Most older drivers are safe drivers and are less likely than younger people to drive recklessly, at high speeds, or under the influence of alcohol.¹ However, motor vehicle injuries are the second leading cause of injury-related deaths among older adults. Very old adults (80 years and over) have higher rates of fatality and injury in motor vehicle crashes per million miles driven than any other age group except for teenagers.¹ Therefore, consider safety screening of all very old drivers plus any older adult with certain high-risk medical conditions, including the following.

NEUROCOGNITIVE DISORDERS

Drivers with Alzheimer disease—the most common type of major neurocognitive disorder (dementia) in older adults in the United States—are at high risk for adverse driving events due to impaired memory, attentiveness, problem-solving skills, multitasking, orientation, judgment, and reaction speed. Even in amnesic mild cognitive impairment—a mild neurocognitive disorder without functional decline—driving skills such as lane control may be impaired.²

Frontotemporal dementia, a less common cause of dementia in older adults, is associated with profound impairments in reasoning, task flexibility, planning, and execution. Persons with frontotemporal dementia are more likely to speed, run stop signs, and suffer more off-road crashes and collisions.³

Discuss driving safety with any patient age 80 or older or one with specific conditions

The diagnosis of dementia, however, is less predictive of driving risk than the stage of dementia. The American Academy of Neurology recommends that health care providers clinically “stage” all demented individuals using a validated tool at diagnosis and periodically afterwards. The Clinical Dementia Rating (CDR) scale is appropriate for staging dementia in the office. The CDR has also been shown to identify people with dementia who are at an increased risk of unsafe driving, with strong  evidence (level of evidence A) relating dementia stage to driving risk.⁴ The CDR assigns a score of 1 for mild dementia (function impaired in at least one complex activity); 2 for moderate dementia (function impaired in at least one basic activity); and 3 for severe dementia. Individuals with a CDR score of 2 or higher are considered to be at very high risk if still driving. These persons should be encouraged to surrender their driving privileges.⁴ Even with mild dementia (CDR score of 1), as few as 41% of drivers may drive safely.⁴ Most persons with mild cognitive impairment (CDR score of 0.5) are safe drivers.

Patients often have poor insight into their driving safety. However, a caregiver’s rating of driving skills as marginal or unsafe is useful in identifying unsafe drivers (level of evidence B) and can be considered a red flag.⁴ Predictors with less support in the literature (level of evidence C) include recent traffic citations, motor vehicle accidents, and self-reported situational avoidance, such as limiting driving to familiar roadways. Additional predictors include Mini-Mental State Examination scores of 24 or less, and/or the emergence of an aggressive or impulsive personality (Table 1). A driver evaluation is helpful when there is mild cognitive impairment or mild dementia with at least one red flag.

Clinicians who are not comfortable with staging dementia as mild, moderate, or severe may consider referring to a neurologist or geriatrician.

There is no evidence to support or refute the benefit of interventional strategies such as driver rehabilitation for drivers with dementia.

PARKINSON DISEASE

Individuals with mild motor disability from Parkinson disease may be fit drivers. As the disease progresses, drivers with Parkinson disease may make more errors than healthy elders in visual scanning, signaling, vehicle positioning, and velocity regulation (eg, traveling so slowly that it may be unsafe).⁵ Clinicians can consider referring a patient with Parkinson disease for a baseline driving evaluation upon diagnosis, and then every 1 to 2 years for reassessment. Alternate transportation should be arranged as the disease progresses.

EPISODIC INCAPACITATION

Approximately 1% to 3% of all motor vehicle accidents are due to sudden incapacitation of an otherwise safe driver.

Syncope. Neurally mediated (vasovagal) syncope accounts for 30% to 35% of syncopal episodes while driving.⁶ Cardiac arrhythmias are the next most common cause and include bradyarrhythmias (7%), supraventricular tachyarrhythmias (2%–15%), and ventricular tachyarrhythmias (5%–17%). Because neurocardiogenic syncope often recurs, consider restricting driving for those with recurrent or severe neurocardiogenic syncopal episodes until symptoms are controlled.

Arrhythmias. Driving recommendations for various arrhythmias^7,8 are listed in Table 2.

Many patients who have an implantable cardioverter-defibrillator (ICD) device experience an unexpected shock. For individuals with a history of ventricular tachycardia or fibrillation, the 5-year actuarial incidence of appropriate ICD shocks ranges between 55% and 70%. However, data indicate that 90% to 100% of drivers who received ICD discharges while driving continued to drive without causing motor vehicle accidents.^9,10

Seizures. States differ in their rules for reporting drivers who have epilepsy or breakthrough seizures. Physicians should refer to their state regulations when counseling these patients.

POLYPHARMACY

Polypharmacy is common in older adults. Many take psychoactive drugs that can impair tracking, alertness, coordination, and reaction time. With the “Roadwise Rx” tool  (www.roadwiserx.com), health care providers and patients can enter the names of medicines to check if they affect driving ability. Nonproprietary on-line tools such as “START” (Screening Tool to Alert doctors to Right Treatment) and “STOPP” (Screening Tool of Older Persons’ Potentially Inappropriate Prescriptions) can be used to prune medication lists.

DRIVING EVALUATION

America is a nation of highways overflowing with cars. Cars provide transportation but also reflect wealth and personality, particularly for men. Practically, the ability to drive a car allows older men and women to socialize in the community, shop for essentials, and take care of themselves without being a burden. Driving cessation can cause social isolation and depressive symptoms and can strain caregiver resources.

Patients’ self-rating of driving correlates poorly with caregivers’ ratings

It is therefore understandable for health care providers to feel reluctant or uncomfortable counseling older adults to give up their driving privileges. A health care provider who identifies driving safety concerns can refer a patient to a geriatrician for further risk  assessment or to a certified driver rehabilitation specialist (CDRS) for a driving evaluation. A CDRS will also offer the patient and caregiver information on local resources for transportation alternatives. A list of local CDRSs can be found on the Association for Driver Rehabilitation Specialists website (www.aded.net). Many hospitals have occupational therapists who are CDRSs.

The evaluation typically involves an assessment of the driver’s knowledge of traffic signs and laws, a cognitive assessment, possibly a simulation, and finally an on-road driving evaluation if deemed appropriate. Medicare coverage depends on diagnosis and the state carrier.

Most older drivers are safe drivers and are less likely than younger people to drive recklessly, at high speeds, or under the influence of alcohol.¹ However, motor vehicle injuries are the second leading cause of injury-related deaths among older adults. Very old adults (80 years and over) have higher rates of fatality and injury in motor vehicle crashes per million miles driven than any other age group except for teenagers.¹ Therefore, consider safety screening of all very old drivers plus any older adult with certain high-risk medical conditions, including the following.

NEUROCOGNITIVE DISORDERS

Drivers with Alzheimer disease—the most common type of major neurocognitive disorder (dementia) in older adults in the United States—are at high risk for adverse driving events due to impaired memory, attentiveness, problem-solving skills, multitasking, orientation, judgment, and reaction speed. Even in amnesic mild cognitive impairment—a mild neurocognitive disorder without functional decline—driving skills such as lane control may be impaired.²

Frontotemporal dementia, a less common cause of dementia in older adults, is associated with profound impairments in reasoning, task flexibility, planning, and execution. Persons with frontotemporal dementia are more likely to speed, run stop signs, and suffer more off-road crashes and collisions.³

Discuss driving safety with any patient age 80 or older or one with specific conditions

The diagnosis of dementia, however, is less predictive of driving risk than the stage of dementia. The American Academy of Neurology recommends that health care providers clinically “stage” all demented individuals using a validated tool at diagnosis and periodically afterwards. The Clinical Dementia Rating (CDR) scale is appropriate for staging dementia in the office. The CDR has also been shown to identify people with dementia who are at an increased risk of unsafe driving, with strong  evidence (level of evidence A) relating dementia stage to driving risk.⁴ The CDR assigns a score of 1 for mild dementia (function impaired in at least one complex activity); 2 for moderate dementia (function impaired in at least one basic activity); and 3 for severe dementia. Individuals with a CDR score of 2 or higher are considered to be at very high risk if still driving. These persons should be encouraged to surrender their driving privileges.⁴ Even with mild dementia (CDR score of 1), as few as 41% of drivers may drive safely.⁴ Most persons with mild cognitive impairment (CDR score of 0.5) are safe drivers.

Patients often have poor insight into their driving safety. However, a caregiver’s rating of driving skills as marginal or unsafe is useful in identifying unsafe drivers (level of evidence B) and can be considered a red flag.⁴ Predictors with less support in the literature (level of evidence C) include recent traffic citations, motor vehicle accidents, and self-reported situational avoidance, such as limiting driving to familiar roadways. Additional predictors include Mini-Mental State Examination scores of 24 or less, and/or the emergence of an aggressive or impulsive personality (Table 1). A driver evaluation is helpful when there is mild cognitive impairment or mild dementia with at least one red flag.

