Aminocaproic acid reduces the risk of secondary hemorrhage in patients with traumatic hyphema. A phase III, multicenter, randomized, placebo-controlled clinical trial of topical aminocaproic acid (Caprogel) in the management of traumatic hyphema. Topical aminocaproic acid in the treatment of traumatic hyphema. Aminocaproic acid decreases secondary hemorrhage after traumatic hyphema. Topical aminocaproic acid to prevent rebleeding in cases of traumatic hyphema. Traumatic hyphema. Failure of steroids to alter its course: a double-blind prospective study. Clinical evaluation of aminocaproic acid for managing traumatic hyphema in children. Aminocaproic acid in the treatment of traumatic hyphema. Tranexamic acid and traumatic hyphaema. A prospective study. Aminocaproic acid versus prednisone for the treatment of traumatic hyphema. A randomized clinical trial. Traumatic hyphema in children. Treatment with epsilon-aminocaproic acid. Impact of stereotactic hematoma evacuation on activities of daily living during the chronic period following spontaneous putaminal hemorrhage: a randomized study. The effect of tranexamic acid on secondary haemorrhage after traumatic hyphaema. Benefits and risks of antifibrinolytic therapy in the management of ruptured intracranial aneurysms. A double-blind placebo-controlled study. Prospective, randomized, controlled trial to determine the effect of early enhanced enteral nutrition on clinical outcome in mechanically ventilated patients suffering head injury. Antithrombin treatment in patients with traumatic brain injury: a pilot study. Effects of 2 patterns of prehospital care on the outcome of patients with severe head injury. Prehospital hypertonic saline resuscitation of patients with hypotension and severe traumatic brain injury: a randomized controlled trial. Surgery for hemorrhagic choroidal neovascular lesions of age-related macular degeneration: ophthalmic findings: SST report no. 13. Double-blind comparison of full and partial anemia correction in incident hemodialysis patients without symptomatic heart disease. Effect of hypervolemic therapy on cerebral blood flow after subarachnoid hemorrhage : a randomized controlled trial.
In a prospective, randomized, double-masked study, 34 patients (34 eyes) with nonperforating ocular injury and traumatic hyphema were treated with either aminocaproic acid (Amicar), 100 mg/kg every four hours, up to a maximum of 30 g/d, or placebo for five days. None of 21 patients who were treated with aminocaproic acid rebled, while three (23%) of 13 patients who were treated with placebo rebled. This difference was statistically significant. Of the three patients who rebled, two required surgical intervention, with one patient requiring four surgical procedures. Although complications following aminocaproic acid therapy included light-headedness, nausea and vomiting, and systemic hypotension, only one patient was withdrawn from the study because of drug-related adverse reactions. This study strongly confirms that aminocaproic acid therapy significantly reduces the incidence of secondary hemorrhage following traumatic hyphema. To determine the safety and efficacy of topical aminocaproic acid (Caprogel) in the management of traumatic hyphema.
                Multicenter, randomized, double-masked, placebo-controlled clinical trial.
                A total of 51 patients participated in this trial (power = 36%, 2-tailed test).
                Patients presenting with traumatic hyphema were randomly assigned to 5-day treatment with topical aminocaproic acid or a placebo gel. Patients were monitored daily with ocular examination and vital sign testing for the 5 days of treatment and at 24 and 48 hours after treatment. General physical examination and laboratory testing were performed at baseline and day 5.
                The main efficacy variable was the rate of rebleeding. Secondary efficacy variables included time to hyphema clearance, intraocular pressure, time to secondary hemorrhage, and visual acuity. Safety variables included adverse events, vital signs, and laboratory measurements.
                Rebleeding occurred in 30% of the placebo group (8 of 27; 95% confidence interval [CI] = 14-50%), versus 8% of the treatment group (2 of 24; 95% CI = 1-27%), for an estimated continuity-corrected difference in percentage of patients with bleeding of 17% (95% CI = -3-38%). Secondary efficacy variables were similar in the groups, except that there was a trend towards more visual improvement in the topical aminocaproic acid group (54%) than in the placebo group (30%) at the last measurement (P = 0.08). Adverse events were similar.
