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7. Hypertensive Disorders: Delivery Management
7.1 Introduction
Hypertensive disorders in pregnancy (HDPs) are on the rise and significantly seen to contribute to maternal morbidity and mortality [1, 2]. Delivering these patients is an additional challenge due to the dynamic nature of the delivery process, compromised maternal fetal unit, and sensitive and hyperresponsive nature of the maternal vascular responses which may suddenly cause an apparently mild HDP mother go into a tumultuous course. Pain, fluids, and alterations in the hemodynamic parameters are significant contributors to such a course. Additionally one has to try and fathom the systemic involvements due to widespread endothelial dysfunction, assess the coagulation system, and remember that every mother with hypertension has a potential risk of developing complications such as placental abruption, postpartum hemorrhage, disseminated intravascular coagulation (DIC), eclampsia, acute renal failure, respiratory distress, cardiomyopathy, and sometimes death. In addition one has to remember that every apparently normotensive woman has a risk of developing hypertension during labor and entails vigilance during the processes of delivery. Preeclampsia is a misnomer and should ideally be called as Gestosis which means disordered pregnancy associated with multisystem involvement [3].
7.2 Background of HDP Context Delivery
It is important to understand some basic physiological changes leading to clinical situation in a hypertensive mother to better understand the management during delivery. Blood pressure measurement that equals 150/100 mm of Hg or more should be considered as severe hypertension in Indian context. The reason being it has been observed that low-risk mothers typically record blood pressure reading of 110/70 mm of Hg when assessed antenatally. Therefore wisdom lies in to starting antihypertensive medications at 150/100 mm of Hg. Rise of blood pressure is the sign which appears at the end of the pathogenesis of the disease process. This therefore mandates investigations and evaluation of the mother carefully. Also sometimes women may be normotensive but still have all the features of HDP, and these can be atypical presentations many times resulting in grave consequences.
7.2.1 Classification
Classification of Hypertension in Pregnancy (ISHDP)
Gestational hypertension | Hypertension that develops after completion of 20 weeks pregnancy, returns to normal within or by 6 weeks, and is not associated with any other features of preeclampsia | 6–7% of all pregnancies |
Preeclampsia/eclampsia | Hypertension occurs after 20 weeks of pregnancy with significant urinary proteins When associated with fits, it is called eclampsia | 5–7% of all pregnancies |
Chronic hypertension | Blood pressure reading of ≤140/90 mm Hg present before pregnancy or before 20th week of pregnancy or recorded during 6 weeks postpartum | 1–5% of all pregnancies |
Preeclampsia superimposed on chronic hypertension | Occurrence of urinary proteins or any other features of preeclampsia in mothers with CHT | 20–25% of all CHTs |
Categorizing HDP thus is important to help in predicting complications and therapy, but increasingly it has been identified to be one disease process. The fundamental difference between gestational hypertension and preeclampsia is proteinuria, and this in some way seems to cause more delirious effects. The above classification is adapted from the National High Blood Pressure Education Program Working Group classification and has better clinical utility. Clinical classification of preeclampsia is useful in predicting complications and thus planning appropriate clinical approach. Proteinuric hypertension before 34 weeks of gestation is called as early-onset preeclampsia (EPE) and is disease of feto-placental origin and associated with severe complications while late-onset preeclampsia (LPE) is disease which is a result of underlying maternal disease or abnormalities in maternal adaptation to pregnancy.
7.2.2 Pathology and Pathogenesis
Systemic involvements associated with preeclampsia
System | Affliction |
|---|---|
Cardiovascular | Cardiac failure, hypertension, thrombocytopenia coagulation failure |
Renal | Oliguria, renal failure, tubular, and/or cortical necrosis |
Respiratory | Acute respiratory distress syndrome (ARDS), pulmonary edema |
CNS | PRES (posterior reversible encephalopathy syndrome, seizures, encephalopathy retinal detachment, cerebral edema, infarction, hemorrhage, cortical blindness |
Liver | HELLP, failure or dysfunction, subcapsular hematoma, hepatic rupture |
Clinical and laboratory assessments should focus on identifying these abnormalities.