Clinicians who are not comfortable with staging dementia as mild, moderate, or severe may consider referring to a neurologist or geriatrician.

There is no evidence to support or refute the benefit of interventional strategies such as driver rehabilitation for drivers with dementia.

PARKINSON DISEASE

Individuals with mild motor disability from Parkinson disease may be fit drivers. As the disease progresses, drivers with Parkinson disease may make more errors than healthy elders in visual scanning, signaling, vehicle positioning, and velocity regulation (eg, traveling so slowly that it may be unsafe).⁵ Clinicians can consider referring a patient with Parkinson disease for a baseline driving evaluation upon diagnosis, and then every 1 to 2 years for reassessment. Alternate transportation should be arranged as the disease progresses.

EPISODIC INCAPACITATION

Approximately 1% to 3% of all motor vehicle accidents are due to sudden incapacitation of an otherwise safe driver.

Syncope. Neurally mediated (vasovagal) syncope accounts for 30% to 35% of syncopal episodes while driving.⁶ Cardiac arrhythmias are the next most common cause and include bradyarrhythmias (7%), supraventricular tachyarrhythmias (2%–15%), and ventricular tachyarrhythmias (5%–17%). Because neurocardiogenic syncope often recurs, consider restricting driving for those with recurrent or severe neurocardiogenic syncopal episodes until symptoms are controlled.

Arrhythmias. Driving recommendations for various arrhythmias^7,8 are listed in Table 2.

Many patients who have an implantable cardioverter-defibrillator (ICD) device experience an unexpected shock. For individuals with a history of ventricular tachycardia or fibrillation, the 5-year actuarial incidence of appropriate ICD shocks ranges between 55% and 70%. However, data indicate that 90% to 100% of drivers who received ICD discharges while driving continued to drive without causing motor vehicle accidents.^9,10

Seizures. States differ in their rules for reporting drivers who have epilepsy or breakthrough seizures. Physicians should refer to their state regulations when counseling these patients.

POLYPHARMACY

Polypharmacy is common in older adults. Many take psychoactive drugs that can impair tracking, alertness, coordination, and reaction time. With the “Roadwise Rx” tool  (www.roadwiserx.com), health care providers and patients can enter the names of medicines to check if they affect driving ability. Nonproprietary on-line tools such as “START” (Screening Tool to Alert doctors to Right Treatment) and “STOPP” (Screening Tool of Older Persons’ Potentially Inappropriate Prescriptions) can be used to prune medication lists.

DRIVING EVALUATION

America is a nation of highways overflowing with cars. Cars provide transportation but also reflect wealth and personality, particularly for men. Practically, the ability to drive a car allows older men and women to socialize in the community, shop for essentials, and take care of themselves without being a burden. Driving cessation can cause social isolation and depressive symptoms and can strain caregiver resources.

Patients’ self-rating of driving correlates poorly with caregivers’ ratings

It is therefore understandable for health care providers to feel reluctant or uncomfortable counseling older adults to give up their driving privileges. A health care provider who identifies driving safety concerns can refer a patient to a geriatrician for further risk  assessment or to a certified driver rehabilitation specialist (CDRS) for a driving evaluation. A CDRS will also offer the patient and caregiver information on local resources for transportation alternatives. A list of local CDRSs can be found on the Association for Driver Rehabilitation Specialists website (www.aded.net). Many hospitals have occupational therapists who are CDRSs.

The evaluation typically involves an assessment of the driver’s knowledge of traffic signs and laws, a cognitive assessment, possibly a simulation, and finally an on-road driving evaluation if deemed appropriate. Medicare coverage depends on diagnosis and the state carrier.

Most older drivers are safe drivers and are less likely than younger people to drive recklessly, at high speeds, or under the influence of alcohol.¹ However, motor vehicle injuries are the second leading cause of injury-related deaths among older adults. Very old adults (80 years and over) have higher rates of fatality and injury in motor vehicle crashes per million miles driven than any other age group except for teenagers.¹ Therefore, consider safety screening of all very old drivers plus any older adult with certain high-risk medical conditions, including the following.

NEUROCOGNITIVE DISORDERS

Drivers with Alzheimer disease—the most common type of major neurocognitive disorder (dementia) in older adults in the United States—are at high risk for adverse driving events due to impaired memory, attentiveness, problem-solving skills, multitasking, orientation, judgment, and reaction speed. Even in amnesic mild cognitive impairment—a mild neurocognitive disorder without functional decline—driving skills such as lane control may be impaired.²

Frontotemporal dementia, a less common cause of dementia in older adults, is associated with profound impairments in reasoning, task flexibility, planning, and execution. Persons with frontotemporal dementia are more likely to speed, run stop signs, and suffer more off-road crashes and collisions.³

Discuss driving safety with any patient age 80 or older or one with specific conditions

The diagnosis of dementia, however, is less predictive of driving risk than the stage of dementia. The American Academy of Neurology recommends that health care providers clinically “stage” all demented individuals using a validated tool at diagnosis and periodically afterwards. The Clinical Dementia Rating (CDR) scale is appropriate for staging dementia in the office. The CDR has also been shown to identify people with dementia who are at an increased risk of unsafe driving, with strong  evidence (level of evidence A) relating dementia stage to driving risk.⁴ The CDR assigns a score of 1 for mild dementia (function impaired in at least one complex activity); 2 for moderate dementia (function impaired in at least one basic activity); and 3 for severe dementia. Individuals with a CDR score of 2 or higher are considered to be at very high risk if still driving. These persons should be encouraged to surrender their driving privileges.⁴ Even with mild dementia (CDR score of 1), as few as 41% of drivers may drive safely.⁴ Most persons with mild cognitive impairment (CDR score of 0.5) are safe drivers.

Patients often have poor insight into their driving safety. However, a caregiver’s rating of driving skills as marginal or unsafe is useful in identifying unsafe drivers (level of evidence B) and can be considered a red flag.⁴ Predictors with less support in the literature (level of evidence C) include recent traffic citations, motor vehicle accidents, and self-reported situational avoidance, such as limiting driving to familiar roadways. Additional predictors include Mini-Mental State Examination scores of 24 or less, and/or the emergence of an aggressive or impulsive personality (Table 1). A driver evaluation is helpful when there is mild cognitive impairment or mild dementia with at least one red flag.

Clinicians who are not comfortable with staging dementia as mild, moderate, or severe may consider referring to a neurologist or geriatrician.

There is no evidence to support or refute the benefit of interventional strategies such as driver rehabilitation for drivers with dementia.

PARKINSON DISEASE

Individuals with mild motor disability from Parkinson disease may be fit drivers. As the disease progresses, drivers with Parkinson disease may make more errors than healthy elders in visual scanning, signaling, vehicle positioning, and velocity regulation (eg, traveling so slowly that it may be unsafe).⁵ Clinicians can consider referring a patient with Parkinson disease for a baseline driving evaluation upon diagnosis, and then every 1 to 2 years for reassessment. Alternate transportation should be arranged as the disease progresses.

EPISODIC INCAPACITATION

Approximately 1% to 3% of all motor vehicle accidents are due to sudden incapacitation of an otherwise safe driver.

Syncope. Neurally mediated (vasovagal) syncope accounts for 30% to 35% of syncopal episodes while driving.⁶ Cardiac arrhythmias are the next most common cause and include bradyarrhythmias (7%), supraventricular tachyarrhythmias (2%–15%), and ventricular tachyarrhythmias (5%–17%). Because neurocardiogenic syncope often recurs, consider restricting driving for those with recurrent or severe neurocardiogenic syncopal episodes until symptoms are controlled.

Arrhythmias. Driving recommendations for various arrhythmias^7,8 are listed in Table 2.

Many patients who have an implantable cardioverter-defibrillator (ICD) device experience an unexpected shock. For individuals with a history of ventricular tachycardia or fibrillation, the 5-year actuarial incidence of appropriate ICD shocks ranges between 55% and 70%. However, data indicate that 90% to 100% of drivers who received ICD discharges while driving continued to drive without causing motor vehicle accidents.^9,10

Seizures. States differ in their rules for reporting drivers who have epilepsy or breakthrough seizures. Physicians should refer to their state regulations when counseling these patients.

POLYPHARMACY

Polypharmacy is common in older adults. Many take psychoactive drugs that can impair tracking, alertness, coordination, and reaction time. With the “Roadwise Rx” tool  (www.roadwiserx.com), health care providers and patients can enter the names of medicines to check if they affect driving ability. Nonproprietary on-line tools such as “START” (Screening Tool to Alert doctors to Right Treatment) and “STOPP” (Screening Tool of Older Persons’ Potentially Inappropriate Prescriptions) can be used to prune medication lists.

DRIVING EVALUATION

America is a nation of highways overflowing with cars. Cars provide transportation but also reflect wealth and personality, particularly for men. Practically, the ability to drive a car allows older men and women to socialize in the community, shop for essentials, and take care of themselves without being a burden. Driving cessation can cause social isolation and depressive symptoms and can strain caregiver resources.

