Incidence

The reported incidence of VTE in patients undergoing THA or TKA varies greatly—up to 4.4%, with TKA patients more likely than THA patients to experience a VTE. The rate of mortality in TJA patients experiencing DVT is thought to increase four- to eightfold. ^{, ,} Additionally, the hospital length of stay (LOS) nearly doubles for patients who experience DVTs. While distal DVTs are common and often asymptomatic, occurring in about 50% of patients who do not receive any postoperative anticoagulation, the development of a PE can be life-threatening. PEs have been reported in up to 1.7% of TJA patients, with a risk of mortality after PE as high as 3.3%. ^{, , , ,}

Risk Factors

Several preoperative factors are thought to impose a risk of VTE. These include smoking, increased body mass index (BMI), increased medical comorbidities, advanced age, cancer, prolonged immobilization, bilateral procedures, increased operative times, and history of prior VTE. ^{, , , ,} In the TJA population, with the exception of history of VTE, there is insufficient evidence to conclude that these factors increase the likelihood of VTE.

Diagnosis

Diagnostic strategy of VTE relies on the assessment of pretest probability (PTP). According to the American Society of Hematology (ASH) guidelines, PTP is determined using validated, standardized clinical prediction rules to assume prevalence of VTE in patients with similar clinical criteria. The Wells and Geneva criteria are the ones commonly used.

In patients with low PTP, the highly sensitive D-dimer assay can exclude DVT, but positive D-dimer results trigger additional studies. If additional testing is required, ultrasound is recommended. It should be noted that the D-dimer assay has limited utility in immediate postsurgical patients due to high frequency of positive results, and the decision to start with D-dimer assumes timely results and offsets costs associated unnecessary ultrasound. Postoperative TJA patients with suspected DVT fall into at least the intermediate PTP category due to recent major surgery. In the intermediate PTP population, whole-leg ultrasound is recommended, with no further testing required if results are negative. In high-PTP patients, whole-leg ultrasound is again recommended. However, serial ultrasound should be obtained if the initial ultrasound is negative and no alternative diagnosis is identified.

In the diagnosis of PE, low- to intermediate-PTP patients should be initially evaluated with D-dimer to exclude PE. If elevated, additional studies include ventilation-perfusion (VQ) scans or computed tomography pulmonary angiography (CTPA). VQ scans are preferred over CTPA due to radiation exposure considerations. In the high-PTP population, CTPA is the initial diagnostic study of choice.

Treatment

Treatment is indicated for patients with proximal lower extremity DVT, symptomatic distal DVT (calf veins), symptomatic upper extremity DVT, or PE. For subsegmental PE, patients at risk for recurrence should be treated, while patients with no proximal DVT and low recurrence risk warrant surveillance. Anticoagulation should be initiated immediately, weighing the risk of bleeding in these patients ( Table 2.1 ) and their comorbidities. TJA patients fall at least in the intermediate-risk category (recent surgery) but are often high risk (age >65 years, nonsteroidal antiinflammatory drug [NSAID] use).

Pharmacologic agents are the mainstay of all treatment phases: acute term (0–7 days), long term (7 days to 3 months), and extended term (3 months to indefinitely). ^∗

∗ All dosing is based on Bartholomew, JR. Update on the management of venous thromboembolism. Cleveland Clinic Journal of Medicine , 2017;84(12 suppl 3):39–46.

In the initial treatment of acute VTE, heparin is generally preferred over LMWH, especially in patients with renal failure. Dosing is weight based at 80 U/kg bolus, followed by 18 U/kg per hour intravenous (IV) infusion. Anti-Xa assay is used to monitor treatment efficacy, with a target of 0.3 to 0.7 IU/mL. In the outpatient setting, heparin may be given subcutaneously with an initial bolus of 333 U/kg followed by 17,500 U twice daily. Enoxaparin (Lovenox) is the most common LMWH used in the United States. In the acute setting, it is administered subcutaneously either once daily (1.5 mg/kg per day) or twice daily (1 mg/kg every 12 hours). Renal patients may need to be dosed appropriately. Typically, no monitoring is required. Fondaparinux may also be used in combination with warfarin, dabigatran, or edoxaban for treatment of acute VTE. For VTE treatment, it is administered subcutaneously with weight-based dosing at 5 mg for patients <50 kg, 7.5 mg for 50 to 100 kg, and 10 mg for >100 kg. For DVT prophylaxis, it is dosed at 2.5 mg daily. It is contraindicated in patients with renal disease (creatinine clearance [CrCl] <30 mL/min) and bacterial endocarditis. Some DOACs (rivaroxaban and apixaban) may also be used in the acute phase. Rivaroxaban is given orally, 15 mg twice daily for 21 days, followed by 20 mg once daily for the long term, and 10 mg or 20 mg daily for the extended term. It is contraindicated in patients with renal disease (CrCl <30 mL/min). Apixaban is given orally, 10 mg twice daily for 7 days, followed by 5 mg twice daily for the long term except in patients 80 years of age or older, weighing 60 kg or less, or with serum creatinine 1.5 mg/dL or greater receiving half the dose. In the extended term, dosing is 2.5 mg or 5 mg twice daily.

