Referral for Long Case

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Associated symptoms may provide important clues to whether other portions of the

nervous system have been effected in addition to motor damage. Complaints of

numbness or tingling, vision disturbance or vertigo suggest broader damage to the

nervous system. The presence of such symptoms may indicate the level of damage to the

nervous system or alert you to the presence of a neurologic syndrome. A change in

character of the voice or problems swallowing (usually choking on water) suggests thatthe weakness may involve the pharyngeal muscles or those of the palate. Myelopathy

(damage to the spinal cord) often produces bilateral symptoms below a certain level on

the body. This may be attended by urgency of bladder function. Another common feature

of damage to spinal cord, or peripheral nerves for that matter, is the combination of

sensory and motor complaints. Some complaints can indicate a potentially serious

neurologic disorder requiring urgent action. This includes rapidly progressive weakness

of both lower extremities, which can be due to acute myelopathy, compressive lesions of

the cauda equina (cauda equina syndrome) or Guillain-Barre syndrome. In any of

these cases urgent evaluation is appropriate due to the need for prompt treatment

Pneumonia - adults (community acquired)

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Pneumonia is a breathing (respiratory) condition in which there is an infection of the lung.

This article covers pneumonia in people who have not recently been in the hospital or

another health care facility (nursing home or rehab facility). This type of pneumonia iscalled community-acquired pneumonia, or CAP.

See also:Hospital-acquired pneumonia

Causes

Pneumonia is a common illness that affects millions of people each year in the United

States. Germs called bacteria, viruses, and fungi may cause pneumonia.

Ways you can get pneumonia include:

Bacteria and viruses living in your nose, sinuses, or mouth may spread to yourlungs.

You may breathe some of these germs directly into your lungs. You breathe in (inhale) food, liquids, vomit, or fluids from the mouth into your

lungs (aspiration pneumonia)
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Pneumonia caused by bacteria tends to be the most serious kind. In adults, bacteria are

the most common cause of pneumonia.

The most common pneumonia-causing germ in adults is Streptococcuspneumoniae (pneumococcus).

Atypical pneumonia, often called walking pneumonia, is caused by certain otherbacteria.

Pneumocystis jiroveci pneumonia is sometimes seen in people whose immunesystem is not working well.

Many other bacteria can also cause pneumonia.

Virusesare also a common cause of pneumonia, especially in infants and young children.

Risk factors that increase your chances of getting pneumonia include:

Chronic lung disease (COPD,bronchiectasis,cystic fibrosis)

Cigarette smoking Dementia, stroke, brain injury,cerebral palsy, or other brain disorders Immune system problem (during cancer treatment or due to HIV/AIDS or organ

transplant)

Other serious illnesses, such asheart disease, livercirrhosis, ordiabetes mellitus Recent surgery or trauma Surgery to treat cancer of the mouth, throat, or neck

Symptoms

The most common symptoms of pneumonia are:

Cough(with some pneumonias you may cough up greenish or yellow mucus, orevenbloody mucus)

Fever, which may be mild or high Shaking chills Shortness of breath(may only occur when you climb stairs)

Other symptoms include:

Confusion, especially in older people Excess sweating and clammy skin Headache Loss of appetite, low energy, andfatigue Sharp or stabbing chest pain that gets worse when you breathe deeply or cough

Exams and Tests
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If you have pneumonia, you may be working hard to breathe, or breathing fast.

The health care provider will hear crackles or abnormal breath sounds when listening toyour chest with a stethoscope. Other abnormal breathing sounds may also be heard

through the stethoscope or by tapping on your chest wall (percussion).

The health care provider will likely order a chest x-ray if pneumonia is suspected.

You may need other tests, including:

Arterial blood gasesto see if enough oxygen is getting into your blood from thelungs

CBCto check white blood cell count CT scan of the chest Culture of your sputumto look for the bacteria or virus that is causing your

symptoms

Pleural fluid cultureif there is fluid in the space around the lungs

Less often patients may need:

Bronchoscopy--a flexible tube with a lighted camera on the end passed down toyour lungs

Thoracentesis--removing fluid from the space between the outside lining of thelungs and the chest wall

Treatment

Your doctor must first decide whether you need to be in the hospital. If you are treated inthe hospital, you will receive:

Fluids and antibiotics in your veins Oxygen therapy Breathing treatments (possibly)

It is very important that you are started on antibiotics very soon after you are admitted

(unless you have viral pneumonia).

You are more likely to be admitted to the hospital if you:

Have another serious medical problem Have severe symptoms Are unable to care for yourself at home, or are unable to eat or drink Are older than 65 or a young child Have been taking antibiotics at home and are not getting better
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However, many people can be treated at home. Your doctor may tell you to take

antibiotics. Antibiotics help some people with pneumonia get better.

Don't miss any doses. Take the medicine until it is gone, even if you start to feelbetter.

Do NOT take cough medicine or cold medicine unless your doctor says it is okay.Coughing helps your body get rid of mucus from your lungs.

Breathing warm, moist (wet) air helps loosen the sticky mucus that may make you feellike you are choking. These things may help:

Place a warm, wet washcloth loosely over your nose and mouth. Fill a humidifier with warm water and breathe in the warm mist. Take a couple of deep breaths two or three times every hour. Deep breaths will

help open up your lungs.

