Date: Fri, 28 Dec 2001 14:23:51 -0700

From: William Wheeler, MD (AAST List)

Subject: Fat embolism and encephalopathy

Ladies & Gentlemen:

Dealing with the trauma we see here in rural Colorado, I rarely see some problems I dealt with too long ago in residency. 25 yo male snowmobiler hit a tree - fractured femur - 24 hours later with impressive diffuse encephalopathy. CT scan is normal, neuro exam is non-focal - he just is not awake and talking. O2 sats still 88% on 1-2 liters nasally. Orthopod plans on putting a plate on the fracture.

I am not anxious for the orthopod to proceed with surgery until we see how sick he is going to get, yet I don't want to heparinize him.

What else would you recommend.

Bill Wheeler, MD
Alamosa, CO

Reply at: Orthopaedic Trauma Association forum

From: William S Lyons MD (AAST List)

Date: Sat, 29 Dec 2001 14:54:12 -0500

I would agree on not proceeding with the surgery until the general condition is better understood. I assume the 88% is from an oximeter. Got a pO2 and chest x-ray?

Date: Sat, 29 Dec 2001 19:36:22 -0600

From: Adam Starr

Hi Dr. Wheeler,

The reason to push to stabilize the femur early is to avoid pulmonary complications. Who knows if it's the stabilization of the fracture or the mobilization of the patient that yields that benefit?

We did a retrospective review here (which included only patients with intracranial injury visible on CT scan - people who I felt had real, honest to God head injuries) and found that head injury complications (worsened GCS, increased ICP, new neuro deficits) were more associated with the severity of the initial head injury (judged by admit CGS and the Marshall head CT scoring system) than by the timing of femur fracture fixation.

So I felt like it was safe to go ahead and fix them - it didn't appear that early stabilization made the chance of a head injury complication any higher.

We also found that patients whose femur stabilization was delayed were more likely to develop pneumonia.

So, my bias is to fix them early.

BUT...our series was retrospective, small, and certainly subject to all the problems you see with any retrospective review.

The best review of this to date is probably the one done by Dunham, Mike Bosse, Bob Ostrum, Attila Poka and others. It was recently pubished in the Journal of Trauma - this year.

They looked critically at the available lit (and there were no class I studies for this question - it was all class 2 or 3) and felt that there was little data to support the idea that early stabilization of long bone fractures in patients with brain injury either worsened or improved outcome.

They said that each case should be individually managed according to how the patient is doing.

So you're on your own.

Since it's known that a "second hit" to the brain (in the form of hypoxia or hypotension) will make the brain outcome worse, I'd try my best to avoid that second hit.

If you've already passed the 24 hour mark, then you're not going to get him into the "early" category. The horse is already out of the barn on that one. If he's not oxygenating very well just sitting there in the ICU (88% isn't so hot in a young guy), I doubt if he'd improve his oxygenation if he was being operated on. Plate fixation in my hands involves more OR time and blood loss than IM nails. I'd be leery of doing the plate.

Now, if this guy has an isolated femur fracture and had a GCS of 15 when he hit the door, maybe you could say that his mental deterioration was caused by fat emboli - maybe he should've been fixed sooner.

But, now that his brain is showing signs of injury, and you've already bit the bullet on the 24 hour mark, and his lungs aren't doing so hot...I think I'd wait.

Good luck.

Adam Starr
Dallas, Texas

Date: Date: Sat, 29 Dec 2001 22:12:31 -0700

From: William Wheeler, MD (AAST List)

Thanks for the comments....

This poor guy got much worse overnite. GCS really down, started posturing. Got intubated and shipped to a neurosurgeon. Never had any significant hypoxia....sat's tend to run a little low here at 7600 feet.

Bill Wheeler

Date: Mon, 31 Dec 2001 12:32:35 -0700

From: Thomas Higgins


What about the argument that the unstabilized femur presents an ongoing insult? It's been pretty well shown that simply tranferring a patient or rolling them in bed with an unstabilized femur results in a transient shower.

Sick or not, do folks think that make sense to stabilize the skeleton to halt the continued insult? We realize that the operation (nail OR plate) we create a shower, but presumably this would halt the ongoing problem.

I was just interested in people's thoughts / feedback on this.

