What you NEED to know at the Bedside, with further reading provided for later.
APRIL 2026
34 F who has a past medical h/o GERD dx by outside ENT prior syncope/Dizziness IDA receiving iron infusions secondary to intolerance to PO iron PTED w/ PTED w/ persistent Odyncophagia=globus sensation "feels like there is something in her throat" over the past 3-4 months. Diagnosed with acid reflux by ENT in 6/2025 Symptoms are not relieved by pantoprazole. Also notes chest heaviness and difficulty breathing with walking. No othopnea pedal edema cough or congestion. Pt is from South Caroling and is attempting to establish care
DATA:
EKG: NSR@80 NSST pattern
LAB:
Blood Gas Profile w/Lytes - Venous: Performed In Lab (03-15-26 @ 18:49)
Blood Gas Venous - Lactate: 1.3 mmol/L (03-15-26 @ 18:49)
9.0
6.93 )-------( 440 ( 15 Mar 2026 18:20 )
31.9
MCV 65%
RDW 19
PT: 11.6 sec; INR: 1.00 ratio PTT:31.1 sec03-15
138 | 102 | 7
----------------------------< 91
4.5 | 23 | 0.54
Ca 9.3 15 Mar 2026 18:20
Phos 3.8 03-15
Mg 2.10 03-15
TPro 8.7[H] / Alb 4.5 / TBili 0.6 / DBili x / AST 34[H] / ALT 18 / AlkPhos 88 03-15
Lipase: 41 U/L (03-15-26 @ 18:20)
Troponin T, High Sensitivity Result: <6 ng/L (03-15-26 @ 18:20)
Urinalysis Basic - ( 15 Mar 2026 18:20 )
Color: Yellow / Appearance: Clear / SG: 1.015 / pH: x
Gluc: 91 mg/dL / Ketone: x / Bili: Negative / Urobili: 0.2 mg/dL
Blood: x / Protein: Negative mg/dL / Nitrite: Negative
Leuk Esterase: Moderate / RBC: 1 /HPF / WBC 18 /HPF
Sq Epi: x / Non Sq Epi: 9 /HPF / Bacteria: Negative /HPF
Which of the following is the most appropriate management?
A . Intramuscular iron dextran
B. Oral ferrous gluconate, three times daily
C. Oral ferrous sulfate, once every other day
D. Serum ferritin measurement
Click Here for Answer
Answer C. The most appropriate treatment is oral ferrous sulfate, once every other day. Although oral ferrous fumarate, ferrous gluconate (Option B), and other oral iron salts are available, none has proven superior to ferrous sulfate in tolerability, efficacy, or cost. Frequent dosing of oral iron two or three times a day every day (the way we used to do it!) may lead to increased hepcidin production, a hormone produced by the liver that reduces iron absorption by reducing binding it in the gut (by breaking down and decreasing production of the enterocyte binding protein ferroportin). So ferrous sulfate every other day is the best option and better tolerated by patients (ironically hepcidin deficiency is one of the causes of hemochromatosis)
Parenteral iron is reserved for patients receiving dialysis or for those who have absorption problems (e.g., patients who have had gastric bypass surgery) or intolerance to oral iron replacement. The availability of newer parenteral iron preparations, which are simpler to administer and have better adverse effect profiles, have lowered the threshold for giving parenteral treatment. The intramuscular (IM) route for iron (e.g., IM iron dextran) (Option A) is generally not preferred because of the risk for local complications.
This patient has IDA that is probably a result of menstrual blood loss. For simple iron deficiency, oral ferrous sulfate is the least expensive and simplest treatment option and is therefore the most appropriate. Several ferrous preparations available over the counter are probably as effective. Since this is simple iron deficiency Option D further testing (ferritin level) is not necessary
The Goal Here? To update everyone on management of Iron Deficiency Anemia (IDA)
For further info read below
IDA may result from blood loss or malabsorption in addition to increased iron requirements. Women of reproductive age may lose enough iron through normal menstrual blood loss to become iron deficient in the absence of uterine or gastrointestinal disease. This patient has IDA that is probably a result of menstrual blood loss. For simple iron deficiency, oral ferrous sulfate is the least expensive and simplest treatment option and is therefore the most appropriate. Several ferrous preparations available over the counter are probably as effective.
Parenteral iron is reserved for patients receiving dialysis or for those who have absorption problems (e.g., patients who have had gastric bypass surgery) or intolerance to oral iron replacement. The availability of newer parenteral iron preparations, which are simpler to administer and have better adverse effect profiles, have lowered the threshold for giving parenteral treatment. The intramuscular (IM) route for iron (e.g., IM iron dextran) (Option A) is generally not preferred because of the risk for local complications.
Although oral ferrous fumarate, ferrous gluconate (Option B), and other oral iron salts are available, none has proven superior to ferrous sulfate in tolerability, efficacy, or cost. Iron two to three times day every day of oral iron ( the way we used to do it!) may make things worse by failure to tolerated and by increased hepcidin production, a hormone that reduces iron absorption by reducing binding it in the gut!
Iron deficiency is a hypoproliferative (low reticulocyte count), microcytic (low MCV), hypochromic (pale RBCs low MCH) anemia. The presence of these features along with a elevated red cell distribution width (RDW), and peripheral blood smear showing microcytosis and anisopoikilocytosis is virtually diagnostic of iron deficiency, especially in premenopausal women; these findings may obviate the need for additional laboratory testing, including serum ferritin measurement (Option D), provided that a follow-up complete blood count is performed to assess response to iron therapy. A low serum iron level, elevated total iron-binding capacity, low transferrin saturation (>15%; iron/total iron-binding capacity × 100), and a serum ferritin level less than 14 ng/mL (14 μg/L) confirm the diagnosis of iron deficiency. The ferritin value is highly specific (99%) but has a low sensitivity (59%), resulting in potentially false-negative results and missed diagnosis of iron deficiency.
Some things to think about; What other Physical findings can patients with IDA have?
Higher level question: what is Plummer Vinson Syndrome? (hint look at the history....this patient might have had it Rouchdy!)
Bibliography
Auerbach M, Adamson JW. How we diagnose and treat iron deficiency anemia. Am J Hematol. 2016;91:31-8. PMID: 26408108 doi:10.1002/ajh.24201