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Laboratory predictors of maternal and foetal outcomes in early onset pregnancy-induced hypertension.

BACKGROUND

Hypertensive disorders during pregnancy constitute 7 to 10% of pregnancies, of which nearly 12-22% have unfavourable outcomes. (1,2) Pregnancy Induced Hypertension (PIH) still remains an ill understood and underestimated disease. The usual markers in developing countries like poor antenatal care, illiteracy, lack of awareness and poverty in developing countries continue to favour these nightmares of pregnant mothers. (1)

Masking of PIH symptoms with simple medications may delay its diagnosis leading to poor maternal and foetal outcomes.

Approximately 1,00,000 women die worldwide per annum because of eclampsia.[3] It is said that preeclampsia and eclampsia contribute to death of a woman every 3 minutes worldwide. (4) Preeclampsia is a common dangerous condition for both mother and baby and is also predictable in onset and progression, cured only by termination of pregnancy.

Hypertensive Disorders of Pregnancy (HDP) are multisystem diseases, which include chronic (pre-existing) hypertension, gestational hypertension, preeclampsia, eclampsia and preeclampsia superimposed on chronic hypertension. (3)

The high perinatal mortality in women with HDP is mainly due to premature delivery and growth restriction. (5,6) A secondary analysis from the World Health Organisation (WHO) multi-country survey has shown that there were about 3- and 5-fold increased risk of perinatal death in women with preeclampsia and eclampsia respectively, as compared to women with no preeclampsia/eclampsia. (7)

Although, there is a large body of literature that described the magnitude and associated complications of HDP, little is done to assess the predictors of perinatal mortality, particularly in low and middle income countries. (8-10) This is despite the fact that the majority of perinatal deaths due to complications of HDP have occurred in the low and middle income countries. [11-14] This study was planned with an objective of determining the clinical and laboratory predictors of maternal and foetal outcomes in early onset pregnancy-induced hypertension, so as to appropriately manage these cases early and prevent their progression to serious forms and complications.

MATERIALS AND METHODS

This prospective observational study enrolled 100 cases of pregnant women with early onset PIH, i.e. rise of BP more than 140/90 with or without proteinuria between 20 to 34 weeks of gestation. The study was conducted in the high risk obstetrics unit of tertiary care referral Wanless Hospital at Miraj, catering to rural and peri-urban population.

The inclusion criteria was all registered diagnosed cases of early onset PIH, i.e. between 20 to 34 weeks of gestation who were categorised as gestational HT, mild preeclampsia, severe preeclampsia, eclampsia and HELLP syndrome.

The exclusion criteria was patients with rise of B.P. 140/90 with or without proteinuria before 20 weeks and after 34 weeks and those with pre-existing medical disorder leading to rise of B.P. like essential hypertensive, chronic hypertension and diabetes.

Study Procedure

1. Pregnant women enrolled in the study were admitted to the ward and a detailed history and examination was carried out as per pre-designed proforma. Details of risk factors for PIH were documented. All mothers underwent following investigations--CBC with peripheral smear, PT APTT, RFT, LFT, Obstetric USG with Doppler. Patients were given bed rest, antihypertensives like Depin, Aldomet or Labetalol orally. Antihypertensives were initiated if B.P. was > 160/100 mmHg. All cases were given Inj. Betamenasone as per standard of care. Expectant line of management included regular maternal and foetal monitoring. Maternal monitoring included B.P. every 6 hrs., daily urine for protein, urine output, daily weight and impending signs of eclampsia. Foetal monitoring included daily foetal kick count, daily NST, biweekly USG and Doppler. Prophylactic Inj. MgSo4 was used if there was evidence of impending eclampsia. Blood and blood products were used if there was evidence of abnormal coagulation profile. Foetal outcomes were measured as intrauterine death, intrauterine growth restriction or appropriate for gestational age. Maternal outcome were measured as mortality or morbidity (abruption placentae, pulmonary oedema, acute renal failure, DIC, cortical venous thrombosis, post-partum haemorrhage).

