Continuing Education Activity
Mean corpuscular volume (MCV) is a measure used to determine anemia etiologies. This activity illustrates the categories of anemia with varying MCVs, the causes of microcytic, macrocytic, and normocytic anemias, the use of MCV in the next step of treatment of anemia, and other elements including pathophysiology, histopathology, treatment, and epidemiology of each category of anemia based on MCV. These components are important for the management of patients with varying types of anemia.
- Define mean corpuscular volume.
- Describe the history and physical examination findings of patients with varying mean corpuscular volume (MCV) values and anemia.
- Summarize the complications expected in patients with abnormal mean corpuscular volume (MCV) values.
- Describe interprofessional team strategies for improving care coordination and communication to advance mean corpuscular volume (MCV) use and improve anemia outcomes.
Mean corpuscular volume (MCV) is a laboratory value that measures the average size and volume of a red blood cell. It has utility in helping determine the etiology of anemia — calculation of the value is by multiplying the percent hematocrit by ten divided by the erythrocyte count. Along with the hemoglobin and hematocrit, MCV can determine the classification of anemia as either microcytic anemia with MCV below the normal range, normocytic anemia with MCV within the normal range, macrocytic anemia with MCV above the normal range. Furthermore, it is useful for calculating the red blood cell distribution width (RDW).
Clinicians can discern definitive diagnoses for the type of anemia based on the MCV value.
Microcytic anemia is a type of anemia where the average erythrocyte is smaller than normal and much smaller than a leukocyte. On the complete blood count (CBC), its measure is under 80 fL while normal MCV is between 80 to 100 fL. It is commonly seen in chronic iron-deficient anemia, anemia of chronic disease, sideroblastic anemia, and thalassemias but can also occur in other conditions. Microcytic cells can appear to have a larger area of central pallor, especially in the setting of iron-deficient anemia and anemia of chronic disease.
Macrocytic anemia is a type of anemia where the average red blood cell volume is larger than normal. On CBC, its MCV is over 100 fL. Macrocytic anemia further subcategorizes as megaloblastic or non-megaloblastic. Megaloblastic anemia is due to impaired DNA synthesis versus normal DNA synthesis in non-megaloblastic anemia. Megaloblastic anemia is commonly secondary to folate (also knowns as folic acid or vitamin B9) deficiency, cobalamin/vitamin B12 deficiency, and orotic aciduria, an autosomal recessive disorder that does not allow conversion of orotic acid to UMP. Non-megaloblastic anemia is due to hepatic insufficiency, chronic alcoholism, or a rare congenital disease Diamond-Blackfan anemia.
Normocytic anemia is anemia with a low hemoglobin and hematocrit range but MCV in the normal range of 80 to 100 fL. This type of anemia can subclassify as hemolytic and non-hemolytic. Normocytic hemolytic can occur intravascularly and extravascularly and can be due to myriad causes. Other laboratory values on the CBC will further indicate the type of anemia.
Non-hemolytic normocytic anemias can present in early anemia of chronic disease, early iron deficiency anemia, aplastic anemia, microangiopathic hemolytic anemias, and even certain plasmodial infections.
The demographics affected by various anemias range depending on the MCV value and etiologies.
The underlying causes of microcytic anemia have epidemiologic variations.
