Table of Contents

2019 Month : September Volume : 6 Issue : 38 Page : 2608-2610


Kapil Lamba1, Shaily Dutt2

1. Senior Consultant, Department of Anaesthesiology, Mata Chanan Devi Hospital, Janakpuri, New Delhi.
2. Senior Resident, Department of Anaesthesiology, Mata Chanan Devi Hospital, Janakpuri, New Delhi.

Corresponding Author:
Dr. Kapil Lamba,
#D-101, 2nd Floor,
Vikaspuri - 110018, New Delhi.
DOI: 10.18410/jebmh/2019/538

Pregnancy induced hypertension (PIH) encompasses a range of disorders including the following four conditions1- Chronic hypertension, gestational hypertension, chronic hypertension with superimposed gestational hypertension with proteinuria and pre-eclampsia-eclampsia.

How to cite this article

Lamba K, Dutt S. Pregnancy induced hypertension (PIH). J. Evid. Based Med. Healthc. 2019; 6(38), 2608-2610. DOI: 10.18410/jebmh/2019/538


Pregnancy induced hypertension (PIH) encompasses a range of disorders including the following four conditions1- Chronic hypertension, gestational hypertension, chronic hypertension with superimposed gestational hypertension with proteinuria and pre-eclampsia-eclampsia.

The incidence of these events during pregnancy is 5-15% of all pregnancies while that of eclampsia i.e. convulsions superimposed on preeclampsia is 1.5%.

Pre-eclampsia is defined as hypertension presenting after 20 weeks' gestation with significant proteinuria (spot urinary protein: creatinine ratio >30 mg mmol−1 or a 24-h urine collection with >300 mg protein).2 The Haemolysis Elevated Liver Enzymes Low Platelets (HELLP) syndrome is an advanced stage of preeclampsia. The diagnostic criteria are : (1) haemolysis, defined by abnormal peripheral bleeding and increased bilirubin levels (1.2 mg dL−1 or more); (2) elevated liver enzymes, defined by glutamic-oxaloacetic transaminase (AST) of 70 U L−1 or more and lactate dehydrogenase (LDH) above 600 U L−1; (3) low platelet count (less than 100,000 mm−3).3 HELLP syndrome may affect 4-12% of patients with severe preeclampsia and may contribute to high maternal (24%) and perinatal (up to 40%) mortality, despite the delivery care in a timely manner.4



A 33 years old patient was received in obstetric department with complaints of headache, dizziness, blurring of vision, pedal oedema with hypertensive crisis (BP 164/108 mmmHg). Patient had no seizures at home or in hospital. She had no known co morbidities before this pregnancy. Her reports included Hb- 9.0 gm%, TLC 6500, DLC- N-60/ L- 16/M-0/ E- 4/B-0. ESR- 30, platelet count- 236, RBS – 103 mg/dl. Liver function test were t. bilirubin- 3.8, indirect bilirubin- 3.0, direct bilirubin- 0.8, SGOT- 184/ SGPT- 176/ ALP - 261. Prothrombin time - 11.8, INR- 2.13, kidney function test showed urea -23, serum creatinine - 0.45. Heart rate was 90/min with blood pressure of 158/104 mmHg. Patient was cannulated with 18 gauze large bore I.V. cannula and I.V. fluids were started. Injection labetalol 20 mg I.V. was given. Magnesium sulphate infusion was started as per obstetric regimen followed. Foetal heart rate was monitored continuously. As the foetal distress was patient was taken to OR, patient was given premedication with injection ranitidine 50 mg I.V. and metoclopramide 10 mg iv. Pre oxygenation was started with oxygen at 5 l/min. propofol 100 mg I.V. with fentanyl 50 microgram and vecuronium 6mg was given, intubated with ET tube size 7, after the delivery of baby injection midazolam 1 mg I.V. and injection oxytocin 15 IU was given in 1 L OF ringer lactate. APGAR score was noted at 1 min. and 5 min. patient was extubated with injection neostigmine 2.5 mg and glycopyrrolate 0.4 mg I.V. after the return of consciousness and reflexes. Patient was monitored in the recovery room for 24 hours with magnesium infusion continued.



Primigravida with 34 weeks 3 days of gestation with gestational hypertension.



  • Lupus flare
  • Preeclampsia/HELLP syndrome
  • Catastrophic antiphospholipid syndrome
  • Hepatorenal syndrome
  • Thrombocytopenia in pregnancy



PIH is a major cause of obstetric and perinatal morbidity and mortality. Among the several mechanisms proposed, the most accepted are impaired trophoblastic cell invasion leading to failure of spiral artery dilation, placental hypoperfusion and consequent hypoxia. Due to hypoxia cytokines, inflammatory mediators are released into the maternal circulation triggering endothelial dysfunction. This leads to5:

  1. Immunologic injury to placenta
  2. Uterine Ischemia and / Or
  3. Development of intravascular coagulation.


It is common in young and elderly primigravidas6 and its incidence is high in patients with multiple gestations, diabetes mellitus, hydatidiform mole etc.


Clinical Features

  1. Hypertension: A blood pressure greater than 140/90 mm Hg or a rise of 30 mm Hg (systolic pressure) above normal or 15 mmHg (diastolic pressure) above normal.
  2. Urinary protein loss over 2 g a day
  3. Oedema may not be readily apparent.

