Aging is an irreversible and progressive physiologic phenomenon characterized by degenerative changes in structure and the functional reserve of organs and the tissues. It produces many physical manifestations due to reduced connective tissue flexibility and elasticity or the degeneration of highly structured molecular arrangements within specialized tissues. Life span is an idealized, species-specific biologic parameter that quantifies maximum attainable age under optimal environmental conditions. Historical anecdote suggests that human life span has remained constant at 110 to 115 years for at least the past 20 centuries.1 In contrast, life expectancy describes an empirical estimate of typical longevity under prevailing or predicted circumstances. Increased life expectancy and reduced mortality from chronic age-related disease continue to enlarge that fraction of the surgical patient population considered elderly (defined arbitrarily as persons over 65 years of age).
These patients are vulnerable to the adverse effects of anaesthesia because of their reduced margin of safety. Morbidity and mortality increases with advancing age, with a steep increase after 75 years of age.2 The frequency of complications related to anaesthesia is 0.5 per cent in patients more than 80 years old. Emergency procedures are associated with a higher mortality rate regardless of age group. Similarly, abdominal and thoracic procedures have a higher complication rate.3
PHYSIOLOGY OF AGING
Nervous System
Central: Brain is the target organ for all general anaesthetic agents in the central nervous system (CNS). Aging produces a decrease in neuronal density and loss of 30 per cent brain mass by the age of 80 years. Neuronal activity, blood flow metabolism, auto-regulation and cerebrovascular response to carbon dioxide (CO2) remain intact in the absence of disease.4 Cerebral blood flow (CBF) is reduced by 10 to 20 per cent, which occurs in response to decreased metabolic requirement of oxygen and decreased cerebral mass. There occurs a reduction as well as destruction of brain neurotransmitters (catecholamines, serotonin, acetylcholine) at an accelerated rate.5 Dopamine uptake sites, transporters and levels are reduced as also are cortical serotonergic, alpha 2, beta and gamma-aminobutyric acid (GABA) binding sites.3
Peripheral: Aging of peripheral CNS is manifested by a loss of motor sensory and autonomic fibres, decrease in afferent and efferent conduction velocities and progressive decline of signal processing rate within the brain stem and spinal cord.3 There is a reduction both in the efficiency of nerve to muscle coupling, and in the number of muscle cells innervated by an axon, leading to denervation and atrophy of muscle. Plasma epinephrine and norepinephrine levels are increased, but responsiveness of the aging autonomic end organs is reduced.
Neuromuscular junction: Aging affects the neuromuscular junction in many ways. The distance between the junctional axon and the motor end-plate is increased, the folds of the motor end-plate are flattened, the concentration of acetylcholine receptors at the motor end-plate is decreased and the amount of acetylcholine in the junctional vesicles and the amount of acetylcholine released is decreased. In spite of all of these changes in the neuromuscular junction, alterations in the pharmacodynamics of nondepolarizing neuromuscular blocking agents in the elderly are largely due to alterations in the pharmacokinetics of these agents. Sensitivity of the acetylcholine receptor to neuromuscular blocking agents is not affected by advanced age. Altered pharmacokinetics are the result of decreases in hepatic and renal blood flow and function that occur with advanced age as well as altered volumes of distribution of relaxants in geriatric patients.
