\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\n'}],latestNews:[{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"},{slug:"intechopen-s-chapter-awarded-the-guenther-von-pannewitz-preis-2020-20200715",title:"IntechOpen's Chapter Awarded the Günther-von-Pannewitz-Preis 2020"}]},book:{item:{type:"book",id:"2068",leadTitle:null,fullTitle:"Understanding Tuberculosis - New Approaches to Fighting Against Drug Resistance",title:"Understanding Tuberculosis",subtitle:"New Approaches to Fighting Against Drug Resistance",reviewType:"peer-reviewed",abstract:"In 1957, a Streptomyces strain, the ME/83 (S.mediterranei), was isolated in the Lepetit Research Laboratories from a soil sample collected at a pine arboretum near Saint Raphael, France. This drug was the base for the chemotherapy with Streptomicine. The euphoria generated by the success of this regimen lead to the idea that TB eradication would be possible by the year 2000. Thus, any further drug development against TB was stopped. Unfortunately, the lack of an accurate administration of these drugs originated the irruption of the drug resistance in Mycobacterium tuberculosis. Once the global emergency was declared in 1993, seeking out new drugs became urgent. 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During this time, she isolated and selected fungi with high cellulose activity for the enzymatic hydrolysis of sugarcane bagasse. \nShe received her Ph.D. in Science from the Soil Science Department (Agricultural Microbiology Program) at ESALQ/USP, with a period of one year as a visiting scholar at the University of California Berkeley and Energy Bioscience Institute. Meanwhile, she worked on the improvement of S. cerevisiae by hybridization for increased tolerance toward inhibitors from second-generation ethanol substrates.\nCurrently, she is Collaborating Professor of Cell Biology and Molecular Genetics at University of Sao Paulo. 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From chapter submission and review to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"49816",title:"The Current Trend of Total Ankle Replacement",doi:"10.5772/62192",slug:"the-current-trend-of-total-ankle-replacement",body:'Total ankle replacement (TAR) was introduced for end-stage arthritis of the ankle joint in the 1970s. Initial poor clinical results due to imperfect prosthesis design and our incomplete knowledge of the biomechanics of the foot and ankle limited the using of TAR. Despite high numbers of failures in early generations of ankle prostheses, there has been a continued and increasing interest in TAR for end-stage arthritis. Nowadays, scientists are working on fourth-generation ankle prostheses, which are characterized by three-part, mobile-bearing, uncemented design. The STARTM ankle prosthesis was one of these fourth-generation ankle prostheses, which was approved for use by the United States Food and Drug Administration (FDA) in May 2009. The clinical outcomes of TAR have been increasing in terms of progress. Newer studies suggested that implant survival rates were 70% to 95% during follow-up periods that ranged from 2 to 12 years. TAR is increasingly used as an alternative to arthrodesis.
The ankle joint is subjected to more weight-bearing force per square centimeter and is more commonly injured than any other joint in the body. Approximately 6% to 13% of all cases of osteoarthritis (OA) involve the ankle joint. While the incidence of severe ankle arthritis is clearly less than that of the hip or knee, OA of the ankle is a main cause of disability, which impairs functional mobility and leads to poor quality of life. Unlike the hip and knee joints, in which the primary causes of degeneration are primary OA and inflammatory diseases, 70–80% of ankle arthritis is post-traumatic and the remaining cases are related to primary OA and rheumatoid arthritis [1, 2, 3].
The treatment options for severe ankle arthritis have changed during the past 10 to 15 years. Currently, treatment options include ankle arthrodesis and TAR. There remains considerable controversy surrounding the benefits of each procedure and treatment option, especially concerning the idea that patients might benefit from one approach more than the other. TAR has some disadvantages such as expensive cost, implant loosening, ankle instability, higher infection rate, and higher re-operation rate [6–9]. TAR remains a less satisfactory solution when compared to other joint replacements; however, TAR offers greater range of motion in the ankle with improved gait kinematics, reduced stress, and potentially causes less arthritis in adjacent joints [3]. In addition, with regards to cost-effectiveness analysis, TAR has better quality-adjusted life years when compared to arthrodesis, albeit at a higher cost [10].
In this chart, we will introduce the decision-making process of whether to use TAR or arthrodesis, as well as discuss the history of TAR, the characteristics of different prosthesis designs, their clinical outcome, and the complications and revisions associated with TAR.
Lord and Marotte introduced an inverted hip prosthesis as a disappointing solution for ankle replacement in 1970 [4]. The original first-generation TAP was non-anatomical, cemented, and restrictive. It is not surprising then that the original first-generation TAP prostheses are associated with severe osteolysis, component loosening, impingement, infection, and soft-tissue breakdown; this has led many surgeons to discredit this procedure. For these reasons, there has been a continuous effort to develop a safe, stable, and long-lasting ankle prosthesis that could replicate the complex anatomy of the ankle joint and better mimic ankle biomechanics.
Implant design played a large role in the effect of loading direction on the magnitude and direction of the joint’s motion. Bone–implant displacements occurred along the directions expected on the basis of the implant interface geometries. Various ankle designs are available, including two-component and three-component systems [5]. After unacceptably high failure rates had been published for the first generation of implants [1–5], the second generation of implants achieved marked improvements in clinical outcomes [6–8]. Second- and third-generation prostheses followed these first implants, and interest in this procedure has resurged in the past decade. These new designs include changes in the geometry and design of the components, as well as the use or non-use of polymethylmethacrylate bone cement, which is termed a two- or three-component design. The third-generation prosthesis is characterized by the non-use of cement, accurate anatomy, and better ROM of the ankle joint. Mobile-bearing implants are designed without constraint to reduce meniscal wear and to increase the longevity of the implant, which features mobile PE inlays. The stability of the bone–implant interface has been explored in an unconstrained, three-piece mobile-bearing implant using the concepts of implant migration and inducible displacement. Fixed-bearing designs, in contrast, are designed to increase stability, reduce micromotion at the bone–implant interface, and decrease bearing dislocation. In addition, the surgical instrumentation and technique are improved and redesigned for the new prosthesis.
The third-generation of ankle prostheses includes the HINTEGRA ankle (New deal, Lyon, France/Integra, Plainsboro, NJ, USA), the INBONE TAR implant (Wright Medical Technology, Arlington, TN, USA), the Agility prosthesis (DePuy Orthopaedic, Warsaw, IN, USA), the STAR prosthesis (Scandinavian TAR), the Mobility prosthesis (DePuy, Leeds, United Kingdom), and the Salto Talaris (Tornier, Edina, MN, USA).
The HINTEGRA prosthesis is a three-component, mobile-bearing ankle replacement with cobalt–chromium tibial and talar components [6]. The polyethylene mobile-bearing element provides axial rotation, physiological flexion, and extension mobility, and it also provides inversion and eversion stability [7, 8]. The HINTEGRA, which is a flat, anatomically shaped component, fully contacts the resected area with fixation of its tibial component. All inserted components have locking pegs on the talar component. The tibial component consists of a flat tray with raised spikes for bone fixation. The anterior side has a flange with holes for screw fixation. The talar component has medial and lateral walls and two fixation pegs; two screws may be used for added fixation, if appropriate. The ingrowth surface is plasma-sprayed titanium with a hydroxyapatite coat [9, 10]. Therefore, the HINTEGRA ankle prosthesis may be used for the treatment of major coronal plane deformities and as a salvage of failed ankle replacements.
