Spinal (con)Fusion goes International!

Last month I travelled with my colleague and Physician Assistant Jack Bagley to Nepal where I was privileged to be a faculty member for the NZAUSA 2018 Conference on Spinal Deformity.  Several months prior I was introduced to Dr. Chet Sutterlin, a renowned orthopedic spine surgeon who runs a small non-profit called Spinal Health International (SHI).   Through SHI, Chet educates surgeons from developing countries on modern techniques in spinal surgery and NZAUSA 2018 was the most recent iteration of his educational efforts (NZAUSA stands for Nepal, New Zealand, Australia and USA where members of the faculty were from.)   As fellow climbers Chet and I were trading mountaineering stories when he mentioned his course in Nepal.  He’d barely gotten the invitation out of his mouth before I’d accepted! 

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Rather than just performing surgeries in-country via the traditional medical mission model, SHI is unique in its goal of educating the local surgeons so that they can become self-sufficient and build robust surgical programs at home.  It’s the old “teach a man how to fish…” idea.   I hesitate to use the word “educate”, though, because it implies some sort of knowledge gap between the Western surgeons and their Nepali counterparts.  In fact, I quickly learned that these surgeons are quite knowledgeable and skilled and that their only limitations stem from a lack of access to the technological resources we have in the U.S.    

I’ve never participated in an international medical education conference before and I approached my lectures as I would for a meeting back stateside.  Here I was, prepared to talk about advanced minimally-invasive (MIS) techniques such as Lateral ALIF (LALIF) or some of the innovative single-position lateral surgery we’re doing.  Man were these Nepali surgeons gonna be impressed!   As we moved through the Q&A sessions after the first few lectures, though, it was evident that these surgeons weren’t going to find my lectures applicable to their own practices at all!  This was a tremendous oversight on my part, as I didn’t really take the time to understand my audience.  Sure, these surgeons are well-trained, very knowledgable and appreciate the benefits of minimally-invasive single-position surgery in theory. The problem is that they can’t even get the basic retractors used to perform the techniques.  To think they’d be able to replicate these techniques, which are so technology-dependent (and thus very expensive), with the limited resources in Nepal was quite obtuse of me.  In the end I was able to tweak the messaging in my talks to focus more on the general themes rather than the technical nuances of these procedures and I think the talks were well received.  I could definitely tell that the Nepali surgeons are eager to learn more about MIS techniques so that they can start using these techniques in their own practices.  Maybe I’ll be invited back to Nepal for future courses!

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Dr. Thomas presents a lecture to Nepali surgeons on spinopelvic parameters at NZAUSA 2018.

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Jack Bagley, PA-C receives a traditional Nepali hat and scarf as a gift for participating as faculty in NZAUSA 2018. 

Ultimately I was left truly humbled by what the Nepali surgeons are able to accomplish with such limited resources and technology.  They’re routinely tackling complicated pathology such as Pott’s Disease (spinal manifestation of tuberculosis which is rampant in Nepal) and severe spinal deformity using very basic spinal instrumentation.  I was particularly humbled when I was asked to scrub in to a case of a severe thoracic spinal fracture.  I’m supposed to be the “expert” in the room but I looked like a fish out of water performing an open spinal procedure without even a fluoroscope to help place pedicle screws!  I was thoroughly impressed with my Nepali counterpart Dr. Bigyan Bhandari’s skill in navigating this complicated case with his assistant of questionable skill (yours truly) at his side.  Now that I’m back home doing cases in the US, with my advanced instrumentation, image guidance and neuromonitoring technology, I feel like I’m cheating!  Maybe it’s a good thing I’m a surgeon here and not in Nepal!

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Image on left shows severe T12/L1 fracture/dislocation in a young male who was left paralyzed after a motor vehicle collision.  Image on right shows Dr. Thomas and Dr. Bhandari performing an open reduction of the spinal fracture. The accident occurred in a remote part of western Nepal and it took the patient 2 days to get to Kathmandu. 

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The entrance to Grande International Hospital which celebrated its 5th anniversary this year.  This is a very modern private hospital with all of the facilities you’d see in a hospital in the U.S.  The image on the right is a view of Kathmandu taken from the helipad on the roof of Grande.  

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We did get out for some sightseeing!  Image on left is Jack Bagley looking down at Everest base camp on the helicopter flight out of the Khumbu Valley.  Image on right is me standing at Gorak Shep with Pumori in the background.  Mt. Everest would be to my left.  We’re at over 18k feet here and while it may not look like it I feel like I’m about to lose consciousness!

Thanks for reading!

J. Alex Thomas, M.D.

What is a Spondylolisthesis?

At this point in our discussion of lumbar pathology we come to one very important topic: spondylolisthesis of the lumbar spine.  First described in the mid-1800s, spondylolisthesis literally means slipping bones.  In this painful condition there is forward slippage of one vertebral body over the body below.  If you want to get academic about it, the severity of this slippage is classified according to the Meyerding Scale:  

  • Grade I: <25% slip
  • Grade II: 25-50% slip
  • Grade III: 50-75% slip
  • Grade IV: 75-100% slip
  • Grade V: >100% slip (the vertebral body above is floating freely in front of the body below.) 

Some patients obsess about grading schemes like these but they’re really not that important for a typical patient with spondylolisthesis.  Grade I is by far the most common grade and if you’ve been told you have a spondylolisthesis this is probably what you have.  I will occasionally operate on a grade II and I can count on one hand the number of times I’ve operated on a grade III.  The higher grades really aren’t seen in adult patients.  They usually require a congenital defect in the bony anatomy of the spine and thus usually are already symptomatic in childhood (which is why, since I’m not a pediatric neurosurgeon, I don’t see these cases.)   A patient with spondylolisthesis may first present with only non-specific back pain.  As the patient ages and their spine degenerates the spondylolisthesis may become unstable and start to progress.  The slip eventually becomes severe enough that the patient develops back and leg pain and they come to see me.  This is the condition for which I most commonly book lumbar fusion procedures.  See figure 1. 

