PRE-ECLAMPSIA

PRE-ECLAMPSIA

Definition:- It is a multi system disorder of unknown etiology characterised by development of hypertension to the extent of 140/90 mm of Hg or more with proteinuria after the 20th week in a previously normotensive or non-proteinuric woman.

PIH (Pregnancy Induced Hypertension)-

Is defined as the hypertension that develops as a direct result result of the gravid state. It includes- GHTN, Pre-eclampsia & eclampsia.

Etiopathogenesis:-

Basic pathology is endothelial dysfunction & intense vasospasm, affecting all the vessels particularly those of uterus,kidney, placental bed or brain.

(A) Hypertension:-

  1. Trophoblast invasion:-

Invasion of endovascular trophoblast into the walls of the spiral arterioles of uteroplacental bed

In 1st trimester endovascular trophoblast invades upto decidual segment

In second trimester another wave of trophoblast invades up to myometrial segment

 ⇓

Muscular arterial wall(endothelial lining by fibrinoid formation)

Spiral arterioles into a low resistance, low pressure, high flow system.

[in pre eclampsia] there is failure of 2nd wave of endovascular trophoblast migration & reduction in blood supply to fetoplacental unit.

 

2. Endothelial dysfunction & vasospasm:-

Endothelial dysfunction due to oxidative stress & inflammatory mediators. Vasospasm due to imbalances of vasodilators (PGI2, NO) & vasoconstrictors (Angiotension 2, TXA2 & endothelin)

  • There is imbalance in different component of prostaglandin, deficiency of vasodilator prostaglandin(PGI2) & increase in synthesis of thromboxane(TXA2) a vasoconstrictor in platelet.
  • Increased vascular sensitivity to the pressor agent angiotensin II, angiotensinase activity is depressed.
  • Nitric oxide(NO)synthsised in the vascular endothelium which relaxes smooth muscle inhibit platelet aggregation & prevent thrombosis. Deficiency of NO cause HTN.
  • Endothelin-1 synthesised by endothelial cells is vasoconstrictor, causes HTN.
  • Inflammatory meditors:- cytokines, TNF(tumour necrosis factor) interleukins(IL) derived from leucocytes causes endothelial injury.
  • Abnormal lipid metabolism causes more oxidative stress by peroxides, superoxide radicals-cause endothelial injury.

(B) Oedema:-

Excessive accumulation of fluid in the extracellular tissues space, due to oxidative stress causes endothelial injury leads to increased capillary permeability & leaky capillaries.

(C) Proteinuria:-

Spasm of afferent glomerular arterioles causes glomerular endotheliosis leads to increased capillary permeability & leakage of protein.

Types :

1.Mild – Include rise of BP 140/90 mmHg but <160/110 mmHg without significant proteinuria.

2.Severe :- Persistent ≥ 160/110mmHg BP, protein excretion >5gm/24 hrs, oliguria (<400 ml/24 hrs), platelet count <100,000/mm3, HELLP syndrome, cerebal or visual disturbance, severe epigastric pain, IUGR, Retinal Haemorrhage, pulmonary Oedema.

Clinical features :-

Frequently occurs in primigravida (70%) usually appears after 20 weeks.

  1. Symptoms –

           Mild symptoms :-

  • slight swelling over the ankles which persist on rising from the bed. Tightness of the ring on the finger, gradually swelling may extended to the face, abdominal wall, vulva or even the whole body.

          Alarming symptoms :-

  • Headache – either over occipital or frontal region
  • Disturbed sleep
  • Diminished urinary output <400ml/24 hr
  • Epigastric Pain – associated with vomiting, may be coffee colour (haemorrhagic gastritis)
  • Eye symptom – bluring dimness of vision or may be complete blindness

2.   Signs –

  • Abnormal weight gain ( 5 pound a month or 1 pound in a week)
  • Rise of blood pressure
  • Oedema over the ankles on rising from the bed.
  • Abdominal examination reveal evidence of placental insufficiency or growth retardation of fetus.

