CONFIRMING DIAGNOSIS Although signs of respiratory distress in a premature neonate during the first few hours of life strongly suggest IRDS, a chest X-ray and arterial blood gas (ABG) analysis are necessary to confirm the diagnosis.
❑ Chest X-ray may be normal for the first 6 to 12 hours (in 50% of neonates with IRDS), but 24 hours after birth it will show the characteristic ground-glass appearance and air bronchograms.
❑ ABG analysis shows decreased partial pressure of arterial oxygen; normal, decreased, or increased partial pressure of arterial carbon dioxide; and decreased pH (from respiratory or metabolic acidosis or both).
❑ Chest auscultation reveals normal or diminished air entry and crackles (rare in early stages).
When a cesarean delivery is necessary before 36 weeks’ gestation, amniocentesis enables the determination of the lecithin/sphingomyelin (L/S) ratio and the presence of phosphatidylglycerol. An L/S ratio of more than 2:1 and the presence of phosphatidylglycerol decrease the likelihood of IRDS.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Lung cancer:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
Typical clinical findings may strongly suggest lung cancer, but firm diagnosis requires further evidence.
❑Chest X-ray usually shows an advanced lesion, but it can detect a lesion up to 2 years before symptoms appear. It also indicates tumor size and location.
❑ Sputum cytology, which is 75% reliable, requires a specimen coughed up from the lungs and tracheobronchial tree, not postnasal secretions or saliva.
❑ Computed tomography (CT) scan of the chest may help to delineate the tumor's size and its relationship to surrounding structures.
❑ Bronchoscopy can locate the tumor site. Bronchoscopic washings provide material for cytologic and histologic examination. The flexible fiber-optic bronchoscope increases the test's effectiveness.
❑ Needle biopsy of the lungs uses biplane fluoroscopic visual control to detect peripherally located tumors. This allows firm diagnosis in 80% of patients.
❑ Tissue biopsy of accessible metastatic sites includes supraclavicular and mediastinal node and pleural biopsy. Directed needle biopsy may be performed in conjunction with CT scan.
❑Thoracentesis allows chemical and cytologic examination of pleural fluid.
Additional studies include preoperative mediastinoscopy or mediastinotomy to rule out involvement of mediastinal lymph nodes (which would preclude curative pulmonary resection).
Other tests to detect metastasis include bone scan, bone marrow biopsy (recommended in small cell carcinoma), CT scan of the brain or abdomen, and positron emission tomography.
After histologic confirmation, staging determines the extent of the disease and helps in planning the treatment and predicting the prognosis. (See Staging lung cancer.)
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Toxic shock syndrome:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
Diagnosis is based on several criteria: fever, hypotension, rash that peels after 1 to 2 weeks, and at least 3 organs with signs of dysfunction. In some cases, blood cultures may be positive for S. aureus. Organs with signs of dysfunction may include:
❑GI effects, including vomiting and profuse diarrhea
❑muscular effects, with severe myalgias or a fivefold or greater increase in creatine kinase levels
❑mucous membrane effects such as frank hyperemia
❑renal involvement with elevated blood urea nitrogen or creatinine levels (at least twice the normal levels)
❑liver involvement with elevated bilirubin, aspartate aminotransferase, or alanine aminotransferase levels (at least twice the normal levels)
❑blood involvement with signs of thrombocytopenia and a platelet count of less than 100,000/µl
❑central nervous system effects such as disorientation without focal signs.
Negative results on blood tests for Rocky Mountain spotted fever, leptospirosis, and measles help rule out these disorders.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Hypovolemic shock:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
No single symptom or diagnostic test establishes the diagnosis or severity of shock. Characteristic laboratory findings include:
❑ elevated potassium, serum lactate, and blood urea nitrogen levels
❑ increased urine specific gravity (more than 1.020) and urine osmolality
❑ decreased blood pH and partial pressure of arterial oxygen and increased partial pressure of arterial carbon dioxide.
In addition, gastroscopy, aspiration of gastric contents through a nasogastric tube, computed tomography scan, and X-rays identify internal bleeding sites; coagulation studies may detect coagulopathy from DIC. Echocardiography or right-heart catheterization can help differentiate between hypovolemic and cardiogenic shock.
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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
Atelectasis:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
Diagnosis requires an accurate patient history, a physical examination, and a chest X-ray. Auscultation reveals diminished or bronchial breath sounds. When much of the lung is collapsed, percussion reveals dullness. However, extensive areas of “microatelectasis” may exist without abnormalities on the chest X-ray. In widespread atelectasis, the chest X-ray shows characteristic horizontal lines in the lower lung zones. With segmental or lobar collapse, characteristic dense shadows commonly associated with hyperinflation of neighboring lung zones are also apparent. If the cause is unknown, diagnostic procedures may include bronchoscopy to rule out an obstructing neoplasm or a foreign body.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Accessory muscle use:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient’s condition allows, examine him more closely. Ask him about the onset, duration, and severity of associated signs and symptoms, such as dyspnea, chest pain, cough, and fever.
Explore his medical history, focusing on respiratory disorders, such as infection or COPD. Ask about cardiac disorders, such as heart failure, which may lead to pulmonary edema; also inquire about neuromuscular disorders, such as amyotrophic lateral sclerosis, which may affect respiratory muscle function. Note a history of allergies or asthma. Because collagen vascular diseases can cause diffuse infiltrative lung disease, ask about such conditions as rheumatoid arthritis and lupus erythematosus.
