Oral and Maxillofacial Trauma in the Geriatric Patient
The older population in the United States is on the rise. A number of factors have contributed to this trend, including early detection and prevention of life-threatening diseases and a more widespread engagement in exercise and fitness activities among the older. As a result, more than half of the current U.S. population can anticipate living to age 80, with a contemporary life expectancy at age 75 of 11 years and at age 85 of 6 years.1 From 1990 to 1994, the older population, defined as 65 years and older, increased 11-fold and the segment of the population younger than 65 years only increased threefold. Based on several variables, including fertility rate, mortality rate, immigration activity, and the aging of the baby boomer generation, the U.S. older population is projected to increase by 18% over the next 10 years and by more than 50% within 50 years.2 It is estimated that by 2050, more than 20% of the population will be 65 years of age or older. The impact of these population trends on the national health care system is significant considering the adjustments that must take place in the delivery of health care and reallocation of resources.
The geriatric population has been an increasing focus of health care providers and therefore is one of the largest consumers of health care in regard to resources and funding. Although older adults make up only 14% of our population, they receive more than 30% of all prescribed medications.3 Trauma is the seventh leading cause of death in older adults, making up 25% of all trauma admissions. The most common mechanisms of injury among older adults are falls and motor vehicle accidents (MVAs). Most deaths occur in the first 24 hours, usually due to head injury. Late mortality is related to severity of organ failure and existence of a premorbid condition. Approximately one third of long-term survivors require nursing home care. The oral and maxillofacial surgeon, as a specialist involved in the care of trauma patients, will see an increasing number of older patients requiring treatment for trauma-related injuries. Increasing age puts a trauma patient into a higher risk category and older patients sustaining major trauma are known to have higher complication and mortality rates than their younger counterparts.4 The purpose of this chapter is to review the biologic effects of the aging process on major organ systems and its effects on the psychological status of older adults, and discuss management of traumatic injuries to the maxillofacial region.
The Biology of Aging
Aging is a biologic process that results in a progressive deterioration of structure and function over time that cannot be stopped or reversed. It is a process that is genetically programmed but modified by environmental influences. Kohn5 has described the aging population as having multiple coexisting diseases that are progressive within a physiologic framework that has a diminished ability to react to stress. This results in increased mortality from injuries and other various insults. Although aging should not be considered a disease, these age-related changes will eventually result in disease and death. Human aging is associated with molecular, cellular, and physiologic changes characterized by a deteriorating homeostatic balance associated with the increasing prevalence of neoplasia and other diseases. At the molecular level, aging has been associated with an increase in DNA point mutations, telomere attrition, and alterations in patterns of methylation.6–9 Each of these can disrupt the normal expression and/or function of proteins involved in cellular growth, maintenance of genomic integrity, responses to cellular stress, and inflammation.7,8
On the cellular level, multiple age-related changes have been observed, including the increase in the number of nucleoli as a result of invagination of nuclear membrane around the clumped nuclear chromatin. Decreased levels of protein production have been attributed to reduction in rough and smooth endoplasmic reticulum. Changes in mitochondrial size and function have been linked to reduced efficiency of fatty acid usage in the aged cell.10,11 In 1968, Harman proposed that mitochondria determine life span due to its damage by free radicals.12 As the cell ages, there is a progressive loss of water from the cytoplasm, causing an increase in the viscosity of the cytoplasm, which reduces the exposure of biologically active cell surfaces.13 Cell membrane permeability also increases and the sodium-potassium pump becomes less efficient. There is a shift of water out of cells, increasing the extracellular space. The total level of intracellular potassium is also reduced.14 These alterations in membrane function have to be considered when managing fluid administration and resuscitation in the older patient. All these changes affect the cell’s ability to produce energy and maintain vital biochemical functions. In its entirety, these age-related cellular changes are directly responsible for the physiologic aberrations that characterize the older patient.
The age-old question of why we age still has to be answered. Throughout the years, many theories have been proposed to answer this question. The popular programmed theory of aging proposes that aging is similar to other biologic processes controlled by the expression of a specific gene.15 This theory is supported by observations that every organism has a physiologic life span that is highly characteristic for its species. In this model, so-called senescence genes, when expressed, are responsible for modulating various cellular functions that begin the aging process. The somatic mutation theory focuses on mitotic errors as an important factor in the aging process. It is thought that the gradual accumulation of genetic errors, which has been observed in older cells, results in chromosomal losses that have a negative impact on cellular metabolism. Others have hypothesized that the aging process is directly related to alterations in immune system function characterized by an increase in the levels of circulating autoantibodies.16 Some have linked aging to the release of a specific hormone that reduces the response of peripheral tissue to the effects of thyroid hormone.17 Harmon12 has proposed that free radicals from the diet, environment, or metabolic cellular processes can accumulate in cells and interfere with cellular oxidation. Older cells, therefore, will have a greater exposure to these agents and are more likely to experience these negative effects.
