Amiodarone is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) while performing chest compressions. The prescribed dose is 300 mg, which should be given as an intravenous bolus. To ensure proper administration, the medication should be diluted in 20 mL of 5% dextrose solution.

In cases where VF/pVT continues after five defibrillation attempts, an additional dose of 150 mg of Amiodarone should be administered. It is important to note that Amiodarone is not suitable for treating PEA or asystole, and its use is specifically indicated for shockable cardiac arrest situations.

Clostridium difficile is a type of bacteria that is Gram-positive, anaerobic, and capable of forming spores. It is found in the intestines of about 3% of healthy adults, according to estimates from the UK Health Protection Agency in 2012.

Clostridium difficile associated diarrhea (CDAD) often occurs after the use of broad-spectrum antibiotics, which disrupt the normal bacteria in the gut and allow Clostridium difficile to multiply. This leads to inflammation and bleeding in the lining of the large intestine, resulting in a distinct pseudomembranous appearance. The majority of Clostridium difficile infections are reported in individuals over the age of 65.

The main symptoms of CDAD include abdominal cramps, severe bloody and/or watery diarrhea, offensive-smelling diarrhea, and fever.

The gold standard for diagnosing Clostridium difficile colitis is a cytotoxin assay. However, this test can be challenging to perform and results may take up to 48 hours to obtain. The most commonly used laboratory test for diagnosing 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%.

In some cases, patients may develop a condition called toxic megacolon, which can be life-threatening, especially in frail or elderly individuals.

The current recommended first-line treatment for CDAD is oral vancomycin. For more information, refer to the guidance provided by the National Institute for Health and Care Excellence (NICE) regarding the risk of Clostridium difficile infection associated with the use of broad-spectrum antibiotics.

During pregnancy, the vena cava can be compressed by the uterus, leading to a decrease in venous return to the heart. This can worsen the shock state in cases of trauma by reducing cardiac output. To alleviate pressure on the inferior vena cava, the ATLS guidelines recommend manually displacing the uterus to the left side during the primary survey.

If spinal immobilization is necessary, the mother should be log rolled to her left side at a 15-30-degree angle, raising the right side by 10-15 cm. To maintain spinal motion restriction while decompressing the vena cava, a bolstering device like a Cardiff wedge should be used to support the mother.

Pregnancy causes an increase in intravascular volume, which means that pregnant patients can lose a significant amount of blood before showing signs of hypovolemia such as tachycardia and hypotension. Despite stable vital signs, the placenta may not receive adequate perfusion, putting the fetus at risk. Therefore, it is crucial to initiate fluid resuscitation, starting with crystalloid fluids and then using type-specific blood if necessary. Vasopressors should only be used as a last resort to restore maternal blood pressure, as they can further reduce uterine blood flow and lead to fetal hypoxia.

If the mother is rhesus D negative, anti-D immunoglobulin should be administered within 72 hours. However, this is not a priority during the primary survey.

Gout and pseudogout are both characterized by the presence of crystal deposits in the joints that are affected. Gout occurs when urate crystals are deposited, while pseudogout occurs when calcium pyrophosphate crystals are deposited. Under a microscope, these crystals can be distinguished by their appearance. Urate crystals are needle-shaped and negatively birefringent, while calcium pyrophosphate crystals are brick-shaped and positively birefringent.

Gout can affect any joint in the body, but it most commonly manifests in the hallux metatarsophalangeal joint, which is the joint at the base of the big toe. This joint is affected in approximately 50% of gout cases. On the other hand, pseudogout primarily affects the larger joints, such as the knee.

Testicular torsion is the correct diagnosis in this case. When a patient presents with sudden, severe, and acute testicular pain, testicular torsion should be assumed until proven otherwise. There are several historical factors that support this diagnosis. These include the pain occurring suddenly, being accompanied by vomiting, happening during sleep (as half of torsions occur during sleep), a previous history of torsion in the other testis, previous episodes that have resolved recently, and a history of undescended testis.

On examination, there are certain findings that further suggest testicular torsion. The testis may be positioned high in the scrotum and too tender to touch. The opposite testis may lie horizontally (known as Angell’s sign). Pain is not relieved by elevating the testis (negative Prehn’s sign), and the cremasteric reflex may be absent.

