Emergency Medicine 3


Emergency Medicine 3

Table 3A.1. Common causes of acute respiratory failure

Failure to Oxygenate

Ventilation-perfusion mismatch (pneumonia, aspiration, ARDS*,

pulmonary embolism)

Decrease in FiO2

Intra/extrapulmonary shunting

Diffusion defects (emphysema, interstitial lung disease)

Restrictive lung disease

Ventilatory failure

Failure to Ventilate

Depressed mental status (drugs, stroke, sepsis, seizures)

Upper airway obstruction (croup, epiglottitis, burns, cancer, trauma)

Lower airway obstruction (asthma, COPD+, cancer)

Chest wall disorders (flail chest, kyphosis, muscular dysfunction)

*ARDS: acute respiratory distress syndrome

+ COPD: chronic obstructive pulmonary disease

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• Arterial blood gas (ABG) may aid in the diagnosis in patients with suspected CO

poisoning. It also allows the physician to assess the degree of hypoxia and hypercapnia

but is not a necessary study in patients with a clinical picture consistent with ARF.

• Portable chest radiograph (CXR) is indicated in all patients with acute or impending

respiratory failure. Findings are often useful for identification of the underlying cause

and may have treatment implications. However, the decision to intubate or administer

other airway interventions is nearly always based on clinical, rather than radiographic

criteria. CXR should also be obtained after endotracheal intubation to assess

tube placement.

• Laboratory results rarely affect management. However these patients are often critically

ill with comorbid illness. Basic studies including complete blood count (CBC),

electrolytes, blood urea nitrogen (BUN), creatinine and glucose as well as an electrocardiogram

(EKG) should be obtained in most patients with ARF. Other studies may

be indicated depending on the presentation.

Treatment

• Supplemental oxygen increases the delivered FiO2 with each liter of oxygen increasing

FiO2 by approximately 4%. Many delivery devices are available but nasal cannulae

and masks are the most commonly used.

• Nasal cannula delivers up to 44% FiO2. Oxygen administered at 1 to 6 L/min.

Nasal cannula may be used for patients with mild hypoxia but is not appropriate in

the setting of severe respiratory distress.

• Nonrebreather mask (NRB) delivers up to 98% FiO2 (almost 100%). Oxygen is

generally administered at 15 L/min. NRB may be used in patients with moderate

to severe hypoxia or as a bridge to more definitive therapy.

• Noninvasive Positive Pressure Ventilation (NPPV)

• NPPV provides positive pressure to airways using either a nasal or face mask. Both

inspiratory pressure (IPAP) and expiratory pressure (EPAP) can be controlled. NPPV

is probably most effective in disorders where treatment may be expected to result in

rapid improvement of respiratory status, such as asthma, COPD, or pulmonary

edema. Use of NPPV may avoid endotracheal intubation. The vast majority of

patients who will fail treatment do so within the first 12 h.

• Most of the studies regarding NPPV have focused on COPD patients. The bulk of

evidence is positive. Several controlled trials have shown improved gas exchange

and lower intubation rates among patients treated with NPPV. Asthma and acute

pulmonary edema have also been treated successfully with NPPV.

• NPPV does not provide airway protection. In order to be a candidate, a patient must

have a clear sensorium, be able to initiate breaths, and be able to tolerate the mask.

• NPPV should be used in conjunction with a respiratory therapist, nurse, or physician

who is skilled in its use. Once instituted, IPAP and EPAP are set independently.

IPAP is adjusted to decrease the work of respiratory muscles and is titrated

to the desired PaCO2. Avoid peak pressures >20 cm H2O. Oxygenation is controlled

by adjusting the FiO2 and EPAP. Common initial settings are an EPAP of

3-5 cm H2O and IPAP of 10 cm H2O.

• Endotracheal intubation is the gold standard for respiratory support and airway management.

Placement of an endotracheal tube (ETT) provides the maximum control of

ventilation, oxygenation, and airway patency.

• Indications for intubation include:

• Severe or progressive hypoxemia

• Severe or progressive acute hypercapnia

• Severe or progressively increased work of breathing

• Airway protection

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• Acute or impending airway occlusion

• Pulmonary support in the critically ill or injured patient

• Need for life-saving diagnostic studies or therapies in uncooperative patients

• Ventilator management varies depending upon the underlying mechanism. A detailed

discussion of ventilator management is beyond the scope of this text.

• Defect in oxygenation: adjust FiO2 and/or positive end expiratory pressure (PEEP)

to achieve desired pO2.

• Defect in ventilation: adjust RR and/or tidal volume to achieve desired pCO2.

• Specific treatment: once the patient’s respiratory status is stabilized, directed therapy

can begin. This might include medical therapy, surgical intervention, and/or specific

ventilator strategies.

Disposition

• All patients with respiratory failure should be admitted to an intensive care unit (ICU).

Patients with impending respiratory failure should be admitted to either an ICU or

another closely monitored bed (e.g., step-down unit).

• Patients with a stable respiratory status who are at very low risk for deterioration can

be admitted to a ward bed.

Part B: Asthma

Asthma is a chronic disease characterized by increased airway responsiveness to

various stimuli. This causes widespread narrowing of the lower airways that reverses

either spontaneously or with treatment. Although the exact pathophysiology of

asthma is complex and poorly understood, inflammation is thought to play a central

role. Pathologic changes that occur in asthma include smooth muscle hypertrophy,

mucosal edema, and mucous plugging. Asthma affects 4-5% of adults and 10% of

children. Onset usually occurs in children and young adults.

Etiology and Risk Factors

• Asthma is commonly classified as allergic (extrinsic) or nonallergic (intrinsic).

• Allergic asthma is more common and is responsible for the majority of childhood

asthma and a significant portion of adult disease. These patients are sensitive to specific

inhaled allergens. Patients with allergic asthma frequently have a personal and

family history of allergic diseases, including allergic rhinitis and atopic dermatitis. In

contrast to patients with intrinsic asthma, those with allergic asthma have increased

levels of immunoglobulin E (IgE). Inhalation of an allergen induces a response in two

phases.

• The early response usually begins within minutes of exposure and lasts up to period

of several hours. Caused by mast cell degranulation. Mediator release subsequently

induces bronchoconstriction and an inflammatory reaction.

• The late response is characterized by airway inflammation that results in further

bronchoconstriction and mucous production. Symptoms may persist for days to

weeks after the initial exposure.

• Nonallergic asthma is associated with numerous stimuli including exercise, emotion,

air pollution, cigarette smoke, medications, and occupational exposures.

Diagnosis

• A definitive diagnosis is made via pulmonary function tests (PFTs) that demonstrate

reversible airway obstruction. PFTs are not practical for use in the emergency department

(ED) where the diagnosis is made clinically.

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• In stable patients, historical information can be obtained that may help guide therapy

and disposition. There are several factors associated with poor outcome.

• History of prior intubations for ARF secondary to asthma

• Multiple or recent hospitalization(s) for asthma exacerbation

• Recent use of corticosteroids

• Other important information includes the time of onset, inciting factors, and use of

medications prior to arrival.

• Patients generally complain of dyspnea and cough. Severity ranges from mild to life

threatening. Note that dyspnea is likely unrelated to hypoxia and may not resolve with

supplemental oxygen. The cough can be either dry or productive. Patients with

“cough-variant asthma” present with a nonproductive cough that tends to be nocturnal.

They may not have audible wheezing. These patients have ventilatory impairments demonstrable

with PFTs and usually experience relief with bronchodilator therapy.

• General appearance, vital signs, and pulmonary evaluation should be assessed as previously

discussed (see ARF). Patients often have tachypnea and tachycardia that should

improve with appropriate treatment. Pulsus paradoxus is associated with acute asthma

but is not a practical aspect of the ED evaluation. Common auscultatory findings

include wheezing, decreased breath sounds, and prolongation of the expiratory phase.

Absence of wheezing may be indicative of severe airway obstruction. Reexamination

after bronchodilator therapy in such patients is often notable for increased wheezing.

AMS, increased work of breathing, hypoxia, and hypercarbia indicate ARF and mandate

immediate intervention.

• While asthma is mainly a clinical diagnosis, various diagnostic modalities can contribute

to management and disposition.

• Pox—Saturation should be continuously monitored on all asthma patients (see Part

A, Diagnosis, for discussion of Pox). Any patient with a saturation <90% should be

considered severely hypoxic and treated accordingly.

• ABG—Blood gas assessment is not routinely indicated but can help guide ventilator

management and determine the degree of hypercarbia/hypoxia in patients with

severe exacerbation. During an acute exacerbation, the ABG usually shows a respiratory

alkalosis. Normal or increasing pCO2 reflects deterioration in ventilation

although this should also be clinically evident.

• Pulmonary function testing/Peak flow—As previously discussed, PFTs are not a

routine aspect of the ED evaluation. Peak expiratory flow rate (PEFR) provides a

means of assessing pulmonary function at the bedside although patient cooperation

is required. PEFR values do not correlate well with prognosis, and there is no

absolute value that mandates admission. It is best used serially to monitor the effects

of therapy on patients with mild to moderate disease. Ideally, PEFR in the ED

is compared against the patient’s known baseline. Measurements can also be compared

to predicted levels using nomograms that consider age, sex, and height. In

general for adults patients, PEFR <300 indicates a mild exacerbation, PEFR <200 a

moderate exacerbation, and PEFR <100 a severe exacerbation.

