Leptin and the post-operative inflammatory response. More insights into the correlation with the clinical course and glucocorticoid administration.

BACKGROUND: Cardiac surgery involving cardiopulmonary bypass (CPB) causes a systemic inflammatory process which can lead to multiple organ failure and postoperative morbidity. Recent animal and human studies suggested a possible involvement of leptin in the systemic inflammatory response. AIM: To characterize the response of leptin to open heart surgery (OHS) and the relationship between the time course of leptin levels and the post-operative clinical course, and to examine the effect of exogenous glucocorticoids. PATIENTS AND METHODS: Forty-seven pediatric patients, undergoing OHS for congenital heart disease were studied. Thirty-four patients (Group 1) received methylprednisolone during CPB while 13 (group 2) did not. Serial blood samples were collected perioperatively and up to 24 h after surgery, and assayed for leptin and cortisol. RESULTS: All patients' leptin levels decreased significantly during CPB (to 44-48% of baseline, p<0.001); they then increased, peaking at 12 h post-operatively. The levels of groups 1 and 2 were similar up to 8 h post-operatively; thereafter, those of group 1 were significantly higher. Recovery of leptin levels in patients with a more complicated post-operative course was comparatively slower. Cortisol levels of all patients increased significantly during CPB (p<0.001), gradually decreasing afterwards. Cortisol and leptin levels were inversely correlated in both patients' groups. CONCLUSIONS: CPB is associated with acute changes in circulating leptin levels. A complicated postoperative course is associated with lower leptin levels which are inversely correlated with cortisol levels. Leptin may participate in post-CPB inflammatory and hemodynamic responses.

Prevention of potential errors in resuscitation medications orders by means of a computerised physician order entry in paediatric critical care.

INTRODUCTION: Computerised physician order entry with clinical decision support system (CPOE+CDSS) is an important tool in attempting to reduce medication errors. The objective of this study was to evaluate the impact of a CPOE+CDSS on (1) the frequency of errors in ordering resuscitation (CPR) medications and (2) the time for printing out the order form, in a paediatric critical care department (PCCD). SETTING: An 18-bed PCCD in a tertiary-care children's hospital. DESIGN: Prospective cohort study. MEASURES: Compilation and comparison of number of errors and time to fill in forms before and after implementation of CPOE+CDSS. Time to fill in conventional, simulated and CPOE forms was measured and compared. RESULTS: There were three reported incidents of errors among 13,124 CPR medications orders during the year preceding implementation of CPOE+CDSS. These represent errors that escaped the triple check by three independent staff members. There were no errors after CPOE+CDSS was implemented (100% error reduction for 46,970 orders). Time to completion of drug forms dropped from 14 min 42 s to 2 min 14s (p < 0.001). CONCLUSIONS: CPOE+CDSS completely eliminated errors in filling in the forms and significantly reduced time to completing the form.

Selective attenuation of acute lung ventilatory injury by methylene blue after liver ischemia-reperfusion: a drug response study in an isolated perfused double organ model.

BACKGROUND: Liver transplantation-related ischemia-reperfusion (IR) is associated with the generation of stress oxidants that can spread damage remotely. Methylene blue (MB) had been shown to reduce lung neutrophils sequestration after in vivo intestinal IR and to have a dose-dependent potential for abrogating oxidant-induced ex vivo aortal ring reperfusion injury after liver IR. We now investigated MB's dose-dependent capabilities in preventing acute lung injury after the same liver IR. METHODS: Wistar rat livers (eight replicates/group) were perfused (control) with modified Krebs-Henseleit solution or put globally in no flow (IR) conditions for 2 hr. Separately prepared lungs were then paired with livers and "reperfused" (15 min) together. The livers were then removed, and the lungs were left to recirculate alone with the accumulated Krebs for 45 min. Three additional control and three IR groups were reperfused with Krebs containing 20, 40, or 60 mg/kg MB at concentrations of 42, 86, or 128 microM. RESULTS: All IR livers had hepatocellular and biochemical abnormalities compared with normal functions in the controls. Liver IR was associated with a 50%-75% increase in lung ventilation and perfusion pressures, vascular resistance and decreased compliance, and abnormal bronchoalveolar lavage (BAL) volume and content. Adding 42 and 86 microM MB selectively maintained normal the vascular parameters, intra-experimental lung weight gain, BAL indices, and wet-to-dry ratios. MB128 microM but not 42 or 86 microM best prevented IR-induced deterioration in lung ventilatory pressure and compliance. CONCLUSIONS: MB selectively affords maintenance of normal lung ventilatory versus vascular measures after liver ischemia-reperfusion. Its proposed differential mechanism of action is discussed.