It is important to recognize that testicular torsion is a surgical emergency that requires immediate assessment and intervention to restore blood flow. Irreversible damage can occur within six hours of onset, so prompt treatment is crucial in this patient.

The use of NSAIDs in the third trimester of pregnancy is linked to several risks. These risks include delayed onset of labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus, which is a condition where bilirubin causes brain dysfunction. Additionally, there is a slight increase in the risk of first-trimester abortion if NSAIDs are used early in pregnancy.

Below is a list outlining commonly encountered drugs that have adverse effects during pregnancy:

ACE inhibitors (e.g. ramipril): If given in the second and third trimester, these drugs can cause hypoperfusion, renal failure, and the oligohydramnios sequence.

Aminoglycosides (e.g. gentamicin): These drugs can cause ototoxicity and deafness.

Aspirin: High doses of aspirin can lead to first-trimester abortions, delayed onset of labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g. 75 mg) do not pose a significant risk.

Benzodiazepines (e.g. diazepam): When given late in pregnancy, these drugs can cause respiratory depression and a neonatal withdrawal syndrome.

Calcium-channel blockers: If given in the first trimester, these drugs can cause phalangeal abnormalities. If given in the second and third trimester, they can lead to fetal growth retardation.

Carbamazepine: This drug can cause hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol: Use of this drug can result in grey baby syndrome.

Corticosteroids: If given in the first trimester, corticosteroids may cause orofacial clefts.

Danazol: If given in the first trimester, this drug can cause masculinization of the female fetuses genitals.

Finasteride: Pregnant women should avoid handling finasteride. Crushed or broken tablets can be absorbed through the skin and affect male sex organ development.

Haloperidol: If given in the first trimester, this drug may cause limb malformations. If given in the third trimester, there is an increased risk of extrapyramidal symptoms in the neonate.

Heparin: Use of heparin during pregnancy can lead to maternal bleeding and thrombocytopenia.

Isoniazid: This drug can cause maternal liver damage

The size of the cannula used for IV fluid infusion determines the maximum flow rate. For a 20g cannula, the maximum flow rate is around 60 ml per minute. As a result, the fastest infusion time through a 20g cannula is approximately 15 minutes for a maximum volume of 1000 ml.

Further Reading:

Peripheral venous cannulation is a procedure that should be performed following established guidelines to minimize the risk of infection, injury, extravasation, and early failure of the cannula. It is important to maintain good hand hygiene, use personal protective equipment, ensure sharps safety, and employ an aseptic non-touch technique during the procedure.

According to the National Institute for Health and Care Excellence (NICE), the skin should be disinfected with a solution of 2% chlorhexidine gluconate and 70% alcohol before inserting the catheter. It is crucial to allow the disinfectant to completely dry before inserting the cannula.

The flow rates of IV cannulas can vary depending on factors such as the gauge, color, type of fluid used, presence of a bio-connector, length of the cannula, and whether the fluid is drained under gravity or pumped under pressure. However, the following are typical flow rates for different gauge sizes: 14 gauge (orange) has a flow rate of 270 ml/minute, 16 gauge (grey) has a flow rate of 180 ml/minute, 18 gauge (green) has a flow rate of 90 ml/minute, 20 gauge (pink) has a flow rate of 60 ml/minute, and 22 gauge (blue) has a flow rate of 36 ml/minute. These flow rates are based on infusing 1000 ml of normal saline under ideal circumstances, but they may vary in practice.

The speed at which local anesthetics take effect is primarily determined by their lipid solubility. The onset of action is directly influenced by how well the anesthetic can dissolve in lipids, which is in turn related to its pKa value. A higher lipid solubility leads to a faster onset of action. The pKa value, which represents the acid-dissociation constant, is an indicator of lipid solubility. An anesthetic agent with a pKa value closer to 7.4 is more likely to be highly lipid soluble.

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.

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.

Warfarin has been found to heighten the likelihood of bleeding events when consumed alongside specific juices, such as cranberry juice and grapefruit juice. As a result, individuals who are taking warfarin should be cautioned against consuming these beverages. For more information on this topic, please refer to the BNF section on warfarin interactions and the interaction between warfarin and cranberry juice.

