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Sub-arachnoid hemorrhage following cardiopulmonary resuscitation
Resuscitation 63 (2004) 221–223
Case report
Sub-arachnoid hemorrhage following cardiopulmonary resuscitation Alexander Lowenthal a , Nimrod Maimon a , Svetlana Waldman b , Yaniv Almog a,∗ a
Medical Intensive Care Unit, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev Beer-Sheva, P.O. Box 151, Beer-Sheva 84101, Israel b Department of Neurology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev Beer-Sheva, Beer-Sheva, Israel
Received 13 November 2003; received in revised form 16 May 2004; accepted 23 May 2004
Abstract We report the case of a 20-year-old male who developed unexplained sub-arachnoid haemorrhage following cardiopulmonary resuscitation. Computed tomography and lumbar puncture performed within 24 h were normal. A CT performed on day 5 revealed massive sub-arachnoid hemorrhage. The patient expired due to brain herniation. We conclude that sub-arachnoid hemorrhage (SAH) may be a late complication of aborted sudden death. We suggest ischaemia-reperfusion injury as a possible mechanism. © 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Sub-arachnoid haemorrhage; Cardiopulmonary resuscitation; Ischaemia-reperfusion injury
Resumo Descrevemos o caso de um jovem do sexo masculino de 20 Anos que desenvolveu uma hemorragia sub-aracnoideia após reanimação cardio-pulmonar. A tomografia computadorizada e a punção lombar realizadas nas primeiras 24 h foram normais. A CT realizada no 5◦ dia revelou uma hemorragia sub-aracnoideia massiva. O paciente faleceu devido a herniação cerebral. Conclu´ımos que a hemorragia sub-aracnoideia (SAH) pode ser uma complicação tardia da“morte súbita abortada”. Sugerimos a lesão de isquemia-reperfusão como um poss´ıvel mecanismo. © 2004 Elsevier Ireland Ltd. All rights reserved. Palavras chave: Hemorragia subaracnoideia; Reanimação cardio-pulmonar; Lesão de isquemia-reperfusão
Resumen Reportamos el caso de un varón de 20 años quien desarrolló una hemorragia subaracnoidea sin explicación después de resucitación cardiopulmonar. Se realizó una tomograf´ıa computarizada (CT) y punción lumbar que fueron normales en las primeras 24 horas. Una CT realizada el d´ıa 5 reveló una hemorragia subaracnoidea (SAH) masiva. El paciente falleció por herniación cerebral. Concluimos que la SAH puede ser una complicación tard´ıa de muerte súbita abortada. Sugerimos la lesión por isquemia y reperfusión como posible mecanismo de lesión. © 2004 Elsevier Ireland Ltd. All rights reserved. Palabras clave: Hemorragia subaracnoidea; Reanimación cardiopulmonar; Lesión por isquemia y reperfusión
1. Introduction Sudden cardiac death is a major public health problem. In the United States alone, more than 225,000 such deaths ∗ Corresponding author. Tel.: +98-972-8-6400640; fax: +98-972-8-6400166. E-mail address: [email protected] (Y. Almog).
occur each year, accounting for 50% of all cardiac deaths [1]. The rate of survival to hospital discharge for patients with a witnessed collapse who are found in ventricular fibrillation is 34% [1]. Complications may be divided into those occurring in the immediate period following CPR, such as aspiration leading to pneumonia and adult respiratory distress syndrome, and to those occurring later due to prolonged ischaemia
0300-9572/$ – see front matter © 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2004.05.015
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A. Lowenthal et al. / Resuscitation 63 (2004) 221–223
and ischaemia related reperfusion injury [2]. Hypoxic or ischaemic encephalopathy is the most frequent neurological complication of CPR. Additional complications include infarcts, brain swelling and mild intracerebral haemorrhage. Sub-arachnoid haemorrhage has never been reported as being associated with CPR. We report a case of sub-arachnoid hemorrhage occurring 5 days after resuscitation with prolonged CPR and propose ischaemia related reperfusion injury as a possible mechanism for this haemorrhage.
