Systemic complications
Important concepts and introduction
Postoperative congestive heart failure
Postoperative cardiac dysrhythmia
Venous thrombosis and thromboembolism
Renal failure or kidney dysfunction
Urinary tract infection versus asymptomatic bacteriuria
IMPORTANT CONCEPTS AND INTRODUCTION
When looking at the topic of systemic complications it is important to view it through the lens of aging. As described in Chapter 2, the aging patient’s complexity is defined not only by their comorbidities but also by the complex physiological changes associated with aging across all systems.
One way of summarizing the accumulative effect of aging is the loss of physiological reserve. In the context of homeostasis, this loss of physiological reserve represents decreasing capacity to maintain homeostasis in the setting of an insult or strain. For the purpose of this chapter we refer to this vulnerable state of maintaining homeostasis as ‘homeostenosis’.1 The homeostenotic baseline affects the response to strain placed on the organism at any given time.
As trauma and surgery will consume much of the already limited physiological reserve, it is important to evaluate these complications in each person and make the appropriate management changes to try and prevent them. Minimizing complications allows much of the physiological reserve to be dedicated to the acute trauma. This has implications for management before and after surgery. It demands astute clinical reasoning to decide whether an abnormality needs gentle homeostenotic support or aggressive intervention for a new disease process.
Cognitive reserve is also one of the homeostenotic physiological systems and has its own special demands throughout the clinical care pathway. Those with added neurodegenerative disorders may require even further input and thought for their care.
Adding further to the complexity is the fact that the field of orthopaedic trauma in the elderly is evolving as orthopaedic surgeons, geriatricians, anaesthesiologists, physical therapists, occupational therapists and others collaborate to better the care and understanding within the field. This means that there is not necessarily a consensus on how to define a complication. We have done our best to use consensus definitions and present complication incidences known at the time of writing. Interdisciplinary collaborations are increasing and may impact on the presented prevalence of complications in this chapter through prevention and early recognition.
Finally, it is impossible to cover all possible systemic complications in one chapter. The authors have chosen some of the most common and those they deem relevant to the clinician and student of musculoskeletal trauma in the elderly.
DELIRIUM
Definition
Delirium is a clinical syndrome consisting of distinct abnormalities in brain function due to a somatic illness. First codified in the Diagnostic and Statistical Manual of Mental Disorders (DSM),2 in the first edition the syndrome was labelled ‘acute brain syndrome’ and finally crystallized as delirium with very specific diagnostic criteria in DSM-III-R.3,4 and 5 To this day delirium remains a purely clinical diagnosis, and so the reference standard for delirium is a psychiatric evaluation in accordance with evolving DSM criteria. The current gold standard is DSM-V (Table 7.1).6
Table 7.1 DSM-V criteria for delirium
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Physiological risk factors/age related changes
Age itself is a risk factor for delirium. In addition to age, cognitive impairment such as dementia increases the risk for delirium. Individuals who are cognitively intact need a larger insult to cause delirium than those with underlying cognitive impairment.7
Incidence/epidemiology
Delirium is a common postoperative complication that increases both mortality and morbidity in elderly patients.8 Delirium has been associated with higher in-hospital mortality (4–17%)9,10 and 11 and postdischarge mortality (22.7-month mortality hazard ratio = 1.95).8 In orthopaedic patients the prevalence and incidence are 17% and 12–51%, respectively.7
Prevention
In the context of delirium, it is hard to separate preventive measures from non-pharmacological treatment. Once delirium occurs, preventive measures become treatment modalities. This stems from the multifactorial nature of delirium and the incomplete understanding of the pathophysiology of delirium.12 A non-pharmacological approach requires a multidisciplinary team which simultaneously attempts to address and manage multiple risk factors for delirium. It can only be implemented through education, reallocation of resources and reorganization of care for older adults by all those involved.