                This study provides evidence that topical aminocaproic acid is safe and demonstrates trends towards reducing the rebleeding rate in the management of traumatic hyphema. However, because the study was terminated before complete enrollment, more definitive recommendations will require a larger trial. To determine whether topically applied aminocaproic acid, like systemic aminocaproic acid, effectively reduces secondary hemorrhage after hyphemas and to compare the safety and effectiveness of topical application with those of systemic use and a control group.
                A prospective, randomized, double-masked, multicenter study.
                Sixty-four patients with traumatic hyphema treated with topical or systemic aminocaproic acid and compared with 54 control patients with hyphema. Daily slitlamp examinations for hyphema grading and corneal clarity, initial and final visual acuity, applanation tonometry, and fundus indirect ophthalmoscopy were studied. Follow-up was 6 months to 5 1/2 years (mean, 2.96 years).
                Compared with the control group, topical and systemic aminocaproic acid was statistically significant in preventing secondary hemorrhage. Only 3% (2/64) of the patients who received topical or systemic aminocaproic acid had secondary hemorrhage compared with 22% (12/54) of the control group (P = .002). Final visual acuity was 20/40 or better in 30 patients (86%) in the topical group compared with 23 patients (43%) in the control group (P < .001). Final visual acuity was 20/40 or better in 20 patients (69%) in the systemic aminocaproic acid group compared with 23 patients (43%) in the control group (P = .04). The topical aminocaproic acid group had a final visual acuity of 20/40 or better in 86% of patients, compared with 69% of patients in the systemic group.
                Topical aminocaproic acid appears to be a safe, effective treatment to prevent secondary hemorrhage in traumatic hyphema. It is as effective as systemic aminocaproic acid in reducing secondary hemorrhage. No systemic side effects were observed with topical use. Topical aminocaproic acid provides an effective out-patient treatment for traumatic hyphemas. Forty-eight patients (49 eyes) had nonperforating traumatic hyphema. Twenty-eight patients (28 eyes with hyphema) received oral aminocaproic acid, an antifibrinolytic agent, in a dosage of 100 mg/kg every four hours for five days, up to a maximum daily dose of 30 g. Twenty patients (21 eyes with hyphema) received placebo in an identical regimen. One eye treated with aminocaproic acid rebled; seven eyes receiving the placebo rebled. The results of this study show a statistically significant reduction in the incidence of secondary hemorrhage in the patients receiving aminocaproic acid. To determine the effect of topical aminocaproic acid on the incidence of rebleeding after traumatic hyphema.
                This randomized double blind clinical trial investigated 132 consecutive cases of traumatic hyphema referred to the emergency room of Farabi Eye Hospital in 1998-1999. The patients were randomly divided into three groups: Group 1 received cycloplegic drops only. Group 2 received cycloplegic drops and 2% carboxy polymethylene (CPM) gel as placebo. Group 3 was treated with cycloplegic drops and 25% aminocaproic acid (ACA) in CPM gel (supplied by Messrs. Sina Darou). All patients were treated for five days on an outpatient basis, with a two-week follow-up. The incidence of rebleeding, time needed for clot absorption, and complications of hyphema were recorded and analyzed using the chi-square and Student's t-tests and logistic regression modeling.
                Rebleeding occurred in 8 eyes of 52 patients in group 1 (15.4%), 7 eyes of the 39 patients in group 2 (17.9%) and 5 eyes of the 41 patients in group 3 (12.2%). This difference was not significant. The time needed for clot absorption in groups 1, 2 and 3 was respectively 9.5 +/- 3.9, 9.3 +/- 4.2 and 11.15 +/- 4.7 days, the difference between group 3 and the other two groups being statistically significant (p<0.04).
                Topical 25% ACA is not effective in reducing the incidence of rebleeding and lengthens the time needed for clot absorption. Forty-three patients with traumatic hypema were studied prospectively in a controlled, double-blind study. Twenty-three patients received prednisone and 20 received a lactose placebo. Secondary hemorrhages occurred in 16% of all patients. There was no significant difference in the incidence of secondary hemorrhage between the two groups (P = .85). There is no evidence that prednisone (40 mg/day) decreases the incidence of secondary hemorrhage. There was no significant difference in final visual acuities between the two groups. Patients with initially larger hyphemas do not appear to have worse final visual acuities. Hyphemas without secondary hemorrhage had a uniformly good prognosis. Although final visual acuities were worse in eyes with secondary hemorrhage, associated ocular injuries rather than blood-related complications accounted for the decreased visual acuity. The purpose of this study is to determine the incidence of secondary hemorrhage after traumatic hyphema in children and to evaluate the efficacy of epsilon aminocaproic acid in reducing this incidence.