Tap your chest gently a few times a day and lie with your head lower than yourchest. This can help bring up mucus from the lungs.

Drink plenty of liquids (as long as your health care provider says it is okay):

Drink water, juice, or weak tea Drink at least 6 to 10 cups a day Do NOT drink alcohol

Get plenty of rest when you go home. If you have trouble sleeping at night, take naps

during the day.

Outlook (Prognosis)

With treatment, most patients will improve within 2 weeks. Elderly or very sick patientsmay need longer treatment.

Those who may be more likely to have complicated pneumonia include:

Older adults or very young children People whose immune system does not work well People with other, serious medical problems such as diabetes orcirrhosis of the

liver

In rare cases, more severe problems may develop, including:

Life-threatening changes in the lungs that require a breathing machine Fluid around the lung (pleural effusion) Lung abscesses
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Your doctor may want to make sure your chest x-ray becomes normal again after you are

treated. However, it may take many weeks for your x-ray to clear up.

When to Contact a Medical Professional

Call your doctor if you have:

A cough that brings up bloody or rust-colored mucus Breathing (respiratory) symptoms that get worse Chest pain that gets worse when you cough or breathe in Fast or painful breathing Night sweats or unexplained weight loss Shortness of breath, shaking chills, or persistent fevers Signs of pneumonia and a weak immune system (for example such as with HIV or

chemotherapy)

Prevention

Wash your hands often, especially after:

Blowing your nose Going to the bathroom Diapering

Also wash your hands before eating or preparing foods.

Don't smoke. Tobacco damages your lung's ability to ward off infection.

Vaccines may help prevent some types of pneumonia. They are even more important for

the elderly and people with diabetes, asthma, emphysema, HIV, cancer, or other long-

term conditions:

Flu vaccineprevents pneumonia and other problems caused by the influenza virus.It must be given each year to protect against new virus strains.

Pneumococcal vaccine(Pneumovax, Prevnar) lowers your chances of gettingpneumonia from Streptococcus pneumoniae.

If you have cancer or HIV, talk to your doctor about ways to prevent pneumonia andother infections.

Alternative Names

Bronchopneumonia; Community-acquired pneumoni
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Background

Anemia is strictly defined as a decrease in red blood cell (RBC) mass. The function of the

RBC is to deliver oxygen from the lungs to the tissues and carbon dioxide from thetissues to the lungs. This is accomplished by using hemoglobin (Hb), a tetramer protein

composed of heme and globin. Anemia impairs the bodys ability for gas exchange by

decreasing the number of RBCs transporting oxygen and carbon dioxide.[1] (See Etiology.)

Anemia, like a fever, is a symptom that requires investigation to determine the underlying

etiology. Often, practicing physicians overlook mild anemia. This is similar to failing to

seek the etiology of a fever. The purpose of this article is to provide a method ofdetermining the etiology of an anemia. (See the image below.) (See Etiology, History,

Physical Examination, and Workup.)

Microcytic anemia.

Methods for measuring RBC mass are time consuming and expensive and usually requiretransfusion of radiolabeled erythrocytes. Thus, in practice, anemia is usually discovered

and quantified by measurement of the RBC count, Hb concentration, and hematocrit(Hct). These values should be interpreted cautiously, because they are concentrations

affected by changes in plasma volume. For example, dehydration elevates these values,

and increased plasma volume in pregnancy can diminish them without affecting the RBC

mass. (See Workup.)

RBCs are lipid membranes encasing fluid Hb and are supported by a cytoskeleton.Abnormalities of the membrane, the chemical composition of the Hb, or certain

glycolytic enzymes can reduce the life span of RBCs to cause anemia. (See Etiology.)

Complications

The most serious complications of severe anemia arise from tissue hypoxia. Shock,hypotension, or coronary and pulmonary insufficiency can occur. This is more common

in older individuals with underlying pulmonary and cardiovascular disease. (See

Pathophysiology.)
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Erythrocyte life cycle

Erythroid precursors develop in bone marrow at rates usually determined by therequirement for sufficient circulating Hb to oxygenate tissues adequately. Erythroid

precursors differentiate sequentially from stem cells to progenitor cells to erythroblasts to

normoblasts in a process requiring growth factors and cytokines. This process ofdifferentiation requires several days. Normally, erythroid precursors are released into

circulation as reticulocytes.

Reticulocytes are so called because of the reticular meshwork of rRNA they harbor. They

remain in the circulation for approximately 1 day before they mature into erythrocytes,

after the digestion of RNA by reticuloendothelial cells. The mature erythrocyte remainsin circulation for about 120 days before being engulfed and destroyed by phagocytic cells

of the reticuloendothelial system.

Erythrocytes are highly deformable and increase their diameter from 7 m to 13 m

when they traverse capillaries with a 3-m diameter. They possess a negative charge ontheir surface, which may serve to discourage phagocytosis. Because erythrocytes have no

nucleus, they lack a Krebs cycle and rely on glycolysis via the Embden-Meyerhof andpentose pathways for energy. Many enzymes required by the aerobic and anaerobic

glycolytic pathways decrease within the cell as it ages. In addition, the aging cell has a

decrease in potassium concentration and an increase in sodium concentration. Thesefactors contribute to the demise of the erythrocyte at the end of its 120-day lifespan.

