A life-saving therapy in Class I HELLP syndrome: Therapeuticplasma exchangeMehmet Ali Erkurt a, Ilhami Berber a,*, Hacı Bayram Berktas b, Irfan Kuku a,Emin Kaya a, Mustafa Koroglu a, Ilknur Nizam a, Fatma Acar Bakırhan b,Mustafa Ozgul a

a Department of Hematology, Faculty of Medicine, Inonu University, Malatya, Turkeyb Department of Internal Medicine, Faculty of Medicine, Inonu University, Malatya, Turkey

A R T I C L E I N F O

Article history:Received 18 August 2014Received in revised form 17 December2014Accepted 19 December 2014

Keywords:HELLP syndromeTherapeutic plasma exchange

A B S T R A C T

HELLP syndrome, which can affect multiple organ systems and cause maternal and fetalmortality, is a serious complication of pregnancy characterized by microangiopathic he-molytic anemia, elevation of liver enzymes, and thrombocytopenia. Delivering the infantusually suffices for the treatment of this syndrome. In cases with Class I HELLP syndrome,however, the clinical picture may rapidly deteriorate despite delivery. In this paper we pre-sented the outcomes with the use of therapeutic plasma exchange in cases with class I HELLPsyndrome. This study included 21 patients diagnosed with the Class I HELLP syndrome atInonu University Faculty of Medicine, Department of Hematology between 2011 and 2014.A central venous catheter was placed and plasma exchange therapy was begun in pa-tients unresponsive to delivery, steroid, and supportive therapy (blood and blood products,antihypertensive therapy, intravenous fluid administration, and antibiotics) within 24 hoursafter the diagnosis of Class I HELLP syndrome according to the Mississippi Criteria. All pa-tients underwent therapeutic plasma exchange for three sessions each with a 1:1 volume.Hemogram and biochemical parameters of the patients were evaluated before and afterthe procedure. According to results, there was a statistically significant decrease in totalbilirubin, LDH, AST, and ALT levels whereas a significant increase in platelet count was ob-served. Hemoglobin levels were increased, although this increase was not statisticallysignificant. HELLP syndrome is primarily treated with the delivery of infant; however, somecases may show disease progression despite completion of delivery. As a potential causeof both maternal and fetal mortality, HELLP syndrome condition should be aggressivelytreated. Therapeutic plasma exchange is one of the available treatment options. Our studyhas found that postpartum use of plasma exchange therapy within 24 hours is an effi-cient and lifesaving treatment choice in Class I HELLP syndrome.

© 2014 Published by Elsevier Ltd.

1. Introduction

HELLP syndrome, which can affect multiple organsystems and cause maternal and fetal mortality, is a seriouscomplication of pregnancy characterized by microangio-pathic hemolytic anemia, elevation of liver enzymes, and

thrombocytopenia. HELLP Syndrome is an acronym wherethe letters in the word are the first letters of Hemolysis, El-evated Liver Enzymes, and Low Platelet Count [1]. Martinet al. described 3 risk categories of HELLP syndrome ac-cording to the Mississippi classification based on the plateletcount: class I: <50.000/microliter (μl), class II: 50.000–100.000/μl, class III: 100.000–150.000/μl [2]. Maternalmortality in HELLP syndrome changes between 1 and 25%,and it is usually due to the severity of disease, delayed di-agnosis, presence of infection, and acute renal failure [3].

* Tel.: +90 422 341 0660, ext. 4203; fax: +90 422 341 07 28.E-mail address: drilhamiberber@hotmail.com.

http://dx.doi.org/10.1016/j.transci.2014.12.0261473-0502/© 2014 Published by Elsevier Ltd.

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Most maternal deaths occur among women with class 1HELLP syndrome [4].

The main treatment in HELLP syndrome is to stabilizethe patient clinically prior to delivery. In clinically mild cases,watchful waiting following high dose corticosteroid therapyuntil after 34th week to allow full maturation of fetaldevelopment is the recommended approach [5,6]. In severecases, however, delivery should be completed within at most24–48 hours by accelerating the fetal lung maturation aftercorticosteroid therapy administered in the same period.Platelet count returns to normal within 24 hours in a ma-jority of patients; however, a low platelet count may persistbeyond delivery [7] in some cases.

