Microcytic Anemia

Name the anemia before you plan around it - CBC with MCV and MCHC, then iron studies. Total iron-binding capacity rises and transferrin saturation falls markedly in iron deficiency, and a ferritin under 12 ng/mL is a reliable indicator - but ferritin is an acute-phase reactant, so a normal value in an inflamed or infected patient does not exclude iron deficiency. Hemoglobin electrophoresis or HPLC when thalassemia is in play; sideroblastic anemia shows normal-to-high iron.

Oxygen delivery - Unless contraindicated, give supplemental oxygen and make sure ventilation is adequate. Anemia is an oxygen transport problem, and a normal saturation on a low hemoglobin is still a low delivery.

Watch the myocardium - Severe anemia produces angina from reduced oxygen delivery to cardiac myocytes, and untreated chronic anemia causes high-output heart failure and arrhythmias. Keep the heart rate controlled, avoid the hypotension that steals coronary perfusion, and watch the ST segments.

Optimize elective cases, don't just transfuse them - Iron replacement must continue for at least three months after iron levels normalize to restore stores, and parenteral iron is an option when oral fails or time is short. That is a preoperative clinic conversation, not a day-of-surgery one.

Transfuse for symptoms and for the case - Symptomatic anemia warrants packed red cells, but transfuse with caution in volume-overloaded patients such as those on hemodialysis or in congestive heart failure. Use your institution's threshold rather than a remembered number.

Find the bleeding - Iron deficiency in an adult male or a postmenopausal female is a GI source until proven otherwise; EGD and colonoscopy are the workup. A patient coming for an unrelated case with a newly-found microcytic anemia needs that referral in the discharge plan.

Thalassemia is a different animal - Beta-thalassemia major depends on chronic transfusion, and iron overload from those transfusions causes the heart failure that is the leading cause of death, plus atrial fibrillation, hypothyroidism, hypoparathyroidism, adrenal insufficiency, diabetes and hypogonadism. Ask for the most recent echo and ferritin, check a TSH, calcium and glucose, and remember these patients run a resting tachycardia with low blood pressure and high cardiac output at baseline. Thromboembolic events including DVT and PE are part of the disease.

Thalassemic airway and spleen - Marrow expansion produces skeletal deformity including frontal bossing and facial bone changes, so look at the face, mouth opening and neck rather than assuming a routine airway. Hypersplenism is common in thalassemia intermedia and major and may have been treated with splenectomy - which makes the patient functionally asplenic and raises the infection stakes.

Do not reflexively give iron - Chronically transfused thalassemia patients are already iron-loaded and at risk of acquired hemochromatosis, and sideroblastic anemia carries normal to high iron rather than depleted stores. X-linked sideroblastic anemia responds to oral pyridoxine; look for alcohol use, isoniazid, lead toxicity, copper deficiency and chemotherapy as secondary causes.

Small findings that matter at the airway - Iron deficiency can produce glossitis and esophageal webs (Plummer-Vinson syndrome) with a sensation of food sticking. Take that history seriously before blind esophageal instrumentation such as a TEE probe or an OG tube.

Microcytic anemia is anemia with an MCV under 80 fL, most often from iron deficiency. Iron is freed by gastric acid, absorbed in the duodenum and upper jejunum through ferroportin under hepcidin control, carried on transferrin and stored as ferritin. Anything that empties those stores - dietary lack, malabsorption, acute or chronic blood loss, or the increased demand of pregnancy, major trauma and surgery - reduces the hemoglobin loaded into each cell, so the cells come out small and hypochromic with a widened central pallor. The differential also includes thalassemia, anemia of chronic disease, sideroblastic anemia and lead toxicity. The perioperative consequence is the same regardless of cause: reduced oxygen-carrying capacity and tissue hypoxia, compensated by tachycardia and tachypnea until it isn't.