Size Of Hemorrhage Research Articles

Determinants of 30-day mortality of spontaneous intracerebral hemorrhage in Pakistan

BACKGROUND The present study was undertaken to evaluate the determinants of acute (30-day) mortality after spontaneous intracerebral hemorrhage (ICH) in a developing country setting, and to compare these findings with those available from studies conducted in the West. METHODS Medical records of 146 patients admitted to a major tertiary hospital in Karachi, Pakistan between 1990 and 1991 with a diagnosis of spontaneous ICH were reviewed. The level and intensity of care provided to these patients was similar to that available at modern neurosurgical centers. The salient prognostic indicators that were studied included hypertension, pulse pressure, GCS score, neurologic deficits, and CT-scan predictors including site, size, and intraventricular spread of hemorrhage. These data were used to determine independent predictors of 30-day mortality by univariate and multivariate analysis. Additionally, 30-day survival probabilities for these outcome predictors were also computed. RESULTS The 30-day mortality after spontaneous ICH was 39.7%. Two-thirds of the patients had a history of hypertension. The important clinical predictors at the multivariate level included GCS score ≤8 and progressive increase in pulse pressure. The CT scan predictors included intraventricular spread of hemorrhage, ventricular enlargement, and size of the bleed. Location of the lesion did not appear to significantly influence mortality. Survival analysis showed a large clustering of deaths within the first 72 hours of hospitalization. CONCLUSIONS The 30-day mortality rate and prognostic predictors for spontaneous intracerebral hemorrhage were found to be similar to those reported in the Western hemisphere. However, the correlation of incremental increase in pulse pressure with deteriorating prognosis was a new and significant finding.

Development and Pathophysiological Basis of Thrombolytic Therapy in Acute Myocardial Infarction: Part III, 1981–1985 Registries of Intracoronary Thrombolytic Therapy and Experimental Reperfusion Studies

The angiographic results of intracoronary thrombolysis were correlated with various outcome parameters in three registries. The West German Registry (n = 232) showed that mortality and improvement of left ventricular function were related to recanalization and prevention of reocclusion. This registry became the core database for the Food and Drug Administration (FDA) approval of thrombolytic agents for myocardial infarction in 1982. The European Registry (n = 414) analyzed changes in left ventricular ejection fraction further. A continuous model suggested that the functional benefit of reperfusion decreases rapidly and in a nonlinear fashion with delays in treatment during the first 3 hours. Reperfusion after > 6 hours was still associated with a significant benefit, which appeared to be related to collateral flow to the infarct zone. Myocardial salvage in experimental reperfusion studies and the reperfusion injury controversy are reviewed. In experimental studies performed by our group, it was found that thrombolytic agents did not exacerbate myocardial hemorrhage or increase infarct size. The Goettingen Registry (n = 152) demonstrated that reperfusion resulted in a steeper slope of the regression line between infarct size determined by ventriculography and cumulative serial creatine kinase release. Furthermore, reperfusion was associated with transient loss of R waves and transient development of Q waves. The implications of these findings regarding the reperfusion injury controversy and assessment of infarct size are discussed. Other analyses of the Goettingen data found that flow patterns to the infarct zone at preintervention angiography correlated with the duration of angina pectoris, incidence of antianginal therapy, and baseline ejection fraction. Assessment of the reliability of the admission ECG showed that half of the patients with infarction due to occlusion of the circumflex artery lacked diagnostic changes. The Goettingen Registery followed the first group of 70 patients ever treated with intracoronary thrombolytic therapy for 3 years. Mortality was low by the standards of the time. Reperfusion was associated with sustained improvement of left ventricular function and often dramatic clinical stabilization not seen before.

Responses of hepatic TNF-alpha mRNA to repeated hemorrhage in the conscious rat.