                In a prospective, randomized, double-blind study performed between November 1987 and February 1994, 94 children admitted for traumatic hyphema were assigned to receive either aminocaproic acid (n = 48) (100 mg/kg every 4 hours; maximum, 30 g daily) or placebo (n = 46) for 5 days. Patients who had ingested aspirin in the week preceding admission were excluded from the study.
                Mean age of the patients was 9.4 years. Black patients comprised 4% of the study population. Secondary hemorrhage occurred in only three patients (3.2%), two from the placebo group and one from the aminocaproic acid group, none of whom had any complications. The duration of hospital stay and the clot resorption times were increased significantly in the aminocaproic acid group (P < 0.001).
                The authors report a very low incidence of secondary hemorrhage compared with most previous studies. This difference is likely related to the small proportion of black patients in our study and to the exclusion of patients having ingested aspirin, two factors that seem to be associated with higher rates of rebleeding. The efficacy of aminocaproic acid could not be determined due to the low incidence of hemorrhage. The results of this study, however, suggest that the incidence of secondary hemorrhage in white patients without prior ingestion of aspirin is insufficient to justify routine use of aminocaproic acid in managing traumatic hyphema. Rather, an individualized decision based on the risk factors of each patient would seem more appropriate to avoid a slower clot resorption time and possible side effects of this medication. Of 59 patients with traumatic hyphema studied prospectively, 32 received aminocaproic acid, an antifibrinolytic agent, to prevent secondary hemorrhage. The remaining 27 patients received placebo in an identical manner. Of the aminocaproic acid-treated patients, only one (3%) rebled, while nine patients (33%) receiving placebo suffered secondary hemorrhage. The results of this study indicate a statistically significant reduction (P less than .01) in the incidence of rebleeding in patients treated with this drug. 112 patients with traumatic hyphaema were investigated prospectively over a period of 3 years. 53 had conservative treatment and 59 tranexamic acid treatment. They were hospitalized, but fully mobilized. Both groups were given supplementary local therapy with glucocorticoids and mydriatics as well as monocular patching. In neither group was any re-bleeding seen. The resorption of blood was delayed in the tranexamic treated patients, which may be taken as indirect proof of the efficacy of the treatment. The longer persistence of blood in the anterior chamber in the tranexamic acid treated group caused no complication. The treatment was well tolerated. In both departments treatment with tranexamic acid had replaced the bed rest treatment. One hundred twelve patients who sustained hyphema after blunt trauma were enrolled in a double-blind randomized clinical trial to determine the relative efficacies of aminocaproic acid (Amicar) and systemic prednisone for reducing the rate of secondary hemorrhage. Fifty-six patients received an oral dosage of 50 mg/kg of aminocaproic acid every 4 hours for 5 days, up to a maximum of 30 g daily, and 56 patients received an oral dosage of 40 mg of prednisone daily (adjusted for weight) in two divided doses. Placebo pills and liquids were given to each patient to mask the treatment schedules. There were no statistically significant differences between the patient populations for any demographic or clinical characteristic (e.g., visual acuity, intraocular pressure [IOP], initial hyphema size) measured in the study. Blacks comprised 53% of the study population, and the mean age of the patients was 23.5 years. Four patients in each of the treatment groups experienced a secondary hemorrhage; the rebleed rate was 7.1% in each group. Forty-nine patients, ages 3 to 18 years, who sustained nonpenetrating unilateral trauma with hyphemas were assigned randomly to receive either 100 mg/kg of epsilon-aminocaproic acid (EACA), an antifibrinolytic agent, orally every 4 hours for 5 days (maximum 30 g/day) or a placebo. No patients ingested acetylsalicylic acid (ASA)-containing compounds before or during admission. Two patients of 24 treated with EACA and 1 of 25 given placebo had rebleeds. The hyphemas in the EACA-treated group took significantly longer to clear (mean, 5.3 versus 2.6 days; P less than 0.001). Because of the low incidence of rebleeds in the placebo group, the efficacy of EACA in reducing the rate of rebleeds could not be determined. Further studies with this drug, controlling for age, race, sickle trait, and pre-admission antiplatelet agents should be undertaken before its routine use in traumatic hyphema management can be recommended. Stereotactic evacuation of hematoma has been reported to reduce the incidence of mortality and to improve functional outcome in patients with spontaneous putaminal hemorrhage. Stereotactic evacuation of hematoma has not been widely accepted as a standard therapy, however, because its effect on functional outcome has been regarded as marginal and there have been no randomized trials with sufficient statistical power to quantify the benefits of this procedure. The authors reassessed the value of stereotactic evacuation of hematoma by analyzing its impact on activities of living during the chronic period following spontaneous putaminal hemorrhage in a randomized study.
