Cerebral hemodynamic and metabolic changes in fulminant hepatic failure / Modificações da hemodinâmica e metabolismo cerebral na insuficiência hepatica fulminante

ABSTRACT Intracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF.

RESUMO O edema cerebral e a hipertensão intracraniana (HIC) são as principais causas de morbidade e mortalidade de pacientes com insuficiência hepática fulminante (IHF). A patogênese dessas complicações tem sido investigada no homem, em modelos experimentais e em sistemas celulares isolados. Atualmente, o mecanismo subjacente ao edema cerebral e HIC na presença de IHF é multifatorial em etiologia e pouco compreendido na literatura. O objetivo deste trabalho é revisar a fisiopatologia das alterações hemodinâmicas e metabólicas cerebrais na IHF, visando melhorar a compreensão da complicação da hemodinâmica encefálica na IHF.

Hipotermia terapêutica como ponte até transplante em pacientes com falência hepática fulminante / Therapeutic hypothermia as a bridge to transplantation in patients with fulminant hepatic failure

Os tópicos mais importantes na falência hepática fulminante são o edema cerebral e a hipertensão intracraniana. Dentre todas as opções terapêuticas, tem sido relatado que a hipotermia sistêmica induzida em níveis entre 33 - 34ºC reduz a elevação da pressão e aumenta o tempo durante o qual os pacientes podem tolerar um enxerto. Esta revisão discutiu as indicações e os efeitos adversos da hipotermia.

The most important topics in fulminant hepatic failure are cerebral edema and intracranial hypertension. Among all therapeutic options, systemic induced hypothermia to 33 - 34ºC has been reported to reduce the high pressure and increase the time during which patients can tolerate a graft. This review discusses the indications and adverse effects of hypothermia.

Relevancia de la hiperglucemia para la evolución y el desenlace de la hemorragia subaracnoidea aneurismática: evidencias y mecanismos / Relevance of hyperglycemia on the course and outcome of aneurysmal subarachnoid hemorrhage: evidence and mechanisms

La hemorragia subaracnoidea aneurismática (HSAa) puede tener un desenlace mortal en unas pocas semanas debido por las complicaciones que presenta, como el vasoespasmo y el edema cerebrales junto con la hiperglucemia. La hiperglucemia podría estar relacionada con el desarrollo del vasoespasmo y el edema cerebrales. Es posible que el control de la glucemia juegue un papel central en la evolución y el desenlace de la HSAa. Se han descrito los mecanismos por los cuales puede darse esta relación, que incluyen el equilibrio de iones, la liberación de aminoácidos excitadores, la estimulación de moléculas vasoconstrictoras y la disminución en la síntesis de vasorrelajantes. Sin embargo, existen estudios que no apoyan la hipótesis sobre la participación de la hiperglucemia en esta enfermedad. En conjunto, estas evidencias sugieren que el control de los niveles de glucosa podría modificar el desenlace de los grupos de pacientes con HSAa dependiendo de las complicaciones que presenten.

Aneurysmal subarachnoid hemorrhage (aSAH) may have a fatal outcome after a few weeks from ictus, due to its complications, like cerebral vasospasm and edema along with hyperglycemia. Hyperglycemia may be involved in the development of brain vasospasm and edema. It is possible that hyperglycemia plays a central role in the outcome of aSAH. Several mechanisms may explain this relationship; they include ion balance, excitatory amino acid release, stimulation of vasoconstrictor molecules and reduced synthesis of vasorelaxants. However, some studies do not support this hypothesis regarding the role of hyperglycemia in aSAH. Taken together, the evidence suggests that the control of glucose levels may influence the aSAH outcome depending on the complications that may develop.

