anemia case study for nursing students

Learn about the nursing care management of patients with anemia .

Table of Contents

What is anemia, classification, hypoproliferative anemia, hemolytic anemia, clinical manifestations, complications, assessment and diagnostic findings, medical management, nursing assessment, planning & goals, nursing interventions, discharge and home care guidelines, documentation guidelines.

Anemia is a condition that is slowly rising in cases across all countries. Every age and every stage can be affected by anemia, and though others may consider this as a simple condition, it could blow out of proportion if left untreated.

• Anemia is a condition in which the hemoglobin concentration is lower than normal.
• Anemia reflects the presence of fever than the normal number of erythrocytes within the circulation.
• Anemia is not a specific disease state but an underlying disorder and the most common hematologic condition.

A physiologic approach classifies anemia according to whether the deficiency in erythrocytes is caused by a defect in their production, by their destruction, or by their loss.

• Hypoproliferative anemias . In hypoproliferative anemias, the marrow cannot produce adequate numbers of erythrocytes.
• Hemolytic anemias . There is premature destruction of erythrocytes that results in the liberation of hemoglobin from the erythrocytes into the plasma ; the released hemoglobin is then converted into bilirubin , therefore bilirubin concentration rises.
• Bleeding anemias . Bleeding anemias are caused by the loss of erythrocytes in the body.

Pathophysiology

The pathophysiology of anemias is drawn according to the cause of the disease.

• Decreased erythrocyte production . There is decreased erythrocyte production, reflected by an inappropriately normal or low reticulocyte count .
• Marrow damage . As a result of marrow damage, inadequate production of erythrocyte occurs due to the medications or chemicals or from a lack of factors.
• Premature destruction . Premature destruction of erythrocytes results in the liberation of hemoglobin from the erythrocytes into the plasma.
• Conversion . The released hemoglobin is converted in large part to bilirubin, resulting in high concentration of bilirubin.
• Erythropoietin production . The increased erythrocyte destruction leads to tissue hypoxia which stimulates erythropoietin production.
• Increased reticulocytes . This increased production is reflected in an increased reticulocyte count as the bone marrow responds to the loss of erythrocytes.
• Hemolysis . Hemolysis is the end result, which can result from an abnormality within the erythrocyte itself or within the plasma, or from direct injury to the erythrocyte within the circulation.

It is usually possible to determine whether the presence of anemia is caused by destruction or inadequate production of erythrocytes on the basis of the following factors.

• Response . The marrow’s response to decreased erythrocytes as evidenced by an increased reticulocyte count in the circulation blood .
• Proliferation . The degree to which young erythrocytes proliferate in the bone marrow and the manner in which they mature as observed in the bone marrow biopsy .
• Destruction . The presence or absence of end products of erythrocyte destruction within the circulation.

In general, the more rapidly the anemia develops, the more aggressive is its symptoms.

• Decreased hemoglobin . A patient with anemia has hemoglobin levels between 9 to 11 g/dL.
• Fatigue . Fatigue occurs because there is inadequate oxygen levels in the tissues that should have been carried by hemoglobin.
• Tachycardia . The heart compensates for the decrease in oxygen by pumping out more blood so it can reach peripheral tissues in the body.
• Dyspnea . Difficulty of breathing occurs because of the decreased concentrations of oxygen in the blood.
• With decreased hemoglobin that serves as the pigment in the red blood cells, the patient may become pale because of the lack or decrease in the pigment that is hemoglobin.

To prevent anemia, lifestyle modifications must be made.

• Diet rich in iron . Ingestion of iron-rich foods could help prevent anemia because it adds to the hemoglobin in the body.
• Iron supplements . Iron supplements can also be taken to increase the hemoglobin levels in the body.

Anemia has general complications and this includes:

• Heart failure . As the heart compensates by pumping faster than the normal rate, the heart muscles gradually weaken until the muscles wear out and the heart fails to function.
• Paresthesias . Paresthesias develop when the muscles do not have enough oxygen delivered to them.
• Delirium . Insufficient oxygen in the brain results in delirium and is considered a fatal complication of anemia.

A number of hematologic studies are performed to determine the type and cause of anemia.

• Blood studies . In an initial evaluation , the hemoglobin, hematocrit, reticulocyte count, and RBC indices, particularly the mean corpuscular volume and red cell distribution width are taken to assess for the presence of anemia.
• Iron studies . Serum iron level, total iron binding capacity, percent saturation, and ferritin, as well as serum vitamin B12 and folate levels, are all useful in diagnosing anemia.
• CBC values . The remaining CBC values are useful in determining whether the anemia is an isolated problem or part of another hematologic condition.

Management of anemia is directed towards correcting or controlling the cause of anemia.

• Nutritional supplements . Use of nutritional supplements should be appropriately taught to the patient and the family because too much intake cannot improve anemia.
• Blood transfusion . Patients with acute blood loss or severe hemolysis may have decreased tissue perfusion from decreased blood volume or reduced circulating erythrocytes, so transfusion of blood would be necessary.
• Intravenous fluids . Intravenous fluids replace the lost volumes of blood or electrolytes to restore them to normal levels.

Nursing Management

The management of anemia by nurses should be accurate and appropriate so that objectives and goals would be achieved.

The assessment of anemia involves:

• Health history and physical exam . Both provide important data about the type of anemia involved, the extent and type of symptoms it produces, and the impact of those symptoms on the patient’s life.
• Medication history . Some medications can depress bone marrow activity, induce hemolysis, or interfere with folate metabolism.
• History of alcohol intake . An accurate history of alcohol intake including the amount and duration should be obtained.
• Family history . Assessment of family history is important because certain anemias are inherited.
• Athletic endeavors . Assess if the patient has any athletic endeavor because extreme exercise can decrease erythropoiesis and erythrocyte survival.
• Nutritional assessment . Assessing the nutritional status and habits is important because it may indicate deficiencies in essential nutrients such as iron, vitamin B12, and folic acid.

Based on the assessment data, major nursing diagnosis for patients with anemia include:

• Fatigue related to decreased hemoglobin and diminished oxygen-carrying capacity of the blood.
• Altered nutrition , less than body requirements , related to inadequate intake of essential nutrients.
• Altered tissue perfusion related to insufficient hemoglobin and hematocrit.

The major goals for a patient with anemia include:

• Decreased fatigue
• Attainment or maintenance of adequate nutrition.
• Maintenance of adequate tissue perfusion .
• Compliance with prescribed therapy.
• Absence of complications.

Nursing interventions are based on the data assessed by the nurse and on the symptoms that the patient manifests.

To manage fatigue :

• Prioritize activities . Assist the patient in prioritizing activities and establishing balance between activity and rest that would be acceptable to the patient.
• Exercise and physical activity . Patients with chronic anemia need to maintain some physical activity and exercise to prevent the deconditioning that results from inactivity.

To maintain adequate nutrition:

• Diet . The nurse should encourage a healthy diet that is packed with essential nutrients.
• Alcohol intake . The nurse should inform the patient that alcohol interferes with the utilization of essential nutrients and should advise the patient to avoid or limit his or her intake of alcoholic beverages.
• Dietary teaching . Sessions should be individualized and involve the family members and include cultural aspects related to food preference and preparation.

To maintain adequate perfusion:

• Blood transfusion monitoring . The nurse should monitor the patient’s vital signs and pulse oximeter readings closely.

To promote compliance with prescribed therapy:

• Enhance compliance . The nurse should assist the patient to develop ways to incorporate the therapeutic plan into everyday activities.
• Medication intake . Patients receiving high-dose corticosteroids may need assistance to obtain needed insurance coverage or to explore alternative ways to obtain these medications.

Included in the expected patient outcomes are the following:

• Reports less fatigue .
• Attains and maintains adequate nutrition.
• Maintains adequate perfusion.

Health education is the main focus during discharge and for the home care.

• Instruct the patient to consume iron-rich foods to help build-up hemoglobin stores.
• Iron supplements. Enforce strict compliance in taking iron supplements as prescribed by the physician.
• Follow-up. Stress the need for regular medical and laboratory follow-up to evaluate disease progression and response to therapies.

The data to be documented consists the following:

• Baseline and subsequent assessment findings to include signs and symptoms.
• Individual cultural or religious restrictions and personal preferences.
• Plan of care and persons involved.
• Teaching plan.
• Client’s responses to teachings, interventions, and actions performed.
• Attainment or progress toward desired outcome.
• Long-term needs, and who is responsible for actions to be taken.

