American Journal of Emergency Medicine (2009) 27, 377.e7377.

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Case Report
Life-threatening iron deficiency anemia and profound
lactic acidosis due to uterine fibroid bleeding
Abstract
A case of a patient with severe lactic acidosis as a result
of profound iron-deficiency anemia (Hb: 1.3 g/dl) due to
chronic uterine bleeding is presented. The pathophysiology
of profound anemia and the reported cases of irondeficiency anemia with very low hemoglobin values
( 2 g/dl) are reviewed and discussed.
Globally, anemia ranks number 9 among 26 risk factors
included in the Global Burden of Disease project during the
year 2000 and accounts for 841 000 deaths per year [1].
Profound anemia in experiments (Hematocrit b 10%)
leads to substantial compromise of arterial oxygen delivery
and rarely to lactic acidocis as a result of a metabolic shift
within cells to anaerobic glucose metabolism [2]. One of the
primary hemodynamic adaptations to diminished arterial
oxygen content pertains to higher cardiac output [3,4] and
lower systemic vascular resistance [4] due to enhanced
endothelium-derived relaxing factor activity [5]. In exceptional cases though, cardiac output remains normal even in
profound anemia (hemoglobin level of approximately 4.5 g/
dL) [4]. Although high cardiac output is not considered a
landmark of severe anemia, hyperlactatemia when present
may be indicative of myocardial anaerobic metabolism and
probably reflect the onset of lethal myocardial injury [2].
A 44-year-old white woman was admitted to the hospital
because of weakness and dyspnea. A 5-year history of
menometrorrhagia with very recent onset of severe orthostatic weakness and dyspnea at rest were reported.
On physical examination, the patient was disoriented, very
pale and cachectic, afebrile, with full regular pulses, 68 beats
per minute, and normal arterial pressure (100/60 mm Hg),
without jugular venous distention, and tachypneic (25 breaths
per minute). Pelvic examination revealed an enlarged uterus
with no blood in the vagina.
Initial screening tests showed a hemoglobin concentration
of 1.3 g/dL, hematocrit of 4.7%, mean corpuscular volume
of 59 femtoliters, reticulocytes of 1.8%, white blood cell
count of 18.700/L, and thrombocytosis (platelet count, 534
000/L). Microscopic examination revealed no schistocytes.
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International normalized ratio was 1.81, activated partial

thromboplastin time of 42.8 seconds, and fibrinogen of
3.86 g/L. Hepatic function tests were abnormal (aspartate
aminotransferase, 391 U/L; alanine aminotransferase,
535 U/L; total bilirubin, 1.65 mg/dL; direct, 0.88 mg/dL).
Blood gases showed severe lactic acidosis (pH, 7.07; lactate,
14.1 mmol/L; bicarbonate, 4 mmol/L), hypocapnia (pCO2,
14 mm Hg), and preserved oxygen saturation (92%).
Sinus rhythm (68 beats per minute) and inverted T waves
(0.2 mV) in leads III, aVF were the electrocardiographic
findings (Fig. 1).
Urgently performed abdominal computed tomography
showed a large uterine mass compatible with uterine fibroid.
The patient was transfused with 6 U of blood and 1 U of
fresh frozen plasma. After transfusion, hemoglobin level and
hematocrit raised to 7.9 g/dL and 23.7%, respectively. The
patient became alert and oriented. Lactate levels normalized
12 hours later (Fig. 2).
Bone marrow aspirate stained with Prussian blue before
transfusions showed absent deposits of iron in macrophages. Serum vitamin B12, folic acid, and erythropoietin
levels were normal.
The patient underwent an uneventful total abdominal
hysterectomy and bilateral oophorectomy. A benign uterine
fibroid tumor was diagnosed by pathologic examination.
The patient was discharged home 1 week after the
operation, on per os iron and folic acid therapy.
Such profound life-threatening anemia with severe
lactic acidosis attributed to chronic uterine bleeding is
very uncommon.
To our knowledge, this is probably the first reported case
of an adult referred to hospital alive with an hemoglobin
value of 1.3 g/dL.
The hemoglobin value measured is undoubtedly correct
for 3 reasons. Firstly, the analyses of all 3 initial blood
specimens before treatment were in accord second, hemodilution as a possible confounding factor was ruled out; and
third, transfusion of 6 U of packed red blood cells resulted to
the expected hemoglobin level increase (7.9 g/dL).
Severe anemia effects a dramatic fall of tissue oxygen
uptake, usually below the critical level of 100 mL/minm2,
and dysoxia with lactic acid overproduction ensues. Lactic
acid values more than 4 mmol/L are thought to be indicative
of a severe oxygen tissue deficit [6].