Amongst the third-generation ankle implants approved by the US FDA, the INBONE TAR implant employs a fixed-bearing design with a modular stem system for both the tibial and the talar components. The INBONE system features a technique that offers potential advantages in improved stem fixation and a unique intramedullary alignment system. It has a broader polyethylene component that conforms to the saddle ankle geometry, and it also provides a large surface area that spreads out stress gradients, leading to possible decreased wear [11]. A. Datir found that only the lateral talar component angle and the mean difference between the pre- and postoperative tibial slope had significant correlations with postsurgical outcomes in INBONE ankle replacement [11].
The Agility TAR System, which is almost exclusively without polymethylmethacrylate cement fixation, was the most commonly used implant in the United States from 1998 to 2007. The design process started in 1978, with prototype completion and cadaver implantation occurring in 1981 [12, 13]. It was first implanted in a patient in 1985 and subsequently marketed in 1992 as the “DePuy Alvine Total Ankle Prosthesis”. From 1985 to 2007, the implant went through a total of four generations and seven phases of implant improvement [13, 14]. The US FDA has cleared it for use only with polymethylmethacrylate cement fixation [15]. The Agility prosthesis is a semi-constrained ankle replacement with a cobalt–chromium talar component, a titanium tibial component, and a fixed polyethylene bearing [16]. It is characterized by a tibial component, which provides a talar component with a larger surface area. The talar component of the Agility system was prone to shift forward and backward along the talar groove during plantar flexion–dorsiflexion loading, and it would also rock about its long axis in inversion–eversion loading. The ingrowth surface consists of cobalt–chromium sintered beads. Fixation on the tibial side is aided by syndesmotic arthrodesis. Fixation on the talar side is achieved with the use of a keel under a flat-cut component.
The STARTM ankle was first approved by the US FDA in 1998 [17]. It was a three-part, mobile-bearing, uncemented ankle replacement. The STAR prosthesis featured a cementless design with a plasma-sprayed titanium coat [18]. Fixation on the tibia was achieved with use of two barrels on the flat tibial component. The talar component was fixed with the use of two sidewalls and a fin on the inferior surface. The tibial component of the STAR was most susceptible to normal motion on the bone surface, especially in plantar flexion–dorsiflexion and inversion–eversion loading. On average, of the three loading directions, the internal–external rotation resulted in the smallest relative motions of both of the STAR components since the device allowed for unconstrained rotation about this axis [19].
The Mobility prosthesis is a mobile-bearing ankle replacement with cobalt–chromium components on the tibial and talar sides, and it also features a sintered bead ingrowth surface [20]. The tibial component has a stem placed into the tibia with an anterior bone window. The talar component has two fins on the inferior surface; no sidewalls are present on the talar component. The talar cut has three surfaces. The prosthesis has not undergone design changes during the course of the study.
The Salto Talaris TAP, with design and instrumentation based on the Salto mobile-bearing TAP, was approved for use by the US FDA in 2006. Although it is a fixed-bearing device, the instrumentation and component trialing incorporate a rotationally mobile tibial trial component that allows for self-alignment on the resected surface of the distal aspect of the tibia, which is determined by the talar component. The final implant has a polyethylene insert that is rigidly fixed to the tibial component and does not allow for rotational or translational motion between the two surfaces.
Normal ankle kinematics attenuates ground reaction impact forces and impact loading on the subtalar joint. The importance of achieving normal ankle kinematics during stance is very important for both function of the ankle and long survivorship of the prosthesis. During a normal gait cycle, the talus has a continuously changing axis of rotation against the tibia as well as a gliding motion against the calcaneus, respectively. The talus and mortise widen slightly anatomically from posterior to anterior. Following talus plantar flexion, the narrowest portion of the talus sits in the ankle mortise and allows for rotational movement between the talus and mortise. When the talus is maximally dorsiflexed, the wider portion of the talar articular surface locks into the ankle mortise, allowing for little or no rotation between the talus and the mortise [21, 22].
Compared to a normal ankle, ankle OA shows a significant deficiency in triplanar ankle movement, the second active maximal vertical and maximal medial ground reaction force, sagittal and transverse ankle joint moments, and ankle joint power [2]. However, J.F. Baumhauer reported that ankle arthrodesis results in a normal gait postoperatively, especially when there is a normal subtalar joint and talonavicular joint [23].
S. Singer reported that TAR with first-generation TAP resulted in increasingly normal gait mechanics during sagittal joint motion, which was maintained, and it also resulted in more normal ankle kinematics when compared with those following arthrodesis [24]. The gait patterns of TAR with the third-ankle prosthesis more closely resembled normal gait during sagittal plane motion and dorsiflexion, and it also resulted in a normal range of tibial tilt when compared with the gait patterns of patients following arthrodesis [24]. Peak plantar flexor moment increased in arthrodesis patients and decreased in TAR patients. TAR appears to regain more natural ankle joint function. R.M. Queen compared the kinetics of TAR with that of the INBONETM or Salto Talaris, as well as that of the normal contralateral ankle in bilateral patients; the results showed that walking speed, step time, step and stride length, and propulsion ground reaction forces improved following TAR. However, peak dorsiflexion did not change. At the same time, the dorsiflexion angle during heel strike was increased on the nonsurgical side [25].
A. Rosello Anon et al. reported that kinetic gait parameters were similar to those of a healthy ankle following TAR with HINTEGRA [26]. M.E. Hahn reported that both arthrodesis and TAR patients were similar in terms of demographics and anthropometrics. Neither group increased their average daily step count [27]. Gait patterns in both treatment groups were not completely normalized [24]; however, both treatment groups did not exhibit equivalent to normal plantar flexion motion, ankle moments, and power when compared with the normal group. Further investigation is needed to determine why patients who have undergone TAR do not use the plantar flexion motion in the terminal-stance phase, as well as to explain the limited increase in power generation at toe-off after replacement [24].
In addition, walking speed, step, and stride length improves from the preoperative phase to each postoperative time point. Peak dorsiflexion did not changed over time or between sides; however, the dorsiflexion angle during heel strike was increased on the nonsurgical side. Peak plantar flexion moment, stance, step time, weight acceptance, and propulsion ground reaction forces improved from the preoperative period to 1 year postsurgery on the surgical side. These results indicated that fixed-bearing TAR was effective at improving gait mechanics in patients with painful end-stage ankle arthritis. In addition, TAR resulted in the maintenance of ankle dorsiflexion during the stance phase; however, a decrease in dorsiflexion angle was present during heel strike on the operative side when compared with the nonoperative side up to 2 years following TAR. Finally, following TAR, the asymmetry in temporal gait variables and peak plantar flexion moment were improved, although differences did remain between the operative and nonoperative limbs for stance, step, and swing time, as well as for the peak plantar flexion moment 2 years following TAR. This remaining gait asymmetry is of potential concern because of the possibility that the patient might overload the contralateral limb and engage compensatory walking mechanics that could lead to secondary injuries following TAR [25].
