Atelectasis

 

 

INTRODUCTION

Background: The term atelectasis is derived from the Greek words ateles and ektasis, which mean incomplete expansion. Atelectasis is defined as diminished volume affecting all or part of a lung. Pulmonary atelectasis is one of the most commonly encountered abnormalities in chest radiology findings. Recognizing an abnormality due to atelectasis on chest x-ray films can be crucial to understanding the underlying pathology. Several types of atelectasis exist; each has a characteristic radiographic pattern and etiology. Atelectasis is divided physiologically into obstructive and nonobstructive causes.

Obstructive atelectasis

Obstructive atelectasis is the most common type and results from reabsorption of gas from the alveoli when communication between the alveoli and the trachea is obstructed. The obstruction can occur at the level of the larger or smaller bronchus. Causes of obstructive atelectasis include foreign body, tumor, and mucous plugging. The rate at which atelectasis develops and the extent of atelectasis depend on several factors, including the extent of collateral ventilation that is present and the composition of inspired gas. Obstruction of a lobar bronchus is likely to produce lobar atelectasis; obstruction of a segmental bronchus is likely to produce segmental atelectasis. Because of the collateral ventilation without a lobe or between segments, the pattern of atelectasis often depends on collateral ventilation, which is provided by the pores of Kohn and the canals of Lambert.

Nonobstructive atelectasis

Nonobstructive atelectasis can be caused by loss of contact between the parietal and visceral pleurae, compression, loss of surfactant, and replacement of parenchymal tissue by scarring or infiltrative disease. Examples of nonobstructive atelectasis are described in the following paragraphs.

Relaxation or passive atelectasis results when a pleural effusion or a pneumothorax eliminates contact between the parietal and visceral pleurae. Generally, the uniform elasticity of a normal lung leads to preservation of shape even when volume is decreased. The different lobes also function differently, eg, the middle and lower lobes collapse more than the upper lobe in the presence of pleural effusion, while the upper lobe may be affected more by pneumothorax.

Compression atelectasis occurs from any space-occupying lesion of the thorax compressing the lung and forcing air out of the alveoli. The mechanism is similar to relaxation atelectasis.

Adhesive atelectasis results from surfactant deficiency. Surfactant normally reduces the surface tension of the alveoli, thereby decreasing the tendency of these structures to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. This is observed particularly in acute respiratory distress syndrome (ARDS) and similar disorders.

Cicatrization atelectasis results from diminution of volume as a sequela of severe parenchymal scarring and is usually caused by granulomatous disease or necrotizing pneumonia. Replacement atelectasis occurs when the alveoli of an entire lobe are filled by tumor (eg, bronchioalveolar cell carcinoma), resulting in loss of volume.

Right middle lobe syndrome is a form of chronic atelectasis that usually results from bronchial compression by surrounding lymph nodes. Partial bronchial obstruction and recurrent infection also may lead to chronic atelectasis and acute or chronic pneumonitis.

Rounded atelectasis represents folded atelectatic lung tissue with fibrous bands and adhesions to the visceral pleura. Incidence is high in asbestos workers (65-70% of cases), most likely due to a high degree of pleural disease. Affected patients typically are asymptomatic, and the mean age at presentation is 60 years.

 

Pathophysiology: The mechanism of obstructive and nonobstructive atelectasis is quite different and is determined by several factors.

Obstructive atelectasis

Following obstruction of a bronchus, the circulating blood absorbs the gas in the peripheral alveoli, leading to retraction of the lung and an airless state within a few hours. In the early stages, blood perfuses the airless lung; this results in ventilation-perfusion mismatch and arterial hypoxemia. A filling of the alveolar spaces with secretions and cells may occur, thereby preventing complete collapse of the atelectatic lung. The uninvolved surrounding lung tissue distends, displacing the surrounding structures. The heart and mediastinum shift toward the atelectatic area, the diaphragm is elevated, and the chest wall flattens.

If the obstruction is removed, any complicating postobstructive infection subsides and the lung returns to its normal state. If the obstruction is persistent and infection continues to be present, fibrosis develops and the lung becomes bronchiectatic.

Nonobstructive atelectasis

The loss of contact between the visceral and parietal pleurae is the primary cause of nonobstructive atelectasis. A pleural effusion or pneumothorax causes relaxation or passive atelectasis. Pleural effusions affect the lower lobes more commonly than pneumothorax, which affects the upper lobes. A large pleural-based lung mass may cause compression atelectasis by decreasing lung volumes.

