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Postoperative Delirium After Hip Fracture
Benjamin D. Robertson, MD1; Timothy J. Robertson, MD2
1 Department of Orthopaedic Surgery, University of Minnesota, 2450 Riverside Avenue South, Suite R200, Minneapolis, MN 55454. E-mail address: benbeckyr@yahoo.com
2 Behavioral Health Department, Luther Midelfort/Mayo Health System, 1400 Bellinger Street, Eau Claire, WI 54702-1510
View Disclosures and Other Information
The authors did not receive grants or outside funding in support of their research for or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

The Journal of Bone and Joint Surgery, Incorporated
J Bone Joint Surg Am, 2006 Sep 01;88(9):2060-2068. doi: 10.2106/JBJS.F.00049
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Image Not Available A hip fracture is sustained by 250,000 Americans every year. The most common complication associated with hip fracture is delirium.Image Not Available Delirium is a serious medical condition that consists of a disturbance of consciousness with a reduced ability to focus, sustain, or shift attention.Image Not Available Multiple studies have shown that patients with postoperative delirium are less likely to return to their preinjury level of function, are more frequently placed in nursing homes, and ultimately have an increased rate of mortality.Image Not Available Delirium can be completely prevented in up to one-third of at-risk patients. When delirium cannot be prevented, the prevalence of severe delirium can be reduced by up to 50%.Image Not Available Optimal treatment of delirium requires excellent teamwork among the orthopaedic surgeon, anesthesiologist, internist or geriatrician, and others.
Image Not Available A hip fracture is sustained by 250,000 Americans every year. The most common complication associated with hip fracture is delirium.
Image Not Available Delirium is a serious medical condition that consists of a disturbance of consciousness with a reduced ability to focus, sustain, or shift attention.
Image Not Available Multiple studies have shown that patients with postoperative delirium are less likely to return to their preinjury level of function, are more frequently placed in nursing homes, and ultimately have an increased rate of mortality.
Image Not Available Delirium can be completely prevented in up to one-third of at-risk patients. When delirium cannot be prevented, the prevalence of severe delirium can be reduced by up to 50%.
Image Not Available Optimal treatment of delirium requires excellent teamwork among the orthopaedic surgeon, anesthesiologist, internist or geriatrician, and others.
A hip fracture is sustained by 250,000 Americans every year1, and that number is expected to double by 20402. The most frequent complication associated with hip fracture in elderly patients is postoperative delirium3, with a prevalence ranging between 5% and 61%, depending on the patient population1,3-8. Delirium is often undetected, misdiagnosed, or undertreated9-11. However, this condition has severe consequences for the patient4,5,11. The focus of this article is to provide an overview of current knowledge regarding the outcomes, pathogenesis, diagnosis, prevention, and treatment of postoperative delirium in elderly patients treated for a hip fracture.
For the purposes of this article, delirium and acute confusional states are synonymous. Delirium consists of a "disturbance of consciousness.... with reduced ability to focus, sustain, or shift attention." There is also "a change in cognition... or the development of a perceptual disturbance that is not better accounted for by a preexisting, established, or evolving dementia."12 The diagnostic criteria for delirium have been established by the American Psychiatric Association (Table I)12. It is important to be aware of, and to use, these criteria because many of the signs and symptoms of delirium are also associated with conditions such as dementia, depression, and psychosis. Table II summarizes some of the distinguishing characteristics of these diagnoses13.
 
Anchor for JumpAnchor for JumpTABLE I  Diagnostic Criteria for Delirium*
Disturbance in consciousness (impaired ability to focus, sustain, or shift attention)
Change in cognition (memory impairment, disorientation, or language disturbance) or perceptual disturbance (misinterpretations, illusions, or hallucinations)
The disturbance develops over a short period of time and fluctuates during the course of the day
There is laboratory or clinical evidence that the delirium state is caused by the direct physiological consequences of a general medical condition
Adapted from: Delirium, dementia, and amnestic and other cognitive disorders. In: Diagnostic and statistical manual of mental disorders: DSM-IV. 4th ed, text revision. Washington, DC: American Psychiatric Association; 2000. p 135-80.
 
Anchor for JumpAnchor for JumpTABLE II  Distinguishing Characteristics of Delirium, Dementia, Psychotic Disorders, and Depression*
Disorder Distinguishing Feature Associated Symptoms Course
Delirium Fluctuating levels of consciousness with decreased attention Disorientation, visual hallucinations, agitation, apathy, withdrawal, impairment in memory and attention Acute onset; most cases remit with correction of underlying medical condition
Dementia Memory impairment Disorientation, agitation Chronic, slow onset, progressive
Psychotic disorders Deficits in reality testing Social withdrawal, apathy Usually slow onset with prodromal syndrome; chronic with exacerbations
Depression Sadness, loss of interest and pleasure in usual activities Disturbances of sleep, appetite, concentration, and energy; feelings of hopelessness and worthlessness; thoughts of suicide Single episode or recurrent episodes; may be chronic
Reprinted, with permission, from: Gleason OC. Delirium. Am Fam Physician. 2003;67:1027-34.
Deep vein thrombosis and the subsequent risk of death from pulmonary embolus have received a great deal of attention in the orthopaedic literature. The morbidity and mortality associated with postoperative delirium are far greater than those associated with deep vein thrombosis6, and yet postoperative delirium has received very little attention in the orthopaedic literature.
Gustafson et al. studied 111 consecutive patients who had undergone surgery for a femoral neck fracture6. They evaluated the patients for preexisting dementia and, with use of the DSM-III6 (Diagnostic and Statistical Manual of Mental Disorders, Third Edition), examined them preoperatively and postoperatively for the development of delirium. Sixty-eight (61%) of the 111 patients became acutely confused: 33% were in an acute confusional state preoperatively and another 28% were in an acute confusional state postoperatively. Gustafson et al. followed all patients for six months after the operation and found a significant difference in the length of the stay in the hospital (p < 0.05) as well as in postoperative complications such as urinary incontinence (p = 0.0005), feeding problems (p = 0.05), and decubitus ulcers (p = 0.01). In addition, patients with delirium had an increased likelihood of dying or being placed in a nursing home for the first time, and they were less likely to regain their prefracture walking level.
In a similar study, Marcantonio et al. evaluated 126 consecutive patients, more than sixty-five years old, who had sustained a hip fracture1. They examined them preoperatively, daily after the operation, and at one and six months postoperatively. Delirium developed in 41% (fifty-two) of the 126 patients; it persisted in fifteen patients at one month and in three patients at six months. Patients who had delirium had a significantly greater decline in activities of daily living (odds ratio, 2.6; 95% confidence interval, 1.1 to 6.1), a significantly greater decline in walking ability (odds ratio, 2.6; 95% confidence interval, 1.03 to 6.5), and a significantly higher rate of death or new placement in a nursing home (odds ratio, 3.0; 95% confidence interval, 1.1 to 8.4) during the follow-up period than those without delirium. In addition, patients whose delirium persisted had worse outcomes in those categories than patients whose delirium resolved.
Edelstein et al. followed 921 patients for the development of delirium after hip fracture5. Although they reported a much lower prevalence (5.1%) than the authors mentioned above, they examined the patients for delirium at only one point in time after the operation and they selected healthier patients with their inclusion and exclusion criteria. They did show that patients with delirium had a significant increase in the length of the overall hospital stay (p < 0.001) and increased mortality (p = 0.02) at one year. In addition, their patients were less likely to regain their prefracture level of walking (p = 0.03) and activities of daily living (p < 0.001).
Medically ill elderly individuals in whom delirium develops during hospitalization have an increased chance of dying during that hospitalization (an 11% rate of death in the first month after discharge and a 25% rate within six months12).
The above reports document the substantial impact of delirium on patient outcomes, with increased rates of mortality or new nursing home placement postoperatively and longer, more expensive14 hospital stays. Prolonged delirium is also a risk factor for the development or worsening of dementia. Finally, delirium is upsetting for the patient and their loved ones. For all of these reasons, delirium requires our attention.
The pathogenesis of delirium is not fully understood. Part of the difficulty in studying delirium stems from the fact that it is transient and may often have multiple underlying causes15-19. Delirium has been considered to be a generalized, nonspecific dysfunction of the higher cortical processes because electroencephalograms of delirious patients have shown diffuse slowing16,18. However, studies of animals15 as well as studies of lesions in patients who have sustained a stroke or traumatic brain injury and functional brain imaging in humans18 offer insight regarding which areas of the brain and which neurotransmitters are primarily affected.
 
