Biomedical subjects

D L Mollitt

Publications and source records attributed to D L Mollitt.

At least 19 recordsLinked to original sources

PubMed2001

Pediatric cervical spine injuries: defining the disease.

BACKGROUND/PURPOSE: Pediatric cervical spine injuries are uncommon. Most previous studies have been hampered by the small number of patients available for evaluation. The purpose of this study is to determine the incidence and characteristics of pediatric cervical spine injury utilizing a multiinstitutional pediatric trauma database, and to assess the impact of age and level of spine injury on mortality rate. METHODS: All children with cervical spine injury entered into the National Pediatric Trauma Registry over a consecutive 10-year period were identified. Patients were stratified by age, mortality, presence or absence of bony injury, level of cervical spine injury, and presence of neurologic deficit. Data were analyzed utilizing Student's t test for continuous variables and chi(2) analysis for categorical variables. Statistical significance was accepted at the P less than .05 level. RESULTS: From a database of 75,172 injured children, 1,098 were identified with cervical spine injury, overall incidence 1.5%. The mean age of the study group was 11 +/- 5 years, and 61% were boys. Nine hundred eight children (83%) had bony spine injury. Distribution of bony injury among upper cervical spine, lower cervical spine, or both was 52%, 28%, and 7%, respectively. The remaining 13% comprised unspecified levels of injury. Upper cervical spine injuries were prevalent among all age groups (42%, age < or = 8; 58%, age > 8), whereas lower spine injuries predominated in older children (85%, age > 8). One third of children in the study group had neurologic injury, and half of these had no radiographic evidence of bony injury. Ninety-four children (24%) had a complete cord injury, and the remaining 76% had an incomplete spinal cord injury. One hundred eleven children (23%) with upper spine injury died compared with 11 children (4%) with lower spine injury. Mortality rate was highest (48%) in those with atlanto-occipital dislocation. CONCLUSIONS: From this, the largest experience with pediatric cervical spine injury, several conclusions can be drawn. (1) Cervical spine injury occurs in 1.5% of injured children. (2) Upper cervical spine injuries are not limited to younger children but are equally prevalent in both age groups. (3) Associated mortality rate is nearly 6-fold higher in patients with upper cervical injury. (4) Seventeen percent of children with cervical spine trauma show no radiologic anomaly, yet 50% of children with cervical spinal cord injury have no initial radiologic abnormalities. (5) Of those in whom cervical spine injury is associated with a neurologic deficit, the deficit is complete in 24% of children.

Adolescent↗

PubMed2000

Infectious complications in critically injured children.

PURPOSE: Infection will complicate the care of a significant number of injured adults. Trauma is the leading cause of mortality in the pediatric population, yet little information is available regarding the incidence of infection in this group. This study evaluates infectious complications in the critically injured child. METHODS: All children admitted to the pediatric intensive care unit from an urban level-1 trauma center during an 80-consecutive-month period were studied. Infection was defined by Centers for Disease Control criteria and was identified by a retrospective review of the medical records. Demographic and clinical information, including microbiologic data, were compiled for all study patients. Data were analyzed using Student's (t)test or chi2 analysis where appropriate. RESULTS: Five hundred twenty-three children were at risk for infection during the study period. Seventy-eight infections were documented in 53 children (incidence, 10.1%). Nosocomial infections accounted for 78% of these with a majority (85%) being device associated. Common infections in this group included lower respiratory (n = 35), primary bloodstream (n = 10), and urinary tract (n = 7). Trauma-related infections were primarily wound (n = 9), intraabdominal (n = 3), or central nervous system (n = 3). Bacterial pathogens predominated, and the most frequent microorganisms recovered were Staphylococcus aureus, Pseudomonas sp, and Haemophilus sp. Children with infectious complications were more severely injured (injury severity score [ISS] 24 versus 17, P < .001) and had a longer hospital stay (21 days v 6 days, P < .001) compared with children without infection during the same period. Overall mortality rate for the study group was 5.7% and was not significantly different from children without infection. CONCLUSIONS: Infection is a significant source of morbidity in the critically injured child. Nosocomial infections predominate, and a majority of these are device related, emphasizing the need for continued vigilance toward prevention in this high-risk group.