Identification/diagnosis
Unfortunately, a complete psychiatric evaluation is labour intensive and impractical to employ on a widespread basis. In one study, the psychiatric evaluation took a mean of 90 minutes.13 Moreover psychiatric resources are scarce in comparison with the sheer number of patients with delirium. As the medical community increasingly recognized the impact of delirium on morbidity, mortality, functional status and length of hospital stay, there was a need for more efficient instruments to diagnose delirium. This led to a proliferation of screening instruments with more than 24 of them described in published studies.2 One of the most widely used clinical algorithms is the Confusion Assessment Method or CAM, which itself was developed from criteria based on the DSM-III-R.13 It has been used in 4000 published studies, extensively validated and has a sensitivity of 94%, specificity of 89% and high reliability compared to expert psychiatric evaluation.2
Table 7.2 Confusion Assessment Method (CAM) short form criteria
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Source: Confusion Assessment Method. © 1998, 2003. Hospital Elder Life Program. All rights reserved. Adapted from Inouye SK, van Dyck CH, Alessi CA, Balkin S, Siegal AP, Horwitz RI. Clarifying confusion: the confusion assessment method. A new method for detection of delirium. Ann Intern Med 1990, 113(12):941–948.
Note: Criteria 1 and 2 are required in addition to either criterion 3 or 4. Once there are at least three criteria, the diagnosis of delirium is established.
CAM has been validated in surgical patients (Table 7.2).2
For the diagnosis of delirium, the presence of the first two criteria is required in addition to either criterion 3 or 4.13 Once there are at least three criteria, the diagnosis of delirium is established.
Historical data on acute onset and fluctuating course are obtained from caregivers or healthcare professionals. Therefore knowledge of baseline cognitive status is essential. Sometimes a detailed history is not available during initial evaluation and a diagnosis of delirium is presumed. However, this underscores the fact that the clinician should make every effort to contact the primary caregiver or the patient’s known health professionals. Fluctuating course is also assessed during daily clinical evaluations in the postoperative period.
Complex attention is one of the neurocognitive domains and describes ability to focus, sustain, divide and shift attention.6 It also describes processing speed. Careful clinical observation during the interview is important to assess an individual’s attention. Is the patient easily distractible, or do questions need to be repeated because the patient’s attention wanders, or does the patient perseverate with an answer to a previous question rather than appropriately shift attention?13 However, simple observation is not enough. Formal evaluation of attention must be done to decrease interobserver variability. A task such as naming days of the week backwards or months of the year backwards can serve as tests of attention.2 Other commonly used methods are forward digit span (four or more random digits) or serially subtracting sevens from 100.2 The test should be congruent to the person’s cognitive ability. It is important to note that attention can be preserved in dementia.
Disorganized thinking is characterized by illogical flows of ideas, irrelevant or rambling conversation and frequent switches from one topic to another.6 Disorganized thinking itself is likely driven in part by disturbances of complex attention and also perceptual abnormalities that might include misinterpretations, illusions and hallucinations in one or more sensory modalities.6 There is no formal scale to quantify disorganized thinking and it is mostly based on the experience of the clinician.
Finally, identification of an altered level of consciousness depends on an observer’s impression of whether a patient looked alert (normal), vigilant (hyperalert), lethargic (drowsy, easily aroused), stuporous (difficult to arouse) or comatose.13 Altered level of consciousness may be formally assessed using the Richmond Agitation and Sedation Scale (RASS), which is a validated measure.14 Additionally there are three variants of delirium based on psychomotor activity and level of consciousness.6 Hyperactive delirium is fairly easily diagnosed and is what most clinicians think of when they mention delirium. It is characterized by psychomotor agitation and disturbed emotional state with patients calling out, screaming, cursing, muttering, moaning or making other sounds. Psychomotor agitation may significantly interfere with patient care, safety as well as the safety of healthcare personnel and is a frequent reason for indiscriminate administration of antipsychotic medications or sedatives. A less recognized form of delirium is the hypoactive variant with decreased level of consciousness and apathy. The hypoactive form has been shown to carry a poorer prognosis.15 Finally, delirium may fluctuate between hyperactive and hypoactive forms, which is referred to a mixed delirium.
Management
The management goals of delirium start with preventing delirium, minimizing its duration and minimizing its severity (Table 7.3).16
Table 7.3 Management goals of delirium
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Source: From Javedan H, Tulebaev S. Clin Geriatr Med 2014;30(2):271–8.
