligated to notify the designated proper officer at their local council or local health protection team (HPT) if they suspect cases of certain infectious diseases.
The Health Protection (Notification) Regulations 2010 specify the diseases that RMPs must report to the proper officers at local authorities. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.
It is worth noting that roseola infantum is not considered a notifiable disease, making it the least likely option among the diseases listed above.

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

Further Reading:

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

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

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

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

There are several factors that are known to increase the risk of violence from patients. These include being male, being young (under 40 years old), having poor levels of self-care, exhibiting coercive behavior, having a history of prior violent episodes, making multiple attendances to the hospital, being intoxicated with alcohol, and experiencing organic psychosis.

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.

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

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

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

Blood transfusion is a crucial medical treatment that can save lives, but it also comes with various risks and potential problems. These include immunological complications, administration errors, infections, and immune dilution. While there have been improvements in safety procedures and a reduction in transfusion use, errors and adverse reactions still occur. One common adverse reaction is febrile transfusion reactions, which present as an unexpected rise in temperature during or after transfusion. This can be caused by cytokine accumulation or recipient antibodies reacting to donor antigens. Treatment for febrile transfusion reactions is supportive, and other potential causes should be ruled out.

Another serious complication is acute haemolytic reaction, which is often caused by ABO incompatibility due to administration errors. This reaction requires the transfusion to be stopped and IV fluids to be administered. Delayed haemolytic reactions can occur several days after a transfusion and may require monitoring and treatment for anaemia and renal function. Allergic reactions, TRALI (Transfusion Related Acute Lung Injury), TACO (Transfusion Associated Circulatory Overload), and GVHD (Graft-vs-Host Disease) are other potential complications that require specific management approaches.

In summary, blood transfusion carries risks and potential complications, but efforts have been made to improve safety procedures. It is important to be aware of these complications and to promptly address any adverse reactions that may occur during or after a transfusion.

The tibial nerve has three main sensory branches that provide sensory function. These branches include the medial plantar nerve, which supplies the skin on the medial sole and the medial three and a half toes. The lateral plantar nerve supplies the skin on the lateral sole and the lateral one and a half toes. Lastly, the medial calcaneal branches of the tibial nerve supply the skin over the heel. Overall, these branches play a crucial role in providing sensory supply to the sole of the foot.

Patients typically initiate dialysis when their glomerular filtration rate (GFR) drops to 10 ml/min. However, if the patient has diabetes, dialysis may be recommended when their GFR reaches 15 ml/min. The GFR is a measure of kidney function and indicates how well the kidneys are able to filter waste products from the blood. Dialysis is a medical procedure that helps perform the function of the kidneys by removing waste and excess fluid from the body.

Thyroid storm is a rare condition that affects only 1-2% of patients with hyperthyroidism. However, it is crucial to diagnose it promptly because it has a high mortality rate of approximately 10%. Thyroid storm is often triggered by a physiological stressor, such as stopping antithyroid therapy prematurely, recent surgery or radio-iodine treatment, infections (especially chest infections), trauma, diabetic ketoacidosis or hyperosmolar diabetic crisis, thyroid hormone overdose, pre-eclampsia. It typically occurs in patients with Graves’ disease or toxic multinodular goitre and presents with sudden and severe hyperthyroidism. Symptoms include high fever (over 41°C), dehydration, rapid heart rate (greater than 140 beats per minute) with or without irregular heart rhythms, low blood pressure, congestive heart failure, nausea, jaundice, vomiting, diarrhea, abdominal pain, confusion, agitation, delirium, psychosis, seizures, or coma.

To diagnose thyroid storm, various blood tests should be conducted, including a full blood count, urea and electrolytes, blood glucose, coagulation screen, CRP, and thyroid profile (T4/T3 and TSH). A bone profile/calcium test should also be done as 10% of patients develop hypocalcemia. Blood cultures should be taken as well. Other important investigations include a urine dipstick/MC&S, chest X-ray, and ECG.

The management of thyroid storm involves several steps. Intravenous fluids, such as 1-2 liters of 0.9% saline, should be administered. Airway support and management should be provided as necessary. A nasogastric tube should be inserted if the patient is vomiting. Urgent referral for inpatient management is essential. Paracetamol (1 g PO/IV) can be given to reduce fever. Benzodiazepines, such as diazepam (5-20 mg PO/IV), can be used for sedation. Steroids, like hydrocortisone (100 mg IV), may be necessary if there is co-existing adrenal suppression. Antibiotics should be prescribed if there is an intercurrent infection. Beta-blockers, such as propranolol (80 mg PO), can help control heart rate. High-dose carbimazole (45-60 mg/day) is recommended.

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

Delayed haemolytic transfusion reactions (DHTRs) typically occur 4-8 days after a blood transfusion, but can sometimes manifest up to a month later. The symptoms are similar to acute haemolytic transfusion reactions but are usually less severe. Patients may experience fever, inadequate rise in haemoglobin, jaundice, reticulocytosis, positive antibody screen, and positive Direct Antiglobulin Test (Coombs test). DHTRs are more common in patients with sickle cell disease who have received frequent transfusions.

These reactions are caused by the presence of a low titre antibody that is too weak to be detected during cross-match and unable to cause lysis at the time of transfusion. The severity of DHTRs depends on the immunogenicity or dose of the antigen. Blood group antibodies associated with DHTRs include those of the Kidd, Duffy, Kell, and MNS systems. Most DHTRs have a benign course and do not require treatment. However, severe haemolysis with anaemia and renal failure can occur, so monitoring of haemoglobin levels and renal function is necessary. If an antibody is detected, antigen-negative blood can be requested for future transfusions.

