infectious arthritis and wounds of jointsvehicular accident, puncture wounds, or bulletwounds. early...

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In: Textbook of Small Animal Orthopaedics, C. D. Newton and D. M. Nunamaker (Eds.) Publisher: International Veterinary Information Service (www.ivis.org), Ithaca, New York, USA. Infectious Arthritis and Wounds of Joints ( 1-Jan-1985 ) S. G. Brown and C. D. Newton Septic Arthritis Open Joint Injuries Prognosis Septic Arthritis PATHOPHYSIOLOGY OF BACTERIAL INFECTION Bacterial infections of joints usually begin suddenly and develop rapidly into an acute suppurative arthritis. Pain, lameness, andlimitation of joint motion occur along with the classic signs ofinflammation, swelling, redness, heat, and tenderness. Jointeffusion is present early, thus providing a very importantdiagnostic tool. The patient usually manifests fever, althoughit may be low-grade. There is often a leukocytosis in thehemogram. Sterile aspiration of the joint will reveal anincreased number of polymorphonuclear leukocytes, from40,000/mm3 to 50,000/mm3 very early in the infection and risingrapidly to 100,000/mm3 or higher depending on the type oforganism and the duration and seventy of the infection. Thesynovial fluid glucose is usually reduced (in contrast to bloodglucose) owing to its metabolism by massive numbers ofpolymorphonuclear leukocytes. In most joint infections thedisease is monarticular, unlike some of the autoimmune diseases.(See Table 88-1.) Suppurativearthritis due to hematogenous spread is most unusual in the dogand, when seen, is most often in the young or debilitatedanimal. Although many pathogenic bacteria have been incriminatedin joint inflections, the ones that most commonly attack thesetissues are staphylococcus, hemolytic streptococcus, andKlebsiella spp from a pneumonic process. The infectingorganism reaches the joint tissue (by hematogenous spread) as aresult of a primary septicemia from a bacterial endocarditis,pneumonia, or abscess in another portion of the body. The mostcommon entry is by a direct penetrating wound or a surgicalwound. Sometimes the infection decompresses into the joint froma metaphyseal bone infection. The infection in the jointtissue manifests itself in a manner similar to infectionselsewhere in the body. There is hyperemia with swelling andlater edema of the synovial tissue. This is followed by aninfiltration with inflammatory cells, principallypolymorphonuclear leukocytes. Small vessels may rupture toproduce petechial hemorrhages, and focal areas of necrosis maydevelop. A copious outpouring of fluid into the joint follows.This fluid is high in protein and has a lowered glucose content(Fig. 88-1). Fibrin and blood clottingmechanisms that do not inhabit the normal joint pour into theinflamed joint. Polymorphonuclear leukocytes are shed into thesynovial fluid to produce purulence. As these polymorphonuclearleukocytes, in particular, and, to a lesser degree, the synovialcells phagocytize bacteria, they are broken down and theirlysosomal enzymes, as well as other enzymes, are released intothe synovial fluid. These enzymes attack and break down thecartilaginous matrix, leaving the collagen fibrils withoutsupport. The fibrin are then broken off mechanically, fragmentedby the wear and tear of the joint motion in this abnormalsituation. Replacement of the normal synovial fluid with theeffusate, suppuration, and fibrin doubtlessly interferes withnutrient and cell waste transport mechanisms making thecartilage even more vulnerable to injury. Fibrin deposition canfurther impair the entrance of nutritional material into thecartilage from synovial fluid and may in fact further impede therelease of metabolites from the cartilage. Fibrin itself canchemotactically attract leukocytes to the joint. Phagocytosis ofthis fibrin and other particulate matter by the leukocytes TABLE 88-1 Analysis ofEffusion

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Page 1: Infectious Arthritis and Wounds of Jointsvehicular accident, puncture wounds, or bulletwounds. Early diagnosis and treatment are of the utmostimportance, although Early diagnosis and

In: Textbook of Small Animal Orthopaedics, C. D. Newton and D. M. Nunamaker (Eds.) Publisher: International Veterinary Information Service (www.ivis.org), Ithaca, New York, USA.