2. Data analysis was done by using Microsoft Excel 2007 and SSPE for logistic regression analysis.

3. Written informed consent from patient and Ethical Committee approval from Institutional Ethical Committee were taken.

RESULTS

The total number of deliveries from April 2011 to March 2013 were 1000, of which early onset PIH (20 to 34 wks.) was seen in 100 cases. The overall incidence of PIH at the centre being 10% with contribution of gestational hypertension 26 (26%), mild preeclampsia 11 (11%), severe preeclampsia 34 (34%) eclampsia 19 (19%) and HELLP syndrome 10 (10%).

In the present study, maximum number of cases 53 (53%) were between the age group of 21 to 25 years with 63 (63%) being primi gravida. Significant risk factor for PIH were booked outside 95 (95%), history of PIH in previous pregnancy 11 (11%) and family history of PIH8 (8%) [Ref. Table 1].

Maximum number (90%) of patients of early onset PIH were having haemoglobin level between 8 to 12 (g/dL) or > 12 (g/dL). Peripheral haemolysis, thrombocytopenia, altered liver and renal functions were observed in severe pre-eclampsia, eclampsia and HELLP syndrome cases. Maximum cases (79.41%) in severe preeclampsia group were having deranged coagulation profile. Serum uric acid levels of > 6 mg% were observed in 65 patients, majority of them were having severe preeclampsia (67.64%), eclampsia (73.68%) and HELLP syndrome (100%). But results are not statistically significant.

For using logistic regression variables which were significantly associated, i.e. p < 0.05, were considered. Among all variables severe hypertension, gestational age, proteinuria, low platelet count, Sr. uric acid levels and deranged liver enzymes were statistically significant.

Using logistic regression, we found that foetal outcome (survival/death) was highly dependent on gestational age, severe hypertension, proteinuria and deranged liver enzymes. Maternal outcome was highly dependent upon severe hypertension, proteinuria, thrombocytopenia and deranged liver enzymes.

There were two maternal deaths due to complications such as ARF, DIC and pulmonary oedema. No patient received expectant line of management.

In the present study expectant line of management was given only in 10 (10.00%) cases, gestational hypertension 7 (26.92%) and mild preeclampsia 3 (27.27%). The prolongation of pregnancy was from 3 days to 8 days. Meticulous maternal and foetal monitoring for earliest diagnosis of complications was done. Immediate termination of pregnancy was required in 90% and the most common indication for delivery was foetal hypoxia on Doppler study (37%). The other indications for delivery were already established labour cases with signs of impending eclampsia, abruptio placentae and patient landed up in one of the complications of pregnancy-induced hypertension. No patients with severe preeclampsia, eclampsia and HELLP syndrome received expectant line of management. Prematurity was noted in all 100 cases of the study and AGA in 12%, IUGR in 47% and all babies were admitted to NICU. Total 41% were perinatal death and IUD.

DISCUSSION

In this prospective observational study, we found out early onset PIH with altered laboratory parameters like proteinuria, platelet count, sr. uric acid levels and deranged liver enzymes were significantly associated with poor maternal and foetal outcomes.

The total cases with pregnancy-induced hypertension were 286 out of 1000 pregnancies during the study period with incidence being 28.6%. The cases with early onset pregnancy-induced hypertension were 100, incidence being 10%. The incidence of gestational hypertension was 26%, preeclampsia 45%--mild preeclampsia 11% and severe preeclampsia 34%, eclampsia 19% and HELLP syndrome 10%. Ganzevoort et al 20075 found similar incidences; however, the incidence of gestational hypertension was more and preeclampsia was less compared to Hwang JL et al, (6) whereas incidence of eclampsia and HELLP was more in our study. This may be because the overall incidence varies with different geographical region and also the availability and accessibility of antenatal services.

Eskenazi et al 1991 (9) and Jophy et al 2004 (15) reported incidence of PIH was more common in primi gravida, which were similar to our observation. Many earlier studies reported risk factors for PIH like history of PIH in previous pregnancy, family history of PIH, thrombophilic disorder, obesity, dyslipidaemia [Eskenazi et al 1991, (9) Cincotta RB et al 1998, (16) Gonzalez et al 2000, (17) Ros HS et al 2000, (18) Sibai BM et al 1997, (19) Branch DW et al 2001 (20)]. Similar results were observed in our study except incidence of family history was less in the present study, may be due to exclusion of patients with chronic hypertension and other medical disorders.