Lactate dehydrogenase is a marker of hemolysis. Besides,stage of the disease advances at HELLP syndrome as throm-bocytopenia gets more apparent. For this reason, bestparameters to be used for follow-up of HELLP syndrome (asthey are measured more objectively compared to clinicalpresentation of the patient) are the increase in platelet countafter therapeutic plasmapheresis and a decrease in LDH [8].

The maternal mortality rate is about 1.1% with HELLP syn-drome. The infant morbidity and mortality rate is anywherefrom 10 to 60% depending on many factors such as gestationof pregnancy, severity of symptoms and the promptness oftreatment. Most deaths in patients with HELLP syndrome occurwith class 1 disease (60%), and neurologic abnormality duemostly to cerebral hemorrhage/stroke is the most commonsystem involved at autopsy (45%) [8–10]. It has been shownthat therapeutic plasma exchange may be effective in HELLPsyndrome not responsive to delivery. Plasma exchange therapywas successfully used in patients who have organ failure orrefractory to treatment [11,12]. Plasmapheresis can replace apatient’s plasma by a donor plasma and remove lots of harmfulsubstances in the bloodstream. It also replaces the coagulat-ing factors, albumin and biologically active substances thatnormally have to be carried out by the liver cells. Plasmapher-esis in theory can lead to the removal of ammonia, endotoxins,bilirubin, and inflammatory cytokines from the circulation.Also, injection of large volumes of FFP (fresh frozen plasma)in this method can help to improve the DIC, and removingrenin angiotensin and other vasoactive factors may improverenal function [13]. All these advantages improve hepatic, renaland neurologic function in patients with HELLP syndrome.Therefore, this treatment especially considering the ad-vanced cases of HELLP syndrome is very important.

Our purpose was to investigate the effects of the post-partum use of plasma exchange therapy within 24 hours onoutcomes of patients with Class I HELLP syndrome.

2. Methods

This study included a total of 21 patients with Class I HELLPsyndrome who underwent therapeutic plasma exchange atInonu University Faculty of Medicine, Department of Hema-tology between 2011 and 2014. The patients were followedat the intensive care unit until after their laboratory and clin-ical symptoms returned to normal upon delivery. The studywas approved by the Ethical Committee of Inonu UniversityMedical School, and written informed consent was obtainedfrom the patients or their relatives. The criteria requiredfor the diagnosis of HELLP syndrome included signs of

hemolysis (LDH > 600 U/L, increased total bilirubin, presenceof fragmented erythrocytes (schistocytes) in peripheral smear),impaired liver function tests (AST > 70 U/L), and a low plate-let count (<150.000/μL). Thrombocyte count was confirmedby a peripheral smear in each patient. The differential diag-noses included other disorders with microangiopathichemolytic anemia (thrombotic thrombocytopenic purpura, he-molytic uremic syndrome, disseminated intravascularcoagulation, fatty liver of pregnancy, preeclampsia and ec-lampsia). ADAMTS13 level could not be studied, owing to lackof equipment. HELLP syndrome was diagnosed based on thefindings of clinical and laboratory examinations. The diagno-sis was confirmed by a favorable response given by all patientsto therapeutic plasma exchange.

A central venous catheter was placed and plasma ex-change therapy was begun in patients unresponsive todelivery, steroid, and supportive therapy (blood and bloodproducts, antihypertensive therapy, intravenous fluid ad-ministration, and antibiotics) within 24 hours after thediagnosis of Class 1 HELLP syndrome according to the Mis-sissippi Criteria [2]. Fresh frozen plasma was used as thereplacement fluid in therapeutic plasma exchange proce-dure. Each patient underwent three sessions of therapeuticplasma exchange on average with a Spectra Optia, and plas-mapheresis was continued until clinical recovery and theplatelet count was over treshold for spontaneous bleeding.This threshold platelet count was accepted over 50.000/μL.

