Udruzenje-hirurga.ba

CEREBRAL ISCHEMIA PRIOR
TO ANEURYSM SURGERY.
PREDICTOR OF POOR PROGNOSIS
Harun Brkić, Goran Bićanin, Mirza Moranjkić, Mirsad Hodžić

ABSTRACT
Objective study.
We have analyzed the prognostic value of post hemorrhage cerebral isch-
emia in aneurismal SAH: the degree of neurological deterioration as graded by the WFNS
and GCS scales, the intensity of ischemia as detected by CT scan and timing of surgery.
Material and methods. A series of 33 patients, consecutively admitted to our hospital over
the last three years, were reviewed retrospectively. The outcome was measured by deter-
mining the one-month mortality rate.
Results. The mean WFNS scale values were 2.45 for the entire analyzed specimen and 3.40
for the mortality group, respectively. There were no statistically significant differences not-
ed between the 2 groups in terms of other factors. Local ischemia was present in 51.5 %,
regional ischemia in 30.3 % and global ischemia in 18.2 % patients. Arterial hypertension
was noted in 93.9% of all patients and 92.3 % of those who experienced lethal outcome. The
percentages of smokers were 87.9 % and 69.2% for the entire group and for the mortality
group, respectively. Diabetes mellitus was present in 21.21% of all patients and 23.1% for
patients who experienced a lethal outcome. The majority of patients underwent surgery
between 4-10 days following the hemorrhage.
Conclusion. We conclude that CT confirmed post hemorrhage cerebral ischemia prior to
aneurysm surgery and earlier surgery is a major cause of poor prognosis.
KEY WORDS: ischemia, post hemorrhage, prognosis.
Harun Brkić
INTRODUCTION
Goran Bićanin
A decreased level of consciousness following the initial subarachnoid hemorrhage (SAH) or Mirza Moranjkić
early re-bleeding may be caused by a cerebral hematoma, subdural hematoma or hydrocepha- Mirsad Hodžić
lus. Only by exclusion should it be assumed that the cause is global brain damage as a result of high pressure and subsequent ischemia. An important notion is that axonal damage may con- University Clinical Center Tuzla tinue well after the primary injury and extend into the period of delayed cerebral ischemia1. Ischemia following subarachnoid hemorrhage is a catastrophic complication and a major cause of in-hospital mortality. The presence of cerebral ischemia after SAH, however, has received little attention as a prognostic variable. This may be due to the fact that ischemia is a difficult occurrence to appreciate and quantify on computed patients with aneurysmal SAH and PCI who were ad- tomography (CT) scans2. Delayed cerebral ischemia mitted to the University Hospital Tuzla in Bosnia and occurs primarily during the first or second week fol- Herzegovina, in the period between January 2003 and lowing aneurismal SAH, in up to one-third of patients, December 2006, all within 4 days after the hemorrhage. depending on case mix operative regimen3. This oc- We analyzed 4 additional characteristics of value in the currence also constitutes a leading cause of disability after aneurismal SAH. The disability and decrease in 1. Neurological status and CT scan. The patient’s clini- the number of productive life years caused by SAH is cal condition had been determined by the World Fed- comparable to that of cerebral infarction, because of eration Neurological Scale (WFNS) criteria and Glas- the relatively young age at onset and poor outcome in gow Coma Scale (GCS) prior to surgery and one month SAH4. It is a common belief that a thus far unidenti- fied factor which induces vasoconstriction and thereby 2. Intensity of cerebral ischemia as seen on the pre-op- secondary ischemia is introduced in the subarachnoid erative CT scan graded as either peri-aneurysmal focal space following the hemorrhage. This report is, in part, ischemia, regional blood vessel ischemia or global isch- the result of advances in intensive care management emia. In our study CT scan was obtained in an interval that have reduced the damage from cerebral ischemia between 2 and 7 days after the bleeding.
