Pulmonary edema associated with child abuse: case reports and review of the literature.

Pulmonary edema has been an unreported finding in the evaluation of abused children. We describe 2 cases of pulmonary edema in abused infants, 1 after confessed suffocation and the other after inflicted head injury. A review of the literature regarding postobstructive and neurogenic pulmonary edema suggests useful inferences for the forensic evaluation of maltreated children who present with this finding.

Age-related differences in acute physiologic response to focal traumatic brain injury in piglets.

INTRODUCTION: The goal of the present study was to determine whether age-related differences in the acute physiologic response to scaled cortical impact injury contribute to differences in vulnerability to traumatic brain injury (TBI). METHODS: Heart rate (HR), mean arterial pressure (MAP), brain temperature (BrT) and cerebral blood flow (CBF) were measured in 22 piglets (7 of age 5 days, 8 of age 1 month, 7 of age 4 months) at baseline and for 3 h following scaled cortical impact injury. RESULTS: There were no age-dependent variations from baseline in HR, MAP or BrT following injury. CBF increased in the 5-day-old animals following injury while CBF in the 1- and 4-month-old animals decreased following injury (p = 0.0049). CONCLUSION: CBF was shown to have a significant age-dependent response to TBI with the youngest animals exhibiting increased CBF following injury.

Early hyperthermia after traumatic brain injury in children: risk factors, influence on length of stay, and effect on short-term neurologic status.

OBJECTIVES: a) To determine the risk factors for early hyperthermia after traumatic brain injury in children; b) to identify the contribution of early hyperthermia to neurologic status at pediatric intensive care unit (PICU) discharge and to PICU length of stay in head-injured children. STUDY DESIGN: Observational cohort study. SETTING: PICU at a tertiary care, university medical center. PATIENTS: Children (n = 117) admitted to a PICU from July 1995 to May 1997 with traumatic brain injury. These children had a median age of 5.4 yrs (3 wks to 15.2 yrs old), and 33.4% were girls. MEASUREMENTS AND MAIN RESULTS: Early hyperthermia (temperature >38.5 degrees C within the first 24 hrs of admission) occurred in 29.9% of patients admitted to the PICU with traumatic brain injury. Risk factors predicting early hyperthermia included Glasgow Coma Scale score in the emergency department < or =8, pediatric trauma score < or =8, cerebral edema or diffuse axonal injury on initial head computed tomography scan, admission blood glucose >150 mg/dL (8.2 mmol/L), admission white cell count >14,300 cells/mm3 (14.3 x 10(9) cells/L), and systolic hypotension. The presence of early hyperthermia significantly increased the risk for Glasgow Coma Scale score <13 at PICU discharge (odds ratio [OR] 9.7, 95% confidence interval [CI] 2.8, 24.4) and PICU stay > or =3 days (OR 13.8, CI 5.1, 37.5). When we used multiple logistic regression models including injury severity and hypotension, early hyperthermia remained an independent predictor of lower Glasgow Coma Scale score at PICU discharge (OR 4.7, CI 1.4, 15.6) and longer PICU length of stay (OR 8.5, CI 2.8, 25.6). CONCLUSIONS: Early hyperthermia is independently associated with a measure of early neurologic status and resource utilization in children with traumatic brain injury serious enough to require PICU admission. These results support the prevention of hyperthermia in the management of traumatic brain injury in children. Further research is required to understand the mechanisms of this response and to identify appropriate preventive or therapeutic interventions.

Pediatric airway issues.

Airway management in the pediatric patient requires an understanding and knowledge of the differences and characteristics unique to the child and infant. New and exciting techniques are currently being explored and developed for management of the pediatric airway. Technology in the area of imaging has allowed clinicians to better visualize the airway and aberrations of it. Presently, there are many different modes and routes of ventilation and oxygenation that are being applied to the pediatric patient for different disease states. Work continues to probe for methods and ways that will allow us to take care of infants and children better and to provide the safest and most effective means of delivering that care. No doubt, there will be more advances and exciting ideas to come that lead to better management of the pediatric airway.

Alterations in ionized and total blood magnesium after experimental traumatic brain injury: relationship to neurobehavioral outcome and neuroprotective efficacy of magnesium chloride.

