Clinical Signs Of Encephalopathy Research Articles

Hydranencephaly in a newborn due to occupational toluene exposure during pregnancy: a case report.

The etiopathogenesis of hydranencephaly remains unclear; however, exposure to toxic substances during pregnancy likely increases hydranencephaly risk. Head computed tomography (CT) was performed in a neonate 9 hours post-delivery because the anterior fontanelle was large and there were clinical signs of encephalopathy. Head CT revealed a lack of both cerebral hemispheres and significant cystic enlargement, while the cerebellar hemispheres and pons were found to have developed normally. History-taking revealed that the mother worked in the automotive industry, specifically in the car paint cleaning business and was exposed to toluene during the pregnancy. The patient was diagnosed with hydranencephaly, central diabetes insipidus and central hypothyroidism. Due to the increased head circumference and tense anterior fontanelle, a ventriculoperitoneal shunt was placed. Toluene exposure during pregnancy should be considered among the causes of hydranencephaly. Furthermore, central diabetes insipidus and central hypothyroidism may develop in such cases.

PULMONARY FINDINGS SUGGESTS COXIELLA BURNETII INFECTION TO A PATIENT WITH HEPATITIS

On 23th of July 2019 a 63y old man, was admitted for acute hepatitis with low-grade fever, myalgia, fatigue, jaundice. Farmer (grows crops, and tends to farm animals). He was known to have a non-replicative chronic B hepatitis virus infection. At admission, moderate increase of prothrombin time, but without clinical signs of encephalopathy. No positive IgM serology for hepatitis viruses (A, B, C, E), CMV, Epstein Barr, or Leptospira spp. CRP was 34mg/L, HBV-DNA undetectable.

ретроспективный анаЛиз резу Льтатов сеЛективного портосистемного шунтирования у боЛьных с портаЛьной гипертензией

Aim — to analyze the results of selective portosystemic shunt in patients with portal hypertension. Material and methods. Analysis is carried out in three study groups: the first group — the implementation phase, which covered the period from 1976 to 1992; the second group — a step of forming a specialized unit of surgery of PH in RSCS (1992—1998); the third group — stage of improvement techniques of DSRS and expanding indications for this type of bypass (1998—2014). The study included 396 patients with PH, whom were performed DSRS, for the periods indicated. Results and discussion. The incidence of hepatic failure and encephalopathy in the implementation phase of PSSH reached 25% and 33,3%, respectively, in the future, after standardization indications for DSRS its frequency decreased to 14,3% and 17,1%, while in the present period developed in 5,1% of cases and the clinical signs of encephalopathy in 10,9% of patients. The frequency of bleeding against the backdrop of a functioning DSRS established in 16 out of 23 of our patients with bleeding from esophageal varices. The growth of ascites averaged a total group of patients with DSRS — in 11,3% of cases. Depending on the chronological period, the frequency of this complication has decreased from 20,8% in the first period to 10,1% in the third period. Selective shunt thrombosis in the immediate postoperative period was 1,8%, bleeding from esophageal varices — 4,7% of cases. Conclusion. Depending on the characteristics of the vascular transformation of splenic vein DSRS in the present period is dominant and performed in more than 50% of cases, and for the older age group or a low compensatory allowance hepatocytes against a background of cirrhosis of the liver, this type of bypass surgery remains a priority, and sometimes and the only way to decompress of portal pool.

Rotavirus Disease in Germany—A Prospective Survey of Very Severe Cases

Rotavirus (RV) gastroenteritis is a notifiable disease in Germany. The reports to the authorities contain few data concerning the severity of disease. The aims of this study were to determine incidence and outcome of very severe cases of RV disease. Cases of very severe RV disease were collected by the German Paediatric Surveillance Unit for rare diseases (Erhebungseinheit für seltene pädiatrische Erkrankungen in Deutschland) using anonymous questionnaires based on hospitalized patients between April 2009 and March 2011. Inclusion criteria were detection of RV antigen in feces, patient aged 0-16 years and 1 or more of the following criteria: intensive care treatment, hypernatremia or hyponatremia (>155 mmol/L or <125 mmol/L), clinical signs of encephalopathy (somnolence, seizures, apnea) and RV-associated death. During 2 years, 130 cases of very severe RV disease were reported, 101 of 130 were verified. Seventeen patients had nosocomial infection, of whom 14 were neonates in intensive care. Among those, 12 infants had verified or suspected necrotizing enterocolitis. Eighty-four community-acquired cases were reported, median age was 10.5 months (0-108 months). The median hospital stay was 6 days, and 48 patients needed intensive care treatment. Among children less than 5 years of age, the yearly incidence of community-acquired very severe RV disease was 1.2 of 100,000 (95% confidence interval: 0.9-1.4/100,000). A total of 26 of 84 and 10 of 84 patients had severe hypernatremia or hyponatremia, respectively, and 58 of 84 patients had signs of encephalopathy. Three deaths were reported (1 nosocomial and 2 community acquired). RV infection in Germany can have a life-threatening course. A substantial number are nosocomial infections.