Ask about recent trauma, especially to the spine or chest. Find out if the patient has recently undergone pulmonary function tests or received respiratory therapy. Ask about smoking and about occupational exposure to chemical fumes or mineral dusts such as asbestos. Explore the family history for such disorders as cystic fibrosis and neurofibromatosis, which can cause diffuse infiltrative lung disease.
Perform a detailed chest examination, noting abnormal respiratory rate, pattern, or depth. Assess the color, temperature, and turgor of the patient’s skin, and check for clubbing. (See Accessory muscle use: Causes and associated findings, page 30.)
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Respirations, grunting:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
After addressing the child’s respiratory status, ask his parents when the grunting respirations began. If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child’s activity level or feeding pattern to determine if the child is lethargic or less alert than usual.
Begin the physical examination by auscultating the lungs, especially the lower lobes. Note diminished or abnormal sounds, such as crackles or sibilant rhonchi, which may indicate mucus or fluid buildup. Characterize the color, amount, and consistency of any discharge or sputum. Note the characteristics of the cough, if any.
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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
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
Salivation, increased [Polysialia, ptyalism]:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
A patient who complains of increased salivation may have overproductive salivary glands or difficulty swallowing. To distinguish these, first test for a gag reflex and observe the patient’s ability to swallow and chew. Is he drooling? Is his chewing uncoordinated? An impaired gag reflex, drooling, and chewing incoordination suggest difficulty swallowing. Does he have related signs and symptoms, such as fatigue, fever, headache, or a sore throat? Ask about exposure to industrial toxins, such as mercury. Is the patient taking any medications? Note especially use of iodides, cholinergics, and miotics.
Inspect the mouth and mucous membranes for lesions. If present, are they painful? Put on gloves and palpate the lesions, which may be suppurative or infectious. Describe them in your notes. Next, inspect the uvula, gingivae, and pharynx. Palpate the lymph nodes, and determine if the parotid glands are swollen or sore.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Tearing, increased [Epiphora]:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient complains of increased tearing, begin by fully exploring this sign. When did it begin? Is it constant or intermittent? Minimal or extensive? Is increased tearing accompanied by pain, irritation, or any other eye drainage or discharge? Next, ask about recent eye trauma and about ocular and systemic disorders. Then record which drugs the patient is taking. Note his occupation and the nature of his work. For example, does he read extensively, look at a computer screen frequently, or work with small or fine objects? Is he exposed to any chemicals or dust in the workplace?
After taking vital signs, examine both eyes—unless the history suggests a perforating or penetrating injury. Carefully inspect the external structures. Do the eyelashes contain debris? Examine the eyelids for lesions and edema. Ask the patient to look straight ahead at a fixed object while you check for ptosis. Are the lid margins turned inward or outward? Examine the eyeballs. Do they appear sunken or bulging? Examine the conjunctivae for redness and abnormal drainage. Also, note the color of the sclera. Hold a flashlight at the side of each eye and examine the cornea and iris for scars, irregularities, and foreign bodies. Evaluate extraocular muscle function by testing the six cardinal fields of gaze. (See Testing extraocular muscles, page 245.) Finally, test the patient’s visual acuity.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
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
Epigastric Distress:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Pain is the usual presentation of epigastric distress. First priority is to ask questions about the onset, intensity, frequency, pattern, and location of the pain. Onset: When did the pain start? Is there any prior history of similar pain?
B. Intensity and quality. Can you describe the pain? (sharp, dull, burning, radiating, pressure). Burning pain is often used to describe GERD. Pressure sensation “like an elephant sitting on me” suggests cardiac ischemia (Chapter 7.1).
C. Frequency and pattern. Does the pain occur at any particular time of day? Is there anything that makes the pain better or worse? Pain that is worse at night when lying down suggests GERD. Pain that occurs after a high fat meal increases the likelihood of gallbladder disease (Chapter 9.1).
D. Location. Where is the pain? Does the pain radiate anywhere? Radiation to the back suggests pancreatitis. Pain radiating to the scapula can indicate gallbladder disease.
E. Associated symptoms. Has there been any nausea, vomiting, or hematemesis? The previous symptoms can indicate a Mallory-Weiss tear or PUD. If diarrhea is present, is there bright red blood or melena in the stool? The presence of blood or melena in the stool requires further workup for GI bleed.
F. Past medical history. Has the patient had any prior GI problems? Obtain a drug history, including the use of aspirin, nonsteroidal antiinflammatory drugs, alendronate sodium (Fosamax), steroids, antibiotics. Is there a history of tobacco or alcohol use? Both tobacco and alcohol use are associated with an increased incidence of GERD and PUD. Multiparity and obesity increase the risk of gallbladder disease. Are there risk factors for sexually transmitted diseases? Hepatitis B and human immunodeficiency virus can be transmitted sexually and can be causative factors in epigastric distress.
Physical examination
A. General assessment. Obtain vital signs. Is the patient febrile—indicating an infectious cause? Tachycardia and hypotension can indicate dehydration or GI bleed. Is the patient in acute distress? Jaundiced?
B. Cardiopulmonary assessment. Evaluate the heart and lungs to rule out any cardiac or pulmonic process that could present with epigastric distress. Is there evidence of an arrhythmia, myocardial infarction, or congestive heart failure? Are there crackles or rales suggesting a pneumonia?
