Surgical site infections (SSI), chest infections, and urinary tract infections make up the majority of infectious complications. The typical onset of an SSI is between day 3 and day 8 postsurgery and is reduced by active surveillance, hand hygiene, attention to nutritional status, glycemic control, and perioperative antibiotic prophylaxis [15].

Chest infections are common and are associated with increased length of stay, worsening morbidity, and increased mortality. Age-related immunosenescence, age-related changes to the lung epithelium, silent aspiration of oropharyngeal secretions, reduced alertness and gag reflex, and immobility all contribute to the development of chest infections in the elderly postoperative patient [16]. Vigilance is key because the elderly patient often will not mount the classical signs of infection such as fever or leukocytosis.

Chest infections are sometimes grouped under the broader category of postoperative pulmonary complications (PPCs), which include atelectasis, pneumonia, respiratory failure, and venous thromboembolism (VTE). VTE will be discussed in more detail separately; however, atelectasis and respiratory failure deserve special mention here.

Atelectasis is common, and postoperative orthopedic patients are prone to this because of immobility, inadequate pain control, body habitus, and preexisting cardiopulmonary disease. Regular pulmonary toilet, incentive spirometry, early extubation, and ambulation must be stressed upon in the postoperative period. Hypercapnic respiratory failure is common as well, most commonly from excessive administration or reduced excretion of centrally acting medications or from undiagnosed sleep apnea. Hypoxic respiratory failure is often multifactorial and can occur from fluid overload, aspiration, atelectasis, venous thromboembolism, and pneumonia.

VTE is a serious and common complication following hip fracture surgery [11] which significantly contributes to worse outcomes in terms of morbidity and mortality. Without prophylaxis, the incidence of VTE is as high as 46–75% [17] with a fatal pulmonary embolism (PE) rate of 4% [18]. Delay in presentation to the hospital or delay in time to surgery increases the risk for developing VTE by almost ten times. Patients are at risk for VTE soon after the time of injury and not after surgical repair; therefore prophylactic anticoagulation should be initiated immediately.

The incidence of VTE can be substantially reduced by the use of appropriate and timely VTE prophylaxis. Mechanical VTE prophylaxis such as intermittent pneumatic compression devices (IPCD) has been shown to reduce deep venous thromboses rates [19]. The American College of Chest Physicians, in its 2012 guidelines, recommends the use of only portable, battery-powered devices that are capable of recording and reporting wear time; additionally, it advises at least 18 h/day of daily compliance [20].

Chemical prophylaxis is key in preventing VTE in patients following hip fractures. Options include heparinoids (unfractionated heparin, low-molecular-weight heparin (LMWH)), fondaparinux, direct oral anticoagulants (DOAC, apixaban, rivaroxaban, dabigatran), vitamin K antagonists (warfarin), and aspirin. Using an agent such as LMWH reduces symptomatic VTE rates to <2% in the first 5 weeks postsurgery. LMWH should be used in preference to other agents, irrespective of the use of IPCD, unless there is a contraindication to doing so. Thromboprophylaxis should be extended to 35 days postoperatively since the risk of VTE is highest during these first 5 weeks. There is no established role for routine prophylactic inferior vena caval filter insertion or Doppler screening for DVT in asymptomatic patients [20].

Because of the high incidence of VTE, a high index of suspicion for PE must be maintained in the perioperative course. Traditional Wells’ criteria for diagnosing PE does not perform well in this population [21], and coexisting pulmonary pathologies such as atelectasis, aspiration, and opiod-induced hypercapnia makes hypoxia an extremely nonspecific finding. [Bedside ultrasonography and the use of end-tidal CO₂ monitoring are exciting tools to use in differentiating the etiology of cardiorespiratory failure in this setting. Lower extremity Doppler examination, biomarkers for right ventricular strain such as troponins and beta-natriuretic peptide, echocardiogram, and imaging such as a CT angiogram or a ventilation/perfusion scan are modalities in the workup for possible PE.]

Treatment largely depends on the cardiopulmonary effects of PE. Non-massive PE and low-risk sub-massive PE are usually treated with anticoagulation alone (either heparinoids or vitamin K antagonists or direct oral anticoagulants), while patients with high-risk sub-massive PE may be candidates for thrombectomy or catheter-directed thrombolysis. IVC filters are reserved for patients in whom anticoagulation is contraindicated or has failed, while systemic thrombolysis is usually a salvage measure for massive PE.

Delirium is common in elderly patients, and its incidence is significantly increased in patients who are hospitalized. There is a large overlap among patients with delirium and those with hip fractures. Common risk factors include age, polypharmacy, gait instability and coexisting dementia, and other medical comorbidities. The incidence of perioperative delirium after hip fracture is high as 60% [22]. At 6 months, patients with delirium were found to have increased hospital length of stay, increased postoperative complications such as urinary incontinence and decubitus ulcers, and an increased chance of dying or being placed in a nursing home.

