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Clinical analysis of traumatic subarachnoid hemorrhage.

Traumatic subarachnoid hemorrhage (TSAH) is regarded as a poor prognostic factor of primary brain stem injury. The aim of the present study is to describe the results of a clinical analysis of 15 patients with TSAH who were hospitalized between March, 1987 and April, 1990. They were classified into three groups on the basis of the initial level of consciousness evaluated by Glasgow Coma Scale (GCS) scores. Fourteen patients had TSAH in the sylvian fissures, while in five the location was the cortical sulci. Four patients had TSAH in the ambient and quadrigeminal cisterns, and another four patients had TSAH in the prepontine and interpeduncular cisterns. TSAH localized to the suprasellar cistern was found in three patients, and five patients were found to have TSAH only in the sylvian fissures. Other accompanying intracranial lesions were as follows: acute subdural hematoma in five patients. Intracerebral hematoma in four and cerebral contusion in three. Three patients, one in the severest group and two in the severe group, had fatal outcomes. The cause of death was more closely associated with the accompanying intracranial lesion than the TSAH. One patient had a fair outcome, and 11 patients had a favorable outcome. In the present study, the outcome was generally good in the patients who had TSAH in a confined area, such as the sylvian fissures or cortical sulci.

Adolescent↗

Factors associated with neurological outcome and lesion progression in traumatic subarachnoid hemorrhage patients.

OBJECTIVE: Traumatic subarachnoid hemorrhage (tSAH) is a frequent finding after closed-head injuries, and its presence is a powerful factor associated with poor outcome. The exact mechanism linking tSAH and an adverse outcome is poorly understood. The aim of this study was to identify the factors that may predict outcomes and changes in the computed tomographic (CT) scans of lesions in a selected population of tSAH patients. METHODS: We evaluated 141 patients admitted consecutively from January 1, 1997, to January 31, 1999, with a CT diagnosis of tSAH. The admission and "worst" CT scans were recorded. CT scan changes were reported as "significant CT progression" (changes in the Marshall classification) or "any CT progression." The amount of subarachnoid blood was recorded using a modified Fisher classification. Outcome was assessed at 6 months after injury with the Glasgow Outcome Scale. RESULTS: Twenty-eight patients (19.9%) had an unfavorable Glasgow Outcome Scale outcome. In the univariate analysis, prognosis was significantly related to age, admission Glasgow Coma Scale score, Marshall CT classification score at admission and on the worst CT scan, amount of tSAH, and volume of the associated brain contusions. From multivariate analysis, the only factors independently related to outcome were the Glasgow Coma Scale score (P < 0.01) and size of the tSAH at admission (P < 0.001). Thirty-four patients (24.1%) had significant CT lesion progression, and 66 patients (46.8%) had some lesion progression. Patients having significant progression of the lesion had a higher risk of an unfavorable outcome (32 versus 10%; P = 0.004). Unadjusted factors predicting CT progression were the Glasgow Coma Scale score at admission, the Marshall classification at admission, the amount of subarachnoid blood, and the presence or volume of associated brain contusions at admission. Independent factors associated with significant CT progression were the amount of tSAH (P < 0.001) and the presence or volume of brain contusions at admission (P < 0.001). CONCLUSION: The outcome of patients with tSAH at admission is related in a logistic regression analysis to the admission Glasgow Coma Scale score and to the amount of subarachnoid blood. These patients also have a significant risk of CT progression. The amount of subarachnoid blood and the presence of associated parenchymal damage are powerful independent factors associated with CT progression, thus linking poor outcomes and CT changes.

Aged↗

ICP and MABP following traumatic subarachnoid hemorrhage in the rat.

