Bilateral Lung Contusion Research Articles

THE EVOLUTION OF ISOLATED BILATERAL LUNG CONTUSION FROM BLUNT CHEST TRAUMA IN RATS: CELLULAR AND CYTOKINE RESPONSES

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 <or=24 h, and returned toward normal by 48 h. Deficits in P-V mechanics were most apparent at 24 h postcontusion. Levels of macrophage inflammatory polypeptide-2, cytokine-induced neutrophil chemoattractant-1, and interleukin 6 in BAL peaked at 24 h, whereas monocyte chemoattractant protein-1 and interleukin 1beta peaked at 24 to 48 h postcontusion. Histology showed early hemorrhagic injury (8 min-12 h), with neutrophilic infiltration at 24 h and areas of bronchiolitis obliterans organizing pneumonia-associated fibrosis at 7 days. Vinblastine-treated neutropenic rats had significantly reduced lung injury based on total lung volume at 4 h and on BAL albumin levels at 24 h postcontusion. Inflammatory injury from isolated bilateral lung contusion in rats is most severe in the acute period (8 min-24 h) after initial blunt trauma, and includes a component of neutrophil-dependent pathology.

Damage Control Orthopaedics

In some groups of polytrauma patients, particularly those with chest injuries, head injuries, and those with mangled extremities, early total care of major bone fractures may be potentially harmful. Delaying all orthopaedic surgery, however, is also not always the best approach. In these situations, damage control orthopaedics, which emphasizes the stabilization and control of the injury rather than repair will add little additional physiologic insult to the patient and is a treatment option that should be considered.

Self-Expanding Metallic Stent Placement for Renal Artery Dissection Due to Blunt Trauma

Posttraumatic renal artery injury is rare and its management is still controversial. We report a case of traumatic renal artery stenosis that was managed using a selfexpanding metallic stent. CASE REPORT A 21-year-old woman was hospitalized with bilateral lung and liver contusions due to a traffic accident. At presentation the patient was in hypovolemic shock, and serum creatinine and blood urea nitrogen were 0.4 mg/dl (normal 0.5 to 1.1) and 28 mg/dl (8 to 20), respectively. Urinalysis revealed 15 red blood cells per high power field. Celiac arteriography showed prominent extravasation from branches of the left hepatic artery, which was successfully managed by transcatheter arterial embolization resulting in improvement of the hypovolemic shock. Although left renal arteriography demonstrated severe stenosis following dissection in the main trunk with impaired parenchymal perfusion, the patient was observed without treatment (fig. 1). The next day she became hypertensive (systolic pressure 140 to 160 mm Hg) and repeat left renal arteriography revealed that arterial dissection remained with significant mean pressure (25 mm Hg). After a 5Fr dual lumen aortic cannula (Cobra catheter, Cardeon Corp., Cupertino, California) was advanced into the narrowed true lumen over a hydrophilic guidewire (Radifocus, Terumo Corp., Tokyo, Japan), a self-expanding metallic stent (Wallstent [6 mm diameter, 30 mm length] Boston Scientific Scimed, Inc., Minneapolis, Minnesota) was placed into the stenotic artery. Satisfactory renal arterial caliber was established, and normal perfusion was recovered immediately after stent placement (fig. 2). Because active bleeding was not seen, the patient received 10,000 IU heparin daily for 48 hours, and subsequently cilostazol and aspirin for 3 months, which caused no drug induced hemorrhage. The systemic hypertension improved and the posttreatment level of plasma renin activity was normal at 1.8 ng/ml per hour. Computerized tomography showed adequate positioning of the endoprosthesis without impaired parenchymal perfusion. On day 11 renal scintigraphy using 99m technetium demonstrated that the effective renal plasma flow in the right and left kidney was 477.9 and 534.4 ml per minute, respectively. The patient was discharged home on postoperative day 15. DISCUSSION

Cardiopulmonary, histological, and inflammatory alterations after lung contusion in a novel mouse model of blunt chest trauma.

