Minimal head trauma in children revisited: is routine hospitalization required?

OBJECTIVE: Children with a question of occult head injury are routinely hospitalized despite having both normal central nervous system (CNS) and computed tomographic (CT) scan examinations. We determined the incidence of significant CNS morbidity after occult head injury to determine whether or not hospital admission was necessary in children after minimal head trauma. METHODS: We reviewed the records of children admitted to a level I trauma center with a question of closed head injury, an initial Glasgow Coma Scale equal to 15, a normal neurologic exam, and a normal head CT scan. Children with associated injuries requiring admission were excluded. The endpoints were deterioration in CNS exam, new CT findings, and the need for a prolonged hospital stay. RESULTS: Sixty-two patients were studied with a mean age of 7 years (range, 1 month to 15 years), and 65% were male. The primary mechanisms of injury were fall (45%) and vehicular crash (23%). The mean injury severity score was 4 +/- 2. The mean length of stay was 1.2 days (range, 1 to 3 days). Prolonged hospitalization occurred in 9 patients (15%). No child developed significant CNS sequelae warranting hospital admission. Total charges for these hospitalizations were $177 874. CONCLUSIONS: Children undergoing emergency department work-up of occult head injury, who have a normal CNS exam and a normal head CT scan, do not seem to be at risk for significant CNS sequelae. These patients can be discharged home with parental supervision and avoid unnecessary and costly hospitalization.

Differential microvascular response to cyclooxygenase blockade in the rat small intestine during acute bacteremia.

To determine whether arachidonic acid metabolites are mediators of regional blood flow changes during sepsis, we examined the effects of cyclooxygenase blockade on intestinal microvascular diameters and blood flow during acute bacteremia, induced in the rat by the intravenous injection of 10(9) live Escherichia coli. Mean arterial pressure, cardiac output, intestinal microvascular diameters, and blood flow were measured in the presence or absence of a topically applied selective cyclooxygenase inhibitor (mefenamate). Bacteremia caused a diffuse constriction of both arterioles and venules and a concomitant 50% decrease in blood flow. Treatment with mefenamate did not affect baseline intestinal microvascular tone or bacteremia-induced arteriolar constriction and hypoperfusion, but did reverse an intense venular constriction. Our results suggest that the small intestinal microcirculation has a differential response to cyclooxygenase products of arachidonic acid metabolism during acute bacteremia. They appear not to be mediators of the intestinal arteriolar constriction and hypoperfusion observed during acute E. coli bacteremia, but profoundly influence the mesenteric venular constriction. These observations support the concept that microvascular control mechanisms are different not only between but within organ specific vascular beds.

Absorptive hyperemia restores intestinal blood flow during Escherichia coli sepsis in the rat.

Enteral nutritional support has been found to result in better maintenance of mucosal integrity during stress than parenterally administered nutritional support. In our experiments, we employed in vivo microvascular techniques to examine the effect of mucosally applied glucose on intestinal microvascular blood flow during hyperdynamic live Escherichia coli bacteremia in the rat. We observed a significant decrease in intestinal microvascular blood flow during bacteremia when the mucosa was suffused with a nonglucose solution. Blood flow was rapidly restored to above-baseline values after glucose was added. The restoration of blood flow resulted from dilation of arterioles at all branch orders and was associated with dilation of premucosal arterioles to above-baseline diameters. Our results show that glucose-induced absorptive hyperemia restores intestinal blood flow during live E coli bacteremia. Restoration of intestinal microvascular blood flow may be a contributing factor to the improved maintenance of mucosal integrity associated with enteral feeding.

Cystic hygroma in the fetus and newborn.

Cystic hygromas are developmental abnormalities of the lymphoid system that occur at sites of lymphatic-venous connection, most commonly in the posterior neck. They are frequently associated with karyotypic abnormalities, various malformation syndromes, and several teratogenic agents. The disease course of an infant with cystic hygroma is unpredictable. When diagnosed prenatally, the overall prognosis is poor. Cystic hygroma diagnosed after birth is usually associated with a good prognosis. This article reviews the embryologic, genetic, and pathologic correlates of these lymphatic system abnormalities, as well as the clinical course and outcome of the fetus and newborn with a cystic hygroma. Management strategies are reviewed, including newer nonsurgical therapies for the neonate with a cystic hygroma.

Colonoscopic decompression for pseudo-obstruction of the colon.

