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Following is a list of causes or underlying conditions (see also Misdiagnosis of underlying causes of Anemia) that could possibly cause Anemia includes:
More causes: see full list of causes for Anemia
The follow list shows some of the possible medical causes of Anemia that are listed by the Diseases Database:
The following conditions have been cited in various sources as potentially causal risk factors related to Anemia:
Gender of Patients for Anemia: More common in females...more »
To research the causes of Anemia, consider researching the causes of these these diseases that may be similar, or associated with Anemia:
Causes of Types of Anemia: Review the cause informationfor the various types of Anemia:
Causes of Broader Categories of Anemia: Review the causal information about the various more general categories of medical conditions:
Other conditions that might have Anemia as a complication may, potentially, be an underlying cause of Anemia. Our database lists the following as having Anemia as a complication of that condition:
Conditions listing Anemia as a symptom may also be potential underlying causes of Anemia. Our database lists the following as having Anemia as a symptom of that condition:
The following drugs, medications, substances or toxins are some of the possible
causes of Anemia as a symptom.
This list is incomplete and various other drugs or substances
may cause your symptoms.
Always advise your doctor of any medications or treatments you are using,
including prescription, over-the-counter, supplements, herbal or alternative treatments.
See full list of 466 medications causing Anemia
When combined, certain drugs, medications, substances or toxins may react causing Anemia as a symptom.
The list below is incomplete and various other drugs or substances may cause your symptoms. Always advise your doctor of any medications or treatments you are using, including prescription, over-the-counter, supplements, herbal or alternative treatments.
See full list of 241 drug interactions causing Anemia
The following medical news items are relevant to causes of Anemia:
As with all medical conditions, there may be many causal factors. Further relevant information on causes of Anemia may be found in:
16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Anemia.
Source: In a Page: Signs and Symptoms, 2004
Microcytic
Source: In a Page: Signs and Symptoms, 2004
Source: In a Page: Signs and Symptoms, 2004
Source: In A Page: Pediatric Signs and Symptoms, 2007
Source: In A Page: Pediatric Signs and Symptoms, 2007
Source: In A Page: Pediatric Signs and Symptoms, 2007
In addition to fatigue, AIDS may cause a fever, night sweats, weight loss, diarrhea, and a cough, followed by several concurrent opportunistic infections.
Mild fatigue, the hallmark of adrenocortical insufficiency, initially appears after exertion and stress, but later becomes more severe and persistent. Weakness and weight loss typically accompany GI disturbances, such as nausea, vomiting, anorexia, abdominal pain, and chronic diarrhea; hyperpigmentation; orthostatic hypotension; and a weak, irregular pulse.
Fatigue following mild activity is commonly the first symptom of anemia. Associated findings vary, but generally include pallor, tachycardia, and dyspnea.
Chronic, unremitting anxiety invariably produces fatigue, typically characterized as nervous exhaustion. Other persistent findings include apprehension, indecisiveness, restlessness, insomnia, trembling, and increased muscle tension.
Unexplained fatigue is commonly the earliest sign of cancer. Related findings reflect the type, location, and stage of the tumor and typically include pain, nausea, vomiting, anorexia, weight loss, abnormal bleeding, and a palpable mass.
Chronic fatigue syndrome, whose cause is unknown, is characterized by incapacitating fatigue. Other findings are a sore throat, myalgia, and cognitive dysfunction. Diagnostic criteria have been determined, but research and data collection continues. These findings may alter the diagnostic criteria.
The earliest and most persistent symptoms of COPD are progressive fatigue and dyspnea. The patient may also experience a chronic and usually productive cough, weight loss, barrel chest, cyanosis, slight dependent edema, and poor exercise tolerance.
Persistent fatigue unrelated to exertion nearly always accompanies chronic depression. Associated somatic complaints include a headache, anorexia (occasionally, increased appetite), constipation, and sexual dysfunction. The patient may also experience insomnia, slowed speech, agitation or bradykinesia, irritability, loss of concentration, feelings of worthlessness, and persistent thoughts of death.
Fatigue, the most common symptom in diabetes mellitus, may begin insidiously or abruptly. Related findings include weight loss, blurred vision, polyuria, polydipsia, and polyphagia.
Persistent fatigue and lethargy characterize heart failure. Left-sided heart failure produces exertional and paroxysmal nocturnal dyspnea, orthopnea, and tachycardia. Right-sided heart failure produces jugular vein distention and, possibly, a slight but persistent nonproductive cough. In both types, mental status changes accompany later signs and symptoms, including nausea, anorexia, weight gain and, possibly, oliguria. Cardiopulmonary findings include tachypnea, inspiratory crackles, palpitations and chest tightness, hypotension, a narrowed pulse pressure, a ventricular gallop, pallor, diaphoresis, clubbing, and dependent edema.
Hypercortisolism typically causes fatigue, related in part to accompanying sleep disturbances. Unmistakable signs include truncal obesity with slender extremities, buffalo hump, moon face, purple striae, acne, and hirsutism; increased blood pressure and muscle weakness are other findings.
Fatigue occurs early in hypothyroidism, along with forgetfulness, cold intolerance, weight gain, metrorrhagia, and constipation.
With chronic infection, fatigue is commonly the most prominent symptom — and sometimes the only one. A low-grade fever and weight loss may accompany signs and symptoms that reflect the type and location of infection, such as burning upon urination or swollen, painful gums. Subacute bacterial endocarditis is an example of a chronic infection that causes fatigue and acute hemodynamic decompensation
With acute infection, brief fatigue typically accompanies a headache, anorexia, arthralgia, chills, a high fever, and such infection-specific signs as a cough, vomiting, or diarrhea.
In addition to fatigue and malaise, signs and symptoms of Lyme disease include an intermittent headache, a fever, chills, an expanding red rash, and muscle and joint aches. In later stages, patients may suffer arthritis, fluctuating meningoencephalitis, and cardiac abnormalities, such as a brief, fluctuating atrioventricular heart block
Easy fatigability is common in patients with protein-calorie malnutrition, along with lethargy and apathy. Patients may also exhibit weight loss, muscle wasting, sensations of coldness, pallor, edema, and dry, flaky skin
The cardinal symptoms of myasthenia gravis are easy fatigability and muscle weakness, which worsen as the day progresses. They also worsen with exertion and abate with rest. Related findings depend on the specific muscles affected
Acute renal failurecommonly causes sudden fatigue, drowsiness, and lethargy. Oliguria, an early sign, is followed by severe systemic effects: an ammonia breath odor, nausea, vomiting, diarrhea or constipation, and dry skin and mucous membranes. Neurologic findings include muscle twitching and changes in the patient’s personality and level of consciousness, possibly progressing to seizures and coma.
With chronic renal failure, insidious fatigue and lethargy occur with marked changes in all body systems, including GI disturbances, an ammonia breath odor, Kussmaul’s respirations, bleeding tendencies, poor skin turgor, severe pruritus, paresthesia, visual disturbances, confusion, seizures, and coma.
Fatigue usually occurs along with generalized aching, malaise, a low-grade fever, a headache, and irritability. Primary signs and symptoms include joint pain and stiffness, a butterfly rash, and photosensitivity. Also common are Raynaud’s phenomenon, patchy alopecia, and mucous membrane ulcers.
All types of valvular heart disease commonly produce progressive fatigue and a cardiac murmur. Additional signs and symptoms vary, but generally include exertional dyspnea, a cough, and hemoptysis
Fatigue occurs along with a headache, dyspnea, and confusion and can eventually progress to unconsciousness and apnea.
Fatigue may result from various drugs, notably antihypertensives and sedatives. In those receiving cardiac glycoside therapy, fatigue may indicate toxicity.
Most types of surgery cause temporary fatigue, probably due to the combined effects of hunger, anesthesia, and sleep deprivation.
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Typically, pallor develops gradually with anemia. The patient’s skin may also appear sallow or grayish. Other effects include fatigue, dyspnea, tachycardia, a bounding pulse, an atrial gallop, a systolic bruit over the carotid arteries and, possibly, crackles and bleeding tendencies.