Adhesive atelectasis is caused by a lack of surfactant. The surfactant has phospholipid dipalmitoyl phosphatidylcholine, which prevents lung collapse by reducing the surface tension of the alveoli. Lack of production or inactivation of surfactant, which may occur in ARDS, radiation pneumonitis, and blunt trauma to the lung, cause alveolar instability and collapse.

Scarring of the lung parenchyma leads to cicatrization atelectasis.

Replacement atelectasis is caused by filling of the entire lobe by a tumor such as bronchoalveolar carcinoma.

Platelike atelectasis

Also called discoid or subsegmental atelectasis, this type is seen most commonly on chest radiographs. Platelike atelectasis probably occurs because of obstruction of a small bronchus and is observed in states of hypoventilation, pulmonary embolism, or lower respiratory tract infection. Small areas of atelectasis occur because of inadequate regional ventilation and abnormalities in surfactant formation from hypoxia, ischemia, hyperoxia, and exposure to various toxins. A mild-to-severe gas exchange abnormality may occur because of ventilation-perfusion mismatch and intrapulmonary shunt.

Postoperative atelectasis

Atelectasis is a common pulmonary complication in patients following thoracic and upper abdominal procedures. General anesthesia and surgical manipulation lead to atelectasis by causing diaphragmatic dysfunction and diminished surfactant activity. The atelectasis is typically basilar and segmental in distribution.

 

Frequency:

  • In the US: Postoperative atelectasis is extremely common. Lobar atelectasis is also common. The incidence and prevalence of this disorder are not well documented.

Mortality/Morbidity: Patient mortality depends on the underlying cause of atelectasis. In postoperative atelectasis, the condition generally improves. The prognosis of lobar atelectasis secondary to endobronchial obstruction depends on treatment of the underlying malignancy.

Race: No racial predilection exists.

Sex: No sexual predilection exists.

Age: The mean age at presentation for rounded atelectasis is 60 years.

CLINICAL

History: Atelectasis may occur postoperatively following thoracic or upper abdominal procedures.

  • Most symptoms and signs are determined by the rapidity with which the bronchial occlusion occurs, the size of the lung area affected, and the presence or absence of complicating infection.
  • Rapid bronchial occlusion with a large area of lung collapse causes pain on the affected side, sudden onset of dyspnea, and cyanosis. Hypotension, tachycardia, fever, and shock may also occur.
  • Slowly developing atelectasis may be asymptomatic or may cause only minor symptoms. Middle lobe syndrome often is asymptomatic, although irritation in the right middle and right lower lobe bronchi may cause a severe, hacking, nonproductive cough.

Physical: The physical examination findings show dullness to percussion over the involved area and diminished or absent breath sounds. Chest excursion in the area is reduced or absent. The trachea and the heart are deviated toward the affected side.

Causes:

  • The primary cause of acute or chronic atelectasis is bronchial obstruction by the following:
    • Plugs of tenacious sputum
    • Foreign bodies
    • Endobronchial tumors
    • Tumors, a lymph node, or an aneurysm compressing the bronchi and bronchial distortion
  • External pulmonary compression by pleural fluid or air (ie, pleural effusion, pneumothorax) may also cause atelectasis.
  • Abnormalities of surfactant production contribute to alveolar instability and may result in atelectasis. These abnormalities commonly occur with oxygen toxicity and ARDS.
  • Resorptive atelectasis is caused by the following:
    • Bronchogenic carcinoma

       

    • Bronchial obstruction from metastatic neoplasm (eg, adenocarcinoma of breast or thyroid, hypernephroma, melanoma)

       

    • Inflammatory etiology (eg, tuberculosis, fungal infection)

       

    • Aspirated foreign body

       

    • Mucous plug

       

    • Malpositioned endotracheal tube

       

    • Extrinsic compression of an airway by neoplasm, lymphadenopathy, aortic aneurysm, or cardiac enlargement
  • Relaxation atelectasis is caused by the following:
    • Pleural effusion

       

    • Pneumothorax

       

    • A large emphysematous bulla
  • Compression atelectasis is caused by the following:
    • Chest wall, pleural, or intraparenchymal masses

       

    • Loculated collections of pleural fluid
  • Adhesive atelectasis is caused by the following:
    • Hyaline membrane disease

       

    • Acute respiratory distress syndrome

       

    • Smoke inhalation

       

    • Cardiac bypass surgery

       

    • Uremia

       

    • Prolonged shallow breathing
  • Cicatrization atelectasis is caused by the following:
    • Idiopathic pulmonary fibrosis

       

    • Chronic tuberculosis

       

    • Fungal infections
    • Radiation fibrosis
  • Replacement atelectasis is caused by alveoli filled by tumor or fluid.
  • Rounded atelectasis is caused by asbestos pleural plaques.

