Efficacy of erythromycin for postpyloric placement of feeding tubes in critically ill children: a randomized, double-blind, placebo controlled study.

BACKGROUND: Erythromycin enhances gastric emptying and has been suggested to facilitate nasoenteric feeding tube placement in adults. Our primary objective was to evaluate the effect of erythromycin on the transpyloric passage of feeding tubes in critically ill children, and second, to evaluate the effect of erythromycin on the distal migration of duodenal feeding tubes. METHODS: Seventy-four children were randomly assigned to receive erythromycin lactobionate (10 mg/kg) IV or equal volume of saline placebo 60 minutes before passage of a flexible weighted tip feeding tube. Abdominal radiographs were obtained 4 hours later to assess tube placement. If the tube was proximal to the third part of the duodenum, two additional doses of erythromycin/placebo were administered 6 hours apart. Those receiving additional doses had repeat radiographs 14 to 18 hours after tube placement. RESULTS: The number of postpyloric feeding tubes was similar in the erythromycin and placebo treated groups 4 hours after tube insertion (23/37 vs 27/37, p = .5). Of those with prepyloric tubes at 4 hours, none in the erythromycin group and 3 in the placebo group had the tube migrate to the postpyloric position by 14 to 18 hours (p < .05). Of those with postpyloric tubes proximal to the third part of the duodenum at 4 hours, additional doses of erythromycin did not cause more tubes to advance further into the intestine than did placebo (p = .6). CONCLUSIONS: Erythromycin does not facilitate transpyloric passage of feeding tubes in critically ill children. The distal migration of duodenal tubes further into the small bowel is also not enhanced by erythromycin.

Heat stress is associated with decreased lactic acidemia in rat sepsis.

BACKGROUND: Elevated plasma lactate has been shown to correlate with mortality in patients with septic shock. Heat stress prior to sepsis has resulted in reduction in acute lung injury and mortality. We investigated whether heat stress resulted in decreased plasma lactate concentration and protected the lung by decreasing the inflammatory response to sepsis. RESULTS: Plasma lactate concentration was elevated in septic rats without prior heat stress. Lactic acid levels were significantly lower in heat-treated septic rats (P < 0.05) and were not significantly different when compared with control rats. Septic rats with or without heat pretreatment had significantly higher myeloperoxidase activity in the lung than did control groups. Heat pretreatment did not prevent neutrophil infiltration or inflammatory mediator production in the lung. CONCLUSION: Prior heat stress ameliorates lactic acidemia in rat sepsis. Heat stress did not attenuate the pulmonary inflammatory process. The mechanism of heat-induced protection from lactic acidemia in sepsis needs to be further explored.

Indicators of postpyloric feeding tube placement in children.

OBJECTIVE: To determine the validity of five indicators (color, pH, and concentrations of bilirubin, pepsin, and trypsin in aspirated gastrointestinal secretions) in predicting postpyloric placement of feeding tubes in critically ill children. DESIGN: Prospective, observational study. SETTING: University teaching hospital. PATIENTS: A total of 96 gastrointestinal aspirates were obtained from 53 children requiring placement of a nasoenteric feeding tube. INTERVENTIONS: Feeding tubes were aspirated by applying suction with a 20-mL syringe. Repeat aspirates from the same patient were obtained on different days. All aspirations were performed within 30 mins of obtaining a radiograph to assess tube position. MEASUREMENTS AND MAIN RESULTS: Aspirates were inspected visually for color. pH and bilirubin concentrations were determined at the bedside by using reagent strips. Pepsin and trypsin concentrations were measured spectrophotometrically in a research laboratory. The sensitivity, specificity, predictive values, and efficiency for each indicator and their 95% confidence intervals were determined based on the position of the feeding tube on the radiograph. Aspirate pH > or =6 had the lowest positive predictive value (76%, range 67% to 85%) but high negative predictive value (94%, range 89% to 99%) for determining postpyloric positioning of the feeding tube. Bilirubin concentration > or =5 mg/dL (> or =86 micromol/L) had the highest positive predictive value (96%, range 91% to 100%) and lowest negative predictive value (88%, range 81% to 95%). Overall efficiency was best for the appearance of a clear yellow aspirate color (93%, range 88% to 98%), pepsin concentration < or =20 microg/mL (94%, range 89% to 99%), and trypsin concentration > or =50 microg/mL (94%, range 89% to 99%). CONCLUSIONS: Simple bedside assessment of gastrointestinal aspirate color, pH, and bilirubin concentration is useful for predicting feeding tube position. Use of these tests may reduce the number of radiographic studies needed to confirm postpyloric positioning. Laboratory-determined pepsin and trypsin concentrations predict tube position with a high degree of accuracy. Development of simple and inexpensive bedside tests for the detection of gastrointestinal enzymes may be useful.