Here is a summary of the main transfusion reactions and complications:

1. Febrile transfusion reaction: Presents with a 1-degree rise in temperature from baseline, along with chills and malaise. It is the most common reaction and is usually caused by cytokines from leukocytes in transfused red cell or platelet components. Supportive treatment with paracetamol is helpful.

2. Acute haemolytic reaction: Symptoms include fever, chills, pain at the transfusion site, nausea, vomiting, and dark urine. It is the most serious type of reaction and often occurs due to ABO incompatibility from administration errors. The transfusion should be stopped, and IV fluids should be administered. Diuretics may be required.

3. Delayed haemolytic reaction: This reaction typically occurs 4-8 days after a blood transfusion and presents with fever, anaemia, jaundice and haemoglobuinuria. Direct antiglobulin (Coombs) test positive. Due to low titre antibody too weak to detect in cross-match and unable to cause lysis at time of transfusion. Most delayed haemolytic reactions have a benign course and require no treatment. Monitor anaemia and renal function and treat as required.

If someone with IBS experiences unintentional weight loss or rectal bleeding, it is important to investigate further as these symptoms are not typical of IBS and may indicate a more serious underlying condition. Other alarm symptoms to watch out for include positive faecal immunochemical test (FIT), change in bowel habit after the age of 60, elevated faecal calprotectin levels, iron deficiency anaemia, persistent or frequent bloating in females (especially if over 50), the presence of an abdominal or rectal mass, or a family history of bowel cancer, ovarian cancer, coeliac disease, or inflammatory bowel disease.

Further Reading:

Irritable bowel syndrome (IBS) is a chronic disorder that affects the interaction between the gut and the brain. The exact cause of IBS is not fully understood, but factors such as genetics, drug use, enteric infections, diet, and psychosocial factors are believed to play a role. The main symptoms of IBS include abdominal pain, changes in stool form and/or frequency, and bloating. IBS can be classified into subtypes based on the predominant stool type, including diarrhea-predominant, constipation-predominant, mixed, and unclassified.

Diagnosing IBS involves using the Rome IV criteria, which includes recurrent abdominal pain associated with changes in stool frequency and form. It is important to rule out other more serious conditions that may mimic IBS through a thorough history, physical examination, and appropriate investigations. Treatment for IBS primarily involves diet and lifestyle modifications. Patients are advised to eat regular meals with a healthy, balanced diet and adjust their fiber intake based on symptoms. A low FODMAP diet may be trialed, and a dietician may be consulted for guidance. Regular physical activity and weight management are also recommended.

Psychosocial factors, such as stress, anxiety, and depression, should be addressed and managed appropriately. If constipation is a predominant symptom, soluble fiber supplements or foods high in soluble fiber may be recommended. Laxatives can be considered if constipation persists, and linaclotide may be tried if optimal doses of previous laxatives have not been effective. Antimotility drugs like loperamide can be used for diarrhea, and antispasmodic drugs or low-dose tricyclic antidepressants may be prescribed for abdominal pain. If symptoms persist or are refractory to treatment, alternative diagnoses should be considered, and referral to a specialist may be necessary.

Overall, the management of IBS should be individualized based on the patient’s symptoms and psychosocial situation. Clear explanation of the condition and providing resources for patient education, such as the NHS patient information leaflet and support from organizations like The IBS Network, can also be beneficial.

The ROME IV criteria are utilized in secondary care to diagnose IBS, as recommended by NICE. The DSM-5 criteria are employed in diagnosing various mental health disorders. Coeliac disease diagnosis involves the use of modified marsh typing. Gastro-oesophageal reflux disease diagnosis relies on the Lyon Consensus.

Further Reading:

Irritable bowel syndrome (IBS) is a chronic disorder that affects the interaction between the gut and the brain. The exact cause of IBS is not fully understood, but factors such as genetics, drug use, enteric infections, diet, and psychosocial factors are believed to play a role. The main symptoms of IBS include abdominal pain, changes in stool form and/or frequency, and bloating. IBS can be classified into subtypes based on the predominant stool type, including diarrhea-predominant, constipation-predominant, mixed, and unclassified.

Diagnosing IBS involves using the Rome IV criteria, which includes recurrent abdominal pain associated with changes in stool frequency and form. It is important to rule out other more serious conditions that may mimic IBS through a thorough history, physical examination, and appropriate investigations. Treatment for IBS primarily involves diet and lifestyle modifications. Patients are advised to eat regular meals with a healthy, balanced diet and adjust their fiber intake based on symptoms. A low FODMAP diet may be trialed, and a dietician may be consulted for guidance. Regular physical activity and weight management are also recommended.

Psychosocial factors, such as stress, anxiety, and depression, should be addressed and managed appropriately. If constipation is a predominant symptom, soluble fiber supplements or foods high in soluble fiber may be recommended. Laxatives can be considered if constipation persists, and linaclotide may be tried if optimal doses of previous laxatives have not been effective. Antimotility drugs like loperamide can be used for diarrhea, and antispasmodic drugs or low-dose tricyclic antidepressants may be prescribed for abdominal pain. If symptoms persist or are refractory to treatment, alternative diagnoses should be considered, and referral to a specialist may be necessary.

Overall, the management of IBS should be individualized based on the patient’s symptoms and psychosocial situation. Clear explanation of the condition and providing resources for patient education, such as the NHS patient information leaflet and support from organizations like The IBS Network, can also be beneficial.