Infectious Arthritis and Wounds of Joints ( 1-Jan-1985 ) S. G. Brown and C. D. Newton

Septic Arthritis Open Joint Injuries Prognosis

Septic Arthritis PATHOPHYSIOLOGY OF BACTERIAL INFECTION Bacterial infections of joints usually begin suddenly and develop rapidly into an acute suppurative arthritis. Pain, lameness, andlimitation of joint motion occur along with the classic signs ofinflammation, swelling, redness, heat, and tenderness. Jointeffusion is present early, thus providing a very importantdiagnostic tool. The patient usually manifests fever, althoughit may be low-grade. There is often a leukocytosis in thehemogram. Sterile aspiration of the joint will reveal anincreased number of polymorphonuclear leukocytes, from40,000/mm3 to 50,000/mm3 very early in the infection and risingrapidly to 100,000/mm3 or higher depending on the type oforganism and the duration and seventy of the infection. Thesynovial fluid glucose is usually reduced (in contrast to bloodglucose) owing to its metabolism by massive numbers ofpolymorphonuclear leukocytes. In most joint infections thedisease is monarticular, unlike some of the autoimmune diseases.(See Table 88-1.)

Suppurativearthritis due to hematogenous spread is most unusual in the dogand, when seen, is most often in the young or debilitatedanimal. Although many pathogenic bacteria have been incriminatedin joint inflections, the ones that most commonly attack thesetissues are staphylococcus, hemolytic streptococcus, andKlebsiella spp from a pneumonic process. The infectingorganism reaches the joint tissue (by hematogenous spread) as aresult of a primary septicemia from a bacterial endocarditis,pneumonia, or abscess in another portion of the body. The mostcommon entry is by a direct penetrating wound or a surgicalwound. Sometimes the infection decompresses into the joint froma metaphyseal bone infection. The infection in the jointtissue manifests itself in a manner similar to infectionselsewhere in the body. There is hyperemia with swelling andlater edema of the synovial tissue. This is followed by aninfiltration with inflammatory cells, principallypolymorphonuclear leukocytes. Small vessels may rupture toproduce petechial hemorrhages, and focal areas of necrosis maydevelop. A copious outpouring of fluid into the joint follows.This fluid is high in protein and has a lowered glucose content(Fig. 88-1). Fibrin and blood clottingmechanisms that do not inhabit the normal joint pour into theinflamed joint. Polymorphonuclear leukocytes are shed into thesynovial fluid to produce purulence. As these polymorphonuclearleukocytes, in particular, and, to a lesser degree, the synovialcells phagocytize bacteria, they are broken down and theirlysosomal enzymes, as well as other enzymes, are released intothe synovial fluid. These enzymes attack and break down thecartilaginous matrix, leaving the collagen fibrils withoutsupport. The fibrin are then broken off mechanically, fragmentedby the wear and tear of the joint motion in this abnormalsituation. Replacement of the normal synovial fluid with theeffusate, suppuration, and fibrin doubtlessly interferes withnutrient and cell waste transport mechanisms making thecartilage even more vulnerable to injury. Fibrin deposition canfurther impair the entrance of nutritional material into thecartilage from synovial fluid and may in fact further impede therelease of metabolites from the cartilage. Fibrin itself canchemotactically attract leukocytes to the joint. Phagocytosis ofthis fibrin and other particulate matter by the leukocytes

TABLE 88-1 Analysis ofEffusion

Page 2: Infectious Arthritis and Wounds of Jointsvehicular accident, puncture wounds, or bulletwounds. Early diagnosis and treatment are of the utmostimportance, although Early diagnosis and

mayresult in leukocyte degeneration and release of more Iysosomalenzymes. When the healing reaction is initiated, a mantle, orpannus, of granulation tissue forms from the synovial surface.It is composed of myriads of new vessels, which when spread overthe articular plate cause further lysis by its penetration andundermining of the cartilage plate.

Even before this stageof infection has been attained within the joint, exudativeinflammatory cells may be demonstrated in the subchondralcancellous tissue. It is believed by some authors that this isgeneral and due to the association of the two sites by a commonlymphatic system. (l) If the articular platebarrier is penetrated, there follows a frank suppurativeosteomyelitis of the epiphysis (Fig.88-2).