Bacterial Infections↗

PubMed2000

Nosocomial pneumonia in the pediatric trauma patient: a single center's experience.

OBJECTIVES: To evaluate a single center's experience with the frequency rate, patterns of occurrence, and impact on outcome of nosocomial pneumonia in the critically injured child. DESIGN: Retrospective review of prospectively collected data. SETTING: Level I university trauma center with a pediatric trauma intensive care unit. PATIENTS: A total of 523 consecutive critically injured children admitted to the pediatric intensive care unit during an 80-month interval. MEASUREMENTS AND RESULTS: Thirty-five episodes of nosocomial pneumonia were identified in 29 children (frequency rate of 5.5%). The mean age of the children was 9.2 yrs, and the mean Injury Severity Score was 27 +/- 9. In 91% of patients (26 children), nosocomial pneumonia was associated with mechanical ventilation. This represented a 13% frequency rate in injured children who were ventilated during the study period. The most common organisms recovered were Staphylococcus aureus (21%), Haemophilus influenzae (19%), Pseudomonas (11%), and Enterobacter (11%). Early pneumonia (diagnosed < or = 7 days after injury) was predominantly caused by Haemophilus species. In contrast, Enterobacter and/or Pseudomonas were isolated primarily in late pneumonia (diagnosed >7 days after injury). Staphylococcus was prominent throughout the hospitalization. Overall, children with nosocomial pneumonia were more severely injured (Injury Severity Score 27 vs. 17, p < .001) and had a longer hospital stay (26 vs. 7 days, p < .001). Despite this, mortality (6.9% vs. 7.9%, p = NS) was not significantly different from injured children without pneumonia. CONCLUSIONS: In this study of a single pediatric trauma center, nosocomial pneumonia occurred in a small but significant percentage of injured children. The frequency rate increased two- to three-fold with mechanical ventilation. Microbiology varied with day of onset. In contrast to the adult, mortality did not seem to be significantly altered by this complication. Analysis of additional pediatric trauma centers is encouraged to confirm these characteristics of nosocomial pneumonia in the injured child.

Adolescent↗

PubMed1998

Complications of retained internal bolster after pediatric percutaneous endoscopic gastrostomy.

PURPOSE: Percutaneous endoscopic gastrostomy (PEG) has been widely accepted as an efficacious means of nutritional support in the infant and child. A well-described technique uses the Gauderer-Ponsky tube (CR Bard Incorporated, Tewksbury, MA) drawn antegrade through the gastric wall and secured by an internal and external SILASTIC (Dow Corning; Midland, MI) bolster. The majority of reported complications attendant to its use occur secondary to insertion. This report details a less well-described complication of tube removal. METHODS: Since 1992, 234 pediatric PEGs have been performed using a Gauderer-Ponsky tube. Approximately 6 weeks after the procedure, all catheters were removed and replaced with gastric buttons. The internal bolster was left within the stomach to pass spontaneously. RESULTS: Five children (2.1%), ages 6 months to 5 years, failed to pass this crossbar. Three subsequently presented with dysphagia and drooling with the internal bolster wedged in the proximal esophagus. All were left with significant residual stricture after endoscopic removal of the crossbar. Two required dilatation and the third underwent operative stricturoplasty. A fourth child returned with intermittent gastric outlet obstruction. The internal bolster was retained in the stomach 4 months after catheter removal. Endoscopic retrieval resulted in resolution of the symptomatology. The final case was found to have an asymptomatic bolster in the stomach approximately 18 months after catheter removal. CONCLUSIONS: These cases highlight a potential sequelae of pediatric percutaneous endoscopic gastrostomy not previously acknowledged. The significant complications associated with the retained bolster in four of these five children suggests that follow-up should be altered to monitor prompt passage of the crossbar after tube removal.

