Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
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ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
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Advances in Clinical and Experimental Medicine

2013, vol. 22, nr 1, January-February, p. 101–109

Publication type: original article

Language: English

Effects of Nimodipine on Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage Treated by Endovascular Coiling

Wpływ nimodypiny na skurcz naczyń mózgowych u chorych z krwotokiem podpajęczynówkowym z pękniętego tętniaka leczonych przez embolizację wewnątrznaczyniową

Milan Mijailovic1,A,D,E,F, Snezana Lukic1,A,D,E,F, Dragomir Laudanovic2,B,C,F, Marko Folic3,C,D,E,F, Nevena Folic3,C,D,E,F, Slobodan Jankovic3,A,C,D,E,F

1 Radiology Department, Medical Faculty, University of Kragujevac and Kragujevac Clinical Center, Kragujevac, Serbia

2 Radiology Department, City Hospital, Uzice, Serbia

3 Pharmacology Department, Medical Faculty, University of Kragujevac and Kragujevac Clinical Center, Kragujevac, Serbia

Abstract

Background. An aneurysmal subarachnoid hemorrhage could be complicated with cerebral vasospasm and resultant ischemia, causing neurological deficit.
Objectives. The aim of this study was to compare early and late outcomes in patients with subarachnoidal hemorrhage (SAH) treated by endovascular coiling, who either received or did not receive prophylaxis of cerebral vasospasm with nimodipine.
Material and Methods. In this retrospective cross-sectional study, the data was collected from the histories of 68 patients (38 females and 30 males, age range 29–71 years) with spontaneous aneurysmal SAH in clinical stage HH I–IV, treated at Kragujevac Clinical Center, Serbia, from January 2008 till June 2009. The study population was divided into two groups: (1) the group of 42 patients who received intravenous prophylaxis with nimodipine for 3 weeks, and (2) the group of 26 patients who did not receive nimodipine prophylaxis.
Results. Prophylactic use of nimodipine did not decrease the rate of neurological deficit after one month, but the rates of both cerebral vasospasm (symptomatic and asymptomatic) and the morphological signs of ischemia using nuclear magnetic resonance imaging (MRI) were significantly lower in the nimodipine-protected group. Cerebral vasospasm was detected by Digital Subtraction Angiography (DSA) in the group protected by nimodipine as discrete in 2 patients (5%), and as apparent in 0 patients (0%). On the other hand, in the group unprotected by nimodipine, cerebral vasospasm was detected by DSA as discrete in 9 patients (35%), and as apparent in 6 patients (23%). Up to one month after the endovascular coiling, in the nimodipine-protected group, the T1W hypointense zones were detected by MRI as “small” in 5 patients (12%), as “medium” in 1 patient (2.5%), as “large” in 1 patient (2.5%), and as “multiple” in 2 patients (5%). In the nimodipine-unprotected group, the T1W hypointense zones were detected by MRI as “small” in 4 patients (16%), as “medium” in 2 patients (8%), as “large” in 3 patients (12%), and as “multiple” in 4 patients (16%). The difference between the groups was significant.
Conclusion. When a patient with SAH is treated with the endovascular clipping procedure, prophylactic administration of nimodipine is mandatory due to the reduced rate of cerebral vasospasm and delayed cerebral ischemia.

