Andreas Raabe and Bertil Romner
Kent D. Yundt, Ralph G. Dacey Jr. and Michael N. Diringer
✓ The authors reviewed clinical and financial data for all patients treated for nontraumatic subarachnoid hemorrhage (SAH) and unruptured cerebral aneurysms at their institution between June 1993 and December 1994. This study sought to identify specific areas of high resource utilization that may be amenable to reduction of expenditures without compromising quality of care. Detailed hospital financial data were correlated with clinical grade and course. Areas of high resource use were identified based on patient charges and category-specific loaded hospital cost. Patients were divided into four groups: Group 1, surgically treated unruptured aneurysms (28 patients); Group 2, acute SAH (42 patients); Group 3, SAH with vasospasm (32 patients); and Group 4, SAH with negative angiogram (10 patients). Total cost per patient (mean ± standard deviation in thousands of U.S. dollars) was highest for Group 3 (38.4 ± 21.3; vs. Group 1, 12.7 ± 8.8; Group 2, 22.6 ± 20.9; and Group 4, 25.0 ± 33.5) and correlated with hospital length of stay, Hunt and Hess grade, and Fisher grade. Areas of highest hospital cost were not always reflected in patient charges. The three areas of highest cost accounted for 48.5% of the total cost and were: 1) intensive care unit (ICU) room (Group 1, 2.5 ± 3.5; Group 2, 7.0 ± 9.2; Group 3, 11.0 ± 7.8; and Group 4, 7.9 ± 14.1); 2) arteriography (Group 1, 1.7 ± 1.2; Group 2, 2.1 ± 1.5; Group 3, 4.1 ± 2.1; and Group 4, 2.2 ± 0.7); and 3) ICU medicosurgical supplies (Group 1, 1.7 ± 0.8; Group 2, 2.0 ± 1.5; Group 3, 3.7 ± 1.7; and Group 4, 2.0 ± 3.0). It is concluded that cost containment strategies should be based on cost rather than charge and novel approaches will be required to reduce the cost of treating patients with SAH. Such approaches might include preventing vasospasm, reducing ICU stay, selective use of arteriography, and reducing the cost of supplies.
R. Loch Macdonald
Michael N. Diringer, Venkatesh Aiyagari, Allyson R. Zazulia, Tom O. Videen and William J. Powers
Recent observations indicate that traumatic brain injury (TBI) may be associated with mitochondrial dysfunction. This, along with growing use of brain tissue PO2 monitors, has led to considerable interest in the potential use of ventilation with 100% oxygen to treat patients who have suffered a TBI. To date, the impact of normobaric hyperoxia has only been evaluated using indirect measures of its impact on brain metabolism. To determine if normobaric hyperoxia improves brain oxygen metabolism following acute TBI, the authors directly measured the cerebral metabolic rate for oxygen (CMRO2) with positron emission tomography before and after ventilation with 100% oxygen.
Baseline measurements of arterial and jugular venous blood gases, mean arterial blood pressure, intracranial pressure, cerebral blood flow (CBF), cerebral blood volume, oxygen extraction fraction, and CMRO2 were made at baseline while the patients underwent ventilation with a fraction of inspired oxygen (FiO2) of 0.3 to 0.5. The FiO2 was then increased to 1.0, and 1 hour later all measurements were repeated.
Five patients were studied a mean of 17.9 ±5.8 hours (range 12–23 hours) after trauma. The median admission Glasgow Coma Scale score was 7 (range 3–9). During ventilation with 100% oxygen, there was a marked rise in PaO2 (from 117 ± 31 to 371 ± 99 mm Hg, p < 0.0001) and a small rise in arterial oxygen content (12.7 ± 4.0 to 13.3 ± 4.6 vol %, p = 0.03). There were no significant changes in systemic hemodynamic or other blood gas measurements. At the baseline evaluation, bihemispheric CBF was 39 ± 12 ml/100 g/min and bihemispheric CMRO2 was 1.9 ± 0.6 ml/100 g/min. During hyperoxia there was no significant change in either of these measurements. (Values are given as the mean ± standard deviation throughout.)
