The apnea test for the determination of brain death

1989 ◽  
Vol 71 (2) ◽  
pp. 191-194 ◽  
Author(s):  
Edward C. Benzel ◽  
Charles D. Gross ◽  
Theresa A. Hadden ◽  
Lee Kesterson ◽  
Michael D. Landreneau
Keyword(s):  
Brain Death ◽  
Average Rate ◽  
Tracheobronchial Tree ◽  
Apnea Test ◽  
Content Type ◽  
Arterial Blood ◽  
Volume Ventilation ◽  
Gas Measurements ◽  
Fine Print

✓ By conventional criteria, an apneic patient's PaCO2 must be greater than 60 mm Hg before apnea can be attributed to brain death. The rate of a PaCO2 increase in the apneic patient traditionally has been thought to be in the range of 3 mm Hg/min. In order to assess the validity of these data and the validity of the “apnea test” for determination of brain death, the results of this test were reviewed in 20 patients. In all patients, arterial blood samples were drawn for blood gas measurements every 2 minutes following the cessation of volume ventilation (with an oxygen cannula at 6 liters O2/min passed into the tracheobronchial tree). The rate of PaCO2 increase was noted to be very erratic. The average rate of rise was 3.7 ± 2.3 mm Hg/min (± standard deviation). This, however, varied from 0.5 to 10.5 mm Hg/min and was not predictable from the variables evaluated. The rate of PaCO2 increase was noted to decline throughout the duration of the test. This ranged from 3.9 ± 1.2 mm Hg/min (for patients with baseline PaCO2 ≤ 30 mm Hg) and 4.5 ± 1.9 mm Hg/min (for patients with baseline PaCO2 ≥ 30 mm Hg) in the first 4 minutes of the test to an average of 0.92 mm Hg/min for patients with test lasted longer than 12 minutes. These unpredictable results might be related to CO2 washout, atelectasis, cardiac ventilations, or other yet-undefined parameters. The nonlinear relationship between rate of PaCO2 increase and time following onset of apnea resulted in the test being prolonged in several patients. In these patients, the PaCO2 approached 60 mm Hg in an asymptotic fashion. These lengthy tests could have been avoided by utilizing a standardized apnea test with a baseline PaCO2 of 40 mm Hg or greater. The observation that a high baseline PaCO2 greatly augments the efficiency and safety of the test allows criteria that have previously been based on conjecture to be documented and applied clinically. A standardized apnea test, utilizing these principles, may satisfy many of the criticisms regarding brain-death testing that have been raised by neurologists, neurosurgeons, and transplant surgeons.

Apnea testing for the determination of brain death: a modified protocol

1992 ◽  
Vol 76 (6) ◽  
pp. 1029-1031 ◽  
Author(s):  
Edward C. Benzel ◽  
Jay P. Mashburn ◽  
Steven Conrad ◽  
Denise Modling
Keyword(s):  
Brain Death ◽  
Apnea Test ◽  
Content Type ◽  
Group I ◽  
The Mean ◽  
Group Ii ◽  
Safe Approach ◽  
Apnea Testing ◽  
Fine Print

✓ The absence of spontaneous respirations at a PaCO2 of 60 mm Hg or above has traditionally been accepted as the respiratory criteria for the determination of brain death. The testing of patients for the presence or absence of apnea has been complicated because the rate of PaCO2 elevation may vary substantially from patient to patient, and a nonlinear relationship exists between the rate of PaCO2 increase and the duration of apnea. In an attempt to refine the apnea test and to further elucidate the physiology of hypercapnia in humans, 11 patients who met all but the respiratory criteria for brain death were evaluated using a modification of a previously utilized apnea testing protocol. All patients were brought to a PaCO2 of 40 mm Hg or above prior to the apnea test. Baseline PaCO2 ranged from 40 to 45 mm Hg in six patients (Group I) and from 46 to 51 mm Hg in five patients (Group II). The mean rate of PaCO2 increase was 5.1 ± 1.4 mm Hg/min in Group I and 6.7 ± 3.1 mm Hg/min in Group II. No problems with cardiovascular instability or hypoxia were encountered during testing in this series. This refinement of the apnea test allows for a streamlined and safe approach to brain death detection.

