Pain Management

develop a multimodal protocol

Neurogenic and inflammatory signaling are the transmission pathways of surgical pain.  Implementing multimodal pain management techniques to target both pathways is one of the biggest advances in arthroplasty surgery over the past decade.  

There are significant side effects associated with over-reliance on narcotics for pain control including ileus, nausea, confusion, and lethargy, which can all contribute to a prolonged hospitalization and increase hospital re-admission,  discharge to nursing facilities, and decrease patient satisfaction. 

Pain management protocols are implemented the morning of surgery, during the surgery itself, and after surgery.  They have been shown to shorten hospital stay, improve pain control and decrease opioid use while allowing successful recovery. 


Peripheral signaling pathways (neurogenic and inflammatory) are triggered at the time of surgery and increase CNS sensitivity to pain stimuli. Preemptive analgesia can dampen the initial peripheral pain signal and prevent central hypersensitivity [1].  Regional anesthesia (ie peripheral nerve blocks), local anesthesia (ie bupivicane infiltration around the surgical site), and systemic anesthesia (ie opioids) offer a robust approach to pain control in TJA. We will look at all of these pathways.

The multimodal regimen often begins in Preop Holding [2] where patients may receive a benzodiazepine, NSAID, and/or gabapentanoid.  Patients are given regional anesthesia. 

In THA either a spinal or epidural is utilized, while peripheral nerve blocks are reserved for TKA.

Regional Anesthesia.  There is a trend to steer away from general anesthesia. Most arthroplasty procedures are performed with neuraxial (ie spinal and epidural) or regional (peripheral nerve blocks) anesthesia.  The THA procedures benefit from spinal anesthesia or a lumbar epidural catheter in conjunction with propofol sedation.  Avoiding general anesthesia has been shown to decrease post-op confusion, nausea and lethargy as compared to general anesthesia. 

Peripheral Nerve Blocks are more relevant to the TKA and UKA procedures.  A single dose femoral nerve block (addresses sensation to the anterior knee), and a single dose tibial nerve block (addresses sensation to posterior knee), and an adductor canal catheter block (provides anterior knee analgesia without impairing quad muscle strength, which is seen with femoral nerve catheters, which can slow physical therapy and risk patient falls). Adductor block seems to provide pain relief without significantly affecting function. Similarly, patients previously received single dose sciatic blocks, however, due to reports of postoperative falls, the tibial block reduces the side effect of muscle weakness. [3] [4] [5] [6] [7]


Patients receive a peri-articular injection (also known as local infiltration analgesia). 

Peri-articular injections (PAI).  There are a number of cocktails that surgeons have developed.  Many include morphine, epinephrine (to increase longevity), ketorolac, depomedrol, bupivacaine, lidocaine, etc.  Other surgeons use the slow-release bupivacaine (liposomal bupivacaine suspension called Exparel®, Pacira).  Multiple studies have failed shown significant benefit of liposomal bupivacaine over the “homemade” cocktails combining bupivacaine, epinephrine and other medications. Nonetheless, all of the periarticular injections have demonstrated significantly positive effect on patient outcomes. 

One RCT blinded patients to PCA (epidural) vs. PAI and showed higher oral opioid use and pain scores in the PAI group, although PCA group had higher opioid related adverse events like nausea/vomiting.  Study suggests PAI has limitations. [8]

Results from RCT suggest patients with periarticular injections report better pain control, decreased opioid use, improved physical therapy and lower complications from opioids such as nausea and vomiting. Its unclear whether injections shorten hospital stay, but clearly otherwise show significant benefits.


Multimodal regimens have been shown it reduce pain scores (VAS) and opioid use, although there does not appear to be a significant effect on early function.  These regimens typically include a combination of the following: NSAIDs, short- and long-acting narcotics (i.e. oxycodone and oxycontin), IV acetaminophen, and IV dexamethasone, and pregabalin postoperatively. [15] [16] [17] [18] [19] [20]


This broad class of drugs include short-acting oral medications (Percocet, Vicodin, Oxycodone, MsContin®, Dilaudid) and long-acting oral medications (OxyContin®, MsContin®), and IV medications (Dilaudid, Morphine, Fentanyl). 

Mechanism:  Opioids block the hand-off of "pain information" from the peripheral nerves to the spinal nerves at the dorsal horn of the spinal cord. The spinal nerves, brain stem, thalamus, and cerebral cortex comprise the ascending pain transmission system.  The opioid receptors are found at the descending inhibitory system that affects spinal transmission of pain both at the pre and post-synaptic sites. There are at least 3 opioid receptors: Mu, Kappa, Delta. 

PCA: Patient-Controlled Analgesia has been a popular form of pain control for many decades.  It has been widely published in the literature as having favorable patient satisfaction and pain control[28]. However, the use of PCA has been more recently associated with higher rates of opioid related adverse events such as nausea and vomiting, constipation.  Further, the dosages given are short acting IV medication, and patients hit the button when they are already in pain.  The goal of modern pain management is to prevent patients from repeating feeling pain stimuli and to provide long-term baseline coverage 

historical note: There are news articles every month discussing the growing opioid epidemic in the United States.  Here is a brief historical perspective. The price of prescription painkillers became inexpensive in the 1990s and rates of drug overdose have increased > 400% (1999 to 2011).  Purdue Pharma introduced OxyContin® in 1996 and aggressively marketed the medication (at that time an unprecedented marketing strategy for a Schedule II opioid). In just 5 years, prescriptions increased 10-fold and drug sales were almost 90% of the company’s revenue.  The company argued that its time-release formula was less addictive than Percocet or Vicodin, despite later findings to the contrary. In 2007 the US Dept of Justice fined the company $634.5 million for misleading the public about risks of OxyContin® addiction.   The lasting result of this marketing campaign was the shift in how pain was understood by the American public.  Pain was once something that was endured.  Now its believed to be something that can be completely eliminated with a pill.  Pain became unacceptable.  In 2015, there were over 250,000,000 opioid pills prescribed, there were >30,000 overdoses, and an estimated 2.6 million people addicted to prescription pain killers.  Over 75% of heroin users started with prescription opioids.


