Preeclampsia and pregnancy induced hypertension (PIH)

January 8, 2021 Gaurab Karki Uncategorized 0




Preeclampsia and pregnancy induced hypertension (PIH)
Preeclampsia and pregnancy induced hypertension (PIH)

What is Preeclampsia?

  • When a woman with gestational hypertension also has elevated protein in her urine, pre-eclampsia (also known as xemia) is diagnosed.
  • Pre-eclampsia is the occurrence of hypertension and proteinuria in pre-normotensive women after the 20th week of gestation or in the early postpartum period.
  • This is diagnosed on the basis of hypertension and proteinuria, when proteinuria is measured as > 1+ on dipstick or >0.3g/L of protein in a random clean catch specimen or an excretion of 0.3gm protein/24hrs.
  • It is a mechanism of multisystem vasospastic disease characterized by haemoconcentration, proteinuria and hypertension.
  • In terms of management, pre-eclampsia is typically classified as moderate or severe.
  • Pre-eclampsia is suspected in the absence of proteinuria when hypertension is followed by symptoms including headache, blurred vision, abdominal (epigostrictrial) pain,   
  • Specifically, low platelet counts and irregular liver enzyme levels, i.e. alanine aminotransferase (ALT), aspirate aminotransferase (AST) and gamma glutamyl transpeptidase, or altered biochemistry (GGT).
  • These signs and symptoms, together blood pressure >160mm Hg systolic or >110 mmHg diastolic and proteinuria of 2+ or 3+ on dipstick demonstrate the more severe form of the disease.

Predisposing factors of Pregnancy induced hypertension (PIH):

  • Primigravida
  • Maternal age <19 years or >40 years
  • Family history (hypertension, pre-eclampsia, eclampsia)
  • Multiple gestations
  • Diabetes
  • Chronic hypertension
  • Chronic renal heart disease
  • RH incompatibility
  • Obesity
  • Placental abnormalities
    • Poor placentation (decreased trophoblastic invasion)
    • Hyperplacentosis (Multiple pregnancies, Rh incompatibility, diabetes)
    • Placenta ischemia
    • Molar pregnancies (hydatiform mole)
  • Genetic disorder
  • Immunological phenomena
  • Pre-existing vascular disease

Etiology of Preeclampsia:

  • Exact etiology remains unrecognized.
  • Present hypotheses relating to Pregnancy induced hypertension (PIH) etiology include:
    • i. Abnormal placenta formation is the primary cause.
    • ii. The maternal immune response causes one or more factors to be released that destroy endothelial cells.
      • Maternal immune response to fetal antigens which obtained from the father and demonstrated in abnormal placental tissue.
      • High prevalence of hypertensive disease in primiravida (decreased incidence after long term exposure to the paternal sperm) enhanced inflammatory substances in the maternal circulation and pathological evidence of organ rejection in the placental tissue.
    • iii. Abnormal placentation and decreased placental perfusion (which can also occur in diabetes, hypertension or thromolophila).
    • iv. Large placental mass such as multiple pregnancy or gestational trophoblastic tissue (hydatiform mole).

Pathophysiology of Preeclampsia:

  • In normal pregnancy, placentation entails the invasion of synctrophoblast decidua.
  • The muscular walls and endothelium of the spiral arteries are eroded during early pregnancy and substituted by trophoblast to ensure the forming blastocyst has an ideal environment.
  • A second stage of this intrusive process occurs when the trophoblast erodes the myometrium of the spiral arteries between 16 and 20 weeks of gestation.
  • Dilated vessels that are incapable of vasoconstriction are resulted by the loss of this musculoelastic tissue.
  • A low pressure system with high blood flow into the placenta is therefore created and optimum placental perfusion is maintained.
  • Trophoblastic invasion of the spiral arteries is prevented in pre-clampsia, resulting in reduced placental perfusion, which can potentially lead to early placental hypoxia.
  • The placenta’s trophoblastic tissue fails to move down the maternal spiral arteries and displaces these arteries’ musculo-elastic structure. Therefore, these arteries do not extend to increase placental perfusion, as they usually do.
  • The resulting placental ischemia stimulates the release of a toxic agent to the endothelial cells that line the blood vessels and provide the integrity of the blood vessel wall.
  • Endothelial cells play a major role in controlling capillary transport, regulating plasma lipid interaction and modulating vascular smooth muscle reactivity in response to various stimuli.
  • They also synthesize prostacycline and nitrous oxide, which are vasodilation mediators and thus inhibit platelet accumulation, repreventing the formation of blood clots.
    • – There is less production of prostacycline and nitric oxide (vasodilators) and increased production of thromboxane, endothelin-1, oxygen-free radical and lipid peroxide with endothelial injury.
    • – As a result, the development of thromboxane (vasoconstrictor) and platelet aggregation stimuli over prostacyclin (vasodilators) and platelet aggregation inhibitors has increased sevenfold, causing a compensatory rise in vascular sensitivity to angiotensin-II.
    • -A drop in the development of nitric oxide by placental vessels, along with an increase in thromboxane, resulting in platelet adhesion to the surface of the trophoblast, resulting in intermediate thrombosis, further altering the flow of blood to the fetus.
  • Damage to the endothelial cells will:
    • – Reduction of prostacyclin and nitrous oxide production.
    • – Increase the efficacy of the vessels to angiotensin II
    • – Triggering the cascade of coagulation and thromboxane production
    • -Increase lipid peroxide production and decrease the production of antioxidants, known as ‘oxidative stress.’
  • The combined effect of these events can cause vasospasm and elevated blood pressure, irregular coagulation and thrombosis, and increased endothelium permeability leading to edema, proteinuria and hypovolemia.
  • These are the pre-eclampsia characteristics that manifest in the body, resulting in pathological changes associated with multi-system disorder.

