The differences between type 1 and type 2 reactions [1, 3, 4, 6, 10, 13].
\r\n\t
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The reactions manifest as acute inflammatory episodes rather than chronic infectious course [1]. These reactions account for about 30–50% of cases with leprosy [2]. Both patients with low and high load of leprosy bacilli are at risk of developing leprosy reactions. Leprosy reactions can occur at any time before, during, or after the treatment. Patients with fewer skin lesions and without nerve involvement are less likely to develop leprosy reactions. The presence of multiple lesions in close proximity to peripheral nerves, facial involvement, and presence of nerve thickening without functional impairment are risk factors for the development of leprosy reactions. Patients developing leprosy reactions are more likely to develop sequelae or deformities [3]. There are mainly two types of leprosy reactions. Type 1 reaction involves exacerbation of old lesions leading to the erythematous appearance. Type 2 reaction is an immune complex-mediated reaction. It is characterized by systemic symptoms along with new erythematous subcutaneous nodules [4].
Type 1 reaction is a delayed hypersensitivity reaction. It mostly occurs in borderline patients as well as in patients with lepromatous leprosy (LL) and those with tuberculoid leprosy (TL) receiving therapy. Reaction can be the first sign of the disease and it often persists for a few weeks or months [5]. Classically, two subtypes of type 1 reactions have been described; first subtype is called reversal reactions, false exacerbation reaction or upgrading reactions and this type of reaction is reversible. Second subtype is called downgrading or downgrading reaction and it is associated with disease worsening. Upgrading (reversal) reactions occur in patients receiving therapy, and downgrading reactions occurs in patients who do not receive therapy. Due to decrease in bacterial load, borderline patients receiving therapy progress to tuberculoid phase of the disease spectrum. Bacterial load increases in patients who do not receive therapy and clinical appearance shifts to the lepromatous phase of the disease spectrum due to impaired cellular immunity [6].
These reactions are associated with cellular immunity and particularly with the reaction of T helper 1 (Th1) cells to mycobacterial antigens. It has been demonstrated that cytokines derived from Th1 cells such as interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), interleukin-2 (IL-2), and interferon gamma-Ƴ (IFN-Ƴ) play a more prominent role. High levels of TNF-α, soluble IL-2 receptors, and adhesion molecules also reflect severity of local inflammation. Borderline leprosy patients with type 1 reaction show increased expression of TNF-α mRNA in peripheral nerves and skin. Type 1 reactions are mediated by Th1 lymphocytes and secreted proinflammatory cytokines IFN-Ƴ and IL-12, and free oxygen radicals [4, 5]. It was demonstrated that macrophages could initiate neural inflammatory process even in the absence of bacilli in the neural tissue [7].
Reversal reaction episodes often occur within the first 6 months of multidrug therapy (MDT) [8]. After initiation of therapy, skin lesions with manifestations of regression or lesions appearing as hypochromic macules become erythematous and edematous, and these lesions, then, become scaled and rarely become ulcerated [9]. The existing lesions show signs of inflammation, but no new lesions occur. Previously unnoticed or invisible patches may become prominent. This may give the impression of the development of new lesions. The lesions are often painless, but tenderness may sometimes be found. The lesions are often accompanied by edema and neuritis in the extremities [6]. Edema in the hands and feet may be sometimes the main symptom of reversal reaction. There may be burning pain in the lesions, pain in the face and extremities, and decrease in muscle strength. Isolated neuritis is commonly observed within the first 12 months of therapy. Nerve thickening and pain may occur and preexisting peripheral neuropathy may become prominent (sensory, motor, or autonomic). Ulnar, median, posterior tibial, fibular, radial, and facial nerves are the most commonly involved nerves. The patients may present with the symptoms of neural dysfunction such as loss of sensation, facial palsy, claw hand, and drop-foot. Hyperesthesia may occur in palmar and plantar areas, associated with widespread nerve damage [1]. The ability to close eyelids is lost due to damage in the facial nerves (lagophthalmos) [10]. Neural damage is important, as it is considered the main cause of deformities and sequelae in the course of reversal reactions. Neuritis episodes may be severe; however, it sometimes has an insidious and even painless course, which is called silent neuritis. Silent neuritis is defined as sensory or motor dysfunction in the absence of skin lesions observed in type 1 and type 2 reactions [11]. It may cause inflammatory eye diseases, including iritis and scleritis, and it may even result in blindness. Systemic symptoms such as weakness, fever, bone pain, lymphadenomegaly, joint pain, and generalized edema are rarely observed and these symptoms indicate the severity of clinical condition. Furthermore, systemic symptoms are minimal in patients close to the TL pole of the spectrum and more commonly observed in patients close to the LL pole. Fever is usually absent and patients’ general condition is good [6, 10].
The risk of type 1 reaction may increase with vaccination, MDT, pregnancy, puerperality, infections, stress, trauma, and oral contraceptive use. The extensiveness of skin lesions has been described as an important risk factor both in patients with low and high bacilli load [1]. It has been shown that the risk of developing neural damage, along with the risk of developing reversal reaction, is 10-fold higher in patients in whom three or more body segments are affected [11]. Facial involvement is a risk factor for the development of reversal reaction, as it is for lagophthalmos [12]. Although factors which can induce type I reactions are not clearly known, recent studies have pointed to genetic factors [5]. Identification of the risk factors, therefore, allows more meticulous follow-up of patients and early treatment [1].
The type 1 reaction is characterized by edema in the upper dermis and disorganized granulomas. The foreign body giant cells, Langhans giant cells accompanied by epidermal erosion and spongiosis, and fibroplasia appear in the dermis. The necrosis, ulcer and inflammatory infiltration by neutrophils may be observed in severe reaction [13]. The cytology of preexisting granulomas is differentiated by the presence of large epitheloid cells and decreased number of bacilli. Inflammatory cells often infiltrate epidermis and increased neural destruction is observed. The edema inside and around the granulomas results in the damage of surrounding tissues and nerves [1].
The main goal of treatment in type 1 reaction is to suppress the cellular immunity. Prevention of nerve damage required early diagnosis and early institution of anti-inflammatory medications. MDT must be continued during the reactions. Corticosteroids are the most effective drugs used to treat reversal reaction. Their main effects are to inhibit activation of cellular immune response and suppress inflammatory response against M. leprae antigens in the skin and nerves. Corticosteroids increases vasodilation by inhibiting the release of mediators such as arachidonic acid (prostaglandins) metabolites and platelet activating factor (PAF), vasoactive amines, neuropeptides, interleukin-1 (IL-1), TNF-α, and nitric oxide (NO). They inhibit adhesion of neutrophils, eosinophils, and lymphocytes to the endothelial cells, their migration to the inflammation site, and decrease vascular permeability. They inhibit phagocytosis and production of oxygen-free radicals [1].
Clinically, corticosteroids change the course of reversal reactions in many ways. They decrease intraneural and cutaneous edema and promote rapid recovery of the symptoms [1]. Earlier initiation of corticosteroid treatment can eliminate the risk of permanent neural dysfunction [3]. Corticosteroids must be continued at immunosuppressive doses for prolonged period. A prednisolone dose of 40 mg has been suggested as the start dose to control many of the type I reactions. However, patients with neural involvement require a dose of 1 mg/kg (60 mg) or sometimes higher doses (2 mg/kg). [14] Prednisolone dose must be reduced only after observing clinical recovery and tapering the dose to 20 mg/day. Recovery is often occurs within 3 months but may sometimes exceed 6 months. Intravenous methylprednisolone pulse therapy has been used to control reactions. Pulse therapy is indicated in severe reversal reactions and in cases of acute or chronic neuritis who have previously received oral corticosteroid therapy for prolonged period. The therapy involves administration intravenous methylprednisolone at a dose of 1 gr/day for consecutive 3 days in the first week and this is followed by a dose of 1 gr/week for consecutive 4 weeks, and finally 1 gr/month for consecutive 4 months. Prednisone 0.5 mg/kg/day is administered between the cycles of pulse therapy [15]. The treatment should be modified with a return to the previous dose in case worsening of clinical condition. Correct start dose and dose tapering regimen for prednisone must be determined on a patient basis, and this decision must rely on the follow-up of the loss of sensory functions and motor examination findings. The recommended duration of treatment is often 4–9 months in patients with borderline tuberculoid (BT) leprosy, 6–9 months in patients with borderline-borderline (BB) leprosy, 6–18 months in patients with borderline lepromatous (BL) leprosy; however, the treatment may last 24 months or longer. Patients with recent neural lesions and particularly those with less than 6-month duration better respond to therapy compared with patients in whom therapy is initiated in late periods [1].
