| Article Access Statistics|
| Viewed||28040 |
| Printed||232 |
| Emailed||10 |
| PDF Downloaded||0 |
| Comments ||[Add] |
| Cited by others ||1 |
Click on image for details.
|Year : 1989 | Volume
| Issue : 3 | Page : 183-5
Pulmonary edema in severe pre-eclampsia (a case report).
MM Motwani, SS Shah, AC Mehta
M M Motwani
Source of Support: None, Conflict of Interest: None
Keywords: Adult, Case Report, Chronic Disease, Female, Human, Hypertension, complications,Pre-Eclampsia, complications,Pregnancy, Pulmonary Edema, etiology,
|How to cite this article:|
Motwani M M, Shah S S, Mehta A C. Pulmonary edema in severe pre-eclampsia (a case report). J Postgrad Med 1989;35:183
| :: Introduction|| |
Pulmonary edema is infrequently encountered in patients with severe pre-eclampsia without associated medical, surgical or obstetric complications. In a study by Sibai et al pulmonary edema was diagnosed in 2.9% of cases complicated by severe pre-eclampsia-eclampsia. One such case is reported here.
| :: Case report|| |
Mrs. K.R., aged 32 years, primipara with 27 weeks amenorrhoea. was admitted in our unit for pre-eclampsia. Her blood pressure at the time of admission was 160/120 Ruin Hg. There was generalised body edema. On abdominal examination, ascites was noticed. The fundal height was 20 cm corresponding to 24 weeks gestation. Foetal heart sounds were heard on Doppler. Other systems including fundus were normal. On investigations, marked albuminuria (+ + + ) was detected. The serum BUN was 15 mg%. uric acid 5.2 mg%, S. creatinine 0.99 mg% and S. proteins 6 mg%. Hemogram and glucose tolerance test were within normal limits. An ultrasonograph carried out after 25 weeks gestation showed pregnancy corresponding to 22 weeks. Therapy with methyldopa, nifedipine and labetotol was started alongwith low dose aspirin (75 mg once a day), following which her BP fluctuated between 160/110 and 150/100 mm Hg.
Four days after admission the patient developed dry cough which persisted inspite of antibiotics. A decreased air entry and dulness on the left base of the lung was noticed and X-ray examination revealed left sided pleural effusion. With the addition of frusemide to the antibiotics, the patient's symptoms decreased.
Three weeks later (at 30 weeks gestation), it was decided to terminate the pregnancy, as the blood pressure shot up to 180/130 mm Hg and the patient developed severe pain in the right hypochondrium alongwith hyperreflexia. Parenteral magnesium sulfate was administered to avoid eclapmsia and labour was induced with prostaglandin-A1 (PGA,) infusion. During induction of labour the blood pressure was decreased to 130/90 mm Hg. After 5 hours, the patient delivered a female child (weighing 750 gm) showing evidence of growth retardation.
The prostaglandin infusion was terminated gradually over a period of 4 hours. Magnesium sulfate therapy was however continued for 24 hours after delivery. The 6 hours postpartum BP was 160/100 mm Hg. and the treatment with methyldopa was started.
With this therapy, the blood pressure was maintained at 130/80 mm Hg. However, the patient complained of sudden onset of breathlessness and cough after 72 hours of delivery. The pulse was 124/min., bilateral rales were present and X-ray chest revealed gross cardiomegaly with evidences of pulmonary edema. ECG showed low voltage pattern. The patient was given frusemide (40 mg) intravenously alongwith spironolactone and ampicillin. She was kept on salt free diet and oral fluids were restricted to 800 ml. Daily monitoring of weight loss and alternate day investigations of serum electrolytes were carried out.
