Hypertensive Disease in Pregnancy Sabaratnam Arulkumaran, Sanjay A Gupte, Evita Fernandez
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Classification and Diagnosis of Hypertensive Disorders of Pregnancy: A Practical Approach1

Sanjay A Gupte,
Girija Wagh
 
INTRODUCTION
The very first step of effective treatment of hypertensive disorders in pregnancy (HTNP) is diagnosis and classification. The literature is rife with several definitions of HTNP for the purpose of research as well as clinical management. In the current context we need to identify the most practical and acceptable definition to aid quick and correct diagnosis. This has to be followed up with the classification of the disorder to identify the systemic involvement, prognosticate the outcome and plan prompt interventions.
Many classifications have been promoted by different groups of experts or representative bodies.1–5 These have led to confusion and difficulties in interpretation. The availability of investigative modalities to identify mothers at risk, fetal compromise and laboratory evaluations for multisystemic involvement were not available when the older classification systems were proposed.6,7 The recent classifications are better for clinical usage and a superior reflection of associated pathophysiology.
 
DEFINITION OF HYPERTENSION DURING PREGNANCY
Hypertension during pregnancy is defined as systolic blood pressure (SBP) greater than or equal to 140 mm Hg or diastolic blood pressure (DBP) greater than or equal to 90 mm Hg with the patient sitting quietly (10 minutes), by a mercury sphygmomanometer with the right arm cuff at the heart level. The 5th Korotkoff (K5) sound is used to mark the DBP. Where K5 is absent, 4th Korotkoff sound should be accepted.8 The reading of 140/90 mm Hg is included in the definition because above these levels both the adverse fetal outcome and perinatal mortality was seen to rise.9
The correct diagnosis and classification of HTNP is essential for proper management of the mother and the baby. The classification proposed by the International Society for the Study of Hypertension in Pregnancy (ISSHP)10 is easy to use in clinical settings (Table 1.1).11,12 It is also self-explanatory and practical.
 
Gestational Hypertension
Gestational hypertension is characterized by mild to moderate elevation of blood pressure after 20 weeks of gestation without proteinuria. Occasionally, severe hypertension may be encountered to begin with which later may manifest other signs and symptoms of preeclampsia. The cause of gestational hypertension is unclear. However, it appears to identify women destined to develop essential hypertension in later life similar to the correlation of gestational diabetes to the subsequent development of type 2 diabetes mellitus.13,14 Blood pressure returns to normal during the immediate puerperium. Thus, the diagnosis of gestational hypertension is always retrospective. Such women may present as hypertensive in all or most of their subsequent pregnancies.15
 
Preeclampsia
Hypertension after 20 weeks of pregnancy with proteinuria is defined as preeclampsia, a condition which is a serious disorder with a broad clinical spectrum.
2
Table 1.1   The ISSHP classification of hypertension in pregnancy11,12
Gestational hypertension
  • Hypertension that:
    • develops beyond 20 weeks of gestation
    • returns to normal within 42nd postpartum day and
    • is not associated with any other features of preeclampsia
6–7% of pregnancies
Preeclampsia/eclampsia
  • Hypertension presenting beyond 20 weeks of gestation with > 300 mg protein in a 24 hour urine collection or 1+ (0.3 g/L) on urine dipstick.
  • Eclampsia is the occurrence of seizures in a pregnant woman with preeclampsia
5–7% of pregnancies
Chronic hypertension
  • Blood pressure—140/90 mm Hg
  • Present before pregnancy, before the 20th week of gestation, or persisting beyond the 42nd postpartum day
1–5% of pregnancies
Preeclampsia superimposed on chronic hypertension
  • The onset of features diagnostic of preeclampsia in a woman with chronic hypertension beyond 20 weeks of gestation
20–25% of chronic hypertension pregnancies
Source: Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol. 2000;183(1):S1–S22. European Society of Gynecology (ESG), Association for European Paediatric Cardiology (AEPC), German Society for Gender Medicine (DGesGM), et al. ESC guidelines on the management of cardiovascular disease during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC). Eur Heart J. 2011;32(24):3147–97.
Preeclampsia is a multisystemic disorder primarily characterized by new onset hypertension and proteinuria in pregnancy. Proteinuria is defined as an excretion of 300 mg / 24 hour, a urine protein/creatinine ratio of 0.3, or a qualitative 1+ dipstick reading.
Preeclampsia is a pregnancy-specific condition characterized by placental dysfunction and a maternal response featuring systemic inflammation with activation of the endothelium and coagulation. This multifactorial disease presents as a syndrome of symptoms and signs with associated hematological and biochemical abnormalities. Most consider hypertension and proteinuria to be the hallmarks of preeclampsia, but the clinical manifestation of this syndrome is heterogeneous. Some women develop severe maternal disease requiring intensive care, whereas others remain asymptomatic with mild hypertension and proteinuria. The condition is also associated with adverse neonatal outcomes. Experience shows that the hostile (immunological) response to the pregnancy by the maternal body is an ongoing process which is usually contained by the protective mechanisms of the body. But there appears to be a “turning point” when suddenly this process of protection is overwhelmed and the cascade of preeclampsia syndrome ensues.
It is also recommended that preeclampsia may be diagnosed when hypertension rises after 20 weeks and is associated with any of the following complications like renal (significant proteinuria, serum or plasma creatinine > 90 μmol/L, oliguria), hepatic (raised serum transaminases, severe epigastric or right upper quadrant pain), hematological [thrombocytopenia, hemolysis, disseminated intravascular coagulation (DIC)] or neurologic involvement (eclampsia, hyperreflexia).16
 