The effect of heat on cytokine production in rat endotoxemia.

OBJECTIVE: To determine whether heat stress protects the endotoxemic rat by up-regulation of the counterinflammatory cytokine interleukin (IL)-10, thereby attenuating the inflammatory response. DESIGN: A total of 16 rats were assigned to either the heat stress group (n = 8) or the control group (n = 8). The heat stress group was warmed to a temperature of >42 degrees C (107.6 degrees F) rectally for 10-15 mins; 20 hrs later, all rats were intubated, paralyzed, and ventilated. After jugular venous and arterial catheterization, endotoxin was given intravenously. Arterial blood was removed at 0, 2, 4, and 5 hrs for blood gases, tumor necrosis factor (TNF)-alpha, nitric oxide metabolites (NO), IL-10, and macrophage inflammatory protein (MIP)-2. The alveolar macrophages were removed, counted, and then incubated for 24 hrs. The supernatant was analyzed for TNF-alpha, NO, IL-10, and MIP-2. SETTING: University research laboratory. SUBJECTS: Male Sprague-Dawley rats (n = 16). INTERVENTIONS: Administration of heat before endotoxin infusion. MEASUREMENTS AND MAIN RESULTS: Alveolar-arterial oxygen gradient was lower in the heat stress group at 4 and 5 hrs after endotoxemia. Plasma and alveolar macrophage supernatant concentrations of TNF-alpha, NO, and IL-10 were not affected by heat. Plasma and alveolar macrophage supernatant MIP-2 concentrations were higher in endotoxemic rats receiving heat pretreatment compared with controls. CONCLUSIONS: Our study demonstrates that heat leads to pulmonary protection of short duration in severe endotoxemia. This protection was not mediated by plasma TNF-alpha, IL-10, or NO. Contrary to our hypothesis, pretreatment with heat increased rather than decreased the plasma MIP-2 concentration and alveolar macrophage production of MIP-2 in endotoxemia. The mechanism of heat-conferred pulmonary protection in endotoxemia remains unclear. Alveolar macrophages do not produce IL-10 in endotoxemia. The increased MIP-2 production by heated alveolar macrophages was not attributable to alterations in production of either TNF-alpha or IL-10. The significance of increased MIP-2 by endotoxin-exposed alveolar macrophages in heated rats is unknown.

End-of-life decision-making and satisfaction with care: parental perspectives.

OBJECTIVES: To evaluate parents' perceptions of the process by which decisions are made to limit or withdraw life support from critically ill children, and to evaluate parents' perceptions of their child's death in the pediatric intensive care unit (ICU) and their satisfaction with the care provided. DESIGN: Survey. SETTING: University teaching hospital. PARTICIPANTS: Seventy-eight parents who experienced the death of a child in the ICU between January 1, 1995 and June 30, 1998. INTERVENTIONS: Structured telephone interviews. MEASUREMENTS AND MAIN RESULTS: Forty-one parents recalled discussing the limitation or withdrawal of life support from their child with a physician. Of these, 31 (76%) felt they had just the right amount of authority to make decisions for their child, 8 (20%) felt they had too little, and 1 (2%) felt they had too much. Those satisfied with their decision-making authority had more trust in their physician than those who were dissatisfied (5 vs. 1, p <.001 by Mann-Whitney U test, where 1 = no trust and 5 = complete trust). Factors identified by parents as being extremely important in the decision-making process included physician recommendations, diagnosis, expected neurologic recovery, and degree of pain and suffering. A total of 51 parents were with their child at the time of death. Although none regretted being present, 17 parents who were not present later wished they had been (p <.001, Fisher's exact test). The quality of care provided to parents by the ICU staff was graded (1 = poor; 5 = excellent). Eleven parents (14%) scored quality of care

Effects of insulin and metformin on glucose metabolism in rat vascular smooth muscle.

