Answer: Epstein-Barr virus

The Epstein–Barr virus is one of eight known human herpesvirus types in the herpes family, and is one of the most common viruses in humans. Infection with Epstein-Barr virus (EBV) is common and usually occurs in childhood or early adulthood.
EBV is the cause of infectious mononucleosis, an illness associated with symptoms and signs like:
fever,
fatigue,
swollen tonsils,
headache, and
sweats,
sore throat,
swollen lymph nodes in the neck, and
sometimes an enlarged spleen.

Although EBV can cause mononucleosis, not everyone infected with the virus will get mononucleosis. White blood cells called B cells are the primary targets of EBV infection.
Petechiae on the palate are characteristic of streptococcal pharyngitis but also can be seen in Epstein–Barr virus infection, Arcanobacterium haemolyticum pharyngitis, rubella, roseola, viral haemorrhagic fevers, thrombocytopenia, and palatal trauma.
Despite the fact that infectious mononucleosis is a self-limiting disease, it may cause serious and lethal complications. The mechanism of splenic rupture secondary to infectious mononucleosis has been controversial. It is commonly believed that it is caused by an increase in intra-abdominal pressure or contraction of the diaphragm with vigorous cough, vomiting and defecation, leading to a compression of the spleen. However, Patel et al. argue that it is primarily the result of an expanding subcapsular haematoma which subsequently tears the capsule and leads to hemoperitoneum. Traditionally, rupture of spleen is treated by splenectomy. The rationale is to prevent the chance of sudden death as an early complication of splenic rupture and the risk from blood transfusion.

The possible causes of post-operative pneumothorax after thoracotomy and esophagectomy include lung parenchymal leak/injury, bronchopleural fistula, ruptured bullae and malpositioned chest drains. When suction is applied to the chest drainage system, active and persistent bubbling may be seen. Although an anastomotic leak may produce a small pneumothorax, a large volume air leak is more indicative of lung injury.

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.

Bile leak may be classified into a minor leak with low output drainage (<300 ml of bile/24 hours) or leaks due to major bile duct injury with high output drainage (>300 ml/24 hours).

The majority of minor bile leak results from Strasberg type A injuries with intact biliary-enteric continuity and includes leaks from cystic duct (CD) stump (55%-71%) or small (less than 3 mm) subsegmental duct in gall bladder (GB) bed (16%) and minor ducts like cholecystohepatic duct or supravesicular duct of Luschka (6%). An injury to the supravesicular duct occurs if the surgeon dissects into the liver bed while separating the gall bladder. This duct does not drain the liver parenchyma.
A leak from the cystic duct stump may occur from clip failure due to necrosis of the stump secondary to thermal injury/pressure necrosis or when clips are used in situations where ties are appropriate (acute cholecystitis) and in a significant majority from distal bile duct obstruction caused by a retained stone and resultant blow out of the cystic stump.
Strasberg type C and type D injuries usually present with a minor leak as well. The former results when an aberrant right hepatic duct (RHD) or right posterior sectoral duct (RPSD) is misidentified as the CD and divided because of the anomalous insertion of CD into either of these ducts.
Type D injuries are lateral injuries to the extrahepatic ducts (EHD) caused by cautery, scissors or clips.

High output biliary fistulas are the result of major transactional injury of EHD (Strasberg type E). Here the common bile duct (CBD) is misidentified as the CD and is clipped, divided and excised. This not only results in a segmental loss of the EHD but often associated with injury or ligation of right hepatic artery as well. Such devastating injuries are peculiar to LC and have been described by Davidoff as “classic laparoscopic biliary injury”.

Early recognition is the most important part of the management of bile leak due to iatrogenic injuries.
Unfortunately, most of the bile duct injuries are not recognized preoperatively. Optimal management of BDI detected postoperatively requires good coordination between the radiologist, endoscopists and an experienced hepatobiliary surgeon.