Atypical Preeclampsia
Hypertension and proteinuria before 20 weeks (e.g in gestational trophoblastic disease), preeclampsia with hypertension but without proteinuria or preeclampsia with proteinuria without hypertension when associated with above mentioned systemic involvement is designated at 3atypical preeclampsia. Preeclampsia arising first time after 48 hours of delivery can also be included in this definition.17 This is an important entity for diagnosis and management of certain unusual cases. This has been elaborated in Chapter 11 by Prof Alex Vidaeff.
Eclampsia is defined as the development of grand mal seizures in a woman with preeclampsia. It is the most severe and life-threatening manifestation, with an estimated incidence of 4–5 cases per 10,000 live births.18 Eclampsia usually is preceded by a history of preeclampsia but rarely may arise in a woman with minimally increased blood pressure and no proteinuria. There is significant risk of cardiorespiratory arrest during or after the seizure. Seventy-two percent of eclamptic seizures occur in the antepartum period, 9% are intrapartum and 28% occur in the postpartum period. Late postpartum seizures, arising more than 48 hours after delivery, are increasingly documented.19 The FOGSI-ICOG (Federation of Obstetrics and Gynaecological Societies of India- Indian College of Obstetrics and Gynaecology) National Eclampsia Registry (NER) reveals eclampsia prevalence among registry patients as 1.9%. This is out of the 111,725 deliveries analyzed and reported by the 175 reporting centers. Interestingly out of all the eclampsia reported in the NER 76.78% were antepartum, 9.5% were intrapartum and 13.72% were postpartum.
 
Gestational Hypertension and Preeclampsia
Gestational hypertension and preeclampsia are separate disease processes with different mechanisms. Nulliparity is a strong preeclampsia risk factor while it is not so for gestational hypertension. Preeclampsia is associated with specific histologic changes in the placenta and kidneys and also increase in antiangiogenic peptides which is not so in gestational hypertension. The total circulating volume is lower in women with preeclampsia compared to women with gestational hypertension.20
 
Chronic Hypertension
It is defined as hypertension that presents before pregnancy or within the first 20 weeks of gestation.21 About 1–5% pregnancies are associated but the incidence may be underestimated.10 Women classified as chronic hypertension have essential hypertension (90%), mostly mild in intensity to begin with and their pregnancies are many a times uncomplicated though some variables may occur with grave outcomes.22 Advanced maternal age, obesity (> 30 kg/m2), heredity, race and diabetes are identified risk factors. They are at an increased risk for the development of superimposed preeclampsia and abruptio placentae.23 Less commonly (10%), chronic hypertension is secondary to specific causes such as underlying kidney disease, collagen vascular diseases (systemic lupus erythematosus, scleroderma and periarteritis nodosa), endocrine disorders (diabetes mellitus, pheochromocytoma, thyrotoxicosis, hyperaldosteronism, Cushing's disease) or other vascular diseases (coarctation of the aorta, renal artery stenosis). Women with such secondary chronic hypertension may have grave obstetric outcomes.24,25 Pheochromocytoma, although rare, may present for the first time during pregnancy and is especially fatal when unsuspected, but if diagnosed it can be managed to a successful outcome, either surgically or pharmacologically, depending on the gestational period.26,27 Chronic hypertension may be masked by physiological hemodynamic changes in pregnancy, in particular the second trimester reduction in arterial blood pressure, secondary to increasing vasodilatation. Women presenting with hypertension in the first half of pregnancy should be evaluated keeping in mind the above mentioned causes.
 
