An operating room fire is rare but a well-known hazard that can result in significant patient morbidity. When it comes to the disposal of surgical spirits, the SPC for chlorhexidine states: ‘The solution is flammable. The risk of surgical fires due to spirit-based skin preparation fluid should be actively reduced. Data from the US show that up to 650 surgical fires occur each year, with up to 5% causing death or serious harm.

Diathermy use electric currents to produce local heat and thereby facilitate haemostasis or surgical dissection. There are two major types of diathermy:
1. Monopolar – current flows through a handheld device, from the tip of the device into the patient. The earth electrode is located some distance away.
2. Bipolar – current flows from one electrode to another however, both electrodes are usually contained within the same device e.g. a pair of forceps. The result is that heating is localised to the area between the two electrodes and surrounding tissue damage is minimised. However this may create a spark and ignite flammable solutions.

The special part of the equipment is the T tube itself. As the name refers, it is a special tube in the shape of T with a shorter transverse part (20 cm) that stays inside the CBD (after trimming) and a long longitudinal part (60 cm) that extends from the middle of the transverse part to an end that connects with a drainage bag. This portion extends from the CBD to outside the abdominal cavity when applied. It comes with different circumference sizes (10, 12, 14, 16, 18 Fr). T tube can be made of different materials like latex, silicone, red rubber and polyvinyl chloride (PVC). PVC is very inert causing the least tissue reaction with lack of tissue tract formation making it the least favourable material for T tube placement purposes. Silicon has many favourable physical properties, but it can disintegrate with poor handling making it not a practical option for long-term placement. Latex has the desired properties to be the most commonly used. Red rubber is an alternative if latex can not be used or is not available.

In 1–10% of all patients with acute middle cerebral artery occlusion, the subsequent ischemic stroke can be classified as “malignant,” defined by ischemic brain tissue large enough to cause a considerable increase of ICP and potential cerebral herniation.
Clinically, the patients present with severe hemispheric symptoms including hemiparesis or hemiplegia, loss of visual field, gaze deviation and, depending on the affected hemisphere, neglect or aphasia. Patients may also show an impaired level of consciousness, nausea, vomiting, papillary changes and papilledema as signs of increased ICP.
Decompressive craniectomy is the only therapeutic approach that is based on data of large randomized controlled trials in this condition. Decompressive craniectomy reduces the mortality rate in these patients, however leaving the majority of patients with at least some disability. Other treatment options like osmotherapy may be used in an individual risk-benefit-assessment, but evidence for these treatments and procedures is scarce.

A massive blood transfusion is defined as the replacement of a patient’s total blood volume in <24 h
The abnormalities which result include effects upon coagulation status, serum biochemistry, acid-base balance and temperature homeostasis.
One of the complications is Transfusion-related acute lung injury
(TRALI) which is the most common cause of major morbidity and death after transfusion. It presents as an acute respiratory distress syndrome (ARDS) either during or within 6 h of transfusion.

Clinical features
Hypoxaemia, dyspnoea, cyanosis, fever, tachycardia and hypotension result from non-cardiogenic pulmonary oedema. The radiographic appearance is of bilateral pulmonary infiltration, characteristic of pulmonary oedema. It is important to differentiate TRALI from other causes of ARDS such as circulatory overload or myocardial or valvular heart disease. Invasive monitoring in TRALI demonstrates normal intracardiac pressures