                Four hundred ninety patients were entered into the study. The severity of their hemorrhages was graded neurologically on admission (neurological grades: 1, eyes are open; 2, eyes are closed but open to weak stimuli; 3, eyes are closed but open to strong stimuli; 4, eyes do not open but extremities move to stimuli; and 5, eyes do not open and extremities do not move to stimuli). Patients with Grade 2 and those with Grade 3 were randomized into two groups with different treatment protocols (Group I, stereotactic evacuation of the hematoma; and Group II, conservative treatment). Patients assigned neurological Grade 4 or 5 were excluded from the study because a large-scale retrospective study in Japan revealed that surgical treatment in patients assigned to these neurological grades does not improve functional outcome. Among the 490 patients, 242 were randomized strictly. This patient population comprised 148 men and 94 women ranging in age from 38 to 80 years (mean 60.5 years). Compared with Group II, Group I treatment resulted in a lower mortality rate and better recovery to functional independence in patients with neurological Grade 3. In patients with Grade 2, Group I treatment contributed to a better recovery of functional outcome and a lower mortality rate, but the difference was not significant. Multivariate analysis confirmed that stereotactic evacuation of the hematoma was contributory to a better recovery in functional outcome.
                Stereotactic evacuation of hematoma is clearly of value in selected patients with spontaneous putuminal hemorrhage, whose eyes are closed but will open in response to strong stimuli (neurological Grade 3) on admission. During the period from March 1978 to November 1979, 232 consecutive patients with traumatic hyphaema were allocated by admission-date to conservative treatment and to treatment with the antifibrinolytic drug tranexamic acid. Secondary haemorrhage occurred in only two of 102 tranexamic acid treated patients, while secondary haemorrhage occurred in 12 out of 130 conservatively treated patients. This difference was statistically significant. Some clinical aspects of the rebleeding cases are presented and briefly discussed. One hundred patients with a verified subarachnoid haemorrhage were studied in a double blind, placebo-controlled trial at a single centre to determine the value and relative risks of tranexamic acid (TXA) in the management of ruptured intracranial aneurysms. The incidence of recurrent haemorrhage between active and placebo groups was identical (12%) and the mortality from recurrent haemorrhage was 7% and 5%, respectively. The overall incidence of cerebral infarction before surgery, at discharge and at 6 months follow-up was greater in the TXA group (27%) than in the control group (11%). Post-operative cerebral ischaemia was significantly more frequent in the active, 18 of 29 as compared to 6 of 32 patients, in the placebo group. In a fifth of the patients in whom cerebral blood flow was estimated there was a significant reduction of cerebral blood flow (CBF) on the side of the ruptured aneurysm in the TXA treated group. It is suggested that this may be the cause of the increased incidence of cerebral ischaemia in this group. There was no significant difference in the incidence of cerebral vasospasm, hydrocephalus, visual disturbances and gastrointestinal disturbances. More fatalities were encountered from ischaemia and recurrent haemorrhage in the TXA group but these differences did not reach statistical significance at the 5% level. Given that disability was due to either vasospasm or recurrent haemorrhage than a patient under TXA treatment was significantly more likely to have disability due to vasospasm (p less than 0.04); the reverse was true for the placebo patient (p less than 0.05). To determine the effect of early enhanced enteral nutrition (EN) on clinical outcome of head-injured patients.
                Prospective, randomized, controlled trial.
                Tertiary neurosurgical and trauma center.
                Eighty-two patients suffering head injury and requiring mechanical ventilation.
