Lisfranc fracture-dislocation precipitating acute Charcot arthropathy

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Lisfranc fracture-dislocation precipitating acute Charcot arthropathy Powered By Docstoc
					Lisfr anc fr actur e-dislocation pr ecipitating acute Char cot ar thr opathy in a

neur opathic diabetic foot: impor tant lessons fr om a case r epor t


1*
     Joey Yeoh, 1Kenneth Ross Muir, 1Ajith Munasinghe Dissanayake, 2Wendy Yu Tzu-Chieh




1
    Department of Endocrinology & Diabetes, Centre for Clinical Research &

    Effective Practice, Room 33, Support Building, Middlemore Hospital,

    Auckland, New Zealand
2
    Department of Orthopaedic Surgery, Middlemore Hospital, Auckland, New Zealand




Email addr esses:

JY        : drjoeyyeoh@gmail.com

KRM : muirk@middlemore.co.nz

AMD : AMDiss@middlemore.co.nz

WYTC : YuW@middlemore.co.nz




Cor r esponding author :

*Joey Yeoh

Email : drjoeyyeoh@gmail.com

Phone : 0064-09-2760044 ext 2138

Fax      : 0064-09-2709737




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Abstr act
       The Lisfranc injury is relatively uncommon yet remains popular in the literature due

to its variable causative mechanisms and subtleties in radiographic features despite its

potential for disabling long term outcomes if treatment is inadequate, inappropriate or

delayed. These injuries are especially pertinent in diabetic patients, especially those with

neuropathy, since they are more common, can lead to Charcot neuropathic joint, ulcers and

have different causative mechanisms compared to the general population. We describe the

case of a neuropathic diabetic patient who presented with a Lisfranc injury which precipitated

the development of acute Charcot arthropathy in the right foot. The case serves to illustrate

several important points about the Lisfranc joint and associated injuries in diabetic patients.


Intr oduction
       Lisfranc fracture-dislocations/injuries involve the Lisfranc joint which is named after

the 18th century French field surgeon, Jacques Lisfranc de Saint-Martin [1]. Although the

tarsometatarsal joint (TMT) was described by Jacques Lisfranc as an amputation level, he did

not describe Lisfranc injuries [2]. Lisfranc injuries can be bony, ligamentous or a

combination of both and can result from direct or indirect and high-velocity or low-velocity

mechanisms [3, 4]. In non-diabetic patients, high-velocity indirect mechanisms which cause

axial loading or rotation on a plantarflexed foot are most common [3]. In diabetic patients,

especially those with peripheral neuropathy, Lisfranc injuries can result from minimal or no

trauma and can be a precipitant and/or manifestation of Charcot arthropathy [3, 4].

       Clinical symptoms include soft tissue swelling, increased warmth, inability to weight

bear and significant pain [1, 3, 4]. Treatment depends on the severity and exact nature of the

Lisfranc injury, ranging from conservative immobilization by casting to open reduction and

internal fixation (ORIF) with Kirschner wires (K-wires), transarticular absorbable screws or

plate and screws [5]. We report a case of a diabetic patient with peripheral neuropathy who

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presented with a Lisfranc injury leading to acute Charcot arthropathy affecting the right foot.

We use the discussion section to illustrate several salient points about the Lisfranc joint and

related injuries in diabetic patients.


Case Pr esentation
        A 56 year old Caucasian male presented to the endocrinology and diabetes ward via

the podiatrist with a 5 day history of a hot, swollen and painful right foot leading to the

inability to weight bear over the past 2 days. The patient had slipped down 2 steps while

walking down a short staircase at home 6 days prior. The podiatrist had been seeing him

regularly in the outpatient diabetic foot clinic for his left 1st metatarsal head plantar

neuropathic ulcer. He had been put into a left total contact cast (TCC) for the past 1 month

following debridement and dressing which resulted in good healing of the ulcer. Other than

the local symptoms affecting the right foot and the inability to mobilize or weight bear due to

pain, the patient was well with no symptoms of overt infection or sepsis.

        The patient is a known Type 1a diabetic since 1982 (26 years duration) with

established microvascular complications due to the long duration of diabetes and chronically

sub-optimal glycaemic control. He has end stage renal failure (ESRF) from diabetic

nephropathy and has been on renal replacement therapy for the past 5 years. He has bilateral

stable proliferative retinopathy with previous multiple laser photocoagulations and residual

visual acuity of 6/36 right and 6/9 left. He also suffers from peripheral neuropathy with

plantar neuropathic ulcers affecting the right and left foot in the past. There is no history of

Charcot arthropathy affecting the ankles or feet. There is also a background of treated

dyslipidaemia and hypertension over the past 12 years.