Trauma victims may suffer from repeated hemorrhage, but responses of cytokines to it have not been described. To study this question, we first detected the time course of changes in serum tumor necrosis factor (TNF) activity and hepatic TNF-alpha mRNA by cytotoxicity against L929 cells and by reverse transcription (RT) and polymerase chain reaction (PCR), respectively, after different sizes of hemorrhage (10-20 ml/kg) with chronically cannulated rats. Then we examined the changes in TNF-alpha mRNA when two sequential 10 ml/kg hemorrhages were performed. TNF activity showed no significant increases after either size of hemorrhage. At mRNA level, both 15 ml/kg and 20 ml/kg hemorrhages induced significant increases after hemorrhage, whereas a 10 ml/kg hemorrhage did not. When the 10 ml/kg hemorrhage was repeated 24 h later, however, TNF-alpha mRNA showed a significant increase. There were no significant differences in blood pressure and heart rate after single and repeated 10 ml/kg hemorrhage. This potentiation persisted for >/=48 h. These results show that responses of hepatic TNF-alpha mRNA are augmented when moderate hemorrhage is repeated.

Acute vasoconstriction after subarachnoid hemorrhage.

Decreased cerebral blood flow (CBF) and cerebral ischemia occurring immediately after subarachnoid hemorrhage (SAH) may be caused by acute microvascular constriction. However, CBF can also be influenced by changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The goal of these experiments was to assess the significance of acute vasoconstriction after SAH and its relationship to changes in CBF, ICP, CPP, and extracellular glutamate concentrations. Three experiments were performed using the endovascular filament technique to produce SAH. In the first experiment, CBF, ICP, and CPP were measured for 60 minutes after SAH (n = 21) and were correlated with the 24-hour mortality rate. In the second experiment, rats undergoing SAH (n = 23) or a sham procedure (n = 7) were perfused 60 minutes after SAH for measurement of the circumference and wall thickness of the internal carotid and anterior cerebral arteries and correlation with CBF, ICP, and CPP. In the third experiment (n = 11), extracellular glutamate concentrations determined by hippocampal and cortical microdialysis and high performance liquid chromatography were correlated with physiological changes. CBF reductions to less than 40% of baseline for 60 minutes after SAH predicted 24-hour mortality with 100% accuracy and were used to define "lethal" SAH. In contrast, ICP and CPP 60 minutes after SAH were not correlated with the mortality rate. The vascular circumference was significantly smaller in lethal than in sublethal SAH or sham-operated rats (P < 0.001). Vessel measurements were correlated with both CBF and hemorrhage size (P < 0.01). Extracellular glutamate concentration increased to 600% of baseline after lethal SAH in both hippocampus and cortex and was inversely correlated with CBF (r = 0.9, P < 0.001) but did not increase after sublethal SAH. Acute vasoconstriction after SAH occurs independently of changes in ICP and CPP and is associated with decreased CBF, larger hemorrhage size, persistent elevations of extracellular glutamate, and poor outcome. Acute vasoconstriction seems to contribute directly to ischemic brain injury after SAH. Further evaluations of pharmacological agents with the potential to reverse acute vasoconstriction may increase CBF and improve outcome.

Morbilidad de la hemorragia intracerebral

Intracerebral hemorrhage (HIC) represents 10-30% of all stroke. Epidemiological studies have shown factors associated with its high mortality, but those which might lead to lower morbidity are little known. To find the factors which may influence the functional state of a series of patients with intracerebral hemorrhage. We made a prospective study of 203 patients with intracerebral hemorrhage. We recorded vascular risk factors, arterial blood pressure, laboratory and neuroimaging parameters obtained on admission. The functional condition when discharged from hospital was evaluated on the Rankin Scale, in three categories: independent (Rankin 0-1), partially dependent (Rankin 2-3) and totally dependent patients (Rankin 4-5). There was a 23.2% death rate. Of the 156 patients who survived, at the time of hospital discharge 35.8% had a score of 0-1, 50.6% a score of 2-3 and 13.4% a score of 4-5 on the Rankin Scale. Age (p < 0.005), hyperglycaemia (p < 0.05) and size of hemorrhage (p < 0.05) were associated with increased morbidity. The functional condition on hospital discharge was better in younger patients with lower levels of glycemia on admission and smaller hematomas on CT.

Subretinal hemorrhages in proliferative diabetic retinopathy.