Iron deficiency anemia is the most common cause of microcytic anemia. It frequently occurs in premenopausal, menstruating women due to menorrhagia and chronic blood loss without proper iron supplementation. However, the most significant concern for men and post-menopausal women over the age of 50 is colorectal cancer until proven otherwise and requires colonoscopy as soon as possible. Anemia of chronic disease ranks as the second most common type of anemia seen worldwide. Because this type of anemia is seen in patients within chronic inflammatory states due to the disturbances in iron homeostasis, the demographics range between men and women and all age ranges. The diseases causing anemia of chronic disease can range from diabetes and rheumatologic diseases to malignancies. Sideroblastic anemia can be congenital or acquired from lead exposure, myelodysplastic disorders, myeloproliferative neoplasms, Vitamin B6 deficiency, isoniazid, chronic alcoholism, or copper deficiency. In fact, the finding of ringed sideroblasts can even assist providers in honing in on the diagnosis of either myelodysplastic disorder or myeloproliferative neoplasms by seeking mutations in the spliceosomes. Myelodysplastic disorders have been found to affect approximately 10000 people per year, more commonly in adult males over the age of 65 years old.Myeloproliferative diseases range in those that are acquired forms as well as familial types of the disease. Thalassemia can separate into beta and alpha thalassemia, which also varies in severity. Alpha Thalassemia is found more in the African, Southern Chinese, Malaysian, and Thai populations. Beta Thalassemia is found more prominently in the African and Mediterranean populations. Both types are congenital diseases.
Macrocytic anemia is common with a prevalence ranging from 1.7% to 3.6%.
Folate deficiency and vitamin B12 deficiencies can affect a wide range of demographics throughout the world due to their acquisition from an unbalanced diet; however, vitamin B12 deficiency tends to appear in patients with vegan diets due to its origin of animal products. Moreover, vitamin B12 deficiency can also occur in malabsorptive diseases, Diphllobathrium latum infection, pernicious anemia, and gastrectomy. Organic acidemias were found to affect 1 in 784 live births in the UK. Hepatic insufficiency varies in demographics; however, chronic alcoholism has been found to have a prevalence of 20 to 36% . Diamond Blackfan anemia is congenital and presents within the first year of life with an estimated range of 1 per 100000 to 1 per 200000 live births with an effect on myriad races and ethnicities.
However, due to the many causes of normocytic anemia, its epidemiology varies across the board between all ethnicities, ages, and genders, especially since many are acquired.
Microcytocytic anemia: Microcytosis can be caused by a deficiency in a component in hemoglobin, causing the cells to appear much smaller on a peripheral blood smear (PBS). Hemoglobin forms from heme and globin molecules. For example, during heme synthesis, the ferrochelatase enzyme inserts iron into the protoporphyrin ring structure to make the heme molecule. As a result, the lack of iron from chronic iron-deficient anemia can make the protoporphyrin rings in the heme molecules defective.
Anemia of chronic disease is due to an evolutionary response of the body to protect its iron from bacteria that use the iron for their growth. Because bacterial infections cause inflammation leading to an increase in acute phase reactants like hepcidin, hepcidin traps iron in macrophages and decreases iron absorption in the GI tract. This effect is very similar to the presentation of iron-deficient anemia. If a patient is iron deficient, has anemia of chronic disease, even sideroblastic anemia secondary to lead poisoning, heme and therefore hemoglobin cannot be fully synthesized and cause the erythrocyte to appear much smaller.
On the contrary, thalassemias have mutations in the alpha or beta globin chains, causing a disruption in hemoglobin synthesis as well. All of these types of hemoglobinopathies produce microcytic erythrocytes.
Macrocytic anemia: Macrocytic anemia can categorize as either megaloblastic anemia versus non-megaloblastic anemia. During pyrimidine synthesis, folate becomes tetrahydrofolate and donates a carbon. Vitamin B12 or cobalamin is a cofactor for the enzyme that transfers the carbon group from tetrahydrofolate. A deficiency of either of these enzymes impairs the process of properly dividing erythrocytes to their normal size. The erythrocytes stop dividing due to the deficient pyrimidines found, causing the enlarged cells.
However, non-megaloblastic anemia has a different effect on macrocytes created. Liver disease can compromise lipid production, and the hypothesis is that the lipids within the phospholipid bilayer of erythrocytes become compromised by liver failure. Additionally, alcoholic cirrhosis secondary to chronic alcoholism can impair folate absorption further causing macrocytic anemia.
Normocytic anemia: Normocytic anemia is commonly due to hemolysis whether it is intravascular or extravascular. However, aplastic anemia is also a cause of normocytic anemia due to the destruction of myeloid stem cells, stem cells from which erythrocytes originate.
