TREATMENTS &
RESEARCH

Search the
latest
treatment
information
here.

Dr. Huntley's
Diagnosis
Checklist

Have a symptom?
See what questions
a doctor would ask.
 
Next Prev
Diseases » Asphyxia » Diagnosis
 

Diagnosis of Asphyxia

Asphyxia Diagnosis: Book Excerpts

Diagnostic Tests for Asphyxia: Online Medical Books

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


DYSPNEA: Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is the dyspnea acute? If the dyspnea is acute onset, one should ask if there is a drug history, particularly a history of mainlining narcotics. If so, adult respiratory distress syndrome should be considered. Furthermore, is there an embolic source for a possible pulmonary embolism? If the onset is gradual, one should move on to consider chronic diseases such as congestive heart failure and pulmonary emphysema and fibrosis.
  2. Is there fever or purulent sputum? Obviously, fever and purulent sputum should make one think of pneumonia.
  3. What kind of rales are there? If there are crepitant rales, one should consider congestive heart failure or pneumonia. If there are sibilant and sonorous rales or wheezing, one should consider bronchial asthma or pulmonary emphysema.
  4. Is there hepatomegaly? Hepatomegaly would be a sign of congestive heart failure. However, in the acute stages it may not manifest immediately. Hepatomegaly may also be an indication of other systemic diseases that are associated with either lung disease or heart disease. The collagen diseases in particular come to mind.

DIAGNOSTIC WORKUP

The basic workup of acute onset dyspnea should include a CBC to exclude anemia; a chest x-ray and arterial blood gases to exclude pneumothorax, pneumonia, and other pulmonic diseases; and an EKG and serial cardiac enzymes to exclude myocardial infarction and some of the causes of congestive heart failure. A sputum smear and culture should always be done when there is adequate sputum. Eosinophils should be sought. It is important to make sure that you have an adequate specimen and, therefore, leukocytes should be reported on the smear.

If there is chest pain accompanied by hemoptysis, arterial blood gases and a ventilation-perfusion scan should be done to rule out pulmonary embolism. Even without chest pain and hemoptysis, a pulmonary embolism may need to be excluded. If the ventilation-perfusion scan is inconclusive, a pulmonary angiography may still need to be done in difficult cases. If routine smears and cultures are negative, cultures for AFB and fungi may need to be done, especially when there is continuing purulent sputum. The clinician should also consider doing skin testing for these diseases.

If congestive heart failure is suspected, an arm-to-tongue circulation time and pulmonary function testing should also be done. Echocardiography may also be diagnostic. A therapeutic trial of a diuretic may be valuable. When there is significant wheezing, a trial of sublingual isoproterenol hydrochloride (IsuprelŪ) or epinephrine 0.3 cc subcutaneously may clear up the confusion.

In chronic dyspnea the chest x-ray and EKG should be complemented by pulmonary function testing, exercise testing, and arterial blood gases. Pulmonary function testing will be very useful in diagnosing asthma and distinguishing pulmonary emphysema from pulmonary fibrosis. A diagnosis of pulmonary fibrosis is substantiated by a reduction in a single-breath carbon monoxide-diffusing capacity. The advice of a pulmonologist should be sought when extensive pulmonary function testing, such as compliance and diffusing capacity, need to be determined. Bronchoscopy may need to be done to exclude a foreign body, neoplasm, or bronchiectasis. Cardiac catheterization and pulmonary angiography may be needed to identify chronic recurrent pulmonary embolism, intracardiac shunts, and pulmonary hypertension. Dyspnea without objective findings on physical examination should prompt a referral to a psychiatrist.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

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

  1. Is the patient an adult or a child? If the patient is a child, acute epiglottitis, acute laryngotracheitis, foreign body, congenital laryngeal stridor, laryngismus stridulus, and a retropharyngeal abscess should be considered. Diphtheria is rarely found nowadays. If the patient is an adult, myasthenia gravis, bulbar and pseudobulbar palsy, recurrent laryngeal palsy, pharyngitis, laryngotracheitis, carcinoma of the larynx or trachea, angioneurotic edema, foreign bodies, thyroid disorders, and disorders of the mediastinum should be considered.
  2. Is it acute or gradual onset? The presence of stridor of acute onset would suggest acute epiglottitis, acute pharyngitis, laryngotracheitis, angioneurotic edema, retropharyngeal abscess, laryngismus stridulus, and foreign body.
  3. Is there fever? The presence of fever would suggest acute laryngotracheitis, diphtheria, subacute thyroiditis, retropharyngeal abscess, and mediastinitis.
  4. Are there abnormalities on the ear, nose, and throat examination? On ear, nose, and throat examination, the clinician may find pharyngitis, acute epiglottitis, a foreign body, tenderness of the thyroid suggesting thyroiditis, and thyroid masses.
  5. Are there neurologic abnormalities on examination? Neurologic abnormalities may be found in myasthenia gravis, bulbar and pseudobulbar palsy, bilateral recurrent laryngeal nerve palsy, and comatose states.

DIAGNOSTIC WORKUP

Routine tests may include a CBC; sedimentation rate; smear and culture of material from the nose, throat, and sputum; x-ray of the chest and sinuses; and, in adults, an EKG. In adults also it might be wise to order a chemistry panel, thyroid profile, and VDRL test, depending on the clinical picture. Direct laryngoscopy can now be done in the office with the fiberoptic laryngoscope. In addition, fiberoptic bronchoscopy may be valuable. A Tensilon test may need to be done. An ear, nose, and throat specialist should be consulted before ordering expensive diagnostic tests. If there are neurologic signs, a neurologist should be consulted.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

SLEEP APNEA: Ask the Following Questions:
(Algorithmic Diagnosis of Symptoms and Signs)

  1. Is there excessive snoring? Excessive snoring would indicate obstructive sleep apnea from large tonsils, deviated nasal septum, cleft palate, other abnormalities, and obesity.
  2. Is there obesity? More than 60% of patients with sleep apnea have obesity, and pickwickian syndrome should be considered in these patients, as well as idiopathic obesity.
  3. Are there abnormalities of the neurologic examination? The presence of neurologic abnormalities should make one think of poliomyelitis, Shy-Drager syndrome, brain stem tumors, and other neurologic disorders.

DIAGNOSTIC WORKUP

The most important diagnostic test is an all-night polygraphic recording (polysomnography). This will differentiate between obstructive and nonobstructive sleep apnea. If obstructive sleep apnea is suspected, a referral should be made to an ear, nose, and throat specialist. If there are abnormalities on the neurologic examination, a neurologic consultation should be sought. If idiopathic nonobstructive sleep apnea is suspected, the patient should be referred to a pulmonologist. A therapeutic trial of continuous positive airway pressure may be done. Some cases should have evaluation for a pituitary tumor, a thyroid profile, and a trial of tricyclic drugs and progesterone.

 

» READ BOOK EXCERPT ONLINE »

Source: Algorithmic Diagnosis of Symptoms and Signs, 2003

Dyspnea: Differential Diagnosis
(In a Page: Signs and Symptoms)

  • Asthma
    –Classic triad of chronic cough, dyspnea, and wheezing
  • COPD; chronic bronchitis
  • Pulmonary edema (acute or chronic)
    –Cardiogenic pulmonary edema: LV failure (e.g., MI, cardiomyopathy), valve disease, high-output states (e.g., thyrotoxicosis), volume overload, hypertensive emergency
    –Noncardiac pulmonary edema: Sepsis, inhalation injury, drugs (e.g., narcotics), renal failure, high altitude, aspiration, pancreatitis, seizure, trauma, emboli (fat, air, amniotic fluid), CNS injury, airway obstruction (e.g., croup, foreign body)
    • Coronary artery disease
      –May present without chest pain (“anginal equivalent”)
    • Pneumonia
      • Pleural effusion
        –Common causes: CHF, pneumonia, cancer, pulmonary embolus, connective tissue disease (e.g., SLE, rheumatoid arthritis), pancreatitis, and renal or liver disease
      • Pulmonary embolism
        –Risk factors (Virchow's triad) present in 90% of cases: Venous stasis (e.g., immobility, pedal edema), endothelial damage (e.g., recent trauma or surgery, burns, indwelling catheters, IV drug use), hypercoagulability (e.g., malignancy, obesity, pregnancy, HRT/OCP)
      • Pneumothorax
        • Interstitial lung disease
          –A group of disorders characterized by inflammation and fibrosis of alveolar walls and the interstitium
        • Pulmonary hypertension
          –Primary pulmonary HTN: No identifiable cause
          –Secondary pulmonary HTN: Due to underlying disease (e.g., mitral stenosis, PE, COPD)
        • Less common etiologies (“zebras”) include pericardial disease, chest wall abnormality, tracheal obstruction, neuromuscular diseases, and psychogenic

        Workup and Diagnosis

        • Thorough history and physical exam
          –Note onset (sudden or chronic, progressive)
          –Timing (persistent or intermittent)
          –Associated symptoms (e.g., chest discomfort, syncope)
        • Initial laboratory studies should include CBC, BUN/creatinine, calcium, electrolytes, thyroid function tests, pulse oximetry (resting, ambulatory, and nocturnal), and chest X-ray
        • ABG will identify barriers to oxygen diffusion (increased A-a gradient), hypoxemia, and chronic hypercapnia
        • ECG may reveal evidence of MI, right ventricular strain (e.g., due to PE, pulmonary hypertension), dysrhythmias, and/or bundle branch block
        • Pulmonary function tests are indicated to identify restrictive or obstructive disease and barriers to diffusion
        • BNP may be useful, if the etiology is uncertain, to distinguish CHF from other causes of dyspnea
        • Echocardiogram to establish a diagnosis of structural heart disease, LV dysfunction, or elevated PA pressure
        • Chest CT scan, V/Q scan, and/or lower extremity dopplers if PE is suspected
        • Sputum culture and blood cultures may be necessary in cases of pneumonia

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    Orthopnea: Differential Diagnosis
    (In a Page: Signs and Symptoms)

    • Congestive heart failure is the most common cause of orthopnea
      –Etiologies include uncontrolled HTN, pulmonary embolus, endocarditis, hyperthyroidism, pericardial disease, endocardial disease (e.g., valvular stenosis, insufficiency, rupture, endocarditis), and myocardial disease (e.g., MI, ischemia, arrhythmias)
    • Aortic regurgitation
      –Most commonly due to rheumatic fever
    • Cardiomyopathies
    • Pleural effusion
      –Common causes: CHF, pneumonia, cancer, pulmonary embolus, connective tissue disease (e.g., SLE, rheumatoid arthritis), pancreatitis, renal or liver disease
    • Aortic stenosis
      –Associated with angina, syncope, and CHF
    • Mitral stenosis
      –Usually secondary to rheumatic heart disease (after 15–40 years)
      –Advanced cases result in pulmonary hypertension and right heart failure
      –Dyspnea is the most significant symptom
      –Classic triad: Diastolic rumble, opening snap, and loud first heart sound
    • Congenital heart disease
      –May see failure to thrive, progressive CHF symptoms, cyanosis, and/or murmur
    • Severe COPD and asthma
    • Severe bilateral apical lung disease
    • Bilateral diaphragmatic paralysis