Continuous arteriovenous hemofiltration after cardiac operations in infants and children.

Acute renal insufficiency after cardiopulmonary bypass can lead to a significant morbidity from fluid overload and electrolyte disturbance, impede pulmonary gas exchange, and postpone weaning from mechanical ventilation. The limitations placed on free water intake result in severe restriction of nutrition while diuretic therapy causes electrolyte imbalance. Artificial renal support either in the form of peritoneal dialysis or hemodialysis may be complicated by sepsis and hemodynamic instability. We reviewed our experience with the use of continuous arteriovenous hemofiltration, an extracorporeal technique for removal of solutes, toxins, and water in critically ill patients with cardiac failure complicated by acute renal insufficiency and hemodynamic instability after cardiopulmonary bypass. Ten infants and children with renal insufficiency caused by low cardiac output had continuous arteriovenous hemofiltration instituted for indications including sepsis, volume overload, oliguria for more than 24 hours nonresponsive to diuretic therapy, and the need for hyperalimentation. All were supported by mechanical ventilation and receiving high-dose inotropic support. Arterial and venous vascular access was successfully obtained by cannulation of the femoral artery and vein in nine patients. Anticoagulation of the circuit was achieved with heparin infusion (6 to 20 micrograms/kg/hr) and monitored by measurement of activated clotting time. The continuous arteriovenous hemofiltration circuit was replaced if there was clot formation, or at 3 days after placement. Dialysis solution (Dianeal) 1.5% or 0.5% was infused as prefilter dilution. With the use of continuous arteriovenous hemofiltration, 20 to 100 m/hr of ultrafiltrate was removed, which allowed correction of hypervolemia, and caloric intake increased from 13.5 kcal/kg/day to 79.5 kcal/kg/day. Continuous arteriovenous hemofiltration was maintained between 5 hours and 8 days and was well tolerated in all patients. Serum urea and creatinine levels declined during continuous arteriovenous hemofiltration. We conclude that continuous arteriovenous hemofiltration is a safe and effective method for fluid and electrolyte homeostasis and that it thus allows hyperalimentation in infants and children after cardiac operations.

Gunshot wounds in brains of children: prognostic variables in mortality, course, and outcome.

A retrospective study of 51 children presenting with craniocerebral gunshot lesions was carried out to identify predictors of outcome. The patients ranged in age from 2 months to 17 years, with a mean of 14.5 years. The outcome was good in 20 patients, and seven and four were moderately and severely disabled, respectively. Twenty patients died. Statistical analysis showed prognostic significance of the admission Glasgow Coma Score (GCS), computerized tomographic findings of intraventricular hemorrhage and midline shift, and metabolic abnormalities, including hypokalemia and hyperglycemia. These prognostic factors may have implications regarding counseling of families, utilization of resources, and organ transplantation.

Apnea testing in suspected brain dead children--physiological and mathematical modelling.

OBJECTIVE: To study the validity and safety of the traditional apnea test in children, and to evaluate a mathematical equation estimating the hemodynamic response to the apnea test. DESIGN: A prospective clinical study. SETTING: Pediatric ICU. PATIENTS AND PARTICIPANTS: 38 pediatric patients suffering severe brain injury aged 2 months to 17 years, undergoing apnea testing for brain death. MEASUREMENTS AND RESULTS: Apnea tests were performed 61 times (once in 19 patients, twice in 15, and 3 times in 4 patients). Mean PaCO2 was 41.1 +/- 10.6 mmHg before apnea and increased to 68.0 +/- 17.6 at 5 min. PaCO2 increased to 81.8 +/- 20.1 and 86.0 +/- 25.6 at 10 and 15 min, respectively. There was a mean PaCO2 increase by 5.38 +/- 1.4 mmHg/min in the first 5 min, and 2.75 +/- 0.5 mmHg/min during the next 5 min. We found a statistically significant (p < 0.05) linear relationship between the natural logarithm of PaCO2, time, and the logarithm of the initial level of PaCO2. An inverse linear relationship (p < 0.05) was found between systemic mean arterial pressure (MAP) and initial level of PaCO2 presented as mathematical correlations and nomograms. CONCLUSIONS: By using our model for predicting MAP and PCO2 prior to apnea testing, hemodynamic embarrassment can be anticipated and prevented, thus allowing a safer procedure in the detection of brain death. Despite the fact that continuous cardiorespiratory monitoring is important, hemodynamic disturbances can be estimated before the apnea test, thus allowing a safer approach to brain death detection.

