monia in adults. Clin Infect Dis. 2007;44:S27-72.

Nazarian DJ, Eddy OL, Lukens TW, et a!. Clinical policy: Critical

issues in the management of adult patients presenting to the

emergency department with community-acquired pneumonia.

Ann Emerg Med. 2009;54:704-73 1.

Pneumothorax

Michelle Sergei, MD

Brian Krieger, MD

Key Points

• Tension pneumothorax is a clinical diagnosis that should

be considered in any patient with shock and respiratory

distress. Treatment should not be delayed for radiologic

confirmation.

• Appropriate treatment of a tension pneumothorax is a

needle thoracostomy, followed by tube thoracostomy.

INTRODUCTION

Pneumothorax is an accumulation of air within the pleural

space. Spontaneous pneumothorax is acquired in the

absence of trauma. A primary spontaneous pneumothorax

is found in patients without underlying pulmonary pathology. A secondary spontaneous pneumothorax is found in

patients with underlying lung disease and damage to the

alveolar-pleural barrier (most commonly seen with chronic

obstructive pulmonary disease [COPD] or asthma).

Spontaneous primary pneumothoraces have the

greatest incidence of occurrence in young adults. They

are more common in males than females (6:1), greater

height-weight ratios, and smokers. Smoking is the most

important modifiable risk factor, with a lifetime risk of

12% compared with 0. 1 o/o in nonsmokers. Spontaneous

secondary pneumothoraces are most common in patients

older than 40 years with COPD. Recurrence rates range

from 30-45%.

The parietal pleura lines the thoracic cavity and closely

adheres to the visceral pleura, which surrounds the lungs.

The potential area between these 2 layers is known as the

pleural space. If air accumulates within this potential

space, the pressure causes the thoracic cavity to expand

and the lung to collapse, creating a pneumothorax.

• Unless a pneumothorax is spontaneous, small ( <20%),

minimally symptomatic, and prima ry, definitive

treatment is tube thoracostomy.

Secondary spontaneous pneumothoraces are the result of

a damaged alveolar-pleural barrier or underlying lung

problems that cause an increase in intrabronchial pressures. Tension pneumothoraces occur when air enters the

pleural space on inspiration but cannot escape on expira ­

tion (known as ball-valve effect). There is progressive

accumulation of air in the pleural space, resulting in collapse of the affected lung and shift of the mediastinal

structures to the opposite side. This ultimately causes

compression of the contralateral lung, impairment of

venous return, decreased cardiac output, and signs of cardiovascular collapse requiring immediate intervention

with a needle thoracostomy.

CLINICAL PRESENTATION

� History

Symptoms can vary, but are predicated on the pneumothorax size, rate of formation, and cardiorespiratory reserve. A

typical history includes a sudden onset of ipsilateral pleuritic chest pain and/or dyspnea with a nonproductive

cough. Patients, however, range from clinically silent to

agitated, restless, altered mental status, and/or cardiac

arrest if severe respiratory compromise is present.

1 05

CHAPTER 24

..... Physical Examination

The physical examination can range from unremarkable to

a patient in shock. Vital signs typically include a mild

tachycardia and tachypnea, although only 5% of patients

have a respiratory rate greater than 24. Findings on the

lung examination may be subtle if there is a small pneumothorax. Decreased breath sounds occur in 85%, whereas

hyperresonance to percussion occurs in less than 33%.

Patients with tension pneumothorax present in extremis

with hypotension, cyanosis, severe respiratory distress, and

tracheal deviation to the contralateral side.

DIAGNOSTIC STUDIES

..... Laboratory

Laboratory studies do not assist in making the diagnosis of

pneumothorax, but may be helpful in evaluating other

causes of the patient's symptoms.

.... Imaging

A standard inspiratory posteroanterior chest x-ray (CXR)

is obtained initially. The edge of the collapsed lung runs

parallel to the chest wall, and lung markings cannot be

identified beyond that border (Figure 24-1). The size of the

pneumothorax can be roughly estimated as a percentage

with each centimeter equal to approximately 10% decreased

lung volume. Pneumothoraces > 2 em are considered large.

