JUST THE FACTS IN EMERGENCY MEDICINE - PART 3 ppt

TABLE 32-2 Causes of Hypercapnia Depressed central respiratory drive Structural central nervous system disease Sedating drugs Exogenous toxins Endogenous toxins Thoracic cage disorders K

obesity, burns, malignancy, estrogen use and other

hypercoagulable states, surgery in the last 3

months, or lower extremity trauma

PATHOPHYSIOLOGY

• The pathophysiologic effects are caused by both

mechanical obstruction of the pulmonary artery

system and the release of vaso- and bronchoactive

mediators These mediators—prostaglandins,

cat-echolamines, serotonin, and histamine—cause

bronchoconstriction as well as vasoconstriction of

the pulmonary artery

• Vasoconstriction is the predominant

pathophysio-logic effect, leading to a ventilation/perfusion

mis-match

• PE tends to be multiple and bilateral, with the

right lower lobe of the lung being the most

com-monly involved lung segment

CLINICAL FEATURES

• Common symptoms, in decreasing order of

fre-quency, include dyspnea, pleuritic chest pain,

anxi-ety, cough, hemoptysis, sweats, nonpleuritic chest

pain, and syncope.4,5

• Common signs, in decreasing order of frequency,

include respirations⬎16/min, rales, pulse ⬎100/

min, temperature⬎37.8⬚C (100.4⬚F), phlebitis or

DVT, cardiac gallop, diaphoresis, edema, and

cya-nosis.4Pleural friction rub and wheezes are

infre-quent signs of PE

• The presence or absence of any symptom or sign

does not confirm or exclude the diagnosis of

pul-monary embolism Chest pain (usually pleuritic)

and dyspnea are the most common symptoms, and

tachypnea (respirations ⬎16/min) is the most

common sign in the diagnosis of PE

• Clinical evidence of DVT occurs in less than 50

percent of patients However, up to 80 percent of

patients with PE have positive venography.2

• Massive PE (5 percent of cases) presents with

hypotension and hypoxia

DIAGNOSIS AND DIFFERENTIAL

• The diagnosis can be excluded or confirmed only

with more sophisticated tests, such as a

ventilation/perfusion (V˙ /Q˙) lung scan or

pulmo-nary angiography

• Hypoxia occurs in about 90 percent of patients

with PE, but the PaO may be normal While a

• Compare the above value with the expected mal A-a gradient calculated with the formulaA-a gradient⫽ patient age/4) ⫺ 4 The A-a gradi-ent is less reliable in the elderly.7Patients with anincreased A-a gradient or hypoxia require furthertesting to confirm or reject the diagnosis of PE

nor-A recent meta-analysis suggests that nor-A-a gradient

is unreliable as a screening test for PE.8

• AD-dimer level less than 500 U/mL has a negativepredictive value of 87 to 97 percent for PE, de-pending on the assay method.8 Clinicians shouldseek out second-generation tests However, theD-dimer assay has a high incidence of false positives,

up to 80 percent

• The most common electrocardiographic (ECG)finding is nonspecific ST-T-wave changes Theclassic S1Q3T3pattern on the ECG is highly sugges-tive of PE but is present in only 12 percent of pa-tients

• The chest x-ray may be normal in up to one-third

of patients.5Infiltrate or atelectasis will appear innearly 50 percent of patients An elevated dome

of one diaphragm is seen in 40 percent of patients,often with pleural effusion.5 Hampton hump, apleura-based, wedged-shaped infiltrate, is un-common

• The Westermark sign, relative oligemia distal toengorged pulmonary arteries, may be seen in pa-tients with massive PE

• A normal chest x-ray in the setting of dyspnea andhypoxemia without evidence of reactive airwaydisease is strongly suggestive of PE.9

• The V˙/Q˙ scan is 98 percent sensitive for PE butonly 10 percent specific.10A high-probability scan

is only 80 percent accurate in diagnosing PE, while

a low-probability scan is only 20 percent accurate

in excluding the disorder The combination of alow-probability scan with a low clinical suspicionhas a 96 percent predictive value of exclusion of

PE, while a high-probability scan in the setting ofhigh clinical suspicion has a 96 percent positivepredictive value.10

• Pulmonary angiography is the ‘‘gold standard’’ fordiagnosing PE and is a much more specific testthan the V˙ /Q˙ scan.5 Angiography exposes pa-

CHAPTER 28•PULMONARY EMBOLISM 103

tients—especially the elderly—to more potential

complications

• Disorders in the differential diagnosis include

re-spiratory disorders, such as asthma, COPD,

pneu-monia, spontaneous pneumothorax, and pleurisy

Cardiac disorders that may mimic PE include MI

and pericarditis Musculoskeletal disorders that

may mimic PE include muscle strain, rib fracture,

costochondritis, and herpes zoster

Intraabdomi-nal disorders that irritate the diaphragm or

stimu-late breathing may also present similarly to PE

Finally, hyperventilation syndrome may mimic

PE; however, this is a diagnosis of exclusion

• Spiral computed tomography (CT) scanning is an

excellent confirmation test (experience may vary

at different medical centers) Spiral CT is 93 to

98 percent specific for pulmonary embolism.8,11

EMERGENCY DEPARTMENT CARE

AND DISPOSITION

• The treatment of PE consists of initial

stabiliza-tion, anticoagulation with heparin, and

thrombo-lytic therapy in emergent cases

• Administer oxygen

• Crystalloid IV fluids should be given initially for

hypotension

• For hypotension in the absence of hypovolemia,

dopamine can be started at 2 to 5애g/kg/min and

titrated to maintain a systolic blood pressure of

90 mmHg

• Start heparin with an IV bolus of 10,000 to 20,000

U, followed by a continuous drip of 1000 U/h to

be adjusted using the partial thromboplastin time,

aiming for an international normalized ratio

(INR) of two to three times normal

Contraindica-tions to anticoagulation include active internal

bleeding, uncontrolled severe hypertension,

re-cent trauma, rere-cent surgery, rere-cent stroke, and

intracranial or intraspinal neoplasm Heparin can

be used safely in the nonbleeding pregnant patient

but must be discontinued prior to delivery

Hepa-rin does not prevent the embolization of

ex-isting clots

• Low-molecular-weight heparin has been shown to

be safe and effective in the treatment of DVT and

PE Examples include enoxaparin 1 mg/kg SQ as

the initial dose

• For persistent hypotension despite medical

man-agement with the above measures, consider

thrombolytic therapy Tissue plasminogen

activa-tor (tPA), 50 to 100 mg IV over 2 to 6 h, has been

recommended Streptokinase can be given in a

dose of 250,000 U IV over 30 min followed by a

continuous IV infusion of 100,000 U/h for the next

12 to 24 h Ideally, consultation with an intensivistshould occur prior to starting thrombolytictherapy

• For patients with contraindications to tion or thrombolytic therapy, a Greenfield filter

anticoagula-is recommended

• Further embolization and shock most commonlyoccur within 4 h of initial symptoms

R EFERENCES

1 Morgenthaler TI, Ryu JH: Clinical characteristics of fatal

pulmonary embolism in a referral hospital Mayo Clin

Proc 70:417, 1995.

2 Hirsch J: Diagnosis of venous thrombosis and pulmonary

embolism Am J Cardiol 65:45C, 1990.

3 Stein PD, Terrin ML, Hales CA, et al: Clinical,

labora-tory, roentgenographic and electrocardiographic finding

in patients with acute pulmonary embolism and no

pre-existing cardiac or pulmonary disease Chest 100:598,

1991.

4 Bell WR, Simon TL, DeMets DL: The clinical features

of submassive and massive pulmonary emboli Am J Med

62:355, 1977.

5 Leeper KV Jr, Popovich J Jr, Adams D, et al: Clinical

manifestations of acute pulmonary embolism: Henry

Ford Hospital experience, a five-year review Henry Ford

Hosp Med J 36:29, 1988.

6 Stein PD, Goldhaber SZ, Henry JW: Alveolar-arterial

oxygen gradients in elderly patients with suspected

pul-monary embolism Ann Emerg Med 22:1177, 1993.

7 Jones JS, VanDeelen N, White L, et al: Alveolar-arterial

oxygen gradients in the assessment of acute pulmonary

embolism Chest 107:139, 1995.

8 Kline JA, Johns KL, Colucciello SA, et al: New

diagnos-tic tests for pulmonary embolism Ann Emerg Med

35:168, 2000.

9 Stein PD, Alavi A, Gottschalk A, et al: Usefulness of

noninvasive diagnostic tools for diagnosis of acute monary embolism in patients with a normal chest radio-

pul-graph Am J Cardiol 67:1117, 1991.

10 PIOPED: Value of the ventilation/perfusion scan in

acute pulmonary embolism: Results of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIO-

PED) JAMA 263:2753, 1990.

11 Gallagher EJ: Clots in the lung Ann Emerg Med

35:181, 2000.

For further reading in Emergency Medicine: A

Comprehensive Study Guide, 5th ed., see Chap.

52, ‘‘Pulmonary Embolism,’’ by Charles N.Schoenfeld

29 HYPERTENSIVE

EMERGENCIES

Jonathan A Maisel

EPIDEMIOLOGY

• Hypertension is the fourth most prevalent chronic

medical condition in the United States, affecting

up to 24 percent of the general adult population.1,2

• The risk of developing serious cardiovascular,

re-nal, or cerebrovascular disease increases with

poorly controlled blood pressure

• Nearly 75 percent of adult Americans with known

hypertension have inadequate control of their

blood pressure, and only one-half are compliant

with prescribed medications.2,3

PATHOPHYSIOLOGY

• At the cellular level, postsynaptic 움1and움2

recep-tors are stimulated by norepinephrine released

from presynaptic sympathetic nerve endings,

lead-ing to the release of intracellular calcium Free

calcium activates actin and myosin, resulting in

smooth muscle contraction, increased peripheral

vascular resistance, and an increase in blood

pres-sure Presynaptic움2receptors help limit this

re-sponse via a negative-feedback loop

• Hypertension develops: (a) as a result of

alter-ations in the contractile properties of smooth

mus-cle in arterial walls, or (b) as a response to failure

of normal autoregulatory mechanisms within

vas-cular beds of vital organs (i.e., heart, kidney,

and brain)

• Long-standing, poorly controlled hypertension

may damage target organs by injuring vascular

beds Endothelial injury leads to deposition of

fibrin within vessel walls, and activation of

media-tors of coagulation and cell proliferation.4A

recur-rent cycle of vascular reactivity develops which

leads to platelet aggregation and myointimal

pro-liferation, and subsequent progressive narrowing

of arterioles

• Hypertension is associated with major

cardiovas-cular risk factors such as smoking, hyperlipidemia,

diabetes mellitus, age⬎60, gender (men and

post-menopausal women), obesity, and a family history

of cardiovascular disease.3 Although no single

cause of hypertension has been identified, a

com-bination of factors such as these are believed to

contribute to ‘‘essential’’ hypertension Several

specific causes do exist, with intrinsic renal andrenovascular disease being the most prevalent ofthe known causes

• Hypertensive emergencies in childhood, defined

as systolic or diastolic blood pressureⱖ95th centile for age and sex, are most commonly caused

per-by intrinsic renal or renovascular disease

CLINICAL FEATURES

• Essential historical features include a prior history

of hypertension; noncompliance with tension medication; overall medication use, in-cluding over-the-counter and illicit drugs; and diet(especially products with sodium or tyramine)

anti-hyper-• Any past medical history of cardiovascular, rovascular, or renal disease; diabetes; hyperlipid-emia; chronic obstructive pulmonary disease; orasthma; or a family history of hypertension orpremature heart disease should be elicited.3

cereb-• Precipitating causes such as pregnancy, illicit druguse (i.e., cocaine and methamphetamine), mono-amine oxidase inhibitors, and decongestantsshould be considered

• Patients should be asked about central nervoussystem (CNS) symptoms (headache, visualchanges, confusion, paresis, seizures), cardiovas-cular symptoms (chest pain, dyspnea, palpitations,pedal edema, tearing pain radiating to the back

or abdomen), and renal symptoms (anuria, turia, edema)

hema-• Blood pressure should be measured with an propriately sized cuff (false elevations with smallcuffs), at least twice if elevated, and in both armsand legs if substantially elevated

ap-• The physical exam should focus on target organinjury and its acuity, including mental statuschanges, focal neurologic deficits, funduscopicchanges (hemorrhages, cotton-wool exudates,disk edema), and cardiovascular findings (carotidbruits, heart murmurs and gallops, asymmetricpulses—coarctation versus dissection, pulmonaryrales, and pulsatile abdominal masses).3

• In the pregnant or postpartum patient, assessmentshould be made for hyperreflexia and peripheraledema, suggesting preeclampsia

• Children present with nonspecific complaints such

as a throbbing frontal headache or blurred vision.Physical findings are similar to those seen in adults

