ED Approach to Anemia


A 57-year-old female presents to the emergency department with fatigue and weakness that have been worsening over a period of several months. She has a past medical history of chronic daily alcohol use, coagulation disorder with increased INR, and anxiety. She does not like to see physicians and has not been to her primary care doctor in several years, but decided to come in today because her fatigue and weakness have become too severe.

She reports that for the past few months she has had a poor appetite and is unable to eat most things without vomiting. Her diet consists mostly of fruit juices. She is still drinking large amounts of alcohol daily, and has smoked half a pack of cigarettes per day for the past 40 years. There is a family history of breast cancer in her mother and her sister. On review of systems, she endorses reduced appetite, chills and fatigue. She also endorses heart palpitations, tinnitus, vomiting, black stools, easy bleeding and loss of balance. 

On exam, she is hypotensive (80/60) and tachycardic (108), her oxygen saturation is 89% on room air and her BMI is 15. She appears ill, intoxicated and very pale. She has severe conjunctival pallor and tachycardia. On rectal exam, she has black stool and a positive occult blood test. At this point, there is a high degree of concern for anemia with gastrointestinal bleeding as the most likely underlying cause. 

Laboratory studies show a critically low hemoglobin level of 2.1, with numerous electrolyte abnormalities. Transfusion of four units of packed red blood cells is initiated, and she is started on a proton pump inhibitor due to concern for gastric ulcers and octreotide in case of varices given her extensive alcohol use. Her condition stabilizes, and she is admitted to the ICU for a gastrointestinal workup.

During her hospital stay, she has an upper endoscopy which shows localized erosions in the gastric antrum without evidence of recent bleeding, and her H. pylori test comes back negative. A colonoscopy shows an erythematous region in the ascending colon, multiple non-bleeding diverticula, a sessile 5-mm polyp, and some moderately-sized internal hemorrhoids. No source of the bleeding is identified, and all biopsy specimens are normal.

After a few days in the hospital, her hemoglobin is stable at 11.8 and her symptoms have improved. She is discharged to a skilled nursing facility on a proton pump inhibitor. 


Over the past 30 years, transfusion thresholds and protocols have become much more conservative in an effort to balance the risks of anemia against the risks and costs of using blood products. For most stable patients, clinical trials support transfusion when the hemoglobin drops below 7 or 8 g/dL; higher thresholds may be used for certain populations, including those undergoing cardiac surgery or those with symptomatic anemia, ongoing bleeding, or cardiac ischemia. 

While the exact timing of blood transfusion is debated for patients who are asymptomatic and moderately anemic, it is clear that severe anemia is dangerous and associated with high mortality. A hemoglobin concentration of less than 6.5 g/dL is generally considered life-threatening, and even healthy patients can generally only tolerate a decrease to 3.5-4 g/dL before a significant increase in death from all etiologies. In a study of Jehovah’s Witness patients who were not transfused when their hemoglobin concentration dropped to 2.0 g/dL or less after surgery, their median survival was 1 day from their lowest Hb value. 

While the patient in this case was severely symptomatic for many months, she was able to survive likely because her bleeding was slow and chronic from one or more of the pathologies found on her upper endoscopy and colonoscopy. Throughout this prolonged, slow decline in hemoglobin concentration, her body underwent a number of hemodynamic and molecular adaptations as a result of long-term anemia. These include vasodilation to allow for higher cardiac output to improve oxygen transport as well as increasing production of reticulocytes by the bone marrow.

We assume that she was unable to compensate by increasing red blood cell output due to the effects of chronic alcohol use on hematopoiesis. Heavy alcohol consumption directly suppresses red blood cell production in the bone marrow, and it also causes the cells that are produced to be defective and unable to mature properly. Therefore, they are destroyed prematurely, resulting in anemia and a poor compensatory response to blood loss. Cytopenias can also occur as a result of hypersplenism secondary to increased portal pressures in liver disease, which is a common result of chronic alcohol use. 

The treatment for alcohol-induced cytopenias is abstinence from alcohol use and nutrient repletion if a poor diet contributed to the problem. Anemia association with nutrient deficiencies should improve within a month of treatment, while alcohol-induced macrocytosis typically takes months to improve. Complications of hypersplenism may not resolve despite alcohol cessation.

Author: Katherine Barry is a fourth year medical student at the Warren Alpert Medical School of Brown University.

Faculty Reviewer: Kristina McAteer, MD is an attending physician at Rhode Island Hospital and Newport Hospital.


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Source: brownemblog.com

ED Approach to Anemia