Preeclampsia in rural Ecuador

PRÁCTICA FAMILIAR RURAL │Vol 1 │ No. 5 │ Julio 2017 www.saludrural.org

 

Case Report: Delayed Post-partum Preeclampsia in rural Ecuador


Obregon M., Betancourt C., Gaus D.

 

 

Abstract

Background: Delayed, Post-partum preeclampsia is an unusual presentation of preeclampsia.  Delay in diagnosis at the time of presentation could result in progression to eclampsia.  Consideration should be given to routine post-partum checkup at 3-4 weeks rather than 6 weeks in countries where home birthing is still common.

Case Presentation: We report a case of delayed, post-partum preeclampsia in a mother 4 weeks post-partum who presented to our emergency department with headache and abdominal pain. Hypertensive urgency was diagnosed.  Subsequently, a 24 hour urine indicated significant proteinuria, and delayed postpartum preeclampsia was established.  Her blood pressure normalized and adequate diuresis was maintained.  Magnesium Sulfate was not initiated.

Conclusion: A high index of suspicion for preeclampsia is required in hypertension in the peripartum period.  This is also true up to one month post partum.  When should magnesium sulfate be discontinued in these patients who have adequate diuresis and normal blood presssures, the signs normally used in the immediate post-partum period that the preeclampsia has resolved?

 

Background

In low income countries (LICs) , hypertensive disorders of pregnancy continue to cause significant morbidity and mortality.  Post partum hypertension can result from pre-existing hypertension, preeclampsia, persistence of gestational hypertension, or present for the first time post partum due to other causes, such as volume overload, medications (NSAIDS, Ergotamine, decongestants), Cerebrovascular Accident, or Thrombotic Thrombocytopenic Purpura. 1 Late onset severe preeclampsia has been reported up tp six weeks post partum. 2 

Evidence has suggested that early detection of preeclampsia and early delivery, even prior to the availability of Magnesium Sulfate therapy or advanced neonatal care, produced significant reductions in eclampsia in high income countries. 3  In low income countries, policy appropriately continues to recommend greater prenatal services to identify prenatal preeclampsia, among other conditions. 

Delayed postpartum preeclampsia is much less common than prenatal or intrapartum preeclampsia.  In rural Ecuador, many childbirths continue to occur in the home, where blood pressure monitoring and proteinuria remain unmeasured.  This complicates the ability to diagnose intrapartum and/or postpartum pre-eclampsia when it does ocurr.

 

Case Report

On the western slopes of the Ecuadorian Andes, in a poor, sub-tropical region, a 41 year old woman presented to the emergency department 28 days post partum with right upper quadrant pain and diffuse headache of seven hours duration.  She has a history of hypertension diagnosed 5 years previously for which she was prescribed enalapril but discontinued therapy after 2 months.  No further evaluation of her hypertension was pursued. She is multiparous with eight pregnancies and seven vaginal deliveries.  Her prenatal care prior to her most recent childbirth revealed blood pressures in the normal range, without proteinuria, and without pharmacological therapy.  During and after an uncomplicated vaginal delivery, her blood pressures remained in the normal with the excpetion of one reading at 150/80.

At the time of presentation to the emergency department, 4 weeks post-partum, nausea and 2 episodes of emesis accompanied her epigastric and right upper quadrant (RUQ) abdominal pain of seven hours duration.  Visual disturbances did not accompany her diffuse headache.  She denied dyspnea.  Her blood pressure was elevated to 180/100 without tachycardia, fever, or tachypnea.   RUQ tenderness was noted on physicial exam.  Jaundice was not present. Neurologic exam was intact, without confusion, disorientation, or hyperreflexia. 

Laboratory evaluation revealed the following: Hgb 13.0 g/dL, WBC 10,300, Plts 244,000, AST 30, ALT 24, Creatinina 0.82mg/dL, BUN 14, Lipase 62, Uric Acid 3.1, LDH 253, Albumina 3.8, Alkaline Phosphatase 368, Total Bilirubin 1.56mg/dL, Urinalysis revealed 1+ proteinuria without hematuria.