If adequate conservative measures for the treatment of end-stage ankle osteoarthritis have failed, surgery may be taken into consideration. M.R. McGuire reported that TAR is indicated in rheumatoid patients with severe ankle involvement who have not responded to medical management. TAR is especially suitable for those patients who will place minimal stress on the ankle, those for whom no destruction of the hip or knee joint is found, and for those who are 65 years of age or older. The elderly may not tolerate the prolonged immobilization or repeated operations that arthrodesis may require. TAR should not be used in young patients with post-traumatic arthritis [28]. J.R. Ramaskandhan found that early outcomes following TAR for patients with post-traumatic OA are comparable with those for patients with OA and rheumatoid arthritis [29]. More importantly, patients whose lifestyle or employment requires them to walk down ramps may have an advantage with TAR when compared with an arthrodesis. In addition, I. Hetsroni reported that TAR has better quality-adjusted life years when compared to arthrodesis, albeit at a higher cost [10].
TAR improves clinical and functional outcomes independent of preoperative tibiotalar alignment when postoperative alignment is restored to neutral at the time of replacement. Therefore, one of the keys to success may be to achieve coronal plane balance by performing additional osseous and soft- tissue procedures in patients with coronal plane deformity [30]. Preoperative talar varus deformity increases the technical difficulty of TAR and is associated with an increased failure rate. Deformity of >20° has been reported to be a contraindication to replacement. T. Trajkovski determined whether clinical outcomes of TAR in patients with ankle arthritis and a preoperative talar varus deformity of 10° were comparable with those of patients with a varus deformity of <10°. Satisfactory results can be achieved in patients with varus malalignment of 10°, which should not be considered a contraindication to TAR [31].
With the population ageing, the absolute number of patients affected by ankle OA is likely to increase, which means that there are more and more potential candidates for TAR. For this reason, there is a trend of increasing indications; as such, clinical guidelines regarding implant migration must be established to ensure successful outcomes [3]. On the other hand, some patients might be younger and have higher physical demands, placing the damaged joint under increased stress [32]. Based on this, young age and high physical demand are currently considered contraindications for TAR.
Taking into account numerous individual criteria, the most appropriate indication substantially influences the outcome of patients with end-stage ankle arthritis who are treated by ankle TAR.
We present a typical case who underwent TAR. She was a 59-years-old woman and had a severe pain on her left ankle. She failed to respond to a trial of conservative treatment for ≥6 months.
The preoperative X ray images showed a severe osteoarthritis in the left ankle.
The picture showed incision and the osteotomy.
The pictures showed that the ankle joint is in a good alignment with the template.
The pictures showed the X rays image of ankle joint after TAR 2 years postoperatively.
Modern TAR systems have either a fixed-bearing or a mobile-bearing design. In the United States, fixed-bearing, two-component designs are more commonly used. S. Noelle reported that STAR prostheses achieved a high satisfaction rate following TAR, and exhibited clear pain relief in patients between March 2005 and May 2010 [33]. J.R. Jastifer reported that the overall implant survival of STAR prosthesis was 94.4% at a minimum of 10 years of follow-up. A total of 39% of patients required additional surgical procedures, most of which were performed more than 9 years postoperatively, and one patient required a revision of the prosthesis. Preoperative VAS pain scale scores, Mean Buechel–Pappas Scale scores, and mean AOFAS Ankle–Hindfoot Scale scores improved from 8.1 to 2.1, from 32.8 to 82.1, and from 32.8 to 78.1 at the latest follow-up, respectively. All patients reported their outcomes as good or excellent. In the current cohort of STAR ankle patients, implant survival, patient satisfaction, pain relief, and function ratings were high. However, the rate of additional procedures was also high, which highlights the need for patient follow-up and additional long-term outcome studies on TAR [17].
Early clinical results indicate that the Salto Talaris fixed-bearing TAR system can provide significant improvements in terms of pain, quality of life, and standard functional measures in patients with end-stage ankle arthritis [34]. Implant survival at a mean follow-up time of 2.8 years was 96% when metallic component revision, removal, or impending failure was used as the endpoint. For the Salto Talaris total ankle implant, a high incidence of bony overgrowth occurs at the margins of the tibial tray. The frequency and amount of overgrowth were directly related to the amount of cortical coverage at the bone–implant interface [35]. Patients who underwent TAR with the INBONETM or Salto Talaris prosthesis demonstrated that they were able to walk faster, and they also exhibited an improvement in gait symmetry. However, this improvement did not appear to return the patient to a symmetric walking pattern by 2 years post-TAR [25].
The Agility prosthesis typically exhibited greater relative motion than did the STAR, with significant differences observed for both the tibial component in inversion–eversion rotation and for the talar component in internal–external rotation. The magnitudes of the relative motions were affected by the loading direction and compression. The motion magnitudes were quite large, with values exceeding 1, 000 mm for the Agility talar component in plantar flexion–dorsiflexion and in inversion–eversion. Large motions at the bone–implant interface, resulting from weak initial fixation, may inhibit implant osseointegration early in the healing process, and it may also contribute to the overall likelihood of implant failure resulting from aseptic loosening [19].
The overall survival rates of the HINTEGRA implant were 94% and 84% after 5 and 10 years, respectively. The mid-term survivorship of the HINTEGRA implant was comparable with that of other third-generation TARs [36]. The mid-term to long-term survivorship of a TAR in which a HINTEGRA implant was used is promising, and it is in agreement with the survivorship findings for other third-generation total ankle implants. There were no polyethylene failures and amputations. The generation category of the prosthesis, the cause of ankle OA, and the age of the patient were identified as independent risk factors for prosthesis failure.
There is a concern that placing a TAP in the setting of a fused hindfoot will create abnormal stresses on the ankle joint and will thus lead to increased early wear or degeneration of the implant. Ipsilateral hindfoot arthrodesis in combination with TAR may diminish functional outcome and prosthesis survivorship when compared to isolated TAR. J.S. Lewis reported that TAR with the STAR performed with ipsilateral hindfoot arthrodesis resulted in significant improvements in pain and functional outcomes, which was in contrast to prior studies; however, overall outcomes were inferior to those observed for isolated TAR [37]. The authors of this study have speculated that the mobile-bearing design may play an important role in the transfer of rotational movement from the tibia into calcaneal inversion/eversion in patients with a fused hindfoot [37].
Future work could examine the effect of normalizing gait asymmetry on long-term outcomes following TAR. Additional work should focus on gait changes following TAR, as well as on gait symmetry results when comparing fixed and mobile-bearing implants to better assess the overall viability of modern TAR prostheses as a long-term solution for the treatment of severe, painful ankle OA.
The first- and second-generation ankle prostheses were cemented and constrained, which led to higher failure rates [11, 12]. With continuously improving design and fewer constraints, third-generation ankle implants are increasingly favored; however, the technical demands of TAR are substantial. There are still some complications that the surgeon should treat carefully. The recorded complication rate of TAR was 23%, while intraoperative bone fracture and wound healing had a failure rate of at least 50% [38]. The short-term complications of TAR included intraoperative malleolar fractures and skin necrosis. The mid-term clinical outcomes showed a 41% complication rate including instability, infections, subtalar arthritis, malalignment, and one tibial bone cyst, which led to the need for subsequent surgery. Adequate patient selection and a thorough knowledge of associated complications are mandatory to reduce the number of complications and increase the rates of ankle replacement survivorship [39, 40].