-celecoxib: Commonly started preop and continued postop.  May be administered as 400 mg preop, then 200 mg BID 5 days post-op.  The use of celecoxib has demonstrated improved pain scores for 72 hours, decreased morphine use 24 hours, no difference in functional outcomes. [21] A similar study looking at 81 TKA, 60 THA also found decreased opioid consumption and improved pain scores during hospitalization in the celecoxib group [22] The dose of celecoxib should be reduced in half with borderline renal failure and those older than 70 years old.

Mechanism: Prostaglandins (PGE1, 2) are not mediators of pain transmission but rather contribute to pain by sensitizing nociceptive nerve endings to stimuli (histamine, bradykinin).  NSAIDS block COX enzymes, reduce prostaglandin production (either reversibly or irreversibly), and prevent nerve sensitization.  Selective COX-2 inhibitors don’t interfere with hemostasis and therefore patients can continue to take medications until the day of surgery (COX-1 continues to produce prostacyclin allowing gastric mucosa protection and allowing platelet aggregation). 

-ketorolac: Typical dosing is 30 mg IV every 6 hours.  Onset is about 10 minutes, peak effect at 2 to 3 hours, and lasts about 6 to 8 hours. Caution in patients with renal insufficiency, and elderly patients with impaired creatinine clearance.

Mechanism: The only IV NSAID.  Analgesic strength has been compared with opioids and 30 mg of ketorolacis equivalent to 12 mg of morphine [23].

IV Acetaminophen. The tradename is Ofirmev® (Mallinckrodt) is given 1000 mg IV Q8H often dosed 1-3 times on postop day #0. Should be held in patients with liver disorders.  Many hospitals are limiting its use due to increased costs (a medication owned by a Private Equity group that increased the cost overnight from under $20 to over $40).  [26]

Mechanism: Inhibits central prostaglandin synthesis without inhibiting peripheral prostaglandin synthesis (weak anti-inflammatory effect, doesn’t inhibit COX).  It has no effect on platelet function or gastric mucosa. 

Gabapentinoids (Gabapentin – Neurontin; Pregabalin – Lyrica).   

Administered 150 mg preop, then 75 mg BID for 1 week post-op in conjunction with 200 mg Celebrex PO BID for 3 days. 

In RCT, shown to decrease PCA morphine use 24 hours after surgery and decrease Percocet use 1 week after surgery with improved pain scores 1 week after surgery (no effect on pain or function at 6 weeks or 3 months) [24]However, a recent meta-analysis looking at 12 RCT comparing gabapentinoids vs. placebo for postoperative pain control found no clinically significant differences in pain at 24, 48, 72 hours. This study recognized a difference in pain scores, however this difference was not clinically significant, and furthermore there was no impact on knee range of motion, and furthermore it was associated with a significant increased risk of sedation. [25]

IV Dexamethasone: This is given as 1 or 2 doses on postop day# 0. Should be held in diabetics. [25] [26] [27]

Blood Management

its all about the txa

Similar to advances in pain management, the perioperative blood loss management has improved dramatically over the past decade. [29] [30] [31]

Tranexamic Acid (TXA) is credited for a large part in decreasing postoperative transfusions after TJA. 

The coagulation cascade is a dynamic balance of continuous formation and degradation of clots, whereby signals from our body tips the scale in favor of one or the other (this is a gross simplification of the process).  The medication is administered just prior to incision and often again during surgery and it minimizes bleeding by preventing degradation of fibrin clots.  Importantly this medication is not associated with increased risk for thrombotic events such as strokes, MI, PE, or DVT.  The medication is shown to decrease transfusions after THA [32]and for TKA [33] [34].

Hemodilution. Another popular technique to minimize blood loss.  By giving a lot of IV fluids during surgery, the hemoglobin becomes diluted within the blood, and therefore less is lost per volume of blood loss. 

Transfusion thresholds.  The dependence on hemoglobin values is decreasing with the greater recognition that everyone is different and that vital signs in conjunction with hemoglobin trends are likely the best guide to transfusion.  Transfusing for hgb >9 g/dL has no effect on risk for complications even if people have a history of cardiac disease, and below 8, patients with cardiac disease or other medical conditions may benefit from transfusion, while younger, healthier patients may do well even if their hemoglobin drops below 7 g/dl.  Generally, all people should be transfused if hemoglobin dips below 6.  Why should we care about transfusions anyway?  There are risks such as allergic reaction, and a low but real risk of viral disease transmission.  Furthermore, studies have suggested that blood transfusion increases the risk for prosthetic joint infection [35].

Antibiotic Prophylaxis

Our skin flora is polymicrobial, with staphylococcus, streptococcus, and p.acnes (all gram-positive bacteria) being the most common and also most commonly associated with SSI and PJI [1] [2].  Polymicrobial and gram-negative infections account for 20-30% of PJI.

Selection of perioperative antibiotics reduces the risk of surgical site infection (SSI) caused by direct inoculation of skin flora during the index procedure.  AAOS recommends 1st and 2nd generation cephalosporins as first line antibiotic prophylaxis to target gram-positive bacteria and about 40% of gram-negative bacteria. [3] Perioperative antibiotics reduce SSI from about 10% to 1%, studied back in the 1950s [4-6].

Cefazolin (ancef) and cefuroxime (ceftin) are the most common prophylactic antibiotics. Cefazolin is given at 1 g for patients < 170 lbs and 2 g for those < 260 lbs (3 g can be considered for those higher).  Ceftin is given as 1.5 g for all patients.  Optimal timing of administration is within 1 hour of incision per AAOS guidelines, although within 30 minutes gives highest concentration as cefazolin has rapid tissue penetration[7, 8].  Antibiotics should be re-dosed intraoperatively in cases >4 hours as tissue concentrations should remain above the MIC thru the critical parts of the procedure to avoid higher infection rates [9].

It is ok to give 2nd generation cephalosporins in patients with a penicillin (PCN) allergy because the cross-reactivity is < 1% in patients with self-reported allergy, and <2.5% in patients with confirmed PCN allergy [10] [11].  The misconception that cross-reactivity is 10% originates in studies in the 1960s where there was PCN contamination of other antibiotics due to processing in the same manufacturing plant and because 1st generation cephalosporins were examined, which do have a higher cross-reactivity as compared to 2nd generation [12].

Patients with anaphylactic PCN allergy should receive alterative antibiotic because the complication is too significant.