Cardiovascular System
Integrated cardiac function changes less than cardiac and vascular anatomy.2 Cardiac output is reduced only in proportion to decreased skeletal muscle and lean tissue mass. Ventricular pump function appears to be largely a reflection of conditioning and aerobic demand rather than chronological age. Aging impairs diastolic filling, chronotropic and inotropic responses of the heart. Therefore, ability of the older patient to cope with stress is reduced leading to a limited capacity to meet the increased metabolic demands when maximal cardiac output and oxygen delivery are limited.6 Heart rate is reduced, due to decreased sympathetic activity, fibrotic infiltration or degenerative changes in conductive system. Loss of elasticity of large arteries produces a progressive rise in systemic BP and widening of pulse pressure. Impedance of stroke volume ejection, produces concentric left ventricular hypertrophy. Reduced ventricular compliance makes the heart, volume sensitive and volume intolerant.7 There occurs a progressive decrease in compliance in the venous system also. This 4decrease exaggerates hypotension resulting from blood loss, as well as from peripheral pooling of blood with general or regional anaesthesia.8 Cardiac output decreases at a rate of 1 per cent per year. At the age of 80 years, it is decreased by 50 per cent as compared to a 30 year old.2 This is due to increased myocardial stiffness, interstitial fibrosis, progressive atherosclerosis and increased amyloid deposits in the myocardium. These patients are at an increased risk of developing hypotension because of decreased baroreceptor sensitivity, decreased response to beta stimulation and decreased response of renin/aldosterone/angiotensin systems.7
Respiratory System
A number of striking anatomic changes occur in the respiratory system with age.3 There occurs an emphysema-like increase in parenchymal compliance that leads to ventilation perfusion mismatch, increased physiological shunting and reduced efficiency of gas exchange. Ventilation-perfusion mismatch causes arterial oxygen tension to fall linearly with age. However, CO2 excretion is minimally affected. There is marked suppression of hyperventilation, in response to imposed hypoxia or hypercapnia putting these patients at a higher risk for developing respiratory failure. Anaesthesia, supine position and use of narcotics worsen hypoxia by increasing ventilation perfusion mismatch in the presence of blunted ventilatory reflexes. Impaired cough and laryngeal reflexes, decreased immune response and mucociliary clearance increases the risk of aspiration and postoperative pneumonia. Four hallmarks of aging that lead to reduced capacity of all pulmonary functions are shown in Table 1.1.
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Laryngeal structures undergo a slow decline in function12. Protective reflexes involved in coughing and swallowing are diminished.13 This results in a reduction of vital capacity, stiffening of the chest wall and reduced compliance of the lung parenchyma. Rate of respiration increases, lung expansion reduces increasing / maldistribution. Alveolar surface area decreases, thereby reducing efficiency of gas 5exchange. Mean arterial oxygen tension (PaO2) while breathing air declines to 73 ± 5 mmHg at 75 years after which it remains more or less constant.14 Anaesthesia compounds / mismatch over and above that present due to age. A rigid pulmonary vasculature blunts the hypoxic pulmonary vasoconstrictor (HPV) reflex reducing the ability of the aged lung to respond to altered / mismatch. A blunted ventilatory response to hypoxia and hypercapnia along with a reduced respiratory reserve can be further compromised by narcotic premedication. Older patients, therefore, may develop ventilatory inadequacy early for any given ventilatory load or increased demand for oxygen, e.g. in atelectasis, collapse or pneumonia. Age related changes are a mix of obstructive and restrictive lung disease. Thus, respiratory inadequacy may not be apparent in the immediate postoperative period but may manifest up to 2 to 3 days postoperatively. Sternotomy or thoracotomy for cardiac surgery may have additive effects. Functional inspired oxygen concentration (FiO2) needs to be increased while providing basic tidal volumes.