Glucose metabolism in vascular smooth muscle cells (VSMCs) is characterized by substantial lactate production even in fully oxygenated conditions. Insulin and metformin, an insulin-sensitizing agent, have direct effects on the vascular tissue metabolism. We investigated whether insulin or metformin can induce a switch in VSMC glucose metabolism from lactate production to pyruvate oxidation, by measuring lactate oxidation as determined by the conversion of [1-14C]-D,L-lactate to [1-14C]-pyruvate and subsequent oxidation to acetyl coenzyme A and 14CO2 by pyruvate dehydrogenase (PDH). Lactate oxidation was measured in control rat aortic cultured VSMCs incubated for 30 minutes in media with and without additional glucose compared with VSMCs cultured in the presence of insulin or metformin. The addition of glucose to VSMCs decreased lactate oxidation (4.6+/-1.7 v 9.6+/-2.4 pmol/cell/min, P < .001). In the absence of additional glucose, metformin decreased lactate oxidation in VSMCs compared with controls (4.9+/-1.4 v 9.6+/-2.4 pmol/cell/min, P < .01). Metformin in the presence of glucose caused the greatest decline in lactate oxidation (2.5+/-0.4 pmol/cell/min, P < .001). In contrast to the effects of metformin, insulin increased lactate oxidation both with (12.9+/-1.5 pmol/cell/min, P < .001) and without (17.9+/-4.4, P < .01) additional glucose. This suggests that insulin facilitates VSMC utilization of lactate as a source of pyruvate and energy production even during noncontractile periods.

Ibuprofen attenuates cardiopulmonary dysfunction by modifying vascular tone in endotoxemia.

Ibuprofen, a cyclooxygenase inhibitor, improves pulmonary and cardiovascular injury in endotoxemia. We studied the mechanism of the beneficial effects of ibuprofen in relation to production of inflammatory mediators which influence vascular tone in endotoxemia. Rats were randomly assigned to one of three groups: (1) control, (2) endotoxemia alone; and (3) ibuprofen pretreatment and endotoxemia. Plasma and lung lavage concentrations of tumor necrosis factor, thromboxane B2 (TXB2), leukotriene (LT) C4,D4,E4 and nitric oxide (NO) were determined over a 2 h period. Pretreatment with ibuprofen resulted in increased survival, and attenuation of pulmonary and cardiovascular dysfunction when compared to the rats receiving endotoxin alone. The marked elevation in plasma TXB2 concentration in endotoxemic rats was prevented by pretreatment with ibuprofen. Similarly, pretreatment with ibuprofen prevented the decrease in lung lavage NO levels in endotoxemic rats. The improved survival and cardiopulmonary protection in endotoxemic rats pretreated with ibuprofen appears to be related to decreased thromboxane production and preservation of endothelial production of nitric oxide.

Syndrome of inappropriate antidiuretic hormone secretion in children following spinal fusion.

