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| CASE REPORT |
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| Year : 2011 | Volume
: 1
| Issue : 2 | Page : 85-87 |
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Misoprostol-induced pulmonary edema in a parturient with postpartum cardiomyopathy
Bikash Ranjan Ray, Puneet Khanna, Vimi Rewari, Renu Sinha, Ajisha Aravindan, Anjan Trikha
Department of Anesthesia and Intensive Care, All India Institute of Medical Sciences, New Delhi, India
| Date of Web Publication | 17-Mar-2012 |
Correspondence Address:
Vimi Rewari
Department of Anaesthesiology, AIIMS
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2249-4472.93993
Misoprostol, a synthetic prostaglandin E1 (PGE1) analogue, although not the first-line drug in the management of postpartum hemorrhage, is frequently used for this purpose due to its safety profile and cost-effectiveness. Cardio-pulmonary complications have been previously reported with use of prostaglandin analogues but not with misoprostol. We describe a case of pulmonary edema after the use of vaginal misoprostol for treatment of postpartum vaginal bleed in an otherwise healthy asymptomatic patient, who was later diagnosed as a case of peripartum cardiomyopathy. Keywords: Misoprostol, peripartum cardiomyopathy, pulmonary edema
How to cite this article:
Ray BR, Khanna P, Rewari V, Sinha R, Aravindan A, Trikha A. Misoprostol-induced pulmonary edema in a parturient with postpartum cardiomyopathy. J Obstet Anaesth Crit Care 2011;1:85-7 |
How to cite this URL:
Ray BR, Khanna P, Rewari V, Sinha R, Aravindan A, Trikha A. Misoprostol-induced pulmonary edema in a parturient with postpartum cardiomyopathy. J Obstet Anaesth Crit Care [serial online] 2011 [cited 2022 May 24];1:85-7. Available from: https://www.joacc.com/text.asp?2011/1/2/85/93993 |
| Introduction | |  |
Misoprostol, a synthetic prostaglandin E 1 (PGE 1 ) analogue, is routinely used for many obstetrical indications such as induction of labor, [1] cervical ripening, [2] and prevention [3] and treatment of postpartum hemorrhage (PPH). [4] The World Health Organization (WHO) recommends that misoprostol can be used to prevent and treat postpartum hemorrhage in situations where no other treatment is available. [5] Use of misoprostol for prevention and treatment of PPH is less effective than oxytocin. [5] However, it is inexpensive, is thermostable (thus does not require refrigeration unlike oxytocin), is easy to administer and has fewer side effects, making it a valuable and frequently used drug. [6]
We encountered a case of pulmonary edema after the use of vaginal misoprostol for postpartum bleeding, in a young female, on postoperative Day 8 of cesarean section. PGE 2 analogues (Sulprostone) have been reported to cause pulmonary edema, [7],[8] but there is no report of misoprostol-induced pulmonary edema in the literature.
| Case Report | | |
A 32-year-old (weight = 50 kg, height = 155 cm) female, having twin pregnancy, was admitted to our hospital for elective cesarean section. During her antenatal check-ups, she was diagnosed as a case of pregnancy-induced hypertension. She had no other comorbidities, her blood investigations were within normal range, and her blood pressure was well controlled on oral methyldopa, 250 mg thrice daily. She underwent elective lower segment cesarean section (at 37 weeks) under subarachnoid block uneventfully and delivered twin healthy babies.
Her postoperative course was uneventful until postoperative Day 8, when she developed vaginal spotting, for which four misoprostol tablets (800 μg each) were inserted per vaginum, in the ward. After 20 minutes, the patient developed sudden respiratory distress with frothing from the mouth. At this time, a probable diagnosis of pulmonary edema was made and management for the same was started.