M.A. Glazebrook classified the complications following TAR into three tiers: high-grade, medium-grade, and low-grade. High-grade complications result in a greater than 50% failure rate in TAR, including deep infection, aseptic loosening, and implant failure. Medium-grade complications are defined as technical error, subsidence, and postoperative bone fracture. Finally, low-grade complications are defined as intraoperative bone fractures and wound healing problems, which should be considered [41]. Recently, R.J. Gad thought that the three-grade classification system of complications did not reliably reflect practitioners’ experiences, and they thus categorized complications as either high or low risk for the early failure of TAR [38].
Initial clinical results were poor, largely because of early loosening [42, 43]. Aseptic loosening is the predominant failure mechanism in TAR; in fact, A. Henricson reported that about 40% of revision cases are due to aseptic loosening [44]. Primary stability may be affected by the initial implant fixation; in addition, known uncemented talar designs rely on bone ingrowth for fixation, which requires minimal relative motion between the implant and the host bone.
The greater magnitudes of relative motion in the Agility prosthesis suggest that primary instability of the implant may contribute to its higher clinically observed aseptic loosening rate. However, large motions at the bone–implant interface, resulting from a weak initial fixation, may inhibit implant osseointegration early in the healing process and contribute to the overall likelihood of failure resulting from aseptic loosening [19]. Future TAR designs will require better fixation to improve outcomes.
Implant migration is a good clinical evaluation tool for the loosening of prosthesis following TAR. Implant migration was defined as a change in implant location from the immediate postoperative radiograph. J.W.-Y. Fong designed a radiostereometric analysis marker insertion protocol to evaluate the stability of the migration of a fixed-bearing design following TAR [45]. The results showed that the migration of a fixed-bearing design was within the normal range.
S.A. Brigido presented a measurement technique to assess implant migration, which was supported by the high level of inter-rater reliability and intraclass correlation. The results showed that the mean INBONETM implant migration was 0.7 mm at 1 year and 1.0 mm at 2 years. Time and sex were significant predictors of implant migration [3].
Although talar subsidence and migration are recognized complications, empirical observations of postoperative patients with a Salto Talaris ankle replacement have suggested a high rate of posterior bony overhang and resultant overgrowth. In addition, it has been noted that a relatively high percentage of these implants were inserted at an angle other than perpendicular to the anatomic axis of the tibia. Specifically, the implants were usually placed in varus and with a positive slope [35].
Inlay fractures are relatively common, which indicates potential for the improvement of implants. The documentation of intraoperative surgical errors leading to revision surgery varies significantly among registers [46]. The results of the present study indicate a high incidence of hypertrophic bone proliferation when the dimensions of the tibial component do not match the anteroposterior depth of the tibia at the plane of resection. Despite the high occurrence rate, the clinical relevance of hypertrophic bone is obscure. After insertion, the position of the components is not expected to change. Disruption of the extraosseous talar blood supply at the time of ankle replacement may be a factor contributing to talar component subsidence—a common mechanism of early failure following ankle replacement [39].
The stable biological coating of prosthesis components and high initial structural stability is critical for successful TAR. Continuing observation of patients who have undergone TAR is warranted for the purpose of conducting long-term analysis of prosthesis failures in order to improve the outcomes associated with this surgical technique.
Deep infection rates following TAR have been reported to be as high as 4.6% [47]. M.S. Myerson retrospectively reported on the patient- and prosthesis-associated demographics of infected TAR and the outcomes following treatment. The results showed that the treatment of deep infections following TAR is dependent on an accurate and timely diagnosis. A more uniform diagnostic approach, including immediate ankle joint aspiration and the evaluation of inflammatory markers before starting antibiotics, may allow for early surgical intervention, as well as for improved monitoring of a patient’s response to treatment. Only a limited number of patients who develop a deep infection following primary or revision TAR can expect to undergo successful joint-preserving revision arthroplasty. However, hindfoot arthrodesis with intramedullary fixation and structural allograft may be a reliable alternative [48].
Patients with a body mass index higher than 30 showed a higher rate of complications after TAR. Cardiovascular and peripheral vascular disease, smoking, osteoporosis, and overweight are risk factors for a worse survival rate. Preoperative MRI and long-leg X-rays to evaluate any angular deformities of other joints are recommended. Additionally, angiography and neurological examination is recommended for selected patients.
In conclusion, adequate patient selection and thorough knowledge of the surgical technique used are mandatory to reduce the number of complications and to increase ankle replacement survivorship.
Design improvements have increased the success of TAR; revision rates of TAR are higher than those for hip and knee replacement. The revision rates of TAR are approximately 10%–17% at 5 years [38, 40]. In the current cohort of STAR patients, implant survival at a minimum of 10 years of follow-up was high. However, 39% of patients required some sort of secondary procedure, most of which occurred after 9 years of follow-up [17]. A. Henricson et al. defined ankle replacement revision as the extraction of one or more bone-incorporated components or the exchange of a broken plastic component without any known trauma’ [49, 50]. Based on the definition, the authors classified the revision of TAR as having either mechanical causes or nonmechanical causes.
Malalignment and periprosthetic fracture are the major sources of mechanical failure in TAR [23]. S. Manegold et al. classified periprosthetic ankle fractures following TAR into three different types, which are based on three items: the cause of the fracture, the anatomic location of the fracture, and prosthesis stability.
The first parameter evaluates the fracture cause—Type 1: an intraoperative fracture; Type 2: a postoperative traumatic fracture; and Type 3: a postoperative stress fracture. The second parameter is the anatomic location of the periprosthetic fracture. The fracture is assigned a letter (A through D). Concomitant injuries involving bimalleolar fractures and diaphyseal lower-leg fractures are classified as AB and BC, respectively. The third parameter involved the stability of the implanted components. If there are no clinical or radiographic signs of implant loosening, or if the fracture does not reach the prosthesis, the implant can be considered stable. In the presence of periprosthetic osteolysis or fracture-related implant loosening, the prosthesis is classified as unstable. This classification is relatively clear and can be conducted on the basis of the treatment options used. However, the effectiveness of the classification system still needs to be confirmed by the treatment results [51].
Coronal plane malalignment at the level of the tibiotalar joint is not uncommon in end-stage ankle arthritis. Restoration of neutral coronal plane alignment is important in TAR. If an ankle joint prosthesis is not well balanced and edge loading occurs, increased contact stresses on the polyethylene insert can result in accelerated polyethylene wear and premature implant failure. Ancillary procedures performed before, during, or after TAR to correct deformities are thus important in preventing failure due to instability in the varus ankle [31].
There are limited choices currently available in the revision of ankle replacements due to the need to correct osteotomy for alignment. However, the “salvage” can be challenging because a lot of bone has been lost. Alternative approaches include direct arthrodesis with shortening, arthrodesis with interposition graft (autograft, allograft, or shape porous metals), or revision ankle replacement with a larger replacement.
The most prevalent cause of non-mechanical revision involves aseptic loosening. Ellington and Myerson provided a grading system that ranged from 1 to 3 to define the severity of talar component subsidence and to predict the outcomes following revision. In grade 1, the subsidence of the talar component is minimal. In grade 2, the talar component has subsided into the talar body, but it has not violated the subtalar joint. In grade 3, the talar component has migrated onto or through the subtalar joint [15, 52].
