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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3156_Библиотеки_им_академика_М_И_Перельмана.pdf
I. BACKGROUND. Cough is the most common reason for outpatient clinical visits in the United
States (1). It accounts for over 200 million episodes of acute illness per year, and chronic cough
is associated with significant morbidity and reduced quality of life (2).
II. PATHOPHYSIOLOGY. Cough is a reflex that clears the upper airways of the respiratory tract. It
is triggered through sensory activation of afferent fibers in the vagus nerve. This visceral reflex
can be controlled by higher cortical centers.
III. EVALUATION
A. History.
A complete history is crucial to determining the etiology.
1. Cough Characteristics. In determining the cause for a cough, a distinction from the
following should be considered:
a. Cough Duration:
i. Acute cough is under 3 weeks in duration
ii. Subacute cough is between 3 and 8 weeks in duration
iii. Chronic cough is over 8 weeks in duration
b. Pediatric versus adult patient
2. Characteristics of the Cough. There are specific causes and clinical symptoms associ-
ated with acute, subacute, and chronic cough. Special consideration for pediatric causes
for chronic cough must also be recognized.
a. Acute cough is most commonly due to self-resolving viral illness, but can be the first
sign of potential and serious life-threatening disease (3). A focused history to rule
out pneumonia, severe asthma exacerbation, chronic obstructive pulmonary disease
(COPD), congestive heart failure (CHF), or pulmonary embolism (PE) should be
undertaken and documented. Complaints such as severe pleuritic chest pain and
hemoptysis may prompt consideration of PE or positional dyspnea, and bilateral leg
swelling may lead to conclusion of CHF. Smoking should be identified and smoking
cessation discussed as it can cause chronic bronchitis and bronchogenic cancer. Travel
history should also be discussed to consider if patient is possibly exposed to tuber-
culosis. Immunization history should also be obtained. Discuss medical history of
preexisting conditions or environmental or occupational exposure to noxious agents.
Once it is established that a non–life threatening diagnosis is likely, the most common
causes are viral upper and lower respiratory tract illness, mild exacerbations of asthma
or COPD, bronchitis, or environmental exposure.
b. Subacute cough can be considered to be caused by postinfectious versus noninfectious
etiologies (3). A history of previous infection with persistence of symptoms may
CHAPTER 8
Respiratory Problems
Christopher Bunt
8.1
Cough
Kenji L. Takano
148
suggest that pneumonia has developed, or that bronchitis has set in. Pertussis should
be considered in patients with an inspiratory whooping sound, paroxysmal coughing,
or post-tussive emesis. Previous conditions such as asthma, if not treated, can lead to
subacute cough. Other etiologies such as gastroesophageal reflux disease (GERD) can
also occur; this is suggested by possible gastrointestinal (GI) complaints such as acid
reflux or heartburn. Upper airway cough syndrome (UACS) is another condition that
can be identified through clinical symptoms in the upper airway such as postnasal drip
or sinus symptoms.
c. Chronic cough has a larger differential diagnosis and includes consideration of
medications such as angiotensin converting enzyme inhibitor (ACE-I), environmental
influences such as smoking, and persistent asthma (4). GERD can also be the cause
for chronic cough and may still be a cause despite a lack of GI symptoms. Usually,
patients in this category have been seen previously for their cough and review of
previous treatments and treatment response can help guide further diagnostic studies.
Chronic cough has many similar etiologies as subacute cough and in many patients is
caused by more than one etiology. Neoplasm should always be considered, especially
with a smoking history, weight loss, and hemoptysis. Chest radiography is usually
indicated in chronic cough evaluation as normal versus abnormal imaging can exclude
infectious conditions, neoplasm, and sarcoidosis.
d. In children, there are some crucial differences in the evaluation of cough (5,6). For
instance, aspiration of foreign body should be considered and early chest radiography
would be indicated. Spirometry should also be considered early in the evaluation if age
appropriate. Children who have cystic fibrosis, tracheoesophageal fistula, or congenital
cardiac abnormalities may also present initially with cough, and further history should
be obtained if suspected. Children may also be sensitive to environmental irritants
such as second-hand smoke. Specific treatment guidelines for pediatric patients should
be followed as medication type and starting dosage such as antibiotics may be different
from adults. In young children, parents should be discouraged from using over-the-
counter cough medications (7).