NON-PHARMACOLOGICAL STRATEGIES
Non-pharmacological measures have always been a foundation of delirium management. Pharmacological management consisting of antipsychotic medications is mostly directed towards agitation, which is a symptom of hyperactive delirium or mixed delirium. It is important to emphasize that antipsychotic medications and benzodiazepines do not treat the underlying causes of delirium and in the case of benzodiazepines may actually trigger delirium. Non-pharmacological management, on the other hand, attempts to address the multifactorial nature of delirium by early identification and elimination of risk factors.
One of the earliest landmark multicomponent intervention studies conducted on general medical wards by Inouye et al. focused on six components that were chosen because of known association with the risk of delirium and amenability to treatment.17 The interventions were directed towards the management of:
Cognitive impairment
Sleep deprivation
Immobility
Visual impairment
Hearing impairment
Dehydration
This strategy was able to decrease delirium incidence by 40% and duration by 35%, but not the severity or recurrence rates.17 It became known as the Hospital Elder Life Program (HELP) and was disseminated in the United States and abroad with some variations tailored to individual institutions. HELP required an interdisciplinary team and staff dedicated to implementation of the program.
Another landmark study by Marcantonio et al. used proactive geriatric consultation on hip fracture patients that also targeted multiple components.20 Interventions included:
Correcting fluid and electrolyte balance
Providing adequate nutritional intake
Actively eliminating medications that could potentially trigger delirium
Early mobility
Appropriate environmental stimuli
This study showed a reduction in delirium incidence of one third and in delirium severity of one half.20
Reorganization of medical care, appropriate resource allocation and education of staff with the focus on delirium prevention has also been shown to reduce duration of delirium and mortality in delirious patients.18 The non-pharmacological measures are usually performed by trained medical staff; however, even intervention by family members who were briefly educated about some aspects of delirium has been shown to be effective.19 Most studies in non-pharmacological management employed different variations and combinations of the strategies given in Table 7.4.
Controversies
Blood transfusion to a haemoglobin of 10 in a multicomponent intervention was helpful20 but when looked at in isolation did not show any improvement.21 Furthermore increased delirium was observed with intraoperative blood transfusions greater than 1000 ml red blood cells.22 Please see the section on anaemia in this chapter for further discussion.
PHARMACOLOGICAL STRATEGIES
The multifactorial nature of delirium makes medications another tool to help address many of the driving and exacerbating factors. Antipsychotics are traditionally thought of as the pharmaceutical approach to delirium. Antipsychotics in delirium do not treat the underlying cause but rather address the symptoms. Agitation for example is a symptom that can escalate to a level that is detrimental to the patient and dangerous to caregivers. At the same time treating pain and sleep deprivation with an appropriate medication addresses one of the underlying causes and can be far more effective than antipsychotics.
Table 7.4 Non-pharmacological interventions
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As a result, the medication and its timing and dosing need to be tailored to the specific patient with constant monitoring and adjustment as all such medications carry risk and side effects. The long-term risks of antipsychotics are well established, but smaller retrospective studies have shown likely safe use in short-term acute circumstances.23,24 Table 7.5 outlines the pharmacological approaches to treating delirium and its symptoms.
Maximal effective dose
Haloperidol has been in use the longest and studies have shown that doses above 3.0 mg/24 hours increase medication side effects without significant added benefit to duration or severity of delirium.33
There is not enough evidence to definitively identify the maximal effective dose in other antipsychotic medications. However, based on geriatric pharmacokinetic principles it is best to use the lowest effective dose, which the authors recommend (Table 7.6).
Timing
The authors recommend evaluating the pattern of agitation throughout the day and giving a low dose of medication at the beginning of the agitation before it escalates. This will prevent escalation to a point where even maximum dosing will be ineffective and allows the overall 24-hour dosing to stay at a minimum.
