CHEST
Spontaneous Hemothorax*
A Comprehensive Review
Hakim Azfar Ali, MD; Michael Lippmann, MD, FCCP; Uday Mundathaje, MD;
and Ghulam Khaleeq, MD
(CHEST 2008; 134:1056 1065)
Key words: coagulopathy; endometriosis; exostoses; fibrothorax;
hemothorax; neoplasia; spontaneous pneumothorax
Abbreviations: AVM arteriovenous malformation; EDS Ehlers-
Danlos syndrome; HCC hepatocellular carcinoma; HHT hered-
itary hemmorhagic telangiectasia; IPFT intrapleural fibrinolytic
therapy; SHP spontaneous hemopneumothorax; VATS video-
assisted thoracic surgery
H emothorax by definition is extraction of pleural
fluid with a hematocrit 50% of the blood
hematocrit. Most cases of hemothorax are related to
open or closed chest trauma or procedures such as
central lines, thoracentesis, pleural biopsy, or cathe-
terization. Spontaneous hemothorax is much less
common, and the causes include malignancies, anti-
coagulant medications, vascular ruptures (aortic dis-
section, arteriovenous malformations [AVMs]), en-
dometriosis, pulmonary infarctions, adhesions with
pneumothorax, and hematologic abnormalities such
as hemophilia.
Pleural fluid imparts a red color indistinguishable
from blood at a hematocrit 5%. It is therefore
always important to measure the hematocrit of any
hemorrhagic pleural effusion. The hematocrit may
be reduced due to secondary dilution to less than the
required 50% that of blood within a few days,
making it appear as a hemorrhagic exudate. The
definition of hemothorax has therefore included
hematocrits ranging from 25 to 50% that of blood.
Hemorrhagic effusions have been associated with
*From the Albert Einstein Medical Center, Philadelphia PA.
The authors have no conflicts of interest to disclose.
Manuscript received March 14, 2008; revision accepted May 6,
2008.
Reproduction of this article is prohibited without written permission
from the American College of Chest Physicians (www.chestjournal.
org/misc/reprints.shtml).
Correspondence to: Hakim Azfar Ali, MD, Division of Pulmonary
and Critical Care, Albert Einstein Medical Center, 5401 Old York
Rd, Philadelphia PA 19141; e-mail: azfarali1@gmail.com
DOI: 10.1378/chest.08-0725
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Special Features
malignancies, tuberculosis, uremia, and vascular pro-
cesses such as pulmonary infarction.
A true hemothorax, however, usually signals a
more blatant compromise of the vascular wall. The
involved vessel could either be a normal vessel
undergoing an abnormal stress or an abnormal vessel
rupturing without precipitating factors.
Most of the data about spontaneous hemothorax
are in the form of scattered case reports and case
series.1 Table 1 gives a summary of the diagnoses
associated with nonpneumothorax-related spontane-
ous hemothoraces. The major etiologies will be
discussed.
Spontaneous Hemopneumothorax
Spontaneous pneumothorax is by far the most
common cause of hemothorax. Our review found
hemothorax to be a complication in 3 to 7% of cases
of spontaneous pneumothorax2 Spontaneous hemo-
pneumothorax (SHP) occurs mostly in young pa-
tients (mean age, 22.1 to 34.0 years).
The earliest reports of the condition have been
traced to Laennec (1828), Whittaker (1876),3 and Pitt
(1900). Approximately 300 cases have been reported in
the literature in the form of cases and case series.4 12
SHP is defined by Ohmori and colleagues13 as the
accumulation of 400 mL of blood in the pleural
cavity in association with spontaneous pneumotho-
rax. Sometimes the patients can present in shock
with blood loss 600 mL and the mechanical effects
of a pneumothorax. There are said to be three
mechanisms of bleeding in hemopneumothorax.14
First, bleeding can result from a torn adhesion
between the parietal and visceral pleura.2 At autopsy,
adhesions have been shown to be present in 50% of
patients 20 years of age who have had no history of
pulmonary disease. According to Barry et al,15 the
site of bleeding is usually a small noncontractile
vessel on the parietal pleura, where vascular adhe-
sions exist. Second, bleeding may result from the
Special Features
 Table 1Etiology of Hemothorax* In a review by Hsu et al16 of 488 patients with
Category Specific Etiology
spontaneous pneumothorax over a 6-year period, 27
patients (5.5%) had an associated hemothorax (25
Pneumothorax SHP men; mean age, 22.3 years). The amount of blood
Coagulopathy Congenital diseases
Hemophilia, Glanzman thrombasthenia
that was drained ranged from 400 to 1,700 mL, with
Acquired a third of the patients in shock. Twenty-one patients
Drug related underwent VATS within 1 day after admission, and 6
Vascular AVM (OWR disease) patients were treated conservatively with tube tho-
VRD racostomy alone with no recurrence of hemopneu-
Aneurysms
EDS type IV
mothorax.
