Simple method for monitoring concentration of inhaled nitric oxide.
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Biomedical subjects
Publications and source records attributed to D Bohn.
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Recurrent fistulas occur in about 10% of infants treated for esophageal atresia with distal tracheoesophageal fistula. Failed repair of a recurrent fistula rarely requires esophageal replacement and removal or diversion of the native esophagus. We present a patient who underwent multiple operations for recurrent tracheosophageal fistula whose native esophagus was eventually replaced with a colonic interposition graft. Over the subsequent 9 years he experienced failure to thrive, respiratory distress, and repeated pulmonary infections attributed to chronic aspiration. Eventually, he developed respiratory failure and required endotracheal intubation and mechanical ventilation. He became increasingly difficult to ventilate and, in spite of aggressive efforts, suffered a cardiac arrest from which he could not be resuscitated. At postmortem, a dilated blind segment of native esophagus, which was compressing and obstructing the malacic trachea, was found in the posterior mediastinum. Death was caused by massive air embolus, which was in turn attributed to the high airway pressures needed to ventilate the patient. Tracheal compression by a remnant of native esophagus should be considered in the differential diagnosis of respiratory failure after esophageal replacement.
OBJECTIVE: To define infection rates in patients with Pediatric Risk of Mortality (PRISM) scores greater than and less than 10 on admission to the pediatric ICU (PICU). DESIGN: Descriptive. SETTING: An 18-bed PICU admitting patients of all ages except nonsurgical neonates; within a 585-bed tertiary care pediatric hospital. PATIENTS: Patients admitted to the PICU from July 1987 to February 1988 inclusive. Of 685 admitted, 480 were followed for greater than or equal to 72 hr. METHODS: The baseline state of the patients on admission was determined by a designated intensivist using the PRISM score. Other variables included age, length of stay, and hospital day of onset of infection. Infections were identified by a designated intensivist who undertook prospective daily bedside observation, chart, radiographic, and laboratory review. MEASUREMENTS AND MAIN RESULTS: Equal portions of patients had PRISM scores less than and greater than 10. Significantly more infections occurred in the high PRISM population (10.8% vs. 3.4%, p less than .001). This association held through age, service, and length of stay. Sensitivity, specificity, positive and negative predictive values of a PRISM score greater than 10 were 75%, 53%, 11%, and 97%, respectively. Bacteremias accounted for 36% of infections, skin/eye/drain site 22%, respiratory 16%, wound 15%, and urine 9%. The most prevalent organisms were coagulase-negative staphylococci (32%), Pseudomonas aeruginosa (23%), Candida sp. (20%), and S. aureus (9%). CONCLUSIONS: A PRISM score greater than 10 on PICU admission characterizes a population within the PICU at increased risk of infection. However, 93% of patients did not develop infection and thus, a negative predictive value of 97% yields little additional information.
Lung disease in patients with severe combined immune deficiency (SCID) undergoing bone marrow transplantation (BMT) is most commonly caused by infection. Noninfectious episodes of pulmonary disease following BMT are more frequently encountered in patients with hematologic disorders or malignancy and are probably related to ablation therapy or graft-versus-host disease (GVHD). In contrast, patients with SCID do not receive chemotherapy before an HLA-identical allogeneic BMT and they do not suffer significant GVHD. We report a patient who developed severe lung disease during the period of rapid engraftment following an HLA-identical allogeneic bone marrow transplantation. Lung biopsy showed dense lymphocytic infiltrates in the alveolar septae and no evidence of infection. Following the idea that the acute recruitment of engrafted lymphocytes may have contributed to or caused the pulmonary disease, we have attempted to suppress cellular immunity by administering high-dose methylprednisolone. The patient's lung disease rapidly improved and eventually completely resolved.