Cholinesterase inhibitors
Anticholinesterases have not been effective in treating delirium.35
Controversies
MYOCARDIAL INFARCTION
Definition
Acute myocardial infarction (MI) is defined as myocardial cell death due to inadequate blood supply according to the Third Universal Definition of Myocardial Infarction which was revised in 2012.38 The definition distinguishes five types of MI. However in the context of the postoperative period, type I and II MI are the most relevant entities due to postoperative stress as well as increased prevalence of coronary atherosclerosis and diminished cardiac reserve in older adults. The distinction between type I and type II MI is important due to different approaches to management.
Table 7.5 Pharmacological interventions.
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Note: IM, intramuscular; IV, intravenous; PO, by mouth (per os); PRN, as needed (pro re nata); QHS, every night at bedtime (quaque hora somni); SL, sublingual.
Table 7.6 Dosing regimens for pharmacological interventions
Drug | Dosage |
|---|---|
Haloperidol | 0.25–1.0 mg PO/IM to be repeated every 30–60 minutes if needed. Maximum dose of 3.0 mg in 24 hours to minimize side effects.33 |
Risperidone | 0.25–0.5 mg PO; repeat every 30–60 minutes if needed. |
Quetiapine | 12.5–50 mg PO; repeat every 30–60 minutes if needed. Consider maximum dose of 175 mg/day.34 |
Olanzapine | 2.5–5.0 mg PO/SL/IM; repeat every 30–60 minutes if needed. |
Lorazepama | 0.25 mg–1.0 mg PO/IM; repeat every 30–60 minutes if needed. |
Source: From Javedan H, Tulebaev S. Clin Geriatr Med 2014;30(2):271–8.
Note: IM, intramuscular; PO, by mouth (per os); SL, sublingual.
a The authors recommend this as a choice of last resort as there is no good evidence to support its use except in alcohol withdrawal. If a benzodiazepine must be used, recommend shorter acting formulations with no active metabolites.
Type I is a spontaneous MI occurring as a result of the rupture of unstable atherosclerotic plaque in one or more coronary arteries with local formation of thrombus that interrupts blood flow to an area of myocardium. These patients usually have underlying coronary artery disease.
Type II MI occurs due to an imbalance between myocardial blood supply and oxygen demand. Examples include conditions that are fairly common in the postoperative period such as tachycardia, anaemia, respiratory failure, hypotension or severe hypertension.
Myocardial injury with non-cardiac surgery (MINS) is an emerging diagnostic entity and is defined as prognostically relevant myocardial injury due to ischaemia that occurs during or within 30 days after non-cardiac surgery.39 It is characterized by isolated troponin elevation in the postoperative period without ischaemic symptoms or EKG changes. The definition of MINS does not apply to non-ischaemic elevation of troponin which may happen, for instance, with pulmonary embolism, sepsis or chronic kidney disease.
Physiological risk factors/age related changes
Aging of the cardiovascular system results in worsening of left ventricular diastolic dysfunction, increased cardiac afterload and increased arterial stiffness.40 In addition, elderly patients have an increased prevalence of comorbidities such as hypertension, dyslipidemia, diabetes mellitus and chronic kidney disease that increase the risk of postoperative coronary events. Tachycardia due to pain or increased levels of catecholamines after surgery, hypotension or hypertension, and anaemia are common in the postoperative period and further increase the risk of either unstable plaque rupture in atherosclerotic coronary arteries or mismatch between oxygen supply and demand in aging myocardium.41
Incidence
There is a paucity of data regarding the incidence of postoperative MI in the setting of musculoskeletal injury in older adults. Most of the investigations report incidence of coronary events either after major non-cardiothoracic surgery or after hip fractures. The incidence of postoperative MI after hip fractures varies across studies and depends on the criteria used to establish the diagnosis. The incidence was reported as high as 10.4–13.8% within first 7 days after hip fracture surgery when the diagnosis relied on a combination of rise in cardiac troponin, ischaemic ECG changes and clinical symptoms.42, 43 It is worth noting that 92% of coronary events occurred in the first 48 hours.
Diagnosis
Currently the diagnosis of MI is based on the Third Universal Definition of Myocardial Infarction.