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Anemia in the Elderly

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#99084: Anemia in the Elderly

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CASE STUDY 1

Patient H is a White woman, 89 years of age, who resides in a skilled nursing facility. She is being evaluated due to an Hgb level of 8.1 g/dL. She is ambulatory with a rolling walker, generally alert, and oriented with some mild cognitive impairment. She is compliant with medical treatments and takes medications as prescribed. Her medical history is positive for congestive heart failure, chronic obstructive pulmonary disease (COPD), chronic kidney disease, and osteoarthritis. She is oxygen dependent on 2 L/minute per nasal cannula. She is bright and outgoing and verbalizes multiple vague physical complaints.

During her last hospitalization, one year ago for pneumonia, the nephrologist and pulmonologist told Patient H there was not much else that could be done for her. Despite the poor prognosis, her multiple medical conditions stabilized and she completed a rehabilitation program. She enjoys participating in activities and has developed friendships with some other residents. Over the past year, she has been treated for multiple infections, including bronchitis and multiple urinary tract infections.

Patient H's chief complaint is of feeling tired and short of breath at times. She also complains of arthritic pains in her neck and hands. Review of systems is notable for hearing loss, dentures, glasses, and dyspnea, mostly with exertion. She has occasional palpitations of the heart and orthopnea at times. Her bowel movements are regular, and she has not noticed any blood in the stool. She has 1+ chronic edema of the legs, which is about usual for her. She has not had a mammogram for five years, and she has not had a dual energy x-ray absorptiometry scan, colonoscopy, or other preventive care recently.

Patient H's record indicates an allergy to sulfa drugs and penicillin. She also has completed advance directives (a do not resuscitate order and a living will). She is taking the following medications:

Amlodipine besylate (Norvasc): 5 mg/day

Calcium carbonate (OsCal) with vitamin D twice daily

Polyethylene glycol powder (Miralax): 17 g in 8 oz liquid daily

Furosemide (Lasix): 40 mg/day

Escitalopram (Lexapro): 20 mg/day

Prednisone: 10 mg/day

Omeprazole (Prilosec): 20 mg/day

Cinacalcet (Sensipar): 30 mg/day

Simvastatin (Zocor): 20 mg at bedtime

Tiotropium oral inhalation (Spiriva): 1 cap per inhalation device daily

Vitamin B12: 1,000 mcg twice daily

Enteric-coated aspirin: 81 g/day

Upon physical examination, Patient H appears well-nourished and groomed. She is mildly short of breath at rest but in no apparent pain or distress. She is 5 feet 6 inches tall and weighs 156 pounds. Her vital signs indicate a blood pressure of 132/84 mm Hg; pulse 72 beats/minute; temperature 97.4 degrees F; respirations 20 breaths/minute; and oxygen saturation 94% on 2 L/minute. Her oropharynx is clear, and her neck is supple. There is no lymphadenopathy. The patient is hard of hearing and wears glasses for distance and reading.

Patient H's heart rate is slightly irregular, with a soft systolic ejection murmur. Evaluation of her lungs indicates diminished breath sounds in the bases with no adventitious sounds. The abdomen is soft and non-tender, with active bowel sounds and no signs of hepatosplenomegaly. As noted, Patient H has 1+ pitting chronic edema and vascular changes to lower extremities. There are no active skin lesions. Neurologic assessment shows no focal deficit. Extremity strength is rated 4 out of 5. A mini-mental status exam is administered, and the patient scores 22/30, indicating mild cognitive impairment.

Blood is drawn and sent to the laboratory for CBC and a basic metabolic panel. The results are:

Leukocytes: 5,700 cells/mcL

RBC: 3.02 million cells/mcL

Hgb: 8.1 g/dL

MCH: 26.5 Hgb/cell

RDW-CV: 15.8%

Platelets: 150,000 cells/mcL

Glucose: 82 mg/dL

Blood urea nitrogen (BUN): 34 mg/dL

Creatinine: 1.4 mg/dL

GFR: 38 mL/minute/1.73 m2

Patient H is in no apparent distress at present, but she appears to have anemia, as evidenced by the low Hgb. She has chronic kidney disease (stage 3), which may be contributing to the anemia. Further laboratory evaluation is necessary to determine the etiology of the anemia and to determine if specialty referral to gastroenterologist or hematologist is necessary. The clinician orders an iron profile, vitamin B12 and folate levels, reticulocyte count, and stool for occult blood. The results of this testing are:

Vitamin B12: 1,996 pg/mL

Folate: 9.9 mcM

Ferritin: 20 ng/mL

Serum iron: 26 mcg/dL

Unsaturated iron binding capacity: 216 mcg/dL

Total iron binding capacity: 242 mcg/dL

Transferrin saturation: 11%

Reticulocyte count: 1%

Stool for occult blood: Negative (three samples)

Vitamin B12 is a water-soluble vitamin that is excreted in urine, so a high level is generally not significant. The folate level is sufficient, while the ferritin level is considered low-to-normal. The iron profile shows a low level of iron in the blood; this may be caused by gastrointestinal bleeding or by inadequate absorption of iron by the body. Patient H has medical conditions that can cause elevated cytokines, which would interfere with iron absorption. If her ferritin level was high, which it is not, it would suggest AI/ACD. Therefore, the patient appears to have anemia secondary to chronic kidney disease and possibly inadequate iron absorption and processing.

Prior to initiating treatment with an ESA, the patient is evaluated for a history of cancer, as these agents may cause progression/recurrence of cancer. Before writing the prescription for darbepoetin alfa, the clinician signs the ESA APPRISE Oncology Patient and Healthcare Professional Acknowledgement Form to document discussing the risks associated with darbepoetin alfa with the patient. The lowest dose that will prevent blood transfusion is prescribed.

The multidisciplinary team works with Patient H to develop a treatment plan. It is determined that treating the anemia will improve the patient's quality of life. The patient is prescribed ferrous sulfate 325 mg twice daily. Because vitamin C facilitates iron absorption, the iron can be given with a glass of orange juice or other citrus juice (not grapefruit). Iron must not be given with calcium, milk products, and certain medications as they can interfere with absorption. The patient should be monitored for the development of constipation and the need for stool softeners. In addition, darbepoetin alfa 40 mcg is prescribed, to be administered subcutaneously every week. This requires significant monitoring. Hgb and HCT should be measured on the day patient is to receive the injection, and the drug should be held if the Hgb is greater than 11.5 g/dL. If a current Hgb level is unavailable, the drug should not be given.

Blood pressure should be measured twice daily after treatment with darbepoetin alfa is initiated. Staff must also monitor for symptoms of a deep vein thrombosis and pulmonary embolus (e.g., unilateral edema, cough, and/or hemoptysis). Daily exercise is encouraged to help reduce the risk of a blood clot.

After one month, Patient H has received darbepoetin alfa weekly for four weeks. She is also taking the ferrous sulfate and a stool softener. The review of systems is unchanged from the previous evaluation. The physical examination is also unchanged aside from a 1-pound weight loss. No new complaints or problems are reported. A review of the patient's vital signs shows a blood pressure of 130/80 mm Hg; pulse 78 beats/minute; temperature 97.8 degrees F; and oxygen saturation 97 on 2 L/minute. Her Hgb levels over the last month have improved:

Week 1: 8.4 g/dL

Week 2: 9.2 g/dL

Week 3: 9.6 g/dL

Week 4: 10.1 g/dL

No side effects from darbepoetin alfa have been observed. Patient H's blood pressure remains stable, with no signs or symptoms of a blood clot.

The clinician orders the weekly monitoring of Hgb and HCT to continue with the darbepoetin alfa held if the Hgb is greater than 11.5 g/dL. If the medication is held more than once, the clinician will re-evaluate the dosage and frequency. The patient may only need the injection once or twice a month after the anemia is stabilized. The clinician also reduces the patient's vitamin B12 supplement to daily (rather than twice daily) and reduces her prednisone dose to 5 mg/day.

Patient H's initial complaint was of shortness of breath and fatigue. These symptoms may have been related to the anemia or may have been a chronic complaint secondary to her congestive heart failure and COPD. The decreased hematocrit level is likely contributing to the patient's symptomatic heart failure. By exploring her condition further, it was determined that treating the anemia might improve the patient's quality of life and prevent the necessity for more extreme interventions (e.g., blood transfusion). Patient H was informed of the potential side effects of darbepoetin alfa and agreed to take it to prevent transfer to the hospital for blood transfusion.

The patient's condition was monitored closely, with weekly blood draws for Hgb. Her blood pressure remained stable, and no signs of complications were detected. Her shortness of breath and fatigue improved as the treatment progressed and her Hgb level rose above 10 g/dL. This allowed her to be more active.