Experimental evidence suggests that magnesium plays a role in the pathophysiological sequelae of brain injury. The present study examined the variation of blood ionized and total magnesium, as well as potassium, sodium, and ionized calcium, after experimental fluid percussion brain injury in rats. Blood ionized magnesium concentration significantly declined from 0.45 +/- 0.02 to 0.32 +/- 0.02 mM by 30 min postinjury and stayed depressed for the 24-h study period in vehicle-treated rats. Blood total magnesium concentration was 0.59 +/- 0.01 mM and remained stable over time in brain-injured vehicle-treated animals. When magnesium chloride (125 micromol/rat) was administered 1 h postinjury, ionized magnesium levels were restored by 2 h postinjury and remained at normal values up to 24 h following brain trauma. Magnesium treatment also significantly reduced posttraumatic neuromotor impairments 1 and 2 weeks after the insult, but failed to attenuate spatial learning deficits. A significant positive and linear correlation could be established between ionized magnesium levels measured 24 h postinjury and neuromotor outcome at 1 and 2 weeks. We conclude that acute ionized magnesium measurement may be a predictor of long-term neurobehavioral outcome following head injury and that delayed administration of magnesium chloride can restore blood magnesium concentration and attenuate neurological motor deficits in brain-injured rats.

Recurrent seizures in a neonate after lidocaine administration.

OBJECTIVE: We report recurrent seizures in a neonate after intravenous lidocaine administration at the recommended dose for intubation and supplementation of general anesthesia. STUDY DESIGN: Further evaluation of this case included determination of serum lidocaine level, serum electrolyte levels, and arterial blood gas values; cerebral spinal fluid analysis; an electroencephalogram; head ultrasonography; brain stem auditory evoked response testing; and a complete developmental evaluation. Previously published literature discussing lidocaine toxicity and pharmacokinetics is reviewed. RESULTS: The lidocaine level in the patient was 0.3 mg/L 2 hours after the last dose was administered. Results of the remaining studies were within normal limits, and the patient had no additional seizures several months after birth. CONCLUSION: We caution that lidocaine administration to newborn infants at previously accepted doses may result in life-threatening side effects, including prolonged seizures.

Increased hematocrit and decreased transfusion requirements in children given erythropoietin before undergoing craniofacial surgery.

OBJECT: This study was undertaken to determine the efficacy of preoperative erythropoietin administration in infants scheduled for craniofacial surgery and, in so doing, to minimize problems associated with blood transfusions. METHODS: Families were offered the option of having their children receive erythropoietin injections before undergoing craniofacial surgery. The children whose families accepted this option received daily iron and 300 U/kg erythropoietin three times per week for 3 weeks preoperatively. Weekly complete blood counts with reticulocyte counts were measured and transfusion requirements were noted. Blood transfusions were administered depending on the clinical condition of the child. A case-matched control population was also evaluated to compare initial hematocrit levels and transfusion requirements. Thirty patients in the erythropoietin treatment group and 30 control patients were evaluated. The dose of erythropoietin administered was shown to increase hematocrit levels from 35.4 +/- 0.9% to 43.3 +/- 0.9% during the course of therapy. The resulting hematocrit levels in patients treated with erythropoietin at the time of surgery were higher compared with baseline hematocrit levels obtained in control patients at the time of surgery (34.2 +/- 0.5%). Transfusion requirements also differed: all control patients received transfusions, whereas 64% (19 of 30) of erythropoietin-treated patients received transfusions. CONCLUSIONS: The authors conclude that treatment with erythropoietin in otherwise healthy young children will increase hematocrit levels and modify transfusion requirements. Erythropoietin therapy for elective surgery in children of this age must be individualized according to the clinical situation, family and physician beliefs, and cost effectiveness, as evaluated at the individual center.

Treatment with the competitive NMDA antagonist GPI 3000 does not improve outcome after cardiac arrest in dogs.

