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53 y/o F hx GERD, presented w/ intermittent chest pain felt as "sharp epigastric vs chest heaviness with walking".
Patient denies melena, hematochezia, diarrhea, constipation, nausea, and vomiting.
- takes omeprazole 40mg qD, no hx PUD, ulcer, H pylori
- cardiac work up neg, HDS
- Hgb 6.7, MCV 57.6, no frank bleeding, 1pRBC
- TSAT 4%, ferritin 26, retic index 0.8 (<2)
- Hgb values: Male <13.5, Female < 12, g/dl
- Things which affect hgb values
General Hx/PE
- Dyspnea, fatigue (oxygen delivery to tissues)
Low amount of RBC, changes in workload of heart -> Tachycardia, dizziness, syncope
- Although anemia causes tachycardia and pallor, DOES NOT cause hypotension w/o BL
- account for full pic of anemia?
(i.e. hemolysis, hypersplenism, etc)
- AoCI (anemia chronic inflammation) -> hypo proliferative
vs
- Hemolysis -> hyperproliferative
- Generally strive for both assessment
- distinguish co-existing dx -> i.e. slow chronic GI bleed from colon CA
- Ferritin vs TSAT %
- latest data on value of different biomarkers but not all useful
- % percentage hypochromic cells
- sTfR (soluble Transferrin Receptor)
Megaloblastic/ Non megaloclasic
Megaloblastic : B12/ Folate: due to impaired DNA synthesis from folate/ B12 deficiency
Folate: diminished intake (alcohol abuse or malnutrition), increased consumption (hemolysis or pregnancy), malabsorption (familial, gastric bypass, or medications like cholestyramine or metformin)
B12: iminished intake (malnutrition), malabsorptive states (atrophic gastritis either autoimmune or non-autoimmune from Helicobacter pylori or Zollinger-Ellison syndrome, Diphyllobothrium tapeworm infection, gastric bypass, ileal resection), or the presence of antagonists (nitrous oxide).
Non megaloblastic absence of hypersegmented neutrophils,: alcohol, liver diz, hypothyroidism, myelodysplastic syndrome
alcohol consumption (RBC toxicity), hereditary spherocytosis (impaired volume regulation increases red cell size), hypothyroidism and liver disease (due to lipid deposition in the cell membrane), and marked reticulocytosis from states of excess RBC consumption such as hemolysis or turnover in pregnancy or primary bone marrow disease (reticulocytes are larger than the average RBCs).
First R/o IDA vs AoCI as are 2 most common
IDA: chronic GI bleed most common, insufficient dietary intake, malabsorption (celiac, chronic gastritis, bariatric surgery), menstruation (normal/high transferrin, TIBC high) (low iron circ, transf sat, low ferritin)
AoCI: Malignancy, autoimmune, chronic infections, DM2, HF (low Transferrin, iron circ, transferrin sat low or may be normal, ferritin normal or high)
Co-existing: Slow chronic GI bleed colon CA: iron, transferrin/TIBC, transf sat all low, ferritin can be low, high or normal
"Assessing iron status: beyond serum ferritin and transferrin saturation"
Clin J Am Soc Nephrol. 2006 Sep;1 Suppl 1:S4-8. doi: 10.2215/CJN.01490506.
- much challenges have come about due to co-existence of inflammatory state
-lack of the biomarker for assessing specifically iron status
- i.e. : Popular dx of chronic Dz: much inflammatory state (inflammatory state inhibits the mobilization of iron from reticuloendothelial stores) -> less useful ferritin acute phase reactant,
Common scenario : ferritin >100 ng/ml (iron overload), TSAT <20% (IDA) common
Ferritin <10 ng/ml -> IDA
IDA predom: TSAT <20%, ferritin <10
Mixed IDA/AoCI: TSAT <20%, Ferritin 10-100
AoCI: Tsat < 20%, Ferritin >100
Special Dx threshold
CHF: ferritin<300, TSAT <40%
ESRD: ferritin <700, TSAT <40%
"How to diagnose iron deficiency in chronic disease: A review of current methods and potential marker for the outcome"
Eur J Med Res
. 2023 Jan 9;28(1):15. doi: 10.1186/s40001-022-00922-6.
- Specifically in pts w/ chronic Dz (CKD, HF), very much suspected ID, IDA, Dx and approach specifically important
- Saw Under Dx of IDA due to elevated ferritin levels
- Ultimately favors at least assessing TSAT level <20%
- Suggestion came for much newer alternative markers for iron status
---% percentage hypochromic red cells
Soluble transferrin receptor: sTfR: formed from cleavage of membrane transferrin receptor on erythroid precursor cells in bone marrow, which enters systemic circ
Measuring this is increased in IDA, vs. chronic inflammation normal sTfR
- Provides info regarding iron availability (available to transport)
- circulating serum iron conc in total blood's iron binding capacity (TIBC)
- TIBC correlates closely to transferrin but are Not the same...
- Very important measure as under normal conditions, 20-45% TIBC loaded with iron (NORMAL TSAT SHOULD BE >20%
Much less influenced by inflammation
Is the pt actively bleeding?
Mixed of both hemolysis and under production
-Specifically if strong suggestion from oncoming hx, hgb f/u from labs
-Don’t forget about retroperitoneal bleed/ other sources of bleed
UGI bleed very common, especially in ICU setting
---Get GI involved, definitely address underlying issue
- reassess w/ f/u eval
hgb/hct
MCV
Circ Iron, transferrin, TSAT/transferrin saturations/ferritin
Hemolysis labs
Retic ct, LDH, indirect bili, haptoglobin, blood smear
Underproduction? Vs hemolysis
At the same time eval w/ Hx/PE/ labs if suspicion for:
-Malnutrition, EtOH dependence
-Established chronic inflammation
--->Low retic ct, low retic index
---> LDH/Indirect bili/haptoglobin: NORMAL
Blood smear: hypochromia
High retic ct, high retic index or High LDH, indirect bili, LOW haptoglobin
Smear: Micro spherocytes, or schistocytes
- R/o HX autoimmune or lymphoproliferative Dz
hx/ PE leading to DIC, TTP or HUS
PMH or FMHx of RBC defect? spherocytosis?
If concerned for autoimmune: then check direct coombs (DAT, direct antiglobulin test)
Most hemolytic conditions with DAT neg, f/u with blood smear
-- R/osevere thrombocytopenia, Schistocytes
: Microangiopathic hemolytic anemia MAHA
-- Septic: DIC
--GI and or neuro sx: TTP vs HUS
-- Pregnant: HELLP vs DIC
--DAT NEG but MCV low, micro cytic: thalassemia:
Hgb electrophoresis
Sickle cells :SCDisease
Heinz bodies/ bite cells: G6PD or oeven thalassemia (denatured Hgb)
Basophilic stippling Thalassemia, alcohol abuse, heavy metal poisoning
RBC parasites: Malaria/ Babesiosis
Spherocytes: hereditary spherocytosis