Traumatic Aortic Disruption (TAD)
Arch is mobile just distal to L subclavian
Can also tear major branches
Secondary to trauma, cpr, t-spine fx
Suspect if deceleration injury or side impact mva, fall >30 feet, steering column or wheel damage.
ChestCT-may give false positive c mediastinal hematoma, necessitates aortogram
Proximal Descending-most common
Ascending-80% have associated cardiac injuries
Manage c esmolol then nitroprusside
Can get spinal cord ischemia and atrial-aortic fistulas
If L hemothorax is seen or periaortic hematoma, strongly consider thoracic dissection/rupture (J Trauma 52 (4):699 2002)
Most recent review supporting helical CT (Emerg Med J 2004; 21:414-419)
Best study to date of CTA for aortic injury shock trauma (J Trauma. 1998 Nov;45(5):922-30)
Two recent papers expand our knowledge of blunt traumatic aortic injury from resusme
UK crash data identified risk factors for low impact blunt traumatic aortic rupture, or LIBTAR (crashes at relatively low speed): age >60, lateral impacts and being seated on the side that is struck are predictive of LIBTAR. This study should raise our index of suspicion of aortic injury in low-impact scenarios since low-impact collisions account for two thirds of fatal aortic injuries.
Low-impact scenarios may account for two-thirds of blunt traumatic aortic rupture Emerg Med J. 2010 May;27(5):341-4
Data from the Victorian State Trauma Registry showed pre-hospital mortality from traumatic thoracic aortic transection was approximately 88.0%, whereas patients who survive to reach hospital have a much lower hospital mortality (33.3%, and once patients who arrived in extremis were removed hospital mortality was reduced to 5.9%). Repair was performed in 46 patients, with 22 receiving initial endovascular repair and 24 receiving initial open repair. Mortality rates following surgery were 9.1% and 16.7%, respectively.
The majority of patients arriving at hospital (57.1%) had an ISS of over 40 highlighting that these patients are unlikely to have only one serious injury and are likely to be more seriously injured than the normal trauma population. An ISS greater than 40 was a main predictor of mortality before repair.
Aortic transection: demographics, treatment and outcomes in Victoria, Australia Emerg Med J. 2010 May;27(5):368-71
Radiographic Clues That Should Prompt Suspicion of a Thoracic Great Vessel Injury (Trauma 6th ed) Fractures Sternum Scapula Multiple left ribs Clavicle in multisystem injured patients (?) First rib Mediastinal Clues Obliteration of aortic knob contour (Fig. 29-3) Widening of the mediastinum >8 cm (Fig. 29-4) Depression of the left mainstem bronchus >140° from trachea Loss of perivertebral pleural stripe Calcium layering at aortic knob “Funny-looking” mediastinum Deviation of nasogastric tube in the esophagus (Fig. 29-5) Lateral displacement of the trachea Lateral Chest X-ray Anterior displacement of the trachea Loss of the aortic/pulmonary window Other Findings Apical pleural hematoma Massive left hemothorax Obvious blunt injury to the diaphragm
Best study (274 patients)
(Fabian T. J Trauma 1997; 42: 374-383)
Wide mediastinum 221 85% Indistinct aortic knob 63 24% Left pleural effusion 49 19% Apical cap 49 19% Tracheal deviation 32 12% NGT deviation 29 11% Bronchus deviation 12 5% Normal chest X-ray 19 7%
X-Ray (90-95% sensitive)
Increased mediastinal width >8 cm at knob
Opacification of space between aorta and pa
Deviation of NGT
Widened paratracheal stripe
Depression of L mainstem
L apical pleural cap
All chest x-ray findings are of mediastinal hematoma which is not the same thing as TAD. 10-20% of mediastinal hematomas will turn out to be TADs. Massive hemothorax is the only direct sign of TAD on C-XR.
Most recent study casts doubts on utility of supine chest film (J Trauma 2004;56:243)
Chest x ray did not show obvious mediastinal widening,but incidentally the space between intimal calcification andthe outer border of the aortic arch was >1 cm, a recognisedradiological sign of aortic dissection (fig 1). Awareness ofthis is crucial. Troponin was normal but D-dimer was raised.A computed tomography scan confirmed aortic dissection typeB, managed conservatively with intravenous labetolol and analgesia,with a good outcome. ( Gartland et al. 24 (4): 310 — Emergency Medicine Journal)
Helical CT in TAD
Author Total TAD Sensitivity NPV Fabian J Trauma 98 494 71 100% 100% Mirvis J Trauma 98 1,104 24 100% 100% Dyer J Trauma 02 1,338 30 100% 100%
Signs of TAD on Helical CT
Well visualized flap
false lumen with flow
obvious aortic disruption
abnormal vessel contours
question of flap on one cut
Most Recent J Trauma Study (Volume 56(2) February 2004 pp 243-250) One center states CT ready for prime time as sole diagnostic test
1. The initial resuscitation should not be aggressive. Keep the BP below 90/- 2. NONE should go to CT. Look at the chest x-ray, mechanism and PE, If you are suspicious of an injury from these screening tests. GO TO AORTOGRAM 3. If the mechanism is suggestive, but the Chest X-ray is NOT, then a CT to look for a mediastinal hematoma is indicated. FOR ANY PATIENT WHO YOU ARE GOING THROUGH ALL THESE EVALUATIONS, THEY SHOULD BE ON BETA BLOCKERS UNTIL DX IS RULED OUT OR OPERATION IS COMPLETED 4. Only ones to go straigtht to OR are those who are unstable. Stable patients should wait till daylight or up to 3 days acutely if they have extensive associated injury. 5. CT is a screening NOT DIAGNOSTIC aid. I know of NO case I have seen in the hospital, or those I have seen in consultation in the court room that the CT ALTERED ANYONES DECISION MAKING. I AM FAMILIAR WITH FAR TOO MANY CASES THAT THE CT AND TEE were misleading and led to spurious decision making. The ATLS does not address the urgency for operation. You will find that in the thoracic surgery and trauma literature.