Pulmonary Function Tests
Pulmonary reserve decreases with increasing age. Vital capacity decreases 25 ml per year after age 20. Forced expiratory volume in one second (FEV1) falls by 0.2 liters per decade after age twenty. PaO2 decreases 4 mmHg per decade after age 20. There is a progressive increase in closing volume which may contribute to post-operative atelectasis. Flow rates including FEV1 decrease by 20 to 30 per cent and maximal breathing capacity is reduced by at least 50 per cent at 70 years.15 Dynamic lung compliance becomes frequency dependent. As breathing rate increases, lung expansion becomes less effective, particularly in some areas, increasing maldistribution of ventilation to perfusion. Decreased efficiency of vascular distensibility and recruitment leads to decreased hypoxic pulmonary vasoconstriction. Elderly patients develop ventilatory inadequacy earlier for any given ventilatory load. The subjective feature of ventilatory inadequacy is dyspnoea.15
Liver
Aging produces a marked reduction in liver size such that 40 to 50 per cent of young adult hepatic tissue mass, involutes by 80 years. Liver and splanchnic blood flow is reduced leading to delayed drug clearance. Hepatic synthesis of cholinesterase is deficient in elderly males. Decreased production of albumin results in reduced plasma protein binding of drugs. Loss of well perfused hepatic tissue plays an important role for drugs, which require biotransformation.156
Kidney
Glomerular filtration rate (GFR) reduces by 6 to 8 per cent per decade. Almost one half of the glomeruli are non-functional by 80 years of age and the glomerular filtration rate decreases from 120 ml/min in the young adult to 60 ml/min at 80 years. Pituitary response to dehydration is compromised. There is a reduced ability to concentrate urine after water deprivation, so the ability to excrete an acid load is reduced. These changes reduce the clinical reserve of the kidneys and drugs, which are dependent on renal excretion for elimination, have a prolonged half life.3 Decreased ability of the kidney to regulate salt balance, especially under stress makes fluid and electrolyte balance more labile. Reabsorption of glucose is decreased in elderly patients, thus glucosuria may be misleading in diagnosis of diabetes mellitus. These alterations are unlikely to have any clinical significance unless challenged by super imposition of an acute illness or stress of surgery or infection.3, 16
Endocrine
There occurs a decrease in the secretion of growth hormone and insulin like growth factor-I (IGF-I) may increase sympathetic nerve activity. Decreased growth hormone is a cause of age related intracellular dehydration, atrophy of skeletal muscle and increase in lipid fraction of total body weight. Progressive decline in androgens may be a cause for change in body composition, leading to decreased muscle mass and total body water, and increase in adipose tissue.17
PHARMACOKINETICS AND PHARMACODYNAMICS IN THE ELDERLY
The elderly tend to maintain higher blood levels of drugs due to changes in volume of distribution, slower drug metabolism, reduced protein binding, loss of skeletal muscle and increase in body fat, reduction in blood volume, loss of hepatic and renal function. There is no ideal anaesthetic for elderly patients but an understanding of the aging process, pharmacological responses, increased intensity of monitoring according to the patient's condition and proposed surgical procedure help offer elderly patients a safe anaesthetic.
Protein-binding
All anaesthetic agents are to some extent protein-bound to plasma proteins. The portion of the drug that is bound to protein is unable to cross membranes to produce the desired drug effect. On the other 7hand, the portion that remains free in plasma is able to cross membranes, including the blood brain barrier, and is responsible for drug effect. In the elderly, protein-binding of anaesthetic drugs is less efficient resulting in an exaggerated pharmacologic effect.
Four factors may explain the reduced drug-binding to serum protein in elderly individuals. First, with aging, the circulating level of serum protein, especially albumin, decreases in quantity, reducing available protein-binding sites for a variety of anaesthetic drugs. Second, qualitative changes may occur in circulating protein that reduces the binding effectiveness of the available protein. Third, co-administered drugs may interfere with the ability of anaesthetic agents to bind to available serum protein-binding sites. Fourth, certain disease states exaggerate this phenomenon. Thus, anaesthetic agents that are highly protein-bound should be delivered to an elderly individual with the expectation that reduced protein-binding will lead to higher free drug levels and an enhanced delivery of the drug to the brain. Figure 1.1 illustrates the effect of decreased plasma protein-binding as a smaller difference between brain and plasma drug levels in the elderly than in young adults.
Change in Body Compartments
Important age-related changes in body composition include a loss of skeletal muscle (lean body mass) and an increase in percentage of body fat. These changes are more exaggerated in women. In addition, it has been suggested that a 20 to 30 percent reduction in blood volume occurs by age 75 years.
Therefore, injection of anaesthetic drugs will initially be dispersed in a contracted blood volume in the elderly patient producing a higher than expected initial plasma drug concentration (Fig. 1.1).