BACKGROUND AND PURPOSE: We previously showed that treatment with a competitive N-methyl-D-aspartate (NMDA) receptor antagonist GPI-3000 (GPI) improved short-term physiological recovery after incomplete global cerebral ischemia complicated by dense acidosis. We tested the hypothesis that GPI administered after resuscitation from cardiac arrest would improve a more long-term recovery as measured by neurobehavioral assessment and neuropathology 4 days after resuscitation. METHODS: Anesthetized dogs were subjected to 7 minutes of cardiac arrest followed by vest cardiopulmonary resuscitation. Neurobehavioral outcomes were scored daily on a score ranging from 0 (normal) to 500 (worst). On the fourth day, the animals were killed, and neuropathology was evaluated in a blinded manner in the hippocampus and the neocortex by hematoxylin and eosin staining and by determination of percentage of injured neurons. Three groups of animals were treated in a randomized, blinded protocol with either saline (SAL), low-dose GPI (5 mg/kg followed by 1 mg/kg per hour for 2 hours), or high-dose GPI (25 mg/kg, followed by 5 mg/kg per hour for 2 hours). RESULTS: The mortality rate was higher in animals receiving GPI than in saline-treated control animals (4 of 15 deaths in SAL, 6 of 15 in the low-dose GPI group, and 9 of 18 in the high-dose GPI group). Neurobehavioral scores were depressed in GPI-treated animals compared with saline-treated control animals in a dose-dependent manner, with 96-hour scores of essentially normal (9+/-2) in saline-treated animals compared with those animals with significant impairment (181+/-47) treated with high-dose GPI. Neuropathological damage in the neocortex was most severe in GPI-treated animals, with the percentage of injured neurons dependent on the dose: 8.3%+/-2.7% SAL, 13.2%+/-6.4% low-dose GPI, and 39.4%+/-10.1%, high-dose GPI. CA1 neuronal damage was severe regardless of treatment. CONCLUSIONS: Contrary to results seen in experimental global and focal cerebral ischemia, in which NMDA receptor antagonism may improve responses to injury, receptor antagonism with GPI does not improve brain outcome after cardiac arrest and resuscitation in the dog. Behavioral and histological outcomes both were worsened by GPI treatment at two doses, and mortality was higher relative to saline control treatment. We speculate that systemic drug effects, as well as potential neurotoxicity of the drug under ischemic conditions, may be responsible for the deleterious outcomes observed in our cardiac arrest model.

Permissive hypercapnia with high-frequency oscillatory ventilation and one-lung isolation for intraoperative management of lung resection in a patient with multiple bronchopleural fistulae.

We report the use of high-frequency oscillatory ventilation in the operating room during repair of multiple bronchopleural fistulae in a 9-year-old boy. In addition, we used principles of permissive hypercapnia to further minimize barotrauma. There were no cardiovascular consequences due to either the high-frequency ventilation or the permissive hypercapnia. Our goals in employing this strategy were to minimize barotrauma, minimize gas flow through the fistulae, and optimize the surgical results.

Parallel antioxidant and antiexcitotoxic therapy improves outcome after incomplete global cerebral ischemia in dogs.

