A 20 yrs-old male jockey fell during a horse-race and the following horse stepped off his neck . He referred to our ED 24 hrs. after the event. Physical examination revealed lateral neck ecchimosis with absence of left carotid pulse. There was no neurologic deficit. Angiography showed thrombosis with complete occlusion of the common, external, and internal left carotid arteries. No ischaemic area in the brain was detected by CT-scan. Due to the cephalad extension of the internal carotid occlusion no surgical procedure was undertaken and the patient is currently treated with subcutaneous heparine. Is this enough? Any suggestion?

Massimo Chiarugi, M.D., F.A.C.S.

Caro Massimo,

My Italian is very bad, but I would explore that neck, because the possibilities of developing a aneurism with time are very high, it can be done with good outcome because his Willis poligon is working, I would think of a graft, since the Intima must be very injured.

Dr. Porfirio Lango
Trauma Surgeon
Hospital General Mazatlan
Mexico

Standard management of patients with blunt carotid artery trauma involves full anticoagulation. In the multitrauma environment this may not be possible and many lesser scenarios (such as sq heparin) have been used. However at this stage, if there are no contraindications, I would have fully anticoagulated the patient with warfarin(coumadin) for 6 months.

Ian Civil,
General, Vascular and Trauma Surgeon,
Director of Trauma Services,
Auckland Hospital, Auckland, NZ.

no idea whether it's enough. my question is more: is it too much ? what's the justification for proceeding to angiography, what's the evidence that heparin makes any difference to anything and just what are you trying to treat ?

I supposed the more damage I see being done by knowlegable academics trying to fix things that aren't broken, the more I'm inclined to do nothing about anything unless the patient has a definite symptom.

Chris Taylor

Chris Taylor ask whether anticoagulation for carotid occlusion is more than the patient needs because the jockey is asymptomatic. My question is why wait for a stroke? If you understand that propagation of thrombus above the level of collateralization is the mechanism by which traumatic occlusions cause symptoms (devastating symptoms) you would be terrorized at the thought of not anticoagulating an acute carotid occlusion. If a well informed patient decided he didn't want any treatment, I could live with that (but think its foolish).

The role of surgery for this condition is controversial. I am trying to defend a surgeon being sued for doing absolutely the right thing for an MVA victim who stroked from carotid occlusion.

Remember that the management of carotid disease is one of the (not the only) purely prophylactic surgical (or medical) treatments we do. Until you find a good way to treat a CVA, preventing one is the biggest favor you can do for a patient. That is: anti coagulate or operate anybody whose risk for stroke is higher than the risk associated with your treatment. Acute blunt traumatic occlusion counts. (I don't know if sub Q heparin is as good as full dose heparin for disease and would bet it's never been studied)

J. Aucar, M.D.

Chris, There are many asymptomatic diseases, involving all organ systems, that are asymptomatic yet morbid/mortal if left untreated. If we let patient symptoms alone dictate treatment, we'd all be both wasting our training and malpracticing.

The question that was actually being asked was "what is the natural history of such an injury?" Without knowledge of natural history of untreated asymptomatic disease, there can be no effective treatment.

Your approach may be the correct one, yet may be oversimplified.

Regards,

I would go one step further: "... can be no effective treatment. And treatment is contraindicated unless it is proven to be effective."

giving heparin in the described case is IMO the moderist equivalent of applying leeches.

... Case of a young girl, who presented neurologically and hemodynamically stable after an MVA. She was admitted to the floor and proceded to develop aphasia, obtundation and a dense right hemiplegia agter about 12 to 18 hours, due to an occluded internal carotid. This scenario is describe as case and as series. This illustrates that not knowing the natural history of a disease is an indication to read.

The mechanism is by propagation of thrombus distally from the point of occlusion. If this propogates into the circle of willis in a patient that has no contraindication to anticoagulation, the next step to take is probably to call your lawyer.

Thrombolytics would have to be considered experimental in cases like this and should only be considered on protocol.

JAA

I agree with everything that's been said, but I'm still short of the answer: where is the objective evidence that heparinization for asymptomatic internal carotid occlusion after trauma is better than doing nothing ?

I'm happy with the reference of just 1 good study that deals with the specific issue.

No references, just a case.

A few months ago, a patient was seen in the ED after a MVC. She was unconscious for about 5 minutes, and was admitted for observation. Two hours later, she became hemiplegic; CTscan was normal, the patient recovered after 90 minutes. She was admitted to the neurology department. Only recently, I found out that a bilateral carotid artery stenosis and a left vertebral artery occlusion was found. No surgeon was consulted, the patient was put on low dose aspirin, and sent home. No neurologic symptoms occured later.

Was this a dangerous thing to do? Your comments, please.

Jan J. De Waele
Surgical Resident
University Hospital Ghent
Belgium

It would be nice if the world would all fit into prospective, double blind, randomized clinical trials, but it doesn't. Some clinical questions are difficult or impossible to study in that manner. Soetimes even case comparisons are not practical, particularly with relatively rare conditions. So we have to resort to extrapolation of principles derived from other clinical scenarios. It is imperative, of course, if we wish to call it science, that the principles be placed in the context of a scientific theory, whose objects are derived from observations. So, while I do not have a reference for you, I'll ask you consider this:

We know from the studies on deep venous thrombosis, that intravascular clots begin at foci of injuries and propagate proximally and distally to the nearest point of increased flow. For example clots often (but not always stop where the saphenous enters the femoral vein). Anticoagulation can reduce the extent of propagation of clot, even in the presence of stagnat flow. When clots mature they adhere and become less likely to propagate or embolize. (Anticoagulation decreases the incidence of PE after DVT from 40% to about 4% by RCT). The same principles are commonly accepted (I know that this is a soft epistomological criterion) to apply to the peripheral arterial system, from the study of lower extremity arterial thrombotic and embolic disease; also to mural cardiac thrombi (we anticoagulate those); and to coronary arterial thrombosis (we anticoagulate those). There is histologic evidence on autopsy studies that thrombus formation and propagation is an important mechanism in myocardial infarction.

So why should we assume that the cerebral circulation follows a different set of "rules". I would, in fact, ask you establish that by studies before refuting the extrapolations that I have suggested. I am pretty sure that a review of blunt carotid injuries will show a general concensus that full anticoagulation is the accepted treatment of choice.

I grant that this is based somwhat on assumptions and would like to see comparative data, but it would be tough to get. Untill then, just remember that it is the patient that takes all the risks.

JAA

I agree. Probably had a flap/dissection of the CCA. If there is no pseudoaneurysm or extravasation of contrast, I would do nothing except anticoagulation. I would probably put him on systemic anticoagulaton for three months.

I think his jockey days should be over.

WBS

I have discussed this case with our vascular radiologists who I was working with today. They believe that this patient would benefit from Urokinase infusion. I agree with others that he probably should sttay away from large ungulate mammals proceding at high speeds, but will defer to my friend Dr. Pauline wong on that matter.

Stephen M. Stowe, M.D.

Based on what you say, I would think your vascular radiologists are not looking at the case appropriately. I think UK would be nuts.

WBS

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William B. Schroder MD FACS
Chief, Section of Vascular Surgery
UMKC School of Medicine

Stephen M. Stowe, M.D.