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Figure 1: Sagittal MRI showing the forward slip of L4 on L5 in a typical spondylolisthesis.  The image on the right is a schematic of the same process (source: SpinePro III for iPad)

Spondylolisthesis is commonly asymptomatic (radiographic studies on normal volunteers tell us that nearly 10% of us are walking around with this condition yet have no pain.)  In my clinic, though, patients with spondylolisthesis have progressed to the point where they now have pain.  Patients with spondylolisthesis typically present with a combination of two types of pain: mechanical back pain from stress on the facet joints as well leg pain from compression of nerves.  As one vertebral body slips forward over the one below, this puts a tremendous amount of stress on the facet joints at the back of the spine (imagine how your knee would feel if was repeatedly bent outside of its normal range of motion.)  As they struggle to maintain the structural integrity of the spine they get stressed, become inflamed and arthritic and thus cause the back pain associated with spondylolisthesis.  Also, as the vertebral body slips forward, the nerves within are guillotined causing severe pain, numbness, tingling and even weakness.  The condition is especially debilitating because both nerves at the level of the slip can be compressed and injured.  First, there is compression of the exiting nerve because of foraminal stenosis caused by the slip and resultant foraminal height loss.  The traversing nerve (the nerve still within the spinal canal that will exit at the foramen below) also gets crushed in the lateral recess underneath the severely degenerated facet joint as one part of the joint slides forward in relation to the other (see figure 2).   For example a slip at L4/5 can cause compression of both the exiting L4 nerve and the traversing L5 nerve.  Both the back pain and leg pain associated with spondylolisthesis get worse as the patient stands up for even a short period of time.  When the patient is upright this loads the spine, aggravates the slippage and thus causes worsening pain. 

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Figure 2: On the left is a sagittal MRI showing severe foraminal stenosis associated with a spondylolisthesis at L4/5 (red arrow); contrast this with a normal foramen at the level above (green arrow).  On the right is an axial MRI of the same patient.  Note the severe lateral recess stenosis crushing the traversing nerve below the facet joint (red arrow).  Also seen is severe facet arthropathy (blue arrow) as indicated by a displaced joint and fluid within the joint.

There are several types of spondylolisthesis described in the textbooks.   The two most common types by far are degenerative spondylolisthesis (DS) and isthmic spondylolisthesis (IS).  DS, the most common form, occurs, as the name would suggest, as the spine degenerates over time.  As the intervertebral disc degenerates it no longer can properly absorb motion.  The facet joint tries to take up the slack but eventually, after enough time as a defacto shock absorber, becomes arthritic and incompetent (the same thing my wife says is happening to me.)  This incompetent facet joint can no longer maintain the structural integrity of the spine and the spine becomes unstable, allowing slippage to occur.  For reasons that aren’t entirely understood, most people with normal, age-related wear and tear of their spine do NOT develop DS.  A small number of unlucky folks are predisposed to this condition, however, perhaps because of the morphology of their facet joints or a genetic predisposition to accelerated disc and facet degeneration (degenerative conditions like this do run in families.)  DS more commonly occurs in older patients at the L4/5 level.

IS, a.k.a. lytic spondylolisthesis, occurs as a result of a fracture of the pars interarticularis, a small bridge of bone connecting the facet joint at one level to that of the level above (see figure 3).   This condition, also referred to as spondyloLYSIS, is thought to begin as an innocuous stress fracture in young athletes.   Only a small percentage of patients with a pars fracture will ever develop pain and an even smaller number will ever develop a slip.  Again, there seems to be a subset of patients who are predisposed to developing a slip in the setting of a pars fracture.  One theory is that patients with a high pelvic incidence (PI) are more likely to progress, mainly because of the force of gravity pulling the spine forward (PI is a measure of the morphology of one’s pelvis usually associated with a steep downward sloping sacrum.  More on this in a later post.) IS more commonly occurs in younger patients at the L5/S1 level (secondary to pars fractures at L5, see figure 4).  Again, as a patient, don’t get too bogged down in the details of different types of spondylolisthesis here.  If you have a spondylolisthesis it’s probably a degenerative one although it may be an isthmic one.  In the end, though, it doesn’t matter as the treatment is the same. 

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Figure 3: Left, posterior view of lumbar spine at L4/5 level (red line indicates location of a fracture across the pars of L5.)  Image on right shows schematic of slip at L4/5 that has developed as a result of a pars fracture at L4 (yellow arrows.)

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Figure 4: Lateral standing Xray showing spondylolisthesis at L5/S1 associated with pars fracture at L5 (thin red lines).  This patient also has a high pelvic incidence with a steeply sloping sacrum (the top of which is indicated by blue line).  You can imagine how the force of gravity is contributing to the development of the slip in this patient by pulling L5 forward and downward (red arrow.)  

Even today there continues to be a great deal of controversy over the treatment of spondylolisthesis.  As I mentioned previously, spondylolisthesis and spondylolysis are commonly asymptomatic.  Interestingly, several large population studies have failed to show a strong correlation between the presence of spondyolysis/spondylolisthesis and pain, even when the slip progresses.  Patients can have this condition, a structural deformity of their spine, and be just fine. IT raises the question: should these patients even be treated at all?  Ultimately, though, once a spondylolisthesis progresses to the point where it’s now an unstable deformity of the spine, patients usually begin to seek treatment.  

When I first see a patient with a spondylolisthesis I’ll begin by offering conservative treatments such as physical therapy (PT) and epidural steroid injections.  PT will relieve pain in patients with spondylolisthesis, even when the slip is unstable and associated with stenosis.  I’ve been amazed at how some patients, with horrible looking MRIs, will do just fine with regular PT.  If nothing else, even if the patients do progress to surgery, I prefer that the patient has completed a course of PT because it strengthens them for recovery after surgery.  Only when PT and injections fail to provide lasting relief of pain do we consider surgical intervention.