before and after surgery. There is an abundance of stud- 3. Risk factors for atherosclerosis including: history of ies regarding the period of greatest risk for developing prior stroke, arterial hypertension, aspirin use (within ischemia after subarachnoid hemorrhage. Several stud- 2 weeks before bleed), cigarette smoking, diabetes and ies have claimed that the highest risk for ischemia is within the first 24 hours, whereas others have shown 4. Timing of surgery and correlation of surgery with the the highest risk to be between days 4 and 9 or after day degree of disability. The timing of surgery was graded as 10. Rates of post-hemorrhage cerebral ischemia (PCI) surgery performed within 3 days after the hemorrhage, range between 24% and 35%, when defined by CT scan between 4-10 days after the hemorrhage and more than and may be as high as 81% when magnetic resonance imaging (MRI) is used for diagnosis5. Identifying isch- All patients were treated according to a standardized emic lesions after SAH is an important issue because protocol. Recording the outcome extended for 1 month the appearance of these lesions on follow-up imaging correlates with a poor outcome. The effect of ischemic lesions seen on CT scans during the first days of treat- ment remains unknown, however6. Factors that predict Over a period of three years we surgically treated 105 the development of ischemic lesions in these patients patients with aneurismal aubrachnoid hemorrhage. In have not been defined and clarified7. Recognizing the 33 patients we detected cerebral ischemia by CT scan. risk factors may have a positive impact on the treat- Overall mortality was 13 patients. We analyzed 33 pa- ment. Some studies have shown that the main reason tients (Group 1) with aneurismal SAH and PCI cere- for poor clinical results in aneurysm surgery is the exis- bral ischemia. Fatal outcome was noted in 13 patients (Group 2). The mean WFNS scale values were 2.45 and 3.4, for the entire analyzed specimen and for the mor- The goal of this study was to assess the patterns of cere- bral infarction caused by SAH and to define what clini-cal variables play a role in determining poor outcome in There were no significant differences between the two groups in terms of age and sex. Ischemic changes were more intensive in group 2 (Table 2). Most patients MATERIAL AND METHODS
presented with local ischemia. All patients with global We retrospectively studied a consecutive series of 33 ischemia experienced a poor outcome (Figure 1).
We found no significant influence of smoking, hyper- Table 1. Results of WFNS and GCS scales
tension, history of stroke or recent use of aspirin and (33 patients)
(13 patients)
Surgery was performed earlier in the mortality group DISCUSSION
All patients with subarachnoid hemorrhage should be evaluated and treated on an emergency basis with maintenance of airway and cardiovascular function. After initial stabilization, patients should be transferred to centers with neurovascular expertise and preferably (33 patients)
(13 patients)
with a dedicated neurologic critical care unit to opti- mize care. Once in the critical care setting, the main goals of treatment are the prevention of re-bleeding, the prevention and management of vasospasm and delayed ischemia as well as treatment of other medical and neu-rologic complications. All patients in our series were Table 2. Distribution of patients according to sex,
admitted to the neurosurgical intensive care unit and vigorously treated prior to and following surgery. It is a well established fact that secondary brain damage caused (33 patients)
(13 patients)
by delayed cerebral ischemia adversely affects the po- tential for recovery8-10. The presentation of the ischemic lesions proved to be a strong predictor of the outcome. Patients who experience cerebral ischemia following Intensity of
SAH harbor an increased risk for a poor outcome. This ischemia
may be due to the micro-vascular spasm resulting in ischemia, induced by blood products in subarachnoid space, auto-regulatory breakdown or abnormalities related to ictal cardiovascular arrest. About 50% of pa-tients who survive do not return to their previous level Figure 1. CT scans depicting local, regional and global ischemic changes.