End-tidal CO2 levels are a reliable indicator of band tightness in pulmonary artery banding.

BACKGROUND: Monitoring of end-tidal CO2 levels, performed routinely nowadays in most operating rooms, is obligatory in our hospital for all anesthesia patients. Levels are dependent on pulmonary blood flow, ventilation, and CO2 content of blood. When ventilation is kept constant, the end-tidal CO2 closely follows pulmonary blood flow. METHODS: Reduction of end-tidal CO2 in the expired air was used to adjust tightness of the pulmonary band in 10 patients with complex cardiac anomalies, all including ventricular septal defect, who underwent pulmonary artery banding. Other parameters were systemic blood pressures and distal pulmonary artery pressures. RESULTS: There were no operative deaths. Average reduction was 3.8 mm Hg (range, 2 to 10 mm Hg; p < 0.001 by paired t test), average increase in systolic blood pressure was 14 mm Hg (range, 4 to 20 mm Hg; p < 0.03 by Wilcoxon sign rank test), distal pulmonary artery pressure was reduced from 56 mm Hg (range, 37 to 79 mm Hg) to 29 mm Hg (range, 20 to 38 mm Hg; p < 0.03 by t test), and postoperative pulmonary artery to systemic pressure ratio averaged 0.36 mm Hg (range, 0.24 to 0.49 mm Hg, difference from preoperative value, p < 0.06). CONCLUSIONS: End-tidal CO2 tension is a simple and convenient, yet highly reliable parameter for adjusting pulmonary artery band tightness.

Beta-chemokine secretion patterns in relation to clinical course and outcome in children after cardiopulmonary bypass: continuing the search to abrogate systemic inflammatory response.

BACKGROUND: Surgery involving cardiopulmonary bypass (CPB) is frequently accompanied by a systemic inflammatory response partly triggered by neutrophils and monocyte-macrophages. Certain cytokines that are powerful leukocyte-chemotactic factors have recently been characterized and shown to be important in evoking inflammatory responses: monocyte chemoattractant protein-1 (MCP-1) has monocyte-macrophage chemotactic activity, and regulated-upon-activation normal T-cell expressed and secreted (RANTES) has a potent chemoattractant activity for mononuclear phagocytes. This prospective cohort study investigated possible roles of these chemokines in the inflammatory response to CPB and relationships between the changes in chemokine levels and the clinical course and outcome. METHODS: Systemic blood of 16 children undergoing CPB was collected after induction of anesthesia (base line); at 15 minutes after bypass onset; at CPB cessation; and at 1, 2, 4, 8, 12, and 24 hours afterward to measure MCP-1 and RANTES. RESULTS: The significant changes of plasma beta chemokine levels following CPB were associated with patient characteristics, operative variables, and postoperative course. Cardiopulmonary bypass of more than 2 hours, longer surgical times, inotropic support, and reoperation were associated with higher MCP-1 levels and lower RANTES levels. CONCLUSIONS: Our results suggest a relation between CPB-induced mediators and clinical effects, implying pathogenic roles for chemokines following CPB. These molecules should be considered as possible targets for therapeutic intervention.

Anaesthesia and critical care considerations in nerve agent warfare trauma casualties.

Nerve agents (NA) (tabun, sarin, suman, VX) have been stocked around the world for some time and still present a major threat to civilian as well as to military populations. Since NA can be delivered through both an aerial spray system and a ballistic system, victims could suffer both NA intoxication and multiple trauma necessitating urgent surgical intervention followed by intensive care. These patients can be expected to be extremely precarious neurologically, respiratorily and haemodynamically. Moreover, their clinical signs can be misleading. Further exacerbating the problem is the fact that interactions of NA with the pharmacological agents used for resuscitation and/or during anaesthesia can aggravate organ instability even more and possibly cause systemic collapse. There are no protocols for perioperative critical care and early assessment or for the administration of anaesthesia for surgical interventions in such combined multiple trauma and intoxicated casualties. We propose a scheme for the administration of critical care and anaesthesia based on the scant anecdotal reports that have emerged after the occurrence of local accidents involving NA intoxication and on the neuropharmacological knowledge of the pesticide organophosphate poisoning database, these compounds being related chemical substances.