If a pneumothorax is not seen on the film, but still highly

suspected, an expiratory, lateral, and/or decubitus film may

help. The intrapulmonary pressure is decreased during

expiration, causing decreased lung volumes and a relative

increase in the size of the pneumothorax. Computed

Figure 24-1. Complete pneumothorax of the left lung.

tomography (CT) has higher sensitivity for the detection

of pneumothoraces, especially in the supine patient. CT

also has high specificity in differentiating bullae from

pneumothoraces. Patients with pneumothoraces identified

solely on a CT, however, uncommonly require treatment.

Ultrasonography is another modality to detect a pneumothorax that capitalizes on changes in artifact when comparing normal lung with collapsed lung. The utility of

ultrasound, however, is vastly tied to the ability of the

operator.

PROCEDURES

Needle decompression is performed if a tension pneumothorax is suspected. Using a long 14- or 16-gauge angiocatheter, puncture the second intercostal space at the

mid-clavicular line on the affected side. A gush of air will

be heard, as the hemodynamics improve. Ultimately, a tube

thoracostomy must be placed. Tube thoracostomy is discussed in detail in Chapter 7.

Complications include re-expansion pulmonary edema,

extrapleural placement, intraparenchymal placement,

empyema, and penetration of solid organs.

MEDICAL DECISION MAKING

Suspicion for a pneumothorax begins with the history and

physical examination. If a pneumothorax is suspected, the

vital signs are critical in the medical decision making.

 

Stable vital signs allow time for chest radiographs, confirming the diagnosis. Pneumothorax with hypotension

equates to a tension pneumothorax requiring needle tho ­

racostomy followed immediately by tube thoracostomy

(Figure 24-2).

TREATMENT

Oxygen is a mainstay of treatment. Reabsorption, normally

occurring at a rate of 1-2% per day, is hastened with 02

(3-4 L/min increases the rate 4-fold). Tube thoracostomy

is indicated in patients with secondary spontaneous pneumothoraces; those greater than 20% in size or expanding

pneumothoraces; bilateral or tension pneumothoraces;

those associated with significant symptoms; or in patients

requiring positive pressure ventilation or air transport.

Small ( <20%) pneumothoraces can be observed and

the patient can be discharged if there is no progression

seen on a CXR repeated after 6 hours. Failure rates, defined

by the eventual need for tube thoracostomy, with observation alone are as high as 40%.

Catheter aspiration reduces a moderate to large pneumothorax to a small one that will resolve on its own. A

CXR is needed immediately after aspiration and again

6 hours later to verify successful aspiration and to ensure

that there is no reaccumulation of air. Catheter aspiration

decreases length of stay without affecting mortality or

complications.

PNEUMOTHORAX

I nspiratory and

expiratory CXR Tension pneumothorax

Perform needle thoracostomy

Administer 02;

observe, aspirate, or

insert chest tube

Tube thoracostomy

.A. Figure 24-2. Pneumothorax diag nostic algorithm. CXR, chest x-ray.

A trend toward discharging patients after insertion

of a small-bore catheter with a small 1 -way valve

attached (ie, Heimlich valve) has emerged. After consultation with a specialist (cardiothoracic surgeon or pillmonologist) , discharge is either completed after an

observation period or immediately with a next-day

follow-up appointment.

DISPOSITION

� Admission

If a chest tube is inserted, patients are admitted to the hospital. The chest tube must be attached to a water seal and

vacuum device (Pleur-Evac). Patient with small (<20%)

traumatic pneumothoraces that are managed conservatively are usually admitted for observation.

� Discharge

If the pneumothorax is small ( <20%) and patients are

healthy, reliable, and minimally symptomatic, they may

be observed. A second CXR 6 hours later should be

performed to ensure that there has been no change in the

size of the pneumothorax before discharge. Close followup with a specialist should be arranged. Patients must

avoid air travel until the pneumothorax shows complete

resolution.

SUGGESTED READING

Humphries RL, Young WF. Spontaneous and iatrogenic pneumothorax. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM,

Cydulka RK, Meckler GD. Tintinalli's Emergency Medicine: A

Comprehensive Study Guide. 7th ed. New York, NY: McGrawHill, 20 1 1, pp. 500-504.

Henry M, Arnold T, Harvey J. BTS guidelines for the management

of spontaneous pneumothorax. Thorax. 2003;58:ii39-ii52.