In cases of acute glandular fever, certain antibiotics like ampicillin and amoxicillin can potentially cause severe rashes that affect the entire body and specifically the extremities. The exact cause of these rashes is still unknown. If there is uncertainty in the diagnosis and the clinician wants to cover the possibility of streptococcal tonsillitis, it is recommended to use phenoxymethylpenicillin (penicillin V) as the preferred treatment.

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.

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

Further Reading:

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

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

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

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

Parkinson’s disease is often accompanied by two prevalent diseases, namely dementia and depression. Dementia is observed in approximately 20 to 40% of individuals diagnosed with Parkinson’s disease. On the other hand, depression is experienced by around 45% of patients with Parkinson’s disease.

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

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

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

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

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

The initial symptoms of ARS usually include feelings of nausea and the urge to vomit. During the prodromal stage, individuals may also experience a loss of appetite and, in some cases, diarrhea, which can vary depending on the amount of exposure. These symptoms can manifest within minutes to days after being exposed to ARS.

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.

This explanation describes the observation of a patient with psoriasis, the most common associated condition in adults. The observations suggest that the patient may be experiencing dehydration, which is a complication of this condition.

Further Reading:

Erythroderma is a rare inflammatory skin condition that affects the majority of a person’s skin surface area. It is characterized by widespread redness, intense itching, and peeling of the skin. The condition can occur in people of all ages and races, but it is more common in males. Erythroderma is considered a dermatological emergency due to the potential for life-threatening complications.

The most common causes of erythroderma are exacerbations of pre-existing skin conditions, such as atopic dermatitis, psoriasis, and lichen planus. However, approximately one-third of cases are idiopathic, meaning the cause is unknown. Other less common skin conditions and systemic illnesses, including certain types of lymphoma and leukemia, can also lead to erythroderma.

Clinical features of erythroderma include generalized redness and swelling of at least 90% of the skin surface area. This is often preceded by a rash or dermatitis. The intense itching associated with the condition can lead to scratching and thickening of the skin. Skin scaling or peeling typically occurs a few days after the onset of redness. Other symptoms may include hair loss, yellowing of the palms and soles, nail abnormalities, and swollen lymph nodes. Patients may also feel generally unwell.

Erythroderma can lead to significant complications, including dehydration, electrolyte imbalances, hypothermia, heart failure, and secondary skin infections. Diagnosis is typically made based on clinical presentation, but further investigations may be done to assess the patient’s overall condition and identify any underlying causes.

Treatment of erythroderma involves addressing the underlying cause, if known. Trigger medications should be discontinued, and supportive measures such as fluid resuscitation, correction of electrolyte imbalances, and treatment of secondary infections should be implemented. Medications for symptom relief, such as painkillers and antihistamines, may also be prescribed. Emollients are often recommended to soothe the skin. In some cases, steroids and immunosuppressants may be used, depending on the underlying cause of the erythroderma.

Chronic hepatitis B infection is characterized by the persistence of serum HbsAg for a duration exceeding six months.

Further Reading:

Hepatitis B is a viral infection that is transmitted through exposure to infected blood or body fluids. It can also be passed from mother to child during childbirth. The incubation period for hepatitis B is typically 6-20 weeks. Common symptoms of hepatitis B include fever, jaundice, and elevated liver transaminases.

Complications of hepatitis B infection can include chronic hepatitis, which occurs in 5-10% of cases, fulminant liver failure, hepatocellular carcinoma, glomerulonephritis, polyarteritis nodosa, and cryoglobulinemia.

Immunization against hepatitis B is recommended for various at-risk groups, including healthcare workers, intravenous drug users, sex workers, close family contacts of infected individuals, and those with chronic liver disease or kidney disease. The vaccine contains HBsAg adsorbed onto an aluminum hydroxide adjuvant and is prepared using recombinant DNA technology. Most vaccination schedules involve three doses of the vaccine, with a booster recommended after 5 years.

Around 10-15% of adults may not respond adequately to the vaccine. Risk factors for poor response include age over 40, obesity, smoking, alcohol excess, and immunosuppression. Testing for anti-HBs levels is recommended for healthcare workers and patients with chronic kidney disease. Interpretation of anti-HBs levels can help determine the need for further vaccination or testing for infection.

In terms of serology, the presence of HBsAg indicates acute disease if present for 1-6 months, and chronic disease if present for more than 6 months. Anti-HBs indicates immunity, either through exposure or immunization. Anti-HBc indicates previous or current infection, with IgM anti-HBc appearing during acute or recent infection and IgG anti-HBc persisting. HbeAg is a marker of infectivity.

Management of hepatitis B involves notifying the Health Protection Unit for surveillance and contact tracing. Patients should be advised to avoid alcohol and take precautions to minimize transmission to partners and contacts. Referral to a gastroenterologist or hepatologist is recommended for all patients. Symptoms such as pain, nausea, and itch can be managed with appropriate drug treatment. Pegylated interferon-alpha and other antiviral medications like tenofovir and entecavir may be used to suppress viral replication in chronic carriers.

The Parkinson-plus syndromes are a group of neurodegenerative disorders that share similar features with Parkinson’s disease but also have additional clinical characteristics that set them apart from idiopathic Parkinson’s disease (iPD). These syndromes include Multiple System Atrophy (MSA), Progressive Supranuclear Palsy (PSP), Corticobasal degeneration (CBD), and Dementia with Lewy Bodies (DLB).

Multiple System Atrophy (MSA) is a less common condition than iPD and PSP. It is characterized by the loss of cells in multiple areas of the nervous system. MSA progresses rapidly, often leading to wheelchair dependence within 3-4 years of diagnosis. Some distinguishing features of MSA include autonomic dysfunction, bladder control problems, erectile dysfunction, blood pressure changes, early-onset balance problems, neck or facial dystonia, and a high-pitched voice.

