Disease relevance of Brain Death

• MAIN OUTCOME MEASURES--Data from children undergoing brain death evaluations including number of coma examinations, number and duration of apnea tests, PCO2 measurements at the end of the apnea test, ancillary tests used to confirm brain death, organ procurement, and reasons for nonprocurement [1].
• INTERPRETATION: Desmopressin can be given to brain-dead donors to limit the harmful effects of diabetes insipidus without any substantial effects to graft function in recipients [2].
• A 37-year-old woman, while being treated with nitroprusside for acute hypertension due to an intramural renal artery hemorrhage, became blind on the fourth hospital day, comatose on the fifth, and brain dead on the seventh [3].
• In patient 3, ATP and PCr were detected with P-31 MR spectroscopy, and now, more than 20 months after brain death, cardiac death has not yet occurred [4].
• Preservation of ischemia and isoflurane-induced preconditioning after brain death in rabbit hearts [5].

Psychiatry related information on Brain Death

• CONCLUSIONS: eEEG provided data that influenced clinical decision-making in the setting of epilepsy related situations, hypoxic encephalopathy and brain death examination [6].
• SPECT brain perfusion imaging has definite value in the evaluation of cerebrovascular disease (particularly acute stroke), dementia, epilepsy, and may have a role in the diagnosis of brain death and head trauma [7].

High impact information on Brain Death

• Brain death sans frontières [8].
• Cardiopulmonary bypass in brain-dead organ donors. The Brain Death Study Group [9].
• Adenylate cyclase concentration was measured in liver tissue from end stage cirrhotic patients and from brain-dead organ donors whose cardiovascular function was maintained in a stable state [10].
• Our study further shows that infants with clinical brain death and those treated with atropine exhibit a similar lack of nonlinear feedback control [11].
• In a first series of experiments, dogs given a sudden rise in ICP (n = 5) showed a hyperdynamic response and a 1,000-fold increase in the level of epinephrine after brain death [12].

Chemical compound and disease context of Brain Death

• In brain-dead pigs, the increases in the aforementioned blood measurements were smaller following glucose/insulin infusion than following saline infusion [13].
• An innocuous intravenous portable radioisotopic test using technetium 99m pertechnetate was employed to demonstrate the deficit of cerebral blood flow associated with brain death [14].
• Four groups of 40-kg pigs were studied: brain-dead and control pigs given isotonic saline or glucose/insulin (7.5 mg glucose/kg/min, 1.25 mU insulin/kg/ min) (n = 5 to 10 in each group) [13].
• A mean lowest creatinine level of 2.0 mg/dL, (range 1.1-3.0 mg/dL), the rate of postoperative dialysis (22%), and a 1-year graft survival rate of 76% for kidneys from NHB-donated kidneys compare favorably to expected results achieved nationally from brain-dead cadaveric donors [15].
• Donors were treated immediately after induction of brain death either with intravenous steroids, which block inflammatory cytokine release, or a soluble P-selectin glycoprotein ligand (sPSGL), which blocks initial selectin-mediated cellular adhesion [16].

Biological context of Brain Death

• This report demonstrates the acquisition of nonlinear heart rate dynamics and possible chaos in developing human infants and its loss in brain death and with the administration of atropine [11].
• Median nerve somatosensory evoked potentials (SEPs) were recorded in a total of 181 patients in coma and brain death [17].
• A massive increase in levels of glutamate, glycerine, and the lactate-pyruvate ratio was measured 24 hours before intracranial pressure elevation was observed and brain death occurred [18].
• Maintenance of liver graft viability in the state of brain death. Synergistic effects of vasopressin and epinephrine on hepatic energy metabolism in brain-dead dogs [19].
• The analysis of serum or plasma concentration patterns of a number of hormonal parameters following brain death does not support the rationale for a routine replacement therapy of total triiodothyronine (TT3) or cortisol to maintain endocrine homeostasis prior to organ harvest [20].

Anatomical context of Brain Death

• Dogs given a gradual rise in ICP (n = 6) showed a lesser hyperdynamic response, almost 200-fold increase in the level of epinephrine after brain death, and mild ischemic damage to the myocardium (23 +/- 1%) [12].
• The present study confirms the onset of a dramatic increase in cardiac norepinephrine release from myocardial nerve endings following brain death, and demonstrate the utility of the new cardiac microdialysis technique to assess changes in interstitial fluid content [21].
• RESULTS: After 6 hr of brain death, influx of polymorphonuclear cells and macrophages and expression of vascular cell adhesion molecule-1 in the donor lungs was increased [22].
• In all patients the hospital records documented coma, fixed dilated pupils, absent brain stem reflexes, apnea, and verification of the diagnosis of brain death by two physicians who were not part of the transplantation team [23].
• CONCLUSIONS: During the initial period after induction of brain death, cerebral and thyroid hormones remained stable while cortico- and medullo-surrenal hormones varied significantly [24].

Gene context of Brain Death

• Levels of monocyte chemotactic protein-1 and transforming growth factor-beta were twice as high after brain death but did not reach significance [25].
• Serum IL-8 levels in patients who died or became brain dead within 1 week after ROSC were significantly higher than those in other patients [26].
• Intrinsic ADH was depleted in the plasma shortly after the diagnosis of brain death [27].
• Shortly after brain death induction, a significant increase in serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6 was demonstrated in a time-dependent manner [28].
• Recent studies have shown that brain death upregulates multiple lymphocyte- and macrophage-derived cytokines and the injured brain itself may be the source of proinflammatory factors such as S100B [29].

Analytical, diagnostic and therapeutic context of Brain Death

• Two isoelectric electroencephalograms obtained 24 hours apart support a clinical diagnosis of brain death in prolonged coma [30].
• Estimation of myocardial interstitial norepinephrine release after brain death using cardiac microdialysis [21].
• Liver transplantation from a cadaver donor with ethylene-glycol-induced brain death [31].
• Ten brain-dead patients had significantly decreased low-frequency heart rate power (p = .008) and plasma norepinephrine (p = .015), epinephrine (p = .03), and dopamine (p = .04) concentrations when compared with six non-brain-dead patients with a Glasgow Coma Scale score of 3 [32].
• Although 24 hours' storage by continuous hypothermic perfusion of hearts taken from control animals led to only a minimal reduction in myocardial function, storage increased the reduction in function associated with brain death when intravenous fluid and dobutamine support had been given to maintain the brain dead pig in a normotensive state [33].

References