Today, because of thedevelopment of specific antibiotic agents and the earlyaggressive treatment, the complete course of suppurativearthritis is seen less often. This is fortunate because thearticular plate has little or no capacity for regenerativehealing. With the loss of articular plates, there is usually anextension of granulation from one subchondral area to the otheracross the joint space. As the granulation ages, it formscollagen scar tissue, and a fibrous ankylosis is the result. Thecollagen often calcifies as it condenses, followed usually byossification/ankylosis. In short, if the joint infectionprogresses to destruction of the articular plate, jointdestruction and patient crippling will be the result. It isimperative that the clinician make an early and accuratediagnosis so that the infection may be treated aggressively andcurbed before irreversible joint damage takes place. Itcannot be emphasized enough that examination of the synovialfluid is probably the most valuable single means of making thecorrect diagnosis. The only early radiographic alteration may bea slight fluid distention of the joint (see Fig. 88-1); by the time the other jointalterations are visible radiographically, irreparable damage hasbeen done (Fig. 88-3). DIAGNOSIS Diagnosis of the infection may at times bedifficult. For example, in a series of 37 children treated atthe Mayo Clinic, cultures of the synovial fluid of some withproven septic arthritis were negative.(10)Even so, a diagnosis of septic arthritis was made if anyfive of the following six clinical conditions were present:

Low-grade fever Pain (localized to the joint) made worseby gentle, passive motion Swelling of the involved joint Systemic signs of lethargy, irritability, or"toxicity" No other demonstrable pathologicprocess, such as leukemia or intrapelvic abscess Satisfactory response to antibiotic therapy

In addition to meeting five of these six clinicalconditions, the patient must have had a positive blood cultureor two of the following three conditions:

Pus aspiratedfrom the joint Marked elevation of the erythrocytesedimentation rate

FIG. 88-1 (A) Photographdemonstrates obvious swelling of the left stifle in a10-week-old Great Dane. (B.) Cranial-caudal and (c)medial-lateral radiographs of the same stifle demonstrate fluiddistention and soft tissue swelling. The distal femoral andproximal tibial epiphyses appear very small owing to the dog'simmaturity.

FIG. 88-2Medial-lateral radiograph of a canine shoulder demonstratesosteomyelitis of the proximal humeral epiphysis secondary toseptic arthritis of the shoulder.

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Specific radiographic changes in theinvolved joint (hip)

Only one third of the children experiencing hematogenousspread had an elevated peripheral leukocyte count, while twothirds had only a shift to the left in the differential. Aslightly widened joint space distended by the exudate may be theonly early radiographic change. Late changes may include apersistent subluxation, destructive arthritis (similar torheumatoid), and evidence of vascular compromise of theepiphysis in the young.

TREATMENT Thefundamental goals of treatment are listed below: 1. To cleanthe joint in order to avoid articular cartilage destruction andadhesion formation 2. To decompress the joint in theimmature patient to avoid vascular embarrassment to theepiphysis 3. To administer adequate doses of antibiotics toeradicate the joint infection and prevent secondary spread There is general agreement that a suppurative joint must bedrained. However, to adequately debride the joint by multipleaspirations is difficulty and possibly harmful to the jointbecause of repeated insults to the cartilage from the needle.(7) In the young animal, multiple aspirationsare not likely to be adequate to prevent the accumulation ofintra-articular debris and pressure. Whatever one's argumentsfor multiple aspirations as opposed to surgical drainage, thistreatment has no place in the management of pyarthrosis ofmovable joints in the immature animal owing to the possibilityof severe consequences if adequate decompression, as well asdebridement, is not carried out early and rapidly.