24 hours postoperative dosing is recommended (studies show no benefit to 3 or 7 days antibiotics for clean, primary TJA). [13-15] [16]

Clindamycin and Vancomycin are alternatives antibiotics.

They can be given to patients with a beta-lactam allergy or to high-risk patients (MRSA history, institutionalized patients, and healthcare workers).  While both offer MRSA coverage, Vancomycin covers a higher percentage of MRSA species, furthermore, Clindamycin is only bacteriostatic, and most surgeons prefer bacteriocidal antibiotics. Clindamycin is recommended at 900 mg dose. 

Vancomycin is recommended at a weight-based dose (15 mg/kg) not a default 1 g to all comers.  Studies suggest that patients given a default 1 g are under dosed in 70% of cases as 1 g only covers people weighing up to ~150 lbs [17].  Vancomycin has slower tissue penetration, and rapid infusion risks histamine release causing hypotension and a skin reaction, and thus should be given 1 hr before incision.  Therefore recommendations are for infusion within 2 hours of incision, and infusion must be completed before use of a tourniquet. Routine use of Vancomycin for primary TJA is controversial.  While some studies have shown lower SII (1.0% vs. 0.5%) and better eradication of infections with I&D alone for those that do occur (22% vs 77%), others have found no significant difference in SSI [18, 19].  Due to conflicting data, AAOS recommends consideration for routine use of vancomycin only if hospitals report a high rate of MRSA prevalence (although there is no definition of a high rate). Patients with prior history of MRSA, but screened negative for MRSA, should be given routine antibiotics. Active MRSA carriers should receive Vancomycin.

Teicoplanin is a glycopeptide antibiotic similar to vanomycin that is commonly used for TJA prophylaxis in Europe[20], yet it is not currently available in North America.  This medication has a long half-life (32-176 hours), low toxicity and excellent tissue penetration.

Routine use of dual antibiotics is not recommended[21].

Other dosing considerations [22].

- Primary and Revision TJA (include megaprosthesis) get the same perioperative antibiotics, although patients being revised at second-stage TJA for infection should received antibiotics to cover cultured organism.

- Patients with poor immune function, either poorly controlled diabetes, on immunosuppressive medication, or autoimmune disease, do not require different antibiotics.

- Patients with asymptomatic bacteriuria can be treated with routine antibiotic prophylaxis.  Patients with acute UTI require treatment prior to TJA[23].  Three studies comparing preoperative bacteriuria with risk for PJI found no correlation[24].   Incidence of bacteriuira increases from 0.5% to 1.0% with a single catheterization, and increases to 10-30% for catheters left for 4 days, and 95% in catheters left for 30 days[25]


1. Pandey R, Berendt AR, Athanasou NA. Histological and microbiological findings in non-infected and infected revision arthroplasty tissues. The OSIRIS Collaborative Study Group. Oxford Skeletal Infection Research and Intervention Service. Arch Orthop Trauma Surg. 2000;120(10):570
2. Lamagni T. Epidemiology and burden of prosthetic joint infections. J Antimicrob Chemother. 2014;69 Suppl 1:i5-10.
3. Bratzler DW, Dellinger EP, Olsen KM, Perl TM, Auwaerter PG, Bolon MK, et al. Clinical practice guidelines for antimicrobial prophylaxis in surgery. Surg Infect (Larchmt). 2013;14(1):73-156.
4. Burke JF. The effective period of preventive antibiotic action in experimental incisions and dermal lesions. Surgery. 1961;50:161-8.
5. Tachdjian MO, Compere EL. Postoperative wound infections in orthopedic surgery; evaluation of prophylactic antibiotics. J Int Coll Surg. 1957;28(6 Pt 1):797-805.
6.  Fogelberg EV, Zitzmann EK, Stinchfield FE. Prophylactic penicillin in orthopaedic surgery. J Bone Joint Surg Am. 1970;52(1):95-8.
7.  Williams DN, Gustilo RB. The use of preventive antibiotics in orthopaedic surgery. Clin Orthop Relat Res. 1984(190):83-8.
8.  Steinberg JP, Braun BI, Hellinger WC, Kusek L, Bozikis MR, Bush AJ, et al. Timing of antimicrobial prophylaxis and the risk of surgical site infections: results from the Trial to Reduce Antimicrobial Prophylaxis Errors. Ann Surg. 2009;250(1):10-6.
9. Wymenga AB, Hekster YA, Theeuwes A, Muytjens HL, van Horn JR, Slooff TJ. Antibiotic use after cefuroxime prophylaxis in hip and knee joint replacement. Clin Pharmacol Ther. 1991;50(2):215-20.
10. Catanzano A, Phillips M, Dubrovskaya Y, Hutzler L, Bosco J, 3rd. The standard one gram dose of vancomycin is not adequate prophylaxis for MRSA. Iowa Orthop J. 2014;34:111-7.
11. Sewick A, Makani A, Wu C, O'Donnell J, Baldwin KD, Lee GC. Does dual antibiotic prophylaxis better prevent surgical site infections in total joint arthroplasty? Clin Orthop Relat Res. 2012;470(10):2702-7.
12. Smith EB, Wynne R, Joshi A, Liu H, Good RP. Is it time to include vancomycin for routine perioperative antibiotic prophylaxis in total joint arthroplasty patients? J Arthroplasty. 2012;27(8 Suppl):55-60.
13. Cranny G, Elliott R, Weatherly H, Chambers D, Hawkins N, Myers L, et al. A systematic review and economic model of switching from non-glycopeptide to glycopeptide antibiotic prophylaxis for surgery. Health Technol Assess. 2008;12(1):iii-iv, xi-xii, 1-147.

DVT Prophylaxis

coag 1.0.jpg

Venous thromboembolism (VTE) refers to abnormal coagulation that develops into deep venous thrombosis (DVT) and/or pulmonary embolism (PE).  

Normal hemostasis is maintained as a balance between Coagulation (clot formation) and Fibrinolysis (clot breakdown) pathways.  Coagulation is driven by the Intrinsic Pathway ("contact activation" when damaged to blood vessels expose sub-endothelium to Factor 7) and the Extrinsic Pathway (activated when damaged cells release a burst of Tissue Factor).  Coagulation Cascade converges on Fibrin. Fibrin forms a sticky mesh (think spiders web) to trap the circulating platelets and form a clot.  The Fibrinolytic system promotes blood flow by activating Plasmin.  The competing activity of Fibrin and Plasmin is balanced unless the  Coagulation Cascade is promoted via Virchow Triad (stasis, endothelial damage, up-regulation tissue factors).  

