Diseases » Anthrax » Diagnosis

Diagnosis of Anthrax

Diagnostic Test list for Anthrax:

The list of medical tests mentioned in various sources as used in the diagnosis of Anthrax includes:

• Anthrax blood tests
• Skin tests
• Respiratory secretion tests
• Antibody blood test

Anthrax Diagnosis: Book Excerpts

• Ask the following questions - EDEMA, GENERALIZED
• Ask the Following Questions - PERIORBITAL EDEMA
• Ask the following questions - EDEMA, LOCALIZED
• Differential Diagnosis - Periorbital Edema
• Differential Diagnosis - Peripheral Edema
• Differential Diagnosis - Periorbital Edema
• Differential Diagnosis - Edema
• Approach to the Diagnosis - EDEMA OF THE EXTREMITIES
• History and physical examination - Pustular rash
• History and physical examination - Edema, generalized
• History and physical examination - Edema of the arm
• History and physical examination - Edema of the leg
• Diagnosis - Plague
• Diagnosis - Anthrax
• Diagnosis - Pulmonary edema
• Diagnostic tests - Introduction Gastrointestinal Disorders
• History and physical examination - Pustular rash
• History and physical examination - Edema, generalized
• History and physical examination - Edema of the arm
• History and physical examination - Edema of the face
• History and physical examination - Edema of the leg
• History - Gastrointestinal Bleeding
• History - Edema
• Differential Overview - Gastrointestinal Bleeding
• Differential Overview - Edema
• Differential Overview - Vesicles/Bullae/Pustules
• Diagnosis - Plague
• Diagnosis - Anthrax
• Diagnosis - Pulmonary edema
• History - Edema, facial
• History - Edema, generalized
• History - Pustular rash
• History - Edema, generalized
• History - Edema of the arm
• History - Edema of the face
• History - Edema of the leg
• Clinical Features and Diagnosis - Gastrointestinal Bleeding
• Clinical Features and Diagnosis - Edema
• History and physical examination - Pustular rash
• History and physical examination - Edema, generalized
• History and physical examination - Edema of the arm
• History and physical examination - Edema of the face
• History and physical examination - Edema of the leg
• Approach to the Diagnosis - EDEMA OF THE EXTREMITIES
• Plague - DIAGNOSIS - Plague

Tests and diagnosis discussion for Anthrax:

Anthrax General: DBMD (Excerpt)

Anthrax is diagnosed by isolating B. anthracis from the blood, skin lesions, or respiratory secretions or by measuring specific antibodies in the blood of persons with suspected cases. (Source: excerpt from Anthrax General: DBMD)

Anthrax: NWHIC (Excerpt)

A person can be exposed to anthrax by coming into contact with anthrax bacteria. However, a person can be exposed without getting the disease. Actual anthrax disease occurs when there is some sign of illness, such as the skin lesion that occurs with cutaneous anthrax. A person who is exposed to anthrax spores but given appropriate antibiotics can avoid getting anthrax. Anthrax is not a contagious disease and cannot be passed from person to person. (Source: excerpt from Anthrax: NWHIC)

Anthrax: NWHIC (Excerpt)

Currently used tests for anthrax in an individual can only confirm an infection, not exposure without infection. The only way exposure can be determined is through a public health investigation. The tests that you hear or read about, such as nasal swabs and environmental tests, are not tests to determine whether an individual should be treated. These kinds of tests are used only to determine the extent of exposure in a given building or workplace and are not reliable in determining if an individual has been exposed to anthrax. When an investigation shows that exposure may have occurred, prophylactic (preventive) therapy with antibiotics is provided to those persons. (Source: excerpt from Anthrax: NWHIC)

Anthrax: NWHIC (Excerpt)

Anthrax is diagnosed by isolating the anthrax bacteria from the blood, skin lesions, or respiratory secretions or by measuring specific antibodies in the blood of persons with suspected cases. (Source: excerpt from Anthrax: NWHIC)

Diagnostic Tests for Anthrax: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about diagnostis of Anthrax.

EDEMA, GENERALIZED: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Does the edema pit on pressure? Edema that pits on pressure is more likely to be due to heart, liver, or kidney disease. Edema that does not pit on pressure is more likely due to myxedema or lymphedema.
2. Is there hepatomegaly? If there is hepatomegaly, one should consider liver disease such as cirrhosis or cardiac disease.
3. Is there ascites? If there is ascites along with hepatomegaly, cirrhosis of the liver is the most likely cause of the edema. However, one should not forget constrictive pericarditis. If there is no ascites along with the hepatomegaly, then congestive heart failure should be considered.
4. Is there jugular vein distention? Jugular vein distention certainly would be most suggestive of congestive heart failure, but other causes of jugular vein distention include superior vena cava syndrome due to a mediastinal mass such as carcinoma of the lung and constrictive pericarditis. Right heart failure secondary to pulmonary emphysema and fibrosis can also cause jugular vein distention.
5. Is there an abnormal urinary sediment? If there is an abnormal urinary sediment, consider nephritis, whether it might be due to chronic glomerulonephritis or whether it is secondary to diabetes mellitus or a collagen disease.
6. Is the patient taking any drugs that could cause the edema? Among the drugs that should be considered are corticosteroids, progesterone, estrogen, anti-inflammatory drugs such as naproxen (Naprosyn®) and ibuprofen (Motrin®), antihypertensive drugs such as methyldopa (Aldomet®) and clonidine hydrochloride, calcium channel blockers, beta-adrenergic blockers, and antidepressants.

DIAGNOSTIC WORKUP

A CBC should be done to rule out significant anemia that may be the cause of the edema. If there is anemia, we need to determine its source. Liver function tests are done to rule out liver disease, and serum protein electrophoresis and tests for BUN and creatinine should be done to exclude renal disease. The urinalysis is very important both for the routine studies and also to examine the urinary sediment for diseases such as chronic glomerulonephritis and collagen disease. If there is significant loss of protein in the urine, one should be considering nephrosis. An EKG, chest x-ray, and venous pressure and circulation time will be extremely helpful in diagnosing congestive heart failure, but pulmonary function tests can be done as the vital capacity is significantly reduced in this disease. When there is a strong suspicion of congestive heart failure, echocardiography or radionuclide-gated blood pool scintigraphy should be done to determine the left ventricular ejection fraction (LVEF). A value of less than 45% is considered abnormal. A thyroid profile should be done to diagnose myxedema. A CT scan of the chest will help diagnose constrictive pericarditis. Occasionally, the edema is due to an abdominal tumor. A CT scan of the abdomen and pelvis will be helpful in those cases. Contrast lymphangiography may be necessary to diagnose lymphedema.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

PERIORBITAL EDEMA: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is there a periorbital or facial rash? The presence of a periorbital or facial rash should suggest contact dermatitis, angioneurotic edema, trichinosis, and herpes zoster. Remember, herpes zoster is usually unilateral.
2. Is there a generalized edema? The presence of generalized edema suggests myxedema, cirrhosis, acute and chronic glomerulonephritis, congestive heart failure, and other disorders.
3. Is there fever? The presence of fever suggests acute sinusitis, cavernous sinus thrombosis, orbital cellulitis, meningitis, and neurosyphilis.

DIAGNOSTIC WORKUP

Routine diagnostic studies include a CBC, sedimentation rate, urinalysis, chemistry panel, thyroid profile, chest x-ray, VDRL test, and x-ray of the sinuses and orbits. If there is fever, a nose and throat culture and blood culture should be done and antibiotics begun without delay. A CT scan of the brain and sinuses probably ought to be done in these cases, but why not get an ear, nose, and throat or neurologic consultation first?

If there is generalized edema, the workup should proceed as outlined on page 138 .

Trichinosis can be diagnosed by the skin test, serologic studies, or a muscle biopsy. Superior vena cava syndrome may be diagnosed by a chest x-ray in many cases, but a CT scan of the mediastinum may be necessary.

 

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

EDEMA, LOCALIZED: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

1. Is the edema acute or chronic? Acute edema, if it is localized, should always bring to mind a deep vein thrombophlebitis. It also should bring to mind acute lymphangitis, particularly if there is erythema in the area. Finally, it should also make one think of trauma or a focal infection such as cellulitis. Chronic localized edema, on the other hand, is more likely related to varicose veins or lymphedema.
2. Is the edema pitting or nonpitting? If the edema pits, it is more likely related to inflammation or venous incompetence. If it is nonpitting, it is more likely due to obstruction of the lymphatics, i.e., lymphedema.
3. Is there erythema, a rash, or focal tenderness, or all three? Erythema and focal tenderness would suggest cellulitis, lymphangitis, thrombophlebitis, angioneurotic edema, insect bite, or snake bite. It also would suggest a sprain or contusion. Focal tenderness alone with pitting edema and no significant erythema or rash would suggest a deep vein thrombophlebitis. When there is no erythema or tenderness in a case of pitting edema of a localized nature, one should consider varicose veins or, in the lower extremities, a popliteal cyst that might be obstructing the veins on a chronic basis.
4. If the edema is of the lower extremities, is there a positive Homans' sign? A positive Homans' sign should always be looked for because this would suggest a deep vein thrombophlebitis. Action must be taken immediately in such cases.

DIAGNOSTIC WORKUP

A venous ultrasound study, impedance plethysmography, and contrast venography are very useful in the diagnosis of deep vein thrombophlebitis. d -dimer testing is also a sensitive indicator of active deep vein thrombophlebitis and the need for anticoagulants. Patients with suspected cellulitis or osteomyelitis should have a CBC, sedimentation rate, and cultures of the blood or any fluid that is available from the site of the lesion, either direct or by aspiration. X-rays and CT scans of the involved area are useful as well. Bone scans are often of value in diagnosing osteomyelitis and fractures. Lymphangiography will be helpful in the diagnosis of carcinomatosis or lymphedema from other causes. A CT scan of the abdomen or pelvis may also demonstrate the malignant lymph nodes. A thyroid profile will diagnose cases of pretibial myxedema due to thyrotoxicosis. Patients with upper extremity edema should have a chest x-ray and CT scan of the mediastinum to determine the causes of superior vena cava syndrome.

