Efeitos da morte cerebral na microvasculatura pulmonar em um modelo experimental de doador de pulmão / Brain death effects on lung microvasculature in an experimental model of lung donor

RESUMO Objetivo A morte cerebral (MC) desencadeia alterações hemodinâmicas e inflamatórias importantes, comprometendo a viabilidade dos órgãos empregados em transplantes. Para compreender melhor as alterações microcirculatórias nos pulmões de doadores com MC, o presente estudo investigou a microcirculação pulmonar em um modelo de roedor com MC via microscopia intravital. Métodos Ratos Wistar machos foram anestesiados e ventilados mecanicamente. Eles foram submetidos a trepanação e a MC induzida por meio do aumento da pressão intracraniana. Os ratos do grupo Sham (SH), utilizado como controle, foram submetidos apenas à trepanação. Em ambos os grupos, foram monitorados o O2 expiratório e o CO2, e, após 3 horas, foi realizada a toracotomia e criada uma janela para observar a superfície pulmonar usando o sistema de microscopia intravital. As expressões pulmonares das moléculas de adesão intercelular (ICAM)-1 e da óxido nítrico-sintase endotelial (eNOS) foram avaliadas por imuno-histoquímica, e as citocinas foram medidas em amostras pulmonares. Resultados Três horas após os procedimentos cirúrgicos, a perfusão pulmonar foi de 73% no grupo SH. Por outro lado, os animais com MC apresentaram uma importante diminuição na perfusão do órgão para 28% (p = 0,036). O comprometimento microcirculatório pulmonar após a indução de MC foi associado a um aumento do número de leucócitos recrutados para o tecido pulmonar, além de uma redução na expressão de eNOS e um aumento na expressão de ICAM-1 nas células endoteliais do pulmão. Os ratos com MC apresentaram valores mais elevados de O2 expiratório e valores mais baixos de CO2 em comparação com os animais SH após 3 horas de monitorização. Conclusões Os dados apresentados demonstraram que a MC desencadeia uma importante hipoperfusão e inflamação nos pulmões, comprometendo a microcirculação pulmonar do doador.

ABSTRACT Objective Brain death (BD) triggers important hemodynamic and inflammatory alterations, compromising the viability of organs suitable for transplantation. To better understand the microcirculatory alterations in donor lungs caused by BD. The present study investigated the pulmonary microcirculation in a rodent model of BD via intravital microscopy. Methods Male Wistar rats were anaesthetized and mechanically ventilated. They were trepanned and BD was induced through the increase in intracranial pressure. As control group, sham-operated (SH) rats were trepanned only. In both groups, expiratory O2 and CO2 were monitored and after three hours, a thoracotomy was performed, and a window was created to observe the lung surface using an epi-fluorescence intravital microscopy. Lung expression of intercellular adhesion molecule (ICAM)-1 and endothelial nitric oxide synthase (eNOS) was evaluated by immunohistochemistry, and cytokines were measured in lung samples. Results Three hours after the surgical procedures, pulmonary perfusion was 73% in the SH group. On the other hand, BD animals showed an important decrease in organ perfusion to 28% (p = 0.036). Lung microcirculatory compromise after BD induction was associated with an augmentation of the number of leukocytes recruited to lung tissue, and with a reduction in eNOS expression and an increase in ICAM-1 expression on lung endothelial cells. BD rats showed higher values of expiratory O2 and lower values of CO2 in comparison with SH animals after three hours of monitoring. Conclusion Data presented showed that BD triggers an important hypoperfusion and inflammation in the lungs, compromising the donor pulmonary microcirculation.