Pathophysiology of preeclampsia

  • During preeclampsia significant changes in following organs are reported;
  • Blood:
    • Hypertension and damage to endothelial cells impact capillary permeability.
    • The leakage of plasma proteins from the damaged blood vessel causes plasma colloid pressure to decrease and edema to increase in intracellular space.
    • The reduced amount of intravascular plasma causes hypovolemia and haemoconcentration, which is referred to as elevated hematocrit,
    • The lungs become congested with fluid in extreme cases, and pulmonary edema occurs, oxygenation is hindered and cyanosis takes place.
    • The coagulation cascade is triggered with vasoconstriction and disturbance of the vascular endothelium.
  • Coagulation system:
    • Thrombocytopenia is produced by increased platelet intake and may be responsible for the production of disseminated intravascular coagulation.
    • Fibrin and platelets are accumulated as the process progresses, which can block blood flow to several organs, especially the kidney, liver, brain and placenta.
  • Kidneys:
    • Hypertension in the kidney contributes to vasospasm of the afferent arterioles, resulting in reduced renal blood flow that causes hypoxia and edema of the glomerular capillary endothelial cells.
    • Glomerulo-endotheliosis (glomerular endothelial damage) enables proteins to fit into the urine, causing proteinuria, predominantly in the form of albumin.
    • Reduced creatinine clearance and increased serum creatinine and uric acid levels are expressed in renal injury.
    • Oliguria progresses as the condition worsens, suggesting significant pre-eclampsia and damage to the kidneys.
  • Liver:
    • Hepatic vascular bed vasoconstriction can result in hypoxia and edema of liver cells.
    • Edematous swelling of the liver in extreme cases causes epigastic pain, which can lead to intracapsular haemorrhage and, in extremely rare cases, liver rupture.
    • Changed liver function is displayed by falling albumin level rise in liver enzyme levels.
  • Brain:
    • Hypertension combined with cerebrovascular endothelial dysfunction increases the permeability of the blood-brain barrier resulting in cerebral oedema and micro haemorrhaging.
    • Clinically this is characterized by the onset of headaches, visual distturbances and convulsions.
    • If the mean arterial pressure (MAP, i.e. systolic blood pressure plus twice the diastolic pressure separated by3) reaches 125 mmHg, cerebral flow autoregulation is impaired, resulting in cerebral vasospasm, cerebral edema, and formation of blood clots.
    • This is known as hypertensive ecephalopathy, which may lead to cerebral haemorrhage and death if left untreated.
  • Fetoplacental unit:
    • In the uterus, hypertension-induced vasoconstriction decreases the flow of uterine blood and vascular lesions occur in the placental bed, which can lead to placental abruption.
    • The reduction in blood flow to the choriodecidual areas reduces the amount of oxygen that diffuses into the fetal bloodstream inside the placenta via the cells of the syncytiotrophoblast and cytotrophoblast.
    •  The consequence is that the placental tissue becomes ischamic, thrombosis of the capillaries in the chorionic villi, and defects occur that lead to restriction of fetal development.
    • With decreased placental activity, hormonal production is also reduced and this has serious consequences for the fetus’s survival.
    • This combination of factors frequently result in preterm labor and birth.