Epinephrine pharmacokinetics and pharmacodynamics following endotracheal administration in dogs: the role of volume of diluent.

OBJECTIVE: to define the optimal volume of dilution for endotracheal(ET) administration of epinephrine (EPI). DESIGN: prospective, randomized, laboratory comparison of four different volumes of dilution of endotracheal epinephrine (1, 2, 5, and 10 ml of normal saline). SETTING: large animal research facility of a university medical center. SUBJECTS AND INTERVENTIONS: epinephrine (0.02 mg/kg) diluted with four different volumes (1, 2, 5, and 10 ml) of normal saline was injected into the ET tube of five anesthetized dogs. Each dog served as its own control and received all four volumes in different sequences at least 1 week apart. Arterial blood samples for plasma epinephrine concentration and blood gases were collected before and 0.25, 0.5, 0.75, 1, 2, 3, 4, 5, 10, 15, 20, 25, 30 and 60 min after drug administration. Heart rate and arterial blood pressure were continuously monitored with a polygraph recorder. MEASUREMENTS AND MAIN RESULTS: higher volumes of diluent (5 and 10 ml) caused a significant decrease of PaO2, from 147 +/- 8 to 106 +/- 10 torr, compared with the lower volumes of diluent (1 and 2 ml), from 136 +/- 10 to 135 +/- 7 torr (P < 0.05). These effects persisted for over 30 min. Mean plasma epinephrine concentrations significantly increased within 15 s following administration for all the volumes of diluent. Mean plasma epinephrine concentrations, maximal epinephrine concentration (Cmax) and the coefficient of absorption (Ka) were higher in the 5 and 10 ml groups. The time interval to reach maximal concentration (Tmax) was shorter in the 5 and 10 ml groups. Yet these results were not significantly different. Heart rate, systolic and diastolic blood pressures did not differ significantly between the groups throughout the study. CONCLUSIONS: Dilution of endotracheal epinephrine into a 5 ml volume with saline optimizes drug uptake and delivery without adversely affecting oxygenation and ventilation.

Ventilation index and outcome in children with acute respiratory distress syndrome.

The purpose of this investigation was to determine the predictive value of the ventilation index (VI) in children with acute respiratory distress syndrome (ARDS). We performed a 10-year retrospective chart review of children who were admitted to the Pediatric Intensive Care Unit with a diagnosis of ARDS. Acute respiratory distress syndrome was defined as acute onset of diffuse, bilateral pulmonary infiltrates of noncardiac origin, and severe hypoxemia, defined as the ratio of the arterial partial pressure of oxygen to the fraction of inspired oxygen of <200 and a positive end expiratory pressure of 6 cmH2O or greater. Records of daily arterial blood gas results and ventilator settings were reviewed, and the ventilation index (VI=partial pressure of arterial CO2 x peak airway pressure x respiratory rate/1,000) was calculated each time the measurements were made. These values were correlated with outcome (survival or nonsurvival). The VI was not different at the time of diagnosis of ARDS in the patients who lived, compared with those who subsequently died. However, by 3 to 5 days after study entry, the VI of nonsurvivors was significantly higher than for survivors (P < 0.05). The VI for survivors remained between 30 and 35 throughout the study period, whereas the VI of nonsurvivors continued to increase with time. A VI of >65 predicted death with a specificity and positive predictive value of >90% on days 3 through 9. We conclude that the VI provides a reliable prognostic marker in children with ARDS, and its increase above 65 indicates a need for orderly intervention with alternative modalities of care.

Atropine pharmacokinetics and pharmacodynamics following endotracheal versus endobronchial administration in dogs.

