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Summary Table

Category	Details
Risk Factors	Post-term pregnancy (>42 weeks), chronic uteroplacental insufficiency, maternal hypertension, preeclampsia, diabetes with vascular disease, bilateral renal agenesis (Potter sequence), NSAID or ACE inhibitor use, twin-to-twin transfusion syndrome (donor twin)
Etiology	Decreased fetal urine production (renal agenesis, obstructive uropathy, uteroplacental insufficiency), premature rupture of membranes (PROM), maternal dehydration, medication-induced (NSAIDs, ACE inhibitors)
Patient Presentation	Fundal height less than expected for gestational age ("small for dates"), decreased fetal movement reported by mother
Classic Physical Exam	Uterus that feels "snug" around fetal parts on palpation, easy palpation of fetal limbs and body, possible signs of amniotic fluid leakage per vagina if PROM is the cause
Key Diagnostic Results	Amniotic fluid index (AFI) < 5 cm or single deepest pocket < 2 cm on ultrasound
Management	Identify and treat underlying cause, maternal oral hydration, amnioinfusion during labor for cord compression, delivery if fetal status is non-reassuring or if term/post-term
Keywords	"Small for dates," "decreased fetal movement," "AFI < 5," "Potter sequence," "pulmonary hypoplasia," "cord compression," "post-term pregnancy"

1. Pathophysiology

Amniotic fluid volume is a dynamic balance governed primarily by two processes: fetal urination (the main contributor to amniotic fluid in the second and third trimesters) and fetal swallowing (the main route of fluid reabsorption). In the first trimester, amniotic fluid is largely a transudate from the fetal skin and the amnion itself. However, by 16 weeks of gestation, the fetal kidneys become the dominant source of amniotic fluid, and the fetal skin keratinizes, eliminating transdermal fluid transfer.

Oligohydramnios develops when there is either reduced production or increased loss of amniotic fluid. Reduced production occurs when fetal renal function is impaired, whether from structural anomalies like bilateral renal agenesis or posterior urethral valves, or from functional reduction in renal perfusion as seen in uteroplacental insufficiency. When the placenta fails to deliver adequate blood flow, the fetus redistributes cardiac output preferentially to the brain and heart at the expense of the kidneys and lungs. This "brain-sparing" redistribution leads to decreased renal perfusion, decreased urine output, and consequently decreased amniotic fluid.

Increased loss of amniotic fluid most commonly results from premature rupture of membranes (PROM), where fluid leaks through a defect in the chorioamniotic membranes. This is a clinical diagnosis often confirmed by pooling of fluid in the posterior vaginal fornix, a positive nitrazine test (turning blue due to alkaline pH of amniotic fluid), or ferning on microscopy.

The consequences of oligohydramnios depend on timing and severity. In early pregnancy (second trimester), severe oligohydramnios leads to pulmonary hypoplasia because the fetus lacks the fluid environment necessary for lung expansion and development. Fetal breathing movements against amniotic fluid are critical for alveolar growth. Without this, the lungs remain underdeveloped, which is often incompatible with postnatal life. Prolonged oligohydramnios also causes limb compression deformities and the characteristic Potter facies (flattened nose, recessed chin, low-set ears, epicanthal folds) due to mechanical compression from the uterine wall directly against the fetus.

In late pregnancy, oligohydramnios increases the risk of umbilical cord compression during labor. Without adequate fluid cushioning, the cord can become trapped between the fetus and the uterine wall, producing variable decelerations on fetal heart rate monitoring. This is the hallmark tracing pattern associated with oligohydramnios in labor.

Medications are a testable cause. NSAIDs (e.g., indomethacin used for tocolysis) cause oligohydramnios by decreasing fetal renal blood flow through prostaglandin inhibition. ACE inhibitors are teratogenic and reduce fetal renal perfusion, causing oligohydramnios, renal dysgenesis, and neonatal renal failure. Both drug classes are high-yield associations.

2. Classification and Clinical Manifestation

Basis	Category	Clinical Features
By Timing	Early-onset (second trimester)	Associated with fetal renal anomalies (bilateral renal agenesis, obstructive uropathy), carries worst prognosis, leads to Potter sequence with pulmonary hypoplasia and limb deformities
By Timing	Late-onset (third trimester)	Associated with uteroplacental insufficiency, post-term pregnancy, PROM; risk of cord compression and fetal distress during labor
By Etiology	Fetal causes	Bilateral renal agenesis, polycystic kidney disease, posterior urethral valves, chromosomal anomalies
	Maternal causes	Hypertension, preeclampsia, dehydration, medications (NSAIDs, ACE inhibitors), diabetes with vascular disease
	Placental causes	Uteroplacental insufficiency, twin-to-twin transfusion syndrome (donor twin), placental abruption
	Idiopathic	No identifiable cause, accounts for a notable proportion of cases
By Severity (AFI)	Borderline	AFI 5 to 8 cm
	Oligohydramnios	AFI < 5 cm
	Severe / anhydramnios	AFI < 2 cm or virtually absent fluid

