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Interesting case today of a Sgt. Major paratrooper who injured right ankle last September when he landed awkwardly after jumping out of plane. He presented with ongoing pain (described as tooth-ache like) in the ankle around the medial malleolus) when running. Previous MRI (December) revealed damage to the anterior talofibular lig.,maybe some damage to calcaneofib, some damage to the deltoid, possibly damage to the trochlear surface and bruising to the tibial marrow- nice. Pain is reproduced with resisted inversion and on weightbearing end RoM dorsiflexion. Peroneal strength was slightly diminished; proprioception poor; RoM no obvious differences from uninjured side. In terms of orthoses, he already had a pair of foamthotic things, which “weren’t doing anything”. Thinking 4D, I used the foamthotics and mocked up chair-side a 6mm heel lift (to try to limit dorsiflexion), 6 degree varus rearfoot post (to reduce stress on deltoid) and 3 degree valgus forefoot post (to reduce stress on ant talofib) which the patient felt gave an instantaneous improvement of symptoms. Has anyone else come across similar injuries / had experience with orthoses in similar cases? Any thoughts please.

 

Good job, Dr. Spooner. That is exactly what I would have done to modify the orthoses. Also, put the patient into a hiking/military boot with at least a 1/2" heel height differential and that has an upper that extends superior to the malleoli (alternatively may use lace-up ankle brace with medial and lateral velcro straps at ankle in a low-cut shoe).

In addition, have the patient ice 20 twice daily to most symptomatic areas and take NSAIDS. Also don't expect rapid relief of all pain, MRI evidenced "bone bruising" sometimes takes months and months to resolve. I see quite a few injuries such as this that are caused by traumatic injuries in the workplace.

 

The most important issue here is that the patient felt instantaneous improvement, and not what the research or I think...but here is my 2 cents.



I can't believe that, despite your forefoot post, that a 6 degree rearfoot post would agree with the lateral ligament pathology. Either, this is very minor in relation to medial stress pathology...or more likely, that this has long healed since September. In fact most structures should have if managed appropriately. The exception would be trochlear damage which may be quite recalcitrant. Pain is reproduced by a short lunge finding, and if the trochlear is relevant, prognosis may be poor.
I think your 6 degree rearfoot post is doing more for the inversion musculature that is painful when resisted. The post is just reducing its workrate and length demand.


On a side issue, my gut feeling is that if you stabilise the rearfoot, passive mid/fore foot supination would provoke vague midfoot symptoms. Just a hunch with the presentation you paint.




Again, the fact that the patient experience significant gains in signs and symptoms means that your treatment is 100%. The question from my end is do we know why?

 

Sounds familiar. May possibly have a crush lesion on the medial wall of the talus or on the deep fibres of the deltoid. If the ATF ligament and the CF ligament are both damaged than it is logical to assume that it has been a significant inversion injury. rarely when this happens you may get one of these "POMI"(POSTERO-MEDIAL IMPINGEMENT) lesions. The symptoms of a pomi are quite similar to those that you ave described and the method af injury appears to be consistant. From my experience of these injuries a medial wedge under the rearfoot does help significantly with pain. My theory on why would be to do with the fact that if there is a crush injry or lesion in the space between med mall and med wall talus, then by limiting any movement in this space you will prevent further aggravation to the deep deltoid ligament and med wall of talus. Physical therapy by way of mobilisation of talocrural joints are very important as part of treatment. For athletes I have found a basket weave with the foot held incerted is very effective, heel locks make this method of taping even better!
There is an excellent article in the american journal of sports medicine that descibes this condition however it discusses surgical options and doesn't mention conservative treatment methods in any depth.

 

But dorsi-flexion is the provocative/limited motion. One would assume that the impingement is anterior. And besides would a POMI enjoy having its rearfoot inverted?

 

I tend to agree. No pain was reproduced from the lateral side. All symptoms were medial, and the resisted inversion pain obviously implicates contractile tissue- basic Cyriax. The forefoot post was added as much to help with the mobile plantarflexed first ray as anything else, which I felt may have contributed to rf pronation but may help prevent any recurrant inversion injury too; given the poor proprioception at this stage. However, if you consider gait as a 4D process (and remember this guys problem is running, not static standing), you can easily justify its use here as a stress reducer for the lateral ligs.