Preeclampsia Superimposed on Chronic Hypertension
The onset of features diagnostic of preeclampsia in a woman with chronic hypertension beyond 20 weeks of gestation is classified as superimposed preeclampsia. This may include new onset of proteinuria, thrombocytopenia (< 100,000/μL) or any other systemic involvement of preeclampsia. Pre-existing hypertension is a strong risk factor for development of eclampsia.
 
Paradox
In spite of such elaborate classification it is tempting to say that there is no need to classify hypertensive disorders in clinical practice. Presence of rising 4blood pressure should alert the clinician to seek evidence for the development of preeclampsia and associated abnormalities of fetal growth and/or maternal renal, cerebral, hepatic or coagulation functions which may necessitate specific interventions. This is more so in low resource countries like India where traditional health workers in remote areas can be provided with modified blood pressure apparatuses with which they may be able to detect only systolic blood pressures (SBP) as the risk factor for early referral and further management.
 
CLINICAL CLASSIFICATION OF PREECLAMPSIA
Classification as early onset preeclampsia and late onset preeclampsia is clinically useful (Table 1.2). Appearance of preeclampsia before 34 weeks is called as early onset preeclampsia. Early preeclampsia is associated with greater morbidity28 (four-fold increased risk of stillbirth in a subsequent pregnancy, higher recurrence risk in subsequent pregnancy than when the disorder presents later). In this context, suggestions are made to subdivide preeclampsia into two groups by time of onset because of differences in prognosis and management.29 This distinction is held important as there is a suspicion that these two are separate entities with distinct predisposing factors.
Table 1.2   Clinical classification of preeclampsia
Early Onset Preeclampsia (Before 34 Weeks)
Late Onset Preeclampsia (After 34 Weeks)
  • A fetal disorder that is typically associated with placental dysfunction
  • Maternal disorder due to underlying maternal constitutional factors
  • Reduction in placental volume
  • Normal or larger placental volume
  • Intrauterine growth restriction
  • Normal fetal growth
  • Abnormal uterine and umbilical artery Doppler evaluation
  • Normal uterine and umbilical artery Doppler evaluation
  • Low birthweight
  • Normal birthweight
  • Adverse maternal and neonatal outcomes
  • More favorable maternal and neonatal outcomes
The early onset disease may be associated with the underlying genetic or environmental factors leading to abnormal placentation. The late onset disease may be the result of obesity, diabetes, cardiovascular abnormalities or multifetal pregnancy.
 
SEVERITY CLASSIFICATION OF PREECLAMPSIA
Preeclampsia is a syndrome with a significant potential for fetal and maternal morbidity and mortality. These specific risks not only depend upon the gestational age at the time of disease onset and/or presence of comorbidities, but also on the severity of the condition. Severe preeclampsia is characterized by advent of coagulation or liver function abnormalities, occurs commonly in nulliparous usually after 20 weeks of gestation, and most frequently near term. Several classifications for disease severity in preeclampsia are proposed. These are based on the severity of hypertension, timing of delivery and pregnancy outcome. The National Institute for Health and Clinical Excellence (NICE, UK) classification of severity is based on blood pressure measurement (Table 1.3). American College of Obstetricians and Gynecologists (ACOG) classifies severity based on blood pressure measurement as well as the presence of signs of systemic involvement (Table 1.4).
 