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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Periorbital Edema: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Conjunctivitis
• Allergy
  –Systemic (e.g., reaction to medication, urticaria/angioedema)
  –Local (e.g., insect bite)
• Contact dermatitis/dermatitis medicamentosa
• Chalazion
  –Zeis or Meibomian gland obstruction of eyelid
• Orbital disease (see “Proptosis/Exophthalmos” entry)
• Preseptal/periorbital cellulitis
• Acute dacryocystitis (infection of the lacrimal ducts)
• Orbital fat herniation through attenuated or dehiscent orbital septum and/or orbicularis oculi muscle (aging changes)
• Herpes simplex/zoster
• Blepharitis/dermatitis
• Trauma/postsurgical (e.g., orbital fracture)
• Dermatomyositis/polymyositis
  –Associated with a heliotropic (violet colored) rash on the upper eyelids
• Chemical, ultraviolet, or thermal burn
• Cardiac failure (generalized edema)
• Renal failure
• Nephrotic syndrome
• Blepharitis/rosacea
• Dacryoadenitis
• Hypothyroidism
  –Associated with fatigue, pretibial edema, and delayed relaxation of reflexes
• Superior vena cava syndrome
• Sebaceous gland carcinoma
• Squamous or basal cell carcinoma
• Discoid lupus
• Ocular cicatricial pemphigoid (symblepharon)

Workup and Diagnosis

• History should include symptom course, exposure history (allergens, irritants, chemicals, ultraviolet, or thermal injury), associated symptoms, past medical and family history, and medication history
• Physical exam, including a full ophthalmologic exam for erythema, tenderness, cutaneous vesicles, discharge, proptosis, vision changes, and conjunctival injection or chemosis
• Initial laboratory evaluation may include CBC with differential, electrolytes, BUN, creatinine, TSH, ESR, ANA, albumin, and urinalysis
• Culture and Gram stain of eye discharge if infection is considered
• Consider CT/MRI of orbits, neck, and/or chest as appropriate
• Consider biopsy of suspicious or persistent lesions
• Consider echocardiogram if heart failure is being considered
• Consider ophthalmology consultation

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Source: In a Page: Signs and Symptoms, 2004

Peripheral Edema: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Venous insufficiency
  –Caused by incompetent venous valves
  –Skin characteristically has superficial varicose veins associated with a reddish-brown pretibial discoloration (“venous stasis skin changes”)
  –Swelling is typically worse after legs are held in a dependent position and is least noticeable after a night's sleep
• Congestive heart failure
  –Associated with pitting peripheral edema
  –Other signs of heart failure include a third heart sound, cardiomegaly, and hepatomegaly
• Cellulitis
  –Usually unilateral
  –Edematous legs are typically red, warm, and inflamed
  –The patient may exhibit signs of systemic toxicity with fever and leukocytosis
  • Deep venous thrombosis
    –Typically unilateral swelling
    –May exhibit a palpable cord representing a thrombosed vein
    –Homan's sign (pain in the calf with passive dorsiflexion of the foot)
    –Virchow's triad (hypercoagulable states, venous stasis, and vessel injury) are risk factors
  • Cirrhosis
    –Advanced liver disease results in hypoalbuminemia and poor venous return through cirrhotic liver tissue
    –Other stigmata of chronic liver disease include caput medusae, ascites, and spider angiomata
  • Nephrotic syndrome
    –Glomerular damage results in protein loss and decreased oncotic pressure
  • Less common etiologies (“zebras”) include filariasis (lymphatic infection by Wuchereria bancrofti worm), myxedema (seen in patients with severe hypothyroidism), Milroy's disease (congenital lymphedema), chronic lymphedema (e.g., lymphatic damage due to surgery, such as vein harvesting for CABG), and gout

  Workup and Diagnosis

  • History and physical examination should focus on time course, associated symptoms (e.g., dyspnea, urinary changes, fever), unilateral versus bilateral involvement, pitting versus nonpitting edema, and risk factors for DVT
  • Initial labs may include CBC, electrolytes, BUN/creatinine, urinalysis, coagulation studies, LFTs, serum albumin, and thyroid function tests
  • Chest X-ray may reveal signs of pulmonary edema or cardiomegaly
  • Duplex ultrasound of the legs is useful in diagnosing deep venous thrombosis
  • Echocardiography may reveal a depressed ejection fraction in cases of congestive heart failure
  • Blood cultures are often indicated in immunocompromised or systemically ill patients
  • Renal or liver biopsy may be necessary to diagnose cirrhosis or renal pathology leading to nephrotic syndrome

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Source: In a Page: Signs and Symptoms, 2004

Periorbital Edema: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Periorbital cellulitis
  –Also described as preseptal cellulitis (infection is anterior to the orbital septum and thus does not affect the orbit or globe)
  –Usual pathogens are streptococcal species, Staphylococcus aureus, and Haemophilus influenzae

• Orbital cellulitis
  –Also described as postseptal and affects the preseptal structures as well as the extraocular muscles and the optic nerve
  –Bacterial pathogens are the same as periorbital cellulitis and may reflect direct spread
  –May be accompanied by orbital abscess and may spread via the sinuses to the brain

• Other infections
  –Conjunctivitis
  –Sinusitis
  –Dental abscess
• Allergic reaction
  –Conjunctivitis
  –Urticaria/angioedema
  –Drug reaction
• Local ocular causes
  –Insect bites
  –Contact dermatitis
  –Trauma
  –Foreign body
• Systemic disorders with generalized edema
  –Hypoproteinemia
  –Renal disease
  –Congestive heart failure
• Malignancy
  –Neuroblastomas: Associated with ecchymoses, “raccoon eyes,” and proptosis
  –Leukemia: Associated with fever, fatigue, anemia, bone pain, lymphadenopathy, splenomegaly

Workup and Diagnosis

• History
  –Onset, duration, progression of symptoms
  –Presence of pain or pruritus
  –History of trauma
  –Systemic symptoms such as fever
• Physical exam
  –Temperature, vital signs, growth parameters
  –Proptosis
  –Ocular range of motion
  –Full physical exam including heart, lung, and extremities
• Labs
  –Electrolytes, BUN, creatinine
  –Serum protein and albumin
  –CBC and blood culture if infection is suspected
  –ESR, LDH if malignancy is suspected
• Studies
  –CT to distinguish periorbital cellulitis from orbital cellulitis
  –CT or MRI to discover orbital or cranial tumors
  –CXR if CHF is suspected
  –Renal ultrasound to evaluate the architecture of the kidneys, Doppler to evaluate renal flow, DMSA to evaluate renal parenchyma if edema is generalized

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Source: In A Page: Pediatric Signs and Symptoms, 2007

Edema: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Kidney disease (nephrotic syndrome)
  –Insidious onset, periorbital and lower extremity edema, abdominal distension
  –Various types include minimal change disease (MCNS), focal segmental glomerulosclerosis, acute and chronic glomerulonephritis
• Chronic renal failure from any cause may result in impaired fluid excretion
• Liver disease from any cause resulting in impaired production of albumin
• Congestive heart failure (CHF)
• Protein losing enteropathy
  –Menetrier disease (typically CMV), inflammatory bowel disease, neuroblastoma, intestinal lymphangiectasia, trypsinogen deficiency
• Celiac disease
• Sepsis, with capillary leak (movement of fluid out of the blood vessels into the interstitium)
• Hereditary angioneurotic edema
  –Intermittent swelling of extremities
  –Often preceded by trauma
  –Decreased C4 and C1 esterase inhibitor
• Rocky Mountain spotted fever
• Stevens-Johnson syndrome
• Vitamin E deficiency
• Hypothyroidism
• Severe malnutrition
  –Marasmus (calorie deficiency)
  –Kwashiorkor (protein deficiency)
• Zinc deficiency
• Hydrops fetalis
• Impaired lymphatic drainage
  –Milroy disease
  –Meigs syndrome
  –Yellow nail syndrome
  –Lymphedema praecox
• Filariasis (nematode infection resulting in elephantiasis)
• Immobility including placement of body casts and paralysis

Workup and Diagnosis

• History
  –Onset, duration, severity
  –History of heart, kidney, or liver disease; GI bleeding, hypertension, weight gain, feeding intolerance
  –Chest pain, shortness of breath, orthopnea (cardiac disease), jaundice, acholic stools, abdominal distension, GI bleeding (liver disease), oliguria, facial edema, headache or vision changes (hypertension), diarrhea, fever

• Physical exam
  –Blood pressure (hypo- or hypertension), cardiac exam (JVD, murmur)
  –Hepatomegaly, splenomegaly, ascites, scleral icterus
  –Periorbital, lower extremity or presacral edema, abdominal distension, poor peripheral perfusion

• Labs
  –Urinalysis (no proteinuria excludes renal protein loss)
  –Serum chemistries: Albumin, triglycerides, liver transaminases
  –Stool for α-1 antitrypsin for protein-losing enteropathy
  –Prothrombin time (impaired hepatic function)

• Abdominal ultrasound (for liver or kidney disease)
• Studies depending on clinical situation
  –Echocardiogram/ECG for cardiac failure
  –Renal biopsy (if kidney disease other than MCNS is suspected)
  –GI imaging or endoscopy

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Source: In A Page: Pediatric Signs and Symptoms, 2007

EDEMA OF THE EXTREMITIES: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Bilateral pitting edema of the lower extremities is usually due to congestive heart failure, nephrosis, or cirrhosis of the liver. Venous pressure and circulation time will rule out congestive heart failure but echocardiography can be more definitive. Serum and urine osmolality can be helpful also. If there is nephrosis, there will be significant lowering of the serum albumin level and proteinuria. Liver function studies will usually confirm cirrhosis or liver disease but ultrasonography can reveal ascites to assist in the diagnosis. Nonpitting edema of the lower extremities will usually be due to lymphatic obstruction but hypothyroidism can be ruled out with a free T4 assay or TSH. Unilateral edema of the lower extremities suggest deep vein thrombosis, which can be confirm by Doppler ultrasound studies, plethysomography, or contrast venography. A CT scan of the chest will help diagnose constrictive pericarditis, which is rarely found today. Spirometry and arterial blood gas analysis will diagnose pulmonary emphysema with cor pulmonale.

