Pain management in the critically ill child.

Children frequently received no treatment, or inadequate treatment, for pain and for painful procedures. The newborn and critically ill children are especially vulnerable to no treatment or under-treatment. Nerve pathways essential for the transmission and perception of pain are present and functioning by 24 weeks of gestation. The failure to provide analgesia for pain results in rewiring the nerve pathways responsible for pain transmission in the dorsal horn of the spinal cord and results in increased pain perception for future painful results. Many children would withdraw or deny their pain in an attempt to avoid yet another terrifying and painful experiences, such as the intramuscular injections. Societal fears of opioid addiction and lack of advocacy are also causal factors in the under-treatment of pediatric pain. False beliefs about addictions and proper use of acetaminophen and other analgesics resulted in the failure to provide analgesia to children. All children even the newborn and critically ill require analgesia for pain and painful procedures. Unbelieved pain interferes with sleep, leads to fatigue and a sense of helplessness, and may result in increased morbidity or mortality.

Predictors of outcome in severely head-injured children.

OBJECTIVE: Determine variables in the acute care period associated with survival and pediatric intensive care unit (PICU) length of stay (LOS) for children with severe traumatic brain injury. DESIGN: Retrospective cohort. SETTING: Level 1 pediatric trauma center. PATIENTS: Children (0-17 yrs) admitted 1991 to 1995 with nonpenetrating traumatic brain injury and admission Glasgow Coma Scale score of or=14. Predictors of outcome were abstracted, including Pediatric Trauma Score, Glasgow Coma Scale score, Pediatric Risk of Mortality, physiologic variables, computed tomography evidence of brain injury, and neuroresuscitative medications. The fatality rate was 24%. Age and gender were similar between groups (p >or= .1). Survival was independently predicted by 6-hr Glasgow Coma Scale score (odds ratio [OR] 4.6; 95% confidence interval [CI] 2.06-11.9; p < .001) and maximum systolic blood pressure (OR 1.05; 95% CI 1.01-1.09; p < .02). Odds of survival increased 19-fold when maximum systolic blood pressure was >or=135 mm Hg (OR 18.8; 95% CI 2.0-178.0; p < .01). By discharge, 67% of patients had an age-appropriate Glasgow Coma Scale score. Median hospital costs were 8,798 dollars for survivors: only mannitol use independently predicted high cost (odds ratio 4.9; 95% CI 1.2-19.1; p < .01). For survivors, median PICU LOS was 2 days, although 25% had LOS >6 days. Six-hour Glasgow Coma Scale score (OR 0.62; 95% CI 0.48-0.80; p < .001) and mannitol (OR 7.9; 95% CI 2.3-27.3; p < .001) were each independently associated with a prolonged LOS among survivors. CONCLUSIONS: Patients with higher 6-hr Glasgow Coma Scale scores were more likely to survive. Adjusting for severity of injury, survival was associated with maximum systolic blood pressure >or=135 mm Hg, suggesting that supranormal blood pressures are associated with improved outcome. Mannitol administration was associated with prolonged LOS, yet conferred no survival advantage. We suggest reevaluation of blood pressure targets and mannitol use in children with severe traumatic brain injury.

Effects of loaded breathing and hypoxia on diaphragm metabolism as measured by (31)P-NMR spectroscopy.

Diaphragm fatigue may contribute to respiratory failure. (31)P-nuclear magnetic resonance spectroscopy is a useful tool to assess energetic changes within the diaphragm during fatigue, as indicated by P(i) accumulation and phosphocreatine (PCr) depletion. We hypothesized that loaded breathing during hypoxia would lead to diaphragm fatigue and inadequate aerobic metabolism. Seven piglets were anesthetized by using halothane inhalation. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi) at end expiration with the airway occluded. A nuclear magnetic resonance surface coil placed under the right hemidiaphragm measured P(i) and PCr during four conditions: control, inspiratory resistive breathing (IRB), IRB with hypoxia, and recovery (IRB without hypoxia). IRB alone resulted in hypercarbia (32 +/- 7 to 61 +/- 21 Torr) and respiratory acidosis but no change in diaphragm force output or aerobic metabolism. Combined IRB and hypoxia resulted in decreased force output (Pdi decreased by 40%; from 30 +/- 17 to 19 +/- 11 mmHg) and evidence of metabolic stress (ratio of P(i) to PCr increased by 290%; from 0.19 +/- 0.09 to 0.74 +/- 0.27). We conclude that diaphragm fatigue associated with inadequate aerobic oxidative metabolism occurs in the setting of loaded breathing and hypoxia. Conversely, aerobic metabolism and force output of the diaphragm remain unchanged from control during loaded normoxic or hyperoxic breathing despite the onset of respiratory failure.

