A flail chest segment may lacerate the underlying lung and create a flap valve. Tension pneumothorax can, therefore, occur by intubation and ventilation in this situation.

Tension pneumothorax is a life-threatening condition that develops when air is trapped in the pleural cavity under positive pressure, displacing mediastinal structures and compromising cardiopulmonary function. The development of a tension pneumothorax can be life-threatening during mechanical ventilation, since with each breath, the pressure within the pneumothorax becomes greater, compromising both ventilatory and cardiovascular function.

Signs and symptoms of tension pneumothorax include:
1. Chest pain that usually has a sudden onset, is sharp, and may lead to feeling of tightness in the chest
2. Dyspnoea and progressive hypoxia
3. Tachycardia
4. Hyperventilation
5. Cough
6. Fatigue

On examination, hyper-resonant percussion note and tracheal deviation are typically found.

CXR shows:
1. Lung collapse towards the hilum
2. Contralateral mediastinal deviation
3. Diaphragmatic depression and increased rib separation
4. Increased thoracic volume
5. Ipsilateral flattening of the heart border

Management options for tension pneumothorax include
immediate needle decompression followed by definitive wide-bore chest drain insertion (without waiting for CXR results).

Answer: Curling’s ulcers

Curling’s ulcer is an acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa. The most common mode of presentation of stress ulcer is the onset of acute upper GI bleed like hematemesis or melena in a patient with the acute critical illness.

A similar condition involving elevated intracranial pressure is known as Cushing’s ulcer. Cushing’s ulcer is a gastro-duodenal ulcer produced by elevated intracranial pressure caused by an intracranial tumour, head injury or other space-occupying lesions. The ulcer, usually single and deep, may involve the oesophagus, stomach, and duodenum. Increased intracranial pressure may affect different areas of the hypothalamic nuclei or brainstem leading to overstimulation of the vagus nerve or paralysis of the sympathetic system. Both of these circumstances increase secretion of gastric acid and the likelihood of ulceration of gastro-duodenal mucosa.

Mallory-Weiss syndrome is characterized by upper gastrointestinal bleeding secondary to longitudinal mucosal lacerations (known as Mallory-Weiss tears) at the gastroesophageal junction or gastric cardia. However, Mallory-Weiss syndrome may occur after any event that provokes a sudden rise in the intragastric pressure or gastric prolapse into the oesophagus, including antecedent transoesophageal echocardiography. Precipitating factors include retching, vomiting, straining, hiccupping, coughing, primal scream therapy, blunt abdominal trauma, and cardiopulmonary resuscitation. In a few cases, no apparent precipitating factor can be identified. One study reported that 25% of patients had no identifiable risk factors.

This patient has a Bankart lesion which is the most common underlying abnormality in recurrent anterior dislocation of the shoulder.

Bankart lesion is an injury of the anterior (inferior) glenoid labrum of the shoulder due to anterior shoulder dislocation. When this happens, a pocket at the front of the glenoid forms that allows the humeral head to dislocate into it. It is usually visualised by CT and MRI scanning and is often repaired arthroscopically.

Shoulder fractures and dislocations usually result from low-energy falls in predominantly elderly females or from high-energy trauma in young males. They can be associated with nerve injury (commonly axillary), and fracture-dislocation of the humeral head. Anterior shoulder dislocation (glenohumeral dislocation) is the most common type of shoulder dislocation (>90%) and is usually traumatic in nature.

Early assessment of shoulder dislocation:
Careful history, examination, and documentation of neurovascular status of the upper limb, in particular the axillary nerve, is important. This should be re-assessed after manipulation. Early radiographs should also be done to confirm the direction of the dislocation.

Initial management of anterior dislocation:
It consists of emergent closed reduction (to prevent lasting chondral damage) under Entonox and analgesia, but often requires conscious sedation. The affected arm should then be immobilised in a polysling. Initial management requires emergent reduction to prevent lasting chondral damage.

Answer: 6

Eye Opening Response
Spontaneous–open with blinking at baseline – 4 points
Opens to verbal command, speech, or shout – 3 points
Opens to pain, not applied to face – 2 point
None – 1 point

Verbal Response
Oriented – 5 points
Confused conversation, but able to answer questions – 4 points
Inappropriate responses, words discernible – 3 points
Incomprehensible speech – 2 points
None – 1 point

Motor Response
Obeys commands for movement – 6 points
Purposeful movement to painful stimulus – 5 points
Withdraws from pain – 4 points
Abnormal (spastic) flexion, decorticate posture – 3 points
Extensor (rigid) response, decerebrate posture – 2 points
None – 1 point

He opens his eyes to pain and groans or grunts. He extends his hands at the elbow on application of painful stimulus. This gives him a Glasgow score of 6: eye opening response of 2, verbal response 2 and motor response 2.

Delayed primary closure is often intentionally applied to lacerations that are not considered clean enough for immediate primary closure. The wound is left open for 5-10 days; then, it is sutured closed to decrease the risk of wound infection. Improved blood flow at the wound edges, which develops increasingly over the first few days, is another benefit of this style of wound healing and can be associated with progressive increases in resistance to infections. The combination of diabetes and steroids makes wound complications more likely. Despite his high risk, a primary skin graft or flap is unlikely to be a safer option.