Immunosuppressive medications such as azathioprine and cyclosporine can be used alone or in combination with corticosteroids [16]. Thalidomide is an effective drug used as an alternative to corticosteroid therapy and it allows long-term disease control [17]. Nerve decompression surgery has a limited place and it is recommended for patients with permanent pain after corticosteroid therapy. Surgery can be performed in patients with TL and BT leprosy with neuralgia and nerve abscesses in whom therapy with immunosuppressive is not feasible [1].
Type 2 reaction or erythema nodosum leprosum (ENL) occurs in patients with high bacilli load as in patients with multibacillar type leprosy (BL and LL) [5]. Type 2 reaction is considered to be more complicated than type 1 reaction due to systemic nature and recurrent episodes [4]. The differences between type 1 and type 2 reactions are summarized in Table 1 [1, 3, 4, 6, 10, 13]. Type 2 reaction course is 1–2 weeks, but may occur multiple recurrences over several months [5]. ENL is identified by Pocaterra et al. as single acute (one ENL episode lasting less than 6 months, recurrence is not), multiple acute (repeated discrete episodes) or chronic (an episode lasting for more than 6 months, continuous episodes) [18].
Parameter | Type 1 reaction | Type 2 reaction |
---|---|---|
Immunological response | Type 1 helper cells | Type 2 helper cells |
Pathogenesis | Type IV hypersensitivity reaction (delayed cell-mediated) | Type III hypersensitivity reaction (immune complex formation and deposition) |
Type of reaction | Reversal reaction Downgrading reaction | Erythema nodosum leprosum Lucio’s phenomenon Erythema multiforme-like reaction |
Clinical phenotype | Tuberculoid, borderline tuberculoid, borderline-borderline Previous treatment (except in downgrading reactions) | Borderline lepromatosis, lepromatosis Previous treatment or not |
Cutaneous features | Acute onset of erythema and swelling of previous lesions No new lesions | New painful subcutaneous nodules in previously unaffected skin Necrotic areas Polymorphous erythematous plaques |
Neurological features | Painful neuritis with or without loss of nerve function Pain or tenderness in one or more nerves Muscle weakness in the hands, feet, or face | Painful neuritis with or without loss of nerve function Pain or tenderness in one or more nerves Muscle weakness in the hands, feet, or face |
Systemic manifestations | Rarely | Common (Fever, weakness, lymphadenitis, iridocyclitis, neuritis, arthritis, dactylitis, orchitis) |
Risk factors | Multidrug therapy Vaccination Pregnancy Puerperality Oral contraceptive Infection Stress Trauma | Lepromatous leprosy Vaccination Pregnancy Puerperality Puberty Infection Stress |
Recurrence | Less likely | Most likely |
Histopathology | Tuberculoid granuloma Superficial dermal edema Dermal fibroplasia Disorganized granuloma and necrosis or ulceration in severe reactions | Neutrophilic infiltrate in the mid-deep dermis and subcutaneous tissue Leukocytoclastic vasculitis of the small and medium vessels |
Treatment | Nonsteroidal anti-inflammatory drug Systemic corticosteroids | Acetylsalicylic acid, pentoxifylline Systemic corticosteroids Clofazimine Thalidomide |
Type 2 reaction is associated with humoral immunity. This is a type 3 hypersensitivity reaction associated with the deposition of immunocomplexes produced by binding of antigens released by the destruction of bacilli with antibodies [6]. Immunocomplexes cannot be phagocytosed by the macrophages, cleared by the kidneys, and they are deposited on the vessel walls [19]. This reaction is also associated with increased levels of proinflammatory cytokines. Release of inflammatory cytokines and followed by neutrophilic infiltration contribute to the development of variable characteristic clinical findings depending on the involved organ. In type 2 reaction, vasculitis and/or concurrent panniculitis occurs with inflammatory infiltration by neutrophils [5].
Type 2 reaction may occur in the early periods of therapy and even after completion of therapy, as it takes long time for the body to eliminate dead bacilli in the macrophages. It often occurs in the first three years after initiation of leprosy treatment. Sudden deterioration in clinical condition may be observed in patients with LL and rarely in patients with BL leprosy [6]. This reaction can involve multiple organs and systems. Immunocomplexes accumulate in the circulation and they are deposited in the skin, eyes, joints, lymph nodes, kidneys, liver, spleen, bone marrow, endothelium, and the testes. The lesions are multiple, bilateral, erythematous, firm, painful, subcutaneous nodules resembling erythema nodosum that are distributed symmetrically. Pustular, bullous ulcerated, and necrotic types have also been reported. Some nodules may persist as a chronic painful panniculitis and lead to scar. The target lesions of erythema multiforme may occur in any region [4, 6]. The lesions more often occur in external surfaces of the body [20]. General symptoms such as fever, weakness, edema, myalgia-arthralgia, dactylitis, bone tenderness, and lymphadenomegaly are observed prior to the occurrence of or concurrent with ENL lesions. Iridocyclitis, episcleritis, eye pain (photophobia), orchitis, liver, or kidney damage can be observed. Neuritis, painful enlarged nerves and nerve function impairment may occur [4, 5]. Necrosis can occur as a result of vascular thrombosis and ischemia. Vascular occlusion is probably associated with vasculitis caused by immunocomplex deposition on the vessel wall and leukocytoclasia. This should not be confused with Lucio’s phenomenon observed with classical LL. In Lucio’s phenomenon, the majority of the bacilli infect capillary endothelium, leading to endothelial proliferation, thrombosis, and vascular occlusion [21]. Laboratory tests show elevated levels of acute phase reactants such as C-reactive protein (CRP), α1-antitrypsin, α1-acit glycoprotein (AGP), and γ-globulins [22].
Lepromatous leprosy forms with high bacilli load, vaccination, infection, puberty, pregnancy, puerperality, with significant hormonal changes occurring in women are risk factors for the development of type 2 reaction. Emotional and psychological stress and associated immunological and hormonal changes have been regarded to trigger these reactions; however, this has yet to be confirmed [4, 10].
Two different histopathological variants have been described in ENL. First variant has been reported by Ridley as “the pink nodule type” or classical ENL (or mild ENL form). Typically, there are clusters of neutrophils accumulated around the foamy macrophages at the center of small granulomas. Eosinophils, plasma cells, and mast cells are present. Classical characteristics of vasculitis affecting small- or medium-sized vessels, necrotizing changes, and thrombosis formation have been reported in almost 25% of the patients. Indeed, vasculitic changes mostly occur in early lesions. Vasculitic changes involving neutrophilic infiltration, hemorrhage, and thrombus formation may be severe in necrotizing ENL. Necrosis in epidermis and dermis, collagen degeneration can be observed and this may result in dermal fibrosis [13]. Intact acid resistant bacilli (ARB) are found in the lesions of untreated patients, whereas granular and fragmented ARB are often found in patients receiving therapy. Lucio’s phenomenon must be histopathologically differentiated from real erythema nodosum, Sweet syndrome, pyoderma gangrenosum, and deep micotic infections [13, 23].
Type 2 reaction often regresses with addition of clofazimine to the MDT. After the use of clofazimine-containing MDT, type 2 reaction prevalence has decreased in leprosy patients under therapy. Suppression of inflammation is the basis of therapy. Bed rest and drugs such as acetylsalicylic acid, corticosteroids, nonsteroidal anti-inflammatory drug (NSAID), chloroquine, antimony compounds, pentoxifylline, and thalidomide are used in the treatment [4, 24, 25].
Corticosteroids and thalidomide are still considered the mainstay of therapy in severe cases of type 2 reaction presenting with orchitis, iridocyclitis with glaucoma, and neuritis that cause neural dysfunction [14]. Administration of high doses of corticosteroids with pulse therapy and rapid dose tapering within 2–3 weeks have been deemed appropriate as type 2 reaction is an episodic disease. If maintenance therapy must be avoided particularly in patients with chronic recurrent ENL, as long term therapy with prednisolone causes dependence to corticosteroid therapy and side effects. Thalidomide seems to be the choice of drug in maintenance therapy. Action mechanism of thalidomide is not clear. It is thought to be effective in the inhibition of TNF-α. It has some side effects which do not necessitate discontinuation of therapy. Neuropathy has been reported in approximately 20–30% of patients. It is often masked by leprosy neuropathy [26]. It is well tolerated at a dose of 100–300 mg/day in cases with recurrent disease and it provides prolonged remission [4]. Clinical trials have shown that thalidomide rapidly controls ENL and it is superior to acetylsalicylic acid and pentoxifylline therapy. On the other hand, thalidomide is teratogenic when used in early periods of pregnancy [25]. Thalidomide analogs chemically resemble thalidomide, but side effects are not the same. Revlimid and aktimid are promising drugs in this category [27].