Pathogenesis
Two different mechanisms for the pathogenesis of TRALI have been identified: immune (antibody-mediated) and non-immune. Immune TRALI results from the presence of leucocyte antibodies in the plasma of donor blood directed against human leucocyte antigens (HLA) and human neutrophil alloantigens (HNA) in the recipient. Antibodies present in the recipient only rarely cause TRALI. In up to 40% of patients, leucocyte antibodies cannot be detected in either donor or recipient. In these cases, it is possible that reactive lipid products released from the membranes of the donor blood cells act as the trigger. This is known as non-immune TRALI.
The target cell in both forms of TRALI is the neutrophil granulocyte. On activation of their acute phase cycle, these cells migrate to the lungs where they become trapped within the pulmonary microvasculature. Oxygen-free radicals and other proteolytic enzymes are then released which destroy the endothelial cells of the lung capillaries. A pulmonary capillary leak syndrome develops with the exudation of fluid and protein into the alveoli resulting in pulmonary oedema. The majority of reactions are severe, and often life-threatening; 70% require mechanical ventilation and 6–9% are fatal. A definitive diagnosis requires antibody detection. The mortality in non-immune TRALI is lower, and the syndrome is encountered predominantly in critically ill patients.
Other Complications of blood transfusion
Early:
– Haemolytic reactions
Immediate
Delayed
– Non-haemolytic febrile reactions
– Allergic reactions to proteins, IgA
– Reactions secondary to bacterial contamination
– Circulatory overload
– Air embolism
– Thrombophlebitis
– Hyperkalaemia
– Citrate toxicity
– Hypothermia
– Clotting abnormalities (after massive transfusion)
Late:
– Transmission of infection
– Viral (hepatitis A, B, C, HIV, CMV)
– Bacterial (Treponeum pallidum, Salmonella)
– Parasites (malaria, toxoplasma)
– Graft-vs-host disease
– Iron overload (after chronic transfusions)
– Immune sensitization (Rhesus D antigen)

Breast cancer frequently metastasizes to the skeleton, interrupting the normal bone remodelling process and causing bone degradation. Breast cancer is the commonest cause of lytic bone metastasis in women of this age, especially from amongst those options given.

Osteolytic lesions are the end result of osteoclast activity; however, osteoclast differentiation and activation are mediated by osteoblast production of RANKL (receptor activator for NFκB ligand) and several osteoclastogenic cytokines. Osteoblasts themselves are negatively affected by cancer cells as evidenced by an increase in apoptosis and a decrease in proteins required for new bone formation. Thus, bone loss is due to both increased activation of osteoclasts and suppression of osteoblasts. The clinical outcomes of bone pain, pathologic fractures, nerve compression syndrome, and metabolic disturbances leading to hypercalcemia and acid/base imbalance severely reduce the quality of life.

Extradural haematoma (EDH) is defined as an acute bleed between the dura mater and the inner surface of the skull. This then causes increased intracranial pressure, which puts vital brain structures at risk. The question asks for the least likely cause, and extradural hematoma would be acute in onset.

The patient’s history and examination point towards a significant visceral injury. FAST scan is associated with a false-negative result in pregnancy which makes the normal result, in this scenario, less reassuring. CT scan of the abdomen remains the gold standard for diagnosis.

Sonography and FAST scanning are established in pregnancy and provide the advantage of avoiding ionising radiations. However, the sensitivity of the FAST scan is reduced in pregnancy especially with advanced gestational age. CT scan remains the first-line investigation in major trauma where significant visceral injury is suspected. The maximum permitted safe dose of radiation in pregnancy is 5 mSv.

Patient-controlled analgesia (PCA) is a delivery system with which patients self-administer predetermined doses of analgesic medication to relieve their pain. The use of PCA in hospitals has been increasing because of its proven advantages over conventional intramuscular injections. These include improved pain relief, greater patient satisfaction, less sedation and fewer postoperative complications.

Dextran 40 and 70 have a higher rate of causing anaphylaxis than either gelatins or starches.

Dextrans are branched polysaccharide molecules, with dextran 40 and 70 available. The high-molecular-weight dextran 70 may persist for up to eight hours. They inhibit platelet aggregation and leucocyte plugging in the microcirculation, thereby, improving flow through the microcirculation. They are primarily used in sepsis.
Unlike many other intravenous fluids, dextrans are a recognised cause of anaphylaxis.