Cardiorespiratory arrest occurring immediately after multiple injuries is usually assumed to be due to severe cerebral injury, acute hemorrhage, or airway obstruction. We have identified a group of 19 children (mean age, 6.3 years) who presented with absent vital signs (VSA) or severe hypotension, unexplained by blood loss, where these findings were caused by injury to the high cervical spine and cord, demonstrated either by X-ray or postmortem examination. Fourteen had radiologic evidence of injury to the spine between C1 and C3. In two patients the bony injury was at the C6-7 level, while in two patients the cervical spine X-ray was normal. Eighteen of the 19 children were initially resuscitated but died from a combination of hypoxic/ischemic encephalopathy and cerebral injury. Sixteen patients underwent postmortem examination and in 13 there was evidence of cord laceration, up to and including cord transection. These findings demonstrate a distinct pattern of "juvenile" cervical spine injury involving the high spine and cord which results in either apnea and cardiorespiratory arrest, or severe hypotension. This previously unrecognized cause of cardiorespiratory arrest should be considered in all children presenting with VSA after multiple trauma, even when there is no apparent radiologic abnormality of the cervical spine.
We reviewed the coroner's records for all pediatric (less than 16 years of age) trauma fatalities in Ontario (population, 9.5 million) for the period January 1, 1985, through December 31, 1987. Twenty-six (8%) of the 322 cases for which complete autopsy data were available had major thoracic vascular injuries. Twenty-five deaths occurred within 6 hours of injury. The majority of patients had at least one AIS 6 injury. The aorta was the most frequently injured vessel. Major thoracic vascular injuries are more common among children than previous reports suggest, probably because they are rapidly fatal. Many deaths occur in the field, at local hospitals, or in transit before the patient can reach a trauma center. Efforts to reduce the number of total thoracic vascular injuries should focus on primary and secondary prevention.
The effect of hypothermia (29 C) on the pharmacokinetics of ethanol was studied in eight piglets serving as their own normothermic controls. Ten milliliters of 12% ethanol per kilogram were infused over 30 minutes, and serum ethanol concentrations were measured for seven hours. Ethanol concentration data were fitted to one-compartment open model assuming Michaelis Menten elimination kinetics. During hypothermia, ethanol concentrations were consistently higher than during normothermia. This observation could be explained by both a significantly smaller distribution volume of ethanol during hypothermia (0.71 +/- 0.03 L/kg at 29 C and 0.84 +/- 0.05 L/kg at 37 C, P less than .02) and a significantly slower maximum velocity of metabolism of ethanol (Vm) during hypothermia (1.12 +/- 0.11 mg/kg.min vs. 1.83 +/- 0.21 mg/kg.min, P less than .01). Our study indicates that during hypothermia, ethanol stays significantly longer in the circulation in piglets. Potentially, this may contribute to a more profound effect from the ethanol.
To improve the efficiency of nosocomial infection detection, a highly structured system combining initial reporting by the bedside night nurse of symptoms possibly related to infection with follow-up by the infection control nurse (ICN) was developed: The Infection Control Sentinel Sheet System (ICSSS). Between July 1, 1987 and February 28, 1988, a prospective comparison of results obtained through ICSSS and daily bedside observation/chart review by a full-time trained intensivist was undertaken in the pediatric intensive care unit (PICU). Ratios of nosocomial infections and nosocomially-infected patients were 15.8 and 7.0 respectively among 685 admissions; included are seven infections identified only through the ICSSS so that the "gold standard" became an amalgamation of the two systems. The sensitivity for detection of nosocomially-infected patients by bedside observation/chart review and ICSSS was 100% and 87% respectively. The sensitivity for detection of standard infections (blood, wound and urine) was 88% and 85% respectively. The sensitivity for detection of nosocomial infections at all sites was 94% and 72% respectively. Missed infections were minor (e.g., drain, skin, eye), required physician diagnosis (e.g., pneumonia), were not requested on the sentinel sheet (SS) (e.g., otitis media), related to follow-up of deceased patients or were minor misclassifications or failures to associate with device (e.g., central-line related). Daily PICU surveillance by the ICN required only 20 minutes a day. The ICSSS appears highly promising and has many unmeasured benefits.
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Intermittent right-posterior accentuated slow waves (irregular theta and/or delta waves: IRP phenomenon) in the EEG showed an incidence of about 5% in the total in-patients of a psychiatric university hospital. The IRP phenomenon was found in 7.5% of patients with schizophrenic psychoses, 2% of patients with affective psychoses and in 2.4% of patients with neurotic and personality disorders. The IRP groups differed from control groups in a number of sociobiographical and clinical characteristics. Having repeatedly confirmed these relationships with different samples, we regard IRP patients, irrespective of the diagnosis given, as having a maturational deficit of brain function.
