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.

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.

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

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.

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.

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

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

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: 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.

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.

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.

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.

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 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.

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: 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

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

Answer: Flail chest injury

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

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

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

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

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.

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: 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.

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.

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.

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.

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).

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.

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 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

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.

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.