Factors predisposing patients to delirium include the use of centrally acting medications, especially benzodiazepines and opiods, poor nutritional status, hypoxia, sepsis, and preexisting dementia [23].

A high level of suspicion for delirium should be maintained in the perioperative setting. Hypoactive delirium may be as common as hyperactive delirium but is more difficult to diagnose. Risk factors for developing delirium should be minimized. Delirium can be prevented in one-third of at-risk patients and can be minimized in the others. If the underlying cause of delirium cannot be corrected and the patient’s behavioral symptoms cannot otherwise safely be controlled, antipsychotics can be considered. Their toxicity, especially cardiac arrhythmias and extrapyramidal side effects, however, should be carefully monitored. Efforts should be taken to institute a multidisciplinary stepwise approach to assess and treat patients who are at high risk for developing delirium.

Pressure sores are common after hip fractures with reported incidence rates of 10–40% [24] and have significant effects such as an increase in pain scores, length of stay, costs of care, medical complications, and mortality [25]. Of note, hospital-acquired pressure ulcers are considered a “never event,” and the Centers for Medicare and Medicaid Services does not reimburse hospitals for the cost of their treatment.

Older patients with hip fractures are at high risk for developing pressure ulcers. Predisposing factors include immobility, poor nutritional status, incontinence, and the presence of coexisting diseases such as diabetes and anemia [24, 25]. Pressure sore prevention is crucial and involves minimizing surgical delay, pressure-relieving mattresses, good skin care, rehabilitation, and regular assessment of the patient’s nutritional status [26].

Pressure ulcers are particularly difficult to heal. Treatment principles include careful assessment of severity, releif of pressure and friction, moist wound healing, removal of debris, and management of bacterial contamination [26]. Severe complications of pressure sores can include osteomyelitis and bacteremia.

The mere presence of a pressure ulcer is a prognostic sign. Only about 10% of ulcers heal by the time of hospital discharge, and as many as two-thirds of patients with pressure ulcers die during acute hospitalization. Patients whose pressure sores heal do significantly better than those in whom the sores persist. Though pressure sores themselves are not causally related to poor outcomes, their existence marks a patient who may have significant risk factors for developing perioperative complications leading to increased mortality and morbidity [27].

The incidence of preoperative and postoperative anemia following hip fracture is high and is associated with increased length of hospitalization and increased 6-month and 12-month mortality [28]. While approximately 40% of patients are anemic on admission, intraoperative blood loss leads to postoperative anemia in almost all patients with hip fractures [29].

A large, well-designed, randomized controlled trial has helped determine optimal transfusion thresholds in patients following hip surgery [30]. In this trial, more than 2000 high-risk patients (as defined by history of or risk factors for cardiovascular disease) were randomized to a liberal transfusion strategy (hemoglobin threshold of 10 g/dL) or a restrictive transfusion strategy (symptomatic anemia or a hemoglobin threshold of 8 g/dL). There was no difference among the two groups in terms of mortality or functional capacity at 60 days; neither were there any differences in in-hospital myocardial infarction or unstable angina.

While early mobilization of the elderly patient with a recent hip fracture can be challenging, there is robust evidence to support aggressive early mobilization following hip fracture surgery. Increased immobility leads to worsening morbidity and mortality [31] and predisposes to postoperative complications such as pressure ulcers, urinary retention, ileus, and VTE. Studies show that early ambulation (first walk on postoperative day 1 or 2) accelerates functional recovery and reduces the need for high-level care compared to delayed ambulation [32]. Processes should be in place to facilitate early mobilization. These include aggressive and timely pain control, removal of indwelling catheters, minimizing sedative medications, and an early assessment by the rehabilitation team.

More than half of hip fracture patients are malnourished [33]. Nutritional deficiency is strongly implicated in the pathogenesis of hip fractures [34], as they accelerate bone loss, predispose to gait instability, and are associated with higher comorbid indices [35]. Therefore it is imperative to pay close attention to the nutritional status of elderly patients to (a) prevent hip fractures, (b) enhance recovery, and (c) prevent recurrence.

Calcium and vitamin D supplementation in elderly patients has been shown to increase bone density and reduce the incidence of hip fractures and is a cost-effective way of managing high-risk patients [36]. Among patients who have developed a hip fracture, macronutrients and micronutrients must be replenished. Macronutrient deficiencies such as low protein intake play a detrimental role in recovery, and replacement aids in reducing complication rates and hospital length of stay. In general, hyperproteic nutritional supplements are recommended in the inpatient care of elderly patients with hip fractures. Micronutrients that play a pathogenic role in the disease process include vitamin D, vitamin K, and calcium, and efforts should be made to replete their deficiencies.