MCV findings can be followed up with a peripheral blood smear (PBS). PBS will show the volume/size of the erythrocytes relative to leukocytes. Microcytes tend to be smaller and have a large central area of pallor in comparison to a normal erythrocyte (if due to iron deficiency or anemia of chronic disease). Depending on the cause of microcytosis, the microcytic erythrocytes can also be associated with target cells and anisopoikilocytosis for thalassemia, or basophilic stippling seen in lead poisoning. Sideroblasts are only present in bone marrow aspirates.
Megaloblastic macrocytosis has enlarged erythrocytes that tend to be the same size as a leukocyte. Hypersegmented polymorphonuclear neutrophils are affected by DNA and RNA synthesis and also, appear with megaloblastic macrocytosis. However, patients with liver failure can appear to have acanthocytes or spur cells and macro-ovalocytes due to lipid dysfunction from hepatic insufficiency.
Normocytic anemia secondary to hemolysis can have a variety of histopathological findings such as sickled cells from sickle cell anemia, spherocytes from hereditary spherocytosis and autoimmune hemolytic anemia, Heinz bodies, Howell-jolly bodies, degmacytes, schistocytes, and many more. These presentations depend on the underlying intrinsic or extrinsic cause of normocytic anemia. Aplastic anemia has to be diagnosed with a bone marrow aspirate that appears “dry” or with multiple white adipocytes lacking erythrocytes, leukocytes or any progenitor cells.
History and Physical
There are many findings when it comes to anemia presentation.
MCV below 80:
Iron deficiency anemia presents with conjunctival pallor, fatigue, cold intolerance, and cold distal extremities, koilonychia, occasionally pica, glossitis, dry, cracked lips, and cheilosis. These patients will generally describe an event with chronic blood loss, chronic inflammation, exposure to lead paint, or a family history of thalassemias. Anemia of chronic disease presents with the disease that is causing chronic inflammation such as arthritis in rheumatoid arthritis or malignancy. Also, these diseases can be asymptomatic. However, these patients may have a family history of cancer, autoimmune disease, or rheumatologic disease that can assist in the diagnosis.
Additionally, thalassemias can present with “chipmunk” facies due to bone marrow expansion and extramedullary hematopoiesis. This process can also present with hepatomegaly and splenomegaly on physical examination. An X-ray may display skeletal deformities. These patients will more than likely have a family history, including one or both of their parents. Patients with lead exposure are commonly exposed to lead paints, especially children in an older home consuming the lead-based paints. Adults are likely to report exposure through occupations such as miners, pipefitters, auto shop workers, and ceramic glazes. Lead poisoning can present with lead lines on the gums and on long bones metaphysis, abdominal pain, peripheral neuropathy, most commonly fibular and radial nerve neuropathies, and fatigue. Children can present with encephalopathy. Because sideroblastic anemia can result from lead poisoning or even by chronic alcohol use, it presents as the underlying etiology.
MCV over 100:
Patients with vitamin B12 deficiency may report a strict vegan lifestyle without supplementation, short bowel syndrome with a history of small bowel resection, pernicious anemia with presentation of nausea, increased flatulence, diarrhea, weight loss, and anorexia, malabsorptive symptoms like steatorrhea, foul-smelling stools, diarrhea, weakness, and/or weight loss. Vitamin B12 deficiency takes many years to manifest due to hepatic storage for approximately three to six years. As a result, when this condition does present, it tends to affect the neurologic system due to its necessity in fatty acid synthesis for myelin sheaths. Patients demonstrate signs of subacute combined degeneration: cerebellar ataxia, bilateral hemiplegia, and decreased vibration and discriminative touch sensations. Folate deficiency can present with glossitis but has few other symptoms seen. However, if pregnant with a folate deficiency, the neonate can suffer from neural tube defects such as spina bifida occulta. These patients will deny the use of supplemental vitamins while pregnant. Also, chronic alcoholism can be a factor in history for a folate deficiency. Orotic aciduria presents early in life with failure to thrive and slow development reported in patients with a family history. Non-megaloblastic anemias present as their underlying causes such as hepatic insufficiency. These patients may also report chronic alcoholism, which is the most common cause. Additionally, they can report symptoms of jaundice, fatigue, spider angiomas, palmar erythema, ascites, peripheral edema, and even easy bleeding and bruising, to name a few symptoms. Diamond Blackfan anemia presents in the first year of life with facial and hand malformations growth retardation and predisposition to malignancies.