B. Physical Examination
1. Focused physical exam. This must include vital signs such as temperature, pulse,
respiratory rate, oxygen saturation, and blood pressure. A complete heart and lung
examination with bare chest should be performed as well. Ear, nose, sinus, and throat
examinations are also essential for the evaluation of cough.
2. Additional physical exam. Based on clinical history, a cardiac evaluation focused on
stigmata of CHF such as jugular venous distention or liver enlargement should be per-
formed. Lymphadenopathy may suggest neoplasm as the cause and evidence of cachexia
and wasting can suggest chronic disease, cancer, or human immunodeficiency virus.
Clubbing of fingers, barrel chest, or peripheral cyanosis may also indicate COPD if not
identified through history.
C. Testing
1. Clinical laboratory tests. The vast majority of causes for acute non–life threatening
cough do not require laboratory testing. If pneumonia is suspected, it would be reason-
able to obtain a complete blood count and blood cultures. In an outpatient setting,
Gram stain and sputum culture would not likely alter treatment strategy and therefore is
unlikely to be practical. If clinical history suggests, a purified protein derivative may be
useful if tuberculosis is suspected. Further lab testing can confirm specific diagnosis such
as testing for pertussis or cystic fibrosis screening.
2. Radiologic tests. Chest radiography should be considered if a lower airway cause such
as pneumonia is suspected. This would be supported by a patient having a fever,
tachypnea, productive sputum, and abnormal physical exam. In children, imaging
may detect a foreign body as the cough etiology. As a general rule, patients with a
chronic cough should have a chest radiography performed unless they have a specific
149
contraindication such as pregnancy. Appropriate imaging for evaluation of PE
should be performed if this is the suspected cause. In a subacute or chronic cough,
sinus computed tomography imaging can determine if the cause for the cough is
sinusitis.
3. Pulmonary function tests. In adults, peak flowmeter measurement with use of a
bronchodilator can often identify asthma. In children and adults of chronic cough non-
responsive to treatment, spirometry should be performed (5). Children aged 6 and older
can reliably perform spirometry (6).
4. Invasive tests. Bronchoscopy is useful as a follow-up to abnormal imaging such as a
foreign body or neoplasm. For patients with chronic GERD, there is a role in using
esophageal pH monitoring or barium esophagography if nonacid GERD is the suspected
cause (8).
IV. DIAGNOSIS
A. Differential Diagnosis.
In general, the acute cough is most likely due to an infectious
etiology, specifically viral. Given this, antibiotics are unlikely to be effective unless the
condition is bacterial in origin. Life-threatening causes should always be considered when
evaluating acute cough such as CHF exacerbation, pneumonia, or PE. Subacute cough can
be the result of postinfectious recovery or the persistence of a chronic cause for cough such
as asthma, GERD, or COPD. Chronic cough has a much longer differential diagnosis
and includes infectious and noninfectious etiologies such as ACE-I use and UACS. UACS
should be considered if a nonsmoking, immunocompetent adult has a chronic cough with
normal chest x-ray. Often, there is more than one specific disease process that causes chronic
coughing. Environmental agents can also cause coughing; unless these are considered and
the exposure is reduced, symptoms will persist.
B. Special Concerns. Failure to improve despite treatment should prompt a more extensive
diagnostic evaluation and possible specialist referral if the etiology is not found or if clinical
response is not obtained. In general, patients such as the very young, old, or immunosup-
pressed warrant close follow-up to ensure clinical recovery.
Disclaimer
The opinions and assertions contained herein are the private views of the author and are not to be
construed as official or as reflecting the views of the U.S. Air Force Medical Service, the U.S. Air
Force or the Department of Defense at large.
REFERENCES
1. Chun-Ju H, Cherry DK, Beatty PC, et al. National Ambulatory Medical Care Survey: 2007 Summary.
US Department of Health and Human Services, CDC November 2010: 27.
2. French CL, Irwin RS, Curley FJ, Krikorian CJ. Impact of chronic cough on quality of life. Arch Intern
Med 1998;158(15):1657–1661.
3. Irwin RS, Baumann MH, Boser DC, et al.; American College of Chest Physicians. Diagnosis and
management of cough executive summary: ACCP evidence-based clinical practice guidelines. Chest
2006;129(1 suppl):1S–23S.