Anchor for JumpAnchor for Jump
+Fig. 1A schematic diagram showing how various risk factors can affect acetylcholine and dopamine levels, leading to delirium. ACH = acetylcholine, DA = dopamine, and HOTN = hypotension.
Similar to specific tracts in the spinal cord, there are tracts within the brain that are involved in our higher cortical functioning. These tracts are best thought of as parallel yet integrated circuits19,20. Wakefulness, attention, mood, and sleep appear to require sustained coherent activity in these various corticothalamic networks. These neural networks seem to be uniquely sensitive to the metabolic and other changes that are thought to generate delirium. Areas in the parietal and temporal cortices related to attention as well as in the reticular activating system in the brainstem are also affected18-23.
Within the brain, there are a number of neurotransmitters that are responsible for overall brain function15-18,24. There are two major neurotransmitters: gamma-aminobutyric acid, which is inhibitory, and glutamate, which is excitatory. There are also four modulatory neurotransmitters that are very important in brain function and dysfunction: acetylcholine, dopamine, serotonin, and norepinephrine. Psychiatrists target these modulatory neurotransmitters with various psychotropic medications in order to treat psychiatric illnesses25-27. Alterations in each of these neurotransmitters have been found in patients with delirium15-19. In addition, these neurotransmitter systems are not mutually exclusive but interact extensively24.
A decrease in acetylcholine and an increase in dopamine appear to have important roles in the development of delirium15,17,19. Decreased acetylcholine is also found in dementia28. Acetylcholine is important in arousal, attention, memory, and rapid eye movement (REM) sleep, all of which can be affected during delirium15,17,19. Delirium can be induced experimentally by administering anticholinergic drugs, and it can be reversed by administering physostigmine (a cholinergic agent) or antipsychotic medications such as haloperidol19. Furthermore, serum levels of anticholinergic activity, which are usually measured only in research settings, are increased during delirium, and higher levels correlate with greater cognitive impairment. Dopamine, on the other hand, is thought to change reciprocally with acetylcholine15,19; intoxication with dopamine can induce delirium19. The use of postoperative opiates can contribute to delirium by increasing dopamine activity while decreasing acetylcholine levels19. Hypoglycemia or hypoxia also can result in decreased levels of acetylcholine and, in susceptible individuals, delirium19,29,30. Finally, anything that causes an inflammatory response, such as infection, trauma, or operative intervention, causes the release of cytokines15,17. Cytokines, which include interleukins, tumor necrosis factor (TNF), and interferon-alpha, also increase dopamine levels and decrease acetylcholine levels15,17,31.
The impact of aging on the brain also needs to be considered17. With aging, there are morphologic changes in the brain, including a decrease in overall volume, a decrease in the number and volume of neurons, and a loss of dendrites and synapses. In addition to these morphologic changes, there are hormonal changes, such as an increased basal level of cortisol. Also, there is an overall decrease in the level of acetylcholine as a result of a decrease in choline acetyl transferase activity, which is important in acetylcholine synthesis, combined with no change in acetylcholinesterase, the enzyme responsible for acetylcholine breakdown. This decrease in acetylcholine contributes to the memory impairment that occurs with aging and, in a more pronounced way, with Alzheimer's dementia. Lastly, there is an increase in the basal release of dopamine. The result of these age-related changes is a decreased brain reserve for handling metabolic and other stresses. The impact of various risk factors on the levels of acetylcholine and dopamine is summarized in Figure 15,17,32,33.
Diagnosing delirium requires a high index of suspicion, with an understanding that delirium will develop in nearly 50% of patients who have sustained a hip fracture. Use of the DSM-IV-TR (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision) criteria (Table I) or an instrument such as the CAM (Confusion Assessment Method) algorithm (Table III)11,16 at the bedside increases the likelihood of making the correct diagnosis7,11,15,34. The CAM, which is based on DSM-III-R criteria, has been validated in a number of settings11,15,34. It has high sensitivity and specificity and can be administered in approximately two to five minutes11,15. As part of the assessment for symptoms of delirium, it is important to understand the patient's baseline level of cognitive and other functioning. If the patient is not displaying symptoms of delirium on admission, baseline cognitive functioning can be assessed at that time with use of the Mini-Mental State Examination35. This simple examination is easy to administer and should be part of the preoperative evaluation36. Baseline functioning can also be determined by interviewing family members and reviewing medical records.
 
