There are two types of infectious agents that can lead to the development of a dendritic ulcer. The majority of cases (80%) are caused by the herpes simplex virus (type I), while the remaining cases (20%) are caused by the herpes zoster virus. To effectively treat this condition, the patient should follow a specific treatment plan. This includes applying aciclovir ointment topically five times a day for a duration of 10 days. Additionally, prednisolone 0.5% drops should be used 2-4 times daily. It is also recommended to take oral high dose vitamin C, as it has been shown to reduce the healing time of dendritic ulcers.

Addison’s disease can be attributed to various underlying causes. The most common cause, accounting for approximately 80% of cases, is autoimmune adrenalitis. This occurs when the body’s immune system mistakenly attacks the adrenal glands. Another cause is bilateral adrenalectomy, which involves the surgical removal of both adrenal glands. Additionally, Addison’s disease can be triggered by a condition known as Waterhouse-Friderichsen syndrome, which involves bleeding into the adrenal glands. Tuberculosis, a bacterial infection, is also recognized as a potential cause of this disease. Lastly, although rare, congenital adrenal hyperplasia can contribute to the development of Addison’s disease.

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

The typical clinical characteristics of acne fulminans are as follows:

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

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

If a patient with a zygoma fracture experiences visual disturbance, limited eye movements (especially upward gaze), or shows a teardrop sign on a facial X-ray, it is important to refer them urgently to ophthalmology or maxillofacial surgeons.

Further Reading:

Zygomatic injuries, also known as zygomatic complex fractures, involve fractures of the zygoma bone and often affect surrounding bones such as the maxilla and temporal bones. These fractures can be classified into four positions: the lateral and inferior orbital rim, the zygomaticomaxillary buttress, and the zygomatic arch. The full extent of these injuries may not be visible on plain X-rays and may require a CT scan for accurate diagnosis.

Zygomatic fractures can pose risks to various structures in the face. The temporalis muscle and coronoid process of the mandible may become trapped in depressed fractures of the zygomatic arch. The infraorbital nerve, which passes through the infraorbital foramen, can be injured in zygomaticomaxillary complex fractures. In orbital floor fractures, the inferior rectus muscle may herniate into the maxillary sinus.

Clinical assessment of zygomatic injuries involves observing facial asymmetry, depressed facial bones, contusion, and signs of eye injury. Visual acuity must be assessed, and any persistent bleeding from the nose or mouth should be noted. Nasal injuries, including septal hematoma, and intra-oral abnormalities should also be evaluated. Tenderness of facial bones and the temporomandibular joint should be assessed, along with any step deformities or crepitus. Eye and jaw movements must also be evaluated.

Imaging for zygomatic injuries typically includes facial X-rays, such as occipitomental views, and CT scans for a more detailed assessment. It is important to consider the possibility of intracranial hemorrhage and cervical spine injury in patients with facial fractures.

Management of most zygomatic fractures can be done on an outpatient basis with maxillofacial follow-up, assuming the patient is stable and there is no evidence of eye injury. However, orbital floor fractures should be referred immediately to ophthalmologists or maxillofacial surgeons. Zygomatic arch injuries that restrict mouth opening or closing due to entrapment of the temporalis muscle or mandibular condyle also require urgent referral. Nasal fractures, often seen in conjunction with other facial fractures, can be managed by outpatient ENT follow-up but should be referred urgently if there is uncontrolled epistaxis, CSF rhinorrhea, or septal hematoma.

Traumatic aortic rupture is a relatively common cause of sudden death following major trauma, especially high-speed road traffic accidents (RTAs). It is estimated that 15-20% of deaths from RTAs are due to this injury. If the aortic rupture is promptly recognized and treated, patients who survive the initial injury can fully recover.

Surviving patients often have an incomplete laceration near the ligamentum arteriosum of the aorta. The continuity is maintained by either an intact adventitial layer or a contained mediastinal hematoma, which prevents immediate exsanguination and death.

Detecting traumatic aortic rupture can be challenging as many patients do not exhibit specific symptoms, and other injuries may also be present, making the diagnosis unclear.