Streszczenie

Wprowadzenie.Krwotok podpajęczynówkowy może być powikłany skurczem naczyń mózgowych i następującym niedokrwieniem, co powoduje deficyt neurologiczny.
Cel pracy. Porównanie wyników wczesnych i odległych u chorych z krwotokiem podpajęczynówkowym (SAH) leczonych przez embolizację wewnątrznaczyniową, którzy otrzymali lub nie otrzymywali nimodypinę jako profilaktykę skurczu naczyń mózgowych.
Materiał i metody. W tym retrospektywnym badaniu przekrojowym zebrano historie 68 pacjentów (38 kobiet i 30 mężczyzn, w wieku 29–71 lat) ze spontanicznym krwotokiem podpajęczynówkowym z pękniętego tętniaka w klinicznym stadium HH I-IV, leczonych w Centrum Klinicznym w Kragujevac, Serbia, od stycznia 2008 do czerwca 2009 roku. Badanych podzielono na dwie grupy: (1) grupa 42 pacjentów, którzy otrzymywali dożylnie profilaktycznie nimodypinę przez 3 tygodnie i (2) grupa 26 pacjentów, którzy nie otrzymywali nimodypiny.
Wyniki. Profilaktyczne stosowanie nimodypiny nie zmniejszyło odsetka deficytu neurologicznego po miesiącu, ale częstotliwość zarówno skurczu naczyń mózgowych (objawowego i bezobjawowego), jak i morfologicznych objawów niedokrwienia w badaniu MRI były istotnie mniejsze w grupie, w której podawano nimodypinę. Skurcz naczyń mózgowych został wykryty za pomocą badania DSA w grupie, w której podawano nimodypinę jako nieciągły u 2 (5%), i jako widoczny u 0 pacjentów (0%). Z drugiej strony, w grupie bez podawania nimodypiny, skurcz naczyń mózgowych wykryto za pomocą metody DSA jako nieciągły u 9 pacjentów (35%), i widoczny u 6 pacjentów (23%). W ciągu jednego miesiąca po embolizacji wewnątrznaczyniowej w grupie, w której podawano nimodypinę hipointensywne obszary T1W zostały wykryte w badaniu MR jako „małe” u 5 chorych (12%), jako „średnie” u 1 chorego (2,5%), jako „duże” u 1 (2,5%), jako „liczne” u 2 (5%). W grupie bez podawania nimodypiny, hipointensywne obszary T1W wykryte w badaniu MR jako „małe” u 4 (16%), jako „średnie” u 2 (8%), jako „duże” u 3 (12%), i jako „liczne” u 4 chorych (16%). Różnica między grupami była istotna statystycznie.
Wnioski. Kiedy pacjent z krwotokiem podpajęczynówkowym jest leczony za pomocą embolizacji wewnątrznaczyniowej, profilaktyczne podawanie nimodypiny jest obowiązkowe ze względu na zmniejszenie ryzyka skurczu naczyń mózgowych i opóźnianie niedokrwienia mózgu.

Key words

subarachnoidal hemorrhage, endovascular coiling, cerebral vasospasm, nimodipine.

Słowa kluczowe

krwotok podpajęczynówkowy, embolizacja wewnątrznaczyniowa, skurcz naczyń mózgowych, nimodypina.

References (48)