Anchor for JumpAnchor for JumpTABLE III  Confusion Assessment Method (CAM) Diagnostic Algorithm*†
Feature 1: acute onset and fluctuating course This feature is usually obtained from a family member or nurse and is shown by positive responses to the following questions: Is there evidence of an acute change in mental status from the patient's baseline? Did the (abnormal) behavior fluctuate during the day, that is, tend to come and go, or increase and decrease in severity?
Feature 2: inattention This feature is shown by a positive response to the following question: Did the patient have difficulty focusing attention, for example, being easily distractible, or having difficulty keeping track of what was being said?
Feature 3: disorganized thinking This feature is shown by a positive response to the following question: Was the patient's thinking disorganized or incoherent, such as rambling or irrelevant conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject?
Feature 4: altered level of consciousness This feature is shown by any answer other than "alert" to the following question: Overall, how would you rate the patient's level of consciousness? (alert [normal]), vigilant [hyperalert], lethargic [drowsy, easily aroused], stupor [difficult to arouse], or coma [unarousable])
Reprinted with permission 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. 1990:113:941-8. †The diagnosis of delirium by CAM requires the presence of features 1 and 2 and either 3 or 4.
Symptoms such as agitation, delusions, or hallucinations are easy to observe but are present in only a minority of cases4. The more common, or core, symptoms are reduced clarity of awareness of the environment with a reduced ability to focus, shift, or sustain attention and cognitive changes such as memory loss, disorientation, or changes in language, including rambling, incoherent, or difficult-to-follow speech7. These findings can be more subtle and in part account for missed diagnoses. Also, recognizing delirium as it is developing may be helpful37. Disorientation and urgent calls for attention by the patient are the most predictive prodromal changes38.
When a diagnosis of delirium is being considered during the perioperative period for a patient with a hip fracture, it is important to keep in mind the differential diagnosis of alcohol withdrawal, delirium tremens, or fat emboli syndrome39,40. These conditions will be discussed only briefly because they are not the focus of this article.
Alcohol withdrawal occurs primarily in heavy drinkers (more than five drinks per day). It is essential to obtain a history regarding alcohol (or other substance) abuse from the patient and family members in order to be alert to the possibility of alcohol or other withdrawal syndromes. Withdrawal symptoms generally begin five to ten hours after the last drink, peak within forty-eight to seventy-two hours, and subside within five to seven days, although they can last longer. Postoperative pain medication can mask withdrawal symptoms as can concurrent illness or an operation39.
Alcohol withdrawal is characterized by symptoms of autonomic hyperactivity such as diaphoresis; tachycardia; systolic hypertension; hand and body tremors; transient tactile, auditory, or visual hallucinations; anxiety; nausea and vomiting; psychomotor agitation; and occasionally seizures. A patient undergoing alcohol withdrawal is alert, oriented, aware of his or her environment, and able to attend. In patients with delirium tremens, alcohol withdrawal is complicated by frank delirium39.
Fat emboli syndrome occurs within twenty-four to forty-eight hours following femoral neck fracture in 0.5% to 3% of individuals. It is characterized by pulmonary distress, changes in mental status, and a petechial rash in nondependent areas such as the axillae, the anterior surface of the neck, the chest, the area around the navel, and the conjunctiva and oropharynx. There can also be fever, tachycardia, jaundice, renal changes, and retinal changes40.
Often, delirium is preventable or its severity can be lessened, but unfortunately there is no single intervention that has been shown to prevent delirium1,7,37. Instead, reducing the incidence and severity of delirium relies on optimizing the medical and surgical care of the patient1,7,37 in order to maximize neuronal functioning. If delirium does develop, treatment then centers on supportive care and identifying and addressing the underlying cause or causes1,41.
Most surgeons direct the postoperative pain control for their patients. Opiates can contribute to delirium by increasing dopamine levels and decreasing acetylcholine levels16,19. However, Morrison et al. demonstrated that delirium can also be associated with too little pain control3. They used multiple logistic regression analysis to identify risk factors in a study of 541 patients with a hip fracture. Severe pain significantly increased the risk of delirium (risk ratio, 9; 95% confidence interval, 1.8 to 45.2). In addition, delirium was more likely to develop in patients who received <10 mg of parenteral morphine sulfate equivalents per day than it was in patients who received more analgesia (risk ratio, 5.4; 95% confidence interval, 2.4 to 12.3). Finally, patients who received meperidine (Demerol) were at increased risk for the development of delirium compared with those who received other opioid analgesics (risk ratio, 2.4). This was probably due to the anticholinergic effects of meperidine.
The type of anesthesia administered does not appear to affect the development of delirium. In the same study by Morrison et al.3, there was no significant difference between the delirium rates associated with regional and general anesthesia. Gustafson et al.6 showed a trend toward increased delirium with spinal anesthesia; however, it was not significant. They found that a drop in blood pressure below 80 mm Hg was more important, and this more commonly occurred with spinal anesthesia. Approximately 90% of their patients who had this decrease in blood pressure went on to have delirium6,33. Edelstein et al.5 reported a higher prevalence of delirium with general anesthesia and postulated that that higher prevalance may be due to cerebral hypoxia during general anesthesia. However, it appears that the ability to maintain oxygen delivery to the brain during surgery is more important than the type of anesthesia administered.
Other investigators have concentrated more on optimizing the perioperative medical care of patients with a hip fracture in an attempt to decrease the prevalence of delirium. The intervention reported by Gustafson et al.33 consisted of preoperative and postoperative geriatric assessments as well as aggressive management of perioperative conditions and postoperative complications. The prevalence of delirium decreased from 61.3% in their observational cohort to 47.6% in their intervention group (p < 0.05). The prevalence of severe delirium was also significantly lower in their intervention group (30% compared with 7%) (p < 0.0001). The hospital stay decreased from seventeen to eleven days (p < 0.001), and rates of postoperative complications such as urinary retention, decubitus ulcers, and severe falls all decreased.
Milisen et al.42 evaluated the impact of increased involvement by nurses on delirium in a prospective, randomized study of two groups of sixty patients with a hip fracture. Their intervention consisted of educating nursing staff to recognize delirium, systematic cognitive screening of patients, a scheduled pain protocol, and the availability of a consulting geriatric nurse or physician. Although they did not find a significant decrease in the prevalence of delirium, they did observe a significant decrease in the duration (p = 0.03) and severity (p = 0.015) of delirium.
Marcantonio et al.8 performed a prospective, randomized, blinded study to investigate the effect of a structured geriatrics consultation on the development of delirium after hip fracture surgery. The intervention group received a proactive geriatrics consult either preoperatively or within twenty-four hours after surgery. The geriatrician made daily visits for the duration of the hospital stay and gave targeted recommendations based on a structured protocol. The prevalence of delirium was 32% in the intervention group compared with 50% in the usual-care group (p = 0.04), and the prevalence of severe delirium was decreased as well (12% compared with 29%). This study emphasized that delirium can be prevented or lessened in many patients but that there is no single intervention that consistently prevents delirium. Efforts to prevent delirium need to focus on minimizing the number of metabolic or other potential central nervous system insults that the patient experiences once admitted to the hospital. A patient's age, cognitive status, fracture, or need for surgery cannot be prevented. In some patients, these four factors alone will be sufficient to induce delirium. However, some patients have enough brain reserve to withstand these insults, and it is other insults, such as a decrease in blood pressure, hypoxia, urinary tract infection, or uncontrolled pain, that eventually trigger delirium. Reducing or eliminating these insults can prevent delirium in many patients or can decrease its severity.
If delirium does develop, treatment then focuses on supportive care, identification of likely precipitants, and treatment of any underlying causes that can be corrected (Table IV)8,33,41. This generally involves a dedicated team including the orthopaedic surgeon, nursing staff, and consulting specialist(s) with experience and expertise in diagnosing and treating delirium. Medical management must be reviewed and optimized, and the team must systematically rule out potential causes of new-onset delirium. Table V provides an organized approach for prevention and treatment of delirium in patients with a hip fracture.
 
Anchor for JumpAnchor for JumpTABLE IV  Important Laboratory Studies To Consider in Work-up for Patients with Delirium
Laboratory Tests To Evaluate
Complete blood-cell count with differential Anemia, infection
Complete metabolic profile Electrolyte disturbance, dehydration, glucose level, kidney or liver abnormalities
Albumin Nutritional deficiency
Urinalysis/culture Urinary tract infection
Chest radiograph Pneumonia, congestive heart failure
Serum ammonia* Hepatic encephalopathy
Thyroid-stimulating hormone and free T4* Thyroid dysfunction
Urine toxicology* Benzodiazepines, tricyclic antidepressants, opioids
Computed tomography scan or magnetic resonance imaging of head* Stroke, hemorrhage, hematoma, space-occupying lesion
Spinal tap* Central nervous system infection
If indicated by history.
 