Broad-spectrumantibiotics are given immediately to maintain anaround-the-clock blood level. Intravenous antibiotics are thefirst choice; intramuscular the alternate. The cephalosporinshave been particularly effective in septic arthritis. Ampicillinhas also been an effective drug. Penicillin in high doses andaminoglycosides have been used successfully. (11,13) (See Table88-2.) These antibiotics are used until culture andsensitivity results are returned. The appropriate antibioticshould then be administered as frequently as possible for aminimum of 10 days. Indications for Surgery Theindications for surgical management are as follows:

Untreated suppurative arthritis of more than 72 hoursduration An infected movable joint that has not responded toother forms of treatment (i.e., in the adult animal a totallyfavorable response to aspiration must have within the first 48to 72 hours to prevent surgical intervention; this does notapply to movable joints in the young animal) Any penetratingwound to the joint A postoperative joint infection

Synovectomy is added to the following procedure when thesynovium is found to be grossly necrotic as a result of theinfectious process or the previous treatment. It should also beperformed if the synovium is grossly thickened, impeding

FIG. 88-3 Cranial-caudal radiographof the stifle in a 6-month old Labrador retriever. Note the deepbony erosion of the lateral femoral condyle.

TABLE 88-2 Broad-SpectrumAntibiotics

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jointmotion or encroaching upon the articular cartilage. Surgical Technique The entire limb is prepared forsurgery, and tourniquet hemostasis is used where possible. Ifanatomically feasible, bilateral incisions into the joint willgive better postoperative drainage. The retinaculum, capsule,and synovium are opened in line with the skin incision. Carefulattention must be paid to the synovium as it is incised.Exudation of pus anywhere along its cut edges indicates abscessformation and necessitates a subtotal synovectomy. At thispoint, samples of the pus and synovium should be taken formicrobial culture and drug sensitivity. Culture material can becentrifuged in an effort to improve the chances of a positiveculture if large volumes of purulent material are found. Thejoint is irrigated thoroughly with copious quantities of salineor lactated Ringer's solution to remove all of the fibrin clots,foreign material, and loose fragments. The thoroughinspection and removal of fibrin is an extremely important partof the procedure, since the fibrin will hold theinfection.(5) Owing to difficulties ofmanagement and iatrogenic infection with suction-irrigationtubes following this surgical debridement, the wound is leftentirely open on both sides. A fine mesh gauze is placed overthe incision, # followed by bulky absorptive dressing* coveredby bulky cotton dressing. In the more peripheral joints, bulkydressings can be removed after 24 hours and the mesh gauzechanged by sterile technique and the incision covered by alooser bandage. In movable joints, an assisted range of motionis useful to aid in the egress of exudate. The range of motionshould be done every day and a light dressing reapplied dailyduring the first week. The wound is allowed to close with theformation of granulation tissue and is not sutured ormarsupialized. Occasionally it is necessary to employ salineirrigation during a bandage change, especially in the shoulderor hip where double incision drainage is not performed or wherepockets of exudate may exist. The hemorrhagic effusage followingsynovectomy will require tube flushing for clot removal once aday during the first 3 days. Chemical debridement, antibioticinstillation, applications of drains and wicks, or attempts toclose the wound early are not necessary in most instances. A 2week program of parenteral antibiotics is the best and mostaggressive antibiotic regimen; one week of parenteralantibiotics, followed by 1 to 3 weeks of oral antibiotics, isthe alternative program. In extremely difficult cases, periodiccultures of the exuding joint fluid can be taken. #Aqua-flow, petrolatum gauze, Cheeseborough Ponds, Inc.,Greenwich, CT * Kerlix, fluffed gauze, Kendall Co., Boston,MA.

Open Joint Injuries A penetrating joint wound has the potential to be apermanently disabling injury. Early and effective treatment maybe relatively simple, but if septic arthritis develops,effective treatment is difficult. Open joint injuries can be theresult of a vehicular accident, puncture wounds, or bulletwounds. Early diagnosis and treatment are of the utmostimportance, although the patient's general condition and thetype and severity of injury, as well as concomitant injuries,may dictate treatment. Nevertheless, when there has been delayin instituting the proper treatment, the presenting problem maybe septic arthritis. DIAGNOSIS The diagnosis ofa septic joint upon admission can at times be difficult.Temperatures may be elevated only slightly, if at all, andperipheral white blood cell counts may be likewise elevated onlyslightly, often presenting a stress-reaction hemogram andthereby being misleading. In one series, about 50% of synovialfluid cultures from proven septic joints were negative.(9) The patients in this series were treatedwith antibiotics, which probably accounts for the finding. Moreimportantly, however, a synovial biopsy was a more reliablesource of positive culture than surface swabs, culture ofsynovial fluid, or foreign bodies.(9) Thepresence and analysis of the effusion is a good diagnostic tool,since all penetrated joints will have an effusion (Table 88-1). Thus the diagnosis of apenetrating joint injury can be based upon the following:

Visible open laceration into the joint A palpableopening into the joint Air seen in the joint radiograph Extravasation of saline from the joint into the wound duringarthrocentesis Extravasation of contrast media duringarthrography, demonstrating a defect in the joint space.