Clofazimine is recommended in the treatment of chronic recurrent reactions. Clofazimine is administered for 12 weeks together with corticosteroids at doses of 100 mg tid, 100 mg bid, or 100 mg/day. Clofazimine is less effective than corticosteroids and it often takes 4–6 weeks to be fully effective. Addition of clofazimine to the therapy is extremely beneficial in reducing corticosteroid doses or discontinuation of corticosteroid therapy in patients who have become dependent on corticosteroids. The total duration of clofazimine therapy should not exceed 12 months [18].
Corticosteroids and thalidomide are the mainstay of therapy in the control of type II reaction. Selective cytokine inhibitors and phosphodiesterase type-4 inhibitors with potential TNF-alpha activity but without T-cell activating effect are new drugs [17].
In general, cutaneous drug reactions, local skin infections, relapses, diabetes, Bell’s palsy, rheumatoid arthritis, rheumatic fever, and disc prolapse must be taken into consideration in differential diagnosis. It may manifest as various cutaneous drug reactions such as urticarial, lichenoid, exanthematous reactions, erythema nodosum, erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis. The patients usually suffer from itching and burning in some of these lesions, whereas these symptoms are not observed in patients with leprosy. Furthermore, new skin lesions do not resemble preexisting lesions. Localized skin infections developing in patients with leprosy are often confined to a particular body site. The lesions do not occur bilaterally and medical history is often remarkable for trauma or insect bites that could cause an infection. New lesions appear if relapse occurs, and this often has an insidious course rather than a severe clinical course. Reaction often occurs within the first 3 years after initiation of leprosy therapy and old lesions exhibit acute pain and tenderness. Diabetic patients are prone to infections and development of peripheral neuropathy. Furthermore, regulation of blood glucose is impaired upon administration of corticosteroids. All patients must be screened for diabetes and referred to an advanced facility if diabetes is diagnosed. Bell’s palsy may mimic facial paralysis caused by leprosy reactions. These patients do not have nerve thickening, sensory loss along the nerve projection, and hypopigmented skin lesions. This condition is better evaluated by the ophthalmologists. In Bell’s paralysis, widening of palpebral fissure is not associated with the drop of lower eyelid. It occurs in women at childbearing age with rheumatoid arthritis, joint pain, joint deformities, fever, skin rash, and multiple organ involvement. Rheumatoid factor is almost always found to be elevated. However, referral to an advanced facility may be sometimes required to differentiate rheumatoid arthritis from leprosy reaction. Patients with rheumatic fever are usually young patients with fever, joint pain, and skin rash for a short period. These patients have high antistreptolysin O titers and valvular involvement can be found that cause murmur on auscultation. Patients with disc prolapse may present with acute onset of neuropathy in the extremities. Patients often report weight lifting in the early periods or stretching in the back. These patients do not show skin lesions or nerve thickening [23, 28].
The reactions can contribute to further deterioration of the quality of life in leprosy. Early diagnosis of reactions can prevent nerve damage and provide early intervention to systemic complications.
We thank ‘NOVA Language Services’ for the English language edition.
Total knee arthroplasty is an effective treatment option which has been applied with increasing rates in recent years with its highly satisfactory results. Recently increased total knee arthroplasty (TKA) procedures increase the number of complications too. In addition to proper patient selection, an accurate surgical technique, early diagnosis, and proper management of complications are required. Complications of TKA have a wide range. Complications vary from small skin problems to mortality. The development of complications may be due to many factors. Some of these are listed below:
Error in surgical technique.
Medical error.
Nurse error.
Patient non-compliance.
Trauma.
Associated comorbid diseases.
Reviewing all the risk factors before surgery and being prepared for the complications that may occur may be lifesaving in TKA, which is currently applied frequently. It is important to recognize, identify, and classify the complications in a timely manner in the correct and effective management of complications. The ambiguity about the complications of TKA in the literature helped identify and classify the complications in a study conducted in 2013 by the knee community [1]. According to this study, 22 complications were described. These are [1]:
Bleeding
Wound problems
Thromboembolism
Neural deficit
Vascular issues
Medial collateral ligament injury
Instability
Malalignment
Stiffness-toughness-contracture
Deep wound infection
Fracture
Extensor mechanism injury
Patellofemoral dislocation
Tibiofemoral dislocation
Bearing surface wear
Osteolysis
Implant loosening
Implant breakage
Reoperation
Revision
Re-hospitalization and mortality [1]
When the complications are examined, it is seen that some of them are simple and easy to overcome with a short-term solution, while some of them can be serious and can go to revision arthroplasty. The number of complications such as implant fracture and polyethylene surface wear has been reduced due to the techniques and innovations in implant materials and designs. In a study, it was shown that the most common cause of revisions in the first 5 years postop was infection, and the reasons for revision in the next 5 years were polyethylene loosening [2]. Complications will be classified as intraoperative, early postoperative, and late postoperative complications (\nTable 1\n\n).\n
\nIntraoperative | \nEarly postoperative | \nLate postoperative | \n
---|---|---|
Vascular injuries | \nBleeding | \nInstability | \n
Neurological complications | \nSuperficial skin problems | \nJoint stiffness | \n
Extensor mechanism injury Patellar tendon injury Quadriceps tendon injury Patella fractures | \nDeep skin problems | \nPeriprosthetic joint infection | \n
Deep vein thrombosis | \nPeriprosthetic fractures | \n|
Pulmonary embolism | \nAseptic loosening | \n|
\n | Osteolysis | \n|
Medial collateral ligament injury | \n\n | Patellofemoral joint problems | \n
Intraoperative, early postoperative, and late postoperative complications.
Although arterial injury during knee replacement is rare, it may have serious results from limb loss to mortality. Arterial injuries can be seen as thromboembolism, direct vascular laceration, pseudoaneurysm, and arteriovenous fistula [3]. The incidence is reported to be 0.03–0.2% in the literature [4].
\nVascular injuries may develop due to the thermal effect of cement polymerization, joint manipulations, dislocations, and excessive manipulation [5]. Considering the issue as specific to the total knee arthroplasty, care should be taken against vascular injury during posterior cruciate ligament and posterior capsular release during femoral condylar cutting. Atypical localization of vascular structures due to changes in adhesions and normal anatomy in revision cases increases the risk of vascular injury twice as compared to primary cases [6]. Nowadays, increasing procedures of TKA bring about the possibility of vascular injuries although they are rare. Therefore, it is necessary to take precautions against vascular injuries that may develop, to identify risky patients and to make an early diagnosis. For this, a good anamnesis and physical examination are essential. It is important to examine the presence of hypertension, diabetes, smoking, and vascular claudication. Coldness of the extremities to be operated during physical examination, skin atrophy and thinning, prominent vascular structures, ulcerative wound, and distal arterial pulse weakness are the findings that need attention. In addition to these findings, the presence of vascular calcifications in radiological scanning, a history of bypass, and an ankle-brachial index below 0.9 are other findings that should be considered. No tourniquet should be used in patients with the abovementioned conditions [7]. Embolism and arterial insufficiency may develop due to tourniquet effect in patients with vascular disease and atheroma plaque in the superficial artery [8]. It has been shown that during the manipulation of the superficial femoral artery fixed during tourniquet effect, intimal damage may occur [9]. Improper placement of retractors can also cause damage by direct mechanical trauma [10]. Particularly during insertion of the posterior retractor, a 1 cm area in the lateral portion of the midline was identified as a risky area [11]. In a cadaver study, neurovascular structures on the tibial side were mapped on a clock diagram. Accordingly, the popliteal vein at 12 o’clock, the popliteal artery at 1 o’clock, and the anterior tibial artery at 2 o’clock for the left knee were shown as in place [12]. Cautious use of the saw between 11 and 3 o’clock defined in the tibial cutting is important in protecting vascular structures [12].