    Workup and Diagnosis

    • Thorough history and physical exam
      –Note onset (sudden or chronic, progressive)
      –Timing (persistent or intermittent)
      –Associated symptoms (e.g., chest discomfort, syncope)
    • Initial labs should include CBC, electrolytes, thyroid function tests, pulse oximetry (resting, ambulatory, and nocturnal), and chest X-ray
    • Arterial blood gas will identify barriers to oxygen diffusion (increased A-a gradient), hypoxemia, and chronic hypercapnia
    • ECG may reveal evidence of MI, right ventricular strain (e.g., due to mitral stenosis), left ventricular hypertrophy (e.g., aortic stenosis), low voltage (cardiomyopathy), and dysrhythmias
    • BNP may be useful if the etiology is uncertain to distinguish CHF from other causes of dyspnea
    • Pulmonary function tests may be indicated to identify restrictive or obstructive disease and barriers to diffusion
    • Echocardiogram to establish a diagnosis of structural heart disease, valve disease, and LV dysfunction
    • Consider cardiac catheterization to evaluate valve disease, cardiomyopathy, and congenital heart disease

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    Paroxysmal Nocturnal Dyspnea: Differential Diagnosis
    (In a Page: Signs and Symptoms)

    • CHF is the most common cause
      –Etiologies include uncontrolled HTN, pulmonary embolus, endocarditis, hyperthyroidism, pericardial disease, endocardial disease (e.g., valvular stenosis, insufficiency, rupture, endocarditis), and myocardial disease (e.g., MI, ischemia, arrhythmias)
    • Mitral stenosis
      –Almost always secondary to rheumatic heart disease (after 15–40 years)
      –Advanced cases result in pulmonary hypertension and right heart failure
      –Dyspnea is the most significant symptom
      –Classic triad: Diastolic rumble, opening snap, and loud first heart sound
    • Aortic regurgitation
      –Most commonly due to rheumatic fever
    • Cardiomyopathies
      –Abnormal myocardium, resulting in impaired cardiac output and CHF
    • Aortic stenosis
      –Due to senile valve degeneration, rheumatic disease, or congenital
      –Associated with angina, syncope, and CHF
    • Congenital heart disease
      –May see failure to thrive, progressive CHF symptoms, cyanosis, and/or murmur
      • “Cardiac asthma”
        –Bronchospasm secondary to pulmonary congestion and interstitial edema that compresses small airways
        –Standing decreases lung congestion
      • Anxiety
      • Severe COPD and emphysema
      • Asthma
      • Obstructive sleep apnea
      • Obesity/hypoventilation
      • Tropical pulmonary eosinophilia (filariasis)

      Workup and Diagnosis

      • Complete history and physical exam with special attention to cardiac and respiratory systems
      • Initial laboratory studies may include CBC, pulse oximetry, electrolytes, BUN/creatinine, glucose, and calcium
      • Chest X-ray to evaluate for effusion and heart size
      • Echocardiogram may be used to evaluate valves, chamber size, and ventricular function
      • ECG
      • Consider cardiology consult
      • Cardiac catheterization may be indicated for valvular disease, cardiomyopathies, and congenital heart disease

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

    Stridor & Wheezing: Differential Diagnosis
    (In a Page: Signs and Symptoms)

    Stridor (inspiratory)

    • Croup (laryngotracheobronchitis)
      –Viral infection with tracheal narrowing due to airway edema
      –“Bark-like” cough, hoarseness
    • Epiglottitis
      –Airway emergency most commonly due to Haemophilus influenzae or group A streptococcus infection
      –Abrupt onset of high fevers, sore throat, hoarseness, dysphagia, respiratory distress
    • Foreign body lodged in the upper airway
      • Allergic reaction/anaphylaxis
        –May have urticaria and angioedema (subcutaneous or mucosal swelling, often of the lips)
    • Trauma
    • Postendotracheal intubation
    • Psychogenic (e.g., paroxysmal vocal cord dyskinesia)
      Stridor (expiratory)
    • COPD (expiratory vocalization to prolong time to airway closure and avoid air trapping)
    • Cardiac failure (expiratory vocalization to prolong increased intrathoracic pressure and unload left ventricle)

    Wheezing
    • Asthma
      –Triad of chronic cough, dyspnea, wheezing
      –Wheezing may be absent in cases of severe obstruction (insufficient air movement)
    • Pulmonary edema
      –Leakage of fluid into the interstitium and alveoli due to elevated capillary pressure (cardiogenic) or abnormal capillary permeability (noncardiogenic)
  • COPD
  • GERD
  • Respiratory infection
    –Upper respiratory infection
    –Bronchiolitis
    –“Atypical” pneumonia
    • Aspirated foreign body
      –Abrupt onset of unilateral wheezing or stridor (if lodged in the upper airway), cough, and decreased breath sounds
  • Allergic reaction/anaphylaxis
    –Urticaria, throat swelling (angioedema), and lip/tongue edema may be present

    • Workup and Diagnosis

    • History and physical examination
    • Initial labs may include CBC with differential, pulse oximetry, electrolytes, BUN/creatinine, calcium, and glucose
    • Consider blood and/or sputum cultures if infectious cause is suspected
    • Chest X-ray helps to differentiate respiratory infection from pulmonary edema, diagnose radiopaque foreign bodies, and shows “steeple sign” in cases of croup
    • Lateral neck X-ray may reveal swelling of the epiglottis in cases of epiglottitis or abscess
    • Chest CT with contrast provides excellent views of the lung parenchyma and helps to identify tumors and bronchiectasis
    • Bronchoscopy may be diagnostic and therapeutic in cases of obstruction due to foreign body
    • Lung biopsy or bronchoalveolar lavage can be performed in cases of suspected malignancy
    • Echocardiogram may be indicated to evaluate for structural heart disease, valve disease, and left ventricular function

    » READ BOOK EXCERPT ONLINE »

    Source: In a Page: Signs and Symptoms, 2004

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

      • Much apnea is physiologic and normal
        –Post-sigh apnea is normal
        –Newborns, especially premature babies, may have irregular breathing as their respiratory control center matures
        –Periodic breathing at high altitude
    • Prolonged apnea is respiratory arrest, and inadequate ventilation is respiratory failure, and both require immediate intervention
    • Apnea may be divided into central, obstructive, and mixed apnea; etiologies vary by age
    • Central apnea in infants
      –Apnea of prematurity
      –Congenital central hypoventilation syndrome (CCHS, or Ondine curse)
      –CNS depression (sepsis, shock, drug effect, RSV, seizure or postictal state)
      –Respiratory muscle failure (e.g., myotonia, infantile botulism)
      • Obstructive apnea in infants
        –Upper airway obstruction (severe laryngomalacia, choanal atresia, macroglossia, micrognathia, subglottic stenosis or web, laryngospasm)
        –Lower airway: Rarely causes obstructive apnea (tracheal stenosis, rings, slings)
      • Central apnea in children
        –CNS (drug-induced CNS depression, CCHS, abnormal CNS brainstem anatomy and function, sepsis/septic shock)
        –Respiratory muscle failure (muscular dystrophy, myotonia, myasthenia gravis)
      • Obstructive apnea in children
        –Upper airway obstruction, obstructive sleep apnea syndrome (OSAS), tonsillar and adenoidal hypertrophy, macroglossia, micrognathia, subglottic stenosis, laryngospasm
      • Mixed apnea
        –CNS depression and decreased upper airway tone
        –Gastroesophageal reflux leading to increased parasympathetic activity and/or laryngospasm
        –Respiratory muscle failure and adenoidal hypertrophy
      • Apparent life-threatening events (ALTE)
      • Trauma may cause apnea at any age

      Workup and Diagnosis

      • Acute or prolonged apnea must be treated immediately with life-support protocols
      • History may determine if apnea is central or obstructive
        –Snoring, stridor, gasps are consistent with obstructive apnea
        –Pauses are consistent with central apnea
        –Ingestion of raw honey can cause infantile botulism
        –Apnea/ALTE may occur in a familial pattern, but such a history should provoke a search for intentional injury
        • Apnea is most often associated with sleep and/or change in stage of sleep, so obtaining data during sleep may be needed to diagnose the cause of the apnea
        • CCHS may be associated with hypoventilation while awake, but is primarily a sleep-related disorder
        • Neuromuscular disease may be accompanied by structural disease (e.g., arthrogryposis, scoliosis)
        • Obstructive disease may have an obvious etiology (e.g., micrognathia), but consider central or CNS disease
        • Radiographic studies not as helpful as physiologic studies; fluoroscopy may diagnose malacia
        • A pneumogram examines heart rate, respiratory rate, chest wall movement, and oxygen saturation, but may miss obstructive disease
        • Preferred test is polysomnography, which adds measures of sleep stage and body movement, EEG, pH, and CO2
        • Covert videotaping in hospital may be needed for suspected abuse

    » READ BOOK EXCERPT ONLINE »

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

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

    • Dyspnea is driven by an aberration in the mechanics of breathing; consider the pathway taken by oxygen to the tissues, and the mechanics of getting it there
    • Hypoxia
      –Low O2 delivery to tissues increases effort to deliver it, including increased respiratory effort
      –Any cause of hypoxia will lead to dyspnea (decreased availability, V/Q mismatch due to pneumonia or other lung disease)
    • Obstructive disease causes increased effort to move air
      –Upper airway: Nasal congestion, choanal atresia, FB, tonsils, adenoids, macroglossia, decreased tone, retropharyngeal abscess, laryngomalacia, VCD/paralysis, laryngeal web or polyp, subglottic stenosis
      –Lower airway: Asthma, BALT, bronchiolitis obliterans, tracheobronchomalacia, bronchial atresia, bronchiectasis, bronchitis, CF, PCD, hemangioma, polyps, TEF
      • Restrictive disease
        –Small or stiff lungs, chest wall disease (e.g., obesity, kyphoscoliosis, chest deformity), respiratory muscle weakness (Duchenne muscular dystrophy, paralysis)
    • Parenchymal disease
      –Pneumonia, congenital lesions
    • Vascular disease
      –Pulmonary hypertension, sequestered lung
      • Cardiac disease
        –Congenital cyanotic heart disease (e.g., TOF, TAPVR, TGA)
        –Pericarditis
        –Myocarditis
    • Compression of the lung
      –Pneumothorax
      –Tumors (e.g., cyst, teratoma)
      –Elevated diaphragm
      –Effusions (e.g., empyema, hemothorax)
    • Pulmonary embolism (rare)