OBJECTIVES: a) To determine if antidiuretic hormone (ADH) is elevated in patients undergoing spinal fusion, especially in those who have clinical evidence of syndrome of inappropriate antidiuretic hormone (SIADH); b) to evaluate the relationship between ADH secretion and the secretion of atrial natriuretic peptide (ANP). SETTING: Tertiary care pediatric intensive care unit (ICU) in a university hospital. DESIGN: A prospective cross-sectional, observational study with factorial design. PATIENTS: Thirty patients > or = 10 yrs of age undergoing spinal fusion admitted to the ICU for postoperative care. INTERVENTIONS: Patients underwent anterior, posterior, or both anterior/posterior spinal fusion. Blood was collected for serial measurements of ADH, ANP and serum electrolyte levels. Heart rate, blood pressure and central venous pressure were measured. MEASUREMENTS AND MAIN RESULTS: Thirty children were studied. Nineteen had idiopathic scoliosis, nine had neuromuscular scoliosis, one had Marfan's disease, and one had congenital scoliosis. Ten (33%) children met clinical criteria of SIADH. There was no difference in duration of surgery, blood loss, volume of iv fluid administration pre- and intraoperatively, or type of scoliosis between those who developed SIADH and those who did not. Hemodynamic variables were similar in both groups. ADH levels increased in both groups immediately postoperatively and at 6 hrs after surgery, but were much more elevated in those patients with SIADH. Patients with SIADH also had significantly higher ADH levels preoperatively. In relation to serum osmolality, ADH was considerably higher in those with SIADH compared with those who did not. Although ANP values tended to be higher in the group with SIADH, this did not reach statistical significance. CONCLUSION: SIADH occurs in a subset of children who undergo spinal fusion. The diagnosis of SIADH can be made easily using clinical parameters which are well-defined. In the face of SIADH, continued volume expansion may be harmful, and should therefore be avoided.

Anti-s antibody-associated delayed hemolytic transfusion reaction in patients with sickle cell anemia.

PURPOSE: Signs and symptoms of delayed hemolytic transfusion reaction (DHTR) may resemble those of vaso-occlusive crises in patients with sickle cell anemia (SCA). The diagnosis of DHTR therefore presents a challenge to the clinician when treating such patients. The current study describes a patient with SCA and DHTR secondary to red cell anti-s antibody, manifesting as painful extremeties, severe hemolytic anemia, and acute oliguric renal failure. PATIENTS AND METHODS: A 17-year-old patient with homozygous hemoglobin S presented 8 days after partial exchange transfusions with severe anemia and signs and symptoms resembling vaso-occlusive crisis. Clinical course was complicated by intravascular hemolysis and acute renal failure. RESULTS: Anti-s antibody was detected in the eluate. Diagnosis of DHTR was made. Treatment included single volume whole blood exchange transfusion and continuous veno-venous hemofiltration with dialysis. CONCLUSIONS: The possibility of DHTR should be considered in a patient with SCA with hemolytic anemia. Acute renal failure is a rare complication of anti-s antibody-associated DHTR. Such reactions can be successfully managed with exchange transfusion and continuous hemofiltration with dialysis.

Altered T cell cytokine production following mechanical trauma.

BACKGROUND: Cell mediated immunity is suppressed following traumatic injury. The Objective is to determine whether there is a shift from T helper type 1 (TH1) to TH2 cell cytokine production following mechanical trauma in a rat model. METHODS: Male Sprague-Dawley rats were anesthetized and subjected to bilateral femur fractures or sham injury. Spleens were removed 3 days later. T cell proliferation and cytokine production were stimulated by culturing spleen cells with the T cell mitogen concanavalin A (con A). Interleukin-2 (IL-2), interferon-gamma (IFN-gamma), IL-10 and IL-4 concentrations were measured in spleen cell supernatants using enzyme linked immunosorbent assays. RESULTS: Con A-induced spleen cell proliferation was decreased in traumatized rats compared to controls (p < 0.05). Spleen cell supernatant concentrations of the TH1 cytokines IL-2 and IFN-gamma were decreased in the trauma group (p < 0.05). Supernatant concentrations of the TH2 cytokine IL-10 were also decreased in traumatized rats (p < 0.01). The IL-4 concentrations were below the detection limit (< 15 pg/mL) in all cell supernatants. CONCLUSIONS: Mechanical tissue injury leads to generalized suppression of T helper cell cytokine production rather than a shift from TH1 to TH2 cell activity. Post-trauma cellular immunosuppression is not mediated via excess IL-10 production by TH2 cells.

Macrophage inflammatory protein-2 predicts acute lung injury in endotoxemia.