Looking at the co-relation between laboratory parameters and maternal and foetal outcomes {Ref. Table 2 and 3} gestational age at presentation, severe hypertension, laboratory parameters such as elevated haemoglobin, proteinuria and thrombocytopenia, liver impairment and hyperuricaemia were associated with adverse maternal outcome. Similar observations were noted by Brown MA et al. (11)

Early onset preeclampsia is particularly involved with placental insufficiency and more than half of babies born before 34 weeks will be growth restricted. As in our study all babies born were premature and majority (65.38%) of the IUGR cases were noted in mothers with gestational hypertension and minority (10%) with HELLP syndrome. This is due to increasing foetal hypoxia with the severity of the disease. All the IUGR and AGA babies were shifted to NICU for further care. In our study, mild preeclampsia and gestational hypertension was associated with good perinatal outcome. In mild preeclampsia, all the 11 cases (100%) required NICU admission and there were no neonatal death, while gestational hypertension group out of 26 babies 9 were perinatal deaths and remaining 17 requires NICU admission. Moore et al 198321 reported that severe preeclampsia occurring early in third trimester is associated with high perinatal mortality. Similar results were observed in our study with 16 (47.05%) perinatal deaths in severe preeclampsia group.

In conclusion, simple laboratory parameters are useful predictors of poor maternal and foetal outcomes in early onset pregnancy-induced hypertension. Early termination of pregnancy will help in reducing poor maternal outcomes. Poor foetal outcomes can be reduced with close pregnancy monitoring and improved premature baby care. Our study has the limitation of a small sample size; hence, to support our findings multicentric studies with larger sample size are needed in future.

DOI: 10.14260/jemds/2016/1688

Financial or Other, Competing Interest: None.

Submission 16-11-2016, Peer Review 08-12-2016, Acceptance 16-12-2016, Published 22-12-2016.

REFERENCES

(1.) Ray JG, Burrows RF, Burrows EA, et al. MOS HIP: McMaster outcome study of hypertension in pregnancy. Early Hum Dev 2001;64(2):129-43.

(2.) Joshi-Kale V, Sapre S. Lowered platelet count: a prognostic index in pregnancy induced hypertension. J Obstet Gynecol India 2004;54(3):235-6.

(3.) Arias F, Daftary S, Bhide A. Practical guide to high risk pregnancy and Delivery. 3rd edn. Elsevier 2008:397-439.

(4.) Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Obstetrics. 22nd edn. McGraw Hill 2005:761-808.

(5.) Ganzevoort W, Rep A, Bonsel GJ, et al. Trial investigators. Dynamics and incidence patterns of the maternal complications in early onset hypertension of pregnancy. BJOG 2007;114(6):741-50.

(6.) Hwang JL, Hsu MC, Yang YS, et al. Hypertensive disorders of pregnancy: analysis of 110 cases. Taiwan Yi Xue Hui Za Zhi 1989;88(6):572-8.

(7.) Burrow GN, Duffy TP, Copel JA. Medical complications during pregnancy. 6th edn. Elsevier 2004:43-68.

(8.) Hauth JG, Ewell MG, Levine RJ. Pregnancy outcomes in healthy nulliparas who developed hypertension. Calcium for preeclampsia prevention study group. Obstet Gynecol 2000;95(1):24-8.

(9.) Eskenazi B, Fenster L, Sidney S. A multivariate analysis of risk factors for preeclampsia. JAMA 1991;266(2): 237-41.

(10.) de Swiet M. Medical disorders in obstetric practice. 4th edn. Blackwell 2002:159-97.

(11.) Brown MA, Buddle ML. Hypertension in pregnancy: maternal and fetal outcomes according to the laboratory and clinical features. MJA 1996;165(7):360-65.

(12.) Ros HS, Cnattingius S, Lipworth L. Comparison of risk factors for preeclampsia and gestational hypertension in a population-based cohort study. Am J Epidemol 1998;147(11):1062-70.

(13.) Sezik M, Ozkaya O, Sezik HT, et al. Expectant management of severe preeclampsia presenting before 25 week of gestation. Med Sci Monit 2007;13(11):CR523-27.

(14.) Dekker G, Sibai BM. Primary, secondary and tertiary prevention of preeclampsia. Lancet 2001; 357:209-15.

