Presence Of Intracranial Hemorrhage Research Articles

Factors associated with balance deficits on admission to rehabilitation after traumatic brain injury: a multicenter analysis.

To evaluate how demographics, measures of injury severity, and acute care complications relate to sitting and standing balance in patients with traumatic brain injury (TBI). Multicenter analysis of consecutive admissions to designated TBI Model Systems of Care (TBIMS). Ten National Institute for Disability and Rehabilitation Research TBI Model System centers for coordinated acute and rehabilitation care. 908 adults with TBI were included in the study. Sitting and standing balance were assessed within 72 hours of admission to inpatient rehabilitation. Age less than 50 years had a significant association with normal sitting and standing balance (P =.001 and.05, respectively). Measures of severity of traumatic brain injury, including admission Glasgow Coma Score, length of posttraumatic amnesia (PTA), length of coma, and acute care length of stay were each significantly related to impaired sitting and standing balance ratings (P <.01). Initial abnormalities in pupillary response had a significant relationship with impairment of sitting (P =.009) but not standing balance. Incidence of respiratory failure, pneumonia, soft tissue infections, and urinary tract infections were all related to impaired sitting balance (P <.01). Presence of intracranial hemorrhages did not have a significant relationship with either sitting or standing balance. Intracranial compression had a significant relationship with standing (P =.05) but not sitting balance. A discriminant function analysis, which included neuroradiological findings, injury severity, and medical complications, could not accurately predict impaired balance ratings. This study demonstrated that rehabilitation admission balance ratings have a significant relationship with age, multiple measures of severity, and acute care medical complications after TBI. Prospective studies are indicated to evaluate the role balance at rehabilitation admission plays in the functional prognosis of patients with TBI.

Use of Factor IX Complex in Warfarin-related Intracranial Hemorrhage

Anticoagulation-treated patients presenting with intracranial hemorrhage, including subdural hematoma, epidural hematoma, subarachnoid hemorrhage, and intracerebral hemorrhage, require urgent correction of their coagulopathy to prevent worsening hemorrhage and to facilitate surgical intervention when necessary. In this study, we compared the use of fresh frozen plasma (FFP) with that of Factor IX complex concentrate (FIXCC) to achieve rapid correction of warfarin anticoagulation. Patients admitted to a tertiary care center with computed tomography-proven intracranial hemorrhage and a prothrombin time of more than 17 seconds were considered for inclusion in the study protocol. Complete data sets were obtained for eight patients randomized to treatment with FFP and five patients randomized to treatment with FFP supplemented with FIXCC. The prothrombin time and International Normalized Ratio were measured every 2 hours for 14 hours. Correction of anticoagulation was defined as an International Normalized Ratio of < or =1.3. A difference in repeated International Normalized Ratio measurements during the first 6 hours of correction was observed between the FIXCC and FFP groups (P < 0.03). The rate of correction was greater (P < 0.01) and the time to correction was shorter (P < 0.01) for the FIXCC-treated group. No difference in neurological outcomes was detected between groups, but a higher complication rate was observed for the FFP-treated group. The use of FIXCC accelerated correction of warfarin-related anticoagulation in the presence of intracranial hemorrhage.

Cerebral blood flow velocity after head injury: transcranial Doppler evaluation. Work in progress.

To study blood flow velocity (BFV) changes, serial transcranial Doppler ultrasound (US) examinations of basal cerebral arteries were performed in 47 patients with head injury. Computed tomographic (CT) scans obtained at admission were analyzed for the presence of intracranial hemorrhages. Glasgow Coma Scale scores were obtained at admission in 46 patients. The prevalence of posttraumatic increased BFV was 77% (n = 36). Two groups of patients were identified according to the time of onset of increased BFV. They differed with respect to duration and severity of changes, Glasgow Coma Scale score, and evidence of intracranial hemorrhagic lesions. Low Glasgow Coma Scale scores were predictive of increased BFV within 72 hours after injury (P < .001). Patients with hemorrhages were significantly more prone to experience increased BFV within 72 hours (P < .05); 34% of patients who did not have hemorrhage, however, developed increased BFV. Increased BFV after head trauma is not uniformly found and cannot be explained by one pathologic mechanism.

Antithrombin III administration in premature infant with intracranial hemorrhage

Intracranial hemorrhage (ICH) is a significant cause of mortality and morbidity in the neonatal intensive care unit. Abnormalities of coagulation have been implicated as one of the important causes of intracranial hemorrhage in premature infants. Recent advances in the technique of ultrasound diagnosis of ICH in premature infants have made it possible for us to determine the presence of ICH even in the early stages of the disease. This study was conducted to ascertain whether antithrombin III (AT III) inhibits the progress of ICH in prematurely born infants.