\nIf vascular injury is suspected the tourniquet should be deflated, and bleeding control should be performed before the incision is closed. The possibility of arterial injury should be taken into consideration in the presence of excessive and pulsatile bleeding and in the absence of peripheral pulses. Although recent studies suggest bleeding control after routine tourniquet deflation prior to incision, its benefit is controversial [13]. The surgeon should perform a postoperative peripheral pulse examination routinely, suspect acute ischemia in the presence of cold and delayed distal capillary filling, and request cardiovascular consultation [14]. Acute ischemia cases with delayed diagnosis of 4–6 hours cause irreversible damage. Prophylactic fasciotomy is performed after revascularization [14].
\nPseudoaneurysm may present with pulsatile swelling in the popliteal fossa due to direct damage to the popliteal artery during surgery. Doppler ultrasonography is useful in the diagnosis. In the treatment, excision of the lesion and repair with vascular graft is applied after embolization [15]. Arteriovenous fistula is less common. It usually occurs due to injury to the medial and lateral geniculate arteries and its branches. It may present with pulsatile swelling in the popliteal region that gives “trill.” Hemarthrosis or pseudoaneurysm may develop. Ultrasound and angiography are used for diagnosis [16]. The detected lesions should be evaluated together with cardiovascular surgery, and treatment should be planned. Embolization, lesion excision, and graft repair are treatment options [15].
\nNerve injuries are rare during TKA. Peroneal nerve injury is the most common of these [17]. Sacral plexopathy and sciatica neuropathy are also seen, although rarely [18]. Risk factors for neurological injury are [19]:
Flexion deformity
Advanced valgus deformity
Presence of an intra-articular hematoma
It has been shown that the risk of nerve injury is increased in patients with rheumatoid arthritis [20]. However, none of these risk factors is directly related to nerve injury [18]. Nerve injury is associated not only with the surgical procedure but also with the anesthesiologist-induced regional anesthesia [21]. Hypertension, diabetes, nerve compression history, presence of tethered cord, and rheumatoid arthritis in the patients increase the risk of neural complications secondary to regional anesthesia [22]. The duration of tourniquet use was associated with nerve injuries. According to this, in the tourniquet applications exceeding 2 hours, the risk of peroneal and tibial nerve injuries including 89% peroneal nerve was determined as 7%. All of these have been shown to get recovery. In procedures exceeding 2 hours, the 10–30-minute break and deflation of the tourniquet reduces the complication rate [19]. Although there is a minimal effect on the functional results of the patients effect on the functional results of the patients during the follow-up, paresthesia and numbness are seen in the distal and lateral site of incision due to the injury of the infrapatellar branch of the saphenous nerve. It is seen in the literature at a rate of 25–76%, and most of these recover spontaneously [23]. Nerve injuries are difficult to detect intraoperatively. In the presence of postoperative nerve injury, physical therapy should be planned immediately. EMG examination is recommended after 3 months [20]. If no improvement is observed, nerve exploration may be planned in the future.
\nThe extensor mechanism in the knee joint consists of quadriceps muscle group, quadriceps tendon, patella, patellar retinaculum, patellar tendon, and tuberositas tibia. Extensor mechanism integrity may be impaired during surgery [20]. Although extensor mechanism injuries occur more frequently postoperatively, they may also occur intraoperative. The incidence is reported to be between 1 and 12% [24]. The treatment of extensor mechanism injuries is quite difficult and the results are not satisfactory.
\nRupture usually occurs at the site of insertion to the tuberositas tibia. The risk of development is less than 1% [25]. Less frequently, intratendinous and infrapatellar tendon rupture may also occur [25]. The risk of injury increases when patellar tendon mobility decreases. These are [26]:
Patella baja
Previous surgery
Severe limitation of movement in the knee
The risk of tendon injury especially on stiffness knees due to forced manipulations and during the tibial bone cutting increases during surgery. The most common injury mechanism after surgery is falling onto the knee while knee is flexed [27]. Patellar tendon injury without trauma is seen by weakening the tendon after repeated contact of the polyethylene insert [27].
\nIn patients with patellar tendon rupture, pain, swelling, loss of extension, and a palpable defect at the infrapatellar side are detected.
\nAge, functional status, tendon rupture localization, and soft tissue status are the determinants of the treatment. Splitting and bracing are considered in patients who do not have functional expectations and are unsuitable for surgery [28]. Treatment of acute patellar tendon rupture intraoperative is primary repair [26]. Several techniques have been described using staple and suture anchors for this purpose [28]. Reconstruction techniques are used in patients with poor soft tissue quality. For this purpose, biological materials (hamstring tendon autograft, achilles, peroneal tendon autograft, and extensor mechanism allograft) and synthetic materials can be used [28, 29, 30].
\nIt is very rare. It is especially seen as a rupture from the intersion side to the patella. Excessive patella cutting, previous quadriceps snip, or V-Y tipping are risk factors [28]. The clinical finding is similar to patellar tendon rupture.
\nGood results have been reported with plaster cast in partial tears [31]. Extensor loss greater than 20° is considered a complete tear and should be treated surgically. It has unsatisfactory results due to high complication rates and tendency to re-rupture depending on tendon quality and soft tissue condition.
\nPatellar fractures are the most common injury among the extensor mechanism injuries [24, 32]. In general, the risk increases with excessive bone cutting while preparing for patellar component. Patellar fracture may occur by direct trauma to the anterior knee or as an avulsion due to the pull of the quadriceps muscle [32].
\nFor diagnosis, pain, swelling, and extensor insufficiency are detected in front of the knee. Lateral knee radiography and tomography in case of clinical suspicion are helpful imaging methods for the diagnosis.
\nA classification has been developed to assess implant stability and extensor mechanism continuity for periprosthetic patella fractures [33]. Type 1, a stable implant and continuous extensor mechanism; Type 2, a stable implant but a discontinuous extensor mechanism; and Type 3, which indicates instable implant and discontinuous extensor mechanism. Patellar bone stock is classified as 3A if good and 3B if poor. Treatment is also determined according to this classification. Conservative treatment methods are preferred for type 1 cases, while surgical treatments are preferred for types 2 and 3 [33]. In recent studies, it is reported that 40–50% of complications occur and more than half strength loss of extensor mechanism is observed [34].
\nDuring total knee replacement, medial collateral ligament (MCL) is important for soft tissue stabilization and coronal plan stability. The incidence of iatrogenic MCL injury is 2.2–2.7% [35]. In the case of surgical injuries, direct repair, constrained prosthesis use, and even revision at the same session are among the options [36]. Unrecognized MCL injuries during surgery cause early instability. This leads to early implant wear and consequently the need for early revision. Therefore, it is important to diagnose and repair the injury during surgery [37]. Sudden instability in the valgus stress test during knee stabilization indicates MCL injury. Injury may occur from femoral insertion, within the tendon or tibial insertion [38]. Primary repair technique varies according to injury level. Fixation with screw is recommended if MCL injury occurs from its femoral insertion site. Otherwise, if it is through tendon, repairing with insoluble suture technique is recommended. Finally, if MCL injury occurs from its tibial insertion site, both insoluble suture anchor technique and fixation with staple technic are recommended [39, 40]. Factors that increase the risk of medial collateral ligament injury during surgery are as follows [39]:
Using a larger saw blade than femoral condyle
Delayed excision of medial side osteophytes
Performing challenging manipulations of varus-valgus
Patients with flexion contractures [39]
Patient-related risk factors include obesity and severe deformities [41, 42].
\nA certain algorithm has not yet been established for the treatment of iatrogenic MCL injuries that occur intraoperative. Many treatment methods with disadvantages and advantages have been used [39, 43, 44]. The traditional method is using constrained prosthesis. However, in this method, it was shown that the stress load on the implant increased and direct repair and treatment with non-constrained prosthesis were recommended instead. In addition, augmentation or increase in polyethylene thickness has been proposed [45]. In one study, it was shown that the risk of instability was 57% in the use of non-constrained prostheses independent of the repair technique after MCL injury [37]. In a 2016 study, four treatment modalities were compared after MCL injury. These are the use of non-constrained prosthesis only, the use of non-constrained prosthesis with primary repair, the use of non-constrained prosthesis only, and the use of constrained prosthesis with primary repair. In 23 patients, the most appropriate treatment method according to the knee community scoring was found to be the use of constrained prosthesis only [46]. However, due to the small number of patients, larger series of studies are needed to determine which treatment is most appropriate.