BACKGROUND AND PURPOSE: We have previously shown that incomplete global cerebral ischemia complicated by dense acidosis produces a profound secondary deterioration of energy metabolism and cerebral blood flow. Antioxidant treatment only partially averts this deterioration, suggesting that parallel or sequential mechanisms are involved in cerebral ischemic injury. We tested the hypothesis that a novel competitive N-methyl-D-aspartate (NMDA) receptor antagonist GPI 3000 (GPI) ameliorates metabolic injury and that the effectiveness of the iron-chelator and antioxidant deferoxamine (DFO) is augmented by combined therapy with GPI after incomplete global cerebral ischemia. METHODS: Anesthetized dogs were treated with 30 minutes of global incomplete cerebral ischemia. Preischemic plasma glucose was raised to approximately 500 mg/dL to exaggerate lactic acidosis. Brain ATP, phosphocreatine, and pH were measured by 31P MR spectroscopy for 180 minutes of reperfusion. Neurophysiological outcomes were assessed by evoked potential monitoring. Five groups were treated with either saline; 75 mg/kg DFO preischemia plus 75 mg/kg at reperfusion onset, followed by 27.5 mg/kg per hour for the remainder of reperfusion (DFO group); 25 mg/kg GPI pretreatment, followed by 5 mg/kg per hour (GPI-pre group); 25 mg/kg GPI at reperfusion, followed by 5 mg/kg per hour (GPI-post group); or DFO and GPI-pre at the same doses (Combined group). RESULTS: Ischemic cerebral blood flow (microspheres: 5 to 8 mL/min per 100 g) was similar among the groups. End-ischemic pHi was also similar; 5.9 in saline, 6.1 in DFO, 6.2 in GPI-pre, 6.2 in Combined, and 6.1 in GPI-post groups. Progressive hypoperfusion was observed in all groups except Combined during reperfusion. Metabolic recovery was improved relative to saline in all drug-treated groups. Phosphocreatine recovery was improved in Combined compared with DFO and GPI-pre groups. Somatosensory evoked potential recovery was not observed in the saline group and incomplete in all treatment groups. At 60 and 90 minutes of reperfusion, DFO, GPI-pre, and Combined groups demonstrated improved recovery relative to the saline group. CONCLUSIONS: Pretreatment and posttreatment with GPI ameliorated postischemic metabolic failure, suggesting that NMDA-mediated mechanisms are more important in global cerebral ischemia complicated by dense, acidosis than early studies indicated. Combined treatment with GPI and DFO improved cerebral blood flow during reperfusion and one indicator of energy recovery. These data support the hypothesis that parallel therapy aimed at antioxidant and antiexcitotoxic mechanisms of ischemic brain injury augment recovery compared with the individual agents.

Polysomnography after adenotonsillectomy in mild pediatric obstructive sleep apnea.

OBJECTIVES: a) To determine the need for intensive monitoring on the first operative night of surgery in children undergoing adenotonsillectomy for mild obstructive sleep apnea; b) to examine the effect of narcotics on postoperative obstructive sleep apnea. DESIGN: Randomized, prospective study. SETTING: University hospital. PATIENTS: Children, ranging in age between 1 and 18 yrs, presented to the Pediatric Otolaryngology Clinic for adenotonsillectomy for mild obstructive sleep apnea defined as from one to 15 obstructive apnea events per hour on preoperative polysomnogram. INTERVENTIONS: Patients were assigned to receive either a narcotic- or a halothane-based anesthetic for adenotonsillectomy. A postoperative polysomnogram was performed in the pediatric intensive care unit on the first operative night. MEASUREMENTS AND MAIN RESULTS: Eighteen patients were recruited, 15 of whom met inclusion criteria: nine patients received a halothane-based anesthetic and six patients received a fentanyl-based anesthetic. When the data were analyzed by pooling both groups, the differences between pre- and postoperative sleep studies demonstrated a reduction in the number of obstructive events and less severe oxygen desaturations on the operative night. Total sleep time between the two sleep studies decreased from 371 +/- 13 to 304 +/- 14 mins. The number of obstructive apnea events/hr decreased as well. The lowest oxygen saturation measured during rapid eye movement sleep was 78 +/- 5% preoperatively and 92 +/- 1% postoperatively. CONCLUSIONS: Our data suggest that children without underlying medical conditions, neuromotor diseases, or carniofacial abnormalities, 1 to 18 yrs of age, who suffer from mild obstructive sleep apnea, have improvements documented by polysomnography on the night of surgery following adenotonsillectomy and do not necessarily need to be monitored intensively. These findings were not significantly affected by the choice of intraoperative anesthetic.

Effect of nitric oxide synthase inhibition on postischemic cerebral hyperemia.