4.
Benich JJ, Carek PJ. Evaluation of the patient with chronic cough. Am Fam Physician 2011;84(8):
887–892.
5. Asilsoy S, Bayram E, Agin H, et al. Evaluation of chronic cough in children. Chest 2008;134(6):
1122–1128.
6. Custer JW, Rau RE, eds. The Harriett Lane Handbook, 18th ed. Philadelphia, PA: Elsevier Mosby,
2009.
7. AAP Practice Guideline: Withdrawal of Cold Medicines, Addressing Parent Concerns 2008. Accessed
at http://practice.aap.org/content.aspx?aid=2254 on Feb 20, 2012.
8. Irwin RS. Chronic cough due to gastroesophageal reflux disease: ACCP evidence-based clinical practice
guidelines. Chest 2006; 129(suppl):805–945.
150
8.2
Cyanosis
Michael J. Gravett
I. BACKGROUND. Cyanosis is a dusky blue discoloration of the skin and mucous membranes
caused by an increased quantity of reduced (deoxygenated) hemoglobin or hemoglobin deriva-
tives in these tissues.
II. PATHOPHYSIOLOGY. In general, cyanosis appears when the concentration of reduced hemo-
globin in the cutaneous tissues exceeds 4 g/dL (1). This represents systemic arterial oxygen
saturations ranging from 60% in a patient with a hemoglobin concentration of 6 g/dL to 88%
in a patient with a hemoglobin concentration of 20 g/dL (2). In addition, skin pigmentation
and thickness also affect the degree of apparent cyanosis. In darkly pigmented individuals, color
changes may not be seen until significantly lower oxygen saturations (1). Cyanosis is categorized
as either central or peripheral based on the underlying abnormality.
A. Central cyanosis occurs with systemic arterial oxygen desaturation, in some anatomic
shunts, and in certain conditions with abnormal hemoglobin molecules (3). Central cyano-
sis is characterized by the discoloration of both skin and mucous membranes. It is usually
caused by one of the following:
1. Obstruction of oxygen intake (epiglottitis, acute laryngotracheobronchitis, asthma,
chronic bronchitis, emphysema, and foreign body aspiration).
2. Decreased oxygen absorption, such as an alveolar capillary block (sarcoidosis, pulmonary
fibrosis, pneumonia, pulmonary edema, alveolar proteinosis) or ventilation-perfusion
(V/Q) defects from emphysema, pneumoconioses, and sarcoidosis.
3. Decreased lung perfusion (septic shock, cardiogenic shock, pulmonary embolus, pulmo-
nary vascular shunts, and congenital heart disease).
4. Reduced intake of oxygen from altitudes above 8,000 to 13,000 ft (1, 4).
5. A defective hemoglobin molecule that is unable to attach to oxygen (methemoglobin-
emia, sulfhemoglobinemia, and other hemoglobinopathies). Note that carbon monoxide
poisoning causes a cherry red appearance rather than a bluish hue. This is not true cya-
nosis but is often considered in the same category.
B. Peripheral cyanosis is the result of decreased blood flow and an abnormally high extraction
of oxygen from arterial blood. It is caused by reduced cardiac output, cold exposure, and
arterial or venous obstruction. In contrast to central cyanosis, the oral mucous membranes
are typically spared (2). The following are the most common causes of peripheral cyanosis:
1. Reduced cardiac output from acute myocardial infarction or other causes of heart
“pump” failure.
2. Local or regional phenomenon from cold exposure, arterial obstruction from embolus or
thrombosis, and venous stasis or obstruction.
3. Generalized cold exposure (Raynaud’s disease).
III. EVALUATION
A. History
1. Onset? Is the cyanosis of recent onset or has it been present since birth? A history of cya-
nosis since birth and “squatting” in childhood suggest congenital heart disease. Chronic
cyanosis caused by methemoglobinemia can be congenital or acquired. Other causes of
chronic cyanosis include chronic obstructive pulmonary disease (COPD), pulmonary
fibrosis, and pulmonary atrioventricular fistula. Acute and subacute cyanosis can be
caused by acute myocardial infarction, pneumothorax, pulmonary embolus, pneumonia,
or upper airway obstruction.