To describe the clinical features of patients with advanced proliferative diabetic retinopathy who underwent vitrectomy and were found to have subretinal hemorrhages. The authors conducted a retrospective study of 49 patients with complications of proliferative diabetic retinopathy requiring pars plana vitrectomy and demonstrating the presence of subretinal hemorrhage. Preoperative, intraoperative, and postoperative clinical characteristics were evaluated. Patients were observed for a minimum of 6 months. The location, size, and clearance of subretinal hemorrhages revealed wide variation. Forty-two patients had focal subretinal hemorrhages, and 14 patients within this group had submacular hemorrhages. A retinal break was observed in 15 patients (31%). Only one patient required drainage of the subretinal hemorrhage to achieve retinal reattachment. Vitreous surgery resulted in 59% of patients achieving a visual acuity > or = 5/200. Seventy-nine percent had stable or improved vision, whereas 20% had worse vision after surgery. Subretinal hemorrhages appear to be an uncommon feature associated with long-term, advanced proliferative diabetic retinopathy and portend a guarded visual prognosis. These hemorrhages may occur spontaneously in previously untreated eyes and are often unsuspected until observed at the time of vitreous surgery. In general, removal of subretinal hemorrhages was not necessary to achieve macular anatomic attachment, and most patients experienced improved visual function after surgery. Diabetic subretinal hemorrhages may indicate a retinal break, and, therefore, careful ophthalmic inspection should be performed in these patients.

Factors predicting failure of endoscopic injection therapy in bleeding duodenal ulcer

Background: The aim of this study was to assess the factors that may cause failure of endoscopic injection in patients bleeding from a duodenal ulcer.Methods: One hundred twenty patients admitted for a bleeding duodenal ulcer with active arterial hemorrhage or a nonbleeding visible vessel were included.Results: Endoscopic injection was not feasible in 14 of 120 (11.6%) patients because of inaccessibility or massive hemorrhage. The remaining 106 patients underwent endoscopic therapy by injection of adrenaline and polidocanol. The efficacy (achievement of definitive hemostasis) of endoscopy therapy was 83% (88 of 106). Univariate analysis showed that failure of endoscopic injection was related to age, presence of shock, ulcer size greater than 2 cm, and hemoglobin level. Multivariate analysis showed that ulcer size greater than 2 cm ( p = 0.005) and the presence of shock ( p = 0.03) were factors predictive of endoscopic treatment failure. Failure to achieve hemostasis ( p < 0.001) and poor physical status measured by American Society of Anesthesiology classification ( p = 0.02) were significantly related to mortality.Conclusions: Ulcer size and severity of hemorrhage are predictive of endoscopic injection failure in patients bleeding from high-risk duodenal ulcers. Survival is determined by clinical status and associated diseases. (Gastrointest Endosc 1996;43:111-6.)

Fetomaternal hemorrhage following funipuncture: Increase in severity of maternal red‐cell alloimmunization

To determine the prevalence of fetomaternal transplacental hemorrhage after funipuncture and its effect on maternal red-cell alloantibody levels.The prevalence and size of transplacental hemorrhages at the Health Sciences Centre were studied in two groups of patients: 174 women who were not alloimmunized or were carrying fetuses whose red cells were negative for the antigen to which they were immunized, and 122 women who were alloimmunized and carrying fetuses whose red cells were positive for the antigen to which they were immunized. In the alloimmunized group with affected fetuses, we surveyed the incidence of maternal antibody increase in titer by two or more doubling dilutions and the Rh(D) antibody increase (in microgram/mL of serum) of more than 50% after funipuncture.One hundred of the 174 women (57.5%) in the nonimmunized group and 69 of the 122 women (56.6%) in the immunized group had evidence of transplacental hemorrhages ranging in volume from 0.03 mL to greater than 5 mL of fetal red blood cells. In the latter group, antibody titer increases of 2 to 9 and doubling dilutions occurred in 37 of 74 women (50%) in whom such measurements were carried out. Increases of anti-D exceeding 50% occurred in 44 of 53 women (83%) in whom quantitative measurements were assayed.Funipuncture carries a high risk of fetal transplacental hemorrhage. In the immunized woman carrying an antigen-positive fetus, this will increase the level of her antibody and probably increase the severity of hemolytic disease in her fetus. In alloimmunized women, funipuncture should rarely be carried out to determine the fetal antigen status. Serial amniocenteses combined with careful serial ultrasound observation of the fetus are safer. Funipuncture should not be done in alloimmunized women before the cord vessels are of adequate size to allow immediate intravascular fetal transfusion, if required.