Patient education

Inform patients of the etiology of their anemia, the significance of their medical condition,

and the therapeutic options available for treatment.

If no effective specific treatment of the underlying disease exists, educate patients

requiring periodic transfusions about the symptoms that herald the need for transfusion.Likewise, they should be aware of the potential complications of transfusion.

For patient education information, seeAnemia.

Pathophysiology

The physiologic response to anemia varies according to acuity and the type of insult.

Gradual onset may allow for compensatory mechanisms to take place. With anemia dueto acute blood loss, a reduction in oxygen-carrying capacity occurs along with a decrease

in intravascular volume, with resultant hypoxia and hypovolemia. Hypovolemia leads tohypotension, which is detected by stretch receptors in the carotid bulb, aortic arch, heart,

and lungs. These receptors transmit impulses along afferent fibers of the vagus and

glossopharyngeal nerves to the medulla oblongata, cerebral cortex, and pituitary gland.
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In the medulla, sympathetic outflow is enhanced, while parasympathetic activity is

diminished. Increased sympathetic outflow leads to norepinephrine release from

sympathetic nerve endings and discharge of epinephrine and norepinephrine from theadrenal medulla. Sympathetic connection to the hypothalamic nuclei increases

antidiuretic hormone (ADH) secretion from the pituitary gland.[2] ADH increases free

water reabsorption in the distal collecting tubules. In response to decreased renalperfusion, juxtaglomerular cells in the afferent arterioles release renin into the renalcirculation, leading to increased angiotensin I, which is converted by angiotensin-

converting enzyme (ACE) to angiotensin II.

Angiotensin II has a potent pressor effect on arteriolar smooth muscle. Angiotensin II

also stimulates the zona glomerulosa of the adrenal cortex to produce aldosterone.

Aldosterone increases sodium reabsorption from the proximal tubules of the kidney, thusincreasing intravascular volume. The primary effect of the sympathetic nervous system is

to maintain perfusion to the tissues by increasing systemic vascular resistance (SVR).

The augmented venous tone increases the preload and, hence, the end-diastolic volume,

which increases stroke volume. Therefore, stroke volume, heart rate, and SVR all aremaximized by the sympathetic nervous system. Oxygen delivery is enhanced by the

increased blood flow.

In states of hypovolemic hypoxia, the increased venous tone due to sympathetic

discharge is thought to dominate the vasodilator effects of hypoxia. Counterregulatory

hormones (eg, glucagon, epinephrine, cortisol) are thought to shift intracellular water tothe intravascular space, perhaps because of the resultant hyperglycemia. This contribution

to the intravascular volume has not been clearly elucidated.

Nutritional etiologies include the following:

Iron deficiency Vitamin B-12 deficiency Folate deficiency Starvation and generalized malnutrition

Physical etiologies include the following:

Trauma Burns Frostbite Prosthetic valves and surfaces

Chronic disease and malignant etiologies include the following:

Renal disease Hepatic disease Chronic infections Neoplasia Collagen vascular diseases


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Infectious etiologies include the following:

Viral - Hepatitis, infectious mononucleosis, cytomegalovirus Bacterial - Clostridia, gram-negative sepsis Protozoal - Malaria, leishmaniasis, toxoplasmosis

Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome may be a

cause of anemia. Hereditary spherocytosis either may present with a severehemolytic

anemiaor may be asymptomatic with compensated hemolysis. Similarly, glucose-6-phosphate dehydrogenase (G-6-PD) deficiency may manifest as chronic hemolytic

anemia or exist without anemia until the patient receives an oxidant medication.

Immunologic etiologies for anemia may include antibody-mediated abnormalities. In theemergency department (ED), acute hemorrhage is by far the most common etiology for

anemia.

Drugs or chemicals commonly cause the aplastic and hypoplastic group of disorders.

Certain types of these causative agents are dose related and others are idiosyncratic. Anyhuman exposed to a sufficient dose of inorganic arsenic, benzene, radiation, or the usual

chemotherapeutic agents used for treatment of neoplastic diseases develops bone marrowdepression with pancytopenia.

Conversely, among the idiosyncratic agents, only an occasional human exposed to thesedrugs has an untoward reaction resulting in suppression of 1 or more of the formed

elements of bone marrow (1:100 to 1:millions). With certain types of these drugs,

pancytopenia is more common, whereas with others, suppression of 1 cell line is usuallyobserved. Thus, chloramphenicol may produce pancytopenia, whereas granulocytopenia

is more frequently observed with toxicity to sulfonamides or antithyroid drugs.

Current evidence, such as the fact that these patients respond to immunosuppressants,

now points to an immune mechanism.[3]

The idiosyncratic causes of bone marrow suppression include multiple drugs in each of

the categories that can be prefixed with anti- (eg, antibiotics, antimicrobials,

anticonvulsants, antihistamines). The other idiosyncratic causes of known etiology areviral hepatitis and paroxysmal nocturnal hemoglobinuria. In approximately one half of

patients presenting withaplastic anemia, a definite etiology cannot be established, and the

anemia must be regarded as idiopathic.