    Workup and Diagnosis

    • History
      –Determine first the urgency of the problem; some patients who appear to be less dyspneic because of fatigue or weakness are at greater risk of respiratory failure
      –Is there dyspnea at rest? Increased O2 consumption with activity increases symptoms; dyspnea at rest suggests a more severe problem, a fixed degree of hypoxia, or diminished compensatory mechanisms (e.g., profound weakness)
      –Does oxygen help? If not, it may represent a fixed mechanical problem (e.g., severe obstruction or chest wall disease), shunt, or other severe V/Q mismatch
      • Physical exam
        –Inspection and palpation are important; abnormal mechanics or hyperinflation may suggest etiology
        –Loud monophonic sounds (stridor, wheeze) suggest large airway obstruction; polyphonic wheezes suggest small airway disease
      • Oximetry is very useful but may not be accurate
      • Labs
        –ABGs (low PaO2 and SaO2 or high PaCO2suggests interventions)
    • Studies
      –Chest film and CT for parenchymal disease
      –MRI/MRA for vascular anatomy; V/Q scan
    • ECG, Echo, or catheterization for cardiac disease
    • Pulmonary function test for obstructive or restrictive disease

    » READ BOOK EXCERPT ONLINE »

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

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

    Nasal cavity and nasopharynx

    • Congenital
      –Piriform aperture stenosis
      –Choanal atresia
      –Lacrimal duct cyst
      –Craniofacial anomaly
      –Nasopharyngeal mass (teratoma)
      • Inflammatory/infectious
        –Rhinosinusitis
        –Adenoid hypertrophy

      Oral cavity, oropharynx, and hypopharynx
    • Congenital
      –Macroglossia
      –Glossoptosis
      –Vallecular cyst
    • Inflammatory/infectious
      –Tonsillar hypertrophy
    • Tumors
      –Lingual thyroid
      –Dermoid
      –Lymphovascular malformation
    • Foreign body

    Laryngeal
    • Congenital
      –Laryngomalacia (#1 cause in infants); usual onset is in the first 2 weeks of life, typically positional; most resolve spontaneously by age 1
      –Saccular cyst
      –Webs
      –Clefts
      –Vocal cord paralysis
    • Inflammatory/infectious
      –Epiglottitis
      –Laryngotracheitis (croup)
      –Gastroesophageal reflux
    • Tumors
      –Papillomas
      –Hemangiomas
      • Trauma
        –Subglottic stenosis
        –Foreign bodies
        –Laryngeal fracture
        –Caustic ingestion
        Tracheobronchial
      • Congenital
        –Tracheomalacia
        –Vascular rings
        –Tracheoesophageal fistula
      • Inflammatory

    Workup and Diagnosis

      • History
        –Duration, onset, severity, character, progression
        –Failure to thrive, feeding problems, cyanosis, apnea
        –Reflux history: Frequent spit-ups, vomiting, heartburn, chest pain, hoarseness
        –Birth, neonatal, and past medical history: Complicated labor, respiratory distress at delivery
        –Prior intubations, neurologic problems, prior episodes of croup, prior neck surgery, foreign body ingestion
        –Immunization history
    • Physical exam
      –Fever, respiratory rate, heart rate, level of consciousness, cyanosis
      –Auscultation: Chest, nose, mouth, neck (phase of stridor: inspiratory, expiratory, biphasic)
      –Nose: Nasal obstruction
      –Mouth: Tonsillar hypertrophy
      –Neck: Retractions, compressive mass, thyroid
      • Studies
        –Flexible nasolaryngoscopy: Check for choanal patency, adenoid size, laryngomalacia, vocal cord mobility
        –Direct laryngoscopy and bronchoscopy (DLB): Controversial whether all children with stridor need DLB
        –MRI: Vascular compression or external mediastinal mass
        –Modified barium swallow or esophagram in children with history of swallowing difficulties

    » READ BOOK EXCERPT ONLINE »

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

    DYSPNEA, TACHYPNEA, AND ORTHOPNEA: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The history and physical examination will almost invariably disclose the cause of dyspnea. To confirm pulmonary disease one will order pulmonary function studies, a chest roentgenogram and arterial blood gases. If routine pulmonary function studies are normal, more sophisticated studies such as the nitrogen washout test and perfusion and ventilatory scans may be necessary. To diagnose cardiac conditions, an ECG and venous pressure and circulation times may be necessary.

    Any patient with dyspnea and normal physical findings deserves a circulation time to rule out early congestive heart failure. A hemogram will diagnose anemias but it will not diagnose methemoglobinemia. A determination of the erythrocytes methemoglobin, arterial oxygen saturation, and diaphorase I test must be done.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    DECREASED RESPIRATIONS, APNEA, AND CHEYNE–STOKES BREATHING: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    Obviously, the association of other signs and symptoms will determine the workup in most cases. The most important things to do are to order a BUN level, electrolytes, FBS, and arterial blood gases, and a drug screen and to check for increased intracranial pressure by examining the eye grounds. If the history or physical findings suggest increased intracranial pressure, and other metabolic studies (e.g., BUN) are normal, a mannitol or urea drip is begun while awaiting the results of other investigations such as CT scan, EEG, and echoencephalogram. A neurosurgeon should be consulted immediately.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    SLEEP APNEA: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    A thorough examination of the upper respiratory system is essential: It may be wise to get an otolaryngologist to do this. A CBC to rule out anemia and arterial blood gases to rule out anoxia and hypercarbia may be helpful. Spirometry, chest x-ray, ECG, and arm-to-tongue circulation time will help rule out pulmonary and cardiovascular disorders. Ultimately, overnight polysomnography will be required to secure the diagnosis. A pulmonologist or otolaryngologist ought to be consulted before ordering this expensive test.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    STRIDOR AND SNORING: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The approach to the diagnosis involves a careful examination of the air passage with the laryngoscope and bronchoscope (if necessary, under anesthesia). If these have negative findings, a thorough neurologic examination should be performed and a Tensilon test may be indicated. Laryngismus stridulus in children may be terminated by putting the child in a steam bath; this helps establish that diagnosis. Skin testing for allergies may be necessary. A sleep study is often necessary to rule out neurogenic or obstructive sleep apnea.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

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

    When the patient’s respiratory and cardiac status is stable, investigate the underlying cause of apnea. Ask him (or, if he’s unable to answer, anyone who witnessed the episode) about the onset of apnea and events immediately preceding it. The cause may become readily apparent, as in trauma.

    Take a patient history, noting especially reports of headache, chest pain, muscle weakness, sore throat, or dyspnea. Ask about a history of respiratory, cardiac, or neurologic disease and about allergies and drug use.

    Inspect the head, face, neck, and trunk for soft-tissue injury, hemorrhage, or skeletal deformity. Don’t overlook obvious clues, such as oral and nasal secretions reflecting fluid-filled airways and alveoli or facial soot and singed nasal hair suggesting thermal injury to the tracheobronchial tree.

    Auscultate over all lung lobes for adventitious breath sounds, particularly crackles and rhonchi, and percuss the lung fields for increased dullness or hyperresonance. Move on to the heart, auscultating for murmurs, pericardial friction rub, and arrhythmia. Check for cyanosis, pallor, jugular vein distention, and edema. If appropriate, perform a neurologic assessment. Evaluate the patient’s level of consciousness (LOC), orientation, and mental status; test cranial nerve function and motor function, sensation, and reflexes in all extremities.

    » READ BOOK EXCERPT ONLINE »

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

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

    Obtain a brief history from the patient, if possible. Alternatively, obtain this information from whoever accompanied him to your facility. Ask if he's experiencing a drug overdose and, if so, try to determine what drugs he took, how much, when, and by what route. Check his arms for needle marks, indicating possible drug abuse. You may need to administer I.V. naloxone, a opioid antagonist.

    If you rule out a drug overdose, ask about chronic illnesses, such as diabetes and renal failure. Check for a medical identification bracelet or an I.D. card that identifies an underlying condition. Also, ask whether the patient has a history of head trauma, brain tumor, neurologic infection, or stroke.

    » READ BOOK EXCERPT ONLINE »

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

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

    If you observe hyperpnea in a patient whose other signs and symptoms signal a life-threatening emergency, you must intervene quickly and effectively. (See Managing hyperpnea, page 348.) However, if the patient’s condition isn’t grave, first determine his level of consciousness (LOC). If he’s alert (and if his hyperpnea isn’t interfering with speaking), ask about recent illnesses or infections, ingestion of aspirin, and ingestion or inhalation of other drugs or chemicals. Find out if the patient has diabetes mellitus, renal disease, or pulmonary condition. Is he excessively thirsty or hungry? Has he recently had severe diarrhea or an upper respiratory tract infection?

    Next, observe the patient for clues to his abnormal breathing pattern. Can he speak, or does he speak only in brief, choppy phrases? Is his breathing abnormally rapid? Examine the patient for cyanosis (especially of the mouth, lips, mucous membranes, and earlobes), restlessness, and anxiety — all signs of decreased tissue oxygenation, as occurs in shock. In addition, observe the patient for intercostal and abdominal retractions, use of accessory muscles, and diaphoresis, all of which may indicate deep breathing related to an insufficient oxygen supply. Next, inspect for draining wounds or signs of infection, and ask about nausea and vomiting. Take the patient’s vital signs, including oxygen saturation, noting a fever, and examine his skin and mucous membranes for turgor, possibly indicating dehydration. Auscultate the patient’s heart and lungs.

    » READ BOOK EXCERPT ONLINE »

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

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

    Begin by asking about a history of cardiopulmonary disorders, such as myocardial infarction, rheumatic heart disease, valvular disease, asthma, emphysema, or chronic bronchitis. Does the patient smoke? If so, how much? Explore associated symptoms, noting especially complaints of coughing, nocturnal or exertional dyspnea, fatigue, weakness, loss of appetite, or chest pain. Does the patient use alcohol or have a history of heavy alcohol use?

    When examining the patient, check for other signs of increased respiratory effort, such as accessory muscle use, shallow respirations, and tachypnea. Also note barrel chest. Inspect the patient’s skin for pallor or cyanosis and the fingers for clubbing. Observe and palpate for edema, and check for jugular vein distention. Auscultate the lungs for crackles, rhonchi, or wheezing. Also auscultate the heart. Monitor the patient’s oxygen saturation.