Kulvatunyou N, Vigayasekaran A, et al. Two-year experience of using

pigtail catheters to treat traumatic pneumothorax: A changing

trend. J Trauma Injury Infect Grit Care. 2011;71:1104-1 107.

Sahn SA, Heffner JE. Spontaneous pneumothorax. N Eng! f Med.

2000;342:868-874.

Wakai A, O'Sullivan R, McCabe G. Simple aspiration versus inter ­

costals tube drainage for primary spontaneous pneumothorax

in adults. Cochrane Database Syst Rev. 201 1;1:CD004479.

Pu l monary Embolism

Harsh Sule, MD

Key Points

• Consider pulmonary embolism (PE) in patients with

complaints of dyspnea, chest pain, hemoptysis, or

syncope.

• Dyspnea, pleuritic chest pain, or tachypnea is present in

92% of patients with PE.

INTRODUCTION

Pulmonary embolism (PE) is a potentially life-threatening

condition associated with a partial or complete obstruction of the pulmonary artery caused by a thrombus that

b

.

reaks off from a peripheral vein, migrates via the right

s1de of the heart, and lodges in the pulmonary artery

circulation. About 90% of emboli originate from venous

thrombi in the lower extremities and pelvis. The presence

of emboli in the pulmonary vasculature blocks normal

blood flow to the lung and increases pulmonary resistance. This, in turn, increases pulmonary artery pressure

and right ventricular pressure. When greater than 50% of

the vasculature is occluded, the patient experiences significant pulmonary hypertension and acute cor pulmonale. Undetected, this leads to long-term morbidity and

death.

PE is the third most common cause of death from

cardiovascular disease, with approximately 650,000

cases of PE occurring per year in the United States. The

diagnosis is frequently missed, with 30% of cases diagnosed antemortem. Massive PE occurs in only 5% of

cases, but has an associated mortality rate of 40%.

Overall, mortality is 3-10% if treated and 1 5-30% if

untreated.

• If PE is considered in the differential, use clinical decision rules (PERC, Wells, Geneva) to help guide decisions

regarding the patient work-up.

• Consider thrombolytics in hemodynamically unstable

patients with confirmed PE.

 

to say "ee" while you are auscultating. Normally, a muffled

long E sound is heard. When "ee" is heard as "ay;' egophony

is present and indicates an underlying consolidation. Tactile

fremitus refers to an increase in the palpable vibration transmitted through the bronchopulmonary system to the chest

wall when a patient speaks. Increased tactile fremitus suggests

an underlying consolidation.

DIAGNOSTIC STUDIES

..... Laboratory

In ambulatory, mildly symptomatic patients who are other ­

wise healthy, no testing may be indicated. The diagnosis of

pneumonia is often clinical, but laboratory studies may aid

in the diagnosis or treatment decisions. There is often an

elevated white blood cell count in patients with bacterial

pneumonia. Obtain a chemistry panel in ill-appearing

patients to rule out metabolic derangements. For patients

who are hospitalized with pneumonia, obtain blood cultures

before initiating antibiotics (if possible). Do not delay anti ­

biotics for critically ill patients. More than 25o/o of hospital ­

ized patients with pneumonia have bacteremia. Sputum

Gram stain and cultures are rarely obtained in the emer ­

gency department (ED), but can help determine the bacte ­

rial pathogen and narrow specific antimicrobial therapy.

..... Imaging

Chest x-ray (CXR) may demonstrate evidence of pneumonia, but cannot be relied on to completely exclude pneumonia (especially in immunocompromised patients). Typical

findings on CXR include lobar consolidation, segmental or

subsegmental infiltrates, or an interstitial pattern (Figure 23-1).

Cavitation is seen with anaerobic, aerobic gram-negative

bacilli, S. aureus, and mycobacterial or fungal infections

(Figure 23-2). Radiologic findings are nonspecific for

PNEUMONIA

.A Figure 23-1 . Chest radiograph showing pneumonia

in the right middle lobe.

.A Figure 23-2. Chest radiograph of a patient with

tubercu losis. Note the bi lateral apical infiltrates and

the cavitary lesion in the left upper lobe .

predicting a particular infectious etiology and can lag behind

clinical findings. Also, radiographic signs of pneumonia can

persist well after clinical resolution.