DIFFERENTIALS

Asbestosis
Ascites
Blunt Chest Trauma
Diaphragmatic Paralysis
Hypersensitivity Pneumonitis
Lung Abscess
Lung Cancer, Non-Small Cell
Lung Cancer, Oat Cell (Small Cell)
Pneumococcal Infections
Pneumonia, Aspiration
Pneumonia, Bacterial
Pneumonia, Community-Acquired
Pneumonia, Fungal
Pneumonia, Viral
Pneumothorax
Pulmonary Embolism
Pulmonary Fibrosis, Idiopathic
Respiratory Failure


Other Problems to be Considered:

Bronchogenic carcinoma, which may present with atelectasis, must be excluded in all patients older than 35 years.

Spontaneous pneumothorax produces clinical findings similar to atelectasis, but during the physical examination, the percussion note is hyperresonant, the heart and mediastinum are pushed to the opposite side, and x-rays films are diagnostic.

Massive pleural effusion may cause dyspnea, cyanosis, weakness, dullness over the hemithorax, and absent breath sounds. However, the heart and mediastinum are deviated away from the involved area.


WORKUP

Lab Studies:

  • Atelectasis of a significant size results in hypoxemia as measured on arterial blood gas determinations. Arterial blood gas evaluation shows that despite hypoxemia, the PaCO2 level is usually normal or low as a result of the increased ventilation.

Imaging Studies:

  • Chest radiographs and CT scans show direct and indirect signs of lobar collapse.
    • Direct signs include displacement of fissures and opacification of the collapsed lobe.
    • Indirect signs include displacement of the hilum, mediastinal shift toward the side of collapse, loss of volume on ipsilateral hemithorax, elevation of ipsilateral diaphragm, crowding of the ribs, compensatory hyperlucency of the remaining lobes, and silhouetting of the diaphragm or the heart border.
  • Complete atelectasis of an entire lung  is characterized as follows:
    • Complete collapse of a lung leads to opacification of the entire hemithorax and an ipsilateral shift of the mediastinum.
    • The mediastinal shift separates atelectasis from massive pleural effusion.
  • Right upper lobe (RUL) collapse  is characterized as follows:
    • The collapsed RUL shifts medially and superiorly, resulting in elevation of the right hilum and the minor fissure. Rarely, the RUL may collapse laterally, producing a masslike opacity that may look like a loculated pleural effusion.
    • The minor fissure in RUL collapse is usually convex superiorly but may appear concave because of an underlying mass lesion. This is called the sign of Golden S.
    • Tenting of the diaphragmatic pleura juxtaphrenic peak is another helpful sign of RUL atelectasis.
    • Upon CT scanning, RUL collapse appears as a right paratracheal opacity, and the minor fissure appears concave laterally.
  • Right middle lobe (RML) collapse  is characterized as follows:
    • RML collapse obscures the right heart border on a posteroanterior (PA) film. Occasionally, a triangular opacity may be observed. The lateral view shows a triangular opacity overlying the heart because the major fissure shifts upward and the minor fissure shifts downward.
    • Upon CT scanning, the atelectatic RML appears as a triangular opacity against the right heart border with the apex pointing laterally and is termed the “tilted ice cream cone sign.”
  • Right lower lobe (RLL) collapse  is characterized as follows:

     

    • The collapsed RLL shifts posteriorly and inferiorly. A triangular opacity obscuring the RLL pulmonary artery may be observed. The major fissure, which normally is not visible, is seen with RLL collapse. The superior mediastinal structure shifts to the right, causing a superior triangle sign. Laterally, the collapsed RLL blurs the posterior third of the right hemidiaphragm.

       

    • Upon CT scanning, a paraspinal masslike appearance is observed.

