Utility of routine laboratory testing for detecting intra-abdominal injury in the pediatric trauma patient.

OBJECTIVE: To assess the prevalence of laboratory abnormalities (complete blood cell count, electrolytes, blood urea nitrogen, creatinine, glucose, aspartate aminotransferase, alanine aminotransferase, amylase, lipase, urinalysis [U/A]) and the sensitivity and specificity of the physical examination (PE) and screening laboratory tests for identifying intra-abdominal injury (IAI) in moderately injured pediatric patients. DESIGN, PARTICIPANTS, AND SETTING: Phase I: Retrospective chart review of 285 consecutive level II (moderately injured) trauma patients seen at a children's hospital emergency department/pediatric trauma center. All patients were received directly from the scene and had the following data recorded: mechanism of injury, Glasgow coma score, trauma score, pediatric trauma score, systematically recorded PE findings, laboratory results, and injuries detected during hospitalization. Phase II: To confirm the sensitivity of the PE and U/A found in phase I, the model was applied to 91 additional trauma patients identified by International Classification of Diseases, 9th revision (ICD-9) codes as having IAI. INTERVENTION: None. RESULTS: Phase I: A total of 3939 tests were ordered for the 285 patients entered in phase I. Aspartate aminotransferase and alanine aminotransferase values were obtained in 59% of patients; glucose level was obtained in 78% of patients; complete blood cell count, U/A, and levels of electrolytes, blood urea nitrogen, creatinine, amylase, and lipase were obtained in more than 85% of patients. The overall prevalence of laboratory abnormalities was 5.7%. Fourteen patients (4.8%) were identified who had a total of 23 significant IAIs (9 pancreatic, 6 splenic, 5 renal, 3 hepatic). The PE combined with U/A showing more than five red blood cells per high-power field had a sensitivity of 100%, specificity of 64%, positive predictive value of 13%, and negative predictive value of 100% for the detection of IAI. The presence of laboratory abnormalities suggesting injury did not increase the sensitivity of the model and significantly decreased both specificity and positive predictive value. Phase II: The PE combined with U/A identified an abnormality in 89 (97.8%) of 91 cases (95% confidence interval = 94.8% to 100%). CONCLUSIONS: In the moderately injured pediatric trauma patient, (1) there is a low prevalence of laboratory abnormalities; (2) the PE combined with U/A is a highly sensitive screen for IAI; and (3) in patients with a normal PE of the abdomen and a normal U/A, laboratory testing seldom identifies unsuspected IAI.

Antisense oligodeoxynucleotide to inducible nitric oxide synthase inhibits nitric oxide synthesis in rat pulmonary artery smooth muscle cells in culture.

BACKGROUND: We recently demonstrated the induced expression of the inducible nitric oxide synthase (iNOS) gene in cultured rat pulmonary artery smooth muscle (RPASM) in response to lipopolysaccharide and cytokines, using a complementary DNA probe to murine macrophage iNOS. Because nitric oxide (NO) can be cytotoxic, iNOS in the pulmonary vasculature may contribute to lung injury in sepsis. We designed an antisense oligodeoxynucleotide complementary to the iNOS messenger RNA (mRNA) sequence to determine whether the probe prevented iNOS translation. METHODS: RPASM, preincubated in the presence of antisense and sense oligodeoxynucleotide to the first 18 bases after the initiation codon of iNOS mRNA, was exposed to interferon-gamma and tumor necrosis factor-alpha to induce NO production (as measured by NO2-, the stable end product of NO formation). RESULTS: Interferon-gamma and tumor necrosis factor-alpha induced NO production in RPASM: The antisense probe caused up to a 36% decrease in cytokine-induced NO2- production in a concentration-dependent manner (1 to 10 mumol/L). The sense probe had no effect. CONCLUSIONS: Increased transcription of iNOS mRNA is an essential step in the induced production of NO by RPASM: Antisense probes partially inhibit iNOS expression in vitro, suggesting its use to inhibit iNOS expression under pathologic conditions.