2. Symptomatic? Asymptomatic patients may have methemoglobinemia (congenital or
drug induced) or sulfhemoglobinemia. Exposures to drugs (prescribed and/or illicit)
151
or environmental factors should be reviewed. Intermittent cyanosis, skin color changes,
and pain with cold exposure suggest Raynaud’s phenomenon. Symptomatic patients,
especially with chest pain and respiratory distress, are more likely to have a cardiac or
pulmonary cause of cyanosis.
3. Risk Factors? Does the patient have known risk factors for cardiac or pulmonary disease,
including smoking, hyperlipidemia, asthma, drug abuse (especially methamphetamines),
severe obesity (sleep apnea), neuromuscular disease, or autoimmune disease? Does the
patient have chest pain or intermittent cyanosis with exercise, suggesting angina? Chest
pain can be present with acute pulmonary emboli or pneumothorax. Is there a cough
and fever suggesting pneumonia? Has the patient had any occupational or environmental
exposures that might cause pulmonary problems?
4. Family History or Past Medical History? Is there a family history of abnormal
hemoglobin or pulmonary disease? Has the patient suffered an episode of hypotension
that could produce adult respiratory distress syndrome (ARDS), such as sepsis or heart
failure?
B. Physical Examination
1. Initial assessment. Vital signs: tachycardia suggests cardiac arrhythmia, shock, volume
depletion, anemia, or fever. An increased or decreased respiratory rate and use of acces-
sory musculature suggest hypoxia. Hypotension can signal vascular collapse.
2. Additional physical examination. Stridor suggests upper airway obstruction. Examine
the pharynx for evidence of obstruction. If epiglottitis or the presence of a foreign
body is suspected, be prepared to intubate the patient. Check the neck for evidence of
jugular venous distention. Auscultate the chest for rales suggestive of pulmonary edema,
wheezing, and rhonchi consistent with reactive airway disease or absence of breath
sounds, suggestive of pneumonia or pneumothorax. Auscultate the heart for murmurs,
arrhythmias, and abnormal heart sounds. Feel the pulses in the extremities to assess for
arterial embolus or venous thrombosis, especially if cyanosis is localized to one extrem-
ity. Examine the abdomen for evidence of intra-abdominal catastrophe or aneurysm.
Examine the nails for evidence of clubbing, which is suggestive of chronic pulmonary
disease.
C. Testing
1. Pulse oximetry estimates oxygen saturation but does not measure it directly. Direct
measurements using arterial blood gases (ABGs) are necessary to assess a patient with
cyanosis. Patients with abnormal hemoglobin types have a normal Pao
2
but decreased
hemoglobin O
2
saturation. A low Pao
2
is caused by respiratory or cardiac problems in
most circumstances.
2. A chest radiograph helps assess heart size and lung parenchyma. Infiltrates suggest
pneumonia, ARDS, or pulmonary edema. Exclude pneumothorax. Look for evidence of
interstitial lung disease. Pleural effusion can represent infection, malignancy, or pulmo-
nary edema.
3. An electrocardiogram may demonstrate acute myocardial infarction, arrhythmia, or peri-
cardial process. P pulmonale, right ventricular hypertrophy, and right axis shift suggest
chronic pulmonary disease.
4. An echocardiogram can help diagnose both diastolic and systolic heart failure, as well
as visualize wall motion abnormalities that may be present in acute or prior myocardial
infarction. Evidence of pulmonary hypertension can also be seen on echocardiogram.
5. Chest computed tomography (CT) may identify pulmonary emboli and provide more
information than chest x-ray in a variety of cardiac and pulmonary diseases.
6. V/Q scanning may also demonstrate pulmonary embolus. It can be helpful in cases
where a CT scan is contraindicated such as in patients with renal disease or contrast
allergy.
7. Pulmonary artery catheterization and pressure measurements can help distinguish car-
diac causes from pulmonary etiologies.
8. Pulmonary function testing can also be a useful adjunct for diagnosis.
152
IV. DIAGNOSIS
A.
Focused history, physical examination, and diagnostic testing usually reveal the cause of
cyanosis. Response to supplemental O
2
can also help pinpoint the cause of cyanosis (4).
Decreased oxygenation secondary to mild-to-moderate V/Q mismatches caused by pneu-
monia, pulmonary embolus, and asthma may be reversible with supplemental oxygen.