As mentioned in a previous post, instability is one of the clearest indications for spinal fusion.  Indeed, patients with back pain and radiculopathy from an unstable spondylisthesis almost uniformly have excellent outcomes with the proper surgical intervention.  There is some controversy on the best surgical approach to address spondylolisthesis.  In my opinion, though, the best intervention is that which, using minimally-invasive approaches, best restores the structural alignment of the diseased level.  This intervention provides stability to relieve back pain and also, through indirect decompression, relieves nerve root compression and thus relieves leg pain.  More on the surgical treatment of spondylolisthesis in upcoming posts…

 

Thanks for reading!

 

J. Alex Thomas, M.D.

Why patients don’t get better after spinal surgery (it’s not always my fault.)

Ok.  I’m going to admit this for you right here and right now: my patients don’t always get better after surgery.  It’s a crazy thought, I know.  But it’s true.  Despite my best efforts to control all variables to ensure that things go smoothly, things can go awry and the patient doesn’t get better (and sometimes gets worse).  Generally speaking there are two categories of variables that must be managed to ensure success in spine surgery.  First, there are the variables that are dependent on me, the surgeon.  These variables stem from the technical, physical and psychological challenges of spine surgery.  I have to correctly diagnose the patient; I have to know the anatomy and technical nuances of the surgical procedure; I have to plan for the patient-specific anatomy of the case; I have to get a good night sleep before my OR day so that I can focus on the case; I have to maintain a level of fitness in order to handle the physical demands of surgery (yes, spine surgery can be quite physically taxing), etc.  No problem.  This is what I signed up for and I’m up for the challenge.  I can manage these variables better than most.  I do want to say one thing about the psychological stress of these cases.  I want every one of my patients to have the best possible outcome.  That itself weighs on my psyche enough.  But when things don’t go as planned and a patient has a poor outcome (I feel as if I hurt them) it can take months for my conscience and confidence to recover.   This isn’t a therapy session though.  I love what I do and overall I think that I handle the stress of it pretty well (my wife is blocked from posting comments on Spinal (con)Fusion, by the way.) 

Here’s what drives me crazy about taking care of spine patients though.  I can control all of the variables on my end and execute perfectly and the patient STILL doesn’t get better.  There isn’t always a direct correlation with my success in the OR and the patient’s outcome.  Why?  Patient-dependent variables, which often are out of my control, also affect outcomes in spine surgery.   Here, I offer a few of the ways patients don’t hold up their end of the doctor-patient relationship.

1)  Patients don’t want to get better.  Ok, so this is a very broad and potentially very damning characterization of some patients.   You could say obese patients or smokers don’t have the discipline to better themselves and thus don’t want to maximize their chances of success after spinal surgery.  As tempting as it is, though, we can’t blame patients for being obese or for smoking.  Both of these are diseases that many patients are incapable of managing on their own.  So while I do think patients in this country should take more responsibility for their own health, we shouldn’t automatically assume that they don’t want to get better because of their weight or their bad habits.    

What I’m referring to here is a more pernicious subset of patients who are actively trying to not get better, the landmines in the minefield that is my clinic.  These patients usually have some sort of secondary gain that they’re after that leads them to consciously or subconsciously fail to improve after surgery.  Maybe they were injured on the job and want to live off of a worker’s compensation claim.  Maybe they don’t want to be in the military anymore.  Maybe they were in a car accident (not their fault) and their lawyer is telling them they can get more money if they appear more severely injured.  Maybe they want more attention from their spouse.  Maybe they just want oxycodone.  You wouldn’t believe what I’ve seen.   And before you come after me for being insensitive, check the literature.  There are dozens of studies correlating secondary gain with poor outcomes in spine surgery. Thankfully as I’ve moved along in my career I’ve gotten better at spotting patients like these and will avoid ever offering them surgery.  That’s the art of spine surgery.

2)  We aren’t good at accurately measuring if a patient is in fact better.  In spine surgery we rely on patient reported outcomes (PROs) measured before and after surgery to assess the patient’s response to the surgery.    PROs generally fall into two categories: those that measure pain severity and those that measure level of disability.   The visual analog scale (VAS) is the most common tool used to assess a patient’s pain level (see figure 1).  In this scale the patient is asked to rate their back or leg pain on an 11-point scale where 0 is no pain and 10 is the worst pain imaginable.  While VAS is useful on a superficial scale, I find that patients’ responses are widely variable thus making the test unreliable.  I frequently will see that a patient has rated their pain a 10/10 on their intake paperwork but when I walk into the exam room they’re sitting comfortably reading a book.  If this is how the patient self-assesses their pain how can I know for sure that the patient in fact got better?  The problem is that pain is so subjective and influenced by so many factors that it’s just hard to quantify objectively.     

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Figure 1: Visual Analog Scale (VAS) for reporting pain. 

Common measures of disability include the Oswestry Disability Index (ODI) and the Short-Form 36 Health Survey (SF-36).  Both of these are quite thorough but again are subject to variability.  The ODI, for example, asks the patient to rate their quality of sleep, sex life and social life.  In my opinion, these are things that are open to wide interpretation (you ask someone about this stuff on a Friday versus a Monday and the answers may vary!).  With so much variability in patients’ responses on VAS and ODI it can be difficult to determine to what extent the patient actually improved after surgery.  Obviously these PROs leave room for improvement.  These days we’re finding that by combining several PRO modalities we can get a more accurate representation of a patient’s progress.

3)  Patients don’t remember how bad they were and thus don’t realize that in fact they’re better.  Recall bias is a well-known entity in medical research.  When asked to recall facts or conditions in the past, research subjects are notoriously inaccurate.  The same applies to spine patients.  A 2017 study out of the Mayo Clinic found significant limitations in how well patients recalled their preoperative VAS scores when asked to recall them a year later. (Aleem et al, 2017)  Also, more than 40% of patients couldn’t remember if it was their back or leg that hurt them more before surgery.  How can a patient tell me if they’re better after my surgery if they don’t remember what was hurting before the surgery. 