Patients’ characteristics including age, numbers of preg-nancy and abortion, methods of delivery, blood pressure, stateof consciousness, and presence of epileptic attacks were re-corded. All patients were evaluated in terms of Glasgow ComaScore [14]. Additionally, serum aspartate aminotransferase(AST), alanine aminotransferase (ALT), blood urea nitrogen(BUN), creatinine (Cr), calcium (Ca), phosphorus, serum totalbilirubin levels, lactic dehydrogenase (LDH), total protein,albumin, hemoglobin (Hgb), leukocyte and platelet counts,prothrombine time (PT), international normalized ratio (INR),activated partial thromboplastin time (aPTT), D-dimers and fi-brinogen levels were determined daily and the worst valueswere taken for statistical comparison. The complete bloodcount test was performed with a Beckman Coulter Immage(Beckman Coulter, California, USA) device using the imped-ance method; Hgb was measured with the photometricmethod and the leucocyte subgroups with the laser method;serum BUN and creatinine were measured with Aeroset Abbott(Abbott Laboratories, Minnesota, USA) device using the spec-trophotometric method. Mortality rate, causes of death,complications including renal failure, dialysis requirement,hepatic impairment, disseminated intravascular coagulopathy(DIC), and infection were recorded.

Statistical analyses were performed using SPSS 17.0 soft-ware package. Shapiro–Wilk test was used to test the normalityof distribution of the quantitative data. Wilcoxon test was usedto test the differences between the measured parametersbefore and after therapeutic plasma exchange.

3. Results

Four (19.04%) patients delivered via vaginal route and 17(80.96%) via caesarean section. Three patients (14.2%) wereprimigravida while 18 (85.8%) patients were multigravida. The

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mean age of the patient population was 31 + 4.9 (23–38) years.All patients were in the third trimester of pregnancy. Theaverage gestational age of the fetuses have been founded to35th gestational weeks. All fetuses were delivered alive. Themost common complication of the therapeutic plasma ex-change procedure was chills and shivering, and no seriouscomplication was observed related to the procedure. MeanGlasgow Coma Scale score of all the patients at the time of di-agnosis was 9.5. Three patients (14.2%) was in coma, 4 (19%)had stupor, 4 (19%) was confused and 10 (47.6%) were ori-ented. All three patients in coma were intubated. One (4%) outof 3 patients in coma passed away. All other patients were dis-charged as oriented after plasmapheresis. In all of the patients,there was a statistically significant decrease in total biliru-bin, LDH, AST, and ALT levels, whereas a significant increasein platelet count was observed. Hemoglobin levels were in-creased, although this increase was not statistically significant.None of our patients experienced any symptoms attribut-able to anemia or thrombocytopenia, and no erythrocyte orthrombocyte supplementation was provided to any of our pa-tients during the therapeutic plasma exchange. The overallcharacteristics of the patients undergoing therapeutic plasmaexchange are shown on Table 1.

Mean creatinine levels of the patients decreased aftertherapeutic plasmapheresis compared to before (2.68–1.67). But this improvement was not statistically significant.Three out of 20 surviving patients had creatinine levels above2 during follow-up after discharge. But none of these pa-tients required renal replacement treatment. All patientsexcept one who had different stages of confusion were dis-charged as oriented after plasmapheresis at this study. Sixpatients had pneumonia. Five patients recovered from pneu-monia while one patient passed away due to pneumonia.The liver functions of all patients except the deceased wereback to normal.

