Preeclampsia

Ans:B.)   Smoking REF: William’s obstetrics 22^nd edition

Although smoking during pregnancy causes a variety of adverse pregnancy outcomes, ironically, smoking has consistently been associated with a reduced risk of hypertension during pregnancy (Bainbridge and associates, 2005; Zhang and colleagues, 1999). Placenta previa has also been reported to reduce the risk of hypertensive disorders in pregnancy (Ananth and colleagues, 1997).

Underlying Causes of Chronic Hypertensive Disorders:

Magnesium sulfate REF: Current Diagnosis & Treatment Obstetrics & Gynecology, 10th edition Chapter 19

In Severe Pre eclampsia During labor, magnesium sulfate is administered for seizure prophylaxis as an IV loading dose of 4-6 g over 20-60 minutes, followed by a maintenance dose of 1-2 g/h.

Ans. is a and c i.e. Early use of conduction anaesthesia & sedation; and Unripe cervix

First stage i.e. the stage of cervical effacement and dilatation and is further divided into 2 phases.

Latent phase

It is the preparatory phase of the uterus & the cervix, before the actual onset of labour. It starts at the point at which the mother perceives regular uterine contractions.

Its duration 8.6 hours in nulliparous (average 6 – 8 hrs.)° & 5.3 hours in multiparous (average 4 – 6 hours).°

• Mainly concerned with cervical effacement

Active phase

It begins with cervical dilatation of 3 – 4 cms, with regular uterine contractions & normal minimum cervical dilatation rate of 1.2 cm/hr for nulliparous°

&  1.5 cm/hr for parous women°. Minimum of 1cm/hr.

• Mainly concerned with cervical dilatation

Prolonged latent phase

Latent phase is said to prolonged if it is – • Greater than 20 hours in nullipara.°

• Greater than 14 hours in multipara.°                      according to fernando
arias

According to Williams 23/e, p 406-Latent-phase should not last longer than 8 hours.

Causes of Prolonged Latent Phase

—         Excessive sedation or conduction analgesia.

—         Poor cervical conditions (e.g., Thick. uneffaced or undilated).

—         False labour (most common cause in multipara).

Diagnosis : The diagnosis of prolonged labour is made by observation of the .- ,iedman’s curve. Management : Either of the 2 options are used for managing prolonged latent phase
              Therapeutic Rest                                                            Oxytocin stimulation

15 mg of morphine is given intramuscularly. Most of the patients are asleep within 1 hour & awake 4 to 5 hours later, in active labour or in no labour.

Amniotomy is not useful and should be avoided in patients in prolonged latent phase. Also, there is no indication of cesarean section in this case.

Ans. is a, b and c i.e. Chromosome pattern is XX; Enlarged ovarian cyst occurs; and Associated with preeclampsia

• The incidence of H. mole is maximum in oriental and south east countries (maximum incidence is in
  Philippines: 1 in 80 pregnancies) Le., it is more common in developing countries option ‘a ruled out).

H, mole can be categorized as either complete or partial mole on the basis of Gross morphology, histopathology and karyotype.

Com^plete H. mole – shows no evidence (If fetal tissue at all,

• Complete hydatiform moles exhibit characteristic swelling and trophoblastic hyperplasia. Most common karyotype is 46XX (10% may have a 46XY karyotype).
• The molar chromosomes are entirely of paternal origin, although mitochondrial DNA is of maternal origin.
• The complete moles arises from an ovum that has been fertilized by a haploid sperm, which then duplicates
  its own chromosomes called as Androgenesr. The ovum nucleus may be either absent or inactivated.

Clinical features;

Symptoms:

• Amenorrhea of varying duration followed by continuous or intermittent brown or bloody discharge (usually not profuse) evident by – 12 weeks.
• Passage of vesicles per vaginum
• Hyperemesis (due to the high levels of circulating HCG).

Signs:

• Uterus:

–     The fundal height of uterus is more than the period of amenorrhea in 50% cases. In 35% it corresponds to the gestational period and in the rest it may be smaller.

–   Uterus is doughy in consistency (due to absence of amniotic fluid).

–    Fetal parts will not be felt.

–    Fetal heart sounds will not be heard (even on doppler).

–    External and internal ballottement can not be elicited.

• Theca lutein cysts :

–     May be felt in the ovaries in about 25 to 60%.

–     Due to overstimulation of the luteal elements by the large amounts of circulating HCG°

–     Persistent trophoblastic disease is more likely in women with theca lutein cysts.

• Early onset preeclampsia

– When hypertension appears before 24 weeks, it is important to rule out hydatidiform mole.