Pallor develops abruptly in the extremity with arterial occlusion, which usually results from an embolus. A line of demarcation develops, separating the cool, pale, cyanotic, and mottled skin below the occlusion from the normal skin above it. Accompanying pallor may be severe pain, intense intermittent claudication, paresthesia, and paresis in the affected extremity. Absent pulses and an increased capillary refill time below the occlusion are also characteristic.
With arterial occlusive disease, pallor is specific to an extremity — usually one leg, but occasionally, both legs or an arm. It develops gradually from obstructive arteriosclerosis or a thrombus and is aggravated by elevating the extremity. Associated findings include intermittent claudication, weakness, cool skin, diminished pulses in the extremity and, possibly, ulceration and gangrene.
Pallor is localized to the frostbitten area, such as the feet, hands, or ears. Typically, the area feels cold, waxy and, perhaps, hard in deep frostbite. The skin doesn’t blanch, and sensation may be absent. As the area thaws, the skin turns purplish blue. Blistering and gangrene may then follow if the frostbite is severe.
With orthostatic hypotension, pallor occurs abruptly on rising from a recumbent position to a sitting or standing position. A precipitous drop in blood pressure, an increase in heart rate, and dizziness are also characteristic. At times, the patient loses consciousness for several minutes.
Pallor of the fingers upon exposure to cold or stress is a hallmark of Raynaud’s disease. Typically, the fingers abruptly turn pale, then cyanotic; with rewarming, they become red and paresthetic. With chronic disease, ulceration may occur.
Two forms of shock initially cause an acute onset of pallor and cool, clammy skin. With hypovolemic shock, other early signs and symptoms include restlessness, thirst, slight tachycardia, and tachypnea. As shock progresses, the skin becomes increasingly clammy, the pulse becomes more rapid and thready, and hypotension develops with narrowing pulse pressure. Other signs and symptoms include oliguria, a subnormal body temperature, and a decreased LOC. With cardiogenic shock, the signs and symptoms are similar but usually more profound.
Source: Handbook of Signs & Symptoms (Third Edition), 2006
This section lists some fetal and placental causes of low birth weight as well as the associated signs and symptoms pres-ent in the neonate at birth.
Abnormalities in the number, size, or configuration of chromosomes can cause low birth weight and possibly multiple congenital anomalies in a premature or SGA neonate
For example, a neonate with trisomy 21 (Down syndrome) may be SGA and have prominent epicanthal folds, a flat-bridged nose, a protruding tongue, palmar simian creases, muscular hypotonia, and an umbilical hernia.
Although low birth weight in cytomegalovirus infection is usually associated with premature birth, the neonate may be SGA
Assessment at birth may reveal these classic signs: petechiae and ecchymoses, jaundice, and hepatosplenomegaly, which increases for several days. The neonate may also have a high fever, lymphadenopathy, tachypnea, and dyspnea, along with prolonged bleeding at puncture sites.
Low birth weight and a wasted appearance occur in an SGA neonate
He may be symmetrically short or may appear relatively long for his low weight. Additional findings reflect the underlying cause. For example, if maternal hyperparathyroidism caused placental dysfunction, the neonate may exhibit muscle jerking and twitching, carpopedal spasm, ankle clonus, vomiting, tachycardia, and tachypnea.
Usually, the low-birth-weight neonate with this congenital rubellais born at term but is SGA
A characteristic “blueberry muffin” rash accompanies cataracts, purpuric lesions, hepatosplenomegaly, and a large anterior fontanel
Abnormal heart sounds, if present, vary with the type of associated congenital heart defect.
Low birth weight is accompanied by cataracts and skin vesicles.
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Aplastic anemias usually develop when damaged or destroyed stem cells inhibit red blood cell (RBC) production. Less commonly, they develop when damaged bone marrow microvasculature creates an unfavorable environment for cell growth and maturation. About one-half of such anemias result from drugs (antibiotics and anticonvulsants), toxic agents (such as benzene and chloramphenicol), or radiation. The rest may result from immunologic factors (unconfirmed), severe disease (especially hepatitis), or preleukemic and neoplastic infiltration of bone marrow.
Idiopathic anemias may be congenital. Two such forms of aplastic anemia have been identified: Congenital hypoplastic anemia (Blackfan-Diamond anemia) develops between ages 2 and 3 months; Fanconi’s syndrome, between birth and age 10. In Fanconi’s syndrome, chromosomal abnormalities are usually associated with multiple congenital anomalies, such as dwarfism, and hypoplasia of the kidneys and spleen. In the absence of a consistent familial or genetic history of aplastic anemia, researchers suspect that these congenital abnormalities result from an induced change in the fetus’development.
Incidence is 0.6 to 6.1 cases per 1 million people. There is no racial predilection.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Folic acid deficiency anemia may result from:
❑ alcohol abuse (alcohol may suppress metabolic effects of folate)
❑ poor diet (common in alcoholics, elderly people living alone, and infants, especially those with infections or diarrhea)
❑ impaired absorption (due to intestinal dysfunction from disorders such as celiac disease, tropical sprue, regional jejunitis, or bowel resection)
❑ bacteria competing for available folic acid
❑ excessive cooking, which can destroy a high percentage of folic acids in foods (See Foods high in folic acid.)
❑ limited storage capacity in infants
❑ prolonged drug therapy (anticonvulsants and estrogens)
❑ increased folic acid requirements during pregnancy; during rapid growth in infancy (common because of recent increase in survival of premature infants); during childhood and adolescence (because of general use of folate-poor cow’s milk); and in patients with neoplastic diseases and some skin diseases (chronic exfoliative dermatitis).
It’s estimated that 10% of the United States population has low folate stores.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Iron deficiency anemia may result from:
❑ inadequate dietary intake of iron (less than 1 to 2 mg/day), such as in prolonged unsupplemented breast-feeding or bottle-feeding of infants or during periods of stress such as rapid growth in children and adolescents
❑ iron malabsorption, such as in chronic diarrhea, partial or total gastrectomy, chronic diverticulosis, and malabsorption syndromes, such as celiac disease and pernicious anemia
❑ blood loss secondary to drug-induced GI bleeding (from anticoagulants, aspirin, and steroids) or due to heavy menses, hemorrhage from trauma, GI ulcers, esophageal varices, or cancer
❑ pregnancy, which diverts maternal iron to the fetus for erythropoiesis
❑ intravascular hemolysis-induced hemoglobinuria or paroxysmal nocturnal hemoglobinuria
❑ mechanical erythrocyte trauma caused by a prosthetic heart valve or vena cava filters.
A common disease worldwide, iron deficiency anemia affects 10% to 30% of the adult population of the United States. It occurs most commonly in premenopausal women, infants (particularly premature or low-birth-weight neonates), children, and adolescents (especially girls). Persons who are at increased risk for iron deficiency include those of low socioeconomic status who don’t get a well-balanced diet that includes iron-rich foods.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Familial incidence of pernicious anemia suggests a genetic predisposition. (It may involve an inherited single dominant autosomal factor.) Significantly higher incidence in patients with immunologically related diseases, such as thyroiditis, myxedema, and Graves’disease, seems to support a widely held theory that an inherited autoimmune response causes gastric mucosal atrophy and, therefore, deficiency of hydrochloric acid and IF. IF deficiency impairs vitamin B12 absorption. The resultant vitamin B12 deficiency inhibits cell growth, particularly of red blood cells (RBCs), leading to insufficient and deformed RBCs with poor oxygen-carrying capacity. It also impairs myelin formation, causing neurologic damage. Iatrogenic induction can follow partial gastrectomy.