Arthroplasty procedures upset normal hemostasis, and therefore, VTE prophylaxis is recommended by AAOS [140] and ACCP (American College of Chest Physicians)[141]THA patients are at higher risk for symptomatic PE compared to TKA, but lower risk for overall DVT.

A multimodal approach using both pharmacotherapy and mechanical prevention is recommended[142].  Overall these recommendations are broad, with many medications available and a wide variety of protocols [143].   The dictum that you see a lot of treatment options when there is no good treatment option appears to be part of the story with DVT prevention.  The rate of DVT decreases significantly with prophylaxis, yet the rate of overall DVT remains surprisingly high (20 -40%) when all patients are routinely scanned.  The rate of symptomatic DVT is considerably lower (~5%) and the rate of symptomatic PE is still lower (~1%).  The wide variation in these numbers underscores the challenge in distinguishing which are significant.   The uncertainty about what to do with this information is why routine screening is broadly discouraged.  At this time its believed that asymptomatic DVTs should be ignored, while symptoms associated with DVT should prompt a doppler ultrasound, and positive findings should be treated as a symptomatic DVT (see complications section).   Symptomatic DVTs pose their own complications (postthrombotic syndrome), and there is a correlation between proximal DVTs and increased risk of propagation.  

Further complicating the matter, one study examined the literature for efficacy of pharmacologic agents in DVT prophylaxis and found 73% were industry sponsored with 96% reporting favorable outcomes, while the few studies that were not funded showed significantly less impressive outcomes, with 20% showing the studied medication was either not effective or not safe [144].  

VTE prophylaxis recommendations by AAOS:  

Current recommendations suggest pharmacologic anticoagulation for 14 days in low risk patients following TJA, and up to 35 days in higher risk patients, in combination with mechanical compression. 

VTE prophylaxis recommendations by CHEST:

2.1.1 In patients undergoing THA or TKA we recommend use of one of the following for a minimum of 10 to 14 days rather than no antithrombotic prophylaxis: LMWH, fondaparinux, apixaban, dabigatran, rivaroxaban, unfractionated heparin, warfarin, aspirin (all grade 1B), or an intermittent pneumatic compression device (grade 1c).

Mechanical Compression.

Sequential compression devices for calf or foot increase peak venous flow to reduce stasis and up-regulate the fibrinolytic pathway.  Independently reduce risk of VTE [145] [146]. [147]. Japanese study examined over 2,000 TJA patients and 45% received only mechanical prophylaxis. These patients had the same VTE rate by Doppler as lovenox or heparin groups (roughly 26%) [124]. Another Asian study similarly looked at mechanical compression alone.  [148], [149]


Irreversible direct inhibitor of COX pathway in platelets, preventing Thromboxane A2 release (required to make platelets aggregate).  

dosing: 325 mg tab BID (vs. 81 mg tab daily) starting 12-24 hrs postop

Aspirin has grown in popularity: 1) due to efficacy of dvt prophylaxis for primary TJA [123, 150, 151], and revision cases[152].; 2) reduced risk of bleeding complications [123]; 3) low cost [153]. It is independently associated with shorter length of stay, leading to decreased costs (if you control for length of stay, aspirin no longer leads to cheaper medical care suggesting the INR monitoring is not a significant expense) [154]. It is recognized by ACCP and AAOS as acceptable agent for DVT prophylaxis.

LMWH (low molecular weight heparin) "enoxaparin/lovenox"

Indirect Factor Xa inhibitor.  Other Indirect factor Xa inhibitor include Unfractionated Heparin, and Fondaparinux (synthetic form). Binds Antithrombin III and Thrombin (Factor IIa)

dosing: 30 mg BID starting 12-24 hrs postop.  In Europe the dosing is 40 mg daily (starting the night before surgery)

Advantages: no monitoring, appears more effective in preventing overall number of DVT, although no difference in preventing symptomatic DVT as compared to warfarin. Risk of bleeding events are similar to warfarin. Superior to Unfractionated Heparin because higher bioavailability (90% vs. 30%), longer half life, lower risk of bleeding.

Renal metabolism. Not recommended with renal insufficiency, not recommended in combination with epidural catheters.

Fondaparinux "arixtra" 

Synthetic Indirect Factor Xa inhibitor

dosing: 2.5 mg/day starting 6-12 hrs postop.

Meta-analysis of 4x randomized clinical trials comparing with lovenox indicated it was superior in preventing DVT [161].  Overall there was no difference in bleeding risk, although 1 of 4 trials found worse bleeding in fondaparinux and its use in North America is limited due to that concern[162].

Rivaroxaban "xarelto"

Direct Factor Xa inhibitor. Other direct factor Xa inhibitors include eliquis (apixaban).

dosing: 10 mg daily starting 12-24 hrs postop. Recommended 12 days TKA, 35 days THA.

Advantages: oral medication, no monitoring required. More effective at preventing total VTE, but equal at preventing symptomatic VTE compared with enoxaparin [155].  One study found prolonged dosing (35 days) was significantly more effective at preventing symptomatic VTE as compared to 10-14 days of enoxaparin [156]There is concern about higher bleeding rates leading to more reoperation[157], and there isnt a good reversal agent.  

Warfarin (coumadin) 

dosing: variable based on INR target starting night of surgery.

A historical standard anticoagulant for DVT prophylaxis due to proven benefit in VTE prevention and reversibility if hemorrhagic complications occur.  Recently fallen out of favor due to the wide variation in metabolism among patients, which leads to high variation in INR values.  Too often patients are overtreated (INR > 3) or undertreated (INR < 1.5) while the target INR (2.0, not 2.0 – 3.0 which risks bleeding) appears slow to achieve (often 3 days postop) and difficult to maintain for 2 weeks (the challenge of obtaining serial INR adds to patient frustration).  Avoid in conjunction with NSAIDS.