Potter Sequence deserves emphasis as a distinct clinical entity. This is not a single disease but a sequence of deformations caused by severe, prolonged oligohydramnios regardless of the underlying etiology. The unifying mechanism is extrinsic compression of the fetus. The classic tetrad includes: (1) pulmonary hypoplasia (the usual cause of death), (2) Potter facies, (3) limb and growth abnormalities, and (4) the underlying renal or urinary tract pathology. The most classic cause tested on exams is bilateral renal agenesis, which is incompatible with life.

3. Diagnostic Workup

Test	Role	Key Findings
Ultrasound (AFI measurement)	Best initial test and primary diagnostic tool	AFI < 5 cm or single deepest pocket < 2 cm confirms oligohydramnios
Detailed fetal anatomy ultrasound	Evaluate for structural cause	Absent kidneys (bilateral renal agenesis), dilated bladder or ureters (obstructive uropathy), absent bladder filling
Sterile speculum exam	Evaluate for PROM	Pooling of fluid in posterior fornix, positive nitrazine test, positive ferning pattern
Fetal Doppler studies	Assess uteroplacental perfusion	Absent or reversed end-diastolic flow in umbilical artery suggests severe placental insufficiency
Non-stress test / Biophysical profile	Assess fetal well-being	Variable decelerations (cord compression), low biophysical profile score
Karyotype / Amniocentesis	If structural anomaly identified	Chromosomal abnormalities may underlie renal or multisystem malformations

The best initial test is always ultrasound with calculation of the amniotic fluid index. The AFI is measured by dividing the uterus into four quadrants and summing the deepest vertical pocket in each quadrant. An AFI below 5 cm, or a single deepest pocket less than 2 cm, defines oligohydramnios. This distinction matters because some institutions prefer the single deepest pocket method, and exam questions may use either threshold.

Once oligohydramnios is confirmed, the next step is determining the cause. A detailed anatomy scan should evaluate the fetal kidneys and bladder. Bilateral renal agenesis presents with absent kidneys bilaterally and a persistently empty bladder on serial imaging. Posterior urethral valves (seen exclusively in males) present with a distended, thick-walled bladder ("keyhole sign") and bilateral hydroureteronephrosis.

If the clinical picture suggests fluid leakage, a sterile speculum examination is performed to evaluate for PROM. Importantly, digital cervical exam should be avoided in suspected PROM because it increases the risk of introducing infection. The three confirmatory findings for PROM are pooling, nitrazine positivity, and ferning. If these are equivocal, AmniSure (detection of placental alpha microglobulin-1) or insulin-like growth factor binding protein-1 (IGFBP-1) testing can confirm the diagnosis.

Doppler velocimetry of the umbilical artery is indicated when uteroplacental insufficiency is suspected. Absent or reversed end-diastolic flow is an ominous finding that often prompts delivery regardless of gestational age.

A biophysical profile (BPP) integrates ultrasound assessment of amniotic fluid volume with fetal tone, movement, breathing, and a non-stress test. Oligohydramnios itself scores 0 out of 2 on the fluid component, and the combination of low fluid with absent fetal movement or breathing often triggers intervention.

4. Management and Treatment

Clinical Scenario	Management
Mild oligohydramnios, term, reassuring fetal status	Increased maternal oral hydration, close surveillance with twice-weekly non-stress testing and AFI
PROM as the cause (preterm)	Expectant management until 34 weeks (if no infection or fetal distress), antenatal corticosteroids (betamethasone 12 mg IM x 2 doses, 24 hours apart) for fetal lung maturity if < 34 weeks, GBS prophylaxis, latency antibiotics (ampicillin + erythromycin for 7 days)
PROM at term (> 37 weeks)	Induction of labor within 12 to 24 hours to reduce infection risk
Cord compression in labor (variable decelerations)	Amnioinfusion: transcervical infusion of normal saline into the uterine cavity to cushion the cord
Non-reassuring fetal status at any gestational age	Emergent delivery (cesarean if indicated)
Post-term pregnancy	Induction of labor
Bilateral renal agenesis	Counseling regarding lethal prognosis; comfort care after delivery
NSAID or ACE inhibitor-induced	Discontinue the offending drug immediately; fluid volume often recovers

Maternal hydration is a simple but tested intervention. Oral hydration (approximately 2 liters of water over 2 hours) has been shown to increase AFI in cases of mild, idiopathic oligohydramnios or dehydration. This is a common "next best step" answer when the vignette describes borderline low fluid without an alarming underlying cause.

