Intern 8901066 凌永耀

• Polytrauma – at least 2 injuries that involve at least 1 vital organ (e

g, lung or liver) – necessitate patient admission to a trauma intensive c

are unit

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 patient

s with chest trauma) – Neuroimaging studies may be difficult to perform – Treatment options are limited because concurrent injuries may preclude t

he use of treatments such as intravenous heparin and systemic thrombolysis

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

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 Treat

ment (TOAST) criteria – treatments– outcome

• Neuroimaging studies (When available)– arteriographic findings– Computed tomographic (CT)

• Outcome was determined using the Modified Rankin Scale (MRS)

Results

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

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.

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.

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

• 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 co

ntrol after the injury (14) • Because of a small posterior fossa subdural hematoma, his warfarin was disc

ontinued; • 18 days later he experienced a fatal stroke in the area of the left middle cereb

ral 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.

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.

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

Outcome

• Died of postischemic brain swelling: 4

• Mild disability (MRS 2): 4,

• Severe neurologic disability (MRS >3) : 5

• Good recovery (MRS 0): 1

Illustrative Cases

1) After 48 hrs, his ICP = 35mmHg

2) Decerebrate posture3) CT was performed

1) After 20 days, the patient was extubated and was able to follow commands2) 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.

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

Discussion and conclusion

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

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

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

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

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

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.

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

Thanks a Lot!!

• 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.