Multiple randomized trials have compared warfarin to LMWH and found no difference in preventing symptomatic DVT, although all studies suggest that LMWH is more effective in preventing asymptomatic clots [158-160].

knee coag.jpg

Other variables

Spinal anesthesia appears to reduce the risk of VTE in the TKA patients. It remains debatable whether patients comply fully with the recommendations. Friedman et al. reported in the GLORY study that only 62% THA and 69% TKA patients complied with medications [163]

4. Length of Hospital Stay

when to discharge a patient 

The first THA procedures kept patients hospitalized for over 3 months.  The average hospital stay after THA has been getting shorter over the past few decades.  Medicare currently recognizes 3 day inpatient stay as the standard of care.  Yet this number is not set in stone, and patient stay continues to shorten as postoperative management continues to improve.

When deciding how long a patient must be hospitalized, we must first ask what is the integral function of the hospital.  Historically hospitalization was required to monitor blood loss, control pain, facilitate ambulation, and monitor for medical complications.  As described above, the significant advances in minimally invasive surgical technique, blood loss management, and patient optimization have reduced the need for blood transfusion.  Furthermore, use of short-acting anesthetics and long-acting local anesthetics have reduced the opioid requirements and the opioid related adverse events.  The combination of these protocols have improved early ambulation for patients. 

Therefore, compared to historical standards, blood loss, pain control, and ambulation are becoming less and less a reason for patients to require hospitalization. 

As a result the average length of stay has continued to decline.  A nationwide study from Denmark showed a 6 day drop in average length of stay after implementing protocols to address pain control and early mobilization [36].  Similar rapid recovery protocols implemented in the United States have effectively shortened hospital stay without increasing complications or emergency room readmissions[37].  Other studies have identified non-medical risk factors for prolonged hospitalization, further highlighting the notion that length of stay is rarely dictated by medical needs and more often due to culture[38].

The question then becomes whether all patients need to be hospitalized for monitoring of medical complications.  One study examined 1,012 patients undergoing primary THA or TKA and found that 84% complications occurred within 24 hours postop and 90% occurring within 4 days.  These patients had higher incidence of major comorbidities such as CHF, CAD, COPD, and liver failure. Older age was an additional risk factor [39].  In contrast however, a similar study that examined the timing of major postoperative complications found that over 90% occurred within the first 4 days of surgery yet almost 60% of cases occurred in patients without significant comorbidities [40].  

Large national databases have been used recently to further identify risk factors for medical complications.

Age (>80), diabetes, BMI > 40, and ASA class (>3, indicator of comorbidities) were all associated with increased risk of 30 day morbidity and mortality after TKA [41].  Age and cardiac disease were associated with 30 day risk in THA [42].  Looking specifically at cardiac complications, hypertension and coronary artery disease comorbities as well as age > 80 were risk factors.[43]. 

These studies highlight the importance of preoperative screening to identify the risk factors that place a patient at risk for medical complications in the acute postoperative period and require hospital monitoring. However, it is apparent that serious medical complications can occur in any patient regardless of overall health. 

Does length of hospital stay affect the risk of complications? One study found no difference in complications in patients that were “short stay” (<3 days) vs. standard (3-4 days).  This study did however find a higher hospital readmission rate in older patients and those with more comorbidities (particular heart failure).  This suggests that patient factors, not length of hospital stay influenced the risk of a protracted recovery [44].  A similar study looked at early discharges and found no increased risk for readmission[45].

If the vast majority of medical complications are seen in patients with preoperative medical comorbidities, it is evident that these high-risk patients require hospitalization during the window associated with a higher incidence of acute complication.  Yet there is a growing cohort of younger patients without comorbidities that are seeking joint replacement for debilitating arthritis.  Since these patients are at low risk for perioperative complications, there has been a shift towards performing total joint arthroplasty in an outpatient or same-day discharge setting.  

The efficacy of protocols to control postop blood loss, pain, and promote early mobilization have diminished the role of the hospital in postop care.

The historic dogma that all TJA patients require postoperative hospitalization has become questioned in the past decade. Even though the number of patients with comorbidities is increasing, the number of complications following TKA and THA is decreasing [46] [47].  Furthermore, if surgeons are able to successfully identify at risk patients, those that fall outside this cohort may be predisposing themselves to actual increased risk of hospital acquired infection by unnecessarily staying in the hospital. 

Several studies have demonstrated that TJA performed as same-day surgery is safe, effective and efficient in the properly selected patient.  These studies found no significant difference in morbidity or functional recovery. [48] [49] [50] [51].  These studies found that nausea was a common cause of delayed discharge, yet < 5% required hospital admission and < 1 % were seen in the emergency room if discharged. 

Unplanned readmissions are one of the measures to suggest that patients were discharged from the hospital too early.  Whether these issues would have been addressed in a standard hospital stay is debatable, as about 10% of complications occur after the standard 3-4 days hospitalization[52].  The overall readmission rate is about 5% within 90 days, with infection and stiffness being the most common cause for TKA. Risk factors for readmission included discharge to a rehab facility and longer (not shorter) hospital stay [53].  In THA population, cardiac issues were the most common cause in the Medicare population, but were unrelated to length of stay [54].  Risk factors for 30 day readmission included discharge to rehab, general anesthesia, Charleson Comorbidity index >2, and longer stay [55].  Difficulty coping with postoperative situation was not a major cause for readmission (5% of readmissions, 0.1% of all patients)[56]. 

5. Discharge Destination

home vs. rehab

Patients that are discharged home after TJA report higher satisfaction, and have demonstrated superior outcomes.  Patients discharged home also have a lower risk for ER readmission [57].  Many would argue that better outcomes occur because these patients are healthy enough to go home leading to selection bias. Yet many of the factors determining home discharge appear to be unrelated to medical comorbidities. 

There are a number of determinants for who goes home after surgery[58].  Studies suggest ethnicity, gender, age, living arrangements, insurance carrier, preop expectations and hospital length of stay all play a role [59] [60] [61] [62].  In combination, these studies suggest that a black female over >70 years old of lower-to-mid socioeconomic status, living alone, undergoing a TKA (vs. THA) with a friend that went to rehab after her TKA has the highest chance of going to a rehab center.  Female gender appears to be the single most important predictor (2x incidence) of discharge to rehab, although other studies suggest preop patient expectation plays the biggest influence [63].  Another study balanced patients for insurance and age and found that ethnicity no longer played a significant role. 