Severe blunt chest trauma remains an important injury with high morbidity and mortality. However, the associated immunological alterations are poorly understood. Existing big animal models require large-scale settings, are often too expensive, and research products for immunological studies are limited. In this study we aimed to establish a new model of blunt, isolated and bilateral chest trauma in mice and to characterize its effects on physiological and inflammatory variables. Male C3H/HeN mice (n = 9-10/group) were anesthetized and a femoral artery was catheterized. The animals were subjected to trauma or sham procedure and monitored for 180 min. Blunt chest trauma was induced by a blast wave focused on the thorax. Trauma intensity was optimized by varying the exposure distance. Blood pressure, heart rate, respiratory rate, arterial blood gases and plasma cytokine levels were measured. Macroscopic and microscopic examinations were performed. In addition, outcome was evaluated in a 10-day survival study. Chest trauma caused a drop (P < 0.05) in blood pressure and heart rate, which partly recovered. Blood gases revealed hypoxemia and hypercarbia (P < 0.05) 180 min after trauma. There was marked damage to the lungs but none to abdominal organs. Histologically, the characteristic signs of a bilateral lung contusion with alveolar and intrabronchial hemorrhage were found. Plasma interleukin-6 and tumor necrosis factor alpha were considerably increased after 180 min. Blunt chest trauma resulted in an early mortality of 10% without subsequent death. On the basis of these findings, this novel mouse model of blunt chest trauma appears suitable for detailed studies on immunological effects of lung contusion.

Blunt Trauma of the Innominate Artery: a Unique Presentation

Radiology, Rambam Medical Center and The Bruce Rappaport Faculty ofMedicine, Technion – Israel Institute of Technology, Haifa, IsraelIntroductionTrauma to the great vessels in the chest most com-monly affects the aorta and the innominate artery.Although well described series are small and includemainly penetrating trauma. Blunt injuries of theinnominate artery typically involve the origin of theartery. Two rare cases of blunt trauma to the distalinnominate artery are reported herein. CTA andselective angiography were obtained for accuratediagnosis. Treatment was achieved via thoracotomyand placement of a synthetic interposition graft with-out the use of a temporary shunt. Endovascular treat-ment option is discussed. Review of the literature wasdone and a possible cause for this rare trauma issuggested.Case ReportsCase 1A 21-year-old motorcyclist, was involved in a roadaccident and transferred to our medical center intu-bated and in hypovolemic shock (Hemoglobin 7.8g%,Hct 24%). Peripheral pulses were intact. Chest x-rayrevealed a widened mediastinum at the thoracic outletwithout pneumothorax. His injuries included: skullfracture without brain hemorrhage, fracture of thesternum and the first rib on the right side, bilaterallung contusion and fractures of the pubis andextremities.CTA demonstrated an irregular innominate arterialoutline (Fig. 1). Angiography was obtained showing alarge pseudoaneurysm in the distal innominate arterynear its bifurcation (Fig. 2). Upper median sternotomywith a lateral extension was carried out. The dissec-tion revealed a 3-cm pseudoaneurysm in the distalinnominate artery. Proximal control was in the prox-imal part of the innominate artery while distal controlwas in the proximal part of the carotid and subclavianarteries. The innominate artery was disrupted withintimal flap reaching almost to the origin of the carotidartery. After debridement a small rim just at the originof the right carotid artery enabeled the insertion of an8mm PTFE as an interposition graft. The procedurewas done without a temporary shunt. Sequentially, allthe fractures were managed by external fixation. Thepostoperative recovery, albeit long, was unremarkableand without severe complications. CTA was per-formed a week later and demonstrated preservedblood flow. On follow up 13 months later the patientis well.Case 2A 26-year-old male was injured in MVA. On admis-sion he was comatose and in shock. His blood pres-sure 80/50mmHg with heart rate of 130beats/min.No peripheral pulses could be found in the right armwith normally palpated axillary and brachial pulses inthe left. His injuries included subdural and subarach-noid hemorrhage without cerebral herniation, left

