case study anemia

  1. Describe the following types of anemia.  Explain the etiology, population at-risk and risk factors associate with it.  
    1. Megaloblastic

Megaloblastic anemia is described as anemia in which the RBCs are larger than normal. This disorder is usually caused by a deficiency of vitamin B12 or folic acid. In the Western world, about 90% of megaloblastic anemias result from either alcohol-induced folate deficiency or B12 deficiency (Davenport, 1996, p. 155). Vitamin B12 deficiency is harder to detect than folic acid deficiency. Population at-risk for folic acid deficiency includes pregnant women and infants, individuals with Celiac Disease, and people taking medications that interact with nutrient absorption (Mahan, Stump, & Raymond, 2012, p. 735).

    1. Pernicious

Pernicious anemia refers to a decrease in RBCs, due to the inability to absorb vitamin B12; this condition is associated with chronic atrophic gastritis. For people with pernicious anemia, malabsorption of vitamin B12 is usually attributed by the intrinsic factor or other origins, such as infections, medicines, operation, or nutrition. This is due to two mechanisms: 1) the progressive destruction of parietal cells from the gastric mucosa leading to intrinsic factor destruction and 2) the binding of blocking autoantibodies to the vitamin B12-binding site of intrinsic factor, preventing the formation of the vitamin B12-intrinsic factor complex (Toh, 1997). Population at-risk for developing pernicious anemia include strict vegetarians or vegans, those with Crohn’s Disease, or other compromised immune systems (Mahan, Stump, & Raymond, 2012, p. 736-737).

    1. Microcytic

Microcytic anemia is when the RBCs are smaller and paler than normal, indicating a lowered concentration of hemoglobin, which is usually related to insufficient iron intake or excessive iron loss. Excessive iron loss is more common in the United States. This is also known as nutritional anemia. Deficiencies in vitamin B12, folic acid, etc., are also known as hypochromic anemia. Population at-risk for iron-depletion includes women of reproductive age, usually caused by menstruation.  In all other adult groups, the cause is usually some disease of the digestive tract that must be ferreted out and treated (Uthman, 1998, p. 44). Risk factors include “inadequate intake of iron-rich foods…” and having heavy menstrual bleeding” (Whitney & Rolfes, 2005, p.392).

    1. Sickle cell anemia

Different from other types of anemia, sickle cell is an inherited form of anemia caused by a blood mutation steaming from malaria. Sickle cell is the result of abnormal hemoglobin, resulting in a sickle-shaped RBC. In sickle cell anemia, normal hemoglobin, hemoglobin A (Hb A), is replaced with sickle cell hemoglobin, hemoglobin S (Hb S) (Bloom, 1995, p. 5). Due to the abnormality of the blood cells, blood vessels become blocked causing “episodes” of pain for those with sickle cell anemia. An at-risk population of sickle cell anemia includes a large proportion of those of African heritage, including many in the United States. Sickle cell can occur among any person with a family history of sickle cell anemia, even those without African descent.

    1. Thalassemia

Thalassemia (Alpha and Beta) are severe anemias that are inherited from the individual’s biological parents and is characterized by “microcytic, hypochromic, and short-lived RBCs [that cause] defective hemoglobin synthesis” (Mahan, Stump, & Raymond, 2012, p. 740). Populations are risk include both sexes, most often among Italian, Greek, Middle Eastern, Southern Asian, and Africans (“What Are Thalassemias?” 2013). Iron is absorbed more readily and overconsumption of this mineral may lead to problems with the heart, liver, and endocrine glands. The gravity of gene alteration determines the gravity of the condition, and some with severe cases require blood transfusions to stay alive. Blood tests are used for diagnosis during early childhood. Thalassemia is not curable.

  1. Describe the Signs/Symptoms for each type of Anemia and explain why the s/s occur.
    1. Megaloblastic

As with most anemia, fatigue and lack of energy are among the first signs due to lack of oxygen carried by reduced RBCs. Some notable signs and symptoms of a persons with megaloblastic anemia is a smooth and shiny tongue and an abnormal Pap smear which may be misread as precancerous (Uthman, 1998, p. 62). Some people with megaloblastic anemia may not show any signs or symptoms other than altered blood work. Extreme symptoms affect neurological and sensory systems; those affected may feel sensations of “pins-and-needles,” in their extremities. Folic acid is a key ingredient in the spinal cord and a deficiency and related anemia can cause a host of problems therein. With a few important exceptions, the clinical presentation of folate deficiency parallels that of cobalamin deficiency (Pearson, 2008, p. 149).