Diagnosis of Pre-eclampsia:

1. Hypertension:

  • Absolute increase in blood pressure of at least 140/90 mm Hg if previous blood pressure is not known or if systolic pressure is at least 30mm Hg or diastolic pressure is at least 15 mm Hg higher than previously known.
  • An increase in blood pressure of at least 140/90 mmHg should occur at least 6 hours apart on two occasions.
  • On the right arm, the blood pressure is determined, with the patient lying horizontally at 30 ° on her side.
  •  Sitting posture is favoured in the outpatient.

2. Edema:

  • After 12 hours of bed rest or rapid weight gain of more than one pound a week or more than 5lb a month in the later month of pregnancy, demonstration of pitting edema over the ankles can be the earliest sign of preclampsia.
  • However, in a normal pregnancy, some amount of edema is prevalent (physiological).

3. Proteinuria/Albuminuria:

  • In the absence of urinary tract infection, the presence of total protein in 24 hours of urine greater than 0.3 gm or > or= to 2 + (1.0 gm/L) on at least two random clean catch urine samples measured > or= to 4 hours apart is considered significant.

Clinical features:

  • Pre-eclampsia generally takes place in primigravidae.
  • Obstetric medical conditions such as multiple births, plohydramnios, pre-existing hypertension, diabetes, etc., are more commonly linked.
  • Clinical manifestations typically occur after the twentieth week.
  • Onset :
    • Incisions typically occur and the signs run a slow course.
    • The onset becomes acute on rare occasions and follows a rapid path.
  • Symptoms:
    • Pre-clampsia is mainly a condition without signs and it is usually late before symptoms appear.
  • Mild symptoms:
    • The early sign of pre-eclampsia edema is mild swelling over the ankles that occurs on rising from the bed in the morning or tightness of the ring on the finger.
    • The swelling can gradually extend to the face, the abdominal wall, the vulva, and even the entire body.
  • Alarming symptoms:
    • The acute onset of the syndrome is typically associated with:
      • – Headache in the occipital or frontal area.
      • – Disturbed sleep
      • – Reduced urinary output, with urinary output of < 400 ml within 24 hours.
  • Epigastric pain:
    • Acute pain associated with vomiting in the epigastric region, coffee color is sometimes due to haemorrhagic gastritis or subcapsular haemorrhage in the liver.
  • Eye symptoms:
    • Vision blurring or dimness can occur, or total blindness at times.
    • Usually, vision is restored within 4-6 weeks of delivery.
    • Eye symptoms are caused by retinal vessel spasms, damage to the occipital lobe, and retinal detachment.
    • Reattachment of the retina occurs after edema subsidence and blood pressure normalization after delivery.
  • Signs of preeclampsia:
  • Abnormal weight gain:
    • – In a short period of time, abnormal weight gain is likely to occur even before apparent edema.
    • There is a substantial rapid weight gain of more than 5 lb per month or more than 1 pound a week later in the month of pregnancy.
  • Rise of BP:
    • -BP’s growth is typically insidious, but can be sudden.
    • – Typically, diastolic pressure appears to increase first, followed by systolic pressure.
  • Edema:
    • Visible edema over the ankles is pathological when getting out of bed in the morning.
    • In untreated cases, edema may spread to another part of the body.
    • eclampsia can be suggested by sudden and generalized oedema.
  • Due to leaky capillaries and low oncotic pressure, pulmonary edema caused
  • Abdominal examination can show signs of chronic placental failure, such as scanty liquor or fetal growth retardation.

Laboratory diagnosis of preeclampsia:

  • 1. Urine:
    • Proteinuria is the last pre-eclampsed characteristic to emerge.
    •  It may be trace or copious at times so that on boiling (10-15gm/L) urine becomes solid.
    • There may be few hyaline casts, epithelial cells or even few reed cells.
    • There should be twenty four hours of urine collection to test protein.
  • 2. Opthalmoscopic examination:
    • In extreme cases, retinal edema, constriction of the arterioles, changes in the usual ratio of the diameter of the veins arteriole from 3:2 to 3:1 and nicking of the veins crossed by the arterioles can occur.
  • 3. Blood values:
    • There are no clear and sometimes contradictory changes in the blood.
    • The level of serum uric acid (pre-eclampsia biochemical marker) greater than 4.5 mg/dl suggests the existence of pre-eclampsia.
    • The level of urea in the blood remains normal or slightly elevated.
    • Serum creatinine levels can be greater than 1 mg/dl.
    • Thrombocytoponia and irregular coagulation profiles to different degrees can be present.
    • There may be elevated levels of hepatic enzymes.