Occurrence Of Cerebral Edema Research Articles

Clinical and biostatistical approach to assessing the severity of physical status of patients with combined midface trauma. Part 2

Objective. To develop a method for predicting mortality among patients with combined midface trauma (CMFT).
 Materials and methods. This study is based on the examination results of 95 patients with CMFT. Depending on the outcome of CMFT, 2 groups of patients were formed: the first group – patients with a favorable outcome (n=50); the second group – patients with an unfavorable outcome (n=45). A group of physiological parameters was measured on the 1st, 3rd, 7th and 14th days of patients’ hospital stays. The creation of the CMFT outcomes predicting method was carried out using factor analysis (principal component method) and discriminant analysis.
 Results. The CMFT outcomes predicting method has been developed in two variants. The first variant (with parameters of the blood gas test) includes the following parameters: leukocyte index of intoxication according to Ya.Ya. Kalf-Kalifu (LII), blood glucose level, concentration of potassium ions in the blood (K+), international normalized ratio, partial pressure of carbon dioxide in arterial blood, partial pressure of oxygen in arterial blood, measured on the 3rd day after injury, and also the age of the patient, evidence of cardiovascular diseases in patient’s medical history and the occurrence of cerebral edema after the injury. The second variant (without the parameters of the blood gas test) includes the following parameters: absolute number of leukocytes (on the 1st day after injury), LII, K+, blood urea level, absolute number of lymphocytes, measured on the 3rd day after injury, as well as patient’s age, evidence of cardiovascular diseases in patient’s medical history and the occurrence of cerebral edema after injury. The classification accuracy when using the first variant was 100%, the second variant – 98.4%.
 Conclusions. Taking into account the set of variables included in our study, and based on the results of this study published in the first and in this part of this article, we can conclude that the optimal time point for predicting the CMFT outcomes is the 3rd day after injury. The method for predicting the CMFT short-term outcomes developed in our study can be used in determining the timing for reconstructive surgery as part of the damage control surgery treatment of patients with this pathology.

The Recipient Vessel Hemodynamic Features Affect the Occurrence of Cerebral Edema in Moyamoya Disease After Surgical Revascularization: A Single-Center Retrospective Study.

ObjectiveIn moyamoya disease (MMD) with direct or combined revascularization, the initially hemodynamic recipient features are likely one of the main causes of acute hemodynamic disruption. Previous studies have explored the relationship between recipient diameter or flow velocity and postoperative complications, but there are still no optimal selection criteria with multiple potential recipient vessels. Cerebral edema is one of the most common radiological manifestations in the acute postoperative period. This study assessed the hemodynamic characteristics of cortex vessels related to postoperative cerebral edema.MethodsAll patients who had undergone direct or combined revascularization with preoperative digital subtraction angiography (DSA) between 2019 and 2021 were eligible for inclusion in this study. The application of DSA was performed and regular radiological examinations were employed after surgery. DSA was analyzed with the hemodynamic features within chosen recipient vessels. Cerebral edema was identified as a low-density image on CT or high signaling in the MRI T2 phase. The recipient hemodynamic characteristics and demographic presentation, as well as clinical data, were retrospectively analyzed in this study.ResultsA total of 103 patients underwent direct or combined revascularization with preoperative DSA. The mean age of this enrolled cohort was 44.31 ± 10.386 years, in which bilaterally involved MMD accounted for the main part. The preliminary correlation analysis found preoperative disease period (p = 0.078), recipients observed in angiography (p = 0.002), and surgery on the left (p = 0.097) may be associated with cerebral edema. The following regression analysis confirmed low occurrence of cerebral edema was accompanied by recipients observed in angiography (p = 0.003). After subdividing by flow direction and hemodynamic sources, the incidence rate of anterograde direction, anterior sources, and posterior sources were significantly lower than undetected recipients.ConclusionsCerebral edema is a common radiological manifestation in MMDs after surgery. In this study, the observation in angiography reliably identifies a variety of physiological or pathological recipient detection, flow direction, and hemodynamic sources in patients with MMD after revascularization, which indicates the selection strategy of potential recipients and highlights the importance of recipient observability in DSA. Meanwhile, vascular conditions determined by recipient hemodynamics meditate the occurrence of postoperative cerebral edema.

Hyponatremia - unfavourable prognostic factor in hepatic cirrhosis.

Hyponatremia is defined by a level of Na in serum below or equal to 136 mEq/L while in hepatic cirrhosis it is classically considered as relevant only at a level of Na below 130 mEq/L. Hyponatremia frequently occurs in patients with end-stage hepatic disease. The frequency and severity are variable but it has been estimated that it occurs with a frequency of 57% in hospitalized patients with cirrhosis and in those on waiting lists for hepatic transplants. Signs and symptoms of hyponatremia are related to dysfunctions of the central nervous system, due to migration of the water from intravascular space to the brain cells, resulting in the occurrence of cerebral edema. Therapeutic options in hyponatremia are limited and are based on restriction of water consumption, exclusion of diuretics and vaptans. Hepatic transplant remains the only definitive treatment for end-stage hepatic diseases in which hyponatremia has occurred.