Emergency endotracheal and endobronchial drug administration provide an effective alternative for intravenous drug delivery during cardiopulmonary resuscitation. The purpose of the present study was to determine the immediate pharmacokinetic and pharmacodynamic properties of atropine following administration by either of these routes. Atropine (0.02 mg/kg) was given to seven anaesthetized mongrel dogs. Each dog was studied twice: once when atropine was injected into the endotracheal tube, and on another day when atropine was given via a flexible catheter wedged into a peripheral bronchus. Plasma atropine concentrations and blood gases were measured during 60 min following drug administration. Both routes of atropine administration differed significantly in three measures: the maximal atropine concentration (Cmax) was significantly higher with the endobronchial administration 40.0 +/- 7.8 ng/ml compared to 23.9 +/- 5 ng/ml endotracheally (P = 0.008); atropine's elimination (t1/2beta) half-life was significantly longer with the endobronchial route (39.3 +/- 5.2 min vs. 28.0 +/- 7.9 min; P = 0.05); Endobronchial administration resulted in an increase of 16% in heart rate, beginning immediately after drug delivery and peaking after 5 min. Other pharmacokinetic parameters were not significantly different. We conclude that endobronchial administration of atropine has a clear advantage over the endotracheal route.

Hemodynamic effects of tracheal administration of vasopressin in dogs.

BACKGROUND: Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) has been shown to be more effective than optimal doses of epinephrine. Earlier studies had been performed on a porcine model, but pigs produce lysine vasopressin hormone, while humans and dogs do not. This study was designed to compare the effects of tracheal vasopressin with those of NaCl 0.9% (placebo) on haemodynamic variables in a dog model. METHODS: Five dogs were allocated to receive either vasopressin 1.2 U/kg or placebo (10 ml of NaCl 0.9%) via the tracheal route after being anesthetized and ventilated. Haemodynamic variables were determined and arterial blood gases were measured. RESULTS: All animals of the vasopressin group demonstrated a significant increase of the systolic (from 135+/-7 to 165+/-6 mmHg, P<0.05), diastolic (from 85+/-10 to 110+/-10 mmHg, P<0.05) and mean blood pressure (from 98.5+/-3 to 142.2+/-5, P<0.05). Blood pressure rose rapidly and lasted for more than an hour (plateau effect). Heart rate decreased significantly following vasopressin (from 54+/-9 to 40+/-5 beats per min, P<0.05) but not in the placebo group. These changes were not demonstrated with placebo injection. CONCLUSION: Tracheal administration of vasopressin was followed by significantly higher diastolic, systolic and mean blood pressures in the vasopressin group compared with the placebo group. Blood gases remained unchanged in both groups. Vasopressin administered via the trachea may be an acceptable alternative for vasopressor administration during CPR, when intravenous access is delayed or not available, however, further investigation is necessary.

Predictors of adverse outcome from candidal infection in a tertiary care hospital.

OBJECTIVES: To retrospectively delineate predictors of adverse outcome by looking at the demographic features, therapy and outcome of systemic candida infection in a large tertiary care university-affiliated medical center. METHODS: We reviewed the clinical data on 186 inpatients with candidemia over a 6-year period. The major reason for their hospital admission was an underlying malignancy or an infection other than candidemia. RESULTS: Candida albicans, tropicalis, parapsilosis, glabrata and krusei caused 54, 22, 13, 8 and 3% of the candidemia episodes, respectively. The overall mortality was 42% and it was highest in patients suffering from candidemia of the glabrata species (73%). Forty-eight (63%) of the 76 patients who received no anti-fungal treatment died compared to 38 (34%) of 110 patients who were treated (P < 0.05). Predictors of adverse outcome were intensive care unit stay, renal failure, thrombocytopenia and the need for mechanical ventilation or inotropic support. CONCLUSIONS: We identified four predictors of mortality from candidemia infection. Their validity should be further assessed and the specific candida strains and their susceptibility need to be methodically identified. Our data support immediate initiation of therapy at first identification of infection.

Systemic inflammatory mediators and cystic fibrosis genotype.