Pernicious anemia primarily affects people of northern European ancestry. It’s rare in children and infants. Onset typically occurs after age 35, and incidence increases with age. It affects about 2% of people older than age 60.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Sickle cell anemia results from homozygous inheritance of the gene that produces HbS (chromosome 11). It's inherited as an autosomal recessive trait. Heterozygous inheritance of this gene results in sickle cell trait, a condition that usually produces no symptoms. (See Sickle cell trait.) Sickle cell anemia is most common in tropical Africans and in people of African descent; about 1 in 10 American blacks carries the abnormal gene. However, sickle cell anemia also appears in other ethnic populations, including people of Mediterranean or East Indian ancestry. If two parents who are both carriers of sickle cell trait (or another hemoglobinopathy) have offspring, each child has a 25% chance of developing sickle cell anemia. (See Inheritance patterns in sickle cell anemia, page 22.) Overall, 1 in every 400 to 600 black children has sickle cell anemia. The defective HbS-producing gene may have persisted because, in areas where malaria is endemic, the heterozygous sickle cell trait provides resistance to malaria and is actually beneficial. The abnormal HbS found in such patients' RBCs become insoluble whenever hypoxia occurs. As a result, these RBCs become rigid, rough, and elongated, forming a crescent or sickle shape. (See Comparing normal and sickled red blood cells.) Such sickling can produce hemolysis (cell destruction). In addition, these altered cells tend to pile up in capillaries and smaller blood vessels, making blood more viscous. Normal circulation is impaired, causing pain, tissue infarctions, and swelling. Such blockage causes anoxic changes that lead to further sickling and obstruction.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Hereditary sideroblastic anemia appears to be transmitted by X-linked inheritance, occurring mostly in young males; females are carriers and usually show no signs of this disorder.
The acquired form may be secondary to ingestion of or exposure to toxins, such as alcohol and lead, or to certain drugs. It can also occur as a complication of other diseases, such as rheumatoid arthritis, lupus erythematosus, multiple myeloma, tuberculosis, and severe infections.
The primary acquired form, known as refractory anemia with ringed sideroblasts, is most common in elderly people. It’s commonly associated with thrombocytopenia or leukopenia as part of a myelodysplastic syndrome.
In sideroblastic anemia, normoblasts fail to use iron to synthesize Hb. As a result, iron is deposited in the mitochondria of normoblasts, which are then termed ringed sideroblasts.
Source: Professional Guide to Diseases (Eighth Edition), 2005
The cause of chronic fatigue syndrome (CFS) is unknown, but researchers suspect that it may be found in human herpes virus-6 or in other herpesviruses, enteroviruses, or retroviruses. Recent studies have shown that inflammation of nervous system pathways, acting as an immune or autoimmune response, may play a role as well. CFS may also be associated with a reaction to viral illness that’s complicated by dysfunctional immune response and by other factors that may include gender, age, genetic disposition, prior illness, stress, and environment.
Source: Professional Guide to Diseases (Eighth Edition), 2005
Besides fatigue, this syndrome may cause fever, night sweats, weight loss, diarrhea, and a cough, followed by several concurrent opportunistic infections.
Mild fatigue, the hallmark of this disorder, initially appears after exertion and stress but later becomes more severe and persistent. Weakness and weight loss typically accompany GI disturbances, such as nausea, vomiting, anorexia, abdominal pain, and chronic diarrhea; hyperpigmentation; orthostatic hypotension; and a weak, irregular pulse.
Fatigue after mild activity is commonly the first symptom of anemia. Associated findings vary but generally include pallor, tachycardia, and dyspnea.
Chronic, unremitting anxiety invariably produces fatigue, often characterized as nervous exhaustion. Other persistent findings include apprehension, indecisiveness, restlessness, insomnia, trembling, and increased muscle tension.
Unexplained fatigue is commonly the earliest sign of cancer. Related findings reflect the type, location, and stage of the tumor and typically include pain, nausea, vomiting, anorexia, weight loss, abnormal bleeding, and a palpable mass.
This syndrome, whose cause is unknown, is characterized by incapacitating fatigue. Other findings are sore throat, myalgia, and cognitive dysfunction.
The earliest and most persistent symptoms of this disease are progressive fatigue and dyspnea. The patient may also experience a chronic and usually productive cough, weight loss, barrel chest, cyanosis, slight dependent edema, and poor exercise tolerance.
Severe fatigue typically occurs late in this disorder, accompanied by weight loss, bleeding tendencies, jaundice, hepatomegaly, ascites, dependent edema, severe pruritus, and decreased level of consciousness.
This disorder typically causes fatigue, related in part to accompanying sleep disturbances. Cardinal signs include truncal obesity with slender extremities, buffalo hump, moon face, purple striae, acne, and hirsutism; increased blood pressure and muscle weakness may also occur.
Persistent fatigue unrelated to exertion nearly always accompanies chronic depression. Associated somatic complaints include headache, anorexia (occasionally, increased appetite), constipation, and sexual dysfunction. The patient may also experience insomnia, slowed speech, agitation or bradykinesia, irritability, loss of concentration, feelings of worthlessness, and persistent thoughts of death.
Fatigue, the most common symptom of this disorder, may begin insidiously or abruptly. Related findings include weight loss, blurred vision, polyuria, polydipsia, and polyphagia.
Persistent fatigue and lethargy characterize this disorder. Left-sided heart failure produces exertional and paroxysmal nocturnal dyspnea, orthopnea, and tachycardia. Right-sided heart failure produces jugular vein distention and possibly a slight but persistent nonproductive cough. In both types, later signs and symptoms include mental status changes, nausea, anorexia, weight gain and, possibly, oliguria. Cardiopulmonary findings include tachypnea, inspiratory crackles, palpitations and chest tightness, hypotension, narrowed pulse pressure, ventricular gallop, pallor, diaphoresis, clubbing, and dependent edema.
Fatigue, lethargy, and weakness usually develop slowly. Other insidious effects may include irritability, anorexia, amenorrhea or impotence, decreased libido, hypotension, dizziness, headache, visual disturbances, and cold intolerance.
Fatigue occurs early in this disorder along with forgetfulness, cold intolerance, weight gain, metrorrhagia, and constipation.
Fatigue is commonly the most prominent symptom—and sometimes the only one—in a chronic infection. Low-grade fever and weight loss may accompany signs and symptoms that reflect the type and location of the infection, such as burning on urination or swollen, painful gums. Subacute bacterial endocarditis is an example of a chronic infection that causes fatigue and acute hemodynamic decompensation.
In an acute infection, brief fatigue typically accompanies headache, anorexia, arthralgia, chills, high fever, and such infection-specific signs as a cough, vomiting, or diarrhea.
Besides fatigue and malaise, signs and symptoms of this tick-borne disease include intermittent headache, fever, chills, an expanding red rash, and muscle and joint aches. Later, patients may develop arthritis, fluctuating meningoencephalitis, and cardiac abnormalities, such as a brief, fluctuating atrioventricular heart block.
Easy fatigability, lethargy, and apathy are common findings in patients with protein-calorie malnutrition. Patients may also exhibit weight loss, muscle wasting, sensations of coldness, pallor, edema, and dry, flaky skin.
The cardinal symptoms of this disorder are easy fatigability and muscle weakness, which worsen as the day progresses. They also worsen with exertion and abate with rest. Related findings depend on the specific muscles affected.
Fatigue can be severe but is typically overshadowed by chest pain. Related findings include dyspnea, anxiety, pallor, cold sweats, increased or decreased blood pressure, and abnormal heart sounds.
One or more of the following characterizes this disorder: hypersomnia, hypnagogic hallucinations, cataplexy, sleep paralysis, and insomnia. Fatigue is a common symptom as well.
Acute renal failure commonly causes sudden fatigue, drowsiness, and lethargy. Oliguria, an early sign, is followed by severe systemic effects: ammonia breath odor, nausea, vomiting, diarrhea or constipation, and dry skin and mucous membranes. Neurologic findings include muscle twitching, personality changes, and altered level of consciousness, which may progress to seizures and coma.
Chronic renal failure produces insidious fatigue and lethargy along with marked changes in all body systems, including GI disturbances, ammonia breath odor, Kussmaul’s respirations, bleeding tendencies, poor skin turgor, severe pruritus, paresthesia, visual disturbances, confusion, seizures, and coma.
Chronic fatigue may accompany the characteristic signs and symptoms: dyspnea, cough, and rapid, shallow respirations. Cyanosis first appears with exertion; later, even at rest.
Fatigue, weakness, and anorexia precede localized articular findings: joint pain, tenderness, warmth, and swelling along with morning stiffness.
Fatigue usually occurs along with generalized aching, malaise, low-grade fever, headache, and irritability. Primary signs and symptoms include joint pain and stiffness, butterfly rash, and photosensitivity. Also common are Raynaud’s phenomenon, patchy alopecia, and mucous membrane ulcers.