To summarize the distinguishing features of the Parkinson-plus syndromes compared to iPD, the following table provides a comparison:

iPD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Typically starts at rest on one side of the body
– Levodopa response: Excellent response
– Mental changes: Depression
– Balance/falls: Late in the disease
– Common eye abnormalities: Dry eyes, trouble focusing

MSA:
– Symptom onset: Both sides equally affected
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

PSP:
– Symptom onset: Both sides equally affected
– Tremor: Less common, if present affects both sides
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Personality changes, depression
– Balance/falls: Within 1 year
– Common eye abnormalities: Dry eyes, difficulty in looking downwards

CBD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

To manage aortic dissection, it is important to lower the systolic blood pressure to a range of 100-120 mmHg. This helps decrease the strain on the damaged artery and minimizes the chances of the dissection spreading further. In this patient, symptoms such as tearing chest pain and a widened mediastinum on the chest X-ray are consistent with aortic dissection.

Further Reading:

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

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

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

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

Based on the patient’s symptoms of suprapubic pain, increased urinary frequency, and foul-smelling urine, along with the presence of nitrites, leukocytes, and blood in the urine dipstick test, the most likely cause of her symptoms is a urinary tract infection (UTI). The most probable causative organism for UTIs is Escherichia coli.

Further Reading:

A urinary tract infection (UTI) is an infection that occurs in any part of the urinary system, from the kidneys to the bladder. It is characterized by symptoms such as dysuria, nocturia, polyuria, urgency, incontinence, and changes in urine appearance and odor. UTIs can be classified as lower UTIs, which affect the bladder, or upper UTIs, which involve the kidneys. Recurrent UTIs can be due to relapse or re-infection, and the number of recurrences considered significant depends on age and sex. Uncomplicated UTIs occur in individuals with a normal urinary tract and kidney function, while complicated UTIs are caused by anatomical, functional, or pharmacological factors that make the infection persistent, recurrent, or resistant to treatment.

The most common cause of UTIs is Escherichia coli, accounting for 70-95% of cases. Other causative organisms include Staphylococcus saprophyticus, Proteus mirabilis, and Klebsiella species. UTIs are typically caused by bacteria from the gastrointestinal tract entering the urinary tract through the urethra. Other less common mechanisms of entry include direct spread via the bloodstream or instrumentation of the urinary tract, such as catheter insertion.

Diagnosis of UTIs involves urine dipstick testing and urine culture. A urine culture should be sent in certain circumstances, such as in male patients, pregnant patients, women aged 65 years or older, patients with persistent or unresolved symptoms, recurrent UTIs, patients with urinary catheters, and those with risk factors for resistance or complicated UTIs. Further investigations, such as cystoscopy and imaging, may be required in cases of recurrent UTIs or suspected underlying causes.

Management of UTIs includes simple analgesia, advice on adequate fluid intake, and the prescription of appropriate antibiotics. The choice of antibiotic depends on the patient’s gender and risk factors. For women, first-line antibiotics include nitrofurantoin or trimethoprim, while second-line options include nitrofurantoin (if not used as first-line), pivmecillinam, or fosfomycin. For men, trimethoprim or nitrofurantoin are the recommended antibiotics. In cases of suspected acute prostatitis, fluoroquinolone antibiotics such as ciprofloxacin or ofloxacin may be prescribed for a 4-week course.

Lidocaine works by blocking voltage-gated sodium channels. These channels are responsible for the propagation of action potentials in nerve fibers. By blocking these channels, lidocaine prevents the influx of sodium ions into the nerve cells, thereby inhibiting the generation and conduction of nerve impulses. This results in local anesthesia, as the transmission of pain signals from the skin to the brain is effectively blocked.

Further Reading:

Local anaesthetics, such as lidocaine, bupivacaine, and prilocaine, are commonly used in the emergency department for topical or local infiltration to establish a field block. Lidocaine is often the first choice for field block prior to central line insertion. These anaesthetics work by blocking sodium channels, preventing the propagation of action potentials.

However, local anaesthetics can enter the systemic circulation and cause toxic side effects if administered in high doses. Clinicians must be aware of the signs and symptoms of local anaesthetic systemic toxicity (LAST) and know how to respond. Early signs of LAST include numbness around the mouth or tongue, metallic taste, dizziness, visual and auditory disturbances, disorientation, and drowsiness. If not addressed, LAST can progress to more severe symptoms such as seizures, coma, respiratory depression, and cardiovascular dysfunction.

The management of LAST is largely supportive. Immediate steps include stopping the administration of local anaesthetic, calling for help, providing 100% oxygen and securing the airway, establishing IV access, and controlling seizures with benzodiazepines or other medications. Cardiovascular status should be continuously assessed, and conventional therapies may be used to treat hypotension or arrhythmias. Intravenous lipid emulsion (intralipid) may also be considered as a treatment option.

If the patient goes into cardiac arrest, CPR should be initiated following ALS arrest algorithms, but lidocaine should not be used as an anti-arrhythmic therapy. Prolonged resuscitation may be necessary, and intravenous lipid emulsion should be administered. After the acute episode, the patient should be transferred to a clinical area with appropriate equipment and staff for further monitoring and care.

It is important to report cases of local anaesthetic toxicity to the appropriate authorities, such as the National Patient Safety Agency in the UK or the Irish Medicines Board in the Republic of Ireland. Additionally, regular clinical review should be conducted to exclude pancreatitis, as intravenous lipid emulsion can interfere with amylase or lipase assays.