Pneumopericardium

A 27-year-old man was admitted to the hospital after a fall from approximately 10 m. He had multiple bone fractures, head trauma (Glasgow Coma Scale: 4/15), bilateral pulmonary contusions and pneumothoraces. We placed bilateral tube thoracostomies, and treated his other injuries. 1 day later, because of severe haemodynamic instability (hypotension and low cardiac output with high central venous pressure), we did transoesophageal echocardiography and found right ventricular compression in the absence of a pericardial effusion. Repeat chest radiographs (figure, left) showed the existing bilateral lung contusions and a new lucent outline of the heart (arrows). Computed tomography of the chest confirmed the diagnosis of post-traumatic pneumopericardium (figure, right, black arrow), bilateral pneumothoraces (white arrows) and lung contusion. The pneumopericardium resolved after we repositioned the left-sided interthoracic tube. A 27-year-old man was admitted to the hospital after a fall from approximately 10 m. He had multiple bone fractures, head trauma (Glasgow Coma Scale: 4/15), bilateral pulmonary contusions and pneumothoraces. We placed bilateral tube thoracostomies, and treated his other injuries. 1 day later, because of severe haemodynamic instability (hypotension and low cardiac output with high central venous pressure), we did transoesophageal echocardiography and found right ventricular compression in the absence of a pericardial effusion. Repeat chest radiographs (figure, left) showed the existing bilateral lung contusions and a new lucent outline of the heart (arrows). Computed tomography of the chest confirmed the diagnosis of post-traumatic pneumopericardium (figure, right, black arrow), bilateral pneumothoraces (white arrows) and lung contusion. The pneumopericardium resolved after we repositioned the left-sided interthoracic tube.

Acute tamponade after blunt chest trauma

We report a case of high-impact blunt chest trauma resulting in bilateral lung contusion and rupture of the right atrial appendage with subsequent hemopericardium leading to acute right heart failure. Although tamponade remains a clinical diagnosis, in this case CT findings confirmed the diagnosis, initially unsuspected, which led to successful therapeutic intervention. We believe that in patients with high-velocity trauma and possible blunt injury to the chest, a cardiac injury should always be searched for and excluded.

鈍的外傷による胸部仮性大動脈りゅうに対するｄｅｌａｙｅｄ ｒｅｐａｉｒの１例

Blunt aortic injury is a major cause of death from blunt trauma. A 50-year-old man was transferred to our emergency center because of a blunt aortic injury. On admission, chest X-ray showed mediastinal widening, multiple rib fractures, and left pleural effusion. Chest CT demonstrated a pseudoaneurysm of the aortic isthmus, mediastinal hematoma, bilateral lung contusions, fractured sternum and ribs, and left partial renal infarction. There were no signs of shock. Graft replacement of the descending thoracic aorta during left heart bypass with a centrifugal pump was performed 12 days after the injury. The intima of the injured aorta was disrupted, and a 7-cm tear in left pericardium was without cardiac luxation was discovered as an incidental finding and repaired directly. The patient's postoperative course was uneventful. We concluded that delayed repair of blunt thoracic aortic injury in trauma patients with multiple injuries is safe. Patients undergoing delayed repair require increased attention to antihypertensive therapy.

Laterality of air volume in the lungs long after blunt chest trauma.

To clarify a cause of the persistent decrease in lung capacity seen several years after blunt chest trauma, 17 patients with blunt chest trauma (10 with unilateral lung contusion, 7 with bilateral lung contusions; 11 of these with unilateral flail chest) inflicted 1 to 6 years previously and 10 normal volunteers (control) were studied. Lung air volumes (AV) were measured by spirometry (AVsp) and by computed tomographic (CT) scan (AVCT = AVCT.Rt+AVCT.Lt) under the same conditions. Hemithoracic spaces were also calculated by CT scan. The average AVsp in patients (76% +/- 8%) was lower than in the controls (98% +/- 5%). AVCT was consistent with AVsp in all the measurements. %AVCT.Rt and %AVCT.Lt, which were adjusted by the ratio of AVCT.Rt to AVCT.Lt in the controls, decreased significantly in unilateral contused lungs (71% +/- 8%). Fifty-eight percent of contused lungs showed small fibrous changes on the CT scans. The ratio of the hemithoracic space on the flail chest side to the opposite side was 0.95 +/- 0.05. These results suggest that the persistent decrease in AV long after blunt chest trauma might be caused by a constriction of contused lung resulting from fibrous changes.

