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.

High-voltage electrical burns are associated with rhabdomyolysis. Acute tubular necrosis may also occur.

Electrical burns occur following exposure to electrical current. Full-thickness burns are third-degree burns. With these types of burns, the epidermal and dermal layers of skin are destroyed, and the damage may even penetrate the layer of fat beneath the skin.

Following the burn, there is a local response with progressive tissue loss and release of inflammatory cytokines. Systemically, there are cardiovascular effects resulting from fluid loss and sequestration of fluid into the third space. There is a marked catabolic response as well. Immunosuppression is common with large burns, and bacterial translocation from the gut lumen is a recognised event. Sepsis is a common cause of death following major burns.

After the initial management and depth assessment of the burn, the patient is transferred to burn centre if:
1. Needs burn shock resuscitation
2. Face/hands/genitals affected
3. Deep partial-thickness or full-thickness burns
4. Significant electrical/chemical burns

Management options include:
1. The initial aim is to stop the burning process and resuscitate the patient. Adults with burns greater than 15% of total body surface area require burn fluid resuscitation. Fluids administration is calculated using the Parkland formula. Half of the fluid is administered in the first eight hours. A urinary catheter should be inserted and analgesics should be started.

2. Conservative management is appropriate for superficial burns and mixed superficial burns that will heal in two weeks. More complex burns may require excision and skin grafting. Excision and primary closure is not generally practised as there is a high risk of infection.

3. Circumferential full-thickness burns affecting a limb or severe torso burns impeding respiration may require escharotomy to divide the burnt tissue.

4. There is no evidence to support the use of antimicrobial prophylaxis or topical antibiotics in burn patients.

Boerhaave’s syndrome is also known as spontaneous oesophageal rupture or effort rupture of the oesophagus. Although vomiting is thought to be the most common cause, other causes include weightlifting, defecation, epileptic seizures, abdominal trauma, compressed air injury, and childbirth, all of which can increase the pressure in the oesophagus and cause a barogenic oesophageal rupture.
It usually follows excessive alcohol intake or overeating, or both, because either of these can induce vomiting.
The rupture is transmural.
A provider should suspect Boerhaave’s syndrome when a patient presents with retrosternal chest pain with or without subcutaneous emphysema when associated with heavy alcohol intake and severe or repeated vomiting. Up to one-third of patients do not present with these symptoms. The actual clinical presentation of Boerhaave syndrome will depend on the level of the perforation, the degree of leakage, and the time since the onset of the injury. Typically, the patient will present with pain at the site of perforation, usually in the neck, chest, epigastric region, or upper abdomen. Cervical perforations can present with neck pain, dysphagia, or dysphonia; intra-thoracic perforations with chest pain; and intra-abdominal perforations with epigastric pain radiating to the shoulder or back. History of increased intra-oesophageal pressure for any reason followed by chest pain should prompt consideration of this condition. Physical exam findings may include abnormal vitals (tachycardia, tachypnoea, fever), decreased breath sounds on the perforated side, mediastinal emphysema, and Hamman’s sign (mediastinal “crackling” accompanying every heartbeat) in left lateral decubitus position.

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.

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.

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.

Percutaneous coronary intervention (PCI), also known as coronary angioplasty, is a nonsurgical technique for treating obstructive coronary artery disease, including unstable angina, acute myocardial infarction (MI), and multivessel coronary artery disease (CAD).

Inferior STEMI is usually caused by occlusion of the right coronary artery, or less commonly the left circumflex artery, causing infarction of the inferior wall of the heart.

The ECG findings of an acute inferior myocardial infarction include the following:
ST segment elevation in the inferior leads (II, III and aVF)
Reciprocal ST segment depression in the lateral and/or high lateral leads (I, aVL, V5 and V6)

Answer: The burn area is extremely painful until skin grafted

Third-degree burns destroy the epidermis and dermis. Third-degree burns may also damage the underlying bones, muscles, and tendons. The burn site appears white or charred. There is no sensation in the area since the nerve endings are destroyed. These are not normally painful until after skin grafting is done since the nerve endings have been destroyed.

Nasal injuries can be challenging to manage and where there is tissue loss, it can be difficult to primarily close them and obtain a satisfactory aesthetic result. Debridement together with a rotational skin flap would produce the best results.

A rotation flap is a semi-circular skin flap that is rotated into the defect on a fulcrum point. It provides the ability to mobilize large areas of tissue with a wide vascular base for reconstruction. Rotation flaps may be pedicled or free. Pedicled flaps are more reliable but are limited in the range of movement. Free flaps have increased range but carry greater risk of breakdown as they require vascular anastomosis.

This patient has presented with a classical picture of cardiac tamponade, suggested by Beck’s triad: hypotension, raised jugular venous pressure (JVP), and muffled heart sounds.

Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent haemodynamic compromise. This condition is a medical emergency, the complications of which include pulmonary oedema, shock, and death.

Patients with cardiac tamponade have a collection of three medical signs known as Beck’s triad. These are low arterial blood pressure, distended neck veins, and distant, muffled heart sounds. The diagnosis may be further supported by specific ECG changes, chest X-ray, or an ultrasound of the heart. If fluid increases slowly, the pericardial sac can expand to contain more than 2 L; however, if the increase is rapid, as little as 200 mL can result in tamponade.

Management options may include pericardiocentesis, surgery to create a pericardial window, or a pericardiectomy.