Cerebrospinal Fluid in Cerebral Hemorrhage and Infarction

Lee, Myoung C.; Heaney, Lois M.; Jacobson, Ronald L.; Klassen, Arthur C.

doi:10.1161/01.str.6.6.638

Cited by 33 publications

(23 citation statements)

References 7 publications

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“…1027 Since red cell counts less than 1,000 may result in clear fluid, attention to the number of red cells may be a more sensitive discriminator. Lee et al 26 found a 26% incidence of absent red cells in HI. Although none of our patients with HI had absent red cells, of eleven spinal fluid examination only three had numbers sufficiently high to be observed as bloody in appearance.…”

Section: Discussionmentioning

confidence: 95%

“…In one autopsy series, 75% of cases with intracerebral hemorrhage, 10% of cases with HI, and no cases with ischemic infarction who had lumbar punctures showed grossly bloody or xanthochromic fluid. 26 In studies comparing CT scan with lumbar puncture in the diagnosis of HI, 10 to 17% of patients with HI on CT had apparently bloody or xanthochromic fluid. 1027 Since red cell counts less than 1,000 may result in clear fluid, attention to the number of red cells may be a more sensitive discriminator.…”

Section: Discussionmentioning

confidence: 99%

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The clinical spectrum of hemorrhagic infarction.

Ott¹,

Zamani²,

Kleefield³

et al. 1986

Stroke

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SUMMARYThe hospital records and head CT scans of 44 patients with hemorrhagic infarction were retrospectively analyzed. The majority of cases (73%) were embolic or possibly embolic In etiology, and 55% were not associated with anticoagulant therapy. Adverse prognosis was most clearly related to infarct size, underlying systemic illness, and symptomatic hemorrhage. Of the nineteen patients hi whom serial CT scans documented conversion from bland to hemorrhagic infarction, 12 exhibited no clinical worsening at the tune that hemorrhagic infarction was observed; the remaining seven, all of whom worsened, were receiving anticoagulant therapy at the tune of documented conversion. Fourteen patients hi whom anticoagulant therapy was used despite the findings of hemorrhagic infarction remained stable or improved during bospitalization. Stroke Vol 17, No 4, 1986HEMORRHAGIC INFARCTION (HI) has long been recognized as a potential complication of embolic stroke. Fisher and Adams postulated that downstream migration of the embolus after its initial impact leads to extravasation of blood via reflow into damaged vessels of the proximally infarcted zone. 1The exact role of anticoagulants in the causation of hemorrhage into infarcted brain tissue remains unknown. Moreover, recent studies have emphasized the efficacy of early anticoagulation (AC) in the prevention of recurrent embolic stroke. Serial CT scanning allows direct observation of the effect of AC on the evolution of embolic infarcts.We have retrospectively analyzed our experience with patients in whom the diagnosis of HI was made by CT during a period of two years. The study sought to clarify the roles of anticoagulation and embolism in producing HI and to explore the clinical significance of hemorrhagic transformation of bland infarction. MethodsThe CT scan reports of all patients studied during the years 1983 and 1984 in two tertiary hospitals were surveyed, and the hospital records reviewed for all cases in whom the diagnosis of HI was made. All scans were reviewed again by one of two neuroradiologists without knowledge of the clinical picture and a neurologist to verify the original diagnosis and tabulate the characteristics of each HI.The radiologic diagnosis of HI was defined as an area of low attenuation conforming to a vascular territory within which a single non-homogeneous area or multiple areas of high attenuation were present with characteristic blood density. Infarct size was described as large if the entire vascular territory of a major vessel (anterior, middle, or posterior cerebral artery) was involved; moderate if a major division of that territory was involved; and small if only a minor branch territory was involved. The extent of hemorrhage was described as severe if greater than 50% of the infarct was of blood density; mild if having the appearance of scattered punctate hemorrhages; and moderate for those of intermediate degree.Cases were classified as "probably cardiac embolism" if: 1) the symptoms appeared suddenly and rapidly achieved maximal inte...

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

The clinical spectrum of hemorrhagic infarction.

Ott¹,

Zamani²,

Kleefield³

et al. 1986

Stroke

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“…Clinical studies have provided evidence that supports the role of leukocytes in ICH. Early studies by Molle (1942) and Lee et al (1975) showed that leukocyte counts in cerebrospinal fluid, especially the polymorphonuclear neutrophilic leukocyte counts, were frequently elevated after ICH. Infants with intraventricular hemorrhage also have greater total numbers of leukocytes than infants without On day 3 after ICH induction in mice, infiltrated neutrophils (arrowheads, MPO + , A) and mature macrophages (arrowheads, F4/80 + , C) can be seen near the hematoma.…”

Section: Leukocytesmentioning

confidence: 99%

Inflammation after Intracerebral Hemorrhage

Wang

Doré

2007

J Cereb Blood Flow Metab

574

609

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Intracerebral hemorrhage (ICH) is a devastating clinical event without effective therapies. Increasing evidence suggests that inflammatory mechanisms are involved in the progression of ICH-induced brain injury. Inflammation is mediated by cellular components, such as leukocytes and microglia, and molecular components, including prostaglandins, chemokines, cytokines, extracellular proteases, and reactive oxygen species. Better understanding of the role of the ICH-induced inflammatory response and its potential for modulation might have profound implications for patient treatment. In this review, a summary of the available literature on the inflammatory responses after ICH is presented along with discussion of some of the emerging opportunities for potential therapeutic strategies. In the near future, additional strategies that target inflammation could offer exciting new promise in the therapeutic approach to ICH.

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“…16 -53~M Although hemorrhagic infarction is frequently noted at autopsy in patients with cerebral embolism it is difficult to detect clinically. CT scan and lumbar puncture may not be helpful in establishing the presence of hemorrhagic infarction, 31 -39 -59 -61 particularly when these procedures are done early, before the hemorrhagic aspect of the infarct has time to develop. The hemorrhagic component of the infarction probably evolves over several days following the onset of the stroke 36 - 37 and it follows that the diagnostic value of lumbar puncture and CT scan would be enhanced if they were obtained after a delay of a few days.…”

Section: Therapeutic Considerationsmentioning

confidence: 99%

Anticoagulant-related hemorrhage in acute cerebral embolism.

Shields¹,

Laureno²,

Lachman³

et al. 1984

Stroke

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Five patients with nonseptic cerebral embolism of cardiac origin are reported in whom early anticoagulant therapy resulted in clinical deterioration or death from frank hemorrhage into the acute infarct. In each patient an initial CT scan excluded the presence of intracerebral hemorrhage and a second CT scan, after clinical deterioration had occurred, documented frank hemorrhage into the infarcted zone. All five patients had large infarctions in the right middle cerebral artery territory and three patients were mildly hypertensive. Four patients received heparin within 36 hours of their stroke and one was on warfarin at time of the embolism. Clinical deterioration occurred after intervals of several hours (2 cases), 5-6 days (2 cases) and 30 days (1 case). In only 2 patients was anticoagulant activity excessive at time of clinical deterioration. This report illustrates the danger of early anticoagulant therapy of acute nonseptic cerebral embolism, particularly in the setting of large infarction.

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Cerebrospinal Fluid in Cerebral Hemorrhage and Infarction

Cited by 33 publications

References 7 publications

The clinical spectrum of hemorrhagic infarction.

The clinical spectrum of hemorrhagic infarction.

Inflammation after Intracerebral Hemorrhage

Anticoagulant-related hemorrhage in acute cerebral embolism.

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