• CXR—In mild to moderate asthma exacerbations, routine CXR is not necessary. It

is helpful for identification of complications such as pneumothorax (PTX). CXR is

also indicated if the patient does not improve with therapy or has fever, focal findings

on pulmonary exam, pleuritic chest pain, or hypoxia. Patients presenting with

a first episode of wheezing and those with an unclear diagnosis should have CXR to

evaluate for underlying pathology.

• Laboratories rarely influence management and are not routinely indicated. The

decision to obtain laboratory screening should be based upon the patient’s age,

medication use, and other comorbid conditions. An increased leukocyte count

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(WBC) is consistent with both infection and steroid use. However, a normal WBC

does not exclude infection. Also consider a theophylline level in patients taking that

medication.

• Differential Diagnosis

• The emergency physician (EP) must always search for a cause of acute exacerbation

especially in those patients with severe symptoms. Allergen exposure is the most

likely but respiratory infection, PTX, and pulmonary embolism (PE) are important

and potentially fatal problems that must be identified.

• The EP should remember that “all that wheezes is not asthma.” Other conditions

to consider include COPD, congestive heart failure, allergic reaction, airway obstruction,

and pulmonary embolism. A directed history and physical examination,

along with proper use of diagnostic testing, will help to differentiate these entities.

Treatment

Respiratory Support

• Oxygen can be given liberally since asthmatic patients do not chronically retain CO2.

The amount and route primarily depend upon the patient’s symptoms and degree of

hypoxia.

• NPPV has been shown to be effective in improving gas exchange and avoiding intubation

in some asthmatic patients (see “Acute Respiratory Failure”). NPPV is not appropriate

for patients with AMS and an obviously ineffective respiratory effort.

• Endotracheal Intubation

• The decision to intubate is purely clinical. There are no ABG parameters or CXR

findings that mandate this intervention. Patients with severe refractory hypoxia,

altered mental status, severely increased work of breathing, and/or ineffective respirations

are candidates for immediate intubation.

• In the conscious patient, rapid sequence induction (RSI) is the safest method for

endotracheal tube placement. Agents commonly used for RSI include a benzodiazepine

in conjunction with a paralytic agent. Ketamine, in addition to its analgesic

and anesthetic properties, is a bronchodilator and therefore should be considered

the induction agent of choice in young asthmatics. In older patients with coronary

artery disease, the cardiovascular risks of ketamine may outweigh the benefits. There

are no specific contraindications to paralytic agents during RSI of the acute asthmatic

patient.

• Preoxygenation should be attempted prior to intubation. However, this is sometimes

not possible for patients in extremis. Furthermore, oxygen saturation may

decline very rapidly during intubation.

• Oral intubation is preferred to nasotracheal intubation because a larger tube can be

inserted. This allows for adequate suction and for bronchoscopy if needed.

• Ventilator Management

• The intubated asthmatic patient is at risk for barotraumatic complications such as

PTX, pneumomediastinum, or subcutaneous emphysema. The goal of mechanical

ventilation is to supply the lowest minute ventilation that yields adequate gas exchange

keeping peak airway pressures (PAP) below 35 cm H2O. Suggested initial

adult ventilator settings include FiO2 of 100%, tidal volume of 6-8 ml/kg, ventilatory

rate of 10, and inspiratory time/expiratory time (I/E) ratio of 1:3 or 1:4. FiO2

can be titrated based on Pox and/or ABG.

• Permissive hypercapnia is a strategy sometimes used to help control PAP. Patients are

intentionally hypoventilated and airway pressures minimized via low tidal volume

and RR. PaCO2 is permitted to rise and pH to fall, generally to a level of around

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7.25. In severe cases, pH can be further decreased and a sodium bicarbonate infusion

initiated. Oxygenation is maintained via high FiO2.

• After intubation, continued sedation and paralysis allow for maximal relief of the

respiratory muscles and for permissive hypercapnia. This can be achieved with longer

acting benzodiazepines and paralytic agents. Subsequent dosing of ketamine is also

appropriate.

• Patients may also develop hypotension secondary to increased intrathoracic pressure

and impaired venous blood return to the right ventricle resulting in decreased

cardiac output. This must be differentiated from tension PTX. Both will also cause

an elevation of PAP. If the former is suspected, the patient should be disconnected

from the ventilator and manually ventilated at a slower rate (6 to 8 breaths per

minute). This will allow for exhalation of trapped air. In addition, a CXR should be

ordered and the patient suctioned. If a tension PTX is suspected, immediate decompression

of the affected side by needle thoracostomy is indicated.

Medications

• Beta2 Agonists

• Inhaled ²2 agonists are the mainstay of therapy for acute asthma exacerbation. These

agents relax bronchial smooth muscles and reverse bronchospasm. Albuterol is the

most commonly used agent and is generally delivered by nebulizer. Onset of action

is <5 min, and repetitive administration produces incremental effect. Nebulized

albuterol is usually given in 2.5-5 mg increments every 15-20 min as needed. It can

be given continuously for patients with severe symptoms. There is no defined maximum

dose. Administration is usually limited only by symptoms (tremor, tachycardia,

nausea).

• Studies have shown that metered dose inhalers (MDIs) are as effective as nebulizers.

However proper MDI use is essential and a severe exacerbation may preclude

proper use.

• Remember that intubation does not cure asthma. Intubated patients should continue

to receive aggressive in-line ²2 agonists.

• Levalbuterol is the single (R) isomer preparation of albuterol, as opposed to traditional

racemic albuterol, which is a 50/50 mixture of the (R) and (S) isomers, the

(S) component being inactive. It is thought to have similar efficacy to racemic

albuterol but fewer nonrespiratory side effects. The cost of levalbuterol is about five

times that of racemic albuterol. The benefit of this new preparation over standard

albuterol is debatable.

• Although multiple studies have demonstrated the advantages of inhaled ²2 agonists

over systemic medications, it has been suggested that inhaled medications may be

unable to reach critical areas in patients with severe asthma and profoundly impaired

airflow. In these severe circumstances, terbutaline or epinephrine may be

administered subcutaneously. The adult dosing for epinephrine is 0.3-0.5 mg of

1:1000 solution every 15-20 min as needed, up to 3 doses. Terbutaline dosage is

0.25-0.5 mg every 15-20 min as needed. Epinephrine should be used with caution

in elderly patients and those with cardiovascular disease.

• Inhaled Anticholinergics

• These agents block muscarinic receptors preventing smooth muscle contraction

and diminishing mucous gland secretions.

• Ipratropium bromide is the most commonly used agent. It is not to be used as single

agent therapy but has been shown to be effective for the treatment of severe asthma

when added to albuterol. Inhaled ipratropium does not appear to result in significant

systemic side effects unlike other anticholinergic agents such as atropine.

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• Ipratropium is delivered by nebulization and can be mixed with albuterol. The dose

is 0.25-0.50 mg every 15-20 min, up to three doses.

• Most of the studies that support the beneficial effect of ipratropium used with small

to moderate doses of albuterol. Thus, it is possible that the same benefit may be

obtained by simply using higher doses of albuterol without ipratropium.

• Corticosteroids

• Corticosteroids suppress inflammation and have been shown to improve patient

outcomes, prevent relapses, and prevent hospital admission. There is little immediate

benefit because of the delayed onset of these agents (about 6 h). Corticosteroids

are probably unnecessary in mild asthma, but should be given in moderate to severe

cases and in any patient who does not respond promptly to inhaled ²2 agonists.

• Oral prednisone and intravenous (IV) methylprednisolone are the most commonly

used agents. There is no difference between these two medications in terms of efficacy

or onset of action. Prednisone is less expensive and more easily administered

and should be given to the majority of patients. Methylprednisolone is preferred in

patients who are unable to take oral medications due to vomiting or respiratory

distress. The adult dose of prednisone is 60 mg and methylprednisolone 125 mg.

• Patients discharged from the ED after being treated with corticosteroids should be

continued on outpatient therapy for 5-7 days. This dosing regimen does not require

tapering.

• Inhaled corticosteroids have few systemic side effects and are beneficial in long-term

management but currently have little use in the ED.

• Methylxanthines

• The methylxanthines have multiple effects including bronchodilation and enhancement

of diaphragmatic contraction. The mechanisms of action are not well defined.

Use of methylxanthines in the ED is discouraged due to side effect profiles,

complicated dosing, and lack of established efficacy.

• If the decision is made to use intravenous aminophylline for a patient with refractory

disease, frequent serum levels are necessary in order to avoid toxicity. Note that

elimination rates are highly variable. For patients already taking theophylline, a

baseline level is mandatory before beginning acute therapy.

• Magnesium sulfate (Mg) is a weak bronchodilator and a second-line agent for asthma

exacerbations. The most recent data suggests that Mg benefits only the most severe

asthmatic patients and should not be given routinely. Mg is inexpensive and safe in

patients with normal renal function. The adult dose is 2 g IV over 10-15 min.