    » READ BOOK EXCERPT ONLINE »

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

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

    When the patient’s condition permits, obtain a patient history from him or a family member. First, find out when the stridor began. Has he had it before? Does he have an upper respiratory tract infection? If so, how long has he had it?

    Ask about a history of allergies, tumors, and respiratory and vascular disorders. Note recent exposure to smoke or noxious fumes or gases. Next, explore associated signs and symptoms. Does stridor occur with pain or a cough?

    Then examine the patient’s mouth for excessive secretions, foreign matter, inflammation, and swelling. Assess his neck for swelling, masses, subcutaneous crepitation, and scars. Observe the patient’s chest for delayed, decreased, or asymmetrical chest expansion. Auscultate for wheezes, rhonchi, crackles, rubs, and other abnormal breath sounds. Percuss for dullness, tympany, or flatness. Finally, note burns or signs of trauma, such as ecchymoses and lacerations.

    » READ BOOK EXCERPT ONLINE »

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

    Paroxysmal nocturnal dyspnea: History and physical examination
    (Handbook of Signs & Symptoms (Third Edition))

    Begin by exploring the patient’s complaint of dyspnea. Does he have dyspneic attacks only at night or at other times as well, such as after exertion or while sitting down? If so, what type of activity triggers the attack? Does he experience coughing, wheezing, fatigue, or weakness during an attack? Find out if he has a history of lower extremity edema or jugular vein distention. Ask if he sleeps with his head elevated and, if so, on how many pillows or if he sleeps in a reclining chair. Obtain a cardiopulmonary history. Does the patient or a family member have a history of a myocardial infarction, coronary artery disease, or hypertension or of chronic bronchitis, emphysema, or asthma? Has the patient had cardiac surgery?

    Next perform a physical examination. Begin by taking the patient’s vital signs and forming an overall impression of his appearance. Is he noticeably cyanotic or edematous? Auscultate the lungs for crackles and wheezing and the heart for gallops and arrhythmias.

    » READ BOOK EXCERPT ONLINE »

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

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

    When the patient’s respiratory and cardiac status is stable, investigate the underlying cause of apnea. Ask him (or, if he’s unable to answer, anyone who witnessed the
    episode) about the onset of apnea and events immediately preceding it. The cause may become readily apparent, as in trauma.

    Take a patient history, especially noting reports of headache, chest pain, muscle weakness, sore throat, or dyspnea. Ask about a history of respiratory, cardiac, or neurologic disease and about allergies and drug use.

    Inspect the head, face, neck, and trunk for soft-tissue injury, hemorrhage, or skeletal deformity. Don’t overlook obvious clues, such as oral and nasal secretions (reflecting fluid-filled airways and alveoli) or facial soot and singed nasal hair (suggesting thermal injury to the tracheobronchial tree).

    Auscultate over all lung lobes for adventitious breath sounds, particularly crackles and rhonchi, and percuss the lung fields for increased dullness or hyperresonance. Move on to the heart, auscultating for murmurs, pericardial friction rub, and arrhythmias. Check for cyanosis, pallor, jugular vein distention, and edema. If appropriate, perform a neurologic assessment. Evaluate level of consciousness (LOC), orientation, and mental status; test cranial nerve and motor function, sensation, and reflexes in all extremities.

    » READ BOOK EXCERPT ONLINE »

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

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

    Obtain a brief history from the patient, if possible, or from whoever accompanied him to your facility. Ask if he’s experiencing a drug overdose and, if so, try to determine which drugs he took, how much, when, and by what route. Check his arms for needle marks, indicating possible drug abuse. You may need to administer I.V. naloxone, an opioid antagonist.

    If you rule out a drug overdose, ask about chronic illnesses, such as diabetes and renal failure. Check for a medical identification bracelet or card that identifies an underlying condition. Also ask whether the patient has a history of head trauma, brain tumor, neurologic infection, or stroke.

    » READ BOOK EXCERPT ONLINE »

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

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

    If the patient can answer questions without increasing his distress, take a complete history. (See Differential diagnosis: Dyspnea, pages 276 and 277.) Ask if the shortness of breath began suddenly or gradually. Is it constant or intermittent? Does it occur during activity or while at rest? If the patient has had dyspneic attacks before, ask if they’re increasing in severity. Can he identify what aggravates or alleviates these attacks? Does he have a productive or nonproductive cough or chest pain? Ask about recent trauma, and note a history of upper respiratory tract infection, deep vein phlebitis, or other disorders. Ask the patient if he smokes or is exposed to toxic fumes or irritants on the job. Find out if he also has orthopnea, paroxysmal nocturnal dyspnea, or progressive fatigue.

    Cultural Cue: Because dyspnea is subjective and is exacerbated by anxiety, patients from cultures that are highly emotional may complain of shortness of breath sooner than those who are more stoic about symptoms of illness.

    During the physical examination, look for signs of chronic dyspnea such as accessory muscle hypertrophy (especially in the shoulders and neck). Also look for pursed-lip exhalation, clubbing, peripheral edema, barrel chest, diaphoresis, and jugular vein distention.

    Check blood pressure and auscultate the lungs for crackles, abnormal heart sounds or rhythms, egophony, bronchophony, and whispered pectoriloquy. Finally, palpate the abdomen for hepatomegaly, and assess the patient for edema.

    » READ BOOK EXCERPT ONLINE »

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

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

    If you observe hyperpnea in a patient whose other signs and symptoms signal a life-threatening emergency, you must intervene quickly and effectively. (See Managing hyperpnea, page 442.) However, if the patient’s condition isn’t grave, first determine his level of consciousness (LOC). If he’s alert (and if his hyperpnea isn’t interfering with speaking), ask about recent illnesses or infections; ingestion of aspirin or other drugs or chemicals; or inhalation of drugs or chemicals. Find out if the patient has diabetes mellitus, renal disease, or any pulmonary conditions. Is he excessively thirsty or hungry? Has he recently had severe diarrhea or an upper respiratory tract infection?

    Next, observe the patient for clues to his abnormal breathing pattern. Is he unable to speak, or does he speak only in brief, choppy phrases? Is his breathing abnormally rapid? Examine the patient for cyanosis (especially of the mouth, lips, mucous membranes, and earlobes), anxiety, and restlessness—all signs of decreased tissue oxygenation, as occurs in shock. In addition, observe the patient for intercostal and abdominal retractions, use of accessory muscles, and diaphoresis, all of which may indicate deep breathing related to an insufficient supply of oxygen. Next, inspect for draining wounds or signs of infection, and ask about nausea and vomiting. Take the patient’s vital signs, including oxygen saturation, noting fever. Also, examine his skin and mucous membranes for turgor, possibly indicating dehydration. Auscultate the patient’s heart and lungs.

    » READ BOOK EXCERPT ONLINE »

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

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

    Begin by asking about a history of cardiopulmonary disorders, such as myocardial infarction, rheumatic heart disease, valvular disease, asthma, emphysema, or chronic bronchitis. Does the patient smoke? If so, how much? Explore associated symptoms, noting especially complaints of cough, nocturnal or exertional dyspnea, fatigue, weakness, loss of appetite, or chest pain. Does the patient use alcohol or have a history of heavy alcohol use?

    When examining the patient, check for other signs of increased respiratory effort, such as accessory muscle use, shallow respirations, and tachypnea. Also note barrel chest. Inspect the patient’s skin for pallor or cyanosis, and the fingers for clubbing. Observe and palpate for edema, and check for neck vein distention. Auscultate the lungs and heart. Monitor the patient’s oxygen saturation.

    » READ BOOK EXCERPT ONLINE »

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

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

    When the patient’s condition permits, obtain a patient history from him or a family member. First, find out when the stridor began. Has he had it before? Does he have an upper respiratory tract infection? If so, how long has he had it?

    Ask about a history of allergies, tumors, and respiratory and vascular disorders. Note recent exposure to smoke or noxious fumes or gases. Next, explore associated signs and symptoms. Does stridor occur with pain or a cough?

    Then examine the patient’s mouth for excessive secretions, foreign matter, inflammation, and swelling. Assess his neck for swelling, masses, subcutaneous crepitation, and scars. Observe the patient’s chest for delayed, decreased, or asymmetrical chest expansion. Auscultate for wheezes, rhonchi, crackles, rubs, and other abnormal breath sounds. Percuss for dullness, tympany, or flatness. Finally, note any burns or signs of trauma, such as ecchymoses and lacerations.

    » READ BOOK EXCERPT ONLINE »

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

    Paroxysmal nocturnal dyspnea: History and physical examination
    (Professional Guide to Signs & Symptoms (Fifth Edition))

    Begin by exploring the patient’s complaint of dyspnea. Does he have dyspneic attacks only at night or at other times as well, such as after exertion or while sitting down? If so, what type of activity triggers the attack? Does he experience coughing, wheezing, fatigue, or weakness during an attack? Find out if he has a history of lower extremity edema or jugular vein distention. Ask if he sleeps with his head elevated and, if so, on how many pillows or if he sleeps in a reclining chair. Obtain a cardiopulmonary history. Does the patient or a family member have a history of a myocardial infarction, coronary artery disease, or hypertension, or of chronic bronchitis, emphysema, or asthma? Has the patient had cardiac surgery?

    Next perform a physical examination. Begin by taking the patient’s vital signs and forming an overall impression of his appearance. Is he noticeably cyanotic or edematous? Auscultate the lungs for crackles and wheezing and the heart for gallops and arrhythmias.

    » READ BOOK EXCERPT ONLINE »

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

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

    A. Characteristics of stridor. When confronted with stridor, check the age of the patient and the duration of the symptoms.

    1. A child aged less than 6 months with stridor of a few weeks to months has a congenital cause of stridor.

    2. Patients aged more than 6 months with stridor lasting hours to days usually have an acquired cause of stridor, most commonly viral croup, epiglottitis, or aspiration of a foreign body.

     3. A typical history is a child aged less than 6 years with a 2- to 3-day history of upper respiratory infection (URI) and gradually worsening cough, especially at night. A barking cough with the inspiratory stridor heralds the diagnosis of croup, which accounts for 90% of all cases of stridor. This condition will classically improve with moist air (1,3).

     4. A history of choking, coughing, or gagging points to aspiration or ingestion of a foreign body.

    5. In older children and adults, a concomitant sore throat and fever may indicate acute supraglottitis, which constitutes an emergency.

    B. Other information

    1. Whether stridor is acute, recurrent, or chronic.

     2. Personal or family history of atopy, would suggest spasmodic croup, which presents with stridor at night, not necessarily associated with a URI.

