Hemorrhage Of Unknown Cause Research Articles

Unfavorably Altered Fibrin Clot Phenotype in Women Following Postpartum Hemorrhage of Unknown Cause: Effect of Lower Coagulation Factors.

Increased clot permeability and susceptibility to lysis have been reported in women with heavy menstrual bleeding. We hypothesized that similar alterations in fibrin clot properties may also be present in women with postpartum hemorrhage (PPH) of unknown cause. To determine fibrin clot properties and their determinants in women after PPH of unknown cause. We studied 52 consecutive women, aged 35 years (27-40), after at least 3 months since PPH of unknown cause and 52 matched controls for age, weight, and fibrinogen. Coagulation factors (F), antithrombin, thrombin generation, along with a comprehensive plasma fibrin clot analysis including fibrin polymerization, clot permeability (K s), and fibrinolysis efficiency were determined. Women with PPH showed reduced activity of FII (-10.3%), FV (-6.6%), FIX (-6.5%), FX (-7.2%), and FXI (-5.7%) compared with the controls, though all values were within ranges (all p < 0.05). There were no intergroup differences in fibrinogen, FVIII, FXIII, and thrombin generation. The PPH group formed with a delay looser plasma fibrin network (K s; +16.3%, p = 0.008) with lower maximum absorbance and shorter clot lysis time (CLT; -13.5%, p = 0.001) compared with the controls. On multivariable logistic regression, PPH was independently associated with higher C-reactive protein (per 1 mg/L, odds ratio [OR] = 1.70, 95% confidence interval [CI]: 1.09-2.68), lower FII (per 1%, OR = 0.93, 95% CI: 0.89-0.98), lower FV (per 1%, OR = 0.93, 95% CI: 0.89-0.97), and shorter CLT (per 1 minute, OR = 0.94, 95% CI: 0.90-0.98). Prohemorrhagic fibrin clot properties, with lower, though normal coagulation factors, characterize women with PPH of unknown cause, which suggests novel mechanisms contributing to this type of bleeding.

Altered fibrin clot phenotype in young adults with intracerebral hemorrhage of unknown cause: A case-control study

BackgroundIntracerebral hemorrhage (ICH) of undetermined etiology occurs infrequently in young and middle-aged adults. We hypothesized that slight decreases in coagulation factors and formation of less compact fibrin clots prone to faster lysis predispose to this type of ICH. MethodsWe recruited 44 consecutive patients aged <50 years following ICH of unknown cause at least 3 months since the event. Subjects free of ICH (n = 47) matched for age, sex, BMI, and hypertension served as the control group. We assessed plasma fibrin clot permeability, turbidity and fibrinolytic capacity, along with thrombin generation, coagulation factors (F) II, FV, FVII, FVIII, FIX, FX, FXI, antithrombin, and fibrinolysis proteins. ResultsICH patients (median age 41 years, 45.5 % women) had 8.4 % lower FII (p = 0.0001) and 10.1 % lower FVII activity (p = 0.0003), 9.4 % higher antithrombin activity (p = 0.0004) and 13.5 % lower platelet count (p = 0.02). Other factors and thrombin generation did not differ between the two groups. The ICH survivors were characterized by impaired fibrin polymerization reflected by 10.1 % longer lag phase of the turbidimetry curve (p = 0.0002), decreased fiber density indicated by 11.8 % lower maximum absorbance (p = 0.004), as well as 11.1 % shorter clot lysis time (p = 0.014) and 10.0 % faster increase of maximal D-Dimer levels (p = 0.000001). ConclusionsWe demonstrated a prohemorrhagic fibrin clot phenotype, along with lower FII, FVII and higher antithrombin activity in adults below 50 years of age who suffered from ICH of unknown cause, which might indicate novel mechanisms contributing to ICH in younger individuals.

Squamous cell carcinoma invading peripheral cerebral blood vessels and causing repeated cerebral hemorrhage : A case report.

Squamous cell carcinoma (SCC) is known to have less brain metastasis, but the reasons are not well established. Herein, we report the case of an 82-year-old man with recurrent cerebral hemorrhage of unknown cause ; upon brain biopsy, SCC was diagnosed infiltrating peripheral blood vessels of the brain and that it was state of micro-metastasis. It is possible that the blood-brain barrier blocked the infiltration of SCC into the brain parenchyma, and it did not form a mass in the brain parenchyma. In addition, because it did not form a mass, it could not be diagnosed as a metastatic brain tumor by contrast-enhanced magnetic resonance imaging or contrast-enhanced computed tomography. Among cases of recurrent cerebral hemorrhage of unknown cause in a short period, there may be cases of vascular infiltration without crossing the blood-brain barrier. Thus, if similar cases of recurrent cerebral hemorrhage of unknown cause is observed, it is necessary to distinguish metastatic brain tumors even if there is no evidence of suspected tumor on contrast-enhanced magnetic resonance imaging scan. J. Med. Invest. 70 : 276-280, February, 2023.