Susceptibility-weighted imaging is suitable for evaluating signal strength in different brain regions of a rabbit model of acute hemorrhagic anemia.

Susceptibility-weighted imaging is suitable for evaluating signal strength in different brain regions of a rabbit model of acute hemorrhagic anemia.

DKA management and outcomes

Diabetic ketocidosis (DKA) is an acute life threatening complication of type 1 diabetes mellitus (T1D). DKA is characterized by the the triad of hyperglycemia, metabolic acidosis and increased total body ketone concentration. These metabolic derangements result from the combination of absolute or relative insulin deficiency and increased levels of counter-regulatory hormones. DKA is associated with both short-term risks and long-term consequences. Recent data have shown that DKA is responsible for up to 73% of causes of deaths during the first decade of diabetes. Mortality is predominantly related to the occurrence of cerebral edema, which occurs in 0.3-1% of patients, whereas only a minority of deaths in DKA is due to other causes. DKA represents the initial manifestation of T1D in 13-80% of cases and it can also occur in 25% of cases of type 2 diabetes at onset. In addition, DKA is a common complication in patients with known diabetes, where it may be the consequence of illness, poor compliance, or malfunction of diabetes care equipment. Early identification and treatment of DKA are two key points to minimizing the risks of this complication. Children with DKA should be treated in experienced centers and adherence to guidelines for the management of this condition is of paramount importance. Treatment of DKA requires strict monitoring of the patient, correction of hyperglycemia, acidosis and ketosis and replacement of fluid and electrolytes losses. Another important point is the identification and treatment of precipitating events. Early recognition of signs indicative of cerebral edema is essential to prevent the morbidity and mortality associated with this complication. Cerebral edema occurs in 0.3-1% of patients in DKA and represents the most common cause of mortality in children with DKA, accounting for 60-90% of all DKA deaths. In addition, 10-25% of survivors have significant residual morbidity. The etiology of cerebral edema is poorly understood, but it is likely related to vasogenic, osmotic, and ischemic mechanisms. Prevention of DKA at diagnosis is of paramount importance and should be based on intensive community interventions and education of health care providers to raise awareness. In addition, preventive strategies should be applied to avoid episodes of DKA in patients with an already known diagnosis of diabetes. This requires patient education and access to specific diabetes programs and services.

Natural course of fulminant hepatic failure: the scenario in Bangladesh and the differences from the west.

Background/Aim:Fulminant hepatic failure (FHF) is a devastating complication of acute viral hepatitis, leading to death in most cases. The etiology and predictors of outcome differ according to the geographical region. This study was conducted with the aim of evaluating the etiology, complications, and outcome of FHF in Bangladesh.Patients and Methods:In this prospective study, we included 67 consecutive cases of FHF presenting to the Department of Hepatology, Bangabandhu Sheikh Mujib Medical University, Dhaka, between November 2003 and May 2008. Thirty-nine of the patients were male and 28 were female. Data was analyzed using SPSS, version 13.0.Results:The mean age of the subjects was 31.9 ± 11.7 years. Hepatitis E virus (HEV) was the commonest etiological factor for FHF (50 cases, 74.6%); of the 50 cases with HEV infection, 43 (64.2%) were not coinfected with any other virus, four cases were Hepatitis B virus (HBV) carriers, and three had coinfection with hepatitis A virus (HAV). HBV was the cause of FHF in nine (13.4%) patients. HCV, paracetamol, and alcohol were not responsible for any of the cases. Most of the patients (57 patients, 85%) developed FHF within 2 weeks of the onset of jaundice. Of the 67 patients, 49 (73.1%) died. Cerebral edema was the single most common cause of death (48 patients, 71.6%). Other complications were renal failure (23 patients, 34.3%), sepsis (15 patients, 22.4%), electrolyte imbalance (12 patients 17.9%), and bleeding tendency (7 patients, 10.4%). Occurrence of cerebral edema, longer prothrombin time, higher grade of encephalopathy, and longer jaundice-to-encephalopathy interval had significant negative influence on outcome.Conclusions:The etiology of FHF in Bangladesh is different from that in the West. Prolongation of prothrombin time and occurrence of cerebral edema are predictors of the worst prognosis.

Acute liver failure: early supportive medical management for the liver is better than delayed intensive care for the brain

Acute liver failure: early supportive medical management for the liver is better than delayed intensive care for the brain

In vivo 1H MR spectroscopic imaging and diffusion weighted MRI in experimental hydrocephalus.