In this disorder, fatigue may accompany characteristic signs and symptoms, including an enlarged thyroid, tachycardia and palpitations, tremors, weight loss despite increased appetite, diarrhea, dyspnea, nervousness, diaphoresis, heat intolerance, amenorrhea and, possibly, exophthalmos.
All types of valvular heart disease commonly produce progressive fatigue and a cardiac murmur. Additional signs and symptoms vary but generally include exertional dyspnea, cough, and hemoptysis.
Fatigue occurs along with headache, dyspnea, and confusion; apnea and unconsciousness may occur eventually.
Fatigue may result from various drugs, notably antihypertensives and sedatives. In those receiving cardiac glycoside therapy, fatigue may indicate toxicity.
Most types of surgery cause temporary fatigue, probably from the combined effects of hunger, anesthesia, and sleep deprivation.
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Typically, pallor develops gradually with this disorder. The patient’s skin may also appear sallow or grayish. Other effects include fatigue, dyspnea, tachycardia, bounding pulse, atrial gallop, systolic bruit over the carotid arteries and, possibly, crackles and bleeding tendencies.
Pallor develops abruptly in the extremity with the occlusion, which usually results from an embolus. A line of demarcation develops, separating the cool, pale, cyanotic, and mottled skin below the occlusion from the normal skin above it. Accompanying the pallor may be severe pain, intense intermittent claudication, paresthesia, and paresis in the affected extremity. Absent pulses and increased capillary refill time below the occlusion are also characteristic.
With this disorder, pallor is specific to an extremity—usually one leg, but occasionally, both legs or an arm. It develops gradually from obstructive arteriosclerosis or a thrombus and is aggravated by elevating the extremity. Associated findings include intermittent claudication, weakness, cool skin, diminished pulses in the extremity and, possibly, ulceration and gangrene.
Cardiac arrhythmias that seriously reduce cardiac output, such as complete heart block and attacks of tachyarrhythmia, may cause acute onset of pallor. Other features include irregular, rapid, or slow pulse; dizziness; weakness and fatigue; hypotension; confusion; palpitations; diaphoresis; oliguria; and, possibly, loss of consciousness.
Palloris localized to the frostbitten area, such as the feet, hands, or ears. Typically, the area feels cold, waxy and, perhaps, hard in deep frostbite. The skin doesn’t blanch and sensation may be absent. As the area thaws, the skin turns purplish blue. Blistering and gangrene may then follow if the frostbite was severe.
With this condition, pallor occurs abruptly on rising from a recumbent position to a sitting or standing position. A precipitous drop in blood pressure, an increase in heart rate, and dizziness are also characteristic. At times, the patient loses consciousness for several minutes.
Pallor of the fingers upon exposure to cold or stress is a hallmark of this disease. Typically, the fingers abruptly turn pale, then cyanotic; with rewarming, they become red and paresthetic. With chronic disease, ulceration may occur.
Two forms of shock initially cause acute onset of pallor and cool, clammy skin. With hypovolemic shock, other early signs and symptoms include restlessness, thirst, slight tachycardia, and tachypnea. As shock progresses, the skin becomes increasingly clammy, pulse becomes more rapid and thready, and hypotension develops with narrowing pulse pressure. Other signs and symptoms include oliguria, subnormal body temperature, and decreased level of consciousness. With cardiogenic shock, the signs and symptoms are similar, but usually more profound.
Sudden onset of pallor immediately precedes or accompanies loss of consciousness during syncopal attacks. These common fainting spells may be triggered by emotional stress or pain and usually last only a few seconds or minutes. Before loss of consciousness, the patient may exhibit diaphoresis, nausea, yawning, hyperpnea, weakness, confusion, tachycardia, and dim vision. He then develops bradycardia, hypotension, a few clonic jerks, and dilated pupils with loss of consciousness.
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
This section lists some fetal and placental causes of low birth weight as well as the associated signs and symptoms present in the neonate at birth.
Abnormalities in the number, size, or configuration of chromosomes can cause low birth weight and possibly multiple congenital anomalies in a premature or SGA neonate. For example, a neonate with trisomy 21 (Down syndrome) may be SGA and have prominent epicanthal folds, a flat-bridged nose, a protruding tongue, palmar simian creases, muscular hypotonia, and an umbilical hernia.
Although low birth weight in this disorder is usually associated with premature birth, some neonates may be SGA. Assessment at birth may reveal these classic signs: petechiae and ecchymoses, jaundice, and hepatosplenomegaly, which increases for several days. The neonate may also have a high fever, lymphadenopathy, tachypnea, and dyspnea, along with prolonged bleeding at puncture sites.
Low birth weight and a wasted appearance occur in an SGA neonate. The neonate may be symmetrically short or may appear relatively long for his low weight. Additional findings reflect the underlying cause. For example, if maternal hyperparathyroidism caused placental dysfunction, the neonate may exhibit muscle jerking and twitching, carpopedal spasm, ankle clonus, vomiting, tachycardia, and tachypnea.
Usually, the low-birth-weight neonate with this disease is born at term but is SGA. A characteristic “blueberry muffin” rash accompanies cataracts, purpuric lesions, hepatosplenomegaly, and a large anterior fontanel. Abnormal heart sounds, if present, vary with the type of associated congenital heart defect.
The low-birth-weight neonate may be either premature or SGA and may have hydrocephalus or microcephalus. Associated findings include fever, seizures, lymphadenopathy, hepatosplenomegaly, jaundice, and rash. Other defects, which may occur months or years later, include strabismus, blindness, epilepsy, and mental retardation.
Low birth weight is accompanied by cataracts and skin vesicles.
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
❑ Infectious mononucleosis
❑ Depression
❑ Diabetes
❑ Hypothyroidism
❑ Drugs
❑ Chronic sleep deprivation
❑ Congestive heart failure
❑ Occult infection
❑ Iron deficiency anemia
❑ Obstructive sleep apnea
❑ Renal failure
❑ Chronic fatigue syndrome
❑ Cushing syndrome
❑ Occult cancer
❑ Addison disease
❑ Myasthenia gravis
Source: Field Guide to Bedside Diagnosis, 2007
❑ Iron deficiency
❑ Chronic disease
❑ Vitamin B12 deficiency
❑ Subacute blood loss
❑ Thalassemia trait
❑ Folate deficiency
❑ Sickle cell trait
❑ Immune hemolytic anemia
❑ Myeloproliferative disease
❑ Aplastic anemia
❑ Sideroblastic anemia
Source: Field Guide to Bedside Diagnosis, 2007
❑ Musculoligamentous strain
❑ Lumbar disc herniation
❑ Osteoarthritis
❑ Compression fracture
❑ Pyelonephritis
❑ Secondary gain
❑ Scoliosis
❑ Spondylolisthesis
❑ Metastatic cancer
❑ Spinal stenosis
❑ Transverse process fracture
❑ Pancreatic cancer
❑ Ankylosing spondylitis
❑ Sacroiliitis
❑ Aortic dissection
❑ Cauda equina syndrome
❑ Vertebral osteomyelitis
❑ Epidural abscess
Source: Field Guide to Bedside Diagnosis, 2007
Aplastic anemias usually develop when damaged or destroyed stem cells inhibit red blood cell (RBC) production. Less commonly, they develop when damaged bone marrow microvasculature creates an unfavorable environment for cell growth and maturation. About half of such anemias result from drugs (antibiotics, anticonvulsants), toxic agents (such as benzene and chloramphenicol), or radiation. The rest may result from immunologic factors (unconfirmed), severe disease (especially hepatitis), or preleukemic and neoplastic infiltration of bone marrow. (See Understanding bone marrow transplantation.)
Idiopathic anemias may be congenital and account for about 50% of all confirmed occurrences. Two such forms of aplastic anemia have been identified: congenital hypoplastic anemia (Blackfan-Diamond anemia), which develops between ages 2 months and 3 months, and Fanconi’s syndrome, which develops between birth and age 10.