Answer: Achalasia

Achalasia is a primary oesophageal motility disorder characterized by the absence of oesophageal peristalsis and impaired relaxation of the lower oesophageal sphincter (LES) in response to swallowing. The LES is hypertensive in about 50% of patients. These abnormalities cause a functional obstruction at the gastroesophageal junction (GEJ).
Symptoms of achalasia include the following:

Dysphagia (most common)

Regurgitation

Chest pain (behind the sternum)

Heartburn

Weight loss

Physical examination is non-contributory.

Treatment recommendations are as follows:

Initial therapy should be either graded pneumatic dilation (PD) or laparoscopic surgical myotomy with a partial fundoplication in patients fit to undergo surgery

Procedures should be performed in high-volume centres of excellence

Initial therapy choice should be based on patient age, sex, preference, and local institutional expertise

Botulinum toxin therapy is recommended for patients not suited to PD or surgery

Pharmacologic therapy can be used for patients not undergoing PD or myotomy and who have failed botulinum toxin therapy (nitrates and calcium channel blockers most common).

The invasion of the oesophageal neural plexus by the tumour can cause nonrelaxation of the LES, thus mimicking achalasia. This condition is known as malignant pseudo achalasia. Since contrast radiography and endoscopy frequently fail to differentiate these 2 entities, patients with a presumed diagnosis of achalasia but who have a shorter duration of symptoms, greater weight loss, and a more advanced age and who are referred for minimally invasive surgery should undergo additional imaging studies, including endoscopic ultrasound and computed tomography with fine cuts of the gastroesophageal junction, to rule out cancer.

Effort rupture of the oesophagus, or Boerhaave syndrome, is a spontaneous perforation of the oesophagus that results from a sudden increase in intraoesophageally pressure combined with negative intrathoracic pressure (e.g., severe straining or vomiting). 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. Shortness of breath is a common complaint and is due to pleuritic pain or pleural effusion.

A pulmonary embolism is a blood clot that occurs in the lungs.

It can damage part of the lung due to restricted blood flow, decrease oxygen levels in the blood, and affect other organs as well. Large or multiple blood clots can be fatal.
The most common symptom of a pulmonary embolism is shortness of breath. This may be gradual or sudden.

Other symptoms of a pulmonary embolism include:
anxiety
clammy or bluish skin
chest pain that may extend into your arm, jaw, neck, and shoulder
fainting
irregular heartbeat
light-headedness
rapid breathing
rapid heartbeat
restlessness
spitting up blood
weak pulse

Answer: Beta 2 transferrin assay

Beta-2-transferrin is a protein found only in CSF and perilymph. Since 1979, beta-2-transferrin has been used extensively by otolaryngologists in the diagnosis of CSF rhinorrhoea and skull-base cerebrospinal fluid fistulas. With sensitivity of 94% – 100%, and specificity of 98% – 100%, this assay has become the gold standard in detection of CSF leakage. CSF rhinorrhoea is characterized by clear or xanthochromic watery rhinorrhoea that may not become apparent until nasal packing is removed.

The most likely diagnosis is aortic dissection.

Aortic dissection occurs following a tear in the aortic intima with subsequent separation of the tissue within the weakened media by the propagation of blood. There are four different classifications of aortic dissection and the commonest one used is the Stanford classification dividing them into type A and type B. A type A dissection involves the ascending aorta and/or the arch whilst type B dissection involves only the descending aorta and occurs distal to the origin of the left subclavian artery.

Aortic dissection in pregnancy occurs most commonly in the third trimester due to the hyperdynamic state and hormonal effect on vasculature. Other common predisposing factors for aortic dissection include Marfans syndrome, Ehlers-Danlos syndrome, and bicuspid aortic valve. Aortic dissection often presents with sudden severe, tearing chest pain, vomiting, and syncope, most often from acute pericardial tamponade. The patient may be hypertensive, clinically. The right coronary artery may become involved in the dissection, causing myocardial infarct in up to 2% of the cases (hence ST-segment elevation in the inferior leads). An aortic regurgitant murmur may be auscultated.

The management options during pregnancy include:
1. <28 weeks of gestation: aortic repair with the foetus kept in utero
2. 28–32 weeks of gestation: dependent on foetal condition
3. >32 weeks of gestation: caesarean section followed by aortic repair in the same operation

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.

This patient requires immediate insertion of an intercostal chest tube and analgesia. In general, all cases of haemopneumothorax should be managed by intercostal chest drain insertion as it can develop into tension pneumothorax until the lung laceration has sealed.

Haemopneumothorax is most frequently caused by a trauma or blunt or penetrating injury to the chest followed by laceration of the lung with air leakage, or injury to the intercostal vessels or internal mammary artery. The main treatment for haemopneumothorax is chest tube thoracostomy (chest tube insertion). Surgical exploration is warranted if >1500ml blood is drained immediately.

Flail chest occurs when the chest wall disconnects from the thoracic cage. It usually follows multiple rib fractures (at least two fractures per rib in at least two ribs) and is associated with pulmonary contusion. Overhydration and fluid overload is avoided in such patients.

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: 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.

Torsade de pointes is an uncommon and distinctive form of polymorphic ventricular tachycardia (VT) characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line. Torsade de pointes, often referred to as torsade, is associated with a prolonged QT interval, which may be congenital or acquired. Torsade usually terminates spontaneously but frequently recurs and may degenerate into ventricular fibrillation. This woman is likely to have hypokalaemia and hypomagnesaemia as a result of vomiting. In addition to this, the erythromycin will predispose her to torsades de pointes. The patient should be given Magnesium 2g over 10 minutes. Knowledge of the management of this peri arrest diagnosis is hence important in surgical practice.

