The clinical spectrum of hemorrhagic infarction.

Abstract

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...

Cerebrovascular disease in Saudi Arabia.

“…6 Cerebral infarct was defined as a hypodense lesion on brain CT, with a topography corresponding to the territory of a cerebral vessel as defined by Damasio 7 and Bories et al 8 Hemorrhagic infarct was identified as an area of low attenuation conforming to a vascular territory within which a single nonhomogeneous area or multiple areas of high attenuation were present with characteristic blood density. 9 Lacunar infarct was defined as a constellation of clinical symptoms and signs showing a high correlation with small, deep, rounded infarcts due to a single penetrating small arterial occlusion as confirmed by CT. 10 We recognized the four lacunar syndromes pure motor stroke, pure sensory stroke, sensorimotor stroke, and ataxic hemiparesis. Border zone infarcts were those occurring in border zones between two main artery territories as defined by Bogousslavsky and Regli, 11 Damasio, 7 and Bories et al 8 Cerebral hemorrhage was diagnosed as a hyperdense area on brain CT with or without intraventricular leak and classified as ganglionic when occurring in the basal ganglion (thalamic, lenticular, or caudate) or lobar when located in the frontal, temporal, parietal, or occipital regions.…”

Early Hemorrhagic Transformation of Brain Infarction: Rate, Predictive Factors, and Influence on Clinical Outcome

“…[2][3][4][5][6][7][8][9][10][11] Furthermore, most of the information on the effect of early HT on clinical outcomes derives from studies on thrombolysis for ischemic stroke, [12][13][14][15][16] and data on early HT in patients not receiving thrombolysis mainly derives from patients randomized to placebo in the thrombolysis trials. 17,18 The aims of this prospective study in consecutive patients were therefore to assess: (1) the rate of early HT in patients admitted for ischemic stroke, (2) the correlation between early HT and functional outcome at 3 months, and (3) the risk factors for early HT.…”

Bilateral intracerebral hemorrhage following CPR

“…These conditions may lead to intracerebral bleeding due to hemorrhagic transformation of the ischemic area in prolonged CPR patients, similar to developing hemorrhage in patients with embolic stroke. (8)(9)(10)(11) There have been several theories on the mechanism of hemorrhagic infarction, but in this particular patient, whose circulatory arrest time was prolonged over 30 minutes, the restitution of blood flow and subsequent development of coagulopathy may have resulted in hemorrhagic transformation of the ischemic infarction. Furthermore, it has been widely stated in the literature that the peak occurrence of hemorrhagic cerebral infarction is in the first week after stroke.…”

“…Furthermore, it has been widely stated in the literature that the peak occurrence of hemorrhagic cerebral infarction is in the first week after stroke. (11,12) Therefore, in this patient, the most appropriate mechanism may be the hemorrhagic transformation of brain infarction, which was due to global ischemia following prolonged CPR. Another possibility is that delayed hyperemia occurred during the post-cardiac arrest period.…”