    1. Pernicious

Since the body stores several years worth of vitamin B12, pernicious anemia could manifest within the body without any signs or symptoms for an extensive period of time. Misdiagnosis can be detrimental to the patient’s health causing folic acid to “mask: the vitamin B12 deficiency (Mahan, Stump, & Raymond, 2012, p. 736). Permanent damage can include numbness and tingling of the extremities, lack of positional relevance, poor coordination, lack of memory, and many other central nervous issues.

    1. Microcytic

Microcytic anemia is the final stage of chronic iron-deficiency. At this point, the patient may exhibit signs including fatigue and diminished physical capacity due to the low levels of oxygen transport in the blood. Unusual conditions such as pica, anorexia, and pagophagia, koilonychias or spoon-shaped nails, slow and abnormal cognitive development from reduced oxygen and the body attempting to supplement iron (Mahan, Stump, & Raymond, 2012, p. 727). Other symptoms may include susceptibility to infection, a weakened immune system, increased risk of contracting lead poisoning, and even fatality (Whitney & Rolfes, 2005, p. 392).

    1. Sickle cell anemia

Signs and symptoms of sickle cell anemia include painful episodes, vulnerability to infection, anemia, organ damage, and gallstones (Bloom, 1995, p. 50). These manifest most commonly in the abdomen but also can be in the skin and other areas. Other symptoms include dehydration and inadequate oxygen, in addition to extreme abdominal and joint pain (Whitney & Rolfes, 2005, p. 187). Since blood is transported to every part of your body there are problems linked to sickle cell anemia in virtually every part of the patient’s system.

    1. Thalassemia

Thalassemia has different signs and symptoms based on how many genes are altered and how severely they are affected (Mahan, Stump, & Raymond, 2012, p. 740). People who carry the thalassemia trait may have anywhere from no symptoms to severe symptoms. Severe thalassemia can cause pale skin, poor appetite, dark urine (break down of RBCs), jaundice, facial bone issues, and enlarged organs (”What Are Thalassemias?”, 2013).

  1. Explain in detail a minimum of four factors that affect iron absorption and utilization (provide answer in the space provided below).

The dietary mineral iron comes in two forms: Heme and non-heme. Heme is predominately found in hemoglobin from animals and non-heme is found in plant sources. Common dietary sources: meat, especially organ meats such as liver; clams and oysters; peas, beans, nuts, seeds, green leafy vegetables, fruits, grains (Levy, 2001, p. 139). Iron absorption can be inhibited by foods such as unleavened bread, soybeans, and some vegetable fibers. Coffees and teas containing caffeine may affect the absorption of iron up to 50%. Taking vitamin C and iron together helps the body absorb the iron (Medline Plus: Iron, 2013).

Review the SH medical record and answer the following questions.

  1. Identify and explain a minimum of five risk factors in her medical, nutritional and lifestyle history that associated with poor pregnancy outcomes.  (Please research and provide references to support your answers)

SH is a smoker, which may pose a significant amount of risk to her baby during this pregnancy, as well as to herself knowing her family’s history of CVD. With this alone, she should take greater initiative in beginning a smoking cessation program, for her and her unborn child’s health. Since she does not take her pre-natal vitamins accordingly, this may lead to birth defects and retard the proper development of the fetus. Her baby could develop neural tube defects or other conditions due to the deficiencies like that of folate (Whitney & Rolfes, 2005). SH’s daily intake of coffee with her meals may be contributing to iron malabsorption, as well as her “picky” food preferences coupled with her known lab values: RBC: 3.8 (L); HCT: 33 (L); and MCV: 72 (L), may be indicating iron-deficiency anemia. Taking iron supplements with coffee or tea can reduce the amount of iron the body absorbs. These beverages can even reduce the amount of iron the body absorbs from food. (MedLine Plus: Iron, 2013).

  1. In your assessment, what are the signs and symptoms of SH that are consistent with her diagnosis of iron deficiency anemia? (Please research and provide references to support your answers)

SH has an appearance of pale skin, face, and eyes and also states that she is much more tired with this pregnancy. She also describes being short of breath, but states it feels like it has started earlier with this pregnancy. Laboratory test are used to confirm of iron deficiency anemia. Transferrin and TIBC [total iron binding capacity] represent the same thing, and both are expected to become elevated in iron deficiency (Uthman, 1998, p. 42).

Her lab work also sheds a light into some to the signs/symptoms SH has been displaying during her pregnancy:

Transferrin: 410(H)

TIBC: 172 (H)

RBC: 3.8 (L)

HGB: 9.1 (L)

HCT: 33 (L)

MCV: 72 (L)

MCH: 23 (L)

MCHC: 28 (L)

RDW: 22 (L)

Calculations from her 24-hour recall, also suggest in addition to iron-deficiency, she is also not consuming enough calories for her pregnancy.