It is important for surgeons to recognize that many factors contributing to discharge are more social than medical.  If patients are happier going home, and many of the factors determining discharge destination are outside of medical treatment, its beneficial for surgeons and patients to understand the best way to make a home discharge possible[64].

6. Activity after TJA

Reference: Knee Society
 Reference: American Hip Society

Reference: American Hip Society

TJA is a great surgery for allowing people to return to daily activities. But what about activities beyond grocery shopping, visiting friends and family and going for walks.  Surgeons have looked into the activities their patients return to, and the incidence of complications to make some recommendations about how active you can be after surgery.    The Baby Boomer Generation is the most active elderly population in history.  Many remain extremely active into their 70s and 80s, playing golf, tennis, swimming and hiking.  

Lets look at the risks of these activities and the current recommendations made by the Knee Society and the American Hip Society. [65]  The concern is that increased activity will accelerate implant bear surface wear and increase risk of falls, which will subsequently lead to prosthetic loosening and fracture, respectively [66, 67]. 

It appears that preop function plays an important role in determining postoperative return to sport. [68]

GOLF.  About 1-8% of people that get a hip replacement actively play golf.  In areas like Florida and Arizona this number is probably much higher.  Golf is considered a low impact sport on the hips and is therefore allowed after hip replacement by 99% of orthopedic surgeons{Mallon, 1992 #356}. To date, there are no published reports of acute hip prosthesis loosening, or hip dislocation during golf.  X-rays of a swing in people with and without a hip replacement show very similar motion within the hip (which is great, because it means that your handicap won't change too much). Similarly there are no significant adverse events reported in TKA after golf.

It is important to note however, that golf is a more demanding sport than many people give it credit for. The golf swing places a high torque on the lower back and hip, and some doctors remain concerned that this repetitive force, over many years, could lead to the hip replacement wearing out prematurely.  

A recent study looked at x-rays of people with hip replacements while swinging their golf club[69].  During a normal golf swing (these people had time to warm up, and had no complaints of pain while swing the club), over 1/3 showed signs that the ball and socket of the hip replacement were improperly bumping into each other (this is called impingement).  This has some orthopedic surgeons concerned that this could lead to premature wearing out of the replacement or it could cause a hip dislocation, although there is no evidence to date that suggests this minor bumping during activities is significant[70].  The impingement was seen in people where the socket was positioned in more anteversion, and the people had a swing that produced more hip external rotation.

TENNIS. High impact and therefore generally discouraged by orthopedic surgeons. Studies on hip [71]and knee [72]replacement in people that played competitive tennis showed significant improvement in pain relief and court mobility after the joint replacement.  So a hip or knee replacement will let you get back to playing tennis, however, there is the concern that a fall could cause significant damage to the affected joint or overuse could lead to premature failure of the join