For patients with terminal or end-stage conditions, treatment of anemia can restore or preserve their quality of life. Treating problems that could potentially cause suffering, while avoiding futile care, is the goal for patients with a life-limiting condition. Anemia affects the quality of life in elders by causing fatigue, poor endurance, and shortness of breath, and alleviating these symptoms can allow for more activity and comfort.

CASE STUDY 2

Patient P is a White man, 92 years of age, who resides in an assisted living facility. He uses a motorized scooter for mobility but can ambulate short distances with his rolling walker. He requires assistance with medication administration and attends community meals three times a day. His daughter visits once a week and assists with laundry and transports to medical appointments.

Patient P is brought to the primary care clinic by his daughter. She states that he is very fatigued and is not performing his usual daily tasks. He sleeps more than is usual and must be coaxed to attend the community meals. At times, he has refused to take medications that the staff attempt to administer. The patient minimizes his symptoms saying, "What do you expect? I'm 92 years old." Patient P's medical history is positive for Parkinson disease, hypertension, COPD, osteoporosis, compression fracture to the lumbosacral spine, and weight loss. He is a widower and reports no tobacco use and rarely drinking beer or wine. His chief presenting complaints are fatigue, shortness of breath, chronic back and leg pain, and poor appetite.

On review of systems, the patient is noted to be hard of hearing and wearing a hearing aid. Vision is adequate with correction. He wears dentures and denies pain or difficulty with mastication. He has difficulty swallowing large pills, and his caregivers crush his medications. He states his appetite is not good; he has lost 15 pounds over the last year. Patient P denies chest pain, but complains of shortness of breath. This occurs when he exerts himself and often when he lays down. He has a regular bowel movement every one to two days and denies nausea, vomiting, or diarrhea. He has not had dyspepsia but does state he does not seem to be able to eat as much as he used to (early satiety). He complains of nonradiating pain in his lower back. All other review of systems is non-contributory. Patient P has previously been tried on antiparkinsonian medications and osteoporosis medications that were discontinued due to unacceptable side effects. He is currently taking the following medications:

Atenolol (Tenormin): 25 mg twice daily

Vitamin D3: 1,000 units/day

Calcium carbonate: 500 mg three times every day

Vitamin B12: 1,000 mcg/day

Amlodipine (Norvasc): 10 mg/day

Omeprazole: 20 mg/day

Multivitamin daily

Acetaminophen (Tylenol): 650 mg three times daily routinely

Stool softener twice daily

Tramadol (Ultram): 50 mg every six hours as needed

Upon physical examination, Patient P appears frail but well groomed; he is in no apparent distress. He is 5 feet 5 inches tall and weighs 134 pounds. His vital signs indicate a blood pressure of 110/64 mm Hg; pulse 82 beats/minute (regular rate and rhythm); temperature 97.8 degrees F; respirations 22 breaths/minute; and oxygen saturation 91% on room air.

As noted, the patient is hard of hearing with hearing aid and wears glasses. There is no evidence of lymphadenopathy or carotid bruit. His oropharynx is clear. His lungs are clear to auscultations, with diminished air flow in lung bases. The abdomen is soft and non-tender, not distended, with bowel sounds active in four quadrants. There is no hepatosplenomegaly. Extremities are clear of edema. Vascular changes are noted on both legs, and the toenails are thickened. The patient displays dry, flaky skin of lower extremities. Tenderness is noted over the lumbar spine with palpation. Disuse atrophy is noted to the extremities. Chronic skin lesions are also present, with actinic keratoses on the nose and forehead. Neurologic assessment reveals fine resting tremor of both hands and flat affect. Strength is equal bilaterally with strong hand grasps. Gait and balance are unsteady.

The clinician orders Patient P's medical records and diagnostics from previous care providers. She also requests a CBC with differential, a complete metabolic profile, and thyroid studies. A home health care evaluation is also recommended to determine if rehabilitation services would be appropriate. Patient P's laboratory studies indicate:

Leukocytes: 5,400 cells/mcL

RBC: 2.95 million cells/mcL

Hgb: 8.7 g/dL

MCH: 29.4 Hgb/cell

MCHC: 33.3%

RDW-CV: 13.7%

Platelets: 289,000 cells/mcL

Glucose: 77 mg/dL

BUN: 20 mg/dL

Sodium: 139 mEq/L

Potassium: 4.5 mEq/L

Chloride: 104 mmol/L

Carbon dioxide: 27 mmol/L

Creatinine: 0.9 mg/dL

Calcium: 8.8 mg/dL

GFR: Greater than 60 mL/minute/1.73 m2

Thyroid-stimulating hormone: 2.88 mIU/L

The low RBC, Hgb, and HCT indicate that the patient has a normocytic, normochromic anemia. However, blood-loss anemia is not ruled out by lack of microcytosis. If the blood loss is recent, changes to the cells may not yet be evident. The RDW-CV is normal, which may indicate a lack of erythropoietic response. Further laboratory evaluation is indicated.

The clinician requests an iron profile, ferritin level, folate level, vitamin B12 level, reticulocyte count, and stool for occult blood. The results of this testing are:

Vitamin B12: 1,006 pg/mL

Folate: 17.2 mcM

Ferritin: 246 ng/mL

Serum iron: 38 mcg/dL

Total iron binding capacity: 197 mcg/dL

Transferrin saturation: 27%

Reticulocyte count: 1.2%

Stool for occult blood: Negative on two samples, mildly positive on third sample

These findings indicate the patient is not deficient in vitamin B12 or folate. The serum iron is low while the ferritin level is high, suggesting adequate iron stores that are not being utilized by the body. This is a diagnostic indicator of anemia of chronic inflammation. The total iron binding capacity is low, showing that the blood's ability to bind transferrin with iron is reduced. Patient P has signs of a "mixed" anemia, the result of both ACI and gastrointestinal blood loss. Elderly patients often have more than one etiology contributing to the anemia, and all the possible causes should be thoroughly evaluated.

One of the stools for occult blood is positive, which may be representative of intermittent gastrointestinal bleeding. The clinician refers the patient to a gastroenterologist for further diagnostic evaluation. An endoscopy and colonoscopy should be performed if the patient and healthcare surrogate are willing. He is also prescribed a 5% lidocaine patch to be applied to his lower back in the morning and to be removed at bedtime.

Patient P visits a gastroenterologist, who performs an endoscopy and a colonoscopy. He is found to have several polyps in the large intestine, which are removed and biopsied during the colonoscopy. He tolerates the procedures well and has no adverse effects. The polyps are found to be benign.

One month later, Patient P returns to the clinic for follow-up. His review of systems is unchanged, although he reports improvement in his lower back pain. His vital signs are all stable. A CBC is completed to monitor the anemia, and the results are:

Leukocytes: 5,600 cells/mcL

RBC: 3.36 million cells/mcL

Hgb: 9.6 g/dL

MCV: 88.0 fL

MCH: 28.7 Hgb/cell

MCHC: 32.5%

RDW-CV: 14.9%

Platelets: 262,000 cells/mcL

Patient P's RBC, Hgb, and HCT have improved slightly. The RDW-CV has also increased, indicating an improved erythropoietic response. The removal of the colon polyps, which may have been causing some intermittent bleeding contributing to the anemia, appears to have improved the patient's condition. Patient P is instructed to return in one month for additional follow-up.

Patient P is a frail, elderly patient with multiple medical problems. From a primary care perspective, it is important to identify any new or existing medical problems that can be treated and improved. Elderly persons often present with multiple vague complaints that do not point to any one disorder. Laboratory evaluation is crucial to narrow down the diagnostic differential.

Because there is an upward trend in the CBC values, the necessity of a blood transfusion is reduced. However, if the anemia worsens, a hematology consult may be necessary. At 92 years of age, the patient is at risk for myelodysplasia, but if present, lower values of leukocytes, RBCs, and platelets would be expected.

While the use of an ESA might result in an improvement in elderly patients, there are multiple side effects and precautions associated with their use. For Patient P, they should be avoided unless truly necessary to prevent the need for transfusions.

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Patient Case Presentation

Patient  Overview

M.J. is a 25-year-old, African American female presenting to her PCP with complaints of fatigue, weakness, and shortness of breath with minimal activity. Her friends and family have told her she appears pale, and combined with her recent symptoms she has decided to get checked out. She also states that she has noticed her hair and fingernails becoming extremely thin and brittle, causing even more concern. The patient first started noticing these symptoms a few months ago and they have been getting progressively worse. Upon initial assessment, her mucosal membranes and conjunctivae are pale. She denies pain at this time, but describes an intermittent dry, soreness of her tongue.