Chest X-ray findings can aid in the diagnosis and include fractures of the 1st and 2nd ribs, a grossly widened mediastinum, a hazy left lung field, obliteration of the aortic knob, deviation of the trachea to the right, presence of a pleural cap, elevation and rightward shift of the right mainstem bronchus, depression of the left mainstem bronchus, obliteration of the space between the pulmonary artery and aorta, and deviation of the esophagus (or NG tube) to the right.

Helical contrast-enhanced CT scanning is highly sensitive and specific for detecting aortic rupture, but it should only be performed on hemodynamically stable patients.

Treatment options include primary repair or resection of the torn segment with replacement using an interposition graft. Endovascular repair is also now considered an acceptable alternative approach.

Patients with mitral regurgitation can go for extended periods without experiencing any symptoms. They may have a normal exercise tolerance and show no signs of congestive cardiac failure. However, when cardiac failure does occur, patients often complain of breathlessness, especially during physical exertion. They may also experience fatigue, difficulty breathing while lying flat (orthopnoea), and sudden episodes of difficulty breathing at night (paroxysmal nocturnal dyspnoea).

In terms of clinical signs, mitral regurgitation can be identified through various indicators. These include a displaced and volume loaded apex beat, which can be felt during a physical examination. A palpable thrill may also be detected at the apex. Additionally, a pansystolic murmur, which is loudest at the apex and radiates to the axilla, can be heard. This murmur is typically most pronounced when the patient holds their breath during expiration. Furthermore, a soft first heart sound and signs of left ventricular failure may be present.

Heat stroke can be differentiated from other heat related illnesses by the presence of systemic inflammatory response syndrome (SIRS). Patients with heatstroke typically have a core body temperature exceeding 40ºC and lack sweating (unlike heat exhaustion where profuse sweating is common). It is important to note that diuretic treatment is not suitable for heat edema and Dantrolene should not be used to treat environmental heat related illnesses.

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

Veins and arteries can be differentiated on ultrasound based on their compressibility, response to valsalva, and shape. When compressed, veins are obliterated while arteries remain unaffected. Additionally, when a patient performs a valsalva maneuver, the neck veins expand. In transverse view, arteries appear circular with a muscular wall, whereas veins tend to have an oval shape. It is important to note that the overall size and internal diameter are not reliable indicators for distinguishing between arteries and veins.

Further Reading:

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

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

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

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

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

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

Pelvic inflammatory disease (PID) is a pelvic infection that affects the upper female reproductive tract, including the uterus, fallopian tubes, and ovaries. It is typically caused by an ascending infection from the cervix and is commonly associated with sexually transmitted diseases like chlamydia and gonorrhea. In the UK, genital Chlamydia trachomatis infection is the most common cause of PID seen in genitourinary medicine clinics.

PID can often be asymptomatic, but when symptoms are present, they may include lower abdominal pain and tenderness, fever, painful urination, painful intercourse, purulent vaginal discharge, abnormal vaginal bleeding, and tenderness in the cervix and adnexa. It is important to note that symptoms of ectopic pregnancy can be similar to those of PID, so a pregnancy test should be conducted for all patients with suspicious symptoms.

To investigate a possible case of PID, endocervical swabs should be taken to test for C. trachomatis and N. gonorrhoeae using nucleic acid amplification tests if available. Mild to moderate cases of PID can usually be managed in primary care or outpatient settings, while patients with severe disease should be admitted to the hospital for intravenous antibiotics. Signs of severe disease include a fever above 38°C, signs of a tubo-ovarian abscess, signs of pelvic peritonitis, or concurrent pregnancy.

Empirical antibiotic treatment should be initiated as soon as a presumptive diagnosis of PID is made clinically, without waiting for swab results. The current recommended outpatient treatment for PID is a single intramuscular dose of ceftriaxone 500 mg, followed by oral doxycycline 100 mg twice daily and oral metronidazole 400 mg twice daily for 14 days. An alternative regimen is oral ofloxacin 400 mg twice daily and oral metronidazole 400 mg twice daily for 14 days.