       

    • Concomitant RML and RLL atelectasis may appear as an elevated right hemidiaphragm or a subpulmonic effusion. An attempt to identify the fissures usually leads to the accurate diagnosis.
  • Left upper lobe (LUL) collapse  is characterized as follows:

     

    • An atelectatic LUL shifts anteriorly and superiorly. In half the cases, a hyperexpanded superior segment of the left lower lobe (LLL) is positioned between the atelectatic upper lobe and the aortic arch. This gives the appearance of a crescent of the aerated lung, called the Luft Sichel sign.

       

    • On lateral views, the major fissure is displaced anteriorly and the hyperexpanded RUL may herniate across the midline. On PA views, an atelectatic LUL produces a faint opacity in the left upper hemithorax, obliterating the left heart border.

       

    • A CT scan shows the inferior location of the collapsed lobe and the shift of the RUL across the midline.
  • LLL collapse  is characterized as follows:

     

    • On frontal views, increased retrocardiac opacity silhouettes the LLL pulmonary artery and the left hemidiaphragm. The hilum shifts downward, and the rotation of the heart produces flattening of the cardiac waist, which is known as the flat-waist sign. The superior mediastinum may shift and obliterate the aortic arch, the top of the aortic-knob sign.

       

    • On lateral radiographs, opacity makes the posterior third of the left diaphragm indistinct.

       

    • A CT scan shows the atelectatic LLL in the inferior posterior location.
  • Rounded atelectasis is characterized as follows:

     

    • This is a segmental or subsegmental atelectasis that occurs secondary to visceral pleural thickening and entrapment of lung tissue.

       

    • Rounded atelectasis is usually located in the lower lobes, the lingula, or the RML.

       

    • On chest radiographs, rounded atelectasis manifests as a subpleural mass, with bronchovascular structures projecting out of the mass toward the hilum. An associated parietal pleural plaque may be present. The swirl appearance of bronchovascular shadows is called the comet-tail sign.

Procedures:

  • Flexible fiberoptic bronchoscopy can be a useful diagnostic and therapeutic procedure.
    • Bronchoscopy helps evaluate the cause of bronchial obstruction. In addition, bronchoscopy helps clear mucous plugs when they cause bronchial obstruction.
    • Bronchoscopy has limitations. Because only the subsegmental bronchi are visualized, a distal endobronchial lesion is not accessible through bronchoscopy.
Histologic Findings: During fiberoptic bronchoscopy, the washing, brushing, and biopsy specimens of any obstructing mass should be examined for evidence of malignancy or Aspergillus mucous plugging (ie, allergic bronchopulmonary aspergillosis).

 

TREATMENT

Medical Care: The treatment of atelectasis depends on the underlying etiology. Treatment of acute atelectasis, including postoperative lung collapse, requires removal of the underlying cause.

For postoperative atelectasis, prevention is the best approach. Anesthetic agents associated with postanesthesia narcosis should be avoided; narcotics should be used sparingly because they depress the cough reflex. Early ambulation and use of incentive spirometry are important. Encourage the patient to cough and to breathe deeply. Nebulized bronchodilators and humidity may help liquefy secretions and promote their easy removal. In the case of lobar atelectasis, vigorous chest physiotherapy frequently helps reexpand the collapsed lung. When these efforts are not successful within 24 hours, flexible fiberoptic bronchoscopy should be performed.

When a mechanically obstructed bronchus is suggested but coughing or suctioning is not successful, bronchoscopy should be performed. If bronchoscopy is successful, any underlying infection, if present, is treated.

Prevention of further atelectasis involves (1) placing the patient in such a position that the uninvolved side is dependent to promote increased drainage of the affected area, (2) giving vigorous chest physiotherapy, and (3) encouraging the patient to cough and to breathe deeply.

Patients may require repeat bronchoscopy if atelectasis recurs. This is particularly true in patients with neuromuscular disease and poor cough.

Therapy with a broad-spectrum antibiotic is started and modified appropriately if a specific pathogen is isolated from sputum samples or bronchial secretions.

Postoperative atelectasis is treated as follows:

  • Postoperative atelectasis is treated with adequate oxygenation and reexpansion of the lung segments.

     

  • Supplemental oxygen should be titrated to achieve an arterial oxygen saturation of greater than 90%.

     

  • Severe hypoxemia associated with severe respiratory distress or hypoxemia should lead to intubation and mechanical support. Intubation not only provides oxygenation and ventilatory support, but also provides access for suctioning of the airways and facilitates performing bronchoscopy, if needed. The positive pressure and larger tidal volumes often help to reexpand collapsed lung segments.

