Interstital Lung Disease.docx

8/12/2019 Interstital Lung Disease.docx

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Interstital Lung Disease

A group of disorders involving the lung interstitium and characterized by inflammation of the

alveolar structures and progressive parenchymal fibrosis.

The most common presenting complaint of patients eith interstitial lung disease is gradual but

progressive dyspnea. It may initially be present only with exertion, but may occur at rest as the

disease progresses.

The physical examination, including auscultation of the chest, may be antirely normal

early in the disease process. Basilar crackles (Velcro rales) signal the presence of

interstitial pulmonary fibrosis. However, the absence of crackles does not exclude the

diagnosis.

Cyanosis and finger clubbing may develop. With advanced disease, cardiac involvement

is common as a consequence of pulmonary hypertension and right sided heart failure.

With the exception of sarcoidosis and the collagen vascular diseases, the physical

findings are generally limited to the chest.

The chest radiograph may be abnormal in the absence of significant symptoms or normal

in a symptomatic patient. Early in the disease process, radiographic changes may be

limited to an increase in interstitial markings, more prominent in the lower lung fields.

Bilateral hilar adenopathy is suggestive of sarcoidosis. A hight resolution CT scan of

the lung can reveal minimal interstitial disease not evident on conventional chest

radiographs.


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Steroids are beneficial. Patients who are not acutely hypoxic and are nontoxic

appearing can be discharged. The patient should be referred to a pulmonologist for

further evaluation and management.

Pleural Effusion

Definitions

A pleural effusion is the presence of an abnormally large amount of fluid in the pleural

space. A parapneumonic effusion is a pleural effusion associated with bacterial

pneumonia, bronchiectasis, or lung abscess. Empyema (or pus in the pleural space) is

present when there is bacteria on Grams stain of the pleural fluid. A hemothorax is blood

in the pleural space, and a chylothorax results from rupture of the thoracic duct.

Epidemiology and risk factors

The most common cause in Western countries is congestive heart failure, followed by

malignancy, bacterialpneumonia, and PE. The leading cause in developing countries is

tuberculosis.

Other conditions include trauma, pancreatitis, myxedema, viral infections of the lung

parenchyma or pleura, cirrhosis, uremia, nephorotic syndrome, collagen vascular diseases

(e.g, systemic lupus erythematosus, rheumatoid arthritis), and intra abdominal

processes (e.g, acute pancreatitis, subphrenic abscess, ascites). Esophageal perforation is

a rare but serious cause of a pleural effusion.


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Table 52-4 Conditions Causing Pleural Effusion

Transudate Exudate

Congestive heart failure Bacterial pneumonia

Cirrhosis with ascites Bronchiectasis

Nephorotic syndrome Lung abcess

Hypoalbuminemia Tuberculosis

Myxedema Malignancy

Renal failure Connective tissue disease (e.g, systemic lupus erythematosus)

Superior vena cava syndrome Gastrointestinal disorders (e.g, pancreatitis, esophageal rupture)

Pulmonary embolism Uremia

Drug reaction

Cylothorax

Pulmonaryembolism

Pathophysiology

Fluid collects in the pleural space, and compresses the lung leading to impaired

ventilation.

Pleural fluid is classified into two categories: transudates or exudates (table 52-4). A

transudate is essentially an ultrafilttrate of plasma that contains very little protein, and

develops when there is an increase in the hydrostatic pressure or decrease in the oncotic

pressure within pleural microvessels. The most common cause is congestive heart failure.

Exudates contain relatively high amounts of protein, reflecting an abnormality of the

pleura it self, and the result of increased membrane permeability or defective

lymphaticdrainage. Parapneumonic effusion and malignancy are the most common

conditions associated with an exudative effusion. The pleural fluid in association with a


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pulmonary embolus can be transudative or exudative and can be found in up to 50% of

patients.

History

Other than when due to trauma or thoracic aortic rupture, the symptoms are slowly

progressive. Symptoms include shortness of breath, dyspnea on exertion, orthopnea,

cough, and pleuritic chest pain.

Physical Examination

Tachypnea, dullness to percussion over the affected lung, or absence of breath sounds

may be found on physical examination.

Diagnostic Testing

A thoracentesis may be performed to determine if the effusion is a transudate or an

exudates (see Chapter 91 for procedure and Appendix for pleural fluid analysis). The

study is both diagnostic and therapeutic. Send samples for Grams stain and culture,

amylase, cell count, protein, glucose, lactate dehydrogenase (LDH), protein, and pH.