Anchor for JumpAnchor for JumpTABLE V  An Organized Approach to the Prevention and Treatment of Delirium in Patients with Hip Fracture
Ensure adequate central nervous system oxygen delivery
    Give supplemental oxygen to keep saturation >95%
    Keep systolic blood pressure >90 mm Hg
    Keep hematocrit >30%
Restore fluid and electrolyte balance
Treat pain
Assess and promote adequate bowel and bladder function
Evaluate medications (including herbal supplements or over-the-counter medications)
    Be alert to recently added medication with anticholinergic or dopamine-increasing properties
    If delirium develops, reduce or eliminate noncritical medication; watch for discontinuation or withdrawal effects
Assess nutritional intake
    Provide dentures, supplements, or nasogastric tube feeding if needed
Provide early mobilization and rehabilitation
Provide appropriate environmental stimuli
    Glasses, hearing aids, clock, calendar, light
Actively manage concurrent medical conditions and postoperative complications
    Myocardial infarction or stroke
    Arrhythmias
    Congestive heart failure, chronic obstructive pulmonary disease
    Liver or renal disease
    Gastrointestinal bleeding
    Urinary tract infection
    Central nervous system conditions like dementia, Parkinson disease, epilepsy
Physical examination should include measurement of vital signs with pulse oximetry, assessment of signs suggestive of alcohol withdrawal, and an investigation for evidence of fat emboli syndrome. It is also important to look for any localizing signs of wound or other infections and to assess hydration. Thyroid, heart, lung, abdominal (including the lower abdomen because a distended bladder can be evidence of anticholinergic excess), and neurological examinations are important as well. A rectal examination is recommended if there is concern about severe constipation or impaction15,16,36,41. Important laboratory and radiographic studies are listed in Table IV.
Any pertinent abnormalities identified through a review of the history, a review of systems, or physical and laboratory examinations should be corrected, with a focus on adequate oxygenation, restoring fluid and electrolyte balance, treating pain, eliminating or weaning the patient off of unnecessary medications, regulating bowel and bladder function, providing adequate nutritional intake, mobilizing the patient if possible, addressing any vision or hearing impairments, normalizing the sleep-wake cycle, and providing appropriate environmental stimuli, reassurance, orientation, and support8,15,16,37,41. Regarding pain control, the natural response when a patient has delirium is to withdraw narcotic medication. However, as Morrison et al.3 demonstrated, inadequate pain control may also contribute to delirium.
If the underlying cause or causes of delirium are corrected, the course of the delirium is often self-limited and the patient recovers completely. If the cause or causes persist, delirium can persist and progress to dementia. Although dementia is a risk factor for delirium, delirium is also a risk factor for dementia9,43. Thus, the prognosis for an episode of delirium appears to improve when the duration is shorter8.
If a patient with delirium is agitated, delusional, or hallucinating or is too inattentive or confused to cooperate with treatment, adjunctive medication may be needed15,36,41. Treating these symptoms can diminish the patient's distress, decrease the risk of patient injury, and reduce excessive energy expenditure. The most frequently used and studied medication in this situation is Haldol (haloperidol), a first-generation antipsychotic medication, although there are few studies to guide treatment15,35,36,41. Haldol; the second-generation antipsychotic medications Zyprexa (olanzapine), Risperdal (risperidone), Seroquel (quetiapine fumarate), and Geodon (ziprasidone); or the third-generation antipsychotic agent Abilify (aripiprazole) can help to reduce confusion, agitation, or hallucinations by decreasing dopamine levels, thereby improving the acetylcholine-todopamine ratio. Because there is a small risk of potentially fatal torsade de pointes (ventricular tachycardia characterized by polymorphic QRS complexes) with intravenous Haldol, baseline and follow-up electrocardiograms (to look for prolongation of the QTc interval) and serum potassium and magnesium monitoring are needed41. Safety is further increased by utilizing continuous cardiac telemetry monitoring19.
The newer antipsychotic agents can be more difficult to regulate than Haldol, which has minimal anticholinergic side effects and no active metabolites44. The newer antipsychotic agents also have pharmacologic effects beyond reducing dopamine levels44 that can make it difficult to determine whether they are diminishing or exacerbating delirium. They are sometimes utilized on a scheduled basis with use of Haldol as an as-needed agent for breakthrough symptoms45.
In addition to extrapyramidal side effects (muscle tightening or Parkinson symptoms), antipsychotic medication can cause akathisia (a subjective sense of restlessness and an inability to sit still) or, rarely, neuroleptic malignant syndrome (which consists of a high fever, muscle rigidity, and autonomic instability). Tardive dyskinesia (abnormal movements of the tongue, mouth, arms, legs, and trunk) primarily occurs with long-term use but can occur with short-term use. Elderly women constitute a group at high risk for tardive dyskinesia44. Also, the United States Food and Drug Administration (FDA) recently determined that second and third-generation antipsychotic medications are associated with a 1.6 to 1.7-fold increase in death (from cardiac-related events such as heart failure or sudden death, or infections, especially pneumonia) of elderly patients with dementia when used to treat behavioral disorders46. The FDA is considering adding a similar warning to Haldol and other first-generation antipsychotics46. Zyprexa and Risperdal are also associated with a small risk of stroke and other adverse cerebrovascular events in elderly patients with dementia47,48. Because of these possible adverse effects, antipsychotic medication should be carefully titrated to the most effective dose and used only as long as it is needed to control the above-noted deleterious behaviors associated with delirium.
Other medications, such as benzodiazepines or physostigmine, are used less frequently41. Benzodiazepines are useful for managing alcohol or sedative-hypnotic withdrawal and delirium tremens39. They can also be used to augment antipsychotic medication in the treatment of delirium when larger doses appear to be needed41. Benzodiazepines are usually not effective as monotherapy for general cases of delirium and can cause behavioral disinhibition, especially in the elderly41. Physostigmine, which is a cholinergic medication, is useful only if the delirium is known to be caused by an anticholinergic medication41. Physostigmine is associated with a higher risk of side effects, including seizures, bradycardia, asystole, bronchospasm, and pulmonary edema, than are antipsychotic medications49. Aricept (donepezil) has been occasionally used as a safer alternative to physostigmine in these situations50.
Delirium is a serious medical condition that consists of a disturbance of consciousness with a reduced ability to focus, sustain, or shift attention. There are also cognitive and/or perceptual changes. Delirium generally develops over a period of hours to days and tends to fluctuate over the course of the day. It is a frequent and dangerous complication of hip fracture in the elderly that has received little attention in the orthopaedic literature. However, multiple studies1,5,6 have shown that postoperative delirium following hip fracture is associated with prolonged hospital stays, higher costs, and poor outcomes. Patients who experience delirium are less likely to return to their prefracture level of walking or activities of daily living. They are also substantially more likely to be placed in a nursing home for the first time and to die.
Although the pathophysiology of delirium is not fully understood, it appears that multiple metabolic and neurochemical insults disrupt neuronal functioning in susceptible areas, especially in the corticothalamic networks. These insults commonly lead to an imbalance in the dopamine-to-acetylcholine ratio in these important brain regions. Prevention and optimal treatment consist of minimizing or correcting these metabolic and other insults. Maintaining oxygen saturation at >90%, systolic blood pressure at >90 mm Hg, and the hematocrit at >30% is important, as is attention to the fluid and electrolyte status. Pain control, careful review of the patient's medications, regulation of bowel and bladder function, adequate nutritional intake, early mobilization and rehabilitation, appropriate environmental stimulation, and normalization of the patient's sleep-wake cycle are also key. Early detection of coexisting or postoperative medical problems, infections, or other complications is crucial. Antipsychotic medication can be used to reduce agitation that interferes with the patient's ability to cooperate with treatment, places the patient in danger of harm, or excessively increases metabolic demands.
There is no single intervention that can eliminate delirium. Treatment and, when possible, prevention require awareness of the diagnosis, reduction or elimination of modifiable risk factors, early diagnosis and treatment, and excellent teamwork among the orthopaedist, anesthesiologist, nursing staff, and other consulting medical specialists.
Note: The authors thank Dr. Marc Swiontkowski and Dr. Terence Gioe.
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Marcantonio ER, Flacker JM, Wright RJ, Resnick NM. Reducing delirium after hip fracture: a randomized trial. J Am Geriatr Soc. 2001;49: 516-22.49516  2001  [CrossRef]
 