Answer: Rupture of the aorta distal to the left subclavian artery

Aortic rupture is typically the result of a blunt aortic injury in the context of rapid deceleration. After traumatic brain injury, blunt aortic rupture is the second leading cause of death following blunt trauma. Thus, this condition is commonly fatal as blood in the aorta is under great pressure and can quickly escape the vessel through a tear, resulting in rapid haemorrhagic shock, exsanguination, and death.
Traumatic aortic transection or rupture is associated with a sudden and rapid deceleration of the heart and the aorta within the thoracic cavity. Anatomically, the heart and great vessels (superior vena cava, inferior vena cava, pulmonary arteries, pulmonary veins, and aorta) are mobile within the thoracic cavity and not fixed to the chest wall, unlike the descending abdominal aorta. Injury to the aorta during a sudden deceleration commonly originates near the terminal section of the aortic arch, also known as the isthmus. This portion lies just distal to the take-off of the left subclavian artery at the intersection of the mobile and fixed portions of the aorta.

Mitral valve stenosis is the most common cause of cardiac abnormality occurring in pregnant women. It is becoming less common in the UK population; however, it should be considered in women from countries where there is a higher incidence of rheumatic heart disease. Physiological changes in pregnancy may cause an otherwise asymptomatic patient to suddenly deteriorate.

Mitral stenosis causes a mid-diastolic murmur which may be difficult to auscultate unless the patient is placed in the left lateral position. These patients are at risk of atrial fibrillation (up to 40%) which can also contribute to rapid decompensation such as pulmonary oedema (hence, whiteout of lungs seen on CXR). Balloon valvuloplasty is the treatment of choice in patients with mitral valve stenosis.

Answer: Aortic rupture

Aortic rupture is typically the result of a blunt aortic injury in the context of rapid deceleration. After traumatic brain injury, blunt aortic rupture is the second leading cause of death following blunt trauma. Thus, this condition is commonly fatal as blood in the aorta is under great pressure and can quickly escape the vessel through a tear, resulting in rapid haemorrhagic shock, exsanguination, and death. Traumatic aortic transection or rupture is associated with a sudden and rapid deceleration of the heart and the aorta within the thoracic cavity.
Features on plain chest radiography that suggest aortic injury and can help guide the further use of angiography include; an abnormal aortic arch contour, left apical cap, loss of the aorticopulmonary window, rightward deviation of the trachea, depression of the left main stem bronchus, and a wide left paravertebral pleural stripe. Also, widening of the mediastinum (greater than 8 cm) has a reported sensitivity of 81% to 100% and a specificity of 60%.

Post-operative fever is very common.
It is known to occur after all types of surgical procedures, irrespective of the type of anaesthesia.
Postoperative fever can occur after minor surgical procedures but is rare and depends on the type of procedure. Overall, both abdominal and chest procedures result in the highest incidence of postoperative fever.

In this case:
Acute Fever
Fever occurs in the first week (1 to 7 POD)
POD 7 (5 to 10): Wound infection: Risk increases if the patient is immunocompromised (e.g., diabetic), abdominal wound, duration of surgery greater than 2 hours or contamination during surgery. Signs include erythema, warmth, tenderness, discharge.
Rule out abscess or collections by physical exam plus ultrasound if needed. If an abscess is present, drainage and antibiotics are needed. Prevention is by careful surgical technique and prophylactic antibiotics (e.g., intravenous cefazolin at the time of induction of anaesthesia as well as postoperatively if needed)

Other causes of Postoperative fever:
An Immediate Fever
Fever occurs immediately after surgery or within hours on postoperative days (POD) 0 or 1.
– Malignant hyperthermia: high-grade fever (greater than 40 C), occurs shortly after inhalational anaesthetics or muscle relaxant (e.g., halothane or succinylcholine), may have a family history of death after anaesthesia. Laboratory studies will reveal with metabolic acidosis and hypercalcemia. If not readily recognized, it can cause cardiac arrest. The treatment is intravenous dantrolene, 100% oxygen, correction of acidosis, cooling blankets, and watching for myoglobinuria.
– Bacteraemia: High-grade fever (greater than 40 C) occurring 30 to 40 minutes after the beginning of the procedure (e.g., Urinary tract instrumentation in the presence of infected urine). Management includes blood cultures three times and starting empiric antibiotics.
– Gas gangrene of the wound: High-grade fever (greater than 40 C) occurring after gastrointestinal (GI) surgery due to contamination with Clostridium perfringens; severe wound pain; treat with surgical debridement and antibiotics.
– Febrile non-haemolytic transfusion reaction: Fevers, chills, and malaise 1 to 6 hours after surgery (without haemolysis). Management: Stop transfusion (rule out haemolytic transfusion reaction) and give antipyretics (avoid aspirin in the thrombocytopenic patient).