    Physical examination

    A. Focused physical examination (PE)

    1. The PE should include vital signs, notably temperature and respiratory rate, and pulse, with emphasis on general appearance and examination of the head and neck, including ears, nose, and throat.

    2. Signs of respiratory distress may be present, including dyspnea, tachypnea, chest retractions, nasal flaring, and stridor. If cyanosis is present, this is an ominous sign (2,4) (Chapter 8.2).

    B. Additional physical examination may reveal:

    1. A toxic-appearing child with high fever, drooling, severe respiratory distress, and preference for a sitting and forward-leaning position (1,4)

    2. Varying degrees of anxiety, which will increase during examination, cause a worsening of stridor (1,4)

    » READ BOOK EXCERPT ONLINE »

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

    Acute Dyspnea: Differential Overview
    (Field Guide to Bedside Diagnosis)

    ❑ Asthma

    ❑ COPD exacerbation

    ❑ Left heart failure

    ❑ Pneumonia

    ❑ Pulmonary embolism

    ❑ Pneumothorax

    ❑ Hyperventilation

    ❑ Pleural effusion

    ❑ Pericardial tamponade

    ❑ Upper airway obstruction

    ❑ Pulmonary hypertension

    ❑ Lung cancer

    ❑ Noncardiogenic pulmonary edema

    ❑ Bilateral diaphragmatic paralysis

    Diagnostic Approach

    Dyspnea is a sensation of inability to take in enough air, which causes anxiety and discomfort. Being caused by factors including tissue hypoxia, reduced lung compliance, and activation of J receptors, it may not correlate reliably with arterial oxygen saturation.

    Paroxysmal nocturnal dyspnea occurs in congestive heart failure (CHF) when the patient awakens with a sense of suffocation. A patient with chronic bronchitis may also awaken with shortness of breath and wheezing caused by mucous plugging; this clears with a cough. Orthopnea is seen in CHF, asthma, and bilateral diaphragmatic paralysis. Sudden onset suggests pneumothorax, pulmonary embolism, or “flash” pulmonary edema.

    Tachypnea can occur without dyspnea in conditions such as metabolic acidosis.

    » READ BOOK EXCERPT ONLINE »

    Source: Field Guide to Bedside Diagnosis, 2007

    Chronic Dyspnea: Differential Overview
    (Field Guide to Bedside Diagnosis)

    ❑ Chronic obstructive pulmonary disease

    ❑ Congestive heart failure

    ❑ Asthma

    ❑ Recurrent pulmonary embolism

    ❑ Interstitial lung disease

    ❑ Lung cancer

    ❑ Chronic pleural effusion

    ❑ Primary pulmonary hypertension

    ❑ Cystic fibrosis

    ❑ Kyphoscoliosis

    ❑ Myasthenia gravis

    ❑ Tracheal stenosis

    ❑ Mitral stenosis

    Diagnostic Approach

    Nonproductive cough may be a “dyspnea equivalent.” Nocturnal coughing to clear the airway of excess secretions can be confused with paroxysmal nocturnal dyspnea.

    Trepopnea, dyspnea lying on one side but not the other, occurs with cardiomegaly, unilateral parenchymal lung disease, and mediastinal or endobronchial tumors.

    » READ BOOK EXCERPT ONLINE »

    Source: Field Guide to Bedside Diagnosis, 2007

    Asphyxia: Diagnosis
    (Handbook of Diseases)

    Patient history and laboratory test results support the diagnosis. Pulse oximetry reveals decreased hemoglobin (Hb) saturation with oxygen except in patients with carbon monoxide poisoning where Hb is bound by the toxicant, falsely elevating the saturation value. Arterial blood gas analysis, the most important test, indicates decreased partial pressure of oxygen (less than 60 mm Hg) and increased partial pressure of carbon dioxide (greater than 50 mm Hg). Chest X-rays may show a foreign body, pulmonary edema, or atelectasis. Toxicology tests may show drugs, or chemicals. Abnormal Hb levels may also be detected in a complete blood count. Pulmonary function tests may indicate respiratory muscle weakness.

    » READ BOOK EXCERPT ONLINE »

    Source: Handbook of Diseases, 2003

    Apnea: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    When the patient is stabilized, obtain a history from the family. Determine the onset and events immediately preceding the event. Determine if there were related events, such as headache, chest pain, muscle weakness, sore throat, or dyspnea. Ask about a history of respiratory, cardiac, or neurologic disease and about allergies and drug use.

    Physical examination

    Inspect the head, face, neck, and trunk for soft-tissue injury, hemorrhage, or skeletal deformity. Don’t overlook obvious clues, such as oral and nasal secretions reflecting fluid-filled airways and alveoli, or facial soot and singed nasal hair suggesting thermal injury to the tracheobronchial tree.

    Auscultate over all lung lobes for adventitious breath sounds, particularly crackles and rhonchi. Percuss the lung fields for increased dullness or hyperresonance. Auscultate the heart for murmurs, pericardial friction rub, and arrhythmias. Assess for cyanosis, pallor, jugular vein distention, and edema. If appropriate, perform a neurologic assessment. Evaluate the patient’s level of consciousness (LOC), orientation, and mental status; test cranial nerve function and motor function, sensation, and reflexes in all extremities.

    » READ BOOK EXCERPT ONLINE »

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

    Bradypnea: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    Obtain a brief history from the patient or his family. Determine if the patient may be experiencing a drug overdose and, if so, try to determine what drugs were ingested, the amount, time, and by what route. Checking extremities for needle marks may indicate possible drug abuse.

    After drug overdose is ruled out, determine any chronic illnesses, such as diabetes and renal failure. Check for a medical identification bracelet or an I.D. card that identifies an underlying condition. Also, ask whether the patient has a history of head trauma, brain tumor, neurologic infection, or stroke.

    Physical examination

    Perform a full respiratory and neurologic assessment, noting respiratory rate and pattern.

    » READ BOOK EXCERPT ONLINE »

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

    Dyspnea: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    If the patient can answer questions without increasing his distress, take a complete history. Ask if the shortness of breath began suddenly or gradually. Is it constant or intermittent? Does it occur during activity or while at rest? If the patient has had dyspneic attacks before, ask if they’re increasing in severity. Can he identify what aggravates or alleviates these attacks? Does he have a productive or nonproductive cough or chest pain? Ask about recent trauma, and note a history of upper respiratory tract infection, deep vein phlebitis, or other disorders. Ask the patient if he smokes or is exposed to toxic fumes or irritants on the job. Find out if he also has orthopnea, paroxysmal nocturnal dyspnea, or progressive fatigue.

    Physical examination

    During the physical examination, look for signs of chronic dyspnea such as accessory muscle hypertrophy (especially in the shoulders and neck). Also look for pursed-lip exhalation, clubbing, peripheral edema, barrel chest, diaphoresis, and jugular vein distention.

    Check blood pressure and auscultate for crackles, abnormal heart sounds or rhythms, egophony, bronchophony, and whispered pectoriloquy. Finally, palpate the abdomen for hepatomegaly, and assess the patient for edema.

    » READ BOOK EXCERPT ONLINE »

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

    Hyperpnea: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    If you’ve ruled out a life-threatening condition, confirmed that the patient’s level of consciousness (LOC) permits, and determined that hyperpnea isn’t interfering with his ability to speak, obtain his history. Has he experienced any recent illnesses or infections, such as severe diarrhea or an upper respiratory tract infection? Ask about ingestion of aspirin, other drugs, or chemicals, and about inhalation of drugs or chemicals. Is he excessively thirsty or hungry? Does he have a history of diabetes mellitus, renal disease, or a pulmonary condition?

    Physical examination

    Observe the patient for clues to his abnormal breathing pattern. Is he unable to speak, or does he speak only in brief, choppy phrases? Is his breathing abnormally rapid? Examine him for cyanosis (especially of the mouth, lips, mucous membranes, and earlobes), restlessness, and anxiety — all signs of decreased tissue oxygenation, as occurs in shock. In addition, observe the patient for intercostal and abdominal retractions, use of accessory muscles, and diaphoresis, all of which may indicate deep breathing related to an insufficient supply of oxygen. Next, inspect for draining wounds or signs of infection, and ask about nausea and vomiting. Take the patient’s vital signs, including oxygen saturation, noting fever, and examine his skin and mucous membranes for turgor, possibly indicating dehydration. Auscultate the patient’s heart and lungs.

    » READ BOOK EXCERPT ONLINE »

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

    Stridor: History
    (Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)

    When the patient’s condition permits, obtain his medical history. First, find out when the stridor began. Has he had it before? Does he have an upper respiratory tract infection? If so, how long has he had it?

    Ask about a history of allergies, tumors, and respiratory and vascular disorders. Note recent exposure to smoke or noxious fumes or gases. Next, explore associated signs and symptoms. Does stridor occur with pain or a cough?

    » READ BOOK EXCERPT ONLINE »

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

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

    Obtain a brief history from the patient if possible. Alternatively, obtain this information from the person who accompanied him to the facility. Ask if he’s experiencing a drug overdose and, if so, try to determine what drugs he took, how much, when, and by what route. Check his arms for needle marks, indicating possible drug abuse. You may need to administer I.V. naloxone, an opioid antagonist.

    If you rule out a drug overdose, ask about chronic illnesses, such as diabetes and renal failure. Check for a medical identification bracelet or an I.D. card that identifies an underlying condition. Also, ask whether the patient has a history of head trauma, brain tumor, neurologic infection, or stroke.

    » READ BOOK EXCERPT ONLINE »

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

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

    If the patient can answer questions without increasing his distress, take a complete history. Ask if the shortness of breath began suddenly or gradually. Is it constant or intermittent? Does it occur during activity or while at rest? If the patient has had dyspneic attacks before, ask if they have been increasing in severity. Can the patient identify what aggravates or alleviates these attacks? Does he have a productive or nonproductive cough or chest pain? Ask about recent trauma, and note a history of upper respiratory tract infection, deep vein phlebitis, or other disorders. Ask the patient if he smokes or is exposed to toxic fumes or irritants on the job. Find out if he also has orthopnea, paroxysmal nocturnal dyspnea, or progressive fatigue.

    CULTURAL CUE:Because dyspnea is subjective and is exacerbated by anxiety, patients from cultures that are highly emotional may complain of shortness of breath sooner than those who are more stoic about symptoms of illness.