Patients with bilateral pleural effusions and a reasonable explanation for the effusion (e.g,

volume overload from congestive heart failure) do not require a thoracentesis in the ED,

but instead should be treated for the underlying cause of the effusion (i.e., diuresis).

Any other laboratory studies should be directed to the suspected underlying cause. It is

helpful to obtain coagulation studies before attempting an invasive procedure.

An upright chest radiograph may demonstrate blunting of the costophrenic angle

(minimal amount to be seen on radiograph is approximately 150 ml) or complete


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opacification. Lateral decubitus views should be obtained to determine if the effusion will

layer to 1 cm thick (another indication for thoracentesis).

A CT scan is superior for demonstrating intrathoracic pathology, and may lead to a

diagnosis of the underlying problem.

ED Management

Depends on the underlying cause. A tube thoracostomy is indicated for an empyema.

Re expansion pulmonary edema may develop if too much fluid (usually >1,5 L) is

withdrawn during the thoracentesis.

Helpful Hints and Pitfalls

Pleuradesis may be required in recurrent effusions.

Obtain a postthoracentesis chest radiograph to evaluate for pneumothorax.

Pneumothorax (Spontaneous)

Epidemiology and Risk factors

Primary spontaneous pneumothorax occurs in individuals without underlying lung

disease. It is more common in tall, thin males. Smoking, substance abuse (heroine,

ectasy, marijuana, speed, and cocaine), and changes in ambient atmospheric pressure are

risk factors.

Secondary spontaneous pneumothorax is a consequence of an underlying pulmonary

disease process. Individuals with Marfans syndrome are at risk due to connective tissue

defects resulting in apical pleural blebs, which then rupture. Other examples include


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COPD, lung cancer, cysticfibrosis, pneumocystis cariniipneumonia (PCP), tuberculosis,

and lung abscess.

Pathophysiology

The visceral and pleura are in close apposition to each other, with only a potencial

space between them. The negative pressure in the intrapleural space helps to keep the

lungs expanded. The alveolar walls and viscerakl pleura form a barrier that separates this

potential space form the intraalveolar spaces, and help maintain the pressure gradient.

Inspired air escapes from a defect in this barrier into the pleural space, becomes trapped,

and destroys the negative intrapleural pressure. As pressure builds and ultimately

becomes higher than atmospheric pressure, the lung will be unable to expand, the trachea

and mediastinum will shift to the opposite side, relaxation of the heart will be impaired,

pressure on the vena cava will compromise cardiac venous return, and blood pressure will

drop. This is known as a tensionpneumothorax and is a lifethreatening event.

History

There is usually a rapid onset of shortness of breath proceeded by pleuritic (made worse

with deep inspiration) chest pain.

Cough is present in a minority of individuals.


There will be a unilateral absence of breath sounds and hyperresonance to percussion.

Subcutaneous emphysema (crepitus to palpation) may be present if the parietal pleura is

disrupted.


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In tension pneumothorax, the patient will appear ill, and present with tachycardia,

tachypnea, dyspnea, and hypotension. Jugulovenous distention (JVD) may be present.

Tracheal deviation and hypotension are late findings. Hypoxemia is early and profound,

but therapy should not be delayed to obtain a chest radiograph or ABG.

Diagnostic Testing

Tension pneumothorax is a clinical diagnosis requiring immediate intervention. A chest

radiograph study is eseful prior and after insertion of the chest tibe for a simple

pneumothorax in the stable patient; expiratory films are preferred. A chest CT scan is

much more accurate than a plain chest radiograph for small pneumothorax, anterior

pneumothorax, and confusinf diseases such as pulmonary blebs. An ultrasound study can

differentiate beween a pneumothorax and a large bleb.

ED Management

Interventions for a pneumothorax are similar to those described in Chapter 13.

For a primary pneumothorax in a stable patient, a small catheter tube thoracostomy may

be performed, and attached to a Heimlich valve. The patient can be evaluated daily, and

treated as an outpatient if social circumstances permit.

If the spontaneous pnemothorax is recurrent, or if there is evidence of pulmonary blebs, a

thoracic surgeon should be consulted since it may be prudent to take the patient to

surgery for removal of the bleb and pleurodesis. The patient should be advised to avoid

air travel and diving.