Successful treatment of life-threatening acute chest syndrome of sickle cell disease with venovenous extracorporeal membrane oxygenation.

PURPOSE: We describe a pediatric patient with sickle cell disease and life-threatening acute chest syndrome who was successfully treated with venovenous extracorporeal membrane oxygenation (ECMO). PATIENT AND METHODS: An 8-year-old boy with sickle cell disease presented with vaso-occlusive crisis, which progressed to fulminant acute chest syndrome requiring a partial exchange transfusion and mechanical ventilation. Despite very high ventilator settings and significant barotrauma, hypoxia persisted and circulatory failure occurred. He was then successfully treated with venovenous ECMO for 11 days. One month after decannulation he had a seizure associated with abnormalities on magnetic resonance images (MRIs). His disease has been managed with a chronic transfusion program since then. Follow-up after 5 years reveals normal pulmonary function tests, a normal magnetic resonance angiogram (MRA), and above-average cognitive skills. CONCLUSION: This is the first report of a pediatric patient with acute chest syndrome successfully managed with venovenous ECMO. His course was complicated by a seizure associated with MRI abnormalities, although the outcome has been excellent. This case suggests that treatment with venovenous ECMO should be strongly considered for sickle cell patients with life-threatening acute chest syndrome, despite maximal conventional support.

In vivo diaphragm metabolism: comparison of paced and inspiratory resistive loaded breathing in piglets.

OBJECTIVE: We hypothesized that spontaneous, loaded diaphragm contractions would lead to diaphragm fatigue, which would correlate with inadequate oxidative metabolism as measured by phosphorus-31 nuclear magnetic resonance spectroscopy. DESIGN: Prospective, randomized, crossover trial. SETTING: University hospital research laboratory. SUBJECTS: Eight piglets, 4 to 6 wks of age. INTERVENTIONS: Each animal underwent, in random order, a 20-min period of diaphragm pacing and a 45-min period of loaded spontaneous breathing, separated by a 20-min recovery period. Mechanical ventilation was used during diaphragm pacing to maintain a PaCO2 of 35 to 45 torr (4.7 to 6.0 kPa) and a PaO2 of > 100 torr (> 13.3 kPa). During spontaneous breathing, inspiratory loading was achieved with a 2.0-mm inner diameter endotracheal tube in the breathing circuit. MEASUREMENTS AND MAIN RESULTS: During pacing, mean transdiaphragmatic pressure decreased by 35%, from 23 +/- 5 (SD) to 15 +/- 3 mm Hg (p < .05), and this decrease correlated with a 335% increase in the ratio of inorganic phosphate to phosphocreatine, from 0.23 +/- 0.1 to 1.0 +/- 0.7 (p < .05). During loaded spontaneous breathing, arterial pH decreased from 7.42 +/- 0.06 to 7.25 +/- 0.05 (p < .05), secondary to an increase in PaCO2 from 41 +/- 4 to 65 +/- 11 torr (5.3 +/- 0.5 to 8.7 +/- 1.5 kPa) (p < .05). Despite respiratory acidosis, there was no decrease in trandiaphragmatic pressure during the period of loaded breathing, nor was any change in the ratio of inorganic phosphate to phosphocreatine seen. CONCLUSIONS: Diaphragm fatigue in a pacing model correlates with inadequate oxidative metabolism. In contrast, severe inspiratory resistive loaded breathing did not result in changes in oxidative metabolism or decreased diaphragm force output, despite hypercapnia and respiratory acidosis.

Ultrasound evaluation of piglet diaphragm function before and after fatigue.

