[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.