(15.) Jophy R, Mhasker A, Misquitta D. Maternal and perinatal outcome associated with HELLP syndrome in PIH/eclampsia. J Obstet Gynaecol India 2004; 54(2):147.

(16.) Cincotta RB, Brennecke SP. Family history of preeclampsia as a predictor of preeclampsia in primigravidas. International Journal of Gynaecology & Obstetrics 1998;60(1):23-7.

(17.) Gonzalez AL, Ulloa Galvan G, Alpuche G, et al. Risk factors for preeclampsia. Multivariate analysis. Ginecol Obstet Mex 2000;68:357-62.

(18.) Ros HS, Lichtenstein P, Lipworth L, et al. Genetic effects on the liability of developing pre-eclampsia and gestational hypertension. Am J Med Genet 2000;91(4):256-60.

(19.) Sibai BM, Ewell M, Levine RJ, et al. Risk factors associated with preeclampsia in healthy nulliparous women. The Calcium for preeclampsia prevention (CPEP) study group. Am J Obstet Gynecol 1997;177(5):1003-10.

(20.) Branch DW, Porter TF, Rittenhouse L, et al. Antiphospholipid antibodies in women at risk for preeclampsia. Am J Obstet Gynecol 2001;184(5):825-34.

(21.) Moore MP, Redman CW. Case control study of severe preeclampsia of early onset. BMJ (Clinical Research Ed) 1983;287(6392):580-3.

Corresponding Author:

Dr. Uday Chandrapalsingh Rajput, C/O. Dr. Mangala Rajput, Doctors' Quarters, Wanless Mission Hospital, Miraj-416410, Sangli, Maharashtra.

E-mail: drudayrajput@gmail.com

Mangala Chandrapalsingh Rajput [1], Uday Chandrapalsingh Rajput [2], Sujata Waman Gandhare [3], Aarti Avinash Kinikar [4]

[1] Professor and HOD, Department of Obstetrics and Gynaecology, Wanless Hospital, Miraj.

[2] Associate Professor, Department of Paediatrics, BJGMC, Pune.

[3] Consultant, Department of Obstetrics and Gynaecology, Wanless Hospital, Miraj.

[4] Professor and HOD, Department of Paediatrics, GMC, Miraj.
Table 1. Socio-Demographic Characteristics (n = 100)

Age Distribution
16 to 20                                13 (13%)
21 to 25                                53 (54%)
26 to 30                                28 (28%)
31 to 35                                 4 (4%)
> 35                                     2 (2%)

Gravida Distribution
G 1                                     63 (63%)
G 2                                     16 (16%)
G 3                                     11 (11%)
G 4                                      7 (7%)
G 5                                      3 (3%)

Risk Factors
History of PIH in previous pregnancy    11 (11%)
Family history of PIH                    8 (8%)
Thrombophilic disorder                   5 (5%)
Obesity                                  2 (2%)
Dyslipidaemia                            2 (2%)
Multi-foetal gestation                   0 (0%)
Booked outside                          95 (95%)
Unbooked                                 5 (5%)

Group 1    Inj. Bupivacaine 0.25%      1 mL/kg
           + Inj. 0.9% normal saline
Group 2    Inj. Bupivacaine 0.25%      1 mL/kg
           + Inj. Ketamine 0.5 mg/kg

Table 2. Laboratory Investigations (n = 100)

                                      Total     Gestational
Laboratory                             (100)    Hypertension
Parameter               Values         n (%)     (26) n (%)

Haemoglobin              > 12         46 (46)     13 (50)
(g/dL)
                        8 to 12       44 (44)    11 (42.30)

                          < 8         10 (10)     2 (7.69)
Haemolysis on
peripheral blood                      13 (13)        0
smear
Thrombocytopenia       < 100,000      13 (13)        0

Altered                PT, aPTT       37 (37)        0
coagulation
profile

Altered liver          AST, LDH       14 (14)        0
enzymes

Altered renal       BUL, Sr. Creat.    7 (7)         0
functions

Sr. uric acid          4.5 to 6       35 (35)    12 (46.15)

                          > 6         65 (65)    14 (53.84)