Sphenoparietal sinus and superficial middle cerebral vein thrombosis: A case report and review of literature

BackgroundCerebral venous sinus thrombosis is rare and might be overlooked by healthcare providers. It often occurs in the transverse sinuses, superior sagittal sinus, and the vein of Trolard. Sphenoparietal sinus (SPS) and/or superficial middle cerebral vein (SMCV) thrombosis is rare and only 12 cases reported in the literature. Case descriptionWe report a 47-year-old woman with iron deficiency anemia associated with myoma uteri who developed left SPS and SMCV thrombosis. She presented with sudden unconsciousness, right hemiplegia, and aphasia. Brain computed tomography showed subcortical hemorrhages in the left frontal and temporal lobes. Magnetic resonance imaging did not reveal the cause of the bleeding. Although antihypertensive treatment with nicardipine was initiated, she deteriorated into coma the next day and underwent emergency decompressive craniectomy. Thrombosis of the SMCV was identified during surgery. Re-examination of preoperative T2 star-weighted imaging revealed thrombosis of the SPS and SMCV. ConclusionAll but one of the reviewed cases had the thrombosis develop on the left side, which may be attributed to anatomical and brain functional laterality. When an edematous change or cortical hemorrhage of unknown cause is encountered within the perisylvian region, especially on the left side, the possibility of SPS and SMCV thrombosis should be considered.

Subarachnoid Hemorrhage of Unknown Cause: Distribution and Role of Imaging.

Subarachnoid hemorrhage of unknown cause represents approximately 10% to 15% of nontraumatic subarachnoid hemorrhages. The key factors in determining the management strategy for a presumed nonaneurysmal subarachnoid hemorrhage are the distribution, location, and amount of subarachnoid blood. Hemorrhage distribution on computed tomography can be categorized as follows: perimesencephalic, diffuse, sulcal, and primary intraventricular. The extent of the workup required in determining the cause of hemorrhage depends on the distribution of blood. The authors review the potential causes, differential diagnoses, and acute and long-term follow-up strategies in patients with subarachnoid hemorrhage of unknown cause.

Vitreous hemorrhage secondary to iridociliary cyst

Case reportAn 18-year-old man, presented a lower vitreous hemorrhage of unknown cause. Multiple tests are performed, including Ophthalmic Ultrasound and Fluorescein Angiography (FA), they did not find justification of bleeding. Finally, we decide to do a Biomocroscopía Ultrasonic (UBM) showing an iridociliary cyst. DiscussionThe iridociliary cysts are single or multiple, primary or secondary. The primaries are usually benign so, they do not require treatment. When the cyst has a considerable size, it may produce a focal plateau iris with or without angle-closure. Our case reveals an unusual complication that should take notice of when you have an unknown vitreous hemorrhage.

Hemovítreo secundario a quiste iridociliar

Case reportAn 18-year-old man, presented a lower vitreous hemorrhage of unknown cause. Multiple tests are performed, including Ophthalmic Ultrasound and Fluorescein Angioghaphy (FA), they did not find justification of bleeding. Finally, we decide to do a Biomocroscopía Ultrasonic (UBM) showing an iridociliary cyst. DiscussionThe iridociliary cysts are single or multiple, primary or secondary. The primaries are usually benign so, they do not require treatment. When the cyst has a considerable size, it may produce a focal plateau iris with or without angle-closure. Our case reveals an unusual complication that should take notice of when you have an unknown vitreous hemorrhage.