We tested the hypothesis that inhibition of nitric oxide synthase (NOS) activity in brain before ischemia decreases postischemic hyperemia. Pentobarbital-anesthetized piglets underwent 15 min of complete global cerebral ischemia induced by elevation of intracranial pressure followed by 20 min of reperfusion. Before ischemia the animals were randomly assigned to receive either intravenous N omega-nitro-L-arginine methyl ester (L-NAME 10 mg/kg, n = 6, or 50 mg/kg, n = 6) or an equal volume of saline (10 ml, n = 8). Serial cerebral blood flow (radiolabeled microspheres) was measured at baseline and during ischemia and reperfusion. Forebrain postischemic hyperemia was documented after administration of saline (42 +/- 4 to 88 +/- 10 ml.min-1.100 g-1) and 10 mg/kg L-NAME (36 +/- 4 to 59 +/- 9 ml.min-1.100 g-1) but not after 50 mg/kg L-NAME (29 +/- 3 to 34 +/- 7 ml.min-1.100 g-1). However, the percent reduction in cerebral vascular resistance (CVR) fell during reperfusion to a similar extent in all three groups because of differences between groups in cerebral perfusion pressure changes during the protocol. CVR fell to the lowest level at 8 min of reperfusion in the saline-treated animals (2.0 +/- 0.16 to 0.68 +/- 0.05 mmHg.ml-1.min.100 g) compared with the L-NAME-treated animals (50 mg/kg: 4.0 +/- 0.3 to 1.8 +/- 0.2 mmHg.ml-1.min.100 g).(ABSTRACT TRUNCATED AT 250 WORDS)

Nitro-L-arginine analogues. Dose- and time-related nitric oxide synthase inhibition in brain.

BACKGROUND AND PURPOSE: The purpose of the present study was to measure cortical nitric oxide synthase (NOS) activity and determine the appropriate doses of N omega-nitro-L-arginine methyl ester (L-NAME) or N omega-nitro-L-arginine (L-NNA) for near-complete enzyme inhibition in dogs, cats, and pigs. We anticipated that NOS inhibition was dose- and time-dependent and questioned if the dose-response relationship was related to the specific drug or animal species. METHODS: Saline or L-NAME or L-NNA in escalating doses was administered to pentobarbital-anesthetized pigs, dogs, and cats. Brain temperature and arterial blood gas, hemoglobin, and blood pressure levels were maintained within the physiological range. Cortical tissue was biopsied at baseline and 30, 120, and 360 minutes after agent administration for measurement of NOS activity by isotopic assay of the conversion of [14C]arginine to [14C]citrulline. RESULTS: L-NAME produced > 70% enzyme inhibition at a dose of 20 mg/kg across the species tested. Arterial blood pressure was elevated at 30 minutes after L-NAME treatment. However, consistent decreases in brain NOS activity required a longer period of time. Near-complete inhibition was apparent in most animals by 120 minutes and persisted for 6 hours after administration. A smaller dose of L-NNA was required for > 70% enzyme inhibition in the cats and dogs (10 mg/kg). Near-complete NOS inhibition was evident in most animals at 30 minutes after L-NNA administration, which also persisted for 6 hours. In pigs, this same level of inhibition required 20 mg/kg. CONCLUSIONS: These results suggest that administration of L-NAME and L-NNA diminishes brain NOS activity in a dose- and time-dependent manner and that the duration of effect is at least 6 hours.

Dihydropyridine ligand binding decreases earlier in adolescent than in infant swine after global cerebral ischemia.

BACKGROUND AND PURPOSE: Voltage-dependent calcium channels (VDCCs) are thought to play a major role in the alteration of calcium homeostasis during ischemia. Tissue functional state as well as responsiveness to therapy with calcium channel blockers may be a function of regional changes in the density of VDCCs. This study determined whether VDCCs are altered by global ischemia in infant and adolescent swine. METHODS: We employed the radioligand 3HPN200-110 to quantify the binding characteristics of VDCCs in cerebral cortex, caudate, and hippocampus by equilibrium binding analysis. Adolescent and infant pigs underwent 3, 5, 10, and 20 minutes of global cerebral ischemia without reperfusion by ligation of the brachiocephalic and left subclavian arteries combined with hypotension to a mean arterial blood pressure of 50 mm Hg. Brain cortex, hippocampus, and caudate samples were taken during ischemia and frozen immediately in liquid nitrogen, and crude synaptosomal membranes were isolated by differential centrifugation/filtration. 3HPN200-110 equilibrium binding assays were performed in the presence or absence of 1.0 mumol/L unlabeled nitrendipine to determine total and nonspecific binding. RESULTS: Infant cortex maximal binding (Bmax) increased to 176% of control after 5 minutes of global cerebral ischemia and remained significantly elevated (172% of control) after 10 minutes before falling to near control levels by 20 minutes. Adolescent cortex Bmax increased to 157% of control levels after 5 minutes but did not remain elevated, falling to 131% of control by 10 minutes and near control by 20 minutes. Infant caudate and hippocampus binding were significantly elevated after 10 (124% and 149% of control, respectively) and 20 (115% and 120% of control, respectively) minutes of ischemia. Adolescent caudate and hippocampus binding was either not significantly different from control levels (hippocampus at 10 minutes) or less than control after 10 and 20 minutes of global cerebral ischemia. The decrease in binding following the initial upregulation, which appeared earlier in the adolescent than the infant pigs, may indicate decreased tolerance to ischemia in the adolescent. CONCLUSIONS: The binding of 3HPN200-110 in brain is altered during 20 minutes of global cerebral ischemia, and these changes are region- and age-dependent.