Patients’ self-rating of driving correlates poorly with caregivers’ ratings

It is therefore understandable for health care providers to feel reluctant or uncomfortable counseling older adults to give up their driving privileges. A health care provider who identifies driving safety concerns can refer a patient to a geriatrician for further risk  assessment or to a certified driver rehabilitation specialist (CDRS) for a driving evaluation. A CDRS will also offer the patient and caregiver information on local resources for transportation alternatives. A list of local CDRSs can be found on the Association for Driver Rehabilitation Specialists website (www.aded.net). Many hospitals have occupational therapists who are CDRSs.

The evaluation typically involves an assessment of the driver’s knowledge of traffic signs and laws, a cognitive assessment, possibly a simulation, and finally an on-road driving evaluation if deemed appropriate. Medicare coverage depends on diagnosis and the state carrier.

A 59-year-old man with autosomal dominant polycystic kidney disease (ADPKD), end-stage renal disease on hemodialysis, hypertension, and diverticulosis presented with acute pain in the left lower abdomen. The pain began 4 days previously, was dull and nonradiating, was relieved partially with hydrocodone-acetaminophen, and had no clear exacerbating factors. Two days before presentation, he developed a fever with chills. He reported no recent dysuria, diarrhea, hematuria, hematochezia, or melena. He had not been taking anticoagulants or nonsteroidal anti-inflammatory drugs, and he had no history of heavy lifting or trauma.

His temperature was 38.5˚C (101.3˚F), blood pressure 141/60 mm Hg (normal for this patient). On examination, his left lower quadrant was tender with voluntary guarding. Also present was a reducible ventral hernia, which was not new.

His hemoglobin level was 10.6 g/dL (reference range 13.0–17.0), which had dropped from a previous value of 13.7 g/dL.

Computed tomography of the abdomen and pelvis revealed a ruptured retroperitoneal hemorrhagic cyst (Figure 1) in the inferior aspect of the left kidney extending into the fascia of Gerota.

Since his vital signs were stable, he was managed supportively during his hospitalization with intravenous fluids, serial hemoglobin checks, and analgesia. He was eventually discharged home in good condition.

CYST HEMORRHAGE IN POLYCYSTIC KIDNEY DISEASE

ADPKD is a relatively common, inherited systemic disease that leads to cyst formation,  primarily in the kidneys but also in the liver (94%), seminal vesicles (40%), pancreas (9%), arachnoid membrane (8%), and spinal meningeal area (2%).¹

In addition to cyst formation in multiple organs, ADPKD can have extrarenal manifestations such as connective-tissue abnormalities (including mitral valve prolapse) (25%), abdominal hernia (10%), and intracranial aneurysm (8%).¹ Management of extrarenal complications of ADPKD is discussed in detail elsewhere.²

The estimated prevalence of ADPKD is 1 of every 400 to 1,000 live births. However, given that ADPKD is often clinically silent, it is diagnosed during the lifetime of fewer than half of people who have it.³

Most ADPKD cases are caused by mutations in either the PKD1 or PKD2 gene.^4,5  Although the mechanism of cyst formation in ADPKD is still unclear, it is known that PKD1 and PKD2 encode proteins called polycystin-1 and polycystin-2, respectively. Polycystin-1 is a membrane protein found in renal tubular epithelia, hepatic bile ductules, and pancreatic ducts. Polycystin-2 is involved in cell calcium signaling and has been identified in the renal distal tubules, collecting duct, and thick ascending limb. Mutations in PKD1 and PKD2 are thought to contribute to cyst formation, with PKD1 mutations associated with earlier onset and more severe development of renal and extrarenal cysts.

Cyst hemorrhage

Hemorrhage of renal cysts is a well-known complication, occurring in up to 70% of patients with ADPKD.6 Renal cyst hemorrhage often presents clinically as flank pain with point tenderness or hematuria, or both. Flank pain results from hemorrhage into a cyst with consequent distention of the renal capsule, whereas hematuria results from rupture of a cyst into the collecting system.

Spontaneous nonfatal retroperitoneal cyst hemorrhage, as in our patient, is  rare. Indeed, in one series reviewing the abdominal computed tomographic findings of 66 patients with ADPKD, only 2 patients (3%) had perinephric hematomas in the absence of recent trauma.⁶

Management of cyst hemorrhage is primarily conservative. Pain associated with cyst hemorrhage is managed conservatively with bed rest, intravenous hydration, and analgesics (but not nonsteroidal anti-inflammatory drugs).

Fewer than half of people with ADPKD are diagnosed with it in their lifetime

Hematuria is also managed conservatively with bedrest and intravenous hydration, and most episodes of hematuria are self-limiting and last 2 to 7 days. However, if excessive bleeding occurs, the patient may be at risk of urinary tract obstruction from clot formation. If obstruction occurs and persists beyond 2 weeks, then ureteral stenting may be necessary. In rare cases of prolonged, severe bleeding with extensive subcapsular or retroperitoneal hematomas, patients require hospitalization, transfusion, or percutaneous transcatheter embolization of the renal artery. If such efforts are not successful, surgery, including nephrectomy, may be required to control the hemorrhage.²

Other causes of abdominal pain

In addition to renal cyst hemorrhage, the differential diagnosis of abdominal pain in a patient with ADPKD includes cyst enlargement causing stretching of the renal capsule or traction on the renal pedicle, cyst infection, nephrolithiasis, pyelonephritis, and rarely, tumors including renal cell carcinoma.

Unlike cyst rupture and hemorrhage, which are associated with point tenderness, cyst infection often manifests as diffuse, usually unilateral flank pain with associated fever, nausea, malaise, and leukocytosis. Our patient had none of these except for fever, which can also occur in cyst hemorrhage.

Nephrolithiasis occurs in up to 35% of patients with ADPKD,⁷ but no kidney stones were seen on computed tomography in our patient.

Pyelonephritis was unlikely in our patient, given that he had no significant white blood cells in his urinalysis and no leukocytosis.

Abdominal and pelvic imaging did not reveal any tumors in our patient.

A 59-year-old man with autosomal dominant polycystic kidney disease (ADPKD), end-stage renal disease on hemodialysis, hypertension, and diverticulosis presented with acute pain in the left lower abdomen. The pain began 4 days previously, was dull and nonradiating, was relieved partially with hydrocodone-acetaminophen, and had no clear exacerbating factors. Two days before presentation, he developed a fever with chills. He reported no recent dysuria, diarrhea, hematuria, hematochezia, or melena. He had not been taking anticoagulants or nonsteroidal anti-inflammatory drugs, and he had no history of heavy lifting or trauma.

His temperature was 38.5˚C (101.3˚F), blood pressure 141/60 mm Hg (normal for this patient). On examination, his left lower quadrant was tender with voluntary guarding. Also present was a reducible ventral hernia, which was not new.

His hemoglobin level was 10.6 g/dL (reference range 13.0–17.0), which had dropped from a previous value of 13.7 g/dL.

Computed tomography of the abdomen and pelvis revealed a ruptured retroperitoneal hemorrhagic cyst (Figure 1) in the inferior aspect of the left kidney extending into the fascia of Gerota.

Since his vital signs were stable, he was managed supportively during his hospitalization with intravenous fluids, serial hemoglobin checks, and analgesia. He was eventually discharged home in good condition.

CYST HEMORRHAGE IN POLYCYSTIC KIDNEY DISEASE

ADPKD is a relatively common, inherited systemic disease that leads to cyst formation,  primarily in the kidneys but also in the liver (94%), seminal vesicles (40%), pancreas (9%), arachnoid membrane (8%), and spinal meningeal area (2%).¹

In addition to cyst formation in multiple organs, ADPKD can have extrarenal manifestations such as connective-tissue abnormalities (including mitral valve prolapse) (25%), abdominal hernia (10%), and intracranial aneurysm (8%).¹ Management of extrarenal complications of ADPKD is discussed in detail elsewhere.²

The estimated prevalence of ADPKD is 1 of every 400 to 1,000 live births. However, given that ADPKD is often clinically silent, it is diagnosed during the lifetime of fewer than half of people who have it.³

Most ADPKD cases are caused by mutations in either the PKD1 or PKD2 gene.^4,5  Although the mechanism of cyst formation in ADPKD is still unclear, it is known that PKD1 and PKD2 encode proteins called polycystin-1 and polycystin-2, respectively. Polycystin-1 is a membrane protein found in renal tubular epithelia, hepatic bile ductules, and pancreatic ducts. Polycystin-2 is involved in cell calcium signaling and has been identified in the renal distal tubules, collecting duct, and thick ascending limb. Mutations in PKD1 and PKD2 are thought to contribute to cyst formation, with PKD1 mutations associated with earlier onset and more severe development of renal and extrarenal cysts.