Characterization of the intestinal graft in a swine hypotensive after brain death model

Abstract Purpose: To establish a hypotensive brain death pig model and observe the effects of hypotension on small bowel donors. Methods: The hypotensive brain death model was produced using the modified intracranial water sac inflation method in ten domestic crossbred pigs. Effects of hypotensive brain death on small bowel tissue morphology were evaluated through changes in intestinal tissue pathology, tight junction protein of the intestinal mucosa and plasma intestinal fatty acid-binding protein (i-FABP) levels. The pathophysiological mechanism was examined based on changes in superior mesenteric artery (SMA) blood flow and systemic hemodynamics. Results: After model establishment, SMA blood flow, and the mean arterial pressure (MAP) significantly decreased, while heart rate increased rapidly and fluctuated significantly. Small bowel tissue morphology and levels of tight junction protein of the intestinal mucosa showed that after model establishment, small bowel tissue injury was gradually aggravated over time (P<0.05). Plasma i-FABP levels significantly increased after brain death (P<0.05). Conclusions: A hypotensive brain death pig model was successfully established using an improved intracranial water sac inflation method. This method offers a possibility of describing the injury mechanisms more clearly during and after brain death.

Severe fat embolism in perioperative abdominal liposuction and fat grafting / Embolia gordurosa grave no peroperatório de lipoaspiração abdominal e lipoenxertia

ABSTRACT BACKGROUND AND OBJECTIVES: Fat embolism syndrome may occur in patients suffering from multiple trauma (long bone fractures) or plastic surgery (liposuction), compromising the circulatory, respiratory and/or central nervous systems. This report shows the evolution of severe fat embolism syndrome after liposuction and fat grafting. CASE REPORT: SSS, 42 years old, ASA 1, no risk factors for thrombosis, candidate for abdominal liposuction and breast implant prosthesis. Subjected to balanced general anesthesia with basic monitoring and controlled ventilation. After 45 min of procedure, there was a sudden and gradual decrease of capnometry, severe hypoxemia and hypotension. The patient was immediately monitored for MAP and central catheter, treated with vasopressors, inotropes, and crystalloid infusion, stabilizing her condition. Arterial blood sample showed pH = 7.21; PCO2 = 51 mmHg; PO2 = 52 mmHg; BE = -8; HCO3 = 18 mEq L-1, and lactate = 6.0 mmol L-1. Transthoracic echocardiogram showed PASP = 55 mmHg, hypocontractile VD and LVEF = 60%. Diagnosis of pulmonary embolism. After 24 h of intensive treatment, the patient developed anisocoria and coma (Glasgow coma scale = 3). A brain CT was performed which showed severe cerebral hemispheric ischemia with signs of fat emboli in right middle cerebral artery; transesophageal echocardiography showed a patent foramen ovale. Finally, after 72 h of evolution, the patient progressed to brain death. CONCLUSION: Fat embolism syndrome usually occurs in young people. Treatment is based mainly on the infusion of fluids and vasoactive drugs, mechanical ventilation, and triggering factor correction (early fixation of fractures or suspension of liposuction). The multiorgânico involvement indicates a worse prognosis.

RESUMO JUSTIFICATIVA E OBJETIVOS: A Síndrome da Embolia Gordurosa (SEG) pode acontecer em pacientes vítimas de politrauma (fratura de ossos longos) ou operações plásticas (lipoaspiração), comprometendo circulação, respiração e/ou sistema nervoso central. O presente relato mostra evolução de SEG grave após lipoaspiração e lipoenxertia. RELATO DO CASO: SSS, 42 anos, ASA 1, sem fatores de risco para trombose, candidata a lipoaspiração abdominal e implante de prótese mamária. Submetida à anestesia geral balanceada com monitorização básica e ventilação controlada. Após 45 minutos de procedimento, houve queda súbita e progressiva da capnometria, hipoxemia e hipotensão grave. Imediatamente foi monitorizada com PAM e cateter central, tratada com vasopressores, inotrópicos e infusão de cristaloides, obtendo estabilização do quadro. Amostra sanguínea arterial mostrou pH = 7,21; PCO2 = 51 mmHg; PO2 = 52 mmHg; BE = -8; HCO3 = 18 mEQ/l e lactato = 6,0 mmol/l. Ecocardiograma transtorácico mostrou PSAP = 55 mmHg, VD hipocontrátil e FEVE = 60%. Diagnóstico de embolia pulmonar. Após24 h de tratamento intensivo, a paciente evoluiu com anisocoria e coma com escala de glasgow 3. Realizada TC de encéfalo que evidenciou isquemia cerebral grave, hemisférica, com sinais de êmbolos de gordura em A. cerebral média D; o ecocardiograma transesofágico mostrou forame oval patente. Finalmente, após 72 h de evolução, a paciente evoluiu para morte encefálica. CONCLUSÃO: A SEG ocorre geralmente em jovens. O tratamento baseia-se principalmente na infusão de líquidos e drogas vasoativas, ventilação mecânica e correção do fator desencadeante (fixação precoce de fraturas ou suspensão da lipoaspiração). O comprometimento multiorgânico indica pior prognóstico.