Both intrinsic and extrinsic hemolytic normocytic anemias can present similarly. Patients have darkened urine secondary to increase urobilinogen. Intravascular hemolysis due to microangiopathic hemolytic anemias or paroxysmal nocturnal hemoglobinuria can present with hemoglobin and hemosiderin in the urine. Many of these diseases are spontaneous, but patients with malaria can report recent travel to endemic areas, recent camping and Ixodes tick bite for babesiosis, undercooked ground beef for hemolytic uremic syndrome, and SLE, and foamy urine indicating proteinuria with epistaxis and hypertension in a pregnant woman over 20 weeks gestation for HELLP syndrome. Aplastic anemia can present with pallor, purpura, petechiae, increased risk of mucosal bleeding, increased risk of infection, and fatigue secondary to pancytopenia.
A complete blood count is necessary, including hemoglobin, hematocrit, and MCV to determine anemia type.
For microcytic anemia, the presentation will determine the types of studies. If a patient is a menstruating woman with an MCV under 80, a Von Willebrand Factor and/or thyroid panel may be obtained to determine the underlying cause of menorrhagia as well as full menstrual history. On the contrary, a patient with microcytic anemia over the age of 50, is required to obtain a colonoscopy to determine if the iron deficiency originates from a polyp or neoplasm within the colon. Other investigations include urea breath test and an upper endoscopy to test for Helicobacter pylori infection if the patient complains of gastritis type pain. Anemia of chronic disease requires myriad tests if the underlying cause is unknown. Many of these tests include rheumatoid factor, Anti-double stranded DNA antibodies, Anti-neutrophil cytoplastic antibodies, anti-myeloperoxidase antibodies, a urine spot test to determine the renal function with GFR, creatinine, and blood urea nitrogen, HLA-B27 screening, and many more rheumatologic antibodies. Also, screening for malignancies with a CT scan or chest X-ray might be a consideration for the anemia of chronic disease. If lead poisoning is a possibility, a blood lead level is the gold-standard test. However, if other causes of sideroblastic anemia are suspected, a bone marrow biopsy is required. Medical history is very important to uncover the underlying etiology. In this case, the patient may be able to avoid a bone marrow biopsy. If beta-thalassemia is suspected based on history and physical examination, hemoglobin electrophoresis will help determine the amount of AA vs. A2 hemoglobin is present. Genetic analysis is superior tests for alpha-thalassemia.
PBS and urine analysis would be beneficial to determine whether the hemolysis is intravascular or extravascular for normocytic anemia. If schistocytes are present and there is hemoglobin in the urine, it is indicative of microangiopathic hemolytic anemia. If there are no schistocytes on PBS and no hemoglobin in the urine analysis but hemolysis is still suspected, the PBS can also give some insight. If there are spherocytes present, a Direct Coombs test is performed to determine whether autoimmune hemolytic anemia or splenic recruitment from hereditary spherocytosis and help determine the diagnosis.
For macrocytic anemia, history and physical examination is very important to determine whether the patient is a chronic alcoholic, is predisposed to liver failure, malabsorptive disease, or has a vegan diet lacking proper vitamin supplementation. Both vitamin B12 and folate levels are necessary, especially since folate can easily mask vitamin B12 deficiency. If orotic aciduria is suspected, urine analysis for orotic acid and ammonia is essential. The ammonia test can differentiate a deficiency in ornithine transcarbamylase versus orotic aciduria. Due to the rarity of Diamond-Blackfan anemia, the history and physical examination with CBC are efficient. However, a follow-up CT scan may be performed to screen for malignancies due to predisposition.
