Republic of the Philippines

Southern Luzon State University

College of Allied Medicine

Lucban, Quezon

A.Y. 2019-2020

OLOGOHYDRAMNIOS

A case analysis

In partial fulfillment

Of the Requirements for the subject

M102 Related Learning Experience

Submitted to:

Mrs. Lorna Cano

(Clinical Instructor)

Submitted by:

Elloso,Dorcas D.

(Midwifery II)

September 2019
I. OBJECTIVES

GENERAL OBJECTIVES

After establishing a midwife patient interaction and providing care to the clients and by a

thorough assessment and careful study of the patient’s condition, students will gain knowledge,

developed skills and enhance attitude through utilization of the nursing process on the care and

management of the patient with Oligohygramnios.

SPECIFIC OBJECTIVES

More specially, to guide the students in the completion of a comprehensive case study,

the student will able:

1. To define what is Vaginal Bleeding and its related complications.

2. To identify the different signs and symptoms.

3. Review the anatomy and physiology of the Reproductive System.

4. To trace the pathophysiology.

5. To establish good midwife-patient interaction and relationship.

6. Determine the status of the patient through:

a. General Data

b. Physical Assessment

c. Present History of the Illness

d. Maternal History

7. To analyze and interpret the laboratory examinations.

8. To familiarize the different diagnostic procedures done to the patient regarding

her condition.

9. Identify the means of preventing Vaginal Bleeding and its related complications.

10. Identify and understand the importance of pharmacological intervention in

relation to patient’s present condition.

11. Render quality nursing care through implementation of Nursing Care Plan.

12. Evaluate the effectiveness of nursing care plan and medical management.
II. INTRODUCTION

As a midwife student, one of our requirements is to present a comprehensive case

analysis that we had encountered during our exposure to our designated area at QMC-OB Gyne

The amniotic fluid that bathes the fetus is necessary for its proper growth and

development. It cushions the fetus from physical trauma, permits fetal lung growth, and provides

a barrier against infection. Normal amniotic fluid volume varies. The average volume increases

with gestational age, peaking at 800-1000 mL, which coincides with 36-37 weeks' gestation. An

abnormally high level of amniotic fluid, polyhydramnios, alerts the clinician to possible fetal

anomalies. An inadequate volume of amniotic fluid, oligohydramnios , results in poor

development of the lung tissue and can lead to fetal death.

Polyhydramnios occurs in 1% of pregnancies, whereas oligohydramnios occurs in about 11% of

pregnancies. No age variables are recognized.

Oligohydramnios is a deficient volume of amniotic fluid; it is associated with maternal

and fetal complications. Diagnosis is by ultrasonographic measurement of amniotic fluid

volume. Management involves close monitoring and serial ultrasonographic assessments.

Polyhydramnios, or hydramnios, is defined as an excessive volume of amniotic fluid

relative to the gestational age. Polyhydramnios may be acute or chronic. Acute polyhydramnios

is usually a fulminant second-trimester process, with fluid accumulating rapidly over a period of

a few days.Chronic polyhydramnios has a more gradual onset and course, often presenting in the

third trimester.
III. ANATOMY AND PHYSIOLOGY

PREVELENCE AN6D EPIDEMIOLOGY

Oligohydramnios complicates 0.5% to 8% of pregnancies, and management and

prognosis depend on gestational age and associated obstetric complications.14,15 Outcomes are

worse with earlier or more severe oligohydramnios (e.g., anhydramnios) (Fig. 120.1).15–
17
Etiologies include preterm premature rupture of membranes (PPROM) (Fig. 120.2), fetal

abnormalities (especially of the genitourinary tract), and placental insufficiency (Fig. 120.3). In a

retrospective review of 128 second-trimester (13–24 weeks, n = 128) and 122 third-trimester

(25–42 weeks, n = 122) fetuses with oligohydramnios, the former were more likely to be

anomalous and less likely to have unexplained oligohydramnios, whereas the reverse was true of

third-trimester fetuses.17 Specifically, among second-trimester fetuses, 50.7% were complicated

by anomalies, 33.6% by PPROM, 7% by abruption, 5% by growth restriction, and only 4% were

unexplained. In contrast, third-trimester fetuses were most likely to have unexplained

oligohydramnios (52.5%), with anomalies noted in 22.1%, growth restriction in 20.5%, PPROM

in 3.3%, and placental abruption in 1.6%. Accordingly, only 10.2% of second-trimester fetuses

survived compared with 85.3% of third-trimester fetuses.

