Sickle cell disease begins with a single amino acid substitution in hemoglobin, producing hemoglobin S, which polymerizes when oxygen tension falls. The result is the characteristic sickle shape: red blood cells become rigid, lose their deformability, and lodge in capillary beds, causing the ischemic pain known as vaso-occlusive crisis. In pregnancy, this biology collides with profound physiologic change. Plasma volume expands, the coagulation system shifts toward hypercoagulability, and inflammatory mediators rise, all of which can heighten the risk of crises, acute chest syndrome, and venous thrombosis. According to the source report, anemia and episodic pain affect more than half of pregnant individuals with sickle cell disease, preterm delivery occurs in 9 to 45 percent of such pregnancies, and fetal growth restriction appears in roughly 8 to 21 percent of cases.

The statistical backdrop is sobering. In a large United States cross-sectional study cited in the report, preeclampsia occurred in 10.9 percent of deliveries among patients with sickle cell disease, compared with 4.5 percent in controls. Preeclampsia itself is defined by the American College of Obstetricians and Gynecologists as new-onset hypertension after 20 weeks of gestation with proteinuria, or severe features even without proteinuria. Those severe features include systolic blood pressures of at least 160 mmHg or diastolic pressures of at least 110 mmHg, thrombocytopenia, impaired liver function, renal insufficiency, pulmonary edema, or new cerebral or visual symptoms. For a patient whose red cells already struggle to perfuse her tissues, the added vascular insult of preeclampsia creates a dangerous physiological double bind.

The patient in this case arrived at 33 weeks and 2 days of gestation in severe pain from a vaso-occlusive crisis. Her history included type 2 diabetes, obesity, and avascular necrosis of the right knee, a classic sickle cell complication in which bone tissue dies from interrupted blood supply. Her outpatient regimen already included buprenorphine, a partial opioid agonist, along with acetaminophen. Two days later she returned with left thigh pain rated 8 out of 10 despite her medications, and her blood pressure measured 143/90 mmHg. Intravenous hydromorphone provided minimal relief, prompting admission for inpatient pain control. Laboratory evaluation revealed a hemoglobin of 9.6 g/dL and a hematocrit of 26.2 percent, while a venous duplex ultrasound ruled out deep vein thrombosis as the cause of her leg pain.

One of the most technically interesting aspects of the case involved blood banking. The patient’s antibody screen was positive with a complex antibody profile, meaning her immune system carried antibodies that could react against common red cell antigens. Finding compatible packed red blood cells became genuinely difficult, a problem compounded by the fact that transfusion in sickle cell disease carries risks of alloimmunization, in which further antibodies develop, along with transfusion-related infection and iron overload. Rather than waiting for an emergency, the team transfused 4 units of crossmatched blood while the patient was clinically stable, raising her hemoglobin ahead of anticipated delivery-related blood loss. Intraoperative cell salvage, a technique that recovers blood lost during surgery for reinfusion, was planned as a backup but ultimately was not needed.

Then came the preeclampsia. During the admission, the patient developed repeated severe-range systolic blood pressures, documented between 165/86 and 167/90 mmHg. Notably, no proteinuria assessment was documented, but severe-range pressures alone satisfied diagnostic criteria. Her kidney function remained intact, with a creatinine of 0.59 mg/dL, indicating that end-organ damage had not yet taken hold. The team initiated oral nifedipine at 60 mg every 12 hours, a calcium channel blocker that relaxes vascular smooth muscle, and planned intrapartum magnesium sulfate for seizure prophylaxis, the standard safeguard against eclamptic convulsions. Serial fetal growth surveillance continued because both sickle cell disease and diabetes elevate the risk of fetal growth abnormalities, with an estimated fetal weight tracking at the 60th percentile.

The delivery decision arrived at 35 weeks when a biophysical profile score of 4 out of 8 signaled fetal compromise. Induction of labor was attempted, but after 7 hours of oxytocin augmentation, the cervix remained dilated at only 4 centimeters. The patient requested a primary cesarean section. Labor analgesia had been established through an epidural catheter, which the team redosed for surgical anesthesia, the preferred approach because neuraxial techniques avoid the airway manipulation and hemodynamic swings of general anesthesia. However, immediately after delivery the patient reported intense intraoperative pressure, and after discussion, the anesthesiologists converted to general anesthesia using fentanyl, propofol, succinylcholine, and ketamine, with midazolam, morphine, and ketorolac added for maintenance and analgesia. Hemodynamics remained stable through induction and emergence, a critical detail given the fragility of a preeclamptic, recently transfused patient.

The pharmacology threaded through this case reflects the delicate calculus of analgesia in pregnancy. Acetaminophen remains first-line for vaso-occlusive pain, though recent studies have raised questions about possible associations with childhood asthma or neurodevelopmental outcomes. Nonsteroidal anti-inflammatory drugs are avoided late in gestation because they can prematurely close the fetal ductus arteriosus and reduce amniotic fluid. Patients maintained on buprenorphine should continue their therapy through labor to prevent withdrawal, with full opioid agonists such as hydromorphone added for breakthrough pain and neonates observed for withdrawal if exposure is prolonged. A systematic review cited in the report found no definitive regimen for treating sickle cell pain crises in pregnancy, which means care rests on early recognition of triggers, timely analgesia, judicious fluids, and close maternal-fetal monitoring rather than any standardized protocol.

The postpartum course underscored that delivery resolves neither disease. Magnesium sulfate continued for 24 hours, nifedipine continued for blood pressure control, and the patient received 6 weeks of enoxaparin for venous thromboembolism prophylaxis, an important measure because preeclampsia and sickle cell disease both amplify clotting risk. Hematology recommended maintaining hemoglobin above 10 g/dL with transfusion support and continuing high-dose folic acid to support red cell production. Endocrinology discontinued insulin in favor of metformin for the diabetes. The neonate, weighing 2.565 kg, thrived. The authors emphasize that the lesson of this case is coordination: hematology, obstetrics, anesthesiology, palliative care, and endocrinology each held one thread of a clinical picture in which a single misstep, an incompatible transfusion, an uncontrolled pressure, an abrupt withdrawal, could have unraveled everything. As more individuals with sickle cell disease reach childbearing age, cases like this one map the terrain that multidisciplinary teams must navigate.

Subject of Research: Peripartum anesthetic management of pregnancy complicated by sickle cell disease and preeclampsia

Article Title: Peripartum Anesthetic Management of a Patient With Sickle Cell Disease and Preeclampsia

Article References: Dow, M., Srinivasan, A., & Ayad, S. (2026). Peripartum Anesthetic Management of a Patient With Sickle Cell Disease and Preeclampsia. Clinical Case Reports, 14(10), Article e73662. https://doi.org/10.1002/ccr3.73662

Image Credits: AI Generated

DOI: 10.1002/ccr3.73662

Keywords: sickle cell disease, preeclampsia, vaso-occlusive crisis, obstetric anesthesia, cesarean delivery, blood transfusion, magnesium sulfate, buprenorphine, pregnancy complications, epidural analgesia, fetal surveillance, multidisciplinary care