MEDICAL DECISION MAKING

The differential diagnosis of patients with a cough and

CXR abnormality includes pulmonary embolism, congestive heart failure, lung cancer, connective tissue disorders,

CHAPTER 23

Cli nical suspicion of

pneumonia

pneumonia

Consider discharge

to home

Search for alternative

diag nosis or treat for

pneumonia presumptively,

based on clinical findings

Figure 23-3. Pneumonia diag nostic algorithm. CXR, chest x-ray.

granulomatous disease, fungal infections, and chemical or

hypersensitivity pneumonitis. The radiographic signs of

pneumonia vary, so it is difficult to predict the causative

organisms by the radiographic appearance alone. The

clinical presentation, in conjunction with CXR findings,

will aid in treatment decisions (Figure 23-3 ).

TREATMENT

Start with supplemental oxygen by nasal cannula or face

mask if the patient is short of breath or hypoxic. For

patients with severe respiratory distress or shock, mechanical ventilation can decrease the work of breathing and can

be lifesaving.

Empiric antibiotics can be started based on the likely

pathogens and overall clinical picture. Timely administration of antibiotics ( <6 hours from presentation) is associated with improved outcomes for patients requiring

hospital admission. The antibiotic recommendations listed

are representative of recommended treatments, but are not

comprehensive (Table 23-1). Other antibiotic regimens

may also be effective, and the clinician should consider

local resistance patterns and allergies.

Consider whether or not your patient requires measures

to prevent transmission of disease. These include droplet

and airborne precautions. When the pathogen has not been

identified, err on the side of caution and apply the precaution based on the suspected pathogen. These measures

PNEUMONIA

Table 23-1. Recommended antibiotic reg imens to treat pneumonia.

Outpatients age <60 years and otherwise Consider azithromycin (500 mg PO for 1 day, then 250 mg PO for 4 days) or levofloxacin (750 mg

healthy PO daily for 14 days) or doxycycline (100 mg PO bid for 14 days)

Outpatients age >60 years or with

comorbidities (without HCAP}

Consider amoxicillin·clavulanate (2 g PO bid for 14 days) plus azithromycin or levofloxacin (750 mg

PO daily for 14 days)

Admitted with CAP Third-generation cephalosporin (ceftriaxone 1 g IV dai ly) and a macrolide (azithromycin 500 mg IV

dai ly}

  as opposed to being deployed on the verge

of intubation as a "rescue therapY:' However, the only absolute contraindications to its use are respiratory arrest, inability to fit the mask, and patient noncompliance. When used

appropriately, BPAP use in patients with COPD exacerbations has been shown to decrease intubation, mortality,

hospital length of stay, and number of days patients spend in

intensive care unit settings.

Most patients presenting with a COPD exacerbation do

not present in extremis but with moderate to severe respiratory distress and hypoxia. Hypoxemia is the critical life

threat in this group of patients and should never be left

untreated. Although it's true that PaC02 levels rise in

COPD patients to whom oxygen is administered, only a

very small fraction of patients experience enough of a rise

to cause CNS depression and a depressed respiratory effort

(called "C02 narcosis"). However, oxygen should be limited to only what is needed, with a target oxygen saturation

(Sa02

) of 90-94% (Pa02 of 60-65 mmHg). Venturi masks

provide a convenient means of titrating oxygen delivery

more accurately.

Despite the prevalence of COPD, there are few evi ­

dence-based guidelines regarding pharmacologic therapy.

However, the conventional triad of short-acting bronchodilators, steroids, and antibiotics remains unchanged. In

COPD patients, beta-adrenergic agonists (albuterol 2.5 mg

in 3 mL of saline) are used in concert with anticholinergic

agents (ipratropium bromide 0.5 mg in 3 mL saline) via a

nebulizer.

Steroids should be given to all patients presenting to the

ED with a COPD exacerbation. Although steroids are not

as effective in COPD patients as in patients with asthma,

steroids reduce treatment failures and obstructive symptoms, as well as hospital length of stay with an uncertain

effect on mortality. In the ED, methylprednisolone is the

preferred parenteral agent (Solu-Medrol 125 mg IV),

although patients with mild exacerbations can be given

80 mg of prednisone orally. All patients should receive a

prescription for 40-60 mg of prednisone to be taken daily

for at least 1 week after discharge. Steroid prescriptions

do not need to be tapered when prescribed for less than

3 weeks.