Child, Preschool↗

PubMed1997

Altered monocyte calcium dynamics in sepsis.

PURPOSE: This study was designed to evaluate monocyte calcium concentration and mobilization in normal and septic surgical patients. METHODS: Monocytes were isolated from 15 "septic" surgical patients, washed, and loaded with the fluorescent calcium chelator, FURA-2. Monocytes from 20 normal volunteers served as controls. Intracellular calcium concentration ([Ca2+]i) was measured by means of fluorescent spectrophotometry before, during, and after stimulation with concanavalin A. Differences were evaluated for statistical significance by analysis of variance. The study was repeated using normal monocytes preincubated in "septic" serum and "septic" monocytes preincubated in normal serum. Additional paired whole blood specimens were obtained from the control group and were incubated with Escherichia coli endotoxin. Monocytes were then isolated and evaluated as described. RESULTS: Sepsis was associated with significantly low resting monocyte calcium concentrations. Although concanavalin A stimulation resulted in marked calcium mobilization in both normal and septic cells, final cellular calcium concentration was significantly lower in the stimulated "septic" monocytes. Similar alterations were seen in normal cells incubated with septic serum, but could not be reproduced by incubation with endotoxin. This deficiency could not be corrected in septic cells incubated in normal serum. CONCLUSION: Sepsis is associated with a significant alteration of monocyte calcium dynamics in both resting and stimulated cells. These changes appear to be modulated by a serum factor other than endotoxin.

Adult↗

PubMed1997

Nitric oxide synthase inhibition negates septic-induced alterations in cytoplasmic calcium homeostasis and membrane dynamics.

This study was undertaken to evaluate the role of nitric oxide (NO) in the sepsis-induced disruption of intracellular calcium homeostasis and membrane dynamics. Anticoagulated whole blood was obtained from 10 healthy volunteers. Equal aliquots were incubated with saline (control), 2 microg/mL Escherichia coli endotoxin (lipopolysaccharide), 8 microg/mL NO inhibitor, N-monomethyl arginine (NMA), and endotoxin plus NO inhibitor (lipopolysaccharide/NMA). Erythrocytes were harvested, washed, and loaded with the calcium chelator, FURA-2AM, and the fluorescent membrane probe TMA-DPH. Cells were evaluated for both intracellular calcium concentration and membrane viscosity (anisotropy) by fluorescent spectrophotometry. Endotoxin induced a significant increase in both intracellular calcium concentration and anisotropy. NMA had no intrinsic affect on either of these cellular characteristics. NMA was, however, effective in preventing the endotoxin-induced changes. These results suggest that NO may play a role in the disruption of intracellular calcium homeostasis and erythrocyte membrane deformability noted in sepsis.

Adult↗

PubMed1997

Blunt hepatic injury in adolescents: age makes a difference.

This analysis of mortality from blunt hepatic injury was performed to define outcome in the adolescent age group in relation to that recorded for children and adults. Children (age 0-10 years) were selected from a multi-institutional trauma registry, adults (age > or = 21 years) from the registry of a Level I trauma center, and adolescents (age 11-20 years) from both. Groups were compared by injury frequency, proportion of severe hepatic injuries (code 864.03 or 864.04 in the International Classification of Diseases, Adapted for Use in the United States 9-CM), immediate laparotomy, mortality, and cause of death. Children had the lowest proportion of severe injury and overall mortality. Torso trauma was the primary cause of death in only three children. Adolescent injury patterns were similar to those of adults in the proportion of severe visceral disruption and incidence of fatal torso trauma. Immediate laparotomy was employed almost twice as commonly in adults as in adolescents. The 64 per cent of adolescents who did not undergo laparotomy had a lower mortality than those who did. Conversely, the 36 per cent of adults without exploration had a significantly higher mortality, which usually occurred before laparotomy could be initiated. Increasing hepatic injury severity brought increasing mortality; however, the cause of death differed with age. Although the incidence of severe liver injury did not differ between adolescents and adults, management and outcome did. These data indicate that individualized management based on overall patient status remains the best approach to care of these injuries.

