Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care
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ability of the patient to sustain inspiratory and expiratory
muscle work. An important concept in the treatment of sta-
tus asthmaticus is that the airway obstruction should not be
expected to reverse as quickly or completely as in mild asthma
exacerbations. Current management focuses on supporting
the patient’s gas exchange without causing further harm while
waiting for anti-inflammatory treatment to take effect.
A. Oxygen—Ninety percent of patients presenting with an asth-
matic attack are hypoxemic to some degree. Hypoxemia
increases respiratory drive and tachypnea, contributing to
increased hyperinflation and possible inspiratory muscle fatigue.
In addition to correcting hypoxemia, oxygen may be helpful in
attenuating some respiratory drive and prolonging expiratory
time, thereby decreasing hyperinflation. Because hypoxemia is
usually due to ventilation-perfusion mismatching, hypoxemia in
most asthmatics can be treated with low concentrations
(30–50%) of supplemental oxygen in sufficient amounts to raise
Pa
O
2
to 80–100 mm Hg. In nonintubated patients, oxygen can be
given by nasal cannula or Venturi-type masks.
B. Bronchodilators—Bronchodilators of all types have been
used in status asthmaticus, including β-adrenergic agonists
(sympathomimetics), methylxanthines (theophylline), anti-
cholinergics, and others (see Chapter 12). β-Adrenergic ago-
nists are the most effective bronchodilator agents in acute
asthma exacerbations. Those that are modified to have greater
specificity for β
2
receptors, such as albuterol, are preferred
because of their decreased effect on heart rate. Aerosolized
formulations are much more potent and better tolerated than
the same drugs given orally, subcutaneously, or intravenously,
having a greater bronchodilator effect and causing less tachy-
cardia and less hypokalemia even in patients who have severe
bronchial obstruction. In moderately severe to severe asthma,
aerosolized β-adrenergic agonists can be given with equal
effectiveness with either a metered-dose inhaler (MDI) with
spacer or hand-held nebulizer. Finally, the effective dose of
β-adrenergic agonists is often higher than was formerly rec-
ommended; the doses should be titrated in individual patients
to tolerance, often using clinical response, tachycardia, tremor,
or other observations as guides to dosage. Beta-adrenergic
agonists may be given in conventional doses as often as hourly
or even by continuous nebulization. Continuous nebulization
has been found to be variably effective. Hypokalemia as a con-
sequence of β-adrenergic agonist therapy—causing increased
transport of potassium into cells—is a known complication
when these drugs are given in large doses.
Subcutaneous epinephrine has a long history of effective
use in acute asthma, but inhalation of selective β-adrenergic
agonists is more effective. The side effects of epinephrine
include tachycardia, increased myocardial oxygen require-
ment, and hypertension. Salmeterol is a long-acting β-
adrenergic agonist that is structurally similar to albuterol but
has a longer side chain that anchors it near the β
2
-receptor
site. This drug has no value in acute severe asthma, and sal-
meterol should be reserved for use only after resolution of
the acute attack.
In severe asthma, aerosolized albuterol is recommended. If
given by MDI, a spacer or reservoir is necessary. A starting
dosage is 2–4 puffs every 1–2 hours, and the number of puffs
can be increased to 6–8 or more, if tolerated. Alternatively, a
nebulized solution of 0.5 mL albuterol (0.5%) diluted in 2.5
mL normal saline can be given by gas-powered nebulizer or
intermittent positive-pressure breathing every 2–6 hours, but
there is no evidence that this is more effective than administra-
tion by MDI. The response to bronchodilators should be meas-
ured objectively, preferably by peak flow. Tachycardia, tremors,
and changes in blood pressure should be monitored carefully,
especially when doses given exceed usual recommendations.
Anticholinergic drugs are generally considered more
effective in chronic bronchitis than in asthma. Studies sup-
port their use in severe asthma in conjunction with opti-
mized β-adrenergic agonist use. The quaternary anticholinergic
drug ipratropium bromide is given via MDI or by nebuliza-
tion. Effective doses of ipratropium bromide may be consid-
erably higher than currently recommended, but its minimal
side effects allow it to be well tolerated. Ipratropium should
be given to asthmatics with severe exacerbations along with
maximal β-adrenergic agonist therapy. By MDI, the starting
dosage should be 2–4 puffs every 4–6 hours. For nebuliza-
tion, an effective dose is 0.5 mg given every 6–8 hours. Even
at the highest doses, side effects of ipratropium are minimal,
and these doses appear to be safe.
The addition of theophylline to optimized regimens of
β-adrenergic agonist therapy confers little or no additional
benefit and increased toxicity and side effects. Some of the
side effects of theophylline are identical to those of β-adrenergic
agonists, and this may limit use of the more beneficial agent.
Theophylline should be considered a third-line bronchodila-
tor drug in status asthmaticus, but it might warrant consid-
eration in selected patients who are not responding to other
therapy. Theophylline is tolerated only when the serum con-
centrations are carefully maintained in the therapeutic range,
and in some patients toxicity occurs even then.
Intravenous magnesium sulfate (MgSO
4
) has been shown to
be an effective bronchodilator in some studies of asthma exac-
erbation. Doses administered have been in the range of 0.5–1
mmol/min over 20 minutes, corresponding to about 3–5 grams
of MgSO
4
. Comparison with β-adrenergic agonists has not been
carried out in the ideal manner for evaluating the precise role of
magnesium sulfate in combination with other drugs. There
have been trials of inhaled magnesium sulfate as well.
C. Corticosteroids—Corticosteroids are a key component
of treatment of status asthmaticus, but the ideal dosage
remains undetermined. In one study, 15 mg methylpred-
nisolone given intravenously every 6 hours did not appear to be
as effective as larger doses such as 40 or 125 mg every 6 hours,
and most clinicians agree that a dose of 10–15 mg/kg per day
of hydrocortisone or equivalent is effective. Larger doses have
not resulted in improved outcome or more rapid resolution.
These recommendations translate into quite large doses,
PULMONARY DISEASE
537
CHAPTER 24
538
such as 120–240 mg prednisone or methylprednisolone per
day in divided doses for average-sized adults. Oral adminis-
tration has been shown to be as effective as intravenous infu-
sion with no difference in time of onset of effect, but
intravenous administration is chosen more commonly.