Thalamic Hemorrhage

The clinical features of thalamic hemorrhage in terms of localization are of great interest in many studies. To better understand the relationship between the localization of thalamic hemorrhage and clinical features. we evaluated the characteristics of patients with four different topographic types of thalamic hemorrhage. We prospectively studied 100 patients with thalamic hemorrhage who were admitted consecutively to our primary care unit. We divided them into two groups according to large (> 2 cm in diameter and/or > 4 mL in volume) and small thalamic hemorrhage. Four topographic subgroups (large and small) were compared to identify clinical syndromes associated with distinct lesion locations. All patients with posterolateral thalamic hemorrhage had severe sensorimotor deficit. Neuropsychological disturbances in patients with posterolateral thalamic hemorrhage were prominent, with primarily transcortical aphasia in those with left-sided lesions and hemineglect and anosognosia in those with right-sided lesions. Several variants of vertical gaze dysfunction, skew ocular deviation, gaze preference toward the site of the lesion, and miotic pupils were frequent in posterolateral thalamic hemorrhage, particularly in the large type. Patients with small and large anterolateral thalamic hemorrhage were characterized by severe motor and sensory deficits; language and oculomotor disturbances were also observed, although less frequently than in posterolateral hemorrhage. Sensorimotor deficits were observed in patients with medial thalamic hemorrhage (moderate in small hemorrhages and severe in large hemorrhages because of involvement of the adjacent internal capsule). Language disturbances in patients with left-sided lesions and neglect in patients with right-sided lesions were seen only in large medial thalamic hemorrhage. Dorsal thalamic hemorrhage was rare and characterized by mild and transient sensorimotor disturbances. Among patients with dorsal thalamic hemorrhages, only those with large lesions had oculomotor and neuropsychological disturbances. We concluded that despite clinical similarity among the four types of thalamic hemorrhage, there was some discrepancy in the clinical features of small and large thalamic hemorrhages. The most important predictors of death were initial consciousness, nuchal rigidity, maximum size, volume and ventricular extension of hemorrhage, and occurrence of hydrocephalus.

Combined Laparoscopic and Endoscopic Approach to Resection of Gastric Leiomyoma

Gastric leiomyoma is an uncommonly found entity. Most leiomyomas are asymptomatic and are found at autopsy or on abdominal exploration for other reasons. Indications for resection include large size and symptoms of compression, obstruction, or hemorrhage. The traditional surgical approach consists of laparotomy and resection. This article describes a technique for minimally invasive resection using a combined laparoscopic and endoscopic approach.

Neodymium:YAG Laser Treatment for Hemorrhages under the Internal Limiting Membrane and Posterior Hyaloid Face in the Macula

A dense premacular hemorrhage may occur from proliferative diabetic retinopathy, a ruptured retinal artery macroaneurysm, or Valsalva retinopathy. Spontaneous clearing of the hemorrhage in Valsalva retinopathy usually occurs, taking several months. In diabetic retinopathy, a traction macular detachment may result as early as 5 weeks after the hemorrhage. In diabetic retinopathy or a macroaneurysm, only a fibrotic epiretinal membrane overlying the macula may develop. Observation or vitrectomy is the current way of managing a dense premacular hemorrhage. This study was undertaken to investigate an alternative, neodymium:YAG (Nd:YAG) laser membranotomy, in treating this type of hemorrhage. Six eyes in six patients had Q-switched Nd:YAG laser treatment to open trapped hemorrhage overlying the macula. One to three laser membranotomies were performed. Colored fundus photographs were obtained before and after the hemorrhage was treated. In some cases, fluorescein angiography was done before the hemorrhage was treated. The size of the pretreated hemorrhage was estimated from the photographs and expressed in disc diameters. Patients with diabetes had panretinal laser before Nd:YAG laser membranotomy. The premacular bleeding originated from proliferative diabetic retinopathy in four eyes and from a retinal artery macroaneurysm in two. Average estimated area of the pretreated hemorrhage was 14 disc diameters. Five eyes had marked clearing of hemorrhage and rapid improvement of vision after Nd:YAG laser membranotomy. Average follow-up after laser treatment was 20 months. One diabetic eye required vitrectomy for rebleeding. One eye had little visual improvement due to pre-existing subretinal bleeding. Neodymium:YAG laser membranotomy seems helpful in rapid clearing of premacular hemorrhage in certain eyes. A randomized prospective study is needed to evaluate observation, vitrectomy, and Nd:YAG laser treatment of dense premacular hemorrhage.