The clinical history combined with parathyroid hormone levels will reveal the cause of hypocalcaemia in the majority of cases

Causes

Vitamin D deficiency (osteomalacia)
Acute pancreatitis
Chronic renal failure
Hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
Pseudohypoparathyroidism (target cells insensitive to PTH)
Rhabdomyolysis (initial stages)
Magnesium deficiency (due to end organ PTH resistance)

Management

Acute management of severe hypocalcaemia is with intravenous replacement. The preferred method is with intravenous calcium chloride, 10ml of 10% solution over 10 minutes
ECG monitoring is recommended
Further management depends on the underlying cause
Calcium and bicarbonate should not be administered via the same route

Chest pain, hypoxia, and clear chest on auscultation in pregnancy should lead to a high suspicion of pulmonary embolism (PE).

PE is one of the leading causes of mortality in pregnancy. Evaluation with low-dose perfusion scintigraphy may be preferable to computed tomographic pulmonary angiography (CTPA).
PE is treated with LMWH throughout pregnancy and for 4–6 weeks after childbirth. Warfarin is contraindicated in pregnancy (though may be continued in women with mechanical heart valves due to a significant risk of thromboembolism).

The diagnosis for this case is acute haemolytic transfusion reaction, due to ABO incompatibility. Haemolysis of the transfused cells can cause loin pain, shock, and hemoglobinemia, which may subsequently lead to disseminated intravascular coagulation. A direct Coombs test should confirm haemolysis. Other tests include unconjugated bilirubin, haptoglobin, serum and urine free haemoglobin.

Delayed haemolytic reactions, however, are normally associated with antibodies to the Rh system and occur 5–10 days after transfusion.

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 or non-immune-mediated.

High-probability ECG features of MI are the following:
ST-segment elevation greater than 1 mm in two anatomically contiguous leads
The presence of new Q waves

Intermediate-probability ECG features of MI are the following:
ST-segment depression
T-wave inversion
Other nonspecific ST-T wave abnormalities
Low-probability ECG features of MI are normal ECG findings. However, normal or nonspecific findings on ECGs do not exclude the possibility of MI.

Special attention should be made if there is diffuse ST depression in the precordial and extremity leads associated with more than 1 mm ST elevation in lead aVR, as this may indicate stenosis of the left main coronary artery or the proximal section of the left anterior descending coronary artery.

Localization of the involved myocardium based on the distribution of ECG abnormalities in MI is as follows:
– Inferior wall – II, III, aVF
– Lateral wall – I, aVL, V4 through V6
– Anteroseptal – V1 through V3
– Anterolateral – V1 through V6
– Right ventricular – RV4, RV5
– Posterior wall – R/S ratio greater than 1 in V1 and V2, and – T-wave changes in V1, V8, and V9
– True posterior-wall MIs may cause precordial ST depressions, inverted and hyperacute T waves, or both. ST-segment elevation and upright hyperacute T waves may be evident with the use of right-sided chest leads.

Hyperacute (symmetrical and, often, but not necessarily pointed) T waves are frequently an early sign of MI at any locus.
The appearance of abnormalities in a large number of ECG leads often indicates extensive injury or concomitant pericarditis.
The characteristic ECG changes may be seen in conditions other than acute MI. For example, patients with previous MI and left ventricular aneurysm may have persistent ST elevations resulting from dyskinetic wall motion, rather than from acute myocardial injury. ST-segment changes may also be the result of misplaced precordial leads, early repolarization abnormalities, hypothermia (elevated J point or Osborne waves), or hypothyroidism.
False Q waves may be seen in septal leads in hypertrophic cardiomyopathy (HCM). They may also result from cardiac rotation.
Substantial T-wave inversion may be seen in left ventricular hypertrophy with secondary repolarization changes.
The QT segment may be prolonged because of ischemia or electrolyte disturbances.
Saddleback ST-segment elevation (Brugada epsilon waves) may be seen in leads V1-V3 in patients with a congenital predisposition to life-threatening arrhythmias. This elevation may be confused with that observed in acute anterior MI.
Diffuse brain injuries and haemorrhagic stroke may also trigger changes in T waves, which are usually widespread and global, involving all leads.
Convex ST-segment elevation with upright or inverted T waves is generally indicative of MI in the appropriate clinical setting. ST depression and T-wave changes may also indicate the evolution of NSTEMI.
Patients with a permanent pacemaker may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.
To summarize, non-ischemic causes of ST-segment elevation include left ventricular hypertrophy, pericarditis, ventricular-paced rhythms, hypothermia, hyperkalaemia and other electrolyte imbalances, and left ventricular aneurysm.

Answer: Adrenaline 1:1000 IM

Early treatment with intramuscular adrenaline is the treatment of choice for patients having an anaphylactic reaction. IM Injection:

Adults: The usual dose is 500 micrograms (0.5ml of adrenaline 1/1000). If necessary, this dose may be repeated several times at 5-minute intervals according to blood pressure, pulse and respiratory function.

Additional measures

Beta2-agonists for bronchospasm: administer salbutamol or terbutaline by aerosol or nebuliser.