Morbidity and mortality in cystic fibrosis patients is mainly attributed to pulmonary infection and inflammation. Chemokines play a pivotal role in the inflammatory process. Although genotype-phenotype correlation in cystic fibrosis patients has been defined, a clear relationship between the defect in the cystic fibrosis transmembrane regulator (CFTR) gene and pulmonary inflammation has not been established. The aim of this study was to assess whether serum chemokines levels in cystic fibrosis patients correlate with genotype and pulmonary function tests, as well as with other clinical characteristics. Serum levels of interleukin-8, RANTES, and monocyte chemoattractant protein-1 were measured in 36 cystic fibrosis patients grouped according to their genotype. Group A included 25 patients who carried two mutations associated with a pathological sweat test and pancreatic insufficiency (deltaF508, W1282X, G542X, N1303K, S549R). Group B included 11 compound heterozygote patients who carried one mutation known to cause mild disease with borderline or normal sweat test and pancreatic sufficiency (3849+10kb C to T, 5T). Associations between chemokine levels, genotype, pulmonary function, Pseudomonas aeruginosa colonization, age, sweat chloride level, and pancreatic and nutritional status were examined. Mean interleukin-8 and monocyte chemoattractant protein-1 levels were significantly higher in group A than group B (11.4 +/- 2.1 pg/ml vs. 5 +/- 0.9 pg/ml and 157 +/- 16 pg/ml vs. 88.8 +/- 16.4 pg/ml, respectively) (P < 0.01). No difference in RANTES levels were found between groups. interleukin-8 levels were inversely related to forced expiratory volume in 1 s (r = -0.37, P < 0.02), while there was no association between the latter and RANTES and monocyte chemoattractant protein-1 levels. The Pseudomonas colonization rate was higher among group A patients than group B (88% vs. 40%, P < 0.01). No relationship was found between measured chemokines and age, sweat chloride levels, and pancreatic and nutritional status. Our study demonstrates an association between interleukin-8, forced expiratory volume, and cystic fibrosis genotype. Hence, elevated interleukin-8 serum levels could serve as an indicator of an early inflammatory process and encourage the initiation of anti-inflammatory treatment.

Serum CA 19-9 levels as a diagnostic marker in cystic fibrosis patients with borderline sweat tests.

Patients with normal or borderline sweat tests present a diagnostic challenge. In spite of the availability of genetic analysis and measurement of nasal potential difference, there is still uncertainty in diagnosing cystic fibrosis in some patients. CA 19-9 is a tumor-associated antigen whose levels were previously found to be elevated in some cystic fibrosis patients. We investigated whether serum CA 19-9 levels can contribute to establishing the diagnosis of cystic fibrosis in patients with a borderline sweat test, and evaluated the influence of different clinical variables on CA 19-9 levels. Serum CA 19-9 levels were measured in 82 cystic fibrosis patients grouped according to their genotype and in 38 healthy individuals. Group A included 50 patients who carried two mutations previously found to be associated with a pathological sweat test and pancreatic insufficiency (DeltaF508, W1282X, G542X, N1303K, and S549R). Group B included 13 compound heterozygote cystic fibrosis patients who carried one mutation known to cause mild disease with a borderline or normal sweat test and pancreatic sufficiency (3849+10kb C-->T, 5T). Group C included 38 normal controls. Nineteen cystic fibrosis patients carried at least one unidentified mutation. An association between CA 19-9 levels and age, pulmonary function, pancreatic status, sweat chloride, previous pancreatitis, serum lipase, meconium ileus, distal intestinal obstruction, liver disease, and diabetes was investigated. The distribution of CA 19-9 levels was significantly different between the three groups ( p<0.01); high CA 19-9 levels were found in 60% (30/50) of group Apatients and in 46.6% (6/13) of group B patients, but in only 5.2% (2/38) of the controls. CA 19-9 levels were inversely related to forced expiratory volume in 1 s, while no association was found with the other clinical parameters examined. Our findings suggest that the serum CA 19-9 in cystic fibrosis patients originates in the respiratory system, and has a useful ancillary role, particularly when diagnostic uncertainty exists. Hence, the diagnosis of cystic fibrosis should be considered in patients with borderline sweat tests and high CA 19-9 levels, but normal levels do not exclude cystic fibrosis.

Abnormal visual evoked potentials in children with "Alice in Wonderland" syndrome due to infectious mononucleosis.