• Pheochromocytoma is another common etiology

in childhood, presenting with nervousness, tations, sweating, blurry vision, and skin flushing

palpi-CHAPTER 29•HYPERTENSIVE EMERGENCIES 105

DIAGNOSIS AND DIFFERENTIAL

• Renal impairment may present as hematuria,

pro-teinuria, red blood cell casts, or elevations in blood

urea nitrogen (BUN), creatinine, and potassium

levels

• An electrocardiogram may reveal ST-T wave

changes consistent with coronary ischemia,

elec-trolyte abnormalities, strain, or left ventricular

hy-pertrophy

• A chest x-ray may help identify congestive heart

failure, aortic dissection, or coarctation

• In patients with neurologic compromise, a

com-puted tomography scan of the head may reveal

ischemic changes, edema, or blood

• A urine or serum drug screen may identify illicit

drug use

• A pregnancy test should be done on all

hyperten-sive women of childbearing age

EMERGENCY DEPARTMENT CARE

AND DISPOSITION

• Though hypertension is defined as either a systolic

blood pressure⬎140 mmHg or a diastolic blood

pressure⬎90 mmHg, management depends more

on the patient’s clinical condition rather than

ab-solute systolic or diastolic values

• Classification of hypertension into four categories

facilitates management:

a Hypertensive emergency: Elevated blood

pressure associated with target organ (CNS,

cardiac, renal) dysfunction Requires

imme-diate recognition and treatment

b Hypertensive urgency: Elevated blood

pres-sure associated with risk for imminent target

organ dysfunction

c Acute hypertensive episode: Systolic blood

pressure ⬎180 and diastolic blood pressure

⬎110 without evolving or impending target

organ dysfunction

d Transient hypertension: Elevated blood

pressure associated with another condition

(e.g., anxiety, alcohol withdrawal, and

co-caine abuse) Patients usually become

nor-motensive once the precipitating event

re-solves

• Patients with hypertensive emergencies require O2

supplementation, cardiac monitoring, and

intrave-nous access Following attention to the ABCs of

resuscitation, the treatment goal is to reduce the

mean arterial pressure [diastolic blood pressure⫹

1/3 (systolic blood pressure⫺ diastolic blood

pres-sure)] by 20 to 25 percent over 30 to 60 min

• For hypertensive encephalopathy, sodium prusside should be used, beginning at 0.5애g/kg/min and titrating to a maximum of 10애g/kg/min.Rapid correction of blood pressure should beavoided to prevent cerebral ischemia secondary tohypoperfusion Nitroprusside is a potent arteriolarand vasodilator, with an onset of action in seconds

nitro-An arterial line should be placed in order toclosely monitor the blood pressure, and the solu-tion and tubing should be wrapped in aluminumfoil to prevent degradation by light Hypotension

is the most common complication of nitroprussideinfusions Cyanide toxicity is seen rarely after pro-longed infusions

• Labetalol is useful as a second line agent for tensive encephalopathy, providing a steady, con-sistent drop in blood pressure without diminishingcerebral blood flow or producing a reflex tachycar-dia It is a competitive, selective 움1blocker, and

hyper-a competitive, nonselective웁 blocker, with the blocking action 4 to 8 times more potent than the움-blocking action It has an onset of action in 5

웁-to 10 min, and a duration of action of 8 h Its useshould be avoided in patients with asthma, chronicobstructive pulmonary disease, congestive heartfailure, and heart block The treatment shouldbegin with incremental boluses of 20 to 40 mgintravenous (IV) and repeated every 10 min untilthe target blood pressure is achieved or a totaldose of 300 mg is reached Alternatively, after aninitial bolus, a continuous infusion of 1 to 2 mg/min may be used, terminating the infusion whenthe target blood pressure has been achieved La-betalol is also ideal for use in syndromes associ-ated with excessive catecholamine stimulation

• Hypertension associated with stroke is often aphysiologic response to the stroke itself (to main-tain adequate cerebral perfusion) and not its im-mediate cause When the diastolic blood pressure

is⬎140 mmHg, it may be slowly reduced by up

to 20 percent using 5 mg increments of IV lol The acute management of hypertension associ-ated with intracranial hemorrhage is controversial

labeta-• For hypertension associated with pulmonaryedema, IV nitroglycerine or nitroprusside may beused Nitroglycerine is both an arteriolar and ve-nous dilator, with greater effect on the venoussystem, and an onset of action within minutes.Initial infusion should be at a rate of 5 to 20애g/min, with 5애g/min incremental increases every 5min until symptoms improve or side effects (head-ache, hypotension, tachycardia) ensue

• For hypertension associated with myocardial emia, IV nitroglycerine is first-line therapy Be-cause it is a better vasodilator of the coronary

isch-vessels than nitroprusside, it is the drug of choice

for severe hypertension complicating acute

coro-nary ischemia or pulmocoro-nary edema

• For hypertension associated with aortic dissection,

reducing the blood pressure and ventricular

ejec-tion force may limit the extent of the dissecejec-tion

Either labetalol alone, or a combination of

nitro-prusside and a beta blocker can be used Esmolol,

an ultra-short-acting 웁1-selective adrenergic

blocker, is very effective, achieving 90 percent of

beta blockade within 5 min of an IV bolus of 0.5

mg/kg, followed by an infusion of 0.05 to 0.3 mg/

kg/min Propranolol and metoprolol are

alterna-tives Esmolol, as well as other beta blockers,

should be avoided in patients with asthma, chronic

obstructive pulmonary disease, and

cocaine-induced cardiovascular complications (because of

unopposed움-adrenergic effects)

• Worsening renal function in the setting of elevated

blood pressure, manifested by elevation of BUN

and creatinine levels, proteinuria, or the presence

of red blood cells or red blood cell casts in the

urine, is considered a hypertensive emergency

Ni-troprusside is the preferred agent

Dialysis-depen-dent patients presenting with volume overload

may require emergent dialysis if they present with

uncontrolled hypertension and other evidence of

end-organ dysfunction

• Renovascular hypertension in children can be

treated with diazoxide 1 to 3 mg/kg IV q5 to 15

min, labetalol 0.3 to 1 mg/kg IV q10 min, or

capto-pril 0.5 to 1 mg/kg per 24 h PO in 3 to 4

di-vided doses

• Treatment of pheochromocytoma requires

surgi-cal excision, managing the elevated blood pressure

with an 움-adrenergic blocker such as

phentol-amine

• The treatment goal in hypertensive urgencies is

the gradual reduction of blood pressure within

24 to 48 h by using oral antihypertensive agents

Useful agents include the following:

a Labetalol 200 to 400 mg PO, repeated every

2 to 3 h Oral labetalol has an onset of action

in 30 min and a duration of action of 6 to

12 h

b Captopril, an angiotensin-converting

en-zyme inhibitor, has an onset of action in 15

to 30 min, a peak effect at 50 to 90 min, and

a duration of effect of 4 to 6 h A 25 mg

oral dose is effective in refractory congestive

heart failure and renovascular hypertension

Common side effects include rash, cough,

and loss of taste, and rarely, life-threatening

angioneurotic edema

c Sublingual nitroglycerine in the form of

spray, or 0.3 to 0.6 mg tablets, are the agents

of choice for patients with angina or tive heart failure The hypotensive effect be-gins in minutes and can last several hours

conges-d Clonidine is a centrally acting,움2-adrenergicagonist that decreases central sympathomi-metic activity, lowering plasma catechola-mine levels Its onset of action is 30 to 60min, with peak effect in 2 to 4 h It is given

as a dose of 0.1 mg hourly until the targetblood pressure is reached, or a total of 0.7

mg has been given A patient treated withclonidine in the emergency department (ED)does not need to be discharged on this drug.Because an adequate response may take up

to 6 h, it is not a first-line agent

e Nifedipine, a dihydropyridine Ca⫹-channelantagonist, had been used commonly for hy-pertensive urgencies via oral and sublingualroutes Serious adverse reactions, such asacute coronary events and stroke, precluderecommending it for the urgent treatment ofhypertension.5

• For nonemergent, nonurgent hypertension, there

is no evidence of a beneficial effect of acute bloodpressure reduction on long-term control or on thechronic effects of hypertension These patients donot require acute intervention, but should be re-ferred for timely follow-up Should an oral agent

be started in the ED, the choice should be based

on coexisting conditions, if any Diuretics, such

as hydrochlorothiazide 25 mg/day, are first-lineagents in the elderly, as well as for patients withrenal disease and congestive heart failure (Con-sider potassium supplementation.) Beta blockers,such as metoprolol 50 mg bid are first-line agentsfor patients with angina, or those postmyocardialinfarction Angiotensin-converting enzyme inhibi-tors, such as captopril 25 mg two to three times aday, can be used in patients with congestive heartfailure or diabetes

• For a discussion of hypertension associated withpregnancy, see Chap 61

R EFERENCES

1 US Department of Health and Human Services:

Preva-lence of selected chronic conditions: United States, 1986–

1988 Vital Health Stat 182:10, 1993.

2 Burt VL, Whelton P, Roccella EJ, et al: Prevalence of

hypertension in the U.S adult population: Results from

CHAPTER 30•AORTIC DISSECTION AND ANEURYSMS 107

the Third Health and Nutrition Examination Survey,

1988–1991 Hypertension 25:305, 1995.

3 Joint National Committee (JNC) on Prevention,

Detec-tion, EvaluaDetec-tion, and Treatment of High Blood Pressure:

The sixth report of the Joint National Committee on

Pre-vention, Detection, Evaluation, and Treatment of High

Blood Pressure Arch Intern Med 157:2413, 1997.

4 Kitiyakara C: Malignant hypertension and hypertensive

emergencies J Am Soc Nephrol 9:133, 1998.

5 McCarthy M: US NIH issues warning on nifedipine

Lan-cet 346:689, 1995.

For further reading in Emergency Medicine: A

Com-prehensive Study Guide, 5th ed., see Chap 53,

‘‘Hypertension,’’ by Melissa M Wu and Arjun

• Incidence of abdominal aortic aneurysms (AAA)

increases with age; most patients are older than 60

• Males are at increased risk

• Other risk factors include connective tissue

dis-ease, Marfan syndrome, atherosclerotic risk

fac-tors (smoking, hypertension, hyperlipidemia, and

diabetes) and a family history of aneurysm

PATHOPHYSIOLOGY

• Destruction of the media of the aorta is a

promi-nent feature in aneurysm pathogenesis with a

re-duction of elastin and collagen Histologic

exami-nation reveals a thinned media and an intima that

is infiltrated with atherosclerosis

• Laplace’s law [wall tension ⫽ (pressure x radius)/

tensile force] dictates that as the aorta dilates, the

force on the aortic wall increases, causing further

aortic dilation Rate of aneurysmal dilation is

vari-able with larger aneurysms expanding more

quickly An average rate may be 25 to 0.5 cm

per year.1

CLINICAL FEATURES

• Four clinical scenarios exist: acute rupture, toenteric fistula, chronic contained rupture, andAAA as an incidental finding

aor-• Acute leakage or rupture is rapidly fatal withoutintervention Classic presentation is an older malewith severe back or abdominal pain who presentswith syncope or hypotension On exam, such pa-tients classically have a tender pulsatile abdominalmass, but this finding may be obscured by obesity.Femoral pulsations are typically normal.2

• Patients usually exhibit a variation of the classicpresentation.3 They may complain of unilateralflank or groin pain, hip pain, or abdominal painlocalized to a specific quadrant Abdominal ten-derness may or may not be present There may

be signs of retroperitoneal hemorrhage such asperiumbilical or flank ecchymosis or scrotal he-matoma

• Aortoenteric fistula presents as gastrointestinalbleeding This is classically seen in a patient whohas undergone prior aortic grafting.4 These pa-tients may present with a deceptively minor ‘‘sen-tinel’’ bleed or massive gastrointestinal hemor-rhage

• Chronic-contained rupture is uncommon but isseen when an AAA ruptures retroperitoneallywith significant fibrosis that limits blood loss.5

These patients may have pain for an extendedtime period and appear well

• Asymptomatic AAAs may be found on physicalexam or during unrelated radiologic evaluation.Those greater than 5 cm are at high risk of rupture

DIAGNOSIS AND DIFFERENTIAL

• Variable presentations of aortic aneurysm present

a diagnostic challenge Diagnoses that might beconsidered are renal colic, musculoskeletal backpain, pancreatic disease or other intraabdominalprocesses (diverticulitis, cholecystitis, mesentericischemia, etc.), scrotal or testicular disorders, anddisorders that cause gastrointestinal bleeding (var-ices, ulcers, tumors, etc.)