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Quantifying the amount of pneumothorax is inaccurate with plain films. A CT scan may

show unexpected multiple pneumothoraces or pulmonary blebs.

Positive pressure ventilation may cause or woren an existing pnemothorax leading to a

tension pneumothorax.

The average reabsorption rate is in the range of 1% to 2% a day and can be increased by a

factor of 4 with the administration of 100%oxygen.

Reexpansion pulmonary edema and reexpansion hypotension are rare occurrences after

rapid evacuation of a large pneumothorax, and relate to how long the pnemothorax was

present before reexpansion (>3days).

Pulmonary Edema

Epidemiology and Risk Factors

Pulmonary edema is clinically differentiated into cardiogenic and noncardiogenic. Most

people who present to the ED have cardiogenic pulmonary edema, which is mainly due to

elevated pulmonary capillary hydrostatic pressure, and occurs with acute coronary

syndrome, cardiomyopathy, valvular heart disease, and hypertensive emergencies.

Noncardiogenic pulmonary edema results from an alteration in the permeability

characteristics of the pulmonary capillary membrane. There are multiple causes which

include drowning, high altitude, sepsis, inhalation injury, drugs or toxins, aspiration,

neurogenic causes, and adult respiratory distress syndrome (discussed earlier).


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Pathophysiology

The underlying etiology can be simplified into acutely elevated afterload (high resistance

failure), acute pump failure, and acute changes in hydrostatic forces. However, elementsn

of all three underlying mechanisms may be present concomitantly.

In elevated afterload, the peripheral resistance that the heart must pump against is

pathologically higher than the pressure that the heart is able to generate. In pump failure,

the left ventricle is unable to create cardiac output to circulate blood from the pulmonary

vessels. Hydrostatic forces can push or pull fluid into the alveoli. Noncardiogenic

pulmonary edema generally results from an alteration in the permeability characteristics

of the pulmonary capillary membrane. The result, regardless of the mechanism, is fluid

collection within the alveoli that decreases gas diffusion and leads to hypoxemia.

History

Patients typically complain of shortness of breath and cough with white or pink sputum.

Chest pain may be present in valvular rupture or myocardial infarction. Dyspnea on

exertion is one of the earliest complaints. Orthopnea is common due to the increased

venous return in the supine position. Paroxysmal nocturnal dyspnea may be present for

the same reason.

Medications, illicit drug use, and recent procedures should be reviewed. Determine

medication compliance and dietary indiscretions.



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Tachypnea, crackles, wheezing, and labored breathing are findings. Edema may be

present. A systolic cardiac murmur suggests mitral regurgitation or aortic stenosis. A

diastolic murmur indicates mitral stenosis or aortic regurgitation.

Evaluate for signs of hypoperfusion such as clammy skin, a thread pulse, or delayed

capillary refill.

Diagnostic Testing

The EKG should be evaluated for patterns of strain ischemia.

Laboratory studies include chemistry, renal function, CBC, coagulation studies, cardiac

enzymes, and a urine toxicology screen (if indicated). Beta natriuretic peptide (BNP)

may help identify CHF as the origin of acute dyspnea. Levels of BNP < 100 pg/mL are

unlikely to be from CHF. Levels 100-500 pg/mL may be CHF, and levels > 500 pg/mL,

are most consistent with CHF. Other conditions that increase right filling pressures may

also increase BNP levels (e.g, pulmonary embolus cirrhosis, end stage renal failure).

An upright chest radiograph may reveal diffuse patchy alveolar infiltrates; cardiomegaly

is usually seen with high resistance and pump failure, where as normal heart size is seen

with noncardiogenic pulmonary edema. In the early stages of CHF, minimal

cardiomegaly and redistribution of the pulmonary vascularity may be seen. As CHF

worsens, fluid may be seen in the interlobular septa at the lateral basal aspects of the lung

(mean capillary wedge pressure of 25 to 30 mm Hg). These are referred to as Kerley B

lines, are always located just inside the ribs, and are horizontal in orientation. As CHF

becomes more pronounced, vessels near the hila become indistinct because of fluid

accumulating in the interstitium. Pleural effusions may be present, and is seen as


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bilateral, predominantly basilar and perihilar alveolar infiltrates ( >30 mm Hg) (figure 52-

1).

Echocardiography is helpful to gauge cardiac contractility, volume status and the

presence of valvular dysfunction.

