CafeDoor

Cafe’Door Hip Surgery

That you are here probably means that somebody missed the boat. This book ought not exist. Yet, here we are. This is not easy stuff. For clarity, we will start from basics, back before anything like this was needed. Children with paralytic dysplasia of the hip [PDH] had, at birth, normal hip anatomy. What they are not: They are not like otherwise healthy BIG babies who were compressed near term in the womb by the womb itself. Compression causes flat noses, folded ears, odd head shapes, twisted feet, and the like. Once out of the womb and positioned properly, that squashing stuff went away. But the less able to self correct hip joints, that were also compressed, were not visible. Not noticed. “Congenital” (aka “Developmental”) dysplastic hips [CDH=DDH] often went unsuspected. But hip muscle power did not undo it and often made it worse as the fetal flexed legs extended once free of the womb. A way to reveal these normal looking but compressed hips nearly immediately after birth was developed and widely adopted. It was and is a kind of ultrasound. With timely repositining the legs ( using suspenders) DDH just kind of disappeared. But DDH [CDH] left a sea of literature in its wake of treatments for cases where early intervention opportunity was missed as early detection was not guaranteed. The term 'developmental' suggested that the hip condition developed over time. Our reality is that, while worsening untreated, it was awareness of its presence that was developing over time. With modern ultrasound detection, that DDH went the way of smallpox. So baby hips are all great now?

No. Other things also improved. Tiny babies that had zero chance of survival are now nearly routinely saved. Also, those with umbilical cord mishaps or whatever birth traumas nature deals out, also survive. A new problem is that these saved kids are not unscathed. Neurological incompleteness direct or by damage from lack of cardiac & great vessel readiness leaves us with neurological damage. The damage of imbalanced circuits early on isn't obvious as even the imbalances are struggling to exist. As health is acquired, the neural wiring – good and bad - starts to manifest and assert itself. Alas, what manifests isn't the norm. Some muscles get ignored. Others get stimulated nonstop. Infinite circuits with infinite ways the brain can be irregular leaves us with infinite possible mixtures of neurological woe. There are just too many to assign all the potential individual names. Collectively, we just call all of it cerebral palsy. Just keep in mind that this very old name, cerebral palsy, is just that, a very old name. Often, the abnormality we deal with in “CP” is neither cerebral nor a palsy, but that name gets the paperwork done. Nobody wants the monumental alternative naming of infinite deficits and excesses. Even so, the weakest links in the chains of building neurological function as well as vascular and metabolic support are the breaks we see most often. From that, are derived the KINDS of CP that do get notice. The kinds, by quality : spastic, dystonic, rigid, athetoid, choreiform and others are by almost 1:1 related to specific injury cause types. Discrete damage to this brain location or that location, such as by bleeding, insufficient blood flow pressure, metabolic abnormality, oxygen absence, and so on, causes discrete kinds of localization of abnormality... flavors, that we recognize by what body parts manifest the injury most. These get awkward Latin or Greek labels showing that doctors can count to 4 in Latin or Greek.

Avoiding kinds, (aware of so many possibilities) clinicians have fallen prey to name calling. Like, sleaze bags on the corner rating girls as 0 to 10, the docs rate kids with 'cerebral palsy' as 1 to 5. 1 = Why are you complaining?. You ain't so bad. Go play. 5 = Whoa, what a mess. Not much we can do to make a desired difference. These grades from 1 to 5 tell us NOTHING about the neural structure nor potential work around possibilities. There's not very much we do for types 1 & 5. So, we are left treating the most challenging CP kids brought in with problems to solve. We have allotted them types 2, 3, & 4. If you find this wanting and prone to erroneous treatment planning then .. good for you!!! Rehabilitation Engineering does not care much for this arm's length 'Naming of Parts' [Henry Reed 1942] in the face of future needs, hopes & desires. In a quest for work-arounds, we begin with INVENTORY. What is working? What is trying to work but is being thwarted? What is in the way of what is trying? Is the funny looking thing the kid is doing a projection of the damaged brain's intent? Or, is it what the struggling child fopund that gets around it what is blocking intent? We do NOT want to point at compensatory things, give them Latin & Greek names and 'cure them'. We do not want to chisel bone in the name of “lever arms” run amok [how-so??]. To communicate we need basic common language. So let's start from basics and keep the language well grounded in observation.

Common descriptions of anatomy will help.

NORMAL ANATOMY

The upper femur (thigh bone) takes a bend (120 degrees) to seat the ball at the top of the femur (“femoral head”) into the pelvic cup (“acetabulum”). The short angled upper segment supporting the femoral head is the femoral “neck” (the 120 degree part). Above we, can't see the ball (femoral head) hiding in the acetabulum nor the neck which is wearing a turtle neck hip capsule which attaches firmly around the edge of the cup to the femur. The capsule is designed to enhance head stability in the cup as the cup is normally somewhat shallow. The blue colored hip capsule area is also called the iliofemoral ligament. It becomes quite tight as the hip extends. It is crazy strong. If it is too short then the hip cannot fully extend. Trying to force it (exercise??) might fracture the femur or batter the acetabulum wall out. Hamstring “stretching” can damage the socket instead of achieving

hamstring length. In CP, the damage is more to the back of the socket. Pulling the tibia straight might stretch the hamstring. It might pile-drive the back of the socket to flat if the leg is not abducted when the 'stretch' is performed. Knees wide apart spares the socket's weakest spot.

