Chapter 33. Pulmonary Emergencies

See also Chapter 13.

Essentials of Diagnosis

Asthma

• Cough, wheezing, chest tightness, often worse at night
• Physical examination:Prolonged expiratory phaseor bilateral wheezing, tachypnea, tachycardia, hypoxia
• Reversible with bronchodilators

Chronic Obstructive Pulmonary Disease

• Smoker with chronic productive cough complains of dyspnea
• Increased sputum production, bilateral wheezing, rales, and rhonchi

General Considerations

Obstructive lung disease is classified into two categories: asthma and chronic obstructive pulmonary disease (COPD). Patients with asthma have disease that is episodic and reversible to a significant degree. Between acute attacks these patients may have relatively normal lung function. However, patients who have persistent inflammation may develop over time permanent changes that contribute to a decline in functional capacity. Patients with COPD, have significant fixed airway obstruction that remains at baseline even when the patient's illness is under optimal control. In addition to the concept of reversibility, there are other characteristics that distinguish these two groups. Asthmatic patients tend to be younger and more likely to have allergic triggers and conditions. A family history is common. Patients with COPD usually have a long history of cigarette smoking and more significant permanent lung injury and chest remodeling. Associated right heart failure does not occur in asthma but is common in advanced cases of COPD.

Many conditions commonly associated with asthma and COPD exacerbations are listed in Table 33–1. Some of these conditions are treatable, and the clinician should ask about them specifically while taking the patient's history.

There are two varieties of COPD: chronic bronchitis and emphysema. Chronic bronchitis is characterized by chronic cough and sputum production and is almost invariably associated with prolonged and heavy cigarette smoking. Such patients usually have increased lung volumes and a barrel-shaped chest with increased lung markings on chest X-ray. In advanced cases they may have cyanosis and peripheral edema due to right heart failure. Patients with emphysema on the other hand are typically thin without cyanosis and breathe through pursed lips. Accessory muscle use is more prominent. The chest X-ray usually shows a paucity of lung markings reflecting tissue destruction. Some patients with emphysema have genetic factors (α1-antitrypsin deficiency) as the basis of their illness, but most have a long history of cigarette smoking.

Clinical Findings

Asthma

History

Most asthmatic patients present with exacerbations of known disease with shortness of breath and cough. They frequently complain of tightness in the chest. Those with significant chest pain, fever, or purulent sputum may have associated pneumonia. Acute attacks are frequently precipitated by upper respiratory infection, exercise, or inhaled allergens.

Physical Examination

Most patients are wheezing and coughing with respiratory distress. Tremor and tachycardia are common due to a combination of sympathomimetic therapy and the stress of the illness. Mild degrees of hypoxia are common. Dehydration due to inadequate oral intake or vomiting is almost always present. Tachypnea and sometimes fever increase insensible losses. Thick and tenacious secretions tend to cause mucous plugging and significantly contribute to impaired gas exchange. Patients with moderate distress typically prefer to sit up and frequently are agitated, tachycardic, and tachypneic with accessory muscle use. Patients with severe distress may be hypoxic even with supplemental oxygen or have marked abnormalities of vital signs. Those with alteration of mental status, CO2 retention, or who begin to tire are in danger of respiratory arrest.

Chronic Bronchitis and Emphysema

History

COPD is a chronic disease and baseline functional limitations are characteristic of the illness. The presentation of an acute exacerbation is increased shortness of breath, wheezing, and cough that becomes progressively worse over several days. An increase in sputum production is frequently seen, especially in patients with chronic bronchitis. Activity tolerance becomes more limited in these patients. Most are dyspneic at rest when they present to the emergency department.

Physical Examination

Emphysema

Patients with emphysema have diminished breath sounds due to the loss of lung parenchyma. Patients with advanced disease are usually thin and appear uncomfortable even at baseline with obvious use of accessory muscles. These patients may be described as “pink puffers” because they are generally not cyanotic or significantly hypoxic and breathe through pursed lips.

Chronic Bronchitis

In addition to wheezing and prolonged expiration, patients with chronic bronchitis usually have a few course rales and prominent rhonchi. Heart tones are usually distant because of a barrel shape to the chest and the loss of pulmonary parenchyma that transmits sound. They frequently are moderately obese. Peripheral edema may be due to right heart failure associated with advanced disease. Patients with chronic bronchitis are not as uncomfortable in appearance as those with emphysema and frequently have minimal symptoms in the face of pronounced CO2 retention and hypoxia. These patients are sometimes referred to as “blue bloaters,” because of the frequent occurrence of cyanosis and edema.

Evaluation

Medical History

In addition to standard medical history, the use of oxygen at home is important. Patients who have required ICU care or intubation are at greater risk for severe disease. Continued smoking contributes more than any other factor to the increased risk of illness and death.

Laboratory and Other Findings

Pulse Oximetry

Pulse oximetry usually gives better information regarding oxygenation than do blood gases because it is available in real time. An accurate reading depends on good blood flow and a thin body part to attach the device. When a good arterial waveform is visible on the monitor the readings are very accurate and reliable.

Blood Gases

The assessment of alveolar ventilation and respiratory acidosis are best evaluated with blood gas analysis. Many patients with COPD but particularly those on home oxygen have a chronic respiratory acidosis (elevated pco2) with metabolic compensation (increased total CO2, or bicarbonate). A low pH is indicative of acute decompensation. Comparing values from previous measurements is helpful in assessing the significance of these abnormalities.

Chest X-Ray

Most patients with mild asthma will not need a chest X-ray unless pneumonia or pneumothorax is suspected. Patients with COPD or advanced age are more likely to have important findings on chest X-ray. Congestive heart failure, pleural effusions along with lung cancer, and associated complications are important diagnoses that may be made or suspected with plain images of the chest. If pulmonary embolism (PE) is suspected, then CT scanning with contrast is necessary.

Peak Expiratory Flow Measurement

Peak expiratory flow (PEF) measurements are a practical way of following the severity of illness and response to therapy in patients with asthma. The values should be compared with predicted peak flow values, which are based on age, sex, and height.

Electrocardiogram

Most patients with significant respiratory distress or abnormal vital signs should be placed on a cardiac monitor and the cardiac rhythm determined. The electrocardiogram provides additional information where the rhythm is not easily determined from a single lead monitor or if cardiac ischemia is suspected.

CBC and Electrolytes

Some patients with COPD are polycythemic due to chronic hypoxia. Metabolic compensation from chronic CO2 retention is usually evident from venous electrolytes in the form of an elevated bicarbonate as reflected in the total CO2.

Microscopic Examination of Sputum

Sputum examination is primarily useful in selected patients when adequate specimens are available and pneumonia is suspected. They also can be useful in the diagnostic evaluation when atypical pathogens such as mycobacteria or Legionella species are suspected.

Drug Levels

Theophylline is no longer commonly used. Patients who do take theophylline may be toxic and drug levels are indicated if toxicity is suspected.