Manejo del potencial donante cadáver / Management of the potential organ donor

Solid organ transplantation is limited by donor availability. The loss of brain function produces hemodynamic, respiratory, hormonal and metabolic changes that lead to hypotension and organ dysfunction. Management of a potential donor is similar to any critically ill patient. Cardiovascular stability and protective ventilatory support must be pursued, aimed at minimizing the local and systemic inflammatory response that is triggered by brain death. There is no consensus on protocols for hormonal supplementation. The administration of vasopressin analogues and steroids may be beneficial under certain conditions. Appropriate medical management helps to optimize the function of different organs prior to transplantation. This may increase the number of harvested organs and improve their functional outcome in the recipient.

Effect of the systemic administration of methylprednisolone on the lungs of brain-dead donor rats undergoing pulmonary transplantation

OBJECTIVE: Most lung transplants are obtained from brain-dead donors. The physiopathology of brain death involves hemodynamics, the sympathetic nervous system, and inflammatory mechanisms. Administering methylprednisolone 60 min after inducing brain death in rats has been shown to modulate pulmonary inflammatory activity. Our objective was to evaluate the effects of methylprednisolone on transplanted rat lungs from donors treated 60 min after brain death. METHODS: Twelve Wistar rats were anesthetized, and brain death was induced. They were randomly divided into two groups (n = 6), namely a control group, which was administered saline solution, and a methylprednisolone group, which received the drug 60 min after the induction of brain death. All of the animals were observed and ventilated for 2 h prior to being submitted to lung transplantation. We evaluated the hemodynamic and blood gas parameters, histological score, lung tissue levels of thiobarbituric acid-reactive substances, level of superoxide dismutase, level of tumor necrosis factor-alpha, and level of interleukin-1 beta. RESULTS: After transplantation, a significant reduction in the levels of tumor necrosis factor-alpha and IL-1β was observed in the group that received methylprednisolone (p = 0.0084 and p = 0.0155, respectively). There were no significant differences in tumor necrosis factor-alpha and superoxide dismutase levels between the control and methylprednisolone groups (p = 0.2644 and p = 0.7461, respectively). There were no significant differences in the blood gas parameters, hemodynamics, and histological alterations between the groups. CONCLUSION: The administration of methylprednisolone after brain death in donor rats reduces inflammatory activity in transplanted lungs but has no influence on parameters related to oxidative stress. .

Influence of brain death and associated trauma on solid organ histological characteristics / Influência da morte encefálica e do trauma associado nas características histológicas de órgãos sólidos

PURPOSE: To evaluate histopathological alterations triggered by brain death and associated trauma on different solid organs in rats. METHODS: Male Wistar rats (n=37) were anesthetized with isoflurane, intubated and mechanically ventilated. A trepanation was performed and a balloon catheter inserted into intracraninal cavity and rapidly inflated with saline to induce brain death. After induction, rats were monitored for 30, 180, and 360 min for hemodynamic parameters and exsanguinated from abdominal aorta. Heart, lung, liver, and kidney were removed and fixed in paraffin to evaluation of histological alterations (H&E). Sham-operated rats were trepanned only and used as control group. RESULTS: Brain dead rats showed a hemodynamic instability with hypertensive episode in the first minute after the induction followed by hypotension for approximately 1 h. Histological analyses showed that brain death induces vascular congestion in heart (p<0.05), and lung (p<0.05); lung alveolar edema (p=0.001), kidney tubular edema (p<0.05); and leukocyte infiltration in liver (p<0.05). CONCLUSIONS: Brain death induces hemodynamic instability associated with vascular changes in solid organs and compromises most severely the lungs. However, brain death associated trauma triggers important pathophysiological alterations in these organs.