Date: Wed, 02 Jan 2002 07:16:19 -0600

From: Adam Starr


there's probably something to that argument. It makes sense, but I don't know of any study that really proves it - the idea that limiting the showering of emboli affects pulmonary problems.

We were talking about doing a trial down here with 3 arms - femurs fixed late, femur fixed early and mobilized, and femurs fixed early and kept in bed for a while.

My statistician told me I'd need around 1200 patients to do the study, so I chickened out.

But those transesophageal echoes look pretty awful with all that fat flying by - hard to believe that stuff does your lungs any good.

Adam Starr
Dallas, Texas

Date: Tue, 01 Jan 2002 07:27:35 -0500

From: Michael Cheatham MD

This appears to be a classic case of cerebral fat embolism with secondary pulmonary fat embolism. We wrote up a similar case (young male, MVC, femur fracture + tib-fib) several years ago and reviewed the world's literature (largely from Japan for some reason). Mental status changes typically occur within 12-48 hrs of traumatic injury with a normal Head CT. MRI, however, will show classic hypodense embolic lesions on the T2-weighted images. It seems to be most common in the young male, especially after tib-fib fractures. No intervention other than supportive therapy (i.e., alcohol, steroids, heparin, etc...) has been demonstrated to have any benefit. The Japanese experience was that if the patient does not develop severe neurologic deficits (as it appears this patient may have), the patient will typically recover after 5-6 weeks (as our patient did). They will commonly have some residual cognitive deficits however. We've encountered several other patients over the past few years who presented similarly, although not as classically as our initial case or this snowboarder.

We went through the same debate on the timing of nailing the femur. Our Ortho guys used a non-reamed nail and a tourniquet 48 hours after injury when we had identified the MRI findings and confirmed the etiology of the mental status changes. His pulmonary insufficiency did not worsen post-op.

My two cents? Get an MRI to document the lesions, let your Ortho team ORIF the femur as above (unless his neuro status is unstable; he may need an ICP monitor), and wait it out.


Michael L. Cheatham, MD, FACS, FCCM
Director, Surgical Intensive Care Units
Orlando Regional Medical Center
Orlando, Florida 32806

Date: Wed, 02 Jan 2002 13:39:04 +0000

From: b.meinhard

A paper was presented at the OTA 13 October 2000 by Greg. Zych at Jackson Memorial Hospital titled: Detection of Fat Embolism in Patients with Femoral Fractures.

He used Transcranial Doppler studies of the middle cerebral artery and Transesophageal Echo Cardiography to detect a patent foramen ovale. Initial TCD was + for fat emboli in 18. Femoral Fx stabilized with im rods in 22 fxs. Postoperative TCD was + in 14. No patient had fat emboli only after the femoral fracture. Of note was that 9 patients had a patent foramen ovale as detected by contrasted TCD. Six had pulmonary compromise. 5 with patent f.o. had neurologic changes. Initially 77% had cerebral fat emboli. Their results indicated that these emboli occurred soon after femoral fracture and are not necessarily produced by the fracture stabilization. Only three patients first developed the emboli intraoperatively. Both the pulmonary and neurologic changes were attributed to the fat emboli. He concluded that with 15% of the pop. having a patent f.o. that the major risk jof early fat embolism is a femoral fracture caused by blunt trauma. The prevalence of this entity could not be determined, in his study, since it was not possible to enroll every patient admitted with a femoral shaft fracture, but the rate of fat emboli in this group was surprisingly high.

..FOOD FOR THOUGHT concerning the previous discussions of hypoxemia and neurologic deterioration of a patient with a fracture of the femur.


Bruce Meinhard
Nassau County Medical Ctr.

Date: Wed, 02 Jan 2002 18:08:03 -0500

From: carl hauser

I expect that you meant "He used Transcranial Doppler studies of the middle cerebral artery and Transesophageal Echo Cardiography to detect fat embolism through a patent foramen ovale" during fracture surgery.

TEE has previously been used to show transit of material from a femur fracture fixation through the right heart and into the lung. So that's not new. But to get from the right heart to the MCA requires a R to L intracardiac shunt. Now, an "anatomic" PFO is present in about 25% of adults, but R to L shunts through such PFO's are actually pretty rare. This is because left atrial pressures normally exceed right atrial pressures. That closes the PFO "flap-valve" so that 99+% of patients with a PFO have a totally normal circulation.