Connective tissue disease Kakaris et al21 reviewed 3,489 patients with spon-
Neoplasia Bone/soft tissue taneous pneumothorax between 1970 and 2000.
Schwannoma (VRD) Seventy-one patients (2%) [63 men and 8 women
Thymic growths aged from 13 to 80 years] presented with hemopneu-
Vascular tumors
Germ cell tumors
mothorax. Conservative treatment alone was effec-
Hepatocellular tive in 16 cases (22.5%). Among the other 55 patients
Lung cancer (77.5%), 28 patients (39.4%) were operated on an
Mesothelioma emergency basis because they were in shock, while
PNET 27 patients (38%) had elective surgery for clot
Miscellaneous Exostoses
Extramedullary hematopoiesis
evacuation, resection of a bulla, ligation of adhesions
Endometriosis between the parietal and visceral pleura, and irriga-
Pulmonary sequestration tion of the pleural cavity.21
GI surgery A retrospective review27 of 24 patients with SHP
*OWR Osler-Weber-Rendu disease; VRD von Recklinghausen that compared 11 patients treated with early VATS
disease; PNET primitive neuroectodermal tumor. and 13 treated with initial conservative treatment
and subsequent surgery when needed demonstrated
that the early VATS group had longer operating
rupture of vascularized bullae and underlying lung time, less preoperative blood loss, less blood trans-
parenchyma.16,17 Third, it may result from torn fusion (465 mL vs 1,044 mL), shorter period of chest
congenitally aberrant vessels between the parietal tube drainage (4 days vs 7 days), and shorter length
pleura and bullae.3,17 In their series of patients with of stay (all p values 0.05).27
SHP, Tatebe and coworkers18 reported the mucoid In summary, although there is still some debate
degeneration and sclerotic changes in the arterial about the management of the patient who stabilizes
wall of aberrant vessels. The factors that disrupt after a chest tube insertion without further blood
normal homeostasis include the fact that bleeding loss, the predominant opinion favors prompt surgical
from the parietal pleura is not subject to control by management for most of the patients with SHP,28
collapse of the lung and that systemic BP is about six particularly in a patient who is in shock, has rebleed-
times that in the pulmonary arterial circulation. ing after lung expansion, or fails conservative man-
Systemic arteries are likely the source of bleeding in agement after 24 h.
the more massive hemopneumothoraces.
Treatment of hemopneumothorax, in addition
to fluid resuscitation and blood transfusion, consists Coagulopathy
of the insertion of an intercostal tube, followed by
surgical intervention, via either video-assisted tho- Hemothorax associated with a coagulopathy is pre-
racic surgery (VATS) or open thoracotomy. This is dominantly a result of anticoagulants administered in
widely considered to be a surgical emergency be- the setting of thromboembolic disease.29,30 There are
cause of the capability of the vessels to bleed freely 20 well-documented cases of anticoagulant-associated
as mentioned above. hemothorax. The coagulation parameters were su-
We found 10 series of patients described in literature pratherapeutic in six cases, and heparin was admin-
with a total of 240 patients, close to 200 of whom istered in intermittent bolus form in eight patients.