Differential Diagnosis

Adults

Most patients with COPD present with a long history of previous exacerbations similar to the present episode. The diagnostic challenge is usually in the identification or exclusion of associated conditions including congestive heart failure, PE, pneumothorax, and cancer of the lung. Most patients are elderly and at risk for all these illnesses. In many cases, the reason for dyspnea may be multifactorial. Patients with fever may have pneumonia or another type of infection. If chest pain is present, associated cardiac disease must be considered. Other pulmonary pathology such as pneumothorax may be present. It cannot be stressed too strongly that many patients who present with wheezing actually have acute heart failure as the primary reason for dyspnea. Impressively elevated blood pressure is a valuable clue to the presence of associated acute heart failure.

Children

Respiratory syncytial virus infection is a significant cause of wheezing and respiratory distress in young children. Rapid testing for these infections helps to identify these patients but usually does not change therapy. The test is used to determine the need for respiratory isolation if the patient requires hospitalization. Most children may be given a diagnosis of reactive airway disease and treated in a similar manner. Foreign body aspiration typically presents with the acute onset of wheezing and respiratory distress in a crawler or young toddler.

Treatment

Asthma by definition should be largely reversible with treatment. Patients with COPD have fixed obstruction but do have episodes when symptoms are exaggerated and can be improved with therapy.

Provide Supplemental Oxygen

Oxygen Therapy

Most patients with mild asthma can be treated with nasal cannula oxygen at 2–4 L/min. Patients whose saturations fall below 90% require higher concentrations by mask. Patients who are anxious, hypoxic, and struggling to breathe should receive high concentrations of oxygen as necessary to achieve adequate oxygen saturations. A nonrebreather mask with an oxygen reservoir can be used to deliver nearly a 100% inspired oxygen concentration if necessary.

CO2 Narcosis

Some patients with advanced COPD, especially those maintained on oxygen at home, may develop CO2 narcosis if high concentrations of oxygen are used. Such patients develop an altered mental status when their hypoxic ventilatory drive is removed, CO2 levels rise, and a respiratory acidosis develops. Most of the time, this is seen when a patient not short of breath is treated with oxygen for another reason such as chest pain.

Hydration

Patients are usually in need of intravenous fluids. This is particularly true of asthmatics and an aspect of treatment that is frequently neglected. Young adults with asthma and without cardiac disease should receive 1–2 L of normal saline over the first hour or two and at 500 cc/h thereafter. Children should be treated with 20 cc/kg of saline as a bolus.

Patients with COPD are usually older and may have associated cardiac disease; therefore, caution is indicated in these patients to avoid fluid overload. A fluid bolus of 250–500 cc of saline is typically appropriate in an elderly patient or someone with known heart disease.

Respiratory Support

If patients begin to tire or show signs that failure of ventilation is developing, they should be supported mechanically.

BiPAP

The technology of noninvasive treatment with Bilevel (BiPAP) support has improved over the last several years. Many patients who otherwise would require intubation can be supported noninvasively and avoid the risks of an artificial airway. An initial setting of 10 cm H2O of inspiratory pressure and 5 cm H2O of expiratory pressure is usually an appropriate initial setting for BiPAP support for either asthma or COPD.

Intubation

If a patient cannot manage their airway either because of confusion, lethargy, or agitation, then they will require an artificial airway (see Chapter 7). Patients may also require intubation because of excessive secretions or a need for frequent suctioning. Controlled rapid sequence intubation is preferable to crash intubation which may be required if the patient suddenly deteriorates. Larger endotracheal tubes facilitate suctioning and bronchoscopy and should be used if possible. Low tidal volume ventilation (Table 33–2) helps to decrease overdistention, air trapping, and resultant barotrauma. Measurement of blood gases is important in guiding therapy when positive pressure support of any kind is used.

β-Adrenergic Agonists

These medications are the mainstay of treatment for asthma and COPD. The ones most commonly used are the short-acting β2-selective agents. These agents cause rapid relaxation of bronchial smooth muscles, resulting in bronchodilation, and reducing airflow obstruction. Albuterol, levalbuterol (the R-isomer of albuterol), and metaproterenol are used most often. Inhalation, through metered-dose inhalers (MDIs) or nebulizers, has been shown to be faster and to deliver higher concentrations of medication to the lungs with fewer systemic side effects than oral preparations. However, MDIs require coordination and a cooperative, alert patient who can hold his or her breath for 5–10 seconds. Therefore, passive nebulized β2-agonists are more often used in moderate and severe exacerbations. For mild disease, albuterol MDI dosing is 4–6 puffs every 20 minutes (up to 4 hours), and nebulized solutions should be given at 2.5 mg every 20–30 minutes. Patients who are severely ill may receive 5 mg every 20–30 minutes or a continuous treatment for an hour or more. Attention to monitoring the patient for tachycardia and for signs of respiratory failure should be continued and not neglected in patients on continuous treatment.

Anticholinergics

Ipratropium nebulized solution, 0.5 mg every 20–30 minutes, can be used. This is frequently mixed with albuterol and given every 20–30 minutes. Hospitalized patients may be scheduled every 4–6 hours.

Systemic Corticosteroids

Steroids are well known to inhibit both inflammatory cell recruitment and the release of inflammatory mediators into the airways. Many patients with moderate to severe obstructive airway disease take chronic steroids. Although steroids do not initially change emergency department management, these medications are crucial to reduce the rate of relapse in moderate to severe exacerbations. They can also be helpful in mild attacks if the patient is not responding well to initial bronchodilator treatments. Consider steroids if the patient is taking oral or inhaled steroids, has had prolonged symptoms, or recently completed a steroid taper. Patients who are severely ill should receive steroids. Steroid doses for adults are prednisone, 40–60 mg orally, or methylprednisolone, 60–125 mg intramuscularly or intravenously. Dosing for children includes prednisone, 2 mg/kg orally, or methylprednisolone 0.5–2 mg/kg intravenously. Discharge the patient to home with a steroid burst (adults: prednisone, 40 mg/d; children: 1 mg/kg, for 3–5 days) or taper (10–14 days) depending on severity.

Antibiotics

Antibiotics are typically not indicated for mild asthma unless evidence of infection is present on physical examination or chest X-ray. Patients with an acute exacerbation of COPD, presenting with worsening dyspnea and increased cough and sputum production, usually benefit from antibiotics. Patients who have associated pneumonia should be treated with antibiotics. (See Pneumonia and Bronchitis, below.)

Other Known Treatment Modalities

Magnesium Sulfate

Magnesium has a direct relaxing effect on bronchial smooth muscle and also helps to stabilize many inflammatory mediators. For patients with severe asthma, magnesium (in conjunction with ongoing treatment) may help improve airway obstruction and avoid intubation. The dosing is 2–3 g intravenously, infused at 1 g/min, with close monitoring of blood pressure. The infusion should stop if hypotension, respiratory depression, or decreased deep tendon reflexes occurs.

Methylxanthines

Theophylline (oral) or aminophylline (intravenous) are moderately effective bronchodilators. However, toxicity, particularly vomiting and resulting dehydration, is a particular problem. These medications are no longer recommended for the treatment of acute exacerbations of asthma or COPD.