Cole MG. Delirium in elderly patients. Am J Geriatr Psychiatry. 2004;12: 7-21.127  2004  [PubMed]
 
Stiefel F. Delirium: is the confusion slowly clearing up [editorial]. Support Care Cancer. 1996;4: 325-6.4325  1996  [PubMed][CrossRef]
 
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: 941-8.113941  1990 
 
Delirium, dementia, and amnestic and other cognitive disorders. In: Diagnostic and statistical manual of mental disorders: DSM-IV. 4th ed, text revision. Washington, DC: American Psychiatric Association; 2000. p 135-80.135  2000 
 
Gleason OC. Delirium. Am Fam Physician. 2003;67: 1027-34.671027  2003 
 
Webster JR, Chew RB, Mailliard L, Moran MB. Improving clinical and cost outcomes in delirium: use of practice guidelines and a delirium care team. Ann Long-Term Care. 1999;7: 128-34.7128  1999 
 
Samuels SC, Neugroschl JA. Delirium. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 1054-68.1054  2005 
 
Winawer N. Postoperative delirium. Med Clin North Am. 2001;85: 1229-39.851229  2001  [PubMed][CrossRef]
 
van der Mast RC. Pathophysiology of delirium. J Geriatr Psychiatry Neurol. 1998;11: 138-45.11138  1998  [PubMed]
 
Trzepacz PT. The neuropathogenesis of delirium. A need to focus our research. Psychosomatics. 1994;35: 374-91.35374  1994  [PubMed]
 
Trzepacz PT. Delirium. Advances in diagnosis, pathophysiology, and treatment. Psychiatr Clin North Am. 1996;19: 429-48.19429  1996  [CrossRef]
 
Lichter DG, Cummings JL, editors. Frontal-subcortical circuits in psychiatric and neurological disorders. New York: Guilford Press; 2001. Introduction and overview; p 1-43.1  2001 
 
Grebb JA. Neural sciences: introduction and overview. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 1-3.1  2005 
 
Zorumski CF, Isenberg KE, Mennerick SJ. Basic electrophysiology. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 99-115.99  2005 
 
Arnsten AFT, Castellanos FX. Neurobiology of attention regulation and its disorders. In: Martin A, Scahill L, Charney DS, Leckman JF, editors. Pediatric psychopharmacology: principles and practice. New York: Oxford University Press; 2003. p 99-109.99  2003 
 
Bronstein YL, Cummings JL. Neurochemistry of frontal-subcortical circuits. In: Lichter DG, Cummings JL, editors. Frontal-subcortical circuits in psychiatric and neurologic disorders. New York: Guilford Press; 2001. p 59-91.59  2001 
 
Bronstein YL, Cummings JL. Neuropharmacology of frontal-subcortical circuits. In: Lichter DG, Cummings JL, editors. Frontal-subcortical circuits in psychiatric and neurologic disorders. New York: Guilford Press; 2001. p 401-20.401  2001 
 
Voeller KKS. Attention-deficit/hyperactivity disorder as a frontal-subcortical disorder. In: Lichter DG, Cummings JL, editors. Frontal-subcortical circuits in psychiatric and neurologic disorders. New York: Guilford Press; 2001. p 334-72.334  2001 
 
Tecott LH, Smart SL. Monoamine neurotransmitters. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 49-60.49  2005 
 
Neugroschl JA, Kolevzon A, Samuels SC, Marin DB. Dementia. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 1068-93.1068  2005 
 
Magistretti PJ, Pellerin L, Martin J-L. Brain energy metabolism: an integrated cellular perspective. . 2000. 
www.acnp.org/G4/GN401000064

 
Breningstall GN. Oxidative metabolism disorders. In: Swaiman KF, Ashwal S, editors. Pediatric neurology. Principles and practice. St. Louis: Mosby; 1999. p 483-93.483  1999 
 
Gustafson Y. Postoperative delirium: a challenge for the orthopedic team [editorial]. Acta Orthop Scand. 2004;75: 375-7.75375  2004  [CrossRef]
 
Lundstrom M, Edlund A, Bucht G, Karlsson S, Gustafson Y. Dementia after delirium in patients with femoral neck fractures. J Am Geriatr Soc. 2003;51: 1002-6.511002  2003  [PubMed][CrossRef]
 
Gustafson Y, Brannstrom B, Berggren D, Ragnarsson JI, Sigaard J, Bucht G, Reiz S, Norberg A, Winblad B. A geriatric-anesthesiologic program to reduce acute confusional states in elderly patients treated for femoral neck fractures. J Am Geriatr Soc. 1991;39: 655-62.39655  1991 
 
Folstein MF, Folstein SE, McHugh PR. "Mini-mental state". A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12: 189-98.12189  1975  [PubMed][CrossRef]
 
Jacobi J, Fraser GL, Coursin DB, Riker RR, Fontaine D, Wittbrodt ET, Chalfin DB, Masica MF, Bjerke HS, Coplin DW, Crippen DW, Fuchs BD, Kelleher RM, Marik PE, Nasraway SA Jr, Murray MJ, Peruzzi WT, Lumb PD; Task Force of the American College of Critical Care Medicine (ACCM) of the Society of Critical Care Medicine (SCCM), American Society of Health-System Pharmacists (ASHP), American College of Chest Physicians. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill adult. Crit Care Med. 2002;30: 119-41. Erratum in: Crit Care Med. 2002;30:726.30119  2002  [PubMed][CrossRef]
 
Hanson MR, Galvez-Jimenez N. Management of dementia and acute confusional states in the perioperative period. Neurol Clin. 2004;22:vii-viii, 413-22.22413  2004  [CrossRef]
 