Cyst hemorrhage

Hemorrhage of renal cysts is a well-known complication, occurring in up to 70% of patients with ADPKD.6 Renal cyst hemorrhage often presents clinically as flank pain with point tenderness or hematuria, or both. Flank pain results from hemorrhage into a cyst with consequent distention of the renal capsule, whereas hematuria results from rupture of a cyst into the collecting system.

Spontaneous nonfatal retroperitoneal cyst hemorrhage, as in our patient, is  rare. Indeed, in one series reviewing the abdominal computed tomographic findings of 66 patients with ADPKD, only 2 patients (3%) had perinephric hematomas in the absence of recent trauma.⁶

Management of cyst hemorrhage is primarily conservative. Pain associated with cyst hemorrhage is managed conservatively with bed rest, intravenous hydration, and analgesics (but not nonsteroidal anti-inflammatory drugs).

Fewer than half of people with ADPKD are diagnosed with it in their lifetime

Hematuria is also managed conservatively with bedrest and intravenous hydration, and most episodes of hematuria are self-limiting and last 2 to 7 days. However, if excessive bleeding occurs, the patient may be at risk of urinary tract obstruction from clot formation. If obstruction occurs and persists beyond 2 weeks, then ureteral stenting may be necessary. In rare cases of prolonged, severe bleeding with extensive subcapsular or retroperitoneal hematomas, patients require hospitalization, transfusion, or percutaneous transcatheter embolization of the renal artery. If such efforts are not successful, surgery, including nephrectomy, may be required to control the hemorrhage.²

Other causes of abdominal pain

In addition to renal cyst hemorrhage, the differential diagnosis of abdominal pain in a patient with ADPKD includes cyst enlargement causing stretching of the renal capsule or traction on the renal pedicle, cyst infection, nephrolithiasis, pyelonephritis, and rarely, tumors including renal cell carcinoma.

Unlike cyst rupture and hemorrhage, which are associated with point tenderness, cyst infection often manifests as diffuse, usually unilateral flank pain with associated fever, nausea, malaise, and leukocytosis. Our patient had none of these except for fever, which can also occur in cyst hemorrhage.

Nephrolithiasis occurs in up to 35% of patients with ADPKD,⁷ but no kidney stones were seen on computed tomography in our patient.

Pyelonephritis was unlikely in our patient, given that he had no significant white blood cells in his urinalysis and no leukocytosis.

Abdominal and pelvic imaging did not reveal any tumors in our patient.

A 59-year-old man with autosomal dominant polycystic kidney disease (ADPKD), end-stage renal disease on hemodialysis, hypertension, and diverticulosis presented with acute pain in the left lower abdomen. The pain began 4 days previously, was dull and nonradiating, was relieved partially with hydrocodone-acetaminophen, and had no clear exacerbating factors. Two days before presentation, he developed a fever with chills. He reported no recent dysuria, diarrhea, hematuria, hematochezia, or melena. He had not been taking anticoagulants or nonsteroidal anti-inflammatory drugs, and he had no history of heavy lifting or trauma.

His temperature was 38.5˚C (101.3˚F), blood pressure 141/60 mm Hg (normal for this patient). On examination, his left lower quadrant was tender with voluntary guarding. Also present was a reducible ventral hernia, which was not new.

His hemoglobin level was 10.6 g/dL (reference range 13.0–17.0), which had dropped from a previous value of 13.7 g/dL.

Computed tomography of the abdomen and pelvis revealed a ruptured retroperitoneal hemorrhagic cyst (Figure 1) in the inferior aspect of the left kidney extending into the fascia of Gerota.

Since his vital signs were stable, he was managed supportively during his hospitalization with intravenous fluids, serial hemoglobin checks, and analgesia. He was eventually discharged home in good condition.

CYST HEMORRHAGE IN POLYCYSTIC KIDNEY DISEASE

ADPKD is a relatively common, inherited systemic disease that leads to cyst formation,  primarily in the kidneys but also in the liver (94%), seminal vesicles (40%), pancreas (9%), arachnoid membrane (8%), and spinal meningeal area (2%).¹

In addition to cyst formation in multiple organs, ADPKD can have extrarenal manifestations such as connective-tissue abnormalities (including mitral valve prolapse) (25%), abdominal hernia (10%), and intracranial aneurysm (8%).¹ Management of extrarenal complications of ADPKD is discussed in detail elsewhere.²

The estimated prevalence of ADPKD is 1 of every 400 to 1,000 live births. However, given that ADPKD is often clinically silent, it is diagnosed during the lifetime of fewer than half of people who have it.³

Most ADPKD cases are caused by mutations in either the PKD1 or PKD2 gene.^4,5  Although the mechanism of cyst formation in ADPKD is still unclear, it is known that PKD1 and PKD2 encode proteins called polycystin-1 and polycystin-2, respectively. Polycystin-1 is a membrane protein found in renal tubular epithelia, hepatic bile ductules, and pancreatic ducts. Polycystin-2 is involved in cell calcium signaling and has been identified in the renal distal tubules, collecting duct, and thick ascending limb. Mutations in PKD1 and PKD2 are thought to contribute to cyst formation, with PKD1 mutations associated with earlier onset and more severe development of renal and extrarenal cysts.

Cyst hemorrhage

Hemorrhage of renal cysts is a well-known complication, occurring in up to 70% of patients with ADPKD.6 Renal cyst hemorrhage often presents clinically as flank pain with point tenderness or hematuria, or both. Flank pain results from hemorrhage into a cyst with consequent distention of the renal capsule, whereas hematuria results from rupture of a cyst into the collecting system.

Spontaneous nonfatal retroperitoneal cyst hemorrhage, as in our patient, is  rare. Indeed, in one series reviewing the abdominal computed tomographic findings of 66 patients with ADPKD, only 2 patients (3%) had perinephric hematomas in the absence of recent trauma.⁶

Management of cyst hemorrhage is primarily conservative. Pain associated with cyst hemorrhage is managed conservatively with bed rest, intravenous hydration, and analgesics (but not nonsteroidal anti-inflammatory drugs).

Fewer than half of people with ADPKD are diagnosed with it in their lifetime

Hematuria is also managed conservatively with bedrest and intravenous hydration, and most episodes of hematuria are self-limiting and last 2 to 7 days. However, if excessive bleeding occurs, the patient may be at risk of urinary tract obstruction from clot formation. If obstruction occurs and persists beyond 2 weeks, then ureteral stenting may be necessary. In rare cases of prolonged, severe bleeding with extensive subcapsular or retroperitoneal hematomas, patients require hospitalization, transfusion, or percutaneous transcatheter embolization of the renal artery. If such efforts are not successful, surgery, including nephrectomy, may be required to control the hemorrhage.²

Other causes of abdominal pain

In addition to renal cyst hemorrhage, the differential diagnosis of abdominal pain in a patient with ADPKD includes cyst enlargement causing stretching of the renal capsule or traction on the renal pedicle, cyst infection, nephrolithiasis, pyelonephritis, and rarely, tumors including renal cell carcinoma.

Unlike cyst rupture and hemorrhage, which are associated with point tenderness, cyst infection often manifests as diffuse, usually unilateral flank pain with associated fever, nausea, malaise, and leukocytosis. Our patient had none of these except for fever, which can also occur in cyst hemorrhage.

Nephrolithiasis occurs in up to 35% of patients with ADPKD,⁷ but no kidney stones were seen on computed tomography in our patient.

Pyelonephritis was unlikely in our patient, given that he had no significant white blood cells in his urinalysis and no leukocytosis.

Abdominal and pelvic imaging did not reveal any tumors in our patient.

A 46-year-old man with a 50-pack-year  smoking history, hepatitis C, and polysubstance abuse presented with worsening joint pain over the past 2 months involving both knees, ankles, wrists, and hands. On examination, along with clubbing of the fingers and toes, he had tenderness and restriction in range of motion in all the affected joints. A fixed, nontender, hard mass was noted in the left axilla extending into the infraclavicular and supraclavicular regions.

Computed tomography (CT) with contrast revealed a mass in the left upper lobe of the lung, eroding the ribs and extending into the axilla, consistent with a suspected diagnosis of lung cancer (Figure 1). Radiography of the hands and feet showed thickening of the periosteal membrane and periosteal formation of new bone (Figure 2). A bone scan revealed diffuse increased uptake in the affected joints with no metastases (Figure 3). A workup for brain and adrenal metastases was negative. CT-guided needle biopsy confirmed adenocarcinoma of the lung.

The final diagnosis was hypertrophic pulmonary osteoarthropathy (HPOA) secondary to stage IIIB: T4N2M0 adenocarcinoma of the lung. Resection of the lung mass was deemed difficult, so the patient was scheduled for neoadjuvant concurrent chemoradiation therapy before resection. Ibuprofen and intravenous pamidronate provided symptom relief.

HYPERTROPHIC PULMONARY OSTEOARTHROPATHY

HPOA is characterized by abnormal proliferation of the skin and periosteal formation of new bone at the distal ends of long bones, metatarsals, metacarpals, and proximal phalanges.