Nitric oxide produced by cytokine-activated pulmonary artery smooth muscle cells is cytotoxic to cocultured endothelium.

BACKGROUND: We recently demonstrated that rat pulmonary artery smooth muscle (RPASM) generates maximal nitric oxide (NO) when exposed to inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma. Our hypothesis is that NO produced by cytokine-stimulated RPASM has local cytotoxic effects on endothelium. Accordingly, we designed a pulmonary smooth muscle and endothelial coculture experiment in which the effects of NO on endothelium can be distinguished from the direct effects of cytokines. METHODS: RPASM cells were incubated with a mixture of TNF-alpha (500 units/ml) and IFN-gamma (100 units/ml) for 24 hours. This cytokine mixture was then removed and the NO-producing smooth muscle cells were incubated in a coculture transwell system with rat pulmonary artery endothelial (RPAE) cells. Subsequent NO production (as measured by nitrite concentration in cell supernatants), and the number of viable attached endothelial cells were then measured at 48 hours. RESULTS: RPASM continued to produce large amounts of NO, in the absence of further cytokine stimulation, after a 24-hour exposure to TNF-alpha and IFN-gamma. This RPASM-generated NO decreased the number of viable attached endothelial cells after 24 hour RPASM-RPAE coculture by 57%. The competitive stereospecific inhibitor of inducible NO synthase (iNOS), NG-monomethyl-L-arginine (NMA), returned the inducible NO production to basal levels and reversed the cytotoxic effects on endothelial cells. The number of viable attached endothelial cells returned to control levels. CONCLUSIONS: The NO produced by cytokine-activated RPASM has local cytotoxic effects on RPAE in coculture. Such NO produced in the vasculature may be a factor in the origin of acute lung injury under conditions of trauma and sepsis.

Perinatal management of a lingual teratoma.

BACKGROUND: Teratomas of the head and neck are rare and occur almost exclusively in neonates. Prenatal diagnosis of these tumors allows for a carefully planned delivery that maintains an open airway and potentially improves perinatal outcome. We report the perinatal management of a huge intrapharyngeal and intra-oral teratoma that had a broad connection to the base of the tongue. CASE: An anterior neck mass (5 x 5 cm) in an otherwise normal-appearing fetus was detected at 19 weeks' gestation. The mass increased in size over the next 10 weeks to 8 x 6.8 x 4.3 cm. Marked fetal head deflexion was noted along with concomitant hydramnios. The mother had spontaneous rupture of membranes with preterm labor at 29 weeks' gestation. A 1860-g male neonate was delivered by classical cesarean delivery. A tracheostomy was performed in the delivery room for ventilation after the upper airway could not be accessed by bronchoscopy. Histologic examination after surgical excision confirmed a congenital teratoma with immature neuroectodermal tissue and alpha-fetoprotein-bearing endodermal sinus tumor components with exclusively polyvesicular vitelline characteristics. The origin of the pharyngeal mass was the base of the tongue. CONCLUSION: The prenatal diagnosis of a pharyngeal teratoma should prompt a careful delivery plan to optimize perinatal outcome.

Prenatal diagnosis and management of massive bilateral axillary cystic lymphangioma.

BACKGROUND: Fetal lymphangiomas can occur in many different anatomic locations, including the most commonly seen nuchal cystic hygroma. CASE: A fetus at 18 weeks' gestation was found to have a massive right axillary hygroma. The fetal karyotype was normal. Serial ultrasound examinations indicated progressive enlargement, but no hydrops. At 32 weeks' gestation, a left axillary hygroma was also diagnosed. The patient underwent cesarean delivery. CONCLUSION: Prenatal diagnosis of nuchal cystic hygromas has a high association with karyotypic abnormalities, hydrops, and fetal demise; however, this association may not apply to cystic lymphangiomas at other locations.

Hemodynamic effects and metabolic fate of inhaled nitric oxide in hypoxic piglets.