Extracorporeal membrane oxygenation for neonatal respiratory failure: A report of 50 cases

From February 1985 through June 1987, 50 newborn infants in whom maximal ventilator therapy failed (80% predicted mortality) were treated with extracorporeal membrane oxygenation (ECMO) according to the following inclusion criteria: arterial oxygen tension less than 50 torr (alveolar-arterial oxygen gradient greater than 630 torr) for 2 hours or arterial oxygen tension less than 60 torr (alveolar-arterial oxygen gradient greater than 620 torr) for 8 hours. Criteria for exclusion from ECMO therapy included birth weight less than 2000 gm, gestational age less than 35 weeks, presence of intracranial hemorrhage, presence of other major congenital anomalies including cyanotic heart disease, and high levels of ventilatory support for more than 7 days. Mean birth weight was 3.28 +/- 0.56 kg, mean gestational age was 39.6 +/- 1.7 weeks, and mean age at the start of ECMO was 48.6 +/- 36.9 hours. Meconium aspiration, usually associated with persistent pulmonary hypertension, was the most common cause of pulmonary failure (62%). Mean pre-ECMO arterial oxygen tension during maximal ventilatory and pharmacologic support was 34.5 +/- 14.5 torr. Mean ventilatory support immediately before the institution of ECMO was as follows: peak inspiratory pressure 46.8 +/- 9.9 cm H2O, positive end-expiratory pressure 4.6 +/- 1.6 cm H2O, and intermittent mandatory ventilation rate 101.0 +/- 22.7 breaths/min with all patients receiving an inspired oxygen fraction of 1.0. Lung management to prevent pulmonary atelectasis during ECMO consisted of moderate levels of positive end-expiratory pressure (mean 10.3 +/- 2.6 cm H2O, range 8 to 14 in 94% of patients. Other mean ventilator parameters during ECMO were as follows: peak inspiratory pressure 22.8 +/- 1.6 cm H2O, intermittent mandatory ventilation rate 11.8 +/- 2.9, and inspired oxygen fraction 0.21. The overall long-term patient survival rate was 90%. Mean values for arterial blood gases and ventilator settings immediately after the discontinuation of ECMO were as follows: oxygen tension 78.4 +/- 22.1 torr, pH 7.39 +/- 0.10, carbon dioxide tension 37.4 +/- 10.7 torr, peak inspiratory pressure 25.2 +/- 3.9 cm H2O, positive end-expiratory pressure 5.6 +/- 1.2 cm H2O, and intermittent mandatory ventilation rate 41.3 +/- 12.6 with an inspired oxygen fraction of 0.42 +/- 0.17. Despite slightly higher levels of ventilator support (peak inspiratory pressure 46.8 versus 45.0 cm H2O, not significant) mean pre-ECMO oxygen tension was significantly lower than that reported from the National ECMO Registry (34.5 versus 42.0 torr, p less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

RISK FACTOR ASSOCIATED WITH HEARING IMPAIRMENT IN NEONATES

Beginning January, 1983, a comprehensive hearing screening program for all infants less than 28 days of age was initiated. 487 infants at risk for hearing impairment were screened using a list of 20 risk criteria. Infants are classified as high risk when they meet one or more of the risk criteria. Testing involves Behavorial Observation Audiometry (BOA), Tympanography (Tymp) and Auditory Brainstem Response (ABR). Hearing impairment was diagnosed when the infant failed BOA, or ABR on two occasions. Any infant who failed Tymp received otologic exam to rule out middle ear disease. To date 440 infants were classified at high risk and 214 have been tested. 8 (3.8%) have been diagnosed as hearing impaired. The most frequent risk factors to appear in the 8 hearing impaired infants were a birthweight <1500gm (6/8), evidence of intracranial hemorrhage (7/8), and aminoglycoside exposure ≥7 days (5/8). No infant who passed hearing screening has been subsequently diagnosed as hearing impaired during developmental follow-up. This data suggests that a comprehensive aeonatal hearing screening program can identify hearing impaired infants in the neonatal period. Although many other factors have been considered as high risk, birthweight <1500gm, presence of intracranial hemorrhage and aminoglycoside exposure seem to be the most important risk factors.

Diagnostic Cytology of Cerebrospinal Fluid by the Cytocentrifuge Method

Seven hundred seventy-five cerebrospinal fluid samples from 748 patients with neurologic and non-neurologic disorders were studied by a modified cytocentrifuge technic for diagnostic evaluation. The technic proved to be simple, rapid, and inexpensive, and provided consistently good artifact-free morphologic detail suitable for differential and cytochemical analysis. Specimens from 525 patients (70%) had normal cytologic characteristics regardless of underlying condition. Examination of the cerebrospinal fluids of 40 patients (5%) revealed hemorrhage, confirming the presence of intracranial hemorrhage. Inflammatory reactions of various types (acute, chronic, and mixed) were encountered in 120 patients (16%). The appearance of neoplastic cells in cerebrospinal fluid was sometimes the first indication of malignancy. Twenty-six patients (4%) had tumor cells of various types in their cerebrospinal fluids on initial examination. Twenty patients (3%) had abnormal cells initially classified as suspect for malignancy; tumor cells subsequently were found in the spinal fluids of 11 of these, while five were proven to have neoplasms at autopsy without having had tumor cells found in their cerebrospinal fluids. There was no false-positive result. Samples of cerebrospinal fluid from 17 patients (2%) were classified as non-diagnostic, usually because of autolysis.

Hepatic Cell Necrosis in the Newborn

One hundred and forty-seven infants who died from birth to 7 days of age were studied for the relation of hepatic cell necrosis to other pathological conditions. Disseminated hepatic necrosis was significantly correlated with congenital heart disease, and hypoplastic left heart complex and coarctation of the aorta were more frequently associated with disseminated hepatic necrosis than were other types of congenital heart disease. The microscopic features of the liver in these types of congenital heart disease are not those of congestive heart failure, and the hepatic changes observed are considered more probably due to decreased arterial blood flow than to passive venous congestion. Localized hepatic necrosis was significantly correlated with gastroschisis, omphalocele, or diaphragmatic hernia, and hemorrhage in portal areas was associated with the presence of intracranial hemorrhage.