It may be an acceptable strategy to stage the injury and then perform delayed repair with interim lowering of BP and HR.
Retrospective Study (J Trauma Jan 2004 56:1) use serial c-xrs to check silhouette
Shoot for MAP<70 with b-blockers and then nitrites
Pacini D, Angeli E, Fattori R, et al. Traumatic rupture of the thoracic
aorta: ten years of delayed management. J Thor Cardiovasc Surg 2005;
The cardiac surgeons of the Massachusetts General Hospital pioneered
the immediate medical and delayed surgical management of patients with
traumatic rupture of the thoracic aorta starting in 1971. Since their initial
report in 1981, several additional series have been published attesting not
only to the feasibility of such management but to the actually improved
outcomes it makes possible. This article from Bologna, Italy, adds to that
collection and contributes a new dimension: a series of patients treated not
only with delayed repair but with endovascular stenting rather than via open
thoracotomy. The charts of 69 patients with traumatic thoracic aortic rupture
seen over 23 years were reviewed. Twenty-one, seen between 1980 and 1993,
were managed with immediate operative repair. Four of these died, and 3
developed paraplegia. Beginning in 1993, patients were treated with initial
medical management, followed by delayed repair. Of these 48, 5 required
urgent repair, 3 via surgery and 2 via endovascular stent placement.
Indications for urgent repair were massive hemothorax and contrast
extravasation on CT, rapid enlargement of the pseudoaneurysm, and
pseudocoarctation. The remaining 43 had delayed repair, 13 with an
endovascular stent and 30 via open surgery. Only 2 of these patients died,
and only 1 developed paraplegia. All 15 stent placements were successful and
uncomplicated. This is real progress and is certainly the direction of
J Trauma Volume 66(4), April 2009, pp 967-973-Delayed repair of stable blunt TAI is associated with improved survival, irrespective of the presence or not of major associated injuries. However, delayed repair is associated with a longer length of ICU stay and in the group of patients with no major associated injuries a significantly higher complication rate.
Patients who need to be transferred to other facilities for definitive repair Severe head injury Severe pulmonary injury Haemodynamically unstable patients Patients who have undergone damage control procedures Patients with coagulopathy, hypothermia & acidosis Patients with severe medical co-morbidities Patients with burns or severe sepsis.
(2) decrease of the rate of the arterial pulse increase (dP/dt) to diminish shearing forces.
The use of beta-adrenergic blockers (β-blockers) is the cornerstone of aortic dissection management. Because nitroprusside increases the heart rate and may also increase the dP/dt, a β-blocker must be started before or in conjunction with sodium nitroprusside to lower the dP/dt. Esmolol is an ultrashort-acting β-blocker that is easily titrated. After mixing 5 g in 500 ml D5W, an initial bolus of 500 μg/kg is given, followed by an infusion of 50 to 200 μg/kg/min. Labetalol has both α-blocking and β-blocking activity and can be used as monotherapy. A suggested dose is an initial 20 mg IV bolus every 5 to 10 minutes, incrementally increased to 80 mg until a target heart rate has been reached or a total of 300 mg is given. A maintenance dose of labetalol is then given at 1 to 2 mg/hr. A target heart rate should be between 60 and 80 beats/min. If a patient is normotensive, a β-blocker should still be used to lower the dP/dt.
Trimethaphan is mixed as a solution of 500 mg in 500 ml D5W and is infused at a rate of 1 to 2 mg/min. Trimethaphan is a ganglionic blocker that reduces both arterial pressure and its rate of increase, thus not requiring the use of concomitant β-blockade. It is more difficult, however, to titrate trimethaphan than to titrate nitroprusside, and tachyphylaxis frequently occurs after 24 to 48 hours. Additionally, the frequency and severity of side effects (e.g., respiratory depression, nausea, urinary retention) limit the use of trimethaphan.
I guess this myth persists still, Karim–in fact ANY patient can get a pretty near-to-uprite film if we want one regardless of their potential injuries or status. You do not have to sit the patient up , that is, bend at the waist , to do this–it is quite easy to put the stretcher in reverse Trendelenberg position, putting the body fairly uprite while keeping the body straight in alignment and shooting the film perpendicular to the body axis–we do this often, there are papers written on it from years back showing its value–we seem to continually forget.
Joseph Ayella, the original trauma radiologist at Maryland Shock Trauma, described this technique. The xray beam must be about ten degrees toward the feet to obtain a “pseudoupright” film. If the patient is completely upright, then you must increase the angle of the xray source. However, you must get the patient somewhat upright so that the xray source can be directed horizontally in stead of the vertical position for a supine film. The value of this technique is that it allows the technologist to increase the film/xray source distance to 72 inches which reduces magnification. The angle allows a proper projection of the mediastinum. The xray source can only go vertically about 40 inches. However, lest i be seen as a die hard advocate of this technique, I would not do it in an unconscious patient or in situations of possible spine instability. Not worth the risk and those patients all have to go to CT anyway, So we can get a better idea of mediastinal width, hemorrhage etc from the CT
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