were treated surgically ( 50% with VATS),16 25 and There were equal number of men and women. Most
the recurrence rate of bleeding was 1% in all of the cases occurred in the setting of treatment with
groups.20 Haciibrahimoglu et al26 found an incidence heparin and warfarin, and there was at least one
of 3% (9 cases out of 291 spontaneous pneumotho- well-documented case with enoxparin.31
races), and conservative treatment was adequate in Overall, hemothorax is very rare in the setting of
seven patients. anticoagulation, and most cases occur within the first

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 week of therapy and on the same side as the initial
symptoms.32 Hemothorax with anticoagulation in the
setting of pulmonary embolism has a high morbidity
and mortality, with 4 patients dying of the 20 patients
reported. Rupture of a pulmonary infarct should be
suspected when a patient with a proven or suspected
pulmonary thromboembolic disease has abrupt cir-
culatory and respiratory insufficiency in association
with a rapidly accumulating unilateral pleural effu-
sion 7 to 10 days out, compared to a slowly develop-
ing effusion in a purely anticoagulant-related hemo-
thorax.33 A rupture of an infarct is a rare complication
of thromboembolic disease because only 10% are
complicated by infarcts.34,35
In our review, two cases of hemothorax with antico-
agulation in the nonpulmonary embolic setting were
reported: one case was after angioplasty,36 and the
other case was in the setting of anticoagulation for an
artificial heart valve.1 Hemothorax has been reported
in the setting of tissue plasminogen activator use for
venous thrombosis in a patient with pneumonia.37
Congenital hemorrhagic disorders are another cause
for a spontaneous hemothorax. Hemophilia was
associated in eight cases, mostly in men,8,38 41 and
Glanzmans thrombasthenia in one.42
Treatment of anticoagulation-induced hemothorax
should focus on the correction of the coagulopathy.
If rupture of a pulmonary infarct is suspected, a
surgical consultation should be obtained for possible
thoracotomy and resection.33
Vascular
Aortic dissection or rupture is a major reported cause
of hemothorax. It occurs mostly on left side, with
hundreds of cases having been reported. We will not
discuss aortic dissection in detail in this review.
We found 32 reported cases of hemothorax asso-
ciated with pulmonary vascular malformations. In
about half the cases, the patients had documented
Osler-Weber-Rendu disease. AVMs are found in 15
to 33% of cases in this disease.43 46
Hemoptysis is more common than hemothorax in
this disease.47 In a review of 143 patients with heredi-
tary hemmorhagic telangiectasia (HHT)-associated pul-
monary AVMs, 6 had hemothorax.48 Contrast echo-
cardiography, blood gas analysis on 100% oxygen,49
and CT angiography50 are the screening measures
shown to be useful to diagnose pulmonary AVMs.
An interesting reported association was that 30 to
50% patients with AVM bleeding were pregnant.51
In all cases, pulmonary hemorrhage occurred in the
second or third trimesters, suggesting that the risk of
spontaneous rupture increases as blood volume and
cardiac output increase. Some authors48 suggest that
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all women with HHT should be screened for pulmo-
nary AVMs before becoming pregnant.
Ehlers-Danlos syndrome (EDS) type IV has been
associated with hemothorax in the setting of internal
mammary artery rupture.52,53 This form of the EDS,
also known as vascular type, results from deficient or
defective type III collagen. Arterial tears are the
most serious complication, and pulmonary manifes-
tations besides hemothorax include hemoptysis from
pulmonary artery rupture or tears in lung paren-
chyma, thick-walled cavities resulting from previous
lung rupture, pneumothoraces, bullous lung disease,
panacinar emphysema, pulmonary cysts, and bron-
chiectasis.54 Hemothorax has been reported with
EDS in the setting of pneumothorax also.55
Another frequent cause of bleeding is von Reck-
linghausens disease, or neurofibromatosis. Bleeding
in the abdominal cavity, retroperitoneum, and soft
tissues has been reported as a result of rupture of
friable vasculature by either vascular invasion by
neurofibromas or arterial dysplasia.56 In this disease,
bleeding occurred either by the rupture of associated
vascular anomalies57 or by direct rupture of a schwa-
nomma.58 The incidence of vascular lesions in neu-
rofibromatosis type 1 have been reported to be only
3.6%.59 Two types of vascular involvement have been
described: (1) stenotic or aneurysmal alterations in
large vessels such as the aorta and its branches like
the intercostal artery, subclavian,60,61 and internal
thoracic, which may rupture or dissect62,63; and (2)
dysplastic features in smaller vessels.