     

  • Continuous positive airway pressure delivered via a nasal cannula or facemask may also be effective in improving oxygenation and reexpanding the collapsed lung.

     

  • Antibiotics are discussed as follows:
    • Because secondary atelectasis usually becomes infected regardless of the cause of obstruction, broad-spectrum antibiotics should be prescribed if evidence of infection is present, such as fever, night sweats, or leukocytosis.

       

    • Obstruction of a major bronchus may cause severe hacking or coughing. Antitussive therapy reduces the cough reflex and may produce further obstruction; thus, it should be avoided.
  • Fiberoptic bronchoscopy is discussed as follows:

     

    • Fiberoptic bronchoscopy is commonly required for diagnosis, particularly if an endobronchial lesion is suggested.

       

    • This procedure has a limited role in the management of postoperative atelectasis. Fiberoptic bronchoscopy is not more effective than standard chest physiotherapy, deep breathing, coughing, and suctioning of patients who are intubated. Therefore, simple and standard respiratory therapy techniques should be administered to patients who spontaneously ventilate or patients on mechanical ventilation.

       

    • Fiberoptic bronchoscopy should be reserved for those situations in which chest physiotherapy is contraindicated (eg, chest trauma, immobilized patient), poorly tolerated, or unsuccessful.
  • Analgesia is discussed as follows:

     

    • Judicious use of perioperative analgesia is an essential adjunct, permitting patients to breathe deeply, cough forcefully, and participate in chest physiotherapy maneuvers.

       

    • In patients with underlying pulmonary disease, use of epidural analgesia has been shown to be a very effective pain control measure, thereby aiding aggressive chest physiotherapy.
  • N-acetylcysteine aerosols commonly are administered in an effort to promote clearance of tenacious secretions; however, their efficacy has not been documented. In addition, N-acetylcysteine may cause acute bronchoconstriction. Its use should be limited to direct instillation at the time of fiberoptic bronchoscopy.

     

  • Prophylactic maneuvers for reducing the incidence and magnitude of postoperative atelectasis in high-risk patients should be encouraged. These techniques are deep-breathing exercises, coughing exercises, and incentive spirometry.

     

  • For maximal benefit, prophylactic measures should be taught and instituted before surgery and used regularly, on an hourly basis, after surgery.
  • Early ambulation of patients after surgery has also been found to be as effective as physical therapy.

Surgical Care: Chronic atelectasis is treated with segmental resection or lobectomy.

MEDICATION

Bronchodilators may be used to encourage sputum expectoration; if underlying airflow is present, these agents may also improve ventilation. Some patients may require broad-spectrum antibiotics to treat the underlying infections, which may occur because of bronchial obstruction. N-acetylcysteine aerosols are not recommended because of the risk of bronchoconstriction and the lack of documented efficacy.