ED Management

Give supplemental oxygen and position the patient for comfort (e.g, head of bed elevated,

feet dangling over the side of the bed).

Hypertensive emergencies (Chapter 39) leading to pulmonary edema require rapid

reduction of the patients afterload. Nitroprusside, labetolol, esmol, and nesiritide are

commonly used afterload reducers. Hydralazine is indicated during pregnancy.

If the patient is hemodynamically stable, therapy begins with dieresis (e.g, furosemide)

and nitrate therapy (IV or SL nitroglycerin). Nitroglycerin decreases preload and dilates

coronary vessels; it reduces afterload at higher doses. Angiotensin converting enzyme

inhibitor (ACES) are used to reduce afterload. Nesiritide may be a useful alternative to

nitroglycerin. It causes venodilation and dieresis with less hypotension.

Patients in true cardiogenic shock often require inotropic and vasopessor therapy, intra-

aortic ballon counter pulsation, and assisted ventilation. Some of these patients mat

require a small fluid challenge (250 ml NS) to correct hypovolemia. Dobutamine may

increase cardiac contractility. Dopamine may also be needed to maintain a reasonable

perfusion pressure.

Pulmonary edema due to changes in hydrostatic forces requires supportive care. Diuretics

may be required if the patient is fluid overloaded.The treatment for HAPE is discussed in

Chapter 65.


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See chapter 90.3 for cardiovascular Pharmacology. Patients in cardiogenic shock often

require endotracheal intubation. Akll should have hemodynamic monitoring in the critical

care setting.

Figure 52-1. Pulmonary edema, or fluid overload, can be manifested by indistinctness of the

pulmonary vessels as they radiate from the hilum (A).This is sometimes termed a bat wing

infiltrate. As pulmonary edema worsens (B), fluid fills the alveoli, and air bronchograms

(arrows) become apparent. (From Mettler E. Essentials of Radiology (2nd

ed). New York:

Elsevier, 2005,p 98).

Helpful hints and Pitfalls

Failure to consider the underlying pathologic mechanism is detrimental to the patient

because treatments are different.

Heart failure is a diagnosis based on the overall clinical impression. Laboratory tests (i.e,

BNP), if obtained, should only be used for confirmation, as levels can be elevated in any

condition that causes ventricular dilatation.

Pulmonary Embolism

Epidemiology and Risk Factors

Pulmonary embolism (PE) is often a difficult diagnosis to make and is often missed. One

must consider the diagnosis to search for it, and the initial presentation can be

misleadingly benign.

Risk factors form the pretest probability. The wells criteria are tools for ca lculating

pretest probability (table 52-5).


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Table 52-5 Pretest Probability for PE

PE is most likely diagnosis 3

Presence of a DVT 3

Heart rate over 100 1,5Immobilized 1,5

Recent surgery 1,5

History of a VTE 1,5

Hemoptysis 1

Malignancy 1

High probability over 6

Moderate probability 2-6

Low probability less than 2DVT, deep venous thrombosis; PE, pulmonary embolism; VTE, venous thromboembolis.From

Well PS, et al. Excluding pulmonary embolism at the bedside without diagnostic

imaging:management of patients with suspected pulmonary embolism presenting to the

emergency department by using a simple clinical model and d dimer. Ann Intern Med

2001;135:98-107.

Pathophysiology

Virchow described a triad of stasis (prolonged bed rest or travel), vascular injury (trauma

or postsurgical). And hypercoagulability as risk factors for the development of a venous

thromboembolism (VTE). A PE is a VTE that dislodges and travels into the pulmonary

circulation creating a ventilationperfusion mismatch.

Hypercoagulation may be due to genetic problems, smoking, pregnancy, obesity,

hormone replacement, contraception, or malignancy.

Most PEs are thought to originate from lower extremity due to a deep vein thrombosis.

The mortality from a PE been estimated between 5% and 10%.


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History

Shortness of breath is the most common symptom. Other patients may have pleuritic

chest pain, syncope, or hemoptysis.

Syncope may also be the initial presentation.


Tachycardia is the most common finding. Lung sounds are nonspecific.

With massive PE, hypotension, diaphoresis, JVD, respiratory arrest, or cardiac arrest may

be initial findings.

The extremity examination may reveal unilateral pain and swelling.

Diagnostic Testing

The EKG is nondiagnostic, and may only demonstrate nonspecific sinus tachycardia.