Visual illusions characterized by distortion of form, size, reciprocal position of objects, movement, or color, labeled as "Alice in Wonderland" syndrome, were discussed in children with infectious mononucleosis, as well as in other clinical conditions, such as migraine, epilepsy, use of certain hallucinogenic drugs, etc. The purpose of our study was to investigate for the first time visual evoked potential results in children with "Alice in Wonderland" syndrome associated with infectious mononucleosis. Five children with "Alice in Wonderland" syndrome associated with infectious mononucleosis underwent visual evoked potential studies during and after their clinical symptoms. Visual evoked potential results during the disease demonstrated statistically significant high amplitudes of P100-N145 in all children compared to the control group. A few weeks later, repeated studies after the resolution of the complaints were normal. Since the same findings can be observed in patients with migraine, we postulate that a common pathophysiologic underlying abnormality, which can cause transient focal decreased cerebral perfusion, could be involved in the disease process of these two conditions.

Adapting prognostic respiratory variables of ARDS in children to small-scale community needs.

PURPOSE: The clinical literature on the incidence and subsequent mortality of adult respiratory distress syndrome (ARDS) has come primarily from the experiences of large tertiary referral centers, particularly in Western Europe and North America. Consequently, very little has been published on the incidence, management, and outcome of ARDS in smaller community-based intensive care units. We aimed to delineate early clinical respiratory predictors of death in children with ARDS on the modest scale of a community hospital. MATERIALS AND METHODS: A retrospective chart review of children with ARDS needing conventional mechanical ventilation admitted to our pediatric intensive care unit from 1984 to 1997. The diagnosis of ARDS was based on acute onset of diffuse, bilateral pulmonary infiltrates of noncardiac origin and severe hypoxemia defined by partial pressure of oxygen <200 mm Hg during positive end-expiratory pressure (PEEP) of 6 cm H2O or greater for a minimum of 24 hours. Demographic, clinical, and physiological data including PaO2/ FIO2, A-aDo2, and ventilation index were retrieved. RESULTS: Fifty-six children with ARDS aged 8 +/- 5.5 years (range, 50 days to 21 years) were identified. The mortality rate was 50%. Early predictors of death included the peak inspiratory pressure (PIP), ventilation index, and PEEP on the third day after diagnosis: Nonsurvivors had significantly higher PIP (35.3 +/- 10.5 cm H2O vs 44.4 +/- 10.7 cm H2O, P < .001), PEEP (8 +/- 2.8 cm H2O vs 10.7.0 +/- 3.5 cm H2O, P < .01), and ventilation index (49.14 +/- 20.4 mm Hg x cm H2O/minute vs 61.6 +/- 51.1 mm Hg cm H2O/minute) than survivors. In contrast, PAO2/FIO2 and A-a DO2 were capable of predicting outcome by day 5 and thereafter. CONCLUSIONS: A small-scale mortality outcome for ARDS is comparable to large tertiary referral institutions. The PIP, PEEP, and ventilation index are valuable for predicting outcome in ARDS by the third day of conventional therapy. The development of a local risk profile may assist in decision-making of early application of supportive therapies in this population.

Acute respiratory distress syndrome in children with malignancy--can we predict outcome?

PURPOSE: The purpose of this study was to delineate early respiratory predictors of mortality in children with hemato-oncology malignancy who developed acute respiratory distress syndrome (ARDS). MATERIALS AND METHODS: We conducted a retrospective chart review of children with malignant and ARDS who needed mechanical ventilation and were admitted to a pediatric intensive care unit from January 1987 to January 1997. RESULTS: Seventeen children with ARDS and malignancy aged 10.5 +/- 5.1 years were identified. Six of the 17 children (35.3%) survived. Sepsis syndrome was present in 70.6% of all the children. Peak inspiratory pressure, positive end-expiratory pressure (PEEP), and ventilation index values could distinguish outcome by day 3. A significant relationship between respiratory data and outcome related to efficiency of oxygenation, as determined by PaO(2)/FIO(2) and P(A-a)O(2), was present from day 8 after onset of mechanical ventilation. CONCLUSIONS: Peak inspiratory pressure, PEEP, and ventilation index values could distinguish survivors from nonsurvivors by day 3. This may assist in early application of supportive nonconventional therapies in children with malignancy and ARDS.

Rhabdomyolysis due to hereditary torsion dystonia.

Following an acute dystonic crisis, a 6-year-old boy with hereditary torsion dystonia developed rhabdomyolysis. To our knowledge, hereditary torsion dystonia has never been reported as a cause of rhabdomyolysis. Early diagnosis and treatment of rhabdomyolysis should be considered in children with severe dystonia in order to prevent renal failure.