Journal of Hematology, ISSN 1927-1212 print, 1927-1220 online, Open Access |
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Letter to the Editor
Volume 8, Number 2, June 2019, pages 86-87
A Quantitative Approach to Dilutional Anemia
Andrew J. Halea, b, e, Daniel N. Ricottac, d, Shoshana J. Herzigc, d, Jeffrey H. Williamc, d, Jason A. Freedc, d
aUniversity of Vermont Medical Center, Burlington, VT, USA
bLarner College of Medicine at the University of Vermont, Burlington, VT, USA
cBeth Israel Deaconess Medical Center, Boston, MA, USA
dHarvard Medical School, Boston, MA, USA
eCorresponding Author: Andrew Hale, University of Vermont Medical Center, Infectious Disease Unit, 111 Colchester Avenue, Mailstop 115 SM2, Burlington, VT 05401, USA
Manuscript submitted May 22, 2019, accepted June 7, 2019
Short title: Letter to the Editor
doi: https://doi.org/10.14740/jh498
To the Editor | ▴Top |
Anemia amongst hospitalized patients is widespread, occurring in up to 75% of inpatients [1]. In addition to primary hematologic diseases, contributing factors include acute illness, phlebotomy and dilutional anemia [2]. In fact, intravenous fluids are given to a majority of inpatients at some point during their hospitalization [3], and studies on fluid resuscitation in sepsis highlight the significant effect of hemodilution on anemia [4, 5]. With increasing recognition of the risks of over-transfusion of red blood cells, properly identifying dilutional anemia is important for patient care [6, 7]. Clinicians may benefit from using a simple, quantitative approach to predict how much a patient’s hemoglobin concentration will change from a given intravenous fluid load.
Consider the following scenario: a 44-year-old woman who weighs 60 kg with minimal past medical history is admitted with Plasmodium falciparum malaria. Her initial hemoglobin concentration is 12 g/dL. She is given 4 L of intravenous 0.9% normal saline and started on anti-malarial medications. The next morning, her hemoglobin has dropped to 9.8 g/dL. Is this a sign of hemolysis from severe malaria, or due to dilutional anemia from the fluid bolus?
The principle underlying this approach is that, in the absence of blood loss, total body hemoglobin is approximately constant over a 24-h period [8]. This fact can be used to account for changes in blood hemoglobin concentration following the steps outlined in Table 1 [9-12].
Click to view | Table 1. Four Steps for Quantitative Assessment of Dilutional Anemia |
Thus, assuming no loss of blood, infusion of 4 L of normal saline into this patient would result in dilutional anemia to a hemoglobin concentration of approximately 9.6 g/dL. Her actual hemoglobin of 9.8 g/dL is well explained by dilutional anemia, and she does not appear to have had significant hemolysis from malaria.
This simple calculation can be applied to scenarios in which the clinician would like to quantitatively estimate what the hemoglobin concentration should be after an intravenous fluid bolus. A fundamental assumption of this calculation is that total body hemoglobin is constant; thus, true loss of hemoglobin would render it inaccurate. Additionally, the equation assumes typical distribution of intravenous fluids, which may be inaccurate in patients with increased capillary permeability and increased hydrostatic or decreased oncotic pressures. Significant isotonic urine or stool output leading to volume loss may attenuate this decrease in hemoglobin, which may be seen in those on high-dose diuretics or secretory diarrhea. Additionally, in patients with obesity or pregnancy, a weight-based calculation of total blood volume may be inaccurate and more nuanced calculations are recommended [11, 13, 14].
Applied in the correct clinical setting, this simple quantitative approach may help clinicians discern when a drop in hemoglobin concentration is related to intravenous fluids or a separate etiology.
Acknowledgments
We give thanks to William Aird, MD, for his invaluable help.
Financial Disclosure
None.
Conflict of Interest
None of the authors report any conflict of interest.
Informed Consent
Not applicable.
Author Contributions
Andrew J. Hale, MD: writing and editing of the manuscript; Daniel N. Ricotta, MD: writing and editing of the manuscript; Shoshana J. Herzig, MD, MPH: writing and editing of the manuscript; Jeffrey H. William, MD: writing and editing of the manuscript; Jason A. Freed, MD: writing and editing of the manuscript. All co-authors have seen and agree with the contents of the manuscript and have contributed significantly to the work.
References | ▴Top |
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