BACKGROUND: Proinflammatory mediators that include tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein-2 (MIP-2) and anti-inflammatory mediators such as interleukin-10 (IL-10) modulate the immune response to endotoxemia. IL-10 downregulates the production of TNF-alpha and MIP-2. Acute lung injury may occur secondary to neutrophil chemotaxis mediated by chemokine MIP-2. We studied the temporal relationship of TNF-alpha, MIP-2, and IL-10 in rat endotoxemia and correlation of MIP-2 concentrations with acute lung injury. METHODS: Ten ventilated rats were randomized to receive an intravenous infusion of 2 mg/kg Escherichia coli lipopolysaccharide (n = 6) or saline placebo (n = 4). Blood pressure was continuously monitored and arterial blood was obtained for lactate, blood gas, TNF-alpha, IL-10, and MIP-2 measurements at baseline, 2, 4, and 5.5 hours after LPS or saline infusion. RESULTS: Endotoxemia resulted in hypotension, lactic acidemia, and increased alveolar-arterial oxygen gradient (A-a O2 gradient) compared with the placebo group. TNF-alpha, MIP-2, and IL-10 levels were increased 2 hours after endotoxemia. Subsequently, TNF-alpha levels declined while IL-10 and MIP-2 levels remained elevated. Control rats had no significant increase in cytokine production at any time point. MIP-2 concentrations correlated with A-a O2 gradient, an indicator of lung injury (r = 0.56, p < 0.001). CONCLUSIONS: MIP-2, possibly released by TNF-alpha stimulation of macrophages, is associated with acute lung injury possibly by inducing neutrophil chemotaxis. IL-10 may exert its counter-inflammatory response by inhibiting the release of TNF-alpha in endotoxemia.

Outcome of children with carbon monoxide poisoning treated with normobaric oxygen.

OBJECTIVE: To evaluate the clinical characteristics and neurologic outcome of children with carbon monoxide poisoning treated with normobaric oxygen therapy. METHODS: We reviewed the medical records of all children with a diagnosis of carbon monoxide exposure admitted during a 10-year period. Exposures were categorized as (1) severely toxic, carboxyhemoglobin level >25%; (2) toxic, carboxyhemoglobin level 10.1 to 25%; (3) suspected toxic, carboxyhemoglobin level < or = 10% with acute neurologic manifestations; or (4) nontoxic, carboxyhemoglobin < or = 10% without acute neurologic manifestations. RESULTS: One hundred six patients (median age, 3.5 years; range, 0.1-14.9 years) were identified, 37 with severe toxic, 37 with toxic, 13 with suspected toxic, and 19 with nontoxic exposures. The most common presenting signs or symptoms included altered level of consciousness, metabolic acidosis, tachycardia, and hypertension. All patients received normobaric oxygen for 5.5 hours (range, 0.6-44 hours). Carboxyhemoglobin levels decreased to less than 3% in 3.6 hours (range, 0-15.5 hours). Fifteen patients died, three from massive burn injury, eight from hypoxic-ischemic encephalopathy after cardiopulmonary arrest at presentation, and four from late complications of burn injury. Seven survivors did not recover their premorbid neurologic state, four of whom had respiratory arrest when rescued. Two patients had initial neurologic recovery followed by transient deterioration at 4 and 14 days after exposure. One patient developed seizures and was found to have bilateral occipital lobe infarctions 51 days after exposure. CONCLUSION: Acute neurologic manifestations after carbon monoxide exposure are common in children. These resolve rapidly with normobaric oxygen, however. Persistent sequelae are primarily related to asphyxia. Delayed neurologic syndromes are uncommon in children treated with normobaric oxygen.

Tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 concentrations in cerebrospinal fluid predict ventriculoperitoneal shunt infection.