This is the upper femur minus the hip capsule showing head (covered in yellow cartilage) & neck (bone, though in the babies the top of neck is still cartilage). The red cap, on the head, like a yarmulke, is the acetabulum (red indicating bone in continuum with the pelvis). It has cartilage on its inner surface which you see peeking out a wee bit. A normal femoral head is NOT fully covered by the socket. The more horizontal the socket, the more stable it is to STANDING. Not more stable. More stable to standing . Standing badly, upright & adducted, uncovers the femoral head more at the top. Being “uncovered” by hip adduction does not equate with being a bad hip joint; though a bad posture to be in. A hip socket needs some depth. It needs reasonable coverage of the top of the femoral head. But, most of all, the center of the cup, a sphere, should coincide with the center of the femoral head. If THAT isn't exact, then the socket wall was damaged.

The lines they draw on x-rays are a throwback to CDH/DDH. Those drawn lines which revealed loss in the upper anterior cup are very insensitive to cup damage on the backside . Often the only clue we get of considerable acetabular damage is that hip ball centering in the cup has drifted.

Good hips on x-ray. The neck shaft angle (green ) looks flat (“valgus”) in the inset view because the leg as seen is rotated. That is what angles do when viewed from an angle – they go flat by projection perspective. The red line (Shenton's) can only be off if the acetabular center and the femoral head center no longer coincide.

Here, BOTH HIPS are “shallow' (sockets not very deep). But, the hip on OUR left (a right hip) has a broken Shenton's line. The socket is no longer spherical. At a minimum it is elliptical - or flattened. Even a small amount of this is NOT “EARLY DETECTION”. You have to have serious deformation of the acetabulum to get this. Note that the uncovering is made worse by adduction (knee going toward or past the body mid-line).

A. B. A= Upright as seen looking from the right side. The rectus femoris muscle runs from kneecap to two tendons at the top, one of which attaches straight ahead to the pelvis (the straight head tendon). The other, the backward traveling branch at the top of the rectus femoris attaches to the side of the pelvis all along the edge of the acetabulum (like an eyebrow to the eye socket). You don't need an x-ray to know where the socket edge is. This “reflected head” tendon of the rectus femoris outlines it. Easy to see. But, it is not seen when VRO surgery is done. None of the hip parts – head, neck, acetabulum are visualized in VRO surgery, allowing wrong perceptions about the socket to persist throughout the surgery – especially when distinguishing CDH/DDH from PDH . B= Also note on the right side of image, looking up the femur from the knee,

shows that the femoral neck angles a bit forward ( anteversion = forward tilt). Babies have extra anteversion to fold flat in the womb. The deRotation part of VRO is (saving 12 years of this anteversion gradually going away) so as to move the femoral head away from the CDH/DDH anterior cup damage. With that pressure turned backward, the cup can heal itself in the front as the causal pressure is gone. Works fine for CDH/DDH. But it points the femoral head right into the trouble spot more so when we have PDH ! Besides, where the femoral head is pointing in CP is much more from where the entire leg is pointing or crossing than anteversion.

Everybody has heard of the shoulder rotator cuff. Well, the hips have them too. It is a stack of short deep muscles that converge from inside and outside the pelvis to the upper femur just behind and above the head/neck area – a lot like the shoulder. We all KNOW [name your favorite] a baseball pitcher or two [or three] whose pitching went bad as their shoulders 'subluxed' (slid off center of the shoulder shallow cup). Why??? Muscle imbalance. Because those muscles were made crazy strong striking out high paid home-run hitters. SOME of the muscles meant to stabilize the ball in the shallow socket were overdeveloped in the throwing direction, but not maintaining balance in the full circular array of the cuff whose normal job is stability – centering the ball, by tension, at dead center. Pitcher? Get a job color commenting. Your pitching days are over.

The hip also has an encircling muscular cuff which in neurological abnormality can regress to a fetal pattern meant to stabilize a curled up baby in the womb or maybe even to a more primitive sling state, as with dinosaurs before hip joints? Whatever. Strong imbalance. Off center neurologically mediated muscular imbalance creates a wrong

tension center which paired with dystonia not only does not match skeletal cup center, it pulls and pushes toward its own tension center – relentlessly. Pain causes dystonia to increase. Bowel distention is a common source. When we can overtly see & visually behold such postural imbalance that we KNOW kills hips... why wait for x-rays to be abnormal to act? Posture is the only early warning. 'Mild' X-ray change is late. OK, the damage has been done. The hip is out. That which caused the damage to the acetabulum is still there wanting another go at it. Just angling a bone or two for “lever arm” nonsense will just give it another go round. VRO? This one that is on way out again (or still?). Shenton's line is way off. Academics did this... and there are more...

