ABRUPTIO PLACENTA CRISIS – NAVIGATING THE UNPREDICTABLE

Introduction

        Severe preeclampsia with abruptio placentae is a life-threatening obstetric emergency associated with significant maternal and fetal morbidity and mortality. It can lead to hemodynamic instability, endothelial dysfunction, and reduced renal perfusion, predisposing to acute kidney injury. In some cases, this may be further complicated by thrombotic microangiopathy, resulting in multi-organ involvement and worsening prognosis. Early recognition and prompt multidisciplinary management are essential to improve outcomes. This case highlights acute kidney injury following severe preeclampsia with abruptio placentae, complicated by thrombotic microangiopathy.

Case Description

        A 30-year-old lady at 31 weeks period of gestation with cephalic presentation, intrauterine fetal demise, severe preeclampsia, and abruptio placentae presented in active labour. Labour was accelerated with injection oxytocin. In view of abruptio placentae, necessary investigations were sent and blood and blood products were arranged. The bladder was catheterized, which revealed nil urine output. Labour was augmented, and she delivered a dead male baby weighing 1.44 kg within one hour of admission, with a retroplacental clot of approximately 400 g noted.

          Following delivery, the patient remained anuric with rising serum creatinine, for which a nephrology opinion was sought and hemodialysis was initiated. Bedside ultrasonography showed bilaterally increased renal cortical echogenicity, while fundoscopy was normal. Despite four cycles of hemodialysis, serum creatinine (4.88 mg/dL) continued to rise, and a drop in hemoglobin was noted, prompting escalation of antibiotics to meropenem.

         Laboratory evaluation revealed markedly elevated lactate dehydrogenase (5190.8 U/L), and peripheral smear showed schistocytes (2.6%), consistent with microangiopathic hemolytic anemia. In view of these findings, a hematology opinion was obtained, and four cycles of plasmapheresis were completed, with plans to initiate eculizumab therapy.

         Despite continued hemodialysis, renal function worsened, necessitating renal biopsy, which revealed acute cortical necrosis (20–30%) with thrombotic microangiopathy and severe acute tubular injury. Next-generation sequencing for atypical hemolytic uremic syndrome was negative. A repeat biopsy later demonstrated patchy healed cortical necrosis with secondary focal segmental glomerulosclerosis and hemosiderosis.

         Over the course of treatment, urine output gradually improved, allowing discontinuation of hemodialysis. The patient was subsequently discharged with a serum creatinine of 6.57 mg/dL.

Discussion

       Acute kidney injury in this patient was likely precipitated by severe preeclampsia with abruptio placentae, leading to hemodynamic instability, endothelial injury, and reduced renal perfusion. The presence of schistocytes, markedly elevated lactate dehydrogenase, and thrombocytopenia suggested an underlying microangiopathic hemolytic process, consistent with thrombotic microangiopathy.

       Despite undergoing multiple sessions of hemodialysis, the patient showed a persistent rise in serum creatinine, indicating ongoing renal injury. Further evaluation with hemato-oncology consultation supported a thrombotic microangiopathy spectrum disorder. Renal biopsy revealed acute cortical necrosis (20–30%) with associated thrombotic microangiopathy and severe acute tubular injury, explaining the severity of renal dysfunction.This case highlights the complex interplay between obstetric complications and thrombotic microangiopathy in causing acute kidney injury. 

       Early recognition and a multidisciplinary approach involving obstetrics, nephrology, and hemato-oncology are crucial. Although aggressive management may improve clinical outcomes, significant renal impairment can still occur, requiring prolonged renal support.

Conclusion

   Pregnancy related conditions like Severe Preeclampsia , HELLP Syndrome, AFLP needs prompt delivery. Majority will recover following delivery . 

✓Early identifying the cause of AKI.  

✓Timely initiation of dialysis.  

✓Immunosuppressive therapy and steroids when indicated .

✓Plasmapheresis and Eculizumab early in TMA ( Thrombotic Microangiopathy ) . 

✓Requires a multidisciplinary team and action.