• Diagnostic studies are needed when the diagnosis

of AAA is unclear Though not the study ofchoice, plain films may reveal a calcified aorta in

65 percent of those with aneurysmal disease.6Inthe unstable patient, bedside abdominal ultra-sound is very sensitive, reliably measuring aorticdiameter and identifying an aneurysm7 withoutthe hazards of transporting a patient away fromthe emergency department Computed tomogra-

phy scanning, however, is preferred in the stable

patient as it better delineates the anatomic details

of the aneurysm and any associated rupture

EMERGENCY DEPARTMENT CARE

AND DISPOSITION

• The patient should be stabilized with

supplemen-tal oxygen, volume resuscitation with isotonic

flu-ids, and/or blood transfusion via multiple large

bore intravenous lines

• For suspected rupturing AAA or aortoenteric

fis-tula, immediate surgical consultation is warranted

No diagnostic testing should delay surgical repair

• A vascular surgeon should be consulted for urgent

repair of chronically contained ruptured AAAs

Admission to the intensive care unit should be

sought

• For incidentally discovered AAA, the patient can

potentially be discharged home depending on

an-eurysm size and comorbid features Consultation

with a vascular surgeon for admission or close

outpatient follow-up is usually adequate

AORTIC DISSECTION

EPIDEMIOLOGY

• Most patients are over the age of 50 years with a

history of hypertension

• A second group of patients are younger than 50

years and have identifiable risk factors such as

congenital heart disease, connective tissue disease,

and pregnancy Twenty-five to 30 percent of

pa-tients with Marfan syndrome develop dissection

Dissection may also be iatrogenic from cardiac

catheterization or surgery

PATHOGENESIS

• Aortic dissection occurs when the intima is

vio-lated, allowing blood to enter the media and

dis-sect between the intimal and adventitial layers

Common sites for tear include the ascending aorta

and the region of the ligamentum arteriosum

• Dissections may extend proximally, distally, or

both and are classified by two separate systems

The Stanford classification system considers any

involvement of the ascending aorta a type A

dis-section and one restricted to the descending aorta

a type B dissection The DeBakey system classifiestype I dissections as those that involve the as-cending aorta, the arch, and the descending aorta.Type II involves only the ascending aorta and typeIII only the descending aorta

CLINICAL FEATURES

• More than 90 percent of patients have abrupt set of severe tearing chest or upper back pain.Accompanying nausea, vomiting, and diaphoresisare common

on-• Clinical presentation depends on the location ofthe dissection with pain patterns often changing

as the anatomic injury migrates.8Presentations clude aortic valve insufficiency with or withoutpericardial tamponade, coronary artery occlusionwith myocardial infarction, stroke symptoms withcarotid involvement, or paraplegia with occlusion

in-of vertebral blood supply The dissection mayprogress distally causing abdominal or flank pain

or limb ischemia

• Physical exam findings also depend on locationand progression of the dissection A diastolicmurmur or aortic insufficiency may be heard.Fifty percent of patients have decreased radial,femoral, or carotid pulses.8 Hypertension andtachycardia are common, but hypotension mayalso be present

DIAGNOSIS AND DIFFERENTIAL

• Ischemic end organ manifestations associated withdissections may confuse the differential diagnosis,which includes myocardial infarction, pericardialdisease, pulmonary disorders, spinal cord injuries,and intraabdominal disorders Rupture of the dis-section back through the intima into the true lu-men may cause a cessation of symptoms leading

to false reassurance

• Chest x-ray shows an abnormal aortic contour 90percent of the time The ‘‘calcium sign’’ may bepresent, with intimal calcium seen distant fromthe edge of the aortic contour

• Computed tomography, angiography, and esophageal echocardiography are all quite sensi-tive and specific Their use varies by institution9

trans-and should be based on availability trans-and patientstability, in conjunction with a vascular or tho-racic surgeon

CHAPTER 31•NONTRAUMATIC PERIPHERAL VASCULAR DISORDERS 109

EMERGENCY DEPARTMENT CARE

AND DISPOSITION

• Patients with suspected aortic dissection require

prompt radiographic confirmation of the

diag-nosis

• Stabilization of the patient requires large-bore

in-travenous access, supplemental oxygen, and

cor-rection of hypotension with judicious fluid and/or

blood product resuscitation

• More commonly patients with dissection require

antihypertensive treatment along with control of

tachycardia to reduce shear force on the intimal

flap of the aorta This is generally accomplished

with negative inotropes (esmolol, metoprolol, or

propranolol) in conjunction with a vasodilator

such as nitroprusside

• Rapid consultation with a surgeon is mandatory

Dissection of the ascending aorta requires prompt

surgical repair Indications for repair of dissections

involving only the descending aorta are

contro-versial.9

R EFERENCES

1 Faggioli GL, Stella A, Gargiulo M, et al: Morphology of

small aneurysms: Definition and impact on risk of rupture.

Am J Surg 168:131, 1994.

2 Satta J, Laara E, Immonen K, et al: The rupture type

determines the outcome for ruptured abdominal aortic

aneurysm patients Ann Chirurg Gynaecol 86:24, 1997.

3 Henney AM, Adiseshiah M, et al: Abdominal aortic

aneu-rysm: Report of a meeting of physicians and scientists,

University College London Medical School Lancet

341:215, 1993.

4 Batounis E, Georgopoulos S: The validity of current

vas-cular imaging methods in the evaluation of aortic

anasto-motic aneurysms developing after abdominal aortic

aneu-rysm repair Ann Vasc Surg 10:537, 1996.

5 Jones CS, Reilly MK, Dalsing MC, Glover JL: Chronic

contained rupture of abdominal aortic aneurysms Arch

Surg 121:542, 1986.

6 Crawford ED, Hess KR: Abdominal aortic aneurysm N

Engl J Med 321:1040, 1989.

7 Graham M, Chan A: Ultrasound screening for clinically

occult abdominal aortic aneurysm Can Med Assoc 138:

627, 1988.

8 Larson EW, Edwards WD: Risk factors for aortic

dissec-tion: A necropsy study of 161 cases Am J Cardiol

53:849, 1984.

9 Cigarroa JE, Isselbacher EM, DeSanctis RW, et al:

Medi-cal progress: Diagnostic imaging in the evaluation of

sus-pected aortic dissection—old standards and new

direc-tions N Engl J Med 328:35, 1993.

For further reading in Emergency Medicine: A

Com-prehensive Study Guide, 5th ed., see Chap 54,

‘‘Aortic Dissection and Aneurysms,’’ by Gary

A Johnson

31 NONTRAUMATIC PERIPHERAL VASCULAR DISORDERS

David M Cline

DEEP VENOUS THROMBOSIS

• Deep venous thrombosis (DVT) is a common tentially life-threatening condition with an esti-mated annual incidence of 5 to 20 million cases

po-in the United States

PATHOPHYSIOLOGY

• The formation of venous clots is related to at leastone of Virchow’s triad of factors: venous stasis,injury to the vessel wall, and a hypercoagulablestate Table 31-1 outlines the clinical risk factorspredisposing to DVT, which can be remembered

by the mnemonic thrombosis.

• Thrombi most commonly form at the venous cusps

of deep veins in the lower extremities, where tered or static blood flow initiates clot formation.CLINICAL FEATURES

al-• The classic features of DVT include swelling ofthe lower extremity, tenderness, pain, redness, in-

TABLE 31-1 Clinical Risk Factors for Deep Venous Thrombosis

R Recreational drugs (IV drugs)

creased local warmth, and possibly low-grade

fever

• The clinical examination is unreliable for the

de-tection or exclusion of DVT Assessment of risk

factors (Table 31-1) may be a stronger predictor

whenever the diagnosis is entertained

• One study showed that a single risk factor is

associ-ated with DVT in 24 percent of patients, while

those with four or more risk factors are virtually

certain to have the diagnosis established.1

• The constellation of pain, redness, swelling,

warmth, and tenderness is present in less than

one-half of patients with confirmed DVT Swelling

and tenderness in the involved extremity are the

most common findings, occurring in 80 and 75

percent, respectively, of patients with DVT

• Pain in the calf with forced dorsiflexion of the

ankle and the leg straight (Hormans’ sign) is not

reliable for DVT

• Symptomatic DVT will be in the popliteal or more

proximal veins in more than 80 percent of cases

• An isolated calf DVT will extend proximally only

20 percent of the time, usually within a week of

presentation.2 Unlike proximal DVT,

nonex-tending calf DVT will rarely cause a pulmonary

embolism

• Uncommon presentations of DVT include

phlegmasia cerulea dolens (painful blue

inflam-mation) and phlegmasia alba dolens (‘‘milk leg’’)

• In phlegmasia cerulea dolens the patient presents

with an extensively swollen, cyanotic leg from

ve-nous engorgement due to massive iliofemoral

thrombosis This high-grade obstruction can

com-promise perfusion to the foot from high

compart-ment pressures and lead to venous gangrene

Pete-chiae and bullae may be present on the skin

• Phlegmasia alba dolens is also due to massive

ilio-femoral thrombosis, but the patient’s leg is pale

or white secondary to associated arterial spasm

DIAGNOSIS AND DIFFERENTIAL

• Less than one-third of patients with clinically

sus-pected DVT are found to have the disease

follow-ing objective investigation.2

• Venography has represented the historical ‘‘gold

standard’’ for the detection of DVT When

con-trast is seen throughout the deep venous system

(not possible in 5 to 10 percent of tests), a

veno-gram reliably excludes DVT

• The most common test used to identify a DVT in

North America is ultrasonography

• A duplex scan with or without color flow is highly

sensitive and specific for a proximal DVT (clot

proximal to the popliteal veins) The positive

pre-dictive value of ultrasound is higher than ance plethysmography (IPG) for DVTs (94 versus

imped-83 percent, respectively)

• D-dimer fragments can be measured as an tor of the presence or absence of DVT or pulmo-nary embolism.3,4Infections, surgery, trauma, car-diovascular disease, and cancer can elevate aD-dimer level Despite a sensitivity less than 250 ng/

indica-mL of over 80 to 90 percent, a D-dimer level isuseful only when it is low.3

• The combination of a normal IPG or ultrasoundand low D-dimer level has a negative predictivevalue of about 99 percent for proximal DVT.2

• The primary objective in treating DVT is the vention of pulmonary embolism The mainstay oftherapy is anticoagulation

pre-• In the setting of ultrasound-documented proximalDVT with other complications, hospital admission

of a bolus of 80 U/kg followed by an infusion of

18 U/kg/h) may be used.5The available LMWHsinclude dalteparin, enoxaparin, or tinzaparin.6Anexample treatment regimen would be enoxaparin

1 mg/kg of lean body weight subcutaneously twicedaily When using unfractionated heparin, the goal

is a PTT of 1.8 to 2.8 times normal

• If anticoagulation is contraindicated, if a clot isextending proximally in spite of medical treat-ment, or if there is significant bleeding with theanticoagulants, consultation should be obtainedfor the placement of a Greenfield filter in theinferior vena cava

• In the setting of ultrasound-documented proximalDVT, discharge to home on LMWH can be con-sidered.6The patient should have few or no comor-bid illnesses, be able to ambulate unassisted, havegood social support at home, have a physicianfamiliar with the use of LMWH who can follow

up with the patient within 24 h, be able and willing

to self-administer injections at home, and have noother reason for admission to the hospital Warfa-rin therapy would then be initiated by the follow-

up physician

• In the setting of unilateral leg swelling and anultrasound negative for venous thrombosis proxi-mal to the popliteal fossa (presumed calf DVT),discharge with a follow-up ultrasound in 5 to 7days is recommended.7Generally, no anticoagula-tion needs to be started except in very high risk

CHAPTER 31•NONTRAUMATIC PERIPHERAL VASCULAR DISORDERS 111

groups including those with previous proximal

DVT or pulmonary embolus, poor ambulation, a

known hypercoagulable state, or extensive

cardio-vascular comorbidity With a known or presumed

calf DVT, the risk of pulmonary embolus within

7 days after an initial negative ultrasound is near

0, even without anticoagulation.2

OCCLUSIVE ARTERIAL DISEASE

EPIDEMIOLOGY

• Intermittent claudication has a prevalence of

be-tween 1 and 7 percent for men above age 50, with

symptomless disease existing in up to 25 percent

of men scanned with noninvasive testing in this

age group.8

• Symptoms of peripheral arterial disease increase

with age and are two to four times more common

in men than in women The vast majority of these

patients have a history of prolonged smoking

• Given that atherosclerosis is the usual pathology

in ischemic limb pain, it is not surprising that at

least one-half of these patients have coronary or

cerebrovascular disease.8

PATHOPHYSIOLOGY

• Acute limb ischemia results from a blood supply

that is inadequate to meet tissue oxygen and

nutri-ent requiremnutri-ents

• Peripheral nerves and skeletal muscle are very

sensitive to ischemia; in them, irreversible changes

occur within 4 h of anoxia at room temperature

• Nonembolic limb ischemia is secondary to

athero-sclerosis in the vast majority of patients.9

• An embolus is the commonest cause of an acute

arterial occlusion in the limb and originates from

the heart in 80 to 90 percent of cases of embolism

Atrial fibrillation and recent myocardial infarction

are the two primary causes of mural thrombus

within the heart

• Other causes include thrombosis, inflammatory

condition, low flow states, and arterial dissection

CLINICAL FEATURES

• Patients with acute limb ischemia will exhibit one

or more of the ‘‘six Ps’’: pain, pallor, polar (for

cold), pulselessness, paraesthesias, and paralysis

A lack of one or more of these findings, however,

does not exclude ischemia

• Pain alone may be the earliest symptom

• Complete arterial obstruction results in visibleskin changes, with initial pallor that may be fol-lowed by blotchy, mottled areas of cyanosis andassociated petechiae and blisters Severe, steadypain in the involved extremity associated with de-creased skin temperature is expected

• Hypoesthesia or hyperesthesia due to ischemicneuropathy is typically an early finding, as is mus-cle weakness

• An absent distal pulse is only so helpful It may

be an abrupt new sign of an occlusive clot or along-standing finding of chronic vascular disease

• Despite the generally held belief that limb salvage

is possible with reperfusion within 4 to 6 h, tissueloss can occur with significantly shorter occlu-sion times

• Disability and tissue loss are inevitable after 6 h

of occlusion anoxic injury

• Chronic peripheral arterial insufficiency is terized by intermittent claudication, which mayprogress to intermittent ischemic pain at rest

charac-• Pain at rest typically localizes to the foot and isaggravated with leg elevation, improves withstanding, and is poorly controlled with analgesics.8

Shiny, hyperpigmented skin with hair loss and ceration, thickened nails, muscle atrophy, vascularbruits, and poor pulses is a hallmark of chronicvascular disease

ul-DIAGNOSIS AND DIFFERENTIAL

• A thorough clinical evaluation is the most usefuldiagnostic tool for the assessment of occlusive ar-terial disease A history of an abruptly ischemiclimb in a patient with atrial fibrillation or recentmyocardial infarction is highly suggestive of anembolus Acute ischemia in the limb of a patientknown to have advanced peripheral vascular dis-ease is more likely due to thrombosis or a lowcardiac output state

• A hand-held Doppler can document the tude of flow or its absence when held over thedorsalis pedis, posterior tibial, popliteal, or femo-ral arteries in the lower limb and over the radial,ulnar, brachia, or axillary arteries in the arm

ampli-• In consultation with a vascular surgeon and duringthe period of preoperative and/or medical man-agement, an arteriogram can be done to confirmthe diagnosis, define the vascular anatomy andperfusion, and guide aggressive management.EMERGENCY DEPARTMENT CARE

AND DISPOSITION

• When the diagnosis of acute limb ischemia isknown or suspected, immediate intravenous hepa-

rinization should be started if no

contraindica-tions exist.9

• Prompt surgical embolectomy is the optimal

ther-apy for an acute arterial embolism causing

limb-threatening ischemia Catheter embolectomy has

been the choice technique for removal of clot ever

since the development of the Fogarty balloon

catheter in 1963.9 It has reduced mortality from

arterial emboli by 50 percent and need for

amputa-tion by 35 percent

• Overall mortality from an arterial embolus is

about 15 percent and is usually due to the

underly-ing cardiovascular disease The limb salvage rate

ranges from 62 to 96 percent.9

• Intraarterial thrombolysis with streptokinase,

uro-kinase, or tissue plasminogen activator (tPA)

in-fused near or into the clot for a few hours to

days is an alternative to surgery, with a rate of

successful reperfusion of 50 to 85 percent.9

• Systemic thrombolysis has been compared with

intraarterial lytic agents in randomized trials and

has been shown to produce inferior results.9

R EFERENCES

1 Venta ZA, Venta ER, Mumford LM: Value of diagnostic

test for deep venous thrombosis: A decision analysis

model Radiology 174:443, 1990.