There is a scope of re-laparoscopy, within 24 hours of surgery, in situations where a low output fistula (<300 ml/day) is confirmed (by reviewing the operative video), to be because of a slipped CD clip. Through lavage, clipping or tying the CD stump with an endoloop may be a simple solution. Such an approach is not useful after 24 hours as inflammatory adhesions and oedema will make the job difficult. If low output controlled biliary fistula is detected after 24 hours, a wait and watch policy should be followed as many of the minor leaks will close within 5 to 7 days. If the leak fails to resolve or if the drainage amount is >300 ml/day (high output), an ERCP should be performed both to delineate the biliary tree and some therapeutic interventions if indicated.

Vomiting usually results in hypokalaemia, and hyponatremia would least likely occur as a result of it. Hyponatremia is a common postoperative finding among patients and hence serum sodium must be carefully monitored. Addison disease, SIADH, diuretic therapy can all cause hyponatremia.

Answer: Malignant hyperthermia

Malignant hyperthermia (MH) is a life-threatening clinical syndrome of hypermetabolism involving the skeletal muscle. It is triggered in susceptible individuals primarily by the volatile inhalational anaesthetic agents and the muscle relaxant succinylcholine, though other drugs have also been implicated as potential triggers. MH is not an allergy but an inherited disorder that is found both in humans and in swine.

In persons susceptible to MH, the ryanodine receptor in skeletal muscle is abnormal, and this abnormality interferes with regulation of calcium in the muscle. An abnormal ryanodine receptor that controls calcium release causes a build-up of calcium in skeletal muscle, resulting in a massive metabolic reaction.

This hypermetabolism causes increased carbon dioxide production, metabolic and respiratory acidosis, accelerated oxygen consumption, heat production, activation of the sympathetic nervous system, hyperkalaemia, disseminated intravascular coagulation (DIC), and multiple organ dysfunction and failure. Early clinical signs of MH include an increase in end-tidal carbon dioxide (even with increasing minute ventilation), tachycardia, muscle rigidity, tachypnoea, and hyperkalaemia. Later signs include fever, myoglobinuria, and multiple organ failure.

Answer: Serum phosphate

Refeeding syndrome can be defined as the potentially fatal shifts in fluids and electrolytes that may occur in malnourished patients receiving artificial refeeding (whether enterally or parenterally. These shifts result from hormonal and metabolic changes and may cause serious clinical complications. The hallmark biochemical feature of refeeding syndrome is hypophosphatemia. However, the syndrome is complex and may also feature abnormal sodium and fluid balance; changes in glucose, protein, and fat metabolism; thiamine deficiency; hypokalaemia; and hypomagnesaemia.
During refeeding, glycaemia leads to increased insulin and decreased secretion of glucagon. Insulin stimulates glycogen, fat, and protein synthesis. This process requires minerals such as phosphate and magnesium and cofactors such as thiamine. Insulin stimulates the absorption of potassium into the cells through the sodium-potassium ATPase symporter, which also transports glucose into the cells. Magnesium and phosphate are also taken up into the cells. Water follows by osmosis. These processes result in a decrease in the serum levels of phosphate, potassium, and magnesium, all of which are already depleted. The clinical features of the refeeding syndrome occur as a result of the functional deficits of these electrolytes and the rapid change in basal metabolic rate.

Symptoms of hypophosphatemia include:

confusion or hesitation
seizures
muscle breakdown
neuromuscular problems
acute heart failure

Deficiency in thiamine can lead to Korsakoff’s syndrome (retrograde and anterograde amnesia, confabulation) and Wernicke’s encephalopathy (ocular abnormalities, ataxia, confusional state, hypothermia, coma). These symptoms are not present in the patient so Thiamine deficiency can be ruled out and there is no need to do tests for Serum vitamin B.

An acute dystonic reaction is characterized by involuntary contractions of muscles of the extremities, face, neck, abdomen, pelvis, or larynx in either sustained or intermittent patterns that lead to abnormal movements or postures. The symptoms may be reversible or irreversible and can occur after taking any dopamine receptor-blocking agents.
The aetiology of acute dystonic reaction is thought to be due to a dopaminergic-cholinergic imbalance in the basal ganglia. Reactions usually occur shortly after initiation of an offending agent or an increased dose of a possible offending agent.
Anticholinergic agents and benzodiazepines, procyclidine are the most commonly used agents to reverse or reduce symptoms in acute dystonic reaction. Acute dystonic reactions are often transient but can cause significant distress to the patient. Although rare, laryngeal dystonia can cause life-threatening airway obstruction.