The patient was hospitalized and initial diagnostic considerations included acute fatty liver of pregnancy, hypertensive urgency, and cholelithiasis.  The absence of “thunderclap” headache, visual disturbance, and neurological deficit suggested this was not consistent with reversible cerebrovascular syndrome (RCVS).

Her hypertension was treated with Enalapril but readings of 180/100 persisted.  Her urine output was 1-2cc/k/hr on day one, and remained in the normal range throughout her hospitalization. On day two, abdominal ultrasound revealed normal hepatic parenchyma and a non-inflammed gall bladder with several 5mm stones.  The common bile duct was not dilated. Head CAT Scan revealed no hemorrhage or abnormal masses.

Atenolol  and HCTZ were added on day three, but blood pressure measurements of 160/90 continued.  Her abdominal pain resolved. Nifedipine was added, at which time the blood pressure began to normalize slowly and her headache dissipated. Delayed, postpartum pre-eclampsia was considered and a 24-hour urine collection revealed 3.7g of protein, confirming the diagnosis of late onset, severe pre-eclampsia.  Due to resolution of symptoms and normalizing blood pressure, the decison was made to not initiate magnesium sulfate. 

Prior to discharge, her headache completely resolved and blood pressures ranged from 120/80 -130/90.  She was discharged 48 hours after headache resolved and blood pressure normalized on one antihypertensive agent.

Discussion and Conclusions

Delayed, post partum preeclampsia was diagnosed due to the patient’s headache, abdominal pain, hypertension, hypereflexia and proteinuria. 4  Her prenatal and intrapartum course did not suggest preeclampsia.  The delay in identification of the likely diagnosis of late onset, severe pre-eclampsia was due to the doubt in such a  presentation so distant from her childbirth.  Her normal hepatic parenchyma and unremarkable liver function did not suggest acute fatty liver of pregnancy. 5 Absence of hemolysis, and normal platelets were not consistent with HELLP Syndrome. Head CT effectively ruled out hemorrhage.   A hypertensive crisis distinct from severe pre-eclampsia seemed unlikely given the normal renal function, particularly in the presence of significant proteinuria.   However, Magnesium Sulfate (MgSO4) was not initiated in this patient, as her blood pressure began to normalize and her headache resolved.  Retrospectively, she should have recieved MgSO4 earlier to prevent progression to eclampsia.    

The particular clinical question that this patient’s condition brought to light is the use of MgSO4 in delayed post partum severe preeclampsia.  Standard of care appears to suggest using MgSO4 for 24 hours or until the blood pressure decreases to reduce the risk of seizure.  However, the traditional sign used in women with peripartum preeclampsia is diuresis.  In this patient with delayed post partum severe preeclampsia, there was no oliguria.  Had MgSO4 been initiated in this case, what clinical parameters would have been useful to determine the timing of discontinuing MgSO4, and based on what evidence?

Furthermore, it might be useful to revisit the recommendation of the routine 6 week post partum followup, which would miss these late post partum presentations of severe preeclampsia, particularly in LICs where home births are prevlaent.

Foot note

1. Sibai BM, Stella CL. Diagnosis and management of atypical preeclampsia- eclampsia. Am J Obstet Gynecol. 2009;200(5):481.e1–481.e7.

2. Gabbe S, Niebyl J, Simpson JL, et al. Hepatic and gastrointestinal diseases. In: Obstetrics: Normal and Problem Pregnancies. 6th ed. Philadelphia: Saunders; 2012:1025.

3. Goldenberg RL, McClure MM, MacGuire ER, et al.  Lessons for low-income regions following the reduction in hypertension-related maternal mortality in high-income countries.  International J of Gynecology and Obstetrics (2011) 113:91-95

4. Tan L, de Swiet M. The management of postpartum hypertension. BJOG 2002;109:733-6.

Goldenberg RL, McClure MM, MacGuire ER, et al.  Lessons for low-income regions following the reduction in hypertension-related maternal mortality in high-income countries.  International J of Gynecology and Obstetrics (2011) 113:91-95

5. Matthys LA, Coppage KH, Lambers DS, Barton JR, Sibai BM. Delayed postpartum preeclampsia: an experience of 151 cases. Am J Obstet Gynecol. 2004;190(5):1464–1466.

 



DOI: http://dx.doi.org/10.23936/pfr.v0i5.177.g238

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