Ketamine

Ketamine has been shown to be a significant bronchodilator and can be used to facilitate intubation of severely agitated patients with refractory disease (status asthmaticus). Usual anesthetic induction dose is 1–2 mg/kg intravenously or 4 mg/kg intramuscularly.

Disposition

Asthma

Asthma patients who demonstrate a good response (PEF > 70% of predicted) and whose symptoms have resolved can be discharged home. Those with an incomplete response to treatment (PEF, 50–70% of predicted), with improved symptoms, and no hypoxia can be discharged if close follow-up and correct use of inhalers can be demonstrated. Most patients that have returned to the emergency department within 3 days should be admitted for continued treatment in the hospital.

Acute Exacerbations of COPD

Acute exacerbations of COPD are more difficult and resolve slower than acute exacerbations of asthma. Most patients with COPD will require admission. Some patients will have significant comorbidities such as pneumonia or associated heart failure. Some are severely ill and require ICU care. Many patients are elderly and social issues such as the availability of home health care, and assistance with the activities of daily living make treatment outside the hospital impractical.

Acute Pulmonary Embolism

Essentials of Diagnosis

• Acute onset of dyspnea, pleuritic chest pain, tachypnea, tachycardia
• Hypoxemia with widened A-a gradient
• Pulmonary angiogram is gold standard

General Considerations

A variety of clinical conditions may cause clots to form in the venous system that when dislodged will cause pulmonary emboli (Table 33–3). Venous thrombosis may result from a generalized hypercoagulable state, venous endothelial injury, or local stasis (Virchow triad). Clots that cause clinically significant pulmonary emboli form most commonly in the iliofemoral and pelvic venous beds. Pulmonary embolization, from veins of the upper extremities or distal lower extremities, is unusual and rarely clinically significant.

When embolization occurs, the manifestations depend on the size of the embolism, the patient's underlying cardiorespiratory status, and whether subsequent infarction of pulmonary tissue occurs. With small to medium sized emboli, obstruction of a localized portion of the pulmonary vascular tree causes local atelectasis with resulting ventilation–perfusion (V/Q) abnormalities and hypoxemia. Reflex hyperventilation with resultant hypocapnia and tachycardia also occurs. With massive embolization (obstructing over 60% of the vascular bed), acute pulmonary hypertension, right heart strain, systemic hypotension, and shock may also occur. Pulmonary emboli may also present with sudden cardiovascular collapse and death.

Clinical Findings

Symptoms and Signs

The illness often begins abruptly, and a predisposing underlying condition is almost always present. Dyspnea and chest pain are the usual presenting symptoms. Tachycardia and hypoxia are the most common clinical signs. Fever, hypotension, cyanosis, pleural friction rub, and pulmonary consolidation may be the result of PE but are usually the result of other illnesses when they occur.

Laboratory and Other Findings

Chest X-Ray

The chest X-ray is abnormal in most patients with pulmonary embolization with infarction but the abnormalities are often nonspecific (eg, atelectasis, pleural effusions, small infiltrates). The Westermark sign (dilated pulmonary vasculature proximal to embolus with oligemia distal) and Hampton's Hump (a pleural-based density with a rounded border facing the hilum) are more suggestive though uncommon findings with pulmonary emboli.

Electrocardiogram

The electrocardiogram is often abnormal, usually demonstrating tachycardia or diffuse nonspecific ST-T abnormalities. The classic finding of acute right heart strain (S1/Q3/T3; T-wave inversion in leads V1–V3) is more specific but somewhat uncommon.

Arterial Blood Gases

A clinically significant PE is usually but not always associated with hypoxemia (oxygen saturation < 90%; Po2 < 80 mm Hg). Hyperventilation and hypocapnia are also common findings. An arterial puncture is required to measure the arterial Pco2 and calculate an alveolar-arterial oxygen gradient (A-a gradient). The value of the A-a gradient over the more easily measured oxygen saturation by pulse oximetry is minimal. Most of the time the additional time, discomfort and expense is not justified by any additional discriminatory ability of the A-a gradient.

D-Dimer

The serum levels of the D-dimer (a degradation product of crosslinked fibrin) have been shown to be a highly sensitive (95%) screening examination for the formation of acute thrombus. The test is nearly always positive in patients with recent trauma or surgery or any process that produces bleeding and requires hemostasis. In patients who are at low risk for PE (low pretest probability) a negative test can be helpful in ruling out PE. Patients who are not at low risk should undergo a more definitive test such as CT scanning.

Geneva Score

The Geneva score is a clinical decision tool that can be used in the diagnostic evaluation of patients with suspected PE. The original score was revised to preclude the need for arterial blood gasses. The revised and simplified Geneva score (Table 33–4) has the same diagnostic utility as the original score and its calculation is more reliable. A simplified score of 0-2 indicates the patient is unlikely to have a PE and when combined with a normal D-dimer test, the clinical probability of a PE is 3% or less.

Diagnostic Imaging

Contrast-Enhanced CT Scan

Contrast-enhanced CT scan allows for rapid evaluation and is accurate but requires intravenous contrast enhancement and expert radiographic interpretation. The technology has improved in recent years and now includes automated bolus injection and fast, high-resolution, multislice CT scanners. CT scanning also provides a wealth of information regarding other chest pathologies, such as pneumonia, pleural effusion, masses, and vascular pathology, such as aneurysms. Contrast allergy is sometimes an issue. Pretreatment with steroids and antihistamines can be done if a contrast allergy is suspected and the study is necessary.

Ventilation–Perfusion Radionuclide Lung Scan (V/Q Scan)

V/Q scanning has been replaced with contrast-enhanced CT scanning except in cases of contrast allergy. A normal perfusion scan essentially excludes significant embolization. In many patients the perfusion scan will not be normal (most commonly with COPD) and the ventilation scan is used to look for areas of mismatched ventilation and perfusion. A high-probability V/Q scan is defined as a large perfusion defect in areas of normal ventilation and is highly specific (but insensitive) for acute pulmonary emboli. An indeterminate V/Q scan (also reported as nondiagnostic, low probability, or intermediate probability) is more difficult to use clinically.

Venous Doppler Ultrasound

Doppler ultrasound is a noninvasive test used in the diagnosis of deep venous thrombosis. The test is sensitive and specific. A positive venous Doppler lends supportive evidence that the patient has thrombosis; however, thrombosis can occur without embolization. Many patients with significant pulmonary emboli are asymptomatic in their lower extremities and have negative lower extremity Doppler studies.

Pulmonary Angiogram

The diagnostic accuracy of pulmonary angiography is considered to be the best of any procedure available. Frequently, CT images are convincing enough to be considered pathognomonic and in that case angiography does not offer a diagnostic advantage. Angiography requires right heart catheterization, which is usually done only as part of thrombolytic treatment for patients hemodynamically compromised by the size of the embolus.

Treatment

Hemodynamic Support

Correct hypoxemia with supplemental oxygen. Patients with large emboli may be hypotensive and require resuscitation with intravenous fluids. Pressors and positive pressure ventilation are poorly tolerated and should be avoided unless absolutely necessary.

