Physiopathology of Crushed Chest Injuries

Garzon, Antonio A.; Seltzer, Bernard; Karlson, Karl E.

doi:10.1097/00132586-196906000-00008

Cited by 6 publications

(9 citation statements)

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“…Garzon et al reported sustained shunt elevation in patients with flail chest (21). Diffusion limitation, as measured by carbon monoxide rebreathing, did not contribute significantly to hypoxemia (21).…”

Section: Discussionmentioning

confidence: 96%

“…Fulton and Peter in a model of pulmonary contusion in dogs reported increased calculated shunt fraction in a group subjected to vigorous (65 ml/kg) resuscitation and reinfusion of shed blood (18). Garzon et al reported sustained shunt elevation in patients with flail chest (21). Diffusion limitation, as measured by carbon monoxide rebreathing, did not contribute significantly to hypoxemia (21).…”

Section: Discussionmentioning

confidence: 99%

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Ventilation-perfusion relationships following experimental pulmonary contusion

Batchinsky¹,

Weiss²,

Jordan³

et al. 2007

Journal of Applied Physiology

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Ventilation-perfusion changes after right-sided pulmonary contusion (PC) in swine were investigated by means of the multiple inert gas elimination technique (MIGET). Anesthetized swine (injury, n = 8; control, n = 6) sustained a right-chest PC by a captive-bolt apparatus. This was followed by a 12-ml/kg hemorrhage, resuscitation, and reinfusion of shed blood. MIGET and thoracic computed tomography (CT) were performed before and 6 h after injury. Three-dimensional CT scan reconstruction enabled determination of the combined fractional volume of poorly aerated and non-aerated lung tissue (VOL), and the mean gray-scale density (MGSD). Six hours after PC in injured animals, Pa(O(2)) decreased from 234.9 +/- 5.1 to 113.9 +/- 13.0 mmHg. Shunt (Q(S)) increased (2.7 +/- 0.4 to 12.3 +/- 2.2%) at the expense of blood flow to normal ventilation/perfusion compartments (97.1 +/- 0.4 to 87.4 +/- 2.2%). Dead space ventilation (V(D)/V(T)) increased (58.7 +/- 1.7% to 67.2 +/- 1.2%). MGSD increased (-696.7 +/- 6.1 to -565.0 +/- 24.3 Hounsfield units), as did VOL (4.3 +/- 0.5 to 33.5 +/- 3.2%). Multivariate linear regression of MGSD, VOL, V(D)/V(T), and Q(S) vs. Pa(O(2)) retained VOL and Q(S) (r(2) = .835) as independent covariates of Pa(O(2)). An increase in Q(S) characterizes lung failure 6 h after pulmonary contusion; Q(S) and VOL correlate independently with Pa(O(2)).

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Ventilation-perfusion relationships following experimental pulmonary contusion

Batchinsky¹,

Weiss²,

Jordan³

et al. 2007

Journal of Applied Physiology

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“…The pathophysiology of lung contusion and blunt chest trauma includes ventilation/perfusion mismatching, increased intrapulmonary shunting, increased lung water, segmental lung damage, and a loss of compliance (5). Clinically, patients display hypoxemia, hypercarbia, and increased work of breathing of varying severity and duration (6), which are treated with supplemental oxygen and mechanical ventilation as indicated.…”

Section: Introductionmentioning

confidence: 99%

The Evolution of Isolated Bilateral Lung Contusion From Blunt Chest Trauma in Rats: Cellular and Cytokine Responses

Raghavendran¹,

Davidson²,

Woytash

et al. 2005

Shock

114

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Lung contusion is the leading cause of death from blunt thoracic trauma in adults, but its mechanistic pathophysiology remains unclear. This study uses a recently developed rat model to investigate the evolution of inflammation and injury in isolated lung contusion. Bilateral lung contusion with minimal cardiac trauma was induced in 54 anesthetized rats by dropping a 0.3-kg hollow cylindrical weight onto a precordial shield (impact energy, 2.45 Joules). Arterial oxygenation, pressure-volume (P-V) mechanics, histology, and levels of erythrocytes, leukocytes, albumin, and inflammatory mediators in bronchoalveolar lavage (BAL) were assessed at 8 min, at 4, 12, 24, and 48 h, and at 7 days after injury. The role of neutrophils in the evolution of inflammatory injury was also specifically studied by depleting these cells with intravenous vinblastine before lung contusion. Arterial oxygenation was severely reduced at 8 min to 24 h postcontusion, but became almost normal by 48 h. Levels of erythrocytes, leukocytes, and albumin in BAL were increased at

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“…The traumatized lung sequesters fluid and secretions, compliance falls, airways resistance multiplies and the work of breathing is increased up to fivefold (Garzon, Seltzer and Karlson 1968). When to this combination of factors there is added post-laparotomy abdominal pain and distension, a situation readily arises where the patient is unable to continue adequate spontaneous breathing.…”

Section: Discussionmentioning

confidence: 99%

Chest Injury: The Indications for Artificial Ventilation

James

Quail

Gibbons

1974

Anaesth Intensive Care

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During the period April, 1968, to April, 1973, all patients admitted to Royal Newcastle Hospital with respiratory failure following chest injury were managed in the Acute Respiratory Unit. The great majority resulted from motor vehicle accidents. A total of 130 patients suffered respiratory failure following chest injury, and were all seen by at least one of us. Only 21 patients had isolated chest injury, 109 having multiple injuries. Twenty-four patients died, nine from associated cerebral contusion. The place of artificial ventilation in the proper management of chest injuries is discussed and particular. stress is laid on those patients with conditions or injuries likely to lead to resptratory fatlure. In this category are those patients with significant flail segment, associated head or abdominal injury, the obese, and those with pre-existing chest disease.

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Physiopathology of Crushed Chest Injuries

Cited by 6 publications

References 0 publications

Ventilation-perfusion relationships following experimental pulmonary contusion

Ventilation-perfusion relationships following experimental pulmonary contusion

The Evolution of Isolated Bilateral Lung Contusion From Blunt Chest Trauma in Rats: Cellular and Cytokine Responses

Chest Injury: The Indications for Artificial Ventilation

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