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Source: Differential Diagnosis in Primary Care, 2007

Pustular rash: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

Have the patient describe the appearance, location, and onset of the first pustular lesion. Did another type of skin lesion precede the pustule? Find out how the lesions spread. Ask what medications the patient takes and if he has applied topical medication to his rash. If so, what type and when did he last apply it? Find out if he has a family history of a skin disorder.

Examine the entire skin surface, noting if it’s dry, oily, moist, or greasy. Record the exact location and distribution of the skin lesions and their color, shape, and size.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Edema, generalized: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

When the patient's condition permits, obtain a complete medical history. First, note when the edema began. Does it move throughout the course of the
day — for example, from the upper extremities to the lower, periorbitally, or within the sacral area? Is the edema worse in the morning or at the end of the day? Is it affected by position changes? Is it accompanied by shortness of breath or pain in the arms or legs? Find out how much weight the patient has gained. Has his urine output changed in quantity or quality?

Next, ask about previous burns or cardiac, renal, hepatic, endocrine, or GI disorders. Have the patient describe his diet so you can determine whether he suffers from protein malnutrition. Explore his drug history, and note recent I.V. therapy.

Begin the physical examination by comparing the patient's arms and legs for symmetrical edema. Also, note ecchymoses and cyanosis. Assess the back, sacrum, and hips of the bedridden patient for dependent edema. Palpate peripheral pulses, noting whether hands and feet feel cold. Finally, perform a complete cardiac and respiratory assessment.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Edema of the arm: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

When taking the patient's history, one of the first questions to ask is, “How long has your arm been swollen?” Then find out if the patient also has arm pain, numbness, or tingling. Does exercise or arm elevation decrease the edema? Ask about recent arm injury, such as burns or insect stings. Also, note recent I.V. therapy, surgery, or radiation therapy for breast cancer.

Determine the edema's severity by comparing the size and symmetry of both arms. Use a tape measure to determine the exact girth, and mark the location where the measurement was obtained in order to make comparative measurements later. Make sure to note whether the edema is unilateral or bilateral, and test for pitting. (See Edema Pitting or nonpitting? page 240.) Next, examine and compare the color and temperature of both arms. Look for erythema and ecchymoses and for wounds that suggest injury. Palpate and compare radial and brachial pulses. Finally, look for arm tenderness and decreased sensation or mobility. If you detect signs of neurovascular compromise, elevate the arm.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Edema of the leg: History and physical examination
(Handbook of Signs & Symptoms (Third Edition))

To evaluate the patient, first ask how long he has had the edema. Did it develop suddenly or gradually? Does it decrease if he elevates his legs? Is it painful when touched or when he walks? Is it worse in the morning, or does it get progressively worse during the day? Ask about a recent leg injury or recent surgery or illness that may have immobilized the patient. Does he have a history of cardiovascular disease? Finally, obtain a drug history.

Begin the physical examination by examining each leg for pitting edema. (See Edema: Pitting or nonpitting? page 240.) Because leg edema may compromise arterial blood flow, palpate or use a Doppler to auscultate peripheral pulses to detect an insufficiency. Observe leg color and look for unusual vein patterns. Then palpate for warmth, tenderness, and cords, and gently squeeze the calf muscle against the tibia to check for deep pain. If leg edema is unilateral, dorsiflex the foot to look for Homans' sign, which is indicated by calf pain. Finally, note skin thickening or ulceration in edematous areas.

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Source: Handbook of Signs & Symptoms (Third Edition), 2006

Plague: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Because plague is rare in the United States, it's commonly overlooked until after the patient dies or multiple cases develop. Characteristic buboes and a history of exposure to rodents in known endemic areas strongly suggest bubonic plague.

CONFIRMING DIAGNOSIS Stained smears and cultures of Y. pestis obtained from a needle aspirate of a small amount of fluid from skin lesions confirm this diagnosis.

Postmortem examination of a guinea pig inoculated with a sample of blood or purulent drainage allows isolation of the organism. Other laboratory findings include a white blood cell count of over 20,000/µl with increased polymorphonuclear leukocytes and hemoagglutination reaction (antibody titer) studies. Diagnosis should rule out tularemia, typhus, and typhoid.

In pneumonic plague, diagnosis requires a chest X-ray to show fulminating pneumonia and stained smear and culture of sputum to identify Y. pestis. Other bacterial pneumonias and psittacosis must be ruled out. Stained smear and blood culture containing Y. pestis are diagnostic in septicemic plague. However, cultures of Y. pestis grow slowly; so, in suspected plague (especially pneumonic and septicemic plagues), treatment should begin without waiting for laboratory confirmation. For a presumptive diagnosis of plague, a fluorescent antibody test may be ordered.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Anthrax: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Anthrax can be diagnosed through cultures of the blood, skin lesions, or sputum of an exposed patient. If B. anthracis is isolated, the diagnosis is confirmed. Additionally, specific antibodies may be detected in the blood.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Pulmonary edema: Diagnosis
(Professional Guide to Diseases (Eighth Edition))

Clinical features of pulmonary edema permit a working diagnosis. Arterial blood gas (ABG) analysis usually shows hypoxia; the partial pressure of arterial carbon dioxide is variable. Profound respiratory alkalosis and acidosis may occur. Chest X-ray shows diffuse haziness of the lung fields and, commonly, cardiomegaly and pleural effusions. Ultrasound (echocardiogram) may show weak heart muscle, leaking or narrow heart valves, and fluid surrounding the heart. Pulmonary artery catheterization helps identify left-sided heart failure by showing elevated pulmonary wedge pressures. This helps to rule out acute respiratory distress syndrome — in which pulmonary wedge pressure is usually normal.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Introduction: Gastrointestinal Disorders: Diagnostic tests
(Professional Guide to Diseases (Eighth Edition))

After physical assessment, several tests can identify GI malfunction.

❑ A barium or gastrografin swallow is used primarily to examine the esophagus. Gastrografin may be used instead of barium. Like barium, gastrografin facilitates X-ray imaging. However, if gastrografin escapes from the GI tract, it’s absorbed by the surrounding tissue, whereas escaped barium isn’t absorbed and can cause complications.

❑ In an upper GI series, swallowed barium sulfate travels through the esophagus, stomach, and duodenum to reveal abnormalities. The barium outlines stomach walls and delineates ulcer craters and defects.

❑ A small-bowel series, an extension of the upper GI series, visualizes barium flowing through the small intestine to the ileocecal valve.

❑ A barium enema (lower GI series) allows X-ray visualization of the colon.

❑ A stool specimen is useful to detect suspected GI bleeding, infection, or malabsorption as well as the presence of parasites. Guaiac test for occult blood, microscopic stool examination for ova and parasites, and tests for fat require several specimens.

❑ In esophagogastroduodenoscopy, insertion of a fiber-optic scope allows direct visual inspection of the esophagus, stomach, and duodenum. These structures are examined for varices, tumors, inflammation, hernias, polyps, ulcers, and obstruction.

❑ Proctosigmoidoscopy permits inspection of the rectum and distal sigmoid colon; colonoscopy is used for inspection of the descending, transverse, and ascending colon. These tests help visualize tumors, polyps, hemorrhoids, or ulcers.

❑ Gastric analysis examines gastric secretions for the presence of high levels of gastrin and the amount of acid produced.

❑ Endoscopic retrograde cholangiopancreatography directly visualizes the esophagus, stomach, proximal duodenum, and fluoroscopic visualization of the pancreatic, hepatic, and biliary ducts. This test can help visualize duct obstruction, benign structures, cysts, anatomic variations, and malignant tumors.

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Source: Professional Guide to Diseases (Eighth Edition), 2005

Pustular rash: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

Have the patient describe the appearance, location, and onset of the first pustular lesion. Did another type of skin lesion precede the pustule? Find out how the lesions spread. Ask what medications the patient takes and if he has applied any topical medication to his rash. If so, what type and when did he last apply it? Find out if he has a family history of a skin disorder.

Examine the entire skin surface, noting if it’s dry, oily, moist, or greasy. Record the exact location and distribution of the skin lesions and their color, shape, and size.

» READ BOOK EXCERPT ONLINE »

Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Edema, generalized: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

When the patient’s condition permits, obtain a complete medical history. First, note when the edema began. Does it move throughout the course of the day—for example, from the upper extremities to the lower, periorbitally, or within the sacral area? Is the edema worse in the morning or at the end of the day? Is it affected by position changes? Is it accompanied by shortness of breath or pain in the arms or legs? Find out how much weight the patient has gained. Has his urine output changed in quantity or quality?

Next, ask about previous burns or cardiac, renal, hepatic, endocrine, or GI disorders. Have the patient describe his diet so you can determine whether he suffers from protein malnutrition. Explore his drug history, and note recent I.V. therapy.

Begin the physical examination by comparing the patient’s arms and legs for symmetrical edema. Also, note ecchymoses and cyanosis. Assess the back, sacrum, and hips of the bedridden patient for dependent edema. Palpate peripheral pulses, noting whether hands and feet feel cold. Finally, perform a complete cardiac and respiratory assessment.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Edema of the arm: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

When taking the patient’s history, one of the first questions to ask is “How long has your arm been swollen?” Then find out if the patient also has arm pain, numbness, or tingling. Does exercise or arm elevation decrease the edema? Ask about recent arm injury, such as burns or insect stings. Also, note recent I.V. therapy, surgery, or radiation therapy for breast cancer.