For status asthmaticus, intravenous methylprednisolone
at 40–60 mg every 6 hours, or similar dosage of oral pred-
nisone or methylprednisolone is recommended. The dose
should be continued, in the absence of acute severe side
effects, for several days even if the patient improves. The rate
of tapering of systemic corticosteroids depends on clinical
response as well as the patient’s recent history of asthma
severity and previous dosage of corticosteroids.
The beneficial effect of corticosteroids is not clinically
apparent until at least 6 hours after administration.
Therefore, if corticosteroids are to be optimally effective, they
should be given early, as soon as a diagnosis of status asth-
maticus is made. Corticosteroids should be continued ini-
tially for at least 36–48 hours and then reduced by
approximately 25–50% depending on clinical response.
Further reduction generally can take place over about a 2-
week period. Most investigators do not believe there is a role
for aerosolized corticosteroids in status asthmaticus because
of concern about delivery to the airways during acute airway
obstruction. However, these agents are quite beneficial as the
systemic corticosteroids are tapered, and relatively soon
(within a few days), highly potent inhaled corticosteroids are
effective.
The major concern of corticosteroid therapy is the side
effects. The usual side effects of high-dose corticosteroids in
critically ill patients include hyperglycemia, altered mental
status, metabolic alkalosis, and hypokalemia. In asthmatics,
acute myopathy has been reported in association with corti-
costeroids. Three mechanisms have been proposed to explain
this phenomenon. First, hypokalemia may develop, especially
with high-dose β-adrenergic agonist use and high-dose corti-
costeroids. Second, acute steroid myopathy has been reported
at the dosages used in status asthmaticus. Finally, there is an
association with prolonged muscle weakness when high-dose
corticosteroids are given in combination therapy with nonde-
polarizing muscle relaxants. In the latter syndrome, tempo-
rary pharmacologic denervation of muscles appears to
potentiate the acute myopathic effects of corticosteroids. This
syndrome, seen in asthmatics and others requiring muscle
relaxants to help them accept mechanical ventilation, may
prolong the need for mechanical ventilation.
Because of the central role of inflammation in status
asthmaticus, other agents that interfere with the inflamma-
tory response have been proposed. Although methotrexate
has been used in stable steroid-dependent asthmatics, there
are no studies of this antimetabolite in status asthmaticus.
Leukotriene antagonists and inhibitors of leukotriene syn-
thesis are effective in modifying asthma and perhaps reduc-
ing exacerbations. They do not appear to have a role in
acute asthma exacerbations but have been used in clinical
trials.
D. Asthma in Pregnancy—Asthma is the most commonly
encountered pulmonary problem in pregnant women, and
asthma may worsen, improve, or remain unchanged in sever-
ity (roughly one-third in each group) during pregnancy. Fetal
outcome is adversely influenced if the mother’s asthma is
poorly controlled, and improvement in asthma control is
rewarded by a better outcome. Guidelines for treatment
developed by the National Asthma Education and Prevention
Program emphasize recommendations similar to those for
nonpregnant patients. These include close monitoring of lung
function, early administration of inhaled corticosteroids or
other anti-inflammatory agents, and rapid therapeutic inter-
vention during acute exacerbations to avoid hypoxemia.
Clinicians may be reluctant to give medications to pregnant
women because of risks to the fetus. Beta-adrenergic agonists
are considered safe, as are inhaled corticosteroids, and sys-
temic corticosteroids should not be withheld if needed during
acute exacerbations. A more complete discussion of this topic
is included in Chapter 39.
E. Mechanical Ventilation—Patients with status asthmati-
cus who require intubation and mechanical ventilation are
identified either by the extreme severity of the airway
obstruction or by anticipating failure of the patient to main-
tain adequate alveolar ventilation. Although most patients
who require intubation and mechanical ventilation develop
altered mental status, acute CO
2
retention, or both, a poor
response to treatment or evidence of impending inspiratory
muscle failure implies a high likelihood of a need for ventila-
tory support.
1. Dynamic hyperinflation and complications from
mechanical ventilation—Mechanical ventilation in sta-
tus asthmaticus was at one time associated with a dispropor-
tionate complication rate and high mortality. Barotrauma
(eg, pneumothorax) and other complications of positive-
pressure ventilation and endotracheal intubation were much
higher in asthmatics than in patients with other forms of res-
piratory failure requiring mechanical ventilation. Possible
reasons for this include failure to recognize the severity and
slow reversibility of status asthmaticus, insufficient attention
to the high airway pressure and progressive hyperinflation
seen during mechanical ventilation of asthmatics, and failure
to understand the importance of hyperinflation or air trap-
ping as a cause of gas-exchange failure. Identified risk factors
for barotrauma in one study included significantly higher
minute ventilation and degree of estimated hyperinflation
compared with those who escaped complications.
Current recommendations for mechanical ventilation
reduce complications and mortality in this disorder to rates
comparable with other causes of acute respiratory failure.
The most important recommendation is limiting the degree
of dynamic hyperinflation. Dynamic hyperinflation occurs
when end-expiratory lung volume increases because there is
insufficient time for the patient to exhale. This increases the
risk of barotrauma because the lung is highly stretched at
PULMONARY DISEASE
539
end expiration and end inspiration. It also results in very
inefficient gas exchange with a large increase in the ratio of
dead space to tidal volume and in hypercapnia. Finally,
because of the high air space pressures it engenders during
both inspiration and expiration, dynamic hyperinflation
may compromise the circulation.
Dynamic hyperinflation results from a combination of
factors. First, expiratory airway resistance is high, and the
tidal volume requires more time to be exhaled. Second,
patients with asthma may have high ventilatory drive owing
to hypoxemia, hypercapnia, or both. High ventilatory drive
increases respiratory rate and decreases the time available for
exhalation. Third, because of the hypercapnia, clinicians may
try to increase minute ventilation by raising tidal volume and
increasing respiratory rate during mechanical ventilation.
High tidal volume and high respiratory rate during status
asthmaticus are predictably associated with high peak airway
pressures, high inspiratory plateau pressures, short expira-
tory times, auto PEEP, and hyperinflation. The magnitude of
dynamic hyperinflation can be remarkable. In one study,
estimates of the volume of “trapped gas” were as much as
12–20 mL/kg above normal end-expiratory volume.