With Fanconi’s syndrome, chromosomal abnormalities are typically associated with multiple congenital anomalies — such as dwarfism and hypoplasia of the kidneys and spleen. In the absence of a consistent familial or genetic history of aplastic anemia, researchers suspect that these congenital abnormalities result from an induced change in the development of the fetus.
Source: Handbook of Diseases, 2003
Folic acid deficiency anemia results from a decreased level or lack of folate, a vitamin that’s essential for red blood cell production and maturation. Causes include:
❑ alcohol abuse (may suppress metabolic effects of folate)
❑ inadequate diet (common in alcoholics, elderly people who live alone, and infants, especially those with infections or diarrhea)
❑ impaired absorption (due to intestinal dysfunction from such disorders as celiac disease, tropical sprue, and regional jejunitis and from bowel resection)
❑ bacteria competing for available folic acid
❑ overcooking, which can destroy a high percentage of folic acids in foods
❑ limited storage capacity in infants
❑ prolonged drug therapy (with anticonvulsants and estrogens)
❑ increased folic acid requirement during pregnancy, during rapid growth in infancy (common because of increased survival rate of preterm infants), during childhood and adolescence (because of general use of folate-poor cow’s milk), and in patients with neoplastic diseases and some skin diseases (chronic exfoliative dermatitis).
Source: Handbook of Diseases, 2003
Iron deficiency anemia may result from:
❑ inadequate dietary intake of iron (less than 2 mg/day) — for example, during prolonged, unsupplemented periods of breast- or bottle-feeding (not eating solid foods after age 6 months) and during periods of stress, such as rapid growth in children and adolescents
❑ iron malabsorption, as in chronic diarrhea, partial or total gastrectomy, and malabsorption syndromes such as celiac disease
❑ blood loss secondary to drug-induced GI bleeding (from anticoagulants, aspirin, or steroids) or due to heavy menses, hemorrhage from trauma, a GI ulcer, cancer, or bleeding varices
❑ pregnancy, which diverts maternal iron to the fetus for erythropoiesis
❑ intravascular hemolysis-induced hemoglobinuria or paroxysmal nocturnal hemoglobinuria
❑ mechanical erythrocyte trauma caused by a prosthetic heart valve or vena cava filters.
Iron deficiency anemia is most common in premenopausal women, infants (particularly premature and low-birth-weight infants), children, and adolescents (especially girls).
Source: Handbook of Diseases, 2003
Familial incidence of pernicious anemia suggests a genetic predisposition. A significantly higher incidence in patients with immunologically related diseases — such as thyroiditis, myxedema, and Graves’ disease — seems to support a widely held theory that an inherited autoimmune response causes gastric mucosal atrophy and, therefore, deficiency of hydrochloric acid and IF.
Deficiency of IF impairs absorption of vitamin B12. The resultant vitamin B12 deficiency inhibits cell growth, particularly of red blood cells (RBCs), leading to insufficient and deformed RBCs with poor oxygen-carrying capacity. Vitamin B12 deficiency also impairs myelin formation, causing neurologic damage. Iatrogenic induction of IF deficiency can follow partial gastrectomy.
Source: Handbook of Diseases, 2003
Sickle cell anemia results from homo-zygous inheritance of the Hb S gene, which causes substitution of the amino acid valine for glutamic acid in the B Hb chain. Heterozygous inheritance of this gene results in sickle cell trait, usually an asymptomatic condition. (See Sickle cell trait, page 774.)
The abnormal Hb S found in RBCs of patients with sickle cell anemia becomes insoluble whenever hypoxia occurs. As a result, these RBCs become rigid, rough, and elongated, forming a crescent, or sickle, shape. Such sickling can produce hemolysis (cell destruction).
In addition, these altered cells tend to pile up in capillaries and smaller blood vessels, making the blood more viscous. Normal circulation is impaired, causing pain, tissue infarctions, and swelling. Such blockage causes anoxic changes that lead to further sickling and obstruction.
Source: Handbook of Diseases, 2003
Hereditary sideroblastic anemia appears to be transmitted by X-linked inheritance, occurring mostly in young males; females are carriers and usually show no signs of this disorder.
The acquired form may be secondary to ingestion of, or exposure to, toxins, such as alcohol and lead, or to drugs, such as isoniazid and chloramphenicol. It can also occur as a complication of other diseases, such as rheumatoid arthritis, lupus erythematosus, multiple myeloma, tuberculosis, and severe infections.
The primary acquired form, known as refractory anemia with ringed sideroblasts, is most common in elderly people. It’s often associated with thrombocytopenia or leukopenia as part of a myelodysplastic syndrome.
In sideroblastic anemia, normoblasts fail to use iron to synthesize Hb. As a result, iron is deposited in the mitochondria of normoblasts, which are then called ringed sideroblasts.
Source: Handbook of Diseases, 2003
Although the cause of CFIDS is unknown, researchers suspect that it may be found in human herpesvirus 6 or in other herpesviruses, enteroviruses, or retroviruses. Rising levels of antibodies to EBV, once thought to implicate EBV infection as the cause of CFIDS, are now considered a result of this disease.
CFIDS may be associated with a reaction to viral illness that’s complicated by dysfunctional immune response and by other factors that may include sex, age, genetic disposition, prior illness, stress, and environment.
Source: Handbook of Diseases, 2003
Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
In addition to fatigue, acquired immunodeficiency syndrome (AIDS) may cause fever, night sweats, weight loss, diarrhea, and a cough, followed by several concurrent opportunistic infections. The patient may also show signs of malnutrition.
Mild fatigue, the hallmark of adrenocortical insufficiency, initially appears after exertion and stress but later becomes more severe and persistent. Weakness and weight loss typically accompany GI disturbances, such as nausea, vomiting, anorexia, abdominal pain, and chronic diarrhea; hyperpigmentation; orthostatic hypotension; and a weak, irregular pulse.
Fatigue following mild activity is commonly the first symptom of anemia. Associated findings vary but generally include listlessness, irritability, inability to concentrate, pallor, tachycardia, and dyspnea.
CULTURAL CUE:To detect anemia-related pallor in the dark-skinned patient, assess his oral mucosa.
Chronic, unremitting anxiety invariably produces fatigue, commonly characterized as nervous exhaustion. Other persistent findings include apprehension, indecisiveness, restlessness, insomnia, trembling, and increased muscle tension.
Unexplained fatigue is commonly the earliest sign of cancer. Related findings reflect the type, location, and stage of the tumor and typically include pain, nausea, vomiting, anorexia, weight loss, abnormal bleeding, and a palpable mass.
Chronic fatigue syndrome, the cause of which is unknown, is characterized by incapacitating fatigue. Other findings are sore throat, myalgia, low-grade fever, painful lymph nodes, sleep disturbances, and cognitive dysfunction.
The earliest and most persistent symptoms of chronic obstructive pulmonary disease (COPD) are progressive fatigue and dyspnea. The patient may also experience a chronic and usually productive cough, weight loss, barrel chest, cyanosis, slight dependent edema, and poor exercise tolerance.
Severe fatigue typically occurs late in cirrhosis, accompanied by weight loss, bleeding tendencies, jaundice, hepatomegaly, ascites, dependent edema, severe pruritus, and decreased level of consciousness (LOC).
Persistent fatigue unrelated to exertion nearly always accompanies chronic depression. Associated somatic complaints include headache, anorexia (occasionally, increased appetite), constipation, and sexual dysfunction. The patient may also experience insomnia, slowed speech, agitation or bradykinesia, irritability, loss of concentration, feelings of worthlessness, and persistent thoughts of death.
Fatigue, the most common symptom in diabetes mellitus, may begin insidiously or abruptly. Related findings include weight loss, blurred vision, polyuria, polydipsia, and polyphagia.
Persistent fatigue and lethargy characterize heart failure. Left-sided heart failure produces exertional and paroxysmal nocturnal dyspnea, orthopnea, and tachycardia. Right-sided heart failure produces jugular vein distention and possibly a slight but persistent nonproductive cough. In both types, mental status changes accompany later signs and symptoms, including nausea, anorexia, weight gain and, possibly, oliguria. Cardiopulmonary findings include tachypnea, inspiratory crackles, palpitations and chest tightness, hypotension, narrowed pulse pressure, ventricular gallop, pallor, diaphoresis, clubbing, and dependent edema.
