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Thromboembolic events in a severely burned patient
514
Bums (1991) 17,(6), 514-515
PrintedinGreat Britain
Thromboembolic
events in a severely burned patient
J. Handel and H. A. Steinbrecher Departments
of Anaesthesia
and Surgery, Salisbury Hospital, UK
A patient with severe burns suffered spontaneous bilateral peribheral arferibl thromboses which were successfully freafed with recombinanf human tissue plasminogen activator (rf PA) (Actilyse). The patient later died from complications of burns.
Introduction Peripheral arterial thromboembolic events in patients with bums are rare (Counce et al., 1988). They are usually unilateral. Treatment is determined by the site of the embolus and the extent of thermal injury. This appears to be the first reported case of bilateral peripheral arterial thromboses in a patient who sustained severe thermal bums.
Case report A 3%year-old man was transferred to the Regional Bums Unit in Salisbury, UK, having sustained 38 per cent full skin thickness bums to his face, neck and chest. The patient had fallen into a fire during an epileptic seizure and had associated inhalation injuries. Current medications were phenytoin and carbamazepine for chronic idiopathic epilepsy. His general health was good and there was no family history of thromboembolic disease. On arrival at the referring hospital, he had been conscious and orientated with a pulse of 95/min and bood pressure of 14W9OmmHg. Apart from bums, there were no other injuries. Orotracheal intubation was necessary due to progressive oedema of the neck and mouth causing airway obstruction. He received appropriate fluid resuscitation with gelatine and albumin solution and was subsequently transferred to the Regional Bums Unit. Initial investigations showed a haematocrit of 0.509, International Normalized Ratio (INR) 1.1, Activated Partial Thromboplastin Time Ratio (APTR) 1.16, and a carboxyhaemoglobin of 2 per cent. The urine contained myoglobin. Management after transfer consisted of intermittent positivepressure ventilation, fluid resuscitation, analgesia and sedation with papaveretum and midazolam respectively. Twenty-four hours following the injury, his left foot was noted to be cold and cyanosed with absent dorsalis pedis and posterior tibia1 pulses, as assessed by palpation and Doppler ultrasound probe. Pulses in the right leg were normal. He had remained normotensive and in sinus rhythm since admission and the lower limb arteries had not been cannulated or punctured. Femoral arteriography demonstrated an occlusion of the left popliteal artery, which was thought to be acute thrombosis or thromboembolism. This was treated with an infusion of rt PA (tissue plasminogen activator, Actilyse, Boeringher Ingelheim) to the ‘c 1991 Butterworth-Heinemann 0305-4179/91/060514-02
Ltd
occlusion site through a left femoral intra-arterial catheter, at 0.5 mg/h with 200 units of heparin using a catheter. After 24 h the pulses had returned and arteriography confirmed almost complete dissolution of the thromboembolic process. He was then commenced on an infusion of heparin 20 000 units per 24 hours. Seventy-two hours after injury, his right foot and lower leg became pale and cold. Both dorsalis pedis and posterior tibia1 pulses were noted to be absent. There was, however, a weak popliteal pulse. All leg and foot pulses on the left were now palpable. Arteriography using a right transfemoral approach demonstrated an occlusion of the anterior tibia1 artery just below the trifurcation of the popliteal artery. This again was successfully treated with an infusion of rt PA. An ensuing echocardiogram was normal and measurements of plasma antithrombin III levels, protein C, protein S levels and anticardiolipin antibodies revealed no evidence of an inherited or acquired thrombophilic state. His condition subsequently deteriorated with the development of pneumonia, bum wound infection and progressive renal failure. He died 11 days following admission. Autopsy revealed no cardiovascular pathology which may have predisposed to arterial thromboembolism. A mild degree of left ventricular hypertrophy was noticed. Interestingly, an area was noted in the lower lobe of the right lung, the appearance of which was suggestive of recent infarction. This raised the possibility of venous thromboembolism; however, there was no evidence of deep venous thrombosis.