Cardiac biomarkers: The measurement of cardiac biomarkers became central to the diagnosis of MI. There should be a rise and/or fall of cardiac troponins (with at least one value above the 99th percentile of the upper reference limit).
ECG changes: Changes suggestive of ischaemia should be present such as either new ST segment elevation or new left bundle branch block or ST segment depression and T wave changes.
Clinical symptoms: Chest discomfort remains a common presentation of acute MI in older adults. However, elderly patients might also present primarily with atypical symptoms such as dyspnoea (49%), diaphoresis (46%), nausea and vomiting (24%) and syncope (19%).44 New onset dysrhythmias or congestive heart failure (CHF) may also point to a possible coronary event.
In the postoperative period, the diagnosis of acute MI may be challenging. Patients may not be experiencing typical ischaemic pain due to the effects of anaesthesia, sedation or a postoperative pain regimen. Elderly patients with cognitive impairment may poorly communicate their symptoms or even manifest their pain with the development of delirium. One of the difficulties in making the diagnosis is that 75% of elderly patients with postoperative MI after hip fracture may be asymptomatic.43 In this case, diagnosis may be established on the basis of cardiac troponin elevation and ischaemic ECG changes.
Another important distinction that should be made is between acute MI and MINS, myocardial injury which manifests itself with isolated troponin elevation without ischaemic symptoms or ECG changes. Elevated troponin may occur in up to 39% of elderly patients in the postoperative period.45 The level of troponin is usually minimally elevated and does not have the rise and fall characteristic of acute MI. However even in the absence of MI, elevated troponin level independently predicted prolonged length of hospital stay, need for long-term care and all-cause mortality. Therefore cardiac troponin may serve as a prognostic factor. The question of whether cardiac troponins should be routinely measured in the postoperative period in the absence of clinical symptoms or EKG changes is controversial.
Management
The optimal management of postoperative MI in the elderly is unclear due to lack of relevant studies. In elderly patients a decision on the treatment modalities for acute myocardial ischaemia should be made in the context of general health, comorbidities and overall life expectancy.46
MYOCARDIAL INJURY WITH NON-CARDIAC SURGERY (MINS)
In patients with MINS, elevated troponin predicts an increase in 30-day and 1-year cardiovascular mortality. Some authors suggest using aspirin and statins to treat MINS since these patients might have coronary artery disease with fixed obstruction.47 However one randomized controlled study failed to show a difference in mortality between standard treatment and involvement of a cardiologist for postoperative troponin elevation after emergency orthopaedic geriatric surgery.48
NON-ST ELEVATION MYOCARDIAL INFARCTION (NSTEMI)
Non-ST segment elevation MI (NSTEMI) can occur as a result of unstable plaque rupture or a fissure (type I MI) or a mismatch between myocardial oxygen supply and demand (type II MI). The treatment decisions should be interdisciplinary and should involve an orthopaedic surgeon, a cardiologist and an internal medicine physician (ideally a geriatrician). The treatment decisions should be patient-centered and reflect his or her goals of care. Geriatric specific factors such as multimorbidity, cognitive impairment, frailty and functional impairment should be taken into account and will need to be discussed with the patient and/or a healthcare proxy. Other factors such as altered pharmacokinetics, presence of acute or chronic kidney failure and polypharmacy should be considered.
Aspirin and a statin should be started.
A P2Y12 receptor blocker is added (e.g. clopidogrel or prasugrel).49
If there are no contraindications, then anticoagulation with unfractionated or low molecular weight heparin should be initiated.
The decision to start a beta blocker should be individualized and will depend on postoperative blood pressure and the presence of dysrhythmias.
Early invasive versus early conservative management will depend on haemodynamic stability, the patient’s risk and again on goals of care reflecting the patient’s overall health.
ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
These patients are at high risk of postoperative death without treatment and will require urgent primary percutaneous coronary intervention. Fibrinolytic treatment is generally not an option given recent surgery and risk of bleeding, but this again is best addressed with interdisciplinary input.