2. Case report A previously healthy soldier aged 20 collapsed during a soccer match. The ambulance team found him 10 min later in ventricular fibrillation. CPR was initiated for approximately 25 min. He required nine consecutive D.C. shocks before sinus rhythm was restored and he was admitted to hospital. His vital signs upon admission were blood pressure of
70/30 mmHg, heart rate 140 min−1 and body temperature of 37.1 ◦ C. Physical examination revealed a comatose patient, with miotic pupils reactive to light. Clinical biochemistry analysis was remarkable only for: creatine-kinase 1392 IU/L (MB fraction 111 IU/L), troponin-I 1.53 ng/ml. The ECG showed sinus rhythm, right bundle branch block pattern and no signs of myocardial ischaemia. Echocardiography revealed severe global left ventricular dysfunction (ejection fraction 10%) with no valvular abnormalities or pulmonary hypertension. Contrast enhanced computed tomography performed 8 h after admission was normal. A lumbar puncture performed 24 h later in order to rule out sub-arachnoid haemorrhage, as a possible cause of his collapse, was also normal. He subsequently developed myoclonic seizures and was treated with clonazepam and sodium valproate. On the fourth day he was transferred to our institution. Upon admission he had right-sided hemi-seizures and anisocoria, an electroencephalogram (EEG) confirmed the clinical suspicion of status epilepticus and IV phenytoin was admin-
Fig. 1. A contrast enhanced CT scan of the brain.
A. Lowenthal et al. / Resuscitation 63 (2004) 221–223
istered. A repeat contrast enhanced CT scan, 5 days after the initial collapse, demonstrated massive sub-arachnoid hemorrhage, with ischaemia in the right temporal and occipital lobes and brain oedema (Fig. 1). A few hours later he developed diabetes insipidus followed by haemodynamic instability. He died 6 days after his initial arrest. He was not treated with thromboembolism prophylaxis.
3. Discussion We describe a case of sub-arachnoid haemorrhage occurring 5 days after CPR and offer ischaemia-reperfusion injury as a possible mechanism. The neurological complications of prolonged CPR are primarily due to ischaemia, typically resulting in anoxic encephalopathy, brain oedema, seizures and infarcts. Subarachnoid haemorrhage has not been previously described as a complication of CPR. However, it is a well-known cause of sudden cardiac arrest [3]. Non-traumatic sub-arachnoid haemorrhage is caused in approximately 85% of the cases by saccular aneurysms [4]. The diagnosis of sub-arachnoid haemorrhage relies on finding blood in the cerebrospinal fluid (CSF). In more than 95% of the cases there is enough blood to be visualized on a high-quality non-contrast CT scan obtained within 72 h. If the scan fails to demonstrate sub-arachnoid haemorrhage and no mass lesion or obstructive hydrocephalus is found, a lumber puncture should be performed to establish the presence of blood in the sub-arachnoid space [5]. In this patient the presence of a Berry aneurysm cannot be completely ruled out, although the normal lumbar puncture and CT scan, performed within 24 h, effectively ruled out sub-arachnoid haemorrhage as the cause of his initial collapse. The development of sub-arachnoid haemorrhage in this patient somewhere between the second and fifth days led us to believe that it was a late sequel of his initial arrest and resuscitation. Several investigators have described pseudo-sub-arachnoid haemorrhage following prolonged anoxia. In these cases findings in a non-contrast CT were falsely interpreted as sub-arachnoid haemorrhage. However, a normal lumbar puncture or autopsy findings indicated that there was no blood in the sub-arachnoid space [6]. In the present case the normal lumbar puncture ruled out sub-arachnoid haemorrhage as the primary event and the second contrast enhanced CT convincingly ruled out the possibility of pseudo-sub-arachnoid haemorrhage. Gueugniaud hypothesized that sub-arachnoid haemorrhage might be a complication of CPR through an elevation of intracranial
223
pressure secondary to external chest compressions resulting in hemorrhage especially in the presence of prior vascular malformations [7]. This explanation is rather unlikely since CPR is rarely associated with a systolic blood pressure greater than 80 mmHg. Moreover, in our patient there was no evidence of cerebral haemorrhage in the first 24 h following CPR. Complex physiological and chemical derangements occur both in the period of total circulatory arrest to the brain and in the postischaemic-anoxic period (cerebral postresuscitation syndrome). This syndrome may lead to delayed protracted inhomogeneous cerebral hypoperfusion, excitotoxicity and free radical-triggered lipid membrane dysfunction [8–10]. Thus, ischaemia-reperfusion injury and its subsequent cascade of events may play a role in the evolution of bleeding diathesis leading to sub-arachnoid haemorrhage.