Surgical Management of Submacular Hemorrhage

The development of a thick submacular hemorrhage usually carries a poor visual prognosis. The surgical removal of submacular blood may improve the otherwise poor outlook in these cases. Forty-seven consecutive patients underwent vitrectomy with surgical removal of submacular hemorrhage. The patient population consisted of two consecutive groups. Group 1 (1989 to 1991) included 23 patients (20 with age-related macular degeneration [ARMD], one with idiopathic submacular hemorrhage, one with presumed ocular histoplasmosis syndrome [POHS], and one with angioid streaks) who underwent mechanical clot extraction. Group 2 (1991 to 1993) included 24 patients (19 with ARMD, two with POHS, two with arterial macroaneurysm, and one with angioid streaks) who underwent tissue plasminogen activator-assisted drainage of thick submacular hemorrhage. The dose of tissue plasminogen activator ranged from 10 to 40 micrograms. All patients had surgery within 72 hours of diagnosis. In group 1, the mean size of the submacular hemorrhage was 11 disc areas (range, 1 to 16 disc areas). Mean follow-up was 40 weeks. Mean postoperative visual acuity for eyes with ARMD was 20/200. (Visual acuity improved in six eyes, was stable in seven eyes, and deteriorated in seven eyes.) All three of the eyes without ARMD had visual improvement with a mean postoperative visual acuity of 20/70. Overall, visual acuity stabilized or improved in 13 (57%) of 23 patients and decreased in 10 (43%) patients. In group 2, the mean size of the submacular hemorrhage was 11 disc areas (range, 3 to 16 disc areas). Mean follow-up was 24 weeks. Mean postoperative visual acuity for eyes with ARMD was 20/480 (visual acuity was stable in 15 eyes, improved in two eyes, and deteriorated in two eyes). Four of five eyes without ARMD had visual improvement and one was stable, with a mean postoperative visual acuity of 20/60. Visual acuity stabilized or improved in 22 (92%) of 24 patients and decreased in two (8%). The degree of clot lysis was variable. Submacular hemorrhage secondary to ARMD has a poor visual prognosis, with or without surgical drainage. The addition of tissue plasminogen activator-assisted clot lysis does not appear to significantly improve the visual outcome following surgery. The determination of whether surgical intervention is appropriate in these cases requires a prospective, randomized clinical trial.

Primary Intracerebral Haemorrhage in the Oxfordshire Community Stroke Project

Sixty-six patients with primary intracerebral haemorrhage were identified in a prospective, community-based register of 675 consecutive patients with first-ever in a lifetime stroke. No patient was lost to follow-up (up to 6 years). The 30-day case fatality rate was 52%. For patients surviving 30 days the average annual mortality rate was 8% per year for the next 5 years. The main cause of early death (≤30 days) was the neurological sequelae of the original stroke (73%, whilst late deaths (> 30 days) were due to either complications of immobility (45%) or vascular disease (55%). Twenty one percent of all patients were independent at 6 months (52% of survivors). The main predictors for death within 30 days were age, reduced conscious level, abnormal proprioception and rupture of blood into the ventricles or subarachnoid space. In addition, the size of the initial haemorrhage was predictive for death at any stage of follow-up, and the degree of limb weakness was predictive of death or dependency at 6 months. Nine patients had 14 recurrent strokes (including 4 definite haemorrhages and 4 definite cerebral infarctions). Five of the recurrences were fatal. The actuarial risk of recurrence in 30-day survivors was 7% per year (14 per 100 patient-years) and the actuarial risk of death or recurrence in 30-day survivors was 11% per year. Seven patients (11%) had at least one seizure during follow-up, the risk of first seizure being 8 per 100 patient-years overall. Patients with primary intracerebral haemorrhage have a high early case fatality but survivors have a similar outcome to patients with cerebral infarction.