System Changes
Cardiovascular System
As a person ages, cardiac function is altered in an age-related manner and a risk of cardiovascular disease increases directly proportional to age. These age-related physiologic changes (Table 30-1) do not include common cardiovascular diseases such as coronary artery and cerebrovascular diseases, which increase in frequency with aging. Clinical manifestations and prognosis of these cardiovascular diseases likely become altered in older persons of advanced age because interactions occur between age-associated cardiovascular changes in health and specific pathophysiologic mechanisms that underlie a disease.18 As a result, these significant changes predispose a person to these diseases and, in many cases, worsen the prognosis, such as a patient with a myocardial infarction (MI). Preexisting age-associated changes in vascular and ventricular properties alter the substrate on which the infarction occurs and probably play a crucial role in the poor prognosis of older patients with acute MI.19
TABLE 30-1
Common Age-Related Cardiovascular Changes and Associated Diseases
| Age-Related Changes | Associated Cardiovascular Disease |
| Decreased heart rate response | Sinus pauses |
| Longer P-R intervals | Second- and third-degree AV block |
| Right bundle branch block | Left bundle branch block |
| Increased atrial ectopy | Atrial fibrillation |
| Increased ventricular ectopy | Sustained ventricular tachycardia |
| Altered diastolic function | Decreased systolic function (ejection fraction) |
| Aortic sclerosis | Aortic stenosis, aortic regurgitation |
| Annular mitral calcification | Mitral regurgitation, stenosis systolic hypertension diastolic hypertension |
It is difficult to measure the direct age-related effect on the cardiovascular system because most studies have eliminated asymptomatic individuals with a clinically significant CAD (coronary artery disease). Wenger20 has found that about 20% of patients older than 80 years of age have clinically manifest CAD, but most older people with significant obstructive CAD are asymptomatic.
As the heart and blood vessels age, there is a gradual decline in the elasticity of these structures as a result of a decrease in the content of elastic tissue and increase in the amounts of collagen, calcium, and smooth muscle. The degree of collagen cross-linking increases with age and results in a stiffer, less compliant ventricle. The reduced elastic recoil of the large- and medium-sized vessels, coupled with atherosclerotic changes, culminates in an increase in total peripheral vascular resistance. Fibrosis and calcification of the aortic valve, which adversely affect left ventricular function, are present in 20% of patients older than 65. The combination of these effects increases the preload and afterload of the heart and results in a decrease in cardiac output (1%/year) and stroke volume (0.7%/year) and an increase in systolic and diastolic pressures. The impact of cardiovascular disease on the surgical mortality in older patients is significant. In a large controlled study, the average mortality of 2.4% increased to 6.6% with the presence of cardiovascular disease.21,22 The mortality rate increased to 7.2% in patients older than 60 years and 14% in patients older than 70 years.
Respiratory System
The respiratory system undergoes anatomic, physiologic, and immunologic changes with age. Due to variability in physiologic respiratory measurements among healthy adults, it is sometimes difficult to differentiate between a diseased state and normal state. Although the overall number of alveoli does not change appreciably with age, structural changes do occur, which affects gas exchange. Alveolar ducts enlarge and septa collapse because of a loss of elastic tissue, resulting in reduced total alveolar surface area.22 The reduction in elastic lung tissue and increased calcifications at rib articulations results in a stiff, less compliant lung. The effort to expand the lung decreases 30% from 20 to 60 years of age.23 Diaphragmatic breathing assumes a greater role in ventilation but is less efficient as it flattens with age, decreasing the muscle length and strength. These changes function to reduce the elastic recoil of the lungs and lead to premature airway closure, air trapping, and increased dead space. The functional residual capacity increases approximately 10% by age 60.24 This will create ventilation and/or perfusion mismatches and shunting, resulting in a lower PaO2. These changes will decrease an older patient’s ability to deliver oxygen to the tissues that are actively involved in respiration. The operative mortality risk associated with symptomatic pulmonary disease is related to the severity of the dysfunction. This can be determined by preoperative quantitative pulmonary function testing. Respiratory system reserve is limited with age and diminished ventilatory response to hypoxia and hypercapnia makes it more vulnerable to ventilatory failure during high-demand states (e.g., heart failure, pneumonia) and possible poor outcomes.25 There is no evidence that the changes in the respiratory system with aging affect day to day function of older adults, but they may become evident under circumstances when physiologic demand reaches the limits of supply.26
Renal System
Age-related renal changes are mainly characterized by decrease in renal mass, renal blood flow, glomerular filtration rate (GFR), tubular secretion and absorption, and creatinine clearance.27 The decrease in GFR can occur with a normal serum creatinine level and may increase the risk of renal failure and mortality from established renal failure. Older patients with end-stage renal disease (ESRD) undergoing dialysis have a substantial and sustained decline in functional status, and are more likely to die in an acute hospital setting. Along with decreased renal function, a number of significant cellular changes occur as a result of aging, including an increase in some renal membrane transporters and renal membrane protein metabolism; also, Na,K-ATPase protein abundance and activity and renal adaptation to a number of challenges are often diminished.28 The age-related kidney disease is characterized by phenotypic changes in mesangial cell progenitors and is an entity distinct from all other causes of renal disease.29 Alternatively, age-related renal changes are accelerated by comorbid conditions such as hypertension, atherosclerosis, and heart failure.30 Bax et al have assessed the data of 1056 patients to study the effect of atherosclerosis on renal size and function and concluded that atherosclerosis accelerates the decrease of renal size and increase of serum creatinine levels with age.31