• Heli-ox is a combination of helium and oxygen that is usually administered in a 70%/

30% mixture. Heli-ox is thought to improve laminar gas flow through airways, resulting

in improved gas exchange and decreased work of breathing. Although early case reports

were positive, subsequent clinical studies have shown little benefit and use of heli-ox

remains controversial. Heli-ox is safe and inexpensive, and many physicians use this as

adjunctive therapy in severe cases or in intubated patients with elevated PAP.

Disposition

• Disposition is dependent upon the patient’s response to therapy. In general, patients

with complete or near-complete resolution of symptoms and a PFR of at least 300 (or

near the patient’s baseline) can be discharged. Patients who don’t meet discharge criteria

who have mild to moderate symptoms can be admitted to a ward bed. Patients with

more severe symptoms should be admitted to a monitored bed where timely respiratory

assessment and therapy is available. Intubated patients and those with the potential for

respiratory failure require ICU admission.

• All patients discharged from the ED should receive bronchodilator therapy ± corticosteroids.

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Part C: Chronic Obstructive Pulmonary Disease

• Chronic obstructive pulmonary disease (COPD) is defined as progressive, chronic

airflow obstruction due to chronic bronchitis, emphysema, or both. The majority of

patients have components of both, although one of these entities will frequently dominate

the clinical picture.

• Emphysema—airspace enlargement distal to the terminal bronchioles due to destruction

of alveolar septa.

• Chronic bronchitis—chronic airway inflammation and bronchospasm. Clinically

defined as productive cough lasting for at least 3 mo over 2 consecutive years.

• Although COPD is irreversible, patients with acute exacerbations do have reversible

bronchospastic and inflammatory components.

Etiology and Risk Factors

• Cigarette smoking, including passive exposure to cigarette smoke, is by far the leading

cause.

• Occupational exposures and hereditary ±-1 antitrypsin deficiency are less common.

Diagnosis

• Clinical diagnosis is based on the presence of dyspnea, wheezing, and/or cough in a

patient with a history of causative exposure and chronic, progressive symptoms. Patients

usually present in the fifth or sixth decades of life. Alpha-1 antitrypsin deficiency

should be suspected in any patient younger than 40 yr old with signs and

symptoms of COPD.

• Presentation may separated into two syndromes, depending on the predominate pathologic

process.

• “Pink puffer” (emphysema dominant)

• Patient is barrel-chested with thin build.

• Cough is nonproductive or has scant sputum only. Exam remarkable for decreased

breath sounds.

• Hypoxemia and hypercarbia occur only in end-stage disease.

• CXR shows hyperinflation, flattened diaphragms, and a small heart.

• “Blue bloater” (bronchitis dominant)

• Patient is overweight with stocky build.

• Patients have prominent, productive cough with wheezes and rhonchi on examination.

• Patients usually retain CO2. Hypoxemia and hypercarbia occur early in disease.

• CXR shows increased vascular markings and a large heart.

• Patients may present with varying degrees of respiratory difficulty. Dyspnea, worsening

cough, and chest tightness are common complaints.

• Physical examination is similar to asthma with varying degrees of audible wheezing,

decreased breath sounds, and prolonged expiratory phase. Patients may also have other

signs such as a barrel chest and stigmata of chronic pulmonary disease such as clubbing.

• Diagnostic Studies

• Pox and ABG—All COPD patients should have continuous Pox monitoring.

Unlike patients with asthma, many with COPD have baseline oxygen saturations

well below 95%. ABG is helpful in critically ill patients and those requiring mechanical

ventilation. Note that COPD patients often have an elevated pCO2 at

baseline. In these patients, ventilatory insufficiency is indicated by a decreased

pH in conjunction with a high pCO2. ABG may be helpful in assessing the severity

of an exacerbation if a baseline pCO2 is available in the patient’s chart.

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• PEFR is sometimes used to monitor the effects of maintenance therapy in patients

with mild to moderate disease but is of little use in the ED.

• CXR—The EP should consider CXR in most patients with COPD exacerbation,

the exception being those with mild exacerbation and prompt response to therapy.

CXR is helpful in diagnosing an underlying source of for acute symptoms including

PTX and pulmonary infiltrates.

• Laboratory testing—As with asthma, routine laboratory evaluation contributes little

to management (see “Asthma”). If a CBC is obtained, the EP may note polycythemia

secondary to chronic hypoxia. The EP may consider electrolytes, renal function

studies, and/or cardiac enzymes as indicated by presentation and comorbidities.

• EKG—Patients in moderate to severe distress require continuous EKG monitoring.

The 12-lead EKG often has findings consistent with right heart strain. An

EKG should be obtained in those patients with chest pain, severe hypoxia, suspected

dysrrhythmia or acute coronary syndrome.

• Differential Diagnosis

• The diagnosis of COPD is usually not difficult. However, the EP should determine

the cause of the acute exacerbation. Respiratory infections, allergen exposure, continued

cigarette smoking, air pollution, and patient noncompliance are common causes.

• Acute PTX, lobar atelectasis, and PE are the most potentially deadly causes of exacerbation.

Unfortunately, PTX and PE can be difficult to diagnose in the COPD

patient but should be suspected in all patients with exacerbation especially those

with acute onset of symptoms.

• Pneumonia occurs frequently in patients with COPD. This diagnosis should be

considered based on clinical findings since CXR may or may not reveal an infiltrate.

Treatment

• To a large degree, this mirrors therapy for asthma (see “Asthma”) with some variations

as discussed below. The most important aspect of therapy is to initiate rapid intervention

for those patients with acute or impending respiratory failure.

• Respiratory support

• Concern exists that aggressive oxygen therapy may thus worsen hypercarbia by

suppression of hypoxic respiratory drive. This concern is somewhat theoretical

and less important in the ED where ventilatory support is immediately available.

A safe approach in the nonintubated patient is to titrate oxygen to achieve saturation

between 90-92%.

• Application of NPPV, endotracheal intubation, and ventilator management in

COPD patients is similar to use as described in “Asthma” section.

• Medications

• Beta2 agonists—The EP should follow the same dosing recommendations as

previously described but should keep in mind that many patients with COPD

are elderly and have cardiovascular comorbid disease. As a result, administration

of ²2 agonists is more likely to be limited by adverse side effects.

• Inhaled Anticholinergics—these agents are very effective in COPD both alone

and in conjunction with ²2 agonists. Ipratropium should be used in all patients

with COPD exacerbation. Dosing is the same as for asthma.

• Corticosteroids, methylxanthines, and magnesium—Indications and dosing are

discussed in the asthma section.

• Antibiotics

• Although the role of bacterial infection in acute bronchitis is controversial, antibiotic

therapy has been shown to improve outcomes for patients with purulent

sputum and severe COPD exacerbation. Trimethoprim-sulfmethoxazole,

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doxycycline, amoxicillin-clavulanate, azithromycin, or clarithromycin are appropriate

choices for both acute bronchitis and outpatient pneumonia therapy.

• Empiric inpatient pneumonia treatment is with second or third generation

cephalosporin and possibly a macrolide to cover atypical organisms. If possible,

sputum cultures should be obtained for all admitted patients to guide

future antibiotic therapy.

Disposition

• Patients who respond rapidly to therapy and return to baseline in the ED can be

discharged with close outpatient follow-up. However, many patients with COPD exacerbation

require admission. This is due to the relatively smaller reversible component

of airway disease that exists in COPD. The EP should also maintain a low threshold

for admission for those with pneumonia. Intubated patients and those at risk for

decompensation require ICU admission.

• All discharged patients should receive appropriate therapy including bronchodilators

± anticholinergics, corticosteroids, and antibiotics.

Suggested Reading

1. Madison MJ, Irwin RS. Chronic obstructive pulmonary disease. Lancet 1998;

352:467-473.

2. Advanced Cardiac Life Support Textbook. Dallas, TX: American Heart Association, 1994.

3. Gammon RB, Strickland JH, Kennedy JI et al.: Mechanical ventilation: A review for the

internist. Amer J Med 1995; 99:553-562.

4. McFadden ER. Asthma. In: Isselbacher KJ, ed. Harrison’s Textbook of Medicine 13th

Ed. New York: McGraw-Hill, 1994.

5. Honig EG, Ingram RH. Chronic bronchitis, emphysema, and airways obstruction. In:

Isselbacher KJ, ed. Harrison’s Textbook of Medicine. 13th Ed. New York: McGraw-Hill,

1994.

6. Mandavia DP, Dailey RH. Chronic obstructive pulmonary disease. In: Rosen Frakes

MA, Richardson LE, eds. Magnesium therapy in certain emergency conditions. Am J

Emerg Med 1997; 15:182-187.

7. West JB. Respiratory physiology-the essentials, 4th ed. Baltimore: Williams & Wilkins,

1990.

8. Emond SD, Camargo CA, Nowak RM. 1997 National Asthma Education and Prevention

Program guidelines: A practical summary for emergency physicians. Ann Emerg

Med 1998; 31(5):579-594.

9. Brenner B, Kohn MS. The acute asthmatic patient in the ED: To admit or discharge.

Am J Emerg Med 1998; 16(1):69-75.

10. Panacek EA, Pollack CV. Medical management of severe acute asthma. In: Brenner BE,

ed. Emergency Asthma. New York: Marcel Dekker Inc., 1999.

11. Stedman’s Medical Dictionary. In: William R. Henyl, ed. Baltimore: William & Wilkens,

1990.