Gradual improvement was observed in terms of reduction of weight and relief of cough. X-ray chest repeated after 9 days of initiation of treatment revealed regression of the heart size to normal and minimum congestion in the left base. Periodical follow up of the patient thereafter was carried out. No abnormality was detected in any systems. (BP was 130/180 mm Hg with normal respiratory, renal and liver functions).
| :: Discussion|| |
The pathogenesis of pulmonary edema complicating pre-eclampsia-eclampsia is a subject of extensive investigation. The patients with pre-eclampsia usually have generalised arterial vasospasm resulting in an increased systemic vascular resistance (increased after load), reduced plasma volume (decreased pre-load), and increased left ventricular stroke work index (hyperdynamic heart)., In addition, renal function is impaired, serum albumin is reduced and capillary permeability is increased due to endothelial damage. All these changes predispose to an increased risk of pulmonary edema. A report by Donnelly and Lock, on 533 patients who died of toxaemia showed that pulmonary edema was a cause of death in 25% cases. However, though it is a major cause of obstetric mortality, its incidence is infrequent in well managed cases of pre-eclampsia.
In a study of 37 cases of pre-eclampsia, Sibai et al reported an incidence of pulmonary edema in 2.9% patients; 30% of these cases developed pulmonary edema antenatally, whilst 70% developed it after delivery, within an average time of 71 hours. The mechanisms responsible for this increased incidence in the post-partum period are recently reviewed by Benedetti et all and Hankins et al, and are related to delayed post-partum mobilisation of extracellular fluids. In our patient, who had antenatal history of anasarca, ascites and pleural effusion, the same mechanism may be contributing to the development of pulmonary edema.
In addition, the incidence of pulmonary edema is influenced by pre-existing chronic hypertension, maternal age and parity e.g. the incidence has been found to be 7.1% in patients with chronic hypertension as compared to l .7% in those with pure pre-eclampsia. Similarly, it has been observed that the pre-eclamptic patients with maternal age of 26. 8 years have higher incidence than those with mean age of 20.7 years. Though our patient was primipara and there was no past history of hypertension, her age was 32 years, a factor predisposing to pulmonary edema.
Several reports, which have described the cardiovascular and haemodynamic findings in patients with pulmonary edema suggest that haemodynamic monitoring with Swan-Ganz catheter More Details is indicated in patients with pre-eclampsia-eclampsia. Such monitoring will not only help in early diagnosis but also in taking rapid steps towards its management.
| :: References|| |
|1.||Benedetti, T. J., Kates, R. and Milliams, V.: Hemodynamic observations in severe pre-eclampsia complicated by pulmonary edema. Amer. J. Obstet. & Gynaecol., 152: 330-334, 1985. |
|2.||Donnelly, J. F. and Lock, F. R.: Causes of death in five hundred thirty-three fatal cases of toxemia in pregnancy. Amer. T. Obstet. & Gynaecol., 86: 184-190, 1954. |
|3.||Cunningham. F. G., Pritchard, J. A., Hankins, D. and Anderson, P. L.: Peripartum heart failure: idiopathic cardiomyopathy or compounding cardiovascular events? Obstet. & Gynaecol., 67: 157-168 1986. |
|4.||Hankins, G. D. V., Wendel, G. D. Jr., Cunningham, F. G. and Leveno, K. J.: Longitudinal evaluation of hemodynamic changes in eclampsia. Amer. J. Obstet. & Gynaecol., 150: 506-512, 1984. |
|5.||Henderson, D. W., Vilos, G. A., Milne, K. J. and Nichol, P. M.: The role of Swan-Ganz catheterization in severe pregnancy -induced hypertension. Amer. J. Obstet & Gynaecol.. 148: 570-574, 1984. |
|6.||Phelan, J. P. and Yurth, D. A.: Severe preeclampsia 1. Peripartum hemodynamic observations. Amer. J. Obstet. & Gynaecol., 144: 17-22, 1982. |
|7.||Sibai, B. M., Mabie, B. C., Harvey, C. J and Gonzalez, A. R.: Pulmonary edema in severe preeclampsia-eclampsia: Analysis of thirty-seven consecutive cases. Amer. J. Obstet. & Gynaecol., 156: 1174-1179 1987. |
|This article has been cited by|
||Fluid management in pre-eclampsia
| ||Engelhardt T, MacLennan FM |
| ||INTERNATIONAL JOURNAL OF OBSTETRIC ANESTHESIA. 1999; 8 (4): 253-259 |