Q waves in V2 and V3 are typically abnormal and indicate a pathological condition. Q waves are negative deflections that occur before an R wave. They can be either normal or abnormal. Small normal Q waves, which are less than 1mm deep, may be present in most leads. Deeper normal Q waves are commonly seen in lead III, as long as they are not present in the adjacent leads II and AVF. On the other hand, pathological Q waves are usually deeper and wider. In particular, Q waves should not be observed in V2 and V3. The specific criteria for identifying pathological Q waves are as follows: any Q wave in leads V2-V3 that is greater than 0.02s in duration or a QS complex in leads V2-V3; a Q wave that is greater than 0.03s in duration and deeper than 1mm, or a QS complex, in leads I, II, aVL, aVF, or V4-V6 in any two leads of a contiguous lead grouping; an R wave that is greater than 0.04s in duration in V1-V2 and has an R/S ratio greater than 1, along with a concordant positive T wave, in the absence of a conduction defect. In healthy individuals, the T-wave is normally inverted in aVR and inverted or flat in V1. T-wave inversion in III is also considered a normal variation. If there is ST elevation in lead V1, it would suggest a ST-elevation myocardial infarction (STEMI) rather than a non-ST-elevation myocardial infarction (NSTEMI).

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

After the third shock is administered to patients with a shockable rhythm, it is recommended to administer two drugs: adrenaline and amiodarone. Adrenaline should be given at a dose of 1 mg intravenously (or intraosseously) for adult patients in cardiac arrest with a shockable rhythm. For adult patients in cardiac arrest who are in ventricular fibrillation or pulseless ventricular tachycardia, amiodarone should be given at a dose of 300 mg intravenously (or intraosseously) after three shocks have been administered. In cases where amiodarone is unavailable, lidocaine may be used as an alternative.

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.

An anion gap greater than 11 is considered high when using modern ion-selective electrode analyzers. This indicates a condition known as high anion gap acidosis. The anion gap can be calculated using the equation: ([Na+] + [K+]) – ([Cl-] + [HCO3-]). In this particular case, the calculation results in a value of 30.4 mmol/l. Anion gaps greater than 11 are considered high.

Further Reading:

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

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

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

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

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

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

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

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

This presentation strongly suggests a diagnosis of whooping cough, which is an infection of the upper respiratory tract caused by the bacteria Bordetella pertussis. The disease is highly contagious and is transmitted through respiratory droplets. The incubation period is typically 7-21 days, and it is estimated that about 90% of close household contacts will become infected.

The clinical course of whooping cough can be divided into two stages. The first stage, known as the catarrhal stage, is similar to a mild respiratory infection with symptoms such as low-grade fever and a runny nose. A cough may be present, but it is usually mild compared to the second stage. This phase typically lasts about a week.

The second stage, called the paroxysmal stage, is characterized by the development of a distinctive cough. The coughing occurs in spasms, often preceded by an inspiratory whoop sound. These spasms are followed by a series of rapid, hacking coughs. Patients may experience vomiting and may develop subconjunctival hemorrhages and petechiae. Between spasms, patients generally feel well and there are usually no abnormal chest findings. This stage can last up to 3 months, with a gradual recovery over this period. The later stages of this phase are sometimes referred to as the convalescent stage.

Complications of whooping cough can include secondary pneumonia, rib fractures, pneumothorax, hernias, syncopal episodes, encephalopathy, and seizures.

Public Health England (PHE) provides recommendations for testing for whooping cough based on the age of the patient, time since onset of illness, and severity of presentation. For infants under 12 months of age, hospitalised patients should undergo PCR testing, while non-hospitalised patients within two weeks of onset should be tested using culture of a nasopharyngeal swab or aspirate. Non-hospitalised patients presenting over two weeks after onset should be investigated with serology for anti-pertussis toxin IgG antibody levels.

For children over 12 months of age and adults, patients within two weeks of onset should be tested using culture of a nasopharyngeal swab or aspirate. Patients aged 5 to 16 who have not received the vaccine within the last year and present over two weeks after onset should have oral fluid testing for anti-pertussis toxin IgG antibody levels.

Rapid tranquillisation involves administering medication through injection (typically into the muscle) when oral medication is not feasible or appropriate and immediate sedation is necessary. The current guidelines from NICE regarding the short-term management of violent and aggressive patients recommend the use of intramuscular lorazepam for rapid tranquillisation in children and young individuals. The dosage should be adjusted based on their age and weight. If there is only a partial response to intramuscular lorazepam, the dosage should be assessed according to the child or young person’s age and weight, and an additional dose may be considered.

For more information, please refer to the NICE guidance on violence and aggression: short-term management in mental health, health, and community settings.

Fractures in the body of the mandible pose a potential risk of injury to the mental nerve. This nerve is responsible for providing sensation to the lower lip, front of the chin, and the labial gingiva of the mandibular front teeth and premolars. Specifically, fractures involving the mental foramen increase the likelihood of damaging the mental nerve.

Further Reading:

Mandibular fractures are a common type of facial fracture that often present to the emergency department. The mandible, or lower jaw, is formed by the fusion of two hemimandibles and articulates with the temporomandibular joints. Fractures of the mandible are typically caused by direct lateral force and often involve multiple fracture sites, including the body, condylar head and neck, and ramus.

When assessing for mandibular fractures, clinicians should use a look, feel, move method similar to musculoskeletal examination. However, it is important to note that TMJ effusion, muscle spasm, and pain can make moving the mandible difficult. Key signs of mandibular fracture include malocclusion, trismus (limited mouth opening), pain with the mouth closed, broken teeth, step deformity, hematoma in the sublingual space, lacerations to the gum mucosa, and bleeding from the ear.