Part D: Pneumonia

Pneumonia is an infection of the gas exchange segments of the lung parenchyma. It

can cause a profound inflammatory response leading to airspace accumulation of purulent

debris. Pneumonia costs are $8 billion annually, accounts for nearly one-tenth of

all hospital admissions, and remains a leading cause of mortality in the United States.

Etiology and Risk Factors

• There are numerous risk factors as discussed in (Table 3D.1).

• The pathogens involved vary depending upon the host (see Table 3D.2).

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Diagnosis

• Pneumonia is sometimes divided into two categories depending upon the causative

agent and presentation (see Table 3D.3). Note that considerable overlap exists between

the two categories and differentiation in the ED may be difficult.

• Patients typically complain of dyspnea, cough, and fever. Depending upon the etiology,

they may also have night sweats, weight loss, myalgias, and localized extrapulmonary

symptoms. History should focus on acuity symptom onset, presence of associated

symptoms, recent travel history, immunization history, and comorbidities. In certain

populations such as the elderly, pneumonia can present with nonspecific symptoms

such as weakness and fatigue.

• Physical exam findings depend upon the etiology and the extent of lung involvement.

Pulmonary exam often reveals rales and decreased or bronchial breath sounds. Although

sometimes difficult to assess in the ED, patients can also have dullness to

percussion, tactile fremitus, and egophony. Associated findings include tachypnea, tachycardia,

diaphoresis, AMS, and increased work of breathing. Note that the pulmonary

examination sometimes does not correlate with CXR findings.

• Laboratory Studies

• Sputum—Because of the low sensitivity of the sputum Gram stains, the clinical utility

in the ED is controversial. This test is most helpful if a single predominant organism

is identified and requires an adequate specimen (>25 WBCs and <10 epithelial cells

Table 3D.1. Risk factors for pneumonia

Risk Factor Comments

Aspiration/absent gag reflex Stroke, intubation, seizure, altered mental status,

sedative use

Mucociliary clearance disorders Smoking, alcohol, COPD, cystic fibrosis, chronic

bronchitis, viral infections

Alteration of normal oral flora Acute illness and antibiotic use

Immunocompromise AIDS*, diabetes, transplant, steroid use, asplenia,

sickle cell disease, uremia, neoplasia, chemotherapy,

extremes of age, complement deficiency

Hematogeonous Indwelling catheters, intrathoracic devices

Geography/environment American southwest (Valley Fever), Ohio/

MississippiValleys (histoplasmosis, blastomycosis),

Southeast Asia (tuberculosis), pigeon droppings

(psittacosis), bovinesources (Q fever), buildings

with contaminated water supply

Community dwelling Dormitory, prison, barracks, nursing home

* AIDS: acquired immune deficiency syndrome

Table 3D.2. Common pathogens in pneumonia

Population Causative Pathogen

Community acquired Streptococcus pneumoniae, Mycoplasma pneumoniae,

viruses, Chlamydia pneumoniae, Haemophilus influenzae,

Legionella, Staphylococcus aureus

Nosocomial (>likely Gram-negative bacilli, Staphylococcus aureus, anaerobes,

to be resistant to and Streptococcus pneumoniae (less frequent)

antibacterial therapy)

Pulmonary Emergencies 65

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per high power field) as well as experienced laboratory personnel. Sputum cultures are

helpful for critically ill or immunocompromised patients but are rarely of use to the

EP and should not be routinely ordered. An acid fast (AFB) stain is indicated patients

with risk factors or presentation consistent with tuberculosis (TB).

• Serum

• There are no specific laboratories for pneumonia although CBC, electrolytes,

and renal function studies are often ordered. These tests should be obtained

routinely in patients who are critically ill or if significant comorbid disease is

present. Note that presence of an elevated WBC does not identify a bacterial

source. Nor does a normal WBC rule it out.

• Serum antibody titers are available for Legionella, Mycoplasma pneumoniae, and

viruses among others but are of little use in the ED.

• CXR

• Ordered in nearly all patients with suspected pneumonia although studies debate

the utility of this study in otherwise healthy people being treated empirically

as an outpatient.

• Certain radiographic patterns have been described depending upon the etiology

(see Table 3D.4). These patterns sometimes vary and do not provide an accurate

means of diagnosis.

• Note that radiographic findings often lag behind clinical symptoms. Patients with

early disease and immunosuppression may not have classic findings.

• Differential diagnosis includes COPD, bronchitis, asthma, allergic reaction, and PE

among others.

Treatment

• Stabilization of cardiopulmonary status is the first priority. Depending on the disease

severity, patients may have respiratory compromise and/or circulatory collapse that

mandate immediate intervention.

• Early antibiotic treatment decreases morbidity and mortality. Empiric therapy should

be started as soon as possible after appropriate resuscitative measures. Many patients

are treated as outpatients, although certain groups are at risk for poor outcome and

should be considered for hospital admission (see Table 3D.5). Admitted patients should

Table 3D.3. Typical and atypical pneumonias

Category Pathogens Presentation

Typical Streptococcus pneumoniae Acute onset

(usually Haemophilus influenzae Shaking chills and high fever

bacterial) Staphylococcus aureus Cough with purulent sputum

Klebsiella pneumoniae Dyspnea

Anaerobes Pleuritic chest pain

Psuedomonas aeruginosa

Atypical Mycoplasma pneumoniae Gradual onset

Viruses Low grade fever

Legionella Scant sputum

Chlamydia pneumoniae Mild respiratory complaints

Mycobacterium tuberculosis Extrapulmonary complaints

Pneumocystis carinii Mycoplasma: myalgias, headache,

sore throat, rash

Viral: upper respiratory symptoms

Legionella: AMS, gastrointestinal

symptoms

66 Emergency Medicine

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receive IV antibiotics and outpatients appropriate oral therapy as indicated for their

age, comorbid conditions, and suspected pathogen (see Table 3D.6).

• All discharged patients should follow-up with their primary care physician.

Suggested Reading

1. Feldman CF. Pneumonia in the elderly. Clin Chest Med 1999; 20(3):563.

2. Dean NC. Use of prognostic scoring and outcome assessment tools in the admission

decision for community-acquired pneumonia. Clin Chest Med 1999; 20(3):521.

3. American Thoracic Society: Guidelines for the initial management of adults with community

acquired pneumonia: Diagnosis, assessment of severity, and initial microbial

therapy. Am Rev Respir Dis 1999; 148:1418.

Table 3D.4. Radiographic presentation of pneumonia

Radiographic Pattern Pathogens

Lobar Streptococcus pneumoniae

Klebsiella pneumoniae (classically RUL, bulging fissure)

Patchy Atypical agents

Haemophilus influenzae

Staphylococcus aureus

Fungi

Viruses

Interstitial Mycoplasma pneumoniae

Viruses

Pneumocystis carinii

Abscess Tuberculosis and other fungi

Staphylococcus aureus

Effusion Streptococcus pneumoniae

Staphylococcus aureus

Mycoplasma pneumoniae

Viruses

Tuberculosis

Apical Tuberculosis

Klebsiella pneumoniae

Table 3D.5. High risk patients

Risk Factor Comment

Abnormal vital signs Tachypnea (>30/min)

Hypotension (<70 mm Hg systolic)

O2 saturation <95% on room air

Extremes of age <6 mos or >60 yr

Comorbid conditions or disease Pregnancy

Congestive heart failure

Renal or hepatic insufficiency

Immunosuppression: HIV, asplenia, diabetes,

alcohol/drug abuse

Recent hospital admission

Patients who fail initial therapy

Risk of aspiration Stroke, AMS, alcohol abuse

Pathogen Suspected tuberculosis

Gram-negative bacilli on sputum examination

Inability to care for self as outpatient

Pulmonary Emergencies 67

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4. Emergency Medicine Reports: Community-acquired pneumonia (CAP) in the geriatric

patient: Evaluation, risk-stratification, and antimicrobial treatment guidelines for inpatient

and outpatient management 2000; 21(20).

5. The Sanford Guide to Antimicrobial Therapy, 31st edition. 2001.

Part E: Hemoptysis

• Definition—Expectoration of blood from the respiratory tract below the level of the

larynx.

• The amount can vary from blood-tinged sputum to mild (<5 ml in 24 h) to moderate

(5-600 ml in 24 h) to severe (>600 ml in 24 h).

• Mortality is often a result of hypoxemia secondary to impaired gas exchange and also

depends upon the underlying disease process (see Table 3E.1).

Etiology

• Neoplasm and TB are responsible for a significant number of cases but there are many

causes of hemoptysis (see Table 3E.1).

Diagnosis

• History should include symptom acuity, and quality/quantity of expectorate, presence

of associated symptoms (i.e., weight loss, fever, etc), past medical history, risk factors for

pulmonary disease (i.e., cigarette smoking), and recent travel history.

• Patients present with varying degrees of respiratory and/or circulatory compromise

depending upon the severity of bleeding and the underlying cause. In cases of massive

hemorrhage, the patient may present with the affected side recumbent to prevent

blood from filling the uninjured lung.