Antihistamines: administer both H1and H2receptor blockers slowly intravenously:
promethazine 0.5-1 mg/kg
and
ranitidine 1 mg/kg or famotidine 0.4 mg/kg or cimetidine 4 mg/kg
Corticosteroids: administer intravenously: hydrocortisone 2-6 mg/kg or dexamethasone 0.1-0.4 mg/kg
Nebulised adrenaline (5 mL of 1:1000) may be tried in laryngeal oedema and often will ease upper airways obstruction. However, do not delay intubation if upper airways obstruction is progressive.

Anaphylaxis is an acute, potentially fatal, multiorgan system reaction caused by the release of chemical mediators from mast cells and basophils. The classic form involves prior sensitization to an allergen with later reexposure, producing symptoms via an immunologic mechanism.

Anaphylaxis most commonly affects the cutaneous, respiratory, cardiovascular, and gastrointestinal systems. The skin or mucous membranes are involved in 80-90% of cases. A majority of adult patients have some combination of urticaria, erythema, pruritus, or angioedema. However, for poorly understood reasons, children may present more commonly with respiratory symptoms followed by cutaneous symptoms. It is also important to note that some of the most severe cases of anaphylaxis present in the absence of skin findings.

Initially, patients often experience pruritus and flushing. Other symptoms can evolve rapidly, such as the following:

Dermatologic/ocular: Flushing, urticaria, angioedema, cutaneous and/or conjunctival injection or pruritus, warmth, and swelling

Respiratory: Nasal congestion, coryza, rhinorrhoea, sneezing, throat tightness, wheezing, shortness of breath, cough, hoarseness, dyspnoea

Cardiovascular: Dizziness, weakness, syncope, chest pain, palpitations

Gastrointestinal: Dysphagia, nausea, vomiting, diarrhoea, bloating, cramps

Neurologic: Headache, dizziness, blurred vision, and seizure (very rare and often associated with hypotension)

Other: Metallic taste, feeling of impending doom

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.

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.

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 clinical symptoms of Superior Orbital Fissure Syndrome can be explained by the nerve involvement on an anatomic basis.
External ophthalmoplegia is secondary to impairment of the oculomotor, trochlear, and abducens nerves.
Ptosis develops because of lost tension and function of the levator palpebrae superior muscle involving the superior branch of the oculomotor nerve, and loss of tone in Muller’s muscle involving the sympathetic fibre arising from the cavernous sinus.
Proptosis is caused by a decreased tension of the extraocular muscles, which normally are globe retractors, thereby allowing forward movement of the globe.
The fixed dilated pupil with loss of accommodation arises from disruption of the parasympathetic fibres coursing with the oculomotor nerve.
Compromise of the lacrimal and frontal nerves of the ophthalmic branches of the trigeminal nerve results in anaesthesia of the forehead and upper eyelid, lacrimal hyposecretion, and possibly in retro-orbital pain and neuralgia along the path of the nerve.
Because of the disruption of the sensory nasociliary nerve, there may be anaesthesia of the cornea and the bridge of the nose with loss of the corneal reflex. When the disruption is partial, the corneal reflex remains intact.
If the optic nerve is also involved including the above-mentioned symptoms, it is known as the orbital apex syndrome.

Thoracic trauma accounts for > 25% of all traumatic injuries and is a leading cause of death in all age groups. The majority of thoracic trauma patients require only conservative management (e.g. analgesia, simple chest drainage). However, a subset of these patients will show signs of deterioration in the emergency department, especially with penetrating injuries. Such patients may require an emergency thoracotomy for rapid access to the thoracic cavity so that pericardial tamponade can be released and haemorrhage controlled. Furthermore, in severe thoracic trauma cases, specific injuries are difficult to confidently rule out or identify, even if they can be anticipated. Therefore, it is recommended to use an approach that provides the most rapid access to all vital chest organs for assessment and control.
Clamshell thoracotomy (also known as bilateral anterolateral thoracotomy) or hemi-clamshell (longitudinal sternotomy and anterolateral thoracotomy) are techniques used to provide complete exposure of the thoracic cavity (heart, mediastinum and lungs). Studies have demonstrated that it is easier to control the cardiac wound using this approach compared to the standard left anterolateral thoracotomy, as it gives wider exposure for all injuries, which are then easier to control surgically through the larger incision.
Contraindications:
Absolute:
– Traumatic cardiac arrest where the underlying pathology is so severe as to render the procedure futile (e.g. severe traumatic brain injury)
Relative:
Blunt cardiac injury with no signs of life or organised cardiac rhythm

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.

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.

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 the collapse of the contained vascular and lymphatic structures and, hence, loss of tissue viability.
Most compartment syndromes associated with a burn injury do not present in the immediate postburn period unless there is associated with traumatic injury or the patient presents in a delayed fashion. As such, compartment syndromes after burns are not commonly observed in the emergency department. Instead, they develop during the first 6–12 h of the initial volume resuscitation period as the administered intravascular volume goes into the interstitial and intracellular spaces resulting in tissue oedema in or under the burned tissue.

Patients with compartment syndrome typically present with pain whose severity appears out of proportion to the injury. The pain is often described as burning. The pain is also deep and aching in nature and is worsened by passive stretching of the involved muscles. The patient may describe a tense feeling in the extremity. Pain, however, should not be a sine qua non of the diagnosis. In severe trauma, such as an open fracture, it is difficult to differentiate between pain from the fracture and pain resulting from increased compartment pressure.
Paraesthesia or numbness is an unreliable early complaint; however, decreased 2-point discrimination is a more reliable early test and can be helpful to make the diagnosis.
The traditional 5 P’s of acute ischemia in a limb (i.e., pain, paraesthesia, pallor, pulselessness, poikilothermia) are not clinically reliable; they may manifest only in the late stages of compartment syndrome, by which time extensive and irreversible soft tissue damage may have taken place.