For severely ill patients in the inpatient setting, initial treatment includes intravenous doxycycline, a single-dose of intravenous ceftriaxone, and intravenous metronidazole. This is then followed by a switch to oral doxycycline and metronidazole to complete a 14-day treatment course. If a patient fails to respond to treatment, laparoscopy is necessary to confirm the diagnosis or consider alternative diagnoses.

Pyloric stenosis is characterized by recurring episodes of projectile vomiting and the presence of a mass in the upper abdomen, often described as an olive. This patient exhibits clinical features that align with pyloric stenosis and possesses several common risk factors, including being a male, being the firstborn son, being bottle-fed, and being delivered via C-section. It is important to note that intestinal atresia is typically diagnosed either during pregnancy or shortly after birth.

Further Reading:

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

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

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

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

Osteoporosis and fragility fractures are more likely to occur in individuals with low levels of estrogen. Menopause, which causes a decrease in estrogen, can lead to estrogen deficiency. Estrogen plays a role in preventing bone breakdown by inhibiting osteoclast activity. After menopause, there is an increase in osteoclast activity, resulting in a rapid decline in bone mineral density. Osteoporosis is also associated with the long-term use of corticosteroids.

Further Reading:

Fragility fractures are fractures that occur following a fall from standing height or less, and may be atraumatic. They often occur in the presence of osteoporosis, a disease characterized by low bone mass and structural deterioration of bone tissue. Fragility fractures commonly affect the wrist, spine, hip, and arm.

Osteoporosis is defined as a bone mineral density (BMD) of 2.5 standard deviations below the mean peak mass, as measured by dual-energy X-ray absorptiometry (DXA). Osteopenia, on the other hand, refers to low bone mass between normal bone mass and osteoporosis, with a T-score between -1 to -2.5.

The pathophysiology of osteoporosis involves increased osteoclast activity relative to bone production by osteoblasts. The prevalence of osteoporosis increases with age, from approximately 2% at 50 years to almost 50% at 80 years.

There are various risk factors for fragility fractures, including endocrine diseases, GI causes of malabsorption, chronic kidney and liver diseases, menopause, immobility, low body mass index, advancing age, oral corticosteroids, smoking, alcohol consumption, previous fragility fractures, rheumatological conditions, parental history of hip fracture, certain medications, visual impairment, neuromuscular weakness, cognitive impairment, and unsafe home environment.

Assessment of a patient with a possible fragility fracture should include evaluating the risk of further falls, the risk of osteoporosis, excluding secondary causes of osteoporosis, and ruling out non-osteoporotic causes for fragility fractures such as metastatic bone disease, multiple myeloma, osteomalacia, and Paget’s disease.

Management of fragility fractures involves initial management by the emergency clinician, while treatment of low bone density is often delegated to the medical team or general practitioner. Management considerations include determining who needs formal risk assessment, who needs a DXA scan to measure BMD, providing lifestyle advice, and deciding who requires drug treatment.

Medication for osteoporosis typically includes vitamin D, calcium, and bisphosphonates. Vitamin D and calcium supplementation should be considered based on individual needs, while bisphosphonates are advised for postmenopausal women and men over 50 years with confirmed osteoporosis or those taking high doses of oral corticosteroids.

Infantile hypertrophic pyloric stenosis is a condition characterized by the thickening and enlargement of the smooth muscle in the antrum of the stomach, leading to the narrowing of the pyloric canal. This narrowing can easily cause obstruction. It is a relatively common condition, occurring in about 1 in 500 live births, and is more frequently seen in males than females, with a ratio of 4 to 1. It is most commonly observed in first-born male children, although it can rarely occur in adults as well.

The main symptom of infantile hypertrophic pyloric stenosis is vomiting, which typically begins between 2 to 8 weeks of age. The vomit is usually non-bilious and forcefully expelled. It tends to occur around 30 to 60 minutes after feeding, leaving the baby hungry despite the vomiting. In some cases, there may be blood in the vomit. Other clinical features include persistent hunger, dehydration, weight loss, and constipation. An enlarged pylorus, often described as olive-shaped, can be felt in the right upper quadrant or epigastric in approximately 95% of cases. This is most noticeable at the beginning of a feed.