2 Kearon C, Julian JA, Math M, et al: Noninvasive diagnosis

of deep venous thrombosis Ann Intern Med 128:663, 1998.

3 Hirsch J, Hull RD, Roskob GE: Clinical features and

diagnosis of venous thrombosis J Am Coll Cardiol

8:114B, 1986.

4 Becker DM, Philbrick JT, Bachhuber TL, et al:D -dimer

testing and acute venous thromboembolism Arch Intern

Med 156:939, 1996.

5 Buller HR, Gent M, Gallus AS, et al:

Low-molecular-weight heparin in the treatment of patients with venous

thromboembolism N Engl J Med 337:657, 1997.

6 Harrison L, McGinnis J, Crowther M, et al: Assessment

of outpatient treatment of deep-vein thrombosis with

low-molecular-weight heparin Arch Intern Med 158:2001,

1998.

7 Birdwell BG, Raskob GE, Whitsett TL, et al: The clinical

validity of normal compression ultrasonography in

outpa-tients suspected of having deep venous thrombosis Ann

Intern Med 128:1, 1998.

8 Golledge J: Lower-limb arterial disease Lancet 350:

1459, 1997.

9 Clagett GP, Krupski WC: Antithrombotic therapy in

pe-ripheral arterial occlusive disease Chest 108:431s, 1995.

For further reading in Emergency Medicine: A

Com-prehensive Study Guide, 5th ed., see Chap 55,

‘‘Nontraumatic Peripheral Vascular Disorders,’’

by Anil Chopra

• Dyspnea is a subjective feeling of difficult,

la-bored, or uncomfortable breathing It is a complex

sensation, without a defined neural pathway,

de-rived from many sources including mechanical,

chemical, and vascular receptors.1

• Mechanical factors include a sense of skeletal

mus-cle effort dependent on work of breathing and

intraparenchymal stretch and irritant receptors in

the lungs that respond to changes in compliance

and edema

• Chemoreceptors in the central medulla and the

carotid body respond to changes in CO2and O2,

respectively Receptors in the atrium(s) and

pul-monary arteries also contribute in a poorly

de-fined manner

• Central and peripheral receptors send afferent

neurons to the central nervous system, where the

information is integrated in a complex manner

CLINICAL FEATURES

• The patient may present with shortness of breath

or breathlessness, tachypnea, tachycardia, use of

accessory respiratory muscles, and stridor

• The complaint of dyspnea must be rapidly

evalu-ated, including abnormal vital signs and the

pri-113

mary survey [airway, breathing, circulation(ABCs)] Airway obstruction, ineffective respira-tory effort, and changes in mental status may ne-cessitate rapid airway control and intervention.2

• Lesser degrees of dyspnea allow for a more tailed history and exam (Table 32-1)

• Ancillary studies useful in determining a diagnosisinclude pulse oximetry and arterial blood gas anal-ysis, but tests should be taken in light of work

of breathing

• A chest x-ray, electrocardiogram, peak flows, and

a hemoglobin or hematocrit may also be useful

• Other ancillary tests include nary function testing, cardiac stress testing, echo-cardiography, exercise testing, electromyography,ventilation/perfusion scan; pulmonary biopsy mayalso be useful in the appropriate setting

spirometry/pulmo-EMERGENCY DEPARTMENT CARE AND DISPOSITION

• The first priority is to recognize threats to life andaggressively support respiratory function Supple-mental oxygen is given to maintain PaO2 ⬎60mmHg (pulse oximeter ⬎91 to 93 percent) Pa-tients with chronic obstructive pulmonary disease(COPD) may tolerate a lower PaO2

• Further interventions include continuous positiveairway pressure (CPAP) or biphasic positive air-way pressure (BiPAP) ventilation, bag-valve-mask ventilation, and intubation with mechani-cal ventilation

• All patients with an unclear cause of dyspnea andhypoxia require admission to a monitored bed

Copyright 2001 The McGraw Hill Companies, Inc Click Here for Terms of Use.

TABLE 32-1 Common Causes of Dyspnea

Airway mass Left ventricu- Asthma Pneumothorax Pulmonary em- Cerebrovascular ac- Anemia

Foreign body Myocardial COPD Pleural effusion Air embolism Phrenic nerve pa- Metabolic acidosis

Angioedema Pericarditis Pneumonia Pleural adhe- Fat embolism Guillain-Barre´ syn- Shock

Airway ste- Pericardial Pulmonary Chest wall Amniotic em- Tick paralysis Low cardiac output

Bronchiectasis Arrhythmia Pulmonary con- Abdominal dis- Pulmonary hy- Botulism Hypoxia

tusion tention pertension Tracheoma- Myocarditis Atelectasis Kyphoscoliosis Venoocclusive Neuropathy Carbon monoxide

Cardiomy- Alveolitis Pectus exca- Sickle cell Myopathy

Intracardiac Pulmonary fi- Pregnancy Vasculitis Deconditioning shunt brosis

Left ventricu- Adult respira- Arteriovenous Fever

lar outflow tory distress fistula obstruction syndrome

order

reflux Psychogenic hyper- ventilation

HYPOXIA

PATHOPHYSIOLOGY

• Hypoxia is defined as the inadequate delivery of

oxygen to the tissues and is caused by one of

five distinct mechanisms Hypoxia is arbitrarily

defined as PaO2 ⬍60 mmHg

• Hypoventilation: Rising PaCO2 displaces oxygen

from the alveolus, lowering the PaO2and

decreas-ing the O2 diffusion gradient across the

pulmo-nary membrane

• Right-to-left shunting: Unoxygenated blood enters

the systemic circulation This may occur secondary

to perfusion of underventilated lung or with

con-genital heart anomalies

• Ventilation/perfusion mismatch: Results from

re-gional alterations of ventilation or perfusion

• Diffusion impairment: Caused by impairment of

the alveolar blood barrier

• Low Fi O 2: The cause of high-altitude hypoxia

CLINICAL FEATURES

• Signs and symptoms are nonspecific, ranging fromtachycardia and tachypnea to central nervous sys-tem (CNS) manifestations such as agitation, sei-zures, and coma

• At PaO2⬍20 mmHg, there is a paradoxical sion of the respiratory drive

depres-• Dyspnea may or may not be present, and cyanosis

is an insensitive indicator of PaO2status

DIAGNOSIS AND DIFFERENTIAL

• Pulse oximetry is a useful screening test, but rial blood gas analysis defines the diagnosis

arte-• Similar ancillary tests used to determine causes

of dyspnea might elucidate abnormalities leading

to hypoxia

CHAPTER 32•RESPIRATORY DISTRESS 115

EMERGENCY DEPARTMENT CARE

AND DISPOSITION

• Hypoxia is treated the same as dyspnea; support,

identify, and aggressively treat underlying

disor-ders, trying to maintain PaO2⬎60 mmHg

• All patients with persistent hypoxia require

hospi-talization until the abnormality is adequately

ad-dressed and stabilized Frequent arterial blood

samples may require an arterial line

HYPERCAPNIA

PATHOPHYSIOLOGY

• Hypercapnia is defined as a PaCO2⬎45 mmHg and

is caused by hypoventilation It is almost never

caused by intrinsic lung disease or increased CO2

production Minute ventilation is dependent on

respiratory rate and tidal volume; decreases in

either will lead to hypoventilation Disorders

lead-ing to hypoventilation and hypercapnia are varied,

but their effect can always be traced to the minute

ventilation relationship

• Alveolar ventilation is less than minute ventilation;

although this term is more appropriately used in

describing ventilation, alveolar ventilation is

im-practical to measure It is dependent on the tidal

volume less the anatomic dead space and the

respi-ratory rate Dead space is the volume of air that

must be inhaled to initially reach the alveolus and

is made up of the large conducting airways

• Both parameters in minute ventilation are

con-trolled via efferent neuronal output from the

che-moreceptor in the medulla

CLINICAL FEATURES

• Signs and symptoms of hypercapnia are

depen-dent on the rate and degree of elevation Acute

rises are associated with an increase in intracranial

pressure, confusion, lethargy, seizures, and coma

On physical exam, asterixis may also be found

• Acute changes to PaCO2⬎100 mmHg may lead to

cardiovascular collapse In acute retention, for

each 10-mmHg increase of PaCO2, the pH will

de-crease 0.1 U

• Chronic changes in PaCO2 may be well tolerated

To maintain a neutral milieu, the kidneys retain

[HCO3 ⫺] In the chronic setting, for every 10

mmHg of PaCO2over 40 mmHg, [HCO3 ⫺] increases

3.5 meq/L

TABLE 32-2 Causes of Hypercapnia

Depressed central respiratory drive Structural central nervous system disease Sedating drugs

Exogenous toxins Endogenous toxins Thoracic cage disorders Kyphoscoliosis Extreme obesity Neuromuscular diseases Intrinsic lung disease associated with increased dead space Chronic obstructive pulmonary disease

DIAGNOSIS AND DIFFERENTIAL

• Given clinical suspicion, the diagnosis will be firmed on arterial blood gas analysis See Table32-2 for further differential diagnosis

con-EMERGENCY DEPARTMENT CARE AND DISPOSITION

• Hypercapnia is treated in the same manner ashypoxia: identify threats to life, evaluate and ag-gressively treat deficiencies in the ABCs Identifi-cation of the underlying etiology will allow fo-cused treatment For example, a narcotic dosecausing respiratory depression will respond to nal-oxone, while ineffective ventilation secondary torespiratory muscle weakness will respond only toassisted or mechanical ventilation

• Supplemental oxygen should be given to maintainthe level considered normal for the patient Oxy-gen should not be withheld based on the worry

of ‘‘decreasing respiratory drive.’’ Hypoxia willkill a patient, while only extreme hypercapnia will

do the same

• BiPAP or CPAP may be used as a bridge until adefinitive diagnosis of hypercapnia and a treat-ment plan can be made, but it is never a long-term option If all else fails, mechanical ventilation

• While wheezes may occur in normal patients, they

are more pronounced in obstructed airways

Air-way obstruction is associated with bronchospasm,

smooth muscle hypertrophy, increased secretions,

and peribronchial inflammation

CLINICAL FEATURES

• Wheezing usually occurs in asthma and other

ob-structive pulmonary diseases, but ‘‘not all that

wheezes is asthma.’’ A clinician must be savvy

enough to recognize these other causes9 (Table

32-3)

• In addition, not every obstructive pulmonary

dis-ease will cause wheezing For example, the patient

with severe asthma may have a quiet chest, not

moving enough air to produce turbulent flow

• One must judge the presence or absence of

wheezes on the basis of the clinical situation

DIAGNOSIS AND DIFFERENTIAL

• Diagnosis is suspected in the proper clinical

situa-tion, and the patient improves with relief of

ob-struction Relief may be judged by decreased work

of breathing, improvement of bedside pulse

ox-imetry, and decreased respiratory rate

• Definitive diagnosis is confirmed by spirometric

testing, but this is impractical at the bedside or

during an acute exacerbation

• A hand-held peak-flow meter is a useful clinical

adjunct that can serve to gauge response to

treat-ment Any obtained value greater than 80 percent

of predicted is considered normal Results of this

TABLE 32-3 Causes of Wheezing

Upper airway (more likely to be stridor, may have element of

Cardiogenic pulmonary edema (‘‘cardiac asthma’’)

Noncardiogenic pulmonary edema [adult respiratory distress

• Other ancillary studies include a chest x-ray andarterial blood gas analysis However, in uncompli-cated obstructive pulmonary disease, these studiesmay not be needed

EMERGENCY DEPARTMENT CARE AND DISPOSITION

• Initial treatment is directed toward identifyingthreats to life and aggressively treating the under-lying condition Supplemental oxygen is given ifthe patient is hypoxic and, depending on the de-gree of obstruction, monitoring may be needed

• Treatment of wheezing is initially directed at lieving bronchospasm by inhaled medications, in-cluding beta agonists and/or anticholinergicagents

re-• Steroids are also used in the acute setting to reduceairway inflammation, but they are of no help inthe acute setting Other agents, but of unprovensignificance in the acute setting, include methyl-xanthine agents, magnesium, and parenteralbeta agonists

• Admission is required for those who have an gen requirement or have the potential for quickdecompensation

oxy-• If patients have failed treatment, mechanical tilation may have to be instituted and other causes

• Typically, 5 g/100 mL of deoxyhemoglobin mustpresent for cyanosis to occur, but this is highlyvariable.10