B. Acute Fever
– Fever occurs in the first week (1 to 7 POD).
POD 1 to 3: atelectasis: After prolonged intubation, the presence of upper abdominal incision, inadequate postoperative pain control, lying supine. Should be prevented by incentive spirometry, semi-recumbent position, adequate pain control, early ambulation. Clinically may be asymptomatic or with increased work of breathing, respiratory alkalosis, chest x-ray with volume loss. Treatment includes spirometry, chest physiotherapy, semi-recumbent position (improves expansion of alveoli by preventing pressure from intra-abdominal organs on the diaphragm and hence improving functional residual capacity)
– POD 3: Unresolved atelectasis resulting in pneumonia (respiratory symptoms, Chest x-ray with infiltrate or consolidation, sputum culture, empiric antibiotics and modify according to culture result and sensitivity), or development of urinary tract infection (urine analysis and culture, treat with empiric antibiotics and modify according to culture result and sensitivity)
– POD 5: Thrombophlebitis (may be asymptomatic or symptomatic, diagnose with Doppler ultrasound of deep leg and pelvic veins and treat with heparin)
– POD 7: Pulmonary embolism (tachycardia, tachypnoea, pleuritic chest pain, ECG with right heart strain pattern (a low central venous pressure goes against diagnosis), arterial blood gas with hypoxemia and hypocapnia, confirm diagnosis with CT angiogram, and treat with heparin, if recurrent pulmonary embolism while anticoagulated with therapeutic INR, Inferior vena cava filter placement is the next step

C. Subacute Fever
Fever occurs between postoperative weeks 1 and 4.
– POD 10: Deep infection (pelvic or abdominal abscess and if abdominal abscess could be sub-hepatic or sub-phrenic). A digital rectal exam to rule out the pelvic abscess and CT scan to localize intra-abdominal abscess. Treatment includes re-exploration vs. radiological guided percutaneous drainage
Drugs: Diagnosis of exclusion includes rash and peripheral eosinophilia

D. Delayed Fever
Fever after more than 4 weeks.
Skin and soft tissue infections (SSTI)
Viral infections

Answer: Myoglobin

When muscle is damaged, a protein called myoglobin is released into the bloodstream. It is then filtered out of the body by the kidneys. Myoglobin breaks down into substances that can damage kidney cells.
Compartment syndrome is a painful condition that occurs when pressure within the muscles builds to dangerous levels. This pressure can decrease blood flow, which prevents nourishment and oxygen from reaching nerve and muscle cells.

Compartment syndrome can be either acute or chronic.

Acute compartment syndrome is a medical emergency. It is usually caused by a severe injury. Without treatment, it can lead to permanent muscle damage.

Chronic compartment syndrome, also known as exertional compartment syndrome, is usually not a medical emergency. It is most often caused by athletic exertion. Compartments are groupings of muscles, nerves, and blood vessels in your arms and legs. Covering these tissues is a tough membrane called a fascia. The role of the fascia is to keep the tissues in place, and, therefore, the fascia does not stretch or expand easily.
Compartment syndrome develops when swelling or bleeding occurs within a compartment. Because the fascia does not stretch, this can cause increased pressure on the capillaries, nerves, and muscles in the compartment. Blood flow to muscle and nerve cells is disrupted. Without a steady supply of oxygen and nutrients, nerve and muscle cells can be damaged.

In acute compartment syndrome, unless the pressure is relieved quickly, permanent disability and tissue death may result. This does not usually happen in chronic (exertional) compartment syndrome.

Compartment syndrome most often occurs in the anterior (front) compartment of the lower leg (calf). It can also occur in other compartments in the leg, as well as in the arms, hands, feet, and buttocks.

Acute compartment syndrome usually develops after a severe injury, such as a car accident or a broken bone. Rarely, it develops after a relatively minor injury.