Nitric oxide and prostanoids contribute to isoflurane-induced cerebral hyperemia in pigs.

BACKGROUND: The mechanism of isoflurane-induced cerebral hyperemia is poorly understood. Data from studies in vitro suggest that volatile anesthetics release a vasodilator prostanoid. We hypothesized that prostanoids and nitric oxide (NO) are mediators of this response in vivo. If true, inhibition of cyclooxygenase by indomethacin (5 mg/kg intravenously) or of nitric oxide synthase by N omega-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg intravenously) should attenuate isoflurane-induced hyperemia. Any response to L-NAME occurring via nitric oxide should be competitively reversed by L-arginine. METHODS: The cerebral blood flow (microsphere) response to 1 MAC isoflurane was tested at three time points (0, 90, and 180 min) in pentobarbital-anesthetized pigs. Isoflurane challenges were separated by 60-min periods of continuous intravenous pentobarbital alone. Control animals (n = 7) received no additional pharmacologic intervention. Experimental animals were randomized to receive L-NAME before the second and indomethacin before the third isoflurane challenge (n = 7); L-NAME before the second and L-arginine (400 mg/kg intravenously) before the third isoflurane challenge (n = 9); or indomethacin before the second and L-NAME before the third isoflurane challenge (n = 8). RESULTS: In control animals, isoflurane reproducibly increased cerebral blood flow (whole brain; 113 +/- 18%, 120 +/- 18%, and 103 +/- 19% increase above baseline at each time point, respectively). Both indomethacin and L-NAME attenuated (10 +/- 10% and 52 +/- 11% increase, respectively) the hyperemic response to isoflurane. The effect of L-NAME was reversed by L-arginine. CONCLUSIONS: We conclude that both prostanoids and nitric oxide contribute to isoflurane-induced hyperemia. We are unable to determine from our data what, if any, interaction exists between these two mechanisms.

Nitric oxide synthase inhibition with NG-mono-methyl-L-arginine reversibly decreases cerebral blood flow in piglets.

OBJECTIVE: We tested the hypothesis that, in piglets, the intravenous administration of the reversible inhibitor of nitric oxide synthase, NG-mono-methyl-L-arginine, decreases cerebral blood flow via a mechanism unrelated to cerebral oxygen consumption. DESIGN: Prospective, randomized, controlled animal study. SETTING: Animal laboratory at a university. SUBJECTS: Pentobarbital-anesthetized piglets (1 to 2 wks of age; 2.6 to 4.0 kg). INTERVENTIONS: Piglets were treated with either 50 mg of NG-mono-methyl-L-arginine, 100 mg of NG-mono-methyl-L-arginine, or an equal volume of saline by intravenous infusion over 10 mins. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure increased after NG-mono-methyl-L-arginine (50 mg dose: 84 +/- 6 to 100 +/- 7 mmHg; 100 mg dose: 82 +/- 4 to 107 +/- 4 mmHg; p < .001). Forebrain blood flow (microspheres) decreased (37 +/- 2 to 30 +/- 2 mL/min/100 g; p < .05) and cerebrovascular resistance increased (2.1 +/- 0.2 to 3.5 +/- 0.3 mmHg/mL/min/100 g; p < .05) only after 100 mg of NG-mono-methyl-L-arginine. Neurohypophysis blood flow decreased to 56 +/- 9% of the control value, while forebrain blood flow decreased only to 81 +/- 4% of the control value after 100 mg of NG-mono-methyl-L-arginine administration. Blood flow returned to control values by 30 mins after infusion. NG-mono-methyl-L-arginine administration had no effect on cerebral oxygen consumption at either dose. Intravenous administration of L-arginine (300 mg) immediately after the infusion of 100 mg of NG-mono-methyl-L-arginine was associated with prompt (by 3 mins) recovery of blood flow to all brain regions that were affected by NG-mono-methyl-L-arginine. CONCLUSIONS: These data suggest that nitric oxide and/or a nitric oxide-containing substance is an important mediator of cerebrovascular tone in piglets, acting via a mechanism unrelated to altering cerebral oxygen consumption.

