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Intraventricular hemorrhage in adults

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Opinion statement

  • Intraventricular hemorrhage (IVH) in adults usually occurs in the setting of aneurysmal subarachnoid hemorrhage or hypertension-related intracerebral hemorrhage. Thus, the underlying cause of IVH is apparent from history and radiographic findings. If the underlying cause of IVH is not apparent, additional studies, including cerebral angiography, magnetic resonance imaging, and toxicology screening, should be performed to identify etiologic agents that may alter management of IVH. Management of IVH is thus done amidst (and must be tempered by) the multiple pharmacologic, surgical, and critical care interventions directed toward the diagnosis and treatment of the underlying cause of IVH.

  • The most immediate threat to life posed by IVH is the development of acute obstructive hydrocephalus. If the hydrocephalus is contributing to a neurologic decline, it must be treated emergently with external ventricular drainage (EVD) through an intraventricular catheter (IVC). The patient with IVH should be evaluated and treated for deficient clotting function before an IVC is inserted. For this purpose, clotting function can be adequately assessed by prothrombin and partial thromboplastin times.

  • Insertion of an IVC may significantly lower intracranial pressure, increasing the transmural pressure difference across the wall of a ruptured cerebral aneurysm and precipitating rerupture of the aneurysm. Therefore, with IVH secondary to a ruptured cerebral aneurysm, it is advisable to delay treatment of hydrocephalus that is not contributing to a neurologic decline until the aneurysm is repaired.

  • Hydrocephalus contributing to significant neurologic decline in the setting of a ruptured aneurysm must be treated immediately despite the unprotected status of the aneurysm. Extreme diligence must be used to allow for the slow, controlled release of cerebrospinal fluid after IVC insertion. This will mitigate the effects of increasing the transmural pressure gradient across the wall of the ruptured aneurysm.

  • In the patient with a neurologic deficit who has IVH-related hydrocephalus and an associated intracerebral hemorrhage, it is best to assume that the hydrocephalus is a significant contributor to the deficit and that it should be treated with EVD. An IVH that is not causing hydrocephalus but is apparently occluding one or both foramina of Monro or the third ventricle should be treated with EVD because obstructive hydrocephalus may develop precipitously and, if unrecognized, may cause irreversible brain damage or death. An IVH that is not likely to cause hydrocephalus because of small volume relative to its location can be followed expectantly.

  • Intraventricular injections of thrombolytic agents through an IVC is a treatment option that may be considered in all patients with IVH that is causing or threatening to cause obstructive hydrocephalus. Unrepaired cerebral aneurysms, untreated cerebral arteriovenous malformations, and clotting disorders are contraindications for this intervention.

  • The surgical evacuation of IVH has a role only in very rare cases in which the IVH is causing a significant mass effect independent of hydrocephalus and associated intraparenchymal brain hemorrhage.

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References and Recommended Reading

  1. Daverat P, Castel JP, Dartigues JF, et al.: Death and functional outcome after spontaneous intracerebral hemorrhage. A prospective study of 166 cases using multivariate analysis. Stroke 1991, 22:1–6.

    PubMed  CAS  Google Scholar 

  2. Adams HP, Torner JC, Kassell NF: Intraventricular hemorrhage among patients with recently ruptured aneurysms: a report of the cooperative aneurysm study [abstract]. Stroke 1992, 23:140.

    Google Scholar 

  3. Broderick JP, Brott T, Tomsick T, et al.: Intracerebral hemorrhage more than twice as common as subarachnoid hemorrhage. J Neurosurg 1993, 78:188–191.

    PubMed  CAS  Google Scholar 

  4. Lisk DR, Pasteur W, Rhoades H, et al.: Early presentation of hemispheric intracerebral hemorrhage: prediction of outcome and guidelines for treatment allocation. Neurology 1994, 44:133–139.

    PubMed  CAS  Google Scholar 

  5. Tuhrim S, Dambrosia JM, Price TR, et al.: Intracerebral hemorrhage: external validation and extension of a model for prediction of 30-day survival. Ann Neurol 1991, 29:658–663.

    Article  PubMed  CAS  Google Scholar 

  6. Tuhrim S, Horowitz DR, Sacher M, et al.: Validation and comparison of models predicting intracerebral hemorrhage survival. Crit Care Med 1995, 23:950–954. Provides an easy-to-use but powerful model for predicting risk of mortality following intracerebral hemorrhage.

    Article  PubMed  CAS  Google Scholar 

  7. Young WB, Lee KP, Pessin MS, et al.: Prognostic significance of ventricular blood in supratentorial hemorrhage: a volumetric study. Neurology 1990, 40:616–619.

    PubMed  CAS  Google Scholar 

  8. Paramore CG, Turner DA: Relative risks of ventriculostomy infection and morbidity. Acta Neurochir (Wien) 1994, 127:79–84.

