4. Stiff or Painful Knees after TKA
손 승 원 계명의대
A. The Stiff TKR;(Norman A. Johanson, 1997.)
1. Introduction & Definitions;
*Recovery period; A Pt. whose knee by clinical exam. has 90` of flex. & comes to within 10` of full exten. & who has no complaints of pain or functional difficulties is not considered to have a stiff knee.
*A Pt. 1 year after TKR who has clinically acceptable motion but who complains of knee stffness, has difficulty getting out of a chair, has pain on climbing stairs, & walks with an observably stiff-knee gait shoud be further evaluated for underlying knee problems.
*Stiffness is closely related to Pt.`s own motivation to gain a functional ROM, and his or her willingness to endure pain to achieve that goal.
Pt. of minimal supportive care; more stiffness complain.
*Stiffness, which is nearly always present during the early postop. period, gradually decreases over time, & is, therefore, a valuable marker of improvement throughout the recovery period.
*Surgical pain is the most important cause of early knee stiffness. It results in both quadriceps & hamstring guard- ing & makes passive flex. & ext. difficult to perform.
*This factor has formed the theoretical basis for implementation of in-hospital continuous CPM. CPM has no capacity to promote knee exten.
*Postop. knee stiffness usually subsides within 6 to 8 wks. Knee ROM generally improves steadily through the first 3 mns, & then less rapid progress may be seen for an additional 9 mns or more.
*If a limited or deteriorating ROM occurs, the following Cx should be considered: 1) infectiom, 2) mechanical Cxs related to the implant or soft tissue, 3) impending arthrofibrosis, & 4) reflex sympathetic dystrophy(if associated with severe pain & vasomotor skin changes).
*The late onset of knee stiffness following a relatively symptom-free period may be suggestive of one of the fol- lowing conditions: 1) infection, 2) overuse synovities or tendinitis, 3) synovitis secondary to RA, particulate wear debris, or recurrent hemarthrosis, & 4) implant loosening or breakage.
2. Pathphysilolgy of joint stiffness;(Shawn W O`Driscoll,2000) The 4 stages of stiffness:
1) Bleeding; The first stage of stiffness, occurring within minutes to hours following articular surgery or trauma.
2) Edema; the second stage, occurs during the next few hours or days.
3) Granulation tissue; The third stage, occurs during the first few days or weeks.
4) Fibrosis; During this fourth stage, the granulation tissue matures, forming dense, rigid scar tissue(collagen type I fibers).
3. Causes of TKR Stiffness;
1) Infection:
Early infection(within the first 6 weeks):
Late infection:
2) Mechanical Problems(Implant/Soft tissue):
*Inadequate bone resection combined with persistent ligamentous imblalance or thightness may result in knee stiffness.
*If, during trial reduction, asymmetric or symmetric tightness is recognized, it can be corrected by either revising the bone cuts, releasing the liagaments, or a combination of the two.
*If a flexion contracture is present, more distal femur should be resected and/or a posterire capsular release per- formed.
*If the residual contracture is severe(>15`), some additinnal bone may be removed from the proximal tibia, provid- ed that doing so does not make the flexion gap too wide. However, if tibial resection is essential & the flex. gap threatens stability in flexion , the femoral component could be set more posteriorly with augmentation, either by cutting more bone anteriorly or by using a larger size fem. component.
*The problem of tightness in flexion is most important from the standpoint of postop. knee stiffness. If tightness is recognized intraop., PCL recession can be considered or the tibia can be cut again at neutral or with a 5` post. slope.
*The selection of an oversized femoral component or the post. placement of the component can lead to a dispro- portionately narrow flexion gap. It is difficult to manage this problem by resecting more tibia, especially if the extension gap is adequate, because resection of additional tibia may lead to an unacceptable amount of laxity in extension. Downsizing the femoral component and resecting more post. femur will expand the flex. gap without affecting stability in exten.