Traumatic subarachnoidal hemorrhage (t-SAH) is a common finding in head-injured patients occurring with a frequency of 39% according to data of the Traumatic Coma Data Bank. The present study is the first description of a t-SAH-model with particular emphasis on patterns of intracranial pressure (ICP) changes and mean arterial blood pressure (MABP) response. Diffuse brain injury was produced in intubated and ventilated adult Sprague-Dawley rats (N = 24) using a brass weight (500 gm) free falling from a predetermined height (1.5 m) on a steel disc glued to the skull of the rat. Before induction of the injury, heparin was administered intra-arterially (i.a.) and antagonised after injury by protamine. MABP-recordings and ICP-recordings were performed continuously. Histopathology was undertaken. Following injury MABP decreased from 138 +/- 14 mmHg to 89 +/- 22 mmHg. During 5 to 15 min ICP increased up to 89.4 +/- 50.4 mmHg, decreasing slowly within 60 min in surviving animals. The mortality rate was 41.6%. All brains showed a severe subarachnoid hemorrhage in the basal cisterns and cell-loss within the brainstem. Experimental t-SAH is possible. Following t-SAH there is a subacute increase of ICP due to the actual bleeding. The model may provide deeper understanding in the basic physiological patterns of t-SAH.

Animals↗

Clinical significance of traumatic subarachnoid hemorrhage.

The clinical significance of traumatic subarachnoid hemorrhage (TSAH) was studied in 20 head-injured patients. They were classified into mild (9) and severe (11) groups by their initial Glasgow Coma Scale (GCS) scores. TSAH detected by computed tomography was localized in the Sylvian fissure in four of the nine mild group patients, but was also found in other basal subarachnoid cisterns in the other five. Except for one patient who developed delayed vasospasm and communicating hydrocephalus, all had favorable outcomes in this group. Massive TSAH was noted in the basal subarachnoid cisterns in 10 severe group patients and only one had a good outcome. Delayed intracerebral hematoma in the frontal or temporal lobe in the vicinity of the Sylvian fissure was found in two mild and two severe group patients with TSAH in the Sylvian fissures. Traumatic parenchymal lesions in the brainstem were minimal in one of the two autopsied patients and no evidence of diffuse axonal injury was found in both cases. Thus, TSAH in the Sylvian fissure is suggestive of focal brain contusion around the fissures. Massive TSAH in the basal subarachnoid cisterns is not necessarily associated with severe parenchymal injury of the brainstem.

Adolescent↗

[Traumatic subarachnoid hemorrhage in acute severe head injury].

Traumatic subarachnoid hemorrhage (TSAH) is a frequent occurrence resulting from acute severe head injury. Computerized tomography (CT) accurately identifies the region, extent and nature of TSAH following trauma. But, to our knowledge, there have been few series detailing the characteristics of TSAH in acute severe head injury. The purpose of this study is to describe the findings, nature and prognosis of TSAH. Over a six and a half year period between April 1977 and September 1983, 414 severely head injured patients were examined by CT within 24 hours of the injury in the Department of Neurological Surgery and Critical Care Medicine, Nippon Medical School. Among them, 97 (23.4%) patients showed the appearance of TSAH in the Sylvian fissures, tentorium cerebelli, cortical sulci, basal cisterns and interhemispheric fissures. Conscious state on admission was defined using the Glasgow Coma Scale (GCS) and clinical outcome was defined using Glasgow Outcome Scale. There were 77 men and 20 women, ranging from 4 months to 83 years in age (means 44.3 years). TSAH therefore appears to be seen in all age groups, but especially in middle age groups. The GCS on admission was 8 or less in all cases; the GCS was 8 in 10 cases, 7 in 7 cases, 6 in 15 cases, 5 in 16 cases, 4 in 23 cases, 3 in 26 cases. The lower GCS scores, the more frequently TSAH was identified, and 67% of the patients had a GCS of 6 or less.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

[The relationship between delayed traumatic intracerebral hematoma and coagulopathy in patients diagnosed with a traumatic subarachnoid hemorrhage].