Treatment consists of thoracotomy and surgical
ligation of the bleeding vessels, primarily indicated in
the presence of active bleeding with associated
hemodynamic compromise. A more conservative ap-
proach with endovascular embolization or nonopera-
tive management can be taken in case of hemody-
namic stability; however, more frequent postprocedural
monitoring is required. Pollak et al64 reviewed 155
patients (148 patients with HHT) with pulmonary
AVMs who underwent embolization during a period
of 3 years. The symptoms during follow-up consisted
of respiratory manifestations (n 13), cerebral isch-
emia (n 4), brain abscess (n 5), hemoptysis
(n 3), and seizure (n 1). The problems were
related to growth of AVMs, recanalization, residual
AVMs, and collateral or accessory feeding vessels.
Clinical and anatomic evaluation after pulmonary
AVM embolization is important in order to detect
these lesions. Patients with persistent, reperfused, or
enlarging lesions often have symptoms, but a signif-
icant minority of patients are asymptomatic. More
frequent assessment may improve detection before
the onset of symptoms.64
Coil embolization is certainly effective for reduc-
ing right-to-left shunt, improving arterial hypoxemia,
Special Features
 and increasing exercise capacity in patients with
large or numerous pulmonary AVMs.65 In the setting
of a hemothorax, particularly with hemodynamic
instability or recurrence, a surgical approach should
be considered.
Neoplasia
The most common neoplasias associated with hemo-
thorax include schwanommas of von Recklinghausen
disease (discussed above) and soft-tissue tumors such
as sarcomas, angiosarcomas, and hepatocellular car-
cinomas. Lung cancer is a distinctly uncommon
cause of hemothorax even in the setting of pleural
extension. Other associated causes are rupture of
thymomas66 or thymic cysts, liver metastasis, pericy-
tomas,67 and some germ cell tumors,68,69 like cystic
chondroblastoma.70
Angiosarcoma is a rare tumor of endothelial cells
that originates in small blood vessels. It can affect
any organ, but it usually occurs in skin, soft tissue,
breast, and visceral organs.71,72 The most common
metastatic site for angiosarcoma is the lung; there-
fore, pulmonary complications such as hemoptysis,
pneumothorax, hemothorax, atelectasis, and postob-
structive pneumonia have been reported in the
literature both from primary thoracic and metastatic
angiosarcomas.7375
The prognosis of patients with angiosarcoma-
associated hemothorax is poor, and we found a 6- to
8-month mortality rate 80% in our review. In a
recent review, Moriya et al76 reported 17 patients
with bloody effusion or bloody pleurisy with vascular
tumors. Most patients in the series presented with
dyspnea, hemoptysis, and chest pain The notable
finding in the series was occurrence of bilateral
spontaneous hemothorax in 9 of the 17 patients.
However the pleural fluid hematocrit in this review
ranged from 25 to 50%, and therefore only a few
patients had true hemothorax by definition but the
mortality was similar to a true hemothorax (90% at
10 months).
Hepatocellular carcinoma (HCC) is another tumor
that can present as a hemothorax, particularly when
it is metastatic to the chest. This is a very rare compli-
cation, with high mortality secondary to uncontrolla-
ble hemorrhage.77 Most of the cases of hemothorax
are reported from Asia and sub-Saharan Africa,
where the cancer is prevalent. The frequent sites of
metastasis for HCC include the lung, lymph node,
adrenal glands, and bones. Metastatic HCCs, like the
primary tumor, are usually highly vascular and can
lead to spontaneous or secondary hemothorax.78 The
most common symptoms reported in different case
reports79 81 included dyspnea and chest pain. Sohara
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et al77 reviewed 10 patients with hemothorax and
HCC; 5 patients had drainage of hemothorax, 3 pa-
tients were managed without chest drainage, 1 patient
had transcatheter arterial embolization, while an-
other patient had transcatheter arterial injection of
alcohol. All patients in this series died within 3 months
of the diagnosis of hemothorax. Specific treatment of
neoplasia-associated hemothorax depends on the tu-
mor, but the prognosis for all malignancy-associated
hemothoraces remains poor.