7.2.3 Hemodynamic Changes
The underlying hemodynamic changes of pregnancy and the ones contributed by the abovementioned complications need to be understood especially in the context of dynamism of delivery. Vasoconstriction is a result of raised arterial tone and stiffness and is a well-known characteristic of preeclampsia. Vasoconstriction leads to arterial resistance. Abnormal uterine artery notching and increased pulsatility index on color Doppler assessment are due to uterine artery resistance a reflection of vasoconstriction [6]. In addition the cardiac adaptation of mothers with preeclampsia is identified to be different from the mothers with uncomplicated pregnancy [7–10]. Venous hemodynamic dysfunction has been identified in women with preeclampsia [11]. This venous dysfunction is present for a longer period and much precedes the disease in early-onset preeclampsia (EPE) and is not seen preceding late-onset preeclampsia. The raised blood pressure is a composite result of raised cardiac output as well as raised peripheral resistance due to vasoconstriction with some studies attributing this more to raised cardiac output. Due to endothelial dysfunction, it is observed that the resultant intravascular volume of the mother is reduced considerably as the plasma is pushed the third compartments such as interstitial spaces, peritoneal cavity, etc. Vasoconstriction also is responsible for generalized hypoxia and poor tissue perfusion. In addition the vascular system is highly sensitive to medications, and therefore antihypertensive medications have to be carefully administered. Cerebral vasculature autoregulation system is altered, and there can be hyperresponsiveness due to micro hemorrhages and possibilities of vessel aneurysms in case of mothers with chronic long-standing hypertension.
During delivery there are major alterations in the cardiovascular and hemodynamic systems, and these have to be correlated with the background changes in women with hypertension. Uterine contractions cause considerable rise in left ventricular stroke volume and cardiac output. Birthing pain causes phenomenal increase in heart rate and cardiac output. All these contribute to nearly 20% rise in blood pressure, and this may be further augmented during the end of second stage when baby is being expelled especially due to the Valsalva maneuver. In addition there is increased oxygen consumption during delivery processes and may lead to acidosis in severe preeclampsia and eclampsia which are conditions characterized by hypoxia.
Placental perfusion is deficient in hypertensive pregnancies leading to growth restriction. Delivery may be induced in severe early-onset preeclampsia before term and the fetus is premature. Growth restricted babies and preterm babies have a higher possibility of suffering birth asphyxia, intrapartum death, and need of neonatal intensive care. Close fetal monitoring usually during active labor is mandatory and correct interpretation of CTG (cardiotocography) is important as these neonates may not withstand the placental perfusion alterations during uterine contraction, placental abruption, or seizure.
7.3 Clinical Assessment
Causes of seizures in pregnancy and during delivery
Eclampsia |
Cerebral vein thrombosis |
Thrombotic thrombocytopenic purpura |
Cerebral infarction |
Drug and alcohol withdrawal |
Hypoglycemia |
Infection |
Antiphospholipid syndrome |
Correct establishment of the gestational age and records of antenatal investigations, scans, and clinical examinations should be done. Sudden or excessive weight gain, gross edema, treatment with antihypertensive medications, blood pressure records, hematocrits, drop in platelet counts, growth restriction, and any pregnancy hemorrhage all should be carefully documented as are associated with HDP. Preeclampsia many a times has nonspecific symptoms, but as a clinical ritual, specific symptoms such as feeling sick, nausea, vomiting, visual disturbances, headaches, epigastric or any abdominal pain, and suddenly risen edema should be asked for.