Table 3D.6. Antimicrobial guidelines for pneumonia

Group Treatment* Alternatives

Outpatient therapy Erythromycin Levofloxacin

Adults 18-65 yr Clarithromycin Second generation

cephalosporin

No comorbid disease Azithromycin (5 days) Doxycycline

Amoxicillin/clavulanate

Outpatient therapy Bactrim

Adult >65 Doxycycline

Alcohol/tobacco use Azithromycin (5 days)

Levofloxacin

Inpatient therapyª Ceftriaxone or cefotaxime + macrolide

General ward Cefuroxime + macrolide

Levofloxacin

Inpatient therapy Azithromycin + ampicillin/sulbactam

Suspected aspiration Levofloxacin + clindamycin

Second or third generation cephalosporin + clindamycin

Inpatient therapy Ticarcillin/clavulanate + aminoglycoside

Ventilated/ICU Piperacillin/tazobactam + aminoglycoside

Ceftazidime + aminoglycoside

Imipenem

* All regimens are for 7-14 days unless otherwise noted

ª All medications for inpatient therapy via IV route

68 Emergency Medicine

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• Both the pulmonary and extrapulmonary exams help identify the cause of the bleeding.

Pulmonary findings may include rhonchi, rales, decreased breath sounds, egophony,

or a pleural rub. Extrapulmonary findings may include a diastolic murmur of

mitral valve stenosis, supraclavicular adenopathy suggestive of cancer, or digital clubbing

in patients with chronic lung disease. Also look for mucosal or cutaneous changes

in patients with vasculitic pathology.

• Diagnostic Studies

• CXR is indicated in all cases and often aids identification of the etiology.

• Sputum examination—True hemoptysis is identifiable by its characteristic bright

red appearance and alkaline pH. Hematemesis is usually darker, has an acidic pH,

and may contain food particles. However, aspiration of gastric hemorrhage may

create confusion. An AFB stain and culture is mandatory in all patients for whom

TB is suspected.

• Laboratory studies—CBC with differential is the most important and commonly

ordered test. Others including PT, electrolytes, glucose, BUN, creatinine, and blood

type and screen may be performed depending upon the patient’s history and presentation.

• An EKG should be obtained in patients with suspected valvular or congestive heart

disease.

• Specialized radiography such as computerized tomography (CT) and ventilation/

perfusion (V/Q) scans are ordered as needed for suspected neoplasm, bronchiectasis

or PE.

• Bronchoscopy is the gold standard for diagnosis and allows for clot removal and

retrieval of material for biopsy and culture. This is often not possible with severe,

uncontrolled bleeding.

Treatment

• Management of the patient’s airway, breathing and circulatory status are paramount. Supplemental

oxygen as well as crystalloid and/or blood product administration should be administered

as needed. Patients with respiratory failure or difficulty maintaining a patent

Table 3E.1. Etiology of hemoptysis

Infectious Chronic bronchitis

Tuberculosis

Fungal and parasitic infections

Necrotizing pneumonia

Pulmonary abscess

Neoplasia Bronchogenic carcinoma

Pulmonary metastasis

Bronchial adenoma

Cardiopulmonary Mitral valve stenosis

Vascular Pulmonary embolus

Alveolar arteriovenous malformation

Other Trauma

Foreign body

Bronchiectasis

Wegener’s granulomatosis

Goodpasture’s syndrome

Systemic lupus erythematosus

Coagulopathy and use of anticoagulant medications

Idiopathic hemosiderosis

Pulmonary Emergencies 69

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airway mandate intubation. Orotracheal intubation with a large (≥8.0) endotracheal tube

is preferred. This facilitates suctioning and allows for subsequent bronchoscopy.

• Temporizing Measures for Hemorrhage Control in those with Severe Bleeding

• Bronchoscopic balloon tamponade by a pulmonologist

• Selective bronchus intubation

• If the bleeding source is the left lung, selective intubation of the right mainstem

bronchus is accomplished by advancing the tube 4-5 cm beyond the usual

position.

• Intubation of the left mainstem bronchus is more difficult. Rotating the endotracheal

tube 90 degrees counter-clockwise so the tube concavity faces the left

during intubation is sometimes successful. If available, a double-lumen endotracheal

tube can be used although there are often complications and most physicians

have little to no experience with the product.

• Definitive Hemorrhage Control

• Treatment should address any underlying condition such as infection, vasculitis, or

coagulopathy.

• Patients with moderate to severe bleeding warrant emergent evaluation by a pulmonary

specialist for bronchoscopy. Arterial embolization by interventional radiology

is an option for those with uncontrolled hemorrhage or when bronchoscopy is not

possible or not successful.

• Some disease processes are amenable to surgical therapy and a thoracic surgery

consult is indicated if other modalities fail to control bleeding.

Disposition

• All patients with respiratory compromise or unstable hemodynamics should be admitted

to an intensive care unit. There is a high incidence of recurrence in patients

with self-limiting massive hemoptysis and these patients also require intensive care

admission.

• Patients with suspected TB should be admitted and kept in respiratory isolation until

appropriate testing is completed.

• Patients with minor, self-limiting hemoptysis can be considered for discharge. Outpatient

treatment should address the underlying etiology. All discharged patients should

follow-up with their primary care provider or a pulmonologist.

Massive Hemoptysis

Expectoration of blood from lower respiratory tract (systemic bronchial vessels

and low pressure pulmonary vessels) >50 ml per episode or 600 ml/24 h. It may be

differentiated from hematemesis and bleeding from a ENT source ( such as epistaxis)

during the course of resuscitation, which must proceed emergently in severe cases.

Primary Survey

Airway: Endotracheal intubation with RSI technique is indicated.

A large diameter ET tube should be used (8.0 or larger if possible) to provide

pulmonary toilet and facilitate bronchoscopy

The ET tube should be advanced to the mainstem bronchus of nonbleeding

lung, if there is persistent bleeding. The right mainstem is easily entered,

the left requires specialized technique and/or equipment.

Until the airway is secured with endotracheal intubation, personnel should

take precautions against respiratory spread of tuberculosis.

Breathing: Both before and after intubation, the patient should be positioned with

bleeding lung dependent to maximize gas exchange and minimize the filling

of the unaffected side with blood.

70 Emergency Medicine

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Sedation and paralysis should be considered to prevent coughing and retching

that may dislodge clot and worsen hemorrhage.

Circulation: IV fluid resusciation may be initiated with normal saline through large

bore IV access, followed by emergent blood transfusion as needed. Blood

type and crossmatch is critical.

Fresh frozen plasma and platelets should both be considered when there is

suspected coagulopathy or severe thrombocytopenia.

Massive, uncontrolled hemoptysis may require a spectrum of emergent

specialty consultation, including cardiothoracic surgery, interventional radiology

and pulmonary medicine.

Disability: A cursory neurological examination should be sought prior to paralysis and

endotracheal intubation so the need to image the head for intracranial pathology

can be assessed.

Resuscitation Phase

Critical Questions: Other coexistent conditions that may require other critical actions

in the setting of massive hemoptysis:

Conditions Actions

Advanced malignancy Consider level of intervention

Seek advance directives, family conference

Pneumonia Sputum cultures and IV antibiotics

Valvular heart lesion Emergent cardiac surgery consultation

Critical investigations: These may also include:

Emergent bronchoscopy To localize and treat source of bleeding

Emergency bronchial arteriography

CT Chest

Suggested Reading

1. Cahill BC, Ingbar DH. Massive hemoptysis: Assessment and management. Clin Chest

Med 1994; 15(1):147.

2. Dweik RA, Stoller JK. Role of bronchoscopy in massive hemoptysis. Clin Chest Med

1999; 20(1):89.

3. Goldman JM. Hemoptysis: Emergency assessment and management. Emerg Med Clin

North Am 1989; 7(2):325.

4. Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care

Med 2000; 28(5):1642.

5. Marshall TJ, Flower CDR, Jackson JE. The role of radiology in the investigation and

managment of patients with haemoptysis. Clin Radiol 1996; 51:391.

Part F: Pleural Effusions

• The pleural space normally contains a minimal amount of fluid. A pleural effusion is

an excessive collection of fluid in the pleural space resulting from an underlying disease

process (see Table 3F.1).

• Effusions may be transudative (resulting from changes in hydrostatic or oncotic pressure)

or exudative (secondary to alterations in capillary permeability or lymphatic/

vascular obstruction).

Diagnosis

• Patients with small effusions are often asymptomatic. Common complaints with symptomatic

effusions are dyspnea, pleuritic chest pain, or cough. Patients may also have

complaints related to their underlying disease or give a history of cancer, heart failure,

or other comorbidity.

Pulmonary Emergencies 71

3

• The physician should note any increased work of breathing or obvious respiratory

distress. Pulmonary exam may also reveal decreased breath sounds, dullness to percussion,

and decreased tactile fremitus. A friction rub is sometimes noted with mediumsized

effusions. Extrapulmonary findings are present depending upon the etiology and

include peripheral edema, jugular venous distension, ascites, abdominal tenderness,

and lymphadenopathy among others.

• Diagnostic Studies

• CXR—As little as 175 ml is visualized as a blunting of the costophrenic angle on a

routine film. A lateral decubitus view can identify even smaller amounts of fluid.

Subpulmonic effusions appear as an elevated hemidiaphragm.

• Laboratory—Selected studies often include a CBC, electrolytes, BUN, creatinine, and

glucose depending upon the suspected etiology. If a thoracentesis will be preformed,

additional tests should include a serum protein and lactate dehydrogenase (LDH).