Adolescent↗

PubMed1997

Acute abdomen. The teenage girl.

The evaluation of abdominal pain in the adolescent female is a common and often challenging problem. The unique anatomy and biology of the postmenarcheal teenager necessitates the consideration of a broad variety of additional genitourinary problems not encountered in the male. Further complicating this issue, the differential diagnoses involves not only pathological considerations, but normal physiological processes that may, in and of themselves, be symptomatic. One must be skillful enough to avoid unnecessary intervention, while aggressively pursuing significant intraabdominal problems. Occasionally, however, only invasive modalities will enable definitive diagnosis, and facility with these techniques significantly enhances both diagnostic and therapeutic capabilities in these patients.

Abdomen, Acute↗

PubMed1996

Death from pelvic fracture: children are different.

This study compares outcome from pelvic fractures in children with that of adults. Data for 23,700 children registered in the National Pediatric Trauma Registry (NPTR) were compared with those of 10,720 adults recorded over 5 years in the registry of our level I trauma center. Patients were categorized by open versus closed fracture and by fracture type as defined by a modification of the Key and Conwell system. Outcome was evaluated by mortality rate and incidence of fracture-induced fatal exsanguination. The 722 pelvic fractures recorded in the NPTR represent 3% of the population and is half the frequency represented by the 532 adults evaluated (P < .001). The overall mortality rate was 5% for children and 17% for adults. Two children died of fracture-related exsanguination; there were 18 such deaths among the adults. Pelvic ring disruption was encountered more commonly among adults, and was associated with a significantly higher mortality rate. Patients with initial hemodynamic instability were more likely to die, although children less so than adults. The authors conclude that children do not die of pelvic fracture-associated hemorrhage as often as adults. Massive blood loss in the child occurs most commonly from solid visceral injury rather than from pelvic vascular disruption.

Adult↗

PubMed1995

Effect of sepsis on erythrocyte intracellular calcium homeostasis.

OBJECTIVES: To examine erythrocyte intracellular calcium dynamics in clinical sepsis and experimental endotoxemia. DESIGN: Prospective, multiexperimental study utilizing in vitro manipulation and evaluation of human erythrocytes. SETTING: University research laboratory. PATIENTS: Healthy, elective surgical patients, "septic" surgical patients, and normal volunteers. INTERVENTIONS: For all experimental studies, whole blood specimens were incubated with 2 micrograms/mL of Escherichia coli endotoxin (experimental) or an equivalent volume of phosphate buffered saline (control). Incubations were performed in specimens pretreated with 0.4 mM of verapamil and/or 50 mM of dantrolene. Incubations were performed in the presence and absence of extracellular calcium. Incubations were also performed utilizing pre- and posttreatment with 1 mM of adenosine 5'-triphosphate (ATP) and/or 30 mM of adenosine. MEASUREMENTS AND MAIN RESULTS: Free cytosolic calcium concentration was determined by fluorescent spectroscopy, utilizing the calcium chelator, FURA-2AM. Sepsis was associated with a significant increase in erythrocyte intracellular calcium concentration as compared with nonseptic controls (96.26 vs. 45.38 nM; p < .001). Similar changes could be induced by endotoxin incubation of whole blood (84.52 vs. 40.45 nM; p < .001). This endotoxin-induced increase was independent of extracellular calcium concentration and was only partially ameliorated by calcium-channel blockade. Inhibition of intracellular calcium release was ineffective in altering the endotoxin-induced increase in the erythrocyte intracellular calcium value. In contrast, pretreatment with either adenosine or ATP minimized these increases. Posttreatment with ATP, but not adenosine, allowed partial reversal of this endotoxin-induced increase in intracellular calcium. CONCLUSIONS: Sepsis induces alterations of erythrocyte intracellular calcium homeostasis. A significant increase in free cytosolic concentrations of intracellular calcium is characteristic of this altered homeostasis. These changes are reproducible by the incubation of whole blood with endotoxin. This increase in cytosolic calcium concentration appears to be independent of extracellular calcium concentration, transmembrane calcium channels, and/or intracellular calcium stores. It can, however, be modulated through provision of high-energy phosphates and/or their precursors to the cell itself.