Intussusception occurs when a section of the bowel folds into another section, causing a blockage. This can be due to a specific underlying issue, like a Meckel’s diverticulum, or it can happen without any specific cause. The condition is most commonly seen in boys between the ages of 5 and 10 months. Symptoms include sudden vomiting and episodes of abdominal pain that come and go. The vomit quickly becomes greenish-yellow in color. Dance’s sign, which is the absence of bowel in the lower right part of the abdomen, may be observed. Redcurrant jelly-like stools are a late indication of the condition. It is believed that more than 90% of cases are caused by a non-specific underlying issue, often viral infections like rotavirus, adenovirus, and human herpesvirus 6.

Reed-Sternberg cells are distinctive large cells that are typically observed in Hodgkin lymphoma. These cells are often found to have two nuclei or a nucleus with two lobes. Additionally, they possess noticeable nucleoli that resemble eosinophilic inclusion-like structures, giving them an appearance similar to that of an owl’s eye.

The probable underlying reason for the patient’s symptoms is central pontine myelinolysis. This condition is characterized by the destruction of the myelin sheath in the pons, a region of the brainstem. It is often caused by a rapid correction of hyponatremia, which is a low level of sodium in the blood. In this case, the patient’s serum sodium level was initially low at 117 mmol/L, and the administration of intravenous 3% sodium chloride solution caused a rapid increase in sodium levels. This sudden change in sodium concentration can lead to the development of central pontine myelinolysis. The initial improvement in the patient’s symptoms may have been due to the correction of hyponatremia, but the subsequent development of lethargy and dysarthria suggests the onset of central pontine myelinolysis.

Further Reading:

Syndrome of inappropriate antidiuretic hormone (SIADH) is a condition characterized by low sodium levels in the blood due to excessive secretion of antidiuretic hormone (ADH). ADH, also known as arginine vasopressin (AVP), is responsible for promoting water and sodium reabsorption in the body. SIADH occurs when there is impaired free water excretion, leading to euvolemic (normal fluid volume) hypotonic hyponatremia.

There are various causes of SIADH, including malignancies such as small cell lung cancer, stomach cancer, and prostate cancer, as well as neurological conditions like stroke, subarachnoid hemorrhage, and meningitis. Infections such as tuberculosis and pneumonia, as well as certain medications like thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs), can also contribute to SIADH.

The diagnostic features of SIADH include low plasma osmolality, inappropriately elevated urine osmolality, urinary sodium levels above 30 mmol/L, and euvolemic. Symptoms of hyponatremia, which is a common consequence of SIADH, include nausea, vomiting, headache, confusion, lethargy, muscle weakness, seizures, and coma.

Management of SIADH involves correcting hyponatremia slowly to avoid complications such as central pontine myelinolysis. The underlying cause of SIADH should be treated if possible, such as discontinuing causative medications. Fluid restriction is typically recommended, with a daily limit of around 1000 ml for adults. In severe cases with neurological symptoms, intravenous hypertonic saline may be used. Medications like demeclocycline, which blocks ADH receptors, or ADH receptor antagonists like tolvaptan may also be considered.

It is important to monitor serum sodium levels closely during treatment, especially if using hypertonic saline, to prevent rapid correction that can lead to central pontine myelinolysis. Osmolality abnormalities can help determine the underlying cause of hyponatremia, with increased urine osmolality indicating dehydration or renal disease, and decreased urine osmolality suggesting SIADH or overhydration.

Cerebral edema is the most significant complication of diabetic ketoacidosis (DKA), leading to death in many cases. It occurs in approximately 0.2-1% of DKA cases. The high blood glucose levels cause an osmolar gradient, resulting in the movement of water from the intracellular fluid (ICF) to the extracellular fluid (ECF) space and a decrease in cell volume. When insulin and intravenous fluids are administered to correct the condition, the effective osmolarity decreases rapidly, causing a reversal of the fluid shift and the development of cerebral edema.

Cerebral edema is associated with a higher mortality rate and poor neurological outcomes. To prevent its occurrence, it is important to slowly normalize osmolarity over a period of 48 hours, paying attention to glucose and sodium levels, as well as ensuring proper hydration. Monitoring the child for symptoms such as headache, recurrent vomiting, irritability, changes in Glasgow Coma Scale (GCS), abnormal slowing of heart rate, and increasing blood pressure is crucial.

If cerebral edema does occur, it should be treated with either a hypertonic (3%) saline solution at a dosage of 3 ml/kg or a mannitol infusion at a dosage of 250-500 mg/kg over a 20-minute period.