Two (of many) big city famous hospital VROs for PDH

Another famous big city hospital VRO for PDH . These are so unstable that relocation requires that there be nearly no muscle power at all to displace the unstable “reduction”. Tension (and power) is removed by 'femoral shortening', removing a large length from the femur bone leaving he long muscles limp (but doing nothing for the cuff muscles). Femoral shortening is the [temporary] patch to the instability at surgery of VRO in PDH. Muscles slowly recover and pull up the slack. Neurological imbalances were NOT altered and so that time bomb is now reactivated and ready to detonate.

One method [adopted by a COUNTRY] to seek acceptable reported rates of failure was to defer VROs until 18 yo. ??? (There was no post operative outcome monitoring as of 19 yo). THAT WORKS! For the numbers...

But, thinking shoulder & rotator cuff... a computer model of paralytic hip dysplasia included relative muscle length and orientation change with varying degrees of subluxation, dislocation, and socket deformity. Ohh computer... ahem... Yes human? Is there a way to reset the muscular cuff such that the muscular tension center

migrates back to the skeletal cup center? “I will tell you. But first you must suffer” Yeah, I know. Build you a working model...

This is a lot to model, but do-able. Must include deformed models and what things become (relationships, lengths, actual surgical planes of access and so on). It took three years to get something that looked like PDH and which failed the way VROs fail. But could we do something to avoid that? Computer, is there a fix? Yes. Do NOT varus & 'derotate' [knew that already – hard way]. Instead, flex & abduct. Like the harnesses used in the nursery, fetal position? Similar, but not nearly that much. What about femoral shortening? Wouldn't need to if the affected pelvis was shortened instead.

That is two gains – easy to do and a great source of needed bone for free.

THIS?? Yes, but not yet...

This. (above) It worked. Fixation metal for VRO simply didn't fit. Shoulder trauma locking plates and screws did work. But those are nasty to apply and as the metal screws and plate self weld, a beast to remove. Plan B : ===>

Plan B had no metal plate nor screws with all the additional surgical dissection those demanded. Through the same visual exposure, use a straight pin down the femur crossing the angled bone plane on which the femoral head, neck & shoulders [trochanters] are spun into flexion abduction – a geometry similar to a Cafe'Door hinge – free to swing but with a central stable spot. Yes, a “saloon door” has the same thing... but come on!

The proximal best flexion + abduction is by its behavior , it's stability. Then hip extension is simply had by extending the femur below to anatomic plus a wee bit for normal 'hyper-extension'. Trim edges if it makes a better contour.

Sitting up with knees bent and shins vertical will maintain neutral rotation until the osteotomy (bone cut) begins to heal. Diligence in the first two weeks to leg rotation is needed. The pin rotation freedom removes high torque from the hip capsule repair for the critical first two weeks. Hip flexion and extension (PT starts post op day #1) is repeated several times per day to maintain functional planes in tissue remodeling. Our goal is standing and begin assisted walking (according to safety & skill level) in 8 weeks. The acetabular repair is also done in Cafe'Door as are SPMLs as is similar to that of the S.L.O.B. acetabular augmentation surgery but uses native bone which is abundant from the pelvic shortening (moves iliacus & glutae down).

Psoas & rectus femoris are both directly reset. The latter also is moved to cover the osteotomy which is sealed before closure. The hip capsule, is advanced and doubly sewn to provide hip socket protection from new bone and add even more hip joint stability.

Stability is so good that the hip is fully exercised to test tension throughout the operation. This surgery does NOT require any bracing. Simple foam wedge between legs, for comfort and turning, is plenty.

Range of motion by PT begins on the day after surgery while teaching the family how to do it as well. No casts. We sit up as soon as comfort allows. On post operative day one, a Dulcolax suppository is used to help stimulate full bowel motility. Water stool softeners are not used as they bloat in the absence of brisk peristalsis. Dual anesthesia is used during surgery. General and local. This wards off “ileus” (reflex shut down of intestines in reaction to pelvic surgery). It also allows much less use of narcotics. No paralytics (curare-like) are used to allow better intraoperative tension appreciation. Temporary filaments are implanted in the wound to deliver superficial and deep local anesthesia which nearly eliminates narcotic use altogether. This way many complications that are known to cause more need for hospital care are avoided. Hospital stay is greatly reduced. There are newer rods which can lock in place as well as many options for wound dressings. Although Cafe'Door hip rebuilding is bigger surgery than a single side VRO, the VRO is seldom ever done to one side only as it would leave the patient lop sided by its very nature. The scope of Cafe'Door is much less than BILATERAL VRO and rarely done to both sides but never, if needed, at the same time. Big surgery requires good metabolism and a healthy nourished preoperative state. Gastrointestinal problems, if present, should be handled first. A preoperative urine screen having a high specific gravity is a warning that there may be blood volume contracture from chronic dehydration.