Vital Signs:

Temperature – 37 C (98.8 F)

HR – 95

BP – 110/70 (83)

Lab Values:

Hgb- 7 g/dL

Serum Iron – 40 mcg/dL

Transferrin Saturation – 15%

Medical History

• Diagnosed with peptic ulcer disease at age 21 – controlled with PPI pharmacotherapy
• IUD placement 3 months ago – reports an increase in menstrual bleeding since placement

Surgical History

• No past surgical history reported

Family History

• Diagnosis of iron deficiency anemia at 24 years old during pregnancy with patient – on daily supplement
• Otherwise healthy
• Diagnosis of hypertension – controlled with diet and exercise
• No siblings

Social History

• Vegetarian – patient states she has been having weird cravings for ice cubes lately
• Living alone in an apartment close to work in a lower-income community
• Works full time at a clothing department store

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A Case of Iron Deficiency Anemia

By David F. Dean (rr)

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“Dolores Welborn,” a 28-year-old attorney, is pregnant with her first child. Lately she has been tiring easily and is often short of breath. She has also had periods of light-headedness, cramping in her legs, and a sore tongue. Students read a brief clinical history and a description of signs and symptoms, then answer a set of directed questions designed to probe the underlying anatomy, physiology, and pathology of the Dolores's condition.  In the process, they learn about the human hemolymphatic system. The case has been used in a sophomore-level course in human anatomy and physiology taught to pre-med and nursing students as well as in senior-level elective course in general physiology taken primarily by pre-med students.

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Date Posted

• The structure of hemoglobin and the role played by iron in the transport of oxygen.
• The means by which iron is transported and stored in the body.
• The incidence and causes of IDA.
• The red blood cell indices and how they are used to characterize anemia.
• How IDA is prevented and treated.

Iron deficiency anemia; hemoglobin; red blood cell indices; transport of oxygen; blood oxygen; apotransferin; transferring; ferritin

Subject Headings

EDUCATIONAL LEVEL

Undergraduate lower division, Undergraduate upper division

TOPICAL AREAS

TYPE/METHODS

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Hemolytic Anemia

Overview – In hemolytic anemia, the red blood cells are destroyed faster than the body can replace them. Hemolytic anemias are classified as intracorpuscular or extracorpuscular

• Intracorpuscular – Defects of the red blood cell (ex: sickle cell anemia and thalassemia)
• Extracorpuscular  – RBCs are damaged due to external factors (ex: red blood cell transfusion, malaria and the presence of microthrombi).

Signs/Symptoms – In addition to the general characteristics of anemia, signs and symptoms of hemolytic anemia include an enlarged spleen and/or an enlarged liver. Patients with very severe or untreated disease may develop heart failure, arrhythmias or an enlarged heart. 

Hemolytic anemia can come on quickly, which causes a rapid decrease in hemoglobin with an increased reticulocyte count (reticulocytes are immature red blood cells.)  The patient may also have dark urine or blood-tinged urine due to hemolysis and circulating free hemoglobin. Additionally the circulating free hemoglobin from destroyed cells can cause acute renal failure, jaundice, thrombus and disseminated intravascular coagulation. Note that mild cases may have no symptoms. 

Sickle cell anemia specifically can cause an  incredibly painful event called vaso-occlusive crisis, making pain a distinguishing symptom of this condition.

Causes/Patho – Hemolytic anemia occurs when RBCs are broken down in the spleen or bloodstream faster than they can be replaced by the body. Hemolysis stimulates the body to produce erythropoietin which, in turn, leads to the production of new RBCs. These new RBCs (reticulocytes) are immature and don’t function optimally.  

While some types of hemolytic anemia are inherited, such as sickle cell anemia and thalassemia, it can also be acquired. Some acquired causes include: 

• Viral and bacterial infections (ex: hepatitis, cytomegalovirus, Epstein-Barr, malaria)
• Mechanical heart valves can damage RBCs leading to hemolysis
• Autoimmune conditions including rheumatoid arthritis and systemic lupus erythematosus
• Bone marrow disorders and blood cancers
• Blood transfusion reaction
• Medications – the most common are cephalosporins (a class of antibiotic). Other culprit medications include NSAIDs, levodopa, quinidine and levofloxacin. 
• Some tumors 
• Venomous snake bites

As for the inherited conditions, thalassemia is a group of inherited disorders that affect the production of hemoglobin. Sickle cell anemia is another form of inherited hemolytic anemia. In sickle cell anemia, the RBCs are rigid and malformed so they don’t flow easily through microvasculature. These cells become lodged in the vessels in a very painful condition known as a vaso-occlusive crisis.

Treatment – As with the other anemias, treatment will focus on the underlying cause. Blood transfusions may be necessary and some patients will require surgical removal of the spleen, which puts them at high risk for infection. 

Specific treatments for thalassemia include blood transfusions, chelation therapy and bone marrow transplant. Chelation therapy may be needed to remove excess iron which can build up with frequent blood transfusions.

Specific treatments for sickle cell anemia include blood transfusions, pain medication during crisis, and medications that are aimed at decreasing hemolysis and the frequency of vaso-occlusive crisis. These include:

• Hydroyxyurea (Hydrea) 
• Voxelotor (Oxbryta) 
• L-glutamine (Endari) 
• Crizanlizumab (Adakveo) 

I hope this quick overview of the different types of anemia helps you understand this complex condition better so you can feel confident in school and at the bedside! Looking for more hematology topics? Explore them here!

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References:

American Society of Hematology. (n.d.). Anemia . https://www.hematology.org:443/education/patients/anemia

Auerbach, M. (2022a, April 14). Treatment of iron deficiency anemia in adults . UpToDate. https://www.uptodate.com/contents/treatment-of-iron-deficiency-anemia-in-adults?search=iron%20deficiency%20anemia&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2

Auerbach, M. (2022b, April 22). Causes and diagnosis of iron deficiency and iron deficiency anemia in adults . UpToDate. https://www.uptodate.com/contents/causes-and-diagnosis-of-iron-deficiency-and-iron-deficiency-anemia-in-adults?search=iron%20deficiency%20anemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

Bajwa, H., & Basit, H. (2022). Thalassemia. In StatPearls . StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK545151/

Baldwin, C., Pandey, J., & Olarewaju, O. (2022). Hemolytic Anemia. In StatPearls . StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK558904/

Brodsky, R. A. (2021, October 12). Diagnosis of hemolytic anemia in adults . UpToDate. https://www.uptodate.com/contents/diagnosis-of-hemolytic-anemia-in-adults?search=hemolytic%20anemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

Cleveland Clinic. (n.d.). Macrocytic Anemia: Causes, Symptoms, Types & Treatment . Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/23017-macrocytic-anemia

Cleveland Clinic. (2022a). Sickle Cell Anemia: Symptoms, What It Is, Causes & Treatment . Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/4579-sickle-cell-anemia

Cleveland Clinic. (2022b, February 7). Pernicious Anemia: Definition, Symptoms, Causes & Treatment . Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/22377-pernicious-anemia

Davis Drug Guide. (n.d.). Davis’s Drug Guide Online + App | DrugGuide.com . https://www.drugguide.com/ddo

Global Blood Therapeutics, Inc. (n.d.). Oxbryta® tablets/Oxbryta® tablets for oral suspension . Oxbryta HCP. https://hcp.oxbryta.com

Harding, M. M. (2020). Lewis’ Medical Surgical Nursing, Assessment and Management of Clinical Problems (11th ed.). Elsevier, Inc.