• Thoracentesis

• Classification of pleural effusions as a transudate includes a ratio of pleural fluid

protein to serum protein <0.5, pleural fluid LDH <200 IU/ml, a ratio of pleural

fluid LDH to serum LDH <0.6, fluid protein <3 g/100 ml, and fluid pH <1.016.

Effusions that exceed these values are classified as exudates.

• Other tests to consider for exudative pleural fluid are cell count and differential,

pH, glucose, Gram stain, bacterial culture, and cytology. Consider amylase if

pancreatitis or esophageal rupture is suspected.

Treatment

• Initial treatment includes oxygenation, and ventilatory and circulatory support if needed.

Large effusions causing respiratory compromise require emergent drainage.

• Patients with effusions should have a diagnostic thoracentesis unless the etiology is

apparent (heart failure, pneumonia, etc). It has been recommended that no more than

1,000-1,500 ml is drained at one time in order to prevent reexpansion pulmonary

edema. This complication is rare and is minimized by the avoidance of excessive negative

pressure.

• Specific treatments are based on the underlying cause of the effusion as determined by

clinical presentation and diagnostic thoracentesis.

• Chest tube placement is required for empyema and hemothorax.

Table 3F.1. Causes of pleural effusions

Transudative Congestive heart failure

Nephrotic syndrome

Renal failure

Cirrhosis

Pulmonary embolism

Exudative Pulmonary infections

Pulmonary embolism

Malignancy (primary or metastatic)

Drug induced effusion

Connective tissue disease

Trauma

Subdiaphragmatic abscess

Esophageal perforation

Pancreatitis

72 Emergency Medicine

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Disposition

• The need for hospital admission is based on the degree of respiratory or circulatory

impairment, as well as the cause of the effusion. Most patients are admitted to the

hospital following a thoracentesis for observation and treatment of the underlying

condition.

• In a minority of cases, well-appearing patients can be discharged home after thoracentesis

following 4-6 h of observation. All patients who have had a thoracentesis must

have a post-procedure CXR to rule out complications such as pneumothorax or hemothorax.

Suggested Reading

1. Berkman N, Kramer MR. Diagnostic tests in pleural effusion—an update. Postgrad

Med J 1993; 69:12-8.

2. Heffner JE. Evaluating diagnostic tests in the pleural space. Differentiating transudates

from exudates as a model. Clin Chest Med 1998; 19:277-93.

3. Light RW. Useful tests on the pleural fluid in the management of patients with pleural

effusions. Curr Opin Pulm Med 1999; 5:245-9.

4. Strange C. Pleural complications in the intensive care unit. Clin Chest Med. 1999;

20:317-27.

5. Ross DS. Thoracentesis. In: Roberts JR, Hedges JR, eds. Clinical Procedures in Emergency

Medicine, 2nd ed. WB Saunders Company, 1991.

Part G: Pneumothorax

• A simple pneumothorax (PTX) is an accumulation of air in the pleural space and no

communication with the atmosphere. It can occur spontaneously or as a result of

trauma. Tension PTX occurs when air continues to enter the pleural space via a one-way

communication with the atmosphere. This causes a collapse of the lung, shifting of

the mediastinum away from the PTX, and compression of the mediastinal vessels. If

untreated, the result is decreased venous return, hypotension, and death.

• Spontaneous PTX is seen in patients with (secondary) and without (primary) underlying

pulmonary disease. Primary spontaneous PTX occurs more commonly in tall

men 20-40 yr of age and has a high rate of recurrence. Secondary spontaneous PTX is

usually associated with chronic obstructive lung disease as well as other pulmonary

disease states such as infection, asthma, neoplasm, and occupational disease.

Diagnosis

• Presentation

• The most common symptoms are dyspnea and acute onset of ipsilateral chest pain.

• Depending on the size of the PTX and the patient’s pulmonary reserve, varying

degrees of respiratory and circulatory distress are noted. Pulmonary exam can

reveal decreased breath sounds on the affected side, crepitus, and hyperresonance

to percussion.

• Signs of a tension PTX include tachycardia, hypotension, hypoxia, agitation, decreased

breath sounds, and jugular venous distension. Tracheal deviation is a late

physical finding.

• Evaluation

• Diagnosis of a tension PTX is based on history and clinical presentation. Relying

on CXR for the diagnosis can result in a fatal delay in treatment.

• CXR can confirm the diagnosis when a simple PTX is suspected. CXR will reveal

hyperlucency with a lack of lung markings at the periphery of the lung on the

affected side. An expiratory or lateral decubitus film is helpful in identifying a small

PTX when inspiratory CXR is not diagnostic.

Pulmonary Emergencies 73

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Treatment

• Oxygen administration will increase the rate of resorption of the air from the pleural

space as well as improve oxygen saturation.

• Definitive therapy is release of air from the pleural space.

• Tension PTX is treated by immediate needle thoracostomy in the second or third

intercostal space at the midclavicular line. This is followed by tube thoracostomy.

• Traumatic PTX is treated by placing a large (36-40 French) thoracostomy tube in

the fourth of fifth intercostal space at the anterior axillary line.

• Primary, spontaneous PTX can be treated by simple aspiration with a 16-gauge needle

through the second intercostal space at the mid-clavicular line, via a small catheter

with a one-way valve (Heimlich), or with a small thoracostomy tube. Aspiration of

the PTX is more likely to succeed when <20% of the involved lung is collapsed. For

a very small PTX, with only a rim of air visible on CXR, observation and close

follow-up is appropriate.

Disposition

• Patients with traumatic PTX require close monitoring as indicated by other injuries.

• Patients with a small PTX who have successful needle aspiration or one-way valve

placement may be discharged home after a period of observation and post-procedure

CXR. 24 h follow-up is recommended.

Suggested Reading

1. Light RW. Management of spontaneous pneumothorax. Ann Rev Respir Dis 1993;

148:245.

2. Miller AC, Harvey JE. Guidelines for the management of spontaneous pneumothorax.

Br Med J 1993; 307:114.

3. Tanaka F, Masatosi I, Esaki J et al. Secondary spontaneous pneumothorax. Ann Thoracic

Surg 1993; 44:372.

Part H: Pulmonary Embolism

Pulmonary embolism (PE) is the third most common acute cardiovascular disease

after ischemic heart disease and stroke. It is a potentially fatal disorder that is

often difficult to recognize and diagnose.

Risk Factors

The strongest risk factor for PE is prior thromboembolic disease including past

PE and deep-venous thrombosis (DVT). PE is detected on perfusion imaging in a

majority of patients with documented DVT even in the absence of clinical findings.

The classic triad of stasis, hypercoaguability, and endothelial injury forms the basis

for the many other causes (see Table 3H.1).

Diagnosis

• Clinical presentation: depends on the size of the clot and the degree of subsequent

hemodynamic compromise. Signs and symptoms can be extremely subtle and nonspecific

(even non-existent) and a high degree of suspicion is often necessary to make

the diagnosis.

• The classic presentation is acute onset of sharp, pleuritic chest pain with associated

dyspnea. Other symptoms include cough, non-pleuritic chest pain, reproducible

chest pain, anxiety, syncope, and hemoptysis.

• Physical findings may include cyanosis, tachypnea, tachycardia, hypotension, diaphoresis,

fever, S3 or S4, or clinical signs of a lower extremity DVT.

74 Emergency Medicine

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• Evaluation

• CXR is normal in only 30% of patients with PE. While the diagnosis is rarely made

by CXR alone, this study can help exclude other diseases with a similar presentation

such as PTX, pneumonia, or pulmonary edema. A wedge-shaped, pleural-based density

that points to the hilum (Hampton’s hump) and a prominent central pulmonary

artery with decreased distal pulmonary vessels (Westermark’s sign) are fairly specific

radiographic findings for PE but are not commonly seen. Other nonspecific findings

include an elevated hemidiaphragm, pleural effusion, or atelectasis.

• EKG should be performed on all patients with suspected PE. The most common

abnormalities are sinus tachycardia and nonspecific ST-segment and T-wave changes.

Evidence of right heart strain, such as right bundle branch block, right axis deviation,

or a right ventricular strain pattern are seen in a minority of patients with PE.

The most specific, although insensitive, EKG finding is a prominent S-wave in lead

I, with an inverted T-wave and prominent Q-wave in lead III (S1Q3T3 pattern).

• ABG can lend support to the diagnosis. Specific findings include hypoxia, hypocapnia

or an elevated alveolar-arterial (A-a) gradient. In the PIOPED study, 85% of

the patients had a PO2 <90 mm Hg, while 80% had an A-a gradient >20. This test

cannot be used to exclude the diagnosis since 5-15% of patients with PE have a

normal ABG.

• D-dimer assays have been suggested to have diagnostic utility. Unfortunately, these

assays lack specificity, and there is a large range of sensitivity depending on the assay

used (69-100%). The most sensitive is the ELISA assay. A normal D-dimer by

ELISA assay decreases the likelihood that a patient has a PE, but by itself cannot

exclude the diagnosis.

