- 3/5/2020:
o 37-year-old brought into ED around noon after head-on collision with cement truck; her car lost its roof and she had been pinned to the dash with brief LOC (per off-duty nurse at scene of crash) and altered mental status.
o CTs of head and spine all read as negative; dx with open right ulna/radius fracture and clavicle fracture.
o Admitted to trauma service
o Taken to OR for I&D and ORIF of forearm
o Started on 72 h of IV abx per open fracture protocol
- 3/6/2020:
o Pt eager for discharge; ortho said OK to f/u on clavicle fx as outpatient
o Pt complaining of blurred vision and floaters in both eyes at least as early as 10 am – trauma surgeon notified and ordered ophthalmology consult
- 3/7/2020:
o Trauma surgeon re-requested ophthalmology consult b/c it hadn’t happened yet
o Ophthalmologist sees pt and orders prednisone and cyclopentolate drops – no consult note so reasons unclear
o Patient starts vomiting around 11 am – given Zofran PO and IV, then Phenergan but keeps vomiting periodically.
o APRN for trauma surgeon notified by nurse re: “increase in symptoms of head and vomiting” at 12:30. Nurse spoke with APRN again at 13:30 re: continued nausea and vomiting.
o Patient complains of headache possibly as early as 12:30 pm; definitely by 11:30 pm
- 3/8/2020:
o Patient still vomiting in morning
o Around noon, pt begins to convulse with family in room; nurse called and witnesses another seizure – GCS score 7 afterwards
o Pt taken for CT head and has another seizure on the way. CT shows new moderately abundant acute SAH in basal cisterns
o CTA head/neck done and shows no sign of aneurysm; shows long segment left vertebral artery dissection
o Pt taken from CT suite to ICU, started on Keppra and Vimpat. Intubated for airway protection.
o MRI brain also shows “unusual” finding of brainstem edema (per neurosurgeon) but no sign of ischemia.
o Interventional neuroradiologist took pt to IR suite for cerebral angio – dx “multiple nonflow limiting small dissections of the bilateral cervical vertebral arteries and the distal cervical left internal carotid artery”; did not find any etiology for SAH. No interventions done.
o Neurologist adds atorvastatin and aspirin to try to prevent thromboembolism from dissections
o Neurosurgeon consulted – did not think he could help.
- 3/9/2020:
o CT head shows stable hemorrhage.
o EEG negative for seizures; Vimpat stopped over concern for low BP.
o Mental status improved by afternoon; following commands.
- 3/10/2020:
o Pt extubated, then had another 2 witnessed seizures. Vimpat restarted, then Keppra increased.
o Pt following complex commands in am, simple commands in pm. GCS score 14-15.
- 3/11/2020:
o In am, pt following some commands and tries to say her name when asked.
o Failed swallow study; NGT placed.
o Fairly stable throughout day.
- 3/12/2020:
o By noon, no longer following commands; GCS score down to 13.
o “Significant” change in mental status just before midnight – GCS score now 6-7.
- 3/13/2020:
o Pt reintubated for airway protection around 2 am.
o CT head showed SAH slightly improved.
o Noted to have possible decerebrate posturing around 4:30 am; neurologist noted decorticate posturing at 9:30 am.
o MRI/MRA brain, neck, and circle of Willis around 12:30 pm. MRI brain showed “extensive multilobar early ischemic change with gyral swelling. Very nominal mass effect on the left quadrigeminal cistern” and MRA neck showed “complete disruption of the left ICA territory including right A2 division.” Radiologist said “based on imaging, the left carotid has completely occluded with cross fill occlusion of the contralateral right A2 vessels through anterior communicating artery pathway.”
o Trauma note following day describes her as having had a “devastating left MCA stroke as well as complete L ICA distribution occlusion.” Another doctor says it was “acute left MCA distribution hemispheric CVA” – this appears to have been attributed to severe vasospasm.
o Interventional neuroradiologist does another cerebral angiogram; this time he also infuses nicardipine into right ICA and left vertebral artery for vasospasm (left ICA and branches not treated for fear of reperfusion hemorrhage), and does bilateral ICA, MCA, and basilar artery angioplasty. Notes that the “previously seen small dissection of the distal cervical left ICA is not identified in this exam.”
- 3/14/2020:
o CT head just after midnight shows cerebral edema with uncal and transtentorial herniation. Also shows interval development of bilateral diffuse subarachnoid hemorrhage and loss of the left cerebral hemisphere gray-white differentiation.
o Clinical exam w/ no reflexes
o Patient is declared braindead that afternoon.
Files:
Q: Was there evidence of facial/head/neck trauma at initial presentation? Was there a CTA neck at initial workup in addition to the CT head/neck?