Weber JB, Coverdale JH, Kunik ME. Delirium: current trends in prevention and treatment. Intern Med J. 2004;34: 115-21.34115  2004  [CrossRef]
 
Duppils GS, Wikblad K. Delirium: behavioural changes before and during the prodromal phase. J Clin Nurs. 2004:13; 609-16.13609  2004  [CrossRef]
 
Chang PH, Steinberg MB. Alcohol withdrawal. Med Clin North Am. 2001;85: 1191-212.851191  2001  [PubMed][CrossRef]
 
Parisi DM, Koval K, Egol K. Fat embolism syndrome. Am J Orthop. 2002;31: 507-12.31507  2002  [PubMed]
 
Practice guideline for the treatment of patients with delirium. American Psychiatric Association. Am J Psychiatry. 1999;156(5 Suppl): 1-20.1561  1999 
 
Milisen K, Foreman MD, Abraham IL, De Geest S, Godderis J, Vandermeulen E, Fischler B, Delooz H, Spiessens B, Broos P. A nurse-led interdisciplinary intervention program for delirium in elderly hip-fracture patients. J Am Geriatr Soc. 2001;49: 523-32.49523  2001  [PubMed][CrossRef]
 
Olofsson SM, Weitzner MA, Valentine AD, Baile WF, Meyers CA. A retrospective study of the psychiatric management and outcome of delirium in the cancer patient. Support Care Cancer. 1996;4: 351-7.4351  1996  [PubMed][CrossRef]
 
Bezchlibnyk-Butler KZ, Jeffries JJ, editors. Clinical handbook of psychotropic drugs. 15th ed. Ashland, OH: Hogrefe and Huber; 2005. p 102.102  2005 
 
Skrobik YK, Bergeron N, Dumont M, Gottfried SB. Olanzapine vs haloperidol: treating delirium in a critical care setting. Intensive Care Med. 2004;30: 444-9.30444  2004  [PubMed][CrossRef]
 
Deaths with antipsychotics in elderly patients with behavioral disturbances. FDA Public Health Advisory. . 2005. 
www.fda.gov/cder/drug/advisory/antipsychotics.htm

 
Zyprexa. Physicians desk reference. 59th ed. Montvale: 2005. p 1901.1901  2005 
 
Risperdal. Physicians desk reference. 59th ed. Montvale: 2005. p 1743.1743  2005 
 
Physostigmine. Thomson MICROMEDEX. 2005.  2005 
 
Donepezil. Thomson MICROMEDEX. 2005.  2005 
 

Submit a comment

Anchor for JumpAnchor for Jump
+Fig. 1A schematic diagram showing how various risk factors can affect acetylcholine and dopamine levels, leading to delirium. ACH = acetylcholine, DA = dopamine, and HOTN = hypotension.
Anchor for JumpAnchor for JumpTABLE I  Diagnostic Criteria for Delirium*
Disturbance in consciousness (impaired ability to focus, sustain, or shift attention)
Change in cognition (memory impairment, disorientation, or language disturbance) or perceptual disturbance (misinterpretations, illusions, or hallucinations)
The disturbance develops over a short period of time and fluctuates during the course of the day
There is laboratory or clinical evidence that the delirium state is caused by the direct physiological consequences of a general medical condition
Adapted from: Delirium, dementia, and amnestic and other cognitive disorders. In: Diagnostic and statistical manual of mental disorders: DSM-IV. 4th ed, text revision. Washington, DC: American Psychiatric Association; 2000. p 135-80.
Anchor for JumpAnchor for JumpTABLE II  Distinguishing Characteristics of Delirium, Dementia, Psychotic Disorders, and Depression*
Disorder Distinguishing Feature Associated Symptoms Course
Delirium Fluctuating levels of consciousness with decreased attention Disorientation, visual hallucinations, agitation, apathy, withdrawal, impairment in memory and attention Acute onset; most cases remit with correction of underlying medical condition
Dementia Memory impairment Disorientation, agitation Chronic, slow onset, progressive
Psychotic disorders Deficits in reality testing Social withdrawal, apathy Usually slow onset with prodromal syndrome; chronic with exacerbations
Depression Sadness, loss of interest and pleasure in usual activities Disturbances of sleep, appetite, concentration, and energy; feelings of hopelessness and worthlessness; thoughts of suicide Single episode or recurrent episodes; may be chronic
Reprinted, with permission, from: Gleason OC. Delirium. Am Fam Physician. 2003;67:1027-34.
Anchor for JumpAnchor for JumpTABLE III  Confusion Assessment Method (CAM) Diagnostic Algorithm*†
Feature 1: acute onset and fluctuating course This feature is usually obtained from a family member or nurse and is shown by positive responses to the following questions: Is there evidence of an acute change in mental status from the patient's baseline? Did the (abnormal) behavior fluctuate during the day, that is, tend to come and go, or increase and decrease in severity?
Feature 2: inattention This feature is shown by a positive response to the following question: Did the patient have difficulty focusing attention, for example, being easily distractible, or having difficulty keeping track of what was being said?
Feature 3: disorganized thinking This feature is shown by a positive response to the following question: Was the patient's thinking disorganized or incoherent, such as rambling or irrelevant conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject?
Feature 4: altered level of consciousness This feature is shown by any answer other than "alert" to the following question: Overall, how would you rate the patient's level of consciousness? (alert [normal]), vigilant [hyperalert], lethargic [drowsy, easily aroused], stupor [difficult to arouse], or coma [unarousable])
Reprinted with permission 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. 1990:113:941-8. †The diagnosis of delirium by CAM requires the presence of features 1 and 2 and either 3 or 4.
Anchor for JumpAnchor for JumpTABLE IV  Important Laboratory Studies To Consider in Work-up for Patients with Delirium
Laboratory Tests To Evaluate
Complete blood-cell count with differential Anemia, infection
Complete metabolic profile Electrolyte disturbance, dehydration, glucose level, kidney or liver abnormalities
Albumin Nutritional deficiency
Urinalysis/culture Urinary tract infection
Chest radiograph Pneumonia, congestive heart failure
Serum ammonia* Hepatic encephalopathy
Thyroid-stimulating hormone and free T4* Thyroid dysfunction
Urine toxicology* Benzodiazepines, tricyclic antidepressants, opioids
Computed tomography scan or magnetic resonance imaging of head* Stroke, hemorrhage, hematoma, space-occupying lesion
Spinal tap* Central nervous system infection
If indicated by history.
Anchor for JumpAnchor for JumpTABLE V  An Organized Approach to the Prevention and Treatment of Delirium in Patients with Hip Fracture
Ensure adequate central nervous system oxygen delivery
    Give supplemental oxygen to keep saturation >95%
    Keep systolic blood pressure >90 mm Hg
    Keep hematocrit >30%
Restore fluid and electrolyte balance
Treat pain
Assess and promote adequate bowel and bladder function
Evaluate medications (including herbal supplements or over-the-counter medications)
    Be alert to recently added medication with anticholinergic or dopamine-increasing properties
    If delirium develops, reduce or eliminate noncritical medication; watch for discontinuation or withdrawal effects
Assess nutritional intake
    Provide dentures, supplements, or nasogastric tube feeding if needed
Provide early mobilization and rehabilitation
Provide appropriate environmental stimuli
    Glasses, hearing aids, clock, calendar, light
Actively manage concurrent medical conditions and postoperative complications
    Myocardial infarction or stroke
    Arrhythmias
    Congestive heart failure, chronic obstructive pulmonary disease
    Liver or renal disease
    Gastrointestinal bleeding
    Urinary tract infection
    Central nervous system conditions like dementia, Parkinson disease, epilepsy

