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J E Irazuzta

Publications and source records attributed to J E Irazuzta.

11 recordsLinked to original sources
PubMed2001

Serum cleaved Tau protein and neurobehavioral battery of tests as markers of brain injury in experimental bacterial meningitis.

Brain injury due to bacterial meningitis affects multiple areas of the brain with a heterogeneous distribution generating a challenge to assess severity. Tau proteins are microtubular binding proteins localized in the axonal compartment of neurons. Brain injury releases cleaved Tau proteins (C-tau) into the extracellular space where they are transported to the cerebral spinal fluid. We hypothesized that C-tau crosses the blood-brain barrier during inflammation and that it can be detected in serum. The correlation between serum C-tau levels and the extent of the meningitic insult was examined. Furthermore, we studied whether the use of a subset of neurobehavioral tasks can assess the extent of brain injury after meningitis. The tests were chosen primarily for their ability to detect deficits in the acoustic system, low brain, reflexive responding, as well as for impaired motor coordination and the higher brain functions of learning and memory. A rat model of group B streptococcal meningitis with variable severity was utilized. At five days after bacterial inoculation followed by antibiotic therapy neurobehavioral tests were performed and serum C-tau and histologic samples of the brain were obtained. Our study shows that during meningitis C-tau appears in serum and reflects the extent of neurologic damage. Neurobehavioral performance was altered after bacterial meningitis and could be correlated with histologic and biochemical markers of neurologic sequelae. We conclude that serum C-tau and a composite of neurobehavioral tests could become useful markers for assessing the severity of neurological damage in experimental bacterial meningitis.

Animals↗
PubMed2001

La Crosse encephalitis in children.

BACKGROUND: La Crosse encephalitis is a mosquito-borne disease that can be mistaken for herpes simplex encephalitis. It has been reported in 28 states but may be underrecognized. METHODS: We investigated the manifestations and clinical course of La Crosse encephalitis in 127 patients hospitalized from 1987 through 1996. The diagnosis was established by serologic testing for IgM and IgG antibodies to La Crosse virus. Data were collected by chart review. RESULTS: Most of the patients were school-aged children (mean [+/-SD] age, 7.8+/-3.5 years; range, 0.5 to 15.0). Symptoms included headache, fever, and vomiting (each in 70 percent or more of the patients), seizures (in 46 percent), and disorientation (in 42 percent). Thirteen percent had aseptic meningitis. Hyponatremia developed in 21 percent, and there were signs of increased intracranial pressure in 13 percent. Six patients, including three with cerebral herniation, underwent intracranial-pressure monitoring. The 13 patients (11 percent) whose condition deteriorated in the hospital had decreases in serum sodium levels (P=0.007), and increases in body temperature (P=0.003) at the time of deterioration. At admission, these patients more often had a history of vomiting (P=0.047) and a score of 12 or lower on the Glasgow Coma Scale (P=0.02) than the others; a trend toward a greater prevalence of seizures at admission was also evident in this group (P=0.07). All the patients survived, but 15 of them (12 percent) had neurologic deficits at discharge. Follow-up assessments, performed in 28 children, suggested an increase in cognitive and behavioral deficits 10 to 18 months after the episode of encephalitis. CONCLUSIONS: La Crosse virus infection should be considered in children who present with aseptic meningitis or encephalitis. Hyponatremia and increasing body temperature may be related to clinical deterioration.

Adolescent↗
PubMed2000

Hypothermia as an adjunctive treatment for severe bacterial meningitis.

Brain injury due to bacterial meningitis results in a high mortality rate and significant neurologic sequelae in survivors. The objective of this study was to determine if the application of moderate hypothermia shortly after the administration of antibiotics would attenuate the inflammatory response and increase in intracranial pressure that occurs in meningitis. For this study we used a rabbit model of severe Group B streptococcal meningitis. The first component of this study evaluated the effects of hypothermia on blood-brain barrier function and markers of inflammation in meningitic animals. The second part of the study evaluated the effects of hypothermia on intracranial pressure, cerebral perfusion pressure and brain edema. This study demonstrates that the use of hypothermia preserves CSF/serum glucose ratio, decreases CSF protein and nitric oxide and attenuates myeloperoxidase activity in brain tissue. In the second part of this study we show a decrease in intracranial pressure, an improvement in cerebral perfusion pressure and a decrease in cerebral edema in hypothermic meningitic animals. We conclude that in the treatment of severe bacterial meningitis, the application of moderate hypothermia initiated shortly after antibiotic therapy improves short-term physiologic measures associated with brain injury.