Johns Hopkins Medicine. (2021, August 8). Hemolytic Anemia . https://www.hopkinsmedicine.org/health/conditions-and-diseases/hemolytic-anemia

Khan, Y., & Tisman, G. (2010). Pica in iron deficiency: A case series. Journal of Medical Case Reports , 4 , 86. https://doi.org/10.1186/1752-1947-4-86

Massey, A. C. (1992). Microcytic anemia. Differential diagnosis and management of iron deficiency anemia. The Medical Clinics of North America , 76 (3), 549–566. https://doi.org/10.1016/s0025-7125(16)30339-x

Mayo Clinic. (n.d.). Thalassemia—Diagnosis and treatment—Mayo Clinic . https://www.mayoclinic.org/diseases-conditions/thalassemia/diagnosis-treatment/drc-20355001

Means Jr, R. T., & Brodsky, R. A. (2022, April 25). Diagnostic approach to anemia in adults . https://www.uptodate.com/contents/diagnostic-approach-to-anemia-in-adults?search=anemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

MedlinePlus. (n.d.). Drug-induced immune hemolytic anemia: MedlinePlus Medical Encyclopedia . https://medlineplus.gov/ency/article/000578.htm

Moffitt Cancer Center. (n.d.). Aplastic Anemia vs. Myelodysplastic Syndrome . Moffitt Cancer Center. https://moffitt.org/cancers/myelodysplastic-syndromes-mds/faqs/what-is-the-difference-between-aplastic-anemia-and-myelodysplastic-syndrome

National Heart, Lung, and Blood Institute. (n.d.). Anemia—Aplastic Anemia . https://www.nhlbi.nih.gov/health/anemia/aplastic-anemia

National Heart, Lung, and Blood Institute. (2022a, March 24). Anemia—Anemia in Pregnancy . https://www.nhlbi.nih.gov/health/anemia/pregnancy

National Heart, Lung, and Blood Institute. (2022b, March 24). Anemia—Hemolytic Anemia . https://www.nhlbi.nih.gov/health/anemia/hemolytic-anemia

National Heart, Lung, and Blood Institute. (2022c, March 24). Anemia—Iron-Deficiency Anemia . https://www.nhlbi.nih.gov/health/anemia/iron-deficiency-anemia

National Heart, Lung, and Blood Institute. (2022d, March 24). Anemia—Vitamin B12–Deficiency Anemia . https://www.nhlbi.nih.gov/health/anemia/vitamin-b12-deficiency-anemia

Olson, T. S. (2022, June 8). Aplastic anemia: Pathogenesis, clinical manifestations, and diagnosis . UpToDate. https://www.uptodate.com/contents/aplastic-anemia-pathogenesis-clinical-manifestations-and-diagnosis?search=aplastic%20anemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

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Nursing Care and Pathophysiology for Anemia

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Pathophysiology: Anemia is when there is a low red blood cell (RBC) count. This is caused b y blood loss, a decrease in red blood cell (RBC) production or increased RBC destruction.

• ↓ Amount of RBCs or hemoglobin in blood
• ↓ Capacity of blood to carry oxygen

Nursing Points

• Inadequate iron supply – 60% of anemias
• Vitamin B12 deficiency
• Lack of Intrinsic Factor
• ↓ Production of all blood cells in the bone marrow
• Sickle Cell Anemia – see Sickle Cell Anemia Lesson
• Tachycardia
• Hypotension
• ↓ Hgb, Hct, RBC levels
• Schilling test (for Pernicious anemia)
• Spoon-like nails
• Pica – craving non-food substances like ice, dirt, clay, starch.

Therapeutic Management

• Assess for occult blood
• Monitory laboratory studies (Hgb, Hct)
• Green leafy vegetables
• Administer IM via Z-track method
• Take PO Iron on an empty stomach
• Will also have ↓ WBCs

Nursing Concepts

• May require supplemental oxygen
• Monitor s/s poor oxygenation
• Assess for dyspnea
• Monitor vital signs
• Assess for chest pain
• If caused by nutritional deficiencies – provide supplements as ordered
• Educate patient on food choices

Patient Education

• Increased intake of iron or B12 containing foods
• Medication instructions for iron or B12 supplements
• Possible Neutropenic or Thrombocytopenic precautions in Aplastic Anemia
• Energy conservation techniques

Nursing Care Plan (NCP) for Anemia

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Med-surg | hematology / oncology / immunology.

The Hematology/Oncology/Immunology course combines discussion of some of the most common blood disorders, cancers, and autoimmune diseases. These three systems are intertwined because they’re all related to blood cells and immune responses. Our bodies are amazing in how these tiny  specialized cells have such powerful effects in our bodies. When any of it isn’t working, it can cause a lot of issues. We’re going to break it down for you and help you see how it all works together to keep us healthy.

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Chapter 6-1:  Approach to the Patient with Anemia - Case 1

Jeremy Smith

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Chief complaint, constructing a differential diagnosis.

• RANKING THE DIFFERENTIAL DIAGNOSIS
• MAKING A DIAGNOSIS
• CASE RESOLUTION
• FOLLOW-UP OF MRS. A
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Mrs. A is a 48-year-old white woman who has had fatigue for 2 months due to anemia.

Figure 6-1.

Diagnostic approach: anemia.

Anemia can occur in isolation, or as a consequence of a process causing pancytopenia, the reduction of all 3 cell lines (white blood cells [WBCs], platelets, and red blood cells [RBCs]). This chapter focuses on the approach to isolated anemia, although a brief list of causes of pancytopenia appears in Figure 6-1 . The first step in determining the cause of anemia is to identify the general mechanism of the anemia and organize the mechanisms using a pathophysiologic framework:

Acute blood loss: this is generally clinically obvious.

Underproduction of RBCs by the bone marrow; chronic blood loss is included in this category because it leads to iron deficiency, which ultimately results in underproduction.

Increased destruction of RBCs, called hemolysis.

Signs of acute blood loss

Hypotension

Tachycardia

Large ecchymoses

Symptoms of acute blood loss

Hematemesis

Rectal bleeding

Vaginal bleeding

After excluding acute blood loss, the next pivotal step is to distinguish underproduction from hemolysis by checking the reticulocyte count:

Low or normal reticulocyte counts are seen in underproduction anemias.

High reticulocyte counts occur when the bone marrow is responding normally to blood loss; hemolysis; or replacement of iron, vitamin B 12 , or folate.

Reticulocyte measures include:

The reticulocyte count: the percentage of circulating RBCs that are reticulocytes (normally 0.5–1.5%).

The absolute reticulocyte count; the number of reticulocytes actually circulating, normally 25,000–75,000/mcL (multiply the percentage of reticulocytes by the total number of RBCs).

The reticulocyte production index (RPI)

Corrects the reticulocyte count for the degree of anemia and for the prolonged peripheral maturation of reticulocytes that occurs in anemia.

Normally, the first 3–3.5 days of reticulocyte maturation occurs in the bone marrow and the last 24 hours in the peripheral blood.

When the bone marrow is stimulated, reticulocytes are released prematurely, leading to longer maturation times in the periphery, and larger numbers of reticulocytes are present at any given time.

For an HCT of 25%, the peripheral blood maturation time is 2 days, and for an HCT of 15%, it is 2.5 days; the value of 2 is generally used in the RPI calculation.

The normal RPI is about 1.0.

However, in patients with anemia, RPI < 2.0 indicates underproduction; RPI > 2.0 indicates hemolysis or an adequate bone marrow response to acute blood loss or replacement of iron or vitamins.

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Iron Deficiency Anemia: 47-Year-Old Male Patient Case Study

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Introduction

Important questions to help explore patient’s disease symptoms, important questions to help explore the patient’s medical history, abnormal and normal findings in the physical examination, interpretation of diagnostic findings, the disease process for iron-deficiency anemia, nursing care plan.

This paper responds to questions concerning the case study provided. It involves a 47 years old man who visited a clinic with gradual onset of dyspnea on exertion and fatigue. In addition, the patient complained of constant dyspepsia with nausea and occasional epigastric pain. The paper begins by illustrating questions which are pertinent to exploring the patient’s disease symptoms and past medical history. Moreover, it discusses the diagnostic tests carried out and shows pertinent positive and negative findings in the physical examination. This is followed by an interpretation of the findings of the diagnostic tests which in turn gives a green light to discuss the disease process related to the hemolytic system. Finally, all appropriate NANDA nursing diagnoses for anemic patients are provided.

The first step in treating the patient’s condition may involve understanding his family history, history of drug use and amount of alcohol consumed per day (Springhouse, 2006). In addition, the patient should be grilled on any pre-existing mental disorder, metabolic conditions, cardiac problems and medication regimen as well as his sleep patterns. More so, it is wise to ask the patient if he ever suffered any head injury in the past and have him describe his smoking habits. Furthermore, he should be asked to explain the condition he is complaining of (dyspepsia) in relation to meals and the effects of remedies taken. Finally, the practitioner may inquire if the patient is undergoing any stress.

The case presented may warrant a medical practitioner to ask about the patient’s critical diseases history and major hospitalizations. The caregiver should inquire about past hematologic setbacks, past surgeries and liver problems as well as breeding abnormalities (Collins, 2003).

In addition, many want to know the patient’s family history, recent medications and bleeding duration. Furthermore, it is recommended to ask if the bleeding is associated with shock and whether the patient bruises easily. Moreover, caregivers should ask about any case of petechie and renal or splenic disease. Finally, a medical officer may want to know whether the patient is allergic. This is done by considering past treatment using drugs like chloramphenicol which are known to cause allergy (Springhouse, 2006). Then, both physical and diagnostic procedures may be taken.