Amnioinfusion is the key intrapartum intervention. When oligohydramnios leads to recurrent variable decelerations during labor, the instillation of isotonic saline through an intrauterine pressure catheter restores fluid cushioning around the cord. This is a procedural concept that appears frequently. It is not used prophylactically in all oligohydramnios cases but rather when cord compression is demonstrated by the fetal heart rate pattern.

For preterm PROM, the management strategy hinges on gestational age. Between 24 and 34 weeks, expectant management is preferred as long as there is no evidence of chorioamnionitis, placental abruption, or non-reassuring fetal testing. Betamethasone is given for lung maturity. Latency antibiotics (the classic regimen is ampicillin 2 g IV every 6 hours for 48 hours, then amoxicillin 250 mg orally every 8 hours for 5 days, plus erythromycin or azithromycin) prolong the latency period and reduce neonatal morbidity. After 34 weeks, delivery is generally recommended because the risks of prematurity become lower than the risks of prolonged membrane rupture.

The management of drug-induced oligohydramnios is straightforward: stop the drug. Indomethacin, when used as a tocolytic, should generally not be continued beyond 32 weeks of gestation because of the risk of oligohydramnios and premature closure of the ductus arteriosus. ACE inhibitors and ARBs are contraindicated throughout pregnancy but cause renal effects predominantly in the second and third trimesters.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Polyhydramnios	Both are disorders of amniotic fluid volume detected by AFI measurement	Polyhydramnios has AFI > 24 cm (excess fluid); associated with fetal macrosomia, esophageal atresia, anencephaly, and maternal diabetes. Oligohydramnios has AFI < 5 cm and is associated with renal anomalies and IUGR
Intrauterine growth restriction (IUGR) alone	IUGR and oligohydramnios often coexist due to shared etiology (placental insufficiency)	IUGR is defined by estimated fetal weight below the 10th percentile; oligohydramnios is defined by AFI < 5 cm. A vignette may present both, but the question stem will ask about the fluid abnormality versus the growth abnormality
Posterior urethral valves	Causes oligohydramnios via obstructive uropathy	Seen only in male fetuses; ultrasound shows dilated, thick-walled bladder with "keyhole sign" and bilateral hydronephrosis. This is a cause of oligohydramnios, not a separate diagnosis
Chorioamnionitis	Can present in the setting of PROM with oligohydramnios	Distinguished by maternal fever > 38 C, uterine tenderness, foul-smelling discharge, maternal and fetal tachycardia. Requires delivery regardless of gestational age plus broad-spectrum antibiotics
Placental abruption	Can reduce amniotic fluid and cause fetal distress	Presents with painful vaginal bleeding, rigid "board-like" uterus, and signs of hypovolemic shock. Ultrasound may show retroplacental clot
Twin-to-twin transfusion syndrome	The donor twin develops oligohydramnios	Occurs only in monochorionic diamniotic twins; donor twin is "stuck" with low fluid while recipient has polyhydramnios. The discordance between the two sacs is the discriminator

6. Traps and High-Yield Pearls

The most common trap with oligohydramnios questions is confusing the direction of the amniotic fluid abnormality. Students must memorize that fetal urinary tract problems cause low fluid (oligohydramnios) while fetal swallowing problems cause high fluid (polyhydramnios). The logic is intuitive once internalized: if the fetus cannot urinate, fluid is not added to the amniotic cavity; if the fetus cannot swallow, fluid is not removed. Esophageal atresia and anencephaly cause polyhydramnios. Renal agenesis and obstructive uropathy cause oligohydramnios.

Another frequent "gotcha" involves drug-induced oligohydramnios. A vignette may describe a pregnant woman treated with indomethacin for preterm labor who now has decreased amniotic fluid. The tested concept is recognizing the causal link between NSAIDs and reduced fetal urine output via prostaglandin inhibition. Similarly, any vignette mentioning ACE inhibitor or ARB use during pregnancy should immediately raise concern for oligohydramnios and fetal renal injury.

Students also commonly miss the Potter sequence connection. When a vignette describes a newborn with flattened facial features, limb deformities, and respiratory failure at birth, the unifying diagnosis is Potter sequence from bilateral renal agenesis, not a primary pulmonary or musculoskeletal disorder. The pulmonary hypoplasia is the consequence, not the primary problem.

Finally, the intrapartum management pearl: variable decelerations on fetal monitoring during labor in a patient with known oligohydramnios should prompt consideration of amnioinfusion. This is distinct from late decelerations (which suggest uteroplacental insufficiency and may require emergent delivery) and early decelerations (which are benign and caused by fetal head compression). The fetal heart rate pattern is the discriminator for the correct intervention.

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