Determine the edema’s severity by comparing the size and symmetry of both arms. Use a tape measure to determine the exact girth. Be sure to note whether the edema is unilateral or bilateral, and test for pitting. (See Edema: Pitting or nonpitting? page 292.) Next, examine and compare the color and temperature of both arms. Look for erythema and ecchymoses and for wounds that suggest injury. Palpate and compare the radial and brachial pulses. Finally, look for arm tenderness and decreased sensation or mobility. If you detect signs of neurovascular compromise, elevate the arm.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Edema of the face: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

If the patient isn’t in severe distress, take his health history. Ask if facial edema developed suddenly or gradually. Is it more prominent in early morning, or does it worsen throughout the day? Has the patient gained weight? If so, how much and over what length of time? Has he noticed a change in his urine color or output? In his appetite? Take a drug history and ask about recent facial trauma.

Begin the physical examination by characterizing the edema. Is it localized to one part of the face, or does it affect the entire face or other parts of the body? Determine if the edema is pitting or nonpitting, and grade its severity. (See Edema: Pitting or nonpitting? page 292.) Next, take vital signs and assess neurologic status. Examine the oral cavity to evaluate dental hygiene and look for signs of infection. Visualize the oropharynx and look for any soft-tissue swelling.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Edema of the leg: History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))

To evaluate the patient, first ask how long he has had the edema. Did it develop suddenly or gradually? Does it decrease if he elevates his legs? Is it painful when touched or when he walks? Is it worse in the morning, or does it get progressively worse during the day? Ask about a recent leg injury or any recent surgery or illness that may have immobilized the patient. Does he have a history of cardiovascular disease? Finally, obtain a drug history.

Begin the physical examination by examining each leg for pitting edema. (See Edema: Pitting or nonpitting? page 292.) Because leg edema may compromise arterial blood flow, palpate or use a handheld Doppler device to auscultate peripheral pulses to detect any insufficiency. Observe leg color and look for unusual vein patterns. Then palpate for warmth, tenderness, and cords, and gently squeeze the calf muscle against the tibia to check for deep pain. If leg edema is unilateral, dorsiflex the foot to look for Homans’sign, which is indicated by calf pain. Finally, note skin thickening or ulceration in the edematous areas.

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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006

Gastrointestinal Bleeding: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

Clinical history accurately points to the source of bleeding in only 40% of cases (3).

 A. Upper GI bleeding. Hematemesis and melena are the most common presentations of acute upper GI bleeding. Important questions to ask: Is there a prior history of bleeding (60% rebleed from the same site) (3)? Is there any family history? Does the patient have any comorbid diseases (peptic ulcer disease, pancreatitis, cirrhosis, cancer)? Is the patient taking any medications (especially nonsteroidal antiinflammatory agents)? Does the patient use recreational drugs, cigarettes, or alcohol? What is the character of the pain? Peptic ulcer pain is epigastric, gnawing, rhythmic, and dull. GI cancers are associated with vague epigastric pain, dysphagia, or weight loss. Was there any retching (Mallory–Weiss tear)? Does the patient have a history of prior surgeries? Patients with a history of vascular grafting are at risk for aortoenteric fistulae, which is often associated with a “herald bleed.”

 B. Lower GI bleeding. How old is the patient? Age is an important feature in discriminating the source of lower GI bleeding. Patients aged less than 50 years usually bleed from infectious causes, anorectal disease, or inflammatory bowel disease. For patients aged more than 50 years, diverticulosis, angiodysplasia, cancer, and ischemia are most common (4). Are there any associated symptoms? Diverticular disease presents as painless, high volume bleeding. Angiodysplasia and cancer present with symptoms of chronic blood loss (fatigue, dyspnea on exertion). Inflammatory bowel disease presents with bloody diarrhea, cramping, weight loss, and fever. A prior history of inflammatory bowel disease, cancer, or radiation to the abdomen is also important.

Physical examination

A. Vital signs. The single most important aspect of the initial physical examination is determining the patient’s hemodynamic stability. Unstable patients should be managed as trauma patients. Placement of a nasogastric (NG) tube is considered the “fifth vital sign” in patients with acute GI bleeding (2).

 B. Focused physical examination. After ensuring hemodynamic stability, the initial physical examination should eliminate a nasal or oropharyngeal source of bleeding. Examine the skin and abdomen carefully for clues to an underlying cause. A rectal examination is mandatory.

1. Skin examination. Ecchymoses, petechiae, and varices should be noted. Conjunctival pallor is a sign of chronic anemia. Numerous mucosal telangiectasias can point to an underlying vascular abnormality.

 2. Abdominal examination. Look for stigmata of chronic liver disease (hepatosplenomegaly, spider angiomata, ascites, palmar erythema, caput medusae, gynecomastia, and testicular atrophy) (Chapter 9.9).

 3. Rectal examination. Rectal varices, hemorrhoids, and fissures should be noted.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Edema: History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)

A. Onset. When the onset of edema is sudden, consider the following possible causes: cellulitis, deep venous thrombosis (DVT), compartment syndrome, trauma, and exacerbation of chronic problems (systemic disease, medications, venous insufficiency, lymphedema).

When the onset is gradual, consider the causes listed below.

B. Clinical course. Is the edema intermittent or recurrent, or is it chronic?

C. Painful edema most likely results from (3):

1. Cellulitis

2. Trauma

3. Ruptured Baker’s cyst

4. Compartment syndrome

5. DVT

D. Painless edema or bilateral edema usually results from a systemic cause.

E. Associated systemic symptoms

1. Fever and chills can be caused by cellulitis, lymphangitis, or venous thrombosis.

2. Dyspnea and orthopnea suggest that the edema is of cardiac origin.

3. Either a history of streptococcal throat infection or recurrent urinary tract infection (UTI) points to renal causes.

F. Medications that can be associated with edema include the following: diazoxide, minoxidil, hydralazine, calcium channel blockers, alpha- and beta-blockers, reserpine, guanethidine, nonsteroidal antiinflammatory drugs (NSAIDs), carbenicillin, amantadine, lithium, phenothiazines, thioridazine, monoamine oxidase (MAO) inhibitors, corticosteroids, testosterone, estrogen, progesterone, or interleukin-2 (2, 3).

G. Endocrine diseases

1. Hypothyroidism can present with pretibial myxedema (Chapter 14.4).

2. Cushing’s syndrome can cause edema.

H. Miscellaneous causes of edema. These include:

1. Pregnancy

2. Sodium overload

3. Malnutrition

4. Stopping laxatives

5. Prolonged dependent position

6. Cyclic edema in women

7. Lymphatic obstruction (neoplastic, parasitic, iatrogenic)

8. Idiopathic

Physical examination

 A. Generalized edema manifests in the most dependent area (e.g., pedal edema in ambulatory patients, presacral edema in bedbound patients).

B. Peripheral edema (3)

1. Sparing of the feet suggests lipedema.

2. Pitting edema present for more than 3 months usually indicates a low serum protein level. Chronic edema can have fibrosis as well.

3. Assessment of color

a. Redness suggests infection or phlebitis.

b. A red-blue color suggests DVT.

c. A slightly cyanotic color bilaterally suggests CHF (Chapter 7.5).

d. The presence of ecchymosis suggests trauma.

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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000

Gastrointestinal Bleeding: Differential Overview
(Field Guide to Bedside Diagnosis)

Upper GI

❑ Peptic ulcer disease

❑ Gastritis

❑ Mallory-Weiss tear

❑ Esophageal varices

❑ Esophagitis

❑ Epistaxis

❑ Esophageal cancer

❑ Gastric cancer

Lower GI

❑ Infectious diarrhea

❑ Diverticular bleeding

❑ Hemorrhoids

❑ Anal fissure

❑ Inflammatory bowel disease

❑ Angiodysplasia

❑ Colon cancer

❑ Mesenteric ischemia

❑ Aortoenteric fistula

DIagnostic Approach

With overt bleeding, determining whether a source is proximal or distal to the ligament of Treitz is key to the further diagnostic evaluation. Hematemesis confirms an upper GI source, and suggests loss of more than a quarter of blood volume. Melena (black, tarry stool) also comes from an upper source unless the bleeding is brisk or large volume and transit is rapid. Melena without hematemesis usually results from a lesion distal to the pylorus (e.g., duodenal ulcer) or to slow bleeding. Tarry stools may be produced by as little as 100 mL of blood. Lower sources produce hematochezia (maroon or clots from the right colon and bright red from the left colon). A small amount of blood only on the toilet tissue nearly always comes from a bleeding hemorrhoid or fissure. Silver stool is said to arise from acholic stools combined with luminal bleeding in an ampullary cancer.

Determine the hemodynamic significance of the bleeding by looking for postural lightheadedness or changes in pulse or blood pressure. Early symptoms of thirst and lightheadedness occur with loss of more than 15% of intravascular volume. An orthostatic blood pressure drop of 10 mm Hg indicates a loss greater than or equal to 20% of volume. Shock with hypotension and pallor develops with 25% to 40% volume loss.

Stools may be falsely colored by ingestants such as bismuth subsalicylate, iron, licorice or charcoal, which turn it black, or beets, which turn it red. These stools are not sticky. A negative stool test for occult blood will usually resolve this.

Hemoccult screening detects blood loss down to 1 to 10 ml/day. Evaluation of a heme positive stool will reveal colon cancer in 5% to 14% of patients, and large adenomatous polyps in another 15% to 35%. Any single positive stool should be evaluated. Hemoccult screening reduces colon cancer mortality by 15% to 33%. An asymptomatic patient with a negative Hemoccult has only a 0.2% chance of having colon cancer (compared with 1.4% prevalence in this population). Using Hemoccult alone as a screening strategy will miss 50% to 60% of colon cancers.