C. Abdominal examination. Are bowel sounds present? Decreased or absent bowel sounds can indicate a small bowel obstruction, acute surgical abdomen (appendicitis, perforated ulcer), or pancreatitis. Rebound tenderness should prompt consideration of an acute surgical abdomen. The right upper quadrant (RUQ) should be palpated. A palpable liver warrants evaluation for other signs of liver disease—jaundice, ascites, skin changes. Murphy’s sign—sudden cessation of the patient’s inspiratory effort during deep palpation of the RUQ—is suggestive of acute cholecystitis (3). Tenderness to palpation of the left upper quadrant can indicate splenic infarct such as seen with sickle cell disease. Tenderness of the midepigastric area can represent peptic ulcer disease, dyspepsia, “nonclassical” presentation of acute appendicitis, or any other of the above-mentioned conditions. A rectal examination with testing for occult blood should be a part of the examination, particularly with any concern about GI bleeding (Chapter 9.7).
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
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
Shock:
Differential Overview
(Field Guide to Bedside Diagnosis)
Cardiogenic
❑ Anterior myocardial infarction
❑ Arrhythmia
❑ Dilated cardiomyopathy
❑ Aortic stenosis
❑ Acute mitral regurgitation
Obstructive
❑ Massive pulmonary embolism
❑ Pericardial tamponade
❑ Constrictive pericarditis
❑ Tension pneumothorax
Hypovolemic
❑ Hemorrhage
❑ Fluid depletion
Distributive
❑ Sepsis
❑ Anaphylaxis
❑ Adrenal insufficiency
❑ Neurogenic
Diagnostic Approach
A patient in shock will lie still, paying little attention to events around him. If agitated, he will answer in a weak voice. The pupils are dilated and react slowly to light. The coloration is gray and pale, with marbling of the skin on the back or the hands and legs, and cyanosis of the lips. The pulse is rapid and thready; temperature and blood pressure are low. Emergence of these findings corresponds to a 20% to 25% reduction in volume in low preload shock, a fall in the cardiac index to below 2.5 L/min/M 2 or activation of mediators of the sepsis syndrome.
Clues to the underlying cause should be carefully searched for on physical examination. HEENT exam may reveal dilated or pinpoint pupils, dry conjunctivae, or scleral icterus. In the neck, jugular venous distension, delayed carotid upstroke, carotid bruits, or meningeal signs may be observed. Lung exam may show tachypnea, shallow breaths, rales, unilateral tympany or absent breath sounds. The cardiovascular exam may reveal tachycardia, bradycardia, irregular rhythm, S3 gallop, right or left ventricular heave, murmurs, distant heart sounds, pulsus paradoxus, or rub. On abdominal exam, tenderness, guarding or rebound, high-pitched or absent bowel sounds, distension, pulsatile mass, hepatosplenomegaly, or ascites may be found. Rectal exam can reveal evidence of bleeding (occult positive, melena, or bright red blood) or decreased tone. The extremities can show a swollen calf or unequal pulses or blood pressures between the arms. Neurologic exam could exhibit agitation, confusion, delirium, obtundation, or coma. Finally, skin exam can reveal cool and clammy skin, warm and hyperemic skin, rashes, petechiae, urticaria, or cellulitis.
Prognosis in cardiogenic shock can be accurately stratified by Killip class, using observable clinical criteria:
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Source: Field Guide to Bedside Diagnosis, 2007
Respiratory distress syndrome:
Diagnosis
(Handbook of Diseases)
Although signs of respiratory distress in a premature neonate during the first few hours of life strongly suggest respiratory distress syndrome, the following tests are necessary to confirm the diagnosis:
❑ Chest X-ray may be normal for the first 6 to 12 hours (in 50% of neonates with respiratory distress syndrome) but later shows a fine reticulonodular pattern.
❑ Arterial blood gas (ABG) analysis shows decreased partial pressure of arterial oxygen (Pao2); normal, decreased, or increased partial pressure of arterial carbon dioxide; and decreased pH (from respiratory or metabolic acidosis or both).
❑ Pulmonary function studies may be necessary.
When a cesarean section is necessary before the 36th week of gestation, amniocentesis allows determination of the lecithin-sphingomyelin ratio, which helps to assess prenatal lung development and the risk of respiratory distress syndrome.
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Source: Handbook of Diseases, 2003
Lung abscess:
Diagnosis
(Handbook of Diseases)
The following tests are used to diagnose a lung abscess:
❑ Auscultation of the chest may reveal crackles and decreased breath sounds.
❑ Chest X-ray shows a localized infiltrate with one or more clear spaces, usually containing air-fluid levels.
❑ Chest computed tomography scan confirms the presence of localized infiltrate or nodular density, occasionally with air-fluid level. Chest imaging may also identify airway masses or foreign bodies that have led to abscess formation.
❑ Percutaneous aspiration of an abscess or bronchoscopy may be used to obtain cultures to identify the causative organism. Bronchoscopy is only used if abscess resolution is eventful and the patient’s condition permits it.
❑ Blood cultures, Gram stain, and sputum culture are also used to detect the causative organism.
❑ White blood cell count commonly exceeds 10,000/µl.
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Source: Handbook of Diseases, 2003
Lung cancer:
Diagnosis
(Handbook of Diseases)
Typical signs and symptoms may strongly suggest lung cancer, but a firm diagnosis requires further evidence, including the following:
❑ Chest X-ray usually shows an advanced lesion, but it can detect a lesion up to 2 years before symptoms appear. It also indicates tumor size and location.
❑ Sputum cytology is marginally helpful in obtaining a diagnosis. It requires a specimen coughed up from the lungs and tracheobronchial tree, not postnasal secretions or saliva.
❑ Computed tomography (CT) scan of the chest may help to delineate the tumor’s size and its relationship to surrounding structures.
