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Introduction ⬇

Hb M is formed when the iron in the heme portion of deoxygenated Hb is oxidized to a ferric form rather than a ferrous form. In the ferric form, oxygen and iron cannot combine. The formation of Hb M is a normal process and is kept within bounds by the reduction of Hb M to Hb. Hb M causes a shift to the left of the oxyhemoglobin dissociation curve. When a high concentration of Hb M is produced in the RBCs, it reduces their capacity to combine with oxygen—anoxia and cyanosis result.

This test is used to diagnose hereditary or acquired methemoglobinemia in patients with symptoms of anoxia or cyanosis and no evidence of cardiovascular or pulmonary disease. Hb M is an inherited disorder of the Hb that produces cyanosis.

Methemoglobinemia is most commonly encountered as an acquired state as a result of medications such as phenacetin, sulfonamides, or ingestion of nitrates.

Normal Findings ⬆ ⬇

0.4%–1.5% or 0.004–0.015 of total Hb

A value of >40% or >0.40 is a critical value.

Clinical Alert

Critical Values

  1. Hb M of 30% (or 0.30) results in headaches and cyanosis.

  2. Hb M of 50% (or 0.50) results in shortness of breath, fatigue, dizziness, and confusion.

  3. Hb M of 70% (or 0.70) is usually fatal.

Procedure ⬆ ⬇

  1. Obtain two 5-mL venous or arterial blood samples in green-topped tubes or lavender-topped tubes anticoagulated with sodium fluoride. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered.

  2. Place on ice immediately and transport to the laboratory in a biohazard bag. Hb M is very unstable and must be tested within 8 hours.

Clinical Implications ⬆ ⬇

  1. Hereditary methemoglobinemia (uncommon) is associated with:

    1. A hemoglobinopathy, Hb M (40% [or 0.40] of the total Hb)

    2. Deficiency of Hb M reductase (autosomal recessive)

    3. Glutathione deficiency (dominant mode of transmission)

  2. Acquired methemoglobinemia is associated with:

    1. Blackwater fever

    2. Paroxysmal hemoglobinuria

    3. Clostridial infection

  3. Toxic effect of drugs or chemicals (most common cause)

    1. Analgesic agents, phenacetin

    2. Sulfonamide derivatives—sulfonamide S

    3. Nitrates and nitrites; nitroglycerin

    4. Antimalarials

    5. Isoniazid

    6. Quinones

    7. Potassium chloride

    8. Benzocaine, lidocaine

    9. Dapsone (most common drug causing methemoglobinemia)

Interventions ⬆ ⬇

Pretest Patient Care

  1. Advise patient of purpose of test. Assess for history of use of Bromo Seltzer or toxic drugs or chemicals.

  2. Follow guidelines in Chapter 1 for safe, effective, informed pretest care.

Posttest Patient Care

  1. Review test results; report and record findings. Modify the nursing care plan as needed. Counsel the patient regarding abnormal findings; explain the need for possible follow-up testing and treatment. Explain the causes, signs, and symptoms of cyanosis and monitor for anoxia.

  2. Treatment includes IV methylene blue and oral ascorbic acid.

  3. Follow guidelines in Chapter 1 for safe, effective, informed posttest care.

Clinical Alert

Because Hb F is more easily converted to Hb M than to Hb A, infants are more susceptible than adults to methemoglobinemia, which may be caused by drinking well water containing nitrites. Bismuth preparations for diarrhea may also be reduced to nitrites by bowel action

Interfering Factors ⬆

  1. Consumption of sausage, processed meats, or other foods rich in nitrites and nitrates

  2. Absorption of silver nitrate used to treat extensive burns

  3. Excessive intake of acetaminophen, sodium bicarbonate, and citric acid (Bromo Seltzer) is a common cause of methemoglobinemia. (The patient appears cyanotic but otherwise feels well.)

  4. Smoking

  5. Use of bismuth preparations for diarrhea (see Appendix E)