The typical acid-base disturbance seen in this condition is hypochloremic metabolic alkalosis. This occurs due to the loss of hydrogen and chloride ions in the vomit, as well as decreased secretion of pancreatic bicarbonate. The increased bicarbonate ions in the distal tubule of the kidney lead to the production of alkaline urine. Hyponatremia and hypokalemia are also commonly present.

Ultrasound scanning is the preferred diagnostic tool for infantile hypertrophic pyloric stenosis, as it is reliable and easy to perform. It has replaced barium studies as the investigation of choice.

Initial management involves fluid resuscitation, which should be tailored to the weight and degree of dehydration. Any electrolyte imbalances should also be corrected.

The definitive treatment for this condition is surgical intervention, with the Ramstedt pyloromyotomy being the procedure of choice. Laparoscopic pyloromyotomy is also an effective alternative if suitable facilities are available. The prognosis for infants with this condition is excellent, as long as there is no delay in diagnosis and treatment initiation.

Viral induced wheeze is a common condition in childhood that is triggered by a viral infection, typically a cold. The wheezing occurs during the infection and can persist for several weeks after the infection has cleared. This condition is most commonly seen in children under the age of three, as their airways are smaller. It is also more prevalent in babies who were small for their gestational age and in children whose parents smoke. It is important to note that viral induced wheeze does not necessarily mean that the child has asthma, although a small percentage of children with this condition may go on to develop asthma. Asthma is more commonly seen in children with a family history of asthma or allergies. Inhalers are often prescribed for the management of viral induced wheeze, but they may not always be effective.

The patient is showing signs of confusion and restlessness. Upon examination, it is found that the patient has high blood pressure, a rapid pulse rate, increased respiration rate, and a high temperature. An ECG reveals rapid atrial fibrillation. Additionally, the patient exhibits crackling sounds in the lower parts of the lungs, pitting edema in both legs below the knee, and a mild yellowish tint in the sclera. The patient’s medical history is obtained from their GP office, which reveals that they have not renewed their prescription for carbimazole and bisoprolol on time. Based on these findings, the most probable diagnosis is a thyroid storm.

Further Reading:

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

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

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

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

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

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

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

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

Transient global amnesia (TGA) is a neurological condition where individuals experience a temporary loss of short-term memory. This disorder is commonly observed in individuals over the age of 50 and is often associated with migraines.

The onset of TGA is typically sudden and can occur after engaging in strenuous exercise, sexual activity, or exposure to cold temperatures. These episodes usually last for a few hours and almost always resolve within 24 hours. One distinctive characteristic of TGA is perseveration, where patients repetitively ask the same question. Interestingly, once the episode has passed, individuals are unable to recall it.

Unlike a transient ischemic attack, TGA does not result in any focal neurological deficits, and the patient’s physical examination will appear normal.

On the other hand, a fugue state also involves temporary memory loss but presents differently. It is characterized by a loss of personal identity, past memories, and personality traits. Individuals experiencing a fugue state may even adopt entirely new identities and often engage in unplanned travel away from familiar surroundings.

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.

The most probable diagnosis in this case is a subarachnoid haemorrhage (SAH).

When assessing patients who present with an SAH, they may exhibit focal neurological signs, which can indicate the potential location of the aneurysm. Common areas where aneurysms occur include the bifurcation of the middle cerebral artery, the junction of the anterior communicating cerebral artery, and the junction of the posterior communicating artery with the internal carotid artery. If there is complete or partial paralysis of the oculomotor nerve, it suggests the rupture of a posterior communicating artery aneurysm.

While hypertension is a risk factor for SAH, a significant increase in blood pressure may occur as a reflex response following the haemorrhage.

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

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

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

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.

This woman is displaying symptoms and signs that are in line with a diagnosis of meningococcal septicaemia. In the United Kingdom, the majority of cases of meningococcal septicaemia are caused by Neisseria meningitidis group B.