Primary HPOA is genetically inherited and accounts for 5% of cases, while secondary HPOA, accounting for the other 95%, is a paraneoplastic syndrome.¹ Secondary HPOA is most commonly associated with lung cancer, usually stage III or IV adenocarcinoma.¹ However, only 1% of lung cancer patients develop HPOA.¹

Other conditions linked to secondary HPOA are mesothelioma, renal cell carcinoma, gastrointestinal cancers, melanoma, thymic cancer, nasopharyngeal cancers, and Hodgkin lymphoma. HPOA is also associated with pulmonary infection, cystic fibrosis, and right-to-left cardiac shunt. Risk factors associated with secondary HPOA are smoking, male sex, and age greater than 55.

Patients often present with unremitting pain, edema, and erythema in the extremities. Radiography reveals periosteal membrane thickening and periosteal new bone formation.¹ Findings on bone scintigraphy that confirm the diagnosis include diffuse increased uptake and bracelet-like uptake.

The prognosis and treatment of secondary HPOA are directly related to the underlying disease. Symptoms can be relieved with nonsteroidal anti-inflammatory drugs, bisphosphonates, and octreotide. Unilateral vagotomy is an option in refractory cases.^1,2

A 46-year-old man with a 50-pack-year  smoking history, hepatitis C, and polysubstance abuse presented with worsening joint pain over the past 2 months involving both knees, ankles, wrists, and hands. On examination, along with clubbing of the fingers and toes, he had tenderness and restriction in range of motion in all the affected joints. A fixed, nontender, hard mass was noted in the left axilla extending into the infraclavicular and supraclavicular regions.

Computed tomography (CT) with contrast revealed a mass in the left upper lobe of the lung, eroding the ribs and extending into the axilla, consistent with a suspected diagnosis of lung cancer (Figure 1). Radiography of the hands and feet showed thickening of the periosteal membrane and periosteal formation of new bone (Figure 2). A bone scan revealed diffuse increased uptake in the affected joints with no metastases (Figure 3). A workup for brain and adrenal metastases was negative. CT-guided needle biopsy confirmed adenocarcinoma of the lung.

The final diagnosis was hypertrophic pulmonary osteoarthropathy (HPOA) secondary to stage IIIB: T4N2M0 adenocarcinoma of the lung. Resection of the lung mass was deemed difficult, so the patient was scheduled for neoadjuvant concurrent chemoradiation therapy before resection. Ibuprofen and intravenous pamidronate provided symptom relief.

HYPERTROPHIC PULMONARY OSTEOARTHROPATHY

HPOA is characterized by abnormal proliferation of the skin and periosteal formation of new bone at the distal ends of long bones, metatarsals, metacarpals, and proximal phalanges.

Primary HPOA is genetically inherited and accounts for 5% of cases, while secondary HPOA, accounting for the other 95%, is a paraneoplastic syndrome.¹ Secondary HPOA is most commonly associated with lung cancer, usually stage III or IV adenocarcinoma.¹ However, only 1% of lung cancer patients develop HPOA.¹

Other conditions linked to secondary HPOA are mesothelioma, renal cell carcinoma, gastrointestinal cancers, melanoma, thymic cancer, nasopharyngeal cancers, and Hodgkin lymphoma. HPOA is also associated with pulmonary infection, cystic fibrosis, and right-to-left cardiac shunt. Risk factors associated with secondary HPOA are smoking, male sex, and age greater than 55.

Patients often present with unremitting pain, edema, and erythema in the extremities. Radiography reveals periosteal membrane thickening and periosteal new bone formation.¹ Findings on bone scintigraphy that confirm the diagnosis include diffuse increased uptake and bracelet-like uptake.

The prognosis and treatment of secondary HPOA are directly related to the underlying disease. Symptoms can be relieved with nonsteroidal anti-inflammatory drugs, bisphosphonates, and octreotide. Unilateral vagotomy is an option in refractory cases.^1,2

A 46-year-old man with a 50-pack-year  smoking history, hepatitis C, and polysubstance abuse presented with worsening joint pain over the past 2 months involving both knees, ankles, wrists, and hands. On examination, along with clubbing of the fingers and toes, he had tenderness and restriction in range of motion in all the affected joints. A fixed, nontender, hard mass was noted in the left axilla extending into the infraclavicular and supraclavicular regions.

Computed tomography (CT) with contrast revealed a mass in the left upper lobe of the lung, eroding the ribs and extending into the axilla, consistent with a suspected diagnosis of lung cancer (Figure 1). Radiography of the hands and feet showed thickening of the periosteal membrane and periosteal formation of new bone (Figure 2). A bone scan revealed diffuse increased uptake in the affected joints with no metastases (Figure 3). A workup for brain and adrenal metastases was negative. CT-guided needle biopsy confirmed adenocarcinoma of the lung.

The final diagnosis was hypertrophic pulmonary osteoarthropathy (HPOA) secondary to stage IIIB: T4N2M0 adenocarcinoma of the lung. Resection of the lung mass was deemed difficult, so the patient was scheduled for neoadjuvant concurrent chemoradiation therapy before resection. Ibuprofen and intravenous pamidronate provided symptom relief.

HYPERTROPHIC PULMONARY OSTEOARTHROPATHY

HPOA is characterized by abnormal proliferation of the skin and periosteal formation of new bone at the distal ends of long bones, metatarsals, metacarpals, and proximal phalanges.

Primary HPOA is genetically inherited and accounts for 5% of cases, while secondary HPOA, accounting for the other 95%, is a paraneoplastic syndrome.¹ Secondary HPOA is most commonly associated with lung cancer, usually stage III or IV adenocarcinoma.¹ However, only 1% of lung cancer patients develop HPOA.¹

Other conditions linked to secondary HPOA are mesothelioma, renal cell carcinoma, gastrointestinal cancers, melanoma, thymic cancer, nasopharyngeal cancers, and Hodgkin lymphoma. HPOA is also associated with pulmonary infection, cystic fibrosis, and right-to-left cardiac shunt. Risk factors associated with secondary HPOA are smoking, male sex, and age greater than 55.

Patients often present with unremitting pain, edema, and erythema in the extremities. Radiography reveals periosteal membrane thickening and periosteal new bone formation.¹ Findings on bone scintigraphy that confirm the diagnosis include diffuse increased uptake and bracelet-like uptake.

The prognosis and treatment of secondary HPOA are directly related to the underlying disease. Symptoms can be relieved with nonsteroidal anti-inflammatory drugs, bisphosphonates, and octreotide. Unilateral vagotomy is an option in refractory cases.^1,2

After 4 decades of clinical practice in a teaching hospital, I believe that the notes we write to document medical consultations are too long. When I review them for my own patients, the only part I read is the consultant’s assessment and diagnostic and therapeutic recommendations. Many of my colleagues and trainees do the same.

In the old days, when medical records were handwritten, the first three pages of my hospital’s four-page consultation form were for the history, review of systems, physical examination, and test results. The top two-thirds of the last page was for diagnostic impressions and recommendations for additional testing and treatment, to be completed by the trainee performing the consultation.

This left only the bottom third of this page for attestation and additional remarks from the senior consultant. Often, this last (but most used) page was just a bullet list of diagnostic possibilities and suggested tests and treatments, with nothing about the critical reasoning underlying the differential diagnosis and recommendations. This was probably the result of fatigue from having to fill in the first three pages by hand, and then having only limited space on the final page.

Even though the written record has been replaced by the electronic medical record in my hospital, consult notes continue to be at least as long as before, without any change in the length of the assessment and recommendations section. I would guess this is true in most institutions and practices that have switched to an electronic record system.

WHY ARE CONSULT NOTES SO LONG?

The main factor contributing to the lengthy consultation document is that the Center for Medicare and Medicaid Services, with other third-party payers following suit, ties the level of reimbursement to detailed documentation of the history (present, past medical, past surgical, medications, allergies, social, and family), review of systems, and physical examination in the consultation.¹ Physicians are under constant pressure from professional fee-coders to meet these requirements.

Avoid repeating what is already in the record, but include your reasoning and teaching points

Since most of this information is already in the medical record, to require that it be documented again in the consultation note is unnecessary duplication. I believe that consultants comply with this requirement mainly to ensure adequate reimbursement, even though they know that the referring medical team will probably not read the repeated information.

Electronic medical record systems, which focus disproportionately on meeting insurers’ requirements governing reimbursement,^2–5 have made it easier to create a lengthy consult note by checking boxes in templates and copying and pasting from other parts of the electronic record.^2,6–12 Although verbatim copying and pasting may result in punitive audits by insurers, this practice remains common,¹³ including, in my experience, in consultations.

WHAT ARE THE NEGATIVE EFFECTS OF A NEEDLESSLY LONG CONSULT NOTE?

Time spent on repeating information—even if less time is required when using an electronic system—is clearly time wasted, since this part of the consult note is hardly ever read. Equally bad, the assessment and recommendations section in consult notes continues to be very short, probably because long-standing physician practices change slowly.