Timing of Neonatal Seizures and Intrapartum Obstetrical Factors

One hundred ninety-three neonates with seizures were available on a neonatal seizure database, which included intrapartum and neonatal factors such as labor duration, fetal heart rate abnormalities, cord blood gas values, Apgar scores and clinical signs of encephalopathy. Regression analyses (analysis of variance) were performed on the entire cohort as well as specific subsets of neonates (eg, neonatal encephalopathy vs no encephalopathy) to assess the relationship between seizure timing and intrapartum/neonatal factors. Seizures were noted earlier for the encephalopathic group than for the nonencephalopathic group. No significant differences were noted for any intrapartum or neonatal factors. Timing of neonatal seizures, with or without an encephalopathy occurs within the first 2 days after birth and is independent of selected intrapartum and neonatal factors, underscoring recent task force recommendations concerning neonatal encephalopathy. Factors other than intrapartum events more likely contribute to the encephalopathic repertoire of the newborn, including seizures.

Mild hypothermia via selective head cooling as neuroprotective therapy in term neonates with perinatal asphyxia: an experience from a single neonatal intensive care unit

The objective of this study was to determine the efficacy of mild hypothermia via selective head cooling as a neuroprotective therapy in term infants with perinatal asphyxia. Full-term newborns who had 5 min Apgar scores <6, first arterial blood gas pH<7.10 or BD>15 mEq/l, and with the clinical signs of encephalopathy were enrolled within 6 h after birth. Patients were randomized to receive mild hypothermia treatment via selective head cooling for a total of 72 h or receive routine treatment as a control. Brain hypoxic-ischemic injury was quantified based on the head computed tomographic scan (CT scan) at postnatal age 5-7 days and a Neonatal Behavioral Neurological Assessment (NBNA) score at 7-10 days of life. A total of 58 patients (30 hypothermia, 28 control) completed the study. Hypothermia was well tolerated in this study and attenuated the hypoxic-ischemic brain injury due to perinatal asphyxia. Head CT scan demonstrated moderate to severe hypoxic-ischemic changes in only 4/30 cases from the hypothermic group. In contrast, 18/28 cases in the control group showed moderate to severe hypoxic-ischemic changes (chi (2)=15.97, P<0.01). Brain hypothermia also significantly improved the NBNA score (32+/-2 in the hypothermic group vs 28+/-3 in the control group, P<0.01). Our results suggest that selective head cooling may be used as a neuroprotective therapy in term neonates with perinatal asphyxia. A long-term follow-up study is needed to further validate the results of this study.

Noncirrhotic portal vein thrombosis exhibits neuropsychological and MR changes consistent with minimal hepatic encephalopathy

Hepatic encephalopathy can arise from portal-systemic shunting in the absence of intrinsic liver disease. However, there are few descriptions of this form of encephalopathy. Portal vein thrombosis is an infrequent disease that causes portal-systemic shunting. Episodic hepatic encephalopathy has been described in patients with portal vein thrombosis, but it is not known if these patients develop minimal hepatic encephalopathy. We designed a study to investigate the neurological consequences of portal vein thrombosis in patients without cirrhosis and no clinical signs of encephalopathy. For this purpose, 10 patients underwent neuropsychological tests, an oral glutamine challenge test, and brain magnetic resonance (MR) imaging. The results were compared with those obtained in 10 healthy controls. Patients with portal vein thrombosis exhibited abnormalities in the results of neuropsychological tests, oral glutamine challenge test, and MR similar to those described in hepatic encephalopathy associated with cirrhosis. MR spectroscopy revealed a decrease in myo-inositol and an increase in glutamine. The increase in glutamine correlated with an increase in ammonia following the oral glutamine challenge test, signs of increased brain water (decrease in magnetization transfer ratio), and impairment of attention tests. In conclusion, patients with noncirrhotic portal vein thrombosis develop subclinical neurological abnormalities compatible with minimal hepatic encephalopathy. These disturbances, which include signs of increase in brain water and a compensatory osmotic response (decrease in brain myo-inositol), appear to be secondary to brain exposure to ammonia induced by portal-systemic shunting.