These may be sufficient for the diagnosis of preeclampsia. If the blood pressure is above 160/110 mmHg and proteinuria exceed 5 g a day, then it is a case of severe preeclampsia. If epileptiform convulsions occur, then it is diagnosed as eclampsia.


Other Features

  1. Hyperreflexia and hyperirritability of central nervous system.
  2. Increased blood uric acid level.
  3. Oedema of upper airway and tracheobronchial tree.
  4. Pulmonary oedema.
  5. Hyperactive uterus.
  6. Coma and cerebral oedema eclamptic convulsion may occur before labour, during labour and in early postpartum period.


Haematological features may vary but may include thrombocytopenia hypofibrinogenemia, increased fibrin degradation products, increased haematocrit value, prolonged thrombin time and prothrombin time-all these resulting in disseminated intravascular coagulation (DIC).

PIH associated complications include7:

  1. HELLP syndrome
  2. Central nervous system dysfunction
  • Hepatocellular injury
  1. Acute disseminated intravascular coagulation(DIC)
  2. Thrombocytopenia
  3. Pulmonary oedema
  • Cerebrovascular events
  • Prematurity, IUGR and intrauterine death in foetus.



In case of mild to moderate preeclampsia i.e. BP 140/90 mmHg - 159/109 mmHg:

  1. Adequate bed rest
  2. Proper fluid and electrolyte balance.
  • Daily assessment of clinician condition.


In case of severe pre-eclampsia (BP > 160/100 mmHg) and eclampsia (convulsions in patient with pre-eclampsia) the definitive treatment is urgent delivery of foetus and placenta.

Antihypertensives: among antihypertensive drugs methyldopa is the drug of choice, labetalol is of comparable efficacy and atenolol, metoprolol, hydralazine, reserpine, nifedipine are safe to use in pregnancy. Magnesium sulphate: An anticonvulsant drug of first line. It is a CNS depressant drug which decreases the acetylcholine release in neuromuscular junction and diminishes the sensitivity of the end plate to acetylcholine and decreases the excitability of muscle membrane. It increases the sensitivity to both depolarizing and non-depolarizing muscle relaxants. Magnesium toxicity is to be taken care of and is avoided by monitoring the hourly urine output, deep tendon reflexes (biceps and patellar reflex) and respiratory rate. The antidote to magnesium toxicity is Calcium gluconate.8 Plasma volume expanders should be given to correct hypovolemia; it reduces blood viscosity and improve the blood flow. Salt poor albumin may be of great help as well. Glucocorticoids are given to promote foetal lung maturity. Monitoring is important throughout the process with central venous pressure to be maintained at around 6-8 mmHg, blood pressure monitoring using manual or continuous arterial monitoring in case of unstable patient, foetal heart rate monitoring. Bladder catheterization to measure urine volume and osmolality. Serum urea, creatinine, serum proteins, electrolytes, liver function tests, haemoglobin, platelet count and coagulation studies are to be obtained.


Management of Anaesthesia

Vaginal delivery in the presence of pregnancy induced hypertension and in the absence of foetal distress is acceptable. A continuous epidural technique is a useful method of analgesia for labour and vaginal delivery because the absence of maternal pushing reduces the associated blood pressure increase and also the vasodilating effect of epidural anaesthesia improve placental blood flow. Before epidural anaesthesia instituted, the patient should be hydrated with intravenous fluid (1 to 2 L of lactated Ringer’s Solution) as guided by the central venous pressure monitoring furthermore coagulation studies should be performed before placement of lumbar epidural catheter. If vaginal delivery is imminent, a spinal anaesthetic limited to the sacral area is an acceptable approach,9 but institution of intravenous hydration before performance of spinal anaesthesia is desirable. The disadvantage of spinal anaesthesia is the possible rapid fall of blood pressure. If the blood pressure decreases more than 30% from the pre-block level, treatment is with left uterine displacement and increased rate of fluid infusion. If hypotension persists a small dose of vasopressor is appropriate. Immediate delivery is indicated for uncontrollable BP, persistent severe systemic symptoms, foetal distress, renal function deterioration and HELLP syndrome. Induction of anaesthesia is often with thiopental (3 to 5 mg/kg body weight) with Succinylcholine (1 to 1.5 mg/kg) to facilitate placement of cuffed tube in trachea. Cricoid pressure is very necessary during intubation. Oedema of the upper airway structures may interfere with visualization of the glottis opening (swollen tongue and epiglottis) and laryngeal swelling may result in the need to insert a smaller endotracheal tube than anticipated. A short duration of laryngoscopy is helpful for minimizing the magnitude and duration of the blood pressure increase, drug interaction between muscle relaxant and magnesium sulphate must be remembered and a PNS used to monitor activity of the neuromuscular junction. Small dose of halogenated agent may prevent awareness. Reversal of the neuromuscular blocked by the appropriate doses of the atropine and neostigmine is very necessary before the removal of endotracheal tube also the estuation to be done in left lateral position when patient is fully awake. The use of synthetic oxytocic to treat uterine atony after delivery must be done cautiously in view of the hypersensitive peripheral vasculature predictably present in these parturient. During the postoperative care patient should be monitored in recovery room for next 12-24 hours and magnesium sulphate infusion should be continued to prevent eclampsia.



Pregnancy Induced Hypertension with Pre-Eclampsia in Primigravida



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