TREATMENT One must act as soon as the diagnosisof penetrating injury is made or suspected. Successful resultsare dependent upon early

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diagnosis and surgical management.(9,13,15) Penetrating joint injuries treatedearly by arthrotomy, debridement, and irrigation have a betterprognosis than those treated several days later, since sepsisand potential irreparable damage may be avoided. A largeincision and very thorough inspection are critical. Thearticular and periarticular tissues should be debrided Carefullyand thoroughly irrigated. Menisci, articular cartilage, bonystock, and ligaments should be preserved as much as possible.The articular cartilage not only forms a barrier to infection,but its continued good health is a primary goal of treatment. The use of antibiotics is similar to their use in thetreatment of septic arthritis. Broad-spectrum antibiotics aregiven immediately to maintain an around-the-clock blood level.Intravenous antibiotics are the first choice, intramuscular thealternate. The cephalosporins have been particularly effectivein the open joint wound and in the open fracture. Ampicillin hasalso been an effective drug. Penicillin in high doses andkanamycin have both been used successfully (Table 88-2). (11,13)These antibiotics are administered until culture andsensitivity results are returned. The appropriate antibioticshould then be administered as frequently as possible for aminimum of 10 days. The patient is prepared for arthrotomy.In treating penetrating injuries, the surgical technique iscritical.(9,13) The animal should be drapedto allow a full range of motion and to permit completeinspection of the joint. The tourniquet is used when possible toallow better vision. At surgery, cultures should be taken of thecartilaginous surface or more importantly still, a piece of thesynovial tissue. All necrotic and contaminated tissue isdebrided very carefully from the outside inwardly. Afterdebridement of all nonviable tissue and cartilage and curettageof all injured and contaminated bone, the joint is lavaged withmassive amounts of normal saline or lactated Ringer's solution(one or more liters for a small to medium size knee). Furtherdamage to articular surfaces or condyles must be carefullyavoided when extracting metal fragments, as in a gunshot wound.Small metal fragments left deep in Cancerous bone do not causefurther damage or sepsis. Only evident or intraarticular piecesof metal are removed. The copious lavage is continued by meansof gravity flow through an intravenous tubing setup, or a dentalirrigating system (Surgi-Lav, Stryker Corporation, Kalamazoo, MIor Water-Pic) may be used. The large volume of irrigant fluid ismost important here. If after relatively early arthrotomy andirrigation the joint is clean and appears to have only viabletissue, the synovium and capsule are closed. Capsular suturesand soft tissue sutures of 3-0, occasionally 4-0, nylon arepreferred. Polyglycolic acids (Dexon, Davis and Geck, AmericanCynamid Co., Pearl River, NY) or polypropylene (Prolene,Ethicon, Inc., Somerville, NJ.) may be used also. The skincan be closed immediately or it can be closed 4 or 5 days lateras a delayed primary closure if there appears to beperiarticular contamination that cannot be removed bydebridement. However, primary closure of the wound without theroutine use of irrigation-suction tubes placed into the joint isthe goal in most cases, regardless of whether debridement isbeing carried out within the 6 hour limit or, as is true in mostcases, 10 to 12 hours later.(13) In woundswith extensive soft tissue damage and loss of skin,contamination that cannot be debrided completely, or an effusionindicating sepsis, a decision must be made either to close thewound with irrigation tubes in place or, as is preferable inmost instances, to leave the entire wound open. If a welldebrided wound with extensive soft tissue loss has been closedfor some unusual reason, treatment must be initiated promptlyshould infection appear or the tube system becomes clogged. Suction-irrigation tubes used in the joint are difficult tomanage and often ineffective. It should be noted that their usecarries a substantial risk of introducing pathogenic organismsinto a joint not already infected. Furthermore, the iatrogeniccontamination may involve gram-negative organisms, and infectionwith these organisms, notably Pseudomonas, Klebsiella,and other bacillary rods, may be quite difficult to eradicate.Therefore, if a tube system is used at all, it is best to use itwith conscientious nursing care and probably for a short periodof time-1 to 4 days. Open abrasion injuries in which thetarsus or carpus has been sheared by dragging on the concreteare treated by debriding only dead tissue, with care taken tocurette the ground-in dirt and to provide a copious lavage.Culturing this wound is optional, since the wound is packedopen. There are two reasons that shearing injuries shouldrarely, if ever, be closed: The dirt is often ground into thebone and thus is difficult to remove. Also, the ligamentous andcapsular structures that have been ground away will need thelarge bed of granulation tissue that forms postoperatively andlater is converted to scar tissue, thereby providingstabilization for the joint. If skin closure is done early, nogranular bed appears. Therefore, the ultimate stability of thisabraded joint is far less than it would be if the granular bedwere allowed to form and subsequently contract. POSTOPERATIVE MANAGEMENT Identification ofcontaminating microorganisms and their sensitivities isobviously important in the postoperative management of thepenetrating joint injury that has been closed primarily. Iffrank sepsis is present, a bilateral incision, if anatomicallyfeasible, is probably desirable to drain the joint.(2) The value of beginning antibioticspreoperatively has been established.(13) Thepenetration of antibiotics into normal and inflamed synovium hasalso been demonstrated.(11) Postoperative febrile episodes may indicate the necessity forreexploration, redebridement, and reculture. It is mostimportant to identify the organism and its antibioticsensitivity both intraoperatively and for any postoperativeinfections.