Discussion systemic response to bums injury in the first 36 h includes changes in blood volume and blood vessel permeability (Sevitt, 1979). There is a transient hypofibrinogenaemia thrombcytopenia followed by and thrombocytosis. Between I and 4 weeks postbum, there is a period of hypercoagulability with shortened prothrombin time (PTT) and elevated plasma fibrinogen (Bartlett et al., 1981). The only measured abnormality in this patient was a transient elevation of the haematocrit which reached 0.509 The
on one occasion. Myocardial dysfunction may cause arrhythmias resulting in arterial thromboembolic events. A
myocardial depressant factor may be involved (Baxter et al., 1970).This patient had no evidence of cardiac dysfunction until shortly before death. Single isolated vascular occlusion due to presumed thrombosis or thromboembolism was reported as occurring in three of 1740 thermally injured patients (Counce et al., 1988). These authors suggest that acute vascular occlusion
Handel and Steinbrecher et al.: Thromboembolic
events in a burned patient
may be related to electrical injury. It is not stated whether their patients were investigated for the presence of an inherited or acquired thrombophilic state. Our patient appears to be the first reported case of bilateral, peripheral arterial occlusion associated with thermal injury. This patient had not sustained electrical injury and investigation revealed no acquired or congenital factors predisposing to thromboembolism. In the absence of further information, trauma and stasis were the only identifiable factors contributing to the aetiology of thromboembolism in this patient. The treatment of peripheral thromboembolic events, both arterial and venous, has become less invasive due to the introduction of fibrinolytic agents. A survey by vascular surgeons showed that this is increasingly becoming an option in the treatment of acute limb ischaemia (Earnshaw and Shaw, 1990). In this survey, the majority of surgeons used streptokinase as the thrombolytic agent, which is considerably less expensive than rt PA. However, rt PA activates plasminogen only at the site of formed clot and therefore may be associated with a lower risk of haemorrhagic complications than streptokinase, which activates plasminogen systemically. Additionally, rt PA may carry a smaller risk of anaphylaxis than streptokinase. The high risk of infection in severly burned patients made thrombolysis the only realistic option available for the treatment of this patient’s limb ischaemia. It is often the late complications of bums that lead to the high mortality in severe thermal injury, as was the case in our patient.
515
Acknowledgements We are grateful to Mr A. Rossi, Consultant Plastic Surgeon, for allowing us to report this patient under his care. We are also grateful to Miss A. Burdus for preparing the manuscript.
References Bartlett R. H., Fang S. W., Marrujo G. et al. (1981) Coagulation and platelet changes after thermal injury in man. Bums 7,370. Baxter C. R., Moncrief J. A., Prager M. D. et al. (1970) A circulating myocardial depressant factor in bum shock. Research in Bums, Transactions of the Third International Congress. Beme: Hans Hueber, p. 499. Counce J. S., Cone J. B., McAlister L. et al. (1988) Surgical complications of thermal injury. Am. 1. Surg. 156, 556. Eamshaw J. J. and Shaw J. F. L. (1990) Survey of the use of thrombolysis for acute limb ischaemia in the UK and Ireland. Br. J. Surg. 77, 1041. Sevitt S. (1979) A review of the complications of burns, their origin and importance for illness and death. 1. Truumm 19, 358. Paper accepted
19 July 1991.
Correspondence should be addressed to: Dr J. Handel, Department of Anaesthesia, Odstock Hospital, Salisbury, Wilts. SP2 SBJ, UK.
Bums (1991) 17,(6), 514-515
PrintedinGreat Britain
Thromboembolic
events in a severely burned patient
J. Handel and H. A. Steinbrecher Departments
of Anaesthesia
and Surgery, Salisbury Hospital, UK
A patient with severe burns suffered spontaneous bilateral peribheral arferibl thromboses which were successfully freafed with recombinanf human tissue plasminogen activator (rf PA) (Actilyse). The patient later died from complications of burns.
Introduction Peripheral arterial thromboembolic events in patients with bums are rare (Counce et al., 1988). They are usually unilateral. Treatment is determined by the site of the embolus and the extent of thermal injury. This appears to be the first reported case of bilateral peripheral arterial thromboses in a patient who sustained severe thermal bums.
Case report A 3%year-old man was transferred to the Regional Bums Unit in Salisbury, UK, having sustained 38 per cent full skin thickness bums to his face, neck and chest. The patient had fallen into a fire during an epileptic seizure and had associated inhalation injuries. Current medications were phenytoin and carbamazepine for chronic idiopathic epilepsy. His general health was good and there was no family history of thromboembolic disease. On arrival at the referring hospital, he had been conscious and orientated with a pulse of 95/min and bood pressure of 14W9OmmHg. Apart from bums, there were no other injuries. Orotracheal intubation was necessary due to progressive oedema of the neck and mouth causing airway obstruction. He received appropriate fluid resuscitation with gelatine and albumin solution and was subsequently transferred to the Regional Bums Unit. Initial investigations showed a haematocrit of 0.509, International Normalized Ratio (INR) 1.1, Activated Partial Thromboplastin Time Ratio (APTR) 1.16, and a carboxyhaemoglobin of 2 per cent. The urine contained myoglobin. Management after transfer consisted of intermittent positivepressure ventilation, fluid resuscitation, analgesia and sedation with papaveretum and midazolam respectively. Twenty-four hours following the injury, his left foot was noted to be cold and cyanosed with absent dorsalis pedis and posterior tibia1 pulses, as assessed by palpation and Doppler ultrasound probe. Pulses in the right leg were normal. He had remained normotensive and in sinus rhythm since admission and the lower limb arteries had not been cannulated or punctured. Femoral arteriography demonstrated an occlusion of the left popliteal artery, which was thought to be acute thrombosis or thromboembolism. This was treated with an infusion of rt PA (tissue plasminogen activator, Actilyse, Boeringher Ingelheim) to the ‘c 1991 Butterworth-Heinemann 0305-4179/91/060514-02
Ltd
occlusion site through a left femoral intra-arterial catheter, at 0.5 mg/h with 200 units of heparin using a catheter. After 24 h the pulses had returned and arteriography confirmed almost complete dissolution of the thromboembolic process. He was then commenced on an infusion of heparin 20 000 units per 24 hours. Seventy-two hours after injury, his right foot and lower leg became pale and cold. Both dorsalis pedis and posterior tibia1 pulses were noted to be absent. There was, however, a weak popliteal pulse. All leg and foot pulses on the left were now palpable. Arteriography using a right transfemoral approach demonstrated an occlusion of the anterior tibia1 artery just below the trifurcation of the popliteal artery. This again was successfully treated with an infusion of rt PA. An ensuing echocardiogram was normal and measurements of plasma antithrombin III levels, protein C, protein S levels and anticardiolipin antibodies revealed no evidence of an inherited or acquired thrombophilic state. His condition subsequently deteriorated with the development of pneumonia, bum wound infection and progressive renal failure. He died 11 days following admission. Autopsy revealed no cardiovascular pathology which may have predisposed to arterial thromboembolism. A mild degree of left ventricular hypertrophy was noticed. Interestingly, an area was noted in the lower lobe of the right lung, the appearance of which was suggestive of recent infarction. This raised the possibility of venous thromboembolism; however, there was no evidence of deep venous thrombosis.