Long-term and extended-term treatment of VTE is achieved with DOACs or warfarin. Warfarin must be coadministered with heparin, LMWH, or fondaparinux initially and overlapped for 5 days until the international normalized ratio (INR) is at least 2.0 for 24 hours. It is the best long-term/extended-term option for patients with liver dysfunction or renal disease and is much less costly than DOACs. For most other patients, DOACs are recommended due of the lack of required monitoring or bridging, fixed dosage, shorter half-life, and rapid onset. Two additional DOACs may be used in the long term and extended term but not in the acute term due to their required 5-day overlap with a parenteral agent. Dabigatran is given orally at 150 mg twice daily in patients without renal disease (CrCl <30 mL/min). Edoxaban is given orally at 60 mg once daily, or 30 mg once daily for patients with CrCl 30 to 50 mL/min, weighing 60 kg or less, or those on certain P-glycoprotein inhibitors.

In postoperative patients with hemodynamically stable PE, echocardiography may be used to determine the presence of right ventricular (RV) dysfunction. Those without RV dysfunction should continue pharmacologic management. In patients with evidence of RV dysfunction, patients hemodynamically unstable despite acute-term treatment with heparin or LMWH, or those with massive PE on CTPA, pulmonary embolectomy is indicated. ^,

Inferior vena cava (IVC) filters for treatment of VTE are reserved for patients with contraindication to anticoagulation, those experiencing complications of anticoagulation, and those with recurrent VTE despite adequate pharmacologic therapy. They may also be indicated for patients with massive PE, iliocaval DVT, free-floating proximal DVT, cardiac or pulmonary insufficiency, poor compliance, and those at high risk from anticoagulation. Concomitant anticoagulation is recommended in those who are able to tolerate it.

Prevention

Though the rates of TJA procedures continue to grow, the rate of VTE has significantly decreased largely due to the implementation of prophylaxis. Current prevention of VTE in TJA patients is based on the guidelines set forth by the American College of Chest Physicians (ACCP) and the American Academy of Orthopaedic Surgeons (AAOS). While the AAOS guidelines do not make recommendations for a particular agent, they recommend pharmacologic and/or mechanical compression devices for the prophylaxis of VTE after elective THA or TKA. In patients with a history of VTE, concomitant use of pharmacologic and mechanical compression is advised. In those with a known bleeding disorder and/or active liver disease, a mechanical compression device is recommended. All patients should be encouraged to mobilize as early as possible.

The ACCP guidelines recommend using LMWH, fondaparinux, dabigatran, apixaban, rivaroxaban, heparin, warfarin, aspirin, and mechanical compression devices rather than no prophylaxis. They also recommend a duration of 10 to 14 days, which can be extended for up to 35 days. The ACCP specifically suggests the use of LMWH as chemoprophylaxis and the concomitant use of mechanical compression devices while inpatient. They also recommend that LMWH be started 12 hours pre- or postoperatively to limit postoperative bleeding.

Incidence

Postoperative pneumonia occurs as frequently as 1 in 135 patients undergoing THA or TKA and is associated with a 32-fold increased risk of mortality. Although the majority of pneumonia diagnoses are made prior to discharge, TJA patients who develop pneumonia following discharge have an inpatient readmission rate greater than 80%.

Risk Factors

Risk factors associated with the development of pneumonia after TJA include chronic obstructive pulmonary disease (COPD), diabetes, advanced age, dyspnea on exertion, dependent functional status, lower BMI, hypertension, current smoking, and male sex. ^, Congestive heart failure (CHF) and hypoalbuminemia are also considered to be strong independent risk factors for postoperative pneumonia. Although the use of general anesthesia over regional anesthesia is believed to increase the risk of any complication following TJA, there is insufficient evidence to suggest an alteration in the risk of pneumonia. In broad literature, however, neuraxial anesthesia is suggested to reduce the risk of pneumonia when compared with general anesthesia. There are no notable differences in the rates of pneumonia between THA and TKA.