Families, brain death, and traditional medical excellence

1984 ◽  
Vol 60 (6) ◽  
pp. 1192-1194 ◽  
Author(s):  
Rosa Lynn Pinkus
Keyword(s):  
Brain Death ◽  
Tertiary Care Hospital ◽  
Tertiary Care ◽  
Care Hospital ◽  
Personal Beliefs ◽  
Content Type ◽  
The Past ◽  
Transplant Center ◽  
Fine Print

✓ Staff neurosurgeons and residents at a tertiary care hospital designated as a transplant center were surveyed regarding personal opinions concerning brain death and family conferences. Compared to an extensive survey done in 1976, the responses indicated that, while a professional consensus regarding the definition and meaning of brain death has emerged in the past 10 years, a range of personal beliefs and opinions regarding the concept still exists. In spite of the professional consensus, it is still difficult for the physician to communicate gently, yet firmly, to families both the scientific groundwork that validates the determination of brain death, the concept, and the finality of the information.

Cerebral hemorrhage and edema following brain biopsy in rats: significance of mean arterial blood pressure

2000 ◽  
Vol 92 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Helene Benveniste ◽  
Katie R. Kim ◽  
Laurence W. Hedlund ◽  
John W. Kim ◽  
Allan H. Friedman
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Neurosurgical Procedures ◽  
Shr Rats ◽  
Mr Microscopy ◽  
Content Type ◽  
Wky Rats ◽  
Arterial Blood ◽  
Fine Print

Object. It is taken for granted that patients with hypertension are at greater risk for intracerebral hemorrhage during neurosurgical procedures than patients with normal blood pressure. The anesthesiologist, therefore, maintains mean arterial blood pressure (MABP) near the lower end of the autoregulation curve, which in patients with preexisting hypertension can be as high as 110 to 130 mm Hg. Whether patients with long-standing hypertension experience more hemorrhage than normotensive patients after brain surgery if their blood pressure is maintained at the presurgical hypertensive level is currently unknown. The authors tested this hypothesis experimentally in a rodent model.Methods. Hemorrhage and edema in the brain after needle biopsy was measured in vivo by using three-dimensional magnetic resonance (MR) microscopy in the following groups: WKY rats, acutely hypertensive WKY rats, spontaneously hypertensive rats (SHR strain), and SHR rats treated with either sodium nitroprusside or nicardipine. Group differences were compared using Tukey's studentized range test followed by individual pairwise comparisons of groups and adjusted for multiple comparisons.There were no differences in PaCO2, pH, and body temperature among the groups. The findings in this study indicated that only acutely hypertensive WKY rats had larger volumes of hemorrhage. Chronically hypertensive SHR rats with MABPs of 130 mm Hg did not have larger hemorrhages than normotensive rats. There were no differences in edema volumes among groups.Conclusions. The brains of SHR rats with elevated systemic MABPs are probably protected against excessive hemorrhage during surgery because of greater resistance in the larger cerebral arteries and, thus, reduced cerebral intravascular pressures.

Apnea Documentation for Determination of Brain Death in Children

PEDIATRICS ◽  
1984 ◽  
Vol 74 (4) ◽  
pp. 505-508
Author(s):  
Thomas W. Rowland ◽  
Joseph H. Donnelly ◽  
Anthony H. Jackson
Keyword(s):  
Brain Death ◽  
Ventilatory Support ◽  
Respiratory Drive ◽  
Test Protocol ◽  
Apnea Test ◽  
Wide Variability ◽  
Adequate Oxygenation

Discontinuing ventilatory support for determination of respiratory drive is a recognized means of assessing clinical brain death. Methodology must include a means for assuring adequate oxygenation during the test as well as providing sufficient duration for appropriate hypercarbia. Nine patients with other findings of clinical brain death were prospectively assessed with a standardized apnea test protocol. None demonstrated spontaneous respirations. Whereas adequate oxygenation was maintained in each case, wide variability was evident in degree of hypercarbia and acidosis.