M.A. Prissel et al. described a technique for the management of extensive talar aseptic osteolysis for the revision of Agility systems with the use of geometric metal-reinforced polymethylmethacrylate cement augmentation. This technique preserves the subtalar joint, provides immediate component stability, and restores component alignment and height [15]. The authors used three or four titanium plasma-coated triangular metallic arthrodesis rods (3 mm or 7 mm) or large-diameter acetabular screws placed in a triangular or quadrangular orientation around the periphery of the remaining talus and the body of the calcaneus. The superior aspects of the rods or screws should create a parallel surface, allowing the talar component to reside at the proper level to restore the anatomic height of the hindfoot and mechanical function of the ankle joint [15].
Collectively, the classification of periprosthetic fractures and the grading system used for component subsidence can facilitate therapeutic decision making, as they allows for the differential analysis of the causes of these conditions; they can also serve as a guide when making the choice between operative and nonoperative treatment options. There were still obvious functional limitations following the revision of TAR, with fewer than half of the patients returning to previous activity levels. However, the revision of TAR is still a cost-effective alternative to other available options and it still allows for additional revision should late failure occur.
Patients with ankle arthritis and deformity who experience severe pain and functional disability, and do not respond to nonoperative treatment modalities, are candidates for TAR [53]. Currently, there is no consensus regarding which treatment, arthrodesis or replacement, is better for end-stage ankle arthritis.
Ankle arthrodesis is still considered to be the gold standard for the treatment of end-stage ankle arthritis. Ankle arthrodesis yielded good radiographic and functional outcomes in primary arthrodesis [54, 55], bilateral ankle arthrodesis [56], or combined ankle and hindfoot arthrodesis, even in revision cases following TAR [57]. Arthroscopic ankle arthrodesis provides not only an alternative to traditional open techniques but also an obvious advantage including decreased complications, reduced postoperative pain, and shorter hospital stays [58, 59, 60, 61]. There exists fair evidence-based literature (grade B) to support a recommendation for the use of ankle arthroscopy for ankle arthrodesis [62].
Ankle arthrodesis has an approximately 10%–40% nonunion rate [23, 53]. Osteonecrosis of the talus and smoking are known risk factors for nonunion [53]. Risk factors associated with prolonged hospital stay were advanced age, female sex, diabetes mellitus, and more than one general or surgery-related complication [63]. The published literature on the long-term follow-up of modern TAR achieved significantly higher implant survival rates, patient satisfaction, pain relief, and range of motion (ROM) and American Orthopaedic Foot and Ankle Society (AOFAS) scores following the third ankle prosthesis [29, 64]. Complication and survivorship rates were comparable between both groups [65]. Compared to arthrodesis, the primary advantages of TAR include maintenance of motion of the ankle and reduced risk of developing adjacent joint arthritis. J.J. Jiang reported that TAR was independently associated with a lower risk of blood transfusion, non-home discharge, and overall complications when compared to ankle arthrodesis during the index hospitalization period. TAR was also independently associated with a higher hospitalization charge, but the length of stay was similar between the two groups [66]. S. Singer reported that improvement in patient-reported Ankle Osteoarthritis Scale and Short Form-36 scores were similar for both arthrodesis and TAR groups [24]. In addition, R. Rodrigues-Pinto reported that complication and survivorship rates were comparable between both TAR arthrodesis groups [65]. A multicenter study showed that the intermediate-term clinical outcomes of TAR with third-generation prostheses were comparable in a diverse cohort in which treatment was tailored to patient presentation; the rates of reoperation and major complications were higher following ankle replacement when compared with arthrodesis [67].
Although the AOFAS hindfoot scale is the most frequently used outcome instrument in TAR studies, its score has been under recent scrutiny with respect to its moderate level of correlation, its satisfactory degree of reliability, and its degree of responsiveness [68, 69, 70]. The SF-36 and Visual Analog Scale (VAS) pain scoring systems are generic, but validated, outcome measures. Therefore, it will be essential to standardize data collection, evaluation, publication, and the assessment of register data in TAR. TAR outcome measurement by means of registers has several specific requirements necessitating additional documentation beyond the basic dataset [46].
In conclusion, the current investigation demonstrated that neither arthrodesis nor TAR replicated normal ankle function, and there were no differences in ankle power, moments, or temporal gait parameters between the two patient groups. Both arthrodesis and TAR achieved good clinical outcomes. Compared with ankle arthrodesis, the rates of complication with TAR are comparable. Although complications following TAR are frequent, the results of TAR are improving and promising; TAR can reliably improve a person’s quality of life. Nevertheless, patient selection and education are essential.
TAR is becoming the modality of choice for the treatment of end-stage degenerative joint disease of the ankle. To maintain the longest function of ankle replacements, the design of the prosthesis should allow for smooth and continuous interaction and normal gait. TAR offers better mobility, improved gait, and reduces the development of subsequent subtalar joint arthritis when compared with ankle arthrodesis. The decision to treat with TAR or ankle arthrodesis depends on the surgeon’s technique, as well as on the patient’s condition. Improved operative techniques, the surgeon’s experience, as well as appropriate patient selection can anticipate better outcomes. Deformities of the ankle and foot should be corrected before TAR is performed. The revision of a replacement is ultimately inevitable due to aseptic loosening and infection. Despite the functional limitations following the revision of TAR, the revision still offers a cost-effective alternative to ankle arthrodesis.
The journey of exploring acid and base starts long before, but in the last century the advancement was remarkable. In 1890, Wilhelm Ostwald electronically measured hydrogen [1]. Svante Arrhenius won the Noble prize in 1903 for the theory of ionization [2]. In 1908, Henderson and Black showed that bicarbonate and phosphate equilibrated with CO2 at normal body temperature in different solution [3]. In 1923, Bronsted first put forward the idea of acid as a substance that ionizes in solution and donate hydrogen and the base accepts the hydrogen from the solution [4]. Bronsted, Henderson and Van Slyke described acid-base balance in the early part of nineteenth century [5]. Handerson invented bicarbonate as the most important buffer system of the body, and Hasselbalch first measured the real blood pH in the early part of nineteenth century [6, 7, 8]. In 1909, S. P. S. Sorensen developed the pH scale [8]. Later Hasselbalch-Henderson developed an equation that helped in relating pH to the blood bicarbonate and PCO2 [7, 9, 10]. In the early 1980s, scientists introduced electrodes specific for each ion. Thereafter, serum electrolyte and the anion gap measurement become routine tools for assessing acidosis.
Acidosis has fatal consequences like CNS damage. Even death is not uncommon. Acidosis is characterized by a decrease in pH, and this change is rapidly corrected by the body buffer systems. Many clinical conditions develop acidosis, as well as ionic derangements and the only correction of the underlying cause can resolve it. There are equal numbers of cations and anions in the blood and among them there are some unmeasured anions. These unmeasured anions can contribute in the clinically important anion gap. In a healthy individual, there is an acceptable range of normal anion gap. But some conditions can increase or decrease this gap. Increased anion gap usually represents metabolic acidosis. Albumin and many other confounding factors influence the anion gap derangements. Accuracy in measuring anion gap is critically important for the evaluation of acidosis.