Page 6: Infectious Arthritis and Wounds of Jointsvehicular accident, puncture wounds, or bulletwounds. Early diagnosis and treatment are of the utmostimportance, although Early diagnosis and

The synovium should be left open in those jointsthat appear to be septic upon presentation. If there ispurulence with a thick, gray, hypertrophic synovium, thesynovium should be removed. When accumulation or drainage ofsynovium fluid has ceased, the delayed skin closure can beperformed, often 4 to 5 days after injury. The synovium usuallycloses itself off in a day or two and does not require closureby itself. If there is an increase in synovial fluid, thesynovium will remain open and allow drainage. In the wound thatis left open, petrolatum gauze is used to allow blood andsynovial fluid to drain freely into fluff gauze. Telfa and wetdressings do not allow free drainage. Immobilization isaccomplished with a cotton compressive (Robert Jones type)dressing, which will prevent edema of the extremity andaccumulation of intra-articular fluid. If for some reason thearthrotomy cannot be performed immediately, aspiration andlavage with a large-bore needle are necessary to prevent theaccumulation of fluid, white cells, and debris, which preventthe proper functioning of antibiotics. The injection ofantibiotics into these joints is usually not recommended, sinceit may lead to a troublesome synovitis.(15)The joint is allowed minor passive motion the first week, andafter another 1 to 2 weeks mobilization of the joint is allowed. FRACTURE FIXATION Open fractures of a joint canbe treated as follows: if the arthrotomy is performed early,preferably within 6 hours, and the amount of soft tissue damageis minimal, a displaced fracture, such as a condylar fracture,can be fixed with rigid internal fixation, such asinterfragmentary lag screw fixation. Apophyseal fractures shouldbe fixed with tension band wiring. 11' there is a possibility ofsepsis in the joint, internal fixation can be delayed from 5 to10 days until the inflection is under control. If collateralligaments are ground away, on the fifth to eighth day screws maybe placed at the origin and insertion of the collateral ligamentto anchor a figure-of-eight wire or Prolene (1-0, 2-0) temporaryprosthesis to increase stability and maximize range of motion.Much of the wound may still be left open. These fixation devicesare removed in approximately 6 weeks.