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

Extradural haematoma is the most likely cause of this patient’s symptomology. The middle meningeal artery is prone to damage when the temporal side of the head is hit.

Patients who suffer head injuries should be managed according to ATLS principles and extracranial injuries should be managed alongside cranial trauma. Inadequate cardiac output compromises the CNS perfusion, irrespective of the nature of cranial injury.

An extradural haematoma is a collection of blood in the space between the skull and the dura mater. It often results from acceleration-deceleration trauma or a blow to the side of the head. The majority of extradural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery. There is often loss of consciousness following a head injury, a brief regaining of consciousness, and then loss of consciousness again—lucid interval. Other symptoms may include headache, confusion, vomiting, and an inability to move parts of the body. Diagnosis is typically by a CT scan or MRI, and treatment is generally by urgent surgery in the form of a craniotomy or burr hole.

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.

A below-knee amputation (“BKA”) is a transtibial amputation that involves removing the foot, ankle joint, and distal tibia and fibula with related soft tissue structures. In general, a BKA is preferred over an above-knee amputation (AKA), as the former has better rehabilitation and functional outcomes. There are three major categories of indications for proceeding with a BKA. These include:
– Urgent cases where source control of necrotizing infections or haemorrhagic injuries outweighs limb preservation.
– Less acutely, urgent BKAs may be performed for chronic nonhealing ulcers or significant infections with the risk of impending systemic infection or sepsis.
– Urgent BKAs may be performed where limb salvage has failed to preserve a mangled lower extremity. Adequate resuscitation and stabilization must always have occurred before such a decision, as judged by vital signs, lactate, base deficit, and the management of concomitant injuries.
This man is hemodynamically unstable and the limb is likely to be non-viable after so many hours of entrapment. Hence, the safest option would be primary amputation of the injured limb.

For a rib fracture to cause pneumothorax, there must also be laceration to the underlying lung parenchyma. This has the risk of developing into a tension pneumothorax. Therefore, a chest drain should be inserted and the patient admitted.

Pneumothorax is a collection of free air in the chest cavity that causes the lung to collapse. The most common cause of pneumothorax is lung laceration with air leakage. In some instances, the lung continues to leak air into the chest cavity and results in compression of the chest structures, including vessels that return blood to the heart. This is known as a tension pneumothorax and can be fatal if not treated immediately. Blunt or penetrating chest trauma that creates a flap-type defect on the surface of the lung can result in this life-threatening condition.

Significant facial fractures may have an intracranial effect. Computerised tomography (CT) scan of the head allows delineation of the injury extent, and a 3D reconstruction of images can be done. An Orthopantomogram (OPT) provides good images of mandible and surrounding bony structures but cannot give intracranial details. X-ray of the skull lacks the details important in modern practice.

Craniomaxillofacial (CMF) injuries in the UK are due to:
1. Interpersonal violence (52%)
2. Motor vehicle accidents (16%)
3. Sporting injuries (19%)
4. Falls (11%)

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.

The latissimus dorsi myocutaneous flap (LDMF) is one of the most reliable and versatile flaps used in reconstructive surgery. It is known for its use in chest wall and postmastectomy reconstruction and has also been used effectively for coverage of large soft tissue defects in the head and neck, either as a pedicled flap or as a microvascular free flap.

The latissimus dorsi may be transferred as a myofascial flap, a myocutaneous flap, or as a composite osteomyocutaneous flap when harvested with underlying serratus anterior muscle and rib. For even greater reconstructive flexibility, the latissimus can be harvested for free tissue transfer in combination with any or all of the other flaps based on the subscapular vessels (the so-called subscapular compound flap or “mega-flap”), including serratus anterior, scapular, and parascapular flaps

As a reconstructive option after extensive surgery, pedicled musculocutaneous flaps offer several advantages in the setting of previous radiotherapy. Rotational skin flaps will comprise of irradiated tissue and thus won’t heal well.

The combination of a high reticulocyte count and severe anaemia indicates aplastic crisis in patients with sickle cell anaemia. Another differential can be that of a transient aplastic crisis due to parvovirus. This is less likely as it causes reticulocytopenia rather than reticulocytosis.

Parvovirus B19 infects erythroid progenitor cells in the bone marrow and causes temporary cessation of red blood cell production. People who have underlying haematologic abnormalities such as sickle cell anaemia are at risk of cessation of red blood cell production if they become infected. This can result in a transient aplastic crisis. It is more common in people of African, Indian, and Middle Eastern backgrounds. Typically, these patients have a viral prodrome followed by anaemia, often with haemoglobin concentrations falling below 5.0 g/dL and reticulocytosis.

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: 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.

Answer: 8

Eye Opening Response
Spontaneous–open with blinking at baseline – 4 points
Opens to verbal command, speech, or shout – 3 points
Opens to pain, not applied to face – 2 point
None – 1 point

Verbal Response
Oriented – 5 points
Confused conversation, but able to answer questions – 4 points
Inappropriate responses, words discernible – 3 points
Incomprehensible speech – 2 points
None – 1 point

Motor Response
Obeys commands for movement – 6 points
Purposeful movement to painful stimulus – 5 points
Withdraws from pain – 4 points
Abnormal (spastic) flexion, decorticate posture – 3 points
Extensor (rigid) response, decerebrate posture – 2 points
None – 1 point

He opens his eyes to pain and groans or grunts. He flexes his forearms away from the painful stimuli This gives him a Glasgow score of 8: eye opening response of 2, verbal response 2 and motor response 4.