Clinically, a noninvasive measure of diaphragm function is needed. The purpose of this study is to determine whether ultrasonography can be used to 1) quantify diaphragm function and 2) identify fatigue in a piglet model. Five piglets were anesthetized with pentobarbital sodium and halothane and studied during the following conditions: 1) baseline (spontaneous breathing); 2) baseline + CO2 [inhaled CO2 to increase arterial PCO2 to 50-60 Torr (6.6-8 kPa)]; 3) fatigue + CO2 (fatigue induced with 30 min of phrenic nerve pacing); and 4) recovery + CO2 (recovery after 1 h of mechanical ventilation). Ultrasound measurements of the posterior diaphragm were made (inspiratory mean velocity) in the transverse plane. Images were obtained from the midline, just inferior to the xiphoid process, and perpendicular to the abdomen. M-mode measures were made of the right posterior hemidiaphragm in the plane just lateral to the inferior vena cava. Abdominal and esophageal pressures were measured and transdiaphragmatic pressure (Pdi) was calculated during spontaneous (Sp) and paced (Pace) breaths. Arterial blood gases were also measured. Pdi(Sp) and Pdi(Pace) during baseline + CO2 were 8 +/- 0.7 and 49 +/- 11 cmH2O, respectively, and decreased to 6 +/- 1.0 and 27 +/- 7 cmH2O, respectively, during fatigue + CO2. Mean inspiratory velocity also decreased from 13 +/- 2 to 8 +/- 1 cm/s during these conditions. All variables returned to baseline during recovery + CO2. Ultrasonography can be used to quantify diaphragm function and identify piglet diaphragm fatigue.

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.

Emergency management of status asthmaticus in children.

Life-threatening status asthmaticus in children is sufficiently common so that all emergency departments receiving children must have a management strategy prepared for this disease. The strategy encompassing both the prehospital and the emergency department phases relies on frequent inhalation of nebulized bronchodilators (typically albuterol and ipratropium), intravenous steroids, and prompt endotracheal intubation in children with obtundation, hypoxia, or inaudible breath sounds. Death should be preventable in this disease if the child receives aggressive medical attention before respiratory arrest has developed. However, the best therapy involves prevention by ensuring that children with a history of severe asthma receive adequate anti-inflammatory therapy usually with inhaled steroids before life-threatening status asthmaticus develops.

Effect of aminophylline on high-energy phosphate metabolism and fatigue in the diaphragm.

BACKGROUND: Diaphragmatic fatigue causes respiratory failure, for which aminophylline has been used as therapy. Because the mechanism of action of aminophylline in reversing diaphragmatic fatigue is unclear, we used in vivo 31P magnetic resonance spectroscopy (MRS) to determine the relation between diaphragmatic activation, force output, and aerobic metabolism. METHODS: Bilateral phrenic stimulation was used to pace the diaphragm in pentobarbital-anesthetized piglets (6-10 weeks old; n = 44). Esophageal and abdominal pressures were measured to calculate transdiaphragmatic pressure (Pdi) (Pdi = abdominal pressure-esophageal pressure) as an index of force output. Activation was determined by the amplitude of the compound action potential of the diaphragmatic electromyogram. Aerobic metabolism was assessed with a 31P MRS surface coil on the right hemidiaphragm with the animal in a 4.7-T magnet. The animals were divided into four groups based on aminophylline loading dose: saline, aminophylline 10 mg/kg (A10), aminophylline 20 mg/kg (A20), and aminophylline 40 mg/kg (A40). After aminophylline loading the diaphragm was paced for 25 min followed by a 10-min recovery. RESULTS: Aminophylline concentrations were 12.2 +/- 0.7, 21.9 +/- 2.4, and 44.9 +/- 3.6 mg/l in the A10, A20, and A40 groups, respectively. Compound action potential amplitude decreased in all groups by 30% after 25 min of pacing. Conversely, Pdi remained at 100 +/- 3% of the initial value after 5 min of pacing in the A40 group but decreased to 75 +/- 3% in the saline group. Pdi recovered completely (103 +/- 17%) in the A40 group but remained depressed (72 +/- 6%) in the saline group. Pdi values were intermediate in the A10 and A20 groups. MRS data revealed inadequate energy supply/demand ratio in the saline group such that the ratio of inorganic phosphate to phosphocreatine (Pi/PCr) increased to 1.01 +/- 0.09 after 5 min of pacing. Pi/PCr remained unchanged in the A40 group and was intermediate in the A10 and A20 groups. beta-Adenosine triphosphate and intracellular pH did not differ among groups or as a function of pacing. Diaphragmatic blood flow increased from a resting value of 35-60 to 300-410 ml.min-1 x 100 g-1 during pacing in all groups and was not affected by aminophylline dose. CONCLUSIONS: Aminophylline, in a dose-dependent fashion, delays the onset of fatigue and improves recovery from fatigue. Delayed fatigue is associated with improved aerobic metabolism as reflected in a low Pi/PCr ratio.