Anticoagulation Therapy

Anticoagulation is the standard treatment and should be administered as soon as the diagnosis of pulmonary embolization is made. If a delay in diagnosis is anticipated and there are no contraindications, patients may be treated presumptively. This most often occurs when CT scanning is not available and the patient must be transferred to another institution or held overnight.

The usual dose of unfractionated heparin (UFH) is an initial 80 IU/kg bolus followed by 18 IU/kg/h infusion. Many institutions have protocols for heparinization and the use of one is recommended. Low-molecular weight heparin (LMWH) (enoxaparin 1 mg/kg SC q 12 hours or dalteparin 200 units /kg/day SC divided qd to BID) and fondaparinux(a factor Xa inhibitor) 7.5 mg SC qd are as effective and safe as UFH and are more convenient. Compared with UFH, LMWH and fondaparinux are more expensive medications but may reduce the total hospital cost and length of stay.

Thrombolytic Therapy

Although anticoagulation is sufficient treatment for most patients with pulmonary emboli, a few patients who present with hemodynamic compromise may benefit from thrombolytic therapy via a pulmonary artery catheter. Peripherally administered thrombolytic treatment has not been shown to be of value.

Surgical Treatment

A transvenous catheter embolectomy or open surgical embolectomy may be a lifesaving maneuver in a patient with massive emboli and refractory hypotension. The usual indication for a vena cava filter is the failure of anticoagulation to prevent thromboembolism.

Disposition

Hospitalize all patients for continued anticoagulation and supportive care. Patients with hemodynamic impairment, or those receiving thrombolytics, should be monitored in the ICU. Patients in whom PE is strongly suspected should be hospitalized for anticoagulation (if no contraindications are present) until a definitive diagnosis can be made.

Hemoptysis

General Considerations

The most common cause of hemoptysis, bronchitis, is primarily a diagnosis of exclusion. The more significant causes such as cancer, tuberculosis, and autoimmune disorders such as Goodpasture's syndrome are uncommon but still deserve consideration in the patient who admits to coughing up blood. A list of conditions that cause hemoptysis is discussed in Table 33–5. Massive hemoptysis is defined in terms of volume as 200–600 cc in 24 hours. This broad range is in part a manifestation of the difficulty of measuring the volume of expectorated blood. Many patients with life-threatening hemopysis are elderly and have associated co-morbid conditions.

Clinical Findings

History

Hemoptysis is the coughing of blood. This needs to be clearly differentiated from the vomiting of blood (hematemesis) as the diagnostic approach is different. If a patient complains of spitting blood, this may mean that the blood is not being coughed into the oropharynx. The blood may be from the mouth, nose, or nasopharynx and not of tracheobronchial origin. It is important to clarify a history of spitting blood.

Physical Examination

The vital signs are important as is the presence of pallor or cyanosis. Physical findings in the chest are generally nonspecific but may indicate the presence of effusions, pulmonary masses, or airspace disease such as that due to bloody fluids in the alveoli. The heart examination may be abnormal due to the presence of a cardiovascular cause of hemoptysis such as mitral stenosis.

Laboratory Evaluation

Patients who appear pale or report significant blood loss should be evaluated for anemia. Coagulation studies should be obtained on patients who take warfarin or have liver disease and blood gases on patients in severe respiratory distress.

Imaging

A chest X-ray is an important study in patients with hemoptysis. CT scanning of the chest should be considered in the diagnostic evaluation if the initial plain film is abnormal and nondiagnostic. Angiography may be necessary if bleeding is massive and offers the possibility of treatment via embolization.

Treatment

Treatment of hemoptysis in the emergency department usually is limited to general supportive care. An upright position is preferred. If the patient must be recumbent they should be positioned with the radiographically normal (presumably nonbleeding) lung up. If intubation is necessary large-bore endotracheal tubes (greater than 7.5) are helpful in facilitating fiberoptic bronchoscopy.

Bronchoscopy

Rigid bronchoscopy and selective intubation of the nonbleeding lung should be considered if bleeding is massive. The use of a double-lumen tube may be preferable but is technically more challenging. Endobronchial therapy during bronchoscopy may be successful in controlling the bleeding.

Interventional Radiology

Ninety per cent of massive hemoptysis is due to bleeding from the bronchial rather than the pulmonary circulation. Selective embolization of the involved bronchial arterial segment is effective in controlling the bleeding in about 90% of patients. The major risk of this technique is spinal cord ischemia, which may be minimized by selective techniques that avoid embolization of the anterior spinal artery.

Surgical Treatment

Surgical resection of the involved lobe or pulmonary segment may be necessary but depends on a localized site of bleeding. The patient must have adequate pulmonary reserve, have focal disease, and be an acceptable surgical candidate.

Disposition

Massive hemoptysis requires ICU admission and a team approach involving the pulmonologist, interventional radiologist, and the thoracic surgeon. Most patients with minimal degrees of hemoptysis due to bronchitis can be managed as outpatients. Patients who are suspected of having pulmonary tuberculosis should be isolated and treated presumptively until definitive studies can be completed.

Pulmonary Arterial Hypertension (PAH)

General Considerations

Essentials of Diagnosis

• Exertional shortness of breath or syncope
• Absence of congestive changes on chest X-ray
• Loud pulmonic closure, P2

Pulmonary hypertension may be secondary to another lung disorder such as COPD, left-sided heart disease, or recurrent pulmonary thrombo-embolic disease. Pulmonary arterial hypertension (PAH) is a diagnosis category that is not a secondary result of the aformentioned causes but does include familial types and those associated with collagen vascular diseases such as scleroderma, HIV infection, and toxic exposures. Anatomically this disorder is characterized by the remodeling of the pulmonary circulation with occlusion of the lumen in the medium-sized and small pulmonary arteries. The afterload of the right ventricle increases as this occurs which causes an obstruction to flow in the pulmonary arterial tree and increases the pressure as the right ventricle attempts to compensate.

Clinical Findings

Symptoms and Signs

Common symptoms are shortness of breath especially with exertion. Exertional syncope may also be a presenting complaint. Pulmonary venous hypertension from congestive heart failure causes shortness of breath while lying flat while PAH typically does not. A loud pulmonic closure, P2 may be present on auscultation. Peripheral edema may occur.

Imaging and Laboratory Findings

PAH, may be suspected, may be identified with echocardiography but diagnosis requires measurements of pressure and flow with a Swan-Ganz catheter. Pulmonary artery wedge pressure should be less than 15 mm Hg and the pulmonary artery pressure greater than 25 mm Hg to make the diagnosis.

Treatment and Disposition

Phosphodiesterase Type 5 Inhibitors

Phosphodiesterase type 5 inhibitors were first developed to treat erectile dysfunction but also are effective in patients with PAH who have symptoms that are mild to moderately severe. Sildenafil is marketed as Revatio(TM) when used to treat PAH instead of Viagra(TM), and tadalafil is marketed as Adciraca(TM) instead Cialis(TM) for this indication.