Superficial burns are confined in the depth of the epidermis, and all dermal appendages and nerve endings are intact. Superficial burns generally heal in 3 to 5 days with minimal intervention and do not leave significant scarring as they typically heal by re epithelialization. Therefore the sweat glands will be intact.

Answer: Thoracotomy in theatre

A high CVP of 13 indicates cardiac tamponade. Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. The condition is a medical emergency, the complications of which include pulmonary oedema, shock, and death.
A pericardiotomy via a thoracotomy is mandatory for lifesaving cardiac decompression in acute traumatic cardiac tamponade in cases of ineffective drainage due to clot formation within the pericardial space. Wherever possible a patient needing surgery for penetrating chest trauma should be moved to an operating theatre where optimal surgical expertise and facilities are available.

Bladder pressures below 5mm Hg are expected in healthy patients. Pressures between 10 to 15 mmHg can be expected following abdominal surgery and in obese patients. Bladder pressures over 25 mmHg are highly suspicious of abdominal compartment syndrome and should be correlated clinically. It is recommended that pressure measurements be trended to show and recognize the worsening of intra-abdominal hypertension. Recommended management at this stage includes fluid resuscitation and if the pressure rises beyond the critical threshold of 25 mmHg, abdominal decompression is required.

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.

Answer: Oculogyric crisis

Oculogyric crisis is an acute dystonic reaction of the ocular muscles characterized by bilateral dystonic elevation of visual gaze lasting from seconds to hours. This reaction is most commonly explained as an adverse reaction to drugs such as antiemetics, antipsychotics, antidepressants, antiepileptics, and antimalarials. Metoclopramide is a benzamide selective dopamine D2 receptor antagonist that is used as an antiemetic, with side effects that are seen frequently in children.1 The most common and most important side effects of metoclopramide are acute extrapyramidal symptoms, which require immediate treatment. Acute dystonic reactions occur as contractions of the muscles, opisthotonos, torticollis, dysarthria, trismus, and oculogyric crisis.

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.

Various definitions of massive blood transfusion (MBT) have been published in the medical literature such as:

– Replacement of one entire blood volume within 24 h

– Transfusion of >10 units of packed red blood cells (PRBCs) in 24 h

– Transfusion of >20 units of PRBCs in 24 h

– Transfusion of >4 units of PRBCs in 1 h when on-going need is foreseeable

– Replacement of 50% of total blood volume (TBV) within 3 h.

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.

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.

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.

Severe pain in the limb following fixation with intramedullary devices should raise suspicion of compartment syndrome, especially in tibial fractures.

Compartment syndrome is a particular complication that may occur following fractures, especially supracondylar fractures and tibial shaft injuries. It is characterised by raised pressure within a closed anatomical space which may, eventually, compromise tissue perfusion, resulting in necrosis.

The clinical features of compartment syndrome include:
1. Pain, especially on movement
2. Paraesthesia
3. Pallor
4. Paralysis of the muscle group may also occur

Diagnosis is made by measurement of intracompartmental pressure. Pressures >20mmHg are abnormal and >40mmHg are diagnostic.

Compartment syndrome requires prompt and extensive fasciotomy. Myoglobinuria may occur following fasciotomy, resulting in renal failure. Therefore, aggressive IV fluids are required. If muscle groups are frankly necrotic at fasciotomy, they should be debrided, and amputation may have to be considered.

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.

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)

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.

Answer: 13

Eye Opening Response
Spontaneous–open with blinking at baseline – 4 points
Opens to verbal command, speech, or shout – 3 points
Opens to pain, not applied to face – 2 point
None – 1 point

Verbal Response
Oriented – 5 points
Confused conversation, but able to answer questions – 4 points
Inappropriate responses, words discernible – 3 points
Incomprehensible speech – 2 points
None – 1 point

Motor Response
Obeys commands for movement – 6 points
Purposeful movement to painful stimulus – 5 points
Withdraws from pain – 4 points
Abnormal (spastic) flexion, decorticate posture – 3 points
Extensor (rigid) response, decerebrate posture – 2 points
None – 1 point

He is seen to be disorientated despite opening his eyes in response to speech and being able to talk. He is also able to obey motor commands. His score is therefore 13: 3 for eye opening response, 4 for verbal response and 6 for motor response.

Answer: Hemopericardium

Hemopericardium refers to the presence of blood within the pericardial cavity, i.e. a sanguineous pericardial effusion. If enough blood enters the pericardial cavity, then a potentially fatal cardiac tamponade can occur. There is a very long list of causes but some of the more common are:
-ruptured myocardial infarction
-ruptured left ventricular aneurysm
-aortic dissection
-pericarditis
-trauma
-blunt/penetrating/deceleration
-iatrogenic, e.g. pacemaker wire insertion
-cardiac malignancies
-ruptured coronary artery aneurysm
-post-thrombolysis

Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise. The condition is a medical emergency, the complications of which include pulmonary oedema, shock, and death.
Symptoms vary with the acuteness and underlying cause of the tamponade. Patients with acute tamponade may present with dyspnoea, tachycardia, and tachypnoea. Cold and clammy extremities from hypoperfusion are also observed in some patients. Other symptoms and signs may include the following:
Elevated jugular venous pressure

Pulsus paradoxus

Chest pressure

Decreased urine output

Confusion

Dysphoria

Colonic injuries that are managed with resection are associated with a high complication rate regardless of whether an anastomosis or colostomy is performed. Colonic resection and anastomosis can be performed safely in the majority of patients with severe colonic injury, including injuries to the left colon. For injuries of the right colon, an ileocolostomy has a lower incidence of leakage than a colocolonic anastomosis. For injuries to the left colon, there remains a role for colostomy specifically in the subgroups of patients with a high ATI or hypotension, because these patients are at greater risk for an anastomotic leak. The role of resection and primary anastomosis versus colostomy in colonic trauma requires further investigation.