Predictors of acute respiratory failure after bone marrow transplantation in children.

OBJECTIVE: To determine factors associated with acute respiratory failure after bone marrow transplantation which can be identified before the onset of lung disease. DESIGN: Population-based, retrospective study. SETTING: A referral-based pediatric intensive care unit and bone marrow transplant center. PATIENTS: Thirty-nine patients with lung disease (abnormal chest radiograph or a need for supplemental oxygen) were identified from a group of 318 pediatric bone marrow transplant patients from 1978 to 1988. Thirty-four of 39 patients with complete data were further classified into patients with mild lung disease (recovery without needing endotracheal intubation, n = 16) and patients with acute respiratory failure (requirement for endotracheal intubation, n = 18). INTERVENTIONS: Regression analyses were performed to define risk factors for development of respiratory failure (multivariate logistic regression) and for a shortened interval between the identification of lung disease and respiratory failure (Cox proportional hazards analysis). MEASUREMENTS AND MAIN RESULTS: Ninety-three percent (15/16) of patients with mild lung disease survived. Conversely, only 9% (2/23) of patients with respiratory failure survived. Predictors of respiratory failure included graft vs. host disease (odds ratio 28.3, 95% confidence interval 1.9-421, p = .015), a prelung disease (baseline) circulating creatinine concentration of > 1.5 mg/dL (> 132.6 mumol/L) (odds ratio 28.4, 95% confidence interval 1.4-577, p = .029), and male gender (odds ratio 14.6, 95% confidence interval 1-210, p = .049). Predictors of a shortened time to onset of respiratory failure included baseline serum creatinine value of > 1.5 mg/dL (> 132.6 mumol/L) (hazard ratio 6.2, 95% confidence interval 1.5-26.5, p = .013) and baseline total bilirubin concentration > 1.4 mg/dL (> 23.9 mumol/L) (hazard ratio 4.5, 95% confidence interval 0.98-20.7, p = .053). The median time to onset of respiratory failure was 4 days in patients with baseline creatinine values > or = 1.5 mg/dL (> 132.6 mumol/L) and 5 days in patients with baseline bilirubin concentrations > or = 1.4 mg/dL (> 23.9 mumol/L) vs. > 26 days in patients with creatinine < 1.5 mg/dL (< 132.6 mumol/L) and > 29 days in patients with bilirubin < 1.4 mg/dL (< 23.9 mumol/L) (Kaplan-Meier analysis). CONCLUSIONS: Renal and liver dysfunction preceded clinical evidence of lung disease in bone marrow transplant patients who developed respiratory failure. Lung disease leading to respiratory failure and adult respiratory distress syndrome appears to develop as one component of the multiple organ failure syndrome in pediatric bone marrow transplant patients.

Disposition and respiratory effects of intrathecal morphine in children.