Right axis deviation or a prominent S1 Q3 T3 pattern may be seen, but is not reliably

seen often enough to confirm the diagnosis.

There are no laboratory tests diagnostic for PE. With low probability pretest screening,

some quantitative d-dimer assays have an excellent negative predictive value and

preclude further workup. If elevated, the d-dimer is neither helpful nor diagnostic. The

test has no value in patient with an intermediate or high pretest probability. An ABG is

not diagnostic, and many patients with a normal blood gas levels have a PE. Small PEs

do not impair pulmonary gas exchange, and many types of pulmonary pathology can

affect the A-a gradient. A large PE often causes an increased A-a gradient, however, a

normal arterial blood gas can be seen in up to 23% of patients with symptomatic PE.

When a PE is present, studies such as factor V leiden, protein C and S, antithrombin III,


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and antiphospholipid studies are ordered to determine if the patient has a hypercoagulable

state.

A chest radiograph should be obtained to look for other diseases and rarely can be read as

a PE. An elevated right hemidiaphragm and atelectasis are common findings. A

Hamptons hump (a wedge-shaped consolidation at the lung periphery is suggestive of

pulmonary infarction) or a Westermarks sign (decreased pulmonary vascular markings)

are rarely seen.

Echocardiography may demonstrate right ventricular dilatation or pulmonary

hypertension.

Ventilation/ perfusion (V/Q) scan requires a table patient and often a normal chest

radiograph findings. Results are reported as normal, low probability, intermediated

probability, or high probability (Table 52-6). There is high likelihood of a PE in a

positive scan with high pretest probability. There is low likelihood of a PE in a patient

with a normal scan and low pre-test probability (approximately 1%). Many V/Q scans are

nondiagnostic and the patient requires further investigation. The V/Q scan is a safe test

for a pregnant patient.

A spiral CT angiogram (CTA) can demonstrate PE down to the subsegments of the

pulmonary arterial system (Figure 52-2), but is not able to detect a subsegmental PE,

which is of unknown clinical significance. A CTA must be combined with clinical pretest

probability to determine disposition. It is also useful to demonstrate alternative diagnoses.

Pulmonary angiography has been considered the most accurate diagnostic imaging study

to reveal PE, but it is an invasive study, and may also miss subsegmental emboli


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(approximately 1%). Most interventional radiologists request a prior imaging study

before proceeding to angiogram such as V/Q scan or CTA.

Ultrasound can be used to diagnose lower extremity deep venous thrombosis in patients

who have a nondiagnostic study, or are unable to have a diagnostic study. Although a

positive study in a patient with chest symptoms clinches the diagnosis, it does not have a

great enough frequency to be of value, even though most PE originate in the leg veins.

An MRI is useful in pregnant patients but has not been extensively studied.

Table 52-6 Ventilationperfusion Scan Interpretation for pulmonary

Result Interpretation

Normal No perfusion defects are seen. At least 2% of patients with

PE have this pattern, and 4% of patients with this pattern

have PE.

Low probability 14% have PE overall; 40% in high clinical suspicion

group, 16% in moderate suspicion, 4% in low suspicion

group.

Intermediate probability Any V/Q abnormality not otherwise classified.

Approximately 40% of patients with PE fall into this

category and 30% of all patients with this pattern have PE.

High probability 41% of patients with PE have this pattern and 87% of

patients with this pattern have PE. In most clinical settings,


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a high- probability scan pattern may be considered positive

for PE.

Figure 52-2. Pulmonary embolus (PE) located in the proximal pulmonary artery (A) as seen on

CT angiogram. (from;Laack TA, Goyal DG. Pulmonary embolism: an suspected killer. Emerg

Med Clim North Am 2004;22:961-883).

Ergency Departement Management

Disposition will depend on pretest probability combined with the results from the chosen

diagnostic study. An algorithm for a general approach to a patient with a suspected PE is

described in Figure 523.

For massive PE with hemodynamic instability, throbolytics are indicated (see Chapter 90.5).

All patients with an intermediate pretest probability should undergo further diagnostic studies. If

the clinical picture is strongly consistent with PE, it may be prudent to anticoagulate with heparin

(preferentially low- molecular- heparin), admit the patient, and obtain further studies after

admission to the hospital.

All patients with confirmed PE should be admitted for anticoagulation, monitoring, and further

evaluation.