Treatment / Management
Iron deficient anemia treatment is with iron supplementation for premenopausal women. Also, some women receive treatment with oral contraceptive pills to regulate the menstrual cycles and shorten their periods, or levothyroxine if secondary to hypothyroidism. Anemia of chronic disease: the underlying disease has to be treated commonly with anti-inflammatories, corticosteroids, and TNF-alpha inhibitors unless it is due to malignancy. In the case of malignancy, the malignancy requires its standard treatment protocol. Lead poisoning and is chelated with dimercaprol and EDTA and succimer for children. Copper deficiency requires copper supplementation. Patients taking isoniazid and vitamin B6 deficient patients should receive vitamin B6 supplementation and/or discontinue isoniazid. Chronic alcohol intake must cease immediately. Thalassemias are treated differently depending on their severity. Most thalassemias do not receive medication or transfusions; however, beta-thalassemia therapy includes chronic blood transfusions. Other types of thalassemia tend to be asymptomatic and do not require treatment. Iron supplementation is contraindicated, especially in patients with chronic transfusions due to the concern of acquired hemochromatosis. If Helicobacter pylori infection is suspected, a urea breath test is necessary. An upper endoscopy can also be obtained for a biopsy as well as assessing severity, mainly because this bacteria is pre-malignant.
Macrocytic anemia treatments range from due to the etiologies. For vitamin B12 deficiency and folate deficiency, folate and vitamin B12 supplementation are the therapeutic response. Patients with chronic alcohol abuse are urged to cease alcohol intake and to have folate supplementation. Patients with orotic aciduria would be to supplement with uridine monophosphate to bypass the deficiency enzyme.
For patients with paroxysmal nocturnal hemoglobinuria, the treatment includes eculizumab, which can improve hemolysis and prevent portal hypertension secondary to venous thromboses. If the anemia is significant, a blood transfusion may be required. Patients with bone marrow failure may be candidates for hematopoietic stem cell transplantation. Patients with macroangiopathic hemolytic anemia secondary to prosthetic heart value or aortic stenosis may be candidates for the repair of their valves or prosthetic. Patients with intravascular hemolysis secondary to malaria or babesiosis must have therapy with anti-malarial or babesiosis medications. Microangiopathic hemolytic anemia can result from thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), systemic lupus erythematosus (SLE), hypertensive emergency, and HELLP syndrome. TTP treatment is with plasmapheresis and corticosteroids. HUS therapy is with plasmapheresis, similar to TTP. SLE is treated with prednisone to decrease flares then hydroxychloroquine, mycophenolate mofetil, and TNF-alpha inhibitors. HELLP syndrome is treated with anti-hypertensives such as labetalol or hydralazine, magnesium sulfate to prevent convulsions, corticosteroids to further develop baby’s lung development before delivery, and blood transfusion if required due to thrombocytopenia. Hereditary spherocytosis requires folate supplementation, blood transfusions if hemoglobin falls below 7g/dL, erythropoietin for babies up to 9 months, and last line treatment would be to vaccinate against encapsulated bacteria prior to splenectomy. Autoimmune hemolytic anemia can be treated glucocorticoids first line and then with cytotoxic drugs like rituximab if refractory. Aplastic anemia is treated with the withdrawal of the offending agent if there is one and often treated with hematopoietic stem cell transplants.
The differential diagnoses for microcytic, normocytic and macrocytic anemias are listed below based on MCV findings in a complete blood count.
