Faculty Bibliography

The need for organ donation has become a growing concern over that last decade as the gap between organ donors and those awaiting transplant widens. According to UNOS, as of 8/2009, there were 102,962 patients on the transplant waiting list and only 6,004 donors in 2009 (UNOS.org. Accessed 4/8/2009). In 2008, an estimated 17 patients died each day awaiting transplant (OPTN.org). Though currently most organ donations come after brain death (DND or donation after neurological death), tissue donation (cornea, skin, bone, and musculoskeletal tissue), and donation after cardiac death (DCD) and are also possible. The term "extended criteria donor" refers to potential donors over 60 years of age or age 50-59 years plus 2 of the 3 following criteria: stroke as the cause of death, creatnine > 1.5 meq/dl, or a history of hypertension. Historically, extended criteria donors have had a lower organ yield per donor. In order to preserve the choice of organ donation for the family, intensive management of the potential organ donor is necessary. Since each potential donor could save seven lives or more, nihilism in the care of such patients can have far reaching ramifications. This article describes intensive care management practices that can optimize organ donation.

To address the gap between organs available for transplant and the number of patients on the transplant waiting list, the Joint Commission on the Accreditation of Healthcare Organizations, Institute of Medicine, United Network for Organ Sharing and the federal government have recommended the increased used of donation after cardiac death (DCD) (JCAHOnline http://www.jointcommission.org/Library/JCAHOnline/jo_06.06.htm ; UNOS, Highlights of the June Board Meeting, 2006). DCD is defined as organ donation once death is declared after irreversible cessation of circulatory and respiratory functions, as opposed to brain death (donation after neurological death). Though DCD is one of the fastest growing categories of organ donors, it comprises only 8% of all deceased donors (Steinbrook in N Engl J Med 357:209-213, 2007). Prior to 1968, when the Ad Hoc Committee of Harvard Medical School proposed a neurological definition of death based on brain-death criteria, organs from deceased donors came from patients who had suffered cardio-pulmonary demise (IOM, Non-heart-beating organ transplantation: practice and protocols, 2000). Early transplantation from DCD donors met with limited success and most transplant surgeons turned to brain-dead donors. Consequently, DCD fell out of vogue and, until recently, has not been the focus of transplant initiatives.

OBJECTIVE: Hypertensive hypervolemic therapy is widely used to treat symptomatic vasospasm after subarachnoid hemorrhage. Few data exist to support a relationship between early clinical response and mortality or functional outcome. METHODS: In a prospective cohort of 580 subarachnoid hemorrhage patients, we studied 95 patients with acute symptomatic vasospasm who received stepwise volume expansion with crystalloid and/or 5% albumin solution followed by intravenous pressors to maintain systolic blood pressure between 180 and 220 mm Hg. We separately assessed the effects of volume expansion and induced hypertension on the neurological examination during the first 2 hours of each intervention. We used multivariate logistic regression analysis to calculate adjusted odds ratios assessing the relationship between clinical response to hypertensive hypervolemic therapy and 3-month outcome, as measured by the modified Rankin Scale. RESULTS: Of 95 patients with symptomatic vasospasm, volume expansion was used in 94% (n = 89), of whom 43% had a clinical response; 85% of the patients (n = 81) received pressors, of whom 68% responded. Early clinical improvement attributable to either volume expansion or pressors was not related to the development of infarction on computed tomography, but response to either modality within 2 hours was independently protective against death (adjusted odds ratio, 0.03; P < 0.05) and death-or-severe-disability (modified Rankin Scale score, 4-6; adjusted odds ratio, 0.1; P < 0.05) after adjusting for age, Hunt-Hess grade, angioplasty, and aneurysm size. CONCLUSION: Subarachnoid hemorrhage patients with symptomatic vasospasm who fail to demonstrate early clinical improvement in response to volume or pressor therapy are at high risk for death or disability. Urgent endovascular intervention in this high-risk patient cohort may be justified.

OBJECTIVE: We sought to determine the frequency, risk factors, and impact on functional outcome and quality of life (QOL) of global cognitive impairment 1 year after subarachnoid hemorrhage. METHODS: We prospectively evaluated global cognitive status 3 and 12 months after hospitalization with the Telephone Interview for Cognitive Status in 232 subarachnoid hemorrhage survivors. Cognitive impairment was defined as a score of 30 or less (scaled 0 = worst, 51 = best). Logistic regression was performed to calculate adjusted odds ratios (AORs) for impairment at 1 year. Basic activities of daily living were evaluated with the Barthel Index, instrumental activities of daily living were assessed with the Lawton scale, and QOL was evaluated with the Sickness Impact Profile. RESULTS: The frequency of cognitive impairment was 27% at 3 months and 21% at 12 months. After the effects of age, education, and race/ethnicity were controlled for, risk factors for cognitive impairment at 12 months included anemia treated with transfusion (AOR, 3.4; P = 0.006), any temperature level higher than 38.6 degrees C (AOR, 2.7; P = 0.016), and delayed cerebral ischemia (AOR, 3.6; P = 0.01). Among cognitively impaired patients at 3 months, improvement at 1 year occurred in 34% and was associated with more than 12 years of education and the absence of fever higher than 38.6 degrees C during hospitalization (P = 0.015). Patients with cognitive impairment at 1 year had worse concurrent QOL and less ability to perform instrumental and basic activities of daily living (all P < 0.001). CONCLUSION: Global cognitive impairment affects more than 20% of subarachnoid hemorrhage survivors at 1 year, is predicted by fever, anemia treated with transfusion, and delayed cerebral ischemia, and adversely affects functional recovery and QOL.

BACKGROUND AND PURPOSE: Vasospasm is an important complication of subarachnoid hemorrhage, but is variably defined in the literature. METHODS: We studied 580 patients with subarachnoid hemorrhage and identified those with: (1) symptomatic vasospasm, defined as clinical deterioration deemed secondary to vasospasm after other causes were eliminated; (2) delayed cerebral ischemia (DCI), defined as symptomatic vasospasm, or infarction on CT attributable to vasospasm; (3) angiographic spasm, as seen on digital subtraction angiography; and (4) transcranial Doppler (TCD) spasm, defined as any mean flow velocity >120 cm/sec. Logistic regression analysis was performed to test the association of each definition of vasospasm with various hospital complications, and 3-month quality of life (sickness impact profile), cognitive status (telephone interview of cognitive status), instrumental activities of daily living (Lawton score), and death or severe disability at 3 months (modified Rankin scale score 4-6), after adjustment for covariates. RESULTS: Symptomatic vasospasm occurred in 16%, DCI in 21%, angiographic vasospasm in 31%, and TCD spasm in 45% of patients. DCI was statistically associated with more hospital complications (N=7; all P<0.05) than symptomatic spasm (N=4), angiographic spasm (N=1), or TCD vasospasm (N=1). Angiographic and TCD vasospasm were not related to any aspect of clinical outcome. Both symptomatic vasospasm and DCI were related to reduced instrumental activities of daily living, cognitive impairment, and poor quality of life (all P<0.05). However, only DCI was associated with death or severe disability at 3 months (adjusted OR, 2.2; 95% CI, 1.2-3.9; P=0.007). CONCLUSIONS: DCI is a more clinically meaningful definition than either symptomatic deterioration alone or the presence of arterial spasm by angiography or TCD.