  1. Mahaney KB, Todd MM, Bayman EO, Torner JC: IHAST Investigators: Acute postoperative neurological deterioration associated with surgery for ruptured intracranial aneurysm: incidence, predictors, and outcomes. J Neurosurg 2012, 116, 1267–1278.
  2. Kassell NF, Torner JC, Jane JA, Haley EC Jr, Adams HP: The International Cooperative Study on the Timing of Aneurysm Surgery. Part 2: Surgical results. J Neurosurg 1990, 73, 37–47.
  3. Solenski NJ, Haley EC Jr, Kassell NF, Kongable G, Germanson T, Truskowski L, Torner JC: Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med 1995, 23, 1007–1017.
  4. Bor-Seng-Shu E, de-Lima-Oliveira M, Teixeira MJ, Panerai RB: Predicting symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Neurosurgery 2011, 69(2), E501–502.
  5. Wartenberg KE, Schmidt M, Fernandez A, Frontera JA, Claassen J, Ostapkovich ND, Badjatia N, Palestrant D, Parra A, Mayer SA: Multiterritorial symptomatic vasospasm after subarachnoid hemorrhage: predictors, associated complications, and impact on outcome. In: International Stroke Conference: Feb 79, 2007, San Francisco. San Francisco, CA, 2007.
  6. Adams HP Jr, Kassell NF, Torner JC, Haley EC Jr: Predicting cerebral ischemia after aneurismal subarachnoid hemorrhage: influences of clinical condition, CT results, and antifibrinolytic therapy. A report of the Cooperative Aneurysm Study. Neurology 1987, 37, 1586–1591.
  7. Dehdashti AR, Mermillod B, Rufenacht DA, Reverdin A, de Tribolet N: Does treatment modality of intracranial ruptured aneurysms influence the incidence of cerebral vasospasm and clinical outcome? Cerebrovasc Dis 2004, 17, 53–60.
  8. Dorsch NW: Therapeutic approaches to vasospasm in subarachnoid hemorrhage. Curr Opin Crit Care 2002, 8, 128–133.
  9. Keller E, Krayenbuhl N, Bjeljac M, Yonekawa Y: Cerebral vasospasm: results of a structured multimodal treatment. Acta Neurochir Supp 2005, l94, 65–73.
  10. Mayberg MR, Batjer HH, Dacey RG Jr, Diringer M, Haley C, Heros RC, Sternau LL, Torner J, Adams HP Jr, Freinberg W, Thies W: guidelines for the management of aneurismal subarachnoid hemorrhage: a statement for health care professionals from a special writing group of the stroke council, American Heart Association. Stroke 1994, 25, 2315–2328.
  11. Sarrafzadeh AS, Haux D, Ludemann L, Amthauer H, Plotkin M, Kuchler I, Unterberg AW: Cerebral ischemia in aneurysmal subarachnoid hemorrhage: a correlative microdialysis-PET study. Stroke 2004, 35, 638–643.
  12. Vajkoczy P, Horn P, Thome C, Munch E, Schmiedek P: Regional cerebral blood flow monitoring in the diagnosis of delayed ischemia following aneurysmal subarachnoid hemorrhage. J Neurosurg 2003, 98, 1227–1234.
  13. Smith RR, Clower BR, Grotendorst GM, Yabuno N, Cruse JM: Arterial wall changes in early human vasospasm. Neurosurgery 1985, 16, 171–176.
  14. Macdonald RL, Weir BK: A review of hemoglobin and the pathogenesis of cerebral vasospasm. Stroke 1991, 22, 971–982.
  15. Borsody M, Burke A, Coplin W, Miller-Lotan R, Levy A: Haptoglobin and the development of cerebral artery vasospasm after subarachnoid hemorrhage. Neurology 2006, 66, 634–640.
  16. Suzuki H, Muramatsu M, Kojima T, Taki W: Intracranial heme metabolism and cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Stroke 2003, 34, 2796–2800.
  17. Fuwa I, Mayberg M, Gadjusek C, Harada T, Luo Z: Enhanced secretion of endothelin by endothelial cells in response to hemoglobin. Neurol Medico-chir 1993, 33, 739–743.
  18. Misra HP, Fridovich I: The generation of superoxide radical during the autoxidation of hemoglobin. J Biol Chem 1972, 247, 6960–6962.
  19. Rubanyi GM: Endothelium-derived relaxing and contracting factors. J Cell Biochem 1991, 46, 27–36.
  20. Claassen J, Bernardini GL, Kreiter K, Bates J, Du YE, Copeland D, Connolly ES, Mayer SA: Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after subarachnoid hemorrhage: the Fisher scale revisited. Stroke 2001, 32, 2012–2020.
  21. Fisher CM, Kistler JP, Davis JM: Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery 1980, 6, 1–9.
  22. Dorhout Mees SM, Molyneux AJ, Kerr RS, Algra A, Rinkel GJ: Timing of aneurysm treatment after subarachnoid hemorrhage: relationship with delayed cerebral ischemia and poor outcome. Stroke 2012, 43, 2126–2129.
  23. Qureshi AI, Sung GY, Suri MA, Straw RN, Guterman LR, Hopkins LN: Prognostic value and determinants of ultraearly angiographic vasospasm after aneurysmal subarachnoid hemorrhage. Neurosurgery 1999, 44, 967–973, discussion 973–974.
  24. de Oliveira JG, Beck J, Ulrich C, Rathert J, Raabe A, Seifert V: Comparison between clipping and coiling on the incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a systematic review and metaanalysis. Neurosurg Rev 2007, 30, 22–30.