2. Ventilator settings—All asthmatics who are receiving
mechanical ventilation potentially can have severe dynamic
hyperinflation, and a trial of reduced tidal volume, respira-
tory frequency, or both should be initiated with careful mon-
itoring of arterial pH and P
CO
2
. Dynamic hyperinflation is
especially likely to occur if hypercapnia is worsening in the
face of recent increases in tidal volume or respiratory fre-
quency. One key adjustment is to minimize dynamic hyper-
inflation by maximizing inspiratory flow rate (if
volume-cycled ventilation is used). This adjustment shortens
inspiratory time and lengthens expiratory time, providing a
greater opportunity to exhale the tidal volume. Inspiratory
flow should be at least 80–100 L/min (1.3–1.6 L/s). The
resulting I:E ratio should be 1:4 or higher.
A second important strategy is to constrain tidal volume
and respiratory rate during volume-cycled positive-pressure
ventilation to keep inspiratory plateau pressure 30 cm H
2
O
or less. Tidal volume should be 6–7 mL/kg of ideal body
weight, and respiratory rate should be adjusted to minimize
estimated auto PEEP (<5 cm H
2
O) and inspiratory plateau
pressure (<30 cm H
2
O). Patients may require sedation but
almost never muscle relaxants to achieve these goals.
Dynamic hyperinflation plays a dominant role in deter-
mining effective gas exchange. Therefore, although seemingly
paradoxical, decreasing tidal volume or respiratory rate (lower
minute ventilation) may result in a lower Pa
CO
2
.However,a
more likely consequence of such changes is worsening hyper-
capnia. Current practice is to allow moderate hypercapnia
(pH >7.25) to avoid the consequences of dynamic hyperinfla-
tion, a far worse complication. Thus “permissive hypercapnia”
is often seen in the management of status asthmaticus.
The decision to increase minute ventilation and reverse
hypercapnia generally is made as peak airway pressure and
auto PEEP decline as the patient’s high airway resistance falls
with treatment. In one study, a 40–60 seconds apnea period
was set for asthmatic patients who were sedated and given
muscle relaxants. The total exhaled gas volume was measured;
this consisted of the previous tidal volume plus any amount
of “trapped gas” that could be exhaled during the prolonged
exhalation period. Patients whose total exhaled gas volumes
exceeded 20 mL/kg had their respiratory frequency reduced
regardless of the measured P
CO
2
. However, the respiratory
frequency was increased in the other patients as much as pos-
sible without exceeding 20 mL/kg total exhaled volume, and
these patients did not have worsening of hypercapnia or evi-
dence of barotrauma. Patients were discontinued from
mechanical ventilation when a P
CO
2
of 40 mm Hg could be
obtained and exhaled gas volume was less than 20 mL/kg.
There is limited published experience with administra-
tion of intravenous sodium bicarbonate to compensate for
the increased P
CO
2
, and this treatment should be used judi-
ciously in selected patients. In one study, no complications of
bicarbonate therapy were identified, but there is concern for
development of paradoxical cerebrospinal fluid acidosis,
hypernatremia, and intravascular volume overload. The use
of other buffers that do not produce additional CO
2
when
they react with acids has been proposed.
Current Controversies and Unresolved Issues
A. General Anesthesia for Refractory Asthma—In
patients undergoing mechanical ventilation, halothane and
ketamine anesthesia has been used in status asthmaticus that
is refractory to conventional management, but this manage-
ment has not been compared with other forms of therapy.
Both agents have bronchodilator properties, but this remains
an unproved and potentially risky therapy. Such treatment is
used very rarely.
B. Mucolytic Administration by Fiberoptic Bronchoscopy—
Recognition that severe refractory airway obstruction in sta-
tus asthmaticus is often due to plugging of small airways
with inspissated mucus led to the use of mucolytic agents
such as acetylcysteine. However, aerosolization of this agent
sometimes led to bronchospasm, and its effectiveness in the
dose and manner administered has been questioned.
Bronchoalveolar lavage with acetylcysteine and saline has
been performed using the fiberoptic bronchoscope. Because
of compromise of the airway with the bronchoscope, this
must be done only during mechanical ventilation with seda-
tion, muscle relaxants, or general anesthesia. The usefulness
of this technique has not been proved, and because of the
high risks to the patient, it should be considered only if other
more conventional treatment has failed. Using a strategy to
reduce dynamic hyperinflation and waiting for resolution of
the underlying asthma in response to corticosteroids is
almost always a better option.
C. Helium-Oxygen Inhalation—Helium-oxygen mixtures
(21–40% oxygen, balance helium) have less density than
CHAPTER 24
540
nitrogen-oxygen mixtures. Because a less dense gas is more
likely to move through airways under conditions resulting in
laminar rather than turbulent flow, helium-oxygen mixtures
may improve distribution of ventilation and reduce airway
pressures needed for effective ventilation. Helium-oxygen has
been used in spontaneously breathing asthmatics to unload
the work of the inspiratory and expiratory muscles. This may
allow enough time for anti-inflammatory therapy to take
effect and avoid intubation and mechanical ventilation.
Mechanical ventilation with 60% helium and 40% oxygen
mixtures has been used with improved arterial blood gases
and markedly decreased airway pressures compared with a
nitrogen-oxygen mixture. Although there have been no con-
trolled studies of helium-oxygen mixtures in status asthmati-
cus, it is reasonable to suppose that this form of treatment
may be beneficial in some refractory asthmatics. The prob-
lems include obtaining the appropriate gas, adapting the ven-
tilator to use the gas mixture, monitoring tidal volume, and
ensuring the adequacy of oxygen in the inspired gas mixture.
D. Noninvasive Ventilation—Non-invasive positive-
pressure ventilation (NiPPV) successfully reduces endotra-
cheal intubation and mechanical ventilation in patients with
chronic obstructive pulmonary disease (COPD) exacerba-
tion and acute pulmonary edema. Surprisingly, there are
numerous studies but limited data supporting its use in sta-
tus asthmaticus, although it would appear that temporary
support by NiPPV of fatiguing inspiratory muscles would be
helpful. NiPPV is a potentially useful adjunct but may be
successful only in carefully selected patients. One danger is
that some patients with status asthmaticus regain lung func-
tion very slowly, and NiPPV may not be tolerated long
enough to preclude intubation.
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intrinsic positive end-expiratory pressure, and dynamic hyper-
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Life-Threatening Hemoptysis
ESSENTIALS OF DIAGNOSIS
Expectoration of blood or blood-tinged sputum in suffi-
cient quantity to compromise lung function.
Either a large volume of hemoptysis in a healthy
patient (>600 mL in 24 hours) or a smaller volume
(<200 mL in 24 hours) in a patient with preexisting lung
or heart disease who is unable to protect their airway,
maintain adequate gas exchange, or has altered level
of consciousness.