The extensive pharmacologic treatment commonly seen in older adults, in combination with a decrease in renal clearance, leads to significant pharmacokinetic changes, which ultimately result in reduced receptor sites for drug binding, an increase in volume of distribution of lipid-soluble drugs, and subsequent prolongation of elimination half-life.32,33 This should be an important consideration when administering anesthetic medications to the geriatric patient or assessing the patient who is on a cardiovascular drug regimen.34 Failure to excrete anesthetics and analgesics normally by the kidneys can lead to toxic levels of these agents and may lead to complications such as oversedation and apnea. There is often a narrow therapeutic index for opioid analgesics related to hepatic and renal insufficiency and an increased sensitivity to central nervous system (CNS) drugs, and so adverse effects must be carefully monitored.35 For example, in older patients, a longer duration of action has been observed following morphine administration due to a prolonged elimination of the drug from the plasma.36 When assessing geriatric patients, dose adjustment should be considered for all medications that are eliminated renally, such as allopurinol, amantadine, most antibiotics, atenolol, carteolol, digoxin, lithium, gabapentin, H2 blockers, procainamide, quinidine, and sotalol.37
From a surgical standpoint, older patients with active renal disease, especially dialysis patients, require optimal perioperative management. The perioperative concerns include a high incidence of CAD and myocardial dysfunction and difficulty adjusting fluid and electrolytes in the perioperative period in patients with diminished renal function.38 Hyperkalemia is the most common complication and may require immediate postoperative dialysis.39 Other surgical complications include increased perioperative bleeding complications and poor blood pressure control, including hypertension and hypotension. In addition, surgery may need to be deferred to nondialysis days due to heparin coadministration during hemodialysis and the possibility of intraoperative hemorrhage.
Nutrition
Adequate nutrition is essential for maintaining homeostasis in the normal state and trauma patient, in whom so many physiologic systems can be stressed. This is particularly significant in older patients for whom protein energy and micronutrient deficiencies are common. Energy intake below 30% of estimated needs and a low serum albumin level have been associated with longer hospital stays, higher readmission rates, higher in-hospital mortality rates, and increased mortality at 90 days and 1 year.40,41 These concerns are compounded by the fact that certain older maxillofacial surgery patients with compromised oral function secondary to postoperative swelling or maxillomandibular fixation (MMF) will not be able to maintain normal oral nutrition. In addition, the stress of trauma and surgery will elicit a series of physiologic and metabolic responses that will markedly alter the nutritional requirements of the trauma patient. The presence of comorbid conditions, such as diabetes, renal disease, and heart failure, will serve to compound this effect. Identifying and correcting nutritional deficiencies preoperatively will have a significant impact on the healing and recovery of the patient. Following a meta-analysis of clinical studies involving hospital patients with malnutrition, Potter et al have reported that patients who began nutritional supplementation on hospital day 3 or sooner have an average length of stay 3 days shorter than those who started later.42
The caloric requirement of older adults declines by 22% from the age of 30 to the age of 80 years.43 This decline is reflective of a decrease in lean body mass and metabolic rate secondary to reduced physical activity. However, in the older trauma patient, caloric needs will be altered according to the clinical setting. An assessment of the caloric requirement must be established before initiating nutritional support (Table 30-2). Although the caloric requirements of older patients are lower than those of younger patients, their protein requirements are the same and may be elevated. The current recommendation for protein intake in older adults is 0.8 g/kg/day. During episodes of physiologic stress (e.g., trauma, surgery) the protein requirement may be as high as 1.0 to 1.5 g/kg body weight.43 Following the stress of surgery or trauma, glycogen stores are depleted within 36 hours. When glycogen stores are depleted, energy demands are met through the process of gluconeogenesis, in which protein from skeletal muscle is converted to glucose. This increases the demand for protein intake. Surgical patients with a low protein intake have a fourfold increase in medical complications and a sixfold increase in mortality, and are more likely to have an extended hospital stay.44,45 In older adults, inadequate intake of protein has been reported in 10% of men and 20% of women.46 Protein-energy malnutrition (PEM), defined as a deficit in energy (in kilocalories [kcal]) and protein, is also common in older patients. In older surgical patients, the incidence of PEM was reported to range from 43% to 50%47,48 and was higher for patients in extended-care facilities.
TABLE 30-2
Caloric Requirements for the Geriatric Patient
| Degree of Stress | Caloric Requirement (kcal/kg/day) |
| Nonstressful activity | 25 |
| Mild stress (mild URI, grade I or II pressure ulcer) | 30 |
| Moderate stress (pneumonia, UTI, grade III pressure ulcer) | 35 |
| Severe stress (major trauma, sepsis, grade IV pressure ulcer) | 40 |
URI, Upper respiratory tract infection; UTI, urinary tract infection.
Adapted from Abbasi A: Nutrition. In Duthie EH, Katz PR, editors: Practice of geriatrics, Philadelphia, 1998, WB Saunders.
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