Adenosine↗

PubMed1995

Leukocyte modulation inhibits endotoxin-induced disruption of intracellular calcium homeostasis.

OBJECTIVE: Sepsis is associated with disruption of intracellular calcium homeostasis. The specific mechanisms responsible for these changes remain unclear. This study attempts to modify endotoxin-induced alterations in erythrocyte intracellular calcium dynamics through modulation of the activated leukocyte and its products. METHODS: Paired anticoagulated whole-blood specimens were obtained from healthy adult volunteers (n = 30). Specimens were incubated with 2 micrograms/mL endotoxin [lipopolysaccharide (LPS)] or saline control in the presence and absence of the white blood cell. Studies were repeated in specimens pretreated with allopurinol, superoxide dismutase, and pentoxifylline (PTX). After incubation, erythrocytes were separated, washed, and loaded with the fluorescent calcium chelator, FURA-2. Free cytosolic calcium concentration was determined on 10(6) cells using fluorescent spectroscopy. Values were computer-calculated every 1.8 seconds for 1 minute, and mean results were used for analysis. Differences were evaluated by analysis of variance. RESULTS: The LPS resulted in a significant increase in intracellular calcium concentration (LPS 70.95 nM vs. control 44.04 nM). This increase was dependent on the presence of the white blood cell and could not be induced in its absence (control 30.15 --> LPS 32.78). Pretreatment inhibited these endotoxin-induced alterations: allopurinol, 50.49 nM; superoxide dismutase, 49.12 nM; and PTX, 40.23 nM (p < 0.01). CONCLUSIONS: Endotoxin induces a significant increase in intracellular calcium concentration. This alteration seems to be mediated by activated neutrophils and can be ameliorated by both leukocyte modulation (PTX) and free radical scavengers.

Allopurinol↗

PubMed1995

Selective management of pediatric esophageal foreign bodies.

Esophageal foreign body is a relatively common consultation from the Pediatric Emergency Room. This study evaluates optimal selective management of esophageal foreign bodies in the pediatric patient. Eighty-six children have been referred for esophageal foreign body. Fifteen had been symptomatic for 48 or more hours before being seen. In eight, there was a known history of previous repair for esophageal atresia. In 88%, the foreign body was opaque, most frequently a coin. The most common nonopaque foreign body was retained food. Upon diagnosis, 72 children were taken to radiology, where balloon extraction under fluoroscopic control was attempted. Fourteen children went directly to the operating room for endoscopy and foreign body removal. Balloon extraction was successful in 62 cases (86%), and the children were discharged directly from the Emergency Department. The foreign body was successfully removed at esophagoscopy in the 10 cases that failed attempts at balloon extraction. Since 1990, successful extraction has been accomplished in 100% of cases (29/29). Neither balloon extraction nor endoscopy was associated with morbidity or mortality. Endoscopy was, however, associated with total hospital charges approximately 400% higher than balloon extraction. Fluoroscopically guided balloon extraction of appropriate esophageal foreign bodies is a safe and cost-effective alternative to endoscopy. Failure of nonoperative management does not complicate subsequent endoscopic removal. Patients with symptoms > 48 hours, a history of prior esophageal atresia, and/or nonopaque esophageal foreign bodies do not preclude attempt at balloon extraction.

Catheterization↗

PubMed1994

The effect of endotoxin on neonatal erythrocyte intracellular calcium concentration.