*Inadequate release of tight capsular and liamentous structures is an important cause of the stiff TKR, but is diffi- cult to measure. Poor flex. & exten. may result from inadequate release or reccession of a tight PCL. Flex. con- tractures most commonly result from inadequate post. capsular release in conjunction with insufficient bone resection. The MCL in varus deformities, and the LCL and iliotibial band in valgus deformities often require release to prevent asymmetric implant wear and to promote optimal range of knee motion. Ext. rotation of the fem. component has been recommended to enhance lig. balancing in flex. & to facilitate optimal pat. tracking.
*Although not necessarily a causative problem in TKR stiffness, pat-fem. dysfunction may cause pain that may promote stiffness because of disuse.
*Conversely, pat.-fem. pain may result from knee stiffness, particularly with flex. contractures. The following pat.
conditions should be considered when evaluating the stiff TKR: 1) pat. not resurfaced. 2) inadequate lat. release, 3) asymmetrical cutting of pat., 4) excessive elevation of the joint line, 5) internal rotation of the fem. component, 6) the formation of intra-articular adhesions that tether pat. to surrounding structures, thereby altering the normal tracking mechanism, 7) pat. fx., and 8) pat. component loosening. All of these problems may be clinically evident by either loss of ROM or by Pt. complaints of stiffness.
*The generation of an excessive volume of wear debris over a given period of time causes synovitis, with pain, stiffness, and swelling being the usual result. Poor quality polyethylene, high Pt. weight and activity level, falure to remove cement and bone debris from knee joint, or implant design factors(contact stresses, poly distribution) are possible causative factors.
3) Patient-Related Factors:
*The availability an efficiency of in-hospital PT has been thought to have a significant impact on the outcome of TKR.
*An important factor in the process is Pt`s motivation to achieve a good clinical result. In addition Pt must be will- ing to undergo a regorous rehabilitation program.
4. Diagnostic considerations 1) PE:
The most important Dx. tool in the evaluation of the stiff TKR is the PE. At least two examminations should be done within the first 6 weeks to assure acceptable progress with ROM and functional status. Pt. who are having prob- lems should be seen more frequently.
2) Radiographic Evaluation:
*Plain radiograghs should be ordered within the first 6 weeks, and repeated if stiffness and pain increases. A-P, lat., & tangential pat. views should be obtained. Findings associated with knee stiffness may include one or more of the following: 1) inadequate bone resecion, 2) oversized fem. implant, 3) evidence of lig. imbalance resulting from asymmetric cement pressurization, and 4) gross maltracking or subluxation of the pat.
*Bone scans are less useful during the early recovery period and through out the first year postoperatively.
3) Aspiration & Culture:
5. Tx Alternatives 1) PT:
In a stiff, noninfected, radiorgaphically satisfactory TKR, the most important initial tx. is an adequately supervised course of sustained intensive PT, which may last from 3 to 6 mns, depending on the initial results.
2) Manipulation:
*If, during the first 3 mns, a plateau in ROM is reached, manipulation of the knee under regional or general anes- thesia should be considered. Manipulation is not necessary within the first postop. month.
*There was a significant loss of motion during the week following manipulation( Fox,1981).
*Preop. ROM is an important predicton of the resulting ROM following TKR.
3) Debridement:
*At localized tethering of the pat. or fibrous nodules that cause clunking of the pat. over the ant. flange of fem.
component; arthroscopic techniques.
*At generalized arthrofibrosis following TKR; open techniques.
4) Revision Surgery:
During revision for TKR stiffness, it is very important to fully release all structures that may have contributed to the condition, including the following: 1) quadriceps tend. & vastus intermedius adhesion to fem. & suprapat. pouch, 2) med. & lat. gutters, 3) collat. lig.s, & 4) lat. pat. retinaculum.
6. Prevention of the Stiff TKR
*The selection should be based on a published track record of satisfactory implant performance over a period of 5 to 10 years, and the technical difficulty should be compatible with the proficiency and experience of the surgeon.
Like a normal knee, a TKR design will have tolerances for tightness(stability) & laxity(flexibility) throughout a given ROM.
*Knowledge of Pt. expectations, goals, and motivations is essential for early detection of potential problems with stiffness following TKR.