Diagnosis

Generally, pneumonia is categorized into community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP), defined as pneumonia acquired more than 48 to 72 hours after hospital admission. HAP may be further classified into ventilator-associated pneumonia (VAP)—if there is a history of intubation/mechanical ventilation for more than 48 to 72 hours—or health care-associated pneumonia (HCAP) in the presence of certain risk factors ( Table 2.2 ). ^, These distinctions are important due to the differences in causative pathogens and, thus, the need for different pharmacologic treatments.

Clinical suspicion for pneumonia should be raised in patients with fever, purulent sputum, leukocytosis, and possibly hypoxia. Chest radiographs typically demonstrate new or progressive infiltrates ( Fig. 2.1 ). In HAP or HCAP, empiric therapy is started based on these findings. The majority of TJA patients do not fall into the VAP category, as they are not routinely intubated for prolonged periods of time.

Chest radiograph demonstrating lobar pneumonia. Homogenous consolidation in the left upper zone ( black arrows ) and concomitant bronchopneumonia in the right middle zone ( white arrows ).

From Chest X-ray manifestations of pneumonia. Surgery . 2009;27(10):435–455

Treatment

Early empiric antibiotic therapy is essential in the treatment of pneumonia and can significantly improve patient survival. The initial choice of antibiotic therapy is determined by the presence of the patient’s risk for multidrug-resistant (MDR) pathogens and the onset time. ^, Generally, patients with MDR risk factors ( Table 2.3 ) or onset on hospital day 5 or later should receive broad-spectrum coverage. Those without should be treated with limited-spectrum antibiotics.

A minimum of 5 days of treatment is recommended, with a goal to transition to oral antibiotics as soon as possible. This depends on the patient’s clinical improvement. The patient should be afebrile for at least 48 hours and have no more than one sign of pneumonia-associated clinical instability :

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  Temperature >37.8° C

  
  
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  Heart rate >100

  
  
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  Respiratory rate >24

  
  
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  Systolic blood pressure <90

  
  
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  O ₂ saturation <90%, or PaO ₂ <60 on room air

  
  
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  Inability to maintain oral intake

  
  
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  Altered mental status

Prevention

Given the high morbidity and mortality, efforts to reduce the risk of postoperative pneumonia have begun. One published prevention program has cited a 43.6% reduction in postoperative pneumonia from preintervention rates. ^, This specific program includes :

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  Education of all surgical ward nursing staff about their role in pneumonia prevention

  
  
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  Cough and deep-breathing exercises with incentive spirometer

  
  
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  Twice daily oral hygiene with chlorhexidine swabs

  
  
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  Ambulation with good pain control

  
  
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  Head-of-bed elevation to at least 30 degrees and sitting up for all meals (“up to eat”)

  
  
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  Quarterly discussion of the progress of the program and results for nursing staff

  
  
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  Pneumonia bundle documentation in the nursing documentation

  
  
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  Computerized physician pneumonia-prevention order set in physician order entry system

While further investigation is warranted, implementation of simple measures such as perioperative oral hygiene, ^, lung expansion exercises (e.g., cough exercises, deep-breathing with incentive spirometry), and patient/staff education into postoperative care protocols may be a cost-effective method to reducing risk a potentially devastating postoperative complication.

Incidence

The true incidence of AKI following TJA varies in the literature but is estimated to affect nearly 10% of primary TJA and 25% of revision TJA patients. Revision procedures are particularly highlighted due to the nephrotoxic nature of the antibiotics used in cement spacers for PJI cases.

Risk Factors

Risk factors associated with the development of AKI in TJA patients include chronic kidney disease (CKD), advanced age, obesity, male sex, diabetes; hypertension, and the presence of cardiovascular, pulmonary, or liver disease. ^{, ,} Perioperative anemia and blood transfusions have been cited as risk factors for postoperative AKI. Interestingly, the presence of benign heart murmurs has also been associated with postoperative AKI in TJA patients.

The use of certain nephrotoxic agents such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), ^, or certain antibiotics such as aminoglycosides and vancomycin, increase the risk of AKI in TJA patients. Perioperative NSAID use is generally thought to increase the risk of postoperative AKI, though evidence has been inconclusive. ^{, ,} Perioperative hypotension is also a known risk factor for postoperative AKI.

Diagnosis

Several classification systems exist for diagnosing and staging AKI. The RIFLE ( r isk, i njury, f ailure, l oss, e nd-stage renal disease), AKIN (Acute Kidney Injury Network), and KDIGO (Kidney Disease Improving Global Outcomes) systems use creatinine-based and urine output-based criteria. Satisfaction of either, not both, sets of criteria is sufficient for the diagnosis of AKI ( Tables 2.4, 2.5, and 2.6 ).