In addition to cerebral edema, there are other complications associated with DKA in children, including cardiac arrhythmias, pulmonary edema, and acute renal failure.

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.

Patients who have myxoedema coma usually show symptoms such as lethargy, bradycardia, hypothermia, worsening mental state, seizures, and/or coma. This patient has hypothyroidism and takes thyroxine regularly, which aligns with the signs and symptoms of myxoedema coma. It is worth noting that infections often act as a trigger, and this patient has developed a cough in the last week.

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 emergency department doctor does not play a role in obtaining consent from the next of kin for tissue or organ donation. Instead, it is important to involve the Specialist Nurse in Organ Donation (SNOD) as early as possible. The SNOD can provide valuable support and guidance to both the medical team and the family. They will assess the patient’s suitability for organ donation and approach the next of kin for consent, if appropriate. On the other hand, for tissue donation, a referral should be made to the tissue donation national referral centre. Retrievals can take place within 24 hours after death. In the UK, referrals can be made by phone to the tissue donation national referral centre (the contact number can be found in the notes below). It is important to note that the responsibility of gaining consent from the next of kin does not fall on the emergency department doctor.

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.

It is recommended to administer prophylactic oral antibiotics to individuals who have experienced a cat bite that has broken the skin and cause bleeding. For patients over one month of age, co-amoxiclav should be prescribed for a duration of 3 days. In cases where the patient is allergic to penicillin, a combination of metronidazole and doxycycline should be given for 3 days. If the wound shows signs of infection, the antibiotic treatment should be extended to 5 days.

Prophylactic oral antibiotics may also be considered for individuals with a cat bite that has broken the skin but has not caused bleeding, especially if the wound is deep.

Debridement, the removal of dead tissue, should be considered for wounds that are damaged, have abscess formation, lymphangitis, severe cellulitis, osteomyelitis, septic arthritis, necrotising fasciitis, or infected bite wounds that are not responding to treatment. Additionally, individuals who are systemically unwell should also undergo debridement.

Antibiotics should also be considered for other animal bites, such as dog bites, that have broken the skin and cause bleeding.

Further Reading:

Bite wounds from animals and humans can cause significant injury and infection. It is important to properly assess and manage these wounds to prevent complications. In human bites, both the biter and the injured person are at risk of infection transmission, although the risk is generally low.

Bite wounds can take various forms, including lacerations, abrasions, puncture wounds, avulsions, and crush or degloving injuries. The most common mammalian bites are associated with dogs, cats, and humans.

When assessing a human bite, it is important to gather information about how and when the bite occurred, who was involved, whether the skin was broken or blood was involved, and the nature of the bite. The examination should include vital sign monitoring if the bite is particularly traumatic or sepsis is suspected. The location, size, and depth of the wound should be documented, along with any functional loss or signs of infection. It is also important to check for the presence of foreign bodies in the wound.

Factors that increase the risk of infection in bite wounds include the nature of the bite, high-risk sites of injury (such as the hands, feet, face, genitals, or areas of poor perfusion), wounds penetrating bone or joints, delayed presentation, immunocompromised patients, and extremes of age.

The management of bite wounds involves wound care, assessment and administration of prophylactic antibiotics if indicated, assessment and administration of tetanus prophylaxis if indicated, and assessment and administration of antiviral prophylaxis if indicated. For initial wound management, any foreign bodies should be removed, the wound should be encouraged to bleed if fresh, and thorough irrigation with warm, running water or normal saline should be performed. Debridement of necrotic tissue may be necessary. Bite wounds are usually not appropriate for primary closure.

Prophylactic antibiotics should be considered for human bites that have broken the skin and drawn blood, especially if they involve high-risk areas or the patient is immunocompromised. Co-amoxiclav is the first-line choice for prophylaxis, but alternative antibiotics may be used in penicillin-allergic patients. Antibiotics for wound infection should be based on wound swab culture and sensitivities.

Tetanus prophylaxis should be administered based on the cleanliness and risk level of the wound, as well as the patient’s vaccination status. Blood-borne virus risk should also be assessed, and testing for hepatitis B, hepatitis C, and HIV should be done.

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.