Erythrocyte membrane deformability is dependent on the maintenance of "normal" intracellular calcium (Ca) levels. Red cell flexibility is known to be altered in the septic neonate. In turn, this adversely affects viscosity and compromises flow in the microcirculation. It has been suggested that this may play a role in the mesenteric hypoperfusion associated with necrotizing enterocolitis. This study was designed to determine the effect of endotoxin on erythrocyte Ca homeostasis in the neonate. Paired specimens were obtained from the umbilical cord of 10 healthy neonates. The samples were incubated with either buffered saline (control) or 2 micrograms/mL of Escherichia coli endotoxin (LPS). Erythrocytes were then isolated, washed, and loaded with the fluorescent Ca chelator, FURA-2. The free cytosolic Ca concentration was determined by spectroscopic analysis of the ratio of fluorescent intensities at 340 nm and 380 nm. Results were obtained every 1.8 seconds for 1 minute, and the mean value was used for analysis. In 10 additional neonates, the white blood cells were removed before incubation in saline and LPS, and the erythrocytes were evaluated as described above. Differences were analyzed statistically by the paired t test. In the presence of white blood cells, endotoxin resulted in a significant increase in free cytosolic Ca concentration (LPS, 42.602 +/- 5.166 nmol; control, 31.661 +/- 4.002 nmol; P < .02). However, no significant difference were detected when cells were incubated in the absence of white blood cells (LPS, 32.374 +/- 2.479 nmol; control, 34.021 +/- 2.549 nmol). Endotoxin induces a significant increase in neonatal free cytosolic Ca concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗

PubMed1994

Sepsis-induced alterations in the erythrocyte membrane.

Sepsis is known to alter red blood cell (RBC) deformability, and this change in flexibility may play a role in the pathophysiology of the hemodynamic alterations characteristic of the septic syndrome. The etiology of this red cell change is unclear. This study evaluates erythrocyte size and cell membrane fluidity during clinical (septic surgical patients) and experimental (endotoxin incubation) sepsis. Membrane lipid viscosity was assessed by fluorescent spectroscopy. Mean corpuscular volume and hemoglobin concentration was determined by automated counter. There was a significant increase in erythrocyte membrane lipid viscosity (P < 0.001) in both the clinical and experimental septic models. No difference was detected, however, in RBC mean corpuscular volume or hemoglobin concentration. These findings suggest that sepsis-induced alterations in erythrocyte deformability are due primarily to an increase in the membrane lipid viscosity and are unrelated to alterations in the cell surface area to volume ratio.

Erythrocyte Membrane↗

PubMed1993

The effect of endotoxin on the neonatal erythrocyte.

Intestinal ischemia is considered a major factor in the development of necrotizing enterocolitis (NEC). Despite this, the majority of affected infants lack documentation of clinical events associated with obvious gut hypoperfusion. Recent evidence in adults suggests that endotoxin may impair flow in the microcirculation through alterations in erythrocyte deformability. As the gut serves as a semipermeable reservoir of endotoxin in the stressed neonate, such localized activity may result in intestinal ischemia at the microcirculatory level through alterations in the red cell membrane. This study evaluates the role of endotoxin on neonatal erythrocyte membrane viscosity. Paired anticoagulated whole blood specimens were obtained from the umbilical cord of 10 neonates at delivery. Samples were incubated with either 2 micrograms/mL of E coli endotoxin (LPS) or an equal volume of saline (control). Following incubation, erythrocytes were isolated, washed, and incorporated with the fluorescent membrane probe TMA-DPH. Membrane viscosity was assessed by spectroscopic analysis of the fluorescent emissions induced by excitation of the probe at 365 nm. Results were calculated as anisotropy and analyzed for differences by ANOVA. Endotoxin resulted in a significant increase in red cell membrane viscosity as compared to control (LPS 291.2 +/- 5.1 v Control 271.7 +/- 3.3, P < .01). As the effects of endotoxin are known to be primarily the result of white blood cell (WBC) activation, this study was repeated in an additional 10 neonates in whom WBCs were removed prior to endotoxin/saline incubation.(ABSTRACT TRUNCATED AT 250 WORDS)

Endotoxins↗

PubMed1993

Role of the leukocyte in endotoxin-induced alterations of the red cell membrane. Second place winner of the Conrad Jobst Award in the Gold Medal paper competition.