Hypercortisolism typically causes fatigue, related in part to accompanying sleep disturbances. Unmistakable signs include truncal obesity with slender extremities, buffalo hump, moon face, purple striae, acne, and hirsutism; increased blood pressure and muscle weakness are other findings.
With hypopituitarism, fatigue, lethargy, and weakness usually develop slowly. Other insidious effects may include irritability, anorexia, amenorrhea or impotence, decreased libido, hypotension, dizziness, headache, visual disturbances, and cold intolerance.
Fatigue occurs early in hypothyroidism, along with forgetfulness, cold intolerance, weight gain, metrorrhagia, and constipation. Related findings include coarse hair and alopecia; anorexia; edema; dry, flaky skin; and thinning nails.
With chronic infection (such as acute bacterial endocarditis), fatigue is commonly the most prominent symptom — and sometimes the only one. Low-grade fever and weight loss may accompany signs and symptoms that reflect the type and location of infection, such as burning upon urination or swollen, painful gums.
With acute infection, brief fatigue typically accompanies headache, anorexia, arthralgia, chills, high fever, and such infection-specific signs as cough, vomiting, or diarrhea.
Besides fatigue and malaise, signs and symptoms of Lyme disease include intermittent headache, fever, chills, expanding red rash, and muscle and joint aches. In later stages of this tick-borne disease, patients may suffer arthritis, fluctuating meningoencephalitis, and cardiac abnormalities, such as a brief, fluctuating atrioventricular heart block.
Easy fatigability is common in patients with protein-calorie malnutrition, along with lethargy and apathy. Patients may also exhibit weight loss, muscle wasting, sensations of coldness, pallor, edema, and dry, flaky skin.
The cardinal symptoms of myasthenia gravis are easy fatigability and muscle weakness, which worsen as the day progresses. They also worsen with exertion and abate with rest. Related findings depend on the specific muscles affected.
With myocardial infarction (MI), fatigue can be severe but is typically overshadowed by chest pain. Related findings include dyspnea, anxiety, pallor, cold sweats, increased or decreased blood pressure, and abnormal heart sounds.
One or more of the following characterizes narcolepsy: hypersomnia, hypnagogic hallucinations, cataplexy, sleep paralysis, and insomnia. Fatigue is a common symptom as well.
Acute renal failure commonly causes sudden fatigue, drowsiness, and lethargy. Oliguria, an early sign, is followed by severe systemic effects: ammonia breath odor, nausea, vomiting, diarrhea or constipation, and dry skin and mucous membranes. Neurologic findings include muscle twitching and changes in personality and LOC, possibly progressing to seizures and coma.
With chronic renal failure, insidious fatigue and lethargy occur with marked changes in all body systems, including GI disturbances, ammonia breath odor, Kussmaul’s respirations, bleeding tendencies, poor skin turgor, severe pruritus, paresthesia, visual disturbances, confusion, seizures, and coma.
Chronic fatigue may accompany the characteristic signs and symptoms of restrictive lung disease: dyspnea, cough, and rapid, shallow respirations. Cyanosis first appears with exertion; later, even at rest.
With rheumatoid arthritis, fatigue, weakness, and anorexia precede localized articular findings: joint pain, tenderness, warmth, and swelling along with morning stiffness. Assessment findings may include enlarged lymph nodes, fever, leukopenia, anemia, subcutaneous nodules, pericarditis, and Raynaud’s phenomenon.
Fatigue usually occurs in patients with systemic lupus erythematosus (SLE), along with generalized aching, malaise, low-grade fever, headache, and irritability. Primary signs and symptoms include joint pain and stiffness, butterfly rash, and photosensitivity. Also common are Raynaud’s phenomenon, patchy alopecia, and mucous membrane ulcers.
With thyrotoxicosis, fatigue may occur with characteristic signs and symptoms, including an enlarged thyroid, tachycardia and palpitations, tremors, weight loss despite increased appetite, diarrhea, dyspnea, nervousness, diaphoresis, heat intolerance, amenorrhea and, possibly, exophthalmos.
All types of valvular heart disease commonly produce progressive fatigue and a cardiac murmur. Additional signs and symptoms vary but generally include exertional dyspnea, cough, and hemoptysis.
With carbon monoxide poisoning, fatigue occurs along with headache, dyspnea, and confusion, and can eventually progress to unconsciousness and apnea.
Fatigue may result from various drugs, notably antihypertensives and sedatives. In persons receiving cardiac glycoside therapy, fatigue may indicate toxicity.
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Typically, pallor develops gradually with anemia. The patient’s skin may also appear sallow or grayish. Other effects include fatigue, dyspnea, tachycardia, bounding pulse, atrial gallop, systolic bruit over the carotid arteries and, possibly, crackles and bleeding tendencies.
Pallor develops abruptly in the extremity with the occlusion, which usually results from an embolus. A line of demarcation develops, separating the cool, pale, cyanotic, and mottled skin below the occlusion from the normal skin above it. Accompanying the pallor may be severe pain, intense intermittent claudication, paresthesia, and paresis in the affected extremity. Absent pulses and increased capillary refill time below the occlusion are also characteristic.
With chronic arterial occlusive disease, pallor is specific to an extremity — usually one leg, but occasionally both legs or an arm. It develops gradually from obstructive arteriosclerosis or a thrombus and is aggravated by elevating the extremity. Associated findings include intermittent claudication, weakness, cool skin, diminished pulses in the extremity and, possibly, ulceration and gangrene.
Cardiac arrhythmias that seriously reduce cardiac output, such as complete heart block and attacks of tachyarrhythmia, may cause acute onset of pallor. Other features include irregular, rapid, or slow pulse; dizziness; weakness and fatigue; hypotension; confusion; palpitations; diaphoresis; oliguria; and, possibly, loss of consciousness.
Palloris localized to the frostbitten area, such as the feet, hands, or ears. Typically, the area feels cold, waxy and, perhaps, hard if the frostbite is deep. The skin doesn’t blanch and sensation may be absent. As the area thaws, the skin turns purplish blue. Blistering and gangrene may then follow if the frostbite is severe.
With orthostatic hypotension, pallor occurs abruptly on rising from a recumbent position to a sitting or standing position. A precipitous drop in blood pressure, an increase in heart rate, and dizziness are also characteristic. At times, the patient loses consciousness for several minutes.
Pallor of the fingers upon exposure to cold or stress is a hallmark of Raynaud’s disease. Typically, the fingers abruptly turn pale, then cyanotic; with rewarming, they become red and paresthetic. With chronic disease, ulceration may occur.
Two forms of shock initially cause acute onset of pallor and cool, clammy skin. With hypovolemic shock, other early signs and symptoms include restlessness, thirst, slight tachycardia, and tachypnea. As shock progresses, the skin becomes increasingly clammy, pulse becomes more rapid and thready, and hypotension develops with narrowing pulse pressure. Other signs and symptoms include oliguria, subnormal body temperature, and decreased level of consciousness. With cardiogenic shock, the signs and symptoms are similar, but usually more profound.
Sudden onset of pallor immediately precedes or accompanies loss of consciousness during syncopal attacks. These common fainting spells may be triggered by emotional stress or pain and usually last only a few seconds or minutes. Before loss of consciousness, the patient may exhibit diaphoresis, nausea, yawning, hyperpnea, weakness, confusion, tachycardia, and dim vision. He then develops bradycardia, hypotension, a few clonic jerks, and dilated pupils with loss of consciousness.
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Acquired immunodeficiency syndrome (AIDS).In addition to fatigue, AIDS may cause a fever, night sweats, weight loss, diarrhea, and a cough, followed by several concurrent opportunistic infections.
Adrenocortical insufficiency.Mild fatigue, the hallmark of adrenocortical insufficiency, initially appears after exertion and stress, but later becomes more severe and persistent. Weakness and weight loss typically accompany GI disturbances, such as nausea, vomiting, anorexia, abdominal pain, and chronic diarrhea; hyperpigmentation; orthostatic hypotension; and a weak, irregular pulse.
Anemia.Fatigue following mild activity is commonly the first symptom of anemia. Associated findings vary, but generally include pallor, tachycardia, and dyspnea.