Le Fort fractures are complex fractures of the midface that involve the maxillary bone and surrounding structures. These fractures can occur in a horizontal, pyramidal, or transverse direction. The distinguishing feature of Le Fort fractures is the traumatic separation of the pterygomaxillary region. They make up approximately 10% to 20% of all facial fractures and can have severe consequences, both in terms of potential life-threatening injuries and disfigurement.

The Le Fort classification system categorizes midface fractures into three groups based on the plane of injury. As the classification level increases, the location of the maxillary fracture moves from inferior to superior within the maxilla.

Le Fort I fractures are horizontal fractures that occur across the lower aspect of the maxilla. These fractures cause the teeth to separate from the upper face and extend through the lower nasal septum, the lateral wall of the maxillary sinus, and into the palatine bones and pterygoid plates. They are sometimes referred to as a floating palate because they often result in the mobility of the hard palate from the midface. Common accompanying symptoms include facial swelling, loose teeth, dental fractures, and misalignment of the teeth.

Le Fort II fractures are pyramidal-shaped fractures, with the base of the pyramid located at the level of the teeth and the apex at the nasofrontal suture. The fracture line extends from the nasal bridge and passes through the superior wall of the maxilla, the lacrimal bones, the inferior orbital floor and rim, and the anterior wall of the maxillary sinus. These fractures are sometimes called a floating maxilla because they typically result in the mobility of the maxilla from the midface. Common symptoms include facial swelling, nosebleeds, subconjunctival hemorrhage, cerebrospinal fluid leakage from the nose, and widening and flattening of the nasal bridge.

Le Fort III fractures are transverse fractures of the midface. The fracture line passes through the nasofrontal suture, the maxillo frontal suture, the orbital wall, and the zygomatic arch and zygomaticofrontal suture. These fractures cause separation of all facial bones from the cranial base, earning them the nickname craniofacial disjunction or floating face fractures. They are the rarest and most severe type of Le Fort fracture. Common symptoms include significant facial swelling, bruising around the eyes, facial flattening, and the entire face can be shifted.

The main treatment options for Bell’s palsy are oral prednisolone and proper eye care. Referral to a specialist is typically not necessary. It is recommended to start steroid treatment within 72 hours of symptom onset. Currently, NICE does not recommend the use of antiviral medications for Bell’s palsy.

Further Reading:

Bell’s palsy is a condition characterized by sudden weakness or paralysis of the facial nerve, resulting in facial muscle weakness or drooping. The exact cause is unknown, but it is believed to be related to viral infections such as herpes simplex or varicella zoster. It is more common in individuals aged 15-45 years and those with diabetes, obesity, hypertension, or upper respiratory conditions. Pregnancy is also a risk factor.

Diagnosis of Bell’s palsy is typically based on clinical symptoms and ruling out other possible causes of facial weakness. Symptoms include rapid onset of unilateral facial muscle weakness, drooping of the eyebrow and corner of the mouth, loss of the nasolabial fold, otalgia, difficulty chewing or dry mouth, taste disturbance, eye symptoms such as inability to close the eye completely, dry eye, eye pain, and excessive tearing, numbness or tingling of the cheek and mouth, speech articulation problems, and hyperacusis.

When assessing a patient with facial weakness, it is important to consider other possible differentials such as stroke, facial nerve tumors, Lyme disease, granulomatous diseases, Ramsay Hunt syndrome, mastoiditis, and chronic otitis media. Red flags for these conditions include insidious and painful onset, duration of symptoms longer than 3 months with frequent relapses, pre-existing risk factors, systemic illness or fever, vestibular or hearing abnormalities, and other cranial nerve involvement.

Management of Bell’s palsy involves the use of steroids, eye care advice, and reassurance. Steroids, such as prednisolone, are recommended for individuals presenting within 72 hours of symptom onset. Eye care includes the use of lubricating eye drops, eye ointment at night, eye taping if unable to close the eye at night, wearing sunglasses, and avoiding dusty environments. Reassurance is important as the majority of patients make a complete recovery within 3-4 months. However, some individuals may experience sequelae such as facial asymmetry, gustatory lacrimation, inadequate lid closure, brow ptosis, drooling, and hemifacial spasms.

Antiviral treatments are not currently recommended as a standalone treatment for Bell’s palsy, but they may be given in combination with corticosteroids on specialist advice. Referral to an ophthalmologist is necessary if the patient has eye symptoms such as pain, irritation, or itch.