Patients who cannot undergo anticoagulation, or who have a recurrent PE while anticoagulated,

will require an inferior vena cava filter.


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Pitfalls include failure to consider the diagnostic and failure ti know the type of d dimer

study available

Other types of emboli include air, amniotic fluid, and foreign bodies but these are not

treated with anticoagulation.

Consider PE in any patient with unexplained shortness of breath or tachycardia.

Pulmonary Hypertension

Decreased left ventricular compliance, lung parenchymal (such as COPD), or decrased

pulmonary artery compliance leads to increased pulmonary artery resistance. Obesity,

COPD, valvular heart disease, and chronic pulmonary emboli are risk factors. Increased

right ventricular pressures lead to dilation and ultimately right heart failure (cor

pulmonale).

Patients present with dyspnea on exertion and evidence of right heart failure (peripheral

edema, JVD and hepatojugular reflux). Tricuspid regurgitation may be present. Lung

sounds are clear.

Pulmonary function tests may be helpful to diagnose underlying lung disease. A chest

radiograph may demonstrate pulmonary artery enlargement. An echocardiogram may

detect right ventricular dilatation or tricuspid regurgitation. Due to stretch in the right

ventricle, BNP levels may be elevated in the absence of left-sided heart failure.


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Treatment is supportive and admission may be required for management of cor

pulmonale and hypoxia. Pulmonary and cardiology consultation is usually required for

further evaluation and management.

Special Considerations

Refer to Chapter 76, pediatric Respiratory Problems.

Immunocompromised Patient

Respiratory complaints in these patients are commonly encountered in the ED. Although

infectious processes may come to mind initially, significant noninfectious conditions also

may occur. Noninfectious pulmonary conditions include therapy- induced pulmonary

toxicity, thromboembolism, pulmonary hemorrhage, and pulmonary progression of the

primary disease process.

Patients with life-threatening conditions may have fever alone or vague constitutional

complaints.

Teaching Points

The dyspneic patient is immediately recognizable at the triage desk. Although there are myriad

causes of dyspnea, all of these patients are seriously ill. They should be triaged quickly, and

placed on oxygen, a cardiac monitor, and pulse oximetry, and have IV access.

It is useful to attempt to immediately separate cardiac from pulmonary causes, but

unfortunately, many patients with chronic lung disease can develop cor pulmonale, and have a

cardiac contribution to the dyspnea.


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If the primary cause is cardiac, quickly distinguish between highresistance pulmonary

edema, and pump failure cardiac edema. The former will have a high blood pressure, and is

unlikely to be having an acute heart attack. The latter will be in shock, and is likely to be having

a myocardial infarction that involves more than 30% of the left ventricle. The former will

respond to lowering the high resistance, with diuretics, morphine, oxygen, and nitrates, and will

probably not have to be intubated. The latter is more consistent with cardiogenic shock, and the

patient will require immediate intubation, pressor therapy, and possibly an intra-aortic balloon

pump. Dyspnea may also be the chest pain equivalent an acute cardiac ischemic event.

If the causes is respiratory, it is useful to separate infectious from chronic lung disease.

This is accomplished by the presence of fever, chest pain, and often chest radiograph findings.

The common causes of chronic lung disease are best divided into reactive airway disease

(asthma), emphysema, and chronic bronchitis. There is clearly some overlap between all of these

entities since they can all have an element of bronchoconstriction and hypersecretion. Asthmatics

are generally younger, have a known history of the disease, are usually taking some asthmatic

medications, and have expiratory prolongation and increased secretions that are often thick and

green. Emphysematous patients often have a prolonged smoking history, have severe muscle

wasting, expanded anteroposterior chest diameter, snd chronic respiratory failure. Patients with a

chronic wet cough. They also are heavy cigarette smokers. They often have severe right-sided

heart failure.

Treatment for all chronis lung disease includes bronchodilatation, steroid administration,

and attempts to improve oxygenation; therapy often is successful without the admission of the


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patient. Patients who fail to respond to vigorous treatment may require endotracheal intubation

and all require admission.

Suspected PE

Pre-test probability

Low Intermediate or high

(-) D-Diner (+) D-Diner V/Q or CT Anigiogram

Discharge V/Q or CT AnigiogramNondiagnostic Positive

Negative Positive

Negative

Admit for further

evaluation (US, angiogram,

CTPA)

Discharge

Admit for treatment Admit for treatm

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