1.         Woolf, C.J. and M.S. Chong, Preemptive analgesia--treating postoperative pain by preventing the establishment of central sensitization. Anesth Analg, 1993. 77(2): p. 362-79.
2.         Mallory, T.H., et al., Pain management for joint arthroplasty: preemptive analgesia. J Arthroplasty, 2002. 17(4 Suppl 1): p. 129-33.
3.         Macfarlane, A.J., et al., Does regional anaesthesia improve outcome after total hip arthroplasty? A systematic review. Br J Anaesth, 2009. 103(3): p. 335-45.
4.         Safa, B., et al., Comparing the effects of single shot sciatic nerve block versus posterior capsule local anesthetic infiltration on analgesia and functional outcome after total knee arthroplasty: a prospective, randomized, double-blinded, controlled trial. J Arthroplasty, 2014. 29(6): p. 1149-53.
5.         Liu, S.S., et al., A comparison of regional versus general anesthesia for ambulatory anesthesia: a meta-analysis of randomized controlled trials. Anesth Analg, 2005. 101(6): p. 1634-42.
6.         Grevstad, U., et al., Effect of adductor canal block versus femoral nerve block on quadriceps strength, mobilization, and pain after total knee arthroplasty: a randomized, blinded study. Reg Anesth Pain Med, 2015. 40(1): p. 3-10.
7.         Abdallah, F.W., et al., The analgesic effects of proximal, distal, or no sciatic nerve block on posterior knee pain after total knee arthroplasty: a double-blind placebo-controlled randomized trial. Anesthesiology, 2014. 121(6): p. 1302-10.
8.         Jules-Elysee, K.M., et al., Patient-controlled epidural analgesia or multimodal pain regimen with periarticular injection after total hip arthroplasty: a randomized, double-blind, placebo-controlled study. J Bone Joint Surg Am, 2015. 97(10): p. 789-98.
9.         Jiang, J., et al., The efficacy of periarticular multimodal drug injection for postoperative pain management in total knee or hip arthroplasty. J Arthroplasty, 2013. 28(10): p. 1882-7.
10.       Joshi, G.P., et al., Techniques for periarticular infiltration with liposomal bupivacaine for the management of pain after hip and knee arthroplasty: a consensus recommendation. J Surg Orthop Adv, 2015. 24(1): p. 27-35.
11.       Lombardi, A.V., Jr., Recent advances in incorporation of local analgesics in postsurgical pain pathways. Am J Orthop (Belle Mead NJ), 2014. 43(10 Suppl): p. S2-5.
12.       Springer, B.D., Transition from nerve blocks to periarticular injections and emerging techniques in total joint arthroplasty. Am J Orthop (Belle Mead NJ), 2014. 43(10 Suppl): p. S6-9.
13.       Bagsby, D.T., P.H. Ireland, and R.M. Meneghini, Liposomal bupivacaine versus traditional periarticular injection for pain control after total knee arthroplasty. J Arthroplasty, 2014. 29(8): p. 1687-90.
14.       Kerr, D.R. and L. Kohan, Local infiltration analgesia: a technique for the control of acute postoperative pain following knee and hip surgery: a case study of 325 patients. Acta Orthop, 2008. 79(2): p. 174-83.
15.       Ranawat, A.S. and C.S. Ranawat, Pain management and accelerated rehabilitation for total hip and total knee arthroplasty. J Arthroplasty, 2007. 22(7 Suppl 3): p. 12-5.
16.       Peters, C.L., B. Shirley, and J. Erickson, The effect of a new multimodal perioperative anesthetic regimen on postoperative pain, side effects, rehabilitation, and length of hospital stay after total joint arthroplasty. J Arthroplasty, 2006. 21(6 Suppl 2): p. 132-8.
17.       Maheshwari, A.V., et al., Multimodal analgesia without routine parenteral narcotics for total hip arthroplasty. Clin Orthop Relat Res, 2006. 453: p. 231-8.
18.       Maheshwari, A.V., et al., Multimodal pain management after total hip and knee arthroplasty at the Ranawat Orthopaedic Center. Clin Orthop Relat Res, 2009. 467(6): p. 1418-23.
19.       Sharma, V., P.M. Morgan, and E.Y. Cheng, Factors influencing early rehabilitation after THA: a systematic review. Clin Orthop Relat Res, 2009. 467(6): p. 1400-11.
20.       Post, Z.D., et al., A prospective evaluation of 2 different pain management protocols for total hip arthroplasty. J Arthroplasty, 2010. 25(3): p. 410-5.
21.       Chen, J., et al., Efficacy of celecoxib for acute pain management following total hip arthroplasty in elderly patients: A prospective, randomized, placebo-control trial. Exp Ther Med, 2015. 10(2): p. 737-742.
22.       Kazerooni, R., et al., Retrospective evaluation of inpatient celecoxib use after total hip and knee arthroplasty at a Veterans Affairs Medical Center. J Arthroplasty, 2012. 27(6): p. 1033-40.
23.       Morley-Forster, P., P.T. Newton, and M.J. Cook, Ketorolac and indomethacin are equally efficacious for the relief of minor postoperative pain. Can J Anaesth, 1993. 40(12): p. 1126-30.
24.       Clarke, H., et al., Pregabalin reduces postoperative opioid consumption and pain for 1 week after hospital discharge, but does not affect function at 6 weeks or 3 months after total hip arthroplasty. Br J Anaesth, 2015. 115(6): p. 903-11.
25.       Hamilton, T.W., L.H. Strickland, and H.G. Pandit, A Meta-Analysis on the Use of Gabapentinoids for the Treatment of Acute Postoperative Pain Following Total Knee Arthroplasty. J Bone Joint Surg Am, 2016. 98(16): p. 1340-50.
26.       Sinatra, R.S., et al., Efficacy and safety of single and repeated administration of 1 gram intravenous acetaminophen injection (paracetamol) for pain management after major orthopedic surgery. Anesthesiology, 2005. 102(4): p. 822-31.
27.       Backes, J.R., et al., Dexamethasone reduces length of hospitalization and improves postoperative pain and nausea after total joint arthroplasty: a prospective, randomized controlled trial. J Arthroplasty, 2013. 28(8 Suppl): p. 11-7.
28.       Pearson, S., I. Moraw, and G.J. Maddern, Clinical pathway management of total knee arthroplasty: a retrospective comparative study. Aust N Z J Surg, 2000. 70(5): p. 351-4.
29.       Sanders, S., et al., Perioperative protocols for minimally invasive total knee arthroplasty. J Knee Surg, 2006. 19(2): p. 129-32.
30.       Albert, T.J., et al., Patient-controlled analgesia in a postoperative total joint arthroplasty population. J Arthroplasty, 1991. 6 Suppl: p. S23-8.
31.       Stulberg, B.N. and J.D. Zadzilka, Blood management issues using blood management strategies. J Arthroplasty, 2007. 22(4 Suppl 1): p. 95-8.
32.       Nelson, C.L., et al., An algorithm to optimize perioperative blood management in surgery. Clin Orthop Relat Res, 1998(357): p. 36-42.
33.       Ahmed, I., et al., Estimating the transfusion risk following total knee arthroplasty. Orthopedics, 2012. 35(10): p. e1465-71.
34.       Sukeik, M., et al., Systematic review and meta-analysis of the use of tranexamic acid in total hip replacement. J Bone Joint Surg Br, 2011. 93(1): p. 39-46.
35.       Seo, J.G., et al., The comparative efficacies of intra-articular and IV tranexamic acid for reducing blood loss during total knee arthroplasty. Knee Surg Sports Traumatol Arthrosc, 2013. 21(8): p. 1869-74.
36.       Yang, Z.G., W.P. Chen, and L.D. Wu, Effectiveness and safety of tranexamic acid in reducing blood loss in total knee arthroplasty: a meta-analysis. J Bone Joint Surg Am, 2012. 94(13): p. 1153-9.
37.       Newman, E.T., et al., Impact of perioperative allogeneic and autologous blood transfusion on acute wound infection following total knee and total hip arthroplasty. J Bone Joint Surg Am, 2014. 96(4): p. 279-84.
