Biomedical subjects

J V Pellicane

Publications and source records attributed to J V Pellicane.

7 recordsLinked to original sources

PubMed1997

Nonocclusive intestinal ischemia: improved outcome with early diagnosis and therapy.

Nonocclusive intestinal infarction (NOII) is described as bowel necrosis at celiotomy or autopsy without evidence of thromboembolism, vasculitis, or mechanical obstruction. The mortality for this entity is as high as 90 per cent in some series. From January 1990 to January 1995, we identified 15 patients who met the criteria for NOII identified at celiotomy or autopsy. We collected data on demographics, comorbidities, presenting signs and symptoms, laboratory workup, time to definitive therapy, and outcome. Our goal was to improve our ability to identify and treat this devastating surgical problem. There was a 4.5:1 female to male ratio, and patients had an average age of 73 +/- 10 years. Significant comorbidities included coronary artery disease (87%) and atrial fibrillation (73%). Eleven patients were diagnosed at celiotomy and four at autopsy. Overall mortality was 67 per cent. The most common presenting symptoms were abdominal pain (93%) and distention (80%) and mental status changes (60%). Peritonitis was less common, present in only 40 per cent of the patients. Leukocytosis, bandemia, increased creatinine, metabolic acidosis, and hypoxemia were common among all patients. There was a significant difference in time to definitive therapy in survivors versus nonsurvivors (1.2 +/- 0.89 vs 4.8 +/- 2.0 days; P < 0.02, t test). These data suggest that NOII is a lethal surgical problem. A history of coronary artery disease and atrial fibrillation was common among all patients. Various nonspecific presenting signs, symptoms, and laboratory values are suggestive of this diagnosis. A high index of suspicion in select patients and early intervention may lead to improved outcome.

Aged↗

PubMed1997

Meckel's diverticulum: a ten-year experience.

Meckel's diverticulum (MD) is the most common congenital anomaly of the small intestine, occurring in up to 4 percent of the population. The majority of MD cases are discovered incidentally; however, they can occasionally cause serious bleeding or obstructive or inflammatory complications. We reviewed the charts of 58 patients with MD from 1984 to 1994 collecting data on age, sex, presentation, therapy, pathology, and surgical complications to try to identify factors suggestive of the need for surgical therapy and the associated morbidity and mortality of resection. There was a 1.3:1 male:female ratio, and although patients with MD were found at all ages, the majority were found in patients in the 4th and 5th decade of life. Forty-five of 58 were incidental, and 13 of 58 were symptomatic. The most common symptom was bowel obstruction (10 of 13). Forty-five of 58 MD cases were managed surgically, 71 percent by diverticulectomy and the remainder by segmental resection, with no associated morbidity or mortality. Symptomatic patients were more often male (77 vs 23%; P 0.06, Fisher's exact test), more often had ectopic mucosa (31 vs 16%; P, not significant), and were evenly distributed over all ages. These data suggest that, with the possible exception of male sex, there is no factor predictive of the development of symptoms in incidentally found MD. In light of this finding, the low operative morbidity and mortality, and the even age distribution in patients with complications of their MD, we recommend that MD be resected when found incidentally in the absence of an absolute contraindication.

Adolescent↗

PubMed1994

Decreased lactate in endotoxin-resistant mice undergoing hemorrhage is independent of tumor necrosis factor availability.

Although C3H/HeJ mice, characterized by a genetic deficiency in macrophage cytokine release in response to endotoxin, have been studied extensively to gain insight into the possible role of various cytokines in sepsis, few past studies have examined the physiologic response to hemorrhagic shock in this "endotoxin-resistant" strain. We utilized a fixed-volume model of hemorrhagic shock and two different levels of hemorrhage severity (50 and 67% blood volume) to compare C3H/HeJ mice to normal C3H/HeN mice. An additional group of endotoxin-sensitive C3H/HeN mice were treated with 2.5 mg/kg of anti-tumor necrosis factor (TNF) antibody to define the possible role of TNF in shock physiology. Hematocrit, circulating neutrophils, and plasma glucose and lactate concentrations were measured following hemorrhage. TNF increased significantly following hemorrhage in normal mice but did not increase in C3H/HeJ mice or in C3H/HeN mice treated with anti-TNF antibody. No difference between groups was identified in hematocrit, circulating neutrophils, or glucose. Whereas plasma lactate increased significantly by 30 min in all groups, lactate returned to baseline levels in C3H/HeJ mice at 60 min, but remained persistently elevated in C3H/HeN mice and in C3H/HeN mice treated with anti-TNF antibody. The data demonstrate attenuated lactate accumulation in C3H/HeJ mice following hemorrhage. Inhibition of circulating TNF activity with anti-TNF antibody failed to reproduce this late decrease in plasma lactate in normal mice. The data suggest that macrophage products other than TNF known to be deficient in C3H/HeJ mice contribute to anaerobic metabolism in hemorrhagic shock.

Animals↗

PubMed1994

The role of inflammatory cytokines in wound healing: accelerated healing in endotoxin-resistant mice.