Prostaglandins

In severe disease epoprostenol (synthetic prostacyclin, marketed as Flolan(TM)) is indicated. Since the drug lasts only 3–5 minutes it must be administered by continuous infusion via a central venous catheter. These patients may be seen in emergency situations with complications from the indwelling catheter but the major issue is that the interruption of the infusion may cause rapid reversal of symptoms. This can be life threatening. Immediate consultation with the patient's pulmonologist should be obtained if this is suspected.

Pneumothorax

See also Chapters 13 and 24.

Essentials of Diagnosis

Pneumothorax

• Pleuritic chest pain
• Acute-onset dyspnea
• Decreased breath sounds on affected side
• Evidence of lung collapse on chest X-ray

Tension Pneumothorax

• Displaced PMI
• Shift of the trachea
• Jugular venous distension

General Considerations

Pneumothorax is the abnormal collection of air within the pleural space. This condition may be classified as either spontaneous (primary or secondary), traumatic, or iatrogenic. Pneumothorax may also be either simple or under tension and further classified as either primary (not associated with underlying lung disease) or secondary to some other disease in the lung.

Primary spontaneous pneumothoraces occur in patients without clinically apparent lung disease (often young, tall men, aged 20–40 years, who usually smoke). Secondary pneumothoraces are a complication of preexisting underlying pulmonary disease such as COPD, pneumonia particularly Pneumocystis jirovecii pneumonia, cystic fibrosis, asthma, or tuberculosis. Traumatic pneumothoraces are due to either blunt or penetrating chest trauma. Iatrogenic pneumothorax may occur during subclavian line placement, thoracentesis, or following lung or pleural biopsy. Pneumothorax may also result from barotrauma during positive pressure ventilation.

Clinical Findings

Symptoms and Signs

Patients usually present with pleuritic chest pain but may also have tachypnea and shortness of breath. Breath sounds are diminished on the affected side. Pneumothorax under tension may cause severe respiratory compromise and cardiovascular collapse. Other clinical findings include tracheal deviation and displacement of the point of maximal impulse (PMI) to the opposite side.

Imaging and Laboratory Findings

Plain chest X-ray (frontal view) is usually diagnostic. Expiratory films may demonstrate small pneumothoraces that are not visible on inspiratory films. Chest CT will often be helpful in identifying associated pathology, such as pneumocystis pneumonia or differentiating pneumothorax from emphysematous blebs in patients with COPD.

Treatment and Disposition

Primary Spontaneous Pneumothorax

A small pneumothorax will usually resolve without treatment. Supplemental oxygen increases the rate of reabsorption slightly and is appropriate during a short period of observation in the emergency department. Patients may also be treated with small-bore catheter attached to a Heimlich valve. Patients with Heimlich valves may be candidates for outpatient treatment provided adequate follow-up arrangements can be made. If the pneumothorax fails to re-expand then a 24F–28F standard chest tube attached to water seal will be required.

Secondary Spontaneous Pneumothorax

Patients with secondary pneumothorax in general, will require standard chest tube drainage with a water seal device and admission to the hospital. The underlying illness often requires additional intervention such as antibiotics, surgery, or additional diagnostic evaluation.

Traumatic Pneumothorax

Most patients with traumatic pneumothorax have associated hemothorax that requires large chest tubes and water seal drainage with suction. The initial tube when hemothorax is suspected should be 32F or larger. The frequent use of chest CT in trauma patients has resulted in some small pneumothoraces being identified. Some of these patients may be placed under observation without chest tubes if positive pressure ventilation is not required.

Tension Pneumothorax

Tension pneumothorax is produced if air continues to enter the pleural space with a valve preventing its exit. This is most common in patients with traumatic pneumothorax. Patients with tension pneumothorax should be treated with immediate decompression and not wait for radiographic confirmation. The best approach, if time permits, is tube thoracostomy. If the patient is in extremis, then needle decompression may be performed with a 14–16-gauge needle inserted in the second intercostal space at the midclavicular line. Such patients will subsequently need tube thoracostomy drainage to a water seal device.

Pneumomediastinum

General Considerations

Pneumomediastinum is gas in the mediastinum outside the lumen of the esophagus or airways of the tracheobronchial tree. This occurs most commonly from ruptured aveoli when the gas dissects centrally along the bronchovascular interstitial sheaths. This is common in asthmatics but also occurs in blunt trauma and occasionally with forceful coughing. Pneumomedistinum also occurs in patients that Valsalva while smoking illicit substances such as crack cocaine. In such situations, pneumomedistinum is benign and the clinician's attention is appropriately focused on the underlying condition. Gas can enter the mediastinum from lacerations of the GI tract particularly the esophagus or from air containing structures in the head or neck. Air may dissect into the medistinum from ruptured retroperotneal structures in the abdomen including the rectum or from a perforated diverticulum.

Clinical Findings

The only specific physical sign of pneumomedistinum is Hamman's crunch, a crunching sound heard over the heart on auscultation of the chest. Otherwise pneumomedistinum is essentially a radiologic diagnosis identified by lucent streaks of gas that outline mediastinal structures. These include the medistinal pleura, the trachea and its branches or the pulmonary artery or aorta. Sometimes pneumomediastinum is more obvious on the lateral than on the frontal view of the chest. Mediastinal gas may also be seen outlining the superior surface of the diaphragm and separating it from the heart. Boerhaave's syndrome is rupture of the esophageal wall due to vomiting. The typical patient develops severe retrosternal chest pain after retching and vomiting often in the setting of heavy alcohol use.

Treatment and Disposition

The treatment of pneumomedistinum is always directed at the underlying disorder whether it be asthma, trauma, or drug abuse. Esophageal rupture as in Boerhaave's syndrome is a fatal disorder without prompt thoracotomy, esophageal repair and wide medistinal drainage. Tracheobronchial rupture must be recognized quickly because continued attempts to ventilate the lungs may force additional air into the medistinum with resultant compression and displacement of other medistinal structures.

Pleural Effusion

Essentials of Diagnosis

• Pleuritic chest pain, dyspnea with or without fever, cough
• Decreased breath sounds, decreased tactile fremitus on affected side
• Thoracentesis is definitive diagnostic and often therapeutic procedure

General Considerations

Pleural effusions are an abnormal collection of fluid between the parietal and visceral pleura as a result of a local disease process or inflammation. Normally 5–15 mL of serous fluid is present in the pleural space. An effusion can be classified as either an exudate or transudate to help in differential diagnosis. Exudative fluid analysis reveals (1) pleural fluid protein to serum protein ratio greater than 0.5, (2) pleural fluid lactate dehydrogenase (LDH) to serum LDH ratio greater than 0.6, and (3) pleural fluid LDH greater than two-third of the upper limit of normal serum LDH. Exudates are associated with direct disease of the pleura itself usually from infection, inflammation, or malignancy. Transudates do not have the above-mentioned characteristics and are most commonly caused by congestive heart failure, cirrhosis with ascites, or nephrotic syndrome. Every patient with a newly diagnosed pleural effusion requires prompt evaluation to determine the cause so that early and appropriate therapy can be given.