The body maintains its normal physiology by the strict balance of acid and base. The body maintains its normal arterial pH close to 7.4 at a range between 7.36–7.44, and the intracellular pH of the human body is 7.2 [11]. Normal acid-base balance is the balance between each hydrogen increase by the intake or production, and that is decreased by elimination. Acid-base balance is measured by measuring pH, CO2 and HCO3. In general, consuming animal protein add acid in the body, and consuming cereals and vegetables add alkali in the body. In oxidative metabolism, CO2 is produced in the tissue, and at a similar rate, that is eliminated by the lungs. So, pCO2 persists at about 5.33 kPa (40 mm of Hg). Different buffer systems of the body play a crucial role in removing excess H+. Metabolism of carbohydrate and fat uses O2 and produce CO2 and H2O. Normal lungs efficiently remove most of the CO2. In oxidation of amino acids, carbon dioxide and water are produced along with the liberation of nitrogen as ammonia, a toxic material in the body. In the liver, the urea cycle utilizes the ammonia, where this toxic NH3 combines with CO2, and produce urea. In the proximal tubule and other renal epithelial cells, ammonia and bicarbonate are also produced from glutamine metabolism. Some of it returns to the body fluid through the renal veins and is metabolized in the liver. And the rest of the NH3 excreted in the lumen. So, NH3 does not exist in the body fluid. Most of the NH3 is excreted in the urine, and it plays an important role in removing H+ to maintain normal acid-base balance. In the urine, NH3 binds hydrogen ion to produce NH4, and it prevents excessive acidification of urine.
Excess acid is eliminated from the body by the lungs and the kidneys. In the lungs, acid is eliminated in the form of CO2, and in the kidneys, acid is excreted as acid phosphatase and ammonium. CO2 is lipid soluble, and it crosses the cell membranes in the lungs. Most of the CO2 produced in the tissue is eliminated by alveolar ventilation. Arterial and brain chemoreceptors can sense the acid and base excess, and respiratory system responds with hyper or hypo ventilation. As a result, pH is increased or decreased by increasing and decreasing pCO2 level. The regulation between CO2 and H2CO3 level is critically maintained when the blood travels through the lung capillaries. When strong acid is added, some HCO3− become H2CO3 and blood PCO2 is increased. In acidosis, carbonic acid dissociate to CO2 and H2O. As a result, respiratory center is stimulated and it leads to hyperventilation. Hyperventilation eliminates these CO2 to maintain normal pH. In alkalosis, CO2 is retained by hypoventilation. This CO2 combines with H2O to produce H2CO3, and pH is maintained.
The kidneys excrete acids, both respiratory and nonrespiratory origin and retain HCO3− to stabilize the pH of blood. HCO3− is predominantly regulated in the kidneys. The nephron reabsorbs all filtered bicarbonate in exchange for H+. The kidneys also produce new bicarbonate to neutralize acids. Tubular cells contain carbonic anhydrase, that converts CO2 and H2O to HCO3− and H+. Newly formed HCO3− is shunted to peritubular capillaries and H+ is excreted in tubular lumen. Bicarbonate is also produced from glutamine metabolism along with ammonium. Some NH4 diffuses to body fluid and converts to urea in the liver. The rest of the them excreted in urine. The tubules are impermeable to bicarbonate, and it cannot be converted back to CO2 and H2O. So, the blood HCO3 level is increased.
In the apical membrane of the kidney tubules, sodium is reabsorbed in exchange for the hydrogen ion. Salts like sulfates, phosphates, ammonia combines the hydrogen ions and excrete it. The kidneys titrate less than half of the excreted acids and the rest is excreted as ammonium [11]. For every ammonium excreted in urine, one HCO3+− is reabsorbed. HCl and H2SO4 are produced during dietary protein metabolism reacts with NaHSO4, and produce NaCl and Na2SO4. These Na salts are excreted by the kidneys as NH4Cl, and (NH4)2SO4.
The kidneys are largely responsible for K+ excretion and most of it is reabsorbed in the proximal tubule and in the loop of Henly. In acidosis, K+ secretion is decreased and K+ absorption is increased in the collecting duct. In alkalosis, hypokalemia develops from increased K+ secretion and reduced K+ absorption in the collecting duct. H+ and K+ exchange occur in the tubules. Serum potassium level also influences the renal acid-base balance. In hyperkalemia, potassium is available in an increased amount in the filtrate, and hydrogen will be scarce for exchange with HCO3 and there will be an imbalance. In hypokalemia, less potassium will be available for H+ and K+ exchange and hydrogen will be available to exchange with bicarbonate.
Na+, K+ and NH4+ are the principle urinary cations, and the principal urinary anion is chloride. Urinary anion gap helps in estimating renal NH4+ excretion, as NH4+ is the urinary unmeasured ion. Chloride is an important anion in neutralizing positive ions, reabsorbed in the proximal convoluted tubule and secreted in urine by the collecting duct. Secreted H+ is also buffered by urinary buffer HPO4− to H2PO4, and is excreted in urine.
Acidosis results from a reduction in serum bicarbonate and cause secondary reduction of PaCO2 resulting in a low blood pH. It develops from the addition of hydrogen or removal of HCO3 from the body. PaCO2 in blood is 38 ± 2 mm of Hg and HCO3 is 24 ± 2 mmol/L. Metabolic acidosis is characterized by the blood pH <7.38 and bicarbonate <22 mmol/L [12].
Acid and base disorders are: respiratory acidosis and respiratory alkalosis, and metabolic acidosis and metabolic alkalosis [13]. In respiratory acidosis, PaCO2 is increased and it is compensated by renal H+ excretion, HCO3 retention and HCO3 generation. In respiratory alkalosis, decreased PaCO2 is compensated by renal HCO3 excretion. In metabolic acidosis, HCO3 is reduced and it is compensated by hyperventilation and PaCO2 reduction. HCO3 is increased in metabolic alkalosis, and it is compensated by increasing PaCO2 by hypoventilation [14]. Usually, respiratory disorders cause derangements of CO2 level in the blood, and change in HCO3 level is developed from metabolic disturbances.
In the blood, Alkali is present mainly in the form of sodium bicarbonate, and bicarbonate is bound to other bases. Increase in BHCO3 and decrease in H2CO3results in alkalosis, and decrease in BHCO3 and increase in H2CO3 results in acidosis [13]. The body contains many acids. They are hydrochloric acid, carbonic acid, citric acid, lactic acid, phosphoric acid and carboxylic acid. Acute metabolic acidosis is developed by the overproduction of organic acids, like lactic acid and keto acid. Chronic acidosis is caused by bicarbonate wasting and impaired urinary acidification.
Blood cells are more acidic than serum, which influences the distribution of electrolyte and water between them. These transports took place with the oxygenation and reduction of hemoglobin and shift of bases (Na+, K+) due to changes in pH. Under normal environment Na+ and K+ do not diffuse through the cell wall. Shifting of water and electrolyte through membrane results from the change in anion (HCO3− and Cl−) and H+ concentration, and that changes in cell volume. CO2, relative electrolyte concentration and weak acid concentrations are three independent variables that regulate blood pH [15].
The body has different buffer systems to maintain the normal pH of the body. Elkinton Jr. reported that multiple level of buffering linked different series of ionic exchanges which includes hydrogen, sodium, potassium, and other anions. The buffers absorb excess hydrogen and hydroxyl ions. They help in the maintenance of neutrality during redistribution of the hydrogen ion [16].