❑ Bronchoscopy can locate the tumor site. Bronchoscopic washings provide material for cytologic and histologic examination. The flexible fiber-optic bronchoscope increases the test’s effectiveness.
❑ A needle biopsy of the lungs uses biplane fluoroscopic visual control or CT guidance to detect peripherally located tumors. This allows a firm diagnosis in 80% of patients.
❑ Tissue biopsy of accessible metastatic sites includes supraclavicular and mediastinal node and pleural biopsies.
❑ Thoracentesis allows chemical and cytologic examination of pleural fluid.
Additional studies include preoperative mediastinoscopy or mediastinotomy to rule out involvement of mediastinal lymph nodes (which would preclude curative pulmonary resection).
Other tests to detect metastasis include a bone scan, positron emission tomography scan, bone marrow biopsy (recommended in small cell carcinoma), and a CT scan of the brain or abdomen.
After histologic confirmation, staging determines the extent of the disease and helps in planning treatment and predicting the prognosis. (See Staging lung cancer.)
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Source: Handbook of Diseases, 2003
Toxic shock syndrome:
Diagnosis
(Handbook of Diseases)
A diagnosis of TSS is based on clinical findings and the presence of at least three of the following:
❑ GI effects, including vomiting and profuse diarrhea
❑ muscular effects, with severe myalgias or a fivefold or greater increase in creatine kinase
❑ mucous membrane effects such as frank hyperemia
❑ renal involvement with elevated blood urea nitrogen or creatinine levels (at least twice the normal levels)
❑ liver involvement with elevated bilirubin, alanine aminotransferase, or aspartate aminotransferase levels (at least twice the normal levels)
❑ blood involvement with signs of thrombocytopenia and a platelet count < 100,000/µl
❑ central nervous system effects such as disorientation without focal signs.
In addition, isolation of S. aureus from vaginal discharge or lesions helps support the diagnosis. Negative results on blood tests for Rocky Mountain spotted fever, leptospirosis, and measles help rule out these disorders.
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Source: Handbook of Diseases, 2003
Hypovolemic shock:
Diagnosis
(Handbook of Diseases)
No single symptom or diagnostic test establishes the diagnosis or severity of shock. Characteristic laboratory findings include:
❑ elevated potassium, serum lactate, and blood urea nitrogen levels
❑ increased urine specific gravity (greater than 1.020) and urine osmolality
❑ decreased blood pH and partial pressure of arterial oxygen and increased partial pressure of arterial carbon dioxide.
In addition, gastroscopy, aspiration of gastric contents through a nasogastric tube, and X-rays identify internal bleeding sites; coagulation studies may detect coagulopathy from DIC.
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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
Acuterespiratory distress syndrome:
Diagnosis
(Handbook of Diseases)
On room air, arterial blood gas (ABG) analysis initially shows a decreased partial pressure of arterial oxygen (Pao2) — less than 60 mm Hg — and a decreased partial pressure of arterial carbon dioxide (Paco2) — less than 35 mm Hg. The resulting pH usually reflects respiratory alkalosis. As ARDS becomes more severe, ABG levels indicate respiratory acidosis (a Paco2 greater than 45 mm Hg) and metabolic acidosis (a bicarbonate level less than 22 mEq/L) as well as a decreasing Pao2, despite oxygen therapy.
Pulmonary artery (PA) catheterization helps identify the cause of pulmonary edema: It allows evaluation of pulmonary artery wedge pressure (PAWP); collection of PA blood, which shows decreased oxygen saturation, indicating tissue hypoxia; measurement of PA pressure; and measurement of cardiac output via thermodilution.
Serial chest X-rays initially show bilateral infiltrates; in later stages, the X-rays show ground-glass appearance and, eventually (as hypoxemia becomes irreversible), “whiteouts” of both lung fields. This is seen more clearly by the use of computed tomography of the chest.
A differential diagnosis must rule out cardiogenic pulmonary edema, pulmonary vasculitis, and diffuse pulmonary hemorrhage. To establish the cause of ARDS, laboratory work should include a sputum Gram stain, culture and sensitivity tests, and blood cultures to detect infections; a toxicology screen for drug ingestion; and, when pancreatitis is a consideration, a serum amylase determination.
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Source: Handbook of Diseases, 2003
Atelectasis:
Diagnosis
(Handbook of Diseases)
An accurate patient history, a physical examination, and a chest X-ray provide baseline data for a diagnosis. In some cases, chest computed tomography scan may be necessary to confirm findings. Auscultation reveals diminished or bronchial breath sounds. When much of the lung is collapsed, percussion reveals dullness. However, extensive areas of “microatelectasis” may exist without abnormalities on the chest X-ray. In widespread atelectasis, the chest X-ray shows characteristic horizontal lines in the lower lung zones and, with segmental or lobar collapse, characteristic dense shadows commonly associated with hyperinflation of neighboring lung zones.
If the cause is unknown, diagnostic procedures may include bronchoscopy to rule out an obstructing neoplasm or a foreign body.
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Source: Handbook of Diseases, 2003
Cardiogenic shock:
Diagnosis
(Handbook of Diseases)
❑ Auscultation detects gallop rhythm, faint heart sounds and, possibly, if the shock results from rupture of the ventricular septum or papillary muscles, a holosystolic murmur.
❑ Pulmonary artery pressure monitoring reveals increased pulmonary artery pressure (PAP) and increased pulmonary artery wedge pressure (PAWP), reflecting a rise in left ventricular end-diastolic pressure (preload) and increased resistance to left ventricular emptying (afterload) resulting from ineffective pumping and increased peripheral vascular resistance. Thermodilution technique measures decreased cardiac output.