The purpose of this report was to review the authors' experience with colonoscopy as a method of treating patients with acute colonic distention. For the period 1981-1987, 19 patients at two teaching hospitals met the selection criteria for this study. In terms of measurable decompression of a colon distention, colonoscopy was successful in 89 per cent of patients, although 41 per cent required repeat endoscopic decompression during their hospital stay. The procedure failed in two patients (11%) and operative decompression was necessary. The authors have found that colonoscopy is a useful procedure for determining the cause of progressive colon distention and for providing safe and effective treatment.

Oxygen-induced vasodilation is blunted in pulmonary arterioles from fetal rats with nitrofen-induced congenital diaphragmatic hernia.

BACKGROUND/PURPOSE: Persistent pulmonary hypertension contributes to the high mortality rate associated with congenital diaphragmatic hernia (CDH). Oxygen is an important stimulus for pulmonary vasodilation in the perinatal period. The authors have investigated the responses of isolated pulmonary arterioles from fetal rats with and without CDH to an increase in oxygen tension. METHODS: CDHs were induced in fetal rats by feeding nitrofen to timed-pregnant rats at midgestation. A third-generation pulmonary arteriole was isolated from the right lung at term. Isolated arterioles were pressurized at their "optimal distending pressure." Diameter changes in response to an increase in oxygen tension from 25 to 40 mm Hg ("hypoxic" conditions) to 90 to 150 mm Hg ("normoxic" conditions) were recorded for K(+) preconstricted arterioles from control rats, from rats with nitrofen-induced CDH, and from rats that were nitrofen exposed but did not have a CDH. RESULTS: "Normoxic" exposure reversed the K(+) preconstriction in control arterioles by 124 +/- 26%. In contrast, arterioles from rats with nitrofen-induced CDH dilated significantly less than controls (20 +/- 15% of the K(+) preconstriction). The responses of arterioles from rats that were nitrofen exposed but did not get a CDH were not different (P >.05) from controls. CONCLUSIONS: Oxygen-induced vasodilation is blunted in pulmonary arterioles from rats with nitrofen-induced CDH. Blunted oxygen-induced vasodilation may contribute to persistent pulmonary hypertension in CDH. J Pediatr Surg 36:593-597.

Pulmonary arterioles from rats with congenital diaphragmatic hernias are hypoplastic but not hyperresponsive.

BACKGROUND: Infants born with congenital diaphragmatic hernias (CDH) frequently die as a result of pulmonary hypertension and persistent fetal circulation. The pulmonary vessels of infants with CDH have decreased total cross-sectional area, increased muscle content, and muscularization of intra-acinar arterioles that are normally not muscularized. These structural alterations are believed to result in exaggerated responses to normal vasoconstrictor stimuli. METHODS: The authors used the nitrofen-induced CDH model in rats to determine whether the vasoconstrictor responses of pulmonary arterioles are exaggerated in this animal model of CDH. The authors compared the responses of isolated third-generation pulmonary arterioles from normal rats and from rats with nitrofen-induced CDH to K+-induced depolarization, phenylephrine, angiotensin II, serotonin, and the thromboxane A2 agonist, U46619. RESULTS: It was found that the intraluminal diameter of third-generation pulmonary arterioles from CDH rats was significantly less than in controls (129 +/- 5 micron v 152 +/- 9 micron, respectively). In addition, the ratio of wall thickness to vessel internal diameter was increased in the third-generation pulmonary arterioles of rats with nitrofen-induced CDH (0.62 +/- 0.4 v 0.50 +/- 0.5 for controls). Responses to K+-induced depolarization, phenylephrine, angiotensin II, serotonin, and U46619, however, were not different for pulmonary arterioles from control and CDH rats. CONCLUSION: These data suggest that the structural alterations of the pulmonary vasculature observed in infants with CDH may not cause exaggerated vasoconstrictor responses to normal vasoconstrictor stimuli.

Hypoxic pulmonary vasoconstriction is impaired in rats with nitrofen-induced congenital diaphragmatic hernia.