Physical tests carried out on the patient revealed several abnormal conditions. General physical examination indicated that the patient had a thin pale coloration and he appeared older than the stated age even though he suffered no stress. Furthermore, the patient’s sclera was pale although it lacked icterus and his mouth’s corner had signs of cheilosis. In addition, his nails were brittle and thin in appearance. Finally, abdominal and rectal tests showed the presence of moderate epigastric tenderness and guaiac positive stool. These are the physical manifestation of anemia (Coya & Lash, 2009). Nevertheless, there were some encouraging results.

The patient had a standard body temperature (37° Celsius) and a normal pulse rate (95 beats per min). In addition, respiratory rate was normal (16 breaths per minute) while the blood pressure was typical at 120/72 mmHg (Coya & Lash, 2009). The patient’s pupils were equal, round and reactive to light and his pharynx was clear and without any postnasal drainage. More encouraging results indicated that the patient suffered no cases of thyromegaly, adenopathy, or bruits.

Moreover, the client had good bilateral lung expansion and lungs were clear to auscultation. More so, the heart rate was proved to be all right although there was a grade II/VI systolic murmur at the left sternal border. Any cases of gallops, heaves or thrills were dispelled. In addition, the patient’s abdomen was non-distended and the liver span was 8cm at the midclavicular line. His prostate was healthy and he seemed to have stamina. Finally, he had normal body strength (5/5), intact sensation, normal gait, and he had deep tendon reflexes that were 2+ and symmetric throughout. After the physical tests, diagnostic procedures were carried out and their findings are interpreted below.

The patient’s hemoglobin was shown to be 8 g/dl instead of 13-18g/dl for normal men (Springhouse, 2006). This means that there was less oxygen in circulation. In addition, Mean Corpuscular Volume (MCV) was normal and this condition may exist in a normocytic anemia. Additionally, the patient’s Mean Corpuscular Hemoglobin Content (MCHC) was slightly decreased. This is associated with conditions like microcytic anemia and it is attributed to factors such as iron deficiency, chronic blood loss and thalassemia (Springhouse, 2006). Moreover, the red cell distribution width was markedly increased while the MCV was normal.

This presented possible cases of early stages of iron deficiency, vitamin B deficiency, and early folate deficiency as well as initial stages of the anemic condition. The diagnostic results also showed mixed microcytic/hypochromic and macrocytic/normochromic red blood cells. The findings can be associated with folate and iron deficiencies (Springhouse, 2006). This condition may also be responsible for normal MCV. The appearance of platelets was normal hence their function in blood clotting was not jeopardized. The further result revealed that Prothrombin Time (PT), Partial Thromboplastin Time (PTT), liver function, electrolytes, and amylase were normal.

Normal PPT meant that coagulation factors such as fibrinogen and prothrombin as well as heparin were up to standard amounts. Normal PT implied that there was good interaction of prothrombin groups V, VII, X and fibrinogen which are useful in determining amounts of oral anti-coagulants. Furthermore, serum ferritin levels were decreased and this is attributed to prolonged bleeding of the digestive tract, iron deficiency or deprived iron absorption due to abnormal intestinal conditions (Springhouse, 2006). This may ultimately lead to anemia. Moreover, the patient’s transferrin saturation was decreased and this is also associated with iron deficiency.

Decreased levels of total iron-binding capacity implied that the patient also suffered from anemia of chronic ailments. Folate and cell folate levels were decreased and this shows depletion of folate storage. More so, a bone marrow biopsy showed megaloblastic changes and low iron stores giving more clues to iron deficiency anemia as well as megaloblastic anemia (Coya & Lash, 2009). Finally, an upper endoscopy revealed a 2cm duodenal ulcer with evidence of recent but no acute hemorrhage. This could be attributed to Helicobacter pylori infection and may cause bleeding. All the findings are therefore contributing to iron deficiency anemia.

Iron deficiency anemia is an abnormal body condition whereby there are not enough erythrocytes in the blood (McCance et al, 2010). The condition is brought about by low amounts of iron which then hinder the production of hemoglobin. The rate of iron absorption in the jejunum and duodenum is very low and dietary iron may fail to supply the required amounts when such foods lack heme iron. Non-heme iron has to be converted to ferrous iron before absorption (Coya & Lash, 2009).

Iron in the blood system binds to transferrin which conveys it to erythroblast receptors and also to cells in the liver and placenta. The erythroblast mitochondria then convert iron to protoporphyrin and then to heme while transferrin is recycled (McCance et al, 2010). An iron that remains after this process is transported and stored as ferritin and hemosiderin. More iron is recycled from dying erythrocytes by transferrin.

When iron absorption is low, bone marrow stores are diminished so that no red blood cell production occurs hence anemia. Nevertheless, a major cause of this disease is blood loss due to prolonged bleeding from gastrointestinal tracts and extended intravascular hemolysis in men (Springhouse, 2006). Low levels of iron intake may also result from upper small bowel malabsorption or from gastrectomy. There are odd situations when the disease is attributed to undernutrition.

Iron deficiency anemia leads to inadequate hemoglobin levels and thus the low amount of oxygen is circulated. A decreased amount makes an individual feel exhausted, feeble and have shortness of breath as well as pale skin (McCance et al, 2010). As the disease progresses, an individual may have cheilosis and brittle nails and suffer from dysphagia. The disease can be detected through conducting Complete Blood Count (CBC) (Springhouse, 2006). The test is used to ascertain hematocrit and hemoglobin levels. Low levels are a sign of anemia. The test also assesses the amount of leukocytes, erythrocytes and blood platelets.

Unusual results signify a body disorder. Finally, the CBC investigates the MCV and MCHC which give clues to possible causes of anemia. In addition to CBC, blood smears are made to observe the shape of erythrocyte (McCance et al, 2010). Furthermore, reticulocyte count test may be conducted to assess the functionality of bone marrow. Quantity of iron in the body may be determined through testing serum ferritin and iron as well as investigating the concentration of transferrin. Moreover, red blood cell protoporphyrin tests as well as stool occult blood procedures are important in establishing an anemic condition.

Clinical manifestations of this disease include fatigue, black stool, dizziness, dyspepsia and ulcers as well as hometochezia (McCance et al, 2010). Iron deficiency anemia can be cured by first treating the root causes such as hemorrhages and then taking iron supplements like ferrous sulphate (Springhouse, 2006). The supplements may come inform of non heme iron or as heme iron. Supplements can be taken orally or through an injection depending on the patient’s reaction. Other treatments may include taking iron rich foods like fish, eggs and raisins. With such treatment, iron level should normalize within two months (Mosby, 2010). There are no associated complications although the disease may reappear. Therefore, one is advised to take regular medical check ups.

According to Doenges (2010), interpretation of all the collected data may lead to nursing diagnoses. Conditions like exhaustion and weakness, lack of breath on exertion as well as low levels of perseverance during activity are signs of ‘activity intolerance’. As such, care plan 1 in table 1 deals with this condition by determining the desired outcome on the patient so as to achieve endurance. This is achieved through appropriate nursing interventions supported by specific scientific rationales. In addition, care plan 2 in table 2 is aimed at treating malnutrition. This plan is as a result of imbalanced diet- inadequate amount nursing diagnoses which was necessitated by conditions like exhaustion and weakness while performing minor duties.

This plan is important as it aims at ensure proper health through appropriate diet. Finally, the nursing diagnoses in care plan 3 in table 3 deals with risk of infection. This is important as the patient has a lesion on the mouth which may lead to contamination. Furthermore, anemic individuals are prone to cross infections. The care plans aims at protecting the patient from such infections and ensure stability of his immunity.

Table 1. Care Plan 1.

Table 2. Care Plan 2.

Table 3. Care Plan 3.

It is wise to know the patients personal, family and medical history where anemia is suspected. This should be followed by physical and diagnostic tests like CBC which help to understand the real situation of anemic condition. The disease may be brought about by loss of blood and failure of the body to make use of iron found in meals. Its various symptoms include fatigue and loss of breath among others. Treatment is through iron supplement and dietary changes. This is achieved through proper nursing diagnoses and care plan as well as medical diagnosis.

Collins, D. (2003). Algorithmic Diagnosis of Symptom . Web.

Coya, S., & Lash, A. (2009). Pathophysiology of anemia and nursing care implications. Web.

Doenges, M., Moorhouse, M., & Murr, A. (2010). Nursing Care Plans: Guidelines for Individualizing Client Car across the Life Span . Philadelphia: F. A. Davis Company.