CHAPTER 22

Suspected COPD

exacerbation

CXR

CBC,

Electrolytes,

 

toms may have a pneumothorax (from a ruptured bleb) or

a pulmonary embolus (PE). Although acute coronary syndrome should also be considered among patients presenting with dyspnea, chest tightness is a common complaint

among patients with relatively uncomplicated COPD or

asthma exacerbations. One helpful historical detail is to

discern whether chest tightness is a common feature of

past COPD exacerbations.

� Physical Examination

Patients with COPD exacerbations frequently present with

tachypnea, tachycardia, and hypoxia. Because the majority

of patients have an underlying respiratory infection, they

may also have a fever. Most of what the clinician needs to

make a quick assessment can be gathered from vital signs

and a quick glance at the patient on entering the room.

Patients with severe exacerbations may be sitting upright or

leaning forward in the "tripod" position with both of their

hands planted on their knees. Such patients may be confused

and diaphoretic, unable to converse comfortably, and use

accessory muscles in the neck and chest wall to help them

breathe. Cyanosis is an ominous, but uncommon finding.

Patients with less severe exacerbations speak in complete

sentences, and the chest exam reveals diffusely diminished

breath sounds with wheezing or a prolonged expiratory

phase. Patients with emphysema pathology are often thin

and frail appearing with a barrel chest. Some patients with

prolonged COPD will have evidence of right heart failure

including jugular venous distension and lower extremity

edema. Finally, although bedside spirometry in the form of

a peak expiratory flow rate (PEFR) assessment is more useful in asthma, it can be a helpful adjunct to the physical exam

of COPD patients because several patients with COPD have

a reversible component to their disease. In patients with a

known baseline, an easy comparison can be made to determine the severity of airflow obstruction. Most patients do

not recall past PEFR values, but a PEFR <200 L/min suggests

a significant component of airflow obstruction.

DIAGNOSTIC STUDIES

� Laboratory

Given that patients with COPD often have several comor ­

bidities, routine laboratory studies including a complete

blood count, electrolytes, and an assessment of renal function should be ordered in most patients. Brain natriuretic

peptide (BNP) appears to be tailor made to help differentiate patients with COPD from those with CHF. BNP levels

less than 100 pg/mL have a very high negative predictive

value for CHF, whereas most patients with CHF have levels

>400 pg/mL. However, many patients have values that

fall somewhere in between, and discordance between BNP

values and patient symptoms occurs often enough that

single measurements need to be interpreted carefully. If

available, the patient's prior records should be sought out

to compare current and past values to determine trends

and to establish a baseline. Furthermore, some patients

may have a mixture of presenting problems contributing to

their dyspnea, so an elevated BNP does not exclude a concomitant COPD exacerbation.

Cardiac markers such as troponin are frequently

ordered, but usually unnecessary. Because patients with

severe COPD exacerbations often suffer from hypoxia and

tachycardia, myocardial oxygen demand is increased, and

many patients will have small troponin elevations owing to

"demand ischemia." In these patients, serial troponin measurements should be used to help exclude an acute coro ­

nary syndrome.

D-dimer levels may also be useful in patients with a

presumed COPD exacerbation to help exclude PE. Given

their comorbidities (CHF, a low flow state), sedentary life ­

style, history of smoking, and increased risk for an underlying malignancy, many patients with COPD are at

increased risk for PE. Because d-dimer levels are also likely

to be falsely elevated in this population, it is wise to limit

d-dimer testing to those patients in whom there is a reasonable clinical suspicion of PE (abrupt onset, unilateral

leg swelling).

Finally, arterial blood gases (ABG) have long been part

of the routine evaluation of patients with severe COPD

exacerbations. ABGs provide information about oxygenation (PaOz), ventilation (PaCOz), and overall acid-base

status (pH). Blood gas readings in patients with significant

COPD exacerbations will reveal a primary respiratory acidosis, with elevated C02 levels (>40 mmHg) resulting in a

decreased pH ( <7.30).