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Source: Field Guide to Bedside Diagnosis, 2007

Edema: Differential Overview
(Field Guide to Bedside Diagnosis)

❑ Congestive heart failure

❑ Venous insufficiency

❑ Hypoalbuminemia

❑ Drugs

❑ Cirrhosis

❑ Deep vein thrombosis

❑ Inferior vena cava obstruction

❑ Lymphatic obstruction

❑ Glomerular injury

❑ Idiopathic edema

❑ Myxedema

❑ Lipedema

❑ Toxemia

❑ Cyclical edema

❑ Refeeding

❑ Filariasis

❑ Milroy

Diagnostic Approach

The degree of edema is influenced by membrane permeability, hydrostatic pressure, and/or oncotic pressure. Edema implies an increase in interstitial volume of several liters. Low protein fluids (hypoalbuminemia, cardiac, and venous edema) pit easily and recover quickly on release. High protein fluids (cellulitis, lymphedema) resist pitting and recover slowly.

The distribution of the edema combined with an estimation of the jugular venous pressure (JVP) can help differentiate heart failure, cirrhosis, renal sodium retention and nephrotic syndrome. Anasarca suggests cardiac, renal, or hepatic disease. Splenomegaly is found more often in patients with cirrhosis than those with congestive heart failure.

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Source: Field Guide to Bedside Diagnosis, 2007

Vesicles/Bullae/Pustules: Differential Overview
(Field Guide to Bedside Diagnosis)

Vesicles

❑ Herpes simplex

❑ Contact dermatitis

❑ Varicella/zoster

❑ Dyshidrotic eczema

❑ Scabies

❑ Erythema multiforme

❑ Coxsackievirus

❑ Dermatitis herpetiformis

Bullae

❑ Friction blister

❑ Bullous impetigo

❑ Diabetic bullae

❑ Fixed drug eruption

❑ Frostbite

❑ Porphyria cutanea tarda

❑ Staphylococcal scalded skin syndrome

❑ Toxic epidermal necrolysis

❑ Coma bullae

❑ Pseudoporphyria

❑ Pemphigus vulgaris

❑ Bullous pemphigoid

❑ Variegate porphyria

Pustules

❑ Acne vulgaris

❑ Rosacea

❑ Folliculitis

❑ Furuncle

❑ Candida

❑ Gonococcemia

❑ Pustular psoriasis

❑ Hiradenitis suppurativa

❑ Ecthyma gangrenosum

Diagnostic Approach

Vesicles are less than 5 mm in diameter, and bullae are larger. If bullae, petechiae, purpura, or necrosis are present, look for an “allergen” such as HSV, strep, deep fungal infection, collagen disease (especially lupus), or occult neoplasm.

Erythema multiforme can be differentiated from a drug reaction by a dusky violet color and petechiae at the center of the lesion. A target or iris lesion is also characteristic of erythema multiforme.

Staphylococcal scalded skin syndrome can be differentiated from toxic epidermal necrolysis by superficial blisters and absence of oral lesions.

Multidermatomal or disseminated zoster in a young adult should suggest HIV infection.

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Source: Field Guide to Bedside Diagnosis, 2007

Plague: Diagnosis
(Handbook of Diseases)

Because plague is rare in the United States, it’s commonly overlooked until after the patient dies or multiple cases develop.

Bubonic plague

Characteristic buboes and a history of exposure to rodents strongly suggest bubonic plague. Stained smears and cultures of Y. pestis (obtained from a small amount of fluid aspirated from skin lesions) confirm this diagnosis.

Postmortem examination of a guinea pig inoculated with a sample of blood or purulent drainage allows isolation of the organism. Other labora-tory findings include a white blood cell count over 20,000/µl with increased polymorphonuclear leukocytes and hemoagglutination reactions (increased antibody titer).

Diagnosis should rule out tularemia, typhus, and typhoid.

Septicemic plague

Stained smear and blood culture containing Y. pestis are diagnostic in septicemic plague.

Pneumonic plague

Diagnosis of pneumonic plague requires a chest X-ray to show fulminating pneumonia and stained smear and culture of sputum to identify Y. pestis. Other bacterial pneumonias and psittacosis must be ruled out.

UNDER STUDY: Researchers have developed a rapid diagnostic test for bubonic and pneumonic plague. It uses monoclonal antibodies to the F antigen of Y. pestis and has a sensitivity and specificity of 100%. Results from the test are available within 15 minutes and have a shelf life of 21 days at 60° F (15.6° C).

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Source: Handbook of Diseases, 2003

Anthrax: Diagnosis
(Handbook of Diseases)

Anthrax can be diagnosed through cultures of the blood, skin lesions, or sputum of an exposed patient. If B. anthracis is isolated, the diagnosis is confirmed. Additionally, specific antibodies may be detected in the blood.

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Source: Handbook of Diseases, 2003

Pulmonary edema: Diagnosis
(Handbook of Diseases)

Clinical features of pulmonary edema permit a working diagnosis. The following tests are also helpful:

❑ Arterial blood gas (ABG) analysis usually shows hypoxia; partial pressure of arterial carbon dioxide varies. Profound respiratory alkalosis and acidosis may occur. Metabolic acidosis occurs when cardiac output is low.

❑ Chest X-ray films show diffuse haziness of the lung fields and, often, cardiomegaly and pleural effusions.

❑ Pulmonary artery catheterization helps identify left-sided heart failure by showing an elevated pulmonary artery wedge pressure (PAWP). This helps to rule out adult respiratory distress syndrome — in which PAWP is usually normal.

❑ An echocardiogram may reveal weak heart muscle, leaking or narrow heart valves, or fluid surrounding the heart.

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Source: Handbook of Diseases, 2003

Edema, facial: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

If the patient isn’t in severe distress, take his health history. Ask if facial edema developed suddenly or gradually. Is it more prominent in early morning, or does it worsen throughout the day? Has the patient gained weight? If so, how much and over what length of time? Has he noticed a change in his urine color or output? In his appetite? Take a drug history and ask about recent facial trauma and dental procedures.

Physical examination

Begin the physical examination by characterizing the edema. Is it localized and distributed over one part of the face, or does it affect the entire face or other parts of the body? Determine if the edema is pitting or nonpitting, and grade its severity. (See Edema: Pitting or nonpitting? page 128.) Next, take vital signs, and assess neurologic status. Examine the oral cavity to evaluate dental hygiene and look for signs of infection. Visualize the oropharynx and look for any soft-tissue swelling.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Edema, generalized: History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

When the patient’s condition permits, obtain a complete medical history. First, note when and where the edema began. Does it move throughout the course of the day — for example, from the upper extremities to the lower, periorbitally, or within the sacral area? Is the edema worse in the morning or at the end of the day? Is it affected by position changes? Is it accompanied by shortness of breath or pain in the arms or legs? Find out how much weight the patient has gained. Has his urine output changed in quantity or quality? 

Next, ask about previous burns or cardiac, renal, hepatic, endocrine, or GI disorders. Have the patient describe his diet so you can determine whether he suffers from protein malnutrition. Explore his drug history, and note recent I.V. therapy.

Physical examination

Begin the physical examination by comparing the patient’s arms and legs for symmetrical edema. Also, note ecchymoses and cyanosis. Assess the back, sacrum, and hips of the bedridden patient for dependent edema. Palpate peripheral pulses, noting whether his hands and feet feel cold. Finally, perform a complete cardiac and respiratory assessment. Also, obtain a baseline weight for this patient.

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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007

Pustular rash: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Have the patient describe the appearance, location, and onset of the first pustular lesion. Did another type of skin lesion precede the pustule? Find out how the lesions spread. Ask what medications the patient takes and if he has applied any topical medication to his rash. If so, what type and when did he last apply it? Find out if he has a family history of a skin disorder.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Edema, generalized: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

When the patient’s condition permits, obtain a complete medical history. First, note when the edema began. Does it move throughout the course of the day — for example, from the upper extremities to the lower, periorbitally, or within the sacral area? Is the edema worse in the morning or at the end of the day? Is it affected by position changes? Is it accompanied by shortness of breath or pain in the arms or legs? Find out how much weight the patient has gained. Has his urine output changed in quantity or quality?

Next, ask about previous burns or cardiac, renal, hepatic, endocrine, or GI disorders. Ask the patient to describe his diet so you can determine whether he suffers from protein malnutrition. Explore his drug history, and note recent I.V. therapy.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Edema of the arm: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

When taking the patient’s history, one of the first questions to ask is “How long has your arm been swollen?” Then find out if the patient also has arm pain, numbness, or tingling. Does exercise or arm elevation decrease the edema? Ask about recent arm injury, such as burns or insect stings. Also, note recent I.V. therapy, surgery, or radiation therapy for breast cancer.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Edema of the face: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

If the patient isn’t in severe distress, take his health history. Ask if facial edema developed suddenly or gradually. Is it more prominent in early morning, or does it worsen throughout the day? Has the patient gained weight? If so, how much and over what length of time? Has he noticed a change in his urine color or output? In his appetite? Take a drug history and ask about recent facial trauma.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Edema of the leg: History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

To evaluate the patient, first ask how long he has had the edema. Did it develop suddenly or gradually? Does it decrease if he elevates his legs? Is it painful when touched or when he walks? Is it worse in the morning, or does it get progressively worse during the day? Ask about a recent leg injury, surgery, or illness that may have immobilized the patient. Does he have a history of cardiovascular disease? Finally, obtain a drug history.

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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007

Gastrointestinal Bleeding: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Upper Gastrointestinal Bleeding

Nose

See Chap.18, Epistaxis.

