Biomedical subjects

Jerry Zimmerman

Publications and source records attributed to Jerry Zimmerman.

5 recordsLinked to original sources

PubMed2006

Epidemiology and peculiarities of pediatric multiple organ dysfunction syndrome in New Delhi, India.

OBJECTIVE: Most pediatric studies on multiple organ dysfunction syndrome derive from developed countries. There is little information regarding the etiologies and outcomes of multiple organ dysfunction syndrome in critically ill children from developing countries. The objective of this study was to examine the differences in epidemiology of multiple organ dysfunction syndrome and the relationship of the Organ Failure Index (OFI) to outcomes from multiple organ dysfunction syndrome in critically ill children from a developing country. DESIGN: Prospective observational study. SETTING: A 10-bed tertiary pediatric intensive care unit. PATIENTS: A total of 1722 children (1 month to 16 years of age) admitted to a pediatric intensive care unit during the study period from January 1998 to June 2003. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Of all the patients admitted to the pediatric intensive care unit, 184 patients (10.6%) had persistent multiple organ dysfunction syndrome. During the study period 136 deaths (7.9%) occurred in the ICU. Multiple organ dysfunction syndrome was associated with nearly half of these deaths, 67/136 (49.2%). Overall survival of all patients with persistent multiple organ dysfunction syndrome was 64% (117/184). In addition to sepsis, falciparum malaria, fulminant hepatic failure, dengue shock syndrome, severe poisonings, post cardiopulmonary bypass, and post cardiac arrest were significant antecedents of multiple organ dysfunction syndrome . Patients with OFI scores of 2, 3, 4-5, and >5 exhibited mortalities of 9%, 29%, 58%, and 100% respectively. CONCLUSIONS: In addition to "traditional" sepsis, common etiologies of multiple organ dysfunction syndrome included falciparum malaria, fulminant hepatic failure, and dengue shock syndrome. In developing countries like India, multiple organ dysfunction syndrome carries a significant risk of mortality which is directly related to the OFI.

Adolescent↗

PubMed2006

Collaborative Pediatric Critical Care Research Network (CPCCRN).

Pediatric critical care was formally recognized as a separate subspecialty in pediatrics in 1987. Since that time the numbers of pediatric intensivists, pediatric intensive care units, and pediatric intensive care beds in the United States have increased dramatically. Research efforts have lagged behind, however, as this new discipline has struggled to identify the necessary time, funding, and other resources to pursue clinical and laboratory investigation. In April 2004, the National Center for Medical Rehabilitation Research of the National Institute for Child Health and Human Development issued a request for applications to establish the Collaborative Pediatric Critical Care Research Network (CPCCRN). The CPCCRN provides an infrastructure to pursue collaborative clinical trials and descriptive studies in pediatric critical care medicine. Six pediatric centers involving seven intensive care units and a data-coordinating center were identified through a competitive application process. Network goals include the support of collaborative clinical trials otherwise impracticable in single institutions and the establishment of a framework for developing the scientific basis for pediatric critical care practice. This article describes how the CPCCRN was established, its organization, and its goals and future plans.

Child↗

PubMed2005

A retrospective cohort study of prognostic factors associated with outcome in pediatric severe sepsis: what is the role of steroids?

OBJECTIVE: Systemic corticosteroids remain controversial in the treatment of pediatric patients with severe sepsis. Recent studies in septic adults have shown decreased mortality with the use of hydrocortisone in patients with relative adrenal insufficiency. We conducted this large retrospective cohort study to further characterize severe sepsis in infants and children and correlates of outcome, including the use of steroids. DESIGN: Retrospective cohort study. SETTING: The Pediatric Health Information System (PHIS), an administrative database of the Child Health Corporation of America (CHCA), was queried for inpatients 0-17 yrs of age with severe sepsis (defined here as an International Classification of Disease 9th edition code for infection with use of simultaneous mechanical ventilation and vasoactive infusions) from 2001 to 2002. In addition to demographic information, use of systemic corticosteroids (hydrocortisone, methylprednisolone, or dexamethasone) concurrent with the ventilatory and vasoactive support was collected. SUBJECTS: Data from PHIS. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients (n = 6693) were identified at 27 PHIS-participating CHCA member hospitals. Overall mortality was 24%; univariate predictors of death included use of steroids (odds ratio [OR], 1.9; 95% confidence interval (CI), 1.7, 2.2), older age (e.g., 13-17 yrs vs. neonates; OR, 1.6; 95% CI, 1.3, 2.0), a hematologic-oncologic diagnosis (OR, 5.87; 95% CI, 4.19, 8.23), and moderate vs. high case volume (OR, 1.25; 95% CI, 1.09, 1.44). Age, hematologic-oncologic diagnosis, case volume, and use of steroids remained independent predictors of mortality in multivariable analysis. CONCLUSIONS: From this administrative database analysis, there is no evidence that steroids are associated with improved outcome in critically ill infants and children with sepsis. Although steroids may be given preferentially to more severely ill children, their use was associated with increased mortality. Clinicians should maintain equipoise on this topic pending prospective randomized clinical trials.