❑ Invasive arterial pressure monitoring shows hypotension from impaired ventricular ejection.
❑ Arterial blood gas (ABG) levels may show metabolic acidosis and hypoxia.
❑ Electrocardiography may reveal evidence of an AMI, myocardial ischemia, or ventricular aneurysm.
❑ Enzyme levels show elevated creatine kinase (CK-MB, troponin T, or troponin I), lactate dehydrogenase (LD), aspartate aminotransferase, and alanine aminotransferase, which point to an MI or myocardial ischemia and suggest heart failure or shock. CK-MB and LD isoenzyme levels may confirm an AMI.
❑ Echocardiography (color-flow Doppler) shows left ventricular function, valvular disease, aneurysmal dilation, and ventricular septal defects.
Additional tests help identify other conditions that can lead to pump dysfunction and failure, such as cardiac arrhythmias, cardiac tamponade, papillary muscle infarct or rupture, ventricular septal rupture, pulmonary embolus, venous pooling (associated with venodilators and continuous intermittent positive-pressure breathing), and hypovolemia.
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Source: Handbook of Diseases, 2003
Electric shock:
Diagnosis
(Handbook of Diseases)
Usually, the cause of electrical injuries is either obvious or suspected. An accurate history can define the voltage and length of contact.
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Source: Handbook of Diseases, 2003
Respirations, grunting:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
After addressing the child’s respiratory status, ask his parents when the grunting respirations began. Is he usually healthy with normal growth and development? If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child’s activity level or feeding pattern to determine if the child is lethargic or less alert than usual.
Physical examination
Begin the physical examination by inspecting the rate, depth, and ease of respirations and any signs of respiratory distress. Auscultate the lungs, especially the lower lobes. Note diminished or abnormal sounds, such as crackles or sibilant rhonchi, which may indicate mucus or fluid buildup. Also, characterize the color, amount, and consistency of discharge or sputum. Note the characteristics of the cough, if any. Observe for abrupt behavior changes and lowered level of consciousness.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
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
Accessory muscle use:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
If the patient’s condition allows, question him thoroughly. Ask him about the onset, duration, and severity of associated signs and symptoms, such as dyspnea, chest pain, cough, or fever.
Explore his medical history, focusing on respiratory disorders, such as infection or COPD. Ask about cardiac disorders such as heart failure, which may lead to pulmonary edema; also inquire about neuromuscular disorders such as amyotrophic lateral sclerosis, which may affect respiratory muscle function. Note a history of allergies or asthma. Because collagen vascular diseases can cause diffuse infiltrative lung disease, ask about such conditions as rheumatoid arthritis and lupus erythematosus.
Ask about recent trauma, especially to the spine or chest. Find out if the patient has recently undergone pulmonary function testing or received respiratory therapy. Ask about smoking and occupational exposure to chemical fumes or mineral dusts such as asbestos. Explore the patient’s family history for such disorders as cystic fibrosis and neurofibromatosis, which can cause diffuse infiltrative lung disease.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Respirations, grunting:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
After addressing the child’s respiratory status, ask his parents when the grunting respirations began. If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child’s activity level or feeding pattern to determine if the child is lethargic or less alert than usual.
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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
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
Salivation, increased:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Ask the patient about related signs and symptoms, such as fatigue, fever, headache, or a sore throat. Also ask about exposure to industrial toxins such as mercury. Is the patient taking any medications? Note especially use of iodides, cholinergics, and miotics.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Tearing, increased:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
If the patient complains of increased tearing, begin by fully exploring this sign. When did it begin? Is it constant or intermittent? Minimal or extensive? Is increased tearing accompanied by pain or irritation? Is there any other drainage or discharge from the eye? Next, ask about recent eye trauma and about ocular and systemic disorders. Then record what drugs the patient is taking. Note his occupation and the nature of his work. For example, does he read extensively, look at a computer screen frequently, or work with small or fine objects. Is he exposed to any chemicals or dust in the workplace?
