High Intracranial Pressure, Brain Herniation and Death in Cerebral Venous Thrombosis

Abstract

HomeStrokeVol. 37, No. 2High Intracranial Pressure, Brain Herniation and Death in Cerebral Venous Thrombosis Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBHigh Intracranial Pressure, Brain Herniation and Death in Cerebral Venous Thrombosis Axel Petzold, MD, PhD and Martin Smith, FRCA Axel PetzoldAxel Petzold The National Hospital for Neurology and Neurosurgery, Tavistock Intensive Care Unit, London, United Kingdom Search for more papers by this author and Martin SmithMartin Smith The National Hospital for Neurology and Neurosurgery, Tavistock Intensive Care Unit, London, United Kingdom Search for more papers by this author Originally published5 Jan 2006https://doi.org/10.1161/01.STR.0000199644.76930.dcStroke. 2006;37:331Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 5, 2006: Previous Version 1 To the Editor:Sir, the study by Canhao and colleagues made the important point that the most frequent cause of death in patients with cerebral venous thrombosis (CVT) is transtentorial herniation and that these patients may potentially have benefited from decompressive hemicraniectomy.1 We would like to corroborate this argument by providing evidence for a rise in intracranial pressure (ICP) preceding brain herniation and death in a patient with CVT.A 29-year-old pregnant woman who presented with confusion and vomiting was admitted to a district general hospital. A right-sided weakness developed within 2 days. A CT brain scan showed a left temporal hemorrhage without mass effect. Her Glasgow Coma Scale score dropped to 8/15; she was intubated and transferred to the neurocritical care unit at the National Hospital. A repeat CT demonstrated worsening of the hemorrhage with obliteration of the 3rd and 4th ventricles, and the diagnosis of a CVT was confirmed by magnetic resonance venography. At this point, the left pupil became fixed. An ICP bolt was inserted (opening pressure 50 mm Hg; Figure). ICP targeted management (propofol, fentanyl, midazolam, ventilation to maintain a pCO2 4.0 to 4.5 kPa and IV norepinephrine to main blood pressure) and anticoagulation with IV heparin were started. Because an ICP <20 mm Hg could not be maintained, paralysis and moderate hypothermia were initiated. Despite these measures ICP continued to rise. A treatment trial with thiopental to lower ICP failed. Both pupils became fixed and dilated on day 6 on ICU. Several intractable peaks of ICP (>60 mm Hg) were followed by development of diabetes insidipus necessitating treatment with desmopressin. At 8:00 am on the 7th day, periods of ventricular tachycardia and fibrillation started to appear leading to severe hemodynamic compromise and elevated ICP. The clinical diagnosis of brain stem herniation was made and treatment was demescalated after an informed discussion with the family took place. Download figureDownload PowerPointICP (diamonds), mean arterial pressure (squares) and cerebral perfusion pressure (dots) are shown over a 5-day period. The horizontal reference line (gray) indicates the upper reference limit for the ICP (20 mm Hg).Mortality in CVT has decreased over the last decades from 30% to 50% to ≈4.3% in the acute phase.1,2,3 There are occasional reports of decompressive hemicraniectomy performed successfully in patients in whom medical treatment failed.4 It is of note that all 3 patients in this report already showed signs of brain herniation at time of operation. The authors pointed out that indications for surgical intervention are almost completely lacking. The decision to proceed with surgery implies that treatment (heparin) needs to be discontinued. In an individual case this may be a difficult decision because of the arguably beneficial effect (small sample sizes and large confidence intervals).5 Furthermore, there is no guide toward the best timing for surgical intervention. Fixed and dilated pupils may be too late a sign and repeated brain imaging is logistically difficult in the critically ill patient. Continuous ICP and arterial blood pressure monitoring as performed in the present case provides important data at the bedside. There is a need to investigate whether decompressive hemicraniectomy would be of benefit in those patients in whom medical management of ICP fails.1 Canhao P, Ferro JM, Lindgren AG, Bousser MG, Stam J, Barinagarrementeria F; ISCVT Investigators. Causes and predictors of death in cerebral venous thrombosis. Stroke. 2005; 36: 1720–1725.LinkGoogle Scholar2 Stam J. Thrombosis of the cerebral veins and sinuses. New Eng J Med. 2005; 352: 1791–1798.CrossrefMedlineGoogle Scholar3 Ameri A, Bousser MG. Cerebral venous thrombosis. Neurol Clin. 1992; 10: 87–111.CrossrefMedlineGoogle Scholar4 Stefini R, Latronico N, Cornali C, Rasulo F, Bollati A. Emergent decompressive craniectomy in patients with fixed and dilated pupils due to cerebral venous and dural sinus thrombosis: a report of three cases. Neurosurgery. 1999; 45: 626–629.CrossrefMedlineGoogle Scholar5 Stam J, de Bruijn, SFTM, deVeber G. Anticoagulation for cerebral sinus thrombosis (Review). The Cochrane Database of Systematic Reviews. 2001; 4: CD002005.Google ScholarstrokeahaStrokeStrokeStroke0039-24991524-4628Lippincott Williams & WilkinsResponse:Canhão Patrícia, , MD and Ferro José M., , MD, PhD01022006We thank Petzold et al for illustrating with this case report the results of our study, regarding the causes of death in patients with cerebral vein and sinus thrombosis.1 Probably, the patient here presented could have been saved if decompressive craniectomy had been performed before fatal clinical deterioration occurred.We consider that the next step for evaluating the role of this intervention should be to carry out an international registry including cerebral vein and sinus thrombosis patients submitted to decompressive craniectomy. Previous Back to top Next FiguresReferencesRelatedDetailsCited By Petzold A (2022) Neuro-Ophthalmic Implications of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Related Infection and Vaccination, Asia-Pacific Journal of Ophthalmology, 10.1097/APO.0000000000000519, 11:2, (196-207) Rai P, Shivaprasad A, Tremont-Lukats I and Tummala S (2021) Central Nervous System Oncologic Emergency Medicine, 10.1007/978-3-030-67123-5_16, (207-223), . Lechanoine F, Janot K, Herbreteau D, Maldonado I and Velut S (2018) Surgical Thrombectomy Combined with Bilateral Decompressive Craniectomy in a Life-Threatening Case of Coma from Cerebral Venous Sinus Thrombosis: Case Report and Literature Review, World Neurosurgery, 10.1016/j.wneu.2018.09.083, 120, (485-489), Online publication date: 1-Dec-2018. 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Bousser M and Ferro J (2007) Cerebral venous thrombosis: an update, The Lancet Neurology, 10.1016/S1474-4422(07)70029-7, 6:2, (162-170), Online publication date: 1-Feb-2007. Anand S, Siddhartha W, Karnad D, Shrivastava M, Ghatge S and Limaye U (2016) Heparin or Local Thrombolysis in the Management of Cerebral Venous Sinus Thrombosis?, Interventional Neuroradiology, 10.1177/159101990601200207, 12:2, (131-140), Online publication date: 1-Jun-2006. February 2006Vol 37, Issue 2 Advertisement Article InformationMetrics https://doi.org/10.1161/01.STR.0000199644.76930.dcPMID: 16397171 Originally publishedJanuary 5, 2006 PDF download Advertisement