4. Conclusion Sub-arachnoid haemorrhage may complicate the course of patients following prolonged CPR. Early recognition of this complication is of importance since it may affect prognosis and management.
References [1] Eisenberg MS, Mengert TJ. Cardiac resuscitation. N Engl J Med 2001;17:1304–13. [2] Neumar RW, Ward KR. Cardiopulmonary arrest. In: Rosen P, Barkin R, editors. Emergency medicine concepts and clinical practice. 4th ed. St. Louis: Mosby; 1998. p. 35–60. [3] Shapiro S. Management of subarachnoid hemorrhage patients who presented with respiratory arrest resuscitated with bystander CPR. Stroke 1996;10:1780–2. [4] van Gijn J, Rinkel GJ. Subarachnoid haemorrhage: diagnosis, causes and management. Brain 2001;(Pt 2):249–78. [5] Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000;1:29–36. [6] Phan TG, Wijdicks EF, Worrell GA, et al. False subarachnoid hemorrhage in anoxic encephalopathy with brain swelling. J Neuroimaging 2000;4:236–8. [7] Gueugniaud PY. Subarachnoid hemorrhage: a complication of CPR? Crit Care Med 1987;3:284–5. [8] Vaagenes P, Ginsberg M, Ebmeyer U, et al. Cerebral resuscitation from cardiac arrest: pathophysiologic mechanisms. Crit Care Med 1996;2(2 Suppl):S57–68. [9] Negovsky VA, Gurvitch AM. Post-resuscitation disease—a new nosological entity. Its reality and significance. Resuscitation 1995;1:23– 7. [10] Hamann GF, Okada Y, del Zoppo GJ. Hemorrhagic transformation and microvascular integrity during focal cerebral ischemia/ reperfusion. J Cereb Blood Flow Metab 1996;6:1373–8.
Case report
Sub-arachnoid hemorrhage following cardiopulmonary resuscitation Alexander Lowenthal a , Nimrod Maimon a , Svetlana Waldman b , Yaniv Almog a,∗ a
Medical Intensive Care Unit, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev Beer-Sheva, P.O. Box 151, Beer-Sheva 84101, Israel b Department of Neurology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev Beer-Sheva, Beer-Sheva, Israel
Received 13 November 2003; received in revised form 16 May 2004; accepted 23 May 2004
Abstract We report the case of a 20-year-old male who developed unexplained sub-arachnoid haemorrhage following cardiopulmonary resuscitation. Computed tomography and lumbar puncture performed within 24 h were normal. A CT performed on day 5 revealed massive sub-arachnoid hemorrhage. The patient expired due to brain herniation. We conclude that sub-arachnoid hemorrhage (SAH) may be a late complication of aborted sudden death. We suggest ischaemia-reperfusion injury as a possible mechanism. © 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Sub-arachnoid haemorrhage; Cardiopulmonary resuscitation; Ischaemia-reperfusion injury
Resumo Descrevemos o caso de um jovem do sexo masculino de 20 Anos que desenvolveu uma hemorragia sub-aracnoideia após reanimação cardio-pulmonar. A tomografia computadorizada e a punção lombar realizadas nas primeiras 24 h foram normais. A CT realizada no 5◦ dia revelou uma hemorragia sub-aracnoideia massiva. O paciente faleceu devido a herniação cerebral. Conclu´ımos que a hemorragia sub-aracnoideia (SAH) pode ser uma complicação tardia da“morte súbita abortada”. Sugerimos a lesão de isquemia-reperfusão como um poss´ıvel mecanismo. © 2004 Elsevier Ireland Ltd. All rights reserved. Palavras chave: Hemorragia subaracnoideia; Reanimação cardio-pulmonar; Lesão de isquemia-reperfusão
Resumen Reportamos el caso de un varón de 20 años quien desarrolló una hemorragia subaracnoidea sin explicación después de resucitación cardiopulmonar. Se realizó una tomograf´ıa computarizada (CT) y punción lumbar que fueron normales en las primeras 24 horas. Una CT realizada el d´ıa 5 reveló una hemorragia subaracnoidea (SAH) masiva. El paciente falleció por herniación cerebral. Concluimos que la SAH puede ser una complicación tard´ıa de muerte súbita abortada. Sugerimos la lesión por isquemia y reperfusión como posible mecanismo de lesión. © 2004 Elsevier Ireland Ltd. All rights reserved. Palabras clave: Hemorragia subaracnoidea; Reanimación cardiopulmonar; Lesión por isquemia y reperfusión
1. Introduction Sudden cardiac death is a major public health problem. In the United States alone, more than 225,000 such deaths ∗ Corresponding author. Tel.: +98-972-8-6400640; fax: +98-972-8-6400166. E-mail address: [email protected] (Y. Almog).