Fig. 120.1. Severe oligohydramnios in a 21-week fetus.

Fig. 120.2. Preterm premature rupture of membranes in a dichorionic diamniotic twin gestation.

TABLE 4-2. Aetiology in the Second and Third Trimesters

Aetiology in the Second
Aetiology in the Third Trimester
Trimester
Idiopathic oligohydramnios (commonest cause
Fetal anomaly 50.7% 52.5%
of oligohydramnios)
Ruptured membranes 33.6% Fetal anomaly 22.1%
Abruption 7.1% Intrauterine growth restriction 20.5%
Intrauterine growth
4.7% Ruptured membranes 3.3%
restriction
Idiopathic 3.9% Abruption 1.6%

Fig. 120.3. Reversed end-diastolic flow and oligohydramnios in a 23-week fetus with growth

restriction; the mother subsequently developed severe preeclampsia.

Pulmonary hypoplasia is the primary cause of mortality in pregnancies complicated by second-

trimester oligohydramnios. Because amniotic fluid is required for the normal development and

expansion of the pulmonary system, lack of adequate fluid at critical stages of lung

development is associated with poor outcome. Pulmonary hypoplasia is more likely with

oligohydramnios during or before 16–24 weeks' gestation, the canalicular phase of lung

development, when the terminal sacs are developing, compared with later in gestation, when the

terminal sacs are developed, and the primary changes to prepare for eventual gas exchange have

occurred.

The association between outcome and severity of oligohydramnios was shown in a review of

almost 29,000 fetuses at 24 to 34 weeks.15 Of these, 166 had oligohydramnios (AFI ≤ 5 cm), 204
had “borderline” fluid (5.1–8 cm), and the remainder were normal (8.1–24 cm).

Major malformations were present in 25% of fetuses with oligohydramnios compared to 10%

with borderline, and 2% with normal fluid. Compared to fetuses with normal fluid, growth

restriction was nine times more likely in fetuses with oligohydramnios, and five times more

likely in those with borderline fluid. Risks of preterm birth and cesarean section were higher with

oligohydramnios and borderline fluid, but morbidity and mortality were not significantly

different with borderline fluid if fetal growth was appropriate. The authors concluded that close

surveillance or delivery for oligohydramnios is warranted, but recommendations are not clear for

borderline fluid.

IV. OVERVIEW OF THE DISEASE

DEFINITION

Oligohydramnios refers to a low level of amniotic fluid during pregnancy.

It is defined by an amniotic fluid index that is below the 5th centile for the gestational age, and

is thought to affect approximately 4.5% of term pregnancies [AJOC, 2004].

In this article, we shall look at the aetiology, investigations and management of oligohydramnios.

By TeachMeSeries Ltd (2019)

Fig 1 – Amniotic fluid centiles during pregnancy. Polyhydramnios is over the 95th centile,

oligohydramnios is below the 5th centile

PATHOPYSIOLOGY

The volume of amniotic fluid increases steadily until 33 weeks of gestation. It plateaus from 33-

38 weeks, and then declines – with the volume of amniotic fluid at term approximately 500ml.

It is predominantly comprised of the fetal urine output, with small contributions from the

placenta and some fetal secretions (e.g. respiratory).

 The fetus breathes and swallows the amniotic fluid. It gets processed, fills the bladder and is

voided, and the cycle repeats. Problems with any of the structures in this pathway can lead to

either too much or too little fluid.

Anything that reduces the production of urine, blocks output from the fetus, or a rupture of the

membranes (allowing amniotic fluid to leak) can lead to oligohydramnios.

ATEOLOGY

The main causes of oligohydramnios are:

 Preterm prelabour rupture of membranes

 Placental insufficiency – resulting in the blood flow being redistributed to the fetal brain rather

than the abdomen and kidneys. This causes poor urine output.