Severe V/Q mismatch caused by intrapulmonary shunting from severe pulmonary edema
or ARDS may be refractory to supplemental O
2
. Moderate V/Q mismatch associated with
ventilatory failure COPD may respond to supplemental O
2
, but be aware of increasing CO
2
levels. ABGs directly measure Pao
2
and O
2
saturation. Abnormal hemoglobin types are also
measured and they can help guide therapy. Hypoxia with an elevated CO
2
suggests COPD
or asthma, whereas hypoxia with a normal or decreased CO
2
suggests pneumonia, ARDS,
pulmonary edema, pulmonary emboli, or interstitial lung disease (5).
B. Once the cause of the cyanosis is determined, the objective is to treat the underlying process.
Causes of pseudocyanosis include argyria or bismuth poisoning (slate blue-gray coloring
of mucous membranes), hemochromatosis (brownish color), or polycythemia (ruddy red
color). For peripheral cyanosis caused by decreased cardiac output, correct the causes of
hypovolemia (e.g., dehydration, shock, heart failure).
Disclaimer
The opinions and assertions contained herein are the private views of the author and are not to be
construed as official or as reflecting the views of the U.S. Air Force Medical Service, the U.S. Air
Force or the Department of Defense at large.
REFERENCES
1. Longo DL, Fauci AS, Kasper DL, et al., eds. Harrison’s Principles of Internal Medicine, 18th ed. New
York, NY: McGraw-Hill; 2012:Vol. 1:287–291.
2. Fathman L, ed. Evidence-Based Physical Diagnosis, Philadelphia, PA: Saunders, 2001:90–95.
3. Alvero R, Ferri FF, Borkan JM, et al., eds. Ferri’s Clinical Advisor 2012: 5 Books in 1, 1st ed.
Philadelphia, PA: Mosby, 2012:1136–1137.
4. Woodley M, Whelan A. Manual of medical therapeutics, Boston, MA: Little, Brown and Company,
1993:179–181.
5. Khan MG. Cardiac and pulmonary management, Philadelphia, PA: Lea & Febiger, 1993:818–825.
8.3
I. BACKGROUND. Hemoptysis is the expectoration of blood or blood-tinged sputum originating
from the lower respiratory tract, encompassing the lung parenchyma, bronchioles, and trachea.
II. PATHOPHYSIOLOGY. Hemoptysis is often an anxiety-provoking symptom, creating fear more
often than being life-threatening. With that being said, cases of massive hemoptysis, defined
in the literature as the expectoration of ≥600 mL/24 h, can indeed be life-threatening, and
impaired oxygenation can occur with as little as 400 mL of blood in the alveolar space (1).
A. Etiology and Epidemiology
a. Infection.
According to the American Thoracic Society, there are greater than
100 possible causes of hemoptysis (2). By far the most common etiology is infection,
accounting for 60–70% of cases presenting to a primary care setting (3). Resulting from
Hemoptysis
Sean P. Wherry
153
its prevalence in Third World countries, tuberculosis (TB) remains the most common
infectious etiology worldwide (4). Within the United States, viral bronchitis and bacterial
pneumonia have surpassed TB as the primary cause (3). It is thought that pulmonary
infections are responsible for superficial mucosal inflammation and rupture of blood ves-
sels, resulting in blood-tinged sputum.
b. Neoplasm. Neoplastic disease is responsible for 19–20% of hemoptysis cases (2).
Bronchogenic carcinomas comprise 90% of these cases, with metastatic disease (renal,
colon, and breast) accounting for the rest (1, 3). Neoplastic causes should be considered
in patients over the age of 40 years with a history of smoking.
c. Pulmonary Venous Hypertension. Conditions that result in elevated pulmonary
artery pressures are known to cause hemoptysis. These include congestive heart failure,
severe mitral stenosis, pulmonary embolism, and pulmonary arterial hypertension (2, 3).
d. Idiopathic. Idiopathic hemoptysis is a diagnosis of exclusion occurring in 7–34% of
patients (3). Typically, these patients do well and do not have any long-term sequela.
Despite this, patients over the age of 40 years with a history of smoking should undergo
close follow-up, as there is evidence for increased incidence of lung cancer (3).