• Various factors affect the presence or absence ofcyanosis, including skin pigmentation and thick-ness, subcutaneous microcirculation, lighting, andambient temperature.11

CLINICAL FEATURES

• The presence of cyanosis signals tissue hypoxia,but this is not always the case The tongue is a

CHAPTER 33•PNEUMONIA AND BRONCHITIS 117

sensitive indicator of cyanosis, while the earlobes,

conjunctiva, and nail beds are less reliable

• Cyanosis may be central or peripheral Central

cyanosis is usually the result of unsaturated

arte-rial blood or abnormal hemoglobin (e.g.,

methe-moglobin) Peripheral cyanosis is caused by

de-creased peripheral circulation and clinical

situations that lead to an increased arterial

extrac-tion of oxygen

DIAGNOSIS AND DIFFERENTIAL

• The presence of cyanosis must be taken in context

with the clinical situation Arterial blood gas

anal-ysis will confirm the diagnosis Other useful initial

ancillary tests include a hematocrit, looking for

anemia or polycythemia; a chest x-ray, an

electro-cardiogram, and tests for abnormal hemoglobin if

clinically indicated See Table 32-4 for

differen-tial diagnosis

• Methemoglobinemia and carbon monoxide

poi-soning, although rare, must always be kept in mind

in cases of cyanosis, since they will artificially alter

peripheral pulse oximetry secondary to pigment

formation in the blood

EMERGENCY DEPARTMENT CARE

AND DISPOSITION

• Supplemental oxygen is supplied as appropriate

If the patient is unresponsive to supplemental O2,

poor perfusion, abnormal hemoglobin, or large

right-to-left shunts may be present

• Specific antidotes such as methylene blue (1 to 2

TABLE 32-4 Common Causes of Cyanosis

Hemoglobinopathies Decreased cardiac output:

Methemoglobinemia: acquired, shock

hereditary Cold exposure

Sulfhemoglobinemia: acquired Venous congestion

Arterial thrombosis or embolus

Decreased arterial oxygen saturation

Pulmonary etiologies: shunt,

A BBREVIATIONS : VSD ⫽ ventricular septal defect; ASD ⫽ atrial

septal defect; TOF ⫽ tetralogy of Fallot.

mg/kg IV) for methemoglobinemia should beused if signs of toxicity are present

R EFERENCES

1 Manning HL, Schwartzstein RM: Pathophysiology of

dyspnea N Engl J Med 333:1547, 1995.

2 Sharma OP: Symptoms and signs in pulmonary medicine:

Old observations and new interpretations Dis Mon

41:577, 1995.

3 American Thoracic Society: Dyspnea Mechanism,

as-sessment and management: A consensus statement Am

J Respir Care Med 159:321, 1999.

4 Mulrow CD, Lucey CR, Farnett LE: Discriminating

causes of dyspnea through clinical examination J Gen

Intern Med 8:383, 1993.

5 Joffe D, Berend N: Assessment and management of

dys-pnea Respirology 2:33, 1997.

6 Morgan WC, Hodge HL: Diagnostic evaluation of

dys-pnea Am Fam Physician 15:711, 1998.

7 Pasterknap H, Kraman SS, Wodicka GR: Respiratory

sounds: Advances beyond the stethoscope Am J Respir

Crit Care Med 156:974, 1997.

8 Meslier N, Charbonneau G, Racineux JL: Wheezes Eur

Respir J 8:1942, 1995.

9 Holden DA, Mehta AC: Evaluation of wheezing in the

nonasthmatic patient Cleve Clin J Med 57:345, 1990.

10 Gross GA, Hayes JA, Burden JGW: Deoxyhemoglobin

concentrations in the detection of central cyanosis

Tho-rax 43:212, 1988.

11 Martin L, Khalil H: How much reduced hemoglobin is

necessary to generate central cyanosis? Chest 97:1, 1990.

For further reading in Emergency Medicine: A

Com-prehensive Study Guide, 5th ed., see Chap 58,

‘‘Respiratory Distress,’’ by J Stephen czynski

Stap-33 PNEUMONIA AND BRONCHITIS

com-million visits to physicians and 600,000 adult

hospi-talizations per year.1

• There is an increasing frequency of atypical or

opportunistic infections.2,3Atypical infections,

in-fections in compromised hosts, and inin-fections at

the extremes of age may present with more subtle

findings.4 Older patients often present with a

change in mental status and frequently do not

manifest respiratory symptoms

PATHOPHYSIOLOGY

• Pneumonia is an infection of the alveolar, or

gas-exchange, portions of the lung

• Bacterial pneumonia, with an intense

inflamma-tory response, tends to cause a productive cough,

whereas other atypical organisms do not lead to

such an intense inflammatory response and may be

associated with only a mild nonproductive cough

• Pneumococcus is still the most common single

agent, followed by viruses and atypical agents such

as Mycoplasma, Chlamydia, and Legionella.

CLINICAL FEATURES

• Patients with bacterial pneumonia generally

pre-sent with some combination of fever, dyspnea,

cough, pleuritic chest pain, and sputum

produc-tion5(see Table 33-1)

• Pneumococcus classically presents abruptly with

fever, rigors, and rusty brown sputum

• Haemophilus influenzae is more common in

smok-ers and those at the extremes of age

• Staphylococcus aureus frequently follows a viral

respiratory illness, especially influenza or measles

• Pneumonia caused by Legionella is spread by

air-borne, aerosolized water droplets rather than by

person-to-person contact This form of pneumonia

presents, as do Mycoplasma, Chlamydia, and viral

pneumonia, with fever, chills, malaise, dyspnea,

and a nonproductive cough Legionella also

com-monly causes gastrointestinal symptoms of

an-orexia, nausea, vomiting, and diarrhea Mental

status changes also may be present

• The physical findings of pneumonia vary with the

offending organisms and the type of pneumonia

each one causes (see Table 33-1), although most

are associated with some degree of tachypnea

and tachycardia

• Lobar pneumonias, such as those caused by

pneu-mococcus and Klebsiella, exhibit signs of

con-solidation, including bronchial breath sounds,

egophony, increased tactile and vocal fremitus,

and dullness to percussion A pleural friction ruband cyanosis may be present

• Bronchopneumonias, such as those caused by H.

influenzae, reveal rales and rhonchi on

examina-tion without signs of consolidaexamina-tion A monic pleural effusion may occur in either setting;

parapneu-empyemas are most common with S aureus,

Kleb-siella, and anaerobic infections.

• Legionella, which begins with findings of patchy

bronchopneumonia and progresses to signs offrank consolidation, has other common signs, in-cluding a relative bradycardia and confusion

• Interstitial pneumonias, such as those caused by

viruses, Mycoplasma, and Chlamydia, may exhibit

fine rales, rhonchi, or normal breath sounds lous myringitis, when present in this setting, is

Bul-pathognomonic for Mycoplasma infection.

• Clinical features of aspiration pneumonitis pend on the volume and pH of the aspirate, thepresence of particulate matter in the aspirate, andbacterial contamination Although acid aspirationresults in the rapid onset of symptoms of tachy-pnea, tachycardia, and cyanosis and often pro-gresses to frank pulmonary failure, most othercases of aspiration pneumonia progress more in-sidiously.6

de-• Physical signs develop over hours and includerales, rhonchi, wheezing, and copious frothy orbloody sputum The right lower lobe is most com-monly involved as a result of the anatomy of thetracheobronchial tree and gravity.6

DIAGNOSIS AND DIFFERENTIAL

• The differential diagnosis includes acute bronchitis; pulmonary embolus or infarction; ex-acerbation of chronic obstructive pulmonary dis-ease (COPD); pulmonary vasculitides, includingGoodpasture’s disease and Wegener’s granuloma-tosis; bronchiolitis obliterans; and endocarditis

tracheo-• The diagnosis of pneumonia is based on the senting signs and symptoms, examination of thesputum, and chest radiography (see Table 33-1)

pre-• Other tests include a white blood cell count with adifferential count, pulse oximetric analysis, bloodcultures, and pleural fluid examination Arterialblood gas analysis may be performed in ill-ap-pearing patients

• If Legionella is being considered, serum chemistry

studies and liver function tests should be formed, as hyponatremia, hypophosphatemia, andelevated liver enzyme levels are found commonly

per-CHAPTER 33•PNEUMONIA AND BRONCHITIS 119

TABLE 33-1 Characteristics of Bacterial Pneumonia

Streptococcus Sudden onset, fever, rig- Rust-colored; gram-posi- Lobar, occasionally Penicillin V 500 mg PO qid

pneumoniae ors, pleuritic chest pain, tive encapsulated diplo- patchy, occasional pleu- for 10 days or

erythromy-productive cough, cocci ral effusion cin 500 mg PO qid for 10

G 10–20 million units/d

IV q 4–6 h or ceftriaxone

1 g IV qd Group A strepto- Abrupt onset, fever, chills, Purulent, bloody; gram- Patchy, multilobar large See above

cocci productive cough, pleu- positive cocci in chains pleural effusion

ritic chest pain and pairs

Haemophilus in- Gradual onset, fever, dys- Short, tiny, gram-nega- Patchy, frequently basilar, Ceftriaxone 1 g IV qd or

cef-fluenzae pnea, pleuritic chest tive encapsulated coc- occasional pleural ef- uroxime 0.75–1.5 g IV q 8

pain; especially in el- cobacilli fusion h or amoxacillin

10 days

Klebsiella pneu- Sudden onset, rigors, dys- Brown ‘‘currant jelly’’; Upper lobes, bulging fis- Cefazolin 0.5–1.0 g q 8 h IV

moniae pnea, chest pain, bloody thick, short, plump, sure sign, abscess for- or gentamicin 3–5 mg/

sputum; especially in al- gram-negative encapsu- mation kg/d divided q 8 h IV coholics or nursing lated paired cocco-

home patients bacilli

Staphylococcus Gradual onset of produc- Purulent; gram-positive Patchy, multilobar; empy- Oxacillin 8–12 g/d IV or

van-aureus tive cough, fever, dys- cocci in clusters ema, lung abscess comycin 500 mg IV q 6 h

pnea, especially just after viral illness

Legionella pneu- Fever, chills, headache, Few neutrophils and no Multiple patchy nonseg- Erythromycin 1g IV q 6 h ⫾

mophila malaise, dry cough, dys- predominant bacterial mented infiltrates; pro- rifampin 600 mg PO qd

pnea, anorexia, diarrhea, species gresses to consolidation, nausea, vomiting occasional cavitation

and pleural effusion

Pseudomonas Recently hospitalized, de- Gram-negative cocco- Patchy with frequent ab- Tobramycin 3 mg/kg divided

aeruginosa bilitated, or immunocom- bacilli scess formation q 8 h IV and either

pipera-promised patient with fe- cillin 100 mg/kg divided q

mg/kg divided q 8 h IV

Chlamydia pneu- Gradual onset, fever, dry Few neutrophils; organ- Patchy subsegmental infil- Erythromycin 500 mg PO

moniae cough, wheezing, occa- isms not visible trates qid for 10 days or

then 250 mg qd for 4 more days or clarithro- mycin 500 mg PO bid for

10 days

Mycoplasma Upper and lower respira- Few neutrophils; organ- Interstitial infiltrates (re- Same as for Chlamydia

pneu-pneumoniae tory tract symptoms, isms not visible ticulonodular pattern), moniae above

nonproductive cough, patchy densities, bullous myringitis, head- sional consolidation ache, malaise, fever

occa-Anaerobic or- Gradual onset, putrid spu- Purulent; multiple neutro- Consolidation of depen- Clindamycin 450–900 mg IV ganisms tum, especially in alco- phils and mixed or- dent portion of lung; ab- q 8 h or ticarcillin-clavula-

holics ganisms scess formation nate 3.1 g IV q 6 h

EMERGENCY DEPARTMENT CARE

AND DISPOSITION

• Therapies directed against specific organisms are

listed in Table 33-1, although empirical antibiotic

coverage generally is recommended unless the

clinical features and sputum Gram’s stain strongly

suggest a specific cause.7,8

• For outpatient management in otherwise healthypatients under 60 years old, erythromycin 500 mgdaily for 10 to 14 days is an excellent choice forempirical therapy Clarithromycin 500 mg twice aday for 10 days and azithromycin 500 mg on day

1 followed by 250 mg daily for 4 additional daysare more expensive alternatives with fewer sideeffects and better compliance Newer fluoro-

quinolones, such as levofloxacin 500 mg daily for

10 to 14 days, are also highly effective but are

expensive and are restricted to patients over 18

years of age.7,8

• Hospital admission should be reserved for

pa-tients at the extremes of life, pregnant women,

and patients with clinical signs of toxicity (i.e.,

tachycardia, tachypnea, hypoxemia, hypotension,

and volume depletion) or serious comorbid

con-ditions (e.g., renal failure, diabetes, and cardiac

disease).9,10

• Patients who require admission generally also

re-ceive empirical antibiotic therapy Recommended

treatments include erythromycin 500 mg

intrave-nously (IV) every 6 h, ceftriaxone 1 to 2 g IV

daily, and levofloxacin 500 mg IV daily

• Aspiration pneumonitides require a different

therapeutic approach.6 Witnessed aspirations

should be treated with immediate tracheal

suc-tioning, and the pH of the aspirate should be

ascer-tained Bronchoscopy is indicated for the removal

of large particles and further clearing of the

air-ways Patients who require intubation also should

be treated with positive end-expiratory pressure

Oxygen should be administered, but steroids and

prophylactic antibiotics are of no value and should

be withheld For patients at risk of aspiration who

present with signs and symptoms of infection,

anti-biotics are indicated Appropriate choices include

clindamycin 450 to 900 mg IV every 8 h and

ticar-cillin-clavulanate 3.1 g IV every 6 h

BRONCHITIS

EPIDEMIOLOGY

• Acute bronchitis may occur in outbreaks as a

re-spiratory virus spreads through a population or

may be sporadic It accounts for more than 7

mil-lion outpatient physician visits annually among

patients older than age 18

PATHOPHYSIOLOGY

• Acute bronchitis, an infection of the conducting

airways of the lung, produces inflammation,

exu-date, and sometimes bronchospasm of the

in-volved airways

• The majority of cases of acute bronchitis are

caused by viruses, including influenza A and B,

adenovirus, parainfluenza virus, rhinovirus,

respi-ratory syncytial virus (RSV), coxsackievirus A21,

and, less commonly, measles virus, rubella virus,herpesviruses, and coronaviruses.11