We describe the hemodynamic effects and metabolic fate of inhaled NO gas in 12 anesthetized piglets. Pulmonary and systemic hemodynamic responses to incremental [NO] (5-80 ppm) were tested during ventilation with high- [0.30 inspired O2 fraction (FIO2)] and low-O2 (0.10 FIO2) mixtures. In six animals, inhalation of 40 ppm NO was maintained over 6 h to test effects of prolonged exposure (0.30 FIO2). In the other six animals, pulmonary hypertension was induced by hypoxic ventilation (0.10 FIO2) and responses to NO were tested. Inhaled low [NO] partially reversed pulmonary hypertension induced by alveolar hypoxia; mean pulmonary arterial pressure decreased from 31.4 +/- 2.3 mmHg during hypoxia to 18.2 +/- 1.2 mmHg during 5 ppm NO. Mean pulmonary arterial pressure at 0.10 FIO2 did not fall further at higher [NO] (10-40 ppm) and never reached control levels. Pulmonary vascular resistance increased with institution of hypoxic ventilation and fell with subsequent administration of NO, ultimately reaching control levels. Inhaled NO did not affect systemic vascular resistance. Plasma levels of NO2- + NO3- and methemoglobin (MetHb) levels increased with increasing [NO]. Over 6 h of NO administration during high-O2 ventilation, MetHb equilibrated at subtoxic levels while NO2- + NO3- increased. Nitrosylhemoglobin, analyzed by electron paramagnetic resonance spectrophotometry was not detected in blood at any time. At the relatively low concentrations (5-80 ppm) that are effective in relieving experimental pulmonary hypertension induced by alveolar hypoxia, inhaled NO gas causes accumulation of NO2- + NO3- in plasma and a small increase in MetHb but no detectable nitrosylhemoglobin.

Efficacy of inhaled nitric oxide in a porcine model of adult respiratory distress syndrome.

OBJECTIVE: To assess the efficacy of inhaled nitric oxide (NO) in reducing pulmonary hypertension in a porcine model of adult respiratory distress syndrome. DESIGN: Nonrandomized, controlled experiment without blinding. SETTING: Surgical research laboratory. PARTICIPANTS: Twelve pigs, matched equally for body weight. INTERVENTION: Acute lung injury was induced by intravenous injection of oleic acid. Animals were then divided into either a control group, for monitoring without any further intervention, or a NO-treatment group, in which NO was administered at concentrations of 10 to 80 ppm, with each step separated by a NO-free interval to assess duration of effect. MAIN OUTCOME MEASURES: Pulmonary artery pressure, systemic blood pressure, PaO2, intrapulmonary shunt fraction, and extravascular lung water. Nitrosylated hemoglobin, arterial methemoglobin, and plasma nitrite and nitrate concentrations. RESULTS: All animals responded to oleic acid injection with rapid development of pulmonary hypertension and deterioration of PaO2 and intrapulmonary shunt fraction. Inhaled NO reversed these changes in a concentration-dependent manner. Cessation of NO administration led to a prompt return of pulmonary hypertension. A small but significant drop in systemic blood pressure was observed only at the highest concentration of NO administered (80 ppm). Extravascular lung water almost doubled following oleic acid injury. This increase was sustained in all animals for the remainder of the experiment. Significant increases in circulating methemoglobin and plasma nitrite and nitrate concentrations were measured during NO inhalation. CONCLUSION: Inhaled NO appears to be a selective pulmonary vasodilator and may prove to be useful in improving gas exchange in adult respiratory distress syndrome.

Kaolin-induced congenital hydrocephalus in utero in fetal lambs and rhesus monkeys.

A model of congenital hydrocephalus in utero in fetal lambs and rhesus monkeys has been produced by the intracisternal injection of kaolin. Initial attempts to produce hydrocephalus using silicone oil were unrewarding. Hydrocephalus had developed by 2 weeks post-injection and could be followed by ultrasonography. The pathological findings were similar to those reported using kaolin in other species. Ventriculoamniotic shunting, when successful, was capable of partially reversing the deleterious effects of hydrocephalus. The major drawback of the present model is that hydrocephalus is produced during the second rather than the first trimester of pregnancy. However, kaolin produces mainly an obstructive hydrocephalus without other associated brain or systemic anomalies.