Moyamoya disease presenting with subarachnoid hemorrhage localized over the frontal cortex: case report

Background In moyamoya disease, intracranial bleeding is known to occur because of the rupture of saccular aneurysms in the circle of Willis or because of the rupture of dilated, fragile moyamoya vessels. The former causes subarachnoid hemorrhage (SAH), and the latter causes intracerebral or intraventricular hemorrhage. Case description In this report, we describe the case of a 34-year-old woman with moyamoya disease who suddenly developed headache and jacksonian seizure. Plain computed tomographic scans on admission revealed SAH localized over the left frontal cortex. The patient was diagnosed with moyamoya disease on cerebral angiography. However, no aneurysm was found on cerebral angiography. Positron emission tomography showed the reduction of CBF and its reactivity to acetazolamide and the elevation of CBV in the left hemisphere. She underwent STA to MCA anastomosis and indirect synangiosis. Intraoperative observations revealed that the pial arterioles were markedly dilated on the brain surface. The CBF in the left hemisphere significantly improved after surgery. The patient has experienced no further episode of cerebral ischemia or intracranial bleeding. Conclusions Subarachnoid hemorrhage of unknown cause is quite rare in moyamoya disease. Based on the findings in the present case, the dilated collateral arteries on the brain surface may rupture and cause SAH over the cerebral cortex, which is the third cause of intracranial bleeding in patients with persistent cerebral ischemia due to moyamoya disease.

A risk score system for identification of patients with upper-GI bleeding suitable for outpatient management

Background The aim of this study was to develop a risk score system for identification of patients with upper-GI hemorrhage who are suitable for outpatient management. Methods From a prospective cohort of 983 consecutive patients with upper-GI hemorrhage not associated with portal hypertension, 581 cases that did not meet pre-established criteria for admission were selected, and a logistic regression analysis was performed to identify factors associated with two adverse outcomes: recurrent bleeding and/or the need for emergency surgery. The risk score system was developed by using the beta coefficients of the logistic model, and its performance was evaluated. The results of this model were combined with pre-established criteria for admission to build a simplified scoring system for identification of patients who can be managed safely on an outpatient basis. Results Chronic alcoholism, active malignancy, prior upper digestive tract surgery, wasting syndrome, hemodynamic compromise, duodenal ulcer as the cause of upper-GI hemorrhage, and hemorrhage of unknown cause were independently associated with a greater risk of unfavorable outcomes in the group that did not meet pre-established criteria for admission. The logistic model showed a high capacity for discrimination (C statistic: 0.87) and good calibration ( p value for Hosmer-Lemeshow goodness-of-fit test, 0.62), with a sensitivity of 100% and specificity of 64%. The simplified score had a sensitivity of 100% and specificity of 29% for adverse outcomes, and sensitivity of 78% and specificity of 38% for mortality. Conclusions The score system developed in this study may be helpful in deciding between hospitalization and outpatient management for patients with upper-GI hemorrhage, but it remains to be validated in patient groups other than those used for its development.

Prognosis and Prognostic Factors for Unexplained Subarachnoid Hemorrhage: Review of 84 Cases

We conducted a retrospective study to investigate the prognosis, possible prognostic factors, and long-term natural history of subarachnoid hemorrhage of unexplained cause. This report contains a retrospective analysis of data for 84 patients with subarachnoid hemorrhage of unknown cause who were monitored for 1 month to 9.5 years, with an average follow-up period of 5.6 years. We evaluated the associations between computed tomographic (CT) scan features, clinical grade, loss of consciousness during hemorrhage, ventricular ratio, angiographic spasm, complications (such as death resulting from ischemia, early rebleeding, late rebleeding, epilepsy, hydrocephalus, and fixed ischemic deficits), and outcomes, using a nonparametric, two-sample, Kolmogorov-Smirnov test. The chi2 test was used to test the independence of two categorical variables. CT class exhibited a significant association with clinical grade (gamma = 0.865, P = 0.006), loss of consciousness during hemorrhage (gamma = 0.69, P = 0.001), and ventricular ratio (gamma = 0.8175, P = 0.01) but a nonsignificant association with angiographic vasospasm (gamma = 0.21, P = 0.2). Death resulting from ischemic complications and fixed ischemic deficits were strongly associated with clinical grade (P = 0.003 and P = 0.008, respectively) but weakly associated with CT class (P = 0.06 and P = 0.084, respectively). Angiographic vasospasm was strongly associated only with fixed ischemic deficits among complications (P = 0.001). Clinical outcome was strongly positively associated with CT class (gamma = 0.685, P = 0.001), clinical grade (gamma = 0.81, P = 0.001), and ventricular ratio (gamma = 0.57, P = 0.002) but weakly positively associated with loss of consciousness during hemorrhage (gamma = 0.459, P = 0.0487) and angiographic vasospasm (gamma = 0.48, P = 0.04). Our study confirms earlier studies reporting a good prognosis for survival, but it does not confirm the earlier statements regarding low morbidity rates. Although clinical grade and the presence and amount of subarachnoid blood on CT scans are the major prognostic factors related to the incidence of ischemic complications, clinical grade and CT class are also the main parameters, with ventricular ratio, indicating clinical outcomes for patients with subarachnoid hemorrhage of unknown cause.