Discussion systemic response to bums injury in the first 36 h includes changes in blood volume and blood vessel permeability (Sevitt, 1979). There is a transient hypofibrinogenaemia thrombcytopenia followed by and thrombocytosis. Between I and 4 weeks postbum, there is a period of hypercoagulability with shortened prothrombin time (PTT) and elevated plasma fibrinogen (Bartlett et al., 1981). The only measured abnormality in this patient was a transient elevation of the haematocrit which reached 0.509 The
on one occasion. Myocardial dysfunction may cause arrhythmias resulting in arterial thromboembolic events. A
myocardial depressant factor may be involved (Baxter et al., 1970).This patient had no evidence of cardiac dysfunction until shortly before death. Single isolated vascular occlusion due to presumed thrombosis or thromboembolism was reported as occurring in three of 1740 thermally injured patients (Counce et al., 1988). These authors suggest that acute vascular occlusion
Handel and Steinbrecher et al.: Thromboembolic
events in a burned patient
may be related to electrical injury. It is not stated whether their patients were investigated for the presence of an inherited or acquired thrombophilic state. Our patient appears to be the first reported case of bilateral, peripheral arterial occlusion associated with thermal injury. This patient had not sustained electrical injury and investigation revealed no acquired or congenital factors predisposing to thromboembolism. In the absence of further information, trauma and stasis were the only identifiable factors contributing to the aetiology of thromboembolism in this patient. The treatment of peripheral thromboembolic events, both arterial and venous, has become less invasive due to the introduction of fibrinolytic agents. A survey by vascular surgeons showed that this is increasingly becoming an option in the treatment of acute limb ischaemia (Earnshaw and Shaw, 1990). In this survey, the majority of surgeons used streptokinase as the thrombolytic agent, which is considerably less expensive than rt PA. However, rt PA activates plasminogen only at the site of formed clot and therefore may be associated with a lower risk of haemorrhagic complications than streptokinase, which activates plasminogen systemically. Additionally, rt PA may carry a smaller risk of anaphylaxis than streptokinase. The high risk of infection in severly burned patients made thrombolysis the only realistic option available for the treatment of this patient’s limb ischaemia. It is often the late complications of bums that lead to the high mortality in severe thermal injury, as was the case in our patient.
515
Acknowledgements We are grateful to Mr A. Rossi, Consultant Plastic Surgeon, for allowing us to report this patient under his care. We are also grateful to Miss A. Burdus for preparing the manuscript.
References Bartlett R. H., Fang S. W., Marrujo G. et al. (1981) Coagulation and platelet changes after thermal injury in man. Bums 7,370. Baxter C. R., Moncrief J. A., Prager M. D. et al. (1970) A circulating myocardial depressant factor in bum shock. Research in Bums, Transactions of the Third International Congress. Beme: Hans Hueber, p. 499. Counce J. S., Cone J. B., McAlister L. et al. (1988) Surgical complications of thermal injury. Am. 1. Surg. 156, 556. Eamshaw J. J. and Shaw J. F. L. (1990) Survey of the use of thrombolysis for acute limb ischaemia in the UK and Ireland. Br. J. Surg. 77, 1041. Sevitt S. (1979) A review of the complications of burns, their origin and importance for illness and death. 1. Truumm 19, 358. Paper accepted
19 July 1991.
Correspondence should be addressed to: Dr J. Handel, Department of Anaesthesia, Odstock Hospital, Salisbury, Wilts. SP2 SBJ, UK.