Mouth and Pharynx

Trauma orforeign body may produce bleeding in mouth or pharynx.

History and physical exam are usuallydiagnostic.

Esophagus

Esophagitis

May presentwith hematemesis and sometimes occult blood loss.

Gastroesophageal reflux and causticingestions are common causes. Less common cause is infection, whichusually occurs in immunocompromised individuals. Pathogens includeherpes simplex virus, adenoviruses, cytomegalovirus, VZV, and Candidaspecies.

Diagnosis of esophagitis may be confirmedby endoscopy and biopsy. These infections may be diagnosed by specificcultures.

Foreign Body

Foreignbody lodged in esophagus may cause difficulty swallowing, pain,and bleeding.

Chest radiography may show radiopaqueforeign body.

Endoscopy is definitive procedure forremoval.

Varices

Consequenceof portal hypertension.

Major causes of portal hypertensionare parenchymal liver disease and anatomic obstruction of portalvein or its major branches.

Acute painless GI bleeding that occasionallycan be massive is often presenting sign. Other findings may includevisible abdominal wall collateral vessels, splenomegaly, and ascites.Hepatomegaly usually indicates liver parenchymal disease, but acirrhotic liver may be small and shrunken.

Endoscopic exam visualizes varices.

Duplication

Usuallyinvolves lower esophagus and may cause dysphagia.

Large duplication also may cause respiratorydistress.

If duplication contains ectopic gastricmucosa, bleeding can occur.

Diagnosis can usually be made by chestCT with oral contrast.

Gastroesophageal Junction

Tears inmucosa at gastroesophageal junction can result from continued forceful vomitingand retching; condition is called Mallory-Weiss syndrome.

Bleeding is usually self-limited.

Endoscopy can confirm diagnosis.

Stomach

Gastritis

In neonates,gastritis may be due to perinatal asphyxia, septicemia, or hypotension, butoften it is unexplained.

In infancy and childhood, epigastricpain and vomiting are frequent findings with gastritis. Viral illnessand drugs (e.g., aspirin and NSAIDs) are predisposing factors.

In adolescence, chronic alcohol intakemay cause gastritis.

In any age group, causes of stressgastritis include head injury, burns, septicemia, and shock.

Gastric aspirate may contain materialresembling coffee grounds or bright red blood.

Ulcer

Gastriculcer may cause acute bleeding with hematemesis or melena.

Another presentation is finding bloodin stool associated with chronic blood loss and anemia.

See Chap.2, Abdominal Pain.

Duplication

Duplicationof stomach usually involves greater curvature near antrum or pylorus.

Neonates may have vomiting, abdominalmass, and abdominal distension.

Vomiting, intermittent abdominal pain,and GI bleeding may occur in childhood.

Abdominal U/S is usually diagnostic.

Vascular Malformation

Angiodysplasticlesions and arteriovenous malformations can occur in stomach and insmall and large intestine.

Any of these lesions can present withrecurrent painless upper or lower GI tract bleeding.

Endoscopy and angiography are bestavailable diagnostic tools.

Neoplasm

Gastricneoplasms are extremely rare in pediatric population, yet can causeGI bleeding.

Benign tumors include teratoma andleiomyoma, whereas malignant tumors include gastric carcinoma, lymphoma,and leiomyosarcoma.

Combination of abdominal U/S,CT, and endoscopy with biopsy are diagnostic.

Duodenum

In addition to conditions detailed below,varices and vascular malformations can cause GI bleeding.

Ulcer

Duodenalulcer can have similar presentation as gastric ulcer.

See Chap.2, Abdominal Pain.

Foreign Body

Occasionallysharp objects may pass from stomach into duodenum and cause bleeding.Swallowed foreign body may be held up in C loop of duodenum or atpoint of constriction (e.g., ligament of Treitz) and cause obstructivesymptoms and hematemesis.

Combination of plain abdominal radiography,abdominal U/S, and endoscopy is usually diagnostic.

Duplication

Tends tocompress first or second portions of duodenum, producing partialobstruction. Presence of ectopic gastric mucosa predisposes to GIbleeding.

Abdominal U/S is usually diagnostic.

Hemobilia

Most commoncause of bleeding into biliary tract in children is abdominal trauma withinjury to liver and biliary tree.

Abdominal U/S and CT are usefulin locating and defining extent of injury. Duodenal endoscopy mayshow blood oozing from ampulla. If this is negative, celiac angiographymay locate site of bleeding if brisk. If bleeding is slower, technetium-sulfurcolloid scan may detect bleeding.

Other

Swallowed Blood

Maternalblood can be swallowed during passage through birth canal or frombreast-feeding if nipples are cracked.

Apt test can determine whether RBCsare fetal or maternal in origin and can be performed on either NGaspirate or stool.

In this test, small amount of NG contents orstool is mixed with tap water (1 part stool:5 parts water).

After centrifugation, 1 mL of 0.25NNaOH is added to 5 mL of pink supernatant fluid; mixture is leftfor 5 mins.

Pink color signifies fetal Hgb, whereasbrownish yellow color signifies maternal Hgb.

Coagulopathy

Bruising,purpura, and bleeding from sites other than GI tract are clues topresence of systemic bleeding disorder.

See Chap.52, Purpura and Bleeding.

Hemorrhagic Disease of the Newborn (Vitamin K Deficiency)

Becauseneonates have low vitamin K stores, they often fail to develop effectivecoagulation function.

At 2–4 days of age, if vitaminK has not been given at birth, hematochezia, melena, or hematemesismay develop. Bleeding also may occur from other sites beside GItract.

Lack of vitamin K administration atbirth, normal platelet count, and reversal of prolonged prothrombintime (PT) and activated partial thromboplastin time (aPTT) withdecreased bleeding after vitamin K administration confirm diagnosis.

Every newborn should receive 0.5–1.0mg IM of vitamin K at birth so this problem can be prevented.

Disseminated Intravascular Coagulation

Predisposingcauses include bacterial meningitis, septicemia, severe hypoxia,necrotizing enterocolitis, and shock.

Patients are seriously ill and havediffuse bleeding from multiple sites from consumption of clottingfactors and destruction of platelets.

Certain lab findings help confirm diagnosis:low platelet count, fragmented RBCs on blood smear, prolonged PTand aPTT, low plasma fibrinogen, and increase in fibrin-split products.

Drugs

GI bleeding may occur with chronic ingestionof aspirin, which causes a defect in platelet aggregation and aprolonged bleeding time. Excessive use of NSAIDs and anticoagulantsalso may cause significant GI bleeding.

Lower Gastrointestinal Tract Bleeding

Intestine

Cow Milk/Soy Protein Sensitivity

Infantsoften present with diarrhea that contains blood. Practical way tomanage this problem is to eliminate cow milk or soy protein fromdiet and monitor for whether symptoms disappear.

See Chap.14, Diarrhea.

Necrotizing Enterocolitis

Common disorderin preterm infants that can occur in term infants. History of perinatalstress (asphyxia, hypotension, septicemia) often exists.

Clinical findings include poor feeding,lethargy, abdominal distension, bilious vomiting, and bloody orblood-streaked stools.

Abdominal radiography that shows gasin bowel wall or in portal venous system helps confirm diagnosis.

Infectious Colitis

Most frequentpathogens in infancy and childhood are Salmonella, Shigella, Campylobacter,and E. coli. Less common is infection with C. difficile and Y. enterocolitica.Most common pathogen associated with HUS is E. coli 0157:H7.

Usual presenting manifestations arefever and bloody diarrhea.

Positive stool culture is diagnostic,except for infection with C. difficile, for which toxin must beidentified.

Henoch-Schönlein Purpura

Lower GIbleeding from the small intestine or colon can be occult or obvious.Typical purpuric rash occurs on buttocks and lower legs.

See Chap.28, Hematuria.

Intussusception

Common causeof lower GI bleeding in children 2 mos–5 yrs of age.

Most common type is ileocolic, whichinvolves telescoping of distal ileum into ascending or transversecolon.

History of intermittent cramping abdominalpain is usually presenting symptom. Vomiting and bloody (currantjelly) stools also may occur. Abdominal mass may be palpable anywherein abdomen.

Abdominal radiography that shows leadingedge of intussusceptum outlined by air is diagnostic, but oftenradiographs are nonspecific. Air-contrast enema can be diagnosticas well as therapeutic. Contraindications to its use are free abdominalair, intestinal obstruction with fluid levels on abdominal radiography,and clinical peritonitis. With any of these findings, surgery shouldbe performed immediately.

Congenital Aganglionic Megacolon (Hirschsprung Disease)

Enterocolitismay occur as complication.

Most common manifestations are abdominaldistension, diarrhea that is often bloody, fever, and vomiting.

See Chap.9, Constipation, and Chap. 14, Diarrhea.

Meckel Diverticulum

Remnantof omphalomesenteric duct that is located in distal ileum.

Usually presents in infancy with painless,episodic, bright red rectal bleeding, which may be massive.

Most diverticula contain gastric mucosa,and technetium 99m–pertechnetate scan can be diagnostic.

False-positive scans are uncommon butsometimes occur with ulcer, hemangioma, or bowel duplication.

Laparoscopy or laparotomy may sometimesbe necessary to confirm diagnosis.

Volvulus with Malrotation

Usuallypresents with intestinal obstruction; however, lower GI bleedingalso can occur.

Abdominal radiography shows dilatedloops of bowel with air-fluid levels. Upper GI series is usuallyperformed; however, with suspected bowel infarction, contrast studiesare unnecessary, and surgery should be performed immediately.

Inflammatory Bowel Disease

Occult GIblood loss or obvious lower GI tract bleeding may occur. Chronicdiarrhea with lower GI bleeding and weight loss should suggest IBD.

Crohn disease and ulcerative colitisare types of IBD.

See Chap.14, Diarrhea.