A buffer system consists of a weak acid with its conjugate base, or a weak base with its conjugate acid. Blood is a strong solution, and it has many important components that maintain the buffer systems. These include hemoglobin, bicarbonate, carbonic acid, plasma proteins, RBCs and plasma phosphate [17]. HCO3/CO2 buffer is the most important buffer system of the body, and plays a major role in regulating pH of the blood. But, the rest of the buffer systems have minimum contribution in pH regulation. In dissolved state, bicarbonate and carbon dioxide ion remains in equilibrium. Bicarbonate reduces strong acid to carbonic acid, whereas carbonic acid neutralizes strong base (Eq. (1)).
When CO2 and water is converted to HCO3 and hydrogen ions, this hydrogen ion is then buffered by hemoglobin [18].
Proteins have a buffering capacity, including hemoglobin. Protein can accept and donate H+, if there is H+ excess or it is reduced. Hemoglobin has a distinct types of buffer action. When blood passes through the capillaries, it loses oxygen and took CO2 to raise the PaCO2 and maintain the pH. Hemoglobin plays an important role in transporting both oxygen and carbon dioxide. In 1914, Douglas, Haldane and Christiansen tried to prove that the hemoglobin binds more CO2 in the reduced form than the oxygenated form [19].
The phosphate buffer system works in the internal environment of all cells. But, in the blood H2PO4− and HPO42− are found in a very low concentration. Sodium dihydrogen phosphate neutralizes strong bases and sodium monohydrogen phosphate neutralizes strong acids. The Phosphate buffer system plays an important role in the kidneys.
Two types of variables, dependent and independent, are important in acid-base balance [20]. Bicarbonate, hydroxyl ion, hydrogen ion or pH, weak acid, anion and carbon trioxide are dependent variables and they are determined by three independent variables pCO2, total weak acid and net strong ion charge [21]. Lungs, kidneys, liver and gut regulated this balance. Traditional bicarbonate/carbon-di-oxide approach, base excess approach and Stewert’s physicochemical methods are widely discussed for measuring the acid base disorders as well as to explore the physiology of body fluid.
HCO3/CO2 buffer system is the basis of this approach. Carbonic acid freely moves in the body fluid and dissociates into bicarbonate automatically when needed. Bicarbonate in the body acts as alkaline reserve. CO2, pH and HCO3 can be calculated by Hasselbalch-Henderson Equation (2) [7, 9].
This equation states that not only HCO3 and CO2, but also their ratio determines the pH. In this equation, PCO2 is the respiratory component and HCO3− is the metabolic component of the acid base imbalance. This buffer system is the largest and independent buffer system of the body and whole body acts as an open system for CO2. In traditional approach balance is determined by the influx and efflux of H+ and HCO3.
Astrup and Siggaard-Anderson introduced base excess approach, which is close to the traditional approach [22, 23]. Base excess can be calculated from bicarbonate concentration and pH of the body [4]. It can estimate the acid base status of non-respiratory origin. If base excess is too high, then it is metabolic alkalosis. If base excess is too low, then it is metabolic acidosis. When a deviation of normal blood pH is corrected by administrating base, then it is called base deficit. Which is a characteristic of metabolic acidosis. Base deficit with increase anion gap suggest the addition of acid in the body fluid. If there is a base deficit with normal anion gap, then there is bicarbonate loss from the body.
Here H+/proton is the preliminary determinant in acid base disturbances, not the CO2 [21]. The dependent variables are H+, OH−, CO32−, HA (weak acid), A−(weak anions), HCO3− and pH. The independent variables are strong ion difference (SID), total non-volatile weak acids (Atot) and PaCO2 [24]. Among them the strong ion difference has maximum effect on the hydrogen ion concentration. With that, acid base disorder can be divided into three categories: 1. respiratory (increase or decrease PaCO2), 2. SID changes (excess or deficit of strong ions or water) and 3. inorganic phosphate or albumin deficit or excess (Atot changes). In Stewart approach, a large number of variables are needed to calculate SID. Sodium, potassium, calcium and magnesium are strong positive ions, and chloride and lactate are the negative ions [25]. Bicarbonate and albumin are the balancing ion in strong ion difference. Strong ion difference (mEq/L) = [strong cations] − [strong anions]. Weak acid dissociates in body fluid (Eq. (3)).
A− Resembles weak anions, that vary with pH. Strong ion difference is filled with this weak A−, and HCO3+−, H+, OH−, CO32− are also present in minute amount, but are less important. There are many unmeasured anions accounts for ion difference. For electrical neutrality, strong ion difference and the total charge of weak ions must be equal [26]. Normal SID is dominated by sodium and chloride. But other negligible, but measurable ions are present there. Here narrowing of SID from an increase in [Na+] has alkalizing effect, whereas an increase in [Cl−] has acidifying effect. From the ionic basis metabolic acid base disturbances are about four major types [25]: (1) The water effect, and it is produced by dilutional effect on SID. Free water intake and intravenous infusion can produce it. (2) The chloride effect is caused by chloride change, and administration of normal saline is the common cause. (3) The protein effect is produced by a change in albumin concentration. (4) There are other factors, and those are influenced by unmeasured anions, that cause a wide anion gap.
In vivo, true ion gap cannot exist. There are many anions and cations in the blood. Blood cations and anions must be equal. Sodium, chloride and bicarbonate have the highest concentrations, and they are calculated for anion gap for their largest variability in different pathologic conditions. Anion gap is the difference between serum sodium ion and bicarbonate plus chloride. There are wide variations in the reported anion gap. Widely accepted anion gap is 8–12 mmol/L [15]. Anion gap is clinically important for assessing acidosis. Normal anion gap (hyperchloremic) acidosis and increased anion gap acidosis [27] are two important types of anion gap acidosis. Common serum cation levels are sodium 138.8 ± 4.56 mmol/L, potassium 4.05 ± 0.21 mmol/L, magnesium 0.98 ± 0.05 mmol/L [ 28] and calcium 2.2–2.7 mmol/L [ 29]. And normal serum anion levels are chloride 97.7 ± 3.42 mmol/L and acetate 0.23 ± 0.04 mmol/L [ 28]. The sum of cations and anions should be equal (Eq. (4)).
There are other ions which are not commonly measured, are unmeasured anions and cations [30]. Under normal conditions, albumin and phosphate accounts for this anion gap. There are many clinical conditions, where urate, lactate, ketone bodies, sulfate, salicylates, penicillin’s, citrate, pyruvate, and acetates are also responsible for increased anion gap [5]. So, anion gap [31] is Eq. (5)
Presence of unmeasured anion in blood is the anion gap and it represents metabolic acidosis [32]. When unmeasured anions like lactate and pyruvate donates proton then that proton is buffered by bicarbonate. And bicarbonate consumption increases the anion gap. The most common causes include lactic acidosis, diabetic ketoacidosis, uremia and acidosis due to drugs and toxins. Methanol, propylene glycol, ethylene glycol, salicylate, and some inborn error of metabolism are other causes of unmeasured anions [33]. Both lactate and β-hydroxybutyrate are increased in both Gram-positive septiceamia [34] and starvation [35]. Krebs cycle intermediate citrate, isocitrate, malate, α-ketogluterate, succinate and D-lactate are increased in different types of acidosis. Intestinal ischemia and short bowel syndrome cause increase in D-lactate [35]. Plasma proteins are mostly anionic comprising 75% of the unmeasured anion [36, 37, 38]. Treatment with Sodium thiosulfate that has no hydrogen can cause severe metabolic acidosis [39].