38.       Husted, H., et al., Reduced length of stay following hip and knee arthroplasty in Denmark 2000-2009: from research to implementation. Arch Orthop Trauma Surg, 2012. 132(1): p. 101-4.
39.       Stambough, J.B., et al., Rapid recovery protocols for primary total hip arthroplasty can safely reduce length of stay without increasing readmissions. J Arthroplasty, 2015. 30(4): p. 521-6.
40.       Inneh, I.A., The Combined Influence of Sociodemographic, Preoperative Comorbid and Intraoperative Factors on Longer Length of Stay After Elective Primary Total Knee Arthroplasty. J Arthroplasty, 2015. 30(11): p. 1883-6.
41.       Courtney, P.M., et al., Who Should Not Undergo Short Stay Hip and Knee Arthroplasty? Risk Factors Associated With Major Medical Complications Following Primary Total Joint Arthroplasty. J Arthroplasty, 2015. 30(9 Suppl): p. 1-4.
42.       Parvizi, J., et al., Total joint arthroplasty: When do fatal or near-fatal complications occur? J Bone Joint Surg Am, 2007. 89(1): p. 27-32.
43.       Belmont, P.J., Jr., et al., Thirty-day postoperative complications and mortality following total knee arthroplasty: incidence and risk factors among a national sample of 15,321 patients. J Bone Joint Surg Am, 2014. 96(1): p. 20-6.
44.       Belmont, P.J., Jr., et al., Morbidity and mortality in the thirty-day period following total hip arthroplasty: risk factors and incidence. J Arthroplasty, 2014. 29(10): p. 2025-30.
45.       Belmont, P.J., Jr., et al., Postoperative myocardial infarction and cardiac arrest following primary total knee and hip arthroplasty: rates, risk factors, and time of occurrence. J Bone Joint Surg Am, 2014. 96(24): p. 2025-31.
46.       Lovald, S.T., et al., Complications, mortality, and costs for outpatient and short-stay total knee arthroplasty patients in comparison to standard-stay patients. J Arthroplasty, 2014. 29(3): p. 510-5.
47.       Vorhies, J.S., et al., Decreased length of stay after TKA is not associated with increased readmission rates in a national Medicare sample. Clin Orthop Relat Res, 2012. 470(1): p. 166-71.
48.       Memtsoudis, S.G., et al., Trends in demographics, comorbidity profiles, in-hospital complications and mortality associated with primary knee arthroplasty. J Arthroplasty, 2009. 24(4): p. 518-27.
49.       Liu, S.S., et al., Trends in mortality, complications, and demographics for primary hip arthroplasty in the United States. Int Orthop, 2009. 33(3): p. 643-51.
50.       Berger, R.A., et al., Minimally invasive quadriceps-sparing TKA: results of a comprehensive pathway for outpatient TKA. J Knee Surg, 2006. 19(2): p. 145-8.
51.       Berger, R.A., et al., Rapid rehabilitation and recovery with minimally invasive total hip arthroplasty. Clin Orthop Relat Res, 2004(429): p. 239-47.
52.       Berger, R.A., et al., Outpatient total knee arthroplasty with a minimally invasive technique. J Arthroplasty, 2005. 20(7 Suppl 3): p. 33-8.
53.       Berger, R.A., et al., Newer anesthesia and rehabilitation protocols enable outpatient hip replacement in selected patients. Clin Orthop Relat Res, 2009. 467(6): p. 1424-30.
54.       Yu, S., et al., Preventing Hospital Readmissions and Limiting the Complications Associated With Total Joint Arthroplasty. J Am Acad Orthop Surg, 2015. 23(11): p. e60-71.
55.       Zmistowski, B., et al., Unplanned readmission after total joint arthroplasty: rates, reasons, and risk factors. J Bone Joint Surg Am, 2013. 95(20): p. 1869-76.
56.       Vorhies, J.S., et al., Readmission and length of stay after total hip arthroplasty in a national Medicare sample. J Arthroplasty, 2011. 26(6 Suppl): p. 119-23.
57.       Mesko, N.W., et al., Thirty-day readmission following total hip and knee arthroplasty - a preliminary single institution predictive model. J Arthroplasty, 2014. 29(8): p. 1532-8.
58.       Avram, V., et al., Total joint arthroplasty readmission rates and reasons for 30-day hospital readmission. J Arthroplasty, 2014. 29(3): p. 465-8.
59.       Jencks, S.F., M.V. Williams, and E.A. Coleman, Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med, 2009. 360(14): p. 1418-28.
60.       Mednick, R.E., et al., Factors Affecting Readmission Rates Following Primary Total Hip Arthroplasty. J Bone Joint Surg Am, 2014. 96(14): p. 1201-1209.
61.       Rossman, S.R., et al., Selective Early Hospital Discharge Does Not Increase Readmission but Unnecessary Return to the Emergency Department Is Excessive Across Groups After Primary Total Knee Arthroplasty. J Arthroplasty, 2016. 31(6): p. 1175-8.
62.       Munin, M.C., et al., Predicting discharge outcome after elective hip and knee arthroplasty. Am J Phys Med Rehabil, 1995. 74(4): p. 294-301.
63.       Sharareh, B., et al., Factors determining discharge destination for patients undergoing total joint arthroplasty. J Arthroplasty, 2014. 29(7): p. 1355-1358 e1.
64.       Bozic, K.J., et al., Predictors of discharge to an inpatient extended care facility after total hip or knee arthroplasty. J Arthroplasty, 2006. 21(6 Suppl 2): p. 151-6.
65.       Barsoum, W.K., et al., Predicting patient discharge disposition after total joint arthroplasty in the United States. J Arthroplasty, 2010. 25(6): p. 885-92.
66.       Lavernia, C.J., et al., Race, ethnicity, insurance coverage, and preoperative status of hip and knee surgical patients. J Arthroplasty, 2004. 19(8): p. 978-85.
67.       Inneh, I.A., et al., Disparities in Discharge Destination After Lower Extremity Joint Arthroplasty: Analysis of 7924 Patients in an Urban Setting. J Arthroplasty, 2016.
68.       Iorio, R., Strategies and tactics for successful implementation of bundled payments: bundled payment for care improvement at a large, urban, academic medical center. J Arthroplasty, 2015. 30(3): p. 349-50.
69.       Jassim, S.S., S.L. Douglas, and F.S. Haddad, Athletic activity after lower limb arthroplasty: a systematic review of current evidence. Bone Joint J, 2014. 96-B(7): p. 923-7.
70.       Healy, W.L., R. Iorio, and M.J. Lemos, Athletic activity after joint replacement. Am J Sports Med, 2001. 29(3): p. 377-88.
71.       Healy, W.L., R. Iorio, and M.J. Lemos, Athletic activity after total knee arthroplasty. Clin Orthop Relat Res, 2000(380): p. 65-71.
72.       Ollivier, M., et al., Pre-operative function, motivation and duration of symptoms predict sporting participation after total hip replacement. Bone Joint J, 2014. 96-B(8): p. 1041-6.
73.       Mallon, W.J. and J.J. Callaghan, Total hip arthroplasty in active golfers. J Arthroplasty, 1992. 7 Suppl: p. 339-46.
74.       Mallon, W.J. and J.J. Callaghan, Total knee arthroplasty in active golfers. J Arthroplasty, 1993. 8(3): p. 299-306.
75.       Hara, D., et al., Dynamic Hip Kinematics During the Golf Swing After Total Hip Arthroplasty. Am J Sports Med, 2016. 44(7): p. 1801-9.
76.       Marchetti, E., et al., Component impingement in total hip arthroplasty: frequency and risk factors. A continuous retrieval analysis series of 416 cup. Orthop Traumatol Surg Res, 2011. 97(2): p. 127-33.
77.       Mont, M.A., et al., Tennis after total hip arthroplasty. Am J Sports Med, 1999. 27(1): p. 60-4.
78.       Mont, M.A., et al., Tennis after total knee arthroplasty. Am J Sports Med, 2002. 30(2): p. 163-6.