Iron Deficiency Anemia

•February 27, 2010 • Leave a Comment

Essentials of Diagnosis

  • Serum ferritin < 12 mcg/L.
  • Caused by bleeding unless proved otherwise.
  • Responds to iron therapy.

General Considerations

Iron deficiency is the most common cause of anemia worldwide. The causes are listed in Table 13–3. Aside from circulating red blood cells, the major location of iron in the body is the storage pool as ferritin or as hemosiderin and in macrophages.

The average American diet contains 10–15 mg of iron per day. About 10% of this amount is absorbed. Absorption occurs in the stomach, duodenum, and upper jejunum. Dietary iron present as heme is efficiently absorbed (10–20%) but nonheme iron less so (1–5%), largely because of interference by phosphates, tannins, and other food constituents. Small amounts of iron—approximately 1 mg/d—are normally lost through exfoliation of skin and mucosal cells. There is no physiologic mechanism for increasing normal body iron losses.

Menstrual blood loss plays a major role in iron metabolism. The average monthly menstrual blood loss is approximately 50 mL, or about 0.7 mg/d. However, menstrual blood loss may be five times the average. To maintain adequate iron stores, women with heavy menstrual losses must absorb 3–4 mg of iron from the diet each day. This strains the upper limit of what may reasonably be absorbed, and women with menorrhagia of this degree will almost always become iron deficient without iron supplementation.

In general, iron metabolism is balanced between absorption of 1 mg/d and loss of 1 mg/d. Pregnancy may also upset the iron balance, since requirements increase to 2–5 mg of iron per day during pregnancy and lactation. Normal dietary iron cannot supply these requirements, and medicinal iron is needed during pregnancy and lactation. Repeated pregnancy (especially with breast-feeding) may cause iron deficiency if increased requirements are not met with supplemental medicinal iron. Decreased iron absorption can on very rare occasions cause iron deficiency and usually occurs after gastric surgery, though concomitant bleeding is frequent.

By far the most important cause of iron deficiency anemia is blood loss, especially gastrointestinal blood loss. Prolonged aspirin use, or the use of other anti-inflammatory drugs, may cause it even without a documented structural lesion. Iron deficiency demands a search for a source of gastrointestinal bleeding if other sites of blood loss (menorrhagia, other uterine bleeding, and repeated blood donations) are excluded.

Chronic hemoglobinuria may lead to iron deficiency since iron is lost in the urine, but this is uncommon; traumatic hemolysis due to a prosthetic cardiac valve and other causes of intravascular hemolysis (eg, paroxysmal nocturnal hemoglobinuria) should also be considered. Frequent blood donors may also be at risk for iron deficiency.

Clinical Findings

Symptoms and Signs

As a rule, the only symptoms of iron deficiency anemia are those of the anemia itself (easy fatigability, tachycardia, palpitations and tachypnea on exertion). Severe deficiency causes skin and mucosal changes, including a smooth tongue, brittle nails, and cheilosis. Dysphagia because of the formation of esophageal webs (Plummer–Vinson syndrome) also occurs. Many iron-deficient patients develop pica, craving for specific foods (ice chips, etc) often not rich in iron.

Laboratory Findings

Iron deficiency develops in stages. The first is depletion of iron stores. At this point, there is anemia and no change in red blood cell size. The serum ferritin will become abnormally low. A ferritin value less than 12 mcg/L is a highly reliable indicator of iron deficiency. Bone marrow biopsy for evaluation of iron stores is now rarely performed because of intraobserver variation in its interpretation.

After iron stores have been depleted, red blood cell formation will continue with deficient supplies of iron. Serum iron values decline to less than 30 mcg/dL and transferrin levels rise, leading to transferring saturation of less than 15%.

In the early stages, the MCV remains normal. Subsequently, the MCV falls and the blood smear shows hypochromic microcytic cells (see blood smear). With further progression, anisocytosis (variations in red blood cell size) and poikilocytosis (variation in shape of red cells) develop. Severe iron deficiency will produce a bizarre peripheral blood smear, with severely hypochromic cells, target cells, hypochromic pencil-shaped cells, and occasionally small numbers of nucleated red blood cells. The platelet count is commonly increased.

Differential Diagnosis

Other causes of microcytic anemia include anemia of chronic disease, thalassemia, and sideroblastic anemia. Anemia of chronic disease is characterized by normal or increased iron stores in the bone marrow and a normal or elevated ferritin level; the serum iron is low, often drastically so, and the total iron-binding capacity (TIBC) is either normal or low. Thalassemia produces a greater degree of microcytosis for any given level of anemia than does iron deficiency. Red blood cell morphology on the peripheral smear is abnormal earlier in the course of thalassemia.