The diagnosis of subclinical hepatic encephalopathy in patients with cirrhosis using neuropsychological tests and automated electroencephalogram analysis

Neuropsychological tests used for the assessment of subclinical hepatic encephalopathy (SHE) may overdiagnose SHE because scores are usually not corrected for age. The aim of this study was to estimate the prevalence of SHE using two easy administrable psychometric tests (Number Connection Test part A [NCT-A], Symbol Digit Test [SDT]) with age-related normal values. In addition, spectral electroencephalogram (EEG) was used, which is the in-house electrophysiological method for quantifying encephalopathy. One hundred and thirty-seven consecutive patients (mean age 49 years, range 17-77) with cirrhosis without any clinical signs of encephalopathy, were screened for SHE. In addition, the Child-Pugh score and the arterial blood ammonia were determined. Patients with concurrent use of alcohol, benzodiazepines or anti-epileptics were excluded. Fifty percent of the patients had an abnormal NCT according to the standard recommended procedure, in contrast only 7% of the patients had an abnormal NCT when scores corrected for age were used. Combining the results of the spectral EEG and the psychometric tests corrected for age yielded a higher prevalence of SHE (23%) than when each test method was used alone (17% vs. 10% abnormal, respectively). Severity of liver disease correlated with the presence of SHE, because the prevalence of abnormal tests increased from 14% in Child-Pugh grade A to 45% in Child-Pugh grade B or C. Age above 40 years and an elevated blood ammonia level were significant determinants related to an abnormal EEG. We conclude that the NCT uncorrected for age markedly overdiagnoses SHE and, therefore, should not be used as a test for the screening of SHE. Using a combination of spectral EEG and two psychometric tests with age-corrected normal values a low prevalence of SHE in patients with Child A liver cirrhosis is found. Older patients with an elevated arterial ammonia are more prone to develop SHE than younger patients with an equal arterial ammonia concentration. (Hepatology 1996 Sep;24(3):556-60)

Encephalopathy and neuropathy in end-stage liver disease before and after liver transplantation

The nervous system involvement of 8 patients with end-stage liver disease was evaluated by means of clinical neurological, neuropsychological, neurophysiological and neuroradiological investigation before and 6-12 months after a successful liver transplantation. Preoperatively, all subjects (7 women, 1 man; mean age 40 years, range 30-54 years) exhibited decreased muscle strength and 2 patients manifested clinical signs of polyneuropathy. In neuropsychological tests, slight visuoconstructive apraxia, and disturbances of verbal memory and cognitive function were observed. Magnetic resonance imaging (MRI) revealed cerebral lesions in two patients. After transplantation, muscle strength reverted to normal in all patients, polyneuropathy improved and in all but 2 patients recovery of neuropsychological functioning was observed. Clinical signs of encephalopathy had disappeared. All patients were emotionally better adjusted after transplantation. Four subjects showed new, albeit mild changes in neurophysiological and neuropsychological tests postoperatively. We conclude that the majority of neurological impairment disappeared after liver transplantation. We want to stress that evaluation of neurological sequelae of liver transplantation needs to be based on assessments both before and after liver transplantation.

Visual evoked potential — a tool in the diagnosis of hepatic encephalopathy?

Visual evoked potentials (VEP) have been suggested to be of value in the diagnosis of subclinical and mild hepatic encephalopathy. In the present study, a comparison between VEP and four psychometric tests (number connection test A and B, digit symbol and word memory test) was periormed in 42 cirrhotic patients, 17 of whom had clinical signs of encephalopathy. The results were compared to sex- and age-matched healthy controls. The VEP latencies for P2 (the second positive wave) and N3 (the third negative wave) were 11% and 26% longer ( P < 0.01–0.001) in the patients than in the controls. Moreover, the latencies for N2 (the second negative wave) and P2 were longer in the encephalopathic as compared to the non-encephalopathic patients ( P < 0.05). There was a significant correlation between the latencies for N2 and number connection tests A and B and digit symbol test. However, of the patients with clinical encephalopathy, less than half had VEP latencies longer then the mean ± 2 S.D. above those for the controls. In contrast, none of the encephalopathic patients had normal results on the psychometric tests. This study demonstrates that although statistically significant differences exist between groups of cirrhotic patients and controls, VEP is not a reliable tool for the diagnosis of encephalopathy in the individual patient.

