[DISCUSSION]
Pulmonary edema following normal vaginal delivery is a rare but
potentially serious complication that requires prompt recognition and
management [5]. While the exact pathophysiology is not fully
understood, it is believed to be multifactorial, involving fluid shifts,
hemodynamic changes, and altered vascular permeability [6].
Postpartum pulmonary edema can be either cardiogenic (peripartum
cardiomyopathy, pre-existing valvulopathies, myocardial ischemia, and
pre-eclampsia causing heart failure) or noncardiogenic (iatrogenic fluid
overload, excessive tocolytic use, thyroid disease, sepsis, and ARDS) in
origin [7]. Studies have shown that there is an increased risk of
pulmonary edema associated with cesarean and spontaneous preterm
delivery. Our patient did not meet the criteria for any of the above
causes. In study done by Kakogawa et al patient was Managed with oxygen,
diuretics, morphine and beta-blockers contrasting from our study where
we used oxygen, diuretics, hydrocortisone and GTN infusion for
management of the case [8]. A new position statement from a European
Society of Cardiology working group on Post-Partum Cardiomyopathy(PPCM)
has expanded the definition of the condition. It now describes PPCM as
an idiopathic heart condition marked by heart failure caused by
decreased left ventricular function occurring towards the end of
pregnancy or in the months post-delivery, with no other identifiable
cause of heart failure [9].
Kakogawa et al study reported that cause of heart failure in the patient
was diastolic dysfunction during the third trimester of pregnancy.
However, in our resource limited setting, echocardiography screening was
done at the bedside which resulted in normal LVEF with no cardiac
abnormality [8].
In Kakogawa et al study an elevated level of serum prolactin was found,
as the 16-kDa cleavage product of prolactin as well as C1 inhibitor
deficiency is a major contributor to PPCM [8, 10]. The deficiency of
C1 inhibitor led to the onset of acute heart failure, marked by a
combined dysfunction in both systolic and diastolic phases, attributed
to the leakage of capillaries throughout the body [11]. However, we
are unable to test serum prolactin and C1 inhibitor due to limited
resources and unavailability of test in peripheral setting. A
retrospective investigation studying BNP levels in pregnancy found that
women who encountered adverse maternal cardiac events during this period
had BNP levels exceeding 100 pg/mL [12].
Although measuring serial BNP levels was helpful there are limited data
available on the value of BNP levels when evaluating volume status
during pregnancy, so in our study, we have not done serial BNP
monitoring. In our case, multidisciplinary management involving
anesthesiologists and obstetricians played a crucial role in the
successful outcome. Prompt initiation of supportive measures, including
supplemental oxygen, diuretic therapy, and GTN, helped alleviate
symptoms and improve respiratory function. Close monitoring and serial
assessments were essential in guiding therapeutic interventions and
ensuring optimal patient care.
[CONCLUSION]Pulmonary edema occurring after a normal vaginal delivery is uncommon
yet can be a serious complication necessitating quick identification and
comprehensive treatment. Anesthesiologists, given their proficiency in
critical care and airway handling, hold a central position in managing
such scenarios, especially in peripheral hospitals with constrained
resources. This instance highlights the significance of timely action,
vigilant supervision, and teamwork in improving outcomes for patients
experiencing postpartum pulmonary edema.