The implementation of a vaccination program for Neisseria meningitidis group C has significantly reduced the prevalence of this particular type. However, a vaccine for group B disease is currently undergoing clinical trials and is not yet accessible for widespread use.

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

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

The most likely organism responsible for causing this patient’s symptoms is Haemophilus influenzae type B. This is indicated by the patient’s symptoms of fever, sore throat, high-pitched breathing noise during inspiration, and muffled voice. These symptoms are consistent with epiglottitis, which is a severe infection of the epiglottis caused by Haemophilus influenzae type B. This bacterium is known to cause respiratory tract infections, and it is particularly common in young children.

Further Reading:

Epiglottitis is a rare but serious condition characterized by inflammation and swelling of the epiglottis, which can lead to a complete blockage of the airway. It is more commonly seen in children between the ages of 2-6, but can also occur in adults, particularly those in their 40s and 50s. Streptococcus infections are now the most common cause of epiglottitis in the UK, although other bacterial agents, viruses, fungi, and iatrogenic causes can also be responsible.

The clinical features of epiglottitis include a rapid onset of symptoms, high fever, sore throat, painful swallowing, muffled voice, stridor and difficulty breathing, drooling of saliva, irritability, and a characteristic tripod positioning with the arms forming the front two legs of the tripod. It is important for healthcare professionals to avoid examining the throat or performing any potentially upsetting procedures until the airway has been assessed and secured.

Diagnosis of epiglottitis is typically made through fibre-optic laryngoscopy, which is considered the gold standard investigation. Lateral neck X-rays may also show a characteristic thumb sign, indicating an enlarged and swollen epiglottis. Throat swabs and blood cultures may be taken once the airway is secured to identify the causative organism.

Management of epiglottitis involves assessing and securing the airway as the top priority. Intravenous or oral antibiotics are typically prescribed, and supplemental oxygen may be given if intubation or tracheostomy is planned. In severe cases where the airway is significantly compromised, intubation or tracheostomy may be necessary. Steroids may also be used, although the evidence for their benefit is limited.

Overall, epiglottitis is a potentially life-threatening condition that requires urgent medical attention. Prompt diagnosis, appropriate management, and securing the airway are crucial in ensuring a positive outcome for patients with this condition.

This woman is displaying symptoms and signs that are consistent with a diagnosis of meningococcal septicaemia. In the United Kingdom, the majority of cases of meningococcal septicaemia are caused by Neisseria meningitidis group B.

In the prehospital setting, the most suitable medication and method of administration is intramuscular benzylpenicillin 1.2 g. This medication is commonly carried by most General Practitioners and is easier to administer than an intravenous drug in these circumstances.

For close household contacts, prophylaxis can be provided in the form of oral rifampicin 600 mg twice daily for two days.

When patients with diabetic ketoacidosis (DKA) are treated with insulin infusion, it is expected that their plasma bicarbonate levels will increase by at least 3 mmol/L per hour. Insulin therapy is aimed at correcting both hyperglycemia and ketoacidosis. However, if capillary ketones are not decreasing by at least 0.5 mmol/L per hour, venous bicarbonate is not rising by at least 3 mmol/L per hour, or plasma glucose is not decreasing by at least 3 mmol/L per hour, the insulin infusion rate should be reevaluated.

Further Reading:

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

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

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

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

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

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

During the examination, the child is observed to be grunting and has had an episode of urinary incontinence. The question asks about the likely complication that has developed.

The most likely complication in this case is cerebral edema. Cerebral edema refers to the swelling of the brain due to an increase in fluid accumulation. It is a severe and potentially life-threatening complication of diabetic ketoacidosis, particularly in children. The symptoms observed, such as headaches, increasing drowsiness, grunting, and urinary incontinence, are indicative of cerebral edema.

Cerebral edema can occur due to various factors, including the rapid correction of hyperglycemia and dehydration, as well as the release of inflammatory mediators. It is crucial to recognize and manage cerebral edema promptly as it can lead to increased intracranial pressure and neurological deterioration.