It has long been recognized that a traumatic insult to brain tissue may result in substantive coagulation abnormalities. The present study was carried out in an attempt to find out the association of coagulopathy and the development of delayed traumatic intracerebral hematoma (DTICH) in patients diagnosed with a traumatic subarachnoid hemorrhage (TSAH). Sixty-three patients were diagnosed as having TSAH from the initial CT scans obtained within 2 hours after trauma. On admission, peripheral blood samples for coagulation studies were taken within 6 hours after injury. All patients had subsequent CT scans performed within 24 hours of admission. Thirty (47.6%) of 63 patients exhibited radiological evidence of DTICH on their subsequent CT scans. There was a significant correlation between the increased value of serum fibrinogen degradation product (FDP > 40 micrograms/ml) and the development of DTICH. We observed that the origin of the hematoma might be caused by those radiographically unidentifiable parenchymal lesions often found with TSAH on the initial CT scan. We conclude that a clotting study at the time of admission is of value in predicting the occurrence of DTICH associated with TSAH.

Adolescent↗

[Can multislice helical computed tomography replace conventional angiography in the diagnosis of non traumatic subarachnoid hemorrhage?].

AIM OF THE STUDY: To evaluate the reliability of CT angiography in the diagnosis of non traumatic subarachnoid hemorrhage. MATERIALS AND METHODS: We prospectively studied 57 patients presenting with non traumatic subarachnoid hemorrhage. In all cases, CT angiography of the circle of Willis was performed, followed by conventional angiography. We compared the results of both techniques, with conventional angiography considered as the gold standard. RESULTS: The specificity of CT angiography for diagnosing intracranial aneurysms was 100% with sensitivity and negative predictive values of 86% and 65% respectively. The aneurysms that were not diagnosed on CT angiography were located on the supra-cavernous internal carotid artery and their size was less than 5mm. Futhermore CT angiography failed to diagnose the other causes of subarachnoid hemorrhage. CONCLUSION: CT angiography can be considered as a first line imaging technique for diagnosis of non traumatic subarachnoid hemorrhage. However, conventional angiography including three dimensional acquisitions must be performed for all cases where the cause of hemorrhage remains undiagnosed at CT angiography.

Cerebral Angiography↗

The influence of traumatic subarachnoid hemorrhage on prognosis of head injury.

OBJECTIVE: To study the influence of traumatic subarachnoid hemorrhage on secondary intracranial damage in GCS 13-15 head injuries and prognosis. METHODS: One hundred and twenty-eight patients with mild head injury, including 64 with subarachnoid hemorrhage and 64 without subarachnoid hemorrhage, were selected and analyzed according to the changes of their conditions after injury. RESULTS: Intracranial abnormality was found in 14 patients (21.87%) with subarachnoid hemorrhage and only in 4 patients (6.25%) without subarachnoid hemorrhage (P<0.01). In the 14 patients, 4 were given surgical treatment. Mild disability was in 2 patients and 2 completely recovered. The rest were conservatively treated and achieved complete recovery at last. CONCLUSIONS: Traumatic subarachnoid hemorrhage, as a factor of intracranial complications in mild head injury should be given much attention. Early drainage of bloody cerebrospinal fluid by lumbar puncture is an effective method for prevention and treatment of complications in mild head injury.

Adolescent↗

Development and validation of a comprehensive prognostic model for 28-day ICU mortality in non-traumatic subarachnoid hemorrhage: an analysis based on the MIMIC-IV database.