Magnetic resonance imaging study on the effect of levemopamil on the size of intracerebral hemorrhage in rats.

Beneficial effects of calcium antagonists in cerebral ischemia and trauma have been attributed in part to improved cerebral blood flow. Enhancement of cerebral blood flow, however, could aggravate the pathological situation if brain injury is associated with intracerebral hemorrhage. In this study we used high-field magnetic resonance imaging in an animal model of intracerebral hemorrhage to determine noninvasively the effect of the calcium and serotonin antagonist levemopamil [international nonproprietary name for (S)-emopamil] when infused in a dose (6 mg/kg) that is known to increase cerebral blood flow. Intracerebral hemorrhage was induced in rats by stereotaxic microinfusion of collagenase into the caudate putamen. Two series of experiments were performed. (1) Levemopamil was intravenously infused 30 minutes after intracerebral infusion of collagenase (0.05 U), which represents the time of intracranial bleeding. Another group of animals was given heparin (55 IU.kg-1.min-1) to evaluate the capability of this animal model to demonstrate drug-induced worsening of intracerebral hemorrhage. (2) The effects of hyperacute infusion of levemopamil (30 minutes after infusion of 0.5 U of collagenase) were compared with those of a 2-hour delayed administration. In both experimental settings, the extent of intracerebral hemorrhage was determined by T1-weighted magnetic resonance images (spin-echo; repetition time, 400 milliseconds; echo time, 23 milliseconds) taken in vivo in a coronal and a transverse brain plane 24 hours after collagenase infusion. (1) Hemorrhagic brain areas measured 10.1 +/- 2.9 mm2, 8.5 +/- 2.1 mm2, and 18.8 +/- 2.5 mm2 in the coronal brain plane (10 mm anterior to the interaural line) of control, levemopamil-, and heparin-infused rats, respectively (8 animals per group, mean +/- SD). In the transverse brain plane (6 mm dorsal to the interaural line) the hemorrhagic area was 11.5 +/- 3.6 mm2, 9.7 +/- 2.4 mm2, and 19.9 +/- 3.3 mm2 in control, levemopamil-, and heparin-infused rats, respectively. (2) Animals with 2-hour delayed levemopamil infusion displayed intracerebral hemorrhage similar in size to that of control rats. (3) Neither small nor large hemorrhagic lesions were increased by levemopamil. Aggravation of intracerebral hemorrhage was not observed by magnetic resonance imaging in levemopamil-infused animals. However, infusion of heparin caused a significant (P < .05), almost twofold increase in the size of intracerebral hemorrhage. These results justify clinical trials with levemopamil in cerebral disorders such as stroke, brain trauma, and peritumoral brain edema, which may be accompanied by intracerebral hemorrhage from the beginning or where transition to intracerebral hemorrhage may occur.

A Clinical Study of the Parameters and Effects of Temporary Arterial Occlusion in the Management of Intracranial Aneurysms

Temporary occlusion of intracranial arteries has emerged as a valuable technical adjunct in the management of intracranial aneurysms. The current study considered 121 patients (from a group of 234 consecutive aneurysm patients treated during a 2-yr period) who underwent elective temporary arterial occlusion. Twenty-one patients were excluded from further study because of an intraoperative rupture of an aneurysm, the elective sacrifice of afferent or efferent vessels, or the performance of an extracranial-intracranial arterial bypass graft; the remaining 100 patients underwent elective temporary occlusion under a standard neuroanesthetic regimen, including etomidate-induced burst suppression, normotension, normovolemia, and normothermia. In the postoperative period, radiographic evidence of ischemic brain injury in the distribution of the arteries occluded was selected as the end point for the failure of occlusion tolerance. The parameters evaluated with respect to this end point included the duration and nature of the temporary arterial occlusion, the number of the occlusive episodes, the specific vascular territory occluded, patient age, neurological status, presence of subarachnoid hemorrhage, vasospasm, and aneurysm size. Several parameters were found to be related to the postoperative development of ischemic injury. Patients more than 61 years of age and those in poor neurological condition (Hunt and Hess Grades III to IV) did not tolerate temporary occlusion as well as patients who were younger and in better condition. Patients occluded for less than 14 minutes routinely tolerated the iatrogenic ischemia; the 95% confidence level for the toleration of occlusion without the development of infarction occurred at 19 minutes. All patients occluded for more than 31 minutes had both clinical and radiographic evidence of cerebral infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracerebral hemorrhage: pathophysiology and management.

