Robert Dinwiddie

Hemorrhagic shock and encephalopathy: clinical, pathologic, and biochemical features.

To further define the clinical, pathologic, and biochemical features of hemorrhagic shock and encephalopathy syndrome, we studied 25 affected children (aged 3 months to 14 years) admitted to a single center between 1982 and 1985. A prodromal illness comprising vomiting, diarrhea, listlessness, and fever was present in 84% of the cases. Acute onset of shock, convulsions and coma, bleeding (or laboratory evidence of disseminated intravascular coagulation), elevated plasma activity of hepatic enzymes, acidosis, and impaired renal function was present in every case. Twenty patients died, and all the survivors are neurologically damaged. At postmortem examination, intravascular microthrombi coexisting with hemorrhages and petechiae were found in most organs. Centrilobular liver necrosis and cerebral edema were prominent features. No microbiologic cause for the disorder was identified, but decreased plasma levels of the protease inhibitors α 1 -antitrypsin and α 2 -macroglobulin, together with increased levels of circulating proteolytic enzymes, were frequently present. An overrepresentation of the uncommon variant phenotypes of α 1 -antitrypsin was found in first-degree relatives of affected patients (four had the MZ phenotype, and one each the MS or MC phenotype, of 19 relatives studied). Abnormal accumulation of α 1 -antitrypsin was detected immunohistochemically in the livers of six of the patients. Defective protease inhibitor production or release may be involved in the pathogenesis of the disorder.

The effects of feeding on arterial blood gases and lung mechanics in newborn infants recovering from respiratory disease

Fifteen infants recovering from neonatal respiratory disease had arterial blood gases and lung mechanics measured 5 minutes before bolus feeds and at 5, 10, 20, and 30 minutes after feeding to determine physiologic effects of feeding. PaO2 fell significantly from prefeeding values at 5, 10, and 20 minutes after feeds. Mean prefeeding pH and base excess values were significantly different from mean postfeeding values at 5, 10, 20, and 30 minutes, respectively. PaCO2 remained unchanged before and after feeding. Heart rate and systolic and diastolic blood pressure did not change throughout the study. Dynamic lung compliance, respiratory, rate, and tidal volume did not change significantly but there was a trend toward increase in tidal volume. Mean minute volume rose with time as a consequence of the increased tidal volume. Work of breathing remained unchanged at 10 and 20 minutes postfeed and increased slightly at 30 minutes; this was due to a small increase in both elastic and viscous work components at this time.

Cardiopulmonary changes in the crying neonate.

Summary: To determine hemodynamic effects of crying, 12 newborn infants recovering from the respiratory distress syndrome (RDS) were studied.When crying, the range of inspiratory esophageal pressure was - 18.8 to −32.5 cm H2O and the range of expiratory pressure was +6.2 to +34.4 cm H2O. The esophageal pressure remained positive for a mean value of 66% of the respiratory cycle. There was a mean significant increase in heart rate of 19 beats/min. The systolic and diastolic blood pressures increased significantly at the beginning of strain to 115 and 135% of the respective control values. There was a progressive decrease in systolic and diastolic pressures during the period of strain and the systolic pressures reached values significantly less than control. With the decrease in systolic and diastolic pressures, there were pronounced reductions in pulse pressures. Three infants reached pulse pressure values less than 1% of control when cries were sustained for nine cardiac cycles.There was a significant mean decrease in arterial oxygen tension (PaO2) of 16.8 mm Hg. There were no changes in arterial carbon dioxide tension (PaCO2), pH, or base excess.Speculation: Asphyxiated nconates and infants with RDS often have a compromised circulation with hypoxemia and hypotension. This study suggests that the circulatory status in such infants may be further compromised by extended periods of crying. In three patients who were relatively stable and normovolemic, a profound decrease in pulse pressure was observed when the cry included seven or more cardiac cycles. These transient periods of no aortic flow might be of clinical significance in critically ill infants. The decreased frequency of crying observed in critically ill neonates may be beneficial to both oxygenation and hemodynamic stability.

EFFECTS OF CRYING ON INTRATHORACIC PRESSURE AND ART ERIAL BLOOD PRESSURE IN INFANTS RECOVERING FROM RESPIRATORY DISTRESS SYNDROME (RDS)

Although crying vital capacity has been recorded in infants recovering from RDS, little is known about physiological effects of vigorous crying at this stage of the illness. Detailed analysis of intraesophageal pressure (Pes) and abdominal & ortic blood pressure (B.P.) tracings were made on 15 patients recovering from RDS. Mean birth weight 2.04 kg (range 1.28-3.08), mean gestation 34 weeks (range 29-40) and mean age studied 63 hours (range 22-137). During crying maximum Pes ranged from -18.0 to -30.5 cm H2O during inspiration and from +6.2 to +34.3 during expiration. Pes remained positive during 66% of the respiratory cycle (range 54 to 85%) and mean Pes during inspiration was -12.3 cm H2O, during expiration mean Pes was +11.2 cm H2O. Heart rate rose significantly, mean increase 15 beats per minute (S.E.+3), P<0.01 and this was accompanied by a rise in B.P., mean systolic increase 5 mm Hg (S.E.±3), mean diastolic increase 9 mm Hg (S.E.±2) P<0.01. Beat to beat variation in B.P. during expiration resembled that seen in adults performing the Valsalva maneuver with sequential narrowing of the pulse pressure during successive heart beats. This study demonstrates the extreme range of intraoleural pressure generated and shows the significant effects of heart rate and blood pressure as a result of crying in patients recovering from RDS.

1175 ACTIVE EXPIRATORY WORK OF BREATHING IN THE NEWBORN

The small lung volume and low total lung compliance of the newborn lung leads to a different pattern of respiration from that of the older child and adult. Respiratory rates are higher and inspiration-expiration times shorter in order to maintain adequate alveolar ventilation. These parameters are best mediated through a work of breathing pattern which requires active expiratory mechanical work in order to prevent air trapping and to stabilize resting lung volume. Transpulmonary pressure (esophageal balloon), air flow (pneumotachograph), and tidal volume enabled·determination of dynamic pressure volume loops. Expiratory work of breathing was studied by planimetry on pressure-volume diagrams obtained from 100 normal newborn infants in the first three days of life. Mean birthweight was 3.39 kg (range 2.91-5.26 kg.), gestational age 38.6 wks. (range 37-42 wks.). Dynamic lung compliance was 1.68 ± 0.06 ml/cm H2O/kg mean ± S.E., resting lung volume 26.1 ± 0.7 ml/kg, respiratory rate 49 ± 1 per min., total work of breathing 32.7 ± 0.4 gm/cm/kg and active expiratory work per breath 2.9 ± 0.3 gm/cm/kg. Active expiratory work was performed in 98% of infants studied. It is concluded that active mechanical work is required even in the normal newborn during quiet respiration in order to overcome the resistive forces to expiration and that insufficient potential energy is stored during inspiration to perform this passively.