• Adults who have contact with children may velop acute bronchitis and pneumonia fromRSV.12

de-• Bacteria known to contribute to acute bronchitis

include Bordetella pertussis, Mycoplasma

pneu-moniae, Chlamydia pneupneu-moniae, and possibly

CLINICAL FEATURES

• The hallmark of acute bronchitis is cough, usuallyproductive, in patients without evidence of pneu-monia, sinusitis, or chronic pulmonary disease.11

• Sputum may be clear or colored, and the presence

of colored sputum does not necessarily indicate

a bacterial infection Patients may complain ofdyspnea or wheezing, usually caused by broncho-spasm

DIAGNOSIS AND DIFFERENTIAL

• Clinical diagnosis is appropriately made when thefollowing findings are present: an acute cough forless than 1 week, no prior lung disease, normalarterial oxygenation, and no auscultatory abnor-malities

EMERGENCY DEPARTMENT CARE AND DISPOSITION

• Nine randomized, double-blind, trolled trials were undertaken between 1966 and

placebo-con-1995 to determine antibiotic effectiveness in ing acute bronchitis.14,15Systematic review did notfind statistical benefit for antibiotic treatment

treat-• There is some evidence that older adults and tients with underlying COPD benefit from antibi-otic treatment for acute bronchitis.15,16

pa-• There is evidence that bronchodilators are useful

in treating acute bronchitis compared with cebo or erythromycin Patients report decreasedcough and a faster return to work when they aretreated with oral or inhaled albuterol.17,18

pla-R EFERENCES

1 Bartlett JG, Mundy LM, Orloff J: Community-acquired

pneumonia N Engl J Med 333:1618, 1995.

2 Fang GD, Fine M, Orloff J, et al: New and emerging

CHAPTER 34•TUBERCULOSIS 121

etiologies for community-acquired pneumonia with

im-plications for therapy Medicine (Baltimore) 69:307,

1990.

3 Marrie TJ, Fine MJ, Coley CM: Ambulatory patients

with community-acquired pneumonia: The frequency of

atypical agents and clinical course Am J Med 101:508,

1996.

4 Metlay JP, SchulzR, Li YH, et al: Influence of age on

symptoms at presentation in patients with

community-acquired pneumonia Arch Intern Med 157:1453, 1997.

5 Metlay JP, Kapoor WN, Fine MJ: Does this patient have

community-acquired pneumonia? Diagnosing

pneumo-nia by history and physical examination JAMA 278:

1440, 1997.

6 Lomotan JR, George SS, Brandstetter RD: Aspiration

pneumonia Postgrad Med 102:225, 1997.

7 Niederman MS, Bass JB, Campbell GD, et al: Guidelines

for the initial empiric therapy of community-acquired

pneumonia: Proceedings of an American Thoracic

Soci-ety Consensus Conference Am Rev Respir Dis 148:

1418, 1993.

8 Bartlett JG, Breiman RF, Mandell LA, File TM:

Guide-lines from the Infectious Disease Society of America:

Community-acquired pneumonia in adults—guidelines

for management Clin Infect Dis 26:811, 1998.

9 Fine MJ, Smith MA, Carson CA, et al: Prognosis and

outcomes of patients with community-acquired

pneumo-nia: A meta-analysis JAMA 274:134, 1996.

10 Fine MJ, Auble TE, Yealy DM, et al: A prediction rule

to identify low-risk patients with community-acquired

pneumonia N Engl J Med 336:243, 1997.

11 Wilson R, Rayner CF: Bronchitis Curr Opin Pulmon

Med 1:177, 1995.

12 Dowell SF, Anderson LJ, Gary HE, et al: Respiratory

syncytial virus is an important cause of

community-ac-quired lower respiratory infection among hospitalized

adults J Infect Dis 174:456, 1996.

13 Wright SW, Edwards KM, Decker MD, Zeldin MH:

Pertussis infections in adults with persistent cough.

JAMA 273:1044, 1995.

14 MacKay DN: Treatment of acute bronchitis in adults

without underlying lung disease J Gen Intern Med

11:557, 1996.

15 Fahey T, Stocks N, Thomas T: Quantitative systematic

review of randomized controlled trails comparing

antibi-otic with placebo for acute cough in adults Br Med J

316:906, 1998.

16 Grossman RF: Guidelines for the treatment of acute

exacerbations of chronic bronchitis Chest 112(suppl):

310S, 1997.

17 Hueston WJ: A comparison of albuterol and

erythromy-cin for the treatment of acute bronchitis J Fam Pract

33:476, 1991.

18 Hueston WJ: Albuterol delivered by metered-dose

in-haler to treat acute bronchitis J Fam Pract 39:437, 1994.

For further reading in Emergency Medicine: A

Com-prehensive Study Guide, 5th ed., see Chap 59,

‘‘Bronchitis and Pneumonia,’’ by Donald A.Moffa, Jr., and Charles L Emerman; and Chap

60, ‘‘Aspiration Pneumonia, Lung Abscess, andPleural Empyema,’’ by Eric Anderson and Max-ime Alix Gilles

• Stronger TB control programs targeting high-riskgroups have reversed this trend; since 1993, TBcase rates have fallen steadily

PATHOPHYSIOLOGY

• Mycobacterium tuberculosis is a slow-growing

aer-obic rod that has a unique, multilayered cell wallcontaining a variety of lipids that account for itsacid-fast property

• Transmission occurs through inhalation of dropletnuclei into the lungs Persons with active tubercu-losis who excrete stainable mycobacteria in saliva

or sputum are the most infectious.3

• Survival of this organism is favored in areas ofhigh oxygen content or blood flow, such as theapical and posterior segments of the upper lobeand the superior segment of the lower lobe of thelung, the renal cortex, the meninges, the epiphyses

of long bones, and the vertebrae.3

CLINICAL FEATURES

• Primary TB infection is usually asymptomatic andnoncontagious, presenting most frequently with

only a new positive reaction to TB skin testing.

Some patients may, however, present with active

pneumonitis or extrapulmonary disease

Immuno-compromised patients are much more likely to

develop rapidly progressive primary infections

• The lifetime reactivation rate after primary TB

infection is 5 to 10 percent Rates are higher in

the very young and the elderly as well as those

with recent primary infection, major chronic

dis-eases, or immune compromise Most patients

pre-sent subacutely with fever, cough, weight loss,

fa-tigue, and night sweats

• Most patients with active TB have pulmonary

involvement characterized by constitutional

symptoms and (usually productive) cough

He-moptysis, pleuritic chest pain, and dyspnea may

develop

• Rales and rhonchi may be found, but the

pulmo-nary exam is usually nondiagnostic.3

• Extrapulmonary TB develops in up to 15 percent

of cases.3 Lymphadenitis, with painless

enlarge-ment and possible draining sinuses, is the most

common example

• Pleural effusion may occur when a peripheral

pa-renchymal focus or local lymph node ruptures

Pericarditis, with typical symptoms, may develop

by extension of infection from local lymph nodes

or pleura

• TB peritonitis usually presents insidiously after

extension from local lymph nodes

• TB meningitis may follow hematogenous spread,

presenting with fever, headache, meningeal signs,

and/or cranial nerve deficits

• Miliary TB is a multisystem disease caused by

massive hematogenous dissemination It is most

common in immunocompromised hosts and

chil-dren Symptoms and findings may include fever,

cough, weight loss, adenopathy,

hepatospleno-megaly, and cytopenias

• Extrapulmonary TB may also involve bone, joints,

skin, kidneys, and adrenals

• Immunocompromised patients, HIV patients in

particular, are extremely susceptible to TB and

far more likely to develop active infections with

atypical presentations.4 Disseminated

extrapul-monary TB is also far more common in HIV

pa-tients and should be considered in the evaluation

of nonpulmonary complaints as well.3,4

• Prior partially treated TB is the major risk factor

for drug-resistant TB It should be considered

when TB is diagnosed, especially among those

with suboptimal prior care, such as immigrants

from endemic areas, prisoners, homeless persons,

and drug users

• Multidrug-resistant TB (MDR TB) is more

com-mon in HIV patients than the general populationand has a high fatality rate in this group.3,4

DIAGNOSIS AND DIFFERENTIAL

• Consider the diagnosis of TB in any patient withrespiratory or systemic complaints so as to facili-tate early diagnosis, protect hospital staff, andmake appropriate dispositions

• Chest radiographs (CXRs) are the most usefuldiagnostic tool for active TB in the ED.3Classicfindings in active primary TB are parenchymalinfiltrates with or without adenopathy Lesionsmay calcify

• Reactivation TB typically presents with lesions inthe upper lobes or superior segments of the lowerlobes Cavitation, calcification, scarring, atelecta-sis, and effusions may be seen.3

• Miliary TB may cause diffuse nodular infiltrates

• Patients coinfected with HIV and TB are larly likely to present with atypical or normalCXRs.4

particu-• Acid-fast staining of sputum can detect teria in 60 percent of patients with pulmonary TB.5

mycobac-Atypical mycobacteria will yield false positives;many patients will have false negatives on a singlesputum sample Microscopy of nonsputum sam-ples (e.g., pleural or cerebrospinal fluid) is less sen-sitive

• Definitive cultures generally take weeks, but newgenetic tests employing DNA probes or polymer-ase chain reaction (PCR) technology can confirmthe diagnosis in days or hours

• Intradermal skin testing with purified protein rivative (PPD) identifies most patients with prior

de-or active TB infection Results are read 48 to 72

h after placement, limiting the usefulness of thistest for ED patients

• Patients with HIV or other immunosuppressiveconditions and patients with disseminated TB may

isonia-• Patients with immune compromise or MDR TBmay require more drugs for longer periods

CHAPTER 35•PNEUMOTHORAX 123

TABLE 34-1 Dosages and Common Side Effects of

Some Drugs Used in TB

POTENTIAL SIDE

INH Adult: 5 mg/kg (300 Hepatitis, neuritis,

ab-mg) dominal pain,

acido-Child: 10–20 mg/kg sis, hypersensitivity

Ethambutol Adult: 15–25 mg/kg Optic neuritis,

head-(2.5 g) ache, peripheral

neu-Child: same ropathy, GI

Streptomycin Adult: 15 mg/kg (1 g) 8th cranial

neuropa-Child: 20–30 mg/kg thy, rash, renal

fail-(1 g) ure, proteinuria

Route: IM

Ciprofloxacin Adult: 750 mg bid Arthropathy, GI

distur-Child: contraindicated bance, CNS

• Table 34-1 summarizes usual initial daily drug

doses and side effects

• Persons with positive PPDs and no active TB

dis-ease should be evaluated for prophylactic

treat-ment with INH to prevent reactivation TB

• Patients with active TB who are discharged from

the ED must have documented immediate referral

to a physician or public health department for

long-term treatment Patients should be educated

about home isolation, follow-up, and screening of

household contacts

• Admission is indicated for clinical instability,

diag-nostic uncertainty (such as a febrile HIV patient

with pulmonary infiltrates), unreliable outpatient

follow-up or compliance, and active known MDR

TB Admission to respiratory or ‘‘droplet’’

isola-tion is mandatory

• ED staff should be trained to identify patients at

risk for active TB as early as possible in their ED

and prehospital course.8 Patients with suspected

TB should be masked or placed in respiratory

isolation rooms They should be transported

wear-ing masks and admitted to respiratory isolation

areas

• Staff caring directly for patients with suspected TB

should wear OSHA-approved respirators/masks

ED staff should receive regular PPD skin testing

to detect new primary infections, rule out activedisease, and consider INH prophylaxis

R EFERENCES

1 Raviglione MC, Snider DE, Kochi A: Global

epidemiol-ogy of tuberculosis: Morbidity and mortality of a

world-wide epidemic JAMA 273:220, 1995.

2 CDC: Tuberculosis morbidity: United States, 1997.

MMWR 47:253, 1998.

3 Rossman MD, MacGregor RR: Tuberculosis New York,

McGraw-Hill, 1995.

4 Barnes PF, Bloch AB, Davidson PT, Snider DE Jr:

Tuber-culosis in patients with human immunodeficiency virus

infection N Engl J Med 324:1644, 1991.

5 CDC: Guidelines for preventing the transmission of

My-cobacterium tuberculosis in health-care facilities, 1994 MMWR 43(RR-13):1, 1994.

6 CDC: Anergy skin testing and preventive therapy for

MMWR 46(RR-15):1, 1997.

7 CDC: Initial therapy for tuberculosis in the era of

multi-drug resistance: Recommendations of the Advisory

Coun-cil for the Elimination of Tuberculosis MMWR

42(RR-7):1, 1993.

8 Behman AJ, Shofer FS: Tuberculosis exposure and

con-trol in an urban emergency department Ann Emerg Med

31:370, 1998.