Fluid distribution kinetics during cardiopulmonary bypass

OBJECTIVE: The purpose of this study was to examine the isovolumetric distribution kinetics of crystalloid fluid during cardiopulmonary bypass. METHODS: Ten patients undergoing coronary artery bypass grafting participated in this prospective observational study. The blood hemoglobin and the serum albumin and sodium concentrations were measured repeatedly during the distribution of priming solution (Ringer's acetate 1470 ml and mannitol 15% 200 ml) and initial cardioplegia. The rate of crystalloid fluid distribution was calculated based on 3-min Hb changes. The preoperative blood volume was extrapolated from the marked hemodilution occurring during the onset of cardiopulmonary bypass. Clinicaltrials.gov: NCT01115166. RESULTS: The distribution half-time of Ringer's acetate averaged 8 minutes, corresponding to a transcapillary escape rate of 0.38 ml/kg/min. The intravascular albumin mass increased by 5.4% according to mass balance calculations. The preoperative blood volume, as extrapolated from the drop in hemoglobin concentration by 32% (mean) at the beginning of cardiopulmonary bypass, was 0.6-1.2 L less than that estimated by anthropometric methods (p<0.02). The mass balance of sodium indicated a translocation from the intracellular to the extracellular fluid space in 8 of the 10 patients, with a median volume of 236 ml. CONCLUSIONS: The distribution half-time of Ringer's solution during isovolumetric cardiopulmonary bypass was 8 minutes, which is the same as for crystalloid fluid infusions in healthy subjects. The intravascular albumin mass increased. Most patients were hypovolemic prior to the start of anesthesia. Intracellular edema did not occur. .

Encefalopatía hepática fulminante vinculada a hiperintensidad de la corteza cerebral en la resonancia magnética / Fulminant hepatic encephalopathy vinculated with hyperintensity of the cerebral cortex in magnetic resonance

Background: The presence of manganese deposits in basal ganglia is an expression of chronic liver damage in neuroimaging, whereas diffuse edema of the white matter and hyperintensity of the internal capsule are seen in MRI in acute decompensation. In fulminant encephalopathy, changes in intensity in the cerebral cortex have been described, suggesting different pathogenic aspects. Purpose: To describe and try to interpret hyperintensities images of the cerebral cortex in fulminant hepatic encephalopathy. Case report: A 42 years old woman, with history of hyperthyroidism treated with propylthiouracil developed abdominal pain, choluria and general malaise, without fever. At admission, she had jaundice, elevated liver enzymes, and hyperammronemia of 481 ug. She developed progressive impairment of consciousness falling into a non-reactive coma with intermediate size and poorly reactive pupils, absence of oculocephalic reflexes and diminished osteotendinous reflexes, with indifferent plantar reflexes. Brain CT showed brain edema without focal lesions. The MRI showed hyperintense signal abnormalities in the fronto-parietal cortex in T2 and FLAIR with restriction in difussion sequency. She became brain dead. Comment: These exceptional images on MRI are considered an expression of cytotoxic damage, consistent with high levels of ammonium in fulminant hepatic encephalopathy. The swelling of astrocytes and cortical neurons is caused by the accumulation of intracellular glutamine, highly osmophilic, and explains the restriction on the difussion and lower values in the ADC. Interstitial edema would be part of the chronic forms by acquisition of compensatory mechanisms capable of preventing the accumulation of glutamine.

Antecedentes: La presencia de depósitos de manganeso en los núcleos basales es una expresión neuroimagenológica de daño hepático crónico, así como el edema difuso de la substancia blanca y la hiperintensidad de la cápsula interna con RM en descompensaciones agudas. En encefalopatías fulminantes se ha visualizado cambio de intensidad en la corteza cerebral, sugiriendo aspectos patogénicos distintos. Propósito: Describir e intentar interpretar imágenes hiperintensas de la corteza cerebral en una encefalopatía hepática fulminante. Caso clínico: Mujer de 42 años, hipertiroidea en tratamiento con propiltiouracilo. Consultó por dolor abdominal, coluria y compromiso del estado general, sin fiebre. Ingresó con ictericia, enzimas hepática elevadas, e hiperamonemia de 481 ug. Desarrolló progresivo compromiso de conciencia cayendo en un coma no reactivo, con pupilas de tamaño intermedio pobremente reactivas, ausencia de reflejos oculocefálicos y reflejos osteotendíneos apagados, con reflejos plantares indiferentes. TAC de cerebro mostró edema cerebral, sin lesiones focales. La RM definió áreas hiperintensas en la corteza fronto-parietal en T2 y FLAIR, que presentaban incremento de señal en la difusión. Evolucionó hasta la muerte cerebral. Comentario: Estas imágenes excepcionales en la RMson consideradas expresión de daño citotóxico, en concordancia con los altos niveles de amonio de una encefalopatía hepática fulminante. El edema de astrocitos y neuronas corticales se origina por la acumulación de glutamina intracelular, altamente osmofílica, y explica la restricción en la difusión y valores menores en el ADC. El edema intersticial, sería atributo de las formas crónicas, debido a la adquisición de mecanismos compensatorios capaces de impedir la acumulación de glutaminas.