        There is a family history of Type 2 diabetes in the father and grandmother. He does

not smoke or consume alcohol and works as a storeman. His list of current medications

include; insulin Lispro (Humalog) 12 units three times a day (TDS) pre-meals subcutaneously

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(S/C), insulin Glargine 42 units once daily (OD) S/C, Metoprolol succinate 23.75 mg OD,

Cilazapril monohydrate 2.5 mg OD, Erythropoietin beta 6000 units thrice weekly S/C,

Simvastatin 40 mg OD, calcitriol 0.5 micrograms thrice weekly, calcium citrate 1200 mg

once weekly, Aspirin 100 mg OD and Omeprazole 20 mg OD. He weighs 101.5 kilograms

(kg) and stands 1.85 metres (m) tall, making the body mass index (BMI) 29.7 kg/m2.

       Cardiovascular, respiratory and abdominal examination revealed no significant

abnormalities. Neurological examination using Semmes-Weinstein 10g (5.07) monofilament

revealed loss of neuroprotective sensation bilaterally. There was also loss of proprioception

and vibration sense bilaterally. Peripheral pulses were normal. The right foot was noted to be

oedematous, erythematous and was tender to palpation around the dorsal midfoot. The

cutaneous temperature of the right foot was 4oC higher than the left. The recently healed left

plantar ulcer was also seen.

       He had bilateral feet and ankle radiography, including weight-bearing films. The left

foot and ankle films were unremarkable, showing no overt neuropathic arthropathy or

Lisfranc joint problems. The right foot dorsoplantar weight-bearing film showed

malalignment with lateral displacement of the 2nd metatarsal by 3 mm and a mild 2 mm

lateral displacement of the first metatarsal consistent with a homolateral (Type B2) Lisfranc

injury (Figure 1). The lateral weight-bearing film showed the classical “step-off” point

caused by the dorsal displacement of the 2nd metatarsal relative to the medial cuneiform

(Figure 2).

       Magnetic resonance imaging (MRI) was subsequently done to provide structural

information about both feet and ankles. Axial and coronal T1 and Short T1 inversion

recovery (STIR) sequences were undertaken. The left foot did not reveal any significant

findings while the right foot scan showed high STIR signal within all the muscles of the

flexor compartment, oedematous thickening of the interosseous muscles and low T1 with


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high STIR signal within the 2nd and 3rd metatarsal bases and tarsal bones consistent with

acute (Stage 1) Charcot changes. Associated oedematous thickening of the dorsal

subcutaneous tissue was also present. A 6 mm lateral displacement of the 2nd and 3rd

metatarsals was also detected. Oblique axial STIR views revealed a complete rupture of the

Lisfranc ligament (Figure 3).

        He was treated initially with bedrest and analgesia followed by TCC for the right

Lisfranc injury and acute Charcot. A prefabricated pneumatic walking brace (PPWB) was

used for the left leg to prevent unequal distribution of pressure and thus possibility of further

ulceration. We discharged the patient with the plan for the TCC to remain for the next 4 – 6

months (with 2 – 3 weekly re-casting) depending on resolution of the acute phase and

achievement of anatomic alignment, followed by bracing. In the long term, custom made

orthotics will be arranged for him. He will be reviewed regularly in outpatient podiatry and

diabetic clinics.


Discussion

        This case depicts a neuropathic diabetic patient with homolateral (Type B2) Lisfranc

injury and complete rupture of the Lisfranc ligament following minimal trauma. These

injuries undoubtedly lead to fragmentation stage (Stage 1) acute Charcot arthropathy.

Important learning points about the Lisfranc joint and associated injuries in diabetic patients

can be derived from this case, but this discussion will be better appreciated if preceded first

by a brief review of the Lisfranc joint complex, classification of Lisfranc injuries and stages

of Charcot arthropathy.

        The Lisfranc joint complex is the articulation between the three cuneiforms and the

cuboid proximally and the base of the five metatarsals distally [1, 3, 4, 6]. It is also known as

the TMT joint and represents the junction between the forefoot and midfoot [1, 3, 4, 6]. The

stability of the joint is dependent on its bony configuration and more importantly,

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surrounding ligamentous attachments [3, 4, 6]. These ligaments are divided into plantar,

dorsal and interosseous components [3, 6]. Importantly, there is no interosseous ligament

between the 1st and 2nd metatarsal bases [3, 6]. Instead, the stability there is contributed

mainly by the strong Lisfranc ligament which extends obliquely from the base of the 2nd

metatarsal to the medial cuneiform, keeping the 2nd metatarsal base (keystone) in place and

stabilizing the medial column of the midfoot [3, 4, 6].