377.e8

Case Report

Fig. 1

Patient's electrocardiogram at admission, showing sinus rhythm and T-wave inversion in leads III and aVF.

In the few cases published with a diagnosis of extreme

iron deficiency anemia (hemoglobin level 2 g/dL), no
acidemia was reported. Severe anemia was etiologically
linked to parasitic infections, nutritional deficiency, or
chronic bleeding [3,7].
In a short report of 100 cases with severe anemia
(hemoglobin level 3.5 mg/dL), only 10% presented
with hemoglobin values below 2 g/dL and surprisingly,
only half of them complained for syncope-like symptoms
on assuming an erect posture [7]. In most patients, sinus
tachycardia was evidenced in electrocardiogram, a
finding, which is in agreement with other previous
investigations [3]. In contrast, no tachycardia was
detected in our patient, which should be carefully
interpreted into a unique adaptation of compensatory
mechanisms to chronic anemia. However, the electrocardiogram abnormalities observed might be attributed to
limited myocardial ischemia due to myocardial oxygen
demand-supply disproportion.
Bone marrow aspiration and peripheral blood smear examination provided a very strong support of iron deficiency
anemia for our case.
Rarely, leiomyoma-related anemia attributed to chronic
inflammation [8], hemorrhagic pleural effusion [9], and
hemolysis from chronic disseminated intravascular coagulation [10].

In conclusion, our case suggests that even life-threatening

chronic anemia resulting to lactic acidemia may not have
lethal consequences in selected cases because of a satisfactory adaptation to profound dysoxia.

Fig. 2 Hemoglobin values and lactate levels during the first 24

hours after the patient's admission.

Case Report

377.e9
Argyrios Ntalianis MD
3rd Cardiology Department
University of Athens School of Medicine
Kostantinos Mandrekas MD
Department of Clinical Therapeutics
University of Athens School of Medicine
Christos Papamichael MD
Department of Clinical Therapeutics
University of Athens School of Medicine
Maria I. Anastasiou-Nana MD
Department of Clinical Therapeutics
University of Athens School of Medicine
Makedonias 24, 104 33 Athens, Greece
E-mail address: jnanas@ath.forthnet.gr

doi:10.1016/j.ajem.2008.08.014

References
[1] Stoltzfus RJ. Iron deficiency: global prevalence and consequences.
Food Nutr Bull 2003;24:S99-S103.

[2] Wilkerson D, Rosen A, Gould S, et al. Oxygen extraction ratio: a valid

indicator of myocardial metabolism in anemia. J Surg Res 1987;42:
629-34.
[3] Bhatia M, Manchanda S, Roy S. Coronary hemodynamic studies in
chronic severe anaemia. Br Heart J 1969;31:365-74.
[4] Duke M, Abelmann W. The hemodynamic response to chronic anemia.
Circulation 1969;39:503-15.
[5] Anand I, Yellapragada CH, Wander G, Chawla L. Endotheliumderived relaxing factor is important in mediating the high output state
in chronic severe anemia. J Am Coll Cardiol 1995;25:1402-7.
[6] Fontana J, Welborn L, Mongan P, et al. Oxygen consumption and
cardiovascular function in children during profound intraoperative
normovolemic hemodilution. Anesth Analg 1995;80:219-25.
[7] Al-Mondhiry H, Al-Hilali A. Severe anemia: clinical observations in
100 patients with very low haemoglobin levels. Arch Intern Med 1979;
139:1053-4.
[8] Witt J, Marks M, Smith E, et al. Leiomyoma presenting as prolonged
fever, anemia and thrombocytosis. Cancer 1983;52:2359-62.
[9] Gianoutsos P, Laverty CR. Uterine fibroid: an unusual cause of
recurrent haemorrhagic pleural effusions. Med J Aust 1975;2:600-2.
[10] Harris MG, Bannatyne P, Russell P, et al. Chronic consumptive
coagulopathy with a uterine leiomyoma. Aust N Z J Obstet Gynaecol
1982;22:54-8.

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