What is the cause of elevated Alkaline Phosphatase (ALP) and Lactate Dehydrogenase (LDH) levels following a Lower Segment Caesarean Section (LSCS), accompanied by Acute Kidney Injury (AKI) and anemia, in the absence of Pregnancy-Induced Hypertension (PIH)?

Elevated ALP and LDH Post-LSCS with AKI and Anemia: Differential Diagnosis

The most likely diagnosis is Acute Fatty Liver of Pregnancy (AFLP) or HELLP syndrome, both of which are obstetric emergencies that can present postpartum with elevated ALP and LDH, acute kidney injury, and anemia even without pre-existing pregnancy-induced hypertension. 1

Primary Diagnostic Considerations

HELLP Syndrome

HELLP syndrome can occur postpartum and presents with the classic triad of hemolysis, elevated liver enzymes, and low platelets. 1

Key diagnostic features:

• LDH elevation is a cardinal feature of HELLP syndrome, reflecting hemolysis and hepatic ischemia from fibrin deposition in hepatic sinusoids 1
• ALP is typically elevated but less dramatically than LDH (ALT usually <500 U/L) 1
• Hypertension is present in only 85% of cases, meaning 15% lack PIH 1
• Microangiopathic hemolytic anemia with thrombocytopenia (<100 × 10⁹/L) 1
• Acute kidney injury occurs as part of multi-organ involvement 1
• Proteinuria and elevated uric acid are common 1

Acute Fatty Liver of Pregnancy (AFLP)

AFLP typically presents in the third trimester or postpartum and is a critical differential. 1

Distinguishing features:

• LDH is markedly elevated (often >500 U/L) 1
• ALP and GGT are elevated 1
• Renal impairment (creatinine >1.7 mg/dL) is part of the Swansea criteria 1
• Hypoglycemia is characteristic and helps differentiate from HELLP 1
• Coagulopathy with prolonged PT and low fibrinogen (DIC in >75% of cases) 1
• Approximately 50% have concurrent pre-eclampsia features, but absence doesn't exclude diagnosis 1
• Hepatic encephalopathy, if present, strongly suggests AFLP over HELLP 1

Diagnostic Algorithm

Immediate Laboratory Assessment

1. Complete blood count with peripheral smear to assess for:

   • Schistocytes indicating microangiopathic hemolysis (HELLP) 1
   • Platelet count (<100 × 10⁹/L suggests HELLP) 1
   • Hemoglobin level to quantify anemia 1

2. Coagulation studies:

   • PT/PTT and fibrinogen levels (prolonged PT and low fibrinogen suggest AFLP) 1
   • DIC panel if coagulopathy present 1

3. Metabolic panel:

   • Glucose level (hypoglycemia <72 mg/dL strongly suggests AFLP) 1
   • Ammonia level (elevated >42 IU/L in AFLP) 1
   • Uric acid (elevated >5.7 mg/dL in both conditions) 1

4. Liver function tests:

   • Total and direct bilirubin (typically <5 mg/dL in both) 1
   • AST/ALT (usually <500 U/L in both conditions) 1
   • GGT to confirm hepatic origin of ALP 2

Imaging Studies

Abdominal ultrasound or CT should be performed urgently to evaluate for: 1

• Hepatic hemorrhage, infarction, or rupture (life-threatening complication of HELLP) 1
• Fatty infiltration of liver (suggests AFLP, though sensitivity is limited) 1
• Ascites (more common in AFLP) 1
• Subcapsular hematoma 1

Alternative Diagnoses to Consider

Hepatic Ischemia ("Shock Liver")

If significant intraoperative hypotension or blood loss occurred during LSCS: 1

• Marked aminotransferase elevation (often >1000 U/L) with rapid response to hemodynamic stabilization 1
• Simultaneous renal dysfunction and potential muscle necrosis 1
• LDH elevation reflects tissue hypoxia 3, 4

Hemolysis from Other Causes

• Blood transfusion reactions (if transfused perioperatively) 5
• Autoimmune hemolytic anemia 1
• Check direct Coombs test and haptoglobin 1

Sepsis-Associated AKI

Given the post-surgical setting: 3, 6

• LDH is an independent predictor of mortality in critically ill patients with AKI 3
• Evaluate for infection sources (endometritis, wound infection, urinary tract infection) 1
• Blood cultures and inflammatory markers 3

Critical Management Principles

If HELLP or AFLP Suspected:

Immediate multidisciplinary consultation with maternal-fetal medicine and hepatology is mandatory. 1

• HELLP complicated by hepatic rupture or acute liver failure requires transfer to a transplant center 1
• AFLP that progresses to acute liver failure may require liver transplantation 1
• Maternal mortality for AFLP has improved to <10% with early recognition but remains significant 1
• Fetal mortality ranges from 9-23% in AFLP and 11% in HELLP 1

Monitoring Requirements:

• Serial LDH and liver enzymes every 6-12 hours initially 1
• Continuous assessment for hepatic encephalopathy 1
• Frequent glucose monitoring (every 2-4 hours if AFLP suspected) 1
• Coagulation parameters every 6-12 hours 1

Important Clinical Pitfalls

1. Do not assume absence of PIH excludes HELLP syndrome - 15% of HELLP cases lack hypertension 1

2. Postpartum presentation is common - both HELLP and AFLP can manifest or worsen after delivery 1

3. Very high isolated LDH (>800 IU/L) warrants investigation for malignancy, infection, or tissue necrosis if obstetric causes are excluded 4

4. ALP elevation alone has limited specificity - must correlate with GGT to confirm hepatic origin 2

5. Renal cortical LDH efflux correlates with tubular injury severity - elevated serum LDH with AKI indicates significant renal parenchymal damage 7

The combination of elevated ALP, markedly elevated LDH, AKI, and anemia in the immediate post-LSCS period most strongly suggests HELLP syndrome or AFLP, with HELLP being more common. 1 Urgent diagnostic workup focusing on hemolysis markers, coagulation studies, glucose levels, and hepatic imaging is essential to differentiate between these life-threatening conditions and guide appropriate management. 1