       Three radiographic classification systems exist for Lisfranc injuries; Quenu and Kuss

(1909), Hardcastle et al. (1982) and Myerson et al. (1986) [3, 6]. Quenu and Kuss divided

injuries into three categories; homolateral, isolated and divergent [3, 6]. Homolateral injuries

involve dislocation of metatarsals in the same direction, isolated injuries involve dislocation

or subluxation of one or two metatarsals dorsally with the rest being stable and divergent

injuries involve displacement of the metatarsals in different directions [3]. The Hardcastle

system divides injuries into types A, B and C [3, 6]. Type A involves complete incongruity of

the Lisfranc joint complex with complete dislocation of all metatarsals, Type B involves

partial incongruity with one or more metatarsals dislocated and Type C involves

displacement of medial and lateral metatarsals in opposite directions (equivalent to divergent

type) [3, 6]. The Myerson system expands the Hardcastle system and further classifies Type

B into B1 and B2 with B1 involving medial dislocation of the 1st metatarsal and B2 involving

lateral dislocation of the 2nd to 5th metatarsals respectively [3, 6]. Myerson also further

classified Type C into C1 and C2 with C1 involving partial displacement and C2 involving

total displacement of metatarsals [3, 6].

       Charcot arthropathy affects 0.16% to 13% of diabetic patients and the incidence of

acute Charcot of the foot and ankle ranges from 0.15% to 2.5% [7, 8]. While a discussion

about Charcot arthropathy is beyond the scope of this report, it is important to understand the

different stages of the disorder as these affect treatment choices. Although there are three


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staging systems available (Eichenholtz, Sella & Barrette and Armstrong & Lavery), the most

commonly used system for midfoot hypertrophic neuropathic arthropathy is the modified

Eichenholtz system [7, 8]. Stage 0 (pre-fragmentation) involves clinical features of local

inflammation; Stage 1 (fragmentation) involves periarticular fractures, joint dislocations and

instability; Stage 2 (coalescence) is characterized by reabsorption of bone debris and Stage 3

(reparative/consolidation) is associated with re-stabilization of the foot with fusion of the

involved fragments [7, 8, 9]. Stage 0 and 1 are collectively known as acute Charcot while

Stage 2 and 3 are known as subacute and chronic Charcot respectively [8].

       We now proceed to discuss the important points about the Lisfranc joint and Lisfranc

injuries in diabetic patients. Firstly, although Lisfranc injuries are rare, accounting for only

1% of orthopaedic injuries, they are more common in the diabetic population [3, 4, 6].

However, the exact prevalence and incidence of Lisfranc injuries in diabetics is currently

unknown [3, 4]. Secondly, Lisfranc injuries in diabetics frequently occur following minimal

trauma (such as slipping or tripping off a step or a curb) or no obvious trauma at all [3, 4].

Diabetic patients with loss of neuroprotective sensation are at higher risk of developing

Lisfranc injuries without antecedent trauma because of the increased likelihood of repeated

unperceived microtrauma similar to the neurotraumatic theory of Charcot pathogenesis [3, 4,

9]. Thirdly, complete rupture of the Lisfranc ligament usually requires a significant amount

of force, but in diabetic patients only minimal force may be required secondary to

calcification of ligaments, repeated microtrauma and poor healing which all result in loss of

tensile strength and susceptibility to rupture [10].

       Fourthly, the Lisfranc joint is the most common site affected in Charcot arthropathy

of the foot and accounts for 45% of cases [9]. In fact, the medial column of the TMT joint is

where early Charcot changes usually begin [7, 8, 9]. Therefore, Lisfranc injuries and the

resultant architectural instability coupled with pre-existing neuropathy can precipitate the


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Charcot process or alternatively be the first sign of an underlying Charcot process [7, 8, 9]. In

addition, Lisfranc injuries and acute Charcot foot may be clinically indistinguishable [3, 4, 7].

It is therefore essential to look closely for Charcot changes on imaging in diabetics with

Lisfranc injuries [3]. Lastly, Lisfranc injuries in diabetics that do not result in an acute

Charcot process may still lead to unequal distribution of pressure in the affected foot and this,

coupled with poor wound healing and the propensity for infections inherent in diabetics will

lead to the development of plantar ulcers if patient presentation and diagnosis is delayed [7,

8, 9].