AM: 2 c. Frosted Flakes, ½ c. whole milk, and black coffee (377 kcal)

Lunch: Hot dog on bun, ½ c. macaroni and cheese (452 kcal)

Dinner: 3 oz. Salisbury steak, 1 c. green beans, 1 roll, 1 c. black coffee (349 kcal)

  1. Calculate her energy, fluid and protein requirements (show calculations for full credit).

Age: 31

Gender: Female

Height: 5’5”; 165.1 cm

Weight:  Pre-pregnancy: 135 lbs.; 61.36 kg

Estimated energy needs:

RMR = (10 x wt.) + (6.25 x ht.) – (5 x age) -161

= (10 x 61.36) + (6.25 x 165.1) – (5 x 31) -161

= (613.6)+ (1031.88) – (155) -161

=  1329.48 ~ 1329 kcal

EER = RMR x (activity factor or injury factor)

= 1329 x (1–1.39) + 340 kcal for 2nd trimester

= 1329 – 1847 kcal + 340 kcal for 2nd trimester

= 1669 – 2187 kcal

Estimated fluid needs:

1 mL fluid/kcal: 1669 – 2187 mL fluid/kcal

Estimated protein needs:

0.8 – 1.0 g/kg body wt.

= 61.36 kg (0.8 – 1.0 g)

= 49.10 – 61.36 g/kg + 25 g due to pregnancy

= 74.10 – 86.36 g/kg body wt.

SH

Age: 31 Gender: Female

ASSESSMENT

31 y.o., WF, c/o abdominal pain and bleeding after falling on ice when retrieving mail, concern of premature labor.

Current Dx: Microcytic, hypochromic anemia, 2 degrees to iron deficiency

PMH: Two previous pregnancies delivered at 38 and 37 weeks, respectively. No other contributory history. Pt. states that she is much more tired with this pregnancy but has related it to having two small children. She also describes being short of breath, which is common with her pregnancies, but states it feels like it has started earlier with this pregnancy.

Family Hx: Mother, cancer; Father, heart problems, HBP; Maternal Grandmother, Arthritis

Medications: Prenatal vitamins

Height: 5’5” Weight:  Pre-pregnancy: 135 lbs.; Pregnancy: 145 lbs. BMI: 22.5

IBW: range: 125 lbs. UBW: 135 lbs. (gained 15-18 lbs. in previous pregnancies)

%IBW/UBW: 116%

Nutrition-related labs: Transferrin: 410(H); TIBC: 172 (H); RBC: 3.8 (L); HGB: 9.1 (L); HCT: 33 (L); MCV: 72 (L); MCH: 23 (L); MCHC: 28 (L); RDW: 22 (L)

Dietary: Picky eater

Current Diet: Regular

Appetite/Intake/Diet History: Pt. states that appetite is good right now. She suffered a lot of morning sickness during her first trimester but is better now.

Usual dietary intake:

AM: Coffee, cereal, occasionally toast

Lunch: Sandwich or soup

Dinner: Casseroles such as Hamburger Helper, hot dogs, soup; sometimes she cooks a full meal with meat and vegetables

24-hour recall (PTA):

AM: 2 c. Frosted Flakes, ½ c. whole milk, and black coffee (377 kcal)

Lunch: Hot dog on bun, ½ c. macaroni and cheese (452 kcal)

Dinner: 3 oz. Salisbury steak, 1 c. green beans, 1 roll, 1 c. black coffee (349 kcal)

Total calorie intake: 1178 kcal

Nutritional Needs:

Estimated energy needs:

EER = 1669 – 2187 kcal

Estimated fluid needs:

1 mL fluid/kcal: 1669 – 2187 mL fluid/kcal

Estimated protein needs:

= 74.10 – 86.36 g/kg body wt.

Food allergies/Intolerances: Pt. says there are a lot of foods she doesn’t like.  Describes herself as a “picky eater”.

Physical Appearance: 31 y.o. Pregnant female, in no acute distress. Skin: Pale, No edema; Sclera: Pale; PERRLA, fundi without lesions; Ears: Clear; Nose: Clear; Throat: Pharynx clear without postnasal drainage

DIAGNOSIS

#1 Problem Inadequate energy intake (NI-1.2)

Etiology related to limited food acceptance (NI-2.9)

Signs/Symptoms as evidenced by patient eating 30% less of her estimated energy requirement during her second trimester.

# 2 Problem Altered nutrition-related laboratory values (transferrin, TIBC, RBC, HGB, HCT, MCV, MCH, MCHC, RDW) (NI-2.2)

Etiology related to inadequate mineral intake, iron (NI-5.10-1)

Signs/Symptoms as evidenced by her frequent consumption of caffeine based beverages per patient interview and 24-hour recall.