Posttreatment with adenovirus-mediated gene transfer of calcitonin gene—related peptide to reverse cerebral vasospasm in dogs

2002 ◽  
Vol 97 (1) ◽  
pp. 136-142 ◽  
Author(s):  
Motoyoshi Satoh ◽  
Eddie Perkins ◽  
Hitoshi Kimura ◽  
Jiping Tang ◽  
Yi Chun ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Cerebral Vasospasm ◽  
Treated Group ◽  
Positive Staining ◽  
Cmv Promoter ◽  
Content Type ◽  
Related Peptide ◽  
Arterial Blood ◽  
Blood Injection ◽  
Fine Print

Object. Gene transfer to cerebral vessels is a promising new therapeutic approach for cerebral vasospasm after subarachnoid hemorrhage (SAH). This study was undertaken to explore whether a delayed treatment with adenovirus encoding the prepro-calcitonin gene—related peptide (CGRP), 2 days after initial blood injection, reduces cerebral vasospasm in a double-hemorrhage model of severe vasospasm in dogs. Methods. In 20 dogs, arterial blood was injected into the cisterna magna on Days 0 and 2. Thirty minutes after the second blood injection, the animals received either adenovirus encoding the prepro-CGRP gene (AdCMVCGRP—treated group, eight dogs) or adenovirus encoding the β-galactosidase gene (AdCMVβgal—treated group, six dogs) under the cytomegalovirus (CMV) promoter. One group of dogs did not receive treatment and served as controls (control SAH group, six dogs). Angiography was performed on Days 0 and 7 to assess cerebral vasospasm. On Day 7 following angiography, the animals were killed and their brains were stained with X-gal to detect the distribution of gene expression. Cerebrospinal fluid (CSF) was also tested for CGRP immunoreactivity. Severe vasospasm was observed in control SAH dogs on Day 7, and the mean basilar artery (BA) diameter was 53.4 ± 5.5% of the value measured on Day 0. Treatment with AdCMVβgal did not alter vasospasm (the BA diameter was 55 ± 3.9% of that measured on Day 0). The leptomeninges and adventitia of the BAs of dogs treated using AdCMVβgal demonstrated positive staining with X-gal. High levels of CGRP were measured in CSF from dogs that received AdCMVCGRP. In the group treated with AdCMVCGRP, vasospasm was significantly reduced (the BA diameter was 78.2 ± 5.3% of that measured on Day 0, p < 0.05 compared with the control SAH group and the AdCMVβgal group). Conclusions. In a model of severe vasospasm in dogs, gene transfer of CGRP after injection of blood attenuated cerebral vasospasm after SAH.

Evaluation of a method for noninvasive intracranial pressure assessment during infusion studies in patients with hydrocephalus

2000 ◽  
Vol 92 (5) ◽  
pp. 793-800 ◽  
Author(s):  
Bernhard Schmidt ◽  
Marek Czosnyka ◽  
Jens Jürgen Schwarze ◽  
Dirk Sander ◽  
Werner Gerstner ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Intracranial Pressure ◽  
Time Course ◽  
Cerebral Blood Flow Velocity ◽  
Absolute Error ◽  
Content Type ◽  
Arterial Blood ◽  
Potential Clinical Benefit ◽  
The Mean ◽  
Fine Print

Object. A mathematical model previously introduced by the authors allowed noninvasive intracranial pressure (nICP) assessment. In the present study the authors investigated this model as an aid in predicting the time course of raised ICP during infusion tests in patients with hydrocephalus and its suitability for estimating the resistance to outflow of cerebrospinal fluid (Rcsf).Methods. Twenty-one patients with hydrocephalus were studied. The nICP was calculated from the arterial blood pressure (ABP) waveform by using a linear signal transformation, which was dynamically modified by the relationship between ABP and cerebral blood flow velocity. This model was verified by comparison of nICP with “real” ICP measured during lumbar infusion tests. In all simulations, parallel increases in real ICP and nICP were evident. The simulated Rcsf was computed using nICP and then compared with Rcsf computed from real ICP. The mean absolute error between real and simulated Rcsf was 4.1 ± 2.2 mm Hg minute/ml. By the construction of simulations specific to different subtypes of hydrocephalus arising from various causes, the mean error decreased to 2.7 ± 1.7 mm Hg minute/ml, whereas the correlation between real and simulated Rcsf increased from R = 0.73 to R = 0.89 (p < 0.001).Conclusions. The validity of the mathematical model was confirmed in this study. The creation of type-specific simulations resulted in substantial improvements in the accuracy of ICP assessment. Improvement strategies could be important because of a potential clinical benefit from this method.