Nitric oxide synthase inhibition attenuates hypoglycemic cerebral hyperemia in piglets.

We tested the hypothesis that nitric oxide (NO) mediates hypoglycemia-induced cerebral vasodilation in piglets. Piglets (1-2 wk old) were made hypoglycemic with insulin (200 U/kg i.v.) with and without an NO synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg i.v.). Electroencephalogram (EEG), cerebral O2 consumption (CMRO2), and cerebral blood flow (CBF) were measured before L-NAME and insulin and for 180 min after insulin. Hypoglycemia led to isoelectric EEG earlier after L-NAME (87 +/- 8 min) than without L-NAME pretreatment (132 +/- 13 min). CBF increased in all brain regions during hypoglycemia at the onset of isoelectric EEG and was associated with increased CMRO2.L-NAME prevented the increase in CMRO2 and attenuated vasodilation in forebrain (154 +/- 37 vs. 400 +/- 60%), cerebellum (251 +/- 52 vs. 386 +/- 52%), and cortical gray matter (183 +/- 47 vs. 524 +/- 93%) but had no effect on CBF responses in brain stem, thalamus, caudate, or hippocampus. We conclude that NO or a NO-containing compound mediates cerebral vasodilation induced by profound insulin-hypoglycemia in piglets and that this vasodilation plays an important role in the adaptation of immature brain to hypoglycemia.

Obstructive sleep apnea, control of ventilation, and anesthesia in children.

Pathologic disturbances in breathing in children become clinically apparent in the syndrome of obstructive sleep apnea. The surgical approach to this syndrome is often removal of hypertrophied tonsils and adenoids. The preoperative, operative, and postoperative concerns with special attention to the role of anesthesia are reviewed.

Purple glove syndrome.

Purple glove syndrome (PGS) often begins with discoloration and progresses to a petechial rash with induration or evidence of infiltration. The etiology of PGS is unknown, although various theories center around i.v. extravasation. We report a case of PGS in a child's foot associated with administration of Dilantin (phenytoin).

Polyethylene glycol-conjugated superoxide dismutase improves recovery of postischemic hypercapnic cerebral blood flow in piglets.

We tested the hypothesis that administering polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) either before global cerebral ischemia or at the time of reperfusion would alter recovery of cerebral blood flow (CBF; microspheres) response to alteration in arterial PCO2 in pentobarbital-anesthetized, mechanically ventilated piglets (1 to 2-wk old). CBF was measured at an arterial PCO2 of approximately 3.3, 5.3, and 8.7 kPa before and 2 h after ischemia (10 min aortic cross clamp). To determine the effect of preischemic versus postischemic treatment with PEG-SOD, each piglet received two i.v. drug injections of either 30,000 U PEG-SOD or an equal volume of PEG diluent in a randomized, blinded fashion before ischemia and just before reperfusion. Cerebral oxygen consumption and somatosensory evoked potentials were measured during reperfusion as an assessment of brain function. During reperfusion, no group demonstrated delayed hypoperfusion. Hypercapnic CBF was less during reperfusion (48 +/- 6 mL/min/100 g) compared with preischemia (69 +/- 10 mL/min/100 g) in PEG/PEG-treated piglets. However, hypercapnic CBF during reperfusion was not different from preischemic values with either preischemic or postischemic PEG-SOD treatment. Improved return of hypercapnic CBF in PEG-SOD-treated piglets was not attributable to improved postischemic cerebral oxygen consumption. Somatosensory evoked potential amplitude was decreased similarly during reperfusion (approximately 25% of preischemic values) in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)