The Manchester Mandibular Fracture Decision Rule uses the absence of five exam findings (malocclusion, trismus, broken teeth, pain with closed mouth, and step deformity) to exclude mandibular fracture. This rule has been found to be 100% sensitive and 39% specific in detecting mandibular fractures. Imaging is an important tool in diagnosing mandibular fractures, with an OPG X-ray considered the best initial imaging for TMJ dislocation and mandibular fracture. CT may be used if the OPG is technically difficult or if a CT is being performed for other reasons, such as a head injury.

It is important to note that head injury often accompanies mandibular fractures, so a thorough head injury assessment should be performed. Additionally, about a quarter of patients with mandibular fractures will also have a fracture of at least one other facial bone.

When suxamethonium is administered for neuromuscular blockade during rapid sequence induction, one of the clinical observations typically seen is muscle fasciculations. However, when rocuronium is used instead, muscle fasciculations are not present.

Further Reading:

Rapid sequence induction (RSI) is a method used to place an endotracheal tube (ETT) in the trachea while minimizing the risk of aspiration. It involves inducing loss of consciousness while applying cricoid pressure, followed by intubation without face mask ventilation. The steps of RSI can be remembered using the 7 P’s: preparation, pre-oxygenation, pre-treatment, paralysis and induction, protection and positioning, placement with proof, and post-intubation management.

Preparation involves preparing the patient, equipment, team, and anticipating any difficulties that may arise during the procedure. Pre-oxygenation is important to ensure the patient has an adequate oxygen reserve and prolongs the time before desaturation. This is typically done by breathing 100% oxygen for 3 minutes. Pre-treatment involves administering drugs to counter expected side effects of the procedure and anesthesia agents used.

Paralysis and induction involve administering a rapid-acting induction agent followed by a neuromuscular blocking agent. Commonly used induction agents include propofol, ketamine, thiopentone, and etomidate. The neuromuscular blocking agents can be depolarizing (such as suxamethonium) or non-depolarizing (such as rocuronium). Depolarizing agents bind to acetylcholine receptors and generate an action potential, while non-depolarizing agents act as competitive antagonists.

Protection and positioning involve applying cricoid pressure to prevent regurgitation of gastric contents and positioning the patient’s neck appropriately. Tube placement is confirmed by visualizing the tube passing between the vocal cords, auscultation of the chest and stomach, end-tidal CO2 measurement, and visualizing misting of the tube. Post-intubation management includes standard care such as monitoring ECG, SpO2, NIBP, capnography, and maintaining sedation and neuromuscular blockade.

Overall, RSI is a technique used to quickly and safely secure the airway in patients who may be at risk of aspiration. It involves a series of steps to ensure proper preparation, oxygenation, drug administration, and tube placement. Monitoring and post-intubation care are also important aspects of RSI.

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. Shock can occur when there is a loss of 20 ml/kg from the intravascular space, whereas clinical dehydration is only noticeable after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children based on their body weight:

Bodyweight: First 10 kg
Daily fluid requirement: 100 ml/kg
Hourly fluid requirement: 4 ml/kg

Bodyweight: Second 10 kg
Daily fluid requirement: 50 ml/kg
Hourly fluid requirement: 2 ml/kg

Bodyweight: Subsequent kg
Daily fluid requirement: 20 ml/kg
Hourly fluid requirement: 1 ml/kg

In general, if a child shows clinical signs of dehydration without shock, they can be assumed to be 5% dehydrated. If shock is also present, it can be assumed that they are 10% dehydrated or more. 5% dehydration means that the body has lost 5 g per 100 g body weight, which is equivalent to 50 ml/kg of fluid. Therefore, 10% dehydration implies a loss of 100 ml/kg of fluid.

In the case of this child, they are in shock and should receive a 20 ml/kg fluid bolus. Therefore, the initial volume of fluid to administer should be 20 x 8 ml = 160 ml.

The clinical features of dehydration and shock are summarized in the table below:

Dehydration (5%):
– Appears ‘unwell’
– Normal heart rate or tachycardia
– Normal respiratory rate or tachypnea
– Normal peripheral pulses
– Normal or mildly prolonged capillary refill time (CRT)
– Normal blood pressure
– Warm extremities
– Decreased urine output
– Reduced skin turgor
– Sunken eyes
– Depressed fontanelle
– Dry mucous membranes

Clinical shock (10%):
– Pale, lethargic, mottled appearance
– Tachycardia
– Tachypnea
– Weak peripheral pulses
– Prolonged capillary refill time (CRT)
– Hypotension
– Cold extremities
– Decreased urine output
– Decreased level of consciousness

The current guidelines from NICE and the BNF suggest that if treatment is necessary for campylobacter enteritis, clarithromycin should be the first choice. Azithromycin and erythromycin can be used interchangeably, and ciprofloxacin is a suitable alternative. It is important to note that many cases of campylobacter enteritis resolve on their own without treatment. However, individuals with severe infections or those who are immunocompromised should receive treatment.

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

Further Reading:

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

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

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

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

This patient’s medical history suggests a diagnosis of Guillain-Barré syndrome (GBS). GBS typically presents with initial symptoms of sensory changes or pain, accompanied by muscle weakness in the hands and/or feet. This weakness often spreads to the arms and upper body, affecting both sides. During the acute phase, GBS can be life-threatening, with around 15% of patients experiencing respiratory muscle weakness and requiring mechanical ventilation.