 Renal agenesis (known as Potter’s syndrome)

 Non-functioning fetal kidneys, e.g. bilateral multicystic dysplastic kidneys

 Obstructive uropathy

 Genetic/chromosomal anomalies

 Viral infections (although may also cause polyhydramnios)

Ultrasonographic assessment of oligohydramnios

Author Populati Larg Oligo Abnor Sensitiv Specific

on est hy- mal ity(%) ity(%)
pock dram endpoi
et nios nt Positive predi Negative predi
criter (%) ctive value ctive value
ia (%) (%)

Crowley(19 >42 Subje 35 Cesarea 100 68 12 100

80)46 weeks ctive n
for “fet
al
distress
”
Author Populati Larg Oligo Abnor Sensitiv Specific
on est hy- mal ity(%) ity(%)
pock dram endpoi
et nios nt Positive predi Negative predi
criter (%) ctive value ctive value
ia (%) (%)

Manning Suspect <1 24 SGA 84 97 90 95

(1981)51 ed cm
IUGR

Philipson Unselec Subje 4 SGA 16 97 40 91

(1983)40 ted ctive

Bottoms Unselec Subje 19 SGA 32 83 23 89

(1986)33 ted ctive

Hill Unselec <1 0 SGA 0 100 — 98

(1983)39 ted cm

Subje 1 SGA 50 100 100 99

ctive

Haddick Retrosp <1 4 SGA 4 — — —

(1984)52 ective cm
SGA
pregnan
cy

Mercer Retrosp <1 3 Apgar 5 — — 8 —

(1984)53 ective cm <7
unselec
ted

Chamberlai Referre Verti 3 SGA 13 98 25 95

n(1984)54 d for cal
biophys 2 cm
ical
profile

Phelan (198 >41 <1 3 Apgar 5 25 98 29 97

5)45 weeks cm <7

Postmat 3 97 17 83
urity

Bastide Referre Verti 0.7 SGA — — 37 —

(1986)55 d for cal <1
biophys
Author Populati Larg Oligo Abnor Sensitiv Specific
on est hy- mal ity(%) ity(%)
pock dram endpoi
et nios nt Positive predi Negative predi
criter (%) ctive value ctive value
ia (%) (%)

ical cm
profile

Patterson Risk Avera 15 SGA 40 91 50 86

(1987)56 for ge
malnutr <3.2
ition cm

Hashimoto >42 “Volu 46 Postmat 90 64 36 97

(1987)43 weeks me” ure
<60

Rutherford “High Sum 8 Cesarea 30 93 11 98

(1987)57 risk” of 4 n for
pregnan vertic “fetal
cy al distress
quadr ”
ants
<5
cm

Silver 41 Mean 54 Deliver 79 55 41 87

(1987)44 weeks of 3 y for
vertic nonreas
al suring
<3.8 fetal
cm heart
rate
trace

Varma “At Verti 3 SGA — — 39 92

(1988)58 risk” cal <2
pregnan cm
cy
 CLINICAL ASSESSMENT

Oligohydramnios is a diagnosis made via ultrasound examination. Therefore, the clinical

assessment of the patient is directed at establishing any underlying cause:

 History

o Inquire about symptoms of leaking fluid and feeling damp all the time (often described as new

urinary incontinence).

 Examination

o Measure the symphysis fundal height.

o Perform a speculum examination (can a ‘pool’ of liquor be seen in the vagina?).

 Ultrasound

o Assess for liquor volume, structural abnormalities, renal agenesis and obstructive uropathy.

o Measure fetal size. Small babies can result from placental insufficiency, which also causes

oligohydramnios. There may also be a rise in pulsatility index of the umbilical artery Doppler in

placental insufficiency.

 Karyotyping (if appropriate) – particularly in cases of early and unexplained oligohydramnios.

When considering ruptured membranes as a cause for oligohydramnios, a bedside test can be

performed to detect the presence of IGFBP-1 (insulin-like growth factor binding protein-1) in the

vagina. This protein is found in amniotic fluid, and if detected, is strongly suggestive of

membrane rupture. The test is particularly useful if the diagnosis is unclear.

-SA 3.0], vi
 Management

The management of oligohydramnios is largely dependent on the underlying cause. The two

most common causes are rupture of the membranes and placental insufficiency.