analyze other complications of surgery, apart from isch- Table 3. Risk factors for atherosclerosis
emia, that might have had an impact on the outcome. Data regarding possible risk factors in patients with poor outcome were often lacking. During the CT analy- (33 patients) (13 patients)
sis, a massive SAH and acute hydrocephalus were noted in many patients. Studies using MRI have revealed that delayed ischemic lesions after SAH are usual y bilateral and multifocal, often involve the frontal lobes and are CONCLUSION
CT confirmed post hemorrhage cerebral ischemia (PCI), occurring during an initial period upon hemor- Table 4. Timing of surgery
rhage and before surgery, is a major prognostic factor. Hypodense lesions detected on CT following subarach- noid haemorrhage seem to be an independent risk fac- tor for poor outcome after SAH, and early lesion devel-opment may be more detrimental to clinical outcome of employment11-13. The prognostic value of the clinical state is stronger than that of previously identified risk REFERENCES
factors, such as the neurological condition on admis-sion and timing of surgery. This might be explained by 1. Petzold A, Rejdak K, Belli A, Sen J, Keir G, Kitch- the fact that both the neurological condition and the en N, et al. Axonal pathology in subarachnoid timing of surgery change over time and thus depend on and intracerebral hemorrhage. J Neurotrauma. the time interval between onset of SAH and admission. Our data suggest that the severity of the initial ischemia 2. Kreiter KT, Copeland D, Bernardini GL, Bates J, is an important factor in the final outcome. We did not Peery S, Claassen J, Connol y ES, Du YE, Stern Y, find that the presence of risk factors for atherosclerosis Mayer SA. Predictors of cognitive dysfunction after and diabetes had a negative impact on outcome. In a re- subarachnoid hemorrhage. Stroke. 2002; 33: 200–9. cent study, cigarette smoking was found to increase the 3. Hijdra A, Van Gijn J, Nagelkerke NJ, Vermeulen M, risk for atherosclerosis and caused difficulties in post van Crevel H. Prediction of delayed cerebral isch- operative recovery14. Our study could not support this emia, rebleeding, and outcome after aneurysmal finding to a significant degree. Analysis of the utiliza- subarachnoid hemorrhage. Stroke. 1988;19:1250–6.
tion of aspirin in the aforementioned study may have 4. Weir B, Grace M, Hansen J, Rothberg C. Time course been unreliable because it was based on data obtained of vasospasm in man. J Neurosurg. 1978;48: 173–8.
from both patients and their relatives15. Our study did 5. Longstreth WT Jr, Nelson LM, Koepsell TD, van not support the role of arterial vasospasm in the patho- Belle G. Clinical course of spontaneous subarach- genesis of ischemia. No measures of vessel spasm by noid hemorrhage: a population-based study in King angiography, TCD or clinical findings were associated County, Washington. Neurology. 1993;43:712–8.
with the clinical state in the present study. A limiting 6. Siironen J, Porras M, Varis J, Poussa K, Hernesni- factor in our study is reflected in the fact that we did not emi J, Juvela S. Early ischemic lesion on computed tomography: predictor of poor outcome among 13. Vilkki J, Jolst P, Ohman J, Servo A and Heikanen survivors of aneurysmal subarachnoid hemorrhage. O. Social outcome related to cognitive performance Journal of Neurosurgery. 2007;6:1074-9.
and computed tomography findings after surgery 7. Van Gijn J. Subarachnoid haemorrhage. Lancet. for a ruptured intracranial aneurysm. Neurosur- 8. Janjua N, Mayer SA. Cerebral vasospasm after 14. Lasner TM, Weil RJ, Riina HA, King JT Jr, Zager EL, subarachnoid hemorrhage. Curr Opin Crit Care. Raps EC, Flamm ES. Cigarette smoking-induced in- crease in the risk of symptomatic vasospasm after 9. Rinkel GJE, Feigin VL, Algra A, Feigin VL, Rinkel aneurysmal subarachnoid hemorrhage. J Neuro- GJ, Lawes CM et al. Calcium antagonists for aneu- rysmal subarachnoid haemorrhage. Cochrane Da- 15. Juvela S. Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. J Neuro- 10. Van Gijn J, Rinkel GJ. Subarachnoid haemor- rhage: diagnosis, causes and management. Brain. 16. Kivisaari RP, Salonen O, Servo A, Autti T, Hernesni- emi J, Ohman J. MR imaging after aneurysmal suba- 11. Ogden JA, Mee E, Henning M. A prospective study rachnoid hemorrhage and surgery: a long-term fol- of psychosocial adaptation following subarachnoid low-up study. Am J Neuroradiol. 2001;22:1143–18.
haemorrhage. Neuropsychol Rehabil. 1994;4:7–30.
17. Sloan MA, Haley EC Jr, Kassell NF, Henry ML, Stew- 12. Powell J, Kitchen N, Heslin J, Greenwood R. Psy- art SR, Beskin RR, Sevil a EA, Torner JC. Sensitivity chosocial outcomes at 18 months after good neu- and specificity of transcranial Doppler ultrasonog- rological recovery from aneurysmal subarachnoid raphy in the diagnosis of vasospasm following suba- haemorrhage. J Neurol Neurosurg Psychiatry. rachnoid hemorrhage. Neurology. 1989;39:1514–8.

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