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Hemothorax

Hemothorax
Author: Mary C Mancini, MD, PhD; Chief Editor: Jeffrey C Milliken, MD more...
Updated: Oct 15, 2014

Background
Hemothorax is the presence of blood in the pleural space. The source of blood may be the chest wall, lung
parenchyma, heart, or great vessels. Although some authors state that a hematocrit value of at least 50% is
necessary to differentiate a hemothorax from a bloody pleural effusion, most do not agree on any specific
distinction.
Hemothorax is usually a consequence of blunt or penetrating trauma. Much less commonly, it may be a
complication of disease, may be iatrogenically induced,[1] or may develop spontaneously.[2]
Prompt identification and treatment of traumatic hemothorax is an essential part of the care of the injured patient.
The upright chest radiograph is the ideal primary diagnostic study in the evaluation of hemothorax (see Workup). In
cases of hemothorax unrelated to trauma, a careful investigation for the underlying source must be performed while
treatment is provided.
Tube thoracostomy drainage is the primary mode of treatment. Video-assisted thoracoscopic surgery (VATS) may
be used. Thoracotomy is the procedure of choice for surgical exploration of the chest when massive hemothorax or
persistent bleeding is present. (See Treatment.)

Historical background
Hemorrhage from or within the chest has been detailed in numerous medical writings dating back to ancient times.
While lesser forms of trauma were commonly treated in the ancient physician's daily practice, major injuries,
especially those to the chest, were difficult to treat and often lethal.
By the 18th century, some treatment for hemothorax was available; however, controversy raged about its form. A
number of surgeons, including John Hunter in 1794, advocated the creation of an intercostal incision and drainage
of the hemothorax. Those of the opposing viewpoint believed that closure of chest wounds without drainage and
other conservative forms of management of bloody collections in the chest were proper treatment.
While Hunter's method was effective in evacuating the hemothorax, the creation of an iatrogenic pneumothorax as
a result of the procedure was associated with significant morbidity. On the other hand, wound closure or
conservative management posed the possible risks of subsequent empyema with sepsis or persistent trapped lung
with permanent reduction of pulmonary function.
Observing the advantages and dangers of both forms of therapy, Guthrie, in the early 1800s, gave credence to both
viewpoints. He proposed the importance of early evacuation of blood through an existing chest wound; at the same
time, he asserted that if bleeding from the chest persisted, the wound should be closed in the hope that existing
intrathoracic pressure would halt the bleeding. If the desired effect was accomplished, he advised that the wound
be reopened several days later for the evacuation of retained clotted blood or serous fluid.
By the 1870s, early hemothorax evacuation by trocar and cannula or by intercostal incision was considered
standard practice. Not long after this, underwater seal drainage was described by a number of different physicians.
This basic technique has remained the most common form of treatment for hemothorax and other pleural fluid
collections to this day.[3]

Anatomy
Normally, the pleural space, which is between the parietal and visceral pleurae, is only a potential space. Bleeding
into the pleural space may result from either extrapleural or intrapleural injury.

Extrapleural injury
Traumatic disruption of the chest wall tissues with violation of the pleural membrane can cause bleeding into the
pleural cavity. The most likely sources of significant or persistent bleeding from chest wall injuries are the
intercostal and internal mammary arteries. In nontraumatic cases, rare disease processes within the chest wall
(eg, bony exostoses) can be responsible.

Intrapleural injury
Blunt or penetrating injury involving virtually any intrathoracic structure can result in hemothorax. Massive
hemothorax or exsanguinating hemorrhage may result from injury to major arterial or venous structures contained
within the thorax or from the heart itself. These include the aorta and its brachiocephalic branches, the main or
branch pulmonary arteries, the superior vena cava and the brachiocephalic veins, the inferior vena cava, the azygos
vein, and the major pulmonary veins.
Injury to the heart can produce a hemothorax if a communication exists between the pericardium and the pleural
space.
Injury to the pulmonary parenchyma may cause hemothorax, but it is usually self-limited because pulmonary

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vascular pressure is normally low. Pulmonary parenchymal injury is usually associated with pneumothorax and
results in limited hemorrhage.
Hemothorax resulting from metastatic malignant disease is usually from tumor implants that seed the pleural
surfaces of the thorax.
Diseases of the thoracic aorta and its major branches, such as dissection or aneurysm formation, account for a
large percentage of specific vascular abnormalities that can cause hemothorax. Aneurysms of other intrathoracic
arteries such as the internal mammary artery have been described and are possible causes of hemothorax if
rupture occurs.
A variety of unusual congenital pulmonary abnormalities, including intralobar and extralobar sequestration,[4]
hereditary telangiectasia, and congenital arteriovenous malformations, can cause hemothorax.
Hemothorax can result from a pathologic process within the abdomen if blood escaping from the lesion is able to
traverse the diaphragm through one of the normal hiatal openings or a congenital or acquired opening.