Pulmonary dysfunction after primary closure of an abdominal wall defect and its improvement with bronchodilators.

To determine the extent of pulmonary dysfunction following primary closure of an abdominal wall defect, we obtained pulmonary function tests (PFT) in 11 newborn infants with gastroschisis and 6 with large omphaloceles admitted to a newborn ICU in a children's hospital. Patients were 1 to 30 days of age at the time of the PFT; all required endotracheal intubation and mechanical ventilation for operative procedures or for postoperative ventilatory support. Full-term infants (n = 21) undergoing minor surgical procedures provided comparative measurements. Flow-volume curves were obtained with manual inflation of the lungs followed by forced deflation using negative pressure, or by passive expiration, under sedation and pharmacologic paralysis. Deflation flow-volume curves gave measurements of forced vital capacity (FVC) and maximal expiratory flow at 25% of vital capacity from residual volume (MEF25). Modified passive mechanics technique gave passive expiratory curves that provided measurements of respiratory system compliance (Crs) and resistance (Rrs). Tests were done: within 48 h (period A), 3-7 days (period B), and 8-30 days after surgical repair (period C). Pulmonary function testing after nebulized 0.1% isoetharine (a bronchodilator), to test for bronchial reactivity, began midway during the study period in 15 patients. Preoperative and postoperative tests were obtained in 5 patients. Closure of an abdominal wall defect decreased FVC, Crs, and MEF25 by up to 50% of normal, reference values after surgery (P less than 0.05). FVC and MEF25 approached values of normal infants by 4 weeks, whereas Crs remained 50% lower.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary function in newborns after repair of congenital diaphragmatic hernia.

Congenital diaphragmatic hernia (CDH) is associated with pulmonary hypoplasia that limits survival, but the nature and extent of pulmonary dysfunction in neonates with CDH have not been studied. We performed pulmonary function tests (PFTs) in eight intubated infants who survived neonatal repair of CDH (wt, 3.33 +/- 0.15 kg; age, 20.1 +/- 2.7 d; mean +/- S.E.M.). PFTs obtained from six full-term infants (wt, 3.56 +/- 0.15 kg; age, 25.0 +/- 3.3 d) with no respiratory illness served as controls. The deflation flow-volume curve technique produced maximum expiratory flow-volume (MEFV) curves, giving reproducible measurements of forced vital capacity (FVC) and maximal expiratory flow at 25% of FVC (MEF25). Respiratory system compliance (Crs) and resistance (Rrs) were obtained with a modified passive mechanics technique. In seven of eight infants PFTs were repeated after nebulized bronchodilator (0.1% isoetharine). In neonates surviving CDH repair, as compared to those with normal lung function, FVC was significantly reduced (20.78 +/- 3.32 vs. 39.83 +/- 3.30 mL.kg-1, P less than 0.05). MEF25 was also markedly reduced (20.78 +/- 3.32 vs. 39.83 +/- 3.30 mL.kg-1.s-1, P less than 0.05), indicating lower airway obstruction. After administration of nebulized bronchodilator, PFTs showed significant increases from control values in both FVC (15.9%) and MEF25 (200%) without changes in Crs and Rrs. These findings indicate that neonates with CDH have restrictive lung defects, reflecting hypoplasia. After surgical repair and mechanical ventilation airway reactivity develops, primarily in smaller airways, and this may complicate the postoperative course.

Bronchial reactivity in infants in acute respiratory failure with viral bronchiolitis.