Rare causes of anemia due to a hypoplastic bone marrow include familial disorders and

the acquired pure red cell aplasias. The latter are characterized by a virtual absence of

erythroid precursors in the bone marrow, with normal numbers of granulocytic precursorsand megakaryocytes. Rare causes of diminished erythrocyte production with hyperplastic

bone marrow include hereditary orotic aminoaciduria and erythremic myelosis.

Prognosis
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Usually, the prognosis depends on the underlying cause of the anemia. However, the

severity of the anemia, its etiology, and the rapidity with which it develops can each play

a significant role in the prognosis. Similarly, the age of the patient and the existence ofother comorbid conditions influence outcome.

Bleeding from esophageal varices

Approximately 30% of patients with cirrhosis die from variceal bleeding. Patients with

Child class C liver disease have a 50% mortality rate. The rate of rebleeding in medicallytreated patients is in excess of 70%.[10]

Aortic rupture

The prognosis for traumatic rupture is very poor, with approximately an 80% prehospital

mortality rate. If untreated, the majority of patients die within 2 weeks. Nontraumaticaneurysmal rupture also has a poor prognosis and is essentially fatal if untreated.

Immediate surgical repair still carries a high mortality rate, often greater than 80%.

Sickle cell anemia

Patients who are homozygous (Hgb SS) have the worst prognosis, because they tend to

have more frequent crises. Patients who are heterozygous (Hgb AS) have sickle cell traits,

and they have crises only under extreme conditions.

Thalassemias

Patients who are homozygous for beta thalassemia (Cooley anemia or thalassemia major)

have a worse prognosis than do patients with any of the other thalassemias (thalassemiaintermedia and thalassemia minor). These few years have witnessed groundbreakingadvancements in the treatment of thalassemias, especially with iron chelation therapies,

allowing thalassemia patients to live well into adulthood.[9] Patients who are heterozygousfor beta thalassemia have mild microcytic anemia that is not clinically significant.

Aplastic anemia

Chances of survival are poorer for patients with idiosyncratic aplasia caused bychloramphenicol and viral hepatitis and better when paroxysmal nocturnal

hemoglobinuria or anti-insecticides are the probable etiology. The prognosis for

idiopathic aplasia lies between these 2 extremes, with an untreated mortality rate ofapproximately 60-70% within 2 years after diagnosis.

The 2-year fatality rate for severe aplastic anemia is 70% without bone marrow

transplantation or a response to immunosuppressive therapy.


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Hyperplasia

Among patients with a hyperplastic bone marrow and decreased production of RBCs, onegroup has an excellent prognosis, and the other is unresponsive, refractory to therapy, and

has a relatively poor prognosis. The former includes patients with disorders of relative

bone marrow failure due to nutritional deficiency in whom proper treatment with vitaminB-12, folic acid, or iron leads to a correction of anemia once the appropriate etiology is

established. Drugs acting as an antifolic antagonist or inhibitor of DNA synthesis can

produce similar effects.

The second group includes patients with an idiopathic hyperplasia that may respond

partially to pyridoxine therapy in pharmacologic doses but more frequently does not.These patients have ringed sideroblasts in the bone marrow, indicating an inappropriate

use of iron in the mitochondria for heme synthesis.

Certain patients with marrow hyperplasia (see the image below) may have refractory

anemia for years, but some of the group eventually develop acute myelogenous leukemia.

Bone marrow aspirate showing erythroid hyperplasia and

many binucleated erythroid precursors.

Other conditions

In ectopic pregnancy, the prognosis with prompt management is excellent, with amortality rate of about 1-2%. In patients with hemophilia, about 15% of them eventuallydevelop inhibitors to factor VIII and may die from bleeding complications. Patients with

idiopathic thrombocytic purpura (ITP) usually respond to immunosuppression or

splenectomy and have an excellent prognosis. Approximately 80-90% of patients whohave TTP and undergo plasmapheresis recover completely.

Hemolytic-uremic syndrome carries a significant morbidity and mortality if untreated. As

many as 40% of those affected die, and as many as 80% develop renal insufficiency.

Differential Diagnoses

Aplastic Anemia Hemolytic Anemia Iron Deficiency Anemia Low LDL Cholesterol (Hypobetalipoproteinemia) Megaloblastic Anemia Myelophthisic Anemia
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Pernicious Anemia Sickle Cell Anemia Spur Cell Anemia Thalassemia, Alpha Thalassemia, Beta

Presently, RBC cellular indices are computer calculated and automatically placed on

laboratory reports. The formulae for calculating these values follow (reference ranges are

in parentheses). RBC is per million cells.

MCV = Hct x 10/RBC (84-96 fL) Mean corpuscular Hb (MCH) = Hb x 10/RBC (26-36 pg) Mean corpuscular Hb concentration (MCHC) = Hb x 10/Hct (32-36%)

A rapid method of determining whether cellular indices are normocytic andnormochromic is to multiply the RBC and Hb by 3. The RBC multiplied by 3 should

equal the Hb, and the Hb multiplied by 3 should equal the Hct. Deviation from the

calculated values suggests microcytosis, macrocytosis, or hypochromia versus thepresence of spherocytes (MCHC >36).