Along the same lines, patients may have improper expectations about their surgery and thus may be disappointed in their outcome even when it’s a good outcome.  For example, often patients with lumbar stenosis and spondylosis present with both back and leg pain.  When I consent them for surgery I explain to them that the minimally-invasive laminectomy that I’m recommending will only relieve their leg pain (by fixing the stenosis) and not their back pain.  Some patients don’t hear that though.  After surgery they’ll come back in and tell me that surgery didn’t help them at all.  The exchange goes something like this:

     Me: “Mr. Smith, you’re two weeks out from your laminectomy.  How’s it going?”

     Mr. Smith: “Horrible.  Surgery didn’t help me doc.  You said you were gonna fix me but I’m no better.”

     Me: “Oh no! Tell me where you hurt?”

     Mr. Smith: “My back hurts, Doc.  You said you were going to help my pain.  What happened?”

     Me: “Well how do your legs feel?  Prior to surgery you told me that you couldn’t even walk to the mailbox because your legs hurt so badly.  

     Mr. Smith: “My legs?  Oh they’re great.  Leg pain was gone when I woke up from surgery.  I walked 2 miles this morning. But my back still hurts.”

     Me: (internally) Sigh

I understand why some patients may not fully absorb what I’m telling them.  They’re scared and distracted when the prospect of surgery becomes a reality.   Prospective patients should be mindful of this, though, and make every effort to listen to and process what their surgeon is telling them.   On my end I’m working on ways to ensure that patients hear what I’m telling them so that they can have accurate expectations about their surgery.  This includes detailed handouts discussing surgery as well as audio/video recordings of preoperative conversations that the patient can refer back to when they’re home with their families.  The most well-informed patients will have the most accurate expectations of surgery and thus are most likely to report that they’re better after surgery.

4)  Patients just don’t get better.  Unfortunately some patients, through no fault of their own or the surgeon, just don’t get better.  As much as we like to think we doctors know everything, we don’t.  I think that we just don’t understand every etiology of back pain.  Is it the degenerated disc?  Is it the facet joint?  Has the brain just learned the pain?  There’s just so much we don’t know.  We do our best to make an accurate diagnosis, assess the patient and prescribe an accurate treatment and yet sometimes even that’s not enough for the patient.  This may be the most frustrating thing about what I do.  All I can do is look at myself in the mirror in the morning and swear that I’m just going to do my best for my patients.  Hopefully it’s enough. 

Ok so maybe there wasn’t much technical information in this post.  That’s OK.  Hopefully by hearing my candid thoughts on the matter you’ll be better equipped when talking to your surgeon about the surgery he’s recommending.  Ultimately I love taking care of my patients and just want them to have the best possible outcome after their surgery.  We’re in it together.  If we both do our parts you, the patient, are going to do fabulously after your surgery.   

 

Thanks for reading!

J. Alex Thomas, M.D.

Sources:

Aleem IS, Duncan J, Ahmed AM, Zarrabian M, Eck J, Rhee J, et al.: Do Lumbar Decompression and Fusion Patients Recall Their Preoperative Status? Spine (Phila Pa 1976) 42:128–134, 2017.

Lateral ALIF is a true single-position strategy for lumbar fusions

I’m back!  I realize there’s been quite a delay since my last post and for that I apologize.   For over a year now I’ve been busy helping to develop a new retractor system for lumbar spine surgery.  This retractor allows surgeons to perform an anterior lumbar interbody fusion (ALIF) in the lateral position, a procedure we (perhaps not so creatively) call lateral ALIF (see figure 1).  Why does that matter?  In my opinion, an ALIF is the most powerful way to fuse a segment of the lumbar spine and correct spinal deformity (hint: it’s because ALIF allows you to insert the largest spacers!). One drawback of ALIF, though, is that since it’s traditionally performed in the supine position (with the patient laying on his back), if the surgeon wishes to place posterior instrumentation he has to close the incision on the front of the patient and then reposition the patient prone to get access to the back of the spine.  This process of repositioning can add nearly an hour of time to the procedure and may also increase risk to the patient.  By keeping the patient on his side, in a single position, the surgeon can harness the power of ALIF and then immediately be ready to place posterior instrumentation, all without having to stop to reposition the patient (see figure 2).  Now, a so-called 360-degree lumbar fusion that used to take 3 hours to perform can now be done in an hour.  This is good for my OR throughput but it’s GREAT for you, the patient, who will avoid that extra time under anesthesia.  This could potentially be the one of the most important innovations in spine surgery in years. 

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Figure 1: The new Lateral ALIF retractor during a recent ALIF at L5/S1.  The patient is in the lateral decubitus position with their left side up.  The patient’s head is at the left of the image.

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Figure 2: Lateral ALIF at L5/S1.  This image gives you an idea of the massive increase in efficiency you get without having to reposition the patient.  Here, I’ve already placed wires for insertion of percutaneous pedicle screws while my physician assistant Jack Bagley continues to close the abdominal lateral ALIF incision.  Patient is right side up with head towards the left of the image. 

The ALIF, first described in the 1930s, is the original interbody fusion in which bone graft is inserted into the cleaned out intervertebral disc (IVD) space to promote fusion and correct spinal deformity (in modern ALIF the bone graft is carried in a spacer or cage).  Since then, many other techniques have been developed to place spacers into the disc space via a posterior approach.   These other –IF procedures, such as posterior lumbar interbody fusions (PLIFs) or transforaminal interbody fusions (TLIFs) represent early attempts at a single position strategy.  These procedures allow surgeons to perform the three standard steps of a spinal fusion: 1) neural decompression (laminectomy or discectomy), 2) interbody fusion, and 3) placement of posterior instrumentation with the patient in the prone position.  Thus, traditional spine surgeons may say “Well I’ve been doing ‘single-position’ lumbar fusions for years.”  Indeed, TLIF and PLIF are the most common way to perform lumbar fusions these days.  The problem with TLIF and PLIF, though, is that in order to place spacers from behind, one or more nerves have to be retracted out of the way to sneak the spacer into the disc space.  That means that for PLIF and TLIF the surgeon is forced to use very small spacers (see figure 3).  Because you’ve read recent Spinal (con)Fusion posts, though, you know that I believe in the power of large intervertebral spacers.  Bigger is better and thus ALIF is a much more powerful technique for spinal fusion than PLIF or TLIF.  Now, by doing the ALIF in the lateral position I can have concurrent access to the back of the patient to perform a decompression and place pedicle screws without “flipping” the patient. 

