Muerte encefálica: repercusión sobre órganos y tejidos / Brain death: Repercussion on the organs and tissues

La muerte encefálica se acompaña de una serie de efectos sistémicos, hemodinámicos, hormonales e inflamatorios que tienen una repercusión relevante en los órganos y los tejidos de la economía. Cada vez hay más evidencias de que los órganos provenientes de donantes fallecidos en muerte encefálica presentan un grado de respuesta inflamatoria secundaria al daño encefálico y, en ocasiones, proporcional a la intensidad y a la velocidad de progresión de éste. Tanto estudios clínicos como estudios experimentales han mostrado que el resultado de los órganos de donantes fallecidos en parada cardíaca o donantes vivos tienen iguales o mejores resultados clínicos que los obtenidos en donantes en muerte encefálica que han presentado el proceso inflamatorio secundario a ésta. Hay pruebas de que esta respuesta inflamatoria acontece en el pulmón, el corazón, los riñones, el hígado y el intestino, e igualmente se incrementan también las pruebas de que el grado de respuesta inflamatoria observada en los órganos tiene una influencia importante en el resultado final del trasplante. En consecuencia, el desarrollo del conocimiento de las vías que interrelacionan el daño encefálico con la respuesta orgánica inflamatoria abre una importante área de conocimiento y posibilita que futuras estrategias terapéuticas encaminadas a modular la respuesta sistémica al daño encefálico permitan mejorar la calidad de los órganos obtenidos para trasplante, así como incrementar la supervivencia del injerto y de los receptores de trasplantes de órganos sólidos (AU)

Brain death is accompanied by a series of hemodynamic, hormonal and inflammatory systemic effects that have an important repercussion on the economy of the organs and tissues. There is increasing evidence that the organs from brain death donors have an inflammatory response grade secondary to brain death and sometimes proportional to the intensity and rate of its progression. Both clinical and experimental studies have shown that the result of organs from heart arrest deceased donors or live donors have the same or better clinical results than those obtained in brain death donors and who have suffered the inflammatory process secondary to it. There is proof that this inflammatory response occurs in the lung, heart, kidneys, liver, intestine. Furthermore, the evidence also shows that the grade of inflammatory response observed in the organs has an important influence on the final outcome of the transplant. Consequently, the development of the knowledge regarding the pathways that interrelate brain death with the inflammatory organ response provides us with an important area of knowledge, which allow for future therapeutic strategies aimed at modulating the systemic response to brain death to improve the quality of the organs obtained for transplant and also to increase graft survival of the solid organ transplant recipients (AU)

[Brain death: repercussion on the organs and tissues]. / Muerte encefálica: repercusión sobre órganos y tejidos.

Brain death is accompanied by a series of hemodynamic, hormonal and inflammatory systemic effects that have an important repercussion on the economy of the organs and tissues. There is increasing evidence that the organs from brain death donors have an inflammatory response grade secondary to brain death and sometimes proportional to the intensity and rate of its progression. Both clinical and experimental studies have shown that the result of organs from heart arrest deceased donors or live donors have the same or better clinical results than those obtained in brain death donors and who have suffered the inflammatory process secondary to it. There is proof that this inflammatory response occurs in the lung, heart, kidneys, liver, intestine. Furthermore, the evidence also shows that the grade of inflammatory response observed in the organs has an important influence on the final outcome of the transplant. Consequently, the development of the knowledge regarding the pathways that interrelate brain death with the inflammatory organ response provides us with an important area of knowledge, which allow for future therapeutic strategies aimed at modulating the systemic response to brain death to improve the quality of the organs obtained for transplant and also to increase graft survival of the solid organ transplant recipients.

Electrolytic disorders, hyperosmolar states, and lactic acidosis in brain-dead patients.