Table 1. Microcytic Hypochromic Anemia (MCV < 83; MCHC < 31) (Open Table in anew window)

ConditionSerum

Iron

Total Iron-Binding

Capacity (TIBC)

Bone

Marrow

Iron

Comment

Iron deficiency 0 Responsive to iron therapy

Chronic

inflammation

++ Unresponsive to iron therapy

Thalassemia

major

N ++++ Reticulocytosis and indirect

bilirubinemia

Thalassemia

minor

N N - ++ Elevation of fetal hemoglobin and Hb

A2, target cells, and poikilocytosis

Lead poisoning N N ++ Basophilic stippling of RBCs

Sideroblastic N ++++ Ring sideroblasts in marrow

Hemoglobin N N ++ Hemoglobin electrophoresis

= decreased; = increased; 0 = absent; +'s indicate the amount of stainable iron in bone
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marrow specimens, on a scale of 0-4; N = normal.

Table 2. Macrocytic Anemia (MCV >95) (Open Table in a new window)

Megaloblastic bone marrow Deficiency of vitamin B-12

Deficiency of folic acid

Drugs affecting deoxyribonucleic acid (DNA) synthesis

Inherited disorders of DNA synthesis

Nonmegaloblastic bone marrowLiver disease

Hypothyroidism and hypopituitarism

Accelerated erythropoiesis (reticulocytes)

Hypoplastic and aplastic anemia

Infiltrated bone marrow

Table 3. Various Forms of RBCs (Open Table in a new window)

Macrocyte Larger than normal (>8.5 m diameter). See Table 2.

Microcyte Smaller than normal (< 7 m diameter). See Table 1.

Hypochromic Less hemoglobin in cell. Enlarged area of central pallor. See Table 1.

Spherocyte Loss of central pallor, stains more densely, often microcytic. Hereditary

spherocytosis and certain acquired hemolytic anemias

Target cell Hypochromic with central "target" of hemoglobin. Liver disease, thalassemia,

hemoglobin D, and postsplenectomy

Leptocyte Hypochromic cell with a normal diameter and decreased MCV. Thalassemia

Elliptocyte Oval to cigar shaped. Hereditary elliptocytosis, certain anemias (particularly

vitamin B-12 and folate deficiency)

Schistocyte Fragmented helmet- or triangular-shaped RBCs. Microangiopathic anemia,


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artificial heart valves, uremia, and malignant hypertension

Stomatocyte Slitlike area of central pallor in erythrocyte. Liver disease, acute alcoholism,

malignancies, hereditary stomatocytosis, and artifact

Tear-shapedRBCs

Drop-shaped erythrocyte, often microcytic. Myelofibrosis and infiltration ofmarrow with tumor. Thalassemia

Acanthocyte Five to 10 spicules of various lengths and at irregular intervals on surface of

RBCs

Echinocyte Evenly distributed spicules on surface of RBCs, usually 10-30. Uremia, peptic

ulcer, gastric carcinoma, pyruvic kinase deficiency, and preparative artifact

Sickle cell Elongated cell with pointed ends. Hemoglobin S and certain types of

hemoglobin C and l

In microcytic hypochromic anemia, seek a source of bleeding. The appropriate laboratorytests are serum iron level and TIBC and either serum ferritin level or stain of bone

marrow specimen for iron. If the serum iron level is decreased and the TIBC is increased,

a diagnosis of iron deficiency can be made, therapy can be initiated, and a search for thecause of the iron deficiency can be started. If this cannot be demonstrated, suspect each

of the other causes of a microcytic anemia listed in Table 1, and the order of investigation

can be influenced by findings in the history, physical examination, or peripheral smear.

Similarly, a reasonable approach with macrocytic anemia is to determine if the bonemarrow aspirate is megaloblastic. If so, attempt to incriminate either vitamin B-12 orfolic acid deficiency with appropriate laboratory studies. Similar to the establishment of a

diagnosis of iron deficiency anemia, a diagnosis of vitamin B-12 or folic acid deficiency

does not stop with an abnormal laboratory value for one of these vitamins. Prompttreatment can be instituted, but a continued search for an underlying cause of the vitamin

deficiency is indicated (seePernicious Anemia).

When a normocytic normochromic anemia is encountered, classify the anemia into 3

possible etiologies (ie, blood loss, hemolysis, decreased production). In most anemias,

one of these causes is the dominant factor. However, in certain anemias, more than a

single cause may play an important role. For example, pernicious anemia ispredominantly due to decreased production of erythrocytes, but hemolysis adds

significantly to the severity of anemia.

Evaluation for Hemolysis

A normal RBC survives in the circulation for 120 days. If the erythrocytic life span is

shortened significantly (< 40 d), the patient has a hemolytic disorder that may be
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demonstrated by showing increased production of erythrocytes, increased destruction, or

both. The former is revealed most readily by the presence of sustained reticulocytosis and

the latter by the occurrence of indirect bilirubinemia (see Table 4, below). Otherlaboratory tests are available to detect hemolysis, but they are either more expensive or

less reliable.