Further Reading:

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

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

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

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

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

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

The Lake Louise score is widely accepted as the standard method for evaluating the seriousness of Acute Mountain Sickness (AMS). The scoring system, outlined below, is used to determine the severity of AMS. A score of 3 or higher is indicative of AMS.

Further Reading:

High Altitude Illnesses

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

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

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

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

The finger has a total of four digital nerves. Two of these nerves, known as the palmar digital nerves, run along the palm side of each finger. The other two nerves, called the dorsal digital nerves, are located on the back side of the finger. However, the dorsal nerve supply changes slightly at the level of the proximal IP joint. Beyond this point, the dorsal nerve supply comes from the dorsal branch of the palmar digital nerve.

Further Reading:

Digital nerve blocks are commonly used to numb the finger for various procedures such as foreign body removal, dislocation reduction, and suturing. Sensation to the finger is primarily provided by the proper digital nerves, which arise from the common digital nerve. Each common digital nerve divides into two proper digital nerves, which run along the palmar aspect of the finger. These proper digital nerves give off a dorsal branch that supplies the dorsal aspect of the finger.

The most common technique for digital nerve blocks is the digital (ring) block. The hand is cleaned and the injection sites are cleansed with an alcohol swab. A syringe containing 1% lidocaine is prepared, and the needle is inserted at the base of the finger from a dorsal approach. Lidocaine is infiltrated under the skin, and the needle is then advanced towards the palmar aspect of the finger to inject more lidocaine. This process is repeated on the opposite side of the finger.

It is important not to use lidocaine with adrenaline for this procedure, as it may cause constriction and ischemia of the digital artery. Lidocaine 1% is the preferred local anesthetic, and the maximum dose is 3 ml/kg up to 200 mg. Contraindications for digital nerve blocks include compromised circulation to the finger, infection at the planned injection site, contraindication to local anesthetic (e.g. allergy), and suspected compartment syndrome (which is rare in the finger).

Complications of digital nerve blocks can include vascular injury to the digital artery or vein, injury to the digital nerve, infection, pain, allergic reaction, intravascular injection (which can be avoided by aspirating prior to injection), and systemic local anesthetic toxicity (which is uncommon with typical doses of lidocaine).

Based on the clinical history and examination, it strongly indicates that the patient has developed a pulmonary embolism due to a deep vein thrombosis in his right leg.

The symptoms commonly associated with a pulmonary embolism include shortness of breath, pleuritic chest pain, coughing, and/or coughing up blood. These symptoms may also suggest the presence of a deep vein thrombosis. Other clinical features that may be observed are rapid breathing and heart rate, fever, and in severe cases, signs of systemic shock, a gallop heart rhythm, and increased jugular venous pressure.

Cauda equina syndrome (CES) is a rare but serious complication that can occur when a disc ruptures. This happens when the material from the disc is pushed into the spinal canal and puts pressure on the bundle of nerves in the lower back and sacrum. As a result, individuals may experience loss of control over their bladder and bowel functions.

There are certain red flags that may indicate the presence of CES. These include experiencing sciatica on both sides of the body, having severe or worsening neurological issues in both legs (such as significant weakness in knee extension, ankle eversion, or foot dorsiflexion), difficulty starting urination or a decreased sensation of urinary flow, loss of sensation in the rectum, experiencing numbness or tingling in the perianal, perineal, or genital areas (also known as saddle anesthesia or paresthesia), and having a lax anal sphincter.

Conus medullaris syndrome (CMS) is a condition that affects the conus medullaris, which is located above the cauda equina at the T12-L2 level. Unlike CES, CMS primarily causes back pain and may have less noticeable nerve root pain. The main symptoms of CMS are urinary retention and constipation.

To confirm a diagnosis of CES and determine the level of compression and any underlying causes, an MRI scan is considered the gold-standard investigation. In cases where an MRI is not possible or contraindicated, a CT myelogram or standard CT scans can be helpful. However, plain radiographs have limited value and may only show significant degenerative or traumatic bone diseases.