Now you could hypothesize that trauma patients have increased pulmonary vascular resistance (they often do) that can open a 'latent' PFO and result in a R to L shunt. Still, it'd be pretty odd if 18/22 ostensibly normal patients with fractures all had L to R shunts through previously asymptomatic PFO's. After all, that's about 3-fold the total incidence of PFO found in the general population in large autopsy series, and then all of the patients would have to have pulmonary hypertension to boot.

So I think I'd be pretty cautions about interpreting this data. TCD's are cool toys that have failed to achieve wide acceptance (except by the people that own them) in the diagnosis of cerebrovascular diseases. Could it be that the specificity of TCD for cerebral fat embolism is not that good ?

Things that make you go "Hmmmmm..."


Date: Wed, 23 Jan 2002 14:11:40 -0500

From: William Obremsky

Several weeks ago members discussed fat embolism encephalopathy.

I want to see if anyone else has seen a patient similar to one I am seeing now.

30 yo healthy male restrained driver T-boned on driver side and sustained a Type 3A open left proximal femur fx, left chest contusions, closed left minmally displaced tibia fx and right closed ankle fx. He was stable at presentation and taken to OR for I&D of wound and antegrade IMN of femur w/o problems. The team decide to splint the other LE fxs that night.

Pt was stable and required NC oxygen only and was alert and oriented. I discussed w/ he and his family definite treatment of his other injuries and the SPRINT study. The next day he had ORIF of left ankle and unreamed IMN of left tibia w/o problems. The patient has never fully regained consciousness and is believed to have fat embolism encephalopathy and an MRI that is consistent w/ it. He does not have a cardiac ASD or VSD. He has never postured, and is beginning to follow simple commands, but has a long way to go. I have not found any other similar reports in the literature of a patient going from normal mentation to severe encephalopthy. Any other thoughts?

Bill Obremskey MD
Univ of North Carolina

From: Renae E. Stafford, MD

Date: Wed, 23 Jan 2002 14:23:09 -0600

Has anyone listened to this man's neck for bruits or done a carotid duplex? Any evidence of ischemia on head CT or MRI? Seat belt marks on the neck? Horner's syndrome? One of the diagnoses in the differential is blunt carotid dissection which may be associated with any of the previosly mentioned.


Date: Wed, 23 Jan 2002 22:31:29 +0100

From: Hans-Christoph Pape

I am not at all surprised. Note the various reports about opening of venoarterialshunts inside the lung. The key issue is the size of the particles.

If they are large, you will find an increase of pulmonary arterial pressure and even acute pulmonary failure (Pape, J. Orthop Trauma 10,6:429, 1996). If they are smaller, they may bypass the lung via these venoarterial shunt systems (Collard, 1974). Experimental studies compared substances that pass the lung (parafin oil) versus substances that are trapped inside the lung (Iodipine). Iodipine only killed the animals when administered in high dosages (1.5-2.5 g/kg bw, i.e. when the pulmonary vasculature is completely blocked), while parafin oil causes death in a small dosage via central mechanisms, (i.e. embolization to the brain (Kroenke, 1957). Halasz performed a dog study and found the same results. He injected fat i.v. and found a biphasic response: First, a pulmonary reaction occured, then the dogs developed tachycardia and cerebral embolization followed by death (Halasz Surgery 1957,41:921). Another interesting mechanism has been described by Kniseley: If you inject small glass beads into the pulmonary vessels, they are distributed in the entire lung, thus supporting the efficacy of intrapulmonary shunting (Kniseley, Am Heart J 54,4:483, 1957). Please let me know if you are interested to know more studies.

Obviously a number of these pathogenetic responses have been well known in the past (remember all those studies performed by Peltier et al. in the 1950ies). However, due to our improved perioperative care, the clinical sequelae may have been mimicked. We only see them in rare circumstances, but if we do, we are more surprised than the orthopaedic surgeons in the previous decades...

It is also interesting to know that the management of the long bone fractures continues to be the first on the list on malpractice claims (inappropriate fixation, malrotation, fat or pulmonary embolism) (AAOS Bulletin Vol. 49:1; 2000).

H.-C. Pape MD
Prof. of Orthopaedic and Trauma Surgery
Hannover Med. School
Hannover, Germany

Date: Wed, 23 Jan 2002 16:21:07 -0500

From: carl hauser, Department of Surgery, UMDNJ

There's insufficient data to understand the pathophysiology here. Was there a LOC at the scene? Was the BP always stable? Was there ever a base deficit? What did the admission CT of the head show? And no, these are not trick questions.