HELLP SYNDROME
HELLP is a severe form of preeclampsia which includes hemolysis (abnormal blood smear, LDH > 600 IU, elevated indirect bilirubin), elevated hepatic enzymes (transaminases > 70 IU) and thrombocytopenia (platelets < 100,000/mL).26
Table 1.3   Severity classification NICE UK based on blood pressure measurement
NICE Severity Classification
Blood Pressure
  • Mild
  • 140–149 mm Hg systolic and/or 90–99 mm Hg diastolic
  • Moderate
  • 150–159 mm Hg systolic and/or 100–109 mm Hg diastolic
  • Severe
  • ≥ 160 mm Hg systolic and/or ≥ 110 mm Hg diastolic
5
Table 1.4   ACOG severity classification—blood pressure along with signs and systemic involvement
  • Mild to Moderate
  • Blood Pressure (BP) is 140–159 mm Hg Systolic and/or 90–109 mm Hg Diastolic
  • Severe
    (any two if present)
  • BP is ≥ 160 mm Hg systolic and/or ≥ 110 mm
    Hg diastolic (on two occasions at least 6 hours apart, while the patient is on bed rest)
  • Proteinuria of ≥ 5 g/24 hours or ≥ 3+ (on two random urine samples, collected at least 4 hours apart).
  • Oliguria < 500 mL/24 hours
  • Cerebral or visual disturbances
  • Pulmonary edema or cyanosis
  • Epigastric or right upper quadrant pain
  • Impaired liver function
  • Thrombocytopenia
This complex syndrome occurs in approximately 10% of patients with preeclampsia and is associated with significant perinatal morbidity and mortality.30 Common presenting complaints are right upper quadrant or epigastric pain, nausea and vomiting which may indicate hepatocellular injury such as subcapsular hematomas.26 None of these symptoms may be present and only nonspecific symptoms such as malaise could be present.30 The clinical features are similar to hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP).31 The clinical evaluation of preeclampsia patient should include a vigilance to detect HELLP syndrome. The maternal complications like acute renal failure, hemorrhage and neonatal complications like acute respiratory failure, hypoxic damage due to placental abruption, low birth weight, sudden neonatal death, are associated.26,30
 
Classification of HELLP
HELLP syndrome is classified either based on the number of abnormalities viz: (1) hemolysis, (2) thrombocytopenia and (3) elevated liver enzymes or by the range of the platelet count.
Table 1.5   HELLP syndrome classified on the basis of platelet count
Class of HELLP
Platelet count
I
  • < 50,000 per mm3 (50 × 109 per L)
II
  • 50,000 to < 100,000 per mm3 (50–100 × 109 per L)
III
  • 100,000–150,000 per mm3 (100–150 × 109 per L)
In the first classification (Tennessee classification) based on the number of the three abnormalities patients are categorized as having partial HELLP syndrome with one or two abnormalities or full HELLP syndrome with all the three abnormalities. Women with full HELLP syndrome are at a higher risk for complications, including DIC, than women with the partial syndrome. Consequently, patients with the full syndrome should be considered for delivery within 48 hours, whereas those with partial HELLP syndrome may be candidates for temporizing.32
Alternatively, HELLP syndrome can be classified on the basis of platelet count as given in Table 1.5. This is the Mississippi or the Martin classification of HELLP.33 Patients with class I HELLP syndrome are at higher risk for maternal morbidity and mortality than patients with class II or III HELLP syndrome. The utility of specific classifications as prognostic tools were compared and it was concluded that both models classified patients according to different criteria but were correlated with mortality. The two models seem to be complimentary. Development of an aggregate classification could refine the models.34
 