Look at a basic kinematic curve for the STJ, when are the medial ligaments under greatest stress? When are the lateral ligaments under greatest stress? Not simultaneously, right?

One of the finest pieces of advice ever given to me as an undergraduate podiatry student in regard to biomechanics was to think 4D (incidently this advice was given to me by a PhD podiatrist specialising in dermatology). When does the rearfoot post of an orthoses have a functional effect? When does the forefoot post have a functional effect?

One of the things that is discussed in mine and Kevin's paper which due for publication in JAPMA in the next month or so is the importance of the phasic change in STJ axial position during gait, that is to say just because you may see someone with a medially deviated STJ axis in RCSP or during early contact, doesn't mean that this same individual cannot have a laterally deviated axial position during propulsion. So if we wish to minimise tissue stress about the subtalar joint, we should attempt to minimise the axial excursion during the joints pronation phase and supination phase. Hence my ongoing taunt that orthotic prescription writing using SALRE is based on many of the same principles of Root based orthotic intervention- hold the STJ axis close to it's mid range = minimise tissue stress / hold the STJ close to neutral = minimise pathology (same thing really, as well you know Prof. Kirby of Kirbyshire ).

Here's a nice poser for all of you:

Kevin is currently discussing sinus tarsi compression in his thought experiments and beautifully demonstrating how pronation and a medially deviated axis can cause this pathology. Of interst though is that sinus tarsi syndrome can also occur as a result of inversion sprains to the ankle. Question how would we orthotically (is that a word?- it is now) manage sinus tarsi syndrome in someone who has chronic lateral instability of the ankle?

 

The forefoot valgus (2-5) wedge may or may not help him (by itself) with his running pain but I would think this wedge would make it more comfortable for his walking activities. Counteropposing moments across STJ axis help stabilize the STJ axis against external forces. This is a similar mechanical idea to the age-old idea of using opposed rigging lines attached to the mast of a sailboat to add stability to the mast by resisting moments created by wind loading forces.

I would agree with many of the principles advocated by Root and I still use many of them to this day. However, the neutral position theories of orthosis prescription are seriously outdated and, in fact, are contraindicated in some instances. SALRE theory and tissue stress make much more sense for orthosis prescription considering our current knowledge, even though they share many common philosophies and orthosis prescription ideas with the ideas of Root et al.

I treat them in much the same way as with a patient with medially deviated STJ axis. However, in patients with previous history of ankle sprains, smaller medial heel and arch wedges and slightly larger forefoot valgus wedges are used.

 

1. How is sinus tarsi assessed and comprehensively diagnosed?

2. We all love labelling things and putting them into neat boxes. I have worked under and with many a pedantic clinician that salivates over a list of pathologies. Your example of sinus-tarsi and chronic lateral instablity, would have most staring into headlights like stunned rabbit.


I assume that sinus tarsi syndrome 'hates' end-range rearfoot eversion. And common-sense suggests that chronic lateral instability would 'hate' end-range inversion. "Orthotically", the latter would not tolerate a rear-foot inversion post, while the STS would not tolerate any forces augmenting rear-foot eversion.

The other thing many forget is prioritising acute injury over chronic. Invariably, treat an acute injury well and it goes. A chronic injury is one that is either poorly managed, and/or involves avascular tissue that is a poor healer. Forget the chronic, plicate the acute, and soon you only deal with one pathology.

And one other thing. If sinus tarsi syndrome exists, why do we all assume that its pathology is compressive??? Doesn't it contain ligamentous structures that could plausibly be stained when the bullet-hole opens beyond its limits? If it is compressive, why has this condition been reported to have resulted post lateral ankle sprain...which involves tension forces on the lateral aspect of the STJ?



Good question, and clinically relevant and challenging; but in terms of STS, I think we are making assumptions on top of assumptions.

 

Good questions, Ron. Sinus tarsi syndrome, or sinus tarsitis, is a condition where the patient describes pain in the area of the sinus tarsi that tends to get worse with increased duration of weightbearing activity. It is generally described as a deep aching or gnawing type of pain that is generally relieved by rest.