Animals↗
PubMed2000

Mercaptoethylguanidine attenuates inflammation in bacterial meningitis in rabbits.

Reactive oxygen and nitrogen species participate in the inflammatory process during meningitis. Among them, superoxide, nitric oxide (NO), and their reaction product peroxynitrite exert cytotoxic effects. Mercaptoethylguanidine (MEG) exerts beneficial effects in in vivo inflammatory conditions by scavenging peroxynitrite and inhibiting the inducible NO synthase. This study was designed to investigate whether MEG may attenuate inflammation and brain injury in experimental meningitis. Meningitis increased nitrite/nitrate, and protein content in the cerebrospinal fluid (CSF). In the brain tissue high levels of malondialdehyde and formation of nitrotyrosine indicated lipid peroxidation and nitrosative stress, respectively. Myeloperoxidase activity was increased indicating accumulation of neutrophils into the brain parenchyma. Treatment with MEG decreased nitrite/nitrate levels whereas it did not affect the bacterial clearance from the CSF. Furthermore, treatment with MEG markedly reduced brain tissue levels of myeloperoxidase and malondialdehyde. These data demonstrate that MEG could have a therapeutic role in meningitis.

Animals↗
PubMed1999

Hypothermia decreases excitatory neurotransmitter release in bacterial meningitis in rabbits.

The excitatory neurotransmitters glutamate (GLU) and aspartate (ASP) are involved in the pathogenesis of neuronal injury in meningitis. Based on past findings that the induction of moderate hypothermia (32-34 degrees C) attenuates the release of GLU in ischemic brain injury, this study was designed to detect if the application of moderate hypothermia decreases the release of excitatory amino acids (EAA) from brain tissue of animals with bacterial meningitis. Also examined was whether meningitis induces the expression of 72-kDa heat shock protein (HSP 70) in the cerebellum and how hypothermia affects it, for induction of HSP 70 has been used as a sensitive marker of neuronal stress in other forms of brain injury. Meningitis was induced by injecting Group B Streptococcus (GBS) into the cisterna magnae of rabbits. Antibiotic treatment began 16 h later. At this time the animals were anesthetized, instrumented, and randomized to normothermic (Nor) or hypothermic (Hy) conditions. Temperatures were strictly regimented for the following 10 h while maintaining stable cardiorespiratory parameters. Cerebrospinal fluid (CSF) samples were then withdrawn to measure concentrations of bacteria, protein, and amino acids. Meningitis causes CSF contents of GLU and ASP to increase significantly. Hypothermia treated animals demonstrated a 40-50% reduction in CSF GLU and ASP. Meningitis induced the expression of HSP 70 in the cerebellum while hypothermic animals experienced a significant decrease HSP 70 induction. These data demonstrate that hypothermia produces an attenuation of the release of excitatory neurotransmitters in meningitis and suggest that this treatment may attenuate neuronal stress.

Animals↗
PubMed1999

Topical nitroglycerin and pain in purpura fulminans.

Topical nitroglycerin has been previously described as an adjunctive therapy to increase perfusion to areas of purpura affected in purpura fulminans. We report a case of purpura fulminans in which topical nitroglycerin was found to provide analgesia after its application to purpuric lesions. The broader role for the use of topical nitroglycerin in pain management deserves further study and evaluation.

Administration, Topical↗
PubMed1997

Outcome and cost of child abuse.

OBJECTIVE: To compare the cases of child abuse (CA) with other admissions in a pediatric intensive care unit (PICU) for differences in patient-specific health care costs, severity of illness (SI) and mortality, and describe their outcome. METHOD: A retrospective cohort study of all patients admitted to the PICU between January 1991 and August 1994. Discharge diagnosis, age, SI, mortality rate, length of stay, hospitalization charges ($Hosp), and mortality were retrieved. RESULTS: There were 937 admissions; 13 were secondary to CA. Cases of CA represented 1.4% of admissions and 17% of deaths. CA patients had the highest SI (61%), $Hosp ($30,684), daily charges ($5,294) and mortality rates (53%) than any other group. In our patients, SI is a factor that affects charges. Even when compared to a cohort group with SI, child abuse patients had higher daily hospitalization charges (p < .05). The medical bills for the acute care of a CA patient averaged $35,641 per case. Even with these expenditures, 70% died and 60% of the survivors had severe residual morbidity. CONCLUSION: These results confirm that interventional medical care in response to severe CA is very costly and the ultimate outcome is significantly worse than other diseases. Therefore, we believe it is imperative to allocate resources to prevention.