The increase in percentage of body fat that occurs with age results in an increased availability of lipid storage sites and a greater reservoir for deposition of lipid-soluble anaesthetic drugs. The greater sequestration of anaesthetic agents in the lipid storage tissues of the elderly allows for a more gradual and protracted elution of anaesthetic agents from these storage sites, increasing the time period required for their elimination and resulting in greater residual plasma concentrations of drugs that contribute to prolonged anaesthetic effects.
A classic example of age-related reduced anaesthetic requirement is the reduced minimum alveolar concentration (MAC) necessary in elderly patients to produce anesthesia with either cyclopropane, halothane, isoflurane or desflurane.18 The requirement for these inhalational agents decreases linearly with patient age. The reduced anaesthetic requirement for geriatric patients applies not only to inhalational anaesthetics but also to local anaesthetics, narcotics, barbiturates, benzodiazepines and other intravenous anaesthetic agents. Elderly patients achieve a comparable level of sedation at diazepam plasma concentrations significantly lower than that required in young adults. Equivalent electroencephalogram (EEG) suppression occurs at lower plasma concentrations of both fentanyl and alfentanil in the aged.19 Similar to narcotics, the induction dose of barbiturates required in 70 year old adults is approximately 30 per cent less than that required for individuals four to five decades younger.20 However, it has been suggested that the greater sensitivity of the elderly to the same dose of thiopental is dependent upon the basis of a reduced initial volume of distribution resulting in a higher plasma concentration following the same administered dose.21
ANAESTHETIC AGENTS
Intravenous Hypnotic Agents
The pharmacology of thiopentone has been extensively studied. There is no alteration in brain sensitivity to thiopentone in the aged although dose requirements are decreased by 50 to 67 per cent in the elderly when compared with adult patients. It has been confirmed that the age-related decrease of the dose requirement to produce a particular drug effect was due to changes in the distribution phase. With increasing age there is a change of rapid intercompartmental clearance while the initial distribution volume does not change with age. Thiopentone concentration will decrease more slowly in the elderly because the rapid intercompartmental clearance is lower in the elderly.
Therefore, after an intravenous bolus, more thiopentone is available for distribution into the brain to create a more pronounced effect in the elderly.20, 21 It also causes greater cardiovascular depression in the elderly which might contribute to the high degree of pharmacokinetic variability. These effects suggest that the dose for induction of anaesthesia must be reduced in the elderly. The age effect will be more evident when readministration or a short infusion is used because they will significantly prolong recovery. Besides thiopentone, requirement of propofol for induction of anaesthesia has also been demonstrated to be less. Scheepstra et al found that 1.7 mg/kg propofol was needed for induction in the elderly whereas 2.5 mg/kg was needed in younger patients. The maintenance doses were 8.6 and 10 mg/kg/h respectively. Nevertheless, recovery was more rapid in adult patients.22 A dose in excess of 1.75 mg/kg can cause significant hypotension and apnoea in the elderly.23 These studies have shown that the dose of propofol in the elderly must be reduced for both pharmacokinetic and pharmacodynamic reasons (Fig. 1.2).22,23 Further, the hypotensive effect requires slow administration of the reduced dose, titrated to effect rather than the pre-selected standardised dose. The dose of propofol should be 1.0 to 1.5 mg/ kg without opioids, 0.5 to 1.0 with opioids especially when midazolam or ketamine are concomitantly administered.3 The increased sensitivity to propofol in the elderly has been confirmed by Schnider et al. The steady-state propofol concentration at which 50 per cent of the patients are asleep in young adults is twice the concentration needed in the elderly.2410
Elderly patients require a reduction in propofol infusion rate of 30 to 50 percent. Moreover, the rapidly equilibrating peripheral compartment and propofol systemic clearance are reduced in the elderly.25 These findings demonstrate that in the elderly patient, induction dose of propofol as well as infusion rate must be lower than young adults to obtain a predetermined plasma concentration.