B. Partial Denervation for the Tx. of Painful Neuromata Cx. TKR;(A.Lee Dellon, 2001)
1. History; Upper extremity(the past two decades), Knee pain( just 8 ys ago).
2. Pathophysiology of Neuroma Formation:
*Sprouting of the proximal nerve fibers(because this is the physiologic response of the cell bodies located in the dorsal root ganglion), and production of nerve growth factor by the distal(denervated) Schwann`cells.
*One of the most common misconceptions about management of the painful neuroma is that resection of the neu- roma always results in another painful neuroma.
*A recurrent painful reuroma will not occur if the proximal end of the nerve is permitted to regenerate into a appropriate end-organ.
3. Tx. of a Painful Neuroma:
1) Identify the correct peripheral nerve that is the source of the pain; this requires careful clinical evaluation, understanding of anomalous innervation, & diagnostic nerve blocks.
2) Resect the end-bulb neuroma, as it is the source of spontaneous C-fiber & A-delta fiber activity that signals pain, & it is mechano & chemosensitive.
3) Relocate the proximal nerve into a site that is growth factor stimulation, & away from usual pysical contact points; intramuscular placement has proven a successful strategy.
4. Cutaneous Innervation of the Knee Region:
*Infrapat. branch of the saphenous nerve-ant. midline of the region below the pat. & the lat. region below the pat.
It does not innervate the skin covering the pat. It may send branches into the distal ant. knee joint capsule.
*Branches of the obturator nerve-innervation of the post. knee capsule.
*Med. cutaneous nerve of the thigh(saph.n.br.); (=ant or med. fem.cut n.); the skin covering the pat. Its branches often lie directly over the med. retinacular nerve, and therefore a local anesthetic block in this region will block both nerves.
*A source of pain from long ant. or med. incisions-The distal saphenous nerve begins distal to the infrapat. branch of the saphenous nerve.; the region distal to the tibial tuberosity.
*The ant. fem. cutaneous nerve originates from the fem. nerve in the groin region and terminates at the pat. region.
There is usually not an identifiable neuroma of this nerve.
*The lat. fem. cut. nerve.; innervation the lat thigh & lat knee skin. ; Although pain can be referred to the knee from compression of the lat. fem. cutaneous nerve at the hip, direct injury to the knee or surgery in the knee region almost never causes a neuroma of this nerve.
*Lateral knee skin pain is almost always due to a neuroma of the medial cutaneous nerve of the thigh or the infrap- at. branch of the saphenous nerve.
5. Innervation of the Knee Joint:
*The lat. retinacular nerve is consistently present. It arises directly from the sciatic nerve, proximal to the popliteal
fossa, and continues laterally to go beneath the lat. retinaculum. It is always accompanied by the recurrent lat.
geniculate vessel & is always just distal to the vastus lat. muscle. It is immediately superficial to the synovial structures of the knee joint.
*The med. retinacular nerve is consistently present. It arises from the branch of the fem. nerve that innervates the vastus med. muscle.
*Nerves to the prepat. bursal structures arise from the terminal branches of fem. nerves that innervate the vastus intermedus muscle.
*Nerves to the post. knee capsule arise from 1) sciatic nerve over a 2-cm distance and widely innervate post. knee structures or 2) obturator nerve(Druner,1927).
6. Innervation of the Proximal Tibiofibular Joint:
The common peroneal nerve gives the branches that innervate the prox. tib-fib. joint. They travel into the struc- tures between the fibular head and Gerdy`s tubercle of the tibia.
7. Rationale for Denervation for Persistent Pain after TKA:
*Pain following TKR may have a structural or biomechnical cause, such as malalignment or loosening,or may have a medical cause, such as infection.
*What happens to the proximal end of these normal nerves after the surgery? Most probably, related to the degree of traction that occurs during the procedure, they retract into proximal tissues and form their neuromas in a quiet region, i.e. they form a nonpainful neuroma. It is hypothesized that the cause of the deep knee pain in 1 to 3% of TKA patients who have persistent pain is the nerves supplying the knee joint.
8. Diagnosis of Knee Pain of Neural Origin:
*Knee pain, in the presence of a relatively normal P.E. of the musculoskeletal system, in the presence of normal x- rays & a normal MRI, & even in the presence of a relatively normal or “negative” arthroscopy, should be consid- ered of neural origin. The diagnosis must be made based upon nerve blocks.