General Considerations
Hemoptysis can be caused by a wide variety of lung condi-
tions. Expectoration of blood sufficient to be acutely life-
threatening is not common, occurring in 5–15% of
hemoptysis patients. Acute hemoptysis was formerly classi-
fied as massive or nonmassive, and the major decision about
whether to perform surgical intervention was based on the
estimated amount of bleeding. There is now recognition that
even large volumes of hemoptysis can be tolerated if the
patient is relatively healthy. Conversely, small amounts of
bleeding can cause severe complications in patients who have
limited cardiopulmonary reserve from COPD, previous lung
resection, tuberculosis, or heart disease. Mortality from
severe hemoptysis does correlate with the estimated amount
of hemoptysis. However, with additional approaches to diag-
nosis and management now available, one considers both the
severity of bleeding and the patient’s ability to tolerate accu-
mulation of blood in the lungs and airways.
Pathophysiology and Pathogenesis
A. Mechanisms of Hemoptysis—Bleeding in the airways
and lungs can result from several different mechanisms and
two major sources, the bronchial arteries (systemic pressure)
and the pulmonary arteries (low pressure system). Disorders
associated with hemoptysis are listed in Table 24–1. The most
common are bronchiectasis, lung cancer, and tuberculosis
(including mycetoma).
1. Inflammation of the bronchi—Inflammation of the
tracheobronchial mucosa is the most common cause of
hemoptysis but is rarely associated with severe bleeding. In
chronic bronchitis, the mucosa develops increased vascular-
ity with engorged and hypertrophied bronchial arteries that
readily bleed in the face of increased inflammation or acute
viral or bacterial infection.
PULMONARY DISEASE
541
2. Infection—Worldwide, tuberculosis remains an impor-
tant cause of hemoptysis both during active infection and as
a consequence of the scarring and cavitation seen with
chronic disease. Active disease may result in hemoptysis from
lung necrosis, often with a cavity visible on chest x-ray.
Tuberculous cavities may cause hemoptysis whether or not
viable mycobacteria are present. Bleeding arises from dilated
vessels in the wall of the cavity, most often fed by an elabo-
rately developed network of vessels arising from bronchial
arteries with interconnections between these and pulmonary
arteries. An important cause of bleeding from tuberculous
cavities is the development of a mycetoma, or fungus ball,
usually formed by Aspergillus species, that seems to further
stimulate bronchial artery hypertrophy and blood flow.
Rarely, aneurysmal dilation of a vessel in the wall of the cav-
ity has been known to be the cause of severe hemoptysis. In
tuberculosis patients without cavities, bleeding can be
caused by broncholiths (ie, calcified lymph nodes) adjacent
to airways that erode through the bronchial wall and by
chronic bronchiectatic changes of the airways. Patients with
other forms of bronchiectasis (eg, previous viral infections,
bronchopulmonary aspergillosis syndrome, or idiopathic
cases), bacterial lung abscess, and fungal infections with cav-
itation may present with hemoptysis, and on occasion these
patients may have a bout of severe and life-threatening
hemoptysis. Bacterial pneumonia sometimes can present
with blood-tinged sputum (eg, “rusty” sputum seen with
Streptococcus pneumoniae or “currant jelly” sputum seen with
Klebsiella pneumoniae), but significant bleeding is rare.
3. Noninfectious causes—Infarction of the pulmonary
parenchyma can result in hemoptysis by causing death of
lung tissue, but most patients with pulmonary embolism do
not have pulmonary infarction. Inflammation of lung owing
to involvement by Wegener’s granulomatosis may be associ-
ated with hemoptysis, occasionally severe. Two autoimmune
diseases for which hemoptysis is a characteristic feature,
Goodpasture’s syndrome and idiopathic pulmonary hemo-
siderosis, are not associated with inflammatory changes in
the lung. In the former, bleeding arises from involvement of
the alveolar-capillary interface by anti-glomerular basement
membrane antibodies. Less frequent causes of hemoptysis
include left ventricular failure and mitral stenosis, with
bleeding resulting from increased pulmonary venous and
capillary pressures. Hemoptysis may be seen with vascular
malformations occurring as isolated abnormalities of the
pulmonary circulation or in association with hereditary
hemorrhagic telangiectasia syndrome (HHT), including
Osler-Weber-Rendu syndrome.
Bronchogenic carcinoma and benign tumors of the tra-
cheobronchial tree are other important causes of hemopty-
sis, with bleeding coming from hypertrophied bronchial
arteries supplying the tumor. Finally, thoracic trauma may
result in hemoptysis owing to rupture of pulmonary vessels,
resulting in bleeding into the lung parenchyma (lung contu-
sion) or laceration of a major airway.
4. Hemoptysis in ICU patients—In ICU patients who
develop hemoptysis unrelated to their primary problems,
some unique mechanisms must be considered. The most
common source of hemoptysis is upper airway bleeding,
which may result from tracheobronchitis owing to infec-
tion or suction catheter trauma. However, other airway
problems should be considered, such as trauma from the
tip of the endotracheal tube or tracheostomy tube or necro-
sis of the tracheal mucosa by the tube cuff. Rarely, bleeding
can arise from pressure necrosis and erosion of the tube
into an innominate or carotid artery or even into the aortic
arch. A recognized cause of severe hemoptysis is rupture of
a pulmonary artery by a pulmonary artery catheter because
of overdistention of the catheter balloon tip, perforation of
the vessel by the tip of the catheter, or eccentric balloon
placement causing rupture during balloon inflation.
Mortality rates with these types of catheter complications
are very high.
Regardless of the cause of hemoptysis, bleeding can be
made worse in patients with coagulopathy, qualitative platelet
dysfunction from uremia or drugs, or thrombocytopenia.
Patients with severe thrombocytopenia may have sponta-
neous alveolar hemorrhage.
Table 24–1. Common causes of hemoptysis.
∗
Airway
Tracheobronchitis
Chronic bronchitis
Bronchogenic carcinoma
Benign tracheobronchial tumors
Bronchiectasis
Cystic fibrosis
Suctioning or bronchoscopic trauma
Post-transbronchial or endobronchial biopsy
Transthoracic needle aspiration or biopsy
Trauma
Lung parenchyma
Pulmonary infarction (pulmonary embolism)
Invasive pulmonary infection (
Aspergillus,
bacteria)
Necrotizing bacterial or fungal pneumonia
Lung abscess
Tuberculosis with or without cavity
Pulmonary vasculitis
Goodpasture’s syndrome
Idiopathic pulmonary hemosiderosis
Trauma
Thrombocytopenia
Cardiovascular
Left-ventricular failure
Mitral stenosis
Pulmonary artery rupture (PA catheter balloon)
Pulmonary artery aneurysm
Aortic aneurysm
Hereditary hemorrhagic telangiectasia
∗
Items in italics are those associated most often with massive
hemoptysis.