For further reading in Emergency Medicine: A

Com-prehensive Study Guide, 5th ed., see Chap 61,

‘‘Tuberculosis,’’ by Janet M Poponick and JoelMoll

re-• Secondary pneumothorax occurs most often in

pa-tients with chronic obstructive pulmonary disease

(COPD), but other underlying lung diseases such

as asthma, cystic fibrosis, interstitial lung disease,

cancer, and Pneumocystis carinii pneumonia have

been implicated.2

• Iatrogenic pneumothorax occurs secondary to an

invasive procedure such as placement of a

subcla-vian line or nasogastric tube or positive-pressure

ventilation and should always be ruled out by a

postprocedure chest x-ray

• Tension pneumothorax is caused by positive

pres-sure in the pleural space, leading to decreased

venous return, hypotension, and hypoxia

PATHOPHYSIOLOGY

• Pneumothorax occurs when air enters the

poten-tial space between the parietal and visceral pleura,

leading to partial lung collapse.3

CLINICAL FEATURES

• Symptoms resulting from a pneumothorax are

di-rectly related to its size, its rate of development,

and the underlying lung disease

• Acute onset pleuritic pain is found in 95 percent

of patients.4

• Dyspnea occurs in 80 percent and predicts a large

pneumothorax.4

• Decreased breath sounds on the affected side are

present 85 percent of the time.4

• Only 5 percent have tachypnea over 24 breaths

per minute.4

DIAGNOSIS AND DIFFERENTIAL

• The diagnosis of tension pneumothorax is based

on clinical features including hypoxia,

hypoten-sion, distended neck veins, displaced trachea, and

unilaterally decreased breath sounds

• The ‘‘gold standard’’ for diagnosis is an upright

posteroanterior (PA) chest x-ray, but this is only

83 percent sensitive

• Expiratory films have not been shown to be more

effective in making the diagnosis.5

• Computed tomography (CT) may be more

sen-sitive

• The differential diagnosis includes

costochon-dritis, angina, myocardial infarction (MI),

pulmo-nary embolism (PE), pericarditis, pleurisy, and

pneumo-• Since pleural air is slowly resorbed, patients withsmall, spontaneous, asymptomatic pneumothora-ces may be observed for 6 h and discharged ifthere is no enlargement on x-ray; however, 23 to

40 percent eventually require tube thoracostomy.6

• Small, asymptomatic pneumothoraces may be pirated using a minicatheter and such patients dis-charged at 6 h if there is no recurrence

as-• Tube thoracostomy is indicated for failed tion, complete lung collapse, recurrent pneumo-thorax, significant dyspnea, underlying lung dis-ease, helicopter transport, general anesthesia, ormechanical ventilation.7

aspira-R EFERENCES

1 Baumann MH, Strange C: The clinician’s perspective on

pneumothorax management Chest 112:822, 1997.

2 JantzMA, Pierson DJ: Pneumothorax and barotrauma.

Respir Emerg 15:75, 1994.

3 Paape K, Fry WA: Spontaneous pneumothorax Chest

4:517, 1994.

4 Abolnik IZ, Lossos IS, Gillis D, Breuer R: Primary

spon-taneous pneumothorax in men Am J Med Sci 305:297,

1993.

5 Seow A, Kazerooni EA, Pernicano PG, Neary M:

Com-parison of upright inspiratory and expiratory chest

radio-graphs for detecting pneumothoraces Am J Roentgenol

166:313, 1996.

6 Baumann MH, Strange C: Treatment of spontaneous

pneumothorax: A more aggressive approach? Chest

112:789, 1997.

7 Light RW: Management of spontaneous pneumothorax.

Am Rev Respir Dis 148:245, 1993.

For further reading in Emergency Medicine: A

Com-prehensive Study Guide, 5th ed., see Chap 62,

‘‘Spontaneous and Iatrogenic Pneumothorax,’’

by William Franklin Young, Jr., and RogerLoyd Humphries

CHAPTER 36•HEMOPTYSIS 125

36 HEMOPTYSIS

David F M Brown

EPIDEMIOLOGY

• Hemoptysis is defined as mild, less than 5 mL of

blood in 24 h; moderate; or massive, more than

600 mL in 24 h or more than 100 mL for 3 days.1

• The most common causes are infection (including

tuberculosis), neoplasm, and cardiovascular

dis-ease No cause is found in 28 percent of cases.2

• Hemoptysis is found in all age groups, with a 60 : 40

male predominance.3

PATHOPHYSIOLOGY

• The lung has dual blood supply from the

pulmo-nary and bronchial arteries Bleeding may be from

either source

• The mechanism of bleeding is increased

intravas-cular pressure, erosion by an inflammatory process

into a blood vessel, or complication of a

bleed-ing diathesis

• Hemoptysis caused by increased intravascular

pressure generally arises from a primary cardiac

abnormality such as congestive heart failure or,

less commonly, mitral stenosis

• Hemoptysis caused by erosion most frequently is

due to infection, malignancy, bronchiectasis,

for-eign-body aspiration, vasculitis, and pulmonary

embolism

CLINICAL FEATURES

• A history of underlying lung disease and tobacco

use should be sought

• The acute onset of fever, cough, and bloody

spu-tum suggests pneumonia or bronchitis A more

indolent productive cough may indicate bronchitis

or bronchiectasis Dyspnea and pleuritic chest

pain are hallmarks of pulmonary embolism Fever,

night sweats, and weight loss may reflect

tubercu-losis (TB) or malignancy Chronic dyspnea and

minor hemoptysis may indicate mitral stenosis or

alveolar hemorrhage syndromes

• The physical examination is aimed at assessing the

severity of hemoptysis and the underlying disease

process but is unreliable in localizing the site of

bleeding

• Common signs include fever and tachypnea

Hy-potension is rare except in massive hemoptysis.Cardiac examination may reveal the diastolic rum-ble of mitral stenosis or a pronounced P2 sugges-tive of pulmonary embolus Lung auscultationmay reveal rales, wheezes, or focal consolidation.More frequently, the heart and lung examinationsare normal

• Careful inspection of the oral and nasal cavities

is warranted to exclude an extrapulmonary source

of bleeding

DIAGNOSIS AND DIFFERENTIAL

• The differential diagnosis of hemoptysis includesinfection (bronchitis, bronchiectasis, bacterialpneumonia, TB, fungal pneumonia, and lung ab-scess), neoplasms (bronchogenic carcinoma, met-astatic carcinoma, and bronchial adenoma), car-diogenic causes (left ventricular failure, mitralstenosis), trauma, foreign body aspiration, pulmo-nary embolism, primary pulmonary hypertension,vasculitis, and bleeding diathesis

• Basic testing should include pulse oximetry andchest radiography, although 20 to 30 percent ofpatients who present with hemoptysis have a nor-mal chest x-ray.2,4

• A hematocrit and a blood bank sample should beobtained in patients with major hemoptysis Othertesting should be ordered as indicated by the clini-cal situation

EMERGENCY DEPARTMENT CARE AND DISPOSITION

• Initial management focuses on the ABCs Cardiacand pulse oximetry monitoring along with nonin-vasive blood pressure machines should be utilized.Large-bore intravenous (IV) lines should beplaced

• Supplemental oxygen should be administered tokeep the oxygen saturation above 95%

• IV crystalloid should be administered initially forhypotension Packed red blood cells should betransfused as needed

• Fresh-frozen plasma should be given to patientswith coagulopathies; platelets should be adminis-tered to those with thrombocytopenia

• Patients with ongoing massive hemoptysis should

be placed in the decubitus position with the ing side down to minimize spilling of blood intothe contralateral lung

bleed-• Cough suppression with codeine (15 to 30 mg) orother opioids is indicated

• Endotracheal intubation should be performed

with a large tube (8.0 mm) for persistent

hemopty-sis and worsening respiratory status This will

opti-mize suctioning and permit bronchoscopy

• Indications for admission include massive

hemop-tysis or minor hemophemop-tysis whose underlying cause

carries a high risk of proximate massive bleeding

Some underlying conditions may warrant

admis-sion regardless of the degree of bleeding

• All admissions should include consultation with

a pulmonologist or thoracic surgeon for help in

making decisions regarding bronchoscopy,

com-puted tomography scanning, or angiography for

bronchial artery embolization.5

• Patients who are discharged should be treated for

several days with cough suppressants, inhaled

beta-agonist bronchodilators, and, if an infectious

etiology is suspected, appropriate antibiotics

Close follow-up is warranted

R EFERENCES

1 Nelson JE, Forman M: Hemoptysis in HIV-infected

pa-tients Chest 110:737, 1996.

2 Marshall TJ, Flower CDR, Jackson JE: Review: The role

of radiology in the investigation and management of

pa-tients with hemoptysis Clin Radiol 51:391, 1996.

3 Hirschberg B, Biran I, Glazer M, Kramer MR:

Hemopty-sis: Etiology, evaluation, and outcome in a tertiary referral

hospital Chest 112:440, 1997.

4 Haponik EF, Chin R: Hemoptysis: Clinician’s

perspec-tives Chest 97:469, 1990.

5 Patel U, Pattison CW, Raphael M: Management of

mas-sive hemoptysis Br J Hosp Med 52:2, 1994.

For further reading in Emergency Medicine: A

Com-prehensive Study Guide, 5th ed., see Chap 63,

‘‘Hemoptysis,’’ by William Franklin Young, Jr.,

and Michael W Stava

37 ASTHMA AND CHRONIC

OBSTRUCTIVE PULMONARY

DISEASE

David L Leader, Jr.

EPIDEMIOLOGY

• Asthma affects approximately 4 to 5 percent of

the population in the United States.1In childhood,

asthma is the most common chronic disease, with

a prevalence of 5 to 10 percent.2 Approximately

7 to 10 percent of the elderly are affected byasthma.3

• Chronic obstructive pulmonary disease (COPD)

is rarely manifest in individuals below age 40, but

it is very common in older individuals Amongthose aged 55 to 85 years, the prevalence of COPD

is approximately 10 percent

• In the United States, COPD is the third mostcommon cause of hospitalization, the fourth mostcommon cause of death, and the only leadingcause of death with an increasing incidence.4

• Among patients hospitalized for a COPD bation, mortality is approximately 5 to 14percent.3,5

exacer-PATHOPHYSIOLOGY

• In asthma, the pathophysiologic hallmark is a duction in airway diameter caused by smooth mus-cle contraction, vascular congestion, bronchialwall edema, and thick secretions

re-• During the acute-response phase of asthma, flammatory mediators are released, causing an in-tense inflammatory reaction with resultant bron-choconstriction, vascular congestion, edemaformation, increased production of mucus, andimpaired mucociliary transport.6

in-• Although many stimuli have been noted to itate an increase in airway responsiveness, viralrespiratory infections are the most common of thestimuli that cause acute exacerbation of asthma.7

precip-• The physiologic consequences of airflow tion in asthma and COPD are demonstrated inincreased airway resistance, decreased maximumexpiratory flow rates, air trapping, increased air-way pressures (resultant barotrauma and adversehemodynamic effects), ventilation/perfusion im-balance (causing hypoxemia/hypercarbia), andincreased work of breathing (causing respiratorymuscle fatigue with ventilatory failure)

obstruc-• An estimated 80 to 90 percent of the risk of oping COPD can be attributed to cigarette smok-ing Factors predictive of COPD mortality includeage of starting, total pack-years, and current smok-ing status.8

devel-• Alpha1-antitrypsin deficiency is the only provengenetic risk factor for COPD

• The primary element in the pathophysiology ofchronic airflow obstruction in COPD is impedance

to airflow, especially expiratory airflow, due toincreased resistance or decreased caliber through-out the small bronchi and bronchioles

CHAPTER 37•ASTHMA AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE 127

CLINICAL FEATURES

• Dyspnea, chest tightness, wheezing, and cough are

frequent complaints of patients presenting with

exacerbations of asthma or COPD

• Physical exam findings include wheezing and a

prolonged expiratory phase Wheezing does not

correlate with the degree of airflow obstruction,

as a ‘‘quiet chest’’ indicates severe airflow

ob-struction

• There are two dominant clinical forms of COPD:

(1) pulmonary emphysema, due to abnormal

per-manent enlargement and destruction of the air

spaces distal to terminal bronchioles, and (2)

chronic bronchitis, a condition of excess mucus

secretion in the bronchial tree, with a chronic

pro-ductive cough occurring on most days for at least

3 months in the year for 2 consecutive years

Ele-ments of both clinical forms are often present,

although one predominates

• Clinical features of COPD patients with severe

attacks include sitting-up and forward posturing,

pursed-lip exhalation, accessory muscle use,

para-doxical respirations, and diaphoresis

• A pulsus paradoxus above 20 mmHg is indicative

of severe asthma/COPD

• Tachypnea, cyanosis, agitation, apprehension, and

hypertension demonstrate hypoxia

• Signs of hypercapnia include confusion, tremor,

plethora, stupor, hypopnea, and apnea

• Indicators in patients who are at higher risk of

respiratory failure with hypoxia and hypercarbia

include attacks lasting more than several days,

dependence on steroids, and prior attacks

requir-ing intubation

DIAGNOSIS AND DIFFERENTIAL

• Emergency department (ED) diagnosis of asthma

or COPD is usually made clinically, with

determi-nation of the severity and any existing

complica-tions

• The forced expiratory volume in 1 s (FEV1) and

the peak expiratory flow rate (PEFR) directly

measure the degree of large airway obstruction.9

• Objective measurements of airflow obstruction,

such as sequential peak expiratory flow rates, have

been shown to be more accurate than clinical

judg-ment in determining the severity of the attack and

the response to therapy

• Initial spirometry (PEFR—personal best of

pa-tient or percent predicted) and response to initial

treatment can be used to predict the need for

hospitalization with 86 percent sensitivity and 96

percent specificity.10

• Pulse oximetry is a useful and noninvasive means

of assessing and monitoring oxygen saturationduring treatment, but it does not aid in predictingclinical outcomes.11