The diagnosis of iron deficiency anemia can be made either by the laboratory demonstration an iron-deficient state or evaluating the response to a therapeutic trial of iron replacement.

Since the anemia itself is rarely life-threatening, the most important part of treatment is identification of the cause—especially a source of occult blood loss.

Oral Iron

Ferrous sulfate, 325 mg three times daily, which provides 180 mg of iron daily of which up to 10 mg is absorbed (though absorption may exceed this amount in cases of severe deficiency), is the preferred therapy. Compliance is improved by introducing the medicine more slowly in a gradually escalating dose with food. Alternatively, in cases of poor tolerance, one pill of ferrous sulfate can be taken at bedtime on an empty stomach. It is preferable to prescribe a lower dose of iron or to allow ingestion concurrent with food than to insist on a more rigorous schedule that will not be followed. An appropriate response is a return of the hematocrit level halfway toward normal within 3 weeks with full return to baseline after 2 months. Iron therapy should continue for 3–6 months after restoration of normal hematologic values to replenish iron stores. Failure of response to iron therapy is usually due to noncompliance, although occasional patients may absorb iron poorly, particularly if the stomach is achlorhydric. Such patients may benefit from concomitant administration of ascorbic acid (250 mg daily). Other reasons for failure to respond include incorrect diagnosis (anemia of chronic disease, thalassemia) and ongoing gastrointestinal blood loss that exceeds the rate of new erythropoiesis.

Parenteral Iron

The indications are intolerance to oral iron, refractoriness to oral iron, gastrointestinal disease (usually inflammatory bowel disease) precluding the use of oral iron, and continued blood loss that cannot be corrected. Because of the possibility of anaphylactic reactions, parenteral iron therapy has been advocated only for use in cases of persistent anemia after a reasonable course of oral therapy. Sodium ferric gluconate is available and has been shown to result in a lower incidence of severe anaphylaxis, allowing wider use of parenteral therapy.

The dose (total 1.5–2 g) may be calculated by estimating the decrease in volume of red blood cell mass and then supplying 1 mg of iron for each milliliter of volume of red blood cells below normal. Approximately 1 g should then be added for storage iron. Total body iron ranges between 2 g and 4 g: approximately 50 mg/kg in men and 35 mg/kg in women. Most (70–95%) of the iron is present in hemoglobin in circulating red blood cells. One milliliter of packed red blood cells (not whole blood) contains approximately 1 mg of iron. In men, red blood cell volume is approximately 30 mL/kg. A 70-kg man will therefore have approximately 2100 mL of packed red blood cells and consequently 2100 mg of iron in his circulating blood. In women, the red cell volume is about 27 mL/kg; a 50-kg woman will thus have 1350 mg of iron circulating in her red blood cells. Thus, a woman whose hemoglobin is 9 g/dL would be treated with a total of 1315 mg of parenteral iron, 315 mg for the increased red blood cell mass and 1000 mg to provide iron stores. The entire dose may be given as an intravenous infusion over 4–6 hours. A test dose of a dilute solution is given first, and the patient should be observed during the entire infusion for anaphylaxis.

When to Refer:

Referral to a hematologist should not generally be necessary. Refer the patient if he or she is not responsive to iron therapy.

Andrews NC. Forging a field: the golden age of iron biology. Blood. 2008 Jul 15;112(2):219–30. [PMID: 18606887]
Chang J et al. Clinical utility of serum soluble transferrin receptor levels and comparison with bone marrow iron stores as an index for iron-deficient erythropoiesis in a heterogeneous group of patients. Pathology. 2007 Jun;39(3):349–53. [PMID: 17558864]
Killip S et al. Iron deficiency anemia. Am Fam Physician. 2007 Mar 1;75(5):671–8. [PMID: 17375513]
Miller HJ et al. Efficacy and tolerability of intravenous ferric gluconate in the treatment of iron deficiency anemia in patients without kidney disease. Arch Intern Med. 2007 Jun 25;167(12):1327–8. [PMID: 17592108]