  25. Gruber A, Ungersbock K, Reinprecht A, Czech T, Gross C, Bednar M, Richling B: Evaluation of cerebral vasospasm after early surgical and endovascular treatment of ruptured intracranial aneurysms. Neurosurgery 1998, 42, 258–267, discussion 267–268.
  26. Macdonald RL, Rosengart A, Huo D, Karrison T: Factors associated with the development of vasospasm after planned surgical treatment of aneurysmal subarachnoid hemorrhage. J Neurosurg 2003, 99, 644–652.
  27. Mocco J, Ransom ER, Komotar RJ, Mack WJ, Sergot PB, Albert SM, Connolly ES Jr: Racial differences in cerebral vasospasm: a systematic review of the literature. Neurosurgery 2006, 58, 305–314.
  28. Qureshi AI, Sung GY, Razumovsky AY, Lane K, Straw RN, Ulatowski JA: Early identification of patients at risk for symptomatic vasospasm after aneurysmal subarachnoid hemorrhage. Crit Care Med 2000, 28, 984–990.
  29. Roos Y, Rinkel G, Vermeulen M, Algra A, van Gijn J: Antifibrinolytic therapy for aneurysmal subarachnoid hemorrhage: a major update of a Cochrane review. Stroke 2003, 34, 2308–2309.
  30. Hop JW, Rinkel GJ, Algra A, van Gijn J: Initial loss of consciousness and risk of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. Stroke 1999, 30, 2268–2271.
  31. Juvela S, Siironen J, Kuhmonen J: Hyperglycemia, excess weight, and history of hypertension as risk factors for poor outcome and cerebral infarction after aneurysmal subarachnoid hemorrhage. J Neurosurg 2005, 102, 998–1003.
  32. Lasner TM, Weil RJ, Riina HA, King JT Jr, Zager EL, Raps EC, Flamm ES: Cigarette smoking-induced increase in the risk of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage. J Neurosurg 1997, 87, 381–384.
  33. Weir BK, Kongable GL, Kassell NF, Schultz JR, Truskowski LL, Sigrest A: Cigarette smoking as a cause of aneurysmal subarachnoid hemorrhage and risk for vasospasm: a report of the Cooperative Aneurysm Study. J Neurosurg 1998, 89, 405–411.
  34. Pickard JD, Murray GD, Illingworth R, Shaw MD, Teasdale GM, Foy PM, Humphrey PR, Lang DA, Nelson R, Richards P et al.: Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ 1989, 298, 636–642.
  35. Soppi V, Karamanakos PN, Koivisto T, Kurki MI, Vanninen R, Jaaskelainen JE, Rinne J: A randomized outcome study of enteral versus intravenous nimodipine in 171 patients after acute aneurysmal subarachnoid hemorrhage. World Neurosurg 2012, 78, 101–109.
  36. Petruk NF, West M, Mohr G, Weir BK, Benoit BG, Gentili F, Disney LB, Khan MI, Grace M, Holness RO et al.: Nimodipine treatment in poor-grade aneurysm patients. Results of a multicenter double-blind placebo-controlled trial. J Neurosurg 1988, 68, 505–517.
  37. Keyrouz SG, Diringer MN: Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage. Crit Care 2007, 11, 220.
  38. Rinkel GJ, Feign VL, Algra A, van den Bergh WM, Vermeulen M, van Gijn J: Calcium antagonist for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2005, CD000277.
  39. Karinen P, Koivukangas P, Ohnima A, Koivukangas J, Ohman J: Cost-effectiveness analysis of nimodipine treatment after aneurysmal subarachnoid hemorrhage and surgery. Neurosurgery 1999, 45, 780–784.
  40. Rinkel GJ, Klijn CJ: Prevention and treatment of medical and neurological complications in patients with aneurysmal subarachnoid haemorrhage. Pract Neurol 2009, 9, 195–209.
  41. Preacher KJ: Calculation for the chi-square test: An interactive calculation tool for chi-square tests of goodness of fit and independence [Computer software]. 2001. Available from http://www.quantpsy.org/chisq/chisq.htm.
  42. Lowry R: VassarStats: Website for Statistical Computation, Calculation for the Fisher exact probability test: An interactive calculation tool for Fisher exact probability test with Freeman-Halton extension [Computer software]. 2001–2010. Available from http://www.vassarstats.net/fisher2x3.html.
  43. van Gijn J, Kerr RS, Rinkel GJ: Subarachnoid haemorrhage. Lancet 2007, 369(9558), 306–318.
  44. Springer MV, Schmidt JM, Wartenberg KE, Frontera JA, Badjatia N, Mayer SA: Predictors of global cognitive impairment 1 year after subarachnoid hemorrhage. Neurosurgery 2009, 65, 1043–1050.
  45. Kaku Y, Yamashita K, Kokuzawa J, Hatsuda N, Andoh T: Treatment of ruptured cerebral aneurysms – clip and coil, not clip versus coil. Acta Neurochir Suppl 2010, 107, 9–13.
  46. Kim JH, Park IS, Park KB, Kang DH, Hwang SH: Intraarterial nimodipine infusion to treat symptomatic cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Korean Neurosurg Soc 2009, 46, 239–244.
  47. González-Pérez MI: Results of treatment of subarachnoid haemorrhage due to a ruptured cerebral aneurysm. Neurocirugia (Astur) 2006, 17, 433–439.
  48. Pearl JD, Macdonald RL: Vasospasm after aneurysmal subarachnoid hemorrhage: need for further study. Acta Neurochir Suppl 2008, 105, 207–210.
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