Differential diagnoses of MCV under 80 include iron deficiency anemia causes, anemia of chronic disease causes, sideroblastic anemia causes, H. pylori infection, and thalassemias. Iron deficiency anemia can have many different differential diagnoses including menorrhagia, colorectal adenocarcinoma, bleeding colonic polyp, bleeding peptic ulcer disease, Helicobacter pylori infection, hematemesis, chronic epistaxis, and duodenal malabsorption or resection. Anemia of chronic disease can have differential diagnoses including malignancy, rheumatologic conditions such as SLE and rheumatoid arthritis, autoimmune diseases such as primary biliary cirrhosis or multiple sclerosis, chronic kidney disease, and chronic infection. Chronic alcoholism, vitamin B6 deficiency, isoniazid use, myelodysplastic disorder, lead poisoning, copper deficiency, and congenital sideroblastic anemia are all differential diagnoses for sideroblastic anemia, causing microcytic anemia. The main types of thalassemia are alpha1, alpha2, alpha3/ hemoglobin H disease, alpha4, which is fatal, beta-thalassemia minor, beta-thalassemia major, and HbS/β thalassemia heterozygote.
Differential diagnoses of MCV above 100 include megaloblastic anemia and non-megaloblastic anemia.
Megaloblastic anemia causes include folate deficiency which can be caused by chronic alcoholism, barbiturate use, phenytoin use, sulfasalazine use, methotrexate use, triamterene use, trimethoprim/sulfamethoxazole use, pyrimethamine use, and duodenal or jejunal malabsorption or resection. Differential diagnoses for vitamin B12 deficiency would include Crohn disease ileitis, short bowel syndrome, strict vegan diet without supplementation, diphyllobothrium latum infection, chronic metformin use, pernicious anemia, atrophic gastritis, orotic aciduria, and Diamond Blackfan anemia. Non-megaloblastic differential diagnoses include those causing hepatic insufficiency or cirrhosis which can be secondary to chronic alcoholism, fulminant hepatitis secondary to drug toxicity, alpha 1 antitrypsin disease, galactosemia, Wilson disease, chronic hepatitis B viral infection, chronic hepatitis C infection, hemochromatosis, autoimmune hepatitis, amyloidosis, chronic decompensated right heart failure, and parasitic infections such as Schistosoma haematobium.
Differential diagnoses of MCV 80 to 100 include those that cause intravascular hemolytic anemia and extravascular hemolytic anemia and aplastic anemia.
Intravascular hemolytic anemia can be caused by paroxysmal nocturnal hemoglobinuria and micro/macroangiopathic hemolytic anemia due to Thrombotic thrombocytopenic purpura, Hemolytic Uremic Syndrome, HELLP Syndrome, disseminated intravascular coagulation, aortic stenosis, and defective prosthetic cardiac valve. Extravascular hemolytic anemia can result from hereditary spherocytosis, sickle cell anemia, glucose 6-phosphate dehydrogenase deficiency, infections like malaria and babesiosis, and autoimmune hemolytic anemia. Some differential diagnoses for autoimmune hemolytic anemia causes would be chronic leukocytic leukemia, systemic lupus, erythematosus, and hematopoietic stem cell transplant. Also, differential diagnoses for aplastic anemia would include Fanconi anemia, paroxysmal nocturnal hemoglobinuria, radiation exposure, the toxicity of drugs like chloramphenicol, sulfonamides, benzene exposure, viral infections such as parvovirus B19, especially in immunocompromised patients, HIV, Ebstein-Barr virus, hairy cell leukemia, and myelodysplastic disorders.
Pertinent Studies and Ongoing Trials
Outside of anemia, MCV along with red blood cell distribution is thought to help determine the risk of cardiovascular events after surgery and/or blood transfusions. Findings are that after surgery and/or blood transfusion, patients with macrocytic anemia or microcytic anemia have a higher risk than patients with normocytic anemia. These values together may help prevent cardiovascular events due to closer monitoring after these procedures. Additionally, MCV can help determine the risk of restenosis after stent placement into the coronary arteries. Microcytic erythrocytes were associated with restenosis of the coronary arteries with stent more than macrocytosis or normocytic erythrocytes.
There are varying prognoses with changes in MCV.
Iron deficient anemia has a good prognosis with iron supplementation. However, if iron deficiency is secondary to chronic blood loss from malignancy, the prognosis is poor and often fatal. The prognosis of anemia of chronic disease varies due to underlying etiology. As stated above, chronic inflammation secondary to malignancy can have a poorer prognosis than a rheumatologic disease controlled by medication. However, sideroblastic anemia is relatively mild and easily treated with supplementation or withdrawal from the causal agent.