\nBleeding is seen in varying rates between 0 and 39% after TKA [47]. This naturally increases the need for blood transfusion. Intraoperatively, care should be taken about bleeding and good bleeding control is established. Thus, the amount of bleeding is reduced to a minimum. As a result, the risks of immunological reaction due to transfusion are reduced.
\nBleeding tolerance is low in patients with comorbid disease and in patients with insufficient cardiac capacity, and the risk of complications increases even in small amounts of bleeding. Preoperative blood preparation before surgery and limitation of the use of anticoagulants are among the measures that can be taken. Precautions during and after TKA surgery can reduce the amount of bleeding. These methods are as follows:
Use of femoral intramedullary plugs [48]
Hypotensive anesthesia [49]
Cryotherapy and Jones bandage [50]
Application of tranexamic acid [55]
Fibrinolysis is activated by surgical trauma and tourniquet use [56]. Increased fibrinolytic activity causes increased bleeding during TKA. Tranexamic acid shows an anti-fibrinolytic effect by inhibiting the conversion of plasmin to plasminogen [57]. Tranexamic acid can be administered in four different ways: intravenous, oral, intramuscular, and intra-articular [55]. Transition to maximum plasma levels is 30 minutes for intramuscular use, 5–15 minutes for intravenous use, and 2 hours after oral use [58]. Patients with total knee arthroplasty may be treated with a fast-acting intravenous route. Many studies have shown that administration of tranexamic acid after tourniquet deflation and postoperative dose repeat reduces the amount of bleeding and the need for transfusion [59, 60, 61]. However, many different protocols for the use of tranexamic acid have been implemented. Preoperative single dose and repeated dose every 8 hours for 3 days have been described in the literature and shown to be effective [62]. In a study conducted in 2011, tranexamic acid was administered at a dose of 10 mg/kg 10 minutes before the tourniquet was opened, and the same dose was repeated 3 hours postoperatively. Five hundred mg tranexamic acid was administered orally 3 times a day for 5 days. At the end of this study, it was shown that the amount of hemorrhage and the rate of transfusion decreased effectively [55].
\nThe incidence of wound problems after TKA is 1–25% [63]. The skin problems may be delayed wound healing, skin necrosis, traumatic or atraumatic separation of the lips of the wound, prolonged serous discharge at the wound site, formation of superficial or deep hematoma, allergic reaction to patch, suture material or dressing materials, bullae formation, fat necrosis, bleeding, keloid formation, and superficial or deep infection [64].
\nEtiologic reasons that may develop the problem before TKA should be determined in advance, and appropriate measures should be taken [65]. Presence of systemic diseases such as diabetes, hypertension, rheumatoid arthritis, and vascular insufficiency, which may adversely affect wound healing before TKA, should be questioned. Since the soft tissues around the knee are thinner than the other parts of the body, even the smallest problem that may occur at the wound site can cause serious complications. Incision planning should be made carefully in the case of a history of operation from the same place and scarring beforehand, and if necessary, plastic surgery assistance should be taken.
\nFactors adversely affecting wound healing are obesity, hypertension, diabetes, smoking, chronic drug use, steroid use, previous radiotherapy, scarring, inflammatory disease, malnutrition, albumin levels below 3.5 g/dl, and hemoglobin levels below 10 g/dl. Transferrin and lymphocyte levels may also contribute to wound healing problems [66]. Therefore, a detailed anamnesis and physical examination and laboratory examination before surgery give an idea about possible skin problems. Accordingly, measures are taken, replacement therapies are given, and surgery may be postponed until the current pathology is corrected, if necessary. Adjustment of fasting blood sugar levels below 200 g/dl and keeping HbA1C below 6.5 in patients with diabetes will reduce the risk of possible wound problems [67].
\nPatients with a body mass index above 30 kg/m2 are 6 times more likely to have infection and wound problems [66]. In obese patients, dietician support should be given before surgery; unnecessary exclusion should be avoided during surgery, and soft tissue surgery should be applied carefully.
\nA study of smoking patients showed that there were 2 times more wound problems [65]. Because of the vasoconstrictor effect of nicotine in the cigarette, it is recommended to quit smoking 60 days before surgery due to decreased blood supply at the wound site.
\nIncision planning should be performed in the presence of scar after previous surgery. In the presence of a single longitudinal incision without problems, the same incision should be used. If the old incision cannot be used, a distance of at least 7–8 cm should be left. If there is more than one old incision scar in the anterior part of the knee, the most lateral scar is used considering that the anterior knee feeding is from the medial perforating artery. In addition, the lateral soft tissue flap should not be dissected too much [65]. Unnecessary retractors and additional soft tissue damage should be avoided during surgery. The wound lips should be exactly opposite to each other. Overstretched closing should be avoided. This should be checked with capillary filling time.
\nEspecially in patients with risk factors, it should be performed without tourniquet or at low pressures [65]. Difficult rehabilitation in the early postoperative period should be postponed if possible until it is ensured that there are no wound problems.
\nHematoma formation increases the risk of infection [65]. Therefore, measures should be taken to prevent the formation of hematoma. These include no dead space during wound closure, good bleeding control, use of a Jones bandage, and avoidance of overdose of the prophylactic anticoagulants used [65, 68]. Once the hematoma has developed, a needle aspiration can be performed. However, if the hematoma is organized and the drainage cannot be achieved, discharge and debridement can be achieved by arthrotomy under operating room conditions.
\nThe presence of necrosis in the wound leads to catastrophic consequences. Respect to soft tissue is the most important step to prevent necrosis development. The depth of necrosis is important. Superficial necrosis can be treated by local intervention. If larger, debridement and full-thickness skin grafts or fasciocutaneous flaps are required [69]. If necrosis includes full-thickness soft tissue, closure with fascial skin or muscular skin graft should be performed after urgent aggressive debridement [70].
\nDespite all current precautions, surgical site infections remain the most serious and feared complications of TKA. After TKA, patients should be followed up with daily dressings, and wound discharge should be evaluated carefully. Prolonged wound discharge is defined as a discharge that lasts more than 48 hours regardless of the amount of drainage [64]. Wet wounds greater than 2×2 cm are considered abnormal after 72 hours and are associated with fat necrosis, hematoma, necrosis, or poor closure of the fascia. They are reported as 1–10% after primary knee replacement [65]. In the early stage of treatment, usually dressing and immobilization for 3–5 days is recommended [71]. Continuous discharge for 72 hours is dangerous. If it exceeds 5 days, debridement should be applied in operating room conditions as it will increase the risk of superficial or deep infection [64].
\nSuperficial infection: It is defined as infection of the soft tissue above the skin—subcutaneous and deep fascia that has not passed under the deep fascia, not opened into the joint cavity. It occurs most frequently in the first 30 days after surgery. The incidence of superficial infection after TKA has been reported as 10% [72]. It may occur through direct contamination or blood. Improper preparation of direct contamination sterilization environment, inadequate surgical field preparation, presence of sloppy surgical team, non-sterile dressing materials, and application may occur as a result of the presence of infected patients in the same environment [73]. The risk of direct contamination can be minimized by precautions. Hematogen contamination can occur if there is any other focus of infection in the body. Therefore, in the presence of a possible infection focus with detailed anamnesis and examination before the operation, the current focus treatment can be planned through detailed examination.
\nInfection after TKA can be evaluated as patient-related risk factors, surgical intervention-related factors, and postoperative factors [66, 68, 74, 75, 76, 77].
\nPatient-related risk factors include advanced age, previous knee surgery, previous knee infection, steroid use, presence of inflammatory disease, obesity, diabetes, smoking, intravenous drug use, hematologic diseases, oncologic diseases, above ASA score 2, immunosuppressive use, regional skin problems, old incision scars, previous radiotherapy procedures, malnutrition, vascular insufficiency, albumin level below 3.5 g/dl, transferrin level below 200 mg/dl, hemoglobin level below 10 g/dl [78, 79].
\nSurgical intervention related risk factors include prolonged surgical time of more than 2 hours, absence of laminar flow in the operating room, transfusion, use of hinged knee prosthesis, failure of surgical team to comply with asepsis, and sterility rules [80].
\nOperative period related risk factors include prolonged hospital stay pre- and postoperative, lack of appropriate antibiotic prophylaxis, hematoma formation, and prolonged wound drainage for more than 5 days [81].
Superficial wound infection is considered with the presence of at least one of the following: discharge from the wound incision, culture of the wound from aseptic conditions, suspicion of infection in clinical evaluation, disproportionate pain, increased temperature, erythema, and localized swelling [79].
