POLYHYDRAMNIOS/ HYDRAMNIOS

Ans. is D. i.e. Complications include placental abruption, uterine dysfunction, and postpartum hemorrhage.

• Polyhydramnios is an excessive quantity of amniotic fluid.
• The frequency of diagnosis varies, but polyhydramnios sufficient to cause clinical symptoms probably occurs in 1 of 1000 pregnancies, exclusive of twins.
• The incidence of associated malformations is about 20%, with CNS and GI abnormalities being particularly common.
• For example, polyhydramnios accompanies about half of cases of anencephaly and nearly all cases of esophageal atresia.
• Edema of the lower extremities, vulva, and abdominal wall results from compression of major venous systems.
• Acute hydramnios tend to occur early in pregnancy and, can leads to labor before the 28th week.
• The most frequent maternal complications are placental abruption, uterine dysfunction, and postpartum hemorrhage.

B/L renal agenesis [Ref. Dutta 6^th/e p 37, 213, 214]

• Polyhydramnios is defined as a state where liquour amni exceeds 2000 ml.
• Amniotic fluid measures about 50 ml at 12 weeks, 400 ml at 20 weeks and reaches its peak of 1 litre at 36-38 weeks.  •
• There after the amount diminishes till at term it measures about 600-800 ml

Amniotic fluid formation:?

– Early pregnancy                           —>         Ultra filtrate of plasma

– Beginning of 2nd trimester                —>         Composed largely of extracellular_.fluid that diffuses through the fetal skin.

– After 20 weeks                             -4         Cornification of fetal skin prevents this diffusion and the amniotic fluid is composed largely of fetal urine.

The fluid in the amniotic fluid is completely changed and replaced in every 3 hours.

Causes of increase in amniotic fluid (Polyhydramnios)

• Because the fetus normally swallows the amniotic fluid and excretes it through urine it has been assumed that this mechanism is one of the ways by which the volume is controlled.
• Thus renal agenesis will lead to oligohydramnios not polyhydramnios.
• Anencephaly causes polyhydramnios because of transudation from exposed meninges and absence of fetal swallowing reflex.
• Open spina bifida leads to polyhydramnios because of transudation of meninges.

Causes of polyhydramnios Maternal

• Ph isoimmunisation
• Diabetes

Placental

• Placental chrioangioma
• Circumvallate placenta syndrome

Fetal

• Multiple pregnancy
• Fetal anomalies

– CNS abnormalities (Anencephaly)

– G.I. abnormalities (Oesophageal or duodenal atresia)

– G. U. abnormalities

– Skeletal malformations – Fetal tumours

– Cardiac anomalies

– Chromosomal abnormalities

– Genetic syndromes

– Hematological disorders

– Intrauterine infections – Miscellaneous

Idiopathic

Complications of Polyhydramnios:

• Most of the maternal complications of polyhydramnios arise purely from pressure exerted within the overdistended uterus and upon adjacent organs. Which are 😕

– Respiratory discomfort

– Premature rupture of membrane

– Premature labour

– Pregnancy induced hypertension

– Abruptio placenta

– Cord prolapse

– Placental insufficiency

– Post partumhemmorrhage

Fetal complications:

• Fetal morbidity and mortality is significant in cases of polyhydramnios.
• The major causes of mortality are congenital abnormalities incompatible with life.

Ans. is C. i.e. Amniocentesis

• In this clinical scenario, amniocentesis is done to relieve the distress and to continue the pregnancy up to term.
• Slow decompression is done at a rate of about 500ml per hour.
• Normally 1-1.5litres of amniotic fluid is removed.
• Because of slow decompression, there is less chance of accidental hemorrhage, but fluid can reaccumulate soon.
• So amniocentesis has to be repeated.

Ans. is B. i.e. Cleft palate

• Cleft palate in the fetus is associated with the development of maternal polyhydramnios, as the facial cleft interferes with the normal swallowing process.

• Polyhydramnios is defined as a state where liquor amnii exceed 2000ml.

• Sonographically diagnosis is made when the amniotic fluid index is >25cm, and a single pool is >8cm.

Causes of Polyhydrdmnios

• The main contributor of amniotic fluid is fetal urine.
• Amount of amniotic fluid will be more (i.e. polyhydramnios) if:

1. Fetus produces more urine for example:

a. Twin/multifetal pregnancy (number of the fetus is more: more of urine)

b. Maternal hyperglycemia/diabetes Maternal hyperglycemia →Fetal hyperglycemia → Fetalpolyuria →increased amniotic fluid.

c. Twin to Twin transfusion syndrome.