OBJETIVO: Avaliar as alterações histopatológicas desencadeadas pela morte encefálica e pelo trauma associado em diferentes órgãos sólidos em ratos. MÉTODOS: Ratos Wistar machos (n=37) foram anestesiados com isoflurano, entubados e mecanicamente ventilados. Foi realizada trepanação e um cateter foi inserido na cavidade intracraniana e insuflado rapidamente para induzir morte encefálica. Após a indução, os ratos foram monitorados por 30, 180 e 360 min para parâmetros hemodinâmicos e exsanguinados pela aorta abdominal. Coração, pulmão, fígado e rim foram removidos e fixados em parafina para avaliação de alterações histológicas (H&E). Ratos falso-operados foram apenas trepanados e usados como grupo controle. RESULTADOS: Ratos com morte encefálica apresentaram instabilidade hemodinâmica com episódio hipertensivo no primeiro minuto após a indução seguido de hipotensão por aproximadamente 1 hora. Análises histológicas demonstraram que a morte encefálica induz congestão vascular no coração (p<0,05) e pulmão (p<0,05); edema alveolar (p=0,001); edema tubular (p<0,05); e infiltrado leucocitário no fígado (p<0,05). CONCLUSÕES: A morte encefálica induz instabilidade hemodinâmica associada com mudanças vasculares em órgãos sólidos e compromete mais severamente os pulmões. Contudo, o trauma associado à morte encefálica desencadeia importantes alterações fisiopatológicas naqueles órgãos.

Paradoxical effects of brain death and associated trauma on rat mesenteric microcirculation: an intravital microscopic study

OBJECTIVE: Experimental findings support clinical evidence that brain death impairs the viability of organs for transplantation, triggering hemodynamic, hormonal, and inflammatory responses. However, several of these events could be consequences of brain death-associated trauma. This study investigated microcirculatory alterations and systemic inflammatory markers in brain-dead rats and the influence of the associated trauma. METHOD: Brain death was induced using intracranial balloon inflation; sham-operated rats were trepanned only. After 30 or 180 min, the mesenteric microcirculation was observed using intravital microscopy. The expression of Pselectin and ICAM-1 on the endothelium was evaluated using immunohistochemistry. The serum cytokine, chemokine, and corticosterone levels were quantified using enzyme-linked immunosorbent assays. White blood cell counts were also determined. RESULTS: Brain death resulted in a decrease in the mesenteric perfusion to 30 percent, a 2.6-fold increase in the expression of ICAM-1 and leukocyte migration at the mesentery, a 70 percent reduction in the serum corticosterone level and pronounced leukopenia. Similar increases in the cytokine and chemokine levels were seen in the both the experimental and control animals. CONCLUSION: The data presented in this study suggest that brain death itself induces hypoperfusion in the mesenteric microcirculation that is associated with a pronounced reduction in the endogenous corticosterone level, thereby leading to increased local inflammation and organ dysfunction. These events are paradoxically associated with induced leukopenia after brain damage.

Muerte encefálica: la necesidad de una causa suficiente y necesaria: a propósito de un caso de deseferentación completa por síndrome de Guillain Barré / Brain death: the need for sufficient and necessary cause: apropos of a complete deseferentation case from Guillain Barre syndrome

La muerte encefálica es una causa válida en la certificación del deceso de un paciente, especialmente en condiciones de donación de órganos. Existen escasas situaciones en las que el legislador ha propuesto la realización de exámenes complementarios para su certificación. Presentamos el caso de un paciente con un síndrome de Guillain Barré, que llegó a simular un estado de muerte encefálica, debido al compromiso motor completo, incluyendo musculatura ocular intrínseca. La falta de una condición suficiente y necesaria para declarar la muerte del paciente lleva a la solicitud de exámenes complementarios, en este caso un electroencefalograma, los que determinan la normalidad de la actividad eléctrica cerebral. Se recalca la necesidad de cumplir estrictamente los criterios para determinar la muerte encefálica y el no inhibirse de solicitar exámenes complementarios en condiciones de duda, aún cuando la ley no siempre lo contemple.