Chronic Otitis Media

•February 16, 2010 • 1 Comment

Chronic infection of the middle ear and mastoid generally develops as a consequence of recurrent acute otitis media, although it may follow other diseases and trauma. Perforation of the tympanic membrane is usually present. This may be accompanied by mucosal changes such as polypoid degeneration and granulation tissue and osseous changes such as osteitis and sclerosis. The bacteriology of chronic otitis media differs from that of acute otitis media. Common organisms include P. aeruginosa, Proteus species, Staphylococcus aureus, and mixed anaerobic infections. The clinical hallmark of chronic otitis media is purulent aural discharge. Drainage may be continuous or intermittent, with increased severity during upper respiratory tract infection or following water exposure. Pain is uncommon except during acute exacerbations. Conductive hearing loss results from destruction of the tympanic membrane or ossicular chain, or both. The medical treatment of chronic otitis media includes regular removal of infected debris, use of earplugs to protect against water exposure, and topical antibiotic drops for exacerbations. The activity of ciprofloxacin against Pseudomonas may help to dry a chronically discharging ear when given in a dosage of 500 mg orally twice a day for 1–6 weeks.

Definitive management is surgical in most cases. Tympanic membrane repair may be accomplished with temporalis muscle fascia. Successful reconstruction of the tympanic membrane may be achieved in about 90% of cases, often with elimination of infection and significant improvement in hearing. When the mastoid air cells are involved by irreversible infection, they should be exenterated at the same time through a mastoidectomy.

Cholesteatoma is a special variety of chronic otitis media (Plate 57). The most common cause is prolonged eustachian tube dysfunction, with resultant chronic negative middle ear pressure that draws inward the upper flaccid portion of the tympanic membrane. This creates a squamous epithelium-lined sac, which—when its neck becomes obstructed—may fill with desquamated keratin and become chronically infected. Cholesteatomas typically erode bone, with early penetration of the mastoid and destruction of the ossicular chain. Over time they may erode into the inner ear, involve the facial nerve, and on rare occasions spread intracranially. Otoscopic examination may reveal an epitympanic retraction pocket, marginal tympanic membrane perforation that exudes keratin debris, or granulation tissue. The treatment of cholesteatoma is surgical marsupialization of the sac or its complete removal. This may require the creation of a “mastoid bowl” in which the ear canal and mastoid are joined into a large common cavity that must be periodically cleaned.

(Plate 57)



Acute suppurative mastoiditis usually evolves following several weeks of inadequately treated acute otitis media. It is characterized by postauricular pain and erythema accompanied by a spiking fever. Radiography reveals coalescence of the mastoid air cells due to destruction of their bony septa. Initial treatment consists of intravenous antibiotics and myringotomy for culture and drainage. Failure of medical therapy indicates the need for surgical drainage (mastoidectomy).

Petrous Apicitis

The medial portion of the petrous bone between the inner ear and clivus may become a site of persistent infection when the drainage of its pneumatic cell tracts becomes blocked. This may cause foul discharge, deep ear and retro-orbital pain, and sixth nerve palsy (Gradenigo syndrome); meningitis may be a complication. Treatment is with prolonged antibiotic therapy (based on culture results) and surgical drainage via petrous apicectomy.

Facial Paralysis

Facial palsy may be associated with either acute or chronic otitis media. In the acute setting, it results from inflammation of the seventh nerve in its middle ear segment, perhaps mediated through bacterially secreted neurotoxins. Treatment consists of myringotomy for drainage and culture, followed by intravenous antibiotics (based on culture results). The use of corticosteroids is controversial. The prognosis is excellent, with complete recovery in most cases.

Facial palsy associated with chronic otitis media usually evolves slowly due to chronic pressure on the seventh nerve in the middle ear or mastoid by cholesteatoma. Treatment requires surgical correction of the underlying disease. The prognosis is less favorable than for facial palsy associated with acute otitis media.

Sigmoid Sinus Thrombosis

Trapped infection within the mastoid air cells adjacent to the sigmoid sinus may cause septic thrombophlebitis. This is heralded by signs of systemic sepsis (spiking fevers, chills), at times accompanied by signs of increased intracranial pressure (headache, lethargy, nausea and vomiting, papilledema). Diagnosis can be made noninvasively by magnetic resonance venography. Primary treatment is with intravenous antibiotics (based on culture results). Surgical drainage with ligation of the internal jugular vein may be indicated when embolization is suspected.

Central Nervous System Infection

Otogenic meningitis is by far the most common intracranial complication of ear infection. In the setting of acute suppurative otitis media, it arises from hematogenous spread of bacteria, most commonly H influenzae and S pneumoniae. In chronic otitis media, it results either from passage of infections along preformed pathways such as the petrosquamous suture line or from direct extension of disease through the dural plates of the petrous pyramid.