Table 4. Classification of the Hemolytic Disorders (Open Table in a new window)

Hereditary Acquired

Intracorpuscular

defect

Hereditary spherocytosis

Hereditary elliptocytosis

Hemoglobinopathies

Thalassemias

Congenital

dyserythropoietic

anemias

Hereditary RBC

enzymatic deficiencies

Rarer hereditary

abnormalities

Vitamin B-12 and folic acid deficiency

Paroxysmal nocturnal hemoglobinuria

Severe iron deficiency


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Extracorpuscular

defect

Physical agents: Burns, cold exposure

Traumatic: Prosthetic heart valves, march

hemoglobinuria, disseminated intravascular

coagulation (DIC), graft rejection

Chemicals: Drugs and venoms

Infectious agents: Malaria, toxoplasmosis,

mononucleosis, hepatitis, primary atypical

pneumonia, clostridial infections, bartonellosis,

leishmaniasis

Hepatic and renal disease

Collagen vascular disease

Malignancies: Particularly hematologic neoplasia

Transfusion of incompatible blood

Hemolytic disease of the newborn


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Cold hemagglutinin

disease

Autoimmune hemolytic anemia Thrombotic

thrombocytopenic purpura (TTP) and hemolytic-

uremic syndrome (HUS)

Anemia solely due to hemolysis does not occur until RBCs are being destroyed at 6-8times the normal rate, reducing the mean RBC life span to less than 20 days because of

the bone marrow's capacity to undergo 6-fold hypertrophy and hyperplasia. Thus, if the

clinician relies on the presence of anemia to detect hemolytic states, the clinician missesmost of them and, perhaps, an important clue to an underlying disorder. On the other

hand, if reticulocytosis and indirect bilirubinemia are used to detect hemolytic states, they

are usually found when the mean life span is less than 40-50 days. More sophisticatedmethods, such as measurements of RBC lifespan, are required to detect less severe

shortening of erythrocyte life span (50-100 d) and are only occasionally needed in

clinical practice.

All patients with reticulocytosis and indirect bilirubinemia have a hemolytic disorder. All

patients with sustained reticulocytosis have a hemolytic disorder. Unfortunately, thecontrary is not the case, and significant hemolysis can occur without reticulocytosis if the

bone marrow is unable to produce cells at an accelerated rate (eg, pernicious anemia,

leukemia, aplasia).

A single demonstration of an elevated reticulocyte count is insufficient to establish adiagnosis of hemolysis, because transient reticulocytosis may occur without hemolysis

(eg, in the treatment of iron deficiency anemia).

Almost all patients with indirect bilirubinemia have a hemolytic disorder. In adults, the

exception is patients with Gilbert disease. These patients can be distinguished from those

with hemolytic disorders and those who have no other obvious stigmata of hemolysis (eg,

anemia, reticulocytosis, Coombs test) by having the patient fast for 3 days. In Gilbertdisease, indirect bilirubin doubles with starvation, whereas in hemolytic disorders, it does

not. Once the presence of hemolysis has been established, the etiology of the increased

rate of RBC destruction can be sought.

All causes of hemolytic disorders are either hereditary or acquired. Similarly, they aredue to either an intrinsic abnormality of the RBC (intracorpuscular defect) or external

factors that shorten the erythrocyte life span (extracorpuscular). Using this nomenclature,


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only 4 groups of hemolytic disorders are possiblehereditary intracorpuscular,

hereditary extracorpuscular, acquired intracorpuscular, and acquired extracorpuscular.

Hereditary hemolytic disorders

All hereditary hemolytic disorders are due to intracorpuscular defects, and most acquired

disorders are due to extracorpuscular abnormalities (see Table 4). Hereditary etiologies of

hemolytic disease are suggested strongly in any patient with a family history of anemia,jaundice, cholelithiasis, or splenectomy. Whenever possible, family members,

particularly parents, siblings, and children, should undergo a hematologic examination,

including a hemogram with reticulocyte count, an indirect bilirubin determination, and acareful examination of the peripheral smear.

If a specific hereditary hemolytic disorder (eg, hereditary spherocytosis,

hemoglobinopathy) is suggested in a patient, examine blood from family members forthat entity by appropriate laboratory methods. Establishment of a hemolytic defect in

other closely related family members permits a presumptive diagnosis of hereditary

intracorpuscular hemolytic disorder in the patient. Showing a similar RBC abnormality(eg, spherocytes abnormal Hb, G-6-PD deficiency) among family members establishes

the basic etiology. Once the probability of a hereditary hemolytic disorder is established,

a planned approach to determine the definitive abnormality is usually simple.

A careful examination of the peripheral smear may reveal spherocytes in hereditary

spherocytosis, ovalocytes in hereditary elliptocytosis, sickle cells in patients with majorhemoglobinopathies associated with sickle Hb, target cells in patients with Hb C or E

disease, and marked poikilocytosis with target cells, microcytes, and hypochromic RBCs

in thalassemia. (See the images below.)

Microcytic anemia.
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Peripheral smear showing ovalocytes, macrocytes, and a hypersegmented polymorphonuclear

leukocyte. Peripheral smear showing classic spherocytes with

loss of central pallor in the erythrocytes.