It usually indicates acidosis. Increase blood lactate, ketoacidosis, uremia (in advanced renal failure), drugs (salicylate and penicillin), ethylene glycol, methanol are contributor of high anion gap acidosis. But the increase anion gap can be due to laboratory error, hyperphosphatemia [30]. Massive rhabdomyelysis, hippurate, oxalate can also cause increased anion gap acidosis [31]. Diabetes, starvation and alcohol are the most common cause of ketoacidosis. In alcoholic ketoacidosis, primary keto acid is β-hydroxybutyrate. It can be missed in conventional assessment of ketonuria. High anion gap and normal lactate level are characteristics of alcoholic acidosis [40]. Starvation alone can cause high anion gap acidosis [41]. In the third trimester of pregnancy, short period of starvation can cause ketogenesis with a very high anion gap acidosis [42]. Septic shock, hypoxemia, hypovolemic shock, cyanide, mesenteric ischemia, CO poisoning, causes hypoxic type of L-lactic acidosis [43]. Non-hypoxic, L-lactic acidosis develops from seizure, thiamine deficiency, metformin, methanol, ethylene glycol, salicylate, propylene glycol, niacin, isoniazide, iron, propofol, toluene, paraldehyde, non-nucleoside reverse transcriptase inhibitor (NNRTI) drugs [12]. Recurrent 5-oxoprolinuria from inborn errors of metabolism is a rare cause if high anion gap metabolic acidosis [44]. Uremia results from not only reduced ammonia secretion but also reduced filtration of sulfate and phosphate anions, and increases the anion gap [45]. Polyclonal gammopathies are also contributor of increased anion gap [46]. Serum albumin is an important contributor to the anion gap and hypoalbuminemia is a common comorbid condition. That is why, albumin correction is crucial for the anion gap calculation [36, 37]. To explore the cause of the metabolic acidosis anion gap must be corrected for albumin as well as lactate [43]. A high anion gap can be masked by a concomitant low anion gap results from hypoalbuminemia.
In anion gap calculation, sodium is the only cation that is measured. But, hypercalcemia, hyperkalemia and hypermagnesemia can produce significant decrements in anion gap. So, clinical correlation and correction of such abnormality is important. Plasma proteins comprise two third of the unmeasured anion, and hypoalbuminemia is a common cause for the low anion gap [31, 36, 37]. The reduced anion gap is usually seen in delusional states, hypernatremia, hypoalbuminemia, hypermagnesemia, hypercalcemia, bromide intoxication, hyperviscosity associated diseases etc. [47]. Sometimes it can be due to laboratory error, paraproteinemia [48, 49], or iodide [30, 50], gastrointestinal bicarbonate loss and diarrhea [31]. It has been reported that Lithium carbonate intoxication can also produce low or absent anion gap [51]. Non-sodium containing paraprotein IgG in multiple myeloma increase the unmeasured cations and reduce the anion gap [48, 52, 53]. Hypercalcemia and hypoalbuminemia in paraproteinemia also contribute to low anion gap [52].
Measuring anion gap is a routine for evaluating acidosis, and normal anion gap is sometimes misleading. As we know, the increase in anion gap is usual in metabolic acidosis. And acidosis is due to acid retention or ingestion. Normal anion gap acidosis is due to loss of HCO3− from the body. Hyperchloremic normal anion gap acidosis is characterized by acidosis with excess chloride ions [54]. Here, the low HCO3 level is a characteristic feature. Reduced negatively charged bicarbonate is compensated by the negatively charged chloride movement into the extracellular space, and normal anion gap is maintained. The causes of gastrointestinal and renal loss of bicarbonate are diarrhea, ureteral diversions, pancreatic and biliary fistulas, toluene ingestion, acetazolamide, ifosfamide, topiramite, tenofovir, renal tubular acidosis. These are the causes of normal anion gap acidosis. Rapid infusion of 0.9% normal saline can also cause hyperchloremic metabolic acidosis [55]. If the blood anion gap is normal, but there is acidosis, then the urinary anion gap Eq. (6) is calculated [12].
The urinary anion gap is negative in diarrhea, sodium infusion and proximal renal tubular acidosis. Whereas, positive urinary anion gap is found in both type 1 and type 4 renal tubular acidosis. Renal tubular acidosis is sometimes the only presenting feature of many chronic diseases and conditions associated with polyclonal gummopathies.
Metabolic acidosis results from gain of anions and loss of cations. Potassium chloride, hydrogen chloride, sodium chloride, arginine hydrochloride, calcium chloride, ammonium chloride, lysine hydrochloride can cause hyperchloremia and increase anion gap. Hyperphosphatemia increases the anion gap. But renal tubular acidosis [33], amiloride and triamterene cause a non anion gap hyperchloraemic acidosis and hyperkalemia due to impaired bicarbonate production.
Anion gap should be measured for all types of metabolic acidosis. High anion gap metabolic acidosis is a subtype of non-respiratory acidosis. Mnemonics were used for remembering the causes of high gap metabolic acidosis such as KUSMALE (Ketoacidosis, Uraemia, Salicylate poisoning, Methanol, ParAldehyde, Lactate, Ethylene glycol) and MUD PILES (Methanol, Metformin uremia, Diabetic ketoacidosis, Paraldehydes, iron, isoniazid, Lactate, ethylene glycol, Salicylates and starvation). As paraldehyde induced acidosis is extremely rare and recently three anion gap generating organic acid has been recognized. They are Short bowel syndrome producing D-lactic acid, chronic paracetamol use induced 5-oxoproline (or pyroglutamic acid) especially in malnourished woman and high dose propylene glycol (used in lorazepum, phenobarbital) infusions generate acidosis. Also, Iron and Isoniazid can cause lactic acidosis. So, GOLD MARK is a new acronym for metabolic acidosis [Glycols (ethylene and propylene), Oxyproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, Ketoacidosis] [56]. Metabolic acidosis also caused by renal bicarbonate loss in type 2 renal tubular acidosis, renal dysfunction in type 4 renal tubular acidosis, type 1 renal tubular acidosis and ingestion of ammonium chloride [31]. Acute rheumatism causes lactate induced acidosis also [57]. Symptomatic correction of acidosis will not eliminate the problem. If the clinical features suggest acidosis, then it should be assessed for anion gap as well. Following anion gap measurement accordingly history of drug, toxins and diseases need to be evaluated for managing the exact pathology thus acidosis will be properly treated.
At normal blood pH 7.4 plasma proteins are mostly anionic. It has been estimated that anion gap decreases by 2.5 mEq/L for every 10 gm/L drop of serum albumin [36, 37]. Several studies had observed that 2–2.5 times changes in albumin influences in anion gap changes [58]. Albumin contributes a greater part of the normal anion gap [46]. Phosphate and lactate contribute some anion gap as well [59]. Consideration of all of these contributors are important in explaining changes in anion gap. Calculation of anion gap is crucial in critically ill patients. Anion gap should be adjusted for Eq. (7) albumin, phosphate and lactate with the following equation [59].
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