McCance, K.L., Huether, S.E., Brashers, V., & Rote (2010). Pathophysiology: The biologic basis for disease in adults and children (6th Ed.). Maryland Heights, MO: Elsevier Mosby. Web.

Springhouse. (2006). Professional Guide to Signs & Symptoms . (5th Ed.). Lippincott Williams & Wilkins.

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39-Year-Old Woman With an Obscure Case of Anemia

Shanique r. palmer.

* Resident in Internal Medicine, Mayo School of Graduate Medical Education, Mayo Clinic, Rochester, MN

Gita Thanarajasingam

† Medical student, Mayo Medical School, Rochester, MN

Alexandra P. Wolanskyj

‡ Adviser to fellow and Consultant in Hematology, Mayo Clinic, Rochester, MN

A 39-year-old woman was referred to our institution for evaluation of anemia. She was known to have multiple comorbidities and had a baseline hemoglobin concentration of approximately 10.5 g/dL. About 6 months before her referral, the patient began having recurrent episodes of severe anemia, with hemoglobin values as low as 3.5 g/dL. She had become transfusion-dependent and had received about 30 units of packed red blood cells (RBCs) in the preceding 3 months. The patient denied any history of easy bruisability, menorrhagia, or overt evidence of bleeding from any site. Additionally, she denied any change in the appearance or color of her urine and had no history of jaundice. There was no family history of anemia or any other hematologic disorder. As an outpatient, she had undergone an extensive evaluation at another institution, but results failed to provide an explanation for her anemia.

The patient's medical history was remarkable for severe asthma, thought to be due to Churg-Strauss syndrome. She had a tunneled central venous catheter for self-administration of intravenous corticosteroids at the earliest sign of an asthmatic exacerbation. Her other medications included bronchodilators, weekly erythropoietin injections, intravenous iron therapy, an antidepressant, and an anxiolytic.

At presentation, the patient's vital signs were normal. Physical examination was unremarkable except for mild generalized pallor. A complete blood count on the day of admission revealed the following (reference ranges shown parenthetically): hemoglobin, 4.9 g/dL (12.0-15.5 g/dL); mean corpuscular volume (MCV), 94.4 fL (81.6-98.3 fL); hematocrit, 13.4% (34.9%-44.5%); leukocyte count, 6.0 × 10 9 /L (3.5-10.5 × 10 9 /L); and platelet count, 203 × 10 9 /L (150-450 × 10 9 /L). The patient's partial thromboplastin time and prothrombin time (PT)/international normalized ratio were normal. These results were obtained within 24 hours of her last transfusion.

• Chronic blood loss
• Acute hemolysis
• Chronic disease
• Myelodysplastic syndrome
• Acquired pure red cell aplasia

Anemia can be categorized as microcytic, normocytic, or macrocytic by examining the MCV. This patient clearly has a normocytic anemia, with her MCV of 94.4 fL, although this must be interpreted with some caution, given her history of multiple transfusions, which can normalize the MCV. Normocytic anemias are classically due to premature destruction or acute loss of RBCs or to decreased bone marrow production. With this in mind, we can approach the proposed list of differential diagnoses. Chronic blood loss usually leads to iron deficiency anemia, which is classically microcytic in nature; however, a normocytic anemia may also be seen. Hemolytic anemias usually result in a normocytic picture. Anemia of chronic disease is usually normocytic and is possible because of this patient's complicated medical history. The myelodysplastic syndromes refer to a heterogeneous group of stem cell disorders characterized by abnormal cellular maturation and, most commonly, chronic cytopenias. They result in macrocytosis, which is classically marked, with MCV sometimes greater than 110 fL. This is the only condition listed that classically results in a macrocytic anemia, rather than normocytic, and was therefore least likely to be the cause of the patient's anemia. Acquired pure red cell aplasia is a primary bone marrow disorder characterized by decreased reticulocytes and the virtual absence of erythroid precursors in the bone marrow. It is often idiopathic but may occur in association with various diseases, such as systemic lupus erythematosus and hematologic malignancies. Regardless of the underlying cause, the anemia is usually normocytic with absolute reticulocytopenia.

With the observation that the patient's anemia was normocytic with an MCV of 94.4 fL, the next task was to narrow the list of differential diagnoses and establish whether this was due to premature destruction or acute loss of RBCs vs decreased bone marrow production.

• Peripheral blood smear
• Absolute reticulocyte count
• Serum ferritin
• Erythropoietin
• Bone marrow biopsy and aspiration

The peripheral blood smear provides useful information that cannot be obtained with the usual complete blood count and can provide clues to a variety of bone marrow disorders, as well as systemic disorders that can have hematologic manifestations. However, it would not be the single best test to provide the necessary information at this point. We needed to establish whether there was an adequate or inadequate (ie, hypoproliferative) bone marrow response. An adequate response is usually due to hemolysis or acute loss of RBCs. The reticulocyte count is a good indicator of this and is the only test listed that could have directly provided this necessary piece of information. Anemia with an absolute reticulocyte count of less than 75 × 10 9 /L provides strong evidence of deficient production of RBCs, whereas a count of greater than 100 × 10 9 /L indicates a brisk and efficient response to hemolysis or blood loss. The region between these 2 limits remains a gray zone, and other clinical and laboratory parameters should be used to interpret the overall picture. The plasma ferritin level generally reflects overall iron storage and is typically used as a part of the panel to evaluate for iron deficiency anemia in a patient with microcytosis. Therefore, it would not be most useful in this patient with a normocytic anemia. Erythropoietin is a growth factor that is the primary stimulus for erythropoiesis. It would not be useful at this juncture in revealing whether the anemia is due to decreased production or increased loss of blood cells or premature destruction. A bone marrow biopsy would show erythroid hyperplasia, a nonspecific finding, if erythropoiesis is increased in response to the anemia. If there is a hypoproliferative state, the marrow may reveal a variety of findings, depending on the underlying diagnosis. Therefore, a bone marrow biopsy would be premature at this point. However, a bone marrow biopsy would be indicated if there was pancytopenia or if the peripheral smear showed abnormal cells, such as blast forms or dysplastic changes.

Our patient had a reticulocytosis of 13.3% (0.60%-1.83%), with an absolute reticulocyte count of 238.8 × 10 9 /L (29.5-87.3 × 10 9 /L).

• Total and indirect bilirubin levels, haptoglobin, lactate dehydrogenase (LDH)
• Direct Coombs test
• Indirect Coombs test
• Activated partial thromboplastin time (aPTT), PT, fibrinogen, soluble fibrin monomer complex, and D-dimers

In this patient with an absolute reticulocytosis, ie, an adequate bone marrow response, the next step would be in differentiating between hemolysis and acute blood loss. Hemolysis is usually characterized by elevated indirect bilirubin concentrations, decreased serum haptoglobin concentrations (with intravascular hemolysis in particular), and increased serum LDH levels, and this series of tests would be most useful in narrowing the differential diagnoses at this point. The peripheral blood smear is less specific, but in the presence of hemolysis, it may reveal abnormally shaped RBCs, including fragmented RBCs (schistocytes, helmet cells), spherocytes, elliptocytes, or RBC inclusions, which may be seen in certain hemolysis-producing infections, such as malaria, babesiosis, and Bartonella . Hemolytic anemias may be acquired and immune, in which case there is immunologic destruction of RBCs mediated by autoantibodies directed against antigens on the patient's RBCs. The direct and indirect Coombs tests detect antibodies on the surface of the patient's RBCs and in the patient's serum, respectively. However, the presence of hemolysis must first be established, especially since a patient may have a mildly positive Coombs test that is clinically insignificant if not associated with ongoing hemolysis. The laboratory findings in disseminated intravascular coagulation and intravascular coagulation and fibrinolysis (DIC/ICF) include elevated D-dimer and soluble fibrin monomer complex levels, low fibrinogen levels, and prolonged PT and aPTT. Therefore, these investigations should be performed when a diagnosis of DIC/ICF is suspected. However, this patient's clinical scenario and laboratory findings to date, ie, lack of thrombocytopenia and normal PT and aPTT, do not suggest underlying DIC/ICF.

The patient had a mildly reduced haptoglobin level at 14 mg/dL (30-200 mg/dL), likely secondary to her multiple transfusions. However, her LDH level was normal at 205 U/L (122-222 U/L), as were her total and direct bilirubin levels at 0.4 mg/dL (0.1-1.0 mg/dL) and 0.1 mg/dL (0.0-0.3 mg/dL), respectively. A peripheral blood smear showed no abnormally shaped RBCs. The overall picture was not in keeping with hemolysis. On the first day of her evaluation, the patient's hemoglobin concentration was 11.1 g/dL. By day 2 of her outpatient work-up, it had decreased to 5.6 g/dL, and she received 4 units of packed RBCs. Despite the transfusions, her hemoglobin concentration decreased further within 24 hours to 4.9 g/dL. At this point, the patient was admitted and received 3 more units of packed RBCs. During this time, she was asymptomatic, and her vital signs remained stable.

