Anthony Scardella

Obstetric admissions to the intensive care unit: outcomes and severity of illness.

OBJECTIVE To determine whether mortality prediction based on a current model of outcome prediction is accurate in obstetric patients. METHODS Consecutive obstetric admissions to a medical intensive care unit from 1991 to 1998 were reviewed to determine whether mortality prediction is feasible in obstetric patients based on a widely used model. The Simplified Acute Physiologic Score (SAPS II) was used to predict the probability of hospital mortality. RESULTS The Simplified Acute Physiologic Score overestimated mortality in all patients (19 predicted deaths, eight observed) but accurately predicted mortality in patients admitted to the intensive care unit for medical reasons (seven predicted, five observed). The Simplified Acute Physiologic Score did not predict mortality in patients admitted for obstetric indications or postpartum hemorrhage. Median SAPS II scores were significantly higher in those patients who died, compared with survivors. For all groups, SAPS II scores were correlated with intensive care unit length of stay but not hospital length of stay. CONCLUSION The Simplified Acute Physiologic Score accurately predicts hospital mortality in obstetric patients admitted to the intensive care unit for medical reasons but not for indications related to pregnancy and delivery. An alternate model that predicts outcomes in obstetric patients admitted for obstetric indications should be developed.

The Role of Endogenous Opioids in the Ventilatory Response to Sustained Respiratory Loads

The potent respiratory depressant effects of exogenous opiates are well known. Morphine and other opiates reduce ventilation, the ventilatory responses to hypercapnia and hypoxia, as well as the respiratory compensation for an acute increase in airway resistance.1-3 The discovery of endogenous opioid peptides such as beta-endorphin and enkephalin led to investigations into the possible role of these peptides in ventilatory control in humans. In one such study Santiago and co-workers found that the opioid antagonist naloxone restored the respiratory compensation for a flow-resistive load in those patients with chronic obstructive pulmonary disease in whom it was found to be absent.4 They postulated that in these patients endogenous opioids were elaborated in response to the stress of chronically increased airway resistance resulting in attenuation of compensation for the flow-resistive load. In a subsequent study in an unanesthetized goat model we tested the hypothesis that shorter periods of stress produced by increased airway resistance would activate the endogenous opioid system and reduce the subsequent ventilatory response.5 We found in animals exposed to two and one-half hours of inspiratory flow-resistive loading that the reduction in tidal volume was partially reversed by naloxone given at the conclusion of the loading period and that levels of immunoreactive beta-endorphin measured in the cisternal cerebrospinal fluid were increased. Our subsequent studies have been directed at defining the effect of activation of the endogenous opioid system on central respiratory output to the respiratory muscles and the peripheral signal responsible for the activation of this system. The results of these studies are discussed in detail below.