Airway reactivity and the effects of bronchodilators in infants are controversial. We studied the response to bronchodilator treatment in 14 mechanically ventilated infants (mean age, 2.74 months; range, 0.6-5.9) in respiratory failure caused by respiratory syncytial virus (RSV)-associated bronchiolitis. Sixteen infants without lung disease, undergoing elective surgery, provided normal values. Maximum expiratory deflation flow-volume (DFV) curves were produced by manual inflation of the lungs with an anesthesia bag to a predetermined static airway pressure followed by rapid deflation with a negative airway pressure before and after administration of bronchodilator. At baseline, the bronchiolitis group had a forced vital capacity (FVC) of 34.5 +/- 3.6 ml/kg compared with 41.8 +/- 1.5 ml/kg in the normal group; maximum expiratory flow rate at 25% of FVC (MEF25) was 10.2 +/- 2.0 ml/kg/s compared with 27.3 +/- 2.0 ml/kg/s in the normal group. The clinical and radiologic impression was severe lower airway obstruction and air trapping. After administration of bronchodilator, FVC did not increase significantly, but MEF25isov increased by over 30% in 13 of 14 infants. Mean MEF25 increased by 148 +/- 43.2% to 21.7 +/- 3.9 ml/kg/s (P less than 0.02). These findings indicate that during the acute phase of severe RSV-positive bronchiolitis most infants have airway reactivity that responds positively to bronchodilator treatment.

Surgery interns' experience with surgical procedures as medical students.

Instruction in the technical aspects of surgery begins in medical school. To identify areas of inexperience among incoming interns, we asked 40 first-year residents to indicate which bedside and emergency room procedures and operations (or parts of operations) they had performed in medical school and to rate how confident they were in performing those procedures as a result of their experiences. Respondents indicated that placement of nasogastric tubes, Foley catheters, and central lines were procedures they commonly performed (78.4% to 97.3%); they less frequently placed arterial and pulmonary arterial lines and chest tubes (21.6% to 64.9%). Many students had opportunities to assist in closure of incisions in actual operations (60%), but only 22% performed other parts of operative procedures. Opportunities to perform procedures did not correlate with the length of time spent on surgical rotations. Nearly half (49%) participated in animal surgery laboratories as part of their surgical rotation. These findings suggest that many interns have not performed some basic procedures by the time they enter their residency. Instruction in technical skills in clinical medicine, frequently surgical, represents a deficiency in medical school curricula. The general inexperience of surgical interns in performing these procedures must be remembered when assigning these duties.

Primary aldosteronism: changing concepts in diagnosis and management.

Unilateral adrenalectomy for benign causes of primary aldosteronism is an established procedure. The established surgical cure for aldosterone-producing adenoma justifies a thorough preoperative evaluation. No single test accurately identifies aldosterone-producing adenomas in patients with primary aldosteronism. However, a useful algorithm combines postural studies, computerized axial tomography, and adrenal vein catheterization for selective hormonal assay, if computerized axial tomography is negative or equivocal and the suspicion of aldosterone-producing adenoma is high. If an adrenal mass is present and biochemical studies suggest a diagnosis of aldosterone-producing adenoma, resection of the affected gland from a limited unilateral approach is indicated. Cure can be expected in 80 percent of cases. In the uncommon circumstance that the adrenal tumor was not an aldosterone-producing adenoma but a hyperplastic nodule, these patients may still be cured or more easily controlled with antihypertensive medications. Thirty-eight patients who underwent unilateral adrenalectomy are presented and discussed.

Nitric oxide and the pulmonary artery smooth muscle cell.

Nitric oxide (NO) is produced by the enzyme nitric oxide synthase (NOS), which exists in different isoforms in various tissues. The inducible NOS (iNOS) isoform of the enzyme is expressed in vascular smooth muscle in response to lipopolysaccharide and inflammatory mediators. When this expression of iNOS occurs in the lung, the NO produced may play a role in the inflammatory process of acute lung injury. This article reviews the research that characterizes iNOS in rat pulmonary artery smooth muscle and discusses current investigation into the role of NO in sepsis and injury.

Differences in trauma care among pediatric and nonpediatric trauma centers.