    » READ BOOK EXCERPT ONLINE »

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

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

    If you observe hyperpnea in a patient whose other signs and symptoms signal a life-threatening emergency, you must intervene quickly. (See Managing hyperpnea, page 367.) If the patient’s condition isn’t grave, first determine his level of consciousness (LOC). If he’s alert (and if his hyperpnea isn’t interfering with speaking), ask about recent illnesses or infections, the ingestion of aspirin or other drugs or chemicals, and the inhalation of drugs or chemicals. Find out if the patient has diabetes mellitus, renal disease, or any pulmonary conditions. Is he excessively thirsty or hungry? Has he recently had severe diarrhea or an upper respiratory tract infection?

    » READ BOOK EXCERPT ONLINE »

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

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

    Begin by asking about a history of cardiopulmonary disorders, such as myocardial infarction, rheumatic heart disease, valvular disease, asthma, emphysema, or chronic bronchitis. Does the patient smoke? If so, how much? Explore associated symptoms, noting especially complaints of cough, nocturnal or exertional dyspnea, fatigue, weakness, loss of appetite, or chest pain. Does the patient use alcohol or have a history of heavy alcohol use?

    » READ BOOK EXCERPT ONLINE »

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

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

    When the patient’s condition permits, obtain a patient history from him or a family member. First, find out when the stridor began. Has he had it before? Does he have an upper respiratory tract infection? If so, how long has he had it?

    Ask about a history of allergies, tumors, and respiratory and vascular disorders. Note recent exposure to smoke or noxious fumes or gases. Next, explore associated signs and symptoms. Does stridor occur with pain or a cough?

    » READ BOOK EXCERPT ONLINE »

    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 ductusarteriosus
  • 2-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. >>

    » READ BOOK EXCERPT ONLINE »

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

    Stertor, Stridor, and Airway Obstruction: Clinical Features and Diagnosis
    (The Diagnostic Approach to Symptoms and Signs in Pediatrics)

    Nose and Nasopharynx

    Congenital

    Choanal Atresia

  • Causes obstructionof nasopharynx that may be unilateral or bilateral.
  • Respiratory distress occurs with bilateraldisease unless the mouth is open because neonates are obligate nosebreathers.
  • Best diagnostic test is flexible endoscopy.CT is used to delineate anatomy prior to surgery.

    • Craniofacial Anomalies

  • 2 autosomal-dominantdisorders, Apert syndrome and Crouzon syndrome, are caused by mutationsin gene encoding fibroblast growth factor receptor-2 on chromosome10q26. In both disorders, midface hypoplasia and shape of palatecontribute to airway obstruction.
  • Apert syndrome is characterized byacrobrachycephaly, coronal craniosynostosis, shallow orbits, proptosis,hypertelorism, cutaneous and osseous syndactyly, broad distal phalanxof thumb and hallux of big toe, and variable mental retardation.
  • Characteristic features of Crouzonsyndrome include craniosynostosis (especially of coronal, sagittal,and lambdoid sutures), shallow orbits, proptosis, hypertelorism,parrot-beaked nose, and variable mental retardation.

    • Midline Masses

  • Nasal dermoidcyst may be suspected when pit or swelling is seen on dorsum ofnose in midline.
  • Encephalocele is herniation of meningesand brain tissue into nasal area producing mass or swelling.
  • CT demonstrates location and extentof these lesions. Biopsy is never performed if there is suspicionof intracranial communication.

    • Infection/Inflammation

    Rhinitis

    Infectious or allergic rhinitis may causeinflammation and edema of nasal mucosa, causing upper airway obstruction(see Chap. 41, Nasal Discharge).

    Adenoid Hypertrophy

  • Recurrentviral URIs and allergic rhinitis contribute to adenoid hypertrophy.
  • Persistent snoring is common finding,and sleep apnea also may occur.
  • History, physical exam, and lateralneck radiograph confirm diagnosis.

    • Polyps

    Nasal polyps can be visualized on nasal examas gray, smooth, soft, mobile masses. Predisposing causes are allergicrhinitis and cystic fibrosis.

    Trauma

  • Trauma tonose and nasopharynx may produce significant swelling and bleeding, whichcause airway obstruction.
  • Plain radiographs and CT provide valuablediagnostic information.

    • Neoplasm

  • In childhood,most common benign tumors of nasal cavity are hemangioma and lymphangioma.In adolescence, most frequent benign tumor is juvenile angiofibroma.Malignant tumors include rhabdomyosarcoma, carcinoma, and lymphoma.
  • Common presenting feature of thesetumors is nasal obstruction.
  • Nasal speculum can be used to examinenasal cavity, while flexible nasopharyngoscopy permits visualizationof nasopharynx.
  • CT of nasal cavity, nasopharynx, andsinuses locates mass and defines its extent. Histologic diagnosisis definitive.

    • Oropharynx and Hypopharynx

    Congenital

    Micrognathia and Other Skull Base Abnormalities

  • Althoughmicrognathia can occur as isolated lesion, also can occur as partof Pierre Robin syndrome, which includes glossoptosis and cleftpalate.
  • Another disorder with significant micrognathiais autosomal-dominant Treacher-Collins-Franceschetti syndrome, whosegene locus has been mapped to chromosome 5q32-33.1. Other characteristicfindings include downward slanting palpebral fissures, colobomaof lower lid, malar hypoplasia, and malformations of external ear(commonly microtia).

    • Macroglossia

    Can be associated with congenital hypothyroidism,Beckwith-Wiedemann syndrome, Hurler syndrome, and glycogen storagedisease type II. Diagnosis may be suspected from history and physicalexam. These disorders are discussed in other chapters.

    Decreased Pharyngeal Muscle Tone

    Decreased tone of pharyngeal musculaturemay contribute to noisy breathing, especially with cerebral palsyand trisomy 21.

    Infection/Inflammation

    Tonsillar Hypertrophy

    Hypertrophy of tonsils may be seen with recurrentviral URI or allergic rhinitis. Tonsils are enlarged and may causeupper airway obstruction.

    Abscess

    Peritonsillar, retropharyngeal, or lateralpharyngeal abscess may cause fever, difficulty swallowing, drooling,neck pain, and respiratory distress, including stridor (see Chap. 61, Sore Throat).

    Foreign Body

  • Foreignbody in pharynx may cause acute onset of choking and airway obstruction.
  • History and physical exam can be diagnostic;however, in some cases neck radiographs and nasopharyngoscopy maybe needed to locate the foreign body.

    • Trauma

  • Any facialor neck injury can cause edema or hematoma formation that compromises airway.
  • History, physical exam, radiographsof face and neck, and nasopharyngoscopy are usually diagnostic.
  • Laryngoscopy and bronchoscopy alsomay be necessary depending on extent of injury. Early tracheostomyshould be considered.
  • Inhalation injury from fire may causesevere edema of mouth, pharynx, and larynx, producing combinationof cough, hoarseness, and stridor. Visualization of larynx may beaccomplished by endoscopy.

    • Neoplasm

  • Benign tumorsof tongue include hemangioma and lymphangioma. Most common malignanttumor of tongue is rhabdomyosarcoma.
  • Hemangioma can usually be diagnosedclinically.
  • CT or MRI defines extent of mass. Histologicdiagnosis is definitive.

    • Supraglottic

    Congenital

    Laryngomalacia

  • Most commoncongenital anomaly affecting larynx.
  • Inward collapse of aryepiglottic foldsis usual mechanism of stridor, which may occur at birth or may bedelayed for a few weeks.
  • Respiratory distress and feeding difficultiesoccasionally occur. Stridor often improves with placement in proneposition, whereas agitation makes it worse.
  • Flexible endoscopy is diagnostic procedureof choice.
  • Resolution usually occurs in firstyear of life when these tissues become firmer. Only in extreme casesis tracheostomy required.

    • Laryngeal Cyst and Laryngocele

  • Unusuallesions that are thought to arise from saccule of laryngeal ventricle.
  • Fluid-filled mass is called cyst andair-filled mass is called laryngocele.
  • Cyst usually causes airway obstructionat birth, whereas laryngocele usually causes airway problems laterin infancy.
  • Lateral neck radiography shows massthat may be seen by flexible laryngoscopy. CT and MRI are usefulin determination of location and extent of mass.

    • Infection/Inflammation

    Supraglottitis

  • Infectionof supraglottic tissues that includes epiglottis.
  • Generally caused by infection of encapsulatedorganisms.
  • Usual age range is 1–5 yrs.
  • Since introduction of H. influenzaetype b vaccine, occurrence of epiglottitis has markedly decreased.Now organisms usually cultured are S. pneumoniae, S. aureus, nontypeableH. influenzae, and group A Streptococcus.
  • Onset is acute, with fever, inspiratorystridor, pain with swallowing, and drooling.
  • Laryngoscopy should be performed toconfirm diagnosis but should be done with utmost caution and withanesthesiologist or otolaryngologist present.

    • Gastroesophageal Reflux

  • Can be associatedwith coughing, gagging, and choking.
  • Persistent stridor may occur as consequenceof severe gastroesophageal reflux, and laryngoscopic visualizationof upper airway may reveal inflammatory changes (see Chap. 55, Regurgitation and Vomiting).

    • Hereditary Angioedema

    Laryngeal edema can occur in this autosomal-dominantdisorder in which serum levels of C1 inhibitor are low or its functionis defective (see Chap. 17, Edema).

    Trauma

    Supraglottic stenosis may be due to traumaor may result from surgical procedures involving the airway.

    Neoplasm

  • Laryngealpapillomas are caused by human papilloma viruses, which can be transmittedduring birth from infected mother to newborn.
  • They may occur anywhere in airway,but most common location is larynx.
  • Flexible laryngoscopy reveals mass,and histologic diagnosis is confirmatory.

    • Glottic

    Congenital

    Laryngeal Web

    Incomplete canalization of laryngeal airwayresults in formation of laryngeal web. This lesion usually occursat glottic level and produces aphonia or weak or husky voice. Stridoralso may occur, and laryngoscopy is diagnostic.

    Laryngeal Cleft

  • Cleft inlarynx is produced by failure of rostral development of tracheoesophageal septum.
  • Stridor is often heard, and attemptsat feeding produce choking and coughing. Recurrent aspiration mayresult in pneumonia.
  • Esophagraphy shows spillage of contrastinto trachea with swallowing. Endoscopy is confirmatory.

    • Vocal Cord Paralysis

  • Vagus nerveby means of recurrent laryngeal nerve helps control vocal cord movement.Any lesion that affects these nerves may cause unilateral or bilateralvocal cord paralysis, which may be congenital or acquired.
  • When 1 vocal cord is involved, airwaycompromise is usually minimal and weak or hoarse cry occurs. Onlywith periods of agitation or stress does stridor appear. Causesof unilateral vocal cord paralysis include recurrent laryngeal nervecompression or injury secondary to neck or mediastinal mass, enlargedleft atrium or pulmonary artery, and surgery, particularly cardiovascularor neck surgery.
  • Stridor is characteristic of bilateralvocal cord paralysis. Cause is usually CNS lesion (e.g., hydrocephalus,intracranial hemorrhage, or Chiari malformation).
  • Diagnosis of vocal cord paralysis canbe made by flexible laryngoscopy. Vocal cord(s) fails to abducton inspiration. Further investigation depends on suspected cause.

