Blood, Sweat, and Tears: Managing Peripartum Complications in the Blood Bank

Pregnancy is a physiological feat—but when complications arise, the blood bank becomes a lifeline. Managing peripartum complications requires careful coordination between the clinical and transfusion teams. In this post, I’ll summarize the critical role of the blood bank in managing pregnancy-related complications, drawing from a recent presentation on this topic.

1. The Pregnant Patient’s Unique Physiology

Pregnancy is characterized by profound hematologic and circulatory changes:

• Total blood volume increases by about 40%, but plasma volume increases by ~50%, leading to a dilutional (physiologic) anemia.

• Uterine blood flow increases from ~100 mL/min (non-pregnant) to ~700 mL/min at term.

  
  

These changes optimize fetal perfusion—but they also create the potential for catastrophic hemorrhage. Any peripartum bleeding event occurs against the backdrop of this expanded yet vulnerable intravascular space.

2. Thrombocytopenia and Microangiopathy in Pregnancy: Distinguishing the Causes

Pregnancy introduces unique diagnostic challenges when a patient presents with thrombocytopenia, hemolysis, and microangiopathic findings. While true thrombotic microangiopathies (TMAs) such as TTP and aHUS are rare, more common conditions like preeclampsia, HELLP syndrome, and acute fatty liver of pregnancy (AFLP) can present with overlapping laboratory abnormalities.

Hypertensive Disorders of Pregnancy: Placental Dysfunction, Preeclampsia, and HELLP

The pathophysiology of preeclampsia begins with abnormal placental development. Impaired trophoblastic invasion leads to defective remodeling of spiral arteries, resulting in placental ischemia. In response, the placenta releases antiangiogenic factors (like soluble fms-like tyrosine kinase-1, sFlt-1) into maternal circulation, triggering widespread endothelial dysfunction.

This cascade manifests clinically as hypertension and end-organ injury—the hallmark of preeclampsia. While preeclampsia itself is not a thrombotic microangiopathy, the endothelial injury can cause thrombocytopenia, microangiopathic hemolysis, and elevated liver enzymes, mimicking features of TMA.

HELLP syndrome represents a severe variant of preeclampsia, defined by hemolysis, elevated liver enzymes, and low platelets. Though it shares some features of TMA, its pathogenesis is rooted in placental dysfunction rather than primary thrombotic microvascular disease.

Management of HELLP includes:

• Delivery of fetus and placenta (definitive treatment)

• Platelet thresholds:

  • Vaginal delivery: ≥20,000/µL

  • Cesarean delivery: ≥50,000/µL

• Hemoglobin target: >7 g/dL

• Coagulopathy: FFP support as needed

  
  

Most cases of HELLP syndrome resolve within 72 hours postpartum following delivery of the fetus and placenta, which removes the underlying source of endothelial injury and inflammatory mediators.

When ongoing thrombocytopenia, hemolysis, or organ dysfunction continues despite delivery and supportive care, therapeutic plasma exchange (TPE) may be initiated as a salvage therapy. While TPE is not routine first-line treatment for HELLP, emerging case series and observational studies suggest it may shorten disease course and reduce morbidity in refractory HELLP, particularly when initiated within 24 hours of delivery.

TPE in this context is thought to remove circulating antiangiogenic factors (like soluble fms-like tyrosine kinase-1, sFlt-1) and other inflammatory mediators contributing to endothelial dysfunction. Additionally, it provides plasma replacement, which may help correct associated coagulopathies.

Clinicians should have a low threshold for transfusion medicine consultation when HELLP does not follow the expected course of recovery, and the decision to initiate TPE should be individualized based on severity, lab trends, and potential overlap syndromes.

True Thrombotic Microangiopathies: TTP and aHUS

In contrast, thrombotic thrombocytopenic purpura (TTP) and atypical hemolytic uremic syndrome (aHUS) are true TMAs caused by ADAMTS13 deficiency and complement dysregulation, respectively. They require specific therapies (plasma exchange for TTP; complement inhibition for aHUS).