Normobaric hyperoxia did not improve brain oxygen metabolism. In the absence of outcome data from clinical trials, these preliminary data do not support the use of 100% oxygen in patients with acute TBI, although larger confirmatory studies are needed.
Michael N. Diringer, Jeffrey R. Kirsch, Daniel F. Hanley and Richard J. Traystman
✓ The authors tested the hypothesis that cerebral blood flow (CBF) reactivity to CO2 was blunted following subarachnoid hemorrhage (SAH). Subarachnoid hemorrhage was produced in five cats by performing four cisterna magna injections of blood in each (SAH Group). A second group of six cats was treated with an antifibrinolytic agent (AF) in addition to four cisterna magna blood injections (SAH + AF Group). Four cats received AF and four cisterna magna injections of saline (Control Group). The presence or absence of basilar artery vasospasm was determined by comparing baseline and follow-up selective angiograms. Cerebral blood flow reactivity was determined by randomly varying the concentration of inspired CO2 to alter PaCO2 from 20 to 75 mm Hg. Regional CBF was measured with radiolabeled microspheres. Basilar artery vasospasm was seen following subarachnoid injection of blood but not of saline. Normocapnic CBF was similar in all three groups in the brain stem (mean ± standard error of the mean: SAH Group 46 ± 6, SAH + AF Group 46 ± 6, and Control Group 44 ± 9 ml/min/100 gm) and in the supratentorial compartment (SAH Group 53 ± 8, SAH + AF Group 61 ±9, and Control Group 51 ± 13 ml/min/100 gm). At intermediate levels of hypercarbia (PaCO2 50 ± 3 mm Hg), CBF increased similarly in all three groups (SAH Group 161% ± 32%, SAH + AF Group 118% ± 33%, and Control Group 174% ± 19% compared to baseline); at higher levels of PaCO2 (60 ± 3 mm Hg), CBF values were SAH Group 265% ± 50%, SAH + AF Group 205% ± 47%, and Control Group 159% ± 30% of baseline. At the highest level of PaCO2 (75 ± 6 mm Hg), supratentorial CBF did not increase as much in the SAH + AF Group as in the Control Group (179% ± 59% vs. 463% ± 58% of baseline, respectively). The authors conclude that, in this model of SAH, there is no change in normocapnic CBF; however, blood flow reactivity to hypercarbia is blunted. It is possible that this may result from a combination of narrowing of proximal large vessels and globally impaired reactivity of small vessels.
Francisco de Assis Aquino Gondim, Venkatesh Aiyagari, Angela Shackleford and Michael N. Diringer
Mannitol is commonly used for acute insults to the central nervous system; acute renal insufficiency is one of its side effects. The cause of mannitol-induced acute renal insufficiency (MI-ARI) is unknown, although elevated osmolality has been implicated as a risk factor. The goal of this study was to determine risk factors and outcomes of MI-ARI and to determine whether osmolality is associated with MI-ARI.
The authors retrospectively reviewed the cases of 95 patients treated with mannitol to determine if MI-ARI (an increase in the creatinine level of > 0.5 mg/dl if the baseline value is < 2 mg/dl or an increase > 1 mg/dl if the baseline value is > 2 mg/dl) is linked to elevated osmolality. The 11 patients (11.6%) in whom MI-ARI developed did not exhibit significant differences in patient age, sex, or race; history of cerebrovascular disease or smoking; baseline renal function; or Glasgow Coma Scale score from those in whom MI-ARI did not occur. Cumulative fluid balance, exposure to nephrotoxic drugs, and the peak osmolality and osmotic gap before onset of renal insufficiency were also similar in the two groups. Factors predictive of the onset of MI-ARI included a higher Acute Physiology and Chronic Health Evaluation (APACHE) II score on admission and a history of diabetes, coronary artery disease, congestive heart failure, and hypertension. The presence of congestive heart failure and a high APACHE II score were the only factors independently associated with a higher likelihood of MI-ARI according to a multivariate analysis. Renal function spontaneously returned to baseline in all patients. With maintenance of normovolemia and monitoring of the osmotic gap, MI-ARI appears to be associated with chronic insults to the kidneys such as a history of diabetes or hypertension, not mannitol dose, or osmolality.