BACKGROUND: Pulmonary hypertension and persistent fetal circulation contribute to the high mortality rate associated with congenital diaphragmatic hernia (CDH). Morphological alterations of the pulmonary vasculature in infants with CDH are thought to contribute to exaggerated vasoconstrictor responses to normal vasoconstrictor stimuli. In the pulmonary circulation, hypoxia is a potent vasoconstrictor. Under pathological conditions, hypoxia-induced vasoconstriction may contribute to the development of pulmonary hypertension. METHODS: The authors have used the nitrofen-induced model of congenital diaphragmatic hernia in rats to investigate the magnitude of the hypoxic vasoconstrictor response. Congenital diaphragmatic hernias were induced in fetal rats by feeding nitrofen (2,4-dichlorophenyl-p-nitrophenyl ether) to pregnant Sprague-Dawley rats at midgestation. Hypoxia-induced vasoconstriction was measured in isolated, perfused third-generation pulmonary arterioles from normal rats and from rats with nitrofen-induced CDH. RESULTS: The hypoxic vasoconstrictor response was significantly blunted in the pulmonary arterioles of fetal rats with nitrofen-induced (2% +/- 1% vasoconstriction), as compared with the responses observed in normal fetal rats (15% +/- 3% vasoconstriction, P = .004). CONCLUSION: Blunting of the hypoxic pulmonary vasoconstrictor response may contribute to ventilation-perfusion mismatching in infants with CDH.

Oxygen dilation in fetal pulmonary arterioles: role of K(+) channels.

BACKGROUND: Oxygen is a potent stimulus for pulmonary vasodilation. Potassium channels have been implicated as both sensors and effectors for oxygen-induced changes in pulmonary vascular tone. We have examined the effect of potassium channel blockers on oxygen-induced vasodilation in isolated pulmonary arterioles from fetal rats at term. MATERIALS AND METHODS: Third generation pulmonary arterioles were isolated from fetal rats on Day 22 of gestation, cannulated, pressurized at constant distending pressures, and preconstricted by suffusion with a salt solution bubbled with a "hypoxic gas" mixture (pO(2)

Prostaglandins mediate the compensatory responses to hemorrhage in the small intestine of the rat.

We examined the effect of fixed-volume hemorrhage (10 ml/kg) on microvascular diameters and blood flow in the small intestine of the rat using in vivo videomicroscopic techniques. We found that hemorrhage in the absence of a potent cyclooxygenase inhibitor results in a transient decrease in intestinal blood flow and a preferential redistribution of intramural blood flow toward the mucosa because of a localized vasodilator response of the premucosal microvessels. In the presence of the selective cyclooxygenase inhibitor, mefenamic acid, the decrease in intestinal blood flow was more substantial and prolonged, and the localized vasodilator response of the premucosal microvasculature was abolished. Our results suggest that vasodilator prostaglandins contribute to the compensatory response of the intestine to hemorrhage and are responsible for the shunting of blood toward the mucosa during hemorrhagic hypotension.

Intestinal blood flow is restored with glutamine or glucose suffusion after hemorrhage.

Intestinal blood flow has been shown to be impaired after resuscitated hemorrhagic shock. Enteral feeding has been proposed as an adjunct for preserving mucosal integrity and decreasing translocation-related morbidities during stress. The purpose of this study was to determine if an ileal mucosal suffusion with an isotonic glucose or glutamine solution begun after resuscitation would prevent development of this blood flow impairment. The distal ileum of anesthetized Sprague-Dawley rats was prepared for in vivo videomicroscopy. Animals were bled to 50% of baseline blood pressure for 60 min and then resuscitated with their shed blood and an equal volume of lactated Ringer's. After resuscitation was complete, the mucosa was suffused with isotonic glucose, glutamine, or saline (control). Resuscitation restored cardiac output and mean arterial pressure to baseline in all groups; however, first-order arteriolar blood flow remained 50% below baseline in the saline group. Glucose-treated animals demonstrated a 34% increase over baseline in first-order arteriolar blood flow 120 min after resuscitation due to submucosal and previllus arteriolar dilation. This effect became evident 30 min after initiating the suffusion, suggesting an effect mediated via locally generated vasodilators. Glutamine suffusion attenuated the flow impairment by dilation of previllus arterioles but to a lesser degree than that observed in glucose-treated animals. These data demonstrate that mucosal suffusion with an isotonic glucose solution overrides the residual effects of hemorrhagic shock on the intestinal microcirculation and suggest a mechanism for preserving mucosal integrity with the addition of glutamine to standard enteral formulations.

Age-related differences in intestinal arteriolar responses to venous pressure elevation in the rat.

