Resuscitation 51 (2001) 207– 211 www.elsevier.com/locate/resuscitation
Case report
Survival of a subarachnoid hemorrhage patient who presented with prehospital cardiopulmonary arrest: case report and review of the literature Joji Inamasu a,*, Ryoichi Saito a, Yoshiki Nakamura a, Kiyoshi Ichikizaki a, Sadao Suga b, Takeshi Kawase b, Shingo Hori c, Naoki Aikawa c a
Department of Neurosurgery, National Tokyo Medical Center, Higashigaoka 2 -5 -1, Meguro-ku, Tokyo 152 -8902, Japan Department of Neurosurgery, Keio Uni6ersity School of Medicine, Shinanomachi 35, Shinjuku-ku, Tokyo 160 -8582, Japan c Department of Emergency Medicine and Critical Care, Keio Uni6ersity School of Medicine, Shinanomachi 35, Shinjuku-ku, Tokyo 160 -8582, Japan b
Received 24 January 2001; received in revised form 11 June 2001; accepted 11 June 2001
Abstract A 63-year-old woman was admitted to the intensive care unit after resuscitation from prehospital cardiopulmonary arrest (CPA). A brain CT scan revealed a subarachnoid hemorrhage (SAH), which was considered to be the cause of the CPA. The patient recovered neurologically after admission, and the elevated intracranial pressure (ICP) was controlled by inducing mild hypothermia. The day after admission, cerebral angiography revealed a ruptured cerebral aneurysm. The aneurysm was successfully treated with detachable coils by an endovascular technique. Mild hypothermia was continued for 3 days, and the patient was gradually rewarmed. After rehabilitation, the patient was discharged to her home with severe disability. Although aneurysmal SAH is one of the most common causes of CPA, survival of SAH patients after CPA is rare. This case illustrates the ability and possibility of multidisciplinary treatment, including the use of endovascular techniques and mild hypothermia, to improve the outcome of SAH patients with CPA who have been considered to be inoperable and untreatable. © 2001 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Subarachnoid hemorrhage; Cardiopulmonary arrest; Cardiopulmonary resuscitation; Endovascular treatment; Mild hypothermia
1. Introduction Aneurysmal subarachnoid hemorrhage (SAH) is one of the most common causes of sudden death [1]. About one-tenth of all the SAH patients that come to medical attention present with prehospital cardiopulmonary arrest (CPA) [2]. The prognosis of SAH patients who are resuscitated from CPA is extremely poor, and they have a low survival rate [2]. The authors describe a patient with SAH who presented with prehospital CPA but had a long-term survival after intensive treatment. The * Corresponding author. Tel.: + 81-3-3411-0111; fax: +81-3-34111627. E-mail address:
[email protected] (J. Inamasu).
world literature is reviewed, and potential therapeutic interventions are considered that can improve the outcome of SAH patients with CPA who have been thought to be inoperable and untreatable.