OBJECTIVE: To determine the diagnostic value of cerebrospinal fluid tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6 released into the cerebrospinal fluid of patients with ventriculoperitoneal shunt infection. DESIGN: Prospective, observational study. SETTING: University teaching hospital. PATIENTS: Sixty-four patients requiring cerebrospinal fluid aspiration for suspected ventriculoperitoneal shunt malfunction. INTERVENTIONS: Cerebrospinal fluid samples were obtained by shunt aspiration at the time of patient presentation. MEASUREMENTS AND MAIN RESULTS: TNF-alpha and IL-1 beta concentrations were measured by enzyme-linked immunosorbent assay, and IL-6 activity by bioassay. The sensitivity, specificity, predictive values, and overall efficiency for each cytokine were determined based on the cerebrospinal fluid culture results. Ten patients had positive cerebrospinal fluid cultures, eight of which yielded Staphylococcus species, and one each Acinetobacter and Pseudomonas. Cerebrospinal fluid TNF-alpha, IL-1 beta, IL-6, protein, and leukocyte concentrations were significantly increased in patients with shunt infection. Cerebrospinal fluid IL-6 activity had the highest diagnostic accuracy of the cytokines evaluated, with sensitivity of 80% and specificity of 98%. CONCLUSIONS: The presence of cerebrospinal fluid inflammatory cytokines strongly suggests ventriculoperitoneal shunt infection. Detection of these cytokines in the cerebrospinal fluid could be used for earlier diagnosis of bacterial infection.

Protective effects of a thromboxane synthetase inhibitor and continuous arteriovenous hemofiltration in rat endotoxic shock.

We determined the efficacy of continuous arteriovenous hemofiltration (CAVH) and a thromboxane synthetase inhibitor (TSI) on survival and their effect on TXA2, PGI2, TNF alpha, and IL-1beta production in rat endotoxemia. Thirty-six endotoxemic rats were randomized to one of 4 groups: (A) no TSI, sham CAVH; (B) no TSI, CAVH; (C) TSI, sham CAVH; and (D) TSI, CAVH. Either CAVH (Group B) or pretreatment with TSI (Group C) resulted in increased survival time. CAVH did not prevent the rise in TX (Group B). TNF alpha levels at 2 h after LPS infusion were higher in Group D compared to Group B (26.1 +/- 3.7 vs 13.2 +/- 4.3 ng/mL, P < 0.05) respectively. IL-1beta was detected earlier in Groups C,D when compared to Groups A,B (P < 0.02). TNF alpha and IL-1beta were not ultrafiltered. CAVH and the inhibition of TX synthesis independently improved survival in endotoxemia, however, their beneficial effects were not additive. While TSI may improve survival by blocking TXA2 production, the salutary effects of CAVH appear to be from removal of an undetermined TXA2 dependent mediator. TNF alpha and IL-1beta concentrations do not appear to influence survival times in this model.

Dexamethasone for the prevention of postextubation airway obstruction: a prospective, randomized, double-blind, placebo-controlled trial.

OBJECTIVE: To determine whether dexamethasone prevents postextubation airway obstruction in young children. DESIGN: Prospective, randomized, double-blind, placebo-controlled study. SETTING: Pediatric intensive care unit of a university teaching hospital. PATIENTS: Sixty-six children, < 5 yrs of age, intubated and mechanically ventilated for > 48 hrs. INTERVENTIONS: Patients were randomized to receive intravenous dexamethasone (0.5 mg/kg, maximum dose 10 mg) or saline, every 6 hrs for six doses, beginning 6 to 12 hrs before elective extubation. MEASUREMENTS AND MAIN RESULTS: Dependent variables included the presence of stridor, Croup Score, and pulsus paradoxus at 10 mins, 6, 12, and 24 hrs after extubation; need for aerosolized racemic epinephrine and reintubation. The dexamethasone and placebo groups were similar in age (median 3 months [range 1 to 57] vs. 4 months [range 1 to 59], p = .6), frequency of underlying airway anomalies (3/33 vs. 3/33, p = 1.0), and duration of mechanical ventilation (median 3.3 days [range 2.1 to 39] vs. 3.5 days [range 2.1 to 15], p = .7). The dexamethasone group had a lower frequency of stridor, Croup Score, and pulsus paradoxus measurement at 10 mins and at 6 and 12 hrs after extubation. Fewer dexamethasone-treated patients required epinephrine aerosol (4/31 vs. 22/32, p < .0001) and reintubation (0/31 vs. 7/32, p < .01). Three patients exited the study early-one patient in the dexamethasone group had occult gastrointestinal hemorrhage and one patient in each group had hypertension. CONCLUSION: Pretreatment with dexamethasone decreases the frequency of postextubation airway obstruction in children.

Idiopathic pulmonary hemorrhage in infancy. Clinical features and management with high frequency ventilation.