To review the pathophysiologic basis for intensive care management of patients with intracerebral hematoma and to present management strategies based on that analysis. Review of English language scientific and clinical literature using BRS Colleague search. Pertinent literature was selected to demonstrate physiologic principles, the clinical presentation, and the natural history of intracerebral hematoma. All clinical treatment trials were reviewed. Literature was reviewed to summarize physiologic principles and the results of clinical trials. The suggested medical management is based on the results of clinical trials and the applications of pathophysiologic principles. Spontaneous intracerebral hematomas acutely increase intracranial volume and reduce intracranial compliance, thus potentially increasing intracranial pressure and reducing cerebral perfusion. Therefore, any physiologic perturbation that could increase cerebral blood volume (hypercarbia, hypoxia, vasodilation) or reduce cerebral perfusion (hypotension) should be avoided. Acute hypertension may be a response to increased intracranial pressure and should be treated conservatively. Treatment of increased intracranial pressure is accomplished initially with hyperventilation, but this approach should be replaced rapidly with cerebrospinal fluid drainage alone or in combination with osmotic therapy employing diuretics, osmotic agents, or hypertonic saline to produce a state of hyperosmolality and euvolemia. Although the role of surgery remains controversial, it may be helpful in selected patients. Careful attention to pulmonary and metabolic status and to the consequences of therapy is required. Outcome is primarily determined by hemorrhage size, location, and initial level of consciousness. Stereotaxic aspiration of hematomas is a promising new therapy. The primary injury from intracerebral hemorrhage is exacerbated by disturbed intracranial physiology. Management should include principles that improve intracranial compliance and reduce intracranial pressure.

Risks of Anticoagulation Therapy after Experimental Corticectomy in the Rat

To determine the optimal postoperative interval after which heparin therapy can be safely initiated, a rat model for experimental craniotomy and corticectomy was developed. In 50 rats (100 lesions), heparin therapy was initiated 1, 2, 3, 5, or 7 days after standardized bilateral frontal corticectomy and was continued for 7 days. Intraperitoneally administered heparin, 75 to 100 U/kg.h, was continuously given to maintain the activated partial thromboplastin time in one of two ranges: therapeutic (1.5-3 times control) or supratherapeutic (> 3 times control). The size of intracranial hemorrhage was determined from coronal brain sections by automated image analysis. No significant hemorrhage was observed in control (saline infusion) animals or in rats receiving therapeutic doses of heparin beginning more than 24 hours after surgery. Small (10-50 mm3) and large (> 50 mm3) hemorrhages were frequent at all intervals up to 5 days in animals with supratherapeutic activated partial thromboplastin time (P < 0.01). Judicious heparin therapy may be safely initiated at 48 hours after craniotomy and corticectomy in rats, whereas supratherapeutic anticoagulation is associated with intracranial hemorrhage at intervals of up to 5 days.

Assessment of postreperfusion myocardial hemorrhage using proton NMR imaging at 1.5 T.