Conditions that may bring on acute compartment syndrome include:

A fracture.
A badly bruised muscle. This type of injury can occur when a motorcycle falls on the leg of the rider, or a football player is hit in the leg with another player’s helmet.
Re-established blood flow after blocked circulation. This may occur after a surgeon repairs a damaged blood vessel that has been blocked for several hours. A blood vessel can also be blocked during sleep. Lying for too long in a position that blocks a blood vessel, then moving or waking up can cause this condition. Most healthy people will naturally move when blood flow to a limb is blocked during sleep. The development of compartment syndrome in this manner usually occurs in people who are neurologically compromised. This can happen after severe intoxication with alcohol or other drugs.
Crush injuries.
Anabolic steroid use. Taking steroids is a possible factor in compartment syndrome.
Constricting bandages. Casts and tight bandages may lead to compartment syndrome. If symptoms of compartment syndrome develop, remove or loosen any constricting bandages.

This patient is malnourished. Although surgery is imminent, it is best for him to be nutritionally optimised first. As he may have reduced surface area for absorption and has a localised perforation, total parenteral nutrition (TPN) is likely the best feeding modality.

The National Institute for Health and Care Excellence (NICE) has laid down guidelines for identifying patients as malnourished or at risk of malnourishment, in order to start oral, enteral, or parenteral nutrition support, alone or in combination.

Following patients are identified as malnourished:
1. BMI <18.5 kg/m2
2. Unintentional weight loss of >10% within the last 3–6 months
3. BMI <20 kg/m2 and unintentional weight loss of >5% within the last 3–6 months

Following patients are at risk of malnutrition:
1. Eaten nothing or little for >5 days and/or likely to eat little or nothing for the next 5 days or longer
2. Poor absorptive capacity and/or
3. High nutrient loss and/or
4. High metabolic rate

Considering the method of parenteral nutrition:
1. For feeding <14 days, consider feeding via a peripheral venous catheter
2. For feeding >30 days, use a tunnelled subclavian line,
continuous administration in severely unwell patients
3. If feed needed for >2 weeks, consider changing from continuous to cyclical feeding
4. Do not give >50% of daily regime to unwell patients in the first 24–48 hours
5. In surgical patients, if malnourished with unsafe swallow or a non-functional GI tract or perforation, consider perioperative parenteral feeding.

Ototoxicity is a recognised adverse reaction with the aminoglycoside antibiotics.

Gentamicin belongs to a class of drugs known as aminoglycoside antibiotics. It is a broad-spectrum antibiotic that is most affective against aerobic gram-negative rods. Gentamicin acts by inhibiting bacterial protein synthesis. This creates a pool of inactive bacterial ribosomes that can no longer re-initiate and translate new proteins.

The hearing loss produced by gentamicin is known as gentamycin-induced ototoxicity. The antibiotic itself is not dangerous. It becomes toxic when it binds to iron in the blood and produces destructive chemical agents known as free radicals.

This is transfusion-associated graft-versus-host disease (GvHD) occurring in an immunosuppressed patient. It can occur 4–30 days after a transfusion and follows a subacute pathway. Patients may also have diarrhoea and abnormal liver function tests. Management involves steroid therapy.

Acute transfusion reactions present during or within 24 hours of a blood transfusion. The most frequent clinical features are fever, chills, pruritus, or urticaria, which typically resolve promptly without specific treatment or complications. Other signs occurring in temporal relationship with a blood transfusion such as severe dyspnoea, pyrexia, or loss of consciousness may be the first indication of a more severe, potentially fatal reaction.

Transfusion reactions may be immune-mediated and non-immune-mediated. GvHD is a condition that might occur after an allogeneic transplant. The donated blood cells view the recipient’s body as foreign and attacks it. Immunosuppressed patients who receive white blood cells from another person are at increased risk of developing GvHD.

There are two forms of the disease:
1. Acute graft-versus-host disease (aGvHD): usually presents with skin and/or liver and/or gut involvement.
2. Chronic graft-versus-host disease (cGvHD).

The diagnosis is clinical and usually one of exclusion; however, biopsy of affected tissues may be helpful in unclear cases.