Brain death is a valid cause of death certification in a patient, especially in terms of organ donation. There are few situations in which the legislator has proposed further examination for certification. We report the case of a patient with Guillain Barré syndrome, which came to simulate a state of brain death due to motor impairment in full, including intrinsic ocular muscles. The lack of a necessary and sufficient condition for declaring the patient's death led to request additional examinations, in this case an electroencephalogram, which determine the normality of brain electrical activity. It emphasizes the need to comply strictly with the criteria for determining brain death and not to request additional examinations inhibited in a position of doubt, even though the law does not always contemplated.

Fulminant Gullian-Baree syndrome mimicking cerebral death: case report

The Guillian-Baree syndrome [GBS] may present with a wide range of clinical pictures and many variants of typical syndrome are now recognized. Sporadic reports have described the occurrence of acute severe inflammatory polyneuropathy leading to a complete areflexic paralysis[2-3]. So, we described a patient that presented with a rapid course of neurological deterioration lapsing into what resembled a clinically brain-dead state that was subsequently ascribed to a fulminant polyneropathy. Investigations [electrophysiological and pathological] and the clinical course suggested an axonal neuropathy. A fulminant neuropathy can result in a clinical state resembling brain-death through diffuse differentiation, although generally attributed to aggressive demyelination with secondary axonal degeneration. A primary axonopathy can also lead to a similar clinical presentation. NB. This case was reported as the first case diagnosed in Farawnya Hospital and the first case reported in Kuwait

Mecanismos fisiopatógicos en la muerte encefálica / Physiopathologic mechanisms in encephalic death

La muerte encefálica se basa en un diagnóstico clínico, y se acepta como sinónimo de muerte del individuo. Se llega a este estado cuando una lesión catastrófica provoca un coma irreversible, con ausencia de reflejos de tronco encefálico y apnea. La muerte encefálica se define como la pérdida irreversible de las funciones de todo el encéfalo, incluyendo los hemisferios cerebrales y el tronco encefálico. Las causas que llevan a la pérdida irreversible de las funciones del encéfalo son las mismas descritas que provocan un coma, las cuales se han agrupado en: estructurales y multifocales-metabólicas-difusas. Las causas estructurales se subdividen en compresivas y destructivas. Las lesiones compresivas causan conflictos de espacio en la cavidad intracraneana dando lugar a un aumento de la presión intracraneana y herniaciones. Las causas destructivas que llevan a la muerte encefálica afectan el diencéfalo, tronco encefálico y hemisferios cerebrales. Las etiologías multifocales-metabólicas-difusas constituyen un grupo muy variado de causas que provocan la pérdida irreversible de las funciones del encéfalo a través de diversos mecanismos bioquímicos y fisiopatológicos. No obstante, las etiologías descritas provocan la ausencia irreversible del flujo sanguíneo cerebral, que es la causa final que da lugar a la destrucción de las estructuras intracraneales. Aunque la muerte encefálica se basa en un diagnóstico clínico, el conocimiento de la fisiopatología de este estado permite estudiar los posibles mecanismos que llevan a que un enfermo evolucione hacia una muerte encefálica, lo que da la certeza acerca de la irreversibilidad de este diagnóstico.