Even in certain rare disorders, abnormal erythrocyte morphology may provide an

important clue. Examples are acanthocytosis in abetalipoproteinemia, stomatocytosis in

the hereditary disorder of this name, and numerous target cells in lecithin cholesterolacyltransferase deficiency. Other laboratory studies of value in the hereditary hemolytic

disorders include the following:[12]

Hereditary spherocytosis - MCHC greater than 36%, incubated osmotic fragility inoxalate, and detection of the underlying molecular defect

Hemoglobinopathies - Sickle cell preparation, Hb electrophoresis at 1 or more pH, heatdenaturation test for unstable Hbs, oxygen disassociation for Hbs with abnormal oxygen

affinity

Thalassemia - A2 and fetal Hb, Hb electrophoresis, characterization of the moleculardefect, quantification of alpha and beta chains

Congenital dyserythropoietic anemias - Demonstration of abnormalities of erythroidprecursors in bone marrow aspirates, positive acid hemolysis (Ham) test, with normal

result of sucrose hemolysis test in one form of this disease (hereditary erythroblasticmultinuclearity with a positive acidified serum test [HEMPAS])

Hereditary RBC enzymatic deficiencies - Specific RBC enzyme assayAcquired hemolytic disorders

Acquired hemolytic disorders occur in a large number of disease states and can varyconsiderably in severity. In addition, hemolysis may be observed as a result of physical

injury to the RBC or following exposure to drugs, chemicals, or venoms. In many

patients, the etiology of the hemolytic disorder is apparent because of other

manifestations of the disease (eg, infections, collagen vascular disease).

A confirmed positive Coombs test result can be extremely helpful in this group of

disorders. It provides assurance that the hemolytic disorder is an acquiredextracorpuscular defect and limits it to the group of disorders associated with

autoimmune hemolytic anemia; these disorders include the following:

Drug-dependent antibodies (eg, to penicillin, quinidine, alpha methyldopa)
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Coexistence of an underlying disease (eg, hematologic malignancies, lupuserythematosus, certain viral infections)

Idiopathic groups in which an underlying disease cannot be demonstratedUsually, the acquired hemolytic disorders with intracorpuscular defects are not difficult

to diagnose. Vitamin B-12 and folic acid deficiencies are associated with macrocyticanemia, the presence of hypersegmented polymorphonuclear leukocytes in the peripheral

smear, megaloblastic bone marrow, physical findings of the underlying cause of the

deficiency state, and abnormal serum levels for the deficient vitamin.

Iron deficiency in the United States is rarely of sufficient severity to cause significant

hemolysis and is merely mentioned herein for the sake of completeness.

Paroxysmal nocturnal hemoglobinuria is diagnosed only if the physician considers it in

the differential diagnosis, and it may manifest by either a pancytopenia or a

hemoglobinuria. However, a sugar-water test can help to exclude this cause of hemolysis.

Evaluation for Decreased RBC Production

Diminished production of RBCs is suggested in all patients without evidence of either

blood loss or hemolysis. Thus, a patient with anemia without evidence of bleeding or iron

deficiency, with normal indirect bilirubin and normal or decreased reticulocyte count,probably has a defect in the production of erythrocytes. Many of these patients have

pancytopenia or other abnormalities of the leukocytes or the platelets that can be detected

with an examination of a peripheral smear.

When this group of disorders is suspected, the most important laboratory test is a bone

marrow biopsy and aspiration (see Imaging and Procedures). The bone marrow biopsypermits categorization of these disorders into 3 separate groups, as shown in the image

below: (1) aplastic or hypoplastic, (2) hyperplastic, and (3) bone marrow replaced with

nonhematopoietic elements (infiltration of bone marrow).

Whenever possible, a cause for the aplastic anemia should be uncovered, becausecessation of exposure may lead to recovery. Identification of the offending agent is

likewise important in determining the prognosis.

Infiltration of the bone marrow with fibrous tissue, neoplastic cells, or other cells that

replace normal hematopoietic tissue can diminish the production of RBCs, granulocytes,

and platelets. The diagnosis of myelofibrosis or neoplastic involvement of bone marrow

is often suggested by evidence of myeloid metaplasia in the peripheral smear (ie,erythroid and granulocyte precursors).

Replacement of bone marrow with nonhemopoietic cells leads to activation of fetal sites

of blood production in organs such as the liver and the spleen, with release of abnormally

shaped erythrocytes and normoblasts, immature granulocytes and normoblasts, immaturegranulocytes, and large platelets into the peripheral blood. Myeloid metaplasia does not


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occur in aplastic disease. Thus, its presence in a patient who is anemic suggests bone

marrow infiltration, even before the biopsy specimen is obtained.

Imaging and Procedures

Imaging studies are useful in the workup for anemia when a neoplastic etiology issuggested. They permit discovery of the neoplasm or centrally located adenopathy.

Occasionally, they are useful in detecting or confirming the existence of splenomegaly.

Investigate GI bleeding by endoscopy and radiographic studies to identify the bleeding

site. However, even these methods may leave a source of GI bleeding undetected,

because these procedures do not detect the bleeding site or the lesion if small. Examplesof these causes include coagulation abnormalities induced by aspirin or platelet

dysfunction, hookworm infestation, hemangiomas of the small bowel, lymphosarcoma

and other tumors, adenomas of the gallbladder, and self-administration of anticoagulants.

Bone marrow aspirates and biopsy findings are particularly useful in establishing the

etiology of anemia in patients with decreased production of RBCs. They help todifferentiate aplasia; megaloblastic hyperplasia; and infiltration of marrow with neoplasia,

myelodysplasia, and myelofibrosis. In addition, they lead to a definitive histologic

diagnosis of leukemias, lymphomas, myelomas, and metastatic carcinomas. Theseprocedures are less useful in detecting hemolytic anemia (except to detect lymphoma or

leukemia), and they are also less useful in diagnosing congenital dyserythropoietic

anemia, in which they reveal the multinuclearity of erythroid precursors. Iron stains of

the bone marrow aspirate can be used to document the existence of iron deficiencyanemia or the sideroblastic anemias.