Clinical Findings

Symptoms and Signs

The patient may complain of pleuritic or nonpleuritic chest pain or dyspnea. Chest examination discloses dullness, decreased breath sounds, and decreased tactile fremitus on the involved side. Large effusions may cause hypoxia and respiratory distress by compressing adjacent lung tissue and limiting expansion of the remaining lung.

Imaging

Upright posteroanterior and lateral chest X-ray can demonstrate pleural fluid in most cases if more than 250 mL of fluid is present (eg, blunting of costophrenic angles). Decubitus films are useful to demonstrate the presence of free flowing pleural fluid suitable for removal by thoracentesis. CT scanning of the chest can be helpful to identify small effusions and identify associated pathology such as pneumonia, tumors, or pulmonary emboli.

Treatment

Oxygen

If dyspnea is present, obtain pulse oximetry or blood gas measurements, and begin supplemental oxygen by mask or nasal cannula.

Thoracentesis

If the chest X-ray shows a large fluid accumulation (ie, most of one hemithorax), and the patient is in respiratory distress, thoracentesis with removal of fluid should be considered for relief of symptoms. Reexpansion pulmonary edema rarely occurs but is a risk of this procedure and should be treated in similar fashion to acute cardiogenic pulmonary edema if it occurs. Recovered fluid should be sent for cell counts, protein, LDH, glucose, and pH. Pleural fluid cytology should be considered if undiagnosed malignancy is a consideration. If the patient is not in distress, thoracentesis may be deferred until after hospital admission.

Empyema

Infection of a pleural effusion is an empyema, literally a purulent effusion. In addition to antibiotic therapy, an empyema will require chest tube drainage if the fluid is grossly purulent or the gram stain is positive. Drainage is also indicated if the pH is < 7.0. If the pH is between 7.0 and 7.2 the management of the effusion should be individualized and repeat thoracentesis considered in 24 to 48 hours.

Disposition

All patients with unexplained pleural fluid accumulations should be hospitalized for diagnosis and treatment. Stable patients with recurrent fluid of known cause (eg, metastatic cancer or heart failure) should be referred to their regular source of medical care or given treatment in the emergency department (eg, by thoracentesis) and discharged unless the underlying illness requires hospitalization.

Pneumonia and Bronchitis

Essentials of Diagnosis

Pneumonia

• Fever, productive cough, dyspnea, pleuritic chest pain
• Rales, rhonchi, wheezing, or hemoptysis
• Decreased breath sounds or dullness to percussion over affected lobe
• Infiltrate on chest radiograph

Bronchitis

• Cough associated with midline chest pain or burning
• Fever, dyspnea

General Considerations

Bronchitis is an inflammatory condition involving the tracheobronchial tree. The diagnosis of pneumonia implies the additional involvement of the pulmonary parenchyma and aveoli. The primary clinical difference between these two entities is the presence of an infiltrate on the chest X-ray in the case of pneumonia. Bronchitis in a patient without underlying lung disease should not cause hypoxia but pneumonia may if the consolidation of the pulmonary parenchyma is large. Fever may be present in both conditions but is more prominent in pneumonia.

Clinical Findings

Acute Bronchitis

Patients complain of cough, fever, and constitutional symptoms. The cough is initially dry but can become productive and is often associated with a midline chest pain or burning. Hemoptysis in small amounts is sometimes present. Rhonchi that clear with coughing is a characteristic finding. The presence of rales is more characteristic of pneumonic consolidation or other condition involving the pulmonary parenchyma such as pulmonary fibrosis. Laboratory tests are not helpful in making the diagnosis. Chest X-ray will show no evidence of infiltrate and is not indicated unless patients are dyspneic, hypoxic, or have significant comorbidities (eg, COPD, dementia). Cigarette smoking is a cause or contributing factor in many cases.

Pneumonia

Symptoms and Signs

Patients present with fever, dyspnea, cough, pleuritic chest pain, and increased sputum production Auscultation of the chest may reveal rales or rhonchi. There may be areas of dullness to percussion over an infiltrate. Bronchial breath sounds are a classic finding over a dense infiltrate that abuts the pleura.

Cultures and Serologic Testing

The results of blood cultures direct the therapy in only a minority of cases but are an important quality measure in patients admitted to the hospital. They should be obtained before antibiotics are given. Sputum gram stain and culture are needed only if an atypical cause is suspected.

Laboratory Evaluation

Some helpful tests include pulse oximetry and blood gas measurements, white cell count, hemoglobin and hematocrit (anemia), and a basic metabolic panel (dehydration, renal insufficiency). Screening for HIV, tuberculosis, Legionella, and Mycoplasma are appropriate for patients at risk for these diseases.

Treatment

Acute Bronchitis

Intravenous fluids should be given to patients who are significantly dehydrated and unable to tolerate oral fluids. Otherwise, treatment with antipyretics and cough suppressants are sufficient in uncomplicated cases. β-Adrenergic MDIs (albuterol) may improve symptoms even if wheezing is not present. Antibiotics are not recommended because the primary cause is likely viral. Many patients are smokers and need to be counseled regarding cessation.

Pneumonia

Community Acquired Pneumonia (CAP)

Outpatient antibiotic therapy for CAP is typically a macrolide antibiotic such as azithromycin or an extended spectrum fluoroquinolone such as levofloxacin. Doxycycline is an acceptable alternative. Each should be given for 7–10 days (except azithromycin, which is used for only 5 days). Patients who require admission should be started on (1) an extended spectrum fluoroquinolone or (2) a macrolide plus a β-lactam/β-lactamase inhibitor.

Health Care Associated Pneumonia (HCAP)

Patients who have a history of recent exposure to high risk area of the health care system (Table 33–6) fall into the category of HCAP. Pneumonia in this case is more likely to be caused by organisms such as hospital acquired methicillin-resistant Staphylococcus aureus (HA-MRSA) or Pseudomonas aeruginosa. Prompt administration of antibiotic therapy is important with a goal of within 6 hours of presentation to the emergency department. The selection of antibiotics is institution dependent but should adhere to published guidelines. As a general rule treatment requires combination therapy using an antipseudomonal cephalosporin, β-lactam, carbapenem or monobactam(aztreonam) plus an antipseudomonal fluoroquinolone or aminoglycoside plus an agent such as linezolid or vancomycin to cover MRSA.

Disposition

Patients should be hospitalized if they require oxygen or are unable to tolerate oral antibiotics. Vomiting or inability to maintain adequate oral intake of fluids with the need for intravenous fluids is another appropriate indication for hospital admission. Various severity indices such as the pneumonia severity score (PORT score) or CURB-65 score have been developed to predict morbidity and mortality in patients with pneumonia. These were not developed to predict the need for hospitalization but the elements that they enumerate such as advanced age, significant comorbidities, alteration of vital signs or alteration of mental status should be considered in the decision to hospitalize patients with pneumonia. Patients who require hemodynamic monitoring or blood pressure support with catacholamines will require ICU admission.