Brain Death

2017 ◽  
Author(s):  
Anupamaa Seshadri ◽  
Ali Salim
Keyword(s):  
Brain Death ◽  
Apnea Test ◽  
Brainstem Reflex ◽  
Practice Parameters ◽  
Confirmatory Tests ◽  
History Of ◽  
Pediatric Populations ◽  
Definition Of

The concept of “brain death” is one that has been controversial over time, requiring the development of clear guidelines to diagnose and give prognoses for patients after devastating neurologic injury. This review discusses the history of the definition of brain death, as well as the most recent guidelines and practice parameters on the determination of brain death in both the adult and pediatric populations. We provide specific and detailed instructions on the various clinical tests required, including the brain death neurologic examination and the apnea test, and discuss pitfalls in the diagnosis of brain death. This review also considers the most recent literature and guidelines as to the role of confirmatory tests making this diagnosis.  Key Words: apnea test, brain death, brainstem reflex, death examination

Autonomic and histopathological effects of percutaneous trigeminal ganglion compression in the rabbit

1990 ◽  
Vol 72 (6) ◽  
pp. 933-940 ◽  
Author(s):  
Mark C. Preul ◽  
Phillip B. Long ◽  
Jeffrey A. Brown ◽  
Manuel E. Velasco ◽  
Michael T. Weaver
Keyword(s):  
New Zealand ◽  
Trigeminal Ganglion ◽  
Zealand White Rabbit ◽  
Sensory Function ◽  
Content Type ◽  
Arterial Blood ◽  
Corneal Reflex ◽  
Hematoxylin And Eosin ◽  
And Control ◽  
Fine Print

✓ The histopathological and autonomic effects of percutaneous trigeminal ganglion compression for trigeminal neuralgia were studied in New Zealand White rabbits. Drops in mean arterial blood pressure of 38% and in heart rate of 30% were observed during compression (p < 0.0001). Corneal reflex, pinprick sensation, and mastication strength were intact in 13 of 14 rabbits after compression. These findings resembled the effects of percutaneous compression in humans and suggested that the New Zealand White rabbit is a useful model for the study of percutaneous compression. Trigeminal sensory roots and ganglia from 14 rabbits killed at intervals from 1 to 84 days after percutaneous compression were sectioned and stained using immunoperoxidase for neurofilaments, hematoxylin and eosin, luxol fast blue, and cresyl echt violet. Focal axonal damage and demyelination were present 7 days after compression. No difference could be detected in the perikaryonal distribution of neurofilaments between compressed and control trigeminal ganglia. Focal demyelination and Schwann cell proliferation preceding remyelination were present in the trigeminal sensory root at 84 days. Differential injury of axons compared to trigeminal ganglion cell bodies suggests that axonal regeneration is possible and may contribute to the recovery of motor and sensory function in patients after percutaneous compression.

Normal position of the aqueduct of Sylvius

1975 ◽  
Vol 42 (5) ◽  
pp. 503-507 ◽  
Author(s):  
Karl Guldberg Krogness
Keyword(s):  
Standard Deviation ◽  
Cerebral Aqueduct ◽  
Posterior Surface ◽  
Normal Position ◽  
Normal Value ◽  
Content Type ◽  
Abnormal Position ◽  
Tuberculum Sellae ◽  
Fine Print

✓ Two new proportional methods for determination of the normal or abnormal position of the cerebral aqueduct are described. The position of the iter is expressed by the quotients and , when d-aq represents the distance between the upper posterior surface of the dorsum sellae and the dorsal center of the air-filled aqueduct. Ts = aq is the distance from the tuberculum sellae to the same point, and Tw is Twining's line. The normal value of the dorsum to aqueduct ratio was 0.32 ± 0.02 standard deviation (SD) and of the tuberculum to aqueduct ratio 0.44 ± 0.03 SD. Both proportional methods are independent of skull dimensions. These are compared to another proportional method described in Part 1 of this report.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

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