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Respiratory Distress and Apnea:
Clinical Features and Diagnosis: Respiratory Distress (Neonatal)
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Upper Respiratory Tract Obstruction
Disorders that cause upper respiratory tractobstruction are discussed in Chap.63, Stertor, Stridor, and Airway Obstruction. Lower Respiratory Tract Disorders
Transient Tachypnea of the Newborn
Delayedresorption of lung fluid or mild immaturity of surfactant systemare most probable explanations for this disorder, which usuallyoccurs in term infants soon after birth.Respiratory rate is commonly 60–80breaths/min but sometimes is >100 breaths/min.Mild intercostal retractions and expiratory grunting also may occur.Characteristic chest radiographic findingsare prominent perihilar markings, hyperaeration, widening of interlobarfissures, and evidence of interstitial and pleural fluid.Most infants require <40% supplementaloxygen. Tachypnea usually resolves in 3 or 4 days. Respiratory Distress Syndrome (Hyaline Membrane Disease)
Respiratorydistress syndrome, which is most common cause of respiratory distress inpreterm infants, is due to inadequate amount of surfactant. Someinfants experience intrapartum asphyxia and fail to expand theirlungs at birth, whereas others develop tachypnea and expiratorygrunting within first 1–2 hrs of life.Spectrum of disease varies from mild(tachypnea and minimal oxygen requirement) to severe (apnea andrespiratory failure). Crackles may be heard on chest exam.Characteristic chest radiograph showsdiffuse reticulogranular infiltrates, atelectasis, and air bronchograms.Diagnosis is clinical and radiographic. Meconium Aspiration and Other Aspiration Syndromes
Neonateswho aspirate meconium are usually those who have had intrapartumasphyxia.Thick meconium in upper airway andmeconium staining of skin and nails are usual findings. Airway obstruction,pneumonia, and respiratory failure can occur.Chest radiography shows irregular distributionof coarse, patchy infiltrates and hyperaeration.Clinical and radiologic findings arediagnostic.Aspiration of feedings sometimes occursin normal infants but is more frequent in those with sucking andswallowing disorders (see Chap.65, Sucking and Swallowing Difficulty). Pneumonia
Pneumoniamay be caused by infections acquired transplacentally, during birthprocess, and postnatally. Viral infections transmitted by transplacentalroute include enteroviruses, adenoviruses, influenza viruses, rubellavirus, varicella-zoster virus, herpes simplex virus, cytomegalovirus,and HIV. Transplacental bacterial infections caused by L. monocytogenes,M. tuberculosis, or T. pallidum are less common than viral infections.Neonatal pneumonia is most commonlyacquired during birth process. Group B Streptococcus is most commonpathogen; other pathogens (e.g., gram-negative enteric bacteria)are less common. Most common viral agents acquired during birthprocess are herpes simplex virus and cytomegalovirus. C. trachomatisis also acquired during delivery and usually presents at 2–8wks of age with staccato cough and wheezing. History of conjunctivalinfection may or may not exist.Inadequate hand washing and exposureto respiratory equipment or humidified incubators may contributeto infection, especially with S. aureus and gram-negative entericbacteria.Other causes of postnatal infectionsinclude respiratory syncytial virus, parainfluenza viruses, influenzaviruses, herpes simplex virus, cytomegalovirus, and fungi (C. albicans).Infants with pneumonia present withrespiratory distress. Chest radiography shows interstitial or alveolarinfiltrates or consolidation. With suspected bacterial pneumoniain newborns, blood and spinal fluid cultures should be performed,and treatment begun immediately while awaiting culture results.Diagnosis of viral infections is discussedin other chapters. Pulmonary Air Leaks
Extrapulmonaryair can accumulate in interstitial spaces of lung (pulmonary interstitialemphysema), mediastinum (pneumomediastinum), pleural space (pneumothorax),and pericardium (pneumopericardium).Common cause of pulmonary interstitial emphysemais positive-pressure mechanical ventilation.Pneumomediastinum results from dissectionof air from interstitial space into mediastinum.Pneumothorax results from mediastinalair rupture into pleural space or rupture of air blebs on surfaceof lung. Most common causes of pneumothorax are respiratory distresssyndrome, meconium aspiration, and high-pressure mechanical ventilation.Pneumopericardium is produced fromdissection of mediastinal air into pericardium. Clinical presentation depends on sizeand location of air leak. Significant unilateral pneumothorax collapsesipsilateral lung and shifts heart and mediastinum to opposite sidewith diminished breath sounds on affected side. Significant pneumopericardiummay compromise cardiac filling and cause diminished cardiac output.Chest radiography is diagnostic ofdifferent types of air leak. Pulmonary Hemorrhage
Predisposingfactors in neonatal period include perinatal asphyxia, septicemia,and mechanical ventilation, especially in those with respiratorydistress syndrome.Accompanying respiratory distress isbloody fluid, which oozes from nose, mouth, or endotracheal tube.Depending on how severe bleeding is,chest radiography may show spectrum of findings ranging from patchyinfiltrates to opacification of lungs. Bronchopulmonary Dysplasia
This form of chronic lung disease developsin neonates treated with prolonged oxygen therapy and positive-pressureventilation for primary lung disorders. Most infants improve duringfirst 1–2 yrs of life, and with time chest radiograph becomesnormal. However, some of these children continue to have abnormalpulmonary function in childhood. Others with severe disease developcor pulmonale and succumb to their illness. Congenital Malformations of Lungs, Bronchi, Diaphragm, andRib Cage
Lung Agenesis and Aplasia
Lung agenesisis complete absence of lung or lobe and its branches, whereas lung aplasiais complete absence of lung tissue except for presence of smalllobar bronchus.Respiratory distress often occurs atbirth with decreased breath sounds on affected side.Chest radiography shows opaque hemithoraxwith displacement of mediastinum and normal lung toward involvedside.Bronchoscopy shows absence of mainbronchus in agenesis and presence of small bronchus in aplasia. Pulmonary Hypoplasia