BACKGROUND: Due to the complex pathophysiology of non-traumatic subarachnoid hemorrhage (SAH), accurate risk prediction remains a challenge. Our aim is to develop and validate a comprehensive prognostic model that integrates demographic characteristics, vital signs, laboratory parameters, and more, to provide clinical decision-making support in real-world practice. METHODS: We conducted a retrospective cohort study of 785 Non-traumatic subarachnoid hemorrhage patients. The cohort was randomly divided into a training set (n&#xa0;=&#xa0;549) and a validation set (n&#xa0;=&#xa0;236). Feature selection was performed using LASSO regression, followed by backward stepwise Cox regression for optimization. A nomogram was constructed based on independent predictive factors, and model performance was assessed using discrimination, calibration, and decision curve analysis. To prevent immortal-time bias, all predictors were anchored to a fixed early (first-24-hour) measurement window, treatment variables were modelled as binary indicators rather than cumulative exposures, and a five-model sensitivity analysis with baseline-severity adjustment was performed. RESULTS: The development of our model followed a systematic approach: first, 15 potential predictive factors were selected via LASSO regression, which were then refined to 12 independent predictors using backward stepwise Cox regression. The final predictive factors included: Ventilation, AHT, Nimodipine 60&#xa0;mg, Age, SAPS.II, Input amount, Calcium total, Platelet count, White blood cells, Anion gap, pH, and Chloride. The integrated model demonstrated excellent predictive ability for 7-day, 14-day, and 21-day mortality in both the training set (AUC: 0.972, 0.934, 0.898) and the validation set (AUC: 0.968, 0.948, 0.911). Calibration curves and decision curve analysis confirmed the model's reliability and clinical utility across different time points. We constructed a nomogram for individualized risk prediction. Univariate Kaplan-Meier survival analysis demonstrated significant stratification of survival outcomes by each predictor, while restricted cubic spline analysis revealed non-linear relationships between continuous variables and mortality risk. Random survival forest analysis identified the top three predictive factors (Nimodipine 60&#xa0;mg, Ventilation, AHT) and compared them with our full 12-variable model, confirming superior performance of the integrated model at all time points. At the 28-day primary endpoint, the model achieved a time-dependent AUC of 0.898 (training) and 0.904 (validation); after restricting predictors to the early baseline window, the leakage-controlled model retained good discrimination (validation C-index 0.803). CONCLUSIONS: Our ICU 28-day mortality prognosis model demonstrated robust performance in predicting ICU 28-day mortality in non-traumatic subarachnoid hemorrhage. The model, through the nomogram, provides individualized risk assessment, aiding clinical decision-making and patient stratification.

Humans↗

[Traumatic subarachnoid hemorrhage: a prospective study of 58 cases].

BACKGROUND: We evaluated the prognostic factors in traumatic subarachnoid hemorrhage (tSAH). METHODS: This study was conducted with 58 patients (44 males, 14 females; mean age 39.2; range 17 to 79 years) with tSAH, between 2001 and 2003. The patients who were admitted to the hospital within in the first 6 hours of head injury were included, whereas patients with gun shot wounds, multiple injured patients and postoperative patients were excluded. Fifty-eight patients with tSAH were prospectively followed. The neurological status of the patients and the outcomes were evaluated using Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS), respectively and computed tomography (CT) examinations were done according to the grading criteria by Hijdra and Fisher. RESULTS: The etiology of tSAH included traffic accidents (73%), falls (20%) and others (7%). The GCS scores of patients at admission were mild (9%), moderate (39%) and severe (52%). In the CT scans, the amount and distribution of bleeding was grade 1 (small SAH) in 21 patients, grade 2 (moderate SAH) in 17 patients, and grade 3 (extensive SAH) in 20 patients according to Hijdra grading system and according to Fisher's criteria. The thickness of blood layer was grade 1 (no blood) in 6 patients, grade 2 (bleeding layer less than 1 mm) in 21 patients, grade 3 (bleeding layer more than 1 mm) in 15 patients and grade 4 (ventricular bleeding) in 16 patients. Neurological outcomes of patients were favorable (good recovery or moderate disability) in 59%, and unfavorable (severe disability, persistent vegetative state or death) in 41% according to GOS. CONCLUSION: We have found in our series that the prognosis was poor in patients with poor admission scores of GCS, cysternal or fissural hemorrhage, tSAH with cerebral contusion or acute subdural hematoma, higher than 13 points according to Hidjra's classification and patients of grade 3 or 4 in Fisher's criteria.

