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Manual Of Definitive Surgical Trauma Care

Manual Of Definitive Surgical Trauma Care

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Published by bovine splendor
More medical text info for those who cannot access conventional resources.
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Published by: bovine splendor on Jul 10, 2013
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07/13/2013

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Thoracic injury constitutes a significant problem in
terms of mortality and morbidity. In the USA during
the early 1990s, there were approximately 180000
deaths per annum from injury. Several investigators
have shown that 50 per cent of fatal injuries are the
result of primary brain injury, 25 per cent of fatal acci-
dents are caused by chest trauma and, in another 25 per
cent (including brain injury), thoracic injury contributes
to the primary cause of mortality.1
Somewhat less clearly defined is the extent of appre-
ciable morbidity after chest injury, most usually the
long-term consequences of hypoxic brain damage. There
are a number of important points to be made in this
regard:

•A definite proportion of these deaths occur virtually
immediately (i.e. at the time of injury), e.g. rapid
exsanguination after traumatic rupture of the aorta
in blunt injury or major vascular disruption after
penetrating injury.
•Of survivors with thoracic injury who reach hospital,
a significant proportion die in hospital as the result
of misassessment or delay in the institution of treat-
ment. These deaths occur earlyas a consequence of

shock, or lateas the result of adult respiratory distress
syndrome (ARDS), multiple organ failure (MOF) and
sepsis.
•Most life-threatening thoracic injuries can be simply
and promptly treated after identification by needle or
tube placement for drainage. These are simple and effect-
ive techniques that can be performed by any physician.
•Approximately 40 per cent of penetrating thoracic
injuries and 20 per cent of blunt thoracic injuries will
require definitive surgery.

Emergency department thoracotomy (ERT) has dis-
tinct and specific indications: these virtually always
relate to patients in extremis with penetrating injury.
Indiscriminate use of ERT will not alter the mortality
and morbidity, but will increase the risk of communic-
able disease transmission to health workers.
Injuries to the chest wall and thoracic viscera can
directly impair oxygen transport mechanisms. Hypoxia
and hypovolaemia resulting from thoracic injuries may
cause secondary injury to patients with brain injury, or
may directly cause cerebral oedema.
Conversely, shock and/or brain injury can secondar-
ily aggravate thoracic injuries and hypoxaemia by dis-
rupting normal ventilatory patterns or causing loss of
protective airway reflexes and aspiration.
The lung is a target organ for secondary injury follow-
ing shock and remote tissue injury. Microemboli formed
in the peripheral microcirculation embolize to the lung
causing ventilation–perfusion mismatch and right heart
failure. Tissue injury and shock can activate the inflam-
matory cascade, which can contribute to pulmonary
injury (reperfusion).

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