• Thyrotoxicosis seen due to the thyrotrophin-like effect of HOG.°
• Spontaneous expulsion occurs at around 18 weeks° and rarely delayed beyond 28 weeks.°

Characteristics of partial H. mole

• Some embryonic or fetal tissue identifiable.
• Partial moles generally have a triploid karyotype (69 chromosomes); the extra haploid set of chromosomes usually is derived from the father
• Chorionic villi of varying size with focal hydatidiform swelling, cavitation, and trophoblastic hyperplasia whereas complete mole shows diffuse hydatidiform swelling and trophoblastic hyperplasia.
• Marked villous scalloping.
• Prominent stromal trophoblastic inclusions.

–    When a fetus is present in conjunction with a partial mole. it generally exhibits the stigmata of triploidy, including growth retardation and multiple congenital malformations such as syndactyly and hydrocephaly.

Pre-eclampsia is a state of hypertension in pregnancy associated with proteinuria but with or without pathological edema.
It is defined as a multi-system disorder of unknown etiology characterised by development of hypertension to the extent of 140/90 mm Hg or more with protienuria after the 20th week of pregnancy in a previously normotensive and a normoproteinuric patient.
The typical pathological features are endothelial dysfunction and intense vasospasm. In pre-eclampsia, the glomerular filtration rate decreases.

The decrease in glomerular filtration rate is as a result of the following physiological changes:
Afferent glomerular arteriolar vasospasm
Occlusion of the lumen of the glomerulus resulting from glomerular endotheliosis and fibrin deposits in the basement membrane
Decreased renal blood flow

Ref: Textbook of Obstetrics By D.C. Dutta, 6th Edition, Pages 221-3131

The risk of developing pre–eclampsia is only mild in chronic glomerulo nephritis and polycystic kidney disease.
The risk is mild to moderate in Renal artery stenosis and severe in Polyarteritis nodosa.

The disease is preeclampsia, which may be complicated by a wide variety of serious conditions.
Historically, the appearance of convulsions defined the transition from preeclampsia to eclampsia; however the concept of eclampsia is probably flawed because many other serious complications can occur even in the absence of seizures.
Statistically, the most common causes of maternal death in preeclampsia are cerebral hemorrhage and pulmonary complications, notably adult respiratory distress syndrome.

MgSO4 is the drug of choice for severe preeclampsia and eclampsia.

Mechanism of action:

• It reduces motor endplate sensitivity to acetylcholine and thereby reduces neuromuscular irritability.
• It also blocks neuronal calcium influx.
• It induces cerebral vasodilatation, dilates uterine arteries, increases production of endothelial prostacyclin and inhibits platelet activation.

Benefits from other regimens:

• No detrimental effects on the neonate within therapeutic level.
• Excellent result with maternal mortality of 0.4%.

Ref: Textbook of Obstetrics by D.C. Dutta, 6th edition, Page 236.

• Phosphatidylglycerol (PG) is a minor constituent of surfactant. 
• It begins to increase appreciably in amniotic fluid several weeks after the rise in lecithin. 
• Its presence is more indicative of fetal lung maturity because PG enhances the spread of phospholipids on the alveoli.

A serum uric acid level (biochemical marker of pre-eclampsia) of more than 4.5 mg/dl indicates the presence of pre-eclampsia.
Blood urea level remains normal or slightly raised.
Serum creatinine level may be more than 1 mg/dl.
There may be thrombocytopenia and abnormal coagulation profile of varying degrees.
Hepatic enzyme levels will be increased.
Ref: Textbook of Obstetrics D C Dutta, 6th edition, Page 227.

The development of new-onset diabetes insipidus in the third trimester is usually due to increased vasopressinase activity either due to increased placental production or decreased hepatic vasopressinase metabolism due to liver damage from various causes including preeclampsia, acute fatty liver of pregnancy, or HELLP, syndrome.
This phenomenon is called transient vasopressin-resistant diabetes insipidus (DI) of pregnancy.
Ref: Mehta N.D., Chen K.K., Monzon C., Rosene-Montella K. (2012). Chapter 223. Common Medical Problems in Pregnancy. In G.V. Lawry, J. Matloff, D.D. Dressler, D.J. Brotman, J.S. Ginsberg (Eds), Principles and Practice of Hospital Medicine.

Risk Factors for Preeclampsia:

• Age 35 years
• Nulliparity
• Multiple gestation
• Hydatidiform mole
• Diabetes mellitus
• Thyroid disease
• Chronic hypertension
• Renal disease
• Collagen vascular disease
• Antiphospholipid syndrome
• Family history of preeclampsia

Ref: Miller D.A. (2013). Chapter 26. Hypertension in Pregnancy. In A.H. DeCherney, L. Nathan, N. Laufer, A.S. Roman (Eds), CURRENT Diagnosis & Treatment: Obstetrics & Gynecology, 11e.

Termination of pregnancy is the only cure for pre-eclampsia. Headache, visual disturbances, or epigastric pain is indicative that convulsions may be imminent, and oliguria is another ominous sign.
Severe preeclampsia demands anticonvulsant and usually antihypertensive therapy followed by delivery.

Uterine artery