Intestinal Polyps

Definedas protrusion of tissue above normal GI surface that can cause bleedingand occasionally intussusception.

Number and location of polyps, theirhistopathology, and family history of colorectal cancer helps determineproper management.

This section focuses on common polyposissyndromes in pediatric population.

Solitary Juvenile Polyps/Juvenile Intestinal Polyposis

Solitaryjuvenile polyps usually present with painless rectal bleeding oranal prolapse of polyp in children 2–10 yrs of age. Mostchildren have single polyp, which should be removed for histopathologicexam.

Children with ≥2 rectosigmoid polypsand family history of polyps should be suspected of having juvenileintestinal polyposis, which is transmitted as autosomal-dominanttrait.

Manypolyps occur in the colon, but they also may be found in small intestineand stomach.

Age of presentation is usually in school-agedchildren.

Clinical manifestations include abdominalpain, rectal bleeding, and anemia.

There is high incidence of colorectalneoplasia in individuals with this disorder.

Adenomatous Polyposis of Colon

Autosomal-dominantdisorder caused by mutations in adenomatous polyposis coli gene,whose locus has been mapped to chromosome 5q21-q22.

Characterized by premalignant adenomaslocated primarily in colon and rectum and less commonly in stomachand small intestine.

Onset is usually in adolescence, whenhundreds to thousands of adenomas may appear. Other manifestationsinclude osteomas (jaw, long bones), skin lesions (cysts, lipomas),and pigmented retinal lesions.

Diagnosis is confirmed by colonoscopyand biopsy.

Peutz-Jeghers Syndrome

Autosomal-dominantdisorder in which hamartomatous polyps occur primarily in smallintestine but also may be found in colon and stomach. Gene locushas been mapped to chromosome 19p13.3.

Besides GI bleeding, characteristicfeature is presence of hyperpigmentation, which is seen most commonlyon buccal mucosa and lips.

Upper and lower GI endoscopy and upperGI radiographic series should be performed.

These individuals are at increasedrisk for adenocarcinoma, especially of stomach, duodenum, and colon.

Benign Lymphoid Hyperplasia

Large aggregatesof lymphoid tissue occur in colon and rectum. Rectal bleeding and sometimesintermittent diarrhea occur.

Proctosigmoidoscopy, colonoscopy, andhistologic exam confirm diagnosis.

Duplication

May be foundin jejunum and ileum. Abdominal pain, partial intestinal obstruction, orGI bleeding can be presenting feature. Sometimes small bowel intussusceptionor volvulus occurs.

May also involve colon and rectum,but bleeding rarely occurs because colonic duplications rarely containgastric mucosa. Affected individuals may present with abdominalpain and partial intestinal obstruction or they may be asymptomatic.

Abdominal U/S is usually diagnostic,although abdominal CT may be useful in some cases.

Vascular Malformation

Althoughrare, angiodysplastic lesions and arteriovenous malformations cancause lower GI bleeding.

Diagnosis is usually made by angiography.

Neoplasm

GI tumorsare rare in children.

Hemangiomas can be found anywhere insmall or large intestine but usually involve sigmoid colon and rectum.Endoscopy is usually diagnostic.

Adenocarcinoma of colon usually appearsafter 10 yrs of age. Persistent vomiting, anorexia, weight loss,abdominal pain, and GI bleeding are common manifestations. Contrastenema and colonoscopy with biopsy are diagnostic.

Rectum and Anus

Anal Fissure

Common causeof blood-streaked stools in neonates and young infants. Common causesare trauma from passage of hard stool and frequent use of rectalthermometer.

Stretching anal skin enables fissureto be visualized.

Trauma

Any foreignbody placed in rectum may cause trauma and bleeding.

History and physical exam are usuallydiagnostic, but proctoscopy may be needed in some cases. Plain radiographsof lower abdomen and pelvis can demonstrate radiopaque objects.

Sexual Abuse

Rectal trauma and bleeding may occur as resultof sexual abuse. History, physical exam, and proctoscopy are diagnostic.

Hemorrhoids

Defined as thrombosed collections of bloodvessels in anal area, which are uncommon in infancy and childhood.Usual cause is chronic constipation.

Other

Other causes of GI bleeding are swallowedblood, coagulopathy, and drugs.

Factitious Bleeding

Factitioushematemesis, hematochezia, or melena may be seen with various foods, medications,and artificial food colorings.

Commercial dyes no. 2 and no. 3 foundin breakfast cereals and fruit drinks may produce reddish colorof vomitus or stool.

Certain substances produce blackishcolor of stools: iron preparations, licorice, blueberries, beets,lead, charcoal, and bismuth.

In Munchausen syndrome by proxy, emesisor stool may be contaminated with blood that is not the child's.

Diagnostic Approach

Determination of Gastrointestinal Bleeding

Determinewhether reddish color of vomitus or stool is blood (e.g., raspberries,beets, and food colorings can give reddish color).

Gastroccult (Smith Kline Diagnostics,San Jose, CA) test may be used to detect presence of blood in vomitusor gastric aspirate. Hemoccult test can be used to confirm presenceof blood in stool.

Severity of Bleeding

If GI bleedingis obvious, most important task is to determine severity.

Important to quantitate amount of bleeding:1–2 drops, 1 teaspoonful, 1 cupful, or massive bleedingwith clot formation. Passage of clots via rectum or vomiting of >1cupful of bright red blood is indicative of significant bleeding.

In such cases, first note vital signsand perform any necessary resuscitation.

Immediate fluid replacement is requiredto stabilize BP.

Site of the Bleeding

Determinethe site of bleeding—whether it is from the upper or lowertract or both. Blood from nose or mouth can be swallowed and subsequentlyvomited or passed in stool. Retching from vomiting also can producesome blood-stained vomitus but is rarely severe.

Except in these instances, NG tubeshould be placed to document level and rate of bleeding.

Gastric aspirate that is positive forblood is highly specific for upper tract bleeding. Negative aspiratesuggests lower tract bleeding but does not totally preclude uppertract bleeding, especially from duodenum.

Specific Diagnosis

Importantfactors to consider in diagnosis are

Age

Clinical findings (e.g., vomiting,diarrhea, fever, constipation, abdominal pain, hepatomegaly, splenomegaly,abdominal distension, weight loss, and jaundice)

History of aspirin, NSAID, or alcoholingestion

Presence of known diseases (e.g., IBDor liver disease)

Diagnostic studies that may identifysource of acute bleeding include endoscopy, radionuclide scanning,and selective angiography.

If upper tract bleeding has stoppedor is intermittent, upper endoscopy can be performed to diagnoseesophagitis, gastritis, gastric or duodenal ulcer, Mallory-Weisstear, and esophageal varices.

If endoscopic exam is impossible to performbecause of continuous bleeding, radionuclide scan or selective angiographycan be performed. Technetium sulfur colloid scan can detect slow ongoingbleeding, whereas technetium red cell scan can detect slow intermittentbleeding. These techniques help localize site of bleeding, so thatother diagnostic studies can be performed.

Sulfur colloid scan can detect bleedingat rate as low as 0.1 mL/min, but only if bleeding is occurringat time of injection because half-life of tracer is <2.5mins. Labeled red cells remain in blood for 24 hrs, so technetiumred cell scan can detect intermittent bleeding.

If these scans fail to disclose siteof bleeding or bleeding is brisk, selective angiography should beperformed—angiography of celiac axis and superior mesentericartery for suspected upper tract bleeding, and superior mesentericand inferior mesenteric artery angiography for suspected lower tract bleeding.

Another advantage of angiography isthat therapeutic measures (e.g., vasopressin infusion and embolization)can be used if necessary.

If the bleeding is massive or uncontrolled,immediate surgery should be considered.

In stable child with lower tract bleeding,anus should be examined for anal fissure and rectum for polyp.

With bloodydiarrhea, bacterial stool culture should be performed, and examof stool for ova and parasites should be considered.

Technetium 99m–pertechnetatescan to identify ectopic gastric mucosa in Meckel diverticulum orintestinal duplication also should be considered. If diagnosis remainsuncertain, proctosigmoidoscopy should be performed. This may befollowed by colonoscopy or contrast studies.

Colonoscopy with biopsy may diagnosepolyps, colitis, IBD, hemangiomas, and malignant lesions. Air-contrastenema may diagnose intussusception.

With persistent undefined bleeding,upper tract endoscopy may be useful to identify ulcer, esophagealor gastric varices, or vascular lesion.

Upper GI radiographic series with smallbowel follow-through may diagnose lesions of esophagus, stomach,and duodenum as well as lesions of small bowel, including Crohndisease

Selective angiography may not revealsite of bleeding if bleeding is too slow, but it may suggest angiodysplasticlesion or tumor by revealing abnormal vascular pattern.

>

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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Edema: Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)

Disorders with Normal Serum Albumin

Increased Capillary Permeability

Skin Disorders

Cellulitis,exfoliative dermatitis, and burns can cause increase in capillarypermeability and edema.

History and physical exam are diagnostic.

Allergic Reaction

Releaseof histamine and other vasoactive mediators can produce localizedor generalized edema.

Drugs, chemical exposure by inhalation,foods (especially milk, eggs, chocolate, nuts), and bee stings arecommon causes of allergic reactions.

Lips, eyelids, and face are frequentlyinvolved, and urticaria also may occur.

Wheezing, laryngospasm, and hypotensionmay be seen with anaphylactic reactions.

History and physical exam are usuallydiagnostic.

Vasculitis

Common causes of vasculitis causing edemainclude Kawasaki disease and collagen vascular disease.

Septicemia

Severe bacterial or rickettsial infectionscan cause increase in capillary permeability and edema.

Vitamin E Deficiency

Uncommonsince addition of vitamin E to infant formulas.

Preterm infants 4–6 wks ofage without normal intake of vitamin E may develop generalized edema,hemolytic anemia, and thrombocytosis.