The dietary prevention of hepatic coma in eck fistula dogs: Ammonia and the carbohydrate to protein ratio

The conventional animal model of human portal systemic encephalopathy is the dog with Eck fistula. Dogs fed standard dog chow after Eck fistula manifest anorexia, weight loss, hepatic atrophy and encephalopathy. This study was done to determine the natural history of dogs undergoing Eck fistulas when adequate nutrition is maintained with a palatable diet. Twenty-four mongrel dogs were divided into four groups—Eck fistula fed standard dry dog chow (EF-SC) (n equals nine); sham-operated fed standard chow (SO-SC) (n equals five); Eck fistula fed a liquid (Isocal) diet (EF-LD), and sham-operated fed a liquid diet (SO-LD) (n equals five). Dogs were sacrificed when they had clinical signs of encephalopathy or up to 120 days after operation. EF-SC dogs had a daily caloric intake approximately 40 per cent of that of the other groups. Two EF-SC dogs died of sepsis within two weeks of the operation, the other seven became encephalopathic between 46 and 91 days (a mean of 63.6 ± 15.6). On other dogs had signs of neurologic deterioration. EF-SC dogs lost 19 ± 9 per cent body weight and the serum albumin level decreased 14.5 per cent while the other groups maintained body weight and serum albumin levels. Both EF-SC and EF-LD groups had decreased liver weight to body weight ratios (LW × 100/BW) compared with sham-operated upon dogs reflecting hepatic atrophy (1.97 ± 0.7 and 2.2 ± 0.23 versus 3.04 ± 0.85 and 3.48 ± 0.44). Results of histologic examination of the liver revealed hepatocyte atrophy, deglycogenation and lipid accumulation in EF dogs. We conclude from these data that providing dogs with Eck fistula a palatable diet prevents weight loss and malnutrition, but not hepatic atrophy. The lack of neurologic signs in well nourished dogs suggests to us that data concerning hepatic coma from the standard Eck fistula model should be interpreted with extreme caution.

The prognostic value of computed tomography as an adjunct to assessment of the term infant with postasphyxial encephalopathy

Prospective follow-up studies were done on 62 term infants who were treated as neonates for clinical evidence of postasphyxial encephalopathy. Computed tomographic studies were done during the first two weeks of life and repeated at six months of age. All children were followed a minimum of 18 months, at which time they underwent a psychometric and a neurologic evaluation. Major neurodevelopmental sequelae consisted of: hydrocephalus; spastic quadriplegia, hemiplegia, or diplegia; or a mean Bayley score less than 70. Major sequelae were present in 29 (47%) of the children: all were severely handicapped. Five other children scored between 70 and 85 on the Bayley test. Computed tomographic scans were highly predictive of status at 18 months. Eleven of the 15 with intraventricular or parenchymal hemorrhage were severely handicapped. Eighteen of 20 with extensive areas of hypodensity of the white and gray matter (neonatal CT) were abnormal at 18 months. All but two were severely handicapped. The results suggest that CT studies are very useful in the care of the asphyxiated term infant who has clinical signs of encephalopathy.

Encephalopathy in toxicity tests on laboratory animals.

Clinical signs of encephalopathy followed administration of lethal doses of a wide range of drugs, foods, pesticides and other agents in 92 reviewed studies on laboratory animals. Common signs of depression of the brain were anorexia, hypokinesia, hypothermia, prostration, ataxia, pallor, and hyporeflexia and of stimulation were convulsions, hyperreflexia, tremors, muscular spasms, and fever. Less common signs included catalepsy, exophthalmos, phonation, piloerection, bradypnea, tachypnea, automatism, flaccidity, a Straub reaction, erection of the penis, nystagmus, spacial disorientation, and hunch back. Aggressiveness took the form of fighting when animals were aggregated and occasionally automutilation when segregated. Certain signs such as vomiting and panting occurred only in cats and dogs. In chronic studies at sublethal daily doses, there were relatively few signs of encephalopathy. At autopsy, the brain was found relatively resistant to changes in weight, to hydration and to dehydration. Histologically there was no evidence of tissue encephalopathy in a third to a half of the studies. In the remaining studies, the brain was found to have participated in the general inflammatory reaction (capillary or capillary-venous congestion) to toxic doses of the agent under study. Less common histopathological reactions included thrombosis, edema, granulocytic infiltrative meningitis and cerebral abscesses.