Perioperative administration of antibiotics is very important for reducing the risks of postoperative wound infection. Clips make infections easier to manage but do not reduce the risks. Drains have no effect on the skin wounds in these cases.

Surgical site infections (SSI) comprise up to 20% of all healthcare-associated infections and at least 5% of patients undergoing surgery will develop an SSI as a result. SSIs may occur following a breach in tissue surfaces and allow normal commensals and other pathogens to initiate infection. The organisms are mostly derived from the patient’s own body.

SSIs are a major cause of morbidity and mortality.
Some preoperative measures that may increase the risk of SSI include:
1. Shaving the wound using a razor (disposable clipper preferred)
2. Tissue hypoxia
3. Delayed administration of prophylactic antibiotics in tourniquet surgery

SSIs can be prevented by taking certain precautionary steps pre-, intra-, and postoperatively.

1. Preoperatively:
a. Do not remove body hair routinely
b. If hair needs removal, use electrical clippers (razors increase the risk of infection)
c. Antibiotic prophylaxis if:
– placement of prosthesis or valve
– clean-contaminated surgery
– contaminated surgery

2. Intraoperatively:
a. Prepare the skin with alcoholic chlorhexidine (Lowest incidence of SSI)
b. Cover surgical site with dressing

3. Postoperatively:
a. Prevention of incisional infection by appropriate cleansing, skin care, and moisture management
b.Tissue viability advice for management of surgical wound healing by secondary intention

Answer: Instillation of warmed intra peritoneal fluid

Hypothermia describes a state in which the body’s mechanism for temperature regulation is overwhelmed in the face of a cold stressor. Hypothermia is classified as accidental or intentional, primary or secondary, and by the degree of hypothermia.
Active central rewarming is the fastest and most invasive method of rewarming. It involves use of warm IV fluids, gastric lavage and peritoneal dialysis by warm fluids. Peritoneal dialysis can be safely done with crystalloid dialysate at 40 to 42°C and it raises the body temperature by 4 to 6°C/hour.

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.

Clinical characteristics associated with increased venous thromboembolism (VTE) risk in children (listed alphabetically, owing to the current lack of expert consensus or robust data regarding relative risk contributions)
-Anticipated hospitalization > 72 h
-Cancer (active, not in remission)
-Central venous catheter presence
-Oestrogen therapy started within the last 1 month
-Inflammatory disease (newly diagnosed, poorly controlled, or flaring)
-Intensive care unit admission
-Mechanical ventilation
-Mobility decreased from baseline (Braden Q‐score < 2)
-Obesity (BMI > 99th percentile for age)
-Post pubertal age
-Severe dehydration, requiring intervention
-Surgery > 90 min within last 14 days
-Systemic or severe local infection (positive sputum/blood culture or viral test result, or empirical antibiotics)
-Trauma as admitting diagnosis

Pharmacological prophylaxis may be instituted in the following risk groups:
Children in an ICU with a CVC and one other risk factor fit a high‐risk profile and may benefit from pharmacological thromboprophylaxis in the absence of strong contraindications.
For children with either a CVC or admission to an ICU (but not both), two risk factors are recommended before the initiation of pharmacological thromboprophylaxis.
For children with neither a CVC nor ICU admission, at least three risk factors should be present before the initiation of pharmacological thromboprophylaxis.

Spleen injuries are among the most frequent trauma-related injuries. At present, they are classified according to the anatomy of the injury. The optimal treatment strategy, however, should take into consideration the hemodynamic status, the anatomic derangement, and the associated injuries. The management of splenic trauma patients aims to restore the homeostasis and the normal physiopathology especially considering the modern tools for bleeding management.