DIAGNOSIS OF HYPERTENSION IN PREGNANCY
Abnormal blood pressure reading is the first clue for the diagnosis of HTNP. Every pregnancy should be considered as a potentially dangerous one for the appearance of preeclampsia and appropriate laboratory tests should be performed. Women with the following features should be more closely evaluated and monitored:31 first pregnancy, older 6maternal age, previous preeclampsia, duration of 10 years or more since last baby, body mass index greater than or equal to 35 kg/m2, family history of hypertension, patient who herself is low birth weight, DBP greater than or equal to 80 mm Hg at booking, proteinuria (≥ +1 on more than one occasion and ≥ 0.3 g/24 hours), multiple pregnancy, underlying medical condition (pre-existing hypertension, diabetes, renal disease, presence of antiphospholipid antibodies, other thrombophilias, and autoimmune disease and infertility).
Hypertension in pregnancy always cannot be diagnosed definitively. Taking this into account both the ACOG8 and the National High Blood Pressure Education Program (NHBPEP) Working Group (2000)11 recommend more frequent prenatal visits even if preeclampsia is only suspected. Traditionally these visits increase in frequency toward the third trimester and this is of help in early detection of HTNP. Abnormal blood pressure reading can act as a starting point for investigations and warn the clinician to better plan the antenatal care. Blood pressure recorded as 140/90 mm Hg or more anytime during pregnancy needs evaluation and classification which would need laboratory investigations to help correctly segregate this diagnosis.
Existing chronic hypertension may be masked in early pregnancy because of the initial decrease in pressure. When the hypertension reappears later in the gestation, it may be misdiagnosed as a gestation-specific disorder. The absence of normal midpregnancy decrease in the DBP has been reported to be an early sign to be associated with hypertension.35 In the past an increase of 15 mm Hg diastolic and 30 mm Hg systolic, respectively, even if the final value of 140/90 mm Hg was absent was also included in the definition. However, data demonstrating similar outcomes irrespective of the magnitude of rise when values remain less than 140/90 mm Hg, have led consensus groups to delete this latter definition. Nevertheless, the NHBPEP consensus report11 stressed that patients with blood pressure readings below the 140/90 mm Hg cutoff who have experienced a 30 or 15 mm Hg rise in systolic and diastolic levels, respectively, be watched closely.
 
Proteinuria
Proteinuria is defined as the presence of 300 mg/L or more protein in a 24 hour urine specimen. This finding many times correlates with a finding of +1 or greater on the uristick measurements. The dipstick value of 1+ has many false-positive and false-negative results and is the least useful.11,36 A diluted (< 1,010 specific gravity) or concentrated (> 1,030 specific gravity) urine or an alkaline specimen (pH > 8) may produce false results when tested with the reagent strips. Accurately, timed urine collections are difficult to obtain during pregnancy, and theoretically a urine creatinine/protein ratio eliminates such errors. Absence of proteins on dipstick needs further evaluation either by 24 hour urinary proteins or micro albuminuria. Like hypertension, proteinuria too is a poor predictor of either maternal (eclampsia, placental abruption) or fetal (still birth, neonatal or infant death or neonatal intensive care unit admission) complications.37 Data from the Preeclampsia Integrated Estimate of Risk (PIERS)38 study supports this observation.39 NICE guideline recommends that once proteinuria is detected repeat measurements are not necessary and should not be used to guide clinical interventions.40
 
Weight Gain and Edema
Rapid weight gain and appearance of edema were considered the harbingers of preeclampsia in the past. Severe generalized edema or sudden weight gain in pregnancy may still prove to be significant early warning signs in the hands of the traditional health workers in remote areas in low resource settings.
 
SYMPTOMS
Preeclampsia is a strange condition which does not have any specific signs or symptoms of its own. Many vague signs and symptoms are associated. These can vary from something as basic as headache, nausea and vomiting to more ominous right upper quadrant or epigastric pain, chest pain or dyspnea and visual disturbances. Most of these symptoms are nonspecific and common in pregnancy and use of these for clinical diagnosis and severity assessment are controversial. Some workers found visual disturbances and epigastric pain to be associated with adverse maternal 7complications41 while others found nausea and vomiting in the presence of HELLP syndrome like picture to be better associated42 PIERS database found chest pain and dyspnea as predictors of adverse maternal outcomes but poor correlation was observed.43 Thus, evidence suggests that symptoms are of limited value in risk assessment and should not guide clinical management.
 