2. Besides producing Amniotic fluid fetus also swallows amniotic fluid. 

→The amount of amniotic fluid will increase if; fetal swallowing is impaired as in case of:

a. Cleft lip and cleft palate

b. Esophageal atresia or stenosis

c. Duodenal atresia or stenosis

d. Bowel obstruction

e. Anencephaly (swallowing is decreased + increased transudation of CSF into amniotic fluid due to absence of cranial vault)

3. Other important causes of polyhydramnios are:

Placental Causes

a. Chorangioma of the placenta and circumvallate placenta.

Fetal Causes

a. Hydrops fetalis

b. Rubella, syphilis, Toxoplasma infection of the fetus.

c. Trisomy (note – Triploidy leads to oligohydramnios)

d. Sacrococcygeal Teratoma

e. Thalassemia of the fetus.

• M/C cause of mild polyhydramnios: idiopathic
• M/C cause of severe polyhydramnios: Gross congenital anomaly i.e. GIT malformations> CNS malformations.

Ans. is B. i.e. polyhydramnios

The most common cause of hypothyroidism in pregnancy is Hashimoto thyroiditis, characterized by glandular destruction from autoantibodies, particularly antithyroid peroxidase antibodies. There is an increased risk of,

• Preeclampsia
• Placental abruption
• Recurrent abortions
• Intrauterine growth restriction
• Prematurity
• Cardiac dysfunction
• Intrauterine fetal demise

2 ltr.

Posterior urethral value

Renal agenesis

Hydramnios

Ans. is b  i.e. Hydramnios

• As explained in the previous question maternal hyperglycaemia leads to fetal hyperglycaemia, which in turn causes polyuria and thus causes polyhydramnios.

–  Polyhydramnios leads to preterm delivery and not post datism.

–  Excessive uterine enlargement because of polyhydramnios and macrosomia causes increased incidence of atonic PPH.

• Diabetes leads to increased incidence of congenital defects in fetus.
• Maternal hyperglycemia          to fetal hyperglycemia              hyperinsulinemia -÷ to neonatal hypoglycemia at birth.

Ans. is ‘a’ i.e., Spinal muscular atrophy

o Out of the given options only spinal muscular atrophy is able to cause hypotonia and hyporeflexia during infancy. Rest of them either present late in childhood or do not give the symptoms.

o Polyhydromnios and decreased fetal movements can occur in any neuromuscular disorder which present during intrauterine life.

o Lets see each option one by one.

Spinal muscular atrophy (SMA)

• SMA is a degenerative disease of motor neurons that begin in fetal life and continue to progress in infancy and childhood.

o The cardinal features are:

Hypotonia

Generalized weakness

Absent tendon stretch refluxes

Involvement of tongue face and jaw muscle but sparing of extraocular muscle and sphincters.

Congenital mytonia

o Congenital myotonia or myotonia congenita is a chloride channel defect of skeletal muscle.

o There is weakness and generalized hypertrophy of muscles.

o Its ruled out as

 Presents in early childhood (2-3 years age)

Deep tendon reflexes are preserved.

Congenital myaesthenia

o Its a disease of neuromuscular junction similar to myasthenia gravis except that its not autoimmune but rather due to genetic mutations.

o It presents in infancy and childhood with symptom similar to myasthenia gravis.

o It can be ruled out as‑

o It does not present in the intrauterine life (so does not cause polyhydramnios).

DTRs are preserved

Muscular dystrophies

o Muscular dystrophy refers to a group of hereditary progressive diseases.

o It includes

•  Duchenes muscular dystrophy   
• Limb-girdle                           
• Congenital myopathies
• Becker                                     
• Myotonic dystrophica

o All of these except congenital myopathies are easily ruled out as they present in childhood age. some may rarely present in infancy but never in the intrauterine life.

o Congenital myopathies are the most difficult one to rule out.

                   They present with hypotonia in infancy.

                   It may also present in intrauterine life.

o Only reason I’m with ‘Spinal muscular atrophy’ is that congenital myopathy is a very rare disease.

Ans. C: Post Dated Pregnancy

• Pre-eclampsia (25%)
• Malpresentations
• Premature rupture of membranes
• Preterm labour
• Accidental hemorrhage

Complications during labour:

• Early rupture of membranes

Cord prolapsed

Uterine inertia

Retained placenta, postpartum hemorrhage