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Figure 3: side-by-side comparison of various intervertebral spacers.  Notice how much larger the XLIF/ALIF spacer  is versus the much smaller TLIF or PLIF spacers. Size matters!

As you can probably tell, I’m very excited about this new retractor and surgical technique (yes, I’m biased.)  In future posts we’ll talk more about the details of a lateral ALIF procedure.  You’ll also see how well lateral ALIF at L5/S1 compliments the extreme lateral interbody fusion (XLIF) at L4/5 and above.  Lots more about single-position lateral surgery to come! 

Thanks for reading!

J. Alex Thomas, M.D.

Believe in Indirect Decompression!

One of the most common procedures that I book patients for is an extreme lateral interbody fusion (XLIF).  This is a minimally-invasive lumbar fusion procedure that has all of the benefits of the classic anterior lumbar interbody fusion (ALIF) without its downsides (all of the bad things that can occur by traversing someone’s abdomen to get to the spine.)   In previous posts we’ve alluded to various types of spinal deformity that can cause pain.  The one constant in all of these types of spinal deformity: stenosis.  Both XLIF and ALIF rely on an old orthopedic principle known as indirect decompression in which properly sized spacers are used to correct spinal deformity and thus correct stenosis. 

Recall from previous discussion that stenosis, or narrowing around nerve roots, typically results after years of spinal degeneration.  The resulting stenosis can be divided into two simplistic types (and these types are just the way that I think about it in my head, don’t go looking for them in textbooks!).  The first type of stenosis is structural stenosis.  Here, the basic anatomical components of the spine are generally unchanged in terms of their shape or volume; it’s just that these parts of the spine have collapsed onto nearby nerve roots thereby causing pain.  I believe that this is the most common form of stenosis by far.  One common example of structural stenosis occurs when the intervertebral disc (IVD) has degenerated and collapsed resulting in loss of foraminal height and foraminal stenosis.  Another example of structural stenosis is seen in spondylolisthesis when one vertebral body slides over the one below it causing a dynamic foraminal stenosis that worsens when the patient stands and loads their spine (more on this topic later.)  Lastly, it is my opinion that the central stenosis that causes neurogenic claudication in the elderly is a form of structural stenosis resulting from buckling of the ligamentum flavum (this is controversial as some believe that the body actually produces reduntant ligamentum flavum which would be more like the reactive stenosis discussed below.) In each of these cases, normal spinal structure and alignment has been lost resulting in stenosis and pain.

The other simplistic type of stenosis is reactive stenosis.  Here, there IS an increase in the shape or volume of a component of the spine, which results in stenosis and compression of nearby nerves. The most common example of this occurs when the facet joint degenerates and becomes larger as it becomes consumed by arthritis.  This leads to osteophyte (fancy word for bone spur) formation, which can cause nerve root compression and radiculopathy. 

To fix reactive stenosis the surgeon must perform a direct decompression procedure, a laminectomy or foraminotomy, to remove all excess bony overgrowth from around the nerves.  In fact, classically this is the way that all nerve compression (regardless of which type of stenosis is causing the compression) is relieved.  The typical neurosurgeon’s mentality (and I can say this because I’m one of them) is that the only way to know that a nerve is decompressed is to remove any overlying bone and actually see the nerve.  But what if this isn’t always necessary?  I believe that in most cases it’s NOT necessary (and trust me, it takes a huge leap of faith on the part of both the surgeon and the patient to come to this realization.)  Because most spinal stenosis is structural and not reactive, restoration of normal structure and alignment of the spine will relieve stenosis and pain without the extra time and risk of a laminectomy.

Recall that loss of normal spinal structure and alignment begins with degeneration and resulting collapse of the IVD.  So, to restore structure and alignment we go to the disc space (remember the post on spacers?)!  Indirect decompression is achieved when a properly sized spacer is inserted into a collapsed disc space to restore the height of the neural foramen (see figures 1 and 2).  This then relieves nerve root compression because the space around the nerve in the foramen is restored; I don’t have to do more work to remove bone that doesn’t need removing!  To be sure, this is a controversial topic.  I know plenty of very good spine surgeons who just don’t believe in indirect decompression and subject their patients to a concurrent laminectomy with every spinal fusion.  They’re paranoid (we surgeons are a VERY paranoid bunch, some are just more so than others) that if they don’t directly decompress the nerve and visually confirm that it’s decompressed then they may not relieve the patient’s pain.  I get it.  Like I said, it’s a leap of faith.  A laminectomy isn’t a benign procedure though.  There’s a 5-10% risk of dural tear and spinal fluid leak for starters.  Typically this is a minor complication but it can be catastrophic.  There’s also the risk of scar tissue formation around exposed nerve roots, which can lead to chronic pain after surgery.  Finally there’s just the risk of being under anesthesia for the extra time needed to perform the laminectomy.  Why would I subject my patients to these risks when I know that the indirect decompression achieved by the spacer will probably suffice?  Believe in indirect decompression!

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Figure 1: A, preoperative image showing severe collapse of the IVD resulting in foraminal height loss and nerve root compression; B, postoperative image demonstrating restoration of disc space and foraminal height after insertion of a large intervertebral spacer.

