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.

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

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.

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.

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: 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.

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.

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 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.

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.

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.

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: 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: 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.

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.

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

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: 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).

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).

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.

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

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

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.

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.

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

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

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

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

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

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

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.

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

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.

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.