An ideal consult note has been described as one that, in addition to addressing the patient care issues, is as brief as possible, avoids duplication of already documented information, and has educational value to the person requesting it.^14,15 The educational value of the consultation is especially important in teaching hospitals.

If the only part of the consultation perused in depth consists merely of lists of diagnoses, recommended tests, and therapy and does not include the consultant’s critical reasoning underlying them, the educational value of the consultation is lost.

HOW CAN THE FORMAT BE MADE SHORTER, YET MORE USEFUL?

The note should begin by briefly documenting the reason the consultation was requested. Ideally, institutions should train their staff to state this very specifically. For example, instead of “clearance for surgery,” it is better to ask, “Please identify risks involved in proposed surgery and suggest ways to reduce them.” The former steers the consultant to merely say “cleared for surgery, but with increased risk,” whereas the latter ensures a more specific and detailed response.

The consulting team must review in detail and verify the accuracy of all available information in the patient’s record. Once this is done, instead of repeating it, a statement that all existing information has been thoroughly reviewed should suffice, with mention in a separate paragraph of only the additional relevant positive or negative points in the history related to the issue the consultant has been asked to address.

The consultant shares with all users of the medical record the responsibility of pointing out and correcting any errors in the previously recorded information, thereby decreasing perpetuation of erroneous “chart lore,” an undesirable consequence of copying and pasting. If only previously unrecorded data and corrections to existing information are documented, the referring team is more likely to read the note because it points out relevant information that has been overlooked.

The main part should consist of a detailed assessment and recommendations section

The main part of the document should consist of a detailed assessment and recommendations section, which should include not only a list of diagnoses and recommendations for testing and treatment, but also the consultant’s reasoning behind them, the results of tests already obtained that support the consultant’s conclusions, and information of value for teaching and cost-effective practice. A critically reasoned assessment and recommendation section not only will prove very educational, but by challenging the consultant to justify his or her choices, may discourage unnecessary testing and questionable therapy^4,14 and thereby contribute to cost-saving.

My suggestions would not shorten the time spent by the consulting team in evaluating the patient, but only eliminate redundant documentation. I believe the consultation document will be shorter but adequate for patient care, the referring team will read and use the entire document, its educational value will be enhanced, and the time spent on redundant documentation will be saved.

A CASE VIGNETTE

The following vignette (from my own subspecialty) of a patient with acute kidney injury illustrates how a consult note can be made shorter but more useful and educational.

A 78-year-old man had a history of long-standing insulin-requiring diabetes mellitus, hypertension (treated with lisinopril and amlodipine), and benign prostatic hypertrophy. One month earlier, his blood urea nitrogen level had been 15 mg/dL and his serum creatinine had been 1.2 mg/dL.

He presented with a 3-day history of vomiting, diarrhea, and fever, presumed to be viral gastroenteritis. His blood urea nitrogen level was 100 mg, serum creatinine 2.5 mg, and blood glucose 450 mg/dL. Urinalysis revealed 2+ albuminuria, 3+ glucosuria, and 6 red blood cells per high-power field.

In the emergency department he received 2 L of normal saline and regular insulin intravenously, and an indwelling bladder catheter was inserted. He was admitted after 6 hours.

Tests obtained on arrival on the inpatient floor revealed a urinary fractional excretion of sodium of 2.5% and a blood glucose level of 295 mg/dL. His admission history and physical listed his home medications as insulin glargine, amlodipine, lisinopril, and tamsulosin. It also listed the differential diagnosis for acute kidney injury as:

• Prerenal azotemia due to volume depletion
• Rapidly progressive glomerulonephritis to be ruled out in view of proteinuria and microhematuria
• Obstructive uropathy to be ruled out.

Ultrasonography the morning after admission showed normal kidneys and no hydronephrosis. The absence of hydronephrosis was interpreted by the primary team as ruling out obstruction secondary to benign prostatic hypertrophy. The nephrology team saw the patient in consultation the day after admission and discovered the following additional information: urinalysis done 6 months earlier had also shown albuminuria and microhematuria, and the patient had been taking over-the-counter ibuprofen 400 mg three times daily for several days prior to admission.

Table 1 compares consultation documentation in the usual format and in the format I am suggesting. The revised format has much more information of educational value (eg, the importance of reviewing past urinalysis results, asking about over-the-counter medications, factors affecting fractional excretion of sodium, effect of bladder catheterization on hydronephrosis due to benign prostatic hypertrophy, and measuring urine protein only after acute kidney injury resolves). It also encourages cost-effective care (ultrasonography could have been delayed or avoided, and the patient could have been cautioned about ibuprofen-like drugs to decrease the risk of recurrent acute kidney injury).

FINAL THOUGHTS

The modifications I have suggested in consult notes will be accepted only if they are reimbursement-neutral. I hope insurers will not equate a shorter note with an opportunity to lower reimbursement and will see the value in not paying for things almost never read. I hope they will recognize and pay for the effort that went into creating a shorter document that contributes adequately to patient care, provides greater educational value, and may promote cost-effective medical practice. Also, not requiring redundant documentation may reduce or even eliminate undesirable copying and pasting.

Accountable-care organizations are an important part of the Affordable Care Act,¹⁶ which went into effect in 2014. Many organizations had already come into existence in the United States before the act became effective, and their numbers and the number of patients covered by them are projected to grow enormously over the next few years.¹⁷

Since the accountable-care organization model will rely heavily on capitated reimbursement to contain costs, these organizations are likely to scrutinize and curtail the use of consultations. I believe that a shorter consultation note—yet one that is more useful for patient care, education, and cost-containment—is more likely to pass such scrutiny, especially if it decreases time spent on documentation. Furthermore, unlike the fee-for-service model, in a capitated-payment system it may not be necessary to lengthen consultation documentation just to ensure adequate reimbursement.

After 4 decades of clinical practice in a teaching hospital, I believe that the notes we write to document medical consultations are too long. When I review them for my own patients, the only part I read is the consultant’s assessment and diagnostic and therapeutic recommendations. Many of my colleagues and trainees do the same.

In the old days, when medical records were handwritten, the first three pages of my hospital’s four-page consultation form were for the history, review of systems, physical examination, and test results. The top two-thirds of the last page was for diagnostic impressions and recommendations for additional testing and treatment, to be completed by the trainee performing the consultation.

This left only the bottom third of this page for attestation and additional remarks from the senior consultant. Often, this last (but most used) page was just a bullet list of diagnostic possibilities and suggested tests and treatments, with nothing about the critical reasoning underlying the differential diagnosis and recommendations. This was probably the result of fatigue from having to fill in the first three pages by hand, and then having only limited space on the final page.

Even though the written record has been replaced by the electronic medical record in my hospital, consult notes continue to be at least as long as before, without any change in the length of the assessment and recommendations section. I would guess this is true in most institutions and practices that have switched to an electronic record system.

WHY ARE CONSULT NOTES SO LONG?

The main factor contributing to the lengthy consultation document is that the Center for Medicare and Medicaid Services, with other third-party payers following suit, ties the level of reimbursement to detailed documentation of the history (present, past medical, past surgical, medications, allergies, social, and family), review of systems, and physical examination in the consultation.¹ Physicians are under constant pressure from professional fee-coders to meet these requirements.

Avoid repeating what is already in the record, but include your reasoning and teaching points

Since most of this information is already in the medical record, to require that it be documented again in the consultation note is unnecessary duplication. I believe that consultants comply with this requirement mainly to ensure adequate reimbursement, even though they know that the referring medical team will probably not read the repeated information.

Electronic medical record systems, which focus disproportionately on meeting insurers’ requirements governing reimbursement,^2–5 have made it easier to create a lengthy consult note by checking boxes in templates and copying and pasting from other parts of the electronic record.^2,6–12 Although verbatim copying and pasting may result in punitive audits by insurers, this practice remains common,¹³ including, in my experience, in consultations.

WHAT ARE THE NEGATIVE EFFECTS OF A NEEDLESSLY LONG CONSULT NOTE?

Time spent on repeating information—even if less time is required when using an electronic system—is clearly time wasted, since this part of the consult note is hardly ever read. Equally bad, the assessment and recommendations section in consult notes continues to be very short, probably because long-standing physician practices change slowly.

An ideal consult note has been described as one that, in addition to addressing the patient care issues, is as brief as possible, avoids duplication of already documented information, and has educational value to the person requesting it.^14,15 The educational value of the consultation is especially important in teaching hospitals.

If the only part of the consultation perused in depth consists merely of lists of diagnoses, recommended tests, and therapy and does not include the consultant’s critical reasoning underlying them, the educational value of the consultation is lost.

HOW CAN THE FORMAT BE MADE SHORTER, YET MORE USEFUL?