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Figue 2: As above in figure 1, image on left is preoperative image demonstrating severely collapsed IVD at L5/S1 with resultant severe foraminal stenosis (pink outline).  The image on the right is a postoperative image after an L5/S1 anterior lumbar interbody fusion (ALIF) with significant increase in disc space, and thus, foraminal height.  This patient’s leg pain was relieved immediately after surgery WITHOUT laminectomy. 

Of course there are times when relying solely on indirect decompression may not be appropriate.  In cases of severe reactive stenosis in which, say, a nerve root is encased in bone (see figure 3), indirect decompression probably isn’t going to work no matter how large of a spacer you put in.  Also, in cases of large concurrent disc herniations or facet cysts (a type of reactive stenosis, I suppose, which I’ll discuss in a later post) I may also be forced to do a direct decompression.  The more cases I do, though, the more I’m surprised at what I can get away with in terms of avoiding a direct decompression.  These days I’ll typically assume that indirect decompression will work but explain to the patient that there is a very small chance that indirect decompression may fail and that we may have to do a small “second stage” laminectomy later.  How small of a chance you ask?  I went back and looked at the data for every one of my lumbar fusions performed since December 2013.  Of nearly 250 patients only 8 needed reoperation for failure of indirect decompression.  That’s a 3% risk.  I’d say those are pretty good odds in favor of direct decompression. 

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Figure 3: Severe “reactive” foraminal stenosis at L4/5 and L5/S1 resulting from severe bony overgrowth around nerve within the neural foramen (red arrows).  This patient failed indirect decompression and required a minimally-invasive foraminotomy a few months after his initial surgery.

Thanks for reading!

J. Alex Thomas, M.D.

Implants in Spinal Surgery Part III: Intervertebral Spacers

In our last post we discussed pedicle screws, the most commonly used form of posterior instrumentation.  Even in the recent past, pedicle screws were the only form of instrumentation used in a spinal fusion.  Unfortunately, these posterior-only fusion constructs didn’t have excellent rates of fusion: nearly 30% of these cases ended up in non-unions.  Today, most spinal fusion constructs utilize pedicle screws at the back of the spine and intervertebral spacers (or cages) in the front of the spine.  These so-called 360-degree constructs (also referred to as interbody fusions) have dramatically decreased the rates of non-union and thus are now the standard way spinal fusions are done.  

Of note, interbody fusion procedures are abbreviated with the suffix –IF. Common examples include the anterior lumbar interbody fusion (ALIF), posterior lumbar interbody fusion (PLIF) and extreme lateral interbody fusion (XLIF).  We’ll highlight the differences between the various –IFs in a future post.  The most commonly used interbody fusion procedure is actually the ACDF which we’ve already discussed here.

In the 1950s anterior interbody fusions were used in the treatment of Pott’s disease, or tuberculosis of the spine.  These anterior fusions proved to be more effective than posterior fusions because they allowed for reconstruction of the front of the spine, which is where most of the destruction of Pott’s disease occurs.  Once the infected vertebral bodies were resected (via a corpectomy), large defects in the front of the spine were reconstructed with pieces of bone fashioned into struts.  These pieces of bone were either harvested from cadavers (allograft), or may have been harvested from somewhere within the patient’s body (autograft) like the fibula or iliac crest.  These bone struts provided immediate support to the front of the spine and also promoted bony fusion.  They were the earliest intervertebral spacers.

While long structural bone struts are important in the reconstruction of the front of the spine after corpectomy for infection, tumor or trauma, the more commonly used intervertebral spacers are smaller spacers inserted into the disc space for fusion for degenerative conditions.  I will be referring to these spacers primarily for the remainder of the post.  The first such anterior interbody fusion utilizing bone inserted into the disc space was reported by Dr. Burns in 1933 for the treatment of lumbar spondylolisthesis (“slipped bones”, to discussed in a future post.)  Unfortunately, in this case, as with early anterior cervical fusions, often only loose shards of bone were packed into the disc space.  While this may have promoted bony fusion across the disc space it certainly didn’t provide any structural support and may have allowed for further collapse of the spinal segment with resultant kyphosis of the spine (see figure 1).  In the subsequent decades since Dr. Burns’ case, intervertebral spacers of various materials and shapes have been developed that are better at providing structural support and are also more readily available than spacers made of bone.  Today most intervertebral spacers are made of a fancy plastic called PEEK (polyetheretherketone) and this is what I use almost exclusively when I perform interbody fusions.  Titanium is also making a comeback (either comprising the entire spacer or as a coating on the surface of a PEEK spacer) as some feel it may be better at incorporating new bone in the early stages of bony fusion (see figure 2).  I could spend multiple posts discussing the merits of different intervertebral spacer materials but that you would likely bore you (and me) to death.  Regardless of what it’s made of, every intervertebral spacer should serve two purposes: a) correct spinal deformity, and b) promote a bony fusion.   

Postoperative Deformity of the Cervical Spine Clinical Gate 

Figure 1: Anterior cervical fusion done with only bone graft and no spacer for structural support.  Note that the fused bones have collapsed somewhat and are now allowing the spine the fall forward  The red line indicates the forward angle of the collapse and should, in fact, be straight (source: Riew et al, 2015).

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Figure 2: Various intervertebral spacers used for lumbar interbody fusion (source: Williams et al, 2005). 

First, let’s talk about the correction of spinal deformity.  In my opinion spinal reconstruction should take place where the degenerative process starts: the disc space.  As we’ve talked about previously, as the intervertebral disc (IVD) degenerates it dries out and collapses.  Without the structural integrity of the IVD the adjacent vertebral bodies fall out of alignment and the spine then becomes deformed.  Spinal deformity is a complicated topic that I won’t delve too far into at this point.  All you need to know now is that a deformed spine causes both back pain and radicular (nerve) pain.  The back pain is caused by the mechanical stress of the deformity.  The radicular pain is caused by foraminal stenosis and the resulting nerve root compression.  Recall that the neural foramen, the hole on the side of the spine where the nerve exits, is an aperture comprised of the top of the pedicle of the vertebral body below and the bottom of the pedicle of the vertebral body above.  As the IVD collapses the diameter of the foramen narrows significantly and the nerve is guillotined within.  An intervertebral spacer inserted into a collapsed disc space corrects deformity by acting like a wedge to a) restore alignment to relieve mechanical stress, and b) restore foraminal height to allow for indirect decompression of compressed nerves.  The concept of indirect decompression is an immensely important one that I’ll get to in an upcoming post.  (See figures 3 and 4.)