Analysis of Variance↗
PubMed1996

Intratracheal administration of fentanyl: pharmacokinetics and local tissue effects.

OBJECTIVE: To study the pharmacokinetics and local tissue effects resulting from the intratracheal administration of preservative-free fentanyl. DESIGN: Prospective, randomized, blinded and controlled animal study. SETTING: University research laboratory. SUBJECTS: Eighteen adult male New Zealand rabbits. INTERVENTIONS: Preservative-free fentanyl citrate or normal saline was administered by the intratracheal (i.t.) and intravenous (i.v.) routes to randomized groups of rabbits. The animals were killed at 24, 48 and 72 h following administration. MEASUREMENTS AND MAIN RESULTS: Plasma concentrations of fentanyl were measured before administration and at 2, 5, 10, 30, 60 and 120 min following administration by a specific radioimmunoassay. A detailed histological examination of the lung and tracheal tissue was performed to identify local side effects. There were no significant differences in the plasma fentanyl concentrations resulting from the i.v. or i.t. route of administration. In both groups, the concentrations of fentanyl were within the therapeutic range (i.t. 2.37 ng/ml, i.v. 2.53 ng/ml) by 2 min after injection and reached a maximum concentration within 5 min. The bioavailability of i.t. fentanyl was 71%. Microscopic examination of the respiratory system did not show significant differences between the two random groups overall. However, in the sub-group of animals killed at 24 h, more animals in the i.t. group showed signs of inflammation in the lung parenchyma. CONCLUSIONS: There is rapid absorption of fentanyl following i.t. administration. Pharmacokinetic parameters for fentanyl were not significantly altered by the route of administration. Although there were no signs that i.t. administration of preservative-free fentanyl produces lung injury, a transient and mild inflammatory response was detected at 24 h after administration.

Analgesics, Opioid↗
PubMed1992

Laser Doppler measurements of skin blood flow before, during, and after lumbar sympathetic blockade in children and young adults with reflex sympathetic dystrophy syndrome.

Changes in the skin capillary blood flow (SBF) and temperature before, during, and 1 hour after unilateral lumbar paravertebral sympathetic blockade (LSB) were studied simultaneously with laser Doppler flowmetry and thermometry in patients with reflex sympathetic dystrophy syndrome. The baseline flow measurements in the toes on the affected limb were significantly lower than in the contralateral limb (p less than 0.01). During LSB, a 10-fold increase in SBF was detected within 4 minutes after injection of a local anesthetic agent when the sympathetic blockade was effective; an increase of more than 1 degrees C in the skin temperature occurred within 11 minutes. Measurements 1 hour after blockade showed an 18-fold (mean) increase in SBF in the toes (p less than 0.0001) and a 2-fold (mean) increase in SBF in the thighs (p less than 0.001). There was a significant decrease in the skin blood flow in the contralateral toes after the sympathetic blockade (p less than 0.01). We conclude that laser Doppler flow measurements can be used to detect immediate onset of sympathetic blockade in patients under general anesthetic or conscious sedation.

Adolescent↗
PubMed1990

Factor VIII related antigen (von Willebrand's factor) in Kawasaki disease.

Kawasaki disease is a systemic vasculitis in which secondary development of coronary artery aneurysms can occur. Because Factor VIII related antigen has been found increased in other vasculiditides, VIII R:Ag was measured serially in patients with Kawasaki disease. Factor VIII related antigen was prospectively evaluated in the acute phase of ten patients with Kawasaki disease, all of whom showed increased values at this stage (p greater than 0001). In six children a second sample was drawn at the convalescent phase, and all were normal. Of the original ten patients, two developed coronary artery aneurysms. Acute Factor VIII related antigen levels were not higher nor did Factor VIII related antigen fail to return to baseline in these two patients. Based on our findings, Factor VIII related antigen is elevated in the acute phase of Kawasaki disease and returns to normal levels in the convalescent phase.

Adolescent↗