ACOG severity classification based on blood pressure along with signs and systemic involvement
Mild to moderate | SBP ≥140–159 and/or DBP ≥90–109 mm of Hg |
Severe (any two if present) | SBP ≥160 and/or DBP ≥110 mm of Hg rechecked in a rested patient Proteinuria ≥2+ on dipstick (can be done on 2 samples 4 h apart) or ≥5 g in a 24 h sample Oliguria <500 mL/24 h Headache, scotoma, or other vision issues Pulmonary edema or reduced oxygen saturation, breathlessness Abdominal pain especially in the epigastrium or retrosternal Elevated liver enzymes, evidence of subcapsular hematoma, infarctions reduced platelets |
All these parameters should be assessed and looked for in mothers presenting with hypertension. Complications and seizures can occur even in the absence of high blood pressure which now is identified as atypical preeclampsia. Therefore presence of any of the other parameters mentioned above in the absence of hypertension should be identified as preeclampsia. Hyperreflexia should be assessed by brisk knee jerks or ankle clonus and is suggestive of cerebral irritability and needs prophylactic magnesium sulfate to be given. Quick obstetric assessment should be done to assess the size of the uterus, presence of uterine contractions, tenderness with hardened uterus typically a sign of abruption, fetal cardiac activity, and preferably admission CTG which can help in identifying fetal well-being. Cervical dilatation, fetal presentation should also be assessed. Systemic assessment for cardiovascular abnormalities such as valvular heart diseases and respiratory abnormalities such as crepitations and reduced air entry should be assessed.
Oxygen saturation by pulse oximetry is an important risk assessment tool at admission which can help in immediate identification of mothers at risk of complications, and if found to be less than 97%, the mother should be taken care of in obstetric ICU (intensive care unit) or HDU (high dependency unit). Careful evaluation of the cardiovascular system to rule out any preexisting cardiac disease should be done; also the respiratory assessment of the rate and presence of basal crepitations should be done in all mothers presenting to labor wards.
Clinical and laboratory assessment interpretation
Investigation for diagnosis | Values | Significance/inference |
|---|---|---|
Proteinuria | Dipstick: ≥1+ on dipstick on a 24 h urine sample: ≥0.3 g/d protein creatinine ratio: ≥30 mg/mmol | Preeclampsia: proteinuria is due to glomerular endotheliosis |
Oxygen saturation: pulse oximetry | SpO2 < 97% | Immediate risk categorization as a critical patient with possibilities of complications |
CBC and blood smear PBS WBCs Platelets | Hemoglobin <11 g/dL is anemia Red cell fragmentation More than 12,000/cmm < 150,000–400,000/(μL) Less than 1,00,000/μL | This can be misleading anemia and can also be due to hemolysis. PCV more than 40 is a sign of hemoconcentration Hemolysis Inflammatory process Thrombocytopenia /HELLP Do coagulation tests |
Liver tests | SGOT/AST > 45 IU/L SGPT/ALT >45 IU/L SAP >17–88 (first trim), 25–126 (second trim), 38–229 IU/L (third trim) LDH > 600 U/L Bilirubin>0.1–1.0 mg/dL Albumin <3.5–5 g/dL | Liver cells are damaged or dying, ALT and AST leak into the bloodstream Levels are high due to increased placental production in third trimester Hemolysis and liver dysfunction Liver dysfunction and red cell destruction Albumin is produced in the liver. Other causes also may exist for deficiency |
Renal functional tests | Uric acid >6.5 mg/dL Creatinine 0.57–1.10 mg/dL BUN >13 mg/dL | Renal parenchymal disease and placental apoptosis Renal failure Reduced glomerular filtration |
Coagulation tests | APTT >9.5–13.8 s PT INR > 9.5–13.8 s Fibrinogen<244–510 (first trim) 291–538 (second trim) 373–619 (third trim) FDP (nonspecific) D-dimer: >1500 μg/L | DIC Liver dysfunction leading to deficient production of clotting factors Exaggerated inflammatory response and endothelial Increased intravascular coagulation increased in fibrinolytic activity DIC |
Funduscopic examination 3 stages | Spastic stage: spasm of retinal arterioles Stage of sclerosis: superimposed changes in the vessels Stage of retinopathy: cotton wool spots, microaneurysms, flame shaped and splinter hemorrhages, hard exudates, disc edema, etc. | Vasoconstriction Chronic hypertension Severe hypertension |
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