Prognosis Delay in diagnosis and treatment appears to be the importantfactor affecting prognosis; however, other determining factorsmay be the organism involved, the adequacy of treatment, and thepresence or absence of metaphyseal osteomyelitis and/orpenetrating joint wounds, in which much of the cartilage andbone stock has been violated. The advantages of arthrotomy arethat a complete decompression, thorough debridement, andirrigation of the joint may be performed. There is also a betterchance of a definitive diagnosis (positive bacteriologicculture). A practical treatment that allows the joint to remainopen has been described. Motion, rather than immobilization, canbe employed to express quantities of exudate from the wound. (14) In this method, the prolonged exposure ofarticular cartilage in the wound has caused some concern.However, this exposure does not appear to be detrimental.(1) Many antibiotics can pass the inflamedsynovial membrane and reach comparable blood levels. Thebroad-spectrum antibiotics in Table 88-1are used until culture results can be obtained. For ourrationale we recant the pathophysiology. The first measurableevent in the degradation of cartilage in septic arthritis is thedepletion of matrix. A number of enzymes are capable of breakingdown the matrix: Iysosomal enzymes (released from cartilage,neutrophils, or synovium); plasmin (plasminogen activated bystaphylokinase); and extracellular proteolytic enzymes producedby Staphylococcus agrees. After 4 days of inflectionthere has been loss of matrix but not of collagen. After thisperiod of time, the loss of collagen ensues.(6) The destruction of the cartilage proceedsnot only from the interference with nutrition but also from thedestructive enzymes in the septic joint fluid. The rationale forSavage, therefore, is that it removes cartilage-destroyingenzymes as well as bacteria, bacterial products, and fibrindeposits covering the articular cartilage. In humans, aseptic arthritis that has been successfully treated byantibiotics is frequently followed several weeks later by anonbacterial acute inflammatory synovitis. The joint continuesto be inflamed for many months and, much like a rheumatoidjoint, often undergoes progressive destruction with loss ofarticular cartilage. There is evidence that part of thissecondary phase of septic arthritis is associated with animmunologic disease of the articular cartilage initiated by theseptic process. (3,6)

References 1. Aegerter E, Kirkpatrick JA Jr.: Orthopaedic Diseases, 3rded, pp 761-763. Philadelphia, WB Saunders, 1968 2. BallardA, Kurkhalter E, Wayfield GW, et al: The functional treatment ofpyogenic arthritis of the adult knee. J Bone Joint Surg 57A:1065, 1975 3. Bobechko WP, Mandell L: Immunology ofcartilage in septic arthritis. Clin Orthop 1975 4. Boyer J.Daniel D, Akeson WH. et al: The effect of salicylate therapy oncartilage destruction in experimental pyarthrosis.

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Clin Orthop302, 1977 5. Curtiss PH Jr: The pathophysiology of jointinfections. Clin Orthop 96:129, 1973 6. Daniel D, Akeson W.Amiel D, et al: Lavage of septic joints in rabbits: Effects ofchondrolysis. J Bone Joint Surg 58A:393, 1976 7. Griffin PO,Green WT: Hip joint infections in infants and children. OrthopTransact 1:195, 1977 8. Marmor L, Peter JB: Candidaarthritis of the knee joint. Clin Orthop 133, 1976 9. MarvelJE, Marsh HO: Management of penetrating injuries of the knee.Clin. Orthop. 268, 1977 10. Morrey BF, Bianco AJ, Rhodes KH:Suppurative arthritis of the hip in children. J Bone Joint Surg58A:388, 1976 11. Nelson JD: Antibiotic drug concentrationsin septic joint effusions. N Engl J Med 284:379, 1971 12. Oh1: Serratia marcescens arthritis in heroin addicts. Clin Orthop228, 1977 13. Patzaris MJ, Dorr LD, Ivler D et al: The earlymanagement of open joint injuries. J Bone Joint Surg 57A:1065,1975 14. Salter SB, Bell RS, Keeley FW: The protectiveeffect of continuous motion on living articular cartilage inacute septic arthritis. Clin Orthop Rel Res 159:223, 1981 15. Waring TL: Acute infectious arthritis and wounds of joints.In Crenshaw AH (ed): Campbell's Operative Orthopaedics, vol. 1,5th ed, p 963. St. Louis, CV Mosby

All rights reserved. This document is available on-line at www.ivis.org. Document No. B0089.0685.