Prenatal diagnosis of cerebellar hemorrhage: Medicolegal implications

Perinatal brain damage and compromised long-term neurologic outcome have been a topic of major concern and continuing debate. Until recently the occurrence of fetal brain injury was attributed to intrapartum events. However, evidence continues to accumulate that neurologic damage can occur during fetal life unrelated to intrapartum events. We report a case of massive cerebellar hemorrhage of unknown cause diagnosed by ultrasonography at 36 weeks of gestation, after decreased fetal movements. Fetal heart rate pattern and Doppler flow study of cerebral arteries are correlated with neuropathologic findings, and the medicolegal aspects of this condition are discussed. Perinatal brain damage and compromised long-term neurologic outcome have been a topic of major concern and continuing debate. Until recently the occurrence of fetal brain injury was attributed to intrapartum events. However, evidence continues to accumulate that neurologic damage can occur during fetal life unrelated to intrapartum events. We report a case of massive cerebellar hemorrhage of unknown cause diagnosed by ultrasonography at 36 weeks of gestation, after decreased fetal movements. Fetal heart rate pattern and Doppler flow study of cerebral arteries are correlated with neuropathologic findings, and the medicolegal aspects of this condition are discussed.

Prenatal diagnosis of cerebellar hemorrhage: Medicolegal implications

Perinatal brain damage and compromised long-term neurologic outcome have been a topic of major concern and continuing debate. Until recently the occurrence of fetal brain injury was attributed to intrapartum events. However, evidence continues to accumulate that neurologic damage can occur during fetal life unrelated to intrapartum events. We report a case of massive cerebellar hemorrhage of unknown cause diagnosed by ultrasonography at 36 weeks of gestation, after decreased fetal movements. Fetal heart rate pattern and Doppler flow study of cerebral arteries are correlated with neuropathologic findings, and the medicolegal aspects of this condition are discussed. (AM J OBSTET GYNECOL 1994;170:1392-5.)

Optic-disc hemorrhages: Cause or result of ischemia?

Visual-field defects may develop after optic-disc hemorrhages. The question whether blood may be a major damaging agent for the optic nerve head will be discussed. A female patient with an optic-disc hemorrhage in the left eye was followed with frequent disc photography and computerized perimetry for a period of two months. This patient presented, subsequently to an optic-disc hemorrhage of unknown cause, a delayed progression of the visual-field defect. The fact that the visual-field defect developed after the hemorrhage and was progressive in the next few days indicates that the hemorrhage may not be the result of an infarct, but rather provokes further damage. The case raises the question whether blood components may be involved in the pathophysiologic process of optic-nerve-head atrophy. In analogy of cerebral vasospasm after subarachnoid hemorrhage as an important cause of cerebral ischemia, the potential involvement of blood-related injury to the optic disc should be considered in such patients.

Thromboelastogram fails to predict postoperative hemorrhage in cardiac patients

To determine the clinical usefulness of the thromboelastogram in the prediction of postoperative hemorrhage ir cardiac patients, we related the results of routine coagulation tests (RCTs) and thromboelastography with the amount of chest tube drainage postoperatively in 101 patients requiring cardiopulmonary bypass. Our data indicated that there was no correlation between RCT results and thromboelastographic variables. No single variable of RCTs and thromboelastography correlated well with the amount of chest tube drainage postoperatively. Before the onset of cardiopulmonary bypass, the most frequent abnormalities detected by thromboelastograms were fibrinolysis and hypocoagulability resulting from factor deficiency. Hypercoagulability detected by thromboelastograms occurred in 13% of patients after cardiopulmonary bypass and usually was not detected by RCTs. The incidence of false-negative thromboelastograms and RCT results in patients who had excessive hemorrhage of unknown cause was 46% and 52%, respectively. The incidence of fibrinolysis as detected by thromboelastograms was similar before and after bypass, but only 2 of the 18 patients with fibrinolysis had excessive hemorrhage postoperatively. Our results indicate that neither RCTs nor thromboelastography predicts the likelihood of excessive hemorrhage in patients after cardiopulmonary bypass. The thromboelastographic results should be interpreted cautiously because of the high rate of unreliable results.