Cerebrovascular complications of diabetic ketoacidosis in children / Complicações cerebrovasculares da cetoacidose diabética em crianças

Neurological deterioration in children with diabetic ketoacidosis (DKA) is commonly caused by cerebral edema. However, subtle cerebral injuries including strokes should also be suspected, since children with hyperglycemia and DKA are prone to thrombosis. In this paper, a case involving a 2 month-old patient that presented cerebral edema and stroke as complications of DKA is reported. In the discussion, the literature on neurological complications of DKA in children is briefly reviewed, emphasizing the prothrombotic tendency of these patients.

Alterações neurológicas em crianças com cetoacidose diabética (CAD) são comuns, sobretudo em decorrência de edema cerebral. Contudo, lesões cerebrais agudas, como acidente vascular cerebral (AVC), também devem ser investigadas, já que as crianças com hiperglicemia e cetoacidose têm maior chance de apresentar essa complicação. Neste relato, descreve-se a história de um paciente de 2 meses de idade que apresentou edema cerebral e AVC como complicações de um quadro de cetoacidose diabética. Durante a discussão, será feita uma breve revisão da literatura sobre as complicações neurológicas da CAD nos pacientes pediátricos enfatizando sua tendência pró-trombótica.

Peritumoral brain edema in intracranial meningiomas / Edema peritumoral em meningiomas intracranianos

Occurrence of peritumoral brain edema (PBE) in meningiomas has been associated with several factors in recent years, although its pathophysiological mechanism has not yet been fully elucidated. The aim of this study was to analyze the correlation between the presence / degree of PBE and factors such as gender, age, size and histological subtype of tumor. We analyzed the MRI images of 74 patients operated on Hospital Beneficência Portuguesa de Porto Alegre for the presence / degree of PBE and data was statistically correlated with the parameters of the patient. PBE was present in 70.1 percent of patients. Tumors with higher volume had more PBE. Tumors of the olfactory groove showed more PBE than sphenoid wing and parassagittal tumors. Transitional subtype showed more PBE than fibroblastic and meningothelial subtypes.

A presença de edema cerebral peritumoral (ECP) em meningiomas tem sido associada a diversos fatores nos últimos anos, embora o seu mecanismo fisiopatológico ainda não tenha sido inteiramente elucidado. O objetivo desse estudo foi analisar a correlação entre a presença/grau de ECP e fatores como sexo, idade, volume e subtipo histológico do tumor. Foram analisadas imagens de RM de 74 pacientes operados no Hospital Beneficência Portuguesa de Porto Alegre quanto à presença/grau de ECP e os dados correlacionados estatisticamente com os parâmetros do paciente. ECP estava presente em 70,1 por cento dos pacientes. Tumores com maior volume apresentaram mais ECP. Tumores da goteira olfatória apresentaram mais ECP que os da asa do esfenóide e que os parassagitais. Meningiomas transicionais apresentaram mais ECP que os fibroblásticos e que os meningoteliais.

Neurocysticercosis in children.