Adolescent↗

[The hemostatic system in traumatic subarachnoid hemorrhage in the Far North].

It was found that in conditions of the extreme North sanation of the cerebrospinal fluid occurs later in patients with traumatic subarachnoidal hemorrhage than in the central regions of the country. In connection with this the hemostasis system was studied in 20 patients with traumatic subarachnoidal hemorrhage and 10 patients with brain tumours (control group). Patients with traumatic subarachnoidal hemorrhage showed significant hypocoagulation changes.

Adult↗

Review on traumatic subarachnoid hemorrhage.

Recent studies demonstrated clinical significance of the presence of traumatic subarachnoid hemorrhage (tSAH) on the initial CT-scan after head injury. Investigations show similarities between traumatic and aneurysmal SAH suggesting that a similar therapeutic approach as used in spontaneous SAH patients might be beneficial in tSAH patients. Evidence of the clinical significance of the finding of tSAH on CT after head injury and the beneficial use of the calcium antagonist nimodipine in tSAH patients are reported.

Calcium Channel Blockers↗

Traumatic subarachnoid hemorrhage visualized with transesophageal echocardiography.

Computed tomography (CT) is the current standard for the early diagnosis of traumatic subarachnoid hemorrhage (tSAH). It is, however, not feasible when a patient is hemodynamically unstable. We report a novel method of visualizing tSAH with transesophageal echocardiography (TEE). The spinal cord was visualized through the intervertebral disc with the transducer directed posteriorly in the esophagus. TEE findings of the spinal cord in three patients with tSAH were compared with those of 19 patients without it. In the former, fibrin-like mobile images were present, the ratio of diameter of spinal cord to internal diameter of spinal canal was significantly larger (0.59 +/- 0.07 vs. 0.45 +/- 0.04, p = 0.0070) and the pia mater was significantly thicker (1.41 +/- 0.12 mm vs. 0.66 +/- 0.15 mm, p = 0.0001). Our findings suggest that TEE may be an alternative way of diagnosing early tSAH at bedside in patients in which CT is not feasible.

Contraindications↗

Does traumatic subarachnoid hemorrhage caused by diffuse brain injury cause delayed ischemic brain damage? Comparison with subarachnoid hemorrhage caused by ruptured intracranial aneurysms.

OBJECTIVE: To examine whether traumatic subarachnoid hemorrhage (TSAH) caused by severe diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome, as does aneurysmal subarachnoid hemorrhage (ASAH). METHODS: We examined 99 patients with diffuse brain injury with TSAH and 114 patients with ASAH. Computed tomographic (CT) findings, cerebral blood flow, and neurological outcomes were assessed during the acute and subacute phases and were compared between the two groups. RESULTS: The distribution of subarachnoid hemorrhage on the CT scans differed between the two groups. Unlike ASAH, TSAH was not limited to cisterns surrounding the circle of Willis but extended to supratentorial regions and interhemispheric fissures. Computed tomography-detected subarachnoid hemorrhage disappeared very early with TSAH and gradually with ASAH. In the ASAH group, mean cerebral blood flow decreased to 75% of normal during the acute phase and decreased a further 10% during the subacute phase. In the TSAH group, mean cerebral blood flow decreased to 85% of normal during the acute phase and increased slightly during the subacute phase. Neurological deterioration and in-hospital death peaked on Day 0 in association with TSAH and showed twin peaks in association with ASAH. The incidence of low-density areas on the CT scans was significantly higher with ASAH than with TSAH. All low-density areas on the CT scans of patients with ASAH corresponded to vascular territories, but low-density areas on the CT scans of patients with TSAH were rarely associated with vascular territories and contained deep-seated or gliding contusion types. CONCLUSION: The findings suggest that the incidence of vasospasm is low in association with TSAH and that the cause is different compared with ASAH. There is no evidence that the presence of TSAH in cases of diffuse brain injury leads to delayed ischemic brain damage and secondary deterioration of outcome.

Acute Disease↗