The note should begin by briefly documenting the reason the consultation was requested. Ideally, institutions should train their staff to state this very specifically. For example, instead of “clearance for surgery,” it is better to ask, “Please identify risks involved in proposed surgery and suggest ways to reduce them.” The former steers the consultant to merely say “cleared for surgery, but with increased risk,” whereas the latter ensures a more specific and detailed response.

The consulting team must review in detail and verify the accuracy of all available information in the patient’s record. Once this is done, instead of repeating it, a statement that all existing information has been thoroughly reviewed should suffice, with mention in a separate paragraph of only the additional relevant positive or negative points in the history related to the issue the consultant has been asked to address.

The consultant shares with all users of the medical record the responsibility of pointing out and correcting any errors in the previously recorded information, thereby decreasing perpetuation of erroneous “chart lore,” an undesirable consequence of copying and pasting. If only previously unrecorded data and corrections to existing information are documented, the referring team is more likely to read the note because it points out relevant information that has been overlooked.

The main part should consist of a detailed assessment and recommendations section

The main part of the document should consist of a detailed assessment and recommendations section, which should include not only a list of diagnoses and recommendations for testing and treatment, but also the consultant’s reasoning behind them, the results of tests already obtained that support the consultant’s conclusions, and information of value for teaching and cost-effective practice. A critically reasoned assessment and recommendation section not only will prove very educational, but by challenging the consultant to justify his or her choices, may discourage unnecessary testing and questionable therapy^4,14 and thereby contribute to cost-saving.

My suggestions would not shorten the time spent by the consulting team in evaluating the patient, but only eliminate redundant documentation. I believe the consultation document will be shorter but adequate for patient care, the referring team will read and use the entire document, its educational value will be enhanced, and the time spent on redundant documentation will be saved.

A CASE VIGNETTE

The following vignette (from my own subspecialty) of a patient with acute kidney injury illustrates how a consult note can be made shorter but more useful and educational.

A 78-year-old man had a history of long-standing insulin-requiring diabetes mellitus, hypertension (treated with lisinopril and amlodipine), and benign prostatic hypertrophy. One month earlier, his blood urea nitrogen level had been 15 mg/dL and his serum creatinine had been 1.2 mg/dL.

He presented with a 3-day history of vomiting, diarrhea, and fever, presumed to be viral gastroenteritis. His blood urea nitrogen level was 100 mg, serum creatinine 2.5 mg, and blood glucose 450 mg/dL. Urinalysis revealed 2+ albuminuria, 3+ glucosuria, and 6 red blood cells per high-power field.

In the emergency department he received 2 L of normal saline and regular insulin intravenously, and an indwelling bladder catheter was inserted. He was admitted after 6 hours.

Tests obtained on arrival on the inpatient floor revealed a urinary fractional excretion of sodium of 2.5% and a blood glucose level of 295 mg/dL. His admission history and physical listed his home medications as insulin glargine, amlodipine, lisinopril, and tamsulosin. It also listed the differential diagnosis for acute kidney injury as:

• Prerenal azotemia due to volume depletion
• Rapidly progressive glomerulonephritis to be ruled out in view of proteinuria and microhematuria
• Obstructive uropathy to be ruled out.

Ultrasonography the morning after admission showed normal kidneys and no hydronephrosis. The absence of hydronephrosis was interpreted by the primary team as ruling out obstruction secondary to benign prostatic hypertrophy. The nephrology team saw the patient in consultation the day after admission and discovered the following additional information: urinalysis done 6 months earlier had also shown albuminuria and microhematuria, and the patient had been taking over-the-counter ibuprofen 400 mg three times daily for several days prior to admission.

Table 1 compares consultation documentation in the usual format and in the format I am suggesting. The revised format has much more information of educational value (eg, the importance of reviewing past urinalysis results, asking about over-the-counter medications, factors affecting fractional excretion of sodium, effect of bladder catheterization on hydronephrosis due to benign prostatic hypertrophy, and measuring urine protein only after acute kidney injury resolves). It also encourages cost-effective care (ultrasonography could have been delayed or avoided, and the patient could have been cautioned about ibuprofen-like drugs to decrease the risk of recurrent acute kidney injury).

FINAL THOUGHTS

The modifications I have suggested in consult notes will be accepted only if they are reimbursement-neutral. I hope insurers will not equate a shorter note with an opportunity to lower reimbursement and will see the value in not paying for things almost never read. I hope they will recognize and pay for the effort that went into creating a shorter document that contributes adequately to patient care, provides greater educational value, and may promote cost-effective medical practice. Also, not requiring redundant documentation may reduce or even eliminate undesirable copying and pasting.

Accountable-care organizations are an important part of the Affordable Care Act,¹⁶ which went into effect in 2014. Many organizations had already come into existence in the United States before the act became effective, and their numbers and the number of patients covered by them are projected to grow enormously over the next few years.¹⁷

Since the accountable-care organization model will rely heavily on capitated reimbursement to contain costs, these organizations are likely to scrutinize and curtail the use of consultations. I believe that a shorter consultation note—yet one that is more useful for patient care, education, and cost-containment—is more likely to pass such scrutiny, especially if it decreases time spent on documentation. Furthermore, unlike the fee-for-service model, in a capitated-payment system it may not be necessary to lengthen consultation documentation just to ensure adequate reimbursement.

After 4 decades of clinical practice in a teaching hospital, I believe that the notes we write to document medical consultations are too long. When I review them for my own patients, the only part I read is the consultant’s assessment and diagnostic and therapeutic recommendations. Many of my colleagues and trainees do the same.

In the old days, when medical records were handwritten, the first three pages of my hospital’s four-page consultation form were for the history, review of systems, physical examination, and test results. The top two-thirds of the last page was for diagnostic impressions and recommendations for additional testing and treatment, to be completed by the trainee performing the consultation.

This left only the bottom third of this page for attestation and additional remarks from the senior consultant. Often, this last (but most used) page was just a bullet list of diagnostic possibilities and suggested tests and treatments, with nothing about the critical reasoning underlying the differential diagnosis and recommendations. This was probably the result of fatigue from having to fill in the first three pages by hand, and then having only limited space on the final page.

Even though the written record has been replaced by the electronic medical record in my hospital, consult notes continue to be at least as long as before, without any change in the length of the assessment and recommendations section. I would guess this is true in most institutions and practices that have switched to an electronic record system.

WHY ARE CONSULT NOTES SO LONG?

The main factor contributing to the lengthy consultation document is that the Center for Medicare and Medicaid Services, with other third-party payers following suit, ties the level of reimbursement to detailed documentation of the history (present, past medical, past surgical, medications, allergies, social, and family), review of systems, and physical examination in the consultation.¹ Physicians are under constant pressure from professional fee-coders to meet these requirements.

Avoid repeating what is already in the record, but include your reasoning and teaching points

Since most of this information is already in the medical record, to require that it be documented again in the consultation note is unnecessary duplication. I believe that consultants comply with this requirement mainly to ensure adequate reimbursement, even though they know that the referring medical team will probably not read the repeated information.

Electronic medical record systems, which focus disproportionately on meeting insurers’ requirements governing reimbursement,^2–5 have made it easier to create a lengthy consult note by checking boxes in templates and copying and pasting from other parts of the electronic record.^2,6–12 Although verbatim copying and pasting may result in punitive audits by insurers, this practice remains common,¹³ including, in my experience, in consultations.

WHAT ARE THE NEGATIVE EFFECTS OF A NEEDLESSLY LONG CONSULT NOTE?

Time spent on repeating information—even if less time is required when using an electronic system—is clearly time wasted, since this part of the consult note is hardly ever read. Equally bad, the assessment and recommendations section in consult notes continues to be very short, probably because long-standing physician practices change slowly.

An ideal consult note has been described as one that, in addition to addressing the patient care issues, is as brief as possible, avoids duplication of already documented information, and has educational value to the person requesting it.^14,15 The educational value of the consultation is especially important in teaching hospitals.

If the only part of the consultation perused in depth consists merely of lists of diagnoses, recommended tests, and therapy and does not include the consultant’s critical reasoning underlying them, the educational value of the consultation is lost.

HOW CAN THE FORMAT BE MADE SHORTER, YET MORE USEFUL?

The note should begin by briefly documenting the reason the consultation was requested. Ideally, institutions should train their staff to state this very specifically. For example, instead of “clearance for surgery,” it is better to ask, “Please identify risks involved in proposed surgery and suggest ways to reduce them.” The former steers the consultant to merely say “cleared for surgery, but with increased risk,” whereas the latter ensures a more specific and detailed response.

The consulting team must review in detail and verify the accuracy of all available information in the patient’s record. Once this is done, instead of repeating it, a statement that all existing information has been thoroughly reviewed should suffice, with mention in a separate paragraph of only the additional relevant positive or negative points in the history related to the issue the consultant has been asked to address.

The consultant shares with all users of the medical record the responsibility of pointing out and correcting any errors in the previously recorded information, thereby decreasing perpetuation of erroneous “chart lore,” an undesirable consequence of copying and pasting. If only previously unrecorded data and corrections to existing information are documented, the referring team is more likely to read the note because it points out relevant information that has been overlooked.