Severe low cardiac output of unknown cause that did not respond to inotropic and ventilatory support developed in a 2-kg infant. Intraaortic balloon pumping was used successfully to acutely improve her cardiac function and peripheral perfusion and to decrease the requirement for inotropic medications. We describe the technique for insertion and the equipment used, as well as our experience with intraaortic balloon pumping in children.
The effect of hypothermia on the disposition of fentanyl was evaluated in 18 children undergoing corrective cardiac surgery. They received a bolus of fentanyl followed by a continuous infusion which was stopped when cardiopulmonary bypass was established and profound hypothermia was achieved (18 degrees C-25 degrees C). Fentanyl plasma concentration remained essentially unchanged during hypothermia (6.45 ng/ml 5 min into hypothermia and 5.26 ng/ml 100-140 min later; p greater than 0.1). In subsequent experiments, the effect of hypothermia on the pharmacokinetics of fentanyl was studied in 4 piglets serving as their own controls. Both distribution volume (Vz) and total body clearance (CL) were significantly smaller during hypothermia. Our studies indicate that being a drug with a large distribution volume and a high hepatic extraction ratio, both CL and Vz are significantly reduced by hypothermia-induced hypoperfusion. In addition, TBC is influenced by the temperature-dependent hepatic metabolism of fentanyl.
We carried out a prospective study in 66 infants with congenital diaphragmatic hernia within the first 6 hours of life to determine whether outcome is related to the degree of underlying pulmonary hypoplasia, as predicted by preoperative PaCO2, when correlated with an index of ventilation (VI = mean airway pressure X respiratory rate) and confirmed by postmortem analysis of the lung. Those infants with PaCO2 greater than 40 mm Hg before surgery had a 77% mortality; when PaCO2 reduction could be achieved only with VI greater than 1000, the mortality was still greater than 50%. After repair, however, the ability to hyperventilate to PaCO2 less than 40 mm Hg proved to be an important determinant of survival; only one of 31 infants in this group died, whereas only two of 27 infants with PaCO2 greater than 40 mm Hg survived. In 16 infants with PaCO2 greater than 40 mm Hg despite hyperventilation, high-frequency oscillatory ventilation was started. This resulted in a rapid fall in PaCO2, but 14 of the 16 infants had only temporary improvement in oxygenation, and died. In five of the infants who died, alveolar number was assessed by postmortem morphometric analysis; there was a severe reduction to less than 10% of published normal neonatal values. Pulmonary vascular changes of increased muscularization were less remarkable than those observed in infants with persistent pulmonary hypertension. Our findings suggest that the degree of pulmonary hypoplasia (which would not be influenced by surgical repair), rather than the pulmonary vascular abnormality, mainly determines survival. Consideration could therefore be given to an initial nonsurgical approach to congenital diaphragmatic hernia, with the expectation that pulmonary function might improve and pulmonary vascular resistance decrease.
Reactive pulmonary hypertension in children after surgical repair of large left-to-right shunts is an important cause of postoperative low cardiac output. Low output may be caused by impaired left ventricular filling from right ventricular dilatation. We studied 12 children during the first 72 hr after surgery by measuring right ventricular pericardial surface pressure with a flat balloon and compared the results with acute changes in pulmonary arterial pressure (PAP). All 12 children (ages 4 to 14 months) had preexisting large left-to-right shunts with systemic PAPs. We found a highly significant linear correlation between acute rises in PAP and rises in the pericardial pressure (PP). The regression equation was PAP = 1.48(PP) + 5.7, R2 = .61, p less than .001. There was an average of 15.6 pulmonary hypertensive episodes per patient during the 72 hr study period, but only 9% of these episodes were associated with either no change or a fall in systemic pressure. We conclude that changes in right ventricular pericardial pressure reflect acute changes in PAP.
Newborn infants with impaired myocardial performance may not respond to inotropic drugs and volume loading. Vasodilator therapy was tried in 10 such patients and in most there was improvement in peripheral perfusion, blood pH, arterial oxygenation, blood pressure and urine output. No complications of these drugs were detected. Vasodilator therapy has a role in the management of the acutely sick newborn infant with clinical signs of low cardiac output.