OBJECTIVE: We previously reported differences in intestinal arteriolar responses of adult and suckling rats to three stressors (hemorrhage, hypoxia, and hypothermia) that decreased intestinal blood flow. The small, premucosal arterioles of adult rats dilated in response to all three stressors, whereas the premucosal arterioles of suckling rats constricted or remained unchanged. One explanation for this difference might be absence of myogenic responsiveness in the premucosal arterioles of the immature rat. METHODS: We used in vitro videomicroscopy to observe the intestinal arteriolar responses to venous pressure elevation (a myogenic stimulus) in adult (8- to 12-week-old) and suckling (8- to 12-day-old) Sprague-Dawley rats. We increased portal venous pressure by 25 and 50% above the baseline pressure. RESULTS: Arterioles in the rats displayed the expected "myogenic" response to venous pressure elevation (diameters decreased 12-29% when venous pressure was increased by 50%). In contrast to adult rats, arterioles in the suckling rats failed to constrict in response to increases in venous pressure (diameters increased 14-21% in response to a 50% increase in venous pressure). CONCLUSIONS: These results suggest that the myogenic constrictor mechanisms for control of the microcirculation appear to be either nonfunctional or suppressed in the intestinal microcirculation of suckling rats.

Identification of a duplicated undescended testicle (polyorchia): an unexpected benefit of laparoscopic localization.

Polyorchidism is an uncommon anomaly resulting from transverse division of the embryonic genital ridge. Up to 50 percent of cases are associated with cryptorchidism. The present case describes a 6-year-old boy who was referred for evaluation of an undescended right testicle. Examination revealed compensatory hypertrophy of the left testis (2 cm length; 2 cc volume; volume twice normal for age). These measurements were consistent with the presence of monorchidism rather than cryptorchidism. Laparoscopy was performed to confirm the absence of the nonpalpable testicle and to localize any testicular remnants. Laparoscopic findings included a hypoplastic testicle at the mid lumbar it level (abdominal testis) and a second hypoplastic testicle just distal to the internal inguinal ring (inguinal testis). Both measured no more than 1 cm in greatest diameter and were excised laparoscopically. Histologic examination revealed two immature tests, with the abdominal testis demonstrating atrophy. It is well recognized that laparoscopy the high undescended testicle, or identification of testicular remnants. In addition, nonpalpable testicle assists in localization of the undescended testicle or identification of the testicular remnants. In addition,laparoscopic high ligation and division of the gonadal vessels can be performed in cases of the high undescended testicle. Moreover, as demonstrated here, laparoscopy may also allow identification of polyorchia, especially in cases where the proximal testicle is intraabdominal. Inguinal exploration alone may result in failure to recognize a higher duplicated gonad. Failure to recognize and excise the duplicated, potentially dysplastic testicle may place the child at risk for subsequent malignant degeneration.

Endothelin-1 pulmonary vasoconstriction in rats with diaphragmatic hernia.

BACKGROUND: Pulmonary hypertension is an important cause of mortality in infants with congenital diaphragmatic hernia (CDH). Endothelin-1 has been implicated as a mediator of pulmonary hypertension. ET-A receptors are increased in the nitrofen model of CDH in rats. We hypothesized that vasoconstrictor responses to endothelin-1 are increased in pulmonary arterioles of rats with nitrofen-induced CDH. MATERIALS AND METHODS: CDH was induced in fetal rats by feeding nitrofen (2,4-dichlorophenyl-p-nitrophenyl ether) to pregnant rats at midgestation. Third-generation pulmonary arterioles were isolated on the final day of gestation. Arterioles were cannulated and perfused at constant pressure with a physiologic salt solution. Diameters of arterioles from control animals (n = 8), CDH animals (n = 5), and animals exposed to nitrofen but without CDH (n = 4) were measured. Responses to endothelin-1 concentrations of 10(-12) to 10(-8) M were compared by Student's t test. RESULTS: CDH arterioles constricted more than controls in response to endothelin-1 at concentrations of 10(-11) M (29 +/- 11% vs 5 +/- 3%, P = 0.02) and 10(-10) M (40 +/- 14% vs 9 +/- 6%, P = 0.04). The log concentration of endothelin-1 that induced half-maximal response (ED50) was lower for CDH arterioles than for control arterioles (-10.3 +/- 0.6 vs -9.1 +/- 0.2, P = 0.03). Responses of arterioles from animals exposed to nitrofen but without CDH were not different from controls (P > or = 0.05). CONCLUSIONS: Exaggerated vasoconstrictor responses to endothelin-1 may contribute to pulmonary hypertension in CDH.

Age-related differences in intestinal microvascular responses to low-flow states in adult and suckling rats.