*Direct injury, previous surgery;
*Rating scale ; 0(no pain) ~ 10(the worst pain they ever had)
*For surgery; 5 or higher.
*1% lidocaine & o.5% bupivacaine, each without epinephrine: 5ml, of a 1:1 mixture of these two anesthetics is used.
*At about 15 minutes after the block, the pat. should be asked to climb a flight of steps, walk in the hall, or kneel on a padded chair.
9. Results of Partial Knee Denervation:
*Each pat. had had pain for at least 6 months after the arthroplasty. All pat.s were subjectively improved after selective denervation at a mean follow-up of 15 months. Knee Society objective scores improved from a mean of 55 points to a mean of 90 points.
*Patial knee denervation(1993-1998);
1) Indication; TKA 255, knee injury 89, total patients 344.
2) Results; Excellent(70%), Good(20%), Improved(5%), No change-poor(5%), Worse(0%).
3) Number of nerves removed; 1(0%), 2(19%), 3(13%), 4(26%), 5(11%), 6(31%).
4) Causes for poor results; Alzheimer`s disease, Drug abuse, Workmen`s compensation.
10. Operative Technique:
*A neuroma is not resected, but rather a segment of nerve, which may pathologically demonstrate fibrosis, is resected. This is technically a denervation rather than a neuroma resection.
*The nerve inplanted loose for a 2-cm length into the muscle. A suture is not needed. Bupivacaine is instilled into the implantation site at this time.
C. PAIN의 정의
실제로 있었거나 있다고 생각되는 조직손상에 의해 직접으로 또는 간접적으로 연관되어 표현되는 감각적 또는 정서적으로 불유쾌한 경험(International Association for the Study of Pain).
즉 조직 손상이 발생할 정도의 침해성 자극이 있어도 불유쾌한 것이 아니면 통증이 아니다. 반면에 조직 손 상 또는 신경 손상이 있은 후에는 비침해성 자극(예; 옷 스침)이라도 불유쾌한 경험을 느끼는 통증(이질통)이 나타날 수 있다.
*PAIN의 종류;
Allodynia(이질통); 비침해성 자극에 의해 통증을 인지하는 상태.
Anesthesia Dolorosa(무감각성 통증); 감각이 없는 부위에 발생되는 통증.
Causalgia(작열통); 말초신경 손상후 화끈거림,이질통,통각과민 등과 발한 이상, 혈관 운동이상을 동반하고 나중에는 이영양증세가 나타난다.
Central pain(중추성 동통); 중추신경계에 병변이 있을 때 동반되는 통증. 특히 뇌혈관 질환시 흔히 나타나므 로 post-stroke pain이라고도 한다.
Deafferentation pain(구심로 차단성 통증); 중추 신경계로의 감각 전도가 상실되어 나타나는 통증.
Dysesthesia(이상감각); 자극에 의해 또는 자극 없이 발생되는 불유쾌한 자각부전.
Paresthesia(이상감각, 지각이상); 자극에 의한 또는 자발적으로 발생되는 비정상적 감각.
Hyperalgesia(통각과민); 침해성 자극에 의한 통증이 증강된 상태.
Hyperpathia(통각과증후군); 통각과민,이질통,이상감각 등 병리적 통증 증후군으로 나타나는 상태. 특히 반 복 자극시 잘 나타나고 자극후에도 오래 지속된다.
D. 1) Is TKR more painful than THR?(Pang WW, 2000)
The deeper & more extensive op. would in THR does not mean that it is a more painful procedure than TKR.
D. 2) Intraarticular, epidural, and intravenous analgesia after TKA.(Klasen JA, 1999)
; Epidural and intravenous analgesia after TKR are equivalent methods of pain relief. In major orthopaedic proce- dures, application of intraarticular morphine does not reduce analgesic requirements.
D. 3) Thigh pain following tourniquet application in simultaneous bilateral TKA.(Worland RL, 1997)
; For TKA, using the tourniquet at a pressure of 100nnHg above the systolic blood pressure is recommended.