CHAPTER 24
542
B. Massive Hemoptysis—A large volume of hemoptysis,
often called massive hemoptysis, usually results from a
smaller number of common disorders causing hemoptysis
(see Table 24–1). The mechanisms are often due to chronic
and severe development of enhanced bronchial blood flow
(eg, tuberculosis, lung abscess, bronchiectasis, and malig-
nancy), necrosis and destruction of lung parenchyma (eg,
abscess, tuberculous cavity, and fungal pneumonia in
immunocompromised host), or disruption of a pulmonary
artery (eg, trauma, rupture by pulmonary artery catheter
balloon). In major series of patients with massive hemopty-
sis, tuberculosis and bronchiectasis are found in a large
majority of patients, whereas bronchogenic carcinoma is
quite unusual as a cause of massive hemoptysis.
Clinical Features
A. Symptoms—Patients, especially those with chronic spu-
tum production (eg, chronic bronchitis or bronchiectasis),
may complain of coughing up blood-tinged sputum. Others
will note expectoration of bright or dark red material only.
The degree of coughing is highly variable, with some patients
having intractable coughing and others noting only that the
blood wells up into the mouth with little stimulation of
cough. Occasionally, patients actually can describe the
approximate location of the intrathoracic source by pointing
to the area of the sensation within their chest. The relation-
ship of prior hemoptysis to massive or life-threatening
hemoptysis is also highly variable. Some patients have pro-
longed minor hemoptysis, whereas others have no premoni-
tory blood in the sputum prior to a life-threatening event.
The degree of dyspnea accompanying hemoptysis is
determined by the volume of blood expectorated and by
the patient’s underlying cardiopulmonary reserve. Patients
with moderate to severe obstructive lung disease, those with
extensive lung destruction from tuberculosis, and those with
other heart or lung disorders will be most likely to have res-
piratory compromise. Fever, night sweats, and weight loss
suggest active tuberculosis, but other infections also should
be considered. A history of cigarette smoking or other risks
for bronchogenic carcinoma should be sought.
An important part of the medical history is to estimate
the amount of bleeding. While this cannot always be meas-
ured accurately, the patient should be asked to provide an
estimate in cups, tablespoons, or other convenient measures
and over as precise a time frame as possible. If admitted to
the hospital, they should be given a cup to collect all their
expectorated sputum over a 24-hour period for a more accu-
rate determination of the amount of bleeding.
B. Signs—Physical examination may not be helpful in eval-
uating the severity of hemoptysis. The upper airway, includ-
ing the nasopharynx and upper larynx, should be carefully
examined to exclude these sites as the source of bleeding.
Localization to the right or left lower respiratory tract by
physical examination alone is often inaccurate. The presence
of blood in the airways may lead to generalized or focal
wheezing, crackles, and dullness to percussion if there is suf-
ficient bleeding to fill a portion of the lungs. In patients with
chest trauma, rib fractures, superficial injury, and other find-
ings may be helpful in assessing the likelihood of lung contu-
sion, but these indicators are insensitive and nonspecific.
Features of heart failure, such as a third heart sound, rales,
and lower extremity edema, may be helpful in the differential
diagnosis, as well as a diastolic murmur suggesting mitral
stenosis. Osler-Weber-Rendu syndrome is suggested by find-
ing single or multiple telangiectases on the skin or mucosal
membranes. The physical examination is most useful in
determining the severity of respiratory and nonrespiratory
diseases that contribute to mortality and complications from
hemoptysis.
C. Laboratory Findings—Sputum should be examined by
acid-fast stain for mycobacteria, by Gram stain for bacteria,
and by cytology for malignant cells. The presence of a large
number of red blood cells often makes these examinations
difficult. Cultures should be obtained from sputum and
blood if bacterial pneumonia is suspected. Coagulation
times, bleeding time, platelet count, and hematocrit should
be determined. Blood for transfusion should be arranged for
but often is not needed to correct a low hematocrit until
operative treatment is indicated. The presence of a coagu-
lopathy or thrombocytopenia, however, should trigger the
administration of replacement of coagulation factors or
platelets to help to control the bleeding process. Arterial
blood gases are helpful in evaluating the adequacy of gas
exchange and the ability to tolerate further aspiration of
blood into the lungs.
The presence of renal insufficiency changes the differen-
tial diagnosis of hemoptysis to include pulmonary-renal syn-
dromes including Goodpasture’s syndrome and Wegener’s
granulomatosis. Therefore, it is important to evaluate the
urine for the presence of hematuria and to determine renal
function. Unfortunately, despite a rigorous evaluation, the
investigators in one study were unable to identify a cause of
hemoptysis in 41% of patients with a serum creatinine level
greater than 1.5 mg/dL and hemoptysis, and the yield of
fiberoptic bronchoscopy was very low.
D. Imaging Studies—Usual procedures such as chest x-rays
and CT scans may show an infiltrate, cavity, atelectasis, or
other features that suggest a lesion from which bleeding is
arising. These findings should be interpreted with caution,
however, because another unsuspected source may be pres-
ent. For example, aspirated blood may cause atelectasis and
infiltrates remote from the actual bleeding site. Lung cavities
are often multiple, bilateral, and involve several lobes, but the
cavity from which blood is coming may not be readily iden-
tified. Cavitary lung disease, especially in the upper lung
zones, may suggest tuberculosis, but active tuberculosis can-
not be diagnosed accurately from imaging studies.
Furthermore, cavities are seen in fungal infection, sarcoido-
sis, necrotizing pneumonia, and other diseases. A mycetoma
PULMONARY DISEASE
543
within a cavity may be identified on chest x-rays or CT
scan—especially if taken with the patient in several positions.
High-resolution CT scans without intravascular contrast
agents are helpful in establishing the cause and location of
hemoptysis. Localization of bleeding, however, may require
bronchial or, rarely, pulmonary angiography (see below).
Treatment
In life-threatening hemoptysis, maintenance of the airway
and removal of blood from the airway take precedence.