The trend in the management of splenic injury continues to favour nonoperative or conservative management. This varies from institution to institution but usually includes patients with stable hemodynamic signs, stable haemoglobin levels over 12-48 hours, minimal transfusion requirements (2 U or less), CT scan injury scale grade of 1 or 2 without a blush, and patients younger than 55 years.
Surgical therapy is usually reserved for patients with signs of ongoing bleeding or hemodynamic instability. In some institutions, CT scan–assessed grade V splenic injuries with stable vitals may be observed closely without operative intervention, but most patients with these injuries will undergo exploratory laparotomy for more precise staging, repair, or removal.

A retrospective analysis by Scarborough et al compared the effectiveness of nonoperative management with immediate splenectomy for adult patients with grade IV or V blunt splenic injury. The study found that both approaches had similar rates of in-hospital mortality (11.5% in the splenectomy group vs 10.0%), however, there was a higher incidence of infectious complications in the immediate splenectomy group. The rate of failure in the nonoperative management was 20.1% and symptoms of a bleeding disorder, the need for an early blood transfusion, and grade V injury were all early predictors of nonoperative management failure.

Answer: Yersinia enterocolitica

Yersinia enterocolitica (see the image below) is a bacterial species in the family Enterobacteriaceae that most often causes enterocolitis, acute diarrhoea, terminal ileitis, mesenteric lymphadenitis, and pseudo appendicitis but, if it spreads systemically, can also result in fatal sepsis. Symptoms of Y enterocolitica infection typically include the following:

Diarrhoea – The most common clinical manifestation of this infection; diarrhoea may be bloody in severe cases

Low-grade fever

Abdominal pain – May localize to the right lower quadrant

Vomiting – Present in approximately 15-40% of cases

Mesenteric adenitis, mesenteric ileitis, and acute pseudo appendicitis
These manifestations are characterized by the following symptoms (although nausea, vomiting, diarrhoea, and aphthous ulcers of the mouth can also occur):

Fever

Abdominal pain

Tenderness of the right lower quadrant

Leucocytosis

Pseudo appendicitis syndrome is more common in older children and young adults. Patients with Y enterocolitica infection often undergo appendectomy; several Scandinavian studies suggested a prevalence rate of 3.8-5.6% for infection with Y enterocolitica in patients with suspected appendicitis.

Analysis of several common-source outbreaks in the United States found that 10% of 444 patients with symptomatic, undiagnosed Y enterocolitica infection underwent laparotomy for suspected appendicitis.

Human clinical Y enterocolitica infections ensue after ingestion of the microorganisms in contaminated food or water or by direct inoculation through blood transfusion.

Y enterocolitica is potentially transmitted by contaminated unpasteurized milk and milk products, raw pork, tofu, meats, oysters, and fish. Outbreaks have been associated with raw vegetables; the surface of vegetables can become contaminated with pathogenic microorganisms through contact with soil, irrigation water, fertilizers, equipment, humans, and animals.

Pasteurized milk and dairy products can also cause outbreaks because Yersinia can proliferate at refrigerated temperatures.

Animal reservoirs of Y enterocolitica include swine (principle reservoir), dogs, cats, cows, sheep, goats, rodents, foxes, porcupines, and birds.

Reports of person-to-person spread are conflicting and are generally not observed in large outbreaks. Transmission via blood products has occurred, however, and infection can be transmitted from mother to new-born infant. Faecal-oral transmission among humans has not been proven.

Patients treated with moderate-dose intravenous thrombolysis within 3 hours after the onset of stroke symptoms benefit substantially from therapy, despite a modest increase in the rate of symptomatic haemorrhage. This patient is within 3h of symptom onset of a stroke, therefore he should be urgently referred to the medical team for thrombolysis, before Aspirin is given. According to the current guidelines, in order to limit the
risk of an intracranial haemorrhagic complication, no antiplatelet treatment should be administered in the 24 hours that follow treatment of an ischemic stroke by intravenous thrombolysis.

