|LETTER TO THE EDITOR
|Year : 2013 | Volume
| Issue : 1 | Page : 50-51
Resistant postpartum atypical preeclampsia
RS Rautela, Chhavi Sarabpreet Sharma, Anjali Kochar, UC Verma
Department of Anesthesiology and Critical Care, University College of Medical Sciences; Guru Teg Bahadur Hospital, New Delhi, India
|Date of Web Publication||1-Jul-2013|
Chhavi Sarabpreet Sharma
B 77, Vivek Vihar Phase 2, New Delhi - 110 095
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Rautela R S, Sharma CS, Kochar A, Verma U C. Resistant postpartum atypical preeclampsia. J Obstet Anaesth Crit Care 2013;3:50-1
|How to cite this URL:|
Rautela R S, Sharma CS, Kochar A, Verma U C. Resistant postpartum atypical preeclampsia. J Obstet Anaesth Crit Care [serial online] 2013 [cited 2019 Sep 23];3:50-1. Available from: http://www.joacc.com/text.asp?2013/3/1/50/114294
Hypertensive disorders are most common complications of pregnancy, with a prevalence of 5-10%.  Classically, most women who develop preeclampsia (triad of hypertension, proteinuria, and edema) present between 20 weeks of gestation to upto 48 h postpartum. 
In recent years, a new term atypical preeclampsia/eclampsia has been used to describe nonclassical forms of hypertensive disorders arising during pregnancy, there is no strict definition, it includes cases with minimal proteinuria or no proteinuria but with hypertension, proteinuria with no or marginally elevated blood pressure or without hypertension or proteinuria. The presentation may be before 20 weeks or more than 48 h postpartum, those resistant to magnesium sulfate therapy and HELLP syndrome (hemolytic anemia, elevated liver enzymes, low platelets) and its variants are also included in atypical category.  We describe successful management of a patient with atypical preeclampsia.
A 35-year-old female (G 3 P 2 ) with 28 weeks of gestation weighing 55 kg and 152cm height, presented with bleeding per vaginumwas posted for emergency caesarean section under general anesthesia in view of abruption placenta with fetal distress, anesthesia was induced with inj. thiopentone sodium 200 mg i.v., rapid sequence induction with cricoid pressure was done using suxamethonium 75 mg and patient's trachea was intubated with oral cuffed endotracheal tube size 7.0. Anesthesia was maintained with oxygen, nitrous oxide (50:50), isoflurane1%with minimum alveolar concentration (MAC) of 1 and inj. vecuronium. After delivery of stillborn baby, inj. morphine 6 mg and inj. oxytocin 15 IU were given. Her vitals were stable preoperatively as well as during intraoperative period. However, the blood pressure started rising after delivery of placentaand reached to 180/100-220/126 mmHg and inj. morphine 3 mg i.v. repeated, causes of intraoperative hypertension were ruled out like endotracheal tube (ETT) position, light anesthesia, surgical stimulation and hypercarbia. Inj. labetalol was given in 20 mg boluses every 10 min to total dose of 80 mg, but the blood pressure was still 180/100 mmHg. In view of unstable hemodynamics, patient was shifted to intensive care unit (ICU) for electiveventilation and monitoring. Meanwhile, invasive lines of arterial pressures and central venous pressures were secured. Central venous pressure (CVP) was 6-8 cm of water and thus, CVP-guided fluid therapy was given. Nitroglycerine infusion was started with dose of 5 μg/min and was increased gradually to 15 μg/kg/min over a period of 3-4 h along with inj. labetalol infusion of 2 mg/min. Midazolam infusion of 2 mg/h was given for sedation. Physician and obstetrician consulted, magnesium sulfate 4 mg was given as boluses followed by 1 mg/h continuous infusion, inj. furosemide 20 mg/12h, and inj. morphine 4.5 mg/6h was added. Over a period of 12-h, patient was gradually weaned-off the ventilator andtrachea was extubated. All the routine investigations, fundus examination, and echocardiography (ECG) were in the normal limit. Also, urine examination did not reveal protenuria.
On second ICU day, patient's 24-h urine sample was investigated for vanillylmandelic acid (VMA) levels andthyroid function test, renal ultrasound, and doppler revealed no abnormality. Inj. magnesium sulfate, inj. labetalol, and inj. nitroglycerin (NTG) were gradually tapered and stopped. Patient was started on oral antihypertensive (tab. amlodipine 5 mg OD and tab. atenolol 25 mg OD) which were gradually tapered and stopped in 6 weeks. Follow-up for another 2 weeks revealed a normotensive state.
In our patient, a diagnosis of atypical preeclampsia was made as blood pressure started rising after the delivery of placenta with no previous history of hypertension, there was no proteinuria and other causes of secondary hypertension (peripartum cardiomyopathy, pheochromocytoma, hyperthyroidism, renovascular disease, and hyperaldosteronism) were specifically ruled out.
Atypical eclampsia constitutes about 8%.  The onset is unpredictable, causing problem in initiating management. Albayrak et al.,  reported four atypical cases of preeclampsia-eclampsia and concluded that absence of either hypertension or proteinuria should not preclude from diagnosing preeclampsia-eclampsia.
In a review by Stella and Sibai,  a stepwise approach towards diagnosis and treatment of patients with atypical features has been described. They have reported many unusual cases of preeclampsia-eclampsia which were unavoidable despite of proper antenatal care (ANC) care and management. 
Thus, atypical preeclampsia should be considered in all pregnant and postpartum patients, even when classic findings are absent and a stepwise approach should be followed for diagnosis and treatment of patients with atypical features. Treatment should be given more importance than waiting for definite diagnosis of atypical hypertension.
| Acknowledgement|| |
We give our sincere thanks to Dr. U. C. Verma, Professor and Head of the Department of Anaesthesiology and Critical Care, University College of Medical Sciences and Guru Teg Bahadur Hospital, Dilshad Garden, Delhi for his kind support and guidance in completion of this work.
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