Miscellaneous
Exostoses
Hemothorax is a rare but well-documented com-
plication of exostoses and has only been described in
about 16 patients (6 with hereditary multiple exos-
toses, and two solitary exostoses) in the English-
language literature.82 84
The etiological mechanisms proposed by most
authors are the shearing of the pleura or diaphragm
by the relatively sharp margins of the intrathoracic
exostosis or erosion of an adjacent vessel that can be
dilated because of chronic frictional irritation85,86 and
inflammation. Most of the cases have been reported
in the first 3 decades of life, with only a couple of
cases in elderly men. Exostoses are hard to detect on
a plain radiograph. A CT with bone windows is better
in delineating the location and angulation of exostoses.
Exostoses are usually solitary87,88 but may be multiple
as part of hereditary multiple exostoses.89 92 A surgical
approach by VATS or a thoracotomy is needed to resect
the exostoses and prevent recurrence.
Endometriosis
Endometriosis is another etiology for spontaneous
hemothorax or hemopneumothorax. This is seen in
menstruating women and may present as symptoms,
signs, and radiographic changes that recur in the
chest concurrent with menses. Such phenomena,
termed catamenial by Dr. Lilington in 1972, may
take on a number of clinical manifestations, includ-
ing pneumothorax, hemothorax, hemoptysis, pulmo-
nary nodules, chest pain, dyspnea, and others.93 Two
thirds of these patients have a pathologic diagnosis of
thoracic endometriosis on surgery, possibly due to
cyclical changes in pathology with menstruation.
Catamenial hemothorax represents a common man-
ifestation of thoracic endometriosis syndrome, oc-
curring in 14% of known cases, and concomitant
pelvic endometriosis was found in 100% of cases.94 It
is unilateral and affects the right side 80% of the
time; however, bilateral hemothorax from thoracic
endometriosis has been reported.95 The majority of
CHEST / 134 / 5 / NOVEMBER, 2008 1059
 these patients are young, nulliparous, black women.96
Patients may be hemodynamically stable with an
effusion. The etiology of thoracic endometriosis is
not clear but includes possible transdiaphragmatic
migration of endometrial tissue via naturally occur-
ring fenestrations and occurring more frequently on
the right side. Hematogenous or lymphatic spread
after uterine manipulation from pelvic procedures is
another possibility. Diagnosis is often delayed for
months or even years, and a high index of suspicion
is necessary.
The goal of medical therapy for the thoracic endo-
metriosis syndrome is to minimize estrogen secre-
tion. A number of hormonal agents are utilized to
achieve this objective. Danazol, a derivative of 17--
ethinyltestostyerone, minimizes the midcycle surge
of leutinizing hormone, thus mimicking the chronic
anovulatory state. Progestational agents have been
given to induce atrophy of endometrial tissue.
Gonadotropin-releasing hormone agonists minimize
follicle-stimulating hormone and leutinizing hormone Figure 1. CT of the chest showing pleural effusion and paren-
secretion, inducing hypogonadotropic gonadism. Oral chymal nodules.
contraceptive pills, which cause amenorrhea, have
also been used.97 In general, medical therapy alone is
insufficient for the treatment of the pleural manifes- CD34 (Fig 3), and factor VIII antigen. The patient
tations of thoracic endometriosis.93 Recurrence often survived only 3 months. Primary or metastatic105
necessitates pleural inspection, with resection of pleural angiosarcoma should be considered a cause
endometrial implants. Repair of diaphragmatic fen- of spontaneous hemothorax, especially in patients
estrations has also been suggested.98 Hysterectomy with bilateral or intractable hemothorax.107
and oopherectomy have also been performed as a
surrogate for hormonal therapy, with varied results.