\nIn superficial wound infection, unlike deep infection, there is no progressive change in erythrocyte sedimentation rate, C-reactive protein level, and peripheral leukocyte count; the increase is below 25% [82]. In addition, leukocytes in synovial fluid are detected less than 2000/ml, and polymorphonuclear leukocytes are detected under 50%. Alpha defensin and leukocyte esterase tests are negative [71].
\nWhen superficial wound infection is detected, the development of deep infection can be prevented by early intervention. Otherwise, it may develop into periprosthetic infection and cause catastrophic results. In the presence of superficial infection, local wound care due to the underlying cause and debridement should be performed if appropriate anti-therapy is required [80]. In the selection of antibiotics, consultation with infectious diseases should be requested. Antibiotherapy is continued after reproduction. If deep infection is excluded in surgical debridement, the joint should not be opened, and the implant should not be touched [83]. Hyperbaric oxygen therapy has a positive effect on appropriate patient selection [84].
\nDeep vein thrombosis is the general name of thrombosis in the venous circulatory system. It occurs most commonly in the deep veins of the lower extremity [85]. From asymptomatic deep vein thrombosis to pulmonary embolism, which can be fatal, it can be confused with clinical manifestations of varying degrees [85]. It is one of the important complications that increase morbidity and mortality after TKA [86]. Even with mechanical or pharmacological methods, the incidence of asymptomatic DVT is 5.1%, and the incidence of symptomatic DVT is 0.4% [87]. The mortality rate due to pulmonary embolism after TKA is 0.08% [88].
\nIt is important to understand the Virchow triad in the pathogenesis of DVT development. There is a slowdown in blood flow (stasis), endothelial damage, and hypercoagulability [89]. The admixture of fat and bone marrow particles into the venous system after engraving of the femoral canal during TKA explains the hypercoagulability branch of the Virchow triad. Hyperflexion of the leg during surgery and anterior manipulation of the tibia with retractors explain endothelial damage. In addition, this manipulation causes obstruction of the popliteal veins and prolonged immobilization of the leg, leading to venous pooling and stasis [89].
\n\n
VTE risk increases after age of 40 and doubles every 10 years after that age [90]. Age increases the risk of VTE regardless of other risk factors.
Genetic factors are also an important parameter that increases the risk of DVT. Factor V Leiden mutation that causes thrombophilia, as well as protein C, protein S, and antithrombin III deficiency are among the factors that increase the risk of DVT.
Although tourniquet use has been reported to cause venous stasis, it has been shown that it does not significantly increase the risk of DVT because of its fibrinolytic effect [91, 92].
The type of anesthesia also affects the risk of developing DVT. General anesthesia has been shown to increase the risk of DVT compared to neuraxial anesthesia (spinal or epidural). Neuroaxial blockade causes vasodilatation in the lower extremities and reduces venous pooling; therefore it explains the mechanism of action [93].
Other risk factors that increase the risk of DVT are immobilization, smoking, oral contraceptive and hormone use, history of VTE, obesity, malignancy, and difficult knee manipulations.
A painful, swollen, and reddened leg after TKA should suggest the possibility of DVT. Incomplete DVTs usually do not show signs. Incomplete DVTs are seen especially after arthroplasty. Clinical findings are seen in 1% of all DVT cases. Physical examination findings include redness, swelling, and Homan’s sign test and Pratt test positivity. Clinical Wells risk score was established for the diagnosis of deep vein thrombosis [94]. Clinical Wells Scoring criteria are malignancy, paralysis (paresthesia or splinting lower extremity), immobilization for more than 3 days, localized tenderness in the deep venous system, swelling of the lower extremity, 3-cm-diameter differentiation from the other leg, pretibial gode positive edema, history of deep vein thrombosis, and collateral superficial veins. The presence of each risk factor was evaluated as 1 point, and clinical scoring of 3 and above was found to be a high risk for the development of deep vein thrombosis.
\nClinical data are not sufficient for the diagnosis of DVT. Therefore, further examination with clinical risk scoring, D-dimer level, Doppler ultrasonography, contrast-enhanced venography, CT, and MRI should be performed. Venography is the best method for the diagnosis of DVT in the lower extremities. The accuracy rate was 97% in the lower extremity veins and 70% in the iliac veins [95]. Venography is not preferred as first-line imaging because it has a 3% risk of DVT and is an invasive method, and also it requires contrast matter that can be toxic to the kidneys. Doppler USG is the most commonly used first-line imaging method because of its cheapness, reproducibility, and patient comfort in the suspicion of DVT. Proximal DVT sensitivity was 96%, distal DVT sensitivity was 44%, and DVT specificity was 93% [96].
\nPulmonary embolism should be suspected in the case of sudden shortness of breath, tachypnea, tachycardia, and chest pain after TKA. However, since there are many other diseases with these findings, risk factor assessment and effective differential diagnosis should be made. Wells pulmonary embolism clinical probability scoring was established [97]. Pulmonary angiography is the gold standard for the diagnosis of pulmonary embolism [85].
\nPrimary treatment of DVT and related pulmonary embolism is very difficult and cost-effective. Therefore, it is more plausible to establish protocols that prevent the development of DVT and to give ideal prophylaxis. Many pharmacological and mechanical prophylaxis methods are available. The aim is to prevent the development of DVT and not to increase bleeding. Therefore the drug or method of choice should be patient-specific:
\nMechanical prophylaxis: The aim is to reduce venous stasis by compressing the lower extremity and to increase fibrinolysis. The risk of hemorrhage is very low, and, if applied correctly, there are almost no complications. Patient compliance is important in mechanical prophylaxis and is the only negative aspect of the method. Mechanical prophylaxis methods include early mobilization, in-bed exercise, use of antithromboembolic socks, and pneumatic compression devices. It has ben shown that intermittent pneumatic compression devices provide as effective prophylaxis as chemical prophylactic agents, and the American College of Chest Physicians (ACCP) recommends the use of mechanical prophylaxis [98].
\nChemical prophylaxis: Many agents are used. They all have their own advantages and disadvantages. Risk factors are determined by patient-based evaluation and the most appropriate agent should be preferred:
\nK vitamin antagonist warfarin: It prevents the formation of fibrin by inactivating 2, 7, 9, and 10 of the clotting factors. It also inhibits the activation of fibrinolysis-causing protein C and S. Since this effect occurs earlier, it creates a temporary clotting condition. Patients with warfarin should therefore be heparinized until the effect on coagulation factors begins. The anticoagulant effects of warfarin are reversible and monitored by the international normalization rate (INR) measurement. Interaction with other drugs, narrow confidence interval, and dual effect have recently reduced the usage of post-TKA [99, 100].
\nHeparin: It acts by inactivating circulating antithrombin III. Antithrombin III also inactivates circulating factors 2, 9, 10, 11, and 12. The use of standard heparin has recently been restricted due to the low risk of bleeding due to low-molecular-weight heparin.
\nAcetylsalicylic acid: It acts as an anticoagulant by blocking thromboxane A2, which is necessary for platelet aggression. Recent studies have shown that VTE can be used prophylactically [101].
Other oral anticoagulants that may be used: rivaroxaban (direct factor Xa inhibitor), apixaban (direct factor Xa inhibitor), and dabigatran (direct thrombin inhibitor).
The development of instability after TKA is the third most common cause of revision (17%) after aseptic loosening and infection [102]. Patients present with signs of pain and swelling with movement and weight loss. There may also be pain, emptiness, or abnormal friction and rattling noise in some range of motion. On the knee during walking, varus or valgus orientation and recurvatum can be seen. Anterior knee pain during sitting up is typical in flexion instabilities. The heaviest table is knee dislocation. The treatment of instability is revision surgery. However, the rate of recurrent instability after revision was 18–60% [103]. This high rate is usually due to the lack of correct identification of the cause of instability.
\nA clinical classification of knee instability was established. Components of this classification are flexion-extension gap mismatch, component alignment problem, isolated ligament failure, extensor mechanism failure, component loosening, and global instability [103].