The exact cause of GBS is unknown, but it is believed to involve an autoimmune response where the body’s immune system attacks the myelin sheath surrounding the peripheral nerves. In about 75% of cases, there is a preceding infection, commonly affecting the gastrointestinal or respiratory tracts.

In this particular case, the most likely underlying cause is Campylobacter jejuni, a gastrointestinal pathogen. This is supported by the recent history of a severe diarrheal illness.

Pericardial friction rub is a common finding in pericarditis and is often described as a sound similar to squeaking leather. This patient exhibits symptoms that are consistent with acute pericarditis, including flu-like illness with muscle pain and fatigue, chest pain that worsens when lying down and improves when sitting up or leaning forward, and the presence of a pleural rub. The gradual onset of symptoms rules out conditions like pulmonary embolism or acute myocardial ischemia. It is important to note that while the pericardial rub is often considered part of the classic triad of clinical features, it is only present in about one-third of patients. Additionally, the rub may come and go, so repeated examinations may increase the chances of detecting this sign.

Further Reading:

Pericarditis is an inflammation of the pericardium, which is the protective sac around the heart. It can be acute, lasting less than 6 weeks, and may present with chest pain, cough, dyspnea, flu-like symptoms, and a pericardial rub. The most common causes of pericarditis include viral infections, tuberculosis, bacterial infections, uremia, trauma, and autoimmune diseases. However, in many cases, the cause remains unknown. Diagnosis is based on clinical features, such as chest pain, pericardial friction rub, and electrocardiographic changes. Treatment involves symptom relief with nonsteroidal anti-inflammatory drugs (NSAIDs), and patients should avoid strenuous activity until symptoms improve. Complicated cases may require treatment for the underlying cause, and large pericardial effusions may need urgent drainage. In cases of purulent effusions, antibiotic therapy is necessary, and steroid therapy may be considered for pericarditis related to autoimmune disorders or if NSAIDs alone are ineffective.

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.

The plasma osmolality for this patient can be calculated by multiplying the sodium concentration by 2, adding the glucose concentration, and then adding the urea concentration. In this case, the calculation would be (2 x 146) + 38 + 21.

Further Reading:

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

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

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

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

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

Wernicke’s encephalopathy is a condition that is commonly associated with alcohol abuse and other causes of thiamine deficiency. It is characterized by a triad of symptoms, including acute confusion, ophthalmoplegia (paralysis or weakness of the eye muscles), and ataxia (loss of coordination). Additional features may include papilloedema (swelling of the optic disc), hearing loss, apathy, dysphagia (difficulty swallowing), memory impairment, and hypothermia. Most cases also involve peripheral neuropathy, which typically affects the legs.

The condition is caused by capillary hemorrhages, astrocytosis (abnormal increase in astrocytes, a type of brain cell), and neuronal death in the upper brainstem and diencephalon. These changes can be visualized using MRI scanning, although CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will develop Korsakoff psychosis. This condition is characterized by retrograde amnesia (loss of memory for events that occurred before the onset of amnesia), an inability to form new memories, disordered time perception, and confabulation (fabrication of false memories).

Patients suspected of having Wernicke’s encephalopathy should receive parenteral thiamine (such as Pabrinex) for at least 5 days. Oral thiamine should be administered after the parenteral therapy.

It is important to note that in patients with chronic thiamine deficiency, the infusion of glucose-containing intravenous fluids without thiamine can trigger the development of Wernicke’s encephalopathy.

When performing CPR on patients with a core temperature of 30-35°C, it is recommended to double the interval between IV drug doses compared to what is used for normothermic patients. However, if the core temperature is above 35°C, standard drug protocols should be followed.

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.

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

Further Reading:

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

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

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

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

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

During the first trimester of pregnancy, the use of warfarin can lead to a condition known as fetal warfarin syndrome. This condition is characterized by nasal hypoplasia, bone stippling, bilateral optic atrophy, and intellectual disability in the baby. However, if warfarin is taken during the second or third trimester, it can cause optic atrophy, cataracts, microcephaly, microphthalmia, intellectual disability, and both fetal and maternal hemorrhage.

There are several other drugs that can have adverse effects during pregnancy. For example, ACE inhibitors like ramipril can cause hypoperfusion, renal failure, and the oligohydramnios sequence if taken during the second and third trimesters. Aminoglycosides such as gentamicin can lead to ototoxicity and deafness in the baby. 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 like diazepam, when taken late in pregnancy, can cause respiratory depression and a neonatal withdrawal syndrome. Calcium-channel blockers, if taken during the first trimester, can cause phalangeal abnormalities, while their use in the second and third trimesters can lead to fetal growth retardation. Carbamazepine can result in hemorrhagic disease of the newborn and neural tube defects. Chloramphenicol can cause gray baby syndrome. Corticosteroids, if taken during the first trimester, may cause orofacial clefts.

Danazol, if taken during the first trimester, can cause masculinization of the female fetuses genitals. Finasteride should not be handled by pregnant women as crushed or broken tablets can be absorbed through the skin and affect male sex organ development. Haloperidol, if taken during the first trimester, may cause limb malformations, while its use in the third trimester increases the risk of extrapyramidal symptoms in the newborn.

Heparin can lead to maternal bleeding and thrombocytopenia. Isoniazid can cause maternal liver damage and neuropathy and seizures in the baby. Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations and spontaneous abortion.

Tetralogy of Fallot (TOF) is the most prevalent cause of cyanotic congenital heart disease. It is characterized by four distinct features: pulmonary infundibular stenosis, overriding aorta, ventricular septal defect, and right ventricular hypertrophy. TOF is often associated with various congenital syndromes, including DiGeorge syndrome (22q11 microdeletion syndrome), Trisomy 21, Foetal alcohol syndrome, and Maternal phenylketonuria.