Diagnostic measures must be deferred until it is established
that the patient can maintain adequate gas exchange with or
without an artificial airway, oxygen, and other measures to
reverse coagulopathies or other bleeding tendencies. After
the patient is stabilized, efforts are directed toward determin-
ing the site of bleeding as rapidly as possible so that defini-
tive control of the bleeding site can be achieved.
The outcome of patients with large-volume hemoptysis is
said to be poor, and this has strongly influenced recom-
mended treatment options. However, much of these data
comes from older studies in which tuberculosis caused the
hemoptysis from severe chronic destruction of the lung
parenchyma. For example, a series of patients from the 1950s
and 1960s demonstrated that patients who coughed up more
than 600 mL of blood within 16 hours had a 75% mortality
rate, whereas those who produced less than 600 mL over
16–48 hours had a mortality rate of only 5%. About three-
fourths of these patients had active or inactive tuberculosis,
with the remainder having lung abscess, bronchiectasis, or
bronchogenic cancer. Another study of patients who expec-
torated more than 600 mL of blood within 24 hours reported
a 22% overall mortality rate.
The term life-threatening hemoptysis is preferred over
massive hemoptysis. Although the volume of expectorated
blood does relate to outcome, asphyxiation rather than
exsanguination is the most common cause of death.
Therefore, the most important risk factors for mortality are
the rapidity of blood loss and the severity of preexisting car-
diopulmonary disease. Other prognostic signs are listed in
Table 24–2, and most reflect the ability to control blood loss,
maintain a patent airway, and provide for adequate gas
exchange. Some studies have pointed out that spontaneous
cessation of bleeding in those who have had massive hemop-
tysis does not necessarily predict a good short- or long-term
outcome. Rebleeding is very common without definitive
treatment and may occur soon after the patient has been
judged to be stable or greatly improved.
A. Localization of Bleeding—Severe hemoptysis occasion-
ally may be misidentified as upper GI bleeding or bleeding
from the nose, nasopharynx, mouth, or upper airway, but the
history and examination should confirm or absolve these
structures as possible sites of bleeding. The evaluation of the
bloody material produced by the patient occasionally can
be helpful in distinguishing between a GI source and a lung
source. The presence of alveolar macrophages or an alkalotic
pH in the absence of acid-suppressing medications is more
likely to represent a respiratory tract specimen, whereas food
particles or an acidic pH is more suggestive of a stomach
source. Once the lungs are suspected, the next step is to
establish whether bleeding is from the trachea or the right or
left lung. Although it is tempting to conclude that an infil-
trate or cavity on chest x-ray or chest CT scan indicates the
site of bleeding, bilateral disease in tuberculosis, infection,
and inflammatory disorders is common. The infiltrate also
may represent a collection of blood brought up from the
contralateral side or from a different lobe or segment.
Bronchoscopy is the procedure of choice for identification
of a bleeding site in the tracheobronchial tree, and flexible
fiberoptic bronchoscopy generally is preferred over rigid
bronchoscopy. Bronchoscopy performed early in the course
of massive hemoptysis increases the likelihood of localization.
The advantages of fiberoptic bronchoscopy are patient com-
fort and the ability to explore further generations of bronchi.
The fiberoptic bronchoscope may be of limited use in severe
hemoptysis because the view is easily obscured by small
amounts of blood, and its suctioning ability is limited by the
small-diameter channel. Although the fiberoptic broncho-
scope can be passed through a large enough endotracheal
tube (usually >8 mm), maintenance of a patent airway may
be very difficult if the patient is actively bleeding. The fiberop-
tic bronchoscope provides limited treatment options, includ-
ing lavage, suctioning, and balloon tamponade. New
techniques have shown value, including direct application of
thrombin or thrombin-fibrinogen. Bronchoscopy-guided
topical hemostatic tamponade therapy (THT) using an oxi-
dized regenerated cellulose (ORC) mesh recently has been
shown to be helpful. On the other hand, the rigid broncho-
scope can be used even during large-volume hemoptysis
because of its better ability to suction blood, maintain the air-
way, and provide adequate ventilation. In general, if hemopt-
ysis subsides and the patient is stable, bronchoscopy can be
delayed for several days so that the fiberoptic instrument can
be used for careful inspection of the tracheobronchial tree. In
more emergent situations, rigid bronchoscopy is the preferred
bronchoscopic technique. Isolation of a bleeding lobe or
segment by endobronchial balloon tamponade using the
Table 24–2. Factors contributing to life-threatening
hemoptysis.
Massive hemoptysis (estimated >600 mL blood over 24 hours)
Decreased pulmonary function (obstructive or restrictive disease)
Altered mental status or level of consciousness
Poor cough due to advanced age, sedation, neuromuscular weakness
Coagulopathy or thrombocytopenia
Mechanism of hemoptysis
Underlying disease
CHAPTER 24
544
fiberoptic or rigid bronchoscope and lavage of the bleeding
site with iced saline or vasoconstrictor agents such as epi-
nephrine should be regarded as minor adjuncts to control of
hemoptysis. Lastly, these procedures may be difficult to per-
form in the face of severe hemoptysis.
Bronchial arteriography may be useful for localization
of bleeding, and bronchial artery embolization (see below)
is used widely for control of severe hemoptysis. The angio-
graphic characteristics of potentially involved bronchial
arteries include hypervascularity, hypertrophy, aneurysms,
and bronchopulmonary anastomoses. Occasionally, no
abnormalities are identified. In tuberculosis and other dis-
orders, these changes may be seen in several locations,
including bilaterally, suggesting that findings do not estab-
lish the site of bleeding with complete confidence. Because
extravasation of contrast material injected into a bronchial
artery is rarely, if ever, seen except with rapid blood loss,
exact localization of a bleeding site is often not confirmed
until after successful embolization. If there is no evidence
of potential bronchial artery abnormalities, some investi-
gators suggest that pulmonary arteriography should be
performed to examine the pulmonary circulation as a
source of bleeding.
B. Medical Treatment—Supportive care consists of main-
taining an adequate airway and introducing measures to
control bleeding. Patients should be at bed rest with the
suspected or known side of bleeding dependent to protect
less involved parts of the lungs from filling with blood.
Cough suppressants such as codeine and sedative drugs
should be used cautiously, with a balance between decreas-
ing irritation of the airway from coughing and losing the
effectiveness of cough in keeping the airways clear. Vitamin
K, fresh-frozen plasma, and platelet transfusions should be
given if coagulopathy or thrombocytopenia is present.
Significant anemia is not usually due to acute hemoptysis,
so erythrocyte transfusions are needed only if the patient
has symptomatic anemia or other sources of blood loss.