LABORATORY EVALUATION
Women with chronic hypertension most likely have essential hypertension and baseline workup should be undertaken. Secondary causes too should be considered and appropriate relevant workup can be commenced. Women with suspected preeclampsia should undergo evaluation for end organ involvement and also to enable differential diagnoses. Hemoglobin may be higher due to hemoconcentration in the absence of microangiopathic anemia. Exaggerated neutrophilia may give rise to raised white blood cell and differential counts. Lower platelet counts aid in diagnosing and classifying HELLP. Peripheral smear showing microangiopathy with red blood cell fragments is characteristic of preeclampsia. Liver enzymes, aspartate aminotransferase; alanine aminotransferase are raised and are signs of liver involvement. Glucose levels are found to be low in acute fatty liver of pregnancy (AFLP). Renal function is assessed by serum creatinine and serum uric acid estimation. Increased breakdown of purines in the ischemic placenta leading to overproduction of uric acid may explain increased serum uric acid levels in preeclampsia. Tests for coagulation, such as activated partial thromboplastin time, international normalized ratio (INR), are recommended in the presence of thrombocytopenia or placental abruption. The validity of these tests either alone or in combination for prediction of adverse outcomes and the critical values for intervention has not been established.44
Initial laboratory test recommended by most of the guidelines for surveillance of severity are platelet count (< 100,000/mL), elevated creatinine (> 0.9 IU) raised liver enzymes, raised lactate dehydrogenase (LDH) (> 600). The SOMANZ45 strongly recommend delivery in view of these parameters. Platelet counts less than 100,000/mL have been found to be associated with adverse maternal and perinatal outcome,46,47 while PIERS38 database showed the utility of this level of platelets to be borderline in predicting adverse maternal outcomes, such an association with adverse fetal outcome is not evaluated. Likewise creatinine levels, uric acid levels, liver enzymes and LDH levels have been identified as risk factors and diagnostic parameters but cannot be used to predict adverse outcomes accurately.48
 
Hemodynamic Investigations
Preeclampsia is characterized by abnormal placentation. Uterine artery Doppler velocimetry may be useful in hypertensive pregnant women to support a placental origin for the hypertension, proteinuria and/or adverse conditions.49 Umbilical artery Doppler velocimetry too may be useful. Absent or reversed end-diastolic flow in the umbilical artery would be more consistent with placental dysfunction than with decreased biological growth potential, incorrect dates, or aneuploidy as a cause of fetal growth restriction.
 
DIFFERENTIAL DIAGNOSIS
Wrong diagnosis is possible in preeclampsia patients especially with liver involvement, epigastric and right upper quadrant pain. Other diagnoses include hepatitis, gallbladder disease, peptic ulcer, gastroenteritis, pyelonephritis, nephrolithiasis, Reye's syndrome, AFLP, TTP and HUS.
Likewise in case of seizures a differential diagnosis of epilepsy, intracranial hemorrhage and thrombosis, rupture of cerebral aneurysm, meningitis, encephalitis, cerebral tumors, cerebral malaria should be borne in mind. Having said so it should be a ground rule that any convulsion in the later part of pregnancy should be considered as eclampsia unless proved otherwise.
 
CHALLENGES IN THE LOW RESOURCE SETTINGS
Low resource settings have altogether different challenges. The first issue is that the actual prevalence of the disease is unknown in most of the low and middle income countries. Low 8utilization and availability of the antenatal care is identified as a single deficiency contributing towards adverse obstetric outcomes. There also is a marked divide of health care access between the rural and urban population and the often observed delays are in triage, transport and treatment. Adoption of the standards of practice can be difficult in these settings due to lack of facility and resources. In such situations task shifting to the community level workers is important so that early detection of the disease can be undertaken based on risk assessment, signs and symptoms. The basic model consisting of increasing awareness amongst the community about the disease, and training community health workers in identifying the basic signs and symptoms and variables like maternal weight gain SBP, dipstick proteinuria can be adopted for early diagnosis.29
 
CONCLUSION
Hypertension in pregnancy is a major cause of maternal mortality and morbidity worldwide. Classification and early diagnosis is a challenge and prediction of adverse outcomes is a further challenge. Many international guidelines are in place for classification and assessment of the HTNP and therefore we have presented a practical guideline which is clinically useful. Some important points to remember have been listed in Box 1.1.

Box 1.1 :  Important points

  • Existing classification systems and the one proposed by ISSHP is of value but has limitations due to its inability to predict adverse outcomes.
  • Severity criteria as a single entity and in combination have limitations. The clinician should understand and take appropriate decisions with a complete overview.
  • Standardization of antenatal interventions and surveillance for women with HTNP has shown improved outcomes and this therefore needs to be stressed.
  • If we truly have to make a difference to the appalling maternal mortality and morbidity, clinical classification is more important for management.
  • We have to find simpler ways of early detection for low resource settings that will bring about early referral to the community health worker to facilitate further treatment.
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