                Patients were randomized to receive standard EN (gradually increased from 15 mL/hr up to estimated energy and nitrogen requirements) or enhanced EN (started at a feeding rate that met estimated energy and nitrogen requirements) from day 1. Good neurologic outcome (Glasgow Outcome Scale score of 4 or 5) was determined at 3 and 6 months after injury, and the incidence of infective and total complications was determined during the hospital stay up to 6 months.
                Disease severity assessed by best preintubation Glasgow Coma Scale score, pupillary responses, Injury Severity Score, Acute Physiology and Chronic Health Evaluation II score, computed tomographic scan categorization, and age was similar in both groups. Intervention patients had a higher percentage of energy (p = .0008) and nitrogen (p<.0001) requirements met by EN in the first week after injury. Neurologic outcome at 6 months was similar between groups, but there was a tendency for more intervention patients to have a good neurologic outcome at 3 months than control patients (61% vs. 39%, p = .08). Fewer intervention patients had an infective complication (61% vs. 85%, p = .02) or more than one total complication (37% vs. 61%, p = .046) compared with control patients. Enhanced EN was associated with a reduction in the ratio of serum concentration of C-reactive protein to albumin up to day 6 after injury (p = .004).
                Enhanced EN appears to accelerate neurologic recovery and reduces both the incidence of major complications and postinjury inflammatory responses. This study will determine if early administration of antithrombin concentrate to patients with traumatic brain injury (TBI) can inhibit or significantly shorten the time of coagulopathy. The progress of brain injury monitored by computed tomographic scan (CT) was also assessed, as was the time needed for intensive care and outcome related to Glasgow outcome scale (GOS). Twenty-eight patients with isolated brain trauma verified with CT were included in either of two parallel groups. The Glasgow coma score (GCS) was mean 7.5, and median 7.0; signifying a moderate to severe traumatic brain injury but with a mortality of only 3.5%. The patients randomized to antithrombin treatment received a total of 100 U/kg BW during 24 hours. To measure hypercoagulability, soluble fibrin (SF), D-dimer (D-d), and thrombin-antithrombin complex (TAT) were assessed together with antithrombin (AT) and routine coagulation tests. Before treatment, SF, D-d, and TAT were markedly increased in both groups. Soluble fibrin and D-dimer (measured after treatment began) appeared to decrease faster in the AT group, and there was a statistically significant difference between the groups at 36 hours for SF and at 36 hours, 48 hours, and at Day 3 for D-d. Thrombin-antithrombin complex levels were very high in both groups but, surprisingly, showed no significant difference between the groups. The authors conclude that antithrombin concentrate administered to patients with severe TBI resulted in a marginal reduction of hypercoagulation. We could not detect any obvious influence by antithrombin on brain injury progress, on CT, or on outcome or time needed for intensive care. A pattern of prehospital care combining advanced life support, physician staffing, and helicopter transport improves the outcome of patients with severe brain injuries, compared with combined expanded basic life support, nurse staffing, and ground transport.
                Inception cohort from the data set of a population-based, prospective study on major trauma.
                Prehospital and hospital trauma systems of an Italian region.
                All patients with major trauma (Injury Severity Score, >or=16) and severe head injury (Abbreviated Injury Scale score for the head, >or=4) rescued alive from March 1, 1998, to February 28, 1999, who received either form of care. Patients with self-inflicted injuries were excluded. The 184 patients who met the entry criteria were divided equally between care groups.
                None.
                Mortality at 30 days and Glasgow Outcome Scale score of survivors.
                After verifying the comparability of the cohorts, no survival or disability benefit could be demonstrated (95% confidence interval [CI] of the odds ratio for mortality [helicopter/ambulance] [95% CI 1], 0.72 to 2.67; 95% CI of the difference in Glasgow Outcome Scale score medians between helicopter and ambulance groups [95% CI 2], 0.0 to 0.0). Similar results were derived from analyses restricted to the subgroups identified by low (<or=90 mm Hg) roadside systolic blood pressure (95% CI 1, 0.58 to 7.17; 95% CI 2, -1 to 2) and by need for urgent neurosurgical intervention (95% CI 1, 0.16 to 2.60; 95% CI 2, 0 to 2). Exclusion from the ambulance group of victims rescued in urban areas did not change the results (95% CI 1, 0.80 to 3.24; 95% CI 2, 0.0 to 0.0). Stratification by age, Injury Severity Score, and Glasgow Coma Scale score demonstrated a small survival benefit (95% CI 1, 1.12 to 2.12) in the ambulance subgroup with Glasgow Coma Scale score from 10 to 12. Multiple logistic regression analysis confirmed that the group did not affect mortality.