Oxygen generally is administered to all hospitalized
patients. Antibiotics are often given to decrease any inflam-
matory component owing to acute bacterial bronchitis. If
active tuberculosis is suspected, antituberculosis therapy
should be instituted.
The best means of maintaining an adequate airway is the
patient’s own cough. The decision to place an endotracheal
tube implies that the rate and volume of hemoptysis exceed
the patient’s ability to cough up blood to keep the airway
clear. A cuffed endotracheal tube can be introduced into the
trachea and the patient suctioned to see if this treatment is
adequate to keep the airway clear. A sufficiently large endo-
tracheal tube—preferably at least 8 mm—is usually needed.
If extensive bleeding continues, selective endobronchial
intubation of the nonbleeding lung for ventilation can be
performed by advancing the endotracheal tube into a main
bronchus to protect the nonbleeding lung. For uncontrolled
right-sided bleeding, the endotracheal tube should be
inserted into the left main bronchus under fluoroscopic or
bronchoscopic guidance. The left lung is selectively venti-
lated, and blood is allowed to come up the trachea around
the tube. For left-sided bleeding, however, the endotracheal
tube cuff should be placed in the trachea, and a balloon-
tipped catheter (eg, Fogarty-type 14F balloon) is used to
seal the left main bronchus while the right lung is selectively
ventilated. This method permits ventilation of the entire
right lung, including the right upper lobe, because its open-
ing is usually close to the carina and is frequently blocked
by the insertion of an endotracheal tube into the right
mainstem bronchus. Placement of the balloon-tipped
catheter may be difficult while there is active bleeding.
Although the use of double-lumen endobronchial tubes
for split lung ventilation during thoracic surgery has been
advocated to separate the bleeding lung from the nonbleeding
lung, these tubes are not placed easily by inexperienced per-
sons and are subject to displacement even if situated properly.
In addition, the two lumens are small, which limits the
amount of blood that can be suctioned. Both Carlens-type
double-lumen tubes and newer plastic double-lumen tubes
with soft low-pressure tracheal and bronchial cuffs have been
used to achieve lung separation in hemoptysis, but only expe-
rienced personnel familiar with these devices should be asked
to insert them. To maintain the position of these tubes,
patients generally require heavy sedation and sometimes even
paralysis.
C. Bronchial Artery Embolization—Bronchial arteriogra-
phy and selective bronchial artery embolization with artifi-
cial material (eg, polyvinyl alcohol, steel coils, and gelatin
sponge) have greatly changed the management of severe
hemoptysis. Control of bleeding is achieved with a high
degree of success in patients with a variety of causes of
hemoptysis. Bronchial artery embolization is performed by
identifying bronchial arteries leading to the affected side, the
usual patterns consisting of one or two bronchial arteries on
each side arising from the aorta between the fifth and sixth
thoracic vertebrae. Branches of these arteries also may supply
anterior spinal arteries and intercostal arteries.
Complications of this procedure include distal arterial
embolization if the catheter is not placed far enough into the
selected artery and spinal cord damage if embolization is
performed into a branch supplying both the bronchial artery
and the spinal cord. If performed with proper care, this pro-
cedure is highly effective and may lead to long-term resolu-
tion of hemoptysis as well as short-term control prior to
definitive therapy. Estimates of immediate control of bleed-
ing by bronchial arterial embolization range as high as 90%
of patients. Recurrent bleeding after successful embolization
may suggest the need for repeat embolization in the same or
other areas. In some patients with chronic inflammatory
lung disease, identification of collateral arterial vessels may
be important. In one study, lasting control of hemoptysis was
achieved in 82% of patients during follow-up for as long as
24 months. Recurrent bleeding was seen with significantly
PULMONARY DISEASE
545
greater frequency in patients with residual pulmonary dis-
ease and mycetomas.
D. Surgical Treatment—Surgical resection of the bleeding
lobe or segment in patients who can tolerate the procedure
removes the threat of recurrent bleeding. Earlier reports of
mortality rates higher than 30% from resectional surgery in
massive hemoptysis are now considered to be due to ongoing
bleeding, poor pulmonary function, and failure of preopera-
tive localization of the bleeding site. Local control of bleed-
ing by airway management or bronchial artery embolization
allows surgery to be performed under more controlled con-
ditions, and emergency surgery is now quite rare, with a cor-
responding decrease in surgical deaths.
On the other hand, many patients with severe hemopty-
sis will not be surgical candidates because of extensive bilat-
eral lung disease and severe reduction of lung function. Of
the remainder, medical management is usually adequate to
control bleeding, and early surgical therapy is reserved for
those with progressive aspiration of blood or inability to
control bleeding.
There is debate about prophylactic surgical resection after
severe hemoptysis has resolved. Recurrent bleeding is com-
mon after medical management in some series (25–40%),
and death from hemoptysis has occurred during the initial
bout of hemoptysis without warning or during a recurrent
bout after bleeding had apparently ceased. This risk of recur-
rent life-threatening hemoptysis has prompted some to per-
form elective resectional surgery in all patients with
hemoptysis in whom surgery is deemed tolerable. However,
while there is nearly universal agreement that surgery is indi-
cated for recurrent hemoptysis from a tuberculous or other
cavity in which a mycetoma is identified, prophylactic sur-
gery is not universally recommended. Potential candidates
for resection include those with well-localized disease, ade-
quate pulmonary function, minimal pleuropulmonary adhe-
sions, and a high likelihood of recurrence. Results of surgical
resection should be compared with the increasingly long-
term experience with arterial embolization (nonsurgical
management) for hemoptysis.
Fartoukh M et al: An integrated approach to diagnosis and man-
agement of severe haemoptysis in patients admitted to the
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Hsiao EI et al: Utility of fiberoptic bronchoscopy before bronchial
artery embolization for massive hemoptysis. AJR 2001;177:
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Jean-Baptiste E: Clinical assessment and management of massive
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moderate, and massive bleeding. Postgrad Med 2002;112:101–9.
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Deep Venous Thrombosis & Pulmonary
Thromboembolism
ESSENTIALS OF DIAGNOSIS
Deep venous thrombosis:
Risk factors include a chronic or acute illness, immobi-
lization, recent surgery or orthopedic injury, hypercoag-
ulable state.
Asymmetric calf or thigh pain or tenderness but may be
asymptomatic.
Confirmation by contrast venography or duplex com-
pression ultrasonography.