The main part should consist of a detailed assessment and recommendations section

The main part of the document should consist of a detailed assessment and recommendations section, which should include not only a list of diagnoses and recommendations for testing and treatment, but also the consultant’s reasoning behind them, the results of tests already obtained that support the consultant’s conclusions, and information of value for teaching and cost-effective practice. A critically reasoned assessment and recommendation section not only will prove very educational, but by challenging the consultant to justify his or her choices, may discourage unnecessary testing and questionable therapy^4,14 and thereby contribute to cost-saving.

My suggestions would not shorten the time spent by the consulting team in evaluating the patient, but only eliminate redundant documentation. I believe the consultation document will be shorter but adequate for patient care, the referring team will read and use the entire document, its educational value will be enhanced, and the time spent on redundant documentation will be saved.

A CASE VIGNETTE

The following vignette (from my own subspecialty) of a patient with acute kidney injury illustrates how a consult note can be made shorter but more useful and educational.

A 78-year-old man had a history of long-standing insulin-requiring diabetes mellitus, hypertension (treated with lisinopril and amlodipine), and benign prostatic hypertrophy. One month earlier, his blood urea nitrogen level had been 15 mg/dL and his serum creatinine had been 1.2 mg/dL.

He presented with a 3-day history of vomiting, diarrhea, and fever, presumed to be viral gastroenteritis. His blood urea nitrogen level was 100 mg, serum creatinine 2.5 mg, and blood glucose 450 mg/dL. Urinalysis revealed 2+ albuminuria, 3+ glucosuria, and 6 red blood cells per high-power field.

In the emergency department he received 2 L of normal saline and regular insulin intravenously, and an indwelling bladder catheter was inserted. He was admitted after 6 hours.

Tests obtained on arrival on the inpatient floor revealed a urinary fractional excretion of sodium of 2.5% and a blood glucose level of 295 mg/dL. His admission history and physical listed his home medications as insulin glargine, amlodipine, lisinopril, and tamsulosin. It also listed the differential diagnosis for acute kidney injury as:

• Prerenal azotemia due to volume depletion
• Rapidly progressive glomerulonephritis to be ruled out in view of proteinuria and microhematuria
• Obstructive uropathy to be ruled out.

Ultrasonography the morning after admission showed normal kidneys and no hydronephrosis. The absence of hydronephrosis was interpreted by the primary team as ruling out obstruction secondary to benign prostatic hypertrophy. The nephrology team saw the patient in consultation the day after admission and discovered the following additional information: urinalysis done 6 months earlier had also shown albuminuria and microhematuria, and the patient had been taking over-the-counter ibuprofen 400 mg three times daily for several days prior to admission.

Table 1 compares consultation documentation in the usual format and in the format I am suggesting. The revised format has much more information of educational value (eg, the importance of reviewing past urinalysis results, asking about over-the-counter medications, factors affecting fractional excretion of sodium, effect of bladder catheterization on hydronephrosis due to benign prostatic hypertrophy, and measuring urine protein only after acute kidney injury resolves). It also encourages cost-effective care (ultrasonography could have been delayed or avoided, and the patient could have been cautioned about ibuprofen-like drugs to decrease the risk of recurrent acute kidney injury).

FINAL THOUGHTS

The modifications I have suggested in consult notes will be accepted only if they are reimbursement-neutral. I hope insurers will not equate a shorter note with an opportunity to lower reimbursement and will see the value in not paying for things almost never read. I hope they will recognize and pay for the effort that went into creating a shorter document that contributes adequately to patient care, provides greater educational value, and may promote cost-effective medical practice. Also, not requiring redundant documentation may reduce or even eliminate undesirable copying and pasting.

Accountable-care organizations are an important part of the Affordable Care Act,¹⁶ which went into effect in 2014. Many organizations had already come into existence in the United States before the act became effective, and their numbers and the number of patients covered by them are projected to grow enormously over the next few years.¹⁷

Since the accountable-care organization model will rely heavily on capitated reimbursement to contain costs, these organizations are likely to scrutinize and curtail the use of consultations. I believe that a shorter consultation note—yet one that is more useful for patient care, education, and cost-containment—is more likely to pass such scrutiny, especially if it decreases time spent on documentation. Furthermore, unlike the fee-for-service model, in a capitated-payment system it may not be necessary to lengthen consultation documentation just to ensure adequate reimbursement.

Bob Dylan’s song “The Times They Are a-Changin’” was released in January 1964. As with many things Dylan, the song’s true intent is a bit unclear, but it remains one of the most invoked lyrical symbols of change 51 years later. In 2015, the Journal, planning to “heed the call,” is changing its online visage. I hope that our intent will not be viewed as unclear.

Our mission is unchanged: to provide our readers with free access to credible, relevant, readable information, and the opportunity to earn free CME credit. So why change the website? Innovations in digital publishing, the ability to offer a broader landscape of medical information—and the chance to more effectively solicit advertising to pay for it all—prompted us to collaborate with another publisher, Frontline Medical Communications.

Frontline describes itself as health care’s largest medical communications company and as a leader in digital, print, and live events. You likely have encountered their products, which include Internal Medicine News, Cardiology News, and Clinical Endocrinology News, and CME courses such as Perspectives in Rheumatic Diseases, which I codirect. Our collaboration will allow us to offer you links to new and, we hope, interesting material. For example, our online readers will have access to MD-IQ, a popular interactive self-test, as well as brief reports and timely commentaries from specialty scientific meetings.

But even though www.ccjm.org has a new look, everything on it remains open to all and free of charge. You will still have easy access to other educational and clinical information offered by Cleveland Clinic, including information about Clinic authors. At your first visit to our revamped site you will be asked to register, but your subsequent visits will be unencumbered except for a request to sign in using your e-mail address if you log in from a different device. The e-mail address is used for identification purposes only, as site sponsors want to know the (depersonalized) demographics of our readership. You will receive occasional e-mails with links to clinical content that may interest you. If you do not wish to receive these e-mails, just follow the instructions to opt out of them. Our goal is to be unobtrusive.

Our free CME process is the same. Each CME article includes a link to the Cleveland Clinic Center for Continuing Education site with instructions on how to complete the activity. Plus, the CME pull-down menu at the top of our home page will provide easy access to all currently active journal CME offerings. We hope the transition glitches will be few and the benefits many. And the option remains for you to read, download, and print our articles in PDF format, just as you always have.

As we start the new year, we at the Journal wish you our readers a happy, healthy, peaceful, and educational 2015.

Bob Dylan’s song “The Times They Are a-Changin’” was released in January 1964. As with many things Dylan, the song’s true intent is a bit unclear, but it remains one of the most invoked lyrical symbols of change 51 years later. In 2015, the Journal, planning to “heed the call,” is changing its online visage. I hope that our intent will not be viewed as unclear.

Our mission is unchanged: to provide our readers with free access to credible, relevant, readable information, and the opportunity to earn free CME credit. So why change the website? Innovations in digital publishing, the ability to offer a broader landscape of medical information—and the chance to more effectively solicit advertising to pay for it all—prompted us to collaborate with another publisher, Frontline Medical Communications.

Frontline describes itself as health care’s largest medical communications company and as a leader in digital, print, and live events. You likely have encountered their products, which include Internal Medicine News, Cardiology News, and Clinical Endocrinology News, and CME courses such as Perspectives in Rheumatic Diseases, which I codirect. Our collaboration will allow us to offer you links to new and, we hope, interesting material. For example, our online readers will have access to MD-IQ, a popular interactive self-test, as well as brief reports and timely commentaries from specialty scientific meetings.

But even though www.ccjm.org has a new look, everything on it remains open to all and free of charge. You will still have easy access to other educational and clinical information offered by Cleveland Clinic, including information about Clinic authors. At your first visit to our revamped site you will be asked to register, but your subsequent visits will be unencumbered except for a request to sign in using your e-mail address if you log in from a different device. The e-mail address is used for identification purposes only, as site sponsors want to know the (depersonalized) demographics of our readership. You will receive occasional e-mails with links to clinical content that may interest you. If you do not wish to receive these e-mails, just follow the instructions to opt out of them. Our goal is to be unobtrusive.

Our free CME process is the same. Each CME article includes a link to the Cleveland Clinic Center for Continuing Education site with instructions on how to complete the activity. Plus, the CME pull-down menu at the top of our home page will provide easy access to all currently active journal CME offerings. We hope the transition glitches will be few and the benefits many. And the option remains for you to read, download, and print our articles in PDF format, just as you always have.

As we start the new year, we at the Journal wish you our readers a happy, healthy, peaceful, and educational 2015.

Bob Dylan’s song “The Times They Are a-Changin’” was released in January 1964. As with many things Dylan, the song’s true intent is a bit unclear, but it remains one of the most invoked lyrical symbols of change 51 years later. In 2015, the Journal, planning to “heed