Chyle leakage is one of the most challenging complications following an esophagectomy and can lead to hypovolemia, metabolic and nutritional depletion, infection, and even death. The leakage occurs in 1.1 to 3.7% of esophagectomy patients; mortality occurs in excess of 50% of patients. Surgeons administer a lipid rich material prior to surgery to facilitate its identification if it occurs.

The clinical presentation of basilar artery occlusion (BAO) ranges from mild transient symptoms to devastating strokes with high fatality and morbidity. Often, non-specific prodromal symptoms such as vertigo or headaches are indicative of BAO, and are followed by the hallmarks of BAO, including decreased consciousness, quadriparesis, pupillary and oculomotor abnormalities, dysarthria, and dysphagia. When clinical findings suggest an acute brainstem disorder, BAO has to be confirmed or ruled out as a matter of urgency. If BAO is recognised early and confirmed with multimodal CT or MRI, intravenous thrombolysis or endovascular treatment can be undertaken. The goal of thrombolysis is to restore blood flow in the occluded artery and salvage brain tissue; however, the best treatment approach to improve clinical outcome still needs to be ascertained.

Aortic injuries not resulting in immediate death may be due to a contained haematoma. Clinical signs are subtle, and diagnosis may not be apparent on clinical examination. Without prompt treatment, the haematoma usually bursts and the patient dies.

Traumatic aortic disruption, or aortic transection, is typically the result of a blunt aortic injury in the context of rapid deceleration. This condition is commonly fatal as blood in the aorta is under great pressure and can quickly escape the vessel through a tear, resulting in rapid haemorrhagic shock and death. A temporary haematoma may prevent the immediate death. Injury to the aorta during a sudden deceleration commonly originates near the terminal section of the aortic arch, also known as the isthmus. This portion lies just distal to the take-off of the left subclavian artery at the intersection of the mobile and fixed portions of the aorta. As many as 80% of the patients with aortic transection die at the scene before reaching a trauma centre for treatment.

A widened mediastinum may be seen on the X-ray of a person with aortic rupture. Other findings on CXR may include:
1. Deviation of trachea/oesophagus to the right
2. Depression of left main stem bronchus
3. Widened paratracheal stripe/paraspinal interfaces
4. Obliteration of space between aorta and pulmonary artery
5. Rib fracture/left haemothorax

Diagnosis can be made by angiography, usually CT aortogram.

Treatment options include repair or replacement. The patient should, ideally, undergo endovascular repair.

Boerhaave syndrome classically presents as the Mackler triad of chest pain, vomiting, and subcutaneous emphysema due to oesophageal rupture, although these symptoms are not always present.
The classic clinical presentation of Boerhaave syndrome usually consists of repeated episodes of retching and vomiting, typically in a middle-aged man with recent excessive dietary and alcohol intake.
These repeated episodes of retching and vomiting are followed by a sudden onset of severe chest pain in the lower thorax and the upper abdomen. The pain may radiate to the back or to the left shoulder. Swallowing often aggravates the pain.
Typically, hematemesis is not seen after oesophageal rupture, which helps to distinguish it from the more common Mallory-Weiss tear.
Swallowing may precipitate coughing because of the communication between the oesophagus and the pleural cavity.

Active, serious haemorrhage due to Warfarin should be treated with four-factor prothrombin complex concentrate (PCC), if available.
While costly, an essential advantage FFP confers to emergency care is that, in contrast to FFP, it results in a more rapid reversal of coagulopathy and does not require thawing or blood group typing. Additionally, it has a reduced risk of volume overload, transfusion-related acute lung injury, transfusion reactions, and infectious disease transmission. Despite these advantages, no mortality benefit has been proven for PCC compared with FFP.
Alternatively, recombinant factor VIIa (rFVIIa) has been reported to be effective in rapidly lowering INR due to warfarin toxicity and may be considered if PCC is not available. FFP is effective at lowering the INR and was historically first-line therapy for warfarin toxicity with serious or life-threatening bleeding, although it has now been superseded by PCC, which lowers the INR more rapidly. If PCC or rFVIIa is not available, 4 units of FFP may be administered instead.
Administer vitamin K1, 10 mg, by slow IV infusion,

Answer: Escharotomy

Escharotomy is the surgical division of the nonviable eschar, which allows the cutaneous envelope to become more compliant. Hence, the underlying tissues have an increased available volume to expand into, preventing further tissue injury or functional compromise.