STUDY OBJECTIVES: To describe the clinical characteristics of infants with severe acute pulmonary hemorrhage and the effects of mechanical ventilation on gas exchange. SETTING: Tertiary care pediatric ICU in a university hospital. PATIENTS AND DESIGN: Case records of patients with severe acute pulmonary hemorrhage from January 1992 to July 1995 were reviewed. Acute pulmonary hemorrhage was defined as hemoptysis and/or epistaxis or blood obtained from endotracheal tube which could not be attributed to cardiac or vascular malformation, infectious process, or known trauma. INTERVENTIONS: Patients were initially managed with conventional ventilation. High frequency ventilation (HFV) was utilized when hypoxemia (PaO2/PAO2 < 0.2) and/or respiratory acidosis (PaCO2 > or = 60 mm Hg with pH < 7.25) persisted. MEASUREMENTS AND RESULTS: Six African-American male infants from Detroit, with a median age 2.3 months, presented with severe acute pulmonary hemorrhage. Chest radiographs showed diffuse bilateral infiltrates or opacification with a normal sized heart. All infants were managed with HFV, four by oscillation and two by jet. The indications for HFV were persistent hypoxemia (2), respiratory acidosis (1), and a combination of both (3). There was an improvement in pH and PaCO2, and a decreased need for oxygen 6 and 24 h after initiating HFV. PaO2/PAO2 and oxygenation index showed a tendency toward improvement. All infants survived, and there were no complications. No cause for pulmonary hemorrhage was found in any of the infants. CONCLUSIONS: Idiopathic acute pulmonary hemorrhage is a potentially life-threatening disorder encountered among inner-city infants. HFV is highly effective and safe in rapidly reversing the severe oxygenation and ventilation deficits in this setting.

Predicting outcome in children with severe acute respiratory failure treated with high-frequency ventilation.

OBJECTIVES: a) To demonstrate the effect of high-frequency ventilation on gas exchange in children with severe acute respiratory failure unresponsive to conventional ventilation; b) to identify patients at high risk of death early after institution of high-frequency ventilation. SETTING: Tertiary care pediatric intensive care unit in a university hospital. DESIGN: A cross-sectional, observational study with factorial design. PATIENTS: Thirty-one patients with severe acute respiratory failure defined as a Pao2/F1o2 of < 150 torr (< 20 kPa) with a positive end-expiratory pressure of > or = 8 cm H2O and/or Paco2 of > 60 torr (> 8 kPa) with an arterial pH < 7.25. INTERVENTIONS: Patients received either high-frequency oscillation or jet ventilation if respiratory failure was unresponsive to conventional ventilation and if the underlying disease process was deemed reversible. MEASUREMENTS AND MAIN RESULTS: Thirty-one children were managed with high-frequency ventilation, 11 children with jet and 20 children with oscillator. Arterial blood gases and level of ventilatory support were recorded before and at 6, 24, 48, 72, and 96 hrs after institution of high-frequency ventilation. There was an improvement in an arterial pH, Paco2, Pao2, and Pao2/FID2 6 hrs after institution of high-frequency ventilation (p < .01). This improvement, along with decreased need for oxygen, was sustained through the subsequent course. Twenty-three (74%) of 31 children treated with high-frequency ventilation survived. Survivors showed an increase in an arterial pH, Pao2, Pao2/FIO2, and a decrease in Paco2 within 6 hrs, whereas nonsurvivors did not. Oxygenation index was the best predictor of outcome. A combination of an initial oxygenation index of > 20 and failure to decrease the oxygenation index by > 20% by 6 hrs after initiation of high-frequency ventilation predicted death with 88% (7/8) sensitivity and 83% (19/23) specificity, with an odds ratio of 33 (p = .0036, 95% confidence interval 3-365). CONCLUSIONS: In patients with potentially reversible underlying diseases resulting in severe acute respiratory failure that is unresponsive to conventional ventilation, high-frequency ventilation improves gas exchange in a rapid and sustained fashion. The magnitude of impaired oxygenation and its improvement after high-frequency ventilation can predict outcome within 6 hrs.