Encephalic death is bases on a clinical diagnosis and it is accepted like a synonym of subject death. The person arrives to this stage when a catastrophic lesion provokes an irreversible coma with a lack of reflexes from the encephalic trunk and apnea. The encephalic death is defined like an irreversible loss of all encephalon including the brain hemispheres and the encephalic trunk. The different causes of irreversible loss of encephalon functions are the same described provoking a coma, which are grouped in: structural and diffuse-metabolic multifocal. The structural causes are subdivided in compressive and destructives. The compressive ones cause space problems in intracranial cavity leading to an increase of intracranial pressure and herniations. The destructive ones leading to encephalic death affect the diencephalon, the encephalic trunk and brain hemispheres. Diffuse-metabolic multifocal etiologies are a very varied group of causes provoking the irreversible loss of encephalon functions through diverse biochemical and physiopathologic mechanisms. However, the etiologies described provoke the irreversible lack of brain blood flux the final cause leading to destruction of intracranial structures. Although the encephalic death is based on a clinical diagnosis, knowledge of physiopathology of this status allows to study the potential mechanisms leading to a patient evolve to an encephalic death and be certain that there is a irreversibility of this diagnosis.

Selección y manejo del potencial donante de órganos / Selection and management of the potential organs donors

In Chile, an average of 135 effective donors in brain death for organs transplants are generated by year; which it means over 330 solid organs transplants annually. This number corresponds at the 85 percent of total transplants made in Chile, whereas 15 percent rest is from living donor. Of all the stages involved in donor generation, two basic pillars exist: Detection/Selection to accurate an increase in the global number of donors and the Donor Management, directly related with quality an security of transplanted organs. Brain Death it associates to haemodynamic, metabolic and internal equilibrium changes what means directly in hypoperfusion of transplanted organs. Considering also in brain death as in donors generation steps, all the health professionals should be involved, this review present recommendations to equal and optimize to the maximum the optimal care of the potential organ donor.

Cuidados em UTI com o potencial doador de múltiplos órgãos / Care in intensive care units with the potential tissue donors

O maior contingente de órgãos para transplantes provém de doadores cadavéricos, definidos por critérios de morte encefálica (ME). Os autores fazem uma revisão bibliográfica sobre as alterações fisiológicas que ocorrem em pacientes em ME, bem como o manejo clínico e cuidados gerais necessários para obter o maior número, com a melhor qualidade, de enxertos

Alteraciones fisiopatológicas en la muerte encefálica: Su importancia para decisiones de manejo y donación de órganos

Los avances tecnológicos en el área médica han permitido el desarrollo de técnicas útiles en la terapia de sujetos que padecen diversas entidades patológicas. Por ejemplo, en las unidades de terapia intensiva dicha tecnología permite la conservación del riego sanguíneo y la oxigenación de los tejidos, aun cuando la muerte encefálica (ME) ya ha ocurrido y el individuo no pueda volver a funcionar como un ser vivo, pues las funciones del corazón, los pulmones y otros órganos, pueden ser sustituidas con aparatos, pero las funciones cerebrales todavía no. Por lo tanto cuando un sujeto cubre los requisitos establecidos médica y legalmente para el diagnóstico de ME, se debe tener bien claro que cualquier medida que se siga aplicando al paciente ya no tendrá ningún objeto para mantener su vida, y aunque el sujeto parece vivo por las medidas de soporte a las que está sometido, cuando la ME se establece, se debe aceptar como muerte definitiva del individuo. Desde luego, como en todos los casos de muerte, se trata de un proceso difícil de admitir, inclusive para el personal de salud; sin embargo, consideramos que es de suma importancia que principalmente el equipo médico y de enfermería, que son los responsables directos de la atención de los enfermos en el área clínica, estén bien informados al respecto para saber las alternativas que existen con los sujetos en ME y poder orientar adecuadamente a quien lo necesite. En el presente trabajo realizamos una revisión bibliográfica sobre el concepto de ME, los principales cambios fisiopatológicos que presenta el sujeto y algunas posibles alternativas de tratamiento para mantenerlo como potencial donador de órganos.

Technological advances in the medical area have allowed for development of useful techniques to treat patients with diverse diseases. For example, at intensive care units this technology allows maintenance blood flow and tissue oxygenation even when brain death (BD) is already established and the individual cannot function. The function of heart, lungs, and other organs can be maintained with different devices, but maintenance of cerebral functions is not not yet possible. Therefore, when a subject fulfills legal and medical requirements for BD, we must be clear that any patient procedure will not keep him alive, although the subject looks alive due to support devices; when BD is present, death must be accepted. Obviously, death is a difficult process to accept, including for health personnel. We consider that it is very important for medical and nursing personnel directly responsible for patient care to receive knowledge on BD and recognize the alternatives with regard this situation, to be able to provide specific orientation when it is required. This paper is a review of the BD concept, main physiopathologic changes, and some possible treatment alternatives to maintain the patient as a potential organ donor.