References

Marcantonio ER, Flacker JM, Michaels M, Resnick NM. Delirium is independently associated with poor functional recovery after hip fracture. J Am Geriatr Soc. 2000;48: 618-24.48618  2000  [PubMed]
 
Cummings SR, Rubin SM, Black D. The future of hip fractures in the United States. Numbers, costs, and potential effects of postmenopausal estrogen. Clin Orthop Relat Res. 1990;252: 163-6.252163  1990  [PubMed]
 
Morrison RS, Magaziner J, Gilbert M, Koval KJ, McLaughlin MA, Orosz G, Strauss E, Siu AL. Relationship between pain and opioid analgesics on the development of delirium following hip fracture. J Gerontol A Biol Sci Med Sci. 2003;58: 76-81.5876  2003  [PubMed][CrossRef]
 
Duppils GS, Wikblad K. Cognitive function and health-related quality of life after delirium in connection with hip surgery. A six-month follow-up. Orthop Nurs. 2004;23: 195-203.23195  2004  [PubMed][CrossRef]
 
Edelstein DM, Aharonoff GB, Karp A, Capla EL, Zuckerman JD, Koval KJ. Effect of postoperative delirium on outcome after hip fracture. Clin Orthop Relat Res. 2004;422: 195-200.422195  2004  [PubMed][CrossRef]
 
Gustafson Y, Berggren D, Brannstrom B, Bucht G, Norberg A, Hansson LI, Winblad B. Acute confusional states in elderly patients treated for femoral neck fracture. J Am Geriatr Soc. 1988;36: 525-30.36525  1988  [PubMed]
 
Bitsch M, Foss N, Kristensen B, Kehlet H. Pathogenesis of and management strategies for postoperative delirium after hip fracture: a review. Acta Orthop Scand. 2004;75: 378-89.75378  2004  [PubMed][CrossRef]
 
Marcantonio ER, Flacker JM, Wright RJ, Resnick NM. Reducing delirium after hip fracture: a randomized trial. J Am Geriatr Soc. 2001;49: 516-22.49516  2001  [CrossRef]
 
Cole MG. Delirium in elderly patients. Am J Geriatr Psychiatry. 2004;12: 7-21.127  2004  [PubMed]
 
Stiefel F. Delirium: is the confusion slowly clearing up [editorial]. Support Care Cancer. 1996;4: 325-6.4325  1996  [PubMed][CrossRef]
 
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: 941-8.113941  1990 
 
Delirium, dementia, and amnestic and other cognitive disorders. In: Diagnostic and statistical manual of mental disorders: DSM-IV. 4th ed, text revision. Washington, DC: American Psychiatric Association; 2000. p 135-80.135  2000 
 
Gleason OC. Delirium. Am Fam Physician. 2003;67: 1027-34.671027  2003 
 
Webster JR, Chew RB, Mailliard L, Moran MB. Improving clinical and cost outcomes in delirium: use of practice guidelines and a delirium care team. Ann Long-Term Care. 1999;7: 128-34.7128  1999 
 
Samuels SC, Neugroschl JA. Delirium. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 1054-68.1054  2005 
 
Winawer N. Postoperative delirium. Med Clin North Am. 2001;85: 1229-39.851229  2001  [PubMed][CrossRef]
 
van der Mast RC. Pathophysiology of delirium. J Geriatr Psychiatry Neurol. 1998;11: 138-45.11138  1998  [PubMed]
 
Trzepacz PT. The neuropathogenesis of delirium. A need to focus our research. Psychosomatics. 1994;35: 374-91.35374  1994  [PubMed]
 
Trzepacz PT. Delirium. Advances in diagnosis, pathophysiology, and treatment. Psychiatr Clin North Am. 1996;19: 429-48.19429  1996  [CrossRef]
 
Lichter DG, Cummings JL, editors. Frontal-subcortical circuits in psychiatric and neurological disorders. New York: Guilford Press; 2001. Introduction and overview; p 1-43.1  2001 
 
Grebb JA. Neural sciences: introduction and overview. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 1-3.1  2005 
 
Zorumski CF, Isenberg KE, Mennerick SJ. Basic electrophysiology. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 99-115.99  2005 
 
Arnsten AFT, Castellanos FX. Neurobiology of attention regulation and its disorders. In: Martin A, Scahill L, Charney DS, Leckman JF, editors. Pediatric psychopharmacology: principles and practice. New York: Oxford University Press; 2003. p 99-109.99  2003 
 
Bronstein YL, Cummings JL. Neurochemistry of frontal-subcortical circuits. In: Lichter DG, Cummings JL, editors. Frontal-subcortical circuits in psychiatric and neurologic disorders. New York: Guilford Press; 2001. p 59-91.59  2001 
 
Bronstein YL, Cummings JL. Neuropharmacology of frontal-subcortical circuits. In: Lichter DG, Cummings JL, editors. Frontal-subcortical circuits in psychiatric and neurologic disorders. New York: Guilford Press; 2001. p 401-20.401  2001 
 
Voeller KKS. Attention-deficit/hyperactivity disorder as a frontal-subcortical disorder. In: Lichter DG, Cummings JL, editors. Frontal-subcortical circuits in psychiatric and neurologic disorders. New York: Guilford Press; 2001. p 334-72.334  2001 
 
Tecott LH, Smart SL. Monoamine neurotransmitters. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 49-60.49  2005 
 
Neugroschl JA, Kolevzon A, Samuels SC, Marin DB. Dementia. In: Sadock BJ, Sadock VA, editors. Kaplan and Sadock's comprehensive textbook of psychiatry. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2005. p 1068-93.1068  2005 
 
Magistretti PJ, Pellerin L, Martin J-L. Brain energy metabolism: an integrated cellular perspective. . 2000. 
www.acnp.org/G4/GN401000064

 
Breningstall GN. Oxidative metabolism disorders. In: Swaiman KF, Ashwal S, editors. Pediatric neurology. Principles and practice. St. Louis: Mosby; 1999. p 483-93.483  1999 
 
Gustafson Y. Postoperative delirium: a challenge for the orthopedic team [editorial]. Acta Orthop Scand. 2004;75: 375-7.75375  2004  [CrossRef]
 
Lundstrom M, Edlund A, Bucht G, Karlsson S, Gustafson Y. Dementia after delirium in patients with femoral neck fractures. J Am Geriatr Soc. 2003;51: 1002-6.511002  2003  [PubMed][CrossRef]
 
Gustafson Y, Brannstrom B, Berggren D, Ragnarsson JI, Sigaard J, Bucht G, Reiz S, Norberg A, Winblad B. A geriatric-anesthesiologic program to reduce acute confusional states in elderly patients treated for femoral neck fractures. J Am Geriatr Soc. 1991;39: 655-62.39655  1991 
 