Pulmonary Tuberculosis

Essentials of Diagnosis

• Fever, weight loss, hemoptysis, night sweats
• Chest X-ray notes hilar adenopathy with parenchymal infiltrates, often upper lobes or apical
• Positive purified protein derivative (PPD) skin test with positive acid-fast bacilli on sputum smear
• Sputum culture for Mycobacterium tuberculosis is definitive diagnosis

General Considerations

Pulmonary infection is caused when susceptible individuals inhale aerosolized droplets infected with Mycobacterium tuberculosis. This disease was reestablished as a major concern in the United States in the mid-1980s when the incidence rose sharply. The major causes for this resurgence has been the HIV epidemic, immigration of people with undiagnosed tuberculosis from high-risk countries in Asia, Africa, and Latin America, previously established suboptimal antimicrobial regimens, and patient noncompliance. The goal in the emergency department is early diagnosis, treatment, and referral for these patients and to protect hospital staff via early patient isolation.

Clinical Findings

Tuberculosis should be considered in patients who present with pneumonia or cough and are members of one of the previously mentioned high risk groups.

Symptoms and Signs

The most common symptom that will call attention to the diagnosis of tuberculosis is a prolonged cough (more than 3 weeks) especially if bloody. Fever is also common, especially during the day with resolution at night. Night sweats are a typical complaint. Fatigue, malaise, and weight loss with anorexia are common. Patients frequently will appear chronically ill. Chest examination may be normal or rales may be present.

X-Ray Findings

Primary tuberculosis may appear on chest X-ray as parenchymal consolidation, atelectasis, pleural effusion possibly with paratracheal lymphadenopathy. A calcified Ghon complex is evidence of healed primary infection. Reactivation tuberculosis often has a predilection for the upper lobes. Immunocompromised patients, especially HIV patients, may present with a myriad of findings on the chest X-ray.

Laboratory Findings

Cultures and Serologic Testing

Tuberculosis is often identified with serologic tests that use nucleic acid amplication with a polymerase chain reaction for the detection of bacterial DNA (PCR tests). Sputum cultures require several weeks but are important because of the emergence of multidrug-resistant tuberculosis. Treatment will depend on susceptibility results. Definitive diagnosis in the emergency department is essentially impossible. For this reason, individuals who are suspected of having the disease should be placed on respiratory isolation to protect the health care workers that come into contact with the patient.

Tuberculosis Skin Testing

If a patient is suspected of having tuberculosis, an intradermal purified protein derivative (PPD) skin test can be administered. This test is not completed and read until 48–72 hours after administration so appropriate follow-up to evaluate the patient will need to be arranged. A positive test (varying diameters of circumferential skin induration depending on risk factors for the disease) indicates previous infection or active infection. Positive PPD tests should be followed with chest X-ray to evaluate for new or active disease. Severely immunocompromised patients or HIV patients may be anergic so skin testing may be unreliable.

Treatment

Confirmed or Suspected Tuberculosis

The treatment of active tuberculosis has been complicated by the emergence of drug-resistant organisms. Patients will require multidrug therapy if they are found to have active disease. Multidrug-resistant tuberculosis is defined as resistance to the two most effective first-line TB drugs: rifampicin and isoniazid. Extensively drug-resistant TB is also resistant to three or more of the six classes of second-line drugs.

Latent Tuberculosis

Latent tuberculosis occurs when patients have positive skin tests but negative chest X-ray and no clinical disease. These patients are at risk of reactivation tuberculosis and are generally treated with 9 months of isoniazid. Tuberculosis is still rare in the United States except in patients who are members of identified high risk groups. Patients at very low risk for tuberculosis should not be screened with skin testing because the problems associated with treating patients with false positive skin tests outweigh the potential benefit.

Reporting Requirements

The local health department must be informed of all cases of tuberculosis to ensure adequate care, availability of treatment resources, and compliance with therapy.

Disposition

Most patients with active disease are usually admitted with respiratory isolation for full workup and evaluation. The routine screening with skin testing for patients thought to be at risk can be utilized provided that the appropriate follow-up can be arranged. Intradermal skin tests will need to be read at 48 to 72 hours

Pulmonary Aspiration Syndrome

Essentials of Diagnosis

• High-risk patients with alteration of mental status
• Immediate respiratory difficulty due to chemical burn with, hypoxemia, rales, and wheezing
• Pulmonary infiltration either diffusely or in dependent areas of the lungs

General Considerations

Pulmonary Aspiration Syndrome

Aspiration of gastric contents will produce a chemical pneumonitis (Pulmonary Aspiration Syndrome) similar to that caused by any irritant that is inhaled or aspirated in significant quantities. Mechanical obstruction by aspirated food particles will further impair gas exchange. Pulmonary infection is not a part of the initial lung injury but may subsequently develop as a result of it. Pulmonary aspiration is a frequent cause or contributor to the development of the acute respiratory distress syndrome (ARDS).

Aspiration Pneumonia

Aspiration of oropharyngeal secretions is typically chronic and may cause a bacterial pneumonia characterized as aspiration pneumonia. The chest X-ray usually shows consolidation in the lung segments which were dependent at the time of aspiration. If the patient was supine the posterior segments of upper or apical segments of lower lobes are involved. The basal segments of lower lobes particularly the right lower lobe are involved if the patient was upright. In individuals with poor dental hygiene and large amounts of dental plaque this commonly results in anaerobic lung abscess.

Clinical Findings

Pulmonary aspiration syndrome occurring in the hospital may occur during anesthesia, cardiopulmonary resuscitation, or other procedures. Community-acquired cases are usually associated with trauma causing an alteration of mental status, drug overdose (including pronounced alcohol intoxication) or seizures. Sometimes vomiting and aspiration is a witnessed event. Within minutes to hours after aspiration, the patient develops productive cough; dyspnea; fever; leukocytosis; and rales on chest auscultation. Chest X-ray shows pulmonary infiltrates which are generally diffuse, although dependent segments of the lung (especially the right lower lobe) are more commonly involved. Food particles may be present on gross examination of sputum. The condition should be considered at least initially to be an inflammatory process in the lung not an infectious one.

Treatment

Provide respiratory support (eg, supplemental oxygen) as necessary on the basis of arterial blood gas measurements (or pulse oximetry) and clinical findings. If the patient has significant dyspnea or respiratory distress, immediately establish airway control with intubation and mechanical ventilation. Witnessed aspirations should be treated by prompt oropharyngeal and tracheal suctioning. Acute obstruction of the upper airway should be treated immediately with the Heimlich maneuver. Retained, aspirated foreign bodies (greatest risk in children) often necessitate bronchoscopy for final diagnosis and removal. Corticosteroids have not been demonstrated to be helpful and may increase susceptibility to infection. Antibiotics for aspiration pneumonia should be given if infection occurs and not for prophylaxis following an episode of aspiration.

Disposition

All patients should be hospitalized for observation and treatment.