Nowadays, many cases of TOF are identified during antenatal screening or early postnatal assessment due to the presence of a heart murmur. Initially, severe cyanosis is uncommon shortly after birth because the patent ductus arteriosus provides additional blood flow to the lungs. However, once the ductus arteriosus closes, typically a few days after birth, cyanosis can develop.

In cases where TOF goes undetected, the clinical manifestations may include severe cyanosis, poor feeding, breathlessness, dyspnea on exertion (such as prolonged crying), hypercyanotic spells triggered by activity, agitation, developmental delay, and failure to thrive. A cardiac examination may reveal a loud, long ejection systolic murmur caused by pulmonary stenosis, a systolic thrill at the lower left sternal edge, an aortic ejection click, and digital clubbing. Radiologically, a characteristic finding in TOF is a ‘boot-shaped’ heart (Coeur en sabot).

Treatment for TOF often involves two stages. Initially, a palliative procedure is performed to alleviate symptoms, followed by a total repair at a later stage.

Posterior epistaxis, which is bleeding from the back of the nose, is typically caused by bleeding from the sphenopalatine artery or its branches. The most common surgical treatment for posterior epistaxis involves tying off the sphenopalatine artery. It is important to note that there is some disagreement in the literature regarding the exact location of the bleeding, with some sources referring to Woodruff’s plexus. However, cadaveric studies suggest that Woodruff’s plexus is more likely a venous anastomosis rather than an arterial one involving branches of the sphenopalatine artery.

Further Reading:

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

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

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

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

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

A recognized criterion for referral to the burns unit is when a burn involves the upper limb, any burn that has not healed in 7 days, any burn with significant blistering, a burn with a pain score on presentation greater than 8 out of 10 on a visual analogue scale, or a burn that covers 3% or more of the total body surface area in an adult.

Further Reading:

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

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

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

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

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

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

The primary cause of upper gastrointestinal bleeding in adults is peptic ulcer disease. Peptic ulcers are open sores that develop on the lining of the stomach or the upper part of the small intestine. These ulcers can be caused by factors such as infection with Helicobacter pylori bacteria, long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs), or excessive alcohol consumption. When a peptic ulcer bleeds, it can result in the vomiting of blood, which may appear as coffee ground vomit or have speckles of fresh red blood. Other symptoms that may accompany an upper gastrointestinal bleed include abdominal pain, nausea, and a feeling of fullness.

Further Reading:

Peptic ulcer disease (PUD) is a condition characterized by a break in the mucosal lining of the stomach or duodenum. It is caused by an imbalance between factors that promote mucosal damage, such as gastric acid, pepsin, Helicobacter pylori infection, and NSAID drug use, and factors that maintain mucosal integrity, such as prostaglandins, mucus lining, bicarbonate, and mucosal blood flow.

The most common causes of peptic ulcers are H. pylori infection and NSAID use. Other factors that can contribute to the development of ulcers include smoking, alcohol consumption, certain medications (such as steroids), stress, autoimmune conditions, and tumors.

Diagnosis of peptic ulcers involves screening for H. pylori infection through breath or stool antigen tests, as well as upper gastrointestinal endoscopy. Complications of PUD include bleeding, perforation, and obstruction. Acute massive hemorrhage has a case fatality rate of 5-10%, while perforation can lead to peritonitis with a mortality rate of up to 20%.

The symptoms of peptic ulcers vary depending on their location. Duodenal ulcers typically cause pain that is relieved by eating, occurs 2-3 hours after eating and at night, and may be accompanied by nausea and vomiting. Gastric ulcers, on the other hand, cause pain that occurs 30 minutes after eating and may be associated with nausea and vomiting.

Management of peptic ulcers depends on the underlying cause and presentation. Patients with active gastrointestinal bleeding require risk stratification, volume resuscitation, endoscopy, and proton pump inhibitor (PPI) therapy. Those with perforated ulcers require resuscitation, antibiotic treatment, analgesia, PPI therapy, and urgent surgical review.

For stable patients with peptic ulcers, lifestyle modifications such as weight loss, avoiding trigger foods, eating smaller meals, quitting smoking, reducing alcohol consumption, and managing stress and anxiety are recommended. Medication review should be done to stop causative drugs if possible. PPI therapy, with or without H. pylori eradication therapy, is also prescribed. H. pylori testing is typically done using a carbon-13 urea breath test or stool antigen test, and eradication therapy involves a 7-day triple therapy regimen of antibiotics and PPI.

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

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

Further Reading:

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

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

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

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

The current gold standard for diagnosing Clostridium difficile colitis is the cytotoxin assay. However, this test has its drawbacks. It can be challenging to perform and results may take up to 48 hours to be available.

The most common laboratory test used to diagnose Clostridium difficile colitis is an enzyme-mediated immunoassay that detects toxins A and B. This test has a specificity of 93-100% and a sensitivity of 63-99%.

Stool culture, although expensive, is not specific for pathogenic strains and therefore cannot be relied upon for a definitive diagnosis of CDAD.

Sigmoidoscopy is not routinely used, but it may be performed in cases where a rapid diagnosis is needed or if the patient has an ileus. Approximately 50% of patients may exhibit the characteristic pseudomembranous appearance, which can be confirmed through a biopsy.

Abdominal X-ray and CT scanning are not typically used, but they can be beneficial in severe cases where complications such as perforation and toxin megacolon are suspected.

It is important to note that a barium enema should not be performed in patients with CDAD as it can be potentially harmful.