At this point in time, she had a heart rate of 110/min, blood pressure of 144/92 mmHg, respiratory rate of 40/min and oxygen saturation of 64% on room air. Chest auscultation revealed bilateral coarse crepitations and wheeze. It was difficult to maintain oxygen saturation of >90% with bag and mask ventilation, even with 100% oxygen. Hence, she was intubated with size 7.5 mm internal diameter endotracheal cuffed tube, after giving 4.5 mg of morphine and 3 mg of midazolam intravenously. She was transferred to the intensive care unit (ICU) for further management.
In the ICU, she was sedated (morphine 3 mg) and was ventilated (assist control mode) with 100% oxygen and positive end-expiratory pressure (PEEP). X-ray chest showed bilateral patchy infiltrates suggestive of pulmonary edema, and blood gas analysis showed evidence of hypoxemia. She received boluses of morphine and loop diuretics (frusemide), and was sedated with 1 mg/h morphine infusion. Central venous access was established through the right internal jugular vein, and the urinary bladder was catheterized. All other laboratory blood investigations were found to be within normal limits.
Pulmonary edema resolved over the next 6 hours, hemodynamic parameters were stable, auscultation revealed bilateral normal vesicular breath sounds with disappearance of crepitations, hypoxemia improved, and the patient sustained a saturation of >96% with 40% inspired oxygen. Ventilatory support was decreased to pressure support ventilation, and fast-track extubation was planned. However, after 2 hours of T-piece trial, she developed respiratory distress and desaturated (SpO2 = 90%). Chest auscultation revealed bilateral course crepitations. Extubation was deferred, full support ventilation was restarted, and she was again treated for pulmonary edema (morphine, loop diuretics and PEEP).
In view of recurrent pulmonary edema, transthoracic echocardiography (ECHO) was done, which showed: normal valve morphology with mild mitral regurgitation, dilated left atrium and ventricle, and global hypokinesia with ejection fraction of 2530%. These ECHO findings helped arrive at a diagnosis of peripartum cardiomyopathy (PPCM), and she was started on angiotensinogen converting enzyme inhibitors.
The rest of her stay in the ICU was uneventful; she was weaned off from the ventilator over the next 3 days and was extubated on Day 5. She was shifted to the ward on Day 6 and was discharged from the ward on Day 10. She was referred to a cardiologist for further management and follow-up.
| Discussion | | |
The likely causes of pulmonary edema in our patient could be cardiac failure in cardiomyopathic heart, fluid overload or misoprostol itself. Fluid overload was not the cause of pulmonary edema in this patient; it could have developed due to misoprostol in a clinical setting of undiagnosed PPCM.
Misoprostol, in obstetrics, has many indications for its use, including both prevention and treatment of postpartum hemorrhage (PPH). It is available in 25- and 200-μgtablets and can be given orally, sublingually, vaginally and rectally. [5] The route of administration is decided in accordance with the patient's preference and the clinical situation. Oral, sublingual and rectal route are most commonly used for treating PPH. [4] Although the intrauterine route has been used for treating PPH, [9] this route is not preferred due to concern regarding absorption of the drug during bleeding. In this case, misoprostol was given vaginally as there were only spots of bleeding.
Oxytocin is the first-line drug for treatment of PPH, [10] but it requires refrigeration, intravenous infusion and skilled healthcare workers for optimum use. A safe and easy-to-administer alternative, misoprostol, is now frequently used for this purpose. A large randomized controlled trial by Winikoff et al.[11] compared the efficacy of oral misoprostol with intravenous oxytocin for control of PPH and found it to be effective in treating PPH. Recently, a WHO expert committee recommended the use of misoprostol for management of PPH if oxytocin is not available or cannot be safely used. [5]
Side effects of misoprostol when used in the postpartum period are shivering, pyrexia, nausea, stomach cramps and diarrhea. [4] Our patient did not exhibit any of these side effects. Rather, she developed pulmonary edema with the use of misoprostol, which is not documented in literature, although it has been reported with use of PGE 2 analogues (sulprostone). [7],[8]
PPCM in our patient was not known before this event, as the patient was not symptomatic. Clinical presentations of PPCM are similar to signs and symptoms of left ventricular dysfunction and heart failure, which are generally present in the last trimester of pregnancy. PPCM is a rare disorder, with unknown etiology, but viral, autoimmune and idiopathic causes may contribute. PPCM in this patient was suspected because of recurrent pulmonary edema and presence of risk factors of PPCM like advanced age (>30 years), multiple gestations and gestational hypertension. [12] The diagnosis of PPCM in our patient was made on the basis of clinical and echocardiographic criteria as described [13],[14] in literature.