• Esophagogastroduodenoscopy
• Colonoscopy
• Computed tomography (CT) of the abdomen and pelvis
• Transfer to the intensive care unit
• Angiography of the gastrointestinal (GI) tract

The patient had no overt signs or symptoms of bleeding, and it would be unlikely for her to have occult GI bleeding that resulted in such dramatic decreases in her hemoglobin concentration. Also, results of fecal occult blood testing were negative. Therefore, neither upper nor lower GI endoscopy would be expected to reveal any useful information. However, the patient could have occult intra-abdominal bleeding, and noncontrast CT of her abdomen and pelvis would be crucial in ruling this out. The patient's mental status remained normal, and she was exhibiting no overt evidence of decreased perfusion or hemodynamic instability other than mild tachycardia. Therefore, she could be deemed clinically stable, and transferring her to the intensive care unit would be unnecessary at this time. She was well compensated despite the severity and acuteness of the anemia, no doubt in part due to her age and lack of other cardiac comorbidities. In this patient who is exhibiting no overt evidence of GI bleeding, angiography would not be the next best step.

Noncontrast CT of her abdomen and pelvis revealed normal findings. During the night of hospital day 2, an astute nurse noticed what appeared to be bloodstains on the patient's gown. The patient reported that she had spilled cranberry juice on the gown. Closer inspection of her room revealed several blood-soaked tissues and Styrofoam cups filled with fresh blood in her wastebasket. The patient was also found to have dried, crusted blood all over her fingernails, and a blood-stained 10-mL syringe, most of its labeling worn away by overuse, was found in her gown pocket ( Figure ).

10-mL syringe allegedly used by the patient for self-phlebotomy.

• Factitious disorder
• Munchausen by proxy
• Malingering
• Somatization disorder
• Hypochondriasis

With the discovery made in the patient's room, in particular the syringe, the patient's self-phlebotomy became evident, leading to a diagnosis of factitious anemia. The most chronic and extreme form of factitious illness, Munchausen syndrome, typically includes travel from hospital to hospital combined with the willingness to submit to multiple procedures for self-fabricated signs of illness, as occurred with our patient before her presentation at our institution. In Munchausen by proxy, caregivers (usually mothers) induce illness in their children to obtain care and support for themselves. In malingering, illness is feigned to gain such external incentives as money or drugs or to avoid such consequences as military service or criminal prosecution. Factitious disorder, in contrast, has no incentive other than being a patient in the sick role. Since we identified no incentive other than obtaining our care, our patient could not be said to be malingering. Somatization refers to the tendency to experience psychological distress in the form of somatic symptoms not intentionally produced, thus differentiating this disorder from factitious illness or malingering. Hypochondriasis refers to a preoccupation with believing one is ill as a result of misconstruing physical symptoms that are not self-generated. By her self-phlebotomizing activity, our patient could not be considered hypochondriacal.

The patient was seen by the psychiatry service, and although she was obviously at risk of purposeful self-harm, she denied suicidal or homicidal ideation. It became evident that she had a history of severe depression, borderline personality disorder, chemical dependency, and a history of repeated episodes of parasuicide by means of wrist cutting. She gave consent for her central line to be removed, and this was done before her dismissal. There was direct communication with her primary care physicians and primary psychiatrist, and she was then dismissed from the hospital with a plan for close and consistent medical attention.

Several cases of factitious anemia have been reported in the literature. 1 , 2 The patient is seldom caught in the act and usually denies the behavior, making the diagnosis difficult to establish incontrovertibly. Patients with this condition often have underlying psychiatric issues and constantly need to assume the sick role. Once the diagnosis is suspected, the patient should be confronted, and removal of any contributing medical device is essential. Early diagnosis is usually difficult but may prevent repeated hospitalizations and the risks associated with invasive diagnostic procedures. 2 Management is usually extremely difficult but should be centered around long-term psychotherapy. 2 A multidisciplinary approach is of utmost importance because patients usually become very uncooperative when they are discovered and may make attempts to break off relations with the current medical staff and seek medical attention elsewhere. Providing optimal management to an uncooperative patient may be difficult without violating the patient's autonomy. Therefore, a psychiatric consultation should be arranged as soon as possible, and seeking assistance from the institution's ethics and legal committees may be prudent.

The current case provides an opportunity to highlight an approach to the patient presenting with anemia. Anemia can be classified according to measurement of RBC size, as seen on the peripheral blood smear and as indicated by the MCV. This morphological approach categorizes the anemias as microcytic, normocytic, or macrocytic, providing a useful starting point to narrow the list of differential diagnoses. By definition, the MCV is normal (80-100 fL) in patients with normocytic anemia, low (<80 fL) in patients with microcytic anemia, and high (>100 fL) in patients with macrocytic anemia. 3

The presence of a microcytic anemia usually indicates a pathologic process involving hemoglobin synthesis. The most common cause is iron deficiency, but other classic causes include the thalassemias and other hemoglobinopathies, lead poisoning, sideroblastic anemia, and, less commonly, anemia of chronic disease. If microcytosis is identified, the next step would be to differentiate among these common causes, and this can be done by assessing serum iron studies, which include serum ferritin, iron, total iron-binding capacity, and transferrin saturation. In iron deficiency, the classic findings are a low serum ferritin value, which is diagnostic, elevated total iron-binding capacity, and low saturation. Other findings include a peripheral blood smear showing anisocytosis and poikilocytosis. If the serum ferritin level and other iron studies are normal, then thalassemia should be considered, and hemoglobin electrophoresis should be performed for the definitive diagnosis. Caution must be taken in interpreting the iron studies in anemia of chronic disease because findings are often inconsistent. The entire clinical scenario must be taken into account. 3 Sideroblastic anemias may be hereditary or acquired, and the latter is characterized by increased RBC distribution width, dimorphic RBCs, and bone marrow ringed sideroblasts.

If the anemia is found to be normocytic, the next step would be to differentiate between RBC destruction/loss and a hypoproliferative state. The presence of an increased reticulocyte response (>100 × 10 9 /L) suggests either loss or destruction of RBCs; thus, differentiation of these 2 conditions must be made. Hemolysis is characterized by elevated indirect bilirubin levels, decreased serum haptoglobin levels, and increased serum LDH levels. Also, the peripheral smear may reveal several abnormalities, such as fragmented RBCs and other abnormally shaped RBCs. If laboratory parameters or the peripheral smear is not suggestive of hemolysis, then a bleeding source should be sought. A normocytic anemia without reticulocytosis indicates an aplastic anemia; myelophthisis in which the bone marrow is replaced by fibrosis, tumor, or other abnormal cells; or lack of erythropoietin, which can be seen classically in renal failure.

The first step in evaluating a macrocytic anemia should be ruling out a marked reticulocytosis (polychromasia). Polychromasia may cause a regenerative macrocytosis. If this is found, evaluation for hemolysis or blood loss should be performed as outlined previously. Macrocytic anemias may be due to defects in DNA synthesis, resulting in oval macrocytes, or increase in the cholesterol/phospholipid ratio in membranes, resulting in round macrocytes.

Oval macrocytosis is classically due to vitamin B 12 or folate deficiency. If neither is present, then a bone marrow biopsy is warranted to look for the presence of a myelodysplastic syndrome. Round macrocytes may be due to severe alcoholism, liver disease, or hypothyroidism. Also, tobacco use and advanced age may result in round macrocytosis without anemia.

Factitious disorders are difficult to diagnose. However, our patient presented with several clues, including her previous psychiatric history and the recurrent dramatic decreases in her hemoglobin concentration, usually when she was unsupervised. Heightened suspicion is the first step in arriving at the correct diagnosis. Additionally, if anemia is approached in a logical stepwise manner, as outlined previously, multiple expensive, unnecessary, and invasive investigations can be avoided, and if due to a factitious disorder, necessary psychotherapy can be implemented in a more timely fashion.

Acknowledgments

We thank J. Michael Bostwick MD, Department of Psychiatry, Mayo Clinic, Rochester MN, for his expertise in the care of this patient and guidance in the preparation of the submitted manuscript.

See end of article for correct answers to questions.

Correct answers: 1. d , 2. b , 3. a , 4. c , 5. a