Folstein MF, Folstein SE, McHugh PR. "Mini-mental state". A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12: 189-98.12189  1975  [PubMed][CrossRef]
 
Jacobi J, Fraser GL, Coursin DB, Riker RR, Fontaine D, Wittbrodt ET, Chalfin DB, Masica MF, Bjerke HS, Coplin DW, Crippen DW, Fuchs BD, Kelleher RM, Marik PE, Nasraway SA Jr, Murray MJ, Peruzzi WT, Lumb PD; Task Force of the American College of Critical Care Medicine (ACCM) of the Society of Critical Care Medicine (SCCM), American Society of Health-System Pharmacists (ASHP), American College of Chest Physicians. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill adult. Crit Care Med. 2002;30: 119-41. Erratum in: Crit Care Med. 2002;30:726.30119  2002  [PubMed][CrossRef]
 
Hanson MR, Galvez-Jimenez N. Management of dementia and acute confusional states in the perioperative period. Neurol Clin. 2004;22:vii-viii, 413-22.22413  2004  [CrossRef]
 
Weber JB, Coverdale JH, Kunik ME. Delirium: current trends in prevention and treatment. Intern Med J. 2004;34: 115-21.34115  2004  [CrossRef]
 
Duppils GS, Wikblad K. Delirium: behavioural changes before and during the prodromal phase. J Clin Nurs. 2004:13; 609-16.13609  2004  [CrossRef]
 
Chang PH, Steinberg MB. Alcohol withdrawal. Med Clin North Am. 2001;85: 1191-212.851191  2001  [PubMed][CrossRef]
 
Parisi DM, Koval K, Egol K. Fat embolism syndrome. Am J Orthop. 2002;31: 507-12.31507  2002  [PubMed]
 
Practice guideline for the treatment of patients with delirium. American Psychiatric Association. Am J Psychiatry. 1999;156(5 Suppl): 1-20.1561  1999 
 
Milisen K, Foreman MD, Abraham IL, De Geest S, Godderis J, Vandermeulen E, Fischler B, Delooz H, Spiessens B, Broos P. A nurse-led interdisciplinary intervention program for delirium in elderly hip-fracture patients. J Am Geriatr Soc. 2001;49: 523-32.49523  2001  [PubMed][CrossRef]
 
Olofsson SM, Weitzner MA, Valentine AD, Baile WF, Meyers CA. A retrospective study of the psychiatric management and outcome of delirium in the cancer patient. Support Care Cancer. 1996;4: 351-7.4351  1996  [PubMed][CrossRef]
 
Bezchlibnyk-Butler KZ, Jeffries JJ, editors. Clinical handbook of psychotropic drugs. 15th ed. Ashland, OH: Hogrefe and Huber; 2005. p 102.102  2005 
 
Skrobik YK, Bergeron N, Dumont M, Gottfried SB. Olanzapine vs haloperidol: treating delirium in a critical care setting. Intensive Care Med. 2004;30: 444-9.30444  2004  [PubMed][CrossRef]
 
Deaths with antipsychotics in elderly patients with behavioral disturbances. FDA Public Health Advisory. . 2005. 
www.fda.gov/cder/drug/advisory/antipsychotics.htm

 
Zyprexa. Physicians desk reference. 59th ed. Montvale: 2005. p 1901.1901  2005 
 
Risperdal. Physicians desk reference. 59th ed. Montvale: 2005. p 1743.1743  2005 
 
Physostigmine. Thomson MICROMEDEX. 2005.  2005 
 
Donepezil. Thomson MICROMEDEX. 2005.  2005 
 
Accreditation Statement
These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
CME Activities Associated with This Article
Subspecialty CME | November 15, 2006
Quarterly CME | October 05, 2006
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Theocharis Chr. Kyziridis
Posted on January 25, 2008
Pulmonary Embolism As a Cause of Postoperative Delirium
University Hospital of Larissa, Larissa, GREECE

To The Editor:

In their excellent review (1), the authors have presented important information on the very serious complication of postoperative delirium. My intention is not to repeat what is already known, but to emphasize the importance of continuous vigilance, clinical suspicion, and early intervention in such cases,by presenting a relevant case report.

An 85 year old man was admitted to our hospital after a traffic accident in which he suffered a hip fracture. The patient had excellent mental status. From his medical history he reported only the presence of arterial hypertension for which he took no medication.He underwent surgery for the hip fracture and on the second postoperative day he was still very mentally alert. Suddenly in the afternoon of the 3rd postoperative day he was found lying immobile in his bed without speaking. He did not give any answers to my questions nor did he know who he was or where he was. This picture was in clear contrast to his previously good mental status. Arterial blood gases, vital signs and ECG pointed to a possible diagnosis of pulmonary embolism. Indeed the diagnosis was confirmed after a perfusion-ventilation CT scan had been made. Proper treatment was immediately instituted and the patient gradually regained normal mental status. Three years after the operation the patient is living an apparently good life, being able to walk with a slight help and maintaining a very good level of everyday functional ability.

Unfortunately hypokinetic postoperative delirium may often go unnoticed. In such cases, diagnosis is delayed, with all the possible sequelae for the patient, the family and the health care providers. Early recognition may save lives and maintain a good functional level for elderly patients.

References: <_1 /> Benjamin D. Robertson and Timothy J. Robertson Postoperative Delirium After Hip Fracture J Bone Joint Surg Am 2006; 88: 2060-2068

The author did not receive any outside funding or grants in support of his research for or preparation of this work. Neither he nor a member of his immediate family received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, division, center, clinical practice, or other charitable or nonprofit organization with which the author, or a member of his immediate family, is affiliated or associated .

Gary Heyburn, MRCPI, MRCGP, DRCOG
Posted on September 29, 2006
Perioperative Delirium
Royal Group of Hospitals, Belfast, UK

To The Editor:

I read with interest the article by Robertson et al.(1) on delirium which properly highlights a common and upsetting complication following a hip fracture. My only concern is that the title of the piece seems to imply that delirium is only a postoperative complication. Delirium is also a preoperative problem (as mentioned in the article several times) exacerbated by pain, painkillers, noise, sleep deprivation, and change of environment to name but a few. Thus, the title of the article reinforces a mis-perception that delirium only occurs postoperatively and is mainly a side effect of anaesthesia.

I would also emphasize the need for an evidence based use of medications to reduce duration of peri-operatuve delirium. Pharmacological interventions in this setting should be strictly controlled and monitored. The recent set of guidelines on the management of delirium released by the British Geriatric Society review the evidence in a comprehansive fashion and is a valuable resource available to those with an interest in this area (2).

The author(s) of this letter to the editor did not receive payment or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the author(s) are affiliated or associated.

References:

1. Robertson BD, Robertson TJ. Postoperative delirium after hip fracture. J Bone Joint Surg Am. 2006;88:2060-2068.

2. Guidelines for the prevention, diagnosis and management of delirium in older people in hospital British Geriatrics Society. January 2006, http://www.bgs.org.uk/Publications/Clinical%20Guidelines/clinical_1-2_fulldelirium.htm. Accessed 10/10/06.

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