The severity and progression of ventricular enlargement, the occurrence of cerebral edema, and the localization of ischemic metabolic changes were investigated in a rat model of hydrocephalus, using in vivo 1H MR spectroscopic imaging (SI) and diffusion weighted MRI (DW MRI). Hydrocephalic rats were studied 1, 2, 4, and 8 weeks after injection of kaolin into the cisterna magna. Parametric images of the apparent diffusion coefficient (ADC) revealed a varying degree of ventriculomegaly in all rats, with different time courses of ventricular expansion. Extracellular white matter edema was observed during the early stages of hydrocephalus, most extensively in cases of progressive ventriculomegaly. In gray matter regions, ADC values were not changed, compared with controls. In case of fatal hydrocephalus, high lactate levels were observed throughout the whole brain. In all other rats, at all time points after kaolin injection, lactate was detected only in voxels containing cerebrospinal fluid. This suggests accumulation of lactate in the ventricles, and/or an ongoing periventricular production of lactate as a consequence of cerebral ischemia in experimental hydrocephalus.

Time course of cerebral edema after traumatic brain injury in rats: effects of riluzole and mannitol.

Brain trauma is the main cause of morbidity and mortality in young adults. One delayed events that occurs after a head trauma and compromises the survival of patients is cerebral edema. The present study examined first the occurrence of cerebral edema after a traumatic brain injury (TBI) induced by moderate fluid percussion in rats. Brain water content was measured from 1 h to 7 days posttrauma, in the hippocampus and cortex, on both ipsi- and contralateral hemispheres. Second, the effects of mannitol, an osmotic agent frequently used in the clinic, and riluzole, a neuroprotective compound, were investigated on regional edema formation. After TBI, the ipsilateral edema began early at 1-6 h, was maximal at 48 h and was resorbed by 5-7 days. No edema was observed in the contralateral hemisphere. Mannitol at 1 g/kg or vehicle was administered iv 15 min, 2 h and 4 h postinjury. At this dose, mannitol significantly attenuated the ipsilateral injured cortex edema measured at 6 h (p < 0.05). Riluzole at 4 and 8 mg/kg or vehicle was administered 15 min (IV) and 6 h, 24 h, and 30 h (SC) post-TBI. Riluzole at 4 x 4 mg/kg significantly reduced edema measured at 48 h, in the ipsilateral hippocampus (p < 0.05), whereas at 4 x 8 mg/kg, the reduction was observed in the hippocampus (p < 0.01) and the injured cortex (p < 0.05). Our results demonstrate that (1) cerebral edema begins early after the injury and is resorbed over 1 week; (2) mannitol could attenuate cerebral edema; and (iii) riluzole in addition to its neuroprotective effects reduces the brain edema. Thus, riluzole could be useful in human TBI treatment.

Studies on pathogenesis of cerebral edema due to experimental cerebral hemorrhage. An approach through energy metabolism (author's transl)

The occurrence of cerebral edema is considered as one of the most important factors, influencing the prognosis of patients with cerebrovascular disorders. To clarify the edema mechanism due to hypertensive cerebral hemorrhage from the aspects of energy metabolism, experimental hemorrhagic models were prepared with spontaneously hypertensive rats (SHR). The specific hemorrhage was created in the cortex of left parietal region by Klatzo's cold injury method, where hematoma was recognized. After inducing the cold injury, the periodically measured changes of brain-water content were compared with those of c--AMP, ATP and lactate in the brain tissue.1) The brain-water content began to increase at 3-6 hours after the injury on the undamaged hemisphere as well as the damaged one, reaching its peak at 24, --, 48 hours. The increase of brain-water content was more remarkable on the damaged hemisphere.2) The disturbance of aerobic brain metabolism was more significant in the cerebral cortex proximal to the damaged region. Although it was less severe on the undamaged than it was on the damaged, the metabolic disturbance was recognized. This suggests that experimental hemorrhage influences the cerebral metabolism simultaneously not only on the damaged but also on the undamaged hemisphere.3) Within the period between the time immediately after the injury and six hours, c. AMP was rapidly increased once and decreased within half an hour and the decrease of ATP and the increase of lactate were recognized in the cortices of parietal and occipital regions and the white matter. The aerobic disturbance of cerebral metabolism may be considered as playing a part in creating cerebral edema within 3′-6 hours after the injury.4) The above-mentioned disturbance of aerobic cerebral metabolism was improved 18 hours later, but the brain-water content reached its peak within 24, . -48 hours. During this period of 24-48 hours after the injury, it was suggested that the enlargement of cerebral edema was due to the factors other than metabolic ones.5) These results suggest that immediately following the cold injury, the metabolic disturbance plays a leading role in producing the cerebral edema (cytotoxic edema), whereas the disturbance of the vascular permeability later plays a leading role (vasogenic edema).