Epidural abscesses arise from direct extension of disease in the setting of chronic infection. They are usually asymptomatic but may present with deep local pain, headache, and low-grade fever. They are often discovered as an incidental finding at surgery. Brain abscess may arise in the temporal lobe or cerebellum as a result of septic thrombophlebitis adjacent to an epidural abscess. The predominant causative organisms are S aureus, S pyogenes, and S pneumoniae. Rupture into the subarachnoid space results in meningitis and often death. (See Chapter 30: Common Problems in Infectious Diseases & Antimicrobial Therapy).


Otosclerosis is a progressive disease with a marked familial tendency that affects the bony otic capsule. Lesions involving the footplate of the stapes result in increased impedance to the passage of sound through the ossicular chain, producing conductive hearing loss. This may be treated either through the use of a hearing aid or surgical replacement of the stapes with a prosthesis (stapedectomy). When otosclerotic lesions impinge on the cochlea (‘cochlear otosclerosis’), permanent sensory hearing loss occurs. Some evidence suggests that hearing loss associated with cochlear otosclerosis may be stabilized by treatment with oral sodium fluoride over prolonged periods of time (Florical—8.3 mg sodium fluoride and 364 mg calcium carbonate—two tablets orally each morning).

from : CURRENT Medical Diagnosis & Treatment 2010

Acute Otitis Media

•February 16, 2010 • Leave a Comment

Acute Otitis Media
CURRENT Medical Dx & Tx > Chapter 8. Ear, Nose, & Throat Disorders > Diseases of the Ear >

Essentials of Diagnosis

* Otalgia, often with an upper respiratory tract infection.
* Erythema and hypomobility of tympanic membrane.

General Considerations
Acute otitis media is a bacterial infection of the mucosally lined air-containing spaces of the temporal bone. Purulent material forms not only within the middle ear cleft but also within the pneumatized mastoid air cells and petrous apex. Acute otitis media is usually precipitated by a viral upper respiratory tract infection that causes eustachian tube obstruction. This results in accumulation of fluid and mucus, which becomes secondarily infected by bacteria. The most common pathogens both in adults and in children are Streptococcus pneumoniae, Haemophilus influenzae, and Streptococcus pyogenes.

Clinical Findings
Acute otitis media is most common in infants and children, although it may occur at any age. Presenting symptoms and signs include otalgia, aural pressure, decreased hearing, and often fever. The typical physical findings are erythema and decreased mobility of the tympanic membrane. Occasionally, bullae will be seen on the tympanic membrane.
Rarely, when middle ear empyema is severe, the tympanic membrane can bulge outward. In such cases, tympanic membrane rupture is imminent. Rupture is accompanied by a sudden decrease in pain, followed by the onset of otorrhea. With appropriate therapy, spontaneous healing of the tympanic membrane occurs in most cases. When perforation persists, chronic otitis media may evolve. Mastoid tenderness often accompanies acute otitis media and is due to the presence of pus within the mastoid air cells. This alone does not indicate suppurative (surgical) mastoiditis. Frank swelling over the mastoid bone or the association of cranial neuropathies or central findings indicates severe disease requiring urgent care.

The treatment of acute otitis media is specific antibiotic therapy, often combined with nasal decongestants. The first-choice oral antibiotic treatment is amoxicillin (20–40 mg/kg/d) or erythromycin (50 mg/kg/d) plus sulfonamide (150 mg/kg/d) for 10 days. Alternatives useful in resistant cases are cefaclor (20–40 mg/kg/d) or amoxicillin-clavulanate (20–40 mg/kg/d) combinations.
Tympanocentesis for bacterial (aerobic and anaerobic) and fungal culture may be performed by any experienced physician. A 20-gauge spinal needle bent 90 degrees to the hub attached to a 3-mL syringe is inserted through the inferior portion of the tympanic membrane. Interposition of a pliable connecting tube between the needle and syringe permits an assistant to aspirate without inducing movement of the needle. Tympanocentesis is useful for otitis media in immunocompromised patients and when infection persists or recurs despite multiple courses of antibiotics.
Surgical drainage of the middle ear (myringotomy) is reserved for patients with severe otalgia or when complications of otitis (eg, mastoiditis, meningitis) have occurred.
Recurrent acute otitis media may be managed with long-term antibiotic prophylaxis. Single daily oral doses of sulfamethoxazole (500 mg) or amoxicillin (250 or 500 mg) are given over a period of 1–3 months. Failure of this regimen to control infection is an indication for insertion of ventilating tubes.
Ramakrishnan K et al. Diagnosis and treatment of otitis media. Am Fam Physician. 2007 Dec 1;76(11):1650–8. [PMID: 18092706]

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•February 16, 2010 • 1 Comment

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