Despite the use of well-accepted protocols for donor maintenance, the severe electrolytic disorders are not infrequent with deleterious consequences to the organs. The objective of our survey was to determine the incidence of episodes of electrolyte disorders among brain-dead patients (despite of rigid protocols of maintenance) and the rate of anaerobic metabolism in these patients (suggestive of an occult systemic hypoperfusion). The study group of 50 brain-dead patients underwent therapy to maintain normal arterial pressure, urine output, and body temperature. Standard monitoring for brain-dead patients was followed, except for a frequent evaluation of electrolytes, including glucose, sodium, potassium, phosphorus, osmolality, base excess, and lactate plasma levels. Our results demonstrate that with frequent determinations of electrolytes, despite following strict protocols of maintenance, there was a high incidence of hyperglycemia, hypophosphotemia, hypokaemia, and hyperosmolality. Interesting findings were the high incidence of elevated lactate, and the relationship between lactate levels and bases deficit as well as hypernatremia. It can be concluded that, even following rigid protocols, the maintenance of brain-dead patients demands a close evaluation of electrolyte levels. Our results also suggest that the inclusion in the monitoring protocol of anerobic metabolism data including lactate levels can help to avoid occult ischemia of organs, and consequently improve their quality for transplantation.

Identification by CT scan of ischemic stroke patients with high risk of brain death.

The identification of patients with high risk of evolution to brain death is one of the more important tasks of transplant coordination teams. Although most of pool of potential donors come from the group of patients who suffer a head injury or hemorrhagic stroke, the procurement of organs from brain-dead patients suffering an ischemic stroke as the cause of brain damage must also be considered. The main objective of this study was to investigate the radiological signs that in the CT scan of admission to a neurological ICU are more frequently associated with progression to brain death. We studied the CT scans of 15 brain-dead patients after an ischemic stroke versus the scans of 15 recovered patients admitted to ICU with the same diagnosis. The radiological signs included: insular ribbon sign, hyperintensities inside the big arteries of the base of the skull, hemispheric hypodensities, midline shift, and compression of the cerebrospinal fluid spaces. There were two signs significantly associated with brain death: midline shifts and the compression of the ambiens cistern. It may be concluded that analysis of the CT scan at admission of patients with an ischemic stroke in the ICU can predict the risk of evolution to brain death.

Diagnosis of brain death by transcranial Doppler sonography: solutions for cases of difficult sonic windows.

Delays in diagnosis of brain death have definite consequences for the organ retrieval and transplantation process. It is advisable to use accurate diagnostic methods. Transcranial Doppler sonography is a well-accepted technique for diagnosing cerebral circulatory arrest. However, in some cases, the access to the intracranial circulation via the temporal window is difficult. In 43 brain-dead patients we evaluated the rate of impossibility of insonation of middle cerebral artery using a temporal window and the usefulness of an orbital window for insonation of the carotid siphon. In 39 patients the usual protocol of insonation (temporal window and foramen magnum window) was sufficient to demonstrate cerebral circulatory arrest. In 10 patients, including all the cases in which it was impossible to use a temporal approach, the carotid siphon was successfully insonated, showing in all the cases the existence of a sonographic pattern compatible with cerebral circulatory arrest. It may be concluded that the use of an orbital window for exploring intracranial circulation by transcranial Doppler sonography can be a useful tool in cases of difficult sonic windows.

Brain death due to supratentorial masses: diagnosis using transcranial Doppler sonography.

Since cadaveric donation is the main source of organs for transplantation in many countries, the diagnosis of brain death is an important issue. The cessation of cerebral circulation is one phenomenon closely related to brain death. Transcranial Doppler sonography is one of the accepted techniques to establish cessation of cerebral circulation. One of the limitations attributed to Doppler is the lack of sensitivity for this diagnosis. The objective of this research was to establish whether transcranial Doppler sonography showed acceptable sensitivity and whether this was affected by the location of the intracranial mass effect. Twenty-four patients underwent transcranial Doppler sonography to establish the incidence of the three sonographic patterns associated with brain death: separation diastole-systole, reverberating flow, and systolic spikes. In all the cases the insonation of the arteries of the base of the skull was performed. In supratentorial lesions, the predominant pattern was a reverberating flow, while in infratentorial lesions systolic spikes pattern was most frequent. Our study showed a high sensitivity of transcranial Doppler sonography for the diagnosis of brain death and the existence of different mechanisms of cerebral circulatory arrest depending on the location of the intracranial pressure wedge.