Pulmonaryhypoplasia refers to smaller than normal lungs. Can be isolatedmalformation or occur in association with space-occupying lesionsof thorax (congenital diaphragmatic hernia, cystic adenomatoid malformation,large pleural effusion), oligohydramnios (renal agenesis, polycystickidney disease), and thoracic and abdominal wall abnormalities (asphyxiatingthoracic dystrophy, large omphalocele).Respiratory distress, chronic cough,and recurrent infection may occur with unilateral hypoplasia. Thoraxis asymmetric because of underdevelopment of 1 side.Chest radiography shows small hemithoraxwith displacement of mediastinum toward affected side. When bilateralhypoplasia occurs as isolated malformation, respiratory distressoccurs at birth and chest radiography shows small but clear lungfields. Pulmonary Sequestration
Mass ofnonfunctioning pulmonary tissue that receives its blood supply fromsystemic circulation.May occur within or outside a lobe.Intralobar sequestration usually occurs in lower lobe of eitherlung, whereas extralobar sequestration usually occurs just aboveor below diaphragm on left side. Whereas intralobar sequestrationis usually isolated malformation, extralobar sequestration is commonly associatedwith other malformations (e.g., diaphragmatic hernia and pulmonaryhypoplasia).Clinical findings include respiratorydistress, hemoptysis, and recurrent pneumonia.Chest radiography shows mass lesion.Chest CT or MRI is usually diagnostic. Lobar Emphysema
Overdistensionof lobe of lung (usually upper lobe). Usually congenital but alsomay be acquired secondary to extrinsic or intrinsic airway obstruction.Respiratory distress occurs with decreasedbreath sounds and hyperresonance on involved side.Chest radiography shows large distendedlobe or lobes with displacement of mediastinum to opposite sideand compression of contralateral lung. Extension of pulmonary vesselsto periphery of hyperexpanded lung almost always distinguishes lobaremphysema from lung cyst or pneumothorax. Cystic Lung Lesions
Bronchogenic Cyst
Abnormalbudding or branching of tracheobronchial tree produces bronchogenic cysts,which are found incidentally or because they are infected. Locationcan be above or at carina or adjacent to 1 of main lobar bronchi.They usually do not communicate withtracheobronchial tree and are usually fluid-filled, but if theycommunicate with airway or esophagus, they may contain air. Airwayor lung compression can cause respiratory distress.CT or MRI is usually diagnostic. Congenital Cystic Adenomatoid Malformation
Usuallyconsists of multiple cysts, frequently within 1 lobe of lung.Size of lesion determines age of presentationand degree of respiratory distress.Chest CT is usually diagnostic. Intrapulmonary Cysts
Can be singleor multiple and involve ≥1 lobes of lung.Respiratory distress may occur duringneonatal period. Older children may develop chronic cough or persistentinfiltrate.Chest radiography usually shows ovalor round translucent area or areas within pulmonary parenchyma containingair or combination of fluid and air.Chest CT usually confirms diagnosis. Congenital Pulmonary Lymphangiectasia
Is the dilatationof lung lymphatics. Can occur as isolated defect, with congenital heartlesions that cause obstruction of pulmonary venous drainage, orwith generalized lymphangiectasia.Respiratory distress usually beginsat birth.Chest radiography shows reticular appearanceof lungs with nodular infiltrates and hyperinflation.Localized form of this disorder, whichis less common, may only involve 1 or 2 lobes of lung and presentlater in life with mild respiratory distress or abnormal chest radiograph.Lung biopsy confirms diagnosis. Chylothorax
Presenceof chylous fluid in the thorax. Usually attributed to trauma fromdelivery or congenital abnormalities of thoracic duct system.Lymph does not become chylous untilingestion of formula or breast milk. If large amount of chyle accumulates,respiratory distress occurs, with decreased breath sounds over affectedthorax.Chest radiography shows large fluidcollection and shift of mediastinum.Thoracentesis reveals chyle, whichappears milky and has high protein and fat content. Bronchial Malformations
Bronchialstenosis usually involves main bronchus with narrowing just distalto carina. Narrowing of lobar bronchus usually results in recurrentinfection or atelectasis of involved lobe. Usual presenting featuresare respiratory distress and recurrent lung infection.Chest radiography may show hyperinflationof involved lung and evidence of recurrent infection or atelectasis.Chest CT or bronchoscopy is usuallydiagnostic. Diaphragm Lesions
Congenital Diaphragmatic Hernia
Congenitaldefect in diaphragm allows herniation of abdominal organs into hemithorax,producing varying degrees of lung hypoplasia. Nearly 90% areon left side.Severe respiratory distress beginsat birth.Diagnostic chest radiograph shows air-filledloops of bowel and occasionally liver in thoracic cavity. Diaphragmatic Eventration
Abnormalhigh position of diaphragm or portion of diaphragm, which is dueto congenital defect of muscularization of diaphragm.Most children are asymptomatic, butmild respiratory distress can occur.Diagnosis is usually made by chestradiography or fluoroscopy. Diaphragmatic Paralysis or Paresis
Occurrenceis usually due to phrenic nerve injury from thoracic surgery.Respiratory distress and asymmetricchest movement can occur.Fluoroscopy or U/S that showsparadoxic movement of affected hemidiaphragm during respirationis diagnostic. Rib Cage Anomalies
Thoracicrib cage anomalies that reduce amount of intrathoracic volume maycause respiratory distress. These include asphyxiating thoracicdystrophy, thanatophoric dysplasia, achondrogenesis, and chondroectodermaldysplasia.Structural anomalies of rib cage andthorax usually are obvious on physical exam.Physical exam, chest radiograph, andskeletal survey are usually diagnostic of specific disorder. Persistent Fetal Circulation
Is the persistenceof high pulmonary vascular resistance after birth with resultinghypoxemia and cyanosis. Affected infants are usually near term,and many have history of perinatal asphyxia.Soon after birth, respiratory distressoccurs. Hyperoxia test with exposure to 100% oxygen for5–10 mins shows small, if any, increase in partial pressureof arterial oxygen (PaO2)(<20 mm Hg). Simultaneous preductal-postductal measurementsof PaO2 inright arm and umbilical artery reveal PaO2 inright arm that is >15 mm Hg higher than in umbilical artery,which is consistent of right-to-left shunt across patent ductusarteriosus2-D echocardiogram with Doppler methodsshould be performed to rule out any form of structural cardiac disease. Cardiac Disorders
Disorders that cause cardiac failure or cyanosismay produce respiratory distress. See Chap.7, Cardiac Failure, and Chap. 12, Cyanosis. Hematologic Disorders
Anemia