occur each year, accounting for 50% of all cardiac deaths [1]. The rate of survival to hospital discharge for patients with a witnessed collapse who are found in ventricular fibrillation is 34% [1]. Complications may be divided into those occurring in the immediate period following CPR, such as aspiration leading to pneumonia and adult respiratory distress syndrome, and to those occurring later due to prolonged ischaemia
0300-9572/$ – see front matter © 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2004.05.015
222
A. Lowenthal et al. / Resuscitation 63 (2004) 221–223
and ischaemia related reperfusion injury [2]. Hypoxic or ischaemic encephalopathy is the most frequent neurological complication of CPR. Additional complications include infarcts, brain swelling and mild intracerebral haemorrhage. Sub-arachnoid haemorrhage has never been reported as being associated with CPR. We report a case of sub-arachnoid hemorrhage occurring 5 days after resuscitation with prolonged CPR and propose ischaemia related reperfusion injury as a possible mechanism for this haemorrhage.
2. Case report A previously healthy soldier aged 20 collapsed during a soccer match. The ambulance team found him 10 min later in ventricular fibrillation. CPR was initiated for approximately 25 min. He required nine consecutive D.C. shocks before sinus rhythm was restored and he was admitted to hospital. His vital signs upon admission were blood pressure of
70/30 mmHg, heart rate 140 min−1 and body temperature of 37.1 ◦ C. Physical examination revealed a comatose patient, with miotic pupils reactive to light. Clinical biochemistry analysis was remarkable only for: creatine-kinase 1392 IU/L (MB fraction 111 IU/L), troponin-I 1.53 ng/ml. The ECG showed sinus rhythm, right bundle branch block pattern and no signs of myocardial ischaemia. Echocardiography revealed severe global left ventricular dysfunction (ejection fraction 10%) with no valvular abnormalities or pulmonary hypertension. Contrast enhanced computed tomography performed 8 h after admission was normal. A lumbar puncture performed 24 h later in order to rule out sub-arachnoid haemorrhage, as a possible cause of his collapse, was also normal. He subsequently developed myoclonic seizures and was treated with clonazepam and sodium valproate. On the fourth day he was transferred to our institution. Upon admission he had right-sided hemi-seizures and anisocoria, an electroencephalogram (EEG) confirmed the clinical suspicion of status epilepticus and IV phenytoin was admin-
Fig. 1. A contrast enhanced CT scan of the brain.
A. Lowenthal et al. / Resuscitation 63 (2004) 221–223
istered. A repeat contrast enhanced CT scan, 5 days after the initial collapse, demonstrated massive sub-arachnoid hemorrhage, with ischaemia in the right temporal and occipital lobes and brain oedema (Fig. 1). A few hours later he developed diabetes insipidus followed by haemodynamic instability. He died 6 days after his initial arrest. He was not treated with thromboembolism prophylaxis.