4. Discussion

HELLP syndrome is a disorder that affects multiple organsystems and causes maternal and fetal mortality [15,16]. InHELLP syndrome, delivery of infant usually suffices for treat-ment. In some cases, however, the clinical picture mayrapidly deteriorate despite delivery. In such circumstances,corticosteroid may be added to the therapeutic regimen[17,18]. Advanced therapeutic regimens are needed to avoid

maternal and fetal mortality in severe cases with low plate-let counts unresponsive to corticosteroids. Only a few studieshave investigated the role of plasma exchange in HELLP syn-drome. So far, the largest case series exploring the role ofplasma exchange in HELLP syndrome studied 26 patients.This study showed that the postpartum application of plasmaexchange therapy was successful for persistent post-partum HELLP syndrome; however, a uniformly favorableresponse could not be obtained in patients who addition-ally had a single or multiple organ injuries [12]. The majorityof the former studies on this subject are case reports. In thesereports, many patients had organ failure or persistent HELLPsyndrome and they rapidly showed a favorable response toplasma exchange therapy [11,19–22]. Compatible with theliterature above, we found that therapeutic plasma ex-change was an efficient and effective treatment modality forpatients with persistent HELLP syndrome in our study.

Lactate dehydrogenase is a marker of hemolysis. Besides,stage of the disease advances at HELLP syndrome as throm-bocytopenia gets more apparent. For this reason, bestparameters to be used for follow-up of HELLP syndrome (asthey are measured more objectively compared to clinicalpresentation of the patient) are the increase in platelet countafter therapeutic plasmapheresis and a decrease in LDH [8].In our patients, after therapeutic plasma exchange, LDH andAST levels decreased and trombocyte count increased.

HELLP syndrome develops in 0.5–0.9% of all pregnan-cies and 10–20% of all preeclampsia cases [18]. Thissyndrome is diagnosed at antenatal period between 26thand 28th weeks of gestation in 70% of cases while 30% ofcases are diagnosed in the postpartum period. The mean ageat the time of diagnosis is 24–28 years [3]. Haram et al. pub-lished about 70% of the cases that developed before delivery,the majority between the 27th and 37th gestational weeks;the rest occurring within 48 hours after delivery [8]. Ourstudy included patients with Class I HELLP syndrome whodeteriorated despite completion of delivery. In our study,all patients were in the third trimester and none of themwas in the postpartum period. The mean age of the patientpopulation was 31 + 4.9 (range 23–38) years and the averagegestational age was 35 weeks.

Maternal and fetal mortality are reportedly high in HELLPsyndrome. The mortality rate of the syndrome has beenreported at 1.1% [23]. This is due to increased rates of car-diopulmonary complications, renal or hepatic failure,

Table 1The overall characteristics of the patients with HELLP syndrome.

Parameters (n = 21) (mean ± standard deviation) Levels before TPE Levels after TPE P

Leukocyte count (μl) (4.300–10.300) 16.500 ± 6.500 12.700 ± 3.070 0.015Hgb (g/dl) (13.6–17.2) 8.8 ± 1.8 10.1 ± 2.5 0.7Platelet count (μl) (150.000–450.000) 32.100 ± 10.100 174.200 ± 110.200 0.001INR (0.8–1.2) 1.15 ± 0.28 1.08 ± 0.19 0.7aPTT (seconds) (28–35) 26.09 ± 12.0 25.8 ± 10.7 0.3AST (U/L) (5–35) 709.8 ± 136.2 68.7 ± 21.5 0.001ALT(U/L) (0–55) 350.6 ± 64.2 47.2 ± 30.6 0.001Total bilirubin (mg/dl) (0.2–1.2) 7.5 ± 5.7 2.3 ± 1.1 0.03Direct bilirubin (mg/dl) (0–0.5) 5.03 ± 3.2 1.7 ± 0.9 0.0001LDH (U/L) (125–243) 1721.1 ± 1053.8 361.3 ± 217.07 0.0001BUN (mg/dl) (8.4–25.7) 39.6 ± 25.5 29.5 ± 12.5 0.134Creatinine (mg/dl) (0.72–1.25) 2.68 ± 1.51 1.67 ± 1.06 0.17

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pulmonary edema, infections, hemorrhage, and DIC[3,24–26]. Literature data suggest a maternal mortality rateof 1–28.5%. Martin et al. found a maternal mortality rate of3.2% in 62 patients with HELLP syndrome, while it was foundat 1.1% in a larger study enrolling 442 patients [15]. Hariset al. reported that patients with HELLP syndrome can beeffectively treated with therapeutic plasma exchange [27].They reported that all patients completely improved and nofatality was observed. Eser et al. reported that 26 patientstreated with therapeutic plasma exchange were cured andnone died [12]. One (4.7%) of our patients died from sepsisamong 21 patients. According to these results, therapeuticplasma exchange performed within 24 hours dramaticallyreduces mortality rates in patients with Class I HELLPsyndrome.