� Imaging

The chest x-ray (OCR) primarily helps to diagnose pneumonia and to exclude alternative conditions s uch as CHF,

a pneumothorax, or significant atelectasis or lobar collapse. The classic findings are hyperinflation and bullous

changes (Figure 22-1). Vascular markings and heart size

are often decreased in patients with emphysema pathology

and increased in patients with chronic bronchitis.

� Electrocardiogram

As with the CXR, electrocardiograms are primarily useful

to exclude alternative diagnoses, such as cardiac ischemia.

In patients with pulmonary hypertension, peaked P waves

CHRONIC OBSTRUCTIVE PU LMONARY DISEASE

F

Figure 22-1 . Chest radiograph of a patient with

chronic obstructive pulmonary disease.

in lead II may be present (p puhnonale), reflecting right

atrial enlargement, whereas other patients may have signs

of right ventricular hypertrophy (large R wave in v1 and v2

with prominent S waves in v5 and v6), a right bundle

branch block, or right axis deviation. Multifocal atrial

tachycardia (MAT) is the classic arrhythmia associated

with COPD patients. MAT is an irregularly irregular

rhythm, like atrial fibrillation (AF), but there are P waves

of differing morphologies before every QRS complex, and

it tends to be slower than AF.

 

smoking) and be provided with appropriate follow-up

information.

SUGGESTED READING

Cydulka RK. Acute astluna in adults. In: Tintinalli JE, Stapczynski

JS, Ma OJ, Clince DM, Cydulka, RK, Meckler GD. Tintinalli's

Emergency Medicine: A Comprehensive Study Guide. 7th ed.

New York, NY: McGraw-Hill, 20 1 1, pp. 504--5 11.

National Heart Lung and Blood Institute. Expert Panel Report 3:

Guidelines for the Diagnosis and Management of Asthma:

Managing Exacerbations of Asthma. http://www.nhlbi.nih.

gov/ guidelines/asthma/, Accessed April l6, 2007, pp. 3 73-405.

Pollart SM, Compton RM, Elward KS. Management of acute

asthma exacerbations. Am Fam Phys. 2007;84:40-47.

Chronic O bstructive

Pu l monary Disease

David H. Rosenbaum, MD

Key Points

• Respiratory infections are responsible for most acute

exacerbations of chronic obstructive pulmonary

disease (COPD).

• Beta-adrenergic agonists and anticholinergic drugs

remain the primary bronchodilators and are most effective when used together.

• Steroids should be given to nearly all patients presenting to the emergency department (ED) with COPD

INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is defined

as an illness characterized by irreversible, progressive air ­

way obstruction that is associated with inflammatory pulmonary changes. It is extraordinarily common, and

patients with exacerbations of COPD will continue to

inundate emergency departments (EDs) in search of respiratory relief. In the United States, COPD is the fourth most

common cause of death.

The use of the term COPD encompasses patients

with chronic bronchitis and emphysema, as well as those

patients with asthma who have a component of irreversible

airflow obstruction. Airflow obstruction is the end result

of a process that begins with particulate air pollution

exposure ( usually from tobacco smoke) . Particulate

exposure initiates a cascade of events, including airway

inflammation and narrowing of the small airways, as

well as airway destruction and remodeling in the setting

of diminished repair mechanisms and fibrosis, resulting

in fixed airflow obstruction and air trapping. Although

there are clearly pathophysiologic differences between

these groups, their evaluation and treatment is largely

the same.

95

exacerbations, and ongoing therapy should be pre ­

scribed for those patients who are discharged.

• Antibiotics are an important adjunct to therapy,

although their use should be gu ided by the patient's

signs and symptoms.

• Noninvasive ventilation is a critical component of

therapy that is best used early in the ED course to avoid

the need for intubation.

A COPD exacerbation is an event characterized by a

worsening of the patient's respiratory symptoms beyond

the normal day-to-day variation. Typically, this involves

one or all of the following: worsening dyspnea, increased

sputum as well as a change in the character of sputum, and

an increase in the frequency and severity of cough.