Diagnosis and Management
Idiopathic
Once a bloody effusion is obtained, the first step
A definite cause for spontaneous hemothorax is should be to check the hematocrit to confirm a
usually identifiable with investigation. If preliminary hemothorax. A hemorrhagic effusion should prompt
investigations remain nondiagnostic, the case may suspicion of a malignancy, infections like tuberculo-
come to a thoracotomy or an autopsy to identify a
definite etiology.99 It is very rare to fail to identify a
cause for hemothorax with only three to four cases in
the literature, which remained truly idiopathic.100 103

Bilateral Spontaneous Hemothorax

This is a very rare entity. We found eight cases in
the literature of spontaneous bilateral hemothorax
reported over the last 50 years. Four of them were
related to vascular tumors, specifically angiosarco-
mas.75,76,104,105 One each was related to a subclavian
artery aneurysm, endometriosis, an iatrogenic coagu-
lopathy,106 and one was idiopathic. The ninth case is
that of a 56-year-old woman we recently encoun-
tered who presented with bilateral spontaneous he-
mothorax and lung nodules (Fig 1). Pathology re-
vealed an epitheloid angiosarcoma, a highly vascular
tumor both in the pleura and the lung (Fig 2), with Figure 2. Lung nodule showing clusters of epitheloid cells with
immunochemistry revealing positivity for CD31, sinusoidal spaces (hematoxylin-eosin, original 200).

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Figure 3. Immunostaining showing strong positivity with vimentin
(original 100).
sis, or pulmonary infarction. A hemothorax identified
by a hematocrit of 25 to 50% that of blood should
lead one to consider workup for a vascular etiology
either a dissecting aneurysm, AVM/arteriovenous
fistula, vascular tumors, coagulopathies, neurofibro-
matosis, or exostoses. It is important to realize that
even a hemothorax can appear to be like a hemor-
rhagic effusion with a lower hematocrit after a few
days because there is significant dilution in 3 to 4
days. This may be a problem because the presenta-
tion with a hemothorax is not always acute, particu-
larly in a young adult with no underlying respiratory
compromise. The flowchart in Figure 4 shows an
algorithmic approach to the various steps in the diag-
nosis. Besides the coagulation parameters, a contrast-
enhanced CT of the chest yields helpful information
about the etiology. An echocardiogram with bubble
study points toward a pulmonary AVM if there is a
delayed appearance of bubbles in the right heart
chambers. The yield from pleural cytology is vari-
able. It is hard to make an unequivocal diagnosis of
the usual neoplastic etiologies such as angiosarcomas
solely on the basis of cytology of the pleural fluid, but
immunochemical markers may increase the yield and
degree of confidence. In case of endometriosis, the
findings usually include nonspecific hemosiderin-

Figure 4. Flowchart showing the steps in the evaluation of a spontaneous hemothorax;

echo echocardiography; TB tuberculosis; AFB acid-fast bacilli; Cr creatinine; PT prothrombin time;
PTT partial thromboplastin time. See Table 1 footnote for expansion of abbreviations.

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 Table 2History and Physical Examination Clues to
Etiology in Hemothorax
Age
Systemic symptoms (weight loss)
Hemoptysis
Trauma or surgery
Medication history (antiplatelets, anticoagulants)
Bleeding tendencies (epistaxis, hematuria, joint effusions)
Periodicity of effusions (association with menstrual cycles)
Caf au lait spots or neurofibromas
Telangiectasias
Myasthenia
Hyperextensible joints
Increased skin laxity
laden histiocytes, but rarely endometrial epithelial
cells may be identified. A good history and physical
examination can yield valuable clues as to the etiol-
ogy of a hemothorax (Table 2).
As far as management is concerned, it depends on
the cause and is discussed under the respective
subheadings. Thoracostomy drainage is usually the
first step in a stable patient. In a hemodynamically
unstable patient or if the rate of bleeding is 500
mL/h in the first hour or 200 to 300 mL/h subse-
quently, an early surgical approach with ongoing resus-
citation is favored. Correction of the coagulopathy
may be all that is needed in cases of anticoagulant-
induced bleeding. Imaging is important if the suspi-
cion is high for an AVM/arteriovenous fistula. This
may include a CT angiogram or rarely an arterio-
gram. Embolization remains an option in treatment
of vascular anomalies. The management of residual
blood is controversial, with a growing number favor-
ing early VATS particularly if a significant amount of
clot is present to prevent fibrothorax and restrictive
physiology.
