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ARTICLES: S. M. Davis, J. Broderick, M. Hennerici, N. C. Brun, M. N. Diringer, S. A. Mayer, K. Begtrup, T. Steiner for the Recombinant Activated Factor VII Intracerebral Hemorrhage Trial Investigators Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage Neurology 2006; 66: 1175-1181 [Abstract] [Full text] [PDF]

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Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage

Gregory Y Chang   (20 July 2006)

Reply from the Authors

Stephen M Davis, Stephen M Davis, Joseph Broderick, Michael Hennerici, Nikolai C Brun, Michael N Diringer,Stephan A Mayer, Kamilla Begtrup, Thorsten Steiner   (13 July 2006)

Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage 20 July 2006
Gregory Y Chang, University of California at Irvine Dept of Neurology, Bldg 55, Rm 121 101 The City Drive, South Orange, CA 92868 Send Correspondence to journal: Re: Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage gychang{at}operamail.com Gregory Y Chang	I read with interest the article by Davis et al [1] in which they noted the hematoma growth within 24 hours as the most common determinant of subsequent mortality and morbidity in 218 prospectively followed patients. A surprisingly high proportion of patients (72%) demonstrated measurable hematoma enlargement. The following case illustrates that the growth of perihematoma edema rather than the enlarging hemorrhage may also be causative. A 42-year old chronically hypertensive woman was awakened in the middle of night with severe headache followed by stupor. She was intubated in the emergency room. Initial examination revealed eye opening with mild left gaze preference and left limb withdrawal only from a painful stimulus. Pupils were midsize and reactive. Emergent CT scan, 3 hours after the symptom onset, showed a left striatocapsular hemorrhage with a rim of edema. (Figure 1A) Hemorrhage measured 4.8x2.9cm. Six mm of maximal midline shift was noted. Mannitol infusion was started. Next day both pupils became unreactive at 2.5mm with otherwise intact brainstem reflexes. Repeat CT scan, now 30 hours after the ictus, showed the hemorrhage did not enlarge but the perilesional edema was more conspicuous. (Figure 1B) Midline shift worsened to 10 mm. Ventriculostomy was inserted with normal intracranial pressure reading of 8mm Hg. (normal <15 mm) On the fourth hospital day, both pupils remained unreactive but now asymmetric with left at 4mm, and right at 2mm. Follow up CT now showed worsening of midline shift to 15mm without expansion of hemorrhage. (Figure C) On the 10th hospital day, pupils were equal in size and sluggishly reactive. On the 12th day, following successful extubation a day earlier, she expired. Along with hemorrhage expansion, perihematoma edema enlargement may also result in subsequent clinical deterioration in many patients with intracerebral hemorrhages. [2] Severity of midline shift mirrored clinical change this case, but as Papo et al [3] noted, intracranial pressure measurement may not correlate. This case reflects difficulties in treatment strategy whether in expanding hemorrhage or perilesional edema. Figure References 1. Davis SM, Broderick J, Hennerici M, et al. Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage. Neurology 2005;66:1175-1181 2. Mayer SA, Sacco RL, Shi T, Mohr JP. Neurologic deterioration in noncomatose patients with supratentorial intracerebral hemorrhage. Neurology 1994;44:1379-1384 3. Papo I, Janny P, Caruselli G, Colnet G, Luomgo A. Intracranial pressure time course in primary intracranial hemorrhage. Neurosurgery 1979;4:504-511. Disclosure: The author reports no conflicts of interest.
Reply from the Authors 13 July 2006
Stephen M Davis, Royal Melbourne Hospital and University of Melbourne Department of Neurology, Grattan St, Parkville, Victoria, Australia 3050, Stephen M Davis, Joseph Broderick, Michael Hennerici, Nikolai C Brun, Michael N Diringer,Stephan A Mayer, Kamilla Begtrup, Thorsten Steiner Send Correspondence to journal: Re: Reply from the Authors stephen.davis{at}mh.org.au Stephen M Davis, et al.	We thank Dr Chang for his letter. The aim of our paper was to demonstrate that hematoma expansion is a significant, independent predictor of adverse outcomes after intracerebral hemorrhage (ICH), over and above established baseline prognostic indicators. [1] We agree that, in addition to hematoma expansion, the development of edema is an important cause of subsequent clinical deterioration following ICH. These pathophysiological sequelae are likely to be closely related. Using CT, there is a correlation between hematoma volume and the extent of absolute perilesional edema, although no correlation between baseline relative edema volume and subsequent hematoma growth was shown in one study. [4] Using more sensitive MRI measures, Butcher at al showed in a multivariate analysis that the volume of edema on MRI was highly correlated with the volume of hematoma on CT. Other determinants of edema included the time to MRI and increased perihematomal rADC values. [5] This study indicated that perilesional edema is associated with enhanced diffusion of water rather than ischemia, and hence vasogenic in origin. [5] Reinforcing this close association, we reported that recombinant activated factor VII (rFVIIa) reduced not only hematoma growth at 24 hours (the primary endpoint of our proof of concept study), but also the total lesion volume at 72 hours, including the volume of ICH, intraventricular hemorrhage and edema. [6] There was also a dose-response relationship. A more detailed analysis of the effects of rFVIIa on perihematomal edema will be reported by the investigators. References 4. Gebel JM Jr, Jauch EC, Brott TG, et al. Natural history of perihematomal edema in patients with hyperacute spontaneous intracerebral hemorrhage. Stroke 2002;33:2631-2635. 5. Butcher KS, Baird TA, MacGregor L, Desmond PM, Tress BM, Davis SM. Peri-hematomal edema in primary intracerebral hemorrhage is plasma derived. Stroke 2004;35:1879-1885. 6. Mayer SA, Brun NC, Begtrup K et al for the Recombinant Activated Factor VII Intracerebral Hemorrhage Trial Investigators. Recombinant Activated Factor VII for Acute Intracerebral Hemorrhage. N Engl J Med 2005;352:777-785. Disclosure: The authors report no conflicts of interest.