Use of osmolality to limit mannitol use and thus prevent MI-ARI may be unwarranted. Prospective studies are needed.
Fang Qu, Venkatesh Aiyagari, DeWitte T. Cross III, Ralph G. Dacey Jr. and Michael N. Diringer
When subarachnoid hemorrhage (SAH) is caused by an aneurysm or other vascular anomaly, surgery or en-dovascular treatment is generally indicated. Nevertheless, some patients with SAH do not receive such therapy. The objective of this study was to characterize the patients who do not receive treatment.
The records of all patients with SAH who were admitted to a tertiary care center during a 9-year period were retrospectively reviewed. Untreated patients were classified into one of three groups based on angiographic results. Demographic, clinical, and neuroimaging findings and outcomes were compared between these three groups and between treated and untreated patients.
Definitive treatment of SAH was provided in 477 patients and 166 were untreated. Untreated patients were older, had a worse neurological status on presentation, and a higher mortality rate (43.4% compared with 11.7%). Among these, 76 had normal angiographic results and a low mortality rate (6.6%). Fifty-two patients in whom no cerebral angiogram was obtained (mostly because of their neurological condition) had the highest mortality rate (92.3%). Of 38 patients with abnormal angiographic results 50% died, mostly due to rebleeding. Among elderly patients or those with a severe neurological deficit, outcome was significantly better in the ones who were treated.
A significant proportion of patients who were admitted with SAH did not receive definitive therapy. Major reasons for this included normal results on angiographic studies and poor clinical grade. Untreated patients with normal angiographic results had a good outcome, whereas those in whom angiography was not performed and those with abnormal angiographic results had a high mortality rate from the consequences of the initial hemorrhage in the first instance or rebleeding in the second. Although among elderly patients and those with a poor clinical grade the mortality rate was lower among those who received treatment, a definitive conclusion favoring treatment in these high-risk groups can only be drawn from a prospective randomized study.
Michael G. Fehlings and Andrew Baker
Rajat Dhar, Michael T. Scalfani, Allyson R. Zazulia, Tom O. Videen, Colin P. Derdeyn and Michael N. Diringer
Critical reductions in oxygen delivery (DO2) underlie the development of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH). If DO2 is not promptly restored, then irreversible injury (that is, cerebral infarction) may result. Hemodynamic therapies for DCI (that is, induced hypertension [IH] and hypervolemia) aim to improve DO2 by raising cerebral blood flow (CBF). Red blood cell (RBC) transfusion may be an alternate strategy that augments DO2 by improving arterial O2 content. The authors compared the relative ability of these 3 interventions to improve cerebral DO2, specifically their ability to restore DO2 to regions where it is impaired.
The authors compared 3 prospective physiological studies in which PET imaging was used to measure global and regional CBF and DO2 before and after the following treatments: 1) fluid bolus of 15 ml/kg normal saline (9 patients); 2) raising mean arterial pressure 25% (12 patients); and 3) transfusing 1 U of RBCs (17 patients) in 38 individuals with aneurysmal SAH at risk for DCI. Response between groups in regions with low DO2 (< 4.5 ml/100 g/min) was compared using repeated-measures ANOVA.
Groups were similar except that the fluid bolus cohort had more patients with symptoms of DCI and lower baseline CBF. Global CBF or DO2 did not rise significantly after any of the interventions, except after transfusion in patients with hemoglobin levels < 9 g/dl. All 3 treatments improved CBF and DO2 to regions with impaired baseline DO2, with a greater improvement after transfusion (23%) than hypertension (14%) or volume loading (10%); p < 0.001. Transfusion also resulted in a nonsignificantly greater (47%) reduction in the number of brain regions with low DO2 when compared with fluid bolus (7%) and hypertension (12%) (p = 0.33).
The IH, fluid bolus, and blood transfusion interventions all improve DO2 to vulnerable brain regions at risk for ischemia after SAH. Transfusion appeared to provide a physiological benefit at least comparable to IH, especially among patients with anemia, but transfusion is associated with risks. The clinical significance of these findings remains to be established in controlled clinical trials.