INTERVENTION

Nutrition Rx:  1700 – 2200 kcal, 75– 90 g protein and 1700 – 2200 mL fluid. No caffeinated beverages.

Goal #1:  Weight gain of 1 – 2 lbs. per week for the remainder of her pregnancy to reach the desired weight gain of 160 – 170 lbs. (25 – 35 lbs. gain).

Intervention #1: Meals and Snacks (ND-1):

Energy-modified diet (ND-1.2): Increase calorie consumption to 1700 – 2200 kcal/day.

Intervention #2: Nutrition Education (E):

Recommended modification (E-1.5): Recommend healthy food alternatives for picky food preferences.

Goal #2:  Decrease transferrin (200-400) and TIBC (65-165); Increase RBC (4-5), HGB (12-16), HCT (37-47), MCV (84-96), MCH (27-31), MCHC (31.5-36), RDW (11.6-16.5) to normal range.

Intervention #1: Meals and Snacks (ND-1):

Mineral modified diet (ND-1.2.10):  Increase intake of iron-rich or enriched foods

Intervention #2:  Supplements (ND-3):

Vitamin and Mineral Supplements (ND-3.2.4): Iron:

Bioactive Substances Management (3.3): Caffeine (decrease or eliminate)

Coordination of Nutrition Care: Referral: None.

MONITORING/EVALUATION

Monitoring: Evaluation:
1.  Weight Pt. current weight is 145 lbs., 116% UBW. Recommend weight gain of 1 – 2 lbs. per week for the remainder of her pregnancy to reach the desired weight gain of 160 – 170 lbs. (25 – 35 lbs. gain). DT recommends energy modified diet of 1700—2200 kcal/day.
Pt. encouraged monitoring weight weekly. DT provided weight log and pt. to bring weight log to next visit.
2. Total Energy Intake Pt. currently consuming approx. 1200 kcal. 24-hour recall reveals the consumption of high caffeine and low caloric intake.

DT recommended healthy food alternatives for picky food preferences.

Pt. encouraged keeping a food diary for 1 week and bringing during next visit for DT review.

3. Transferrin, TIBC, RBC, HGB, HCT, MCV, MCH, MCHC, RDW Transferrin, TIBC, RBC, HGB, HCT, MCV, MCH, MCHC, RDW are not WNL.

DT provided nutrition education on modification.

Pt. Rx’d ferrous sulfate to take TID.

DT to monitor Transferrin, TIBC, RBC, HGB, HCT, MCV, MCH, MCHC, RDW in two weeks.

Follow-Up Plan: Re-Evaluation in 2 weeks; follow-up appt. scheduled

Performed by: (Krystal Wright, DT Student, April 18, 2014)

References

Bloom, M. (1995). Understanding Sickle Cell Disease. Jackson: University Press of Mississippi.

Crohn’s & Colitis. (n.d.). CCFA: What is Crohn’s Disease. Retrieved April 19, 2014, from http://www.ccfa.org/what-are-crohns-and-colitis/what-is-crohns-disease/

Davenport J. Macrocytic anemia. Am Fam Phys. 1996;53:155-162.

Iron: MedlinePlus Supplements. (n.d.). U.S National Library of Medicine. Retrieved April 19,

2014, from http://www.nlm.nih.gov/medlineplus/druginfo/natural/912.html

Levy, T. E. (2001). Optimal Nutrition for Optimal Health. Chicago: Keats Pub.

Mahan, L.K., Escott-Stump, S., & Raymond, J.L. (2012). Krause’s Food and the Nutrition

Care Process (13th ed.). St. Louis, Missouri: Elsevier Saunders.

Pearson, H. A., & Bridges, K. R. (2008). Anemias and Other Red Cell Disorders. New York:

McGraw-Hill Medical.

Toh B-H, van Driel IR, Gleeson PA. Mechanisms of disease: pernicious anemia. NEJM.

1997;337:1441-1448.

Uthman, E. (1998). Understanding Anemia. Jackson [Miss.]: University Press of Mississippi.

What Are Thalassemias?. (n.d.). – NHLBI, NIH. Retrieved April 19, 2014, from http://www.nhlbi.nih.gov/health/health-topics/topics/thalassemia/

What Causes Pernicious Anemia?. (n.d.). – NHLBI, NIH. Retrieved April 19, 2014, from

https://www.nhlbi.nih.gov/health/health-topics/topics/prnanmia/causes.html

Whitney, E., & Rolfes, S.R. (2005). Understanding Nutrition (10th ed.). Belmont, CA: Thomson

Wadworth.