Drug Category: Bronchodilators -- Decrease muscle tone in both the small and large airways in the lungs, thereby increasing ventilation. Includes subcutaneous medications, beta-adrenergic agents, methylxanthines, and anticholinergics.
Drug Name
 Albuterol (Proventil, Ventolin) -- Beta-agonist for bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta-2 receptors, with little effect on cardiac muscle contractility. Most patients (even those with no measurable increase in expiratory flow) benefit from treatment. Inhaled beta-agonists initially are prescribed prn. Frequency may be increased; institute regular schedule in patients on anticholinergic drugs who are still symptomatic.
Available as a liquid for nebulizer, metered-dose inhalers (MDI), and dry-powder inhalers.
Adult Dose MDI: 2 puffs q3-4h
Nebulizer: 0.2-0.3 mL of 5% solution diluted to 2.5 mL with NS tid/qid
Pediatric Dose MDI
<12 years: Not recommended
>12 years: Administer as in adults
Nebulizer
Infants and children: 0.01-0.02 mL of 5% solution diluted in 2-3 mL NS q4-6h
Adolescents: Administer as in adults
Contraindications Documented hypersensitivity; preexisting cardiac arrhythmia associated with tachycardia
Interactions Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation; cardiovascular effects may increase with MAOIs, inhaled anesthetics, TCAs, and sympathomimetic agents
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Adverse effects include muscle tremor, nervousness, insomnia, transient hypoxemia, and tachycardia; caution in hyperthyroidism, diabetes mellitus, hypertension, ischemic heart disease, seizures, and pheochromocytoma
Drug Name
 Metaproterenol (Alupent) -- Relaxes bronchial smooth muscle by action on beta-2 receptors, with little effect on cardiac muscle contractility. Most patients (even those with no measurable increase in expiratory flow) benefit from treatment. Inhaled beta-agonists initially are prescribed prn. Frequency may be increased; institute regular schedule in patients on anticholinergic drugs who are still symptomatic.
Available as a liquid for nebulizer, MDI, and dry-powder inhaler.
Adult Dose MDI: 2 puffs q3-4h
Nebulizer: 0.2-0.3 mL of 5% solution diluted to 2.5 mL with NS tid/qid
Pediatric Dose MDI
<12 years: Not recommended
>12 years: Administer as in adults
Nebulizer
Infants and children: 0.01-0.02 mL of 5% solution diluted in 2-3 mL of NS q4-6h
Adolescents: Administer as in adults
Contraindications Documented hypersensitivity; arrhythmia associated with tachycardia
Interactions Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation; cardiovascular effects may increase with MAOIs, inhaled anesthetics, TCAs, and sympathomimetic agents
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in hypertension, cardiovascular disease, congestive heart failure, hyperthyroidism, diabetes, and seizures; not recommended during breastfeeding; adverse reactions include tachycardia, headache, nervousness, dizziness, tremor, GI upset, hypertension, paradoxical bronchospasm, and cough
Drug Category: Mucolytics -- N-acetylcysteine is only recommended for direct instillation via fiberoptic bronchoscopy or in an intubated patient. Therapy with mucolytics may promote sputum removal of thick mucous plugs and, therefore, helps treat atelectasis in many patients.
Drug Name
 N-acetylcysteine (Mucomyst) -- Inhalations may be tried to encourage sputum expectoration in patients with tenacious sputum and mucous plugging.
Adult Dose 5-10 mg dissolved in 3 mL NS
Pediatric Dose Not established
Contraindications Documented hypersensitivity
Interactions None reported
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Inhalations may exacerbate bronchospasm; GI distress may occur
Drug Category: Antibiotics -- To treat underlying bronchitis or postobstructive infection.
Drug Name
 Cefuroxime (Zinacef) -- Second-generation cephalosporin maintains gram-positive activity of first-generation cephalosporins; adds activity against Proteus mirabilis, Haemophilus influenzae, Escherichia coli, Klebsiella pneumoniae, and Moraxella catarrhalis.
Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration.
Adult Dose 2 g IV q6-8h
Pediatric Dose 80-160 mg/kg/d IV divided q4-6h
Contraindications Documented hypersensitivity
Interactions Alcoholic beverages consumed <72 h after taking may produce disulfiramlike reactions; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patients receiving potent diuretics (eg, loop diuretics); coadministration with aminoglycosides increases nephrotoxic potential
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Administer half dose if CrCl is 10-30 mL/min and quarter dose if CrCl <10 mL/min; fungal and microorganism overgrowth may occur with prolonged therapy
Drug Name
 Cefaclor (Ceclor) -- Second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods.
Determine proper dosage and route based on condition of patient, severity of infection, and susceptibility of causative organisms.
Adult Dose 500 mg PO tid for 10 d
Pediatric Dose 20-40 mg/kg/d q8-12h
Contraindications Documented hypersensitivity
Interactions Alcoholic beverages consumed <72 h after taking may produce disulfiramlike reactions; may increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics (eg, loop diuretics) and aminoglycosides may increase nephrotoxicity; monitor renal function closely
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Reduce dosage by half if CrCl is 10-30 mL/min and by one fourth if CrCl <10 mL/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy

FOLLOW-UP

Complications:

  • Acute pneumonia
  • Bronchiectasis
  • Hypoxemia and respiratory failure
  • Postobstructive drowning of the lung
  • Sepsis
  • Pleural effusion and empyema

MISCELLANEOUS

Medical/Legal Pitfalls:

  • Failure to consider lobar or segmental collapse when a loss of volume is observed on chest x-ray films
  • Failure to exclude an endobronchial abnormality when evaluating a patient with lobar collapse
  • Failure to recognize that the lung collapse is a medical emergency because patients may develop respiratory distress and hypoxemia
  • Failure to consider bronchoscopy as a diagnostic and therapeutic procedure for patients with lung collapse