Ruptured Membranes

If oligohydramnios is due to ruptured membranes, labour is likely to commence within 24-48

hours in most pregnancies.

In cases of preterm rupture of membranes (i.e. before 37 weeks’ gestation), and where labour

doesn’t start automatically, induction of labour should be considered around 34-36 weeks (in the

absence of infection).

A course of steroids should be given to aid fetal lung development, and antibiotics to reduce the

risk of ascending infection.

Placental Insufficiency

In women where oligohydramnios is caused by placental insufficiency, the timing of delivery

depends on a number of factors:

 Rate of fetal growth

 Umbilical artery and middle cerebral artery Doppler scans

 Cardiotocography

These babies are likely to be delivered before 36-37 weeks.

Complications

Complications may include cord compression, musculoskeletal abnormalities such as facial

distortion and clubfoot, pulmonary hypoplasia and intrauterine growth restriction. Amnion

nodosum is frequently also present (nodules on the fetal surface of the amnion).[1]

The use of oligohydramnios as a predictor of gestational complications is controversial.[2][3]

Potter syndrome is a condition caused by oligohydramnios. Affected fetuses develop pulmonary

hypoplasia, limb deformities, and characteristic facies. Bilateral agenesis of the fetal kidneys is

the most common cause due to the lack of fetal urine.

Causes

The cause is not known but is often associated with some:

 fetal chromosomal anomalies like triploidy

 intra uterine infections

 premature rupture of membrane

 drugs; COX inhibitors like indomethacin, ACE inhibitors

 renal agenesis or obstruction of the urinary tract of the fetus preventing micturition such as

posterior urethral valves in males

 intrauterine growth restriction (IUGR) associated with placental insufficiency

 amnion nodosum; failure of secretion by the cells of the amnion covering the placenta

 postmaturity (dysmaturity)

Diagnosis

 uterine size is much smaller than the period of amenorrhoea

 fewer fetal movements,

 the uterus "full of fetus" because of scanty liquid,

 malpresentation (breech)

 evidences of IUGR of the fetus,

 sonographic diagnosis is made when largest liquid pool is less than 2 cm,

 visualization of normal filling and emptying of fetal bladder essentially rule out urinary tract

abnormality,

 Oligohydramnios with fetal symmetric growth retardation is associated with increased

chromosomal abnormality.
Treatment

A Cochrane review concluded that "simple maternal hydration appears to increase amniotic fluid

volume and may be beneficial in the management of oligohydramnios and prevention of

oligohydramnios during labour or prior to external cephalic version."

In severe cases oligohydramnios may be treated with amnioinfusion during labor to

prevent umbilical cord compression. There is uncertainty about the procedure's safety and

efficacy, and it is recommended that it should only be performed in centres specialising in

invasive fetal medicine and in the context of a multidisciplinary team.[5]

In case of congenital lower urinary tract obstruction, fetal surgery seems to improve survival,

according to a randomized yet small study.

V. CASE STUDY PROPER

DEMOGRAPHIC DATA

Patient’s profile

 Name:

 Age:

 Address:

 Civil status: Married

 Religion: Roman Catholic

 Nationality: Filipino

 Chief Complaint:

 Admitting Diagnosis: Date admitted: September 4, 2019

  Final Diganosis: G1P1 (1001) Pregnancy uterine 401/7 weeks cephalic delivered

operatively to a live baby girl

 Date of Discharge:

History of present illness:

Maternal history:

PHYSICAL ASSESSMENT

General condition:
VI. COURSE IN THEWARD

DIAGNOSTIC PROCEDURE

VII. EVALUATION

A. PATIENT

B. OVERALL

VIII. BILIOGRAPHY

https://www.msdmanuals.com/professional/gynecology-and-obstetrics/abnormalities-of-

pregnancy/oligohydramnios

https://www.google.com/search?q=physiology+of+oligohydramnios&rlz=1C1GGRV_enPH831PH831&oq

=physiology+of+oligohydramn6&aqs=chrome.1.69i57j0l2.12511j0j7&sourceid=chrome&ie=UTF-8

https://www.sciencedirect.com/topics/medicine-and-dentistry/oligohydramnios

https://www.glowm.com/section_view/heading/Amniotic%20Fluid:%20Physiology%20and%20Assessm

ent/item/208