Pulmonary thromboembolism:
Dyspnea, tachycardia, pleuritic chest pain, and tachyp-
nea; if severe, hypotension, syncope, cyanosis, or shock.
May have evidence of deep venous thrombosis.
Mild to moderate hypoxemia, increased P(A–a)
O
2
, and
mildly reduced Pac
O
2
.
Suggested by a clinical syndrome consistent with pul-
monary embolism in the presence of a confirmed deep
vein thrombosis
Confirmation by ventilation-perfusion radionuclide
scan, pulmonary angiogram, or CT angiography (helical
CT scan).
General Considerations
Venous thromboembolism is a disease thought to affect
approximately 1 in every 1000 hospitalized patients in the
United States and Europe. Some studies suggest that this
process accounts for or contributes to over 200,000 deaths
annually in the United States. Because of the difficulty in rec-
ognizing and diagnosing this syndrome, this figure may be
an underestimate of its true prevalence.
CHAPTER 24
546
Deep venous thrombosis and pulmonary thromboem-
bolism present three primary problems in the ICU. First,
patients with pulmonary thromboembolism may present
with severe respiratory failure or hemodynamic instability.
Second, critically ill patients with a variety of medical and
surgical disorders can develop pulmonary thromboem-
bolism complicating their underlying conditions. The diag-
nosis of venous thromboembolism in these ICU patients is
often especially difficult to make or confirm. The usual
method of treatment with anticoagulation is hazardous and
may be contraindicated in some of these patients. Finally,
there is increased emphasis on the prevention of deep venous
thrombosis and pulmonary thromboembolism in ICU
patients given that they tend to have multiple risk factors for
this disease. The causative relationship between the two dis-
orders means that the diagnosis, treatment, and prevention
of both must be considered together.
Pathophysiology and Pathogenesis
A. Deep Venous Thrombosis—The pathophysiology of
deep venous thrombosis centers around Virchow’s triad of
stasis of blood flow, intimal vascular injury, and a hypercoag-
ulable state. It is often the failure of mechanisms that prevent
the normally circulating blood from clotting in the intravas-
cular space, which leads to clot formation. A systemic hyper-
coagulable state can be either inherited or acquired and is
identified in only a small fraction of patients with venous
thromboembolism. In general, these thrombophilic states do
not cause a clinical thrombotic event without the presence of
a second acquired risk factor or precipitating circumstance.
Factor V Leiden or activated protein C resistance has been
identified in up to 5% of the Caucasian population in the
United States. Other hypercoagulable states include congen-
ital or acquired deficiency of circulating anticoagulants (eg,
deficiency of protein C, protein S, or antithrombin III), pro-
thrombin gene mutation (ie, G20210A), abnormalities in fib-
rinolysis, the presence of a lupus-associated anticoagulant,
and increased procoagulant activity such as occurs in some
malignant diseases and severe generalized trauma.
Assessment for the presence of one of these thrombophilic
states can only in part be performed at the time of the acute
thromboembolic event because the clotting process itself can
contribute to low of protein C and S levels. These low protein
C or S levels during the acute phase may not represent a true
deficiency of these factors, but may actually represent con-
sumption of these factors. Factor V Leiden and anticardi-
olipin, and antiphospholipid antibodies, on the other hand,
are not affected by the acute clotting process. More often,
however, patients with deep venous thrombosis have a com-
bination of venous stasis plus local damage to the venous
endothelium, exposing subendothelial procoagulant tissue
factor to the blood. Obstruction of venous flow leads to
edema and pain in the area drained by the affected veins.
On occasion, the intravenous clot is palpable on examina-
tion as a cord. Destruction of venous valves and persistent
venous occlusion by this process may lead to venous
insufficiency or permanent localized discomfort, edema, and
pain known as the postphlebitic syndrome.
Risk factors for deep venous thrombosis include pro-
longed immobilization, trauma to the extremity or pelvis,
generalized trauma, preexisting venous insufficiency, periph-
eral arterial disease, recent surgery, pregnancy or recent deliv-
ery, obesity, nephrotic syndrome, congestive heart failure,
acute myocardial infarction, malignancy, estrogen therapy,
and advanced age. Another important risk group consists of
patients with neurologic diseases leading to immobility
including strokes and spinal cord injury with subsequent
paralysis. Severe acute illness necessitating hospital admission
is also associated with an increased incidence of deep venous
thrombosis. Lastly, the increasing use of central venous
catheters in the ICU setting has led to an increasing incidence
of upper as well as lower extremity deep venous thromboses.
Deep venous thrombosis develops most frequently in the
posterior tibial vein, the popliteal vein just above the knee,
and the common femoral vein in the thigh. A smaller number
of patients with deep venous thrombosis have thrombi in the
pelvic veins. While the calf vein is probably the most common
site of deep venous thrombosis, only about 15–20% of these
lesions will extend proximally into deep veins above the knee.
In addition, it appears that upper extremity deep venous
thrombosis may occur more frequently than previously spec-
ulated owing to the use of short- and long-term central
venous catheters inserted into the internal jugular or subcla-
vian veins in ICU patients. Thrombi also may be found in the
right atrium in patients with chronic atrial fibrillation and in
the ventricles of patients with dilated cardiomyopathy or ven-
tricular aneurysms. Hypercoagulable states may cause clots to
form in the superior and inferior vena cava, the renal veins
(especially in nephrotic syndrome), and the hepatic veins (in
Budd-Chiari syndrome).
B. Pulmonary Thromboembolism—As many as 90% of
patients with pulmonary thromboembolism have blood clots
arising from proximal veins of the lower extremities (deep
femoral veins), with the remainder having thrombi coming
predominantly from pelvic veins. In a study of patients with
deep venous thrombosis, perfusion lung scans were uni-
formly negative in those with thrombosis limited to calf
veins only. This emphasizes the importance of identifying
high-risk thrombi located in popliteal and thigh veins or
extension of clot from calf to proximal veins. Thrombosis of
superficial veins is rarely associated with significant pul-
monary embolism. With increasing use of central venous
catheters and transvenous pacemakers, there has been a
reported rise in venous thrombosis and subsequent pul-
monary thromboembolism from the upper extremity. A
7–20% risk of embolization has been cited in patients with
symptomatic upper extremity thromboses.
The finding of lower extremity proximal deep venous
thrombosis has become part of several algorithms for the diag-
nosis of pulmonary embolism because of the association
between proximal leg deep venous thrombosis and pulmonary
embolism. These data are obtained from the overall population