The patient in this case had neither any prior history of cardiac failure nor any signs and symptoms suggestive of cardiac failure. Misoprostol probably precipitated pulmonary edema in a previously compromised heart due to its effect on pulmonary vasculature. Sulprostone, which is used for atonic uterine hemorrhage, has been reported to cause pulmonary edema [7],[8] and coronary artery spasm. [15] Pulmonary artery hypertension was implicated as the cause of edema in these previously reported cases. Recently, a study on human pulmonary rings demonstrates that both sulprostone and misoprostol are potent contractile agents, with misoprostol being 5-10 times less active than sulprostone. [16] These contractions are mediated by EP3 receptors present on the human pulmonary vasculature. Although there are no reports of pulmonary edema with misoprostol, pulmonary hypertension superimposed on a previously compromised heart was probably the cause in the present case. PGE 2 in animal models has been shown to increase the hydrostatic pressure and vascular permeability of the pulmonary vascular bed, [8] which can lead to pulmonary edema, but no such evidence is present for PGE 1 analogues.
Since the mechanism of pulmonary edema after misoprostol is not completely understood, the mainstay of therapy remains supportive including sedation, intubation and mechanical ventilation. Loop diuretics probably do not help much because fluid overload is not the primary cause.
Cardiopulmonary complications, although rare with the use of misoprostol, can be seen in a clinical scenario of preexisting underlying heart disease, as in the present case. Both the obstetrician and anesthesiologist should be aware of this potential problem. All patients receiving misoprostol should be monitored, and the drug should not be used in a known case of PPCM.
| Conclusion | | |
A case of pulmonary edema following misoprostol administration is reported in an asymptomatic healthy patient having undiagnosed PPCM. Misoprostol, although safe, may cause pulmonary edema when administered to a patient having compromised cardiac function, hence should be used cautiously.
| References | | |
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| 2. | Fonseca L, Wood HC, Lucas MJ, Ramin SM, Phatak D, Gilstrap LC 3rd, et al. Randomized trial of preinduction cervical ripening: Misoprostol vs oxytocin. Am J Obstet Gynecol 2008;199:305.e1-5.
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| 11. | Winikoff B, Dabash R, Durocher J, Darwish E, Nguyen TN, León W, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women not exposed to oxytocin during labour: A double-blind, randomised, non-inferiority trial. Lancet 2010;375:210-6.
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| 12. | Demakis JG, Rahimtoola SH, Sutton GC, Meadows WR, Szanto PB, Tobin JR, et al. Natural course of peripartum cardiomyopathy. Circulation 1971;44:1053-61.
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| 13. | Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD, et al. Peripartum cardiomyopathy. National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendation and review. JAMA 2000;283:1183-8.
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| 14. | Hibbard JU, Lindheimer M, Lang RM. A modified definition for Peripartum cardiomyopathy and prognosis based on echocardiography. Obstet Gynecol 1999;94:311-6.
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| 15. | Fliers E, Duren DR, van Zwieten PA. A prostaglandin analogue as a possible cause of myocardial infraction in a young woman. BMJ 1991;302:416.
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| 16. | Qian YM, Jones RL, Chan KM, Stock AI, Ho JK. Contractile action of EP3 receptor agonists on the human pulmonary artery. Br J Pharmacol 1994;113:368-74.
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