Answer: Flail chest injury

Flail chest is a life-threatening medical condition that occurs when a segment of the rib cage breaks due to trauma and becomes detached from the rest of the chest wall. Two of the symptoms of flail chest are chest pain and shortness of breath.

It occurs when multiple adjacent ribs are broken in multiple places, separating a segment, so a part of the chest wall moves independently. The number of ribs that must be broken varies by differing definitions: some sources say at least two adjacent ribs are broken in at least two places, some require three or more ribs in two or more places. The flail segment moves in the opposite direction to the rest of the chest wall: because of the ambient pressure in comparison to the pressure inside the lungs, it goes in while the rest of the chest is moving out, and vice versa. This so-called paradoxical breathing is painful and increases the work involved in breathing.

Flail chest is usually accompanied by a pulmonary contusion, a bruise of the lung tissue that can interfere with blood oxygenation. Often, it is the contusion, not the flail segment, that is the main cause of respiratory problems in people with both injuries.

Surgery to fix the fractures appears to result in better outcomes.

Answer: It may result in metabolic complications such a refeeding syndrome, resulting in hyperkalaemia, hypermagnesemia, and hyperphosphatemia.

Refeeding syndrome can be defined as the potentially fatal shifts in fluids and electrolytes that may occur in malnourished patients receiving artificial refeeding (whether enterally or parenterally. These shifts result from hormonal and metabolic changes and may cause serious clinical complications. The hallmark biochemical feature of refeeding syndrome is hypophosphatemia. However, the syndrome is complex and may also feature abnormal sodium and fluid balance; changes in glucose, protein, and fat metabolism; thiamine deficiency; hypokalaemia; and hypomagnesaemia.
During refeeding, glycaemia leads to increased insulin and decreased secretion of glucagon. Insulin stimulates glycogen, fat, and protein synthesis. This process requires minerals such as phosphate and magnesium and cofactors such as thiamine. Insulin stimulates the absorption of potassium into the cells through the sodium-potassium ATPase symporter, which also transports glucose into the cells. Magnesium and phosphate are also taken up into the cells. Water follows by osmosis. These processes result in a decrease in the serum levels of phosphate, potassium, and magnesium, all of which are already depleted. The clinical features of the refeeding syndrome occur as a result of the functional deficits of these electrolytes and the rapid change in basal metabolic rate.

Because of the substantial risk of thromboembolism early after valve replacement, perioperative initiation of anticoagulation is necessary, despite the increased risk for bleeding. Anticoagulation should be initiated within 24 h after the procedure with unfractionated heparin or low-molecular-weight heparin (LMWH).
Heparin is monitored by checking the activated partial thromboplastin time or anti-Xa activity.
Oral anticoagulants are monitored by INR.

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.

Answer: Re-open the neck wound

Thyroidectomy: complications
Airway obstruction (compressing hematoma, tracheomalacia)

Incidence of hematoma is 1-2%, tracheomalacia incidence is <1%. Acute airway obstruction from hematoma may occur immediately postoperatively and is the most frequent cause of airway obstruction in the first 24 hours. Definitive therapy is opening the surgical incision to evacuate the hematoma. Re-intubation may be lifesaving for persistent airway obstruction. Consider awake fibreoptic intubation.

Chemotherapy for acute myeloid leukaemia (AML) requires long-term therapy and multiple blood tests. Therefore, an indwelling device, such as Groshong line, is preferable.

Tunnelled lines such as Groshong and Hickman lines are popular devices for patients with long-term therapeutic requirements. These devices are usually inserted, using ultrasound guidance, into the internal jugular vein and then tunnelled under the skin. A cuff of woven material is sited near the end and helps to anchor the device into the tissues. These cuffs require formal dissection to allow the device to be removed.

Clostridium difficile is an anaerobic, gram-positive, spore-forming bacillus that is responsible for the majority of cases of antibiotic-associated diarrhoea in surgical patients. While the spectrum of disease may range from asymptomatic carrier state to life-threatening toxic megacolon, the typical presentation in surgical patients is diarrhoea developing in the first few days after initiation of antibiotic therapy, including single-dose prophylactic perioperative antibiotics.
In routine cases with bile spillage, surgeons generally do use antibiotic prophylaxis; 80% give one dose only while 88% give one or more prophylactic doses of an antibiotic. Co-amoxiclav is the most commonly used antibiotic in all settings.