To characterize pediatric trauma care, state trauma registry data from all designated trauma centers in Pennsylvania were divided into three categories, that from: (1) pediatric centers, (2) urban nonpediatric centers, (3) and rural nonpediatric centers. From October 1, 1986 through September 30, 1989 (3 years), 4,615 patients less than 15 years old were admitted to 28 trauma centers in Pennsylvania. Nonpediatric centers cared for the majority of children (2,734, 59.2%), but the average number of children treated per nonpediatric institution (105.1 per year) was far fewer than the average treated in the pediatric centers (940.5). Pediatric trauma centers in the state treated a younger population (6.4 +/- 4.2 years, mean +/- SD) compared with urban and rural nonpediatric centers (8.4 +/- 4.2 and 8.1 +/- 4.3 years, respectively; P less than .05). Pediatric centers received proportionately more children by transfer (56.2%), victims of falls (34.6%), pedestrian injuries (16.8%), and head and neck injuries (41.8%, all P less than .05). Nonpediatric centers received children directly from the scene of injury more frequently than transferred from other hospitals. The male:female sex ratio in urban nonpediatric centers was significantly higher (70.1%, P less than .05) than in the other two groups. Rural nonpediatric centers cared for a higher proportion of motor vehicle passengers (28.5%) and patients classified as "other" in the state registry, a category to which bicycle injuries are assigned (28.2%, P less than .05). Mortality was highest in rural nonpediatric centers (6.2%). The death rate in pediatric centers and urban nonpediatric centers were similar (4.1%) and significantly lower (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Audit filters in quality assurance in pediatric trauma care.

Quality assurance (QA) systems use audit filters to help identify not only deaths and medical complications, but also cases that reflect deficiencies in the timeliness or appropriateness of care. Through our trauma center QA process, we studied three groups of audit screens for trauma care: two set forth by the Committee on Trauma of the American College of Surgeons, a minimum set of 12 audit filters proposed in 1987 and an expanded version recently proposed in 1990 (studied retrospectively), and one set of filters already in use in our system. A peer review committee determined whether deaths and complication were preventable, and judged the timeliness and appropriateness of care. From July 1, 1989, through June 30, 1990, 844 admitted trauma patients came under QA review. During this period 13 (1.5%) died; 35 (4.1%) suffered at least one medical complication. 140 children (16.6%) violated one of the 12 minimum audit filters suggested by the Committee on Trauma (which includes deaths and medical complications), one of the additional filters used by the Trauma Program QA system, or both. Ninety patients (10.6%) failed one of the 12 minimum audit filters; 104 (12.3%) failed one of the additional filters used by the Trauma Program QA system. Filters that involved medical management issues (late operations, return to operating room, airway, failed reduction, infections, missed injuries, readmissions to intensive care unit, return to the emergency department) frequently involved aspects of inappropriate care (72.5%, 37/51 violations) and were associated with actual deaths or medical complications (52.9%, 27/51).(ABSTRACT TRUNCATED AT 250 WORDS)

Prognosis of posterior urethral valves presenting at birth.

Urethral obstruction due to posterior urethral valves (PUV) is a more lethal condition in the newborn than is commonly recognized. To study its prognosis when the diagnosis of PUV is made shortly after birth, cases of PUV presenting in the first week of life were reviewed. Eleven cases were seen at the University of California, San Francisco from 1974 to 1982. Five babies died, three within two hours of birth of respiratory insufficiency secondary to severe pulmonary hypoplasia, and two within three weeks with rapidly progressive renal failure. Of the six survivors, four exhibited respiratory difficulty (prolonged ventilatory support required in two, and bilateral pneumothoraces in two), three developed renal failure despite early urinary diversion, and one had renal tubular dysfunction. Only two infants had normal renal function after undergoing a successful series of reconstructions. Prune-belly syndrome and limb deformities were present in two surviving and two fatal cases. Although most cases of congenital hydronephrosis can be successfully treated after birth, those presenting in the newborn period represent a subset with high morbidity and mortality. With advances in prenatal diagnosis of congenital hydronephrosis, salvage of severe cases detected early in gestation may require more aggressive management in the prenatal period.