                This study was conceived to emphasize the supposed advantages of the combined helicopter, physician, and advanced life-support rescue. No increased benefit compared with the simpler rescue group could be demonstrated. Prehospital hypertonic saline (HTS) resuscitation of patients with traumatic brain injury (TBI) may increase survival but whether HTS improves neurological outcomes is unknown.
                To determine whether prehospital resuscitation with intravenous HTS improves long-term neurological outcome in patients with severe TBI compared with resuscitation with conventional fluids.
                Double-blind, randomized controlled trial of 229 patients with TBI who were comatose (Glasgow Coma Scale score, <9) and hypotensive (systolic blood pressure, <100 mm Hg). The patients were enrolled between December 14, 1998, and April 9, 2002, in Melbourne, Australia.
                Patients were randomly assigned to receive a rapid intravenous infusion of either 250 mL of 7.5% saline (n = 114) or 250 mL of Ringer's lactate solution (n = 115; controls) in addition to conventional intravenous fluid and resuscitation protocols administered by paramedics. Treatment allocation was concealed.
                Neurological function at 6 months, measured by the extended Glasgow Outcome Score (GOSE).
                Primary outcomes were obtained in 226 (99%) of 229 patients enrolled. Baseline characteristics of the groups were equivalent. At hospital admission, the mean serum sodium level was 149 mEq/L for HTS patients vs 141 mEq/L for controls (P<.001). The proportion of patients surviving to hospital discharge was similar in both groups (n = 63 [55%] for HTS group and n = 57 [50%] for controls; P =.32); at 6 months, survival rates were n = 62 (55%) in the HTS group and n = 53 (47%) in the control group (P =.23). At 6 months, the median (interquartile range) GOSE was 5 (3-6) in the HTS group vs 5 (5-6) in the control group (P =.45). There was no significant difference between the groups in favorable outcomes (moderate disability and good outcome survivors [GOSE of 5-8]) (risk ratio, 0.99; 95% confidence interval, 0.76-1.30; P =.96) or in any other measure of postinjury neurological function.
                In this study, patients with hypotension and severe TBI who received prehospital resuscitation with HTS had almost identical neurological function 6 months after injury as patients who received conventional fluid. To present best-corrected visual acuity (BCVA) findings and other clinical outcomes from eyes of patients enrolled in one of the Submacular Surgery Trials (SST) evaluating surgical removal versus observation of predominantly hemorrhagic subfoveal choroidal neovascularization (CNV) associated with age-related macular degeneration.
                Randomized clinical trial (SST Group B Trial).
                Eligible patients had subfoveal choroidal neovascular lesions greater than 3.5 disk areas (8.9 mm2) composed of at least 50% blood (either blood or CNV underlying the center of the foveal avascular zone) and BCVA of 20/100 to light perception in the study eye.
                Patients were assigned randomly at time of enrollment to observation or surgical removal of blood and any associated CNV.
                A successful outcome was defined a priori as either improvement in visual acuity (VA), no change in VA, or a decline in VA of no more than 1 line (7 letters) from baseline to the 24-month examination based on an intent-to-treat analysis.
                Of 336 patients enrolled, 168 were assigned to each treatment arm; treatment arms were balanced by baseline characteristics. Of 1501 expected examinations 3 months through 36 months after baseline, 1370 (91%) were performed. Loss of > or =2 lines (> or =8 letters) of VA occurred in 56% of surgery eyes, versus 59% of observation eyes examined at 24 months. Although severe loss of VA was not the primary outcome of interest, surgery more often prevented such loss: 36% in the observation arm versus 21% in the surgery arm at the 24-month examination (chi2 P = 0.004). Of initially phakic eyes, the cumulative percentage that had undergone cataract surgery by 24 months was 44% in the surgery arm, compared with 6% in the observation arm. Twenty-seven eyes (16%) in the surgical arm, compared with 3 eyes (2%) in the observation arm, had a rhegmatogenous retinal detachment (RD).