The increased apparent volume of distribution of all benzodiazepines in the elderly induces an increase of the elimination half-life. The use of benzodiazepines must be cautious in elderly patients because they are also more sensitive to their central depressant effects. The slow decrease of midazolam plasma concentrations in the elderly is due to both an increased volume of distribution and a reduced plasma clearance. Although no age-related differences have been observed in benzodiazepines receptors activity, there is an increased brain sensitivity to midazolam in the elderly.26 It is usually accepted that the dose of midazolam should be reduced by more than 50 per cent in the elderly.
The main advantage of etomidate in the elderly is its haemodynamic stability. Arden et al found an age-related decrease of the dose of etomidate needed to reach a predetermined EEG endpoint. The initial distribution volume for etomidate decreases significantly with increasing age, implying that a higher initial blood concentration in the elderly following any given dose of etomidate is part of the cause of the lower dose requirement in the elderly patient.27 The incidence of apnoea and respiratory depression are less in elderly patients receiving etomidate than in those receiving thiopentone.28
Inhalational Agents
There is a reduction in the requirement of halogenated agent and minimum alveolar concentration (MAC) with increasing age. The reduction is regardless of the inhalational agent and it can be as much as 30 percent. It has been shown that the MAC for isoflurane is 1.28 per cent in young adults and 1.05 per cent at age 64 years. MAC for desflurane and sevoflurane is 7.25 per cent and 1.71 per cent in young adults respectively versus 5.17 per cent and 1.48 per cent in elderly patients, respectively.29, 30 The decrease in anaesthetic requirements could be due to decreased cell density, decreased cerebral oxygen consumption and decreased cerebral blood flow. Awakening occurs at lower end-tidal concentrations of isoflurane and sevoflurane in the elderly. Awakening concentrations decrease at a similar rate as the decrease in MAC with increasing age. Therefore, the ratios of awakening concentration to MAC are fairly constant, being 0.34 for both sevoflurane and isoflurane.31
The rate of uptake of inhaled agents is dependant on both ventilation and cardiac output. In the elderly, minute ventilation decreases because of reduced metabolic rate. The simultaneous decrease in cardiac output will counteract decreased alveolar ventilation and decreased blood-gas partition coefficient. The overall effect is that the rate of uptake of inhaled agents is not markedly changed by aging. It has been demonstrated that arterial wash-in of isoflurane occurred at the same rate in healthy elderly patients as in the young despite the physiological changes (Fig. 1.3).32 Although aging delays elimination of inhaled anaesthetics and increases the apparent volume of distribution at steady state,33 the fall in end-tidal concentrations occurs at the same rate in the young and the elderly for the first 24 hours after anaesthesia.
These changes might be due to decreased tissue perfusion and an increase in the fat/lean body weight ratio in the elderly. It is likely that the use of less soluble halogenated agents should minimize the effects of ageing.
Opioids
The dose requirements of opioids are decreased and their effects are more prolonged in the elderly because the elimination half life of 12commonly used drugs is prolonged (Table 1.2). However, they show an opposite pattern to that of intravenous hypnotics because the main mechanism of increased sensitivity to narcotics in the elderly is primarily, increased brain sensitivity. It has been found that dose requirement for fentanyl and alfentanil decreased by approximately 50 per cent with increasing age. Using the EEG as a measure of opioid effect, the concentration associated with 50 per cent of maximal EEG response was significantly decreased in the elderly.34
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When using clinical end points (heart rate, blood pressure, movements or swallowing) after surgical stimulation, Lemmens et al were unable to demonstrate an effect of age on the plasma concentration-effect relationship of alfentanil. However, the dose requirement in elderly patients was 25 per cent lower than in the younger patients.35 It is likely that the increased sensitivity in older patients may be due to the change in the number of opiate receptors or opiate receptor binding (Fig. 1.4). In contrast to other agents, pharmacokinetic parameters did not correlate with age for fentanyl.