         One final but crucial point regarding imaging of Lisfranc injuries in diabetic patients

is that radiographic findings are frequently subtle, easily missed and may not properly

represent the underlying degree of diastasis [4, 6]. This is aptly demonstrated by the case

presentation where the subluxation/dislocation of the 2nd metatarsal on MRI was 6 mm

compared to 3 mm on plain radiography. In fact, up to 10% of subtle injuries such as those

associated with minor or no trauma in diabetics can spontaneously reduce and thus be missed

if weight-bearing radiographic views are not obtained [6]. Therein lies the value of MRI

examination which allows optimal evaluation of malalignment in the midfoot, with the

oblique axial plane allowing visualization of the entire length of the Lisfranc ligament and

therefore allow detection of partial or complete ruptures of this important structure [6].


Conclusion
         Lisfranc injuries are relatively uncommon injuries affecting the midfoot which

frequently have different characteristics in the diabetic population. Understanding these

differences allow us to diagnose, treat and monitor the resolution of the injuries effectively

and therefore prevent poor anatomic alignment which can have particularly dire

consequences in diabetic patients.



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Consent
Written informed consent was obtained from the patient for publication of this case report. A

copy of the written consent is available for review by the Editor-in-Chief of this journal.


Competing Inter ests
The authors of this case report declare that they have no competing or financial interests that

could influence the preparation of the manuscript.


Author s' Contr ibutions
KRM collected the details of the case and was responsible for compiling the case

presentation. WYTC were responsible for the literature search. JY coordinated the entire

process and was responsible for the literature review and preparation of the first draft of the

manuscript. AMD managed the patient during in-patient hospital stay. All the authors read

and approved the final manuscript.


Refer ences
   1. Sands AK, Grose A: Lisfranc injuries. Injury Int J Care Injured 2004; 35:SB71-SB76.

   2. Cassebaum WH: Lisfranc fracture-dislocations. Clin Orthop 1963; 30:116-129.

   3. Desmond EA, Chou LB: Current concepts review: Lisfranc injuries. Foot Ankle Int

       2006; 27:653-660

   4. Crim J: MR imaging evaluation of subtle Lisfranc injuries: the midfoot sprain. Magn

       Reson Imaging Clin N Am 2008;16(1):19-27.

   5. Zgonis T, Roukis TS, Polyzois VD: Lisfranc fracture-dislocations: current treatment

       and new surgical approaches. Clin Podiatr Med Surg 2006; 23:303-322.

   6. Gupta RT, Wadhwa RP, Learch TJ, et al: Lisfranc injury: imaging findings for this

       important but often-missed diagnosis. Curr Probl Diagn Radiol 2008; 37:115-126.


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7. Armstrong DG, Peters EJG: Charcot’s arthropathy of the foot. Int Diab Mon 2001;

   13(5):1-5.

8. Sommer TC, Lee TH: Charcot foot: the diagnostic dilemma. Am Fam Physician 2001;

   64:1591-8.

9. Schon LC, Easley ME, Weinfeld SB: Charcot neuroarthropathy of the foot and ankle.

   Clin Orthop 1998; 349:116-31.

10. Wyatt LH, Ferrance RJ: The musculoskeletal effects of diabetes mellitus. J Can

   Chiropr Assoc 2006; 50(1):43-50.



Figur e Legends


Figur e 1. Dor soplantar weight-bear ing film of the r ight foot. The radiograph shows a

3 mm lateral displacement of the 2nd metatarsal and a mild 2 mm lateral displacement of

the first metatarsal consistent with a homolateral (Type B2) Lisfranc injury.


Figur e 2. Later al weight-bear ing film of the r ight foot. This radiograph shows the

characteristic “step-off” point (arrow) caused by dorsal displacement of the 2nd metatarsal

relative to the medial cuneiform.


Figur e 3. STIR sequence oblique axial view of the r ight foot. This shows the 6 mm

lateral displacement of the 2nd and 3rd metatarsals and a completely ruptured Lisfranc

ligament which should usually be seen crossing the 1st metatarsal space obliquely. The

ruptured ligament would explain why the typical “fleck sign” was absent on the plain

radiograph as a ruptured ligament will not avulse the lateral border of the medial

cuneiform or the medial border of the 2nd metatarsal base.




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Figure 1
Figure 2
Figure 3

				
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