Key differentiating features:

Feature	HELLP	TTP	aHUS
Timing	Late pregnancy/postpartum	Any trimester/postpartum	Any trimester/postpartum
ADAMTS13 activity	Normal/mildly low	Severely low (<10%)	Normal
Creatinine	Mild elevation	Normal/slightly elevated	Markedly elevated
Platelets	Low	Very low	Low
Hemolysis	Present	Present	Present

Acute Fatty Liver of Pregnancy: The Great Mimicker

AFLP is another critical diagnosis in the differential. Its pathophysiology involves hepatocellular microvesicular steatosis and apoptosis, leading to impaired hepatic function. While AFLP can mimic TMA with thrombocytopenia and coagulopathy, hemolysis is not a defining feature and is often absent.

Key distinguishing findings favoring AFLP include:

• Profound hypoglycemia

• Elevated ammonia

• Prolonged PT/INR

• Low fibrinogen

• Hepatic encephalopathy

  
  

Management of AFLP centers on prompt delivery and aggressive correction of coagulopathy with plasma, cryoprecipitate, and platelets to prevent bleeding.

3. Managing Massive Obstetric Hemorrhage: Obstetric MTP

Obstetric hemorrhage is the leading cause of maternal mortality worldwide. Unlike trauma, obstetric massive transfusion protocols (MTP) must account for pregnancy-specific hemostatic challenges and the unique pathophysiology of peripartum bleeding.

Common inciting events for obstetric MTP include:

✅ Placenta previa

✅ Placental abruption

✅ Uterine rupture

✅ Placenta accreta spectrum (accreta, increta, percreta)

Management considerations:

• Recommended ratio: 1:1.5:1 (RBC:FFP:platelets)

• Early cryoprecipitate: Hypofibrinogenemia is common and correlates with poor outcomes; administer cryo in the first round if fibrinogen <200 mg/dL.

• Tranexamic acid (TXA): First-line therapy for postpartum hemorrhage per WOMAN trial.

• Antibody monitoring: While pregnant patients are not inherently at higher risk of alloantibody formation, any newly formed red cell antibodies following obstetric MTP pose a risk for hemolytic disease of the fetus and newborn (HDFN) in subsequent pregnancies. Therefore, meticulous post-transfusion follow-up with repeat antibody screening is critical to identify alloimmunization.

  
  

4. In Pregnancy, All Roads Lead to DIC

A central truth of obstetric medicine is that almost every severe complication of pregnancy can induce disseminated intravascular coagulation (DIC). From preeclampsia to placental abruption, AFLP to sepsis, DIC is a common pathway of maternal decompensation.

One of the most dramatic examples is amniotic fluid embolism (AFE).

Amniotic Fluid Embolism: A Rare but Catastrophic Event

AFE is a sudden, unpredictable complication resulting from entry of amniotic fluid into maternal circulation, triggering an anaphylactoid reaction. Risk factors include:

✅ Advanced maternal age

✅ Multiparity

✅ Rapid labor

✅ Cesarean delivery

✅ Instrumental delivery

✅ Placenta previa or accreta

Clinically, AFE presents with acute hypoxia, hypotension, cardiovascular collapse, and DIC. Maternal mortality remains high despite optimal supportive care.

Blood bank support during AFE focuses on:

✅ Massive transfusion with RBCs, FFP, platelets, and cryoprecipitate to correct consumptive coagulopathy

✅ Maintaining platelets ≥50,000/µL (cesarean) or ≥20,000/µL (vaginal)

✅ Rapid fibrinogen replacement to target fibrinogen >200 mg/dL

✅ Anticipating ongoing bleeding despite lab correction

Key Takeaways for the Blood Bank Team

✅ Anticipate hemorrhagic risk in patients with placenta accreta spectrum, previa, abruption, or uterine rupture

✅ Tailor MTP for obstetrics: early cryoprecipitate and TXA are critical

✅ Differentiate causes of thrombocytopenia: preeclampsia/HELLP vs. TTP vs. aHUS dictates treatment

✅ Monitor for DIC in any critically ill pregnant patient

✅ Provide close antibody monitoring: alloantibodies may impact future pregnancies via HDFN even if not problematic in the index pregnancy

Pregnancy is a state of delicate balance—and when that balance is lost, the blood bank’s interventions can mean the difference between life and death.

Have you encountered these challenges in your practice? Share your experiences and insights below!