Furthermore, the thalassemias have ranging prognoses. Hemoglobin Bart’s disease or alpha-thalassemia major is fatal, causing hydrops fetalis and has a very poor prognosis in utero. Beta-thalassemia major also has improved with increasing treatment of iron chelation with chronic blood transfusions, and patients can live reasonably normal lives. However, the outlook is poor due to the early mortality of these patients from restrictive diseases secondary to acquired hemochromatosis. Patients with other forms of alpha- and beta-thalassemia generally live normal lives without significant complications and have excellent prognoses.
Megaloblastic anemias secondary to folate and cobalamin deficiencies tend to have good prognoses with proper supplementation therapy. However, vitamin B12 deficiency with severe subacute combined degeneration can be fatal and has a poor prognosis. This condition is preventable with appropriate supplementation via vitamins, food intake, or injections. Folate deficiency has a good prognosis in patients that are not pregnant. However, the prognosis for neonates with folate-deficient mothers is poor depending on the neural tube defect etiology. Patients with spina bifida occulta have a good prognosis and many times are unaware of their condition. However, patients with rachischisis have a very poor prognosis and happen to die in utero. Patients with orotic aciduria and Diamond Blackfan anemia can have a good prognosis depending on chronic supplementation. If these patients are not adherent to supplementation, their anemias can have a poor prognosis, can become severe, and fatal. Non-megaloblastic anemias tend to have poor prognoses. Patients with chronic alcoholism have many vitamin defects ranging from folate to thiamine. These deficiencies can also cause neurologic issues, cerebellar damage, and hepatic insufficiency. Hepatic insufficiency and cirrhosis also have a poor prognosis depending on how severe. Many of these patients suffer from portal hypertension, esophageal varices with the risk of rupture, and hemorrhage, and can, in turn, acquire hepatorenal syndrome, become encephalopathic, which can lead to their demise.
Normocytic anemias tend to have poorer prognoses due to their chronic hemolysis and declining conditions. Intravascular hemolysis such as paroxysmal nocturnal hemoglobinuria has improved prognosis with newer treatments. However, without treatment, the patient can present with pancytopenia and suffer from aplastic anemia, which can lead to their demise. Microangiopathic hemolytic anemias tend to have better prognoses if treated; however, patients must be adherent to their treatments. Extravascular hemolytic diseases like sickle cell anemia have a poor prognosis and life expectancy ranging from 30 to 40 years old. These patients suffer from chronic vaso-occlusive crises, which can, in turn, lead to their deaths.
The most common complication for anemias with varying MCV is the lack of treatment and increased mortality. Patients with iron-deficient anemia without supplementation can develop high output heart failure. In addition, lead poisoning can also be fatal without the chelation and removal of the causal agent. Patients with diseases such as SLE can suffer from renal insufficiency without treatment, which is the most common cause of death in these patients. Patients with beta-thalassemia major are the most likely to undergo complications from treatment, such as acquired hemochromatosis. Without chronic chelation, these patients can die from iron intoxication as well as restrictive pericarditis secondary to iron deposition in the pericardium.
As previously stated, folate deficiency can be complicated in pregnant patients causing neural tube defects. Patients with vitamin B12 deficiency can have complications of subacute combined degeneration. Unfortunately, without supplementation, orotic aciduria and Diamond Blackfan anemia are fatal. Patients with hepatic insufficiency or cirrhosis can incur a large number of complications ranging from hyperammonemia, ascites, portal hypertension, cardiomegaly, esophageal varices with rupture and hemorrhage, internal hemorrhoids, hepatorenal syndrome, and hepatic encephalopathy. Chronic alcoholism can also lead to these complications due to alcoholic cirrhosis in addition to Wernicke-Korsakoff syndrome from thiamine deficiency.
Patients with normocytic anemia can have complications ranging from hemoglobinuria, hematuria, syncope, petechial rashes, high fevers, and death. These patients must be treated to avoid complications.
