1. Intern 8901066 凌永耀

2. Polytrauma –at least 2 injuries that involve at least 1 vital organ (eg, lung or liver) –necessitate patient admission to a trauma intensive care unit

3. Introduction Trauma  stroke or Stroke  Trauma ?? Scant Data Putative Mechanisms –Craniocervical artery dissection –Shock –Cardiac injury to the ventricular wall and valves –Abnormalities of coagulation have been suggested Difficult to recognize stroke symptoms –Altered state of consciousness –Sedative and neuromuscular blocking drugs (control ventilation in patients with chest trauma) –Neuroimaging studies may be difficult to perform –Treatment options are limited because concurrent injuries may preclude the use of treatments such as intravenous heparin and systemic thrombolysis

4. Patients and Methods -1 Retrospectively reviewed January 1, 1985, and December 31, 2001, with diagnoses of stroke and trauma Not considered: stroke  trauma –the trauma was mild or caused only a single injury –the injuries were possibly a result of a stroke –patients with severe closed head injury were not considered to avoid confusion between the diagnoses of cerebral infarction and contusions

5. Patients and Methods-2 Demographics, Descriptions of the nature of the trauma, Types of simultaneous injuries, The Glasgow Coma Scale (GCS) score and Revised Trauma Score Stroke characteristics –including the vascular territory involved, –timing, –presumed mechanism according to the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria –treatments –outcome Neuroimaging studies (When available) –arteriographic findings –Computed tomographic (CT) Outcome was determined using the Modified Rankin Scale (MRS)

6. Results

8. Patients The 14 patients –8 women and 6 men –21 to 86 years (median, 40 years). All in motor vehicle crashes, –13 involving cars and –1 involving a snowmobile 12 drivers –4 seat belt restrained –2 were unrestrained –6 unknown

9. Nature of trauma and injuries 13 fractures –6 long bone fractures, –7 rib fractures, –5 skull or facial fractures –3 had spinal injuries. 9 cardiothoracic injury, –pneumothorax –pulmonary and cardiac contusions –a ruptured diaphragm –a transection of the aorta. 4 traumatic splenic or hepatic lacerations.

10. GCS/ RTS scores GCS: ranged from 3 to 15. –4 GCS score of 8 or less. The Revised Trauma Score: ranged from 6 to 12.

12. Nature and mechanism of stroke 13 ischemic stroke: –10 anterior circulation, 4 with bilateral involvement –2 posterior circulation Both with bilateral involvement –1 both circulations 7 of 13 craniocervical artery dissection (followed by distal embolism in 6 ) –5 carotid arteries 1 with bilateral carotid dissections, hypoperfusion could be implicated –2 vertebrobasilar arteries

13. 4 of 13 cardioembolic strokes (7, 9, 11, 14) –2 direct cardiac injury (young and had no risk factors for cardiac disease) Echo: regional ventricular wall motion abnormalities –hemopericardium (9) –a ruptured left diaphragm and lacerated spleen (11) –1 new-onset atrial fibrillation after the trauma (7) –1 had a history of atrial fibrillation and experienced difficulty with rate control after the injury (14) Because of a small posterior fossa subdural hematoma, his warfarin was discontinued; 18 days later he experienced a fatal stroke in the area of the left middle cerebral artery. 1 of 13 Shock contributed to stroke (with a systolic blood pressure level of 40 mmHg); 1 of 13pontine hemorrhage –in the setting of treatment: resistant hypertension after the trauma.

14. Hospital Course The time of onset of stroke symptoms –arrival at the hospital to 23 days after the initial trauma In 6 (43%) of 14 patients: stroke symptoms began within 48 hours after the trauma –Only 1 patient had obvious focal signs at admission. In the 8 patients with a GCS score of 14 or 15 –no obvious signs of stroke at admission –his complication was not considered on initial evaluation.

