🧬 Acute Fatty Liver of Pregnancy (AFLP)


🔷 INTRODUCTION

Acute fatty liver of pregnancy (AFLP) is a rare but life-threatening complication occurring typically in the third trimester (usually after 30 weeks) or early postpartum period. It results from microvesicular fatty infiltration of hepatocytes, leading to acute liver failure and multiorgan dysfunction.

It is considered an obstetric emergency requiring prompt diagnosis and delivery.


🔷 INCIDENCE & RISK FACTORS

  • Incidence: 1 in 7,000–20,000 pregnancies
  • Mortality: Up to 18% maternal; 10–20% fetal
  • Risk Factors:
    • Primigravida
    • Multiple gestation
    • Male fetus
    • Previous AFLP
    • Deficiency of LCHAD (Long-chain 3-hydroxyacyl-CoA dehydrogenase) in fetus or mother causes defective fatty acid β-oxidation


🔷 PATHOPHYSIOLOGY

AFLP is associated with mitochondrial dysfunction and impaired fatty acid oxidation, particularly due to fetal LCHAD deficiency. This leads to accumulation of toxic fatty acid metabolites in maternal liver hepatocellular damage hepatic failure coagulopathy, hypoglycemia, renal failure, and DIC.


🔷 CLINICAL FEATURES

Often non-specific, hence high clinical suspicion is key.

System

Features

GI

Nausea, vomiting, abdominal pain (esp. RUQ/epigastric)

Hepatic

Jaundice, hepatomegaly, LFTs

Neurological

Encephalopathy, confusion, coma

Hematological

Bleeding diathesis, thrombocytopenia

Renal

Oliguria, AKI

Constitutional

Malaise, fatigue, fever

Others

Hypertension and proteinuria may mimic preeclampsia


🔷 DIFFERENTIATING AFLP FROM HELLP

Parameter

AFLP

HELLP

Platelets

or N

↓↓↓

AST/ALT

Mild–mod

Marked

Bilirubin

↑↑

Usually mild

Glucose

Normal

Uric acid

↑↑

Ammonia

↑↑

Normal

Hypoglycemia

Common

Rare

Coagulopathy

Prominent

Variable

Encephalopathy

Frequent

Rare

Liver biopsy

Microvesicular steatosis

Sinusoidal fibrin deposition


🔷 INVESTIGATIONS

🧪 Key Labs:

  • LFTs: AST, ALT, bilirubin
  • Glucose: (often < 70 mg/dL)
  • Coagulation: PT/INR, fibrinogen
  • CBC: platelets, anemia
  • Creatinine/BUN: (AKI)
  • Ammonia:
  • Uric acid:
  • ABG: Metabolic acidosis

🩻 Imaging:

  • USG: May show fatty infiltration, but not diagnostic
  • MRI: Can detect microvesicular steatosis

📋 Swansea Criteria (≥6 criteria = suggestive of AFLP):

Criteria

Vomiting

Abdominal pain

Polydipsia/polyuria

Encephalopathy

Elevated bilirubin

Hypoglycemia

Elevated uric acid

Leukocytosis

Elevated AST/ALT

Elevated ammonia

Renal impairment

Coagulopathy

Microvesicular steatosis (liver biopsy)


🔷 MANAGEMENT OVERVIEW

Immediate delivery is the cornerstone of management.

Goals

Measures

Maternal stabilization

Fluids, glucose correction, ICU care

Correct coagulopathy

FFP, cryoprecipitate, vitamin K

Treat hypoglycemia

IV glucose infusions

Correct acidosis

Sodium bicarbonate if severe

Monitor organ function

LFTs, RFTs, coags, ABG

Plan delivery

Vaginal if stable; cesarean if fetal/maternal compromise

Neonatal support

NICU; test for LCHAD deficiency


🔷 ANESTHETIC CONSIDERATIONS

📍 Pre-Anesthesia Evaluation

  • Airway: Risk of edema anticipate difficult intubation
  • Coagulopathy: Platelets, PT, INR, fibrinogen essential
  • Hepatic function: risk of drug sensitivity and encephalopathy
  • Renal function: Drug clearance, fluid handling affected


💉 Regional Anesthesia

Usually contraindicated:

  • Platelets <75,000/mm³
  • INR
  • bleeding risk

🧠 Also avoid if altered mental status or encephalopathy


🌡️ General Anesthesia

Preferred in most AFLP cases due to:

  • Coagulopathy
  • Urgency
  • Hepatic encephalopathy

💡 Precautions:

  • Rapid sequence induction (RSI) with cricoid pressure
  • Propofol or thiopentone for induction
  • Rocuronium (dose adjustment if hepatic failure)
  • Avoid hepatotoxic drugs
  • Maintain normoglycemia
  • Maintain euvolemia


🩺 Monitoring

  • Arterial line: Beat-to-beat BP, ABG, frequent labs
  • CVP: For fluid management
  • Urinary catheter: Strict output charting
  • Invasive cardiac monitoring: If hemodynamic instability


🔷 POSTPARTUM CARE

  • Most women recover within 1–2 weeks after delivery
  • Continue glucose monitoring, liver function tests, INR
  • Monitor for DIC, renal failure, hepatic failure
  • Liver transplant is rare but may be required if hepatic necrosis ensues
  • Counsel family on risk of LCHAD deficiency in baby and future pregnancies


🔷 COMPLICATIONS

Maternal

Fetal

Hypoglycemia

Prematurity

DIC

IUGR

Renal failure

Stillbirth

Liver failure

Neonatal metabolic disorders

Encephalopathy

Hypoglycemia

Hemorrhage

NICU admission

Death



🔷 MCQ PEARLS

Question

Answer

First sign of AFLP

Nausea & vomiting

Most consistent lab abnormality

Hypoglycemia

Diagnostic criteria

Swansea

Definitive treatment

Immediate delivery

Pathophysiological defect

Defective fatty acid oxidation (LCHAD)

Contraindication to spinal

Coagulopathy