• V/Q scan has classically been the diagnostic study of choice although helical CT

is now being used in many centers. The results of V/Q scanning are reported as

normal, low probability, intermediate probability, and high probability. Clinical

interpretation of results depends on the degree of clinical suspicion for PE. A

normal or scan in combination with a low clinical suspicion makes the diagnosis

of PE unlikely. A high probability scan in combination with a high clinical suspicion

makes the diagnosis of PE very likely although not definite. All other combinations

of V/Q scan results and clinical suspicion are not definite enough to

either rule in or out PE and additional diagnostic testing is indicated.

• Helical CT scan can also be used to identify a PE. This scan may be useful in

patients with significantly abnormal CXR when there is a high likelihood that the

V/Q scan will be nondiagnostic. Although in most studies this test is very sensitive

for diagnosing PE in the larger pulmonary vessels, it has been shown to lack sensi-

Table 3H.1. Risk factors for pulmonary embolism

Causative Factor Comment

Stasis Immobility (bed rest, casting, air/car travel), paralysis, obesity,

heart failure, varicose veins, myocardial infarction

Hypercoagulability Prior thromboembolic disease, malignancy, inflammatory

disease, nephrotic syndrome, sepsis

Hematologic Disorder Protein C & S deficiencies, antiphospholipid antibodies,

antithrombin III deficiency, polycythemia

Increased Estrogen Pregnancy and <3 mo postpartum, oral contraceptive use

Endothelial Injury Trauma, intravenous drug use, surgery, central venous catheters

Pulmonary Emergencies 75

3 tivity for emboli in the smaller, subsegmental branches. Therefore a negative CT

scan does not rule out the diagnosis.

• Lower extremity venous studies may aid in the diagnosis for patients with intermediate

probability V/Q scans. A lower extremity DVT is present 50-70% of all patients

with a proven PE. Evaluation for DVT can be done by impedance plethysmography,

doppler ultrasound, or venogram. The gold standard for diagnosis of a

DVT is the venogram; however this is an invasive procedure and is technically

difficult. The duplex ultrasound is the most commonly used tool for the diagnosis

of a DVT. It has 93% sensitivity and 98% specificity for diagnosis of proximal

DVT. The sensitivity is much lower for calf DVTs (60%). Note that a negative

venous study does not rule out PE—the tests are only helpful if positive.

• The gold standard for diagnosis of PE is the pulmonary angiogram although even

angiography can miss small, distal emboli. It is an invasive procedure with a low risk

of mortality. However, in most institutions this study is not available 24 h a day. It is

generally used only to confirm the diagnosis in patients with nondiagnostic V/Q

scans or when results of V/Q scanning does not correlate with clinical suspicion.

• Echocardiography is useful when evaluating a hemodynamically unstable patient

with suspected PE. This modality can help diagnose other potential etiologies and

can identify changes consistent with PE such as right ventricular enlargement, pulmonary

artery dilatation, and tricuspid regurgitation.

• Treatment

• Support of airway, breathing, and circulation is the initial goal of therapy.

• Treatment of the stable patient consists of anticoagulation. This should be started

prior to final diagnosis when there is a high degree of clinical suspicion for PE.

There are two options for anticoagulation. Low molecular weight heparin (LMWH)

has been shown to effective in patients with PE. The most commonly used agent is

enoxaparin 1 mg/kg SQ every 12 h. The alternative is standard heparin administered

as an initial bolus of 80 units/kg followed by an intravenous drip of 18 units/

kg/h. Relative contraindications to anticoagulation include recent stroke or major

surgery, advanced liver or kidney failure, or bleeding diathesis.

• Fibrinolytics should be considered in hemodynamically unstable patients. The dosing

differs from the protocols used for myocardial infarction (see Table 3H.2).

• Surgical embolectomy is the final option for hemodynamically unstable patients

who have failed medical therapy or who have a contraindication to fibrinolytics.

Disposition

All patients with suspected PE should be admitted to a telemetry bed for monitoring

and anticoagulation. Intensive care unit admission is necessary for patients

with hemodynamic compromise.

Table H2. Fibrinolytic dosing for pulmonary embolism

Urokinase 4400 IU/kg over 10 min then 4400 IU/kg/h

for 12 h

Streptokinase 250,000 IU over 30 min then 100,000 IU/h

for 24 h

Tissue Plasminogen Activator 100 mg over 2 h

76 Emergency Medicine

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Suggested Reading

1. Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the

prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED

Investigators. JAMA 1990; 263:2753-9.

2. Curtin JJ, Mewissen MW, Crain MR, Lipchik RJ. Postcontrast CT in the diagnosis and

assessment of response to thrombolysis in massive pulmonary embolism. J Comput Assist

Tomogr 1994; 18:133-5.

3. Fisman DN, Malcolm ID, Ward ME. Echocardiographic detection of pulmonary embolism

in transit: Implications for institution of thrombolytic therapy. Can J Cardiol

1997; 13:685-7.

4. Goldhaber SZ. Treatment of pulmonary thromboembolism. Intern Med 1999; 38:620-5.

5. Kline JA, Johns KL, Colucciello SA, Israel EG. New diagnostic tests for pulmonary

embolism. Ann Emerg Med 2000; 35:168-80.

6. Perrier A, Desmarais S, Miron MJ et al. Non-invasive diagnosis of venous thromboembolism

in outpatients. Lancet 1999; 353:190-5.

7. Rathbun SW, Raskob GE, Whitsett TL. Sensitivity and specificity of helical computed

tomography in the diagnosis of pulmonary embolism: A systematic review. Ann Intern

Med 2000; 132:227-32.

CHAPTER 1

CHAPTER 4

Emergency Medicine, edited by Sean Henderson. ©2006 Landes Bioscience.

Neurologic Emergencies

Jacquelyn Hasler Salas

Part A: Headache

Anatomy

• Headache, or cephalgia, is defined as pain in various parts of the head, not confined to

the area of distribution of any nerve.

• Headache is caused by distention, traction, displacement, inflammation, vascular spasm,

dilation, or compression of the pain-sensitive structures in the head and neck. The

pain-sensitive structures of the supratentorial space refer pain via the trigeminal nerve,

which innervates the anterior scalp and face. Pain-sensitive structures in the infratentorial

space refer pain via cranial nerves IX, and X, and the second and third cervical nerves;

thus, pain originating in the posterior fossa may be referred to the ear or throat, or the

posterior area of the head and neck.

• Intracranial sources of head pain include the cranial sinuses and afferent veins; the

anterior and middle meningeal arteries; the trigeminal (V), glossopharyngeal (IX),

and vagus (X) nerves; falx cerebri; the dura at the base of the skull; the major arteries at

the base of the brain; the brain stem periaqueductal gray matter; and the sensory

nuclei of the thalamus.

• Muscles frequently involved in extracranial causes of cephalgia include the masseter,

frontalis, temporal, occipital, trapezius, sternocleidomastoid, and deep cervical muscles.

In addition, the skin, the periosteum of the skull, the subcutaneous tissues and arteries,

the eyes, ears, teeth, sinuses, oropharynx, and the mucous membranes of the nasal

cavity may be sources of pain.

Etiology/Risk Factors

Primary headaches are benign, usually recurrent, and have no underlying cause.

These include migraine, cluster, and tension-type headaches. Secondary headaches,

on the other hand, are a symptom of underlying organic disease. Risk factors for

secondary headache disorders include:

• “First or worst” headache

• Very sudden onset

• Nausea and vomiting

• Systemic illness

• Ocular findings

• History of head trauma

• History of immunodeficiency or cancer

• Increased frequency or severity

• Focal neurologic deficits, or altered mental status

• Onset after age 50, or before 3

• Fever, neck stiffness, or meningeal signs

• Headache that begins with exertion or is positional

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Diagnosis

History

• The most important task in evaluating a patient with headache is to identify or exclude

underlying pathology based on the history and physical examination. A detailed

history should be taken to include the following elements:

• Was the onset sudden, gradual, or subacute? Was the patient awakened from sleep?

Are there any precipitating or aggravating factors (e.g., activity, stress, menses/hormonal

therapy, medications/medication withdrawal, foods, cough/Valsalva maneuver,

environmental exposures, position changes, trauma)? Episodes of migraine are often

concentrated around the menstrual period. Exposure to tyramine- or amine-containing

foods, nitrates, MSG, or ethanol may precipitate a migraine; stress, weather changes,

changes in sleep patterns, and caffeine withdrawal are also potential triggers.

Tension-type headaches are often stress-related. Alcohol is reported to precipitate cluster

headaches. The use of cocaine is a risk factor for subarachnoid hemorrhage (SAH).

Are there any alleviating factors?

• Is there a prodrome (e.g., visual, auditory, or olfactory aura or hallucinations; numbness,

paresthesias or motor weakness; speech impairment)? An aura may precede a migraine

headache by up to an hour; patients without aura may have other symptoms suggesting

the onset of a migraine, including lethargy, depression, hyperactivity, or food craving.

• Where is the pain located (e.g., unilateral or bilateral; ocular/retro-ocular; paranasal; frontal

or occipital; at the vertex; in the pharynx or external auditory meatus)? What is the

character of the pain (e.g., sharp, stabbing; dull, steady ache; burning; lancinating; “worst

headache ever”)? Tension-type headaches are described as a diffuse pressure or tightness.

Migraines are typically unilateral, with a pulsating quality. Cluster headaches are excruciating,

sharp, unilateral headaches. Does the pain radiate?