UNLABELLED: The role of cytokines in normal wound healing remains poorly defined. In vitro, tumor necrosis factor alpha (TNF-alpha) decreases collagen accumulation, perhaps by increasing collagenase activity. The current study was undertaken to test the hypothesis that cytokines impair wound healing and collagen production. Wounds in C3H/HeJ (J) mice, which are characterized by a genetic defect in macrophage production of TNF and other cytokines in response to endotoxin, were compared with wounds in normal endotoxin-sensitive C3H/HeN (N) mice. METHODS: TNF (by murine ELISA) and collagenolytic activity (CA by in vivo labelled collagen fibril degradation assay) were measured in wound fluid from silicone reservoirs on post-wounding days 1, 3, and 5 (n = 5 per group). Hydroxyproline (HOP, nmol/mg sponge) incorporation (by HPLC) in polyvinylacohol sponges and breaking strength (BS, as determined by tensiometry) in linear wounds were assessed on days 5, 7, 10, and 14 (n = 5 per group). The data demonstrate significantly increased BS at 5 and 7 days in endotoxin-resistant J mice compared with that in endotoxin-sensitive N mice. An early, significant reduction in TNF production in J mice corresponded with a significant increase in CA on day 1, increased collagen production at day 7, and increased procollagen gene transcription at early time points. Conclusion. The reduced production of inflammatory cytokines including TNF in the wound fluid of J mice corresponded with an early improvement in wound tensile strength. An accelerated accumulation of collagen in the wounds of J mice, perhaps resulting from a significant decrease in collagenolytic activity or increased collagen production, are potential mechanisms. The data suggest that cytokines produced in normal healing of clean wounds may contribute to a delay in increased tensile strength.

Animals↗

PubMed1993

Hemorrhagic shock in endotoxin-resistant mice: improved survival unrelated to deficient production of tumor necrosis factor.

Although tumor necrosis factor (TNF) has been implicated in sepsis-induced mortality, its role in the pathophysiology of hemorrhagic shock (HS) remains ill defined. We studied three groups of acutely anesthetized mice undergoing HS to determine the role of TNF in HS mortality. Shock was initiated in each group after heparinization by arterial bleeding of 4 mL/100 g body weight followed by 12 mL/100 g body weight resuscitation with normal saline at 1 hour. The C3H/HeJ mice (n = 14), characterized by a genetic defect in macrophage production of TNF and other cytokines in response to endotoxin, were compared with the closely related C3H/HeN strain (n = 18), which do produce TNF. A second group of C3H/HeN mice were passively immunized to TNF by pretreatment with 2.5 mg/kg anti-murine TNF antibody (Ab) before HS. In contrast to the high TNF levels measured following HS in C3H/HeN controls, post-HS TNF was undetectable in C3H/HeJ mice. Five-day survival rate and survival time were significantly greater in C3H/HeJ mice when compared with C3H/HeN controls. Anti-TNF Ab pretreatment of C3H/HeN mice abolished the increase in TNF but did not improve survival. The data demonstrate a striking improvement in survival of TNF-deficient C3H/HeJ mice following severe HS. However, the improved survival does not appear to result from deficient TNF production, since Ab pretreatment did not decrease HS mortality. The improved survival in C3H/HeJ mice suggests that cytokines other than TNF may play a role in the pathophysiology of HS.

Animals↗

PubMed1993

Interleukin-1 receptor antagonist improves survival and preserves organ adenosine-5'-triphosphate after hemorrhagic shock.

BACKGROUND: This study was designed to determine the role of interleukin-1 (IL-1) in hemorrhagic shock death. METHODS: Pentobarbital anesthetized C3H/HeN mice (n = 59) were prepared with a femoral arterial catheter and were randomized to treatment with an IL-1 receptor antagonist (IL-1ra, 10 mg/kg, n = 29) or an equal volume of phosphate-buffered saline solution (vehicle, n = 30) by subcutaneous bolus injection at 15 minutes before hemorrhage and again at 120 minutes. Continuous posthemorrhage delivery of IL-1ra or vehicle was performed in each group (1.5 mg IL-1ra in 30 microliters/day) through a subcutaneous osmotic pump. Rapid hemorrhage of 4 ml/100 gm weight was followed by normal saline resuscitation of 12 ml/100 gm 60 minutes later. RESULTS: Survival analysis by Wilcoxon rank sum analysis revealed a significantly improved 5-day survival in IL-1ra-treated mice (n = 15, 20%) as compared with vehicle-treated mice (n = 14, 6%, p < 0.001). To determine a possible mechanism of this survival advantage, the remaining mice in each treatment group were killed at 30 minutes to obtain blood and tissue samples from the heart, liver, and kidney for measurement of adenosine-5'-triphosphate (ATP). No difference in hematocrit, circulating neutrophils, or levels of glucose, lactate, or tumor necrosis factor was identified between groups to explain the improved outcome. IL-1ra prevented hemorrhage-induced ATP depletion observed in vital organs of vehicle-treated mice. CONCLUSIONS: The data implicate IL-1 in shock-induced ATP depletion and suggest IL-1ra may improve hemorrhagic shock survival by preventing ATP depletion in vital organs.

Adenosine Triphosphate↗

PubMed1992

Preventable complications and death from multiple organ failure among geriatric trauma victims.

We reviewed 374 consecutive trauma patients over age 65 years to determine (1) if the emergency room Trauma Score (TS) could predict mortality, thereby improving ICU triage, and (2) the frequency of preventable complications in patients who died (n = 31). Fifty-two percent of deaths (n = 16) occurred in patients with TS = 15 or 16. Multiple organ failure/sepsis (MOF/S) was the most common cause of death overall (42%) and was also the most frequent cause of death in patients with a TS = 15-16 (63%). Nonsurvivors in the TS = 15-16 subgroup were older (80.9 +/- 2.0 vs. 74.9 +/- 0.5 years, p less than 0.02) and had greater ISSs (15.8 +/- 3.7 vs. 8.0 +/- 0.4, p = 0.001) than survivors. Patients with a TS less than 15 suffered high overall mortality (45%). Preventable complications contributed to mortality in 32% of all deaths and in 62% of MOF/S deaths. Aggressive care to prevent avoidable complications may improve survival in elderly trauma victims.

Age Factors↗