We used in vivo videomicroscopic techniques to compare the intestinal microvascular responses of 8- to 12-wk-old adult rats with those observed in 8- to 12-day-old suckling rats. Changes in intestinal microarteriolar diameters and blood flow were measured during hemorrhage (5 and 10 ml/kg), hypoxia (10% O2 breathing environment), and hypothermia (surface cooling to 34 degrees C and 31 degrees C). Intestinal blood flow (as measured by optical Doppler velocimetry) was decreased by a similar amount in both adult and suckling rats during all three periods of stress. Large arteriolar diameter changes were also similar in adult and suckling rats. In contrast, there were substantial differences in the responses of the small premucosal arterioles. These premucosal arterioles selectively dilated in adult rats, suggesting a redistribution of blood flow toward the mucosa during each of the three periods of stress. These same microvessels failed to dilate in the suckling rats during each of the three periods of stress, suggesting that the intestinal microvasculature in the immature rat lacks vasodilator mechanisms that are active in the adult rat. We propose that altered microvascular control could make the developing intestine prone to mucosal damage during periods of decreased perfusion.

Oxygen-induced vasodilation in pulmonary arterioles from fetal rats.

BACKGROUND: Oxygen is a potent stimulus for pulmonary vasodilation in the perinatal period. Little information is available regarding mediators of oxygen-induced pulmonary vasodilation in fetal rats. We have investigated the effect of blocking several proposed mediators of oxygen-induced vasodilation on the responses of isolated, third-generation pulmonary arterioles from term fetal rats to an increase in oxygen tension. MATERIALS AND METHODS: Third-generation pulmonary arterioles were isolated from fetal rats at term. Arterioles were preconstricted by suffusion with "hypoxic" (pO(2) 25-40 mm Hg) solution containing 40 mM KCl. The vasodilation induced by suffusion with "normoxic" (pO(2) 90-150 mm Hg) 40 mM KCl solution was recorded for control pulmonary arterioles and for arterioles pretreated with inhibitors of nitric oxide synthase and cyclooxygenase, and blockers of bradykinin receptors and purinergic receptors. Responses to oxygen suffusion were also recorded for pulmonary arterioles denuded of endothelium. RESULTS: Control arterioles dilated 113 +/- 28% of the potassium-induced preconstriction after 60 min of normoxic suffusion. Pretreatment with indomethacin completely blocked oxygen-induced vasodilation. Inhibitors of nitric oxide synthase, blockers of bradykinin and purinergic receptors, and removal of the endothelium did not significantly change normoxic vasodilation. CONCLUSIONS: Our results are most consistent with a vasodilator product of cyclooxygenase metabolism as a primary stimulus for oxygen-induced vasodilation in isolated, third-generation pulmonary arterioles from fetal rats.

Molecular analysis of the adaptive response of intestinal bile acid transport after ileal resection in the rat.

BACKGROUND & AIMS: The apical sodium-dependent bile acid transporter is critical for intestinal reclamation of bile salts. Its expression and activity, along with the ileal lipid-binding protein, were studied before and after intestinal resection in the rat. METHODS: The effects of surgical resection and bile acid feeding on the expression of ileal bile acid transport were assessed by a combination of functional (taurocholate uptake into crude brush border membrane vesicles) and molecular assays (Northern and Western blotting). RESULTS: Transport, apical sodium-dependent bile acid transporter and ileal lipid-binding protein messenger RNA and protein expression were restricted to the distal 30 cm of ileum. After resection, transport and expression were limited to the remaining portions of this segment. Limited ileal resection increased protein mass and, therefore, transport in the terminal 5 cm of ileum without a specific increase in transporter gene expression. Increased bile acid presentation to the terminal ileum did not induce ileal hyperplasia. Eighty-five percent intestinal resection led to ileal hypertrophy and a specific repression in bile acid transport activity. CONCLUSIONS: Native and compensatory bile acid transporter gene expression occur predominantly in the terminal 30 cm of ileum. The specific ileal responses to intestinal resection are dependent on the extent of resection.

Percutaneous needle aspiration of small interloop abscesses in children.

Treatment of small postoperative interloop abscesses (ILA) can be challenging. In children, these collections have usually been drained surgically at a second operation. This article describes three children with small postoperative ILAs who were treated by percutaneous needle aspiration and parenteral antibiotics, with good outcomes. The advantages of this technique and its utilization in the management of children with ILAs are discussed.