Sepsis and endotoxemia are known to be associated with alterations in the red cell membrane that result in diminished flexibility. This decreased flexibility may be responsible, in part, for the microcirculatory abnormalities accompanying sepsis. The etiology of these sepsis-associated changes remains unclear. This study evaluates the role of the white blood cell in these abnormalities. Specimens were obtained from 44 volunteers and divided into two treatment groups. Group I specimens were incubated with Escherichia coli endotoxin (2 micrograms/ml) followed by removal of the white blood cells. The white blood cells were removed from group II specimens before endotoxin incubation. Paired, saline-incubated samples served as controls. After incubation, washed erythrocytes were evaluated for deformability and membrane viscosity. Deformability was assessed by filtration through 4.7-microns membranes. Red cell deformability was expressed as filtration rate (volume of cells per second per square centimeter). Membrane viscosity was assessed by fluorescent spectroscopy of cells into which the membrane probe 1(4-(trimethylamino)-phenyl)-6-phenyl-1,3,5-hexatriene had been incorporated. Results were expressed as anisotropy. Endotoxin resulted in a significant increase in erythrocyte membrane viscosity (experimental, 0.296 +/- 0.002 vs. control, 0.284 +/- 0.002, P < 0.001). This was reflected by a significant decrease in cellular deformability (experimental, 142.55 +/- 6.55 vs. control, 157.86 +/- 8.63, P < 0.01). However, these alterations are not a direct effect of endotoxin, but require the presence and participation of the white blood cell and/or its mediators (experimental, 0.301 +/- 0.002 vs. control, 0.300 +/- 0.001, P = NS).

Awards and Prizes↗

PubMed1991

The role of pentoxifylline in endotoxin-induced alterations of red cell deformability and whole blood viscosity in the neonate.

Endotoxin induces alterations in the neonatal red cell membrane that result in decreased deformability and an increase in whole blood viscosity. These rheologic alterations are detrimental to flow in the microcirculation. Pentoxifylline (PTX), a methyl xanthine derivation, increases red cell deformability presumably through its effect on intracellular adenosine 5-triphosphate. The purpose of this study was to evaluate the effect of PTX on endotoxin-induced alterations in the neonatal red blood cell. Anticoagulated whole blood specimens obtained from the cord of 12 neonates at birth were used to study the effects of Escherichia coli endotoxin (LPS) with and without PTX (50 micrograms/mL) on red cell deformability and whole blood viscosity. LPS resulted in a significant (P less than .001) decrease in deformability compared with controls. PTX reversed these endotoxin-induced alterations (P less than .01), normalizing deformability to control values (P = NS). LPS resulted in a significant increase (P less than .005) in blood viscosity that was reversed by PTX (P = NS). Pentoxifylline reverses the detrimental rheologic effect of endotoxin in the neonate. This activity may be helpful in sustaining normal microcirculation in neonatal sepsis.

Blood Viscosity↗

PubMed1991

Error in fluid and calorie calculation in the surgical neonate.

Nutritional management has become an integral part of the care of the surgical neonate. In most teaching institutions, this is the responsibility of the resident staff with varying degrees of supervision. The purpose of this study was to assess the accuracy of this management. Eleven parameters of fluid and nutritional status were determined daily on all surgical newborns in the neonatal intensive care unit (NICU). The values were calculated by the housestaff in traditional fashion, based on available bedside data, and entered into the charts. Similar values were calculated, based on the same data, by a trained clinical nurse specialist using a preprogrammed, hand-held computer. Values were then compared for significant difference. Approximately 2,500 calculations were analyzed. Overall, there was a statistically significant error detected in the housestaff evaluation of both fluid and nutritional status. This discrepancy was greatest in infants weighing less than 2 kg. Similarly, there was an inverse correlation between the degree of error and houseofficer level. These data indicate a potential risk in the management of the surgical neonate. This risk is greatest in the small infant, indicating the need for close supervision of critical physiological computations within the teaching NICU.

Computers↗