CLINICAL PRESENTATION

..... History

The critical aspects of the history in evaluating patients

with dyspnea due to a presumed COPD exacerbation are

to establish the patient's baseline function, assess the sever ­

ity of the exacerbation, determine a cause, and rule out

disorders that may mimic a COPD exacerbation. Most

patients experiencing a COPD exacerbation present with

complaints of increased dyspnea in the setting of a recent

onset respiratory infection (ie, upper respiratory infec ­

tion). As a result, they may complain of a productive or

sometimes a nonproductive cough that differs from their

baseline cough, rhinorrhea and nasal congestion, and

fevers and chills, as well as the constitutional symptoms

that frequently accompany systemic illness. Most such

CHAPTER 22

patients are chronically ill and often quite frail, so the key

to determining the severity of the exacerbation is establishing their baseline health. To do this, it helps to ascertain

their oxygen use, their current treatment regimen, their

level of function and ability to perform activities of daily

living, the frequency of hospitalizations and the timing of

their most recent hospitalization, their history of mechanical ventilation, and any comorbid illnesses ( eg, ischemic

heart disease and congestive heart failure [CHFJ).

Patients who present with symptoms that seem to

develop over a long period of time may actually have

underlying CHF, whereas patients with abrupt onset symp ­

 Anaphylaxis may present with wheezing, but the

patient will often have urticaria and sometimes gastrointestinal symptoms. CHF may present with "cardiac

wheezing;' but the patient will often have "wet" lungs

sounds with rales in the bases, an enlarged heart on CXR,

peripheral edema, and jugular venous distention. CHF

ASTHMA

Figure 21-2. Pea k flow meter.

can have many underlying causes, but often these individuals will have underlying heart disease and other

comorbidities. The presence of wheezing is common in

COPD, but unless the patient has a history of

a1

-antitrypsin deficiency, this type of presentation is

found in patients with smoking history and who are

..A.Figure 21-3. Handheld nebul izer treatment.

CHAPTER 21

Suspected asthma

exacerbation

Alternate diag nosis

(CHF, PE, upper

airway obstruction)

Treatment

• 02

• Albutero l

• Steroids

• +/- Atrovent

• +/- CXR

r Good

response to

treatment

Discharge

Poor

response to

treatment

Admission

Magnesiu m, terbutaline,

epinephrine; consider

intubation and ICU if no

improvement

Figure 21-4. Asthma diag nostic algorithm. CHF, congestive heart fa ilure; CXR, chest x-ray; ICU, intensive care

unit; PE, pulmonary embolism.

typically over the age of 40 years. Patients with pneumo ­

nia may have underlying wheezing, but typically have a

fever and an infiltrate of CXR. Other diagnoses such as

foreign body aspiration, PE, and upper airway obstruction should also be considered. Stridor is an indicator of

upper airway swelling and should be differentiated from

wheezing in the lung fields.

Once the diagnosis of asthma has been made, the treatment decisions are based on the severity of illness (Figure 21-4).

Mild exacerbations can be treated with beta-1 agonists and

other supporting medications, and the patient can be discharged. Moderate disease may require further treatments

with beta-2 agonists, and the disposition will depend on the

response to treatment. Severe presentations will require

aggressive management with serial or continuous beta-agonist

treatments and can require other medications such as magnesium and epinephrine.

TREATMENT

Patients who present with difficulty breathing should have

oxygen applied via nasal cannula or facemask and titrated

to keep the level of oxygenation >94%. Cardiac monitoring

and IV access should be used in moderate to severe asthmatics. In conjunction with these, beta-2 agonist therapy

should be instituted as the first-line therapy. Patients who

are started on beta-2 agonists will still receive oxygen

though the nebulized treatment. There are several other

therapies that should be considered during an exacerbation, depending on the severity. All medications discussed

here are safe to use during pregnancy except epinephrine,

which is associated with congenital malformations and

premature labor.

Beta Agonists. Albuterol is the most commonly used

beta-2 agonist agent and is considered first-line therapy. It

causes bronchodilation by increasing cyclic adenosine

monophosphate and relaxing airway smooth muscles. Its

onset of action is <5 minutes. The nebulized form consists

of albuterol 2.5 mg in 3 mL of saline given every 20 minutes x 3, or as a continuous nebulizer for severe asthmatics

using albuterol 10 mg over a period of 1 hour. A metered

dose inhaler (MDI) delivers albuterol using 2 puffs with a

spacer every 20-30 minutes and requires active participa ­

tion.