Neurocysticercosis (NCC) is a common cause of seizures and neurologic disease. Although there may be variable presentations depending on the stage and location of cysts in the nervous system, most children (> 80%) present with seizures particularly partial seizures. About a third of cases have headache and vomiting. Diagnosis is made by either CT or MRI. Single enhancing lesions are the commonest visualization of a scolex confirms the diagnosis. Some cases have multiple cysts with a characterstic starry-sky appearance. Management involves use of anticonvulsants for seizures and steroids for cerebral edema. The use of cysticidal therapy continues to be debated. Controlled studies have shown that cysticidal therapy helps in increased and faster resolution of CT lesions. Improvement in long - term seizure control has not yet been proven. Children with single lesions have a good outcome and seizure recurrence rate is low. Children with multiple lesions have recurrent seizures. Extraparenchymal NCC has a guarded prognosis but it is rare in children. In endemic areas NCC must be considered in the differential diagnosis of seizures and various other neurological disorders.

Edema agudo cerebral de altura / High altitude acute cerebral edema

La ciudad de La Paz - Bolivia, ubicadageográficamente en la cordillera de Los Andes, presentapropiedades ambientales propias, tales comodisminución de la presión parcial de oxígeno en el aireambiente, menor densidad del aire, mayor sequedaddel aire, variaciones significativas de la temperaturaambiental y radiaciones solares no ionizantes(radiaciones ultravioleta). La primera de estascaracterísticas es atribuida como factor desencadenante principal del edema cerebral de altura (EACA). Cuando una persona no aclimatada asciende rápidamente por encima de los 3.000 metros de altura sobre el nivel del mar (m.s.n.m), recibe en algún grado el impacto de la hipoxia hipobárica ambiental que puede producir innumerables efectos fisiológicos enel cuerpo humano, siendo los más importantes los percibidos sobre el rendimiento físico, desempeñomental y sueño

Complicações hiperglicêmicas agudas no diabetes melito tipo 1 do jovem: [revisão] / Hyperglycemic acute crisis in type 1 diabetes mellitus in youth: [review]

A principal complicação hiperglicêmica no diabetes melito tipo 1 (DM1) é a cetoacidose diabética (CAD). Embora variações nos protocolos possam ocorrer, os princípios básicos que norteiam o tratamento devem ser os mesmos. A recuperação inicial da capacidade circulatória, com a infusão rápida de solução salina na dose de 20 mL/kg, que pode ser repetida, é o ponto de partida para o tratamento. A partir daí, a reposição de volume é relativamente lenta, e o objetivo principal é corrigir gradualmente os distúrbios metabólicos instalados, sem ocasionar variações muito intensas e muito rápidas na osmolalidade, fator de risco para complicações. Atenção ao desenvolvimento de edema cerebral que, uma vez suspeitado, deve ser imediatamente corrigido, sob pena de óbito ou seqüelas neurológicas. A administração de insulina ultra-rápida, por via subcutânea, mostra-se eficaz e simplifica o atendimento do paciente. A CAD é uma situação grave, ainda com alta mortalidade, e seu tratamento deve ser dirigido aos pontos principais que levaram ao quadro clínico, com correções graduais, sob risco de se agravar o quadro.

Diabetic ketoacidosis (DKA) is the main hyperglycemic complication in type 1 Diabetes Mellitus (DM1). The basic principles in treatment have to be followed carefully. The patient with DKA has a very deep volume depletion. To restore the circulatory capacity is the first step. From this point on, the restoration of the lost fluids is slow, around 1 percent per hour, aiming at the correction of the metabolic disturbance already on and avoiding great fluctuations in osmolality, which increases the risk of having complications. Attention to the development of cerebral edema, which, once suspected, deserves an urgent treatment plan, trying to avoid neurologic sequelae or even death. Subcutaneous ultra-rapid insulin has been demonstrated to be efficient and easier to use. As the perfusion gets improved and the levels of insulin increase, the lipolysis is blocked, as well as the generation of ketones and so the acidemia tends to be solved. DKA is still a high-mortality condition. And to be in a hurry frequently leads to neurologic sequelae and even to a fatal outcome.