                Submacular surgery as performed in the SST Group B Trial did not increase the chance of stable or improved VA (the primary outcome of interest) and was associated with a high risk of rhegmatogenous RD, but did reduce the risk of severe VA loss in comparison with observation. This article contains additional online-only material available at http://www.ophsource.com/periodicals/ophtha. It is unclear whether physiologic hemoglobin targets lead to cardiac benefit in incident hemodialysis patients without symptomatic heart disease and left ventricular dilation. In this randomized, double-blind study, lower (9.5 to 11.5 g/dl) and higher (13.5 to 14.5 g/dl) hemoglobin targets were generated with epoetin alpha over 24 wk and maintained for an additional 72 wk. Major eligibility criteria included recent hemodialysis initiation and absence of symptomatic cardiac disease and left ventricular dilation. The primary outcome measure was left ventricular volume index (LVVI). The study enrolled 596 patients. Mean age, duration of dialysis therapy, baseline predialysis hemoglobin, and LVVI were 50.8 yr, 0.8 yr, 11.0 g/dl, and 69 ml/m2, respectively; 18% had diabetic nephropathy. Mean hemoglobin levels in the higher and lower target groups were 13.3 and 10.9 g/dl, respectively, at 24 wk. Percentage changes in LVVI between baseline and last value were similar (7.6% in the higher and 8.3% in the lower target group) as were the changes in left ventricular mass index (16.8 versus 14.2%). For the secondary outcomes, the only between-group difference was an improved SF-36 Vitality score in the higher versus the lower target group (1.21 versus -2.31; P = 0.036). Overall adverse event rates were similar in both target groups; higher (P < 0.05) rates of skeletal pain, surgery, and dizziness were seen in the lower target group, and headache and cerebrovascular events were seen in the higher target group. Normalization of hemoglobin in incident hemodialysis patients does not have a beneficial effect on cardiac structure, compared with partial correction. Cerebral blood flow (CBF) is reduced after subarachnoid hemorrhage (SAH), and symptomatic vasospasm is a major cause of morbidity and mortality. Volume expansion has been reported to increase CBF after SAH, but CBF values in hypervolemic (HV) and normovolemic (NV) subjects have never been directly compared.
                On the day after aneurysm clipping, we randomly assigned 82 patients to receive HV or NV fluid management until SAH day 14. In addition to 80 mL/h of isotonic crystalloid, 250 mL of 5% albumin solution was given every 2 hours to maintain normal (NV group, n=41) or elevated (HV group, n=41) cardiac filling pressures. CBF ((133)xenon clearance) was measured before randomization and approximately every 3 days thereafter (mean, 4.5 studies per patient).
                HV patients received significantly more fluid and had higher pulmonary artery diastolic and central venous pressures than NV patients, but there was no effect on net fluid balance or on blood volume measured on the third postoperative day. There was no difference in mean global CBF during the treatment period between HV and NV patients (P=0.55, random-effects model). Symptomatic vasospasm occurred in 20% of patients in each group and was associated with reduced minimum regional CBF values (P=0.04). However, there was also no difference in minimum regional CBF between the 2 treatment groups.
                HV therapy resulted in increased cardiac filling pressures and fluid intake but did not increase CBF or blood volume compared with NV therapy. Although careful fluid management to avoid hypovolemia may reduce the risk of delayed cerebral ischemia after SAH, prophylactic HV therapy is unlikely to confer an additional benefit.
Traumatic hyphema in the absence of other intraocular injuries, uncommonly leads to permanent loss of vision. Complications resulting from secondary hemorrhage could lead to permanent impairment of vision, especially in patients with sickle cell trait/disease. We found no evidence to show an effect on visual acuity by any of the interventions evaluated in this review. Although evidence is limited, it appears that patients with traumatic hyphema who receive aminocaproic acid or tranexamic acid are less likely to experience secondary hemorrhaging. However, hyphema in patients on aminocaproic acid take longer to clear.
Other than the possible benefits of antifibrinolytic usage to reduce the rate of secondary hemorrhage, the decision to use corticosteroids, cycloplegics, or non-drug interventions (such as binocular patching, bed rest, or head elevation) should remain individualized because no solid scientific evidence supports a benefit. As these multiple interventions are rarely used in isolation, further research to assess the additive effect of these interventions might be of value.