🧬 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 |