Unexplained cardiac arrest during closure of craniotomy: case report and review of literature

Hypotension and bradycardia after application of suction to a subgaleal drain, or stimulus inside or outside the skull, have been reported in the medical literature. The commonly reported occurrence is stimulation of the Trigeminal nerve along its distribution and is the main factor that sets off the whole reflex arc through the Vagus nerve ending in a series of serious hemodynamic changes that institute severe bradycardia, asystole and severe hypotension. Another less common but possible pathology caused by a suction drain is Pseudo-Hypoxic Brain Swelling [PHBS]. We report a case of transient cardiac arrest after the application of theatre suction to a subgaleal drain at the closure of an uneventful craniotomy and discuss the possibilities as well as review the literature

Brain edema after intracerebral hemorrhage in rats: the role of inflammation.

BACKGROUND: Intracerebral hemorrhage (ICH) results in secondary brain edema and injury that may lead to death and disability. ICH also causes inflammation. It is unclear whether inflammation contributes to brain edema and neuron injury or functions in repairing the brain tissue. AIMS: To understand the effect of inflammation in ICH, we have carried out an investigation on the various aspects and the dynamic changes of inflammation. SETTINGS AND DESIGN: An ICH model was generated by injecting 50 microl autologous tail artery blood stereotactically into the right caudate nucleus of 30 rats, which were randomly divided into five ICH groups. Similarly, five Sham control groups were generated by inserting the needle to the right caudate nucleus of rats. MATERIALS AND METHODS: Rat behavior was evaluated over the time course (6 h, 24 h, 48 h, 72 h and 7 d) in each group. The rats were then killed by administering an overdose of pentobarbital. Following the euthanasia, the brain water content, neuronal loss, glia proliferation, inflammatory infiltration and brain morphology of the rats were measured. Additionally, the expression of TNF-alpha, IL-6, ICAM-1, VEGF, NF-kappaB, C3 and CR2 was analyzed by immunohistochemistry. STATISTICAL ANALYSIS: The data were analyzed by student's t test. RESULTS: Rat brain water content increased progressively over the time course and reached its peak at 48 h followed ICH. The maximum of inflammatory infiltrate (especially neutrophils) and immunopositive cells of TNF-alpha, IL-6 and NF-kappaB, were at 48 h. The expression of C3 and CR2 reached their peaks at 48-72 h, while the expression ICAM-1 and VEGF were at maximum at 72 h followed ICH. CONCLUSIONS: The results suggested that the inflammatory cytokines, complement system and VEGF may have a function in the development of the brain edema and neuron injury followed ICH.

Cerebral edema in diabetic ketoacidosis.

Cerebral edema is the most important complication of diabetic ketoacidosis in children. It has a high mortality rate of 20 to 90% in different series. Twenty to 40% of survivors suffer from neurologic sequelae. The pathogenetic mechanisms are still controversial and the risk factors which are thought to predict its occurrence do not consistently correlate with cerebral edema in various studies. Prevention and recognition of early warning signs, such as decreased arousal, lethargy after initial improvement, headache, vomiting, relative bradycardia and relative hypertension, are crucial. Therapeutic guidelines to prevent cerebral edema in diabetic ketoacidosis include slow rehydration over about 48 hours, avoidance of hypotonicity and of unnecessary alkali therapy. Early recognition of cerebral edema and prompt institution of hypertonic therapy with mannitol may prevent permanent neurological sequelae.

Hyperthermia induced brain oedema: current status and future perspectives.

Recent years have witnessed a large number of deaths due to hyperthermia and heat-related illnesses across the globe in human population resulting in great social and medical problems. The detailed mechanisms and probable therapeutic measures have still not been worked out. Sporadic autopsy reports show profound brain swelling leading to compression of vital centers that could be responsible for instant death. Increased permeability of the blood-brain barrier (BBB) and brain swelling is also seen in experimental models of heat stress. It appears that hyperthermia is instrumental in opening of the BBB either directly or indirectly leading to vasogenic oedema formation, a feature crucial to molecular and cellular alteration in the brain inducing cell and tissue injury. The probable mechanisms and functional significance of heat induced brain oedema and BBB damage in relation to neurodegenerative changes are discussed.

