Every OB has seen it: by the second trimester, due to hemodilution, a patient’s hemoglobin tanks, her ferritin is barely measurable, and she’s exhausted despite a choking down her pregnancy version of AG1 and a full bottle of iron pills sitting on her nightstand. Every OB has seen it: by mid-pregnancy, plasma volume surges, blood dilutes, and we’re left quietly praying that our patient’s hemoglobin holds at 10. We know her body is working harder than at any other point in her life—building blood, a placenta, a whole human—and yet, we still rely on a treatment (oral iron) that often doesn’t work when she needs it most. It’s 2025, with med spas on every corner, yet we’re treating iron deficiency anemia like it’s 1885, prescribing fixes straight out of “Dr. Williams’ Pink Pills for Pale People” ads. What happens when we stop scrambling to catch up with anemia in pregnancy, and instead play offense—making iron the central pillar of maternal care rather than a side note?
Why Pregnancy Wrecks Iron Metabolism
Pregnancy isn’t just a glow-up; it’s a metabolic upheaval. By 28 weeks, blood volume surges by nearly 50%, diluting hemoglobin in a process called hemodilution. The fetus and placenta act like tiny iron vampires, siphoning off stores to build red blood cells, myoglobin for muscles, and the scaffolding of a developing brain. Meanwhile, hepcidin—the hormone that regulates iron absorption—starts to rise later in pregnancy, making it easier for the body to absorb dietary or oral iron just when needs triple.
This isn’t news to clinicians. We see the labs: hemoglobin tanking, ferritin plummeting (if we even test it at all). Yet we keep handing out oral iron like it’s the only tool in the shed. Why? Because it’s familiar. But familiarity isn’t the same as effective.
Why Oral Iron Fails So Many Women
We hand out oral iron like candy because it feels familiar. But physiologically, it’s often a poor match for pregnancy. Absorption is notoriously inefficient—and while nature designed pregnancy to help by suppressing hepcidin (the hormone that blocks iron absorption), modern health realities can derail that plan. Conditions marked by inflammation—like preeclampsia, diabetes, and obesity—can raise hepcidin levels, shutting down absorption just when iron demand peaks.
This is why we sometimes find ourselves scratching our heads. There’s no genetic explanation. The patient is reliable, taking her pills as prescribed. Yet her hemoglobin barely moves.
The Role of Hepcidin and Inflammation
Here’s what’s actually happening: under normal conditions, hepcidin levels drop in the second trimester and remain low through the third. This suppression is what allows dietary and supplemental iron to be absorbed and mobilized from maternal stores to meet the demands of both mother and fetus. The drop is driven by massive iron utilization maternal red cell expansion, placental development, and fetal growth all of which lower iron stores and transferrin saturation, signaling the body to keep hepcidin low.
But if inflammation blunts that suppression, hepcidin stays elevated. The result? Poor iron absorption, limited transfer to the fetus, and rising risks for growth restriction and neurodevelopmental issues. Add in the nausea, constipation, and general misery oral iron causes, and adherence becomes another battle.
When to Know It’s Not Working
The quiet truth is this: if oral iron hasn’t moved hemoglobin by at least 1 g/dL within two weeks, it probably won’t. That’s why ACOG now recommends considering IV iron by 13 weeks for women with hemoglobin <10–10.5 g/dL and ferritin <30 ng/mL, particularly when oral iron fails or isn’t tolerated.
The Case for IV Iron in Pregnancy
The data is stronger than most clinicians realize. Meta-analyses of randomized trials show that IV iron corrects anemia faster, reduces the risk of transfusion during delivery, and measurably improves maternal energy and quality of life.
Modern formulations like Feraheme (ferumoxytol) allow a full 1,000 mg dose to be given in a single session, safely, without the multi-visit burden older products required. Anaphylaxis rates are extremely low (well below 0.01%). Most patients are in and out in 90 minutes, with no need for ongoing oral supplementation once iron stores are replete.
And acog says its safe, ACOG does not provide a specific preferred IV iron formulation or dosing regimen, but clinical practice typically uses preparations such as iron sucrose or ferric carboxymaltose, administered according to product labeling and patient needs. Universal iron supplementation in pregnancy is recommended with low-dose oral iron, except in conditions such as hemochromatosis
What IV Iron Looks Like in Practice
When to Refer
- Confirm the labs. Hemoglobin <10–10.5 g/dL after 13 weeks and ferritin <30 ng/mL? That’s your candidate.
- Refer for infusion. One 1,000 mg dose of Feraheme (ferumoxytol) is typically given to women ≥50 kg. For most, this single infusion restores iron stores for the rest of pregnancy.
- Follow up. Recheck labs in 4–6 weeks. Most women do not need ongoing oral iron afterward.
This isn’t exotic or “alternative.” It’s evidence-based, covered by insurance, and one of the simplest, most effective ways to reduce maternal fatigue, avoid transfusion, and optimize outcomes at delivery.
Why You Should Be Checking Ferritin
Symptoms that Should Prompt Testing
Ferritin testing isn’t routinely ordered in pregnancy, but it should be considered when women present with symptoms like:
- Persistent fatigue
- Pallor
- Shortness of breath
- Headaches or dizziness
- Cold hands and feet
- Restless legs
- Brittle hair or nails
- Heart palpitations
- Cravings for ice (pica)
Why Waiting for Hemoglobulin to Drop is Too Late
In other words, nearly every pregnant woman reports at least some of these symptoms. That’s why ferritin can be a powerful tool to identify women who are iron deficient before their hemoglobin drops to concerning levels. Early detection allows us to act proactively, rather than waiting for anemia to become severe.
Why This Matters for Clinicians
The goal isn’t just to push hemoglobin up on a lab report. It’s to give women the energy to function, to lower their risk of transfusion and complications, and to ensure their babies get the iron they need for growth and neurological development.
When we normalize IV iron as part of routine prenatal care for those who need it, we shift from playing catch-up at delivery to proactively optimizing maternal health.
How I Explain IV Iron to Patients
Patients often see “IV” and think “serious.” I tell them:
- “This isn’t a blood transfusion. It’s the same iron in your prenatal, just delivered in a way your body can use.”
- “It’s safe for you and your baby. Side effects are rare and mild.”
- “One infusion is usually enough. You don’t have to choke down pills for the rest of your pregnancy.”
Most are relieved, not scared. They just want to feel better—and quickly.
The Bottom Line
Iron deficiency isn’t rare, and it isn’t benign. It drains mothers, increases their risk of complications, and affects babies. Oral iron works for some, but not most. IV iron, particularly with modern agents like Feraheme, lets us correct the problem safely, effectively, and fast.
If your patient is past 13 weeks, symptomatic, and not improving on pills, IV iron isn’t a last resort—it’s the right next step.
At Materna, we work with OB/GYNs and family doctors to assess, treat, and monitor iron deficiency so expectant mothers can focus on the joy—not the exhaustion—of pregnancy. Contact us to discuss referral or treatment options for your patients.