The patient suffers from hyperkalaemia as an adverse effect of RBCs transfusion, which causes his ECG changes.
The potassium concentration of blood increases during storage, by as much as 5–10 mmol u−1. After the transfusion, the RBC membrane Na+–K+ ATPase pumping mechanism is re-established and cellular potassium reuptake occurs rapidly. Hyperkalaemia rarely occurs during massive transfusions unless the patient is also hypothermic and acidotic.
The total extracellular potassium load, which is <0.5 mmol for fresh RBC units and only 5-7 mmol for units at expiration, rarely causes problems in the recipient because of rapid dilution, redistribution into cells, and excretion. An abnormally high potassium level (>5 mmol/l or ≥1.5 mmol/l net increase) within an hour of transfusion is classified as transfusion-associated hyperkalaemia.
Irradiation enhances potassium leakage.

ASA-V: A moribund patient who is not expected to survive without the operation. Examples include (but not limited to): ruptured abdominal/thoracic aneurysm, massive trauma, intracranial bleed with mass effect, ischemic bowel in the face of significant cardiac pathology or multiple organ/system dysfunction

ASA Grading
1 – No organic physiological, biochemical or psychiatric disturbance. The surgical pathology is localised and has not invoked systemic disturbance
2 – Mild or moderate systemic disruption caused either by the surgical disease process or though underlying pre-existing disease
3 – Severe systemic disruption caused either by the surgical pathology or pre-existing disease
4 – Patient has severe systemic disease that is a constant threat to life
5 – A patient who is moribund and will not survive without surgery

The patient has Pulmonary embolism (PE).
PE is when a thrombus becomes lodged in an artery in the lung and blocks blood flow to the lung. Pulmonary embolism usually arises from a thrombus that originates in the deep venous system of the lower extremities; however, it rarely also originates in the pelvis, renal, upper extremity veins, or the right heart chambers. After travelling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise.
The classic presentation of PE is the abrupt onset of pleuritic chest pain, shortness of breath, and hypoxia. However, most patients with pulmonary embolism have no obvious symptoms at presentation. Rather, symptoms may vary from sudden catastrophic hemodynamic collapse to gradually progressive dyspnoea.
Physical signs of pulmonary embolism include the following:
Tachypnoea (respiratory rate >16/min): 96%
Rales: 58%
Accentuated second heart sound: 53%
Tachycardia (heart rate >100/min): 44%
Fever (temperature >37.8°C [100.04°F]): 43%
Diaphoresis: 36%
S3 or S4 gallop: 34%
Clinical signs and symptoms suggesting thrombophlebitis: 32%
Lower extremity oedema: 24%
Cardiac murmur: 23%
Cyanosis: 19%
Management
Anticoagulation and thrombolysis
Immediate full anticoagulation is mandatory for all patients suspected of having DVT or PE. Diagnostic investigations should not delay empirical anticoagulant therapy.
Thrombolytic therapy should be used in patients with acute pulmonary embolism who have hypotension (systolic blood pressure< 90 mm Hg) who do not have a high bleeding risk and in selected patients with acute pulmonary embolism not associated with hypotension who have a low bleeding risk and whose initial clinical presentation or clinical course suggests a high risk of developing hypotension.
Long-term anticoagulation is critical to the prevention of recurrence of DVT or pulmonary embolism because even in patients who are fully anticoagulated, DVT and pulmonary embolism can and often do recur.
Thrombolytic agents used in managing pulmonary embolism include the following:
– Alteplase
– Reteplase

Heparin should be given to patients with intermediate or high clinical probability before imaging.
Unfractionated heparin (UFH) should be considered (a) as a first dose bolus, (b) in massive PE, or (c) where rapid reversal of effect may be needed.
Otherwise, low molecular weight heparin (LMWH) should be considered as preferable to UFH, having equal efficacy and safety and being easier to use.
Oral anticoagulation should only be commenced once venous thromboembolism (VTE) has been reliably confirmed.
The target INR should be 2.0–3.0; when this is achieved, heparin can be discontinued.
The standard duration of oral anticoagulation is: 4–6 weeks for temporary risk factors, 3 months for first idiopathic, and at least 6 months for other; the risk of bleeding should be balanced with that of further VTE.