Bifrontal decompressive craniotomy for malignant edema

To review the outcome of bifrontal decompressive craniotomy used for the treatment of malignant brain edema due to different etiologies. The study was carried out at King Khalid University Hospital, Riyadh, Kingdom of Saudi Arabia during the period from January 2000 to June 2005, and included all patients who had malignant brain edema due to different etiology and were treated with bifrontal decompressive craniotomy after failure of aggressive medical treatment. Ten patients were included in the study, 6 males and 4 females; the mean age was 24 years. Seven patients had severe head injury, 2 had aneurysmal subarachnoid hemorrhage, and one had large calcified olfactory groove meningioma. Clinically, all patients, except one, had Glasgow coma scores more than 3 before surgery, and operation was performed in all patients once clinical deterioration was observed and diagnosis confirmed by CT brain scan. The outcome of surgery was good in 70%, poor in 20%, and mortality was 10%. The mean hospital stay was 85 days. Bifrontal decompressive craniotomy offers immediate reduction of intracranial pressure to its normal levels, and improves the outcome of malignant brain edema whatever its cause, it should be performed once clinical deterioration is observed

Bifrontal decompressive craniotomy for malignant brain edema

To review the outcome of bifrontal decompressive craniotomy used for the treatment of malignant brain edema due to different etiologies. The study was carried out at King Khalid University Hospital, Riyadh, Kingdom of Saudi Arabia during the period from January 2000 to June 2005, and included all patients who had malignant brain edema due to different etiology and were treated with bifrontal decompressive craniotomy after failure of aggressive medical treatment. Ten patients were included in the study, 6 males and 4 females; the mean age was 24 years. Seven patients had severe head injury, 2 had aneurysmal subarachnoid hemorrhage, and one had large calcified olfactory groove meningioma. Clinically, all patients, except one, had Glasgow coma scores more than 3 before surgery, and operation was performed in all patients once clinical deterioration was observed and diagnosis confirmed by CT brain scan. The outcome of surgery was good in 70%, poor in 20%, and mortality was 10%. The mean hospital stay was 85 days. Bifrontal decompressive craniotomy offers immediate reduction of intracranial pressure to its normal levels, and improves the outcome of malignant brain edema whatever its cause, it should be performed once clinical deterioration is observed

Cerebral edema associated to scorpion sting: a two-case sting report

Scorpionism is a public health problem in some places in Mexico. The clinical symptoms of envenomation by scorpion sting are by sympathetic and parasympathetic stimulation, developing systemic and local symptoms. The Central Nervous System (CNS) is one of the organs that are affected. In some cases, cerebral edema develops. In this report we present two pediatric cases with the association of envenomation by scorpion sting and cerebral edema. The first case developed severe cerebral edema, which progressed to a fatal outcome; and the other case developed mild cerebral edema with a satisfactory evolution. The pathophysiology of this complication is not well known and probably is the consequence of hypoxia, secondary to respiratory failure, laryngospasm and seizures that are manifestations of envenomation by scorpion sting

Leucoencefalopatía posterior reversible secundaria a glomerulonefritis postestreptocócica: a propósito de un caso / Posterior leukoencephalopath syndrome in poststretococcal acute glomerulonephritis

La leucoencefalopatía posterior reversible (LEPR) es una entidad clínico radiológica que afecta habitualte la sustancia blanca de los hemisferios cerebrales. Se asocia con frecuencia a hipertensión arterial aguda y al tratamiento inmunosupresor, entre otras causas. La presentación clínica es variada, con cefales, náuseas, vómitos, deterioro de conciencia y alteración en el comportamiento, convulsiones y transtornos visuales, síntomas que frecuentemente retroceden . La tomografía axial computada (TAC) y la resonancia magnética nuclear (RMN) muestran imágenes con edema de la sustancia blanca predominando en regiones posteriores del encéfalo. Se presenta un niño de 10 años con LEPR en el curso de un síndrome nefrítico secundario a una glomerunefritis difusa aguda (GNDA) postestreptocócica.