III. EVALUATION. The initial evaluation of patients with hemoptysis is similar regardless of the
rate of bleeding. Despite this, the mortality from a massive bleed decreases with expeditious
evaluation (2). Regardless of the rate, the initial step in the evaluation is to differentiate whether
the patient truly has hemoptysis versus bleeding from another source, e.g., hematemesis or
pseudohemoptysis (bleeding originating in the naso/oropharynx).
A. History. Close attention should be paid to the nature of the hemoptysis and its associated
symptoms to include the presence of a productive cough, documented fevers, and increased
dyspnea. Even though it is often exaggerated by the patient, an attempt should be made
to assess the volume of expectorant. Frothy, bright red/pink, or clotted appearance is more
likely to be associated with true hemoptysis, whereas dark brown/black, coffee ground
appearance is likely to be gastric in origin. Likewise, the presence of nausea and emesis,
a history of gastric or hepatic disease, or a history of epistaxis decrease the likelihood of a
pulmonary source. If a pulmonary source is suspected, a thorough review of systems and
review of the patient’s past medical history will often be enlightening as to the etiology of the
hemoptysis. A history of anticoagulant use, breast/colon/renal cancer, calf tenderness/swell-
ing, pleuritic chest pain, cardiac disease/heart failure, orthopnea, recent travel, hematuria,
unintentional weight gain/loss, chronic obstructive pulmonary disease, and smoking may
assist in the diagnosis and management of hemoptysis (3).
B. Physical Exam. Vital signs should include heart rate, blood pressure, temperature, respira-
tory rate, and oxygen saturation. Any signs of shock, hypovolemia, hypoxia, or respiratory
failure should be identified and acted upon immediately. A thorough ENT exam should
be performed. The presence of saddle nose with rhinitis and a septal perforation may be
seen with Wegener’s granulomatosis. The presence of oral or genital ulcers should raise the
concern for Behçet’s disease (4). The pulmonary exam should note the work of breathing,
any chest wall abnormalities, as well as the presence of stridor, rales, wheezes, or decreased
breath sounds. A cardiac exam should be done with particular attention paid to the presence
of murmurs, an S4 heart sound, and jugular venous distention. An exam of the patient’s
extremities should note the presence of edema, clubbing of the digits, or cyanosis. Cervical,
axillary, and inguinal lymph nodes should be assessed for lymphadenopathy.
C. Diagnostic Evaluation
a. Labs.
The severity of the patient’s symptoms, the patient’s comorbidities, and the
associated symptoms will dictate what laboratory tests will be appropriate. In all patients
with signs of respiratory distress, an arterial blood gas should be obtained (1). In most
patients, routine blood work to include a complete blood count, renal function panel,
coagulation profile, electrolytes, and urinalysis should be performed (1, 2). Sputum
should be analyzed and cultured for the presence of bacteria (Gram stain, potassium
hydroxide, acid fast). Sputum cytology should be performed in all smokers older than
40 years and in any patient where there is concern for neoplasm (4).
154
b. Imaging. Following a thorough history and physical, all patients presenting with
hemoptysis should obtain a chest radiograph to evaluate lung parenchyma, heart, and pul-
monary vasculature (1–5). Evidence of cavitary lesions, tumors, infiltrates, and atelectasis
may be demonstrated and aid in diagnosis and management (4); 20–40% of chest radio-
graphs are interpreted as normal (1). In stable patients with a normal chest radiograph
who have no risk factors for neoplasm and do not have recurrent episodes of hemoptysis,
no further evaluation is needed, and a course of observation is warranted. In patients with
abnormal chest radiographs, recurrent symptoms, or risk factors for neoplasm, a high-
resolution computed tomography should be performed (3).
c. Bronchoscopy. Bronchoscopy may be performed in patients in whom there is a strong
concern for neoplasm (3). Advantages include direct visualization of the endobronchial
processes to include site of bleeding, and it allows for immediate intervention to con-
trol bleeding. Rigid bronchoscopy is recommended for massive hemoptysis requiring
immediate intervention. This is due to its greater suctioning capabilities and its ability
to maintain a patent airway. It does, however, require general anesthesia and often fails
to visualize the upper lobes (4). Fiber-optic bronchoscopy is often reserved for mild
hemoptysis typically 24–48 hours after presentation (3), can be done at the bedside, and
may reach more peripheral lesions (4).
Disclaimer
The opinions and assertions contained herein are the private views of the author and are not to be
construed as official or as reflecting the views of the U.S. Air Force Medical Service, the U.S. Air
Force or the Department of Defense at large.