Full-thickness circumferential and near-circumferential skin burns result in the formation of a tough, inelastic mass of burnt tissue (eschar). The eschar, by virtue of this inelasticity, results in the burn-induced compartment syndrome. This is caused by the accumulation of extracellular and extravascular fluid within confined anatomic spaces of the extremities or digits. The excessive fluid causes the intracompartmental pressures to increase, resulting in collapse of the contained vascular and lymphatic structures and, hence, loss of tissue viability. The capillary closure pressure of 30 mm Hg, also measured as the compartment pressure, is accepted as that which requires intervention to prevent tissue death.

The circumferential eschar over the torso can lead to significant compromise of chest wall excursions and can hinder ventilation. Abdominal compartment syndrome with visceral hypoperfusion is associated with severe burns of the abdomen and torso. (A literature review by Strang et al found the prevalence of abdominal compartment syndrome in severely burned patients to be 4.1-16.6%, with the mean mortality rate for this condition in these patients to be 74.8%). Similarly, airway patency and venous return may be compromised by circumferential burns involving the neck.

Performing an escharotomy will therefore improve ventilation.

Giardia is a microscopic parasite that causes the diarrheal illness known as giardiasis. Giardia (also known as Giardia intestinalis, Giardia lamblia, or Giardia duodenalis) is found on surfaces or in soil, food, or water that has been contaminated with faeces from infected humans or animals.

Giardia is protected by an outer shell that allows it to survive outside the body for long periods of time and makes it tolerant to chlorine disinfection. While the parasite can be spread in different ways, water (drinking water and recreational water) is the most common mode of transmission.

Signs and symptoms may vary and can last for 1 to 2 weeks or longer. In some cases, people infected with Giardia have no symptoms.

Acute symptoms include:

Diarrhoea
Gas
Greasy stools that tend to float
Stomach or abdominal cramps
Upset stomach or nausea/vomiting
Dehydration (loss of fluids)
Other, less common symptoms include itchy skin, hives, and swelling of the eye and joints. Sometimes, the symptoms of giardiasis might seem to resolve, only to come back again after several days or weeks. Giardiasis can cause weight loss and failure to absorb fat, lactose, vitamin A and vitamin B12.

In children, severe giardiasis might delay physical and mental growth, slow development, and cause malnutrition.

If pain occurs between regular doses of morphine (‘breakthrough pain’), an additional dose (‘rescue dose’) of immediate-release morphine should be given. Breakthrough dose = 1/6th of daily morphine dose

The total daily morphine dose is 30 * 2 = 60 mg, therefore the breakthrough dose should be one-sixth of this, 10 mg.

Answer: Bradycardia

Prolonged bed rest and immobilization inevitably lead to complications. Such complications are much easier to prevent than to treat. Musculoskeletal complications include loss of muscle strength and endurance, contractures and soft tissue changes, disuse osteoporosis, and degenerative joint disease. Cardiovascular complications include an increased heart rate (tachycardia), decreased cardiac reserve, orthostatic hypotension, and venous thromboembolism.