    Article  CAS  Google Scholar 

  9. Holloway KL, Barnes T, Choi S, et al.: Ventriculostomy infections: the effect of monitoring duration and catheter exchange in 84 patients. J Neurosurg 1996, 85:419–424.

    Article  PubMed  CAS  Google Scholar 

  10. Schultz M, Moore K, Foote A: Bacterial ventriculitis and duration of ventriculostomy catheter insertion. J Neurosci Nurs 1993, 25:158–164.

    PubMed  CAS  Google Scholar 

  11. Bullock R, Chesnut RM, Clifton G, et al.: Guidelines for the Management of Severe Head Injury. Park Ridge, IL: The American Association of Neurological Surgeons; 1995. The best available overview of the scientific basis for current clinical management of severe head injury. Highly recommended for all neurosurgeons and critical care neurologists.

    Google Scholar 

  12. Pang D, Sclabassi RJ, Horton JA: Lysis of intraventricular blood clot with urokinase in a canine model. Part 3: Effects of intraventricular urokinase on clot lysis and post-hemorrhagic hydrocephalus. Neurosurgery 1986, 19:553–572. An elegant study that remains the best animal model demonstrating the efficacy of intraventricular thrombolysis.

    Article  PubMed  CAS  Google Scholar 

  13. Findlay JM, Grace MG, Weir BK: Treatment of intraventricular hemorrhage with tissue plasminogen activator. Neurosurgery 1993, 32:941–947.

    Article  PubMed  CAS  Google Scholar 

  14. Findlay JM, Weir BK, Stollery DE: Lysis of intraventricular hematoma with tissue plasminogen activator. J Neurosurg 1991, 74:803–807.

    PubMed  CAS  Google Scholar 

  15. Mayfrank L, Lippitz B, Groth M, et al.: Effect of recombinant tissue plasminogen activator on clot lysis and ventricular dilatation in the treatment of severe intraventricular hemorrhage. Acta Neurochir (Wien) 1993, 122:32–38.

    Article  CAS  Google Scholar 

  16. Shen PH, Matsuoka Y, Kawajiri K, et al.: Treatment of intraventricular hemorrhage using urokinase. Neurol Med Chir (Tokyo) 1990, 30:329–333.

    CAS  Google Scholar 

  17. Todo T, Usui M, Takakura K: Treatment of severe intraventricular hemorrhage by intraventricular infusion of urokinase. J Neurosurg 1991, 74:81–86.

    Article  PubMed  CAS  Google Scholar 

  18. Rohde V, Schaller C, Hassler W: Intraventricular recombinant tissue plasminogen activator for lysis of intraventricular hemorrhage. J Neurol Neurosurg Psychiatry 1995, 58:447–451. A recent clinical series of patients treated with intraventricular thrombolysis.

    PubMed  CAS  Google Scholar 

  19. Akdemir H, Selcuklu A, Pasaoglu A, et al.: Treatment of severe intraventricular hemorrhage by intraventricular infusion of urokinase. Neurosurg Rev 1995, 18:95–100.

    Article  PubMed  CAS  Google Scholar 

  20. Zabramski JM, Spetzler RF, Lee KS, et al.: Phase I trial of tissue plasminogen activator for the prevention of vasospasm in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg 1991, 75:189–196.

    PubMed  CAS  Google Scholar 

  21. Mizoi K, Yoshimoto T, Takahashi A, et al.: Prospective study on the prevention of cerebral vasospasm by intrathecal fibrinolytic therapy with tissue-type plasminogen activator. J Neurosurg 1993, 78:430–437.

    PubMed  CAS  Google Scholar 

  22. Sasaki T, Ohta T, Kikuch H, et al.: Preliminary clinical trial of intrathecal rt-PA (TD-2061) for the prevention of cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. No To Shinkei 1992, 44:1001–1008.

    PubMed  CAS  Google Scholar 

  23. Usui M, Saito N, Hoya K, et al.: Vasospasm prevention with postoperative intrathecal thrombolytic therapy: a retrospective comparison of urokinase, tissue plasminogen activator, and cisternal drainage alone. Neurosurgery 1994, 34:235–244.

    Article  PubMed  CAS  Google Scholar 

  24. Findlay JM, Kassell NF, Weir BKA, et al.: A randomized trial of intraoperative, intracisternal tissue plasminogen activator for the prevention of vasospasm. Neurosurgery 1995, 37:168–176. A well-designed multicenter randomized trial of intracisternal thrombolysis evaluating the efficacy of delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage.

    Article  PubMed  CAS  Google Scholar 

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Naff, N.J. Intraventricular hemorrhage in adults. Curr Treat Options Neurol 1, 173–178 (1999). https://doi.org/10.1007/s11940-999-0001-0

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  • DOI: https://doi.org/10.1007/s11940-999-0001-0

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