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 iron- deficiency 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 excep- tional 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 ortho- static 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/uL, and thrombocytosis (platelet count, 534 000/uL). Microscopic examination revealed no schistocytes.

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 macro- phages. 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, hemo- dilution 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/min.m^-2, 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].

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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 electro- cardiogram abnormalities observed might be attributed to limited myocardial ischemia due to myocardial oxygen demand-supply disproportion.

Bone marrow aspiration and peripheral blood smear exa- mination 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 coagula- tion [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 satisfac- tory 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

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