In this study, 0.051% of patients developed AKI following TJA, and the rate remained unchanged from 2011 to 2018. Diabetes, bilateral procedure, BMI, higher preoperative BUN levels, and lower preoperative hematocrit were significant risk factors. AKI was associated with prolonged hospitalization, non-home discharge, readmission, and higher mortality.
The overall incidence of AKI in this study was much lower (0.051%) than reported in previous studies (0.3 –16.2%) [7, 10, 12, 21, 22]. In a retrospective review of 8,127,282 TKA patients using Nationwide Inpatient Sample, Singh et al. [11] found the incidence of AKI was 1.3%. However, that study was based on a more dated sample (1998–2014) and relied on ICD-9 codes for diagnoses without clearly distinguishing if AKI was present at the time of surgery. In contrast, the key advantage of the ACS-NSQIP database is that it is based on manual chart abstraction, which is less prone to errors due to billing codes. Another possible explanation for the discrepancy in the rates of AKIs is that different measures were used, such as risk, injury, failure, loss of kidney function, and end-stage kidney disease (RIFLE) and acute kidney injury network (AKIN) classifications [6].
The risk factors for AKI based on the multivariate analyses were higher BMI, diabetes, bilateral procedure, higher preoperative BUN and lower preoperative hematocrit. Multiple studies have shown that increased BMI was an independent risk factor for AKI as well as other complications [23, 24]. In an analysis of 22,808 patients from the Veteran Affairs Surgical Quality Improvement Program database, Ward et al. [25] showed, via multivariable regression, that BMI > 40 was an independent risk factor for AKI following THA, with OR = 1.79. Similarly, other studies have shown that diabetes and elevated creatinine were also risk factors for the development of AKI [23, 26]. Creatinine level is often used as screening marker for glomerular filtration rate and, therefore, kidney function. In this study, we found that in addition to creatinine, AKI was correlated with higher BUN and lower hematocrit respectively. Lower preoperative hematocrit has been shown to be a risk factor for the postoperative development of AKI in the revision arthroplasty setting [27]. Simultaneous TKA has also been shown previously to pose higher risk for the development of AKI. In a single center retrospective review, Koh et al. compared the risk of AKI for those undergoing staggered (< 7 days between procedures), staged (8 days-1 year between procedures), and simultaneous TKA [28]. The simultaneous TKA group had the highest risk of AKI (OR 7.7, P < 0.001).
Few studies have examined the change in the incidence of AKI following TJA. One of the cornerstones of multimodal analgesia is the use of NSAIDs [13]. The main drawback of NSAIDs is their potential adverse event profile on the cardiovascular, gastrointestinal, and renal systems [14]. The renal toxicity of NSAIDs is attributed to the inhibition of cyclooxygenase (COX) 1 and 2, which are responsible for the production of prostaglandins that mediate the vasodilation of the renal tubules [15]. NSAIDs have been found to be associated with AKI [15]. However, few studies examined the association of perioperative use of NSAIDs with AKI following TJA. Gharaibeh et al. [21] failed to find an association between perioperative NSAIDs use and postoperative AKI, but they noted that this failure might be attributed to confounders, as those with significant comorbidities, such as CKD and heart failure, had significantly less exposure to NSAIDs.
To our knowledge, only two studies examined the change in AKI rates over time following TJA. In a meta-analysis of THA studies reporting incidence of perioperative AKI, Thongprayoon et al. [6] found that between 2012 and 2018, there was a trend of decreasing AKI incidence after THA. In a single institution review, Yayac et al. showed fairly constant rates of AKI between 2005 and 2017, ranging from 2.1–5.5 %[12] although no statistical analysis was performed. The current study found that AKI rates varied between 0.04% and 0.1% from 2011 to 2018, but there were no statistically significant differences overall. This suggests that AKI incidence has been fairly stable even with the increasing use of recent perioperative advancements such as hypotensive anesthesia and multimodal analgesia.
“Bundle-busters” are drawing scrutiny as the medical system shift towards value-based care since they can make a TJA episode of care financially non-viable. This study showed that the development of AKI within 30 preoperative days is significantly associated with increased LOS, non-home discharge, readmission, and mortality, which all have serious health as well as financial implications. In a single center retrospective case-controlled review of 1719 primary TJA, Abar et al. [21] found that AKI was associated with increased LOS and a mean cost differential of $81,781 in total hospital charges. Similarly, in an analysis of the NIS database of patients undergoing TKA, Singh and Cleveland [11] demonstrated that increased risk of complications was associated with AKI, including implant infection, transfusion, revision surgery, death, and longer LOS which translated to higher mean hospital charges, $71,385 vs. US$42,067. Risk-adjustment of bundles have previously been advocated for non-modifiable factors such as those undergoing TJA due to oncologic reasons or conversions as well as other socioeconomic factors [29,30,31]. Therefore, risk adjustment for factors leading to AKI should be given serious consideration in future bundle payment models.
This study is significant because it lends further credence to the notion that AKI is a potential bundle buster complication. TJA, by virtue of being elective procedures, allows orthopedic surgeons to optimize the medical status of patients preoperatively. Surgeons should be aware of the modifiable risk factors that can help avoid postoperative AKI. In a prospective study, Lands et al. [32] achieved a significant reduction in AKI rates, after the implementation of a targeted protocol, from 6.3 to 1.2%. Some of the risk factors found in the current study to be associated with the development of AKI can be carefully optimized prior to surgery, namely, avoidance of bilateral procedures and optimization of hematocrit levels especially in patients with diabetes, obesity or lower kidney function. Furthermore, given that diabetes and CKD are non-modifiable risk factors, this highlights the need for risk-adjusted bundle payment programs.
Despite the strengths of this study, including the use of a large validated national sample of patients undergoing TJA, there were several limitations. AKI was identified based on chart review at each individual site. However, there are many different criteria for defining AKI, so using a single one may underestimate its incidence, and the NSQIP database does not provide a clear definition of AKI [6]. Second, although CKD was determined based on preoperative creatinine data, additional qualifiers on severity of CKD was not assessed since the GFR was not available. Furthermore, the adverse events were only collected for up to 30 days postoperatively, so this might underestimate the true rates as well as additional adverse outcomes associated with AKI.