POSTOPERATIVE CONGESTIVE HEART FAILURE
Definition
CHF is defined as an inability of the heart to pump sufficient blood to meet the metabolic needs of the body. It combines both pump failure that leads to fatigue and poor exercise tolerance, and neurohormonal activation that leads to fluid retention and symptoms of congestion.
Physiological risk factors/age related changes
CHF is more complex in older adults due to the intersection of age related cardiovascular changes and non-cardiac comorbidities. Chronic kidney disease, anaemia, altered regulation of fluid volume, hypertension and other chronic conditions predispose to heart failure and stress in an already homeostenotic cardiovascular system. Heart failure is essentially a geriatric syndrome and needs to be viewed as a multifactorial condition.50,51
Incidence/epidemiology
The preoperative prevalence of CHF in hip fractures was reported to be 6–27%. The presence of CHF predisposes the elderly to musculoskeletal trauma. Osteopenia or osteoporosis is present in a significant number of CHF patients and there is an association between CHF severity, as expressed by lower left ventricular ejection fraction (LVEF) or higher New York Heart Association (NYHA) class, and bone mineral density (BMD) measurements.52 In a population-based cohort of more than 16,000 elderly patients followed up for 1 year, heart failure was associated with a fourfold higher risk of sustaining any fracture requiring hospitalization compared with other cardiovascular diagnoses. This result remained significant after adjustment for age, sex, concurrent medications and other conditions associated with osteoporosis related fracture.53
Diagnosis
In the postoperative period, practitioners may encounter both typical and atypical presentations of CHF. One of the earliest indicators of CHF could be exercise intolerance that will manifest with fatigue and dyspnoea during physical therapy. The patient should be asked about their tolerance of physical therapy. Daily review of physical therapy notes and personal communication with a physical therapist is important for early detection of heart failure. However fatigue and dyspnoea on exertion are relatively non-specific signs and may be present in patients with lung problems, anaemia or general deconditioning. One should bear in mind that older adults frequently have multiple medical problems and a symptom can be a manifestation of several conditions at the same time. For instance dyspnoea on exertion might be caused by a combination of anaemia, chronic obstructive pulmonary disease (COPD) and worsening heart failure. The patient should be questioned about orthopnoea daily. Orthopnoea, which is shortness of breath in the recumbent position, may also manifest as a nocturnal cough. Orthopnoea is relieved by sitting upright or raising the head off the bed. Nursing request for cough medication at night in orthogeriatric patients should prompt assessment of volume status and daily fluid balance. Paroxysmal nocturnal dyspnoea (PND) is shortness of breath, cough or wheezing that awakens the patient from sleep, usually 1–3 hours after the onset of sleep, and is one of the major Framingham criteria for CHF (Table 7.7).54 Patients with cognitive impairment may have difficulties articulating their complaints and therefore nursing observation of poor sleep should alert a clinician to the possibility of orthopnoea or PND. Heart failure may also manifest with gastrointestinal symptoms such as anorexia, nausea and early satiety as a consequence of bowel oedema. Neurological symptoms such as confusion, disorientation and sleep disturbances may also occur due to underlying heart failure. Since the clinical manifestations in older adults may be diverse and atypical and there is a high prevalence in the elderly, clinicians should maintain a high index of suspicion with regard to the presence of heart failure.
Table 7.7 Framingham criteria for congestive heart failure
Major criteria Complaints Paroxysmal nocturnal dyspnoea Physical exam Neck vein distension Hepatojugular reflux Coarse crackles S3 gallop Other Radiographic cardiomegaly (increasing heart size on chest radiography) Acute pulmonary oedema Increased central venous pressure (16 cm H2O at right atrium) Weight loss of 4.5 kg in 5 days in response to treatment Minor criteria Complaints Dyspnoea on ordinary exertion Nocturnal cough Physical examination Bilateral ankle oedema Hepatomegaly Tachycardia (heart rate of 120 beats per minute) Other Pleural effusion Decrease in vital capacity by one third from maximum recorded |
Source: Klein L. Heart failure with reduced ejection fraction. In: Crawford MH, ed. Current Diagnosis & Treatment: Cardiology. 4th ed. New York: McGraw-Hill Medical; 2014.
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