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 most probable diagnosis in this case is vaginal thrush. Vaginal thrush is characterized by symptoms such as vulval irritation and itching, vulval redness, and a discharge that is often described as cheesy. Some women may also experience dysuria, which is pain or discomfort during urination, but without an increase in frequency or urgency. The recommended treatment for vaginal thrush is the use of antifungal agents, with topical azoles like clotrimazole or miconazole being commonly prescribed. It is important to note that breastfeeding patients should avoid taking oral terbinafine as it can pass into breast milk.

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. Re-warming methods include passive re-warming with warm blankets or Bair hugger/polythene sheets, surface re-warming with a water bath, core re-warming with heated, humidified oxygen or peritoneal lavage, and extracorporeal re-warming 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.

The explanation states that the increased activity of the enzyme kininogenase is caused by hormonal factors, specifically oestrogen, as well as genetic factors.

Further Reading:

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

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

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

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

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

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

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

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.

NSAIDs are known to have a relaxing effect on the ureter, but a randomized controlled trial found no difference between NSAIDs and a placebo in terms of this effect. Currently, only two classes of drugs, calcium channel blockers and alpha-blockers, are considered effective as medical expulsive therapy (MET). Calcium channel blockers work by blocking the active calcium channel pump that the smooth muscle of the ureter uses to contract, resulting in relaxation of the muscle and improved stone passage. Alpha-blockers, on the other hand, are commonly used as the first-line treatment to enhance stone passage. They reduce the basal tone of the ureter smooth muscle, decrease the frequency of peristaltic waves, and lower ureteric contraction. This leads to a decrease in intraureteric pressure below the stone, increasing the chances of stone passage. Patients treated with calcium channel blockers or alpha-blockers have been shown to have a 65% higher likelihood of spontaneous stone passage compared to those not given these medications.

Rapid tranquillisation involves the administration of medication through injection when oral medication is not feasible or appropriate and immediate sedation is necessary. The current guidelines from NICE recommend two options for rapid tranquillisation in adults: intramuscular lorazepam alone or a combination of intramuscular haloperidol and intramuscular promethazine. The choice of medication depends on various factors such as advanced statements, potential intoxication, previous responses to these medications, interactions with other drugs, and existing physical health conditions or pregnancy.

If there is insufficient information to determine the appropriate medication or if the individual has not taken antipsychotic medication before, intramuscular lorazepam is recommended. However, if there is evidence of cardiovascular disease or a prolonged QT interval, or if an electrocardiogram has not been conducted, the combination of intramuscular haloperidol and intramuscular promethazine should be avoided, and intramuscular lorazepam should be used instead.

If there is a partial response to intramuscular lorazepam, a second dose should be considered. If there is no response to intramuscular lorazepam, then intramuscular haloperidol combined with intramuscular promethazine should be considered. If there is a partial response to this combination, a further dose should be considered.

If there is no response to intramuscular haloperidol combined with intramuscular promethazine and intramuscular lorazepam has not been used yet, it should be considered. However, if intramuscular lorazepam has already been administered, it is recommended to arrange an urgent team meeting to review the situation and seek a second opinion if necessary.

After rapid tranquillisation, the patient should be closely monitored for any side effects, and their vital signs should be regularly checked, including heart rate, blood pressure, respiratory rate, temperature, hydration level, and level of consciousness. These observations should be conducted at least hourly until there are no further concerns about the patient’s physical health.

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

This patient has developed an acute auricular subchondral haematoma. It occurs when blood and serum collect in the space between the cartilage and the supporting perichondrium due to a shearing force that separates the perichondrium from the underlying cartilage.

It is important to differentiate this condition from cauliflower ear, which is a common complication that arises when an auricular haematoma is not treated. If a subchondral haematoma is left untreated, the damaged perichondrium forms a fibrocartilage plate, leading to scarring and cartilage regeneration. This results in an irregular and thickened pinna, typically along the helical rim.

The management of an auricular haematoma involves the following steps:

1. Infiltration with a local anaesthetic, such as 1% lidocaine.
2. Drainage or needle aspiration of the haematoma.
3. Application of firm packing and compression bandaging to prevent re-accumulation.
4. Administration of broad-spectrum antibiotics.

By following these management steps, the patient can effectively address and treat the auricular haematoma.