3. Discussion We describe a case of sub-arachnoid haemorrhage occurring 5 days after CPR and offer ischaemia-reperfusion injury as a possible mechanism. The neurological complications of prolonged CPR are primarily due to ischaemia, typically resulting in anoxic encephalopathy, brain oedema, seizures and infarcts. Subarachnoid haemorrhage has not been previously described as a complication of CPR. However, it is a well-known cause of sudden cardiac arrest [3]. Non-traumatic sub-arachnoid haemorrhage is caused in approximately 85% of the cases by saccular aneurysms [4]. The diagnosis of sub-arachnoid haemorrhage relies on finding blood in the cerebrospinal fluid (CSF). In more than 95% of the cases there is enough blood to be visualized on a high-quality non-contrast CT scan obtained within 72 h. If the scan fails to demonstrate sub-arachnoid haemorrhage and no mass lesion or obstructive hydrocephalus is found, a lumber puncture should be performed to establish the presence of blood in the sub-arachnoid space [5]. In this patient the presence of a Berry aneurysm cannot be completely ruled out, although the normal lumbar puncture and CT scan, performed within 24 h, effectively ruled out sub-arachnoid haemorrhage as the cause of his initial collapse. The development of sub-arachnoid haemorrhage in this patient somewhere between the second and fifth days led us to believe that it was a late sequel of his initial arrest and resuscitation. Several investigators have described pseudo-sub-arachnoid haemorrhage following prolonged anoxia. In these cases findings in a non-contrast CT were falsely interpreted as sub-arachnoid haemorrhage. However, a normal lumbar puncture or autopsy findings indicated that there was no blood in the sub-arachnoid space [6]. In the present case the normal lumbar puncture ruled out sub-arachnoid haemorrhage as the primary event and the second contrast enhanced CT convincingly ruled out the possibility of pseudo-sub-arachnoid haemorrhage. Gueugniaud hypothesized that sub-arachnoid haemorrhage might be a complication of CPR through an elevation of intracranial
223
pressure secondary to external chest compressions resulting in hemorrhage especially in the presence of prior vascular malformations [7]. This explanation is rather unlikely since CPR is rarely associated with a systolic blood pressure greater than 80 mmHg. Moreover, in our patient there was no evidence of cerebral haemorrhage in the first 24 h following CPR. Complex physiological and chemical derangements occur both in the period of total circulatory arrest to the brain and in the postischaemic-anoxic period (cerebral postresuscitation syndrome). This syndrome may lead to delayed protracted inhomogeneous cerebral hypoperfusion, excitotoxicity and free radical-triggered lipid membrane dysfunction [8–10]. Thus, ischaemia-reperfusion injury and its subsequent cascade of events may play a role in the evolution of bleeding diathesis leading to sub-arachnoid haemorrhage.
4. Conclusion Sub-arachnoid haemorrhage may complicate the course of patients following prolonged CPR. Early recognition of this complication is of importance since it may affect prognosis and management.
References [1] Eisenberg MS, Mengert TJ. Cardiac resuscitation. N Engl J Med 2001;17:1304–13. [2] Neumar RW, Ward KR. Cardiopulmonary arrest. In: Rosen P, Barkin R, editors. Emergency medicine concepts and clinical practice. 4th ed. St. Louis: Mosby; 1998. p. 35–60. [3] Shapiro S. Management of subarachnoid hemorrhage patients who presented with respiratory arrest resuscitated with bystander CPR. Stroke 1996;10:1780–2. [4] van Gijn J, Rinkel GJ. Subarachnoid haemorrhage: diagnosis, causes and management. Brain 2001;(Pt 2):249–78. [5] Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000;1:29–36. [6] Phan TG, Wijdicks EF, Worrell GA, et al. False subarachnoid hemorrhage in anoxic encephalopathy with brain swelling. J Neuroimaging 2000;4:236–8. [7] Gueugniaud PY. Subarachnoid hemorrhage: a complication of CPR? Crit Care Med 1987;3:284–5. [8] Vaagenes P, Ginsberg M, Ebmeyer U, et al. Cerebral resuscitation from cardiac arrest: pathophysiologic mechanisms. Crit Care Med 1996;2(2 Suppl):S57–68. [9] Negovsky VA, Gurvitch AM. Post-resuscitation disease—a new nosological entity. Its reality and significance. Resuscitation 1995;1:23– 7. [10] Hamann GF, Okada Y, del Zoppo GJ. Hemorrhagic transformation and microvascular integrity during focal cerebral ischemia/ reperfusion. J Cereb Blood Flow Metab 1996;6:1373–8.