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Figure 3: Image on left shows collapsed disc with resultant foraminal stenosis and nerve root compression.  Image on right shows the result after a spacer is inserted with restored foraminal height and indirect nerve decompression.   

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Figure 4: Preoperative MRI showing a focal coronal deformity with unilateral foraminal stenosis and nerve root compression resulting in severe R leg pain (the red lines, indicating the vertebral endplates, should be parallel and instead are collapsed to one side.)  Image on right is a postoperative anterior view Xray after a spacer (with plate) is inserted.  Notice that the vertebral endplates (red lines) are now parallel after the deformity has been corrected.  Of note, because it is PEEK the spacer isn’t seen well on Xray and instead the borders of the spacer are indicated by markers within.  

The other important function of the intervertebral spacer is to promote bony fusion.  Recall from previous posts that it’s the bone graft material that is applied between parts of the spine that promotes the new bone growth in a spinal fusion.  There are many types of graft material used in spine surgery that I’ll discuss in a later post.  Most modern intervertebral spacers have large chambers within their structure where bone graft is packed prior to insertion into the disc space (see figure 5).  These chambers then hold the graft material in place, nicely apposed against the adjacent vertebral bodies, in order to promote bony ingrowth (see figure 6).  

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Figure 5: standard ALIF spacer used in lumbar fusions.  Note the large graft chambers (red arrows) that are packed with bone graft material prior to insertion into the disc space. Source: Globus Medical. 

 

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Figure 6: Lateral postoperative CAT scan demonstrating robust bone growth (red arrow) across intervertebral spacer (spacer material isn’t seen in this cut of the scan.)  

Lastly, I believe that bigger is better when selecting an intervertebral spacer in an interbody fusion.   Not only do larger spacers provide more structural support for deformity correction but they can also carry more graft material to better promote bony fusion.  THIS is why I prefer anterior procedures such as XLIF or ALIF with their large spacers rather than TLIF or PLIF with their quite puny spacers.  More on that later.

Thanks for reading!

J. Alex Thomas, M.D.

 Sources:

1) Riew et al, 2015, Postoperative Deformity of the Cervical Spine, online access at iKnowledge: https://clinicalgate.com/postoperative-deformity-of-the-cervical-spine/.

2) Williams et al, 2005, CT Evaluation of Lumbar Interbody Fusion: Current Concepts, ANJR, 20: 2057-2066, September 2005.

 

 

 

 

 

 

 

 

Implants in Spinal Surgery Part II: pedicle screws and other (very rarely used) forms of posterior spinal instrumentation

In our last post we discussed how various types of spinal implants help stabilize the spine to promote a more robust bony fusion.  Recall that the main goal of a spinal fusion procedure is to promote bone growth which in turn will stabilize a painful unstable or deformed segment of the spine.  Historically, non-instrumented in-situ fusions had very high rates of non-union in which the spine didn’t fuse despite weeks of bedrest and bracing.  This may have required subsequent revision surgeries and often left the patient severely disabled.

In order to mitigate the problem of non-union, surgeons developed forms of posterior instrumentation (instrumentation applied to the back of the spine) to help stabilize the spine.  These implants also provided surgeons a more powerful way to restore alignment to the spine to correct spinal deformity.  The most primitive form of posterior spinal instrumentation, first described in the late 19th century, was posterior spinal wiring.  Here, various parts of the spine (usually the spinous process or lamina) were wired together for immobilization during spinal fusion.  While useful in the cervical spine (see figure 1), this technique never proved to be effective in the thoracic and lumbar spine, where larger forces prevail, and thus has largely been abandoned today. 

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Figure 1: Cahill technique of posterior spinous wiring in the cervical spine.  Source: Omeis et al

In the 1950s Paul Harrington began performing spinal fusions using long rods anchored to the spine with hooks under the lamina (see figure 2).  The rod construct was periodically lengthened to slowly straighten the deformed spines of scoliosis patients. Harrington rod systems were state of the art for decades and I’ll still see patients in clinic today with these long rods in their spine.  Unfortunately, with only a few points of fixation anchoring the long, straight rod in place, these constructs were prone to failure and also predisposed patients to a painful “flat back” deformity.  (When a surgeon fuses a spinal segment without being mindful of its normal degree of curvature he may inadvertently cause more harm by creating spinal deformity.  More on this very important topic in later posts.)  Moving away from Harrington rods, surgeons began to develop new forms of segmental instrumentation in which each segment of the fused section of the spine was anchored with instrumentation (versus the long Harrington rod which spanned multiple non-instrumented segments.)  This segmental instrumentation vastly increased the strength and stability of the fusion construct and therefore further decreased the rate of non-union.  Early forms of segmental instrumentation include variations of trans-facet screws described by King in 1944 and Boucher in 1959 (the latter incorporated part of the pedicle in the screw trajectory and thus is considered by some to be the first pedicle screw.)  In 1970 Roy Camille described the precursor to today’s pedicle screw systems.  In his system he attached screws inserted via the pedicle to a multi-holed plate which would span across two spinal segments from screw to screw.  The screw-plate concept was expanded upon in the U.S. by Dr. Arthur Steffee in the early 1980s with his Steffee Plate/VSP stainless steel pedicle screw system (see figure 3).  Steffee’s company AcroMed was the subject of a 1993 ABC 20/20 expose which profiled several patients who were left disabled after Steffee’s VSP pedicle screws broke (all pedicle screws will eventually break, by the way, if the spinal segment doesn’t fuse properly.)  This prompted hundreds of pedicle screw-related lawsuits around the country in the mid 1990s (part of the issue was that the FDA never cleared the VSP screw for use specifically in the spine).  Ultimately most of the pedicle screw litigation was thrown out.  Today pedicle screws are a mainstay of treatment of a variety of thoracic and lumbar spinal pathology. 