REFERENCES
1. Corder R. Hemoptysis. Emerg Med Clin N Am 2003;21:421–435.
2. Lenner R, Schilero G, Lesser M. Hemoptysis: diagnosis and management. Comp Ther 2002;28(1):7–14.
3. Bidwell JL, Pachner RW. Hemoptysis: diagnosis and management. Am Fam Physician 2005;72(7):
1253–1260.
4. Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care Med
2000;28(5):1642–1647.
5. Marshall TJ, Flower CDR, Jackson JE. The role of radiology in the investigation and management of
patients with haemoptysis. Clin Radiol 1996;51:391–400.
8.4
I. BACKGROUND. Pleural effusions represent an imbalance between the formation and removal of
pleural fluid and are characterized by an excessive accumulation of fluid in the pleural space (1).
There are many medical conditions that may cause pleural effusions, but the most common
causes in adults are congestive heart failure, infection, pulmonary embolism, and malignancy (2).
II. PATHOPHYSIOLOGY. Causative mechanisms for pleural effusion include an increased hydro-
static pressure in the microvascular circulation such as in congestive heart failure, a decreased
oncotic pressure in the microvascular circulation which may be secondary to hypoalbuminemia,
and increased negative pressure in the pleural space suggestive of atelectasis. Other common
mechanisms include separation of the pleural spaces from a trapped lung, increased permeabil-
ity of the microvascular circulation due to inflammatory mediators from infectious processes,
impaired lymphatic drainage from the pleural surface due to blockage by tumor or fibrosis, and
movement of ascitic fluid from the peritoneal space through diaphragmatic lymphatics (1).
Pleural Effusion
Kenisha R. Heath
155
III. EVALUATION
A. History
1. Pulmonary. Symptoms experienced by the patient are largely dependent upon the
amount of accumulated fluid in the pleural space. With significant fluid accumulation,
patients may report pleuritic pain, dyspnea, and a nonproductive cough. With minimal
fluid accumulation, patients may remain asymptomatic.
2. Associated Symptoms. Patients may also experience fever in the presence of infection;
hemoptysis in the presence of pulmonary embolism and lung cancer; or weight loss in
the presence of malignancy, tuberculosis, or infection (2).
3. Past Medical History. Patients with a recent history of abdominal surgery may expe-
rience postoperative pleural effusion or effusion secondary to pulmonary embolism.
Pleural effusion secondary to malignancy should be excluded (2). Congestive heart
failure should be considered in patients with multiple cardiac risk factors.
4. Family History. Consideration of family history of malignancy, heart disease, and infec-
tious diseases should be discussed.
5. Social History. Patients with a history of alcohol abuse, misuse, or pancreatic disease
may have pleural fluid accumulation secondary to a pancreatic effusion. Chronic and
prolonged exposure to asbestos may cause effusion secondary to mesothelioma or benign
asbestos pleural effusion (2).
B. Physical Exam
1. Focused Pulmonary Exam. The patient’s respiratory rate, respiratory effort, and breath
sounds should be thoroughly evaluated. Possible findings on exam suggestive of pleural
effusion may include dullness to percussion, decreased or absent breath sounds, and
reduced tactile fremitus. Presence or absence of the findings may be dependent upon the
severity of the effusion.
2. Additional Physical Exam. The presence of a heart murmur and cardiomegaly on imag-
ing suggests possible heart failure, whereas ascites may suggest the presence of hepatic
hydrothorax. Consider pulmonary embolism in patients exhibiting swelling of a lower
extremity and pericarditis in those with the presence of a pericardial friction rub (2).
C. Testing
1. Radiography. Anteroposterior (AP) and lateral chest radiographs should be completed
when concern for pleural effusion exists. In the upright position, free pleural fluid will
flow beneath the lung, causing the following on imaging: blunting of the costophrenic
angle, lateral displacement of the dome of the diaphragm, and elevation of the hemitho-
rax (1). Views of the lateral decubitus are helpful in viewing smaller effusions, as typically
only effusions of 200 mL or larger are seen on the AP view (3).
2. Ultrasound. The use of ultrasonography is helpful in identifying small effusions unde-
tectable by radiograph. It is also helpful in differentiating between solid and liquid
components. Additionally, an ultrasound may be used to guide thoracentesis for small
or loculated effusions (1).