On clinical examination there is mild tenderness on slight palpation and moderate severe tenderness on deep palpation of the sinus tarsi with the subtalar joint (STJ) held in a slightly supinated position (to open up the sinus tarsi and allow palpation of the contents of the sinus tarsi). Another very characteristic clinical examination finding, and one which I have never seen written within the medical literature, is that these patients will have a feeling of pain within the sinus tarsi with the foot pushed into its maximally supinated position (this maneuver won't cause pain on the unaffected side). They describe this pain as eminating from the sinus tarsi area and the pain becomes worse with increased STJ supination moment applied manually.

I see two distinct categories of patients with sinus tarsi syndrome:

I. Those patients with no history of significant inversion ankle sprains but that do have significant medial deviation of the STJ axis.

II. Those patients with a history of one or multiple inversion ankle sprains that are maximally pronated in gait or undergo late midstance pronation during gait.

I believe that type I sinus tarsi syndrome (STS) is caused primarily by increased compression forces between the lateral process of the talus and the floor of the sinus tarsi of the calcaneus, causing either bone bruising or soft tissue damage, due to the high STJ pronation moments during gait. To my knowledge, this idea that excessive STJ pronation moments from ground reaction force (GRF) acting across a medial deviated STJ axis are responsible for sinus tarsi syndrome was first described in the medical literature within my paper on STJ axis rotational equilibrium from 1989 (Kirby KA: Rotational equilibrium across the subtalar joint axis. JAPMA, 79: 1-14, 1989).

Type II STS is most likely caused by some form of scarring or irritation of the soft tissue structures within the sinus tarsi that have been primarily damaged by prior traumatic inversion ankle sprains. In these patients, there is likely an increase in bulk or a decrease in compliance in these structures so that when the sinus tarsi is closed and the sinus tarsi soft tissue structures are compressed during STJ pronation, these damaged structures become inflamed and painful. In these patients, just the act of being in a maximally pronated position during weightbearing activities may cause pain so that these patients don't even need to have a medially deviated STJ axis. They can simply demonstrate late midstance pronation during gait (in an otherwise fairly normal appearing foot) that causes enough compression of the sinus tarsi to elicit the pain.

It is rare to find patients with type I STS that do not enjoy complete relief of their symptoms with a medial heel skive orthosis (Kirby KA: The medial heel skive technique: improving pronation control in foot orthoses. JAPMA, 82: 177-188, 1992) that has been modified to decompress the sinus tarsi. However, patients with type II STS may need very little varus wedging in the rearfoot but may also need valgus wedging in the forefoot to prevent late midstance pronation from occurring to have improvement of their symptoms. Patients with type II STS are not as easily made asymptomatic with orthoses and I assume that this is a result of their scarring of the lateral ankle and sinus tarsi soft tissue structures from prior inversion ankle sprains.

The above analysis of sinus tarsi syndrome is based on my 20+ years clinical experience of seeing numerous patients with this condition (probably over a thousand) and noting their response to clinical tests and various orthosis modifications. My clinical observations are further supported by mechanical modelling of the forces acting across the sinus tarsi region of the foot http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=1869.

 

One problem I have is with the palpation technique. How do you know you are not hitting part of the lateral ligament complex in you ST palpation? Furthermore, in an inverted position, the pathologic ATFL, particularly its more caudal aspect, would not appreciate palpation, let alone firm palpation.

Kevin, as usual, you have described this pathology quite well, and better than I could ever hope. And you have gone further to differentiate one condition into 2 completely opposing syndromes; one compressive and one tensile.

That is why, I think, musculo-skeletal education should be concerned about compressive versus tensile patterns...and not be obsessed with pedantic diagnostic descriptions that fit neatly into a box.

If you teach a student to understand compressive versus tensile pathology patterns; if you teach a student to somehow understand your thought experiments; rather than teach for "sinus tarsi syndrome" go to recipe page 42 and do this plan a.; we will get practitioners that "understand" and be able to be pragmatic to deal with the spectrum of different presentations in the clinical environment, rather than a dogmatic one-trick-pony that "remembers" how to regurgitate plan "a" that "should work".