Patients with burns of more than 20% – 25% of their body surface should be managed with aggressive IV fluid resuscitation to prevent “burn shock.
Rule of 9’s for Adults: 9% for each arm, 18% for each leg, 9% for head,18% for front torso, 18% for back torso.
A variety of formulas exist, like Brooke, Galveston, Rule of Ten, but the most common formula is the Parkland Formula. This formula estimates the amount of fluid given in the first 24 hours, starting from the time of the burn.
Four mL lactated ringers solution × percentage total body surface area (%TBSA) burned × patient’s weight in kilograms = total amount of fluid given in the first 24 hours.
One-half of this fluid should be given in the first eight hours.
For example, a 75 kg patient with 55% total body surface area burn would need; 4 mL LR × 75kg × 55% TBSA = 16,500 mL in the first 24 hours, with 8,250 mL in the first eight hours or approximately 1 litre/hr for the first eight hours.
For paediatric patients, the Parkland Formula can be used plus the addition of normal maintenance fluids added to the total.
Whichever formula is used, the important point to remember is the fluid amount calculated is just a guideline. Patient’s vital signs, mental status, capillary refill and urine output must be monitored and fluid rates adjusted accordingly. Urine output of 0.5 mL/kg or about 30 – 50 mL/hr in adults and 0.5-1.0 mL/kg/hr in children less than 30kg is a good target for adequate fluid resuscitation.
Other management for severe burns includes nasal gastric tube placement as most patients will develop ileus. Foley catheters should be placed to monitor urine output. Cardiac and pulse oximetry monitoring is indicated. Pain control is best managed with IV medication. Finally, burns are considered tetanus-prone wounds and tetanus prophylaxis are indicated if not given in the past five years. In any severe flame burn, you should always consider possible associated inhalation injury, carbon monoxide or cyanide poisoning.

Early ECG changes of hyperkalaemia, typically seen at a serum potassium levels of 5.5-6.5 mEq/L, include the following:
– Tall, peaked T waves with a narrow base (best seen in precordial leads)
– Shortened QT interval
– ST-segment depression

Perihepatic packing is a surgical procedure used in connection with surgery to the liver. In this procedure the liver is packed to stop non arterial bleeding, most often caused by liver injury.

During this surgery laparotomy pads are placed around the site of the bleeding. The main purpose of hepatic packing is to prevent the person from succumbing to the trauma triad of death. Under- or over-packing of the liver can cause adverse outcomes, and if the bleeding cannot be controlled through this surgical method, the Pringle manoeuvre is an alternate technique that can be utilized.

Rebleeding, constant decline of haemoglobin and increased transfusion requirement, as well as the failure of angioembolization of actively bleeding vessels are a few factors which indicate the need for laparotomy.

The operative approach has also evolved over the last two decades. Direct suture ligation of the parenchymal bleeding vessel, perihepatic packing, repair of venous injury under total vascular isolation and damage control surgery with utilization of preoperative and/or postoperative angioembolization are the preferred methods, compared to anatomical resection of the liver and use of the atriocaval shunt.

Answer: Excision biopsy of a lymph node

Hodgkin lymphoma is an uncommon cancer that develops in the lymphatic system, which is a network of vessels and glands spread throughout your body. In Hodgkin lymphoma, B-lymphocytes (a particular type of lymphocyte) start to multiply in an abnormal way and begin to collect in certain parts of the lymphatic system, such as the lymph nodes (glands). The affected lymphocytes lose their infection-fighting properties, making you more vulnerable to infection. The most common symptom of Hodgkin lymphoma is a painless swelling in a lymph node, usually in the neck, armpit or groin.
A histologic diagnosis of Hodgkin lymphoma is always required. An excisional lymph node biopsy is recommended because the lymph node architecture is important for histologic classification.

Features of Hodgkin lymphoma include the following:

Asymptomatic lymphadenopathy may be present (above the diaphragm in 80% of patients)

Constitutional symptoms (unexplained weight loss [>10% of total body weight] within the past 6 months, unexplained fever >38º C, or drenching night sweats) are present in 40% of patients; collectively, these are known as B symptoms

Intermittent fever is observed in approximately 35% of cases; infrequently, the classic Pel-Ebstein fever is observed (high fever for 1-2 week, followed by an afebrile period of 1-2 week)

Chest pain, cough, shortness of breath, or a combination of those may be present due to a large mediastinal mass or lung involvement; rarely, haemoptysis occurs

Pruritus may be present

Pain at sites of nodal disease, precipitated by drinking alcohol, occurs in fewer than 10% of patients but is specific for Hodgkin lymphoma

Back or bone pain may rarely occur

A family history is also helpful; in particular, nodular sclerosis Hodgkin lymphoma (NSHL) has a strong genetic component and has often previously been diagnosed in the family.