3. Computed Tomography (CT). CT is used in cases where plain radiography and ultra-
sound are unsuccessful in identifying anatomy. It is helpful for detecting small effusions
as well as differentiating pleural fluid from pleural thickening (2).
4. Thoracentesis. Thoracentesis should be performed in cases where the cause of effusion is
not known following history and physical exam. Not all effusions, however, will require
a thoracentesis.
a. Relative contraindications. Thoracentesis should not be performed in several circum-
stances: patients with obvious heart failure, effusions that are too small to be aspirated
safely, patients who have recently underwent thoracic or abdominal surgery (1), and
patients with severe chronic obstructive pulmonary disease or bilateral lung or pleural
involvement (4).
b. Transudate or exudate? Pleural fluid should be evaluated for protein, lactate dehy-
drogenase (LDH), pH, Gram stain, acid fast bacilli (AFB) stain, cytology, and micro-
biologic culture (4). Evaluation of the fluid obtained will assist in determining if the
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effusion is transudative, due to an imbalance in hydrostatic and oncotic forces, or
exudative, due to increased permeability of the pleural surfaces and blood vessels or
impaired lymphatic drainage of the pleural space (3). Transudative effusions are com-
monly caused by congestive heart failure and cirrhosis. They require no further workup
and usually respond to treatment of the causative condition. Exudative effusions, how-
ever, have many more possible causes to include malignancy and infection and require
more investigation.
Light’s criteria is a reliable tool for differentiating between exudative and transuda-
tive effusions. This tool compares the LDH and protein levels of serum and pleural
fluid (3). The presence of at least one of the following three criteria would classify the
fluid as an exudates:
1. Pleural fluid protein/serum protein ratio greater than 0.5
2. Pleural fluid LDH/serum LDH ratio greater than 0.6.
3. Pleural fluid/LDH greater than two-thirds the upper limit of the laboratory’s nor-
mal serum LDH (Table 8.4.1).
c. Other measures have been used to identify exudative pleural effusions and include
pleural fluid cholesterol, triglycerides, glucose, and albumin (3).
IV. DIAGNOSIS. Pleural effusion analysis is an essential component to diagnosis.
A. If the pleural fluid is found to be transudative, the causative condition is commonly conges-
tive heart failure, hypoalbuminemia, atelectasis, or nephrotic syndrome (3). Using clinical
clues from the H&P is now required.
B. Typical causes of exudative effusion are pneumonia and other infections, malignancy, tuber-
culosis, pulmonary embolism, lung entrapment, and connective tissue diseases. Exudative
effusions, however, have a vast number of causes and thus further investigation is warranted
with glucose level, cell count, pH level, amylase, and triglycerides. Thoracoscopy, bronchos-
copy, repeat thoracentesis, or pleural biopsy may also be helpful.
C. In the majority of cases, a diagnosis can be determined based on the patient’s exam and tho-
racentesis results, but in a small number of cases, no diagnosis is ever established (5). When
no diagnosis is made, the patient should be closely monitored and pulmonary consultation
should be obtained.
REFERENCES
1. Yataco JC, Dweik RA. Pleural effusions: evaluation and management. Cleveland Clin J Med
2005;72:854–872.
2. Porcel JM, Light RW. Diagnostic approach to pleural effusion in adults. Am Fam Physician
2006;73(7):1211–1220.
3. Heffner JE. Diagnostic evaluation of a pleural effusion in adults: initial testing. Accessed at http://www
.uptodate.com/contents/diagnostic-evaluation-of-a-pleuraleffusion-in-adults-initial-testing on June 2012.
4. Medford A, Maskell N. Pleural effusion. Postgrad Med J 2005;81:702–710.
5. Rodriquez-Panadero F, Janssen J.P, Astoul P. Thoracoscopy: general overview and place in the diagno-
sis and management of pleural effusion. Eur Resp J 2006;28,2:409–422.
TABLE 8.4.1 Light’s Criteria
Pleural fluid protein/
serum protein
Pleural fluid LDH/
serum LDH
Pleural fluid LDH/upper
limit normal serum LDH
Exudate
>0.5 >0.6 >2/3
Transudate
≤0.5 ≤0.6 ≤2/3
LDH, lactate dehydrogenase.
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