\nThe success of total knee replacement depends on the correct alignment of the lower limb mechanical axis. It is recommended that the postoperative lower limb mechanical axis should be in neutral alignment. The tibial cut surface in the coronal plane should be made perpendicular to the mechanical axis of the tibia. Similarly the femoral cut in the coronal plane should be made perpendicular to the mechanical axis of the femur. It is necessary for a stable knee to obtain a rectangular gap in both flexion and extension after bone incisions and soft tissue release in TKA. Balancing the gaps is important to ensure stability and for full range of motion. Flexion gap controlled by posterior femoral condylar cut and tibial cut. Extansion gap controlled by distal femoral condylar cut and the tibial cut. If there is a symmetric gap problem, tibial bone cut is adjusted first; otherwise if there is asymmetric gap problem, adjust femoral bone cut first. For example, if the knee is tight both in extension and flexion, it is called symmetrical gap problem, and its solution is to cut more proximal tibia. The asymmetric gap is one of the most common causes of instability. In some patients, the underlying cause increases the risk of instability. These reasons can be listed as follows:
Knee with advanced deformity.
Regional muscle weakness.
Neuromuscular disease.
Internal side ligament or posterior cruciate ligament failure.
Obesity and rheumatoid arthritis.
Charcot arthropathy
It is necessary for a stable knee to obtain a rectangular gap in both flexion and extension after bone incisions and soft tissue release in TKA. If the cavity is larger than the prosthesis, the term symmetrical discrepancy is used. The reason for this instability is that the distal femoral incision or the tibial incision is more than necessary [85].
\nIf the tibial incision is excessive, both extension and flexion will be loose. If this condition is noticed intraoperatively, it is thought that the problem is solved with a thicker insert, but in fact, both the patellofemoral joint problems can arise as the joint line will go down more inferiorly and the early relaxation and fixation problems can arise because the tibial component will sit on the narrower surface.
\nIf the distal femoral incision is excessive, there will be looseness in the extension range. The use of a thick insert during surgery will improve the looseness of the extension, but there will be tightness in flexion [104]. In addition, as the joint line will increase, both the effective distance of collateral ligament will decrease, and patellofemoral joint problems will occur. Therefore, if the distal femoral incision is excessive, the use of distal femoral augment should be preferred instead of the use of a thick insert [105].
\nAsymmetric mismatches occur when the joint space is trapezoidal rather than rectangular. It occurs mostly during surgery after excessive loosening of the soft tissue and is most commonly seen in extension. In this case, the transition to the restrictive prosthesis should be considered [106].
\nOne of the reasons that greatly affect patient satisfaction after TKA operations is the amount of joint range of motion. To achieve good results, a flexion range of at least 90° is required. Sixty-five degrees of flexion is required during walking; 106° of flexion is required when sitting on a chair and tying shoes. Postoperative limited and painful joint movements significantly reduce patient comfort. A flexion range of less than 90° for 6 weeks after TKA surgery is defined as a rigid knee [107].
\nHip osteoarthritis, heterotropic ossification, and reflex symptomatic dystrophy can be considered as independent factors. Inadequate posterior femoral incision and inadequate medial collateral ligament releasing of the knee with severe varus deformity may be among the causes for a rigid knee due to surgical technique [108, 109]. In one study, it was observed that joint stiffness occurred more frequently than unilateral knee arthroplasty in patients who underwent bilateral total knee arthroplasty in the same session, and manipulation was required under anesthesia [110].
\nExcessive tight extension and flexion gap, tight PCL, malrotation of components, and inadequate tibial slop angle may lead to joint stiffness [108].
\nOne of the most important indicators of joint stiffness is the extremely limited range of motion in the knee before surgery [109]. The range of motion obtained within the surgery should be considered in the determination of joint stiffness. A sudden loss of motion should suggest a mechanical problem, loosening, and infection.
\nArthrofibrosis is the most treatment-resistant cause of joint stiffness. It develops due to excessive increase of fibrous tissue in the joint [108].
\nThe strongest determinant of postoperative flexion movements is the degree of preoperative flexion. Other than that, age, preoperative diagnosis, and severity of deformity are other factors [111].
\nThe efficacy of conservative treatment is limited in joint stiffness after TKA. Aggressive range of motion improvement of 3.1° was observed with aggressive physical therapy for almost 1 year [112]. It has been shown that the use of continuous passive motion device (CPM) in the early postoperative period reduces bleeding and is beneficial in preventing joint stiffness by reducing the formation of fibrosis [113].
\nAlthough there is no consensus in the literature, manipulation under anesthesia should be performed in cases where knee flexion is below 90° between 2 weeks and 3 months. Revision rates are lower in patients with early manipulation [114]. Manipulation is performed under general anesthesia using a muscle relaxant until the knee and hip reach at least 90°. After this procedure, an average gain of 30–47° was reported [115].
\nIf the joint movement limitation continues despite these methods, surgical procedures are performed. These are arthroscopic release, open release and limited revision knee arthroplasty, and total revision knee arthroplasty [116].
\nDeep infection after TKA is the most common cause of revision. Systemic complications such as septicemia and cardiopulmonary insufficiency may also occur in patients with periprosthetic infection [117]. As a result, it increased mortality rates. Nowadays, the incidence of deep infection after TKA varies between 0.4 and 2% [74]. Factors that pave the way for infection in the postoperative period include the presence of rheumatoid arthritis, diabetes, hemophilia, malignancy, HIV, obesity, smoking, intravenous drug addiction, knee septic arthritis and osteomyelitis, prolonged surgical time, malnutrition, steroid use, and prolonged skin problems.
\nAntibiotic prophylaxis is the most effective method to prevent infection [118]. Prophylaxis should be administered 30–60 minutes. Before skin incision [119]. It has been shown that short postoperative antibiotherapy is more beneficial than the longer one [120].
\nFewer people entering the operating room, using drapes to prevent superficial contamination, providing laminar air flow, effective sterilization of surgical instruments, and keeping the surgical time 150 minutes below are also necessary to prevent infection [121].
\nRisk groups of patients should be identified before the operation, and a separate planning should be made for each patient according to comorbid diseases. Antibiotic cement has been shown to reduce the infection rate in patients at risk [122]. However, it has been reported that the use of antibiotic cement in the patient group with no risk may cause premature loosening [123].
\nThe most common organisms produced after infected knee arthroplasties are Staphylococcus aureus, coagulase negative Staphylococcus, and Streptococcus bacteria [124]. However, many microorganisms can also be active. Variations have occurred in microorganisms due to the unnecessary antibiotics used recently, and this has led to the development of resistance. Of these microorganisms, the most common isolates are methicillin-resistant Staphylococcus aureus (MRSA) and many antibiotics [125]. Fungal infections are not common, but the most common causative agents in these isolated are Candida species [126].
\nBacteria that cause prosthetic infection form a biofilm layer on the implant. This biofilm layer increases the virulence of the agent. In addition, it forms resistance to treatment because of its limitation on antibiotic permeability. The best antibiotic to cross the biofilm layer is rifampicin [127]. There are studies suggesting the addition of rifampicin to antibiotic treatment specific for the reproductive bacteria [127, 128].
\nDetailed anamnesis and detailed physical examination should be performed in the diagnosis of periprosthetic infection. In addition, the presence of a progressive radiolucent area around the prosthesis with direct radiographs, osteopenia, or osteolysis extending to the subchondral bone and the formation of new bone in the periosteal area can be evaluated in favor of infection [129]. The pain caused by rest is unique. However, increasing severity of pain and prolonged drainage at the wound site can also be evaluated in favor of infection. Arthrocentesis is then performed. In the case of active isolation, the necessary treatment is started. Empirical antibiotic therapy should be avoided. Wait until the agent is isolated. Because empirical antibiotherapy will suppress a possible infection and may cause deep infection due to delayed diagnosis of prosthesis infection that may be saved by debridement and may require removal of the prosthesis [130].
\nCRP and sedimentation values should be evaluated in diagnosis. However, it should be remembered that CRP returns to its previous level after 14–21 days postoperatively [131]. Alpha defensin, lactoferrin, ELA-2, BPI, procalcitonin, and synovial CRP values are other parameters that can be used in diagnosis [132].
\nCurrent consensus has been reached in the diagnosis of periprosthetic infection [133]. Accordingly:
Major criteria
Generation of the same agent in two positive cultures.
Presence of sinus mouth associated with prosthesis. In the presence of one of them, the diagnosis is established [133].
Minor criteria
Calculated weights of high serum CRP (>1 mg/dL), D-dimer (>860 ng/mL), and erythrocyte sedimentation rate (>30 mm/h) are also 2, 2, and 1 points, respectively.