15. Treatment Aspirin: 1 Intravenous heparin: 2 Antihypertensive medication: 1 Posterior fossa decompression: 1 (patient no. 4 with a cerebellar stroke) No specific stroke therapy: 9

16. Outcome Died of postischemic brain swelling: 4 Mild disability (MRS 2): 4, Severe neurologic disability (MRS >3) : 5 Good recovery (MRS 0): 1

17. Illustrative Cases

18. 1)After 48 hrs, his ICP = 35mmHg 2)Decerebrate posture 3)CT was performed 1) After 20 days, the patient was extubated and was able to follow commands 2) After 2 months of inpatient rehabilitation, he was discharged home. 3) After 2 years of follow-up, living independently at home with some residual right hemiataxia, mild cognitive impairment, and palatal myoclonus.

19. A seat belt–restrained driver of a car struck from behind by a truck 1)An unsuccessful attempt at anterior fusion and fixation of a C6 vertebral fracture 4 days after the trauma  difficult-to-control hypertension (180~200 mmHg) 2)At 21 days after the initial injury, the patient underwent surgery again for posterior fusion of the cervical spine, which was successful  BP <160mmHg walking with the assistance of a Zimmer frame

20. Discussion and conclusion

21. Stroke 11 poly-trauma with fractures –cervical artery dissection –cardiac injury –subsequent embolism –systemic hypotension 3 patients –discontinuation of anticoagulant medication –uncontrolled hypertension –atrial fibrillation Fat embolism was considered in all patients with fractures –no evidence petechial rash sudden pulmonary edema tachycardia

22. Facial fracture vs Craniocervical artery dissection 5 of the 7 patients with stroke –related to dissection had either skull or facial fractures –Trauma severe enough to cause such fractures likely leads to shearing and torsion stresses that damage craniocervical arteries GCS scores lower than 6 Diffuse axonal brain injury Petrous skull and LeFort II and III fractures  Some have recommended this technique as a screening test in high-risk patients  Besides noninvasive imaging techniques such as CT angiography and magnetic resonance angiography

23. Pontine hemorrhage Pontine hemorrhage (patient no 5) –Previously: use of anticoagulant or thrombolytic agents –In our patient: was probably due to hypertension related to pain; this cause of in-hospital pontine hemorrhage, to our knowledge, has not been reported previously. –Delayed posttraumatic primary brainstem hemorrhage was a consideration but unusual in this location rarely seen on CT without other contusions

24. CT of stroke Physician delay Hypodensity was already evident on CT in 9 patients, –stroke possibly had been present for as long as 12 hours The reasons for this delay –Sedation –Neuromuscular junction blockers to facilitate ventilation –The presence of a limb injury on the side of the paresis –Difficulties with transporting patients in unstable condition

25. Conclusion-1 Potential stroke risk –Polytrauma –Facial fractures Facial fractures might be markers of possible craniocervical artery dissection, the most common mechanism for stroke in our study. –Cardiac injury the second most common mechanism Limb fractures ipsilateral to paresis from stroke may be one factor in delayed recognition of stroke. Limited potential treatments( thrombolysis) –the late recognition of stroke –other injuries that might lead to hemorrhagic complications

26. Conclusion-2 Improved and earlier recognition of stroke might reduce secondary neurologic complications, such as –Massive cerebral edema –herniation This improvement may result from –more frequent neurologic consultations, –judicious use of sedation in patients with facial injury –serial CT scanning and arterial imaging in patients in whom stroke is suspected.

27. Polytrauma as an important cause of in-hospital stroke needs careful prospective assessment before outcome can be improved

28. Thanks a Lot!!

29. 14 patients with polytrauma –experienced a stroke (13 ischemic and 1 hemorrhagic). Craniocervical artery dissection was the most common mechanism (7 patients) –skull or facial fractures were a possible marker for this (5 of 7 patients). –Polytrauma with limb fracture on the side of the paresis (5 of 6 patients)  frequent delays in identifying stroke –Four patients died of postischemic brain swelling, and 5 had major neurologic impairment.