Intramyocardial hemorrhage occurs frequently after reperfusion of acute myocardial infarction. However, its significance has not yet been established, mainly because of the lack of methods for detecting such hemorrhage. The following ex vivo study was carried out to assess the potential of nuclear magnetic resonance (NMR) imaging to detect and quantitate postreperfusion intramyocardial hemorrhage. Sixteen adult mongrel dogs underwent 3 hours of coronary occlusion followed by 1 hour of reperfusion, and three dogs underwent 4 hours of occlusion without reperfusion. Radiolabeled microspheres and 51Cr-labeled red blood cells were used to assess flow and evaluate the extent of hemorrhage. These results were later compared with both NMR and histology. Spin-echo NMR imaging was performed on the excised hearts using a 1.5-T system. Macroscopic assessment of the sliced myocardium revealed the existence of hemorrhage in 14 of the 16 dogs that underwent reperfusion but in none of those with occlusion only. In all 16 dogs with reperfusion, zones of increased signal intensity (SI) ratio (1.68 +/- 0.41 compared with control, p less than 0.05) were seen in regions relating to the distribution of the occluded coronary artery, whereas in 13 of the 16 dogs, areas of decreased SI within the zone of increased SI ratio (0.81 +/- 0.16 compared with control, p less than 0.05) were also seen, corresponding to regions with macroscopic hemorrhage. In contrast, in the three dogs without reperfusion, no macroscopic hemorrhage was observed, and likewise, no NMR zones of reduced SI were detected. Hemorrhage size by NMR (decreased SI zones), correlated well with hemorrhage size calculated from tissue slices (r = 0.96, SEE = 0.92%, p less than 0.01), or by 51Cr labeling (r = 0.78, SEE = 1.5, p = 0.1). In the reperfusion group, T2 relaxation times in the infarcted hemorrhagic zone (58 +/- 9 msec) were significantly lower than the infarcted zones without hemorrhage (98 +/- 13 msec, p less than 0.001). In contrast, when compared with control (964 +/- 72 msec), T1 relaxation times were significantly increased in both infarct zones, either with (1,284 +/- 176 msec) or without (1,266 +/- 103 msec) hemorrhage. The selective shortening of T2 relaxation times in the hemorrhagic regions is consistent with the paramagnetic effects of deoxyhemoglobin. NMR imaging may provide a noninvasive approach for the detection and quantitation of intramyocardial hemorrhage. This observation may provide a means to further characterize pathological processes associated with acute myocardial infarction and assess the role of myocardial hemorrhage after reperfusion therapy.

Intracerebral hemorrhage: External validation and extension of a model for prediction of 30‐day survival

We report validation of a previously reported logistic regression model for predicting 30-day survival after supratentorial intracerebral hemorrhage using independent, prospectively collected data. The original model, using initial Glasgow Coma Scale score, hemorrhage size, and pulse pressure, accounted for mortality or survival at 30 days in 92% of patients in the Pilot Stroke Data Bank with a sensitivity of 0.84 and a specificity of 0.96. For external validation, the model was used to predict 30-day status for each patient in the Main Phase Stroke Data Bank for whom complete risk factor information was available. Overall, 90% of patients' outcomes were correctly predicted with a sensitivity of 0.85 and a specificity of 0.92. Two factors not collected in the Pilot Stroke Data Bank, hyperglycemia and intraventricular hemorrhage extension, were assessed to determine if they provided additional predictive information on 30-day mortality. Intraventricular hemorrhage extension contributed significant predictive information in a logistic regression, whereas hyperglycemia did not. The resulting four-factor model with an interaction term (intraventricular hemorrhage extension and Glasgow Coma Scale score) correctly classified the survival status of 94% of patients at 30 days. A more general outcome, death or failure to achieve a "good" Activities of Daily Living Score by one year, was analyzed with respect to the same four factors. The resulting model correctly classified 95% of the patients in the cohort.

Death and functional outcome after spontaneous intracerebral hemorrhage. A prospective study of 166 cases using multivariate analysis.

Using death and functional status as end points, we prospectively analyzed the outcome 6 months after spontaneous intracerebral hemorrhage in 166 patients admitted to an acute-care stroke unit on the first day of their stroke. Seventy-one patients (43%) died, 69 (42%) had a satisfactory outcome, and 26 (16%) had a poor functional outcome. Early (30-day) survival was correlated with morphologic parameters on the initial computed tomogram (hemorrhage size, midline shift, and intraventricular spread of the hemorrhage), while later (6-month) survival was correlated with age. Using logistic regression, we found five independent predictors of satisfactory outcome at 6 months: age, hemorrhage size, intraventricular spread of the hemorrhage, limb paresis, and communication disorders. Of these, age was the most important predictor by far.