Severe acute or chronic anemia may causerespiratory distress. Pallor usually is evident. Low Hct or Hgbconfirms presence of anemia. Diagnostic approach to anemia is discussedin Chap. 45, Pallor (Anemia). Polycythemia
Common occurrence in infants who have haddelayed clamping of umbilical cord or in infants of diabetic mothers.Venous Hct is greater than 65%, and mild respiratory distressmay occur. Metabolic Disorders
Hypothermia
May occur in preterm low-birth-weight infantswho are otherwise normal, or in ill newborns who have bacterialmeningitis, septicemia, or intracranial hemorrhage. Oxygen consumptionis significantly increased, and hypoxemia as well as metabolic acidosismay occur. Hypoglycemia
Irregularrespirations, apnea, seizures, and alteration of consciousness mayoccur in infants with hypoglycemia.Low blood glucose is diagnostic (see Chap. 59, Seizures). Metabolic Acidosis
Increase in minute ventilation is compensatoryresponse to metabolic acidosis and lowered blood pH. Normal aniongap with reduced bicarbonate may occur with diarrhea or renal tubularacidosis. Increased anion gap with accumulation of fixed acid occurswith lactic acidosis (lactate), diabetic ketoacidosis (beta-hydroxybutyrate,acetoacetate), and organic acidemias (organic acids). Neurologic and Muscle Disorders
Brain Disorders
Respiratory distress and apnea may occurwith intracranial hemorrhage or cerebral edema as consequence ofperinatal asphyxia or birth trauma. Other causes of depressed respirationand apnea include cerebral malformations (Chiari, Dandy-Walker),bacterial meningitis, viral encephalitis, and brain tumors. Spinal Cord Injury
Injury tospinal cord in neonates may occur with vaginal breech delivery orshoulder dystocia.Fractures of vertebrae with transectionof the cord may result in irregular respirations and apnea, as wellas absence of spontaneous movements.Neurologic findings depend on locationand severity of lesion. Neuromuscular Disorders
Disorders affecting neuromuscular system(spinal muscular atrophy, myasthenia gravis, congenital myopathies)may produce slow and shallow respirations with hypoventilation andrespiratory failure (see Chap.33, Hypotonia and Weakness). Drugs
Drugs (e.g., magnesium sulfate, morphine,and meperidine) that are given to some mothers during labor cancause neonatal respiratory depression. Neonatal drug withdrawalsyndrome may produce tachypnea as 1 of its manifestations. >>
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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
Accessory muscle use:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient's condition allows, examine him more closely. Ask him about the onset, duration, and severity of associated signs and symptoms, such as dyspnea, chest pain, cough, sputum production, or fever.
Explore his medical history, focusing on respiratory disorders, such as infection or COPD. Ask about cardiac disorders, such as heart failure, which may lead to pulmonary edema; inquire about neuromuscular disorders, such as amyotrophic lateral sclerosis, which may affect respiratory muscle function. Note a history of allergies or asthma. Because collagen vascular diseases can cause diffuse infiltrative lung disease, ask about such conditions as rheumatoid arthritis and lupus erythematosus.
Ask about recent trauma, especially to the spine or chest. Find out if the patient has recently undergone pulmonary function tests or received respiratory therapy. Ask about smoking and occupational exposure to chemical fumes or mineral dusts such as asbestos. Explore the family history for such disorders as cystic fibrosis and neurofibromatosis, which can cause diffuse infiltrative lung disease.
Perform a detailed chest examination, noting an abnormal respiratory rate, pattern, or depth. Assess the patient's chest for equal expansion during inspiration. Check the trachea for midline position. Assess the color, temperature, and turgor of the patient's skin, and check for clubbing. Auscultate the lungs for adventitious breath sounds.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Respirations, grunting:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
After addressing the child's respiratory status, ask his parents when the grunting respirations began. If the patient is a premature infant, find out his gestational age. Ask the parents if anyone in the home has recently had an upper respiratory tract infection. Has the child had signs and symptoms of such an infection, such as a runny nose, cough, low-grade fever, or anorexia? Does he have a history of frequent colds or upper respiratory tract infections? Does he have a history of respiratory syncytial virus? Ask the parents to describe changes in the child's activity level or feeding pattern to determine if the child is lethargic or less alert than usual.
Begin the physical examination by auscultating the lungs, especially the lower lobes. Note diminished or abnormal sounds, such as crackles or sibilant rhonchi, which may indicate mucus or fluid buildup. Characterize the color, amount, and consistency of any discharge or sputum. Note the characteristics of the cough, if any. Note the respiratory rate. Assess accessory muscle use for breathing and cyanosis.
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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, 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
HYPOTENSION AND SHOCK:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
The workup of shock must be vigorous with emergency CBC, blood
cultures, blood gases, ECG, electrolytes, blood urea nitrogen (BUN), and
type- and cross-match of blood at the same time that vigorous antishock
measures are applied. Checking the GI tract for blood loss with a rectal and
nasogastric tube can be both diagnostic and therapeutic. To work up chronic
hypotension, one should not forget venous pressure and circulation times (to
diagnose decreased cardiac output and CHF), serial electrolytes and cortisol
levels (to rule out adrenal insufficiency), and sedimentation rate and
cultures of various body fluids (to exclude a chronic infectious disease
[e.g., TB]).
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Source: Differential Diagnosis in Primary Care, 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.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
ALKALOSIS (INCREASED pH):
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Taking a drug history and noting hyperventilation or vomiting during
the clinical evaluation will assist in the diagnosis. Serial electrolytes,
arterial blood gases, and drug screen are first-line laboratory tests to
assist in the diagnosis.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
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