Pathophysiology
Bleeding into the pleural space can occur with virtually any disruption of the tissues of the chest wall and pleura or
the intrathoracic structures. The physiologic response to the development of a hemothorax is manifested in two
major areas: hemodynamic and respiratory. The degree of hemodynamic response is determined by the amount
and rapidity of blood loss.

Hemodynamic response
Hemodynamic changes vary, depending on the amount of bleeding and the rapidity of blood loss. Blood loss of up
to 750 mL in a 70-kg man should cause no significant hemodynamic change. Loss of 750-1500 mL in the same
individual will cause the early symptoms of shock (ie, tachycardia, tachypnea, and a decrease in pulse pressure).
Significant signs of shock with signs of poor perfusion occur with loss of blood volume of 30% or more (1500-2000
mL). Because the pleural cavity of a 70-kg man can hold 4 L of blood or more, exsanguinating hemorrhage can
occur without external evidence of blood loss.

Respiratory response
The space-occupying effect of a large accumulation of blood within the pleural space may hamper normal
respiratory movement. In trauma cases, abnormalities of ventilation and oxygenation may result, especially if
associated with injuries to the chest wall.
A large enough collection of blood causes the patient to experience dyspnea and may produce the clinical finding
of tachypnea. The volume of blood required to produce these symptoms in a given individual varies depending on a
number of factors, including organs injured, severity of injury, and underlying pulmonary and cardiac reserve.
Dyspnea is a common symptom in cases in which hemothorax develops in an insidious manner, such as those
secondary to metastatic disease. Blood loss in such cases is not so acute as to produce a visible hemodynamic
response, and dyspnea is often the predominant complaint.

Physiologic resolution of hemothorax

Blood that enters the pleural cavity is exposed to the motion of the diaphragm, lungs, and other intrathoracic
structures. This results in some degree of defibrination of the blood so that incomplete clotting occurs. Within
several hours of cessation of bleeding, lysis of existing clots by pleural enzymes begins.
Lysis of red blood cells results in a marked increase in the protein concentration of the pleural fluid and an
increase in the osmotic pressure within the pleural cavity. This elevated intrapleural osmotic pressure produces an
osmotic gradient between the pleural space and the surrounding tissues that favors transudation of fluid into the
pleural space. In this way, a small and asymptomatic hemothorax can progress into a large and symptomatic
bloody pleural effusion.

Late physiologic sequelae of unresolved hemothorax

Two pathologic states are associated with the later stages of hemothorax: empyema and fibrothorax. Empyema
results from bacterial contamination of the retained hemothorax. If undetected or improperly treated, this can lead
to bacteremia and septic shock.
Fibrothorax results when fibrin deposition develops in an organized hemothorax and coats both the parietal and
visceral pleural surfaces. This adhesive process traps the lung in position and prevents it from expanding fully.
Persistent atelectasis of portions of the lung and reduced pulmonary function result from this process.

Etiology
By far the most common cause of hemothorax is trauma. Penetrating injuries of the lungs, heart, great vessels, or
chest wall are obvious causes of hemothorax; they may be accidental, deliberate, or iatrogenic in origin.[5] In
particular, central venous catheter and thoracostomy tube placement are cited as primary iatrogenic causes.[6, 7,
8]

Blunt chest trauma can occasionally result in hemothorax by laceration of internal vessels.[9] Because of the
relatively more elastic chest wall of infants and children, rib fractures may be absent in such cases.[10, 11]
The causes of nontraumatic or spontaneous hemothorax include the following:

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Neoplasia (primary or metastatic)

Blood dyscrasias, including complications of anticoagulation
Pulmonary embolism with infarction
Torn pleural adhesions in association with spontaneous pneumothorax
Bullous emphysema
Necrotizing infections
Tuberculosis
Pulmonary arteriovenous fistulae
Hereditary hemorrhagic telangiectasia [12]
Nonpulmonary intrathoracic vascular pathology (eg, thoracic aortic aneurysm or aneurysm of the internal
mammary artery)
Intralobar and extralobar sequestration [4]
Abdominal pathology (eg, pancreatic pseudocyst, splenic artery aneurysm, or hemoperitoneum)
Catamenial [13]
Case reports involve associated disorders such as hemorrhagic disease of the newborn (eg, vitamin K deficiency),
Henoch-Schnlein purpura, and beta thalassemia/hemoglobin E disease.[14, 15, 16, 17] Congenital cystic
adenomatoid malformations occasionally result in hemothorax.[18] A case of massive spontaneous hemothorax
has been reported with Von Recklinghausen disease.[19] Spontaneous internal thoracic artery hemorrhage was
reported in a child with type IV Ehlers-Danlos syndrome.
Hemothorax has also been reported in association with costal cartilaginous anomalies.[20, 21, 22, 23] Rib tumors
have rarely been reported in association with hemothorax. Intrathoracic rupture of an osteosarcoma of a rib caused
hemorrhagic shock in a 13-year-old girl.[24]
Hemothorax has been noted to complicate a small fraction of spontaneous pneumothorax cases. Although rare, it
is more likely to occur in young adolescent males and can be life-threatening secondary to massive bleeding.[25]