BACKGROUND: The extent and duration of respiratory depression after opioid administration are poorly defined in infants and children. METHODS: The disposition and respiratory effects of intrathecal morphine were studied in ten patients (ages 4 months-15 yr) after repair of craniofacial defects. Morphine, 0.02 mg/kg, was administered intrathecally before the end of surgery. Postoperatively, we determined the minute ventilation (VE) in response to increasing partial pressure of end-tidal carbon dioxide (PETCO2) during carbon dioxide rebreathing. The slope (VE/PETCO2) and intercept (VE at PETCO2 60 mmHg, VE 60) of the carbon dioxide response curve were calculated at 6, 12, and 18 h after morphine administration. Cerebrospinal fluid (CSF) and blood were analyzed for morphine concentration by radioimmunoassay. RESULTS: Mean VE/PETCO2 decreased from a preoperative value of 35.1 +/- 3.7 to 16.3 +/- 2.8 ml.kg-1 x min-1 x mmHg-1 at 6 h after morphine, and remained depressed to 23.4 +/- 2.9 and 23.5 +/- 3.3 ml.kg-1 x min-1 x mmHg-1 at 12 h and 18 h, respectively, compared to preoperatively). The infants' (n = 3) VE/PETCO2 at 6 h were 21, 4, and 27 ml.kg-1 x min-1 x mmHg-1. Mean VE 60 decreased from 874 +/- 125 to 276 +/- 32 ml x kg-1 x min-1 at 6 h, but then recovered at 12 and 18 h to 491 +/- 68 and 567 +/- 82 ml.kg-1 x min-1, respectively. The infants' VE 60 at 6 h were 350, 142, and 245 ml.kg-1 x min-1. Mean CSF morphine concentration was 2,860 +/- 540 ng/ml at 6 h, and decreased to 640 +/- 220 and 220 +/- 150 ng/ml at 12 and 18 h, respectively. CONCLUSIONS: Intrathecal morphine, 0.02 mg/kg, depressed the ventilatory response to carbon dioxide for up to 18 h concomitant with increased CSF morphine concentrations. Infants (4-12 months of age) did not exhibit greater ventilatory depression than did children (2-15 yr of age).

Cardiorespiratory responses to epidural analgesia in the awake child: a retrospective review of postoperative patients.

The authors retrospectively evaluated the cardiorespiratory effects of epidural administration of bupivacaine in 17 awake children during the immediate postoperative period. Responses to dosing were assessed by comparing heart rate, blood pressure, and respiratory rate before and after administration. Additionally, hourly heart rates were compared between those patients receiving intermittent bolus doses and those receiving a continuous infusion. The patients included 11 boys and 6 girls, ranging in age from 4 months to 12 1/2 years and in weight from 7.4 to 48 kg. All catheters were placed after the induction of general anesthesia. Surgical procedures included exploratory laparotomy (9 patients), bladder reconstruction (4 patients), wound debridement and skin grafting (2 patients), amputation (1 patient), and Nissen fundoplication (1 patient). A total of 37 bolus doses of 0.25% bupivacaine were administered to 7 patients. A significant (P < .001) decrease in heart rate (187 +/- 2 to 137 +/- 1 beats/min), respiratory rate (42 +/- 2 to 25 +/- 1 breaths/min), and systolic blood pressure (125 +/- 3 to 86 +/- 1 mm Hg) was noted after administration. When postdosing cardiorespiratory parameters were compared with preoperative values obtained the day before surgery during the preoperative anesthesia evaluation, there was no significant difference in heart rate (131 +/- 14 versus 137 +/- 13 beats/min), respiratory rate (21 +/- 7 versus 25 +/- 1.0 breaths/min), and systolic blood pressure (93 +/- 9 versus 86 +/- 2 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragmatic fatigue assessed by 31P-magnetic resonance spectroscopy in vivo.