• Are there any associated symptoms (e.g., fever/chills; nausea/vomiting; neck pain or

stiffness; seizures; focal neurologic deficits; ataxia; speech deficit; dizziness/vertigo;

visual changes or eye pain; altered mental status or transient loss of consciousness; jaw

claudication; myalgias; weight loss)? Migraine headaches are frequently associated with

photophobia or phonophobia. Symptoms accompanying a cluster headache include

conjunctival injection, lacrimation, rhinorrhea, ptosis, myosis, and ipsilateral forehead

sweating. Suspicion should be raised for SAH when nausea and vomiting, photophobia,

neck stiffness, or loss of consciousness accompanies the headache.

• What is the frequency of the pain (e.g., intermittent, chronic, seasonal)? Are the headaches

increasing in frequency or severity? How long does the pain last? Cluster headaches

occur once or twice daily—generally at the same time each day—and last about

30 to 90 min. The symptoms may recur for several weeks, and then the patient may

remain pain-free for months or years. Headaches that persist for more than 10 wk,

without associated symptoms, are unlikely to be caused by a neoplasm.

• Is there a family history of headaches? Are there any ongoing medical problems or

recent illnesses? The presence of polycystic kidney disease, Ehlers-Danlos or Marfan’s

syndrome, Grave’s disease, fibromuscular dysplasia, coarctation of the aorta or abdominal

aortic aneurysm, sickle cell disease, atherosclerosis, or hypertension places

the patient at increased risk for SAH or unruptured aneurysm. Is there an HIV history

or risk? Are there any close contacts with similar symptoms? Patients with mild carbon

monoxide poisoning may complain of nonspecific headache and flu-like symptoms;

frequently, members of the same household will have the same toxic exposure and

thus present with similar symptoms.

Vital Signs

• Vital signs may reveal an elevated temperature or blood pressure; tachycardia;

or tachypnea.

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Physical Exam

• A detailed examination of the head may reveal tenderness of the scalp, temporomandibular

joint (TMJ), temporal artery, or sinuses; evidence of head trauma; or disorders

of the eyes, ears, nose, or teeth.

• Examine the neck for bruits, range of motion, and tenderness.

• Examination of the skin may reveal a focal cellulitis, a generalized rash, neurofibromas

or café au lait spots, or cutaneous angiomas.

• A complete neurologic exam is essential, including level of consciousness, mental status,

pupillary responses, cranial nerves, deep tendon reflexes, motor and sensory function,

gait, cerebellar function, and pathologic reflexes.

Differential Diagnosis

Primary Headache

• Migraine

• Tension-type

• Cluster headache

Secondary Headache

• Associated with head trauma

• Post-traumatic headache syndromes

• Associated with vascular disorders

• Infarction, transient ischemic attack (TIA), SAH, unruptured vascular malformation,

arteritis, carotid or vertebral artery pain (arterial dissection, carotidynia), intracranial

hematoma, venous thrombosis, acute arterial hypertension

• Associated with nonvascular intracranial disorders

• High and low CSF pressures, infection, intracranial mass, sarcoidosis, other granulomatous/

inflammatory diseases

• Associated with exposure or use of substances or their withdrawal

• Associated with noncephalic infection

• Associated with metabolic disorders

• Hypoxia, hypercapnia, dialysis, hypoglycemia, hypo- or hyperthyroidism, hypoadrenalism

• Associated with facial or cranial structures

• Skull, neck, eyes, ears, nose, sinuses, teeth and jaws, mouth, TMJ joint, or other

facial or cranial structures

• Paget’s disease, skull metastases, cervical arthritis, acute angle closure glaucoma,

retro-orbital infection, sinusitis, dental caries

• Cranial neuralgias, nerve trunk pain, and deafferentation pain

• Optic neuritis, zoster (post-herpetic neuralgia), trigeminal neuralgia, glossopharyngeal

neuralgia, occipital neuralgia, pain of cranial nerve origin

• Other causes of headache pain

• Idiopathic stabbing headache, external compression headache, cold stimulus headache,

benign exertional headache, benign cough headache, associated with sexual

activity

• High-altitude, anemia, hypotension

Evaluation

Laboratory

• A CBC may be useful in cases of suspected infection, hematologic disorders, or

vasculitis.

80 Emergency Medicine

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• A CD4 count of <500 or 200 in HIV-infected individuals increases the risk for:

• Meningitis (cryptococcal, tuberculous, syphilitic, and lymphomatous);

• Focal brain lesions (toxoplasmosis, CNS lymphoma, PML, abscess, crypotococcoma)

• Diffuse brain lesions (CMV, HSV, toxoplasmosis).

• An erythrocyte sedimentation rate (ESR) of at least 55 mm/h—and usually over 100—

is seen in 90% of patients with temporal arteritis.

• A carboxyhemoglobin level is obtained if carbon monoxide poisoning is suspected.

• A lumbar puncture with analysis of the cerebrospinal fluid (CSF) is essential in the

evaluation of several headache disorders:

• Meningitis—CSF may be cloudy, with elevated WBC and protein, and low glucose.

Specimens should also be sent for stat Gram stain and culture, and—in specific

cases—VDRL, India ink, bacterial antigens, and CSF antibody detection (for

viral encephalitis).

• Subarachnoid hemorrhage—opening pressure may be increased; fluid may be bloody

or xanthochromic (discolored supernatant of centrifuged CSF, as a result of hemolysis),

with increased RBC and protein, and normal glucose. (In the setting of a negative

head CT, LP must still be performed to exclude small SAH not identified by CT.)

• Benign intracranial hypertension—opening pressure is elevated (above 200 mm

H2O); other CSF components are normal; relief from headache with removal of

fluid may be diagnostic.

Imaging

• A panorex radiograph may reveal a dental etiology in selected patients.

• A cervical spine series may be warranted in the setting of trauma or suspicion of cervical

arthritis.

• Emergent neuroimaging is performed in order to identify treatable lesions (e.g., tumors,

AVMs, SAH, cerebral sinus thrombosis, subdural and epidural hematomas, and

hydrocephalus). Computed tomography (CT) scanning of the head without contrast

is indicated when certain historical or physical “red flags” are identified in the evaluation

of a new-onset headache:

• Acute onset, severe headache

• Any neurologic deficit

• History of seizures

• Ocular abnormalities including papilledema, visual impairment, or diplopia

• Persistent or frequent vomiting preceded by recurrent headaches

• Changing character of the patient’s headache

• Extremes of age (patients <3 or over 50)

• Children with neurofibromatosis

• Diabetes insipidus, HIV

• Antecedent head trauma

• Patients with signs of increased intracranial pressure (e.g., papilledema or absent venous

pulsations on funduscopic exam, altered mental status, or focal neurologic deficits)

should be scanned prior to having a lumbar puncture.

• Contrast-enhanced head CT should be considered in patients with a history of immunodeficiency

or malignancy (after a negative noncontrast CT).

• Magnetic resonance imaging (MRI) of the brain may be preferable to CT in cases in

which the posterior fossa must be specifically evaluated but is generally not as readily

available as CT.

Treatment

Primary Headache

• Migraine

Neurologic Emergencies 81

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• Patients with new onset migraine may respond to simple analgesics such as acetaminophen

or oral nonsteroidal anti-inflammatory drugs (NSAIDs). A maximal dose should

be given for prompt relief. Parenteral NSAIDs (ketorolac) may be useful in patients

who present later in the course of their symptoms or have nausea or vomiting.

• Serotonin (5-HT) receptors have been shown to modulate neurogenic peptide release

and vasoconstrict dilated dural vessels. As a result they are the main focus of

pain management. Many medications traditionally employed in the management

of migraine headaches—dihydroergotamine (DHE), prochlorperazine, and

metaclopramide—act at a variety of serotonin and other aminergic receptors.

Metoclopramide and prochlorperazine also act as dopamine antagonists and are

often successful in relieving both the pain and the nausea associated with migraine.

Side effects include orthostatic hypotension, akathesia, and dystonic reactions.

• Ergotamine derivatives are potent vasoconstrictors and are contraindicated in

pregnancy, renal or hepatic disease, uncontrolled hypertension, and in patients

with known or suspected coronary artery disease or Prinzmetal’s angina. In addition,

they tend to cause nausea and are generally given in combination with an

antiemetic.

• The triptans—selective 5-HT1 receptor agonists—can be effective in reducing or

eliminating migraine pain without significant sedation. Side effects include chest,

neck, and/or throat tightness, heaviness, pressure, or pain; paresthesias, and flushing.

They have the same contraindications as DHE; in addition, they should not be

used in patients suffering from basilar or hemiplegic migraine.

• Corticosteroids may be useful, especially in aborting status migrainosus.

• Narcotic agents should be used only when other medications are contraindicated or

ineffective. Rather than terminating the headache, they merely dull the pain. They

are associated with nausea, sedation, and orthostatic hypotension.

• Tension-Type Headache

• Tension-type headaches generally respond to NSAIDs. Other medications used to

treat migraine headaches are generally effective.

• Cluster Headaches

• The same medications used to treat migraine headaches are effective for cluster

headaches. In addition, acute cluster attacks frequently respond to inhalation of

100% oxygen by nonrebreathing face mask over 10 to 15 min. For refractory pain,

intranasal 4% lidocaine or dexamethasone (8 mg/day for 3-4 days) should be

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