Epidemiology
Quantifying the frequency of hemothorax in the general population is difficult. A very small hemothorax can be
associated with a single rib fracture and may go undetected or require no treatment. Because most major
hemothoraces are related to trauma, a rough estimate of their occurrence may be gleaned from trauma statistics.
Approximately 150,000 deaths occur from trauma each year. Approximately three times this number of individuals
are permanently disabled because of trauma, and the majority of this combined group have sustained multiple
trauma. Chest injuries occur in approximately 60% of multiple-trauma cases; therefore, a rough estimate of the
occurrence of hemothorax related to trauma in the United States approaches 300,000 cases per year.[26]
In a 34-month period at a large level-1 trauma center, 2086 children younger than 15 years were admitted with
blunt or penetrating trauma; 104 (4.4%) had thoracic trauma.[27] Of the patients with thoracic trauma, 15 had
hemopneumothorax (26.7% mortality), and 14 had hemothorax (57.1% mortality). Many of these patients had
other severe extrathoracic injuries. Nontraumatic hemothorax carries a much lower mortality.
In another series of children with penetrating chest injuries (ie, stab or gunshot wounds), the morbidity was 8.51%
(8 of 94).[28] Complications included atelectasis (3), intrathoracic hematoma (3), wound infection (3), pneumonia
(2), air leak for more than 5 days (2), and septicemia (1). Note that these statistics apply only to traumatic
hemothorax.

Prognosis
At present, the general outcome for patients with traumatic hemothorax is good. Mortality associated with cases
of traumatic hemothorax is directly related to the nature and severity of the injury. Morbidity is also related to
these factors and to the risks associated with retained hemothorax, namely empyema and fibrothorax/trapped
lung. Empyema occurs in approximately 5% of cases. Fibrothorax occurs in about 1% of cases.
Retained hemothorax with or without one of the aforementioned complications occurs in 10-20% of patients who
sustain a traumatic hemothorax, and most of these patients require evacuation of this collection. Prognosis after
the treatment of one of these complications is excellent.
Short-term and long-term outcome for individuals who develop a nontraumatic hemothorax is directly related to the
underlying cause of the hemothorax.

Contributor Information and Disclosures

Author
Mary C Mancini, MD, PhD Professor and Chief of Cardiothoracic Surgery, Department of Surgery, Louisiana
State University School of Medicine in Shreveport
Mary C Mancini, MD, PhD is a member of the following medical societies: American Association for Thoracic
Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, and Society of
Thoracic Surgeons
Disclosure: Nothing to disclose.
Coauthor(s)
Thomas Scanlin, MD Chief, Division of Pulmonary Medicine and Cystic Fibrosis Center, Department of
Pediatrics, Rutgers Robert Wood Johnson Medical School
Thomas Scanlin, MD is a member of the following medical societies: American Association for the
Advancement of Science, American Society for Biochemistry and Molecular Biology, American Thoracic

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Society, Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.
Denise Serebrisky, MD Associate Professor, Department of Pediatrics, Albert Einstein College of Medicine;
Director, Division of Pulmonary Medicine, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center;
Director, Jacobi Asthma and Allergy Center for Children
Denise Serebrisky, MD is a member of the following medical societies: American Thoracic Society
Disclosure: Nothing to disclose.
Specialty Editor Board
Charles Callahan, DO Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center
Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics,
American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic
Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Shreekanth V Karwande, MBBS Chair, Professor, Department of Surgery, Division of Cardiothoracic
Surgery, University of Utah School of Medicine and Medical Center
Shreekanth V Karwande, MBBS is a member of the following medical societies: American Association for
Thoracic Surgery, American College of Chest Physicians, American College of Surgeons, American Heart
Association, Society of Critical Care Medicine, Society of Thoracic Surgeons, and Western Thoracic Surgical
Association
Disclosure: Nothing to disclose.
Michael R Bye, MD Professor of Clinical Pediatrics, State University of New York at Buffalo School of
Medicine; Attending Physician, Pediatric Pulmonary Division, Women's and Children's Hospital of Buffalo
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American
College of Chest Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.
Chief Editor
Jeffrey C Milliken, MD Chief, Division of Cardiothoracic Surgery, University of California at Irvine Medical
Center; Clinical Professor, Department of Surgery, University of California, Irvine, School of Medicine
Jeffrey C Milliken, MD is a member of the following medical societies: Alpha Omega Alpha, American
Association for Thoracic Surgery, American College of Cardiology, American College of Chest Physicians,
American College of Surgeons, American Heart Association, American Society for Artificial Internal Organs,
California Medical Association, International Society for Heart and Lung Transplantation, Phi Beta Kappa,
Society of Thoracic Surgeons, Southwest Oncology Group, and Western Surgical Association
Disclosure: Nothing to disclose.
Additional Contributors
The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous
authors Jane M Eggerstedt, MD, and Allen Fagenholz, MD, to the development and writing of the source
articles.

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