Acute Lung Injury and Acute Respiratory Distress Syndrome

Essentials of Diagnosis

• Recent known exposure to high-risk systemic or pulmonary etiologic agent
• Acute-onset of impaired gas exchange with a gradient between the inspired and arterial po2 (Pao2/FiO2 < 300 for acute lung injury and Pao2/FiO2 < 200 for ARDS)
• No chemical evidence of cardiogenic or volume overload pulmonary edema (pulmonary capillary wedge pressures < 18 mm Hg)
• Chest X-ray shows diffuse bilateral infiltrates

General Considerations

Acute lung injury is defined as the acute onset of impaired gas exchange with a widened gradient between inspired and arterial po2 (Pao2/FiO2 < 300) and the presence of bilateral alveolar or interstitial infiltrates and the absence of congestive heart failure. The ARDS is used in acute lung injury when the impairment of oxygenation is severe (PaO2/FiO2 < 200). These conditions are characterized by diffuse alveolar damage and increased permeability of the alveolar–capillary membrane. Edema fluid and plasma proteins leak from the vasculature into the alveolar spaces. The primary result of this is impaired gas exchange principally involving oxygen. Any process that causes diffuse alveolar damage may cause this syndrome. Common causes presenting the emergency department are sepsis with or without a pulmonary focus, trauma, pulmonary aspiration syndrome, and thermal or chemical inhalation injury to the lung. Severe systemic illnesses such as pancreatitis and burns may cause this syndrome as can multiple blood transfusions. It is important to avoid overzealous fluid administration in these patients as this may aggravate the exudation of fluid into the aveoli. Over distension of the lung during positive pressure ventilation may also aggravate the injury to the lung particularly in children.

Clinical Findings

Symptoms and Signs

The symptoms of the underlying illness are complicated by the impairment of oxygenation. If hypoxia is uncorrected then this may contribute impairment of essential metabolic functions such as the maintenance of cardiac output. The chest X-ray will also demonstrate the opacity caused by the increase of fluids in the aveoli. Rales are the primary physical findings on auscultation of the chest. Heavy wet lungs increase the work of breathing and will increase the patients sense of dyspnea and malaise and make ventilation more difficult in the intubated patient.

Imaging and Laboratory Findings

Chest imaging always shows extensive infiltration depending on the inciting event. Most often opacity is diffuse and bilateral. Other processes such as pleural effusions and fractured ribs in trauma patients are common. The presence of pneumonia or PE may be present and very difficult to ascertain. If hypoxia is uncorrected then this will contribute to anaerobic metabolism and a lactic acidosis. Carbon dioxide exchange is much less affected and the pco2 may be normal or a respiratory alkalosis may develop as ventilation is increased to attempt to compensate for hypoxemia. Pulmonary artery occlusion pressures (pulmonary capillary wedge pressures) less than or equal to 18 mm Hg are consistent with acute lung injury and not fluid overload. All these patients are significantly stressed by their illness and the WBC count will usually be greatly elevated even in the absence of infection.

Treatment

Provide Respiratory Support

Supplemental Oxygen

Provide high initial oxygen concentration (FiO2 = 50–100%), continue to monitor oxygen saturation with pulse oximetry, and titrate to the lowest FiO2 to keep oxygen saturation greater than 90%.

Intubation and Mechanical Ventilation

Use low tidal volumes and permissive hypercapnia to limit peak airway pressures (Table 33–2).

Maintain Circulation

Avoid both dehydration and vigorous hydration. Central venous pressure monitoring is indicated and the CVP pressure should be kept between 8 and 12 mm Hg.

Treat Underlying Clinical Cause

Prompt evaluation with rapid identification of the underlying cause is paramount for the survival of these patients. Specific treatment for the inciting disorder (most commonly sepsis) should begin as soon as possible in the emergency department.

Disposition

Hospitalize all patients who meet the criteria for ARDS severe (PaO2/FiO2 < 300) in the ICU. Almost all these patients will require intubation. Mild forms of acute lung injury often progress despite appropriate therapy and worsening of oxygenation should be anticipated.

Cystic Fibrosis

Clinical Findings

Cystic fibrosis is an autosomal recessive disease, which causes thick and viscous mucus with subsequent obstruction and damage to organs with exocrine function. Patients will have a history of chronic lung disease with a gradual decline in pulmonary function, pancreatic insufficiency, and gastrointestinal complaints. Most symptoms of disease and many complications develop at an early age (2–20 years). Pulmonary disease is characterized by chronic infections with multiple organisms, with periodic acute exacerbations with increased sputum production and cough. Staphylococcus aureus and Haemophilus influenza are prevalent during childhood. Most patients eventually develop chronic infection with Pseudomonas aeruginosa or other virulent gram-negative organisms.

Treatment

Pulmonary Infections

Antibiotic therapy is used to treat acute exacerbations of lung disease, either orally, parenterally, or via inhalation. Maintenance therapy with macrolide antibiotics particularly azithromycin has been shown to improve pulmonary function and reduce the number of respiratory exacerbations.

Other Therapy

Short-acting inhaled β-2-adrenergic receptor agonists are helpful especially in patients known to respond to them. Additional treatments include DNase I (dornase alfa) and hypertonic saline via nebulizer. High-dose ibuprofen is helpful in children and young adolescents with good lung function. Severe cystic fibrosis lung disease is a common indication for lung transplantation.

Disposition

Patient with cystic fibrosis are best treated in close consultation with the patient's pulmonologist. Hospitalization is a particular problem in these patients because of the problem of antibiotic resistance in the hospital environment.

Interstitial Pulmonary Disease

General Considerations

A variety of conditions may produce diffuse progressive pulmonary interstitial inflammation and fibrosis, including drugs, pneumoconiosis, collagen diseases, sarcoidosis, organic and inorganic dusts, and illnesses of unknown cause with pathologic features involving chiefly the lungs (eg, idiopathic interstitial fibrosis). Most of these illnesses are relatively uncommon. The principal feature of all of them is that dyspnea begins gradually and seldom occurs acutely without a background of increasing shortness of breath. When dyspnea of acute onset does occur, it is often due to inter-current illness (eg, pulmonary infection). Patients also have pulmonary function tests that demonstrate restrictive lung dysfunction and impaired gas exchange.

Clinical Findings

Many patients with interstitial pulmonary disease will know their diagnosis; if not, it can seldom be made with certainty in the emergency department setting, because lung biopsy or bronchoalveolar lavage is often required.

Symptoms and Signs

Gradually increasing dyspnea, especially on exertion, is the only reliable symptom. Chest pain, cough, sputum production, and other symptoms may occur but are inconsistent. Physical findings are variable, but dry crackles (rales) at the bases of the lungs are common. Cyanosis and clubbing may be present as well.

Imaging

Chest X-ray usually shows interstitial infiltrates. Prior chest X-rays are helpful to identify chronic interstitial disease (interstitial fibrosis). CT scan of the chest is also helpful in assessing these patients. Other changes may be present depending on the disease process (eg, hilar adenopathy in sarcoidosis, conglomerate fibrosis in silicosis).

Treatment and Disposition

Provide respiratory support as needed, and treat inter-current disease (eg, infection). Hospitalize patients with respiratory failure or recent marked worsening of symptoms or those in whom acute infection is suspected. Refer all patients not already under care to a pulmonary disease specialist. Early lung transplantation offers a surgical therapeutic option for selected patients.