We tested whether fatigue of the piglet diaphragm is associated with inadequate oxidative metabolism as measured by magnetic resonance spectroscopy (MRS). An MRS measured ratio of inorganic phosphate to phosphocreatine (Pi/PCr) > or = 1 was taken as evidence of inadequate oxidative metabolism. Piglets (n = 10) underwent phrenic nerve pacing for 90 min with stimulation frequency of 30 Hz and duty cycle of 0.33. In a separate group of six piglets PCr, Pi, ATP, and intracellular pH were measured by in vivo MRS, and diaphragmatic blood flow was measured with radioactive microspheres at control, 2, 10, 45, 60, and 90 min of pacing. Transdiaphragmatic pressure fell from 25 +/- 3 to 15 +/- 2 mmHg (61 +/- 5%) at 2 min and remained depressed in a separate group of four piglets (P < 0.05). Conversely, compound action potential amplitude remained constant for the first 10 min of pacing and fell to 68 +/- 5% of control at 45 min (P < 0.05). Pi/PCr rose from a control value of 0.32 +/- 0.06 to 0.92 +/- 0.23 at 2 min and 0.79 +/- 0.03 at 10 min (P < 0.05) before returning toward control at 45-90 min. O2 delivery increased from 4.6 +/- 1.2 to 24.7 +/- 4.8 ml.min-1.100 g-1 at 2 min and 18.4 +/- 2.2 ml.min-1.100 g-1 at 10 min (P < 0.05) but then fell to lower levels at 45-90 min. ATP and intracellular pH remained constant except for a decline in pH to 6.98 +/- 0.09 at 45 min (P < 0.05) from the control value of 7.26 +/- 0.06.(ABSTRACT TRUNCATED AT 250 WORDS)

Millions to benefit from the Safe Medical Devices Act (SMDA) of 1990.

The need and desire for quality improvements in patient care, coupled with consumer desire to assume increasing responsibility for their own healthcare, signals a strong future for services like the International Implant Registry.

Preinduction of anesthesia in children with rectally administered midazolam.

The authors evaluated the efficacy of rectally administered midazolam for preinduction (i.e., premedication/induction) of anesthesia in 67 pediatric patients, ASA physical status 1 or 2, undergoing a variety of elective surgical procedures. In phase 1, 41 children weighing 12 +/- 3 kg (range 7-20 kg) and 31 +/- 16 months (range 8-67 months) of age (mean +/- SD) received midazolam, 0.4-5.0 mg.kg-1, in an attempt to produce unconsciousness. Only one child lost consciousness (4.5 mg.kg-1). However, at all doses, inhalational induction of anesthesia was facilitated because children were tranquil and calmly separated from their parent(s). There were no clinically significant changes in arterial blood pressure, heart rate, oxyhemoglobin saturation, and end-tidal carbon dioxide concentration, 10 min after drug administration. In phase 2, 26 children weighing 17 +/- 4 kg (range 10-26 kg) and 44 +/- 19 months (range 17-84 months) months of age undergoing tonsil and/or adenoid surgery were studied to determine the optimal sedative dose of rectally administered midazolam. Patients received 0.3, 1.0, 2.0, or 3.0 mg.kg-1 of midazolam in a randomized, double-blind fashion. One third (3 of 9) of patients receiving 0.3 mg.kg-1 struggled during mask induction. All patients receiving greater than or equal to 1.0 mg.kg-1 were adequately sedated (P less than 0.008). Discharge from the postanesthesia care unit (PACU), however, was delayed (greater than 60 min) in children receiving greater than or equal to 2.0 mg.kg-1 (P less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragmatic performance during recovery from acute ventilatory failure in Guillain-Barré syndrome and myasthenia gravis.

Diaphragmatic muscle performance during acute ventilatory failure due to Guillain-Barré syndrome and myasthenia gravis was assessed to evaluate (1) diaphragmatic function during weaning from ventilatory support and (2) diaphragmatic tension-time integral (TTdi) during ventilatory failure. We used a multilumen nasogastric tube and a pneumotachograph to measure transdiaphragmatic pressure per breath (Pdi), maximum transdiaphragmatic pressure (Pdimax), tidal volume (VT), and inspiratory time fraction during 74 spontaneous breathing trials in nine patients. Diaphragmatic performance was poor in all patients. The Pdi, Pdimax, and VT improved significantly, but values for Pdi and Pdimax remained low even after weaning. Improvement in Pdimax was the best predictor of recovery (r = 0.48; p less than 0.001). Maximal inspiratory force correlated with Pdimax (r = 0.48; p less than 0.005), but FVC did not. The TTdi rarely exceeded the expected fatigue threshold of 0.15 in spite of the patient's inability to sustain ventilation. Although our patients demonstrated diaphragmatic weakness, TTdi did not demonstrate diaphragmatic fatigue.