• Testing of arterial blood gases (ABGs) should bereserved for sicker patients with severe exacerba-tions and those who are not responding to therapy.This can help to assess for hypoventilation withcarbon dioxide retention and respiratory acidosis

• A normal or slightly elevated PCO2in the setting

of an acute asthmatic attack is an ominous finding

if the patient is doing poorly This is an indication

of extreme airway obstruction and fatigue withpossible onset of acute respiratory failure

• A chest x-ray (CXR) should be obtained if there

is clinical suspicion of a complication such as mothorax, pneumomediastinum, pneumonia, orother medical concern such as congestive heartfailure (CHF), pleural effusion, or pulmonary neo-plasia

pneu-• X-ray findings in emphysematous disease mayshow signs of hyperaeration, such as increasedanteroposterior (AP) diameter, flattened dia-phragms, increased parenchymal lucency, and at-tenuation of arterial vascular shadows

• Laboratory examinations are of limited value andshould be used selectively

• Findings on electrocardiography (ECG) in ate to severe pulmonary disease may reveal rightventricular strain, abnormal P waves, or nonspe-cific ST-T-wave abnormalities; these may resolvewith treatment Arrhythmias can develop, includ-ing multifocal atrial tachycardia (MAT)

moder-• The differential diagnosis of decompensatedasthma and COPD includes CHF (‘‘cardiacasthma’’), upper airway obstruction or aspiration

of a foreign body or gastric acid, pulmonary plasia, pleural effusions, interstitial lung diseases,pulmonary embolism, and exposure to asphyx-iants

neo-EMERGENCY DEPARTMENT CARE AND DISPOSITION

• Patients with COPD often have more underlyingillness than do asthmatics, but the therapy foracute bronchospasm and inflammation in each issimilar

• All patients should be placed on a cardiac monitor,pulse oximeter, and noninvasive blood pressuremonitor; patients with moderate to severe attacksshould have IV access

• Administer oxygen In COPD, the need for gen must be balanced against progressive hyper-carbia and suppression of hypoxic ventilatory

oxy-drive.12Arterial saturation should be corrected to

above 90 percent

• Beta-adrenergic agonists are the drugs of choice

to treat bronchospasm and should be used as

first-line therapy in aerosolized or parenteral forms in

critical settings Albuterol and metaproterenol are

the most beta2-specific agents.13Subcutaneous

ter-butaline sulfate (0.25 to 0.5 mL) or epinephrine

(1 : 1000) (0.1 to 0.3 mL) may also be administered

• Steroids should be given immediately to patients

with severe attacks as well as to those who are

currently taking or have recently taken these

drugs Prednisone 60 to 180 mg/d is the optimal

daily dose; IV methylprednisolone 60 to 125 mg

may be used if the patient is unable to take oral

medications A 3- to 10-day daily course of

ste-roids (prednisone 40 to 60 mg/d) should be given

to discharged patients

• Anticholinergics are useful adjuvants when given

with other therapies; when they are used with beta

agonists, the effects may be additive.14

Ipratro-pium is the agent of choice (500 mg ⫽ 2.5 mL)

and is available as a nebulized solution or

metered-dose inhaler (MDI) A combined

ipra-tropium and albuterol inhaler is available The

effects of ipratropium peak in 1 to 2 h and last 3

to 4 h Dosages may be repeated every 1 to 4 h

• The role of methylxanthines in the treatment of

acute asthma and COPD has been seriously

chal-lenged.13 Theophylline is no longer considered a

first-line agent for acute asthma or COPD

• Broad-spectrum antibiotics: All current guidelines

recommend antibiotics for the treatment of

bacte-rial respiratory infections, especially if there is

evi-dence of infection (fever, CXR findings, and

abnormal mucus production)

Trimethoprim-TABLE 37-1 Criteria for Hospital Admission in

Acute Asthma

Emergency visit within the preceding 3 days

Failure of subjective improvement following treatment

Failure of posttreatment FEV 1 to increase by ⬎500 mL, or

abso-lute value ⬍1.6 L

Failure of posttreatment PEFR to increase more than 15% above

initial value, or absolute value ⬍200 L/min, or PEFR ⬍50%

A BBREVIATIONS : FEV 1 ⫽ forced expiratory volume; PEFR ⫽ peak

expiratory flow rate.

TABLE 37-2 Criteria for Hospital Admissions in Acute Exacerbation of Chronic Obstructive Pulmonary Disease

One or more of the following: inability to walk between rooms,

to sleep or eat due to dyspnea, or to manage at home without additional resources, which are not available

Prolonged or progressive symptoms prior to ED visit Altered mental status

Worsening hypoxia, hypercarbia, or acidosis (pH ⬍ 7.30) High-risk comorbid conditions or complications Unresponsive new or worsening cor pulmonale Planned invasive procedure that may worsen pulmonary function Respiratory muscle fatigue

sulfamethoxazole double strength, doxycycline,macrolides, cephalosporins, and newer fluoro-quinolones may be used

• Heliox: several studies have demonstrated that an

80 : 20 mixture of helium and oxygen (Heliox) canlower airway resistance and act as an adjunct in thetreatment of very severe asthma exacerbation.15

• In selective cooperative patients, noninvasive itive-pressure ventilation (intermittent, continu-ous, or biphasic) may avert artificial ventilationwhen the patient begins to exhibit signs of acuteventilatory failure.16

pos-• Assisted mechanical ventilation is indicated forinability to maintain oxygen saturation above 90%

or severe hypercarbia associated with stupor, tered mental status, exhaustion, narcosis, or acido-sis Oral intubation is preferred, since larger endo-tracheal tubes that facilitate suctioning andventilator weaning can be used

al-• Criteria for admission in asthma patients are listed

in Table 37-1 and for COPD patients in Table 37-2

• In patients being discharged, continued treatmentwith beta2agonists and oral steroids is important

In addition, patient education and close medicalfollow-up is essential

R EFERENCES

1 Mannino DM, Home DM, Pertowski CA, et al:

Surveil-lance for asthma: United States, 1960–1995 MMWR

47:1, 1998.

2 Centers for Disease Control and Prevention: Asthma

mortality rates and hospitalization among children and

young adults: United States, 1980–1993 MMWR

45:350, 1966.

3 Cydulka RK, McFadden ER, Emerman CL, et al:

Pat-CHAPTER 37•ASTHMA AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE 129

terns of hospitalization in elderly patients with asthma

and chronic obstructive pulmonary disease Am J Respir

Crit Care Med 156:1807, 1997.

4 Fiel SB: Chronic obstructive pulmonary disease

mortal-ity and mortalmortal-ity reduction Drugs 52(suppl 2):55, 1996.

5 Fuso L, Incalzi RA, Pistilli R, et al: Predicting mortality

of patients hospitalized for acutely exacerbated chronic

obstructive pulmonary disease Am J Med 98:272, 1995.

6 Fabbri LM, Caramori G, Beghe B, et al: Physiologic

consequences of long-term inflammation Am J Respir

Crit Care Med 157(suppl 1):5195, 1998.

7 Busse WW, Gern JE: Viruses in asthma J Allergy Clin

Immunol 100:147, 1997.

8 American Thoracic Society: Standards for the diagnosis

and care of patients with chronic obstructive pulmonary

disease Am J Respir Crit Care Med 152:578, 1995.

9 McFadden ER Jr: Clinical physiologic correlates in

asthma J Allergy Clin Immunol 77(1pt 1):1, 1986.

10 Rodrigo G, Rodrigo C: A new index for early prediction

of hospitalization in patients with acute asthma Am J

Emerg Med 15:8, 1997.

11 Harden R: Oxygen saturation in adults with acute

asthma J Accid Emerg Med 13:28, 1996.

12 Dunn WF, Nelson SB, Hubmayr RD: Oxygen induced

hypercarbia in obstructive pulmonary disease Am Rev

Respir Dis 144:526, 1991.

13 National Asthma Education and Prevention Expert

Panel: Report 2: Guidelines for Diagnosis and

Manage-ment of Asthma NIH publication 97–4051 Bethesda

MD, National Institutes of Health, 1997.

14 Cydulka RK, Emerman CL: Effects of combined

treat-ment with glycopyrrolate and albuterol in acute

exacer-bations of chronic obstructive pulmonary disease Ann

Emerg Med 25:470, 1995.

15 Manthous CA, Hall JB, Caputo MA, et al: Heliox

im-proves pulsus paradoxus and peak expiratory flow in

non-intubated patients with severe asthma Am J Respir

Crit Care Med 151(2 pt 1):310, 1995.

16 Manthous CA, Hall JB, Caputo MA, et al: A comparison

of non-invasive positive-pressure ventilation and ventional mechanical ventilation in patients with acute

con-respiratory failure N Engl J Med 339:429, 1998.

For further reading in Emergency Medicine: A

Com-prehensive Study Guide, 5th ed., see Chap 64,

‘‘Acute Asthma in Adults,’’ by Rita K Cydulkaand Sorabh Khandelwal, and Chap 65, ‘‘ ChronicObstructive Pulmonary Disease,’’ by Rita K Cy-dulka and Sorabh Khandelwal

• Data from the U.S National Center for Health

Statistics indicate that abdominal pain was the

single ‘‘most frequently mentioned’’ reason

of-fered by patients for visiting the emergency

de-partment (ED) in 1996 (annual incidence is

ap-proximately 57 of 1000 adult ED visits.1

• Admission rates for abdominal pain vary

mark-edly, ranging from 18 to 42 percent, with rates as

high as 63 percent reported in patients over 65

years of age.2

PATHOPHYSIOLOGY

• Visceral abdominal pain is usually caused by

stretching of fibers innervating the walls or

cap-sules of hollow or solid organs, respectively Less

commonly, it is caused by early ischemia or

in-flammation

• Foregut organs (stomach, duodenum, and biliary

tract) produce pain in the epigastric region; midgut

organs (most of the small bowel, appendix, and

cecum) cause periumbilical pain; and hindgut

or-gans (most of the colon, including the sigmoid) as

well as the intraperitoneal portions of the

genito-urinary system tend to cause pain initially in the

suprapubic or hypogastric area

• Visceral pain is usually felt at the midline

• Parietal or somatic abdominal pain is caused by

irritation of fibers that innervate the parietal

• Referred pain is felt at a location distant from thediseased organ

CLINICAL FEATURES

• The principal characteristics of abdominal paininclude location, quality, severity, onset, duration,aggravating and alleviating factors, and change inany of these variables over time

• Associated symptoms should be sought: trointestinal, genitourinary, and gynecologicsymptoms

gas-• Contrary to conventional teaching, absent or minished bowel sounds provide little clinicallyuseful information This is supported by the obser-vation that, in a series of 100 patients with opera-tive confirmation of peritonitis due to perforation

di-of peptic ulcer, about half were noted to havenormal or increased bowel sounds.3

• Hyperactive/obstructive bowel sounds, although

of limited value, are somewhat more helpful, asreflected by their presence in about half of 100patients with small bowel obstruction (SBO), incontrast to only 5 to 10 percent of patients with

500 other surgical diagnoses However, fully 25percent of those with SBO had absent or dimin-ished bowel sounds.3

• ‘‘Rebound’’ tenderness, often regarded as the

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clinical criterion standard of peritonitis, has

sev-eral important limitations In patients with

perito-nitis, the combination of rigidity, referred

tender-ness, and especially ‘‘cough pain’’4 usually

provides sufficient diagnostic confirmation that

lit-tle is gained by eliciting the unnecessary pain of

re-bound.5

• False-positive rebound tenderness occurs in about

one patient in four without peritonitis,5 perhaps

because of a nonspecific startle response Indeed,

more recent work has led some authors to

con-clude that rebound tenderness, in contrast to

cough pain, is of ‘‘no predictive value.’’6

• There is little evidence that rectal tenderness in

patients with right-lower-quadrant (RLQ) pain

provides any useful incremental information

be-yond what has already been obtained by other,

less uncomfortable components of the physical

examination.7

DIAGNOSIS AND DIFFERENTIAL

• Based upon three studies comprising a total of

over 1800 patients, a white blood cell (WBC)

count exceeding the threshold value of 10,000

to 11,000/mm3only doubled the odds of

appendi-citis, while a WBC below this cut the odds in

half.8–10

• For acute cholecystitis, the likelihood ratios (LRs)

of the WBC count are virtually identical to those

seen in appendicitis and are of equally limited

clinical value.8–10

• In one large, well-conducted series of nonspecific

abdominal pain (NSAP), 18 percent (95 percent

CI, 22 to 34 percent) of patients were reported to

have WBC counts⬎10,500/mm3.11

• Recent work has concluded that plain films

tinue to be markedly overutilized One study

con-cluded that restriction of the plain abdominal

radi-ography (PAR) to patients with suspected

obstruction, perforation, ischemia, peritonitis, or

renal colic would have had no impact on

manage-ment and the use of PARs would have been

re-duced by 80 percent.12

• It is clear that diagnostic error in adults with

ab-dominal pain increases in proportion to age,

rang-ing from a low of 20 percent if only young adults

are considered to a high of 70 percent in the

Nonspecific abdominal pain 34%

Incomplete abortion 5% Subtotal, gynecologic 100%

• The small bowel, which is supplied by the superiormesenteric artery, has a warm ischemia time ofonly 2 to 3 h

TABLE 38-2 Causes of Acute Abdominal Pain Stratified by Age 8–10

ⱖ50 YEARS OLD ⬍50 YEARS OLD

Biliary tract disease 21% 6% Nonspecific abdominal 16% 40% pain