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.

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.

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: 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.

Answer: Flail chest injury

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

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

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

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

Answer: 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.

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: 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.

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.

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

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.

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.

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: 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

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.

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: 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 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.

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

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.

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.

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.

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.

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.

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.

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

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.

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.

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

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.