    • Infection/Inflammation

    Laryngitis

    Usually associated with hoarseness and notwith stridor, unless inflammation is so severe that airway obstructionoccurs (see Chap. 31, Hoarseness).

    Laryngeal Spasm

    May be caused by repeated attempts at intubation,allergic reactions, and hypocalcemia. Manifestations of allergicreaction include urticaria, wheezing, and hypotension. Carpopedalspasm suggests tetany, in which case serum calcium should be measuredand intravenous calcium given immediately.

    Foreign Body

    Foreign body in glottic area may cause acuteonset of choking and coughing. Persistent stridor may be only manifestationof retained foreign body. Diagnosis may be suspected from historyand confirmed by neck radiography or laryngoscopy.

    Trauma

    Granuloma formation may occur secondary toendotracheal intubation. Obstruction can be minimal or severe.

    Neoplasm

    Laryngeal papillomas are discussed in thesection Supraglottic: Neoplasm.

    Subglottic

    Congenital

    Subglottic Stenosis

  • Biphasicstridor usually occurs with congenital subglottic stenosis, yetvoice remains normal.
  • Neck radiography may demonstrate subglotticnarrowing.
  • Diagnosis is confirmed by rigid endoscopyunder general anesthesia.

    • Cysts

    Subglottic cysts can be congenital or occursecondary to airway intubation. Rigid endoscopy under general anesthesiais diagnostic.

    Infection/Inflammation

    Croup

  • In viralcroup subglottic edema produces airway obstruction and stridor.Most common cause is parainfluenza viral infection. Influenza viruses,rhinoviruses, respiratory syncytial virus, adenoviruses, and enterovirusesalso can cause croup. Age range is usually 6–36 mos.
  • Symptoms of upper respiratory infectionare followed in 12–24 hrs by barky cough and stridor. Feveris variable finding. This is usually self-limited illness lasting3–7 days.
  • Neck radiography may be performed ifpresentation is unusual or puzzling and diagnosis is uncertain. "Steeplesign" indicates airway obstruction and is consistent withdiagnosis of croup.
  • Except for signs of infection, spasmodiccroup cannot be distinguished from viral croup. Onset is sudden,and episodes usually occur during night. Although pathogenesis remainsuncertain, episodes usually resolve during day and subside in afew days. Diagnosis is clinical.

    • Bacterial Tracheitis

  • Usuallyfollows preexisting viral infection.
  • Usual pathogens are S. aureus, S. pneumoniae,M. catarrhalis, and nontypeable H. influenzae.
  • Average age of onset is 5 yrs.
  • Clinical presentation is similar tothat of viral croup except these children appear more toxic. Theyhave worsening stridor with purulent tracheal secretions and areless responsive to racemic epinephrine. In most cases, trachealintubation is required because of severe airway obstruction.
  • Radiography shows subglottic edemaand irregular tracheal densities. Flexible nasopharyngoscopy canidentify purulent secretions in airway, and rigid endoscopy shouldbe performed for debridement. This diagnosis should be consideredin older child with unusually severe croup.

    • Trauma

  • Acquiredsubglottic stenosis is usually complication of prolonged endotrachealintubation and is generally more severe than congenital subglotticstenosis.
  • Although airway films may be diagnostic,flexible endoscopy should be performed to visualize larynx and otherstructures above vocal cords. Occasionally, view of subglottis ispossible. Rigid endoscopy confirms diagnosis.

    • Neoplasm

  • Subglottichemangioma is benign tumor that usually becomes symptomatic by 3–6 mosof age.
  • Stridor may be inspiratory or biphasic.Barky cough and hoarseness also may occur.
  • Neck radiography may show asymmetricsubglottic narrowing. CT or MRI is used to determine extent of thelesion.
  • Diagnosis is confirmed by endoscopicexam under general anesthesia.

    • Tracheobronchial

    Congenital

    Tracheomalacia

  • Presenceof misshapen or deficient tracheal cartilage rings contributes toabnormal collapse of trachea, called tracheomalacia.
  • Onset is insidious and often episodic.Crying, coughing or feeding may lead to acute exacerbation. Stridoris typically expiratory. Cartilage becomes firmer with growth, andstridor usually resolves by 12–18 mos of age.
  • Diagnosis can be confirmed by fluoroscopyor bronchoscopy, which demonstrates inspiratory collapse of extrathoracictrachea and expiratory collapse of intrathoracic trachea.

    • Tracheal Web

    Local narrowing of trachea produced by fibroustissue, and bronchoscopy is diagnostic.

    Tracheal Cysts

  • Usuallyasymptomatic, but large or infected ones may produce stridor and cough.
  • Chest radiography usually shows cysticmediastinal structure adjacent to trachea.
  • Other useful diagnostic tests includeesophagraphy, CT, and bronchoscopy.

    • Tracheal Stenosis

  • Fibrousstrictures that narrow airway may occur anywhere in trachea, andbronchoscopy is diagnostic.
  • Tracheal ring involves individual trachealrings or segmental areas of trachea that may not increase in sizewith growth. Rings resemble cartilage and lack membranous posteriorsegment.
  • Chest radiography may show narrow orfunnel-shaped trachea. Bronchoscopy confirms diagnosis.

    • Vascular Anomalies

  • Double aorticarch can compress trachea and esophagus and cause stridor, dysphagia, andapnea. Esophagraphy shows characteristic indentations of esophagus,with higher and larger indentation caused by right aortic arch andlower indentation caused by left aortic arch. MRI is confirmatory.
  • Anomalous innominate artery originatesmore distally from aortic arch than normal and compresses rightanterior aspect of trachea just above carina. Stridor, persistentcough, and apnea may occur. Chest radiography shows anterior indentationof trachea. Demonstration of anterior compression of distal tracheaby pulsatile vessel at bronchoscopy is diagnostic.
  • In pulmonary artery sling, left pulmonaryartery arises as branch of right pulmonary artery, courses betweentrachea and esophagus to reach left lung, and compresses right mainbronchus and esophagus. Chest radiograph shows anterior bowing ofright main bronchus, deviation of lower trachea to the left, unequalaeration of lungs, and mediastinal density between trachea and esophagus.Esophagraphy may show anterior indentation of esophagus just abovelevel of carina. MRI or cardiac catheterization with pulmonary angiographyis diagnostic.

    • Infection/Inflammation

  • Retroesophagealabscess may cause fever and stridor due to compression of trachea.
  • Chest radiography, esophagraphy, andCT are useful in diagnosis. Confirmation of diagnosis may only bepossible at surgery.

    • Foreign Body

  • Trachealforeign bodies may produce choking and gagging followed by persistent coughingand stridor. Radiopaque foreign body may be recognized on chestradiograph; otherwise, bronchoscopy is confirmatory.
  • Esophageal foreign body may compresstrachea and cause stridor, cough, and respiratory distress, sometimeswithout any esophageal symptoms (e.g., drooling, dysphagia, or pain).
  • Chest radiography may show its location,whereas esophagraphy usually shows filling defect.
  • Esophagoscopy is confirmatory.

    • Trauma

    Tracheal stenosis may occur from complicationsof intubation or, less commonly, tracheostomy. Bronchoscopy is diagnostic.

    Neoplasm

    Tracheal

  • Rare inpediatric population.
  • Benign tumors include squamous papilloma,chondroma, and hemangioma, whereas malignant tumors include varioussarcomas and carcinomas.
  • Presenting symptoms include persistentcough, expiratory stridor, and hemoptysis.
  • Chest and airway radiography may identifymass lesion. Combination of tests that includes bronchoscopy, CT,and MRI can locate site and extent of lesion.
  • Histologic diagnosis is definitive.

    • Thyroid

    Thyroid neoplasm may compress trachea andcause stridor. CT can demonstrate compression. See further discussionof thyroid neoplasms in Chap.42, Neck Masses.

    Mediastinal Masses

  • Some mediastinalmasses including teratoma, lymphangioma, and lymphoma may compresstrachea and cause stridor.
  • Combination of tests, including chestCT and MRI as well as bronchoscopy, can locate and determine extentof lesion.
  • Histologic diagnosis is definitive.

    • Psychogenic

  • In pediatricpopulation, this type of stridor is most common in adolescent girls.Often history of psychologic stress exists.
  • Stridor may be heard in inspiration,expiration or both. Associated findings include cough, hoarseness,and dyspnea.
  • In some cases, flexible laryngoscopymay reveal paradoxic vocal cord motion, in which vocal cords adductrather than abduct in inspiration.

    • Diagnostic Approach

  • Stertorand stridor are signs of upper airway obstruction. With seriousairway obstruction, establishing control of the airway and maintainingventilation are the most important immediate priorities. In absenceof life-threatening airway obstruction, prompt but thorough investigationis essential.
  • Age of onset is useful in diagnosis.Onset of stridor at birth or during neonatal period suggests laryngomalacia,laryngeal web, vocal cord paralysis, or vascular ring. In infancyand childhood, onset of acute stridor suggests croup, supraglottitis,or foreign body. Most common cause of persistent stertor in children2–8 yrs of age is adenoid or tonsillar hypertrophy.
  • Phase of respiration in which stridoroccurs, pitch of the sound, character of voice or cry, and changein position help in assessing degree of obstruction and its localization.

  • The phaseof respiration associated with different levels of airway obstructionhas already been described.
  • Variation in pitch depends on leveland degree of obstruction. Coarse low-pitched snoring sounds (stertor)localize lesion to nose, nasopharynx, or oropharynx. Harsh inspiratorystridor may occur with supraglottic, glottic, or subglottic lesions.Stridor associated with deep barking cough signifies subglotticor tracheal obstruction, whereas stridor associated with hoarsenessor change in character of voice or cry signifies glottic lesion.
  • When infants with laryngomalacia orinnominate artery compression are placed in prone position withneck extended, stridor decreases.
  • After history and physical exam, othertests may be useful depending on suspected diagnosis. These includeneck and chest radiography and flexible laryngoscopy. If resultsof these tests are normal, upper GI radiographic series with attentionto the pharynx and esophagus should be considered. With suspectedobstruction below glottis, bronchoscopy is necessary. Usefulnessof esophagoscopy, CT, and MRI depends on suspected diagnosis.
  • Histologic diagnosis is necessary forany suspected neoplasm except perhaps hemangioma, which can usuallybe recognized clinically.