Adolescent↗

PubMed2002

Global effects of xanthine oxidase stress on alveolar type II cells.

OBJECTIVE: To delineate biochemical details of graded xanthine oxidase stress toward cultured alveolar type II cells, particularly oxidant-mediated damage of type II cell nucleic acid, protein, and lipid, as an in vitro model of distant ischemia-reperfusion lung injury. DESIGN: In vitro injury model using native rat and immortalized mouse alveolar type II cells and exogenous xanthine oxidase. SETTING: Research laboratory. Measurement: Cultured type II cells were subjected to xanthine oxidase-derived reactive oxygen stress at variable concentrations and incubation times. Reduction of type II cell double-stranded DNA, inhibition of de novo phosphatidyl choline synthesis, enhancement of lipid peroxidation, and suppression of mitochondrial redox capacity were analyzed in relation to high-intensity (xanthine oxidase, 25 munits/mL) oxidant stress. Alterations in type II cell cellular glutathione-related antioxidant repertoire were assessed at both high-intensity and low-intensity (xanthine oxidase, 1 munits/mL) oxidant stress. MAIN RESULTS: High-intensity xanthine oxidase stress significantly increased type II cell DNA strand breakage, inhibited de novo phosphatidyl choline synthesis, diminished mitochondrial integrity, and enhanced lipid peroxidation in the absence of overt cytolysis. This injury was modulated with addition of exogenous glutathione peroxidase, or catalase/superoxide dismutase, but not glutathione or N-acetylcysteine. Although aspects of the glutathione antioxidant repertoire were similarly diminished with high-intensity xanthine oxidase stress, low-dose (long duration) xanthine oxidase stress augmented the activities of type II cell glutathione peroxidase and gamma-glutamyl transferase (the rate-limiting enzyme in glutathione synthesis). CONCLUSION: High-intensity xanthine oxidase stress (in vitro model of in vivo ischemia-reperfusion) may overwhelm type II cell antioxidant defenses and mediate oxidant injury to nucleic acid, protein, and lipid in the absence of cell lysis. Immortalized murine type II cells seem to appropriately model xanthine oxidase-mediated nucleic acid and protein injury of native rat type II cells. Exogenous glutathione peroxidase reduces oxidant injury in this in vitro model. Depending on magnitude (and possibly duration) of the xanthine oxidase stress, type II cell glutathione antioxidant elements may be diminished or enhanced.

Journal Article↗

PubMedDate not supplied

Feeding intolerance as a result of small-intestine intussusception in a child with major burns.

Feeding intolerance is common in critically ill children. We present an unusual case of jejunojejunal intussusception causing feeding intolerance in a child with major burns. An 18-month-old female was admitted to the intensive care unit after sustaining a 65% TBSA burn. Following a decompressive laparotomy for abdominal compartment syndrome, nasojejunal feeds were started immediately after surgery, which she did not tolerate. A plain abdominal radiograph revealed a collection of intraluminal air and an abdominal CT revealed a proximal jejunojejunal intussusception. The patient underwent laparotomy and an uncomplicated reduction of the small-bowel intussusception (SBI). Successful enteral feedings were commenced on hospital day 24, and the patient was discharged to home after approximately a 4.5-month hospitalization. The major learning point is that SBI can cause feeding intolerance in the child with major burns. Despite the low incidence of SBI in critically ill children, arriving at a timely diagnosis is essential because the consequences of a missed or delayed diagnosis include intestinal ischemia, necrosis, or perforation. Because SBI defies diagnosis by techniques traditionally used to diagnose intussusception involving the colon, clinical suspicion for intussusception is needed to facilitate the urgent diagnosis and correction of feeding intolerance caused by mechanical obstruction.

Burns↗