Deterrence and Patient Education
MCV is an essential value for determining the type of anemia and risk of cardiovascular events, but it is not the only value on the CBC used. Some physicians do not pay as much attention to MCV, especially if a patient could have a cause of microcytic and macrocytic anemia together. It is crucial that clinicians treat patients based on history, physical examination, and multiple values outside of MCV to eventually inform their patients of their underlying etiologies and ensure proper treatment and management of their conditions.
Enhancing Healthcare Team Outcomes
MCV in the use of diagnosing types of anemia can experience some challenges. Patients with anemia can have a range of anemia types to a combination of anemias ranging from chronic alcoholism, causing folate deficiency with macrocytosis and bleeding esophageal varices causes microcytosis. Though the history and physical examination are crucial to determining the underlying cause of anemia, MCV can be the determining factor as to what is most important to treat primarily.
Nurse practitioners and primary care physicians whether it is an internist, family practice physician or pediatrician, are generally the first physicians that discover the disturbance in MCV laboratory values with routine visits or investigation of underlying complaints. (Level III) However, there are other clinicians and health care workers that are just as important in the interprofessional team to care for the patients. If the patient is in an inpatient setting, the nurses play a critical role in the patients' care. Nurses play a crucial role in regularly checking vitals, ensuring that the patient is not showing signs of hematemesis, hematuria, hematochezia, or hemorrhage from any other orifices is critical in the care and management of MCV and anemia and can determine patient’s condition is improving or declining. Also, hematologist and oncologists are among the most important physicians in managing a patient blood disorder that involves a change in hemoglobin, hematocrit, and MCV. They can further diagnose and recommend treatment plans for patients with anemia based on their history, physical examination findings, and CBC values as well as treat the patient if the underlying cause of MCV change and anemia is due to malignancy. Other specialists like gastroenterologists are important for investigating upper GI hemorrhages in contrast to lower GI vital and treatment of these conditions. If these conditions are untreatable via the gastroenterologists, then general surgery or trauma can also have an input to treat the patients.
Some patients with a change in MCV and hemoglobin and hematocrit ratio require surgery. There is also the management of patients in the post-operative period by nurses to make sure that the patients initiate and continue inspiratory spirometry to prevent atelectasis and pneumonia and to obtain and monitor laboratory values that are found abnormal especially in the following week after an operation. Physical therapists are also important to ensure that the patients begin moving and maintain physical activity to avoid decubitus ulcers, deep venous thromboses, urinary tract infections, pulmonary embolisms and other preventable surgical complications due to immobility.
Managing proper supplementation is pertinent for the proper care of a patient with MCV changes. As previously stated, patients can suffer from microcytic anemia, which might require iron supplementation, vitamin B6 supplementation, medication changes or even lead chelation. Patients with megaloblastic anemia may require supplementation. The pharmacists are very important for dosage, and reminding providers of contraindications with certain conditions causing anemia.
Pharmacists must assist the clinical team in monitoring the patients for complications of therapy and report back when issues such as constipation develop. They also need to assist in patient education, making sure that appropriate fluid intake is maintained and encourage the clinicians to order a laxative if constipation develops.
Interprofessional healthcare practices are used to improve communication between providers and overall care of the patients. Many of the patients that suffer from changes in MCV are in the elderly population; this population has been found to benefit more with a stronger interprofessional team and meet with their primary care providers to establish a plan targeting their needs (Level III). It is also essential for providers to continue developing interprofessional skills with constant communication and documentation coordinated between clinicians, nurses, and the pharmacy staff. Even simulations during training can build stronger interprofessional collaboration and improve overall patient care (Level II).
Evaluation of patient status and treatment as a team instead of just the primary care can improve the value of the patient’s outcome. These roles in a team can drastically change the type of care for the patient and possibly improve the quality of life of a patient with MCV changes. MCV is a valuable tool in diagnosis, but optimizing its full value requires full coordination from the interprofessional healthcare team. [Level V]