    • » READ BOOK EXCERPT ONLINE »

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

    Apnea: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    When the patient's respiratory and cardiac status is stable, investigate the underlying cause of apnea. Ask him (or, if he's unable to answer, anyone who witnessed the episode) about the onset of apnea and events immediately preceding it. The cause may be readily apparent, as in trauma.

    Take a patient history, noting reports of headache, chest pain, muscle weakness, sore throat, or dyspnea. Ask about a history of respiratory, cardiac, or neurologic disease and about allergies and drug use.

    Inspect the head, face, neck, and trunk for soft-tissue injury, hemorrhage, or skeletal deformity. Don't overlook obvious clues, such as oral and nasal secretions reflecting fluid-filled airways and alveoli or facial soot and singed nasal hair suggesting thermal injury to the tracheobronchial tree.

    Auscultate all lung fields for adventitious breath sounds, particularly crackles and rhonchi, then percuss for increased dullness or hyperresonance. Next, auscultate the heart for murmurs, pericardial friction rub, and arrhythmias. Check for cyanosis, pallor, jugular vein distention, and edema. If appropriate, perform a neurologic assessment. Evaluate the patient's level of consciousness (LOC), orientation, and mental status; test cranial nerve function and motor function, sensation, and reflexes in all extremities.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Bradypnea: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Obtain a brief history from the patient if possible. Alternatively, obtain this information from whoever accompanied him to the facility. Ask if he's experiencing a drug overdose and, if so, try to determine what drugs he took, how much, when, and by what route. Check his arms for needle marks, indicating possible drug abuse. You may need to administer I.V. naloxone, an opioid antagonist.

    If you rule out a drug overdose, ask about chronic illnesses, such as diabetes and renal failure. Check for a medical identification bracelet or an I.D. card that identifies an underlying condition. Ask whether the patient has a history of head trauma, brain tumor, neurologic infection, or stroke.

    Perform a complete physical examination, especially noting abnormalities of the respiratory system.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Dyspnea: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If the patient can answer questions without increasing his distress, take a complete history. Ask if the shortness of breath began suddenly or gradually. Is it constant or intermittent? Does it occur during activity or while at rest? If the patient has had dyspneic attacks before, ask if they're increasing in severity. Can he identify what aggravates or alleviates these attacks? Does he have a productive or nonproductive cough or chest pain? Ask about recent trauma, and note a history of upper respiratory tract infection, deep vein phlebitis, or other disorders. Ask the patient if he smokes or is exposed to toxic fumes or irritants on the job. Find out if he also has orthopnea, paroxysmal nocturnal dyspnea, or progressive fatigue.

    During the physical examination, look for signs of chronic dyspnea such as accessory muscle hypertrophy (especially in the shoulders and neck). Also look for pursed-lip exhalation, clubbing, peripheral edema, barrel chest, diaphoresis, and jugular vein distention.

    Check blood pressure and auscultate for crackles, abnormal heart sounds or rhythms, egophony, bronchophony, and whispered pectoriloquy. Finally, palpate the abdomen for hepatomegaly, and assess the patient for edema.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Hyperpnea: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    If you observe hyperpnea in a patient whose other signs and symptoms signal a life-threatening emergency, you must intervene quickly and effectively. (See Managing hyperpnea, page 334.) However, if the patient's condition isn't grave, first determine his level of consciousness (LOC). If he's alert (and if his hyperpnea isn't interfering with speaking), ask about recent illnesses or infections, ingestion of aspirin, and ingestion or inhalation of other drugs or chemicals. Find out if the patient has diabetes mellitus, renal disease, or pulmonary condition. Is he excessively thirsty or hungry? Has he recently had severe diarrhea or an upper respiratory tract infection?

    Next, observe the patient for clues to his abnormal breathing pattern. Can he speak, or does he speak only in brief, choppy phrases? Is his breathing abnormally rapid? Examine the patient for cyanosis (especially of the mouth, lips, mucous membranes, and earlobes), restlessness, and anxiety—all signs of decreased tissue oxygenation, as occurs in shock. In addition, observe the patient for intercostal and abdominal retractions, use of accessory muscles, and diaphoresis, all of which may indicate deep breathing related to an insufficient oxygen supply. Next, inspect for draining wounds or signs of infection, and ask about nausea and vomiting. Take the patient's vital signs, including oxygen saturation, noting a fever, and examine his skin and mucous membranes for turgor, possibly indicating dehydration. Auscultate the patient's heart and lungs.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Orthopnea: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Begin by asking about a history of cardiopulmonary disorders, such as myocardial infarction, rheumatic heart disease, valvular disease, asthma, emphysema, or chronic bronchitis. Does the patient smoke? If so, how much? Explore associated symptoms, noting especially complaints of coughing, nocturnal or exertional dyspnea, fatigue, weakness, loss of appetite, or chest pain. Does the patient use alcohol or have a history of heavy alcohol use?

    When examining the patient, check for other signs of increased respiratory effort, such as accessory muscle use, shallow respirations, and tachypnea. Also note barrel chest. Inspect the patient's skin for pallor or cyanosis and the fingers for clubbing. Observe and palpate for edema, and check for jugular vein distention. Auscultate the lungs for crackles, rhonchi, or wheezing. Also auscultate the heart. Monitor the patient's oxygen saturation.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Stridor: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    When the patient's condition permits, obtain a patient history from him or a family member. First, find out when the stridor began. Has he had it before? Does he have an upper respiratory tract infection? If so, how long has he had it?

    Ask about a history of allergies, tumors, and respiratory and vascular disorders. Note recent exposure to smoke or noxious fumes or gases. Next, explore associated signs and symptoms. Does stridor occur with pain or cough?

    Then examine the patient's mouth for excessive secretions, foreign matter, inflammation, andswelling. Assess his neck for swelling, masses, subcutaneous crepitation, and scars. Observe the patient's chest for delayed, decreased, or asymmetrical chest expansion. Auscultate for wheezes, rhonchi, crackles, rubs, and other abnormal breath sounds. Percuss for dullness, tympany, or flatness. Finally, note burns or signs of trauma, such as ecchymoses and lacerations.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    Paroxysmal nocturnal dyspnea: History and physical examination
    (Nursing: Interpreting Signs and Symptoms)

    Begin by exploring the patient's complaint of dyspnea. Does he have dyspneic attacks only at night or at other times as well, such as after exertion or while sitting down? If so, what type of activity triggers the attack? Does he experience coughing, wheezing, fatigue, or weakness during an attack? Find out if he has a history of lower extremity edema or jugular vein distention. Ask if he sleeps with his head elevated and, if so, on how many pillows or if he sleeps in a reclining chair. Obtain a cardiopulmonary history. Does the patient or a family member have a history of a myocardial infarction, coronary artery disease, or hypertension or of chronic bronchitis, emphysema, or asthma? Has the patient had cardiac surgery?

    Next perform a physical examination. Begin by taking the patient's vital signs and forming an overall impression of his appearance. Is he noticeably cyanotic or edematous? Auscultate the lungs for crackles and wheezing and the heart for gallops and arrhythmias.

    » READ BOOK EXCERPT ONLINE »

    Source: Nursing: Interpreting Signs and Symptoms, 2007

    DYSPNEA, TACHYPNEA, AND ORTHOPNEA: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The history and physical examination will almost invariably disclose the cause of dyspnea. To confirm pulmonary disease one will order pulmonary function studies, a chest roentgenogram, and arterial blood gases. If routine pulmonary function studies are normal, more sophisticated studies such as the nitrogen washout test and perfusion and ventilatory scans may be necessary. To diagnose cardiac conditions, ordering an ECG and measuring venous pressure and circulation times may be necessary. Any patient with dyspnea and normal physical findings deserves a circulation time to rule out early CHF. A hemogram will diagnose anemias but it will not diagnose methemoglobinemia. A determination of the erythrocytes methemoglobin, arterial oxygen saturation, and diaphorase I test must be done.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    DECREASED RESPIRATIONS, APNEA, AND CHEYNE–STOKES BREATHING: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    Obviously, the association of other signs and symptoms will determine the workup in most cases. The most important things to do are to order a blood urea nitrogen (BUN) level, electrolytes, fasting blood sugar (FBS), arterial blood gases, and a drug screen and to check for increased intracranial pressure by examining the eye grounds. If the history or physical findings suggest increased intracranial pressure, and other metabolic studies (e.g., BUN) are normal, a mannitol or urea drip is begun while awaiting the results of other investigations such as computed tomography (CT) scan, electroencephalogram (EEG), and echoencephalogram. A neurosurgeon should be consulted immediately.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    SLEEP APNEA: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    A thorough examination of the upper respiratory system is essential: It may be wise to get an otolaryngologist to do this. A CBC to rule out anemia and arterial blood gases to rule out anoxia and hypercarbia may be helpful. Spirometry, chest x-ray, echocardiogram (ECG), and arm-to-tongue circulation time will help to rule out pulmonary and cardiovascular disorders. Ultimately, overnight polysomnography will be required to secure the diagnosis. A pulmonologist or otolaryngologist ought to be consulted before ordering this expensive test.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007

    STRIDOR AND SNORING: Approach to the Diagnosis
    (Differential Diagnosis in Primary Care)

    The approach to the diagnosis involves a careful examination of the air passage with the laryngoscope and bronchoscope (if necessary, under anesthesia). If these have negative findings, a thorough neurologic examination should be performed and a Tensilon test may be indicated. Laryngismus stridulus in children may be terminated by putting the child in a steam bath; this helps to establish that diagnosis. Skin testing for allergies may be necessary. A sleep study is often necessary to rule out neurogenic or obstructive sleep apnea.

    » READ BOOK EXCERPT ONLINE »

    Source: Differential Diagnosis in Primary Care, 2007


     » Next page: Signs of Asphyxia

    Rate This Website

    What do you think about the features of this website? Take our user survey and have your say:

    Website User Survey

    Medical Tools & Articles:

    Next articles:

    Tools & Services:

    Medical Articles:

    Forums & Message Boards
     
    HONcode We subscribe to the HONcode principles

    By using this site you agree to our Terms of Use. Information provided on this site is for informational purposes only; it is not intended as a substitute for advice from your own medical team. The information on this site is not to be used for diagnosing or treating any health concerns you may have - please contact your physician or health care professional for all your medical needs. Please see our Terms of Use.

    Home | Symptoms | Diseases | Diagnosis | Videos | Tools | Forum | About Us | Terms of Use | Privacy Policy | Site Map | Advertise

    Copyright © 2009 Health Grades Inc. All rights reserved.