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Figure 2: AP (A) and lateral (B) postoperative Xrays demonstrating a single Harrington rod used in correction of a thoracic scoliosis.  Note in image B how flat the fused segment is. 

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Figure 3: Steffee plate and VSP pedicle screw system in L4-S1 fusion.  Source: Kabins et al.

Today’s pedicle screws are generally made of titanium and have polyaxial heads in which a rod is seated and locked in place using a locking cap.  The rod is used in favor of Camille’s and Steffee’s plates as it allows for easier insertion as well as contouring to correct spinal deformity (see figure 4). Screws vary in size depending on the size of the patients and the part of the spine being instrumented (i.e. smaller screws in the thoracic spine and larger screws for the lumbar spine.)  Typically in lumbar spine fusions I will use screws that are 6.5mm in diameter and 45mm long with a 4.5mm diameter rod.   Once the screws are inserted various attachments can be used to manipulate the screws to rotate, compress or distract across spinal segments in order to correct spinal deformity prior to fusion. 

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Figure 4: Modern pedicle screw with polyaxial head and rod locked in place. Source: Zimmer Biomet.

As you can probably guess, a “pedicle” screw traverses part of the vertebral body called the pedicle.  This bridge of bone connects the anterior elements of the spine (i.e. the vertebral body) with the posterior elements (i.e. lamina, facets, spinous process, see figure 5).  In order to properly insert a screw into the pedicle the surgeon must access a starting point at the junction of the transvers process and the facet complex, several centimeters off of midline.  In traditional open spinal surgery via midline incisions the surgeon has to do quite a bit of destructive, bloody dissection to get a wide enough exposure to access this starting point of the pedicle.  Often, in order to gain enough laxity in the tissue to get out to the starting point, the surgeon must also expose the level above and below the level that is being fused.  This “collateral damage” of healthy levels in open spinal surgery is what sets patients up for adjacent segement degeneration and other problems later in life. 

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Figure 5: Axial (left) and lateral (right) views of lumbar spine demonstrating pedicle (outlined in red) bridging the anterior and posterior elements.

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Figure 6: Small stab incisions used to placed 4 percutaneous pedicle screws for an L4/5 spinal fusion.  The red line indicates the length of incision that would have been needed to place the same number of screws using traditional open techniques. 

In order to avoid the increased blood loss and tissue destruction of open spinal surgery, I insert pedicle screws percutaneously with tiny, minimally-invasive incisions off midline (see figure 6.) I’ll first identify the starting point of the pedicle using a fluoroscope (like an xray machine) and then will hammer in a large needle into the pedicle via the starting point.  I can identify the correct starting point not only using imaging but also with the tactile feedback of the hard bone of the pedicle starting point.  Once I’m happy with my position in the pedicle I’ll insert a long, rigid wire called a K-wire into the pedicle and will remove the needle.  The pedicle is tapped to make a pilot hole and the screw is then inserted over the wire (see figure 7.)  The nerve that exits the spine passes just below the pedicle so one potential complication of pedicle screw insertion is nerve injury resulting from improper positioning of the screw within the pedicle. In order to avoid this complication I always use electromyographic (EMG) monitoring in which the insertion needle and tap are stimulated with low-voltage electrical current.  If the screw trajectory is too close to a nerve the current will stimulate the nerve, the corresponding muscles in the leg will twitch and I’ll be alerted to the problem so that I can plan a new trajectory.  After the screws are inserted a rod is passed through the heads of the screw and locked in place.  While some surgeons will try to get away with placing only unilateral screws, I always place bilateral pedicle screws (i.e. on both sides of the spine), as this is the gold standard for maximum spinal stabilization (see figure 8.)  Finally, recall that the screws just serve as an internal brace to allow the bony fusion to occur.  Theoretically we could remove the screws in a year after the fusion has healed but we almost never do this.

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Figure 7: 4 K-wires placed prior to placement of percutaneous pedicle screws for lumbar fusion (red wire).  Note that wires and thus screws can be placed with the patient in the lateral position (in this case patient’s right side is up.) 

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Figure 8: Axial CT image (left) and schematic image (right) demonstrating bilateral pedicle screws traversing the lumbar pedicles. Source for schematic: DePuy Synthes

There are other types of posterior instrumentation that are used in the lumbar spine.  These include interspinous clamps as well as facet screws.  I don’t believe that these implants provide the same amount of stability as a bilateral pedicle screw construct and therefore I never use them.  Not discussed here are specialized screws used in posterior cervical spine fusions called lateral mass screws (named for the part of the cervical vertebral body that they enter.)  These are very similar to thoracic and lumbar pedicle screws (titanium, polyaxial heads, connected by rods passed through the heads) but are much smaller with a typical diameter of 3.5mm and a length of 12-14mm.  

In summary, pedicle screws act as an internal brace to immobilize the spine so that a more robust bony fusion may occur. These screws can be safely inserted into the spine using minimally-invasive percutaneous techniques.

Thanks for reading!

J. Alex Thomas, M.D.

Sources:

  1. Hasler CC: A brief overview of 100 years of history of surgical treatment for adolescent idiopathic scoliosis. J Child Orthop 7:57–62, 2013.
  2. Omeis I, DeMattia J a, Hillard VH, Murali R, Das K: History of instrumentation for stabilization of the subaxial cervical spine. Neurosurg Focus 16:E10, 2004.
  3. Kabins MB, Weinstein JN: The History of Vertebral Screw and Pedicle Screw Fixation. Iowa Orthop J 11:127–136, 1991.