Answer: Thoracotomy

Cardiac arrest after penetrating chest trauma may be an indication for emergency thoracotomy. A successful outcome is possible if the patient has a cardiac tamponade and the definitive intervention is performed within 10 minutes of loss of cardiac output.
EMERGENCY “CLAM SHELL” THORACOTOMY

Indication:

Penetrating chest/epigastric trauma associated with cardiac arrest (any rhythm).

Contraindications:
Definite loss of cardiac output for greater than 10 minutes.

Any patient who has a cardiac output, including hypotensive patients.

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%.

Aortic transection was the underlying cause of death in this patient.

Aortic transection, or traumatic aortic rupture, 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 types of thoracic trauma include:
1. Tension pneumothorax and pneumothorax
2. Haemothorax
3. Flail chest
4. Cardiac tamponade
5. Blunt cardiac injury
6. Pulmonary contusion
7. Diaphragm disruption
8. Mediastinal traversing wounds

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.

The use of intravenous diltiazem or verapamil is contraindicated in patients with ventricular tachycardia. The IV administration of a calcium channel blocker can precipitate cardiac arrest in such patients.
Marked hemodynamic deterioration and ventricular fibrillation have occurred in patients with wide-complex ventricular tachycardia (QRS >= 0.12 seconds) treated with IV verapamil.

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).

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.

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.

Unstable angina is a common cardiovascular condition associated with major adverse clinical events. Over the last 15 years, therapeutic advances have dramatically reduced the complication and mortality rates of this serious condition. The standard of therapy in patients with unstable angina now incorporates the combined use of a potent antithrombotic (aspirin, clopidogrel, heparin and glycoprotein IIb/IIIa receptor antagonists) and anti-anginal (β-blockade and intravenous nitrates) regimens complemented by the selective and judicious application of coronary revascularisation strategies.
Increasingly, these invasive and non-invasive therapeutic interventions are being guided not only by the clinical risk profile but also by the determination of serum cardiac and inflammatory markers.
Moreover, rapid and intensive management of associated risk factors, such as hypercholesterolaemia, would appear to have potentially substantial benefits even within the acute in-hospital phase of unstable angina. Aspirin 300mg should be given as soon as possible. If the patient has a moderate to high risk of myocardial infarction, then Clopidogrel should be given with a low molecular weight heparin. Thrombolysis or urgent percutaneous intervention should be given if there are significant ECG changes.

The flattened appearance of the face is a classical description of the dish-face deformity associated with Le Fort III fracture of the midface.

The term Le Fort fractures is applied to transverse fractures of the midface involving the maxillary bone and surrounding structures in either a horizontal, pyramidal, or transverse direction. There are three grades of Le Fort fractures:

1. Le Fort I
It is the horizontal fracture of the maxilla. Violent force over a more extensive area above the level of the
teeth will result in this type of fracture. Horizontal fracture line is seen above the apices of the maxillary teeth, detaching the tooth-bearing portion of the maxilla from the rest of the facial skeleton. Floating maxilla and Guerin’s sign is seen in such patients.

2. Le Fort II
It is a pyramidal or subzygomatic fracture. Violent force in the central region extending from glabella to the alveolus results in this type of fracture, resulting in ballooning or moon-face facial deformity.

3. Le Fort III
It is a high-level transverse or suprazygomatic fracture associated with craniofacial disjunction. The entire facial skeleton moves as a single block as a result of the trauma. The patient develops a characteristic panda facies and dish-face deformity.

There is strong evidence to support haemostatic resuscitation in the setting of massive haemorrhage due to trauma. This advocates the use of 1:1:1 ratio.

Uncontrolled haemorrhage accounts for up to 39% of all trauma-related deaths. In the UK, approximately 2% of all trauma patients need massive transfusion. Massive transfusion is defined as the replacement of a patient’s total blood volume in less than 24 hours or the acute administration of more than half the patient’s estimated blood volume per hour. During acute bleeding, the practice of haemostatic resuscitation has been shown to reduce mortality rates. It is based on the principle of transfusion of blood components in fixed ratios. For example, packed red cells, FFP, and platelets are administered in a ratio of 1:1:1.

In adults 50% of the cases of brain death follow severe head injury, 30% are due to subarachnoid haemorrhage and 20% are due to a severe hypoxic-ischaemic event. Thus supra-tentorial catastrophes lead to pressure effect which cause the irretrievable death of the brain-stem.

The Criteria for Diagnosis of Brain-Stem Death

All the pre-conditions must be satisfied and
there should be demonstrably no pharmacological or
metabolic reason for the coma before formally testing the
integrity of the brain-stem reflexes.