                              Preeclampsia

Laboratory          Mild (11)    Severe (34)   Eclampsia
Parameter             n (%)         n (%)      (19) n (%)

Haemoglobin         9 (81.81)    14 (41.17)    9 (47.36)
(g/dL)
                    2 (18.18)    15 (44.11)    9 (47.36)

                        0         5 (14.70)     1 (5.26)
Haemolysis on
peripheral blood        0         3 (8.82)     3 (15.78)
smear
Thrombocytopenia        0         2 (5.88)      1 (5.26)

Altered                 0        27 (79.41)    4 (21.05)
coagulation
profile

Altered liver           0         1 (2.94)     3 (15.78)
enzymes

Altered renal           0         4 (11.76)        0
functions

Sr. uric acid       7 (63.63)    11 (32.35)    5 (26.31)

                    4 (36.36)    23 (67.64)    14 (73.68)

Laboratory            HELLP
Parameter           (10) n (%)   P value

Haemoglobin           1 (10)     P > 0.05
(g/dL)
                      7 (70)     P > 0.05

                      2 (20)     P > 0.05
Haemolysis on
peripheral blood      7 (70)     P > 0.05
smear
Thrombocytopenia     10 (100)    P > 0.05

Altered               6 (60)     P > 0.05
coagulation
profile

Altered liver        10 (100)    P > 0.05
enzymes

Altered renal         3 (30)     P > 0.05
functions

Sr. uric acid           0        P > 0.05

                     10 (100)    P > 0.05

Table 3. Maternal Outcome and Foetal Outcome

                                         Maternal Outcome
                     Total
                    No. of     Morbidity     Mortality
Gestational Age      Cases       n (%)         n (%)        P value

24 wks. to            22      10 (45.45)     1 (4.54)      P > 0.05
28 wks.

29 wks. to            78      27 (34.61)     1 (1.28)
34 wks.

Severe                61      31 (50.81)     2 (3.27)     P < 0.01 **
hypertension

Protein     3+        13       9 (69.23)         0        P < 0.001#

Uria        4+        50        27 (54)        2 (4)

Haemoglobin           46      25 (54.34)     1 (2.17)      P > 0.05
> 12 g/dL

Thrombocytopenia      13      11 (84.61)     2 (15.38)    P < 0.001#
< 100,000

Sr. Protein           17       7 (41.17)     1 (5.88)      P > 0.05
levels total
< 4.5

Hyperuricaemia        65      29 (44.61)     2 (2.89)     P < 0.05 *
> 6.0

Deranged Liver        14      12 (85.71)     2 (14.28)    P < 0.01 **
enzymes AST, ALT

Sr. Creatinine        59      23 (38.98)     1 (1.69)      P > 0.05
> 0.8

                                            Foetal Outcome

Gestational Age     IUGR n (%)    IUD n (%)    AGA n (%)    P value

24 wks. to           3 (13.63)    19 (79.16)       0        P < 0.01
28 wks.

29 wks. to          38 (48.71)    22 (28.20)    18 (23)
34 wks.

Severe              26 (42.62)    28 (45.90)   7 (11.47)    P < 0.05
hypertension

Protein     3+       6 (46.15)    5 (38.46)    2 (15.38)    P < 0.05

Uria        4+        19 (38)      27 (54)       4 (8)

Haemoglobin         22 (47.82)    12 (26.08)   12 (26.08)   P > 0.05
> 12 g/dL

Thrombocytopenia     2 (15.38)    11 (84.61)       0        P > 0.05
< 100,000

Sr. Protein          4 (23.52)    9 (52.94)    4 (23.52)    P > 0.05
levels total
< 4.5

Hyperuricaemia        26 (40)     31 (47.69)    8 (12.3)    P > 0.05
> 6.0

Deranged Liver       3 (21.42)    11 (78.57)       0        P < 0.01
enzymes AST, ALT

Sr. Creatinine      25 (42.37)    25 (42.37)   9 (15.25)    P > 0.05
> 0.8
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Title Annotation:Original Research Article
Author:Rajput, Mangala Chandrapalsingh; Rajput, Uday Chandrapalsingh; Gandhare, Sujata Waman; Kinikar, Aart
Publication:Journal of Evolution of Medical and Dental Sciences
Article Type:Report
Date:Dec 22, 2016
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