2. Case report A 63-year-old woman with a prior medical history of Parkinson’s disease complained of sudden onset of headache while asleep, and immediately fell into a coma with a gasping respiration pattern. By the time the emergency medical service reached the scene, the patient’s respiration had ceased and no carotid pulse could be palpated. Bystander cardiopulmonary resusci-
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tation (CPR) had already been initiated by a family member, and the return of spontaneous circulation (ROSC) was observed 10 min after the onset of the CPA. The return of spontaneous respiration was observed about 20 min after the onset of CPA. On arrival at our emergency room, the patient’s vital signs were: blood pressure 115/68 mmHg, heart rate 86/min, respiration rate 16/min, body temperature 35.9 °C. Her consciousness level was E1V1M2 on the Glasgow Coma Scale (GCS). The patient’s pupils were miotic and did not respond to light. The patient was intubated and an intravenous fluid line placed. An ECG showed diffuse elevation of the ST segment, suggesting the presence of myocardiac ischemia. Clinical chemistry revealed mildly elevated serum cardiac markers, including creatine kinase and troponin T. The results of cardiac ultrasonography augmented the ECG findings by showing diffuse hypokinesis of the left ventricle. A chest X-ray and blood gas analysis revealed the typical ‘butterfly shadow’ pattern and severe hypoxia, respectively, indicating the presence of pulmonary edema. After the patient’s condition had stabilized, a brain CT scan revealed a diffuse subarachnoid hemorrhage (SAH). The patient was rated as grade V on the Hunt and Hess Scale clinically [3], and group 3 by Fisher’s CT score (Fig. 1) [3]. Two hours after admission to the intensive care unit, the patient recovered neurologically to E1V1M3 on the GCS, with pupils reactive to light. Intracranial pressure (ICP) measurement was initiated by insertion of a parenchymal sensor (Camino, USA) and showed an ICP of more than 40 mmHg. After obtaining informed-consent from the patient’s family, mild hypothermia therapy was induced with a watercirculating blanket to lower the ICP and to provide brain protection. Midazolam and vecronium were continuously infused as a sedative and muscle relaxant, respectively. The patient’s brain temperature decreased to 34.5 °C within 3 h after induction of hypothermia, and the ICP dropped to below 20 mmHg. The day after admission, cerebral angiography revealed a saccular aneurysm at the bifurcation of the left internal cerebral artery and posterior communicating artery that was considered to be a source of the bleeding (Fig. 2A). The cerebral arteries were not affected by vasospasm, and the aneurysm was successfully obliterated with Guglielmi detachable coils by an endovascular technique (Fig. 2B). After embolization, mild hypothermia was continued for 3 days, and the patient was gradually rewarmed to 37.5 °C at a rate of 1 °C/day. ICP was optimally controlled during and after hypothermia therapy. During hypothermia, the patient became hypotensive with systolic blood pressure of less than 90 mmHg, necessitating continuous infusion of dobutamine. However, the wall motion of the left ventricle evaluated with the cardiac ultrasonography was not hypokinetic, and clinical chemistry showed no elevation
Fig. 1. A brain CT scan immediately after arrival, showing a diffuse subarachnoid hemorrhage.
of the serum cardiac markers. After rewarming, the blood pressure gradually returned to normal without the use of catecholamines. The patient became alert, but remained tetraparetic and aphasic for several weeks after the onset. By 2 months after the onset, the patient was still tetraparetic but could utter words and obey verbal commands. After a rehabilitation program, the patient was discharged to her home about a year after the onset. A CT scan at the time of discharge showed mild atrophy of the cerebral cortex. The long-term outcome evaluated on the Glasgow Outcome Scale was severe disability.
3. Discussion Aneurysmal SAH is one of the most common causes of sudden death and accounts for about 10% of patients that present with CPA [1]. Another 10% of SAH patients that come to medical attention are reported to arrive at the emergency room in CPA [2]. The pathophysiology of CPA in SAH patients has been attributed to: (1) a sudden increase in ICP caused by massive SAH, resulting in brainstem compression, brain hernia-
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Fig. 2. Left carotid angiogram showing a cerebral aneurysm at the bifurcation of the left internal carotid artery and the posterior communicating artery that was the source of the bleeding (A). After embolization, the aneurysm was completely obliterated (B).