The only minor change was a slight decrease of the rapid intercompartmental clearance. The only change in alfentanil pharmacokinetics was a decrease of total body clearance with age, volumes of distribution being unchanged.36 To summarize, for pharmacodynamic reasons, fentanyl and alfentanil are about twice as potent in elderly as compared to younger patients. However, offset will be as rapid in elderly patients as in younger patients when an appropriately reduced dose is given.
Pharmacokinetic parameters were not found to differ significantly for sufentanil in elderly patients when compared to younger patients with the exception of a smaller central compartment volume in the elderly.37
The age-related differences in the action of sufentanil in their study cannot be accounted for by the observed differences in the initial volume of distribution which may only affect the plasma concentrations for the first few minutes. Helmers et al confirmed that the sufentanil plasma concentration-time curves for young adult and elderly patients could be superimposed.38 It is likely that alterations in pharmacodynamic effects explain the prolonged sufentanil effect observed in the elderly.
The volume of the central compartment and the plasma clearance has been shown to decrease by 20 to 30 per cent from age 20 years to 80 years respectively. As already described for fentanyl and alfentanil, the concentration required to obtain a predetermined EEG effect is reduced by 50 per cent in the elderly.39
The increase of the half-time of plasma-effect site equilibration might prolong the onset and offset of the drug in the elderly. When the dose of remifentanil has been appropriately reduced, elderly patients should recover as fast as younger subjects.
Muscle Relaxants
There is no difference in the initial dose requirement for non depolarising muscle relaxants in the elderly. The ED95 for pancuronium was 0.078 mg/kg and 0.081 mg/kg in middle-aged adults and elderly patients, respectively.40 The dose-response curves of atracurium, pancuronium and vecuronium were slightly shifted to the right for the adult subjects, however, there was no significant difference.41 After a bolus dose of pancuronium, no significant difference was observed at any of the plasma concentrations corresponding to a fixed degree of neuromuscular block. These findings confirm that non depolarising muscle relaxants are as potent in elderly as in young adult patients. The onset of neuromuscular block can be delayed and can be correlated 14with age. This age-related effect is probably caused by circulatory factors such as a decrease in cardiac output and an increase in circulation time in the elderly.42 The onset of neuromuscular block of rocuronium was prolonged to 3.7 from 3.1 min in the elderly. Similarly, the onset of cisatracurium is approximately a minute longer in the elderly.43 A prolongation of the duration of action of non-depolarising muscle relaxants and a decrease in dose requirements for the maintenance of neuromuscular block has been observed with several currently available muscle relaxants in the elderly. These results are explained by pharmacokinetic changes in the elderly. The distribution and elimination may be altered by anyone of the multitude of physiological changes that accompany the ageing process. These changes include an increase in body fat and decreases of the lean body mass, total body water, renal blood flow, glomerular filtration and hepatic blood flow. Pancuronium has a delayed recovery in the elderly because of decreased plasma clearance secondary to delayed urinary excretion. The clinical duration of action was prolonged from 44 to 73 minutes in elderly patients. The dose requirements of vecuronium to maintain a constant neuromuscular block were decreased by approximately 36 per cent in patients over 60 years and spontaneous recovery was significantly longer in the older patients.44 Lien et al have shown that plasma clearance was reduced by more than 50 per cent and elimination half-life prolonged by 60 per cent in the elderly patients. The prolongation of action of vecuronium appears to be secondary to decreased drug elimination consistent with age-associated decrease in hepatic and renal blood flows.45 The duration of action of rocuronium and the recovery index are also increased in the elderly. The prolongation of action can be explained by a 27 per cent decrease in plasma clearance.
Atracurium has multiple routes of elimination. Degradation by Hofmann elimination and ester hydrolysis is independent of the liver and the kidney and is not affected by age. Consequently, the dose requirement during a continuous infusion, the duration of action and the recovery index are independent of age. Cisatracurium is mainly eliminated by Hofmann elimination. Unlike atracurium, cisatracurium does not undergo hydrolysis by non-specific esterases. The minor differences in the pharmacokinetics of cisatracurium between elderly and young patients are not associated with significant changes in the duration of action or the recovery profile. Although elderly patients have about 30 per cent decrease of plasma cholinesterase, it is unlikely that succinylcholine metabolism is affected by these changes.