Pneumatic dilatation and operative treatment of achalasia in children.

The therapeutic approach to children with achalasia of the esophagus is controversial. Both pneumatic dilatation (PD) and Heller esophageal myotomy (EM) are considered effective, while bougienage has been discarded by most authorities. To determine the best place for each in the therapy of achalasia, 19 cases treated since 1964 were reviewed. Ages ranged from 9 months to 17 years (median 11 years), and duration of symptoms ranged from 4 months to 8 years (median 1 year). Three patients had symptoms from infancy. Two patients underwent a successful EM as their sole procedure. Two underwent bougienage as their initial therapy. Dysphagia recurred quickly and both required operation. Fifteen underwent PD under intravenous sedation with a Brown-McHardy dilator placed under fluoroscopy. Seven underwent a single dilatation; seven underwent two; and one underwent four. Relief of dysphagia was achieved in 11 patients, but four required surgery. The patients who experienced adequate relief with dilatation alone were clinically identical to those in whom it failed with respect to age, race, sex, symptom duration, and manometric data. Those who required EM following PD experienced only a brief period of relief following PD (median 1 month) compared with those who enjoyed lasting results (median 18 months). Three patients suffered prolonged chest pain or fever following PD, but without esophageal leakage and with full recovery. Two of eight operative patients developed late postoperative reflux. There were no deaths. Both PD and EM are safe and effective treatments for achalasia. Our results indicate that dilatation is the logical first therapeutic step, but rapid recurrence of symptoms may identify those patients who will require operative myotomy.

Pancreatic injuries in childhood due to blunt trauma.

The records of 22 children who suffered pancreatic injury in whom laparotomy confirmed the diagnosis were reviewed. First, we wished to define diagnostic factors that would distinguish transections and injuries that resulted in pseudocysts (which we termed major injuries) from contusions and lacerations that required no specific operation (minor injuries). Second, we wanted to determine how the timing of diagnosis and treatment of major injuries influenced hospital course. There were 13 major injuries (ten transections, three pseudocysts) and nine minor injuries. Abdominal tenderness (present in 83%) failed to distinguish major from minor injuries. Major injuries appeared to be associated with rising values of serum amylase taken serially over 24 to 48 hours (P = .05). Computerized tomography and ultrasound obtained in the first days after injury gave nonspecific findings and failed to give a definitive diagnosis. Of 13 patients with major injuries, seven underwent laparotomy within 24 hours of injury; six, two days or more. The mean hospital stay in the early group (16.7 days) was significantly shorter than that in the late group (38.8 days). Our review suggests that timely diagnosis of major pancreatic injuries and prompt surgical treatment can shorten hospitalization without increasing morbidity. The diagnosis of surgically significant pancreatic injuries continues to be a primary clinical challenge.

Quality assessment in the pediatric trauma care system.

The goal of the pediatric trauma care system is to prevent death, disability, and suffering of injured children. Quality assessment (QA), the evaluation of clinical performance and quality, is essential not only for formal accreditation processes, but also for day-to-day trauma center operation. QA involves three basic types of performance measures: input, process, and outcome. Input measures are inventories of the resources of a given institution, such as the availability of a surgeon on a 24-hour-a-day in-house basis. They give baseline descriptions of facilities and do not monitor performance directly. Process measures attempt to verify that the system is using its resources appropriately in response to demands, which at Children's Hospital of Pittsburgh (CHP), involves tracking all admitted patients from injury to discharge with the assistance of a system of audit screens to help identify problem cases. The methodology of the Major Trauma Outcome Study (MTOS) provides basic outcome data by identifying unexpected survivors and deaths. However, the few cases identified (four of 316 patients submitted to MTOS; 1.3%) limit conclusions regarding trauma center performance. Performance measures, when applied to admitted trauma patients, allow timely recognition of individual complications and problem trends. QA provides necessary data for important clinical decisions and resource allocations that affect trauma center operation.