Anxiety.Chronic, unremitting anxiety invariably produces fatigue, typically characterized as nervous exhaustion. Other persistent findings include apprehension, indecisiveness, restlessness, insomnia, trembling, and increased muscle tension.
Cancer.Unexplained fatigue is commonly the earliest sign of cancer. Related findings reflect the type, location, and stage of the tumor and typically include pain, nausea, vomiting, anorexia, weight loss, abnormal bleeding, and a palpable mass.
Chronic fatigue syndrome.Chronic fatigue syndrome, whose cause is unknown, is characterized by incapacitating fatigue. Other findings are a sore throat, myalgia, and cognitive dysfunction. Diagnostic criteria have been determined, but research and data collection continue. These findings may alter the diagnostic criteria.
Chronic obstructive pulmonary disease (COPD).The earliest and most persistent symptoms of COPD are progressive fatigue and dyspnea. The patient may also experience a chronic and usually productive cough, weight loss, barrel chest, cyanosis, slight dependent edema, and poor exercise tolerance.
Depression.Persistent fatigue unrelated to exertion nearly always accompanies chronic depression. Associated somatic complaints include a headache, anorexia (occasionally, increased appetite), constipation, and sexual dysfunction. The patient may also experience insomnia, slowed speech, agitation or bradykinesia, irritability, loss of concentration, feelings of worthlessness, and persistent thoughts of death.
Diabetes mellitus.Fatigue, the most common symptom in diabetes mellitus, may begin insidiously or abruptly. Related findings include weight loss, blurred vision, polyuria, polydipsia, and polyphagia.
Heart failure.Persistent fatigue and lethargy characterize heart failure. Left-sided heart failure produces exertional and paroxysmal nocturnal dyspnea, orthopnea, and tachycardia. Right-sided heart failure produces jugular vein distention and, possibly, a slight but persistent nonproductive cough. In both types, mental status changes accompany later signs and symptoms, including nausea, anorexia, weight gain and, possibly, oliguria. Cardiopulmonary findings include tachypnea, inspiratory crackles, palpitations and chest tightness, hypotension, a narrowed pulse pressure, a ventricular gallop, pallor, diaphoresis, clubbing, and dependent edema.
Hypercortisolism.Hypercortisolism typically causes fatigue, related in part to accompanying sleep disturbances. Unmistakable signs include truncal obesity with slender extremities, buffalo hump, moon face, purple striae, acne, and hirsutism; increased blood pressure and muscle weakness are other findings.
Hypothyroidism.Fatigue occurs early in hypothyroidism, along with forgetfulness, cold intolerance, weight gain, metrorrhagia, and constipation.
Infection.With chronic infection, fatigue is commonly the most prominent symptom—and sometimes the only one. A low-grade fever and weight loss may accompany signs and symptoms that reflect the type and location of infection, such as burning upon urination or swollen, painful gums. Subacute bacterial endocarditis is an example of a chronic infection that causes fatigue and acute hemodynamic decompensation.
With acute infection, brief fatigue typically accompanies a headache, anorexia, arthralgia, chills, a high fever, and such infection-specific signs as a cough, vomiting, or diarrhea.
Lyme disease.In addition to fatigue and malaise, signs and symptoms of Lyme disease include an intermittent headache, a fever, chills, an expanding red rash, and muscle and joint aches. In later stages, patients may suffer arthritis, fluctuating meningoencephalitis, and cardiac abnormalities, such as a brief, fluctuating atrioventricular heart block.
Malnutrition.Easy fatigability is common in patients with protein-calorie malnutrition, along with lethargy and apathy. Patients may also exhibit weight loss, muscle wasting, sensations of coldness, pallor, edema, and dry, flaky skin.
Myasthenia gravis.The cardinal symptoms of myasthenia gravis are easy fatigability and muscle weakness, which worsen as the day progresses. They also worsen with exertion and abate with rest. Related findings depend on the specific muscles affected. (See Managing the patient with myasthenia gravis.)
Renal failure.Acute renal failure commonly causes sudden fatigue, drowsiness, and lethargy. Oliguria, an early sign, is followed by severe systemic effects: an ammonia breath odor, nausea, vomiting, diarrhea or constipation, and dry skin and mucous membranes. Neurologic findings include muscle twitching and changes in the patient's personality and level of consciousness, possibly progressing to seizures and coma.
With chronic renal failure, insidious fatigue and lethargy occur with marked changes in all body systems, including GI disturbances, an ammonia breath odor, Kussmaul's respirations, bleeding tendencies, poor skin turgor, severe pruritus, paresthesia, vision disturbances, confusion, seizures, and coma.
Systemic lupus erythematosus (SLE).Fatigue usually occurs with SLE along with generalized aching, malaise, a low-grade fever, a headache, and irritability. Primary signs and symptoms include joint pain and stiffness, a butterfly rash, and photosensitivity. Also common are Raynaud's phenomenon, patchy alopecia, and mucous membrane ulcers.
Valvular heart disease.All types of valvular heart disease commonly produce progressive fatigue and a cardiac murmur. Additional signs and symptoms vary, but generally include exertional dyspnea, a cough, and hemoptysis.
Carbon monoxide poisoning.Fatigue occurs with carbon monoxide poisoning along with a headache, dyspnea, and confusion and can eventually progress to unconsciousness and apnea.
Drugs.Fatigue may result from various drugs, notably antihypertensives and sedatives. In those receiving cardiac glycoside therapy, fatigue may indicate toxicity.
Surgery.Most types of surgery cause temporary fatigue, probably due to the combined effects of hunger, anesthesia, and sleep deprivation.
Source: Nursing: Interpreting Signs and Symptoms, 2007
Anemia.Typically, pallor develops gradually with anemia. The patient's skin may also appear sallow or grayish. Other effects include fatigue, dyspnea, tachycardia, a bounding pulse, an atrial gallop, a systolic bruit over the carotid arteries and, possibly, crackles and bleeding tendencies.
Arterial occlusion (acute).Pallor develops abruptly in the extremity with arterial occlusion, which usually results from an embolus. A line of demarcation develops, separating the cool, pale, cyanotic, and mottled skin below the occlusion from the normal skin above it. Accompanying pallor may be severe pain, intense intermittent claudication, paresthesia, and paresis in the affected extremity. Absent pulses and an increased capillary refill time below the occlusion are also characteristic.
Arterial occlusive disease (chronic).With arterial occlusive disease, pallor is specific to an extremity—usually one leg, but occasionally, both legs or an arm. It develops gradually from obstructive arteriosclerosis or a thrombus and is aggravated by elevating the extremity. Associated findings include intermittent claudication, weakness, cool skin, diminished pulses in the extremity and, possibly, ulceration and gangrene.
Frostbite.Pallor is localized to the frostbitten area, such as the feet, hands, nose, or ears. Typically, the area feels cold, waxy and, perhaps, hard in deep frostbite. The skin doesn't blanch, and sensation may be absent. As the area thaws, the skin turns purplish blue. Blistering and gangrene may then follow if the frostbite is severe.
Orthostatic hypotension.With orthostatic hypotension, pallor occurs abruptly on rising from a recumbent position to a sitting or standing position. A precipitous drop in blood pressure, an increase in heart rate, and dizziness are also characteristic. At times, the patient loses consciousness for several minutes.
Raynaud's disease.Pallor of the fingers upon exposure to cold or stress is a hallmark of Raynaud's disease. Typically, the fingers abruptly turn pale, then cyanotic; with rewarming, they become red and paresthetic. With chronic disease, ulceration may occur.
Shock.Two forms of shock initially cause an acute onset of pallor and cool, clammy skin. With hypovolemic shock, other early signs and symptoms include restlessness, thirst, slight tachycardia, and tachypnea. As shock progresses, the skin becomes increasingly clammy, the pulse becomes more rapid and thready, and hypotension develops with narrowing pulse pressure. Other signs and symptoms include oliguria, a subnormal body temperature, and decreased LOC. With cardiogenic shock, the signs and symptoms are similar but usually more profound.
Source: Nursing: Interpreting Signs and Symptoms, 2007
This section lists some fetal and placental causes of low birth weight as well as the associated signs and symptoms present in the neonate at birth.