Approach ConsiderationsThe purpose of establishing the etiology of an anemia is to permit selection of a specific

and effective therapy. For example, corticosteroids are useful in the treatment of

autoimmune hemolytic anemia.

Therapy and medical care vary considerably in the group of hereditary disorders.Splenectomy has been advantageous in hereditary spherocytosis and hereditary

elliptocytosis, in some of the unstable hemoglobinopathies, and in certain patients with

pyruvic kinase deficiency. It has little value in most other hereditary hemolytic disorders.

Drugs and chemicals capable of producing aplasia or a maturation arrest of erythroid

precursors should be discontinued or avoided. Similarly, diseases known to be associatedwith anemia should be appropriately treated. Guidelines related to the treatment of

chemotherapy-associated anemia are available.

Surgery is useful to control bleeding in patients who are anemic. Most commonly,

bleeding is from the GI tract, uterus, or bladder. Patients should be hemodynamicallystable before and during surgery. A blood transfusion may be needed.


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Follow-up

Patients with chronic anemia can usually be cared for on an outpatient basis. Follow-upcare is necessary to ensure that therapy is being continued and to assess the efficacy of

treatment.

Ferrous Sulfate Therapy

The appropriate treatment of anemia due to blood loss is correction of the underlyingcondition and oral administration of ferrous sulfate until the anemia is corrected and for

several months afterward to ensure that body stores are replete with iron. Relatively few

indications exist for the use of parenteral iron therapy, and blood transfusions should be

reserved for the treatment of shock or hypoxia.

A study in Iran demonstrated that once-weekly, low-dose iron supplementation can be

effective in improving iron status and in treating iron deficiency anemia.[14] Mozaffari-

Khosravi et al randomly selected and assigned 193 adolescent girls aged 14-16 years toreceive either 150 mg ferrous sulfate once weekly for 16 weeks or no iron

supplementation. Before and after intervention, the percentage of anemia, iron deficiencyanemia, and iron deficiency were measured in both groups of girls.

Although the parameters measured before the intervention were not significantly different,at the end of 16 weeks, the group that received the ferrous sulfate had significant

improvement in the same parameters.[14] In addition, all cases of iron deficiency anemia

were resolved in the group receiving the low-dose iron supplementation.

Nutritional Therapy and Dietary ConsiderationsNutritional therapy is used to treat deficiencies of iron, vitamin B-12, and folic acid.Pyridoxine may be useful in the treatment of certain patients with sideroblastic anemia,

even though this is not a deficiency disorder. A strict vegetarian diet requires iron and

vitamin B-12 supplementation.

Iron deficiency anemia is prevalent in geographic locations where little meat is in the diet.

Many of these locations have sufficient dietary inorganic iron to equal the iron content inpersons residing in countries in which meat is eaten. However, heme iron is more

efficiently absorbed than inorganic food iron. Folic acid deficiency occurs among people

who consume few leafy vegetables. Coexistence of iron and folic acid deficiency iscommon in developing nations.

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Splenectomy

Splenectomy is useful in the treatment of autoimmune hemolytic anemias and in certain

hereditary hemolytic disorders (ie, hereditary spherocytosis and elliptocytosis, certainunstable Hb disorders, pyruvic kinase deficiency). Improvement in survival rates has

been reported in patients with aplastic anemia, but splenectomy is not the preferentialtherapy. Leg ulcers have shown improvement in some patients with thalassemia. Prior tosplenectomy, patients should be immunized with polyvalent pneumococcal vaccine.

Preferably, this should be administered more than 1 week prior to surgery.

Management of Aplastic Disorders

Treatment of aplastic disorders includes removal of the offending agent whenever it can

be identified, supportive therapy for the anemia and thrombocytopenia, and prompttreatment of infection. Avoid transfusion in patients with a potential bone marrow donor,

because transfusion worsens the probability of cure from transplantation. Certain patientsseem to develop a salutary response with immunosuppressive therapy (ie, antithymocyte

globulin, cyclosporin). Splenectomy may provide sufficient improvement for patientswith hypoplastic, but not totally aplastic, marrow so that transfusion is not necessary and

platelet and granulocyte counts increase to less dangerous levels.

Medication Summary

Therapeutic approaches to treat anemia include blood and blood products,

immunotherapies, hormonal/nutritional therapies, and adjunctive therapies. The goal oftherapy in acute anemia is to restore the hemodynamics of the vascular systems and to

replace lost RBCs. To achieve this, the practitioner may use mineral and vitamin

supplements, blood transfusions, vasopressors, histamine (H2) antagonists, andglucocorticosteroids.

Documentation of the etiology of anemia is essential in the selection of therapy. Not all

microcytic anemias are caused by iron deficiency; some are iron-overloading disorders.

Similarly, not all megaloblastic anemias are associated with either vitamin B-12deficiency or folic acid deficiency. Hereditary hemolytic disorders do not improve with

corticosteroid therapy.


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Referral for Long Case

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