High synovial fluid white cell count (>3000 cells/μL), alpha defensin (signal cutoff ratio > 1), leukocyte esterase (++), polymorphonuclear percentage (>80%), and synovial CRP (>6.9 mg/L) were arranged as 3, 3, 3, 2, and 1 points, respectively.
Patients with a total score equal to or greater than 6 were considered infected.
\nThe goal of infection treatment in total knee arthroplasty is eradication of the infection, pain relief, and maintenance of limb function. Treatment options are antibiotic pressure, debridement, single- or double-stage revision, arthrodesis, resection arthroplasty, and amputation. Revision surgery also has single-stage or double-stage revision options [134, 135, 136].
\nPeriprosthetic fractures around the knee are fractures that occur during or after surgery within 15 cm of the knee joint or within 5 cm of the intramedullary part of the prosthesis, if any [137]. The incidence of these fractures after TKA is 0.3–2.5% for femur and 0.4 01% for tibia [138, 139].
\nThe main risk factor related to the patient is the age of the patient. This risk is due to an increased risk of falling due to the patient’s age and osteoporosis associated with age [140]. Corticosteroid use, diseases that may increase the risk of falling with rheumatoid arthritis (epilepsy, Parkinson’s, cerebellar ataxia, myasthenia gravis) can be counted as other patient-related risk factors [141].
\nIntraoperative diaphyseal femoral fractures may occur due to incorrect placement of the intramedullary guide and osteopenia [142]. Unsuitable bone incisions, aggressive impaction of the ligamentous posterior stabilized femoral component, and eccentric placement of trial components are also risk factors for femoral fracture. It has been shown to increase the frequency of periprosthetic fractures due to increased resistance in flexion and rotation movements in anterior femoral notching [143]. The possibility of periprosthetic fracture is increased in revision TKA cases [144]. Periprosthetic fractures are more common due to the rotational forces of restrictive prosthesis using shear forces in the prosthesis [141].
\nDue to the stronger structure of the tibia, fracture development is rare.
\nFor femoral periprosthetic fractures, there is a classification that questions fracture displacement and component fixation.
Type 1 describes fractures with non-displaced and stable components.
Type 2 refers to component stable fractures with displacement of more than 5 mm or angulation of more than 5°.
Type 3 indicates loose fractures [145].
The femur fractures vertically more than the metaphyseal region. A stable periosteum prevents displacement. It is followed conservatively without any additional intervention. For fractures penetrating the femoral cortex, whether or not a bone graft is used, the penetration level should be treated with a stem prosthesis that is at least twice the diameter of the femoral canal [146].
\nWhen non-displaced fractures and stable prosthesis occur after TKA, conservative treatment may be preferred. Four to six weeks of non-weight procedure, long leg plaster, or hinged orthosis is followed.
\nDisplaced and unreducible supracondylar fractures are almost always treated surgically in the presence of adequate bone stock (\nFigure 1\n) [147].
\nLocked compression plates are preferred for knee periprosthetic fractures [144]. Prosthetic revision should be performed in fractures that cause prosthesis loosening and malposition. In these cases, stented prosthesis of sufficient length should be placed to obtain a stable fixation of the intact bone [138]. Knee replacement revision after periprosthetic fractures is often associated with the loss of range of motion (ROM) [148].
\nSupracondylar periprosthetic femur fracture treated with open reduction and internal fixation.
The majority of tibial periprosthetic fractures during surgery involve the plateau region and are generally non-displaced [146, 149]. If prosthetic loosening is present, revision surgery using a stem component long enough to cross the fracture line is required [150].
\nPostoperative tibial fractures can be examined in four groups. In type 1 fracture, revision is recommended because tibial component will be in varus alignment. The medial defect should be closed with bone graft or metal support [150]. Type 2 fractures are treated with nonsurgical treatment if the component is stable and there is minimal displacement [149]. Displaced type 2 fractures are treated with internal fixation. If the component is unstable, it must be revised using a long tibial stem to cross the fracture line [149]. Internal fixation should be performed for type 3 and 4 fractures [145].
\nThe deterioration of the relationship between prosthesis and bone is defined as loosening. The loosening may be between the prosthetic cement and the cement bone. Loosening is inevitable in long-term prostheses. It is useful to distinguish the concepts of osteolysis and loosening. Without prosthesis osteolysis, loosening of the cement may occur. The mechanisms that cause loosening are micromotion, component collapse, and periprosthetic osteolysis [151].
\nOveruse and osteopenia are the causes of patient-related loosening. Implant design may also be the cause of loosening. According to this, loosening is more likely in cementless prosthesis and constrained prosthesis. One of the most important causes of aseptic loosening is malalignment. It has been shown that a 4 mm medial collapse of the tibial component and varus deformity of more than 2° increases the likelihood of loosening [152]. In the early period, a radiolucent line is seen between the component and bone on radiography, and a collapse occurs as the loosening progresses. Loosening is more common around the tibial component [152]. In the presence of loosening around the whole component, septic loosening should be considered, and differential diagnosis should be performed.
\nIn the case of loosening, the treatment is decided according to symptoms and progress. If pain is associated with instability and there are X-ray findings, early revision surgery is recommended for bone stock preservation.
\nOsteolysis usually occurs due to inflammatory reactions caused by worn polyethylene particles or in the presence of infection. Metal particles can also cause osteolysis. Titanium causes more osteolysis than cobalt and chromium. Giant cells that develop against abrasive particles act by forming a membrane [153]. Particle size is important for this mechanism. The particle sizes range from 1 to 100 micrometers under the electron microscope. Large parts do not cause osteolysis [153]. There is no osteolysis if the parts are not spread to the cancellous bone, so osteolysis is not seen when the cancellous bone is properly covered with cement [154]. On the other hand, the incidence of osteolysis increases when pres-fit prosthesis is applied; screw fixation without cement is used or cement breaks [155]. Osteolysis is closely related to prosthetic design. Osteolysis usually occurs after 2 years of TKA. Occurrence is rare before 2 years [156]. Osteolysis is mostly seen in the tibia [157]. Diagnosis includes pain, joint effusion, and synovitis due to joint instability. Focal bone destruction may be seen on radiolucent line and X-ray. It can be seen that there is no continuity of trabeculae and bone cortex in cancellous bone. Therefore, control X-rays are very important in patient follow-up and must be compared with old radiographs in controls. CT and MRI can be used for osteolysis that cannot be detected on direct radiography [158].
\nIf the lesion is small in treatment and the prosthesis is stable, observation is sufficient. Bisphosphonate and calcium supplementation can be initiated [159]. If the prosthesis is instable, two options can be applied. The first one is debridement, polyethylene replacement, and curettage, followed by impaction of the defect with bone graft. The second is revision [159].
\nPatellofemoral joint problems after TKA generally cause anterior knee pain. Patients’ ability to tolerate this pain rarely causes patellofemoral joint problems to be revised [160]. It should be kept in mind that not only patellar component-related procedures but also procedures involving the tibiofemoral joint may cause this problem. Even in revision surgery due to a problem of patellofemoral origin, it is often caused by a component in the tibia and femur [161]. In a study, patella and malrotation were among the eight most common causes of failed TKA [162].
\nAdvanced valgus alignment, previous high tibial osteotomy, or tuberositas tibia osteotomy increases the rate of patellofemoral joint problems in TKA [160].
\nThere are many points to be considered in the surgical technique to prevent patellofemoral joint problems. These are [163]:
\nComponent placement: If the femoral component is placed medially, anteriorly, or flexed, or if there is internal rotation and if the component is excessive in size, patellofemoral problems may occur finally. Likewise, the medialization and internal rotation of the tibial component increases the risk.
\nSurgical approach type: Midvastus and subvastus interventions that protect the extensor mechanism more can reduce PF joint problems.
\nLateral release: The need for lateral retinacular release increases PF joint problems.
\nPatella resection amount: When patellar component is used, resection of the patella with anterior–posterior reduction of 12 mm increases the risk of PF joint problems [164, 165].
Patellar surface replacement is controversial today. However, in a recent study, it was found that anterior knee pain was less common in patients who underwent patellar surface change than those who did not. In the same study, the causes of PF joint revision were more common in patients without patella surface changes [166].
\nThe results in patients with patellar articular surface alteration due to persistent anterior knee pain after TKA are not as successful as those with surface replacement during primary TKA [167]. In the treatment of anterior knee pain after TKA, mechanical causes should be investigated after the exclusion of an underlying infection.
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\n\nPolicy last updated: 2018-09-11
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