Serum concentration of vitamin E islow.

Hereditary Angioedema

Deficiencyor functional defect of C1 inhibitor is responsible for this disorder,which is transmitted as autosomal-dominant trait. Gene locus hasbeen mapped to chromosome 11q11-q13.1.

In most common form (type I), serumlevels are 5–30% of normal and functional activityis diminished, whereas in type II, serum levels are normal or increased,but functional activity is decreased.

The 2 types are clinically indistinguishable.Episodic edema may involve face, trunk, and extremities. Most worrisomefeature is edema of larynx and upper airway. Episodes last severaldays, and interval between attacks can be days, months, or years.

Low serum C4 concentration is mostuseful screening test for this disease. Serum C3 concentration isnormal.

Diagnosis is confirmed by measurementof C1 inhibitor and assay of its activity.

Increased Hydrostatic Pressure

Increased Blood Volume

Administrationof excessive amounts of sodium or fluid can produce volume overloadand edema.

In cardiac failure, diminished renalblood flow leads to decrease in glomerular filtration rate (GFR)and edema.

Renal disease (e.g., glomerulonephritis)or any cause of renal failure also may lead to decrease in GFR andedema.

Increased Venous Pressure

Increasedvenous pressure from deep venous thrombosis, constrictive pericarditis, portalhypertension, or impaired venous drainage from tumor may produceedema.

Deep venous thrombosis in thigh orcalf produces pain and swelling of leg distal to thrombus. U/Sis usually diagnostic.

See Chap.30, Hepatomegaly, and Chap. 62, Splenomegaly,for discussion of constrictive pericarditis and portal hypertension.

Increased Lymph Pressure

Lymphedemais excessive accumulation of lymph in interstitial space and isprincipal cause of increased lymph pressure.

Can be congenital or acquired, sporadicor familial, and may appear at birth or in childhood or adolescence.

Abnormal development or dysfunctionof lymphatic vessels, lymph node obstruction, and venous stasisare common mechanisms producing lymphedema.

Common presentation is unilateral,painless edema of leg; however, pain may occur with massive edemaor cellulitis.

U/S and MRI are useful indetection of lymphatic malformations and obstructive lesions.

Disorders with Decreased Serum Albumin (Decreased OncoticPressure)

Disorders with Proteinuria

Any renaldisorder causing severe proteinuria may produce edema. Nephroticsyndrome and acute glomerulonephritis are common examples.

UA confirms presence of proteinuria.

See Chap.50, Proteinuria.

Disorders without Proteinuria

Acute and Chronic Liver Disease

Decreasein synthesis of albumin in liver produces hypoalbuminemia.

Serum albumin of <2.5 g/dLcauses decrease in plasma oncotic pressure and edema.

See Chap.30, Hepatomegaly, and Chap. 36, Jaundice, fordiscussion of causes of acute and chronic liver disease.

Gastrointestinal Disease

Loss ofserum albumin in GI tract leads to decreased plasma oncotic pressureand edema.

Causes of protein-losing enteropathyinclude cow milk protein sensitivity, cystic fibrosis, celiac disease,inflammatory bowel disease, and intestinal lymphangiectasia.

Screening test for protein loss instool is measurement of alpha₁-antitrypsinin spot stool sample.

See Chap.14, Diarrhea.

Protein-Calorie Malnutrition

Severe protein-caloriemalnutrition can produce edema because of decrease in serum albumin.

Growth failure, decreased muscle mass,diarrhea, hepatomegaly, anemia, pigment changes of hair and skin,fatigue, and apathy are other findings.

Edema resolves with adequate calorieand protein intake.

Congenital Albumin Deficiency

Severe edemaoccurs with congenital albumin deficiency, which is rare.

Very low or undetectable serum albuminconcentration in absence of other causes of hypoalbuminemia confirmsdiagnosis.

Hydrops Fetalis: Immune and Nonimmune

Hydrops fetalis is term used to describesevere generalized edema in fetus or newborn.Because of use of anti-D immune globulinfor Rh isoimmunization, most cases of hydrops are nonimmune type(Table 17.1 ). >

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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006

Pustular rash: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

Have the patient describe the appearance, location, and onset of the first pustular lesion. Did another type of skin lesion precede the pustule? Find out how the lesions spread. Ask what medications the patient takes and if he has applied topical medication to his rash. If so, what type and when did he last apply it? Find out if he has a family history of a skin disorder.

Examine the entire skin surface, noting if it's dry, oily, moist, or greasy. Record the exact location and distribution of the skin lesions and their color, shape, and size.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

Edema, generalized: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

When the patient's condition permits, obtain a complete medical history. First, note when the edema began. Does it move throughout the course of the day—for example, from the upper extremities to the lower, periorbitally, or within the sacral area? Is the edema worse in the morning or at the end of the day? Is it affected by position changes? Is it accompanied by shortness of breath or pain in the arms or legs? Find out how much weight the patient has gained. Has his urine output changed in quantity or quality?

Next, ask about previous burns or cardiac, renal, hepatic, endocrine, or GI disorders. Have the patient describe his diet so you can determine whether he suffers from protein malnutrition. Explore his drug history, and note recent I.V. therapy.

Begin the physical examination by comparing the patient's arms and legs for symmetrical edema. Also, note ecchymoses and cyanosis. Assess the back, sacrum, and hips of the bedridden patient for dependent edema. Palpate peripheral pulses, noting whether hands and feet feel cold. Finally, perform a complete cardiac and respiratory assessment.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

Edema of the arm: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

When taking the patient's history, one of the first questions to ask is, “How long has your arm been swollen?” Then find out if the patient also has arm pain, numbness, or tingling. Does exercise or arm elevation decrease the edema? Ask about recent arm injury, such as burns or insect stings. Also, note recent I.V. therapy, surgery, or radiation therapy for breast cancer.

Determine the edema's severity by comparing the size and symmetry of both arms. Use a tape measure to determine the exact girth, and mark the location where the measurement was obtained in order to make comparative measurements later. Make sure to note whether the edema is unilateral or bilateral, and test for pitting. (See Edema: Pitting or nonpitting?page 226.) Next, examine and compare the color and temperature of both arms. Look for erythema and ecchymoses and for wounds that suggest injury. Palpate and compare radial and brachial pulses. Finally, look for arm tenderness and decreased sensation or mobility. If you detect signs of neurovascular compromise, elevate the arm.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

Edema of the face: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

If the patient isn't in severe distress, take his health history. Ask if facial edema developed suddenly or gradually. Is it more prominent in early morning, or does it worsen throughout the day? Has the patient gained weight? If so, how much and over what length of time? Has he noticed a change in his urine color or output? In his appetite? Take a drug history and ask about recent facial trauma.

Begin the physical examination by characterizing the edema. Is it localized to one part of the face, or does it affect the entire face or other parts of the body? Determine if the edema is pitting or nonpitting, and grade its severity. (See Edema: Pitting or nonpitting?page 226.) Next, take the patient's vital signs, and assess his neurologic status. Examine the oral cavity to evaluate dental hygiene and look for signs of infection. Visualize the oropharynx and look for soft-tissue swelling.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

Edema of the leg: History and physical examination
(Nursing: Interpreting Signs and Symptoms)

To evaluate the patient, first ask how long he has had the edema. Did it develop suddenly or gradually? Does it decrease if he elevates his legs? Is it painful when touched or when he walks? Is it worse in the morning, or does it get progressively worse during the day? Ask about a recent leg injury or recent surgery or illness that may have immobilized the patient. Does he have a history of cardiovascular disease? Finally, obtain a drug history.

Begin the physical examination by examining each leg for pitting edema. (See Edema: Pitting or nonpitting?page 226.) Because leg edema may compromise arterial blood flow, palpate or use a Doppler to auscultate peripheral pulses to detect an insufficiency. Observe leg color and look for unusual vein patterns. Then palpate for warmth, tenderness, and cords, and gently squeeze the calf muscle against the tibia to check for deep pain. If leg edema is unilateral, dorsiflex the foot to look for Homans'sign, which is indicated by calf pain. Finally, note skin thickening or ulceration in edematous areas.

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Source: Nursing: Interpreting Signs and Symptoms, 2007

EDEMA OF THE EXTREMITIES: Approach to the Diagnosis
(Differential Diagnosis in Primary Care)

Bilateral pitting edema of the lower extremities is usually due to CHF, nephrosis, or cirrhosis of the liver. Venous pressure and circulation time will rule out CHF, but echocardiography can be more definitive. Serum and urine osmolality can be helpful also. If there is nephrosis, there will be significant lowering of the serum albumin level and proteinuria. Liver function studies will usually confirm cirrhosis or liver disease, but ultrasonography can reveal ascites to assist in the diagnosis. Nonpitting edema of the lower extremities will usually be due to lymphatic obstruction, but hypothyroidism can be ruled out with a free thyroxine (T₄) or thyroid-stimulating hormone (TSH) assay. Unilateral edema of the lower extremities suggests deep vein thrombosis, which can be confirmed by Doppler ultrasound studies, plethysomography, or contrast venography. A CT scan of the chest will help diagnose constrictive pericarditis, which is rarely found today. Spirometry and arterial blood gas analysis will diagnose pulmonary emphysema with cor pulmonale.

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Source: Differential Diagnosis in Primary Care, 2007

Plague: Plague - DIAGNOSIS
(The 5-Minute Pediatric Consult)

Pitfalls:

• Patients who present with fever, tachycardia, or tachypnea, rather than lymphadenitis, are at higher risk for delayed diagnosis and serious sequelae (i.e., septicemic plague).
• Failing to consider septicemic plague in the appropriate epidemiologic setting and withholding appropriate antibiotics or using an empiricโ-lactam
• Failing to treat suspect bubonic plague with antibiotics when needle aspiration of the bubo shows no organisms on direct stain and while awaiting culture results.

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008

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