By the way, what is the MR appearance of the brain in fat embolism, and how can it be discriminated from the MR appearance of the brain in an trauma patient with fractures who is obtunded for other reasons?


Date: Wed, 23 Jan 2002 14:39:01 -0800 (PST)

From: Zsolt Balogh

Was the patient hemodynamically stable during his hospital course?

Any signs of supra-aortic vessel injury?

Zsolt Balogh, MD

Date: Wed, 23 Jan 2002 20:49:38 EST

From: TRToalJr

Several years ago, in Denver, I treated a 24 year old female paramedic for bilateral femur fractures after an MVA. She required extrication from her vehicle -- and arrived about 4 hours after the accident, and was initially oxygenating and mentating normally. After another 2 hours in the hospital, just before anesthesia, her O2 saturation dropped, and this was felt secondary to MSO4. Initial chest xray was felt to be normal. After successful bilateral reamed femoral nailing, she never regained consciousness. Brain function deteriorated to the point where life support was withdrawn at about 48 hours.

Autopsy revealed massive fat emboli in every tissue sampled: brain, lung, kidney... No cardiac septal defect identified. The pulmonary changes seem fairly obvious, but the encephalopathy without any ASD/VSD was never adequately explained.

Tom Toal, MD

Date: Thu, 24 Jan 2002 06:49:20 -0500

From: William Obremsky

Has anyone listened to this man's neck for bruits or done a carotid duplex? Any evidence of ischemia on head CT or MRI? Seat belt marks on the neck? Horner's syndrome? One of the diagnoses in the differential is blunt carotid dissection which may be associated with any of the previosly mentioned.

No evidence of cerebral vascular injury on CT or MRI..

Date: Fri, 25 Jan 2002 02:50:18 +0100

From: Josep M. Munoz Vives

Three years ago I saw a 18 yo male patient that sustained a multiple injury of his left lower limb (posterior column of the acetabulum, closed femoral fracture and closed tibial fracture)

He was neurologically intact at arrival. I obtained written consent for the surgery so he was mentally very alert. He was put in traction waiting for surgery. 12 hours post injury his girl friend called the nurse because she couldn't wake him up (GCS 6). He went to the ICU where he developed a severe ADRS that needed ventilation in 'prone' position with NO (still in traction). They didn't let me operate on him till 15 days later (nailing of long bones and plating posterior column).

Echocardiography: no evidence of Auricular or Ventricular communication.

MRI -> Diffuse encephalopaty, my colleagues couldn't decide if this was secondary to 'brain fat emboli' or to hypoxia.

After 2 month he was transfered from our hospital to a location for reeducation, at that moment he didn't speak, didn't recognize people, wasn't able to eat by himself.

Final result: He is not a bright mind but he is now able to speak normally, he walks, works and has a 'normal life'.

Josep Munoz-Vives
Orthopedic Surgery Dept.
Hospital Dr. Josep Trueta
Girona - Catalunya, Spain

Date: Fri, 25 Jan 2002 00:53:45 -0600

From: Gregory J Schmeling

I have three patients with FES encephalopathy. All three have MRI and CT findings consistent with multiple CNS embolisms. All three had normal carotids, no cardiac defects and no pulmonary findings. There are ten such cases in the old literature and a recent report in JOT ( I Think ) on two cases. All three of my cases had severe CNS depression but all three have recovered normal CNS function (< 45 days).

There are two mechanisms postulated for CNS FES without ARDS: mechanical and biochemical. The lung is only about 80% efficient as a filter and there are many small AV fistulas. The mechanical theory believes that the marrow elements pass through the lung and hit the brain. This can occur without any L/R cardiac shunts because of the lungs 80% filtering efficiency. The second theory is that the marrow elements breakdown into free fatty acids and these pass through the lung. They coalesce in the brain and block the blood flow. I am not sure it matters which theory you believe. The care in my three cases was supportive.

Gregory J Schmeling
MCW Orthopaedics

Date: Fri, 25 Jan 2002 08:04:20 -0700

From: Thomas A. DeCoster

I concur completely with Dr. Schmeling's description. I don't think it is all that uncommon.

Tom DeCoster