Marked Growth of a Cerebral Arteriovenous Malformation: Case Report and Review of the Literature

A case demonstrating the marked growth of an angiographically occult arteriovenous malformation is presented. A review of 58 cases in which an increase in the size of an arteriovenous malformation occurred suggested that the patient's initial age may have had an important role in such growth and that both the age and the duration of follow-up were related to the extent of growth. Follow-up neuroradiological examinations are thought to be necessary for patients who have had an episode of intracranial hemorrhage of unknown cause during childhood, even if the initial angiograms revealed no vascular lesion.

Marked growth of a cerebral arteriovenous malformation

A case demonstrating the marked growth of an angiographically occult arteriovenous malformation is presented. A review of 58 cases in which an increase in the size of an arteriovenous malformation occurred suggested that the patient's initial age may have had an important role in such growth and that both the age and the duration of follow-up were related to the extent of growth. Follow-up neuroradiological examinations are thought to be necessary for patients who have had an episode of intracranial hemorrhage of unknown cause during childhood, even if the initial angiograms revealed no vascular lesion.

Corticosteroid Use and Peptic Ulcer Disease: Role of Nonsteroidal Anti-inflammatory Drugs

To estimate the relative risk for peptic ulcer disease that is associated with the use of oral corticosteroids. A nested case-control study. Tennessee Medicaid program. The case patients (n = 1415) were hospitalized between 1984 and 1986 for gastric or duodenal ulcer or for upper gastrointestinal hemorrhage of unknown cause. The controls (n = 7063) were randomly selected from Medicaid enrollees not meeting the study criteria for inclusion as case patients. The estimated relative risk for the development of peptic ulcer disease among current users of oral corticosteroids was 2.0 (95% CI, 1.3 to 3.0). However, the risk was increased only in those who concurrently received nonsteroidal anti-inflammatory drugs (NSAIDs); these persons had an estimated relative risk associated with current corticosteroid use of 4.4 (CI, 2.0 to 9.7). In contrast, the estimated relative risk for those corticosteroid users not receiving NSAIDs was 1.1 (CI, 0.5 to 2.1). Persons concurrently receiving corticosteroids and NSAIDs had a risk for peptic ulcer disease that was 15 times greater than that of nonusers of either drug. Discrepant findings among earlier studies regarding steroids and the risk for peptic ulcer disease could in part be due to differences in the use of NSAIDs among study participants. The high risk for peptic ulcer disease associated with combined use of NSAIDs and corticosteroids indicates the need to prescribe this drug combination cautiously.

Cerebral amyloid angiopathy as a cause of subarachnoid hemorrhage.

Cerebral amyloid angiopathy is a pathologic condition characterized by the deposition of amyloid in the walls of small vessels in the cerebral cortex and meninges. Intracerebral hemorrhage is common in persons with this condition, but pure subarachnoid or subdural hemorrhage is rarely seen. Recently, the existence of two types of amyloid proteins related to cerebral amyloid angiopathy, beta protein and cystatin C, has been reported, and immunohistochemical methods using antisera to these proteins have become available. We describe a patient with fatal subarachnoid hemorrhage presumably caused by beta protein-type cerebral amyloid angiopathy, which was demonstrated immunohistochemically by using a monoclonal antibody to a synthetic peptide corresponding to residues 8-17 of beta protein. We suggest that beta protein-type cerebral amyloid angiopathy is a possible etiologic factor in subarachnoid hemorrhage of unknown cause.

Subarachnoid hemorrhage of unknown cause

Subarachnoid hemorrhage of unknown cause

Prevention of rebleeding after operation for subarachnoid hemorrhage of unknown cause.

This study is presented to promote prophylactic operation to prevent rebleeding after subarachnoid hemorrhage (SAH) of unknown cause. Twenty-two cases of nontraumatic SAH of unknown cause of a total of 254 cases of SAH treated during a 5-year period (1980-1984) were available for this study. A follow-up study (4 to 61 months after treatment; median, 43 months) revealed a 4.5% mortality rate. Four patients chosen from among the 22 SAH cases underwent prophylactic operation. The decision to operate was based on repeated angiography showing regional cerebral vasospasm corresponding to a limited hyperdense area on the computed tomographic scan at the time of the onset of SAH. Microsurgery revealed a minute protrusion (less than 2 mm in diameter) or thinning of the arterial wall with old hematoma of the surrounding brain in all 4 cases, and treatment required only coating of the abnormal site. All 4 patients are now fully recovered. Frequently, abnormal changes of such cerebral arteries as the anterior communicating artery, the internal carotid artery (C-1 and C-2), and the middle cerebral artery (M-1) may occur. Therefore, the authors emphasize the necessity of surgical treatment for specific cases of SAH with an unknown cause.