Peripartum Hypoxemic Respiratory Failure
June 1, 1998
Peripartum Hypoxemic Respiratory Failure
ABSTRACT & COMMENTARY
Synopsis: An acute illness marked by dyspnea, hypoxemia, and radiographic acute pulmonary edema may occur in the peripartum period, but is unusual and seen mainly in the context of hypertension, premature membrane rupture, fetal distress, and antepartum maternal infection.
Source: Karetzky M, Ramirez M. Medicine 1998;77(1): 41-49.
Karetzky and ramirez reviewed the medical records of all peripartum women who required admission to the ICU at Newark Beth Israel Medical Center from 1989 through 1992 in order to identify all patients who developed acute hypoxemic respiratory failure (AHRF). They defined AHRF as acute dyspnea associated with hypoxemia and radiographic evidence of acute pulmonary edema, and they excluded patients with serious underlying illness such as collagen-vascular disease or HIV infection. Patient data collected included demographics, reproductive and obstetrical history, use of tocolytic agents, amniotic fluid characteristics, and outcome of the delivery. The clinical course, associated laboratory findings, management, and outcome of the episode of AHRF were also noted.
During the four-year study period, there were 19 cases of peripartum AHRF out of 10,852 deliveries (incidence, 0.2%) and 4886 ICU admissions. Study patients' ages ranged from 18 to 40, with an average of 26.8 years. All but two were multigravida, and average gestation was 29.7 weeks. Essentially all of the patients who developed AHRF had had complicated pregnancies or prior obstetrical problems. Compared with the entire obstetric population, AHRF patients had more cesarean sections, premature rupture of the membranes, hypertension, fetal distress, and antepartum infection (P < 0.05 for each factor). Ethnic and socioeconomic factors were not different between the two groups. Five of the 19 AHRF patients had received tocolytic agents.
The clinical presentations and associated findings varied. Nine patients (47%) developed dyspnea before delivery, two during delivery or at the time of cesarean section, and eight after delivery. Five patients who developed postpartum respiratory distress had received transfusions. The acute illness was characterized by fever, hypoxemia, moderate leukocytosis, a fall in hematocrit, and, in the 11 of 19 who underwent pulmonary artery catheterization, a hyperdynamic state without elevated filling pressures. Mechanical ventilation was required in seven of 19 patients, and two of them died. Karetzky and Ramirez discuss a number of possible mechanisms for development of AHRF in the peripartum period. They recommend that maternal oxygenation be monitored routinely in the peripartum period so that respiratory abnormalities can be detected early, intervention undertaken, and progression prevented.
COMMENT BY DAVID J. PIERSON, MD
Karetzky and Ramirez begin by identifying several factors, including decreased expiratory reserve volume, a hyperdynamic circulatory state, and hemodilution, that they hypothesize would predispose the pregnant woman to development of AHRF. They then characterize 19 patients with peripartum dyspnea, hypoxemia, and radiographic findings of pulmonary edema in terms of possible predisposing factors and certain clinical features, based on a retrospective chart review. Subsequently, they provide an in-depth discussion of possible etiologies and mechanisms for development of peripartum AHRF.
The clinical experience provided in this paper offers little new information about the syndrome of peripartum AHRF (if indeed it is a distinct entity), but Karetzky and Ramirez provide a thoughful discussion of the processes that can lead to AHRF in this setting. Conditions that have been associated with acute respiratory failure in pregnancy include aspiration, sepsis, transfusion reactions, abruptio placentae, amniotic fluid embolism, toxemia and preeclampsia, and the administration of tocolytic agents.
Aspiration of gastric contents during anesthesia for delivery, with wheezing, acute respiratory distress, and pulmonary edema, was first reported by Mendelson in 1946. This complication occurred in 45 patients, or 0.15% of deliveries in Mendelson's series, and was a self-limited acute illness without fatality except when massive aspiration of solid material occurred.
Maternal infection, especially acute pyelonephritis, is known to be associated with peripartum AHRF, and was present in seven of 19 patients in the present series. Karetzky and Ramirez propose that inflammatory mediators generated in response to such infection might stimulate the pregnant uterus, precipitating labor, and also facilitating entry of amniotic fluid into the maternal circulation, leading to an enhanced systemic inflammatory response and AHRF. Unquestionably, sepsis is an important risk factor for acute lung injury and the acute respiratory distress syndrome; whether additional factors are operating when AHRF occurs in the peripartum period is unclear.
Transfusion reactions, or more specifically leukoagglutinin reactions, which typically occur when both the donor and the recipient of the blood transfused are multiparous, present with acute respiratory distress and pulmonary edema, although they generally do not progress to full-blown ARDS. Five of the patients in this series were thought to have had leukoagglutinin reactions.
Abruptio placentae consists of premature separtion of the placenta from the uterus, with release of placental thromboplastic and fibrinolytic activators into the circulation. It has been reported to occur in up to 50% of cases of amniotic fluid embolism, in which entry of fetal debris into the maternal circulation is believed to account for the dramatic clinical features of this syndrome.
Pregancy-induced hypertension and its variant, the HELLP syndrome (hemolysis, elevated liver enzymes, low platelets), are associated with a variety of systemic effects, including multiple systems organ dysfunction, especially in the postpartum period. Acute respiratory failure, while unusual in this setting, may be a manifestation of the same pathophysiology. In both preeclampsia and the use of tocolytic agents for premature labor, acute pulmonary edema may occur, although its pathogenesis remains controversial. Both hydrostatic factors from excessive volume administration and increased permeability due to circulating mediators of inflammation have been invoked as possible mechanisms.
Whether all these processes, which vary from hypothetical to well-established, together comprise a syndrome of peripartum AHRF seems somewhat dubious to me. Amniotic fluid embolism is a distinct entity, as are sepsis and aspiration of gastric acid, but are they linked by common mechanisms? Perhaps they are, to a lesser or greater degree, although I am unsure how helpful this is to the clinician. All of the entitites discussed above can be associated with ARDS, a condition for which no known prophylaxis or treatment exists, at least in its more common clinical circumstances.
One thing that is clear is that AHRF in the peripartum period is, fortunately, quite uncommon-it occurred in 0.2% of deliveries in this report and in 0.3% in another large series (Smith JL, et al. West J Med 1990;153:508-510). Rather than subjecting all women to intensive peripartum monitoring for development of AHRF as suggested by Karetzky and Ramirez, it might be more cost-effective to concentrate on those individuals with the risk factors identified in this study, such as hypertension, fetal distress, antepartum infection, and premature rupture of the membranes.
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