Pre Conditions
1. The patient is comatose and mechanically ventilated
for apnoea.
2. The diagnosis of structural brain damage has been
established or the immediate cause of coma is known.
3. A period of observation is essential.

Exclusions
1. Drugs are not the cause of coma e.g. barbiturates.
Neuromuscular blockade has been demonstrably reversed.
2. Hypothermia does not exist.
3. There is no endocrine or metabolic disturbance.

Testing for Brain-Stem Death
Reflexes involving brain-stem function.
1. No pupillary response to light.
2. No corneal reflex.
3. No vestibulo ocular reflex (Caloric test).
4. Doll’s eye reflex
5. No motor response to pain – in the Vth nerve distribution.
6. No gag reflex in response to suction through endotracheal tube or tracheostomy.
7. Apnoea persists despite a rise in PaCO2 to greater than 50 mmHg (6.6kPa) against a background of a normal PaO2.

Diagnosis is to be made by two doctors who have been registered for more than five years and are competent in the procedure. At least one should be a consultant. Testing should be undertaken by the doctors together and must always be performed completely and successfully on two occasions in total.

The goal of fluid management in major burn injuries is to maintain the tissue perfusion in the early phase of burn shock, in which hypovolemia finally occurs due to steady fluid extravasation from the intravascular compartment.

Burn injuries of less than 20% are associated with minimal fluid shifts and can generally be resuscitated with oral hydration, except in cases of facial, hand and genital burns, as well as burns in children and the elderly. As the total body surface area (TBSA) involved in the burn approaches 15–20%, the systemic inflammatory response syndrome is initiated and massive fluid shifts, which result in burn oedema and burn shock, can be expected.

The ideal burn resuscitation is the one that effectively restores plasma volume, with no adverse effects. Isotonic crystalloids, hypertonic solutions and colloids have been used for this purpose, but every solution has its advantages and disadvantages. None of them is ideal, and none is superior to any of the others.
Crystalloids are readily available and cheaper than some of the other alternatives. RL solution, Hartmann solution (a solution similar to RL solution) and normal saline are commonly used. There are some adverse effects of the crystalloids: high volume administration of normal saline produces hyperchloremic acidosis, RL increases the neutrophil activation after resuscitation for haemorrhage or after infusion without haemorrhage. d-lactate in RL solution containing a racemic mixture of the d-lactate and l-lactate isomers has been found to be responsible for increased production of ROS. RL used in the majority of hospitals contains this mixture. Another adverse effect that has been demonstrated is that crystalloids have a substantial influence on coagulation. Recent studies have demonstrated that in vivo dilution with crystalloids (independent of the type of the crystalloid) resulted in a hypercoagulable state.
Despite these adverse effects, the most commonly used fluid for burn resuscitation in the UK and Ireland is Hartmann’s solution (adult units 76%, paediatric units 75%). Another study has revealed that RL is the most popular type of fluid in burn units located in USA and Canada.

This patient has developed a tension pneumothorax following a blunt trauma.

Tension pneumothorax is a life-threatening condition that develops when air is trapped in the pleural cavity under positive pressure, displacing mediastinal structures and compromising cardiopulmonary function. Blunt or penetrating chest trauma that creates a flap-type defect on the surface of the lung can result in this life-threatening condition.

Signs and symptoms of tension pneumothorax include:
1. Chest pain that usually has a sudden onset, is sharp, and may lead to feeling of tightness in the chest
2. Dyspnoea and progressive hypoxia
3. Tachycardia
4. Hyperventilation
5. Cough
6. Fatigue

On examination, hyper-resonant percussion note and tracheal deviation are typically found. Treatment is immediate without waiting for the CXR result and includes needle decompression and chest tube insertion.

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.

The classic presentation of arterial injury include the five Ps: pallor, pain, paraesthesia, paralysis, and pulselessness. In the extremities, the tissues most sensitive to anoxia are the peripheral nerves and striated muscles. Early development of paraesthesia and paralysis indicates that there is significant ischaemia present, and therefore, immediate exploration and repair are warranted. Presence of a palpable pulse does not exclude an arterial injury because this may represent a transmitted pulsation through a blood clot.

When severe ischaemia is present, the repair must be completed within six to eight hours to prevent irreversible muscle ischaemia and loss of limb function. Delay to obtain a conventional angiogram or to observe for change needlessly prolongs the ischaemic time. Fasciotomy may be required but should be done in conjunction with and after re-establishment of arterial flow. Local wound exploration is not recommended because brisk haemorrhage may be encountered without prior securing of vascular control.

Answer: Intravenous naloxone

Naloxone is a medication approved by the Food and Drug Administration (FDA) to prevent overdose by opioids such as heroin, morphine, and oxycodone. It blocks opioid receptor sites, reversing the toxic effects of the overdose. Naloxone is administered when a patient is showing signs of opioid overdose. The medication can be given by intranasal spray, intramuscular (into the muscle), subcutaneous (under the skin), or intravenous injection.

Several conditions and drugs can cause pinpoint pupils, including:
Prescription opioids or narcotics
Some medications have opioids or narcotics in them. Opioids, including morphine, are drugs commonly used for pain relief. Opioids can affect a person psychologically and are highly addictive.

People often take prescription opioids in pill form to treat severe post-surgical pain, such as from dental surgery, or for long-term pain, as with some cancers.

Prescription opioids that may cause pinpoint pupils include:

oxycodone
morphine
hydrocodone
codeine
methadone