Diagnostic criteria-

  • An absolute rise of blood pressure of at least 140/90 mm Hg, if previous BP is not known or rise in systolic pressure at least 30 mm Hg or rise in diastolic pressure of at least 15 mmHg over the previously known BP.
  • A rise of 20 mm Hg MAP over previous reading or when MAP is 105 mm Hg or more.
  • Mean Arterial pressure by Page – [ MAP ]

            = systolic pressure + (diastolic pressure * 2) / 3

  • Oedema – Pitting oedema over the ankle after 12 hours bed rest or rapid gain in weight 5 lb a month or 1 lb a week.
  • Proteinuria – Presence of protein in 24 hrs >3 gm or ≥ 2+ (1 gm/L) on at least 2 random clean catch urine sample tested ≥ 4 hours apart in absence of UTI is considered to be significant.

Diagnostic evaluation-

  • Urine test
  • Blood values (serum uric acid >4.5 mg/dl),(serum creatimine > 1 mg/dl)
  • Antenatal fetal well being monitoring – by fetal kick count, USG for fetal growth or liquor pockets, CTG etc
  • Opthalmoscopic examnation

Complication-

(a) Immediate-

     1.Maternal –

During Pregnancy –

  • Eclampsia
  • Oliguria & Anuria
  • Dimness of vision or Blindness
  • Preterm Labour
  • Cerebral haemorrhage
  • HELLP syndrome (Haemolysis, elevated liver enzyme & low platelet count
  • ARDS ( Acute respiratory distress syndrome)

During Labour –

  • Eclampsia
  • PPH

During puerperium –

  • Eclampsia
  • Shock
  • Sepsis (operative interference)

2.Fetal –

  • Intrauterine death (spasm of utero-placental bed)
  • Intrauterine growth restriction (placental insufficiency)
  • Asphyxia
  • Prematurity – due to spontaneous premature labour

 (b) Remote-

  • Residual HTN – persist even after 6 month following delivery.
  • Recurrent pre-eclampsia
  • Chronic renal disease
  • Placental abruption

Management :-

Objectives –

  • To stabilize HTN & to prevent its progression to severe pre-eclampsia
  • To prevent complication
  • Delivery of a healthy baby in optimal time.
  • Restoration of the health of the mother in peurperium.

General management:-

  • Ideally all patient are to be admitted in the hospital for effective supervision. She should be warned against the ominous symptom such as headache, visual disturbance, vomiting epigastric pain or scanty urine.
  • Proper rest in bed in left lateral position lessen the effects of venacaval compression. Also increased renal blood flow → diuresis. Also reduces blood pressure or increase placental perfusion by uterine blood flow.
  • Diet with adequate amount of daily protein (100 gm), usual salt intake is permitted, fluid need not to be restricted, total calorie approximately 1600 cal/day.

Drugs :-

1.Diuretics –

  • In case of cardiac failure, pulmonary oedema or along with antihypertensive drug (where BP reduction is associated with fluid retention).Oedema is not relieved by rest, use it with precaution as it causes – decreased placental perfusion & harm to baby by electrolyte imbalance.
  • Frusemide 40 mg – 5 day/ week – PO (orally)

2.Antihypertensive –

Use while persistent rise of BP along with proteinuria is found.

  • Methyldopa – 250-500 mg TDS ( central & peripheral anti adrenergic)
  • Labetalol – 100 mg TDS ( adrenoceptor antagonist) (α or β blockers)
  • Nifedipine – ( calcium channel blokers) 10-20 mg BD
  • Hydralazine – 10-25 mg BD (vascular smooth muscle relaxant)

Method of delivery :-

  • Induction of labour
  • If aggravation of the pre-eclampsia in spite of medical treatment & appearance of epigastric pain.
  • If cervix is ripe, surgical induction by low rupture of membrane.
  • If cervix is unripe prostaglandin (PGE2) gel 500 mg intracervical in the posterior fornix is inserted after ripning, low rupture of membrane can be performed.
  • Caesarean section –When the urgent termination is indicated & cervix is unfavourable (unripe or closed) associated with complicated factor malpresentation CPD etc.

Note – I/M ergometrine following delivery of baby is withheld as it may cause further rise of BP.