It has been demonstrated that the duration of action of neostigmine is prolonged in the elderly. The duration of maximal response to 15neostigmine increased from 11 to 32 minutes in the elderly.46 A shift to the right of the dose-response relationship for neostigmine antagonism of vecuronium-induced neuromuscular block in the elderly has been shown.47
EMERGENCE
End tidal gas monitoring significantly underestimates brain concentration of inhaled agents during emergence. This hysteresis effect is more marked with the more soluble agents isoflurane and sevoflurane than desflurane. Failure to take this into account leads to prolonged emergenqce. Use of beta blockers towards the end of surgery helps in giving haemodynamic stability when inhalation agents are being withdrawn.48
Postoperative Cognitive Dysfunction (POCD)
Aging CNS with reduced functional reserve makes the elderly patient more POCD susceptible. Acute disturbance in consciousness and cognitive function is twice as common in the elderly as the young adults. The symptoms for POCD may be related to, further decreases in already low levels of neurotransmitters. Under anaesthesia etiological factors are hypotension, hypoxia, drug interaction, depression, dementia, alcohol abuse and metabolic disturbances. Anaesthetics which can produce delirium are ketamine, benzodiazepines and propofol, anticholinergics, atropine and scopolamine. Preoperative neurological disease increases the POCD incidence. Risk factors are increasing age, duration of anaesthesia, second surgery, postoperative infection, preoperative neurologic disease and respiratory compromise. No particular anaesthesia technique is implicated. The fact is that not much is known as to what anaesthetic drugs or techniques do to the elderly brain, and in what way their actions are different from their actions on the younger brain.28 Until more definitive studies are available, it is better to avoid hypoxia, hypercarbia and provide adequate postoperative pain relief.3,15,17
Postoperative Pain
Inadequately controlled postoperative pain can lead to slow recovery and POCD consequently.49 The physicians are hesitant to give a “good” dose of pain medication because of the side effects of narcotics. Dementia, aphasia and cognitive impairment renders it very difficult for the physician to assess the level of pain. For geriatric patients, the oral route is simple and cost effective as intramuscular injections are painful, and absorption is unpredictable due to less muscle and more 16fat. Parenteral non steroidal anti-inflammatory drugs/opiods with short half lives can be prescribed for mild to moderate pain, being careful of gastro-intestinal, renal and platelet effects. Pethidine should be used with caution as its metabolites rely on renal elimination. It is best to start with 25 to 50 per cent of usual adult dose and the patients should be monitored for excessive sedation and respiratory depression.
FUTURE DIRECTIONS
Aging is an all-encompassing, multifactorial process that results in a decreased capacity for adaptation and a gradual decrease in functional reserve of many of the organ systems. Different individuals age in different ways and different degrees, thus their anaesthetic requirements need to be individualised. Intensity of monitoring during and following anaesthesia will likely be greater than that selected for younger patients but should be determined on an individual basis taking into consideration the patient's condition and proposed surgical procedure. Also, there is need for guidelines for the management of pain in the elderly. By offering geriatric patients the safest anaesthetic possible that is customized to their needs, we can contribute to the revolutionary increase in lifespan of our citizenry and directly enhance not only the lifespan but in maintaining qualitatively as good a function as possible up to the end of life.
CONCLUSIONS
A thorough understanding of the physiological changes that occur with aging and the altered pharmacokinetic and pharmacodynamic responses of the elderly to a variety of anaesthetic drugs is necessary in the design of an optimal anaesthetic technique for an elderly patient. Many of the drugs used during anaesthesia have a greater initial effect and a more prolonged effect in elderly patients. The adage “start low, go slow” still holds true, however, individualized care, knowledge of the effects of coexisting disease and careful titration of drugs and greater vigilance must be exercised in dealing with elderly surgical patients.
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