Chromosomal aberrations.Abnormalities in the number, size, or configuration of chromosomes can cause low birth weight and possibly multiple congenital anomalies in a premature or SGA neonate. For example, a neonate with trisomy 21 (Down syndrome) may be SGA and have prominent epicanthal folds, a flat-bridged nose, a protruding tongue, palmar simian creases, muscular hypotonia, and an umbilical hernia.
Cytomegalovirus infection.Although low birth weight in cytomegalovirus infection is usually associated with premature birth, the neonate may be SGA. Assessment at birth may reveal these classic signs: petechiae and ecchymoses, jaundice, and hepatosplenomegaly, which increases for several days. The neonate may also have a high fever, lymphadenopathy, tachypnea, and dyspnea, along with prolonged bleeding at puncture sites.
Placental dysfunction.With placental dysfunction, low birth weight and a wasted appearance occur in an SGA neonate. He may be symmetrically short or may appear relatively long for his low weight. Additional findings reflect the underlying cause. For example, if maternal hyperparathyroidism caused placental dysfunction, the neonate may exhibit muscle jerking and twitching, carpopedal spasm, ankle clonus, vomiting, tachycardia, and tachypnea.
Rubella (congenital).Usually, the low-birth-weight neonate with congenital rubella is born at term but is SGA. A characteristic “blueberry muffin” rash accompanies cataracts, purpuric lesions, hepatosplenomegaly, and a large anterior fontanel. Abnormal heart sounds, if present, vary with the type of associated congenital heart defect.
Varicella (congenital).With congenital varicella, low birth weight is accompanied by cataracts and skin vesicles.
Source: Nursing: Interpreting Signs and Symptoms, 2007
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Medical Articles:
Sickle cell anemia:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Sideroblastic anemias:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Chronic fatigue syndrome:
Causes
(Professional Guide to Diseases (Eighth Edition))
Fatigue:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Acquired immunodeficiency syndrome
Adrenocortical insufficiency
Anemia
Anxiety
Cancer
Chronic fatigue syndrome
Chronic obstructive pulmonary disease
Cirrhosis
Cushing’s syndrome (hypercortisolism)
Depression
Diabetes mellitus
Heart failure
Hypopituitarism
Hypothyroidism
Infection
Lyme disease
Malnutrition
Myasthenia gravis
Myocardial infarction
Narcolepsy
Renal failure
Restrictive lung disease
Rheumatoid arthritis
Systemic lupus erythematosus
Thyrotoxicosis
Valvular heart disease
Other causes
Carbon monoxide poisoning
Drugs
Surgery
Pallor:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Anemia
Arterial occlusion (acute)
Arterial occlusive disease (chronic)
Cardiac arrhythmias
Frostbite
Orthostatic hypotension
Raynaud’s disease
Shock
Vasopressor syncope
Low birth weight:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Chromosomal aberrations
Cytomegalovirus infection
Placental dysfunction
Rubella (congenital)
Toxoplasmosis (congenital)
Varicella (congenital)
Fatigue:
Differential Overview
(Field Guide to Bedside Diagnosis)
Anemia:
Differential Overview
(Field Guide to Bedside Diagnosis)
Low Back Pain:
Differential Overview
(Field Guide to Bedside Diagnosis)
Aplastic and hypoplastic anemias:
Causes
(Handbook of Diseases)
Folic acid deficiency anemia:
Causes
(Handbook of Diseases)
Iron deficiency anemia:
Causes
(Handbook of Diseases)
Pernicious anemia:
Causes
(Handbook of Diseases)
Sickle cell anemia:
Causes
(Handbook of Diseases)
Altered cells
Sideroblastic anemias:
Causes
(Handbook of Diseases)
Chronic fatigue and immune dysfunction syndrome:
Causes
(Handbook of Diseases)
Pallor:
Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Anemia
Typically, pallor develops gradually with anemia. The patient’s skin may also appear sallow or grayish. Other effects include fatigue, dyspnea, tachycardia, bounding pulse, atrial gallop, systolic bruit over the carotid arteries and, possibly, crackles and bleeding tendencies.
Arterial occlusion (acute)
Pallor develops abruptly in the extremity with the occlusion, which usually results from an embolus. A line of demarcation develops, separating the cool, pale, cyanotic, and mottled skin below the occlusion from the normal skin above it. Accompanying the pallor may be severe pain, intense intermittent claudication, paresthesia, and paresis in the affected extremity. Absent pulses and increased capillary refill time below the occlusion are also characteristic.
Arterial occlusive disease (chronic)
With chronic arterial occlusive disease, pallor is specific to an extremity — usually one leg, but occasionally, both legs or an arm. It develops gradually from obstructive arteriosclerosis or a thrombus and is aggravated by elevating the extremity. Associated findings include intermittent claudication, weakness, cool skin, diminished pulses in the extremity and, possibly, ulceration and gangrene.
Cardiac arrhythmias
Serious reductions in cardiac output caused by complete heart block and attacks of tachyarrhythmia may lead to pallor. Other features include an irregular, rapid, or slow pulse as well as dizziness, weakness and fatigue, hypotension, confusion, palpitations, diaphoresis, oliguria and, possibly, loss of consciousness.
Frostbite
Palloris localized to the frostbitten area, such as the feet, hands, or ears. Typically, the area feels cold, waxy and, perhaps, hard in deep frostbite. The skin doesn’t blanch and sensation may be absent. As the area thaws, the skin turns purplish blue. Blistering and gangrene may then follow if the frostbite is severe.
Orthostatic hypotension
With orthostatic hypertension, pallor occurs abruptly on rising from a recumbent position to a sitting or standing position. A precipitous drop in blood pressure, an increase in heart rate, and dizziness are also characteristic. At times, the patient loses consciousness for several minutes.
Raynaud’s disease
Pallor of the fingers upon exposure to cold or stress is a hallmark of Raynaud’s disease. Typically, the fingers abruptly turn pale and then cyanotic; with rewarming, they become red and paresthetic. With chronic disease, ulceration may occur.
Shock
Two forms of shock initially cause an acute onset of pallor and cool, clammy skin. With hypovolemic shock, other early signs and symptoms include restlessness, thirst, slight tachycardia, and tachypnea. As shock progresses, the skin becomes increasingly clammy, the pulse becomes more rapid and thready, and hypotension develops with narrowing pulse pressure. Other signs and symptoms include oliguria, subnormal body temperature, and a decreased LOC. With cardiogenic shock, the signs and symptoms are similar, but usually more profound.
Vasopressor syncope
The sudden onset of pallor immediately precedes or accompanies loss of consciousness during syncopal attacks. These common fainting spells may be triggered by emotional stress or pain and usually last only a few seconds or minutes. Before loss of consciousness, the patient may exhibit diaphoresis, nausea, yawning, hyperpnea, weakness, confusion, tachycardia, and dim vision. He then develops bradycardia, hypotension, a few clonic jerks, and dilated pupils with loss of consciousness.
Fatigue:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Acquired immunodeficiency syndrome
Adrenocortical insufficiency
Anemia
Anxiety
Cancer
Chronic fatigue syndrome
Chronic obstructive pulmonary disease
Cirrhosis
Depression
Diabetes mellitus
Heart failure
Hypercortisolism
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Infection
Lyme disease
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Myasthenia gravis
Myocardial infarction
Narcolepsy
Renal failure
Restrictive lung disease
Rheumatoid arthritis
Systemic lupus erythematosus
Thyrotoxicosis
Valvular heart disease
Other causes
Carbon monoxide poisoning
Drugs
Pallor:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Anemia
Arterial occlusion (acute)
Arterial occlusive disease (chronic)
Cardiac arrhythmias
Frostbite
Orthostatic hypotension
Raynaud’s disease
Shock
Vasopressor syncope
Fatigue:
Principal Causes of Fatigue
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Pallor (Anemia):
Principal Causes of Pallor (Anemia)
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Fatigue:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Other causes
Pallor:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Low birth weight:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
» Next page: Risk Factors for Anemia
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Copyright © 2010 Health Grades Inc. All rights reserved. Last Update: 8 February, 2010 (23:53)
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