A: EMS reported that an off-duty nurse had said patient was unconscious immediately after the accident, and the patient was confused and repetitive in the ED. But she did not have visible signs of head trauma. No CTA neck done with initial workup.
Q: Prior to development of her neurologic symptoms, was the patient only kept in the hospital for the IV antibiotics? The note says "patient eager for discharge." Does that imply she was suitable to go home with outpatient ortho follow up?
A: Appears she was kept only for IV abx and pending the ophthalmology consult once ordered. Ortho note 3/6 said OK to discharge after IV abx and f/u for clavicle as OP. Trauma surgeon had started her discharge summary on 3/8 before the seizures.
Q: Did they patient receive anticoagulation or anti platelet agents during her course?
A: On prophylactic Lovenox 3/6 to 3/8. After SAH was diagnosed 3/8, switched to aspirin. Lovenox restarted 3/12 and Heparin given w/ angiography 3/8 and 3/13.
Do you believe there might have been medical error?
The CTA neck obtained after the neurologic symptoms demonstrated a Left vertebral artery dissection. Had the patient undergone a CTA neck at initial workup, this may have been identified and she may have been treated (eg with aspirin) to mitigate the risk of a CVA from the dissection. However, if there was no strong indication for a CTA neck in the first place (eg evidence facial trauma), standard of care doesn't suggest getting a CTA neck on all trauma patients. The presence/absence of error hinges on this. The presence of blurred vision may have been a sign of neurologic injury but if it was bilateral, I would be less suspicious. The onset of nausea/vomiting would make me suspicious, but narcotic medication and antibiotics may provoke that as well. In a patient who had a CT head without obvious injury, and one who was clinically well enough to go home, one would require a very high degree of suspicion to jump to a intracranial cause of non focal signs like that. Furthermore, the fact that the neuroradiologist could not identify a source of the SAH makes it difficult to draw the link between a missed diagnosis of dissection and her outcome. Her subsequent devastating stroke seems related to vasospasm based on this reading.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
As above, it seems the outcome follows from the Left vertebral dissection, but the failure to diagnose the dissection at admission is not an error UNLESS there were clear indications to order a CTA neck
What makes you a good expert for this case?
I am a trauma surgeon who practices surgical critical care as well. I have treated numerous patients with blunt cerebrovascular injury like this one. These are challenging injuries - young patients without comorbidities can windup with neurologic deficits even despite anticoagulation or anti platelet therapy.
How often do you encounter cases similar to this one in your practice?
Patients with blunt cerebrovascular injury: 1-2 monthly Patients with devastating sequelae of BCVI: 1-2 yearly
Do you believe there might have been medical error?
When there is a change in mental status in a victim of blunt trauma (especially one where there was loss f consciousness) and there is a normal CT head and neck, a CT angio of the neck should be done to rule out blunt cerebral vascular injury. BCVI are difficult to diagnose until there is a catastrophic and often permanent change in neuro exam. I realize that cerebral vascular imaging was done, but it could be argued that it should have been done as soon as the patient exhibited symptoms consistent with a neurologic compromise such as pain and vomiting. The long segment vertebral artery dissection could have been identified on post trauma day one should have been treated with ASA or heparin (the outcomes are the same per the available data). That may have prevented the subsequent neurologic compromise
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
the lack of timely cerebral vascular imaging after neurologic symptoms developed resulted in the delay of ASA dosing and this delay may have caused the poor outcome
What makes you a good expert for this case?
I have 13 years of experience in a busy level one trauma center and I am board certified in general surgery and surgical critical care.
How often do you encounter cases similar to this one in your practice?
we care for blunt cerebral vascular injury or patients with the potential of BCVI several times per week
Do you believe there might have been medical error?
Suspicion of blunt cerebrovascular injury (BCVI) is mostly based on injury pattern to the head, face and neck. With a negative initial CT head and neck there would be a low suspicion for an injury. The vision changes, headache and nausea individually would not be specific for BCVI, but given new onset and persistent, a repeat CT head would be reasonable...but again, given an initial negative CT in a young patient with stable GCS and not on any blood thinners, index of suspicion for interval development of a head injury would have been low.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
Had the vertebral artery dissection been picked up earlier, I am assuming there would have been an intervention from neuro IR. She would have also been started on seizure prophylaxis earlier if the SAH had been picked up earlier as well and may not have had a clinical seizure.
What makes you a good expert for this case?
I have been a Trauma surgeon from 9 years, all spent at Level 1 Trauma Centers.
How often do you encounter cases similar to this one in your practice?
This is in general a rare occurrence.
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