Vasopressina e morte encefálica / Vasopressin and brain death

A morte encefálica (ME) resulta numa perda completa dos mecanismos centrais de regulação da estabilidade hemodinâmica mesmo em pacientes com suporte adequado da ventilação, correção hidroeletrolítica e ácido-básica e suporte farmacológico convencional máximo da circulação. Acredita-se que a diminuição da vasopressina circulante influencia de maneira preponderante a estabilidade cardiocirculatória de pacientes com ME, sendo a sua administração exógena defendida por alguns autores no manuseio do potencial doador de órgãos. O artigo analisa e discute alguns estudos experimentais e clínicos relevantes em relação ao comportamento da vasopressina na ME e seu papel na manutenção da estabilidade cardiocirculatória, bem como sua potencial utilidade no manuseio destes pacientes. Desta análise concluímos que o comportamento da vasopressina na ME e o seu real valor na manutenção do potencial doador ainda não estão totalmente esclarecidos, necessitando de investigações futuras.

Brain death and organ donation.

Brain death is the irreversible cessation of all brain functions. Brainstem death is the 'physiological core' of brain death. The Indian Parliament has given legal recognition to brain death though it applies only in the context of performance of organ transplantation. Brain death is diagnosed if there is irreversible loss of consciousness, absence of brainstem reflexes and apnoea. Care and diligence in the application of the criteria for brain death provide important safeguards for Individual patients and the community in general. These criteria also allow death to be diagnosed with certainty prior to the occurrence of circulatory arrest. Solid organ transplantation has become possible through the diagnosis of brain death but is not the primary consideration; the management of a potential organ donor, who is brain dead, is also vital. If optimal preservation of organs for transplantation is to be achieved the clinician needs to understand the pathophysiology and consequences of changes occurring in various organs after brain death and active management is required to reverse or control these changes. Discussions about organ donation with relatives of brain deed patients are never easy. These should always be frank and sympathetic. It has been suggested that those whose interests lie in transplantation must bear the responsibility of educating the general public. This will help intensivists who expose themselves knowingly to the unpleasant aspects of organ donation.

Cuidado y soporte del donante en muerte encefálica / Care and support of donor in brain death

Luego de diagnosticar la muerte encefálica, el cuidado del paciente pasa a ser mantenimiento del donante. El objetivo fundamental del equipo encargado de estos "cadaveres latentes" debe ser el mantenimiento de la función óptima de los órganos a transplantar. Debe haber un viraje en el énfasis terapéutico dirigido previamente a la protección cerebral, hacia la protección de los órganos a ser donados. Durante las horas previas a la extracción orgánica, pueden surgir diferentes problemas a resolver. Esto incluye la reposición y el mantenimiento del volumen intravascular, y del gasto cardíaco, para mantener un aporte de oxígeno adecuado a los tejidos del donante. Incluye también la reanimación del paro cardíaco, la evaluacíon y reversión de la poliuria, el manejo de la poiquilotermia y de los efectos de la hipotermia, y el tratamiento del hipopituitarismo y otros posibles cambios a nivel de las hormonas circulantes

Hemorragia cerebral postraumática tardía / Delayed traumatic intracerebral hemorrhage

La hemorragía intracerebral traumática tardía es difícil de reconocer. Se asocia con una alta mortalidad si no se diagnostica en forma temprana. En estos pacientes es de gradn utilidad el monitoreo completo para el diagnóstico y manejo óptimo. Existe un grupo de pacientes con traumatismo craneoencefálico que tiene mayor riesgo de sufrir hemorragia intracerebral traumática tardía. informamos sobre un caso de hemorragia intracerebral traumática tardía y hacemos una revisión de la literatura