Therapeutic plasma exchange clears the antibodies fromplasma [8]. Hence, it may be suggested that therapeuticplasma exchange reduces mortality by improving hepatic,renal, respiratory, and cerebral functions and correctingcoagulopathy. Considering that these patients are mothers,therapeutic plasma exchange also reduces maternal mor-tality. All patients except one who had different stages ofconfusion were discharged as oriented after plasmapher-esis at this study. Six patients had pneumonia. Five patientsrecovered from pneumonia while one patient passed awaydue to pneumonia. The liver functions of all patients exceptthe deceased were back to normal.

Renal failure is one of the most important cause of mor-tality in HELLP syndrome [25]. Martin et al., in a 777-patient study, reported a renal failure rate of 1.2% [28]. Twostudies reported rates of renal failure of 3.2% and 7.7%[16,29]. Eser et al. found acute renal failure incidence of 17.2%in 26 patients with HELLP syndrome. In their study, only 2patients had permanent renal injury, one of whom laterunderwent peritoneal dialysis [12]. We found acute renalfailure rate of 42.8% (9 of 21 patients). Acute renal failureimproved with therapeutic plasma exchange in 6 (28.5%)patients while 3 (14.2%) patients progressed to perma-nent renal failure, all of whom are currently under dialysis-free follow up.

Although HELLP syndrome tends to spontaneouslyimprove after delivery, affected patients should be moni-tored for 48 hours after birth. This is because patients maydevelop pulmonary edema, hepatic failure, renal failure, andcerebrovascular disorder due to microthrombus [3,30]. Weobserved no cases of pulmonary edema and liver failure im-proved after therapeutic plasma exchange. Eleven (52.3%)patients with impaired consciousness at the time of diag-nosis returned to normal after therapeutic plasma exchange.

Limitations to our study are not being able to evaluateADAM TS 13 and complement levels due to technical in-sufficiency, and having no control group. There is noprospective study regarding plasma exchange and its effectin HELLP syndrome. Plasma exchange for the HELLP syn-drome has not yet been classified in the ASFA (AmericanSociety For Apheresis) guideline. There are suggestions inthe National Therapeutic Apheresis Guide, because treat-ment delay for HELLP syndrome is an important reason ofmortality for both mother and infant in our country. Plas-mapheresis should be started within 24 hours HELLPsyndrome is diagnosed, especially in class I patients [31].

In conclusion, HELLP syndrome is an important cause offetal and maternal mortality. Thus, it is of paramount im-portance to timely diagnose and manage this deadly disorder.Plasma exchange therapy applied within 24 hours shouldbe remembered and carried out at once when delivery andsteroid therapy are not sufficient and thrombocytopeniaworsens. Our study suggests that postpartum use of plasmaexchange within 24 hours was discovered to be an effi-cient and lifesaving treatment option in Class I HELLPsyndrome. In order to enlighten this issue, further prospec-tive studies with more patients are required in the future.

Consent

Written informed consent was obtained from thepatient’s next of kin for publication of this manuscript andaccompanying images. A copy of the written consent is avail-able for review by the Editor-in-Chief of this journal.

Authors’ contributions

This report reflects the opinion of the authors and doesnot represent the official position of any institution orsponsor. MAE was responsible for reviewing previousresearch, journal hand searching, and drafting the report.HBB, MK, IN, FAB, MO were responsible for provision ofpublished trial bibliographies, and preparing photographs.EK, IK contributed to the final draft of the manuscript andanalysis of relevant data. IB was responsible for projectcoordination. All authors read and approved the finalmanuscript.

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