Answer: Admit the child to the high dependency unit for close monitoring.

Grade 3: This mid-stage rupture is a tear more than 3 cm deep. It can also involve the splenic artery or a hematoma that covers over half of the surface area. A grade 3 rupture can also mean that a hematoma is present in the organ tissue that is greater than 5 cm or expanding.
The trend in management of splenic injury continues to favour nonoperative or conservative management.
Most haemodynamically stable injuries can be managed non-operatively (especially Grades I to III).

Repair of an inguinal hernia under local anaesthesia has a short operative time, and patients are usually ambulant immediately after. Furthermore, the family history of this patient is unlikely to be significant and therefore, he is at a very low risk of developing a pulmonary embolism (PE).

Deep vein thrombosis (DVT) may develop insidiously in many surgical patients. If left untreated, it may progress to PE. The following surgical patients are at increased risk of developing DVT:

1. Surgery greater than 90 minutes at any site or greater than 60 minutes if the procedure involves lower limbs or pelvis
2. Acute admissions with inflammatory process involving the abdominal cavity
3. Expected significant reduction in mobility
4. Age over 60 years
5. Known malignancy
6. Thrombophilia
7. Previous thrombosis
8. BMI >30 kg/m2
9. Taking hormone replacement therapy or contraceptive pills
10. Varicose veins with phlebitis

Thromboprophylaxis can be mechanical or therapeutic. The former includes:
1. Early ambulation after surgery: cheap and effective
2. Compression stockings (contraindicated in peripheral arterial disease)
3. Intermittent pneumatic compression devices
4. Foot impulse devices

Therapeutic agents for thromboprophylaxis are:
1. Low-molecular-weight heparin (LMWH)
2. Unfractionated heparin
3. Dabigatran

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.

Atrial fibrillation occurring after a colonic resection most likely represents an anastomotic leak. The best modality to visualize this would be an abdominal CT scan. Any bowel anastomosis can leak, sometimes as a result of technical failings and at other times, its patient factors such as background disease that contribute. As a general rule, rectal resections carry the highest risk of anastomotic leak. Indeed, low anterior resections are routinely defunctioned with loop ileostomy to mitigate the clinically effects of a leak. Left sided colonic resections carry a higher risk of anastomotic leak than right sided resections. The reason for this is that an ileocolic anastomosis (or indeed any small bowel anastomosis) has a very low risk of leak (provided the small bowel is otherwise healthy). Where a leak is suspected (new AF and raised inflammatory markers 5 days post resection), the correct course of action is to arrange cross sectional imaging with a CT scan. If a leak is confirmed and the patient is septic, then they should go back to theatre, the anastomosis taken down and the bowel ends exteriorized.

Retroperitoneal liposarcoma (RLS) is a rare, biologically heterogeneous tumour that presents considerable challenges due to its size and deep location.
RPS generally measure >5 cm, and mostly >10 cm diameter at presentation

Liposarcoma occurs in three main biologic forms: (1) well-differentiated liposarcoma; (2) myxoid and/or round cell; and (3) pleomorphic. The latter is a rare high-grade type with a high recurrence rate and poor prognosis.

CT scanning is superior to MRI in detailing cortical bone erosion and tumour mineralization, whereas MRI is useful in providing views of the long axis of the limb and in depicting the fatty nature of the tumour.
Most liposarcomas have well-defined and mostly lobulated margins. The well-differentiated liposarcomas are composed of mainly fat with septa or nodules.
Chest radiography may be used as an initial screening for pulmonary metastases; however, the definitive test for detection of pulmonary metastases is chest CT scanning.