Chest Injuries Sustained in Severe Traffic Accidents by Seatbelt Wearers

In Finland during the period 1972-1985, there occurred 3,468 severe traffic accidents in which one or more of the drivers or passengers sustained an injury leading to a fatal outcome within 30 days. Of the victims who had been wearing seatbelts, 207 had fatal and 73 had severe chest injuries. The four leading causes of fatalities resulting from chest injuries were ruptures of the aorta (37%), ruptures of the heart (28.4%), and bilateral lung contusions (31.1%) or lacerations (15.5%). Seatbelt wearers with heart ruptures more often had concomitant rib fractures, lung injuries, and sternum fractures than those who had sustained ruptures of the aorta. The side of rib fractures was associated with the victim's location in the car, drivers seated on the left having more right-sided and right front passengers more left-sided rib fractures. In addition to chest injuries, 87% of the victims had other concomitant injuries, the most common abdominal injuries being liver injuries (40.2%) and spleen ruptures (26.5%). In seatbelt wearers chest injuries with a fatal outcome appear to be caused by impacts of exceptional severity, since in more moderate accidents seatbelt wearing has proved to save lives.

Genesis of respiratory and circulatory changes in blast injury.

ArticleGenesis of Respiratory and Circulatory Changes in Blast InjuryCarl-Johan Clemedson, and H. PetterssonCarl-Johan ClemedsonFrom the Medical Division, Research Institute of National Defense, Sundbyberg, Sweden, and H. PetterssonFrom the Medical Division, Research Institute of National Defense, Sundbyberg, SwedenPublished Online:01 Aug 1953https://doi.org/10.1152/ajplegacy.1953.174.2.316MoreSectionsPDF (925 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByDiabetes exacerbates brain pathology following a focal blast brain injury: New role of a multimodal drug cerebrolysin and nanomedicineModeling trauma in rats: similarities to humans and potential pitfalls to consider5 September 2019 | Journal of Translational Medicine, Vol. 17, No. 1Introduction to Blast in the Context of Blast-Induced TBI30 July 2019Management of Blast Related Injuries25 October 2016Alveolar macrophage depletion increases the severity of acute inflammation following nonlethal unilateral lung contusion in miceJournal of Trauma and Acute Care Surgery, Vol. 76, No. 4Blast Wave Loading Pathways in Heterogeneous Material Systems–Experimental and Numerical Approaches9 May 2013 | Journal of Biomechanical Engineering, Vol. 135, No. 6Brain injury risk from primary blastJournal of Trauma and Acute Care Surgery, Vol. 73, No. 4Brain Injuries from Blast20 October 2011 | Annals of Biomedical Engineering, Vol. 40, No. 1Survival Risk Assessment for Primary Blast Exposures to the HeadJournal of Neurotrauma, Vol. 28, No. 11Blast Injury19 January 2011Bilateral Vagotomy Inhibits Apnea and Attenuates Other Physiological Responses After Blunt Chest TraumaJournal of Trauma: Injury, Infection & Critical Care, Vol. 64, No. 6THE EVOLUTION OF ISOLATED BILATERAL LUNG CONTUSION FROM BLUNT CHEST TRAUMA IN RATS: CELLULAR AND CYTOKINE RESPONSESShock, Vol. 24, No. 2Exposure to sublethal blast overpressure reduces the food intake and exercise performance of ratsToxicology, Vol. 121, No. 1Die nervöse Steuerung der AtmungBlast injury of the chestClinical Radiology, Vol. 20, No. 4ACUTE INJURIES TO THE LUNGDie nervöse Steuerung der AtmungErgebnisse der Physiologie Biologischen Chemie und Experimentellen Pharmakologie, Vol. 54, No. 1THE EFFECT OF HIGH EXPLOSIVE BLAST ON THE CEREBRAL VASCULAR PERMEABILITY1 March 1957 | APMIS, Vol. 40, No. 2The Electrocardiogram of Rabbits in Blast InjuryActa Physiologica Scandinavica, Vol. 33, No. 2-3 More from this issue > Volume 174Issue 2August 1953Pages 316-320 Copyright & PermissionsCopyright © 1953 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1953.174.2.316PubMed13080453History Received 8 March 1953 Published online 1 August 1953 Published in print 1 August 1953 Metrics