Untreated Hemothorax
Drainage of hemothorax 200 to 300 mL of
blood is necessary for symptomatic management as
well as the prevention of long-term complications of
leaving it untreated. A retained hemothorax can lead
to infection, chronic fibrothorax, lung entrapment,
and impaired pulmonary function. If the pleural
effusion persists despite tube thoracostomy, a diag-
nosis of clotted or retained hemothorax can be made,
which in the trauma literature is defined as an absence
of radiologic improvement despite tube thoracostomy
on the second or third day after the event.108
Once the clot has been allowed to organize, it will
adhere to the lung and pleura, making it difficult to
remove. The agitation of cardiac and respiratory move-
ment rapidly defibrinates the blood, and a fibrin clot
thus formed is deposited on the visceral and parietal
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pleura, setting the stage for a trapped lung. In its
early development, this thin membrane has little
substance and is attached very loosely to the under-
lying pleural surface. By the seventh day, there is an
angioblastic and fibroblastic proliferation. The mem-
brane continues to thicken by progressive deposition
and organization of the coagulum within the cavity.
An understanding of the pathologic features of a
clotted hemothorax makes it clear that, if possible,
the clotted hemothorax should be evacuated within 7
to 10 days of injury. If, however, the hemothorax is
not evacuated by the tenth day, the clotted blood
cannot be easily removed and a decortication is
usually required.109,110 This complication can occur
in as many as 5 to 30% of patients,108 and up to 40%
of these patients will require further surgical inter-
vention for nonresolving, complicated intrapleural
collections, empyema, or fibrothorax. The placement
of additional chest tubes to treat a retained hemo-
thorax is ineffective because of the presence of
clotted blood and loculations.111
VATS is believed to be the best available modality
for the management of clotted hemothorax, with
efficacy rates upwards of 80%. VATS is an accurate,
safe, and reliable operative therapy for retained post-
traumatic pleural collections, even in patients present-
ing later than the conventionally accepted 3- to 5-day
postevent window.112
VATS was found to be superior to intrapleural
fibrinolytic therapy (IPFT), both in terms of de-
creased hospital stay and need for thoracotomy.108
However, fibrinolysis with streptokinase is an effec-
tive adjunctive treatment in hemothorax as shown by
multiple case reports and reviews. In a multicenter
trial113 of 48 patients with loculated effusions includ-
ing 14 patients with nonmalignant hemothorax and 4
patients with malignant hemothorax, the authors
found a 92% success rate for fibrinolysis. The same
success rate has been reported by other authors.114
Kimbrell et al115 studied 25 patients with 300 mL
of hemothorax after 3 days of tube thoracostomy by
administration of 250,000 IU of streptokinase or
100,000 IV of urokinase mixed in 50 mL of sterile
saline solution with dwell time of 4 h for 6 days, and
achieved resolution in 23 patients (90%) without
bleeding complications.
IPFT has been found to be safe without major
concern for systemic fibrinolysis, although some side
effects like nausea, fever, and myalgias, and one case
of hemorrhage have been reported.116 As proposed
by some authors,116 a reasonable approach in a stable
patient can be to first utilize IPFT and, if unsuccess-
ful, can proceed to surgical therapy; however, dura-
tion of hospital stay may be a deterrent to its use.
IPFT is not an option in cases in which the hemo-
thorax is related to a coagulopathy or vascular lesions
Special Features
 such as AVMs and angiosarcomas because it may
worsen the bleeding. In such cases, a surgical ap-
proach may be the only option.
Summary
We have reviewed the major etiologies of sponta-
neous (nontraumatic) hemothorax. The major points
that were emphasized include the following: (1)
distinguishing hemorrhagic effusions from true he-
mothorax because these two entities point toward a
different set of differential diagnoses; (2) differential
diagnosis with attention to major etiologies and an
algorithmic approach to the diagnosis; and (3) gen-
eral management of hemothorax with conservative
and surgical approaches with attention to etiology
specific treatments.
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