tion, and subsequent respiratory arrest and to (2) ‘sympathetic storm’, i.e. excessive release of catecholamines resulting in lethal cardiac arrhythmia and/or pulmonary edema and subsequent cardiac arrest [2,4,5]. Even when ROSC is observed after successful CPR, the chance of long-term survival by such patients is very small, and the prognosis is poor even among survivors. Kitahara et al. [2] and Isayama et al. [6] separately reported that the long-term survival rate of SAH patients with prehospital CPA in whom ROSC was observed after resuscitation was 1.8% (1/57 cases) and 1.6% (2/129 cases), respectively. These figures are consistent with the survival rate in our institution, in which only one of the 60 (1.7%) consecutive SAH patients with prehospital CPA between January 1995 and December 2000 survived. These results are in contrast to those for prehospital CPA of cardiogenic etiology, in which the long-term survival rate was much higher, between 10 and 15%, once ROSC was observed [7]. Similarly, SAH patients with respiratory arrest alone (without cardiac arrest) have a much higher long-term survival rate: Shapiro reported that five of 26 SAH patients with respiratory arrest had a functional long-
term survival [1]. Hypoxic/ischemic brain damage due to complete cessation of the cerebral blood flow by CPA, in addition to the primary brainstem damage due to the elevated intracranial pressure (ICP) resulting from massive SAH, explains why the survival of SAH patients who present with CPA is worse. Most patients remain brain dead even after ROSC is achieved, and therapeutic intervention is usually not indicated in them. A literature review showed reports of only five cases of SAH with CPA on arrival with long-term survival including our own (Table 1) [2,6,8]. These patients had certain background factors in common: (1) bystander CPR was initiated within a few minutes of the onset; (2) return of spontaneous circulation and spontaneous respiration were achieved shortly after CPR was initiated. They had few common characteristics in terms of the location of aneurysm, pretreatment CT grade, age, or gender, due to small number of patients. The authors think that the endovascular obliteration of the aneurysm in the acute stage was effective in our patient. SAH patients with CPA have been considered to be grade V, the poorest grade, and surgical treatment
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Case
Age, sex
Time from onset to CPR
Time from onset Time from onset to return of to ROSC respiration
Pretreatment Fisher CT score
Location of aneurysm
Treatment modality
Long-term outcome (GOS)
Isayama et al. [6] Isayama et al. [6] Kitahara et al. [2] Kinoshita et al. [8] Reported case
n.d.
2 min
B10 min
B30 min
n.d.
ACoA
Clipping
Moderate disability
n.d.
2 min
B10 min
B30 min
n.d.
ACoA
Clipping
45 F
n.d.
n.d.
n.d.
n.d.
BA top
Clipping
Persistent vegetative state Moderate disability
54 F
Immediately after 10–15 min collapse Immediately after 10 min collapse
10–15 min
3
Rt IC bif
25 min
3
Lt IC-PC
Clipping hypothermia Endovascular hypothermia
63 F
Severe disability Severe disability
a ACoA, anterior communicating artery; BA, basilar artery; bif, bifurcation; CPR, cardiopulmonary resuscitation; GOS, Glasgow outcome scale; IC, internal carotid artery; n.d., not described; ROSC, return of spontaneous circulation.
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Table 1 Clinical and radiographic characteristics, treatment, and outcome of SAH patients with CPA who had a long-term survivala
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has not been indicated in the acute stage because of the high risk of the surgery and general anesthesia, even after successful resuscitation [3]. The ‘wait and see’ strategy, in which the patients are considered as surgical candidates only if they recover neurologically and their general condition remains stable until the chronic stage, has been adopted in these patients [3]. However, some resuscitated SAH patients with the potential for recovery may have been lost to rebleeding by their aneurysms during the waiting period for surgery in the chronic stage. The less invasive nature of endovascular treatment has enabled treatment of poor grade SAH patients in the acute stage [9], and if signs of recovery are observed neurologically and electrophysiologically, it may also be indicated in SAH patients resuscitated from CPA. Similarly, the use of mild hypothermia for brain protection may have been beneficial in this case. Mild hypothermia has been reported to improve the outcome of survivors of out-of-hospital cardiac arrest [10]. Hypothermia also reduces elevated ICP and has been used clinically as a means of controlling ICP in patients with hemispheric infarction due to embolic occlusion of the middle cerebral artery [11]. Mild hypothermia effectively controlled the ICP in our patient. Since the efficacy of mild hypothermia for ICP control and brain protection in severe SAH patients has not been reported, large, controlled studies are warranted. In summary, a rare case of a patient with an aneurysmal SAH who survived prehospital CPA has been reported. Although the prognosis is still poor, by widening their extremely narrow therapeutic window, the authors think that multidisciplinary, intensive treatment has the potential to improve the survival rate and the functional outcome of SAH patients with pre-
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hospital CPA who were previously considered untreatable. References [1] Shapiro S. Management of subarachnoid hemorrhage patients who presented with respiratory arrest resuscitated with bystander CPR. Stroke 1996;27:1780 – 2. [2] Kitahara T, Masuda T, Soma S. The etiology of sudden cardiopulmonary arrest in subarachnoid hemorrhage. No Shinkei Geka 1996;21:781 – 6 in Japanese. [3] Kassell NF, Torner JC, Halley EC Jr. The international cooperative study on timing of aneurysm surgery. Part 1: Overall management results. J Neurosurg 1990;73:18 – 36. [4] Schievink WI, Wijdicks EF, Parisi JE, Piepgras DG, Whisnant JP. Sudden death from subarachnoid hemorrhage. Neurology 1995;45:871 – 4. [5] Tabbaa MA, Ramirez-Lassepas M, Snyder BD. Aneurysmal subarachnoid hemorrhage presenting as cardiopulmonary arrest. Arch Intern Med 1987;147:1661 – 2. [6] Isayama K, Kobyashi S, Ikeda Y, Nakazawa S. Fatal subarachnoid hemorrhage: patients with cardiac arrest on arrival. Nippon Rinsho 1993;51(Suppl.):359 – 64 in Japanese. [7] Plaisance P, Lurie KG, Vicaut E, Adnet F, Petit JL, Epain D, Ecollan P, Gruat R, Cavagna P, Biens J. A comparison of standard cardiopulmonary resuscitation and active compression – decompression resuscitation for out-of-hospital cardiac arrest. N Engl J Med 1999;341:569 – 75. [8] Kinoshita K, Hayashi N, Jo N, Utagawa S, Watanabe G. A case of subarachnoid hemorrhage resuscitated from cardiopulmonary arrest with mild hypothermia. Kanto J Jpn Assoc Acute Med 1995;16:270 – 1 in Japanese. [9] Graves VB, Strother CM, Duff TA. Early treatment of ruptured aneurysm with Guglielmi detachable coils: effect on subsequent bleeding. Neurosurgery 1995;37:640 – 8. [10] Bernard SA, Jones BM, Horne M. Clinical trial of induced hypothermia in comatose survivors of out-of-hospital cardiac arrest. Ann Emerg Med 1997;30:146 – 53. [11] Schwab S, Schwarz S, Spranger M, Keller E, Bertram M, Hacke W. Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction. Stroke 1998;29:2461 –6.
Portuguese Abstract and Keywords Uma mulher de 63 anos foi admitida numa unidade de cuidados intensivos depois de uma paragem cardio-respirato´ ria (PCR) pre´ -hospitalar. O TAC cerebral revelou uma hemorragia subaracnoideia (HSA) que foi considerada a causa da PCR. A doente recuperou neurologicamente depois da admissa˜ o e a hipertensa˜ o intra craniana foi tratada com hipotermia moderada. No dia seguinte a´ admissa˜ o foi realizada uma angiografia cerebral que evidenciou um aneurisma cerebral em ruptura. O aneurisma foi tratado por te´ cnica endovascular com a colocac¸ a˜ o de ‘coils’. Continuou-se a hipotermia moderada por mais 3 dias. E depois a doente foi gradualmente aquecida. A doente teve alta para casa com incapacidade grave. Apesar de a HSA ser uma causa frequente de PCR a sobreviveˆ ncia nestes casos e´ rara. Este caso ilustra a utilidade do tratamento multidisciplinar, incluindo o uso de te´ cnica endovascular e hipotermia moderada, para melhorar o progno´ stico dos doentes com HSA considerados sem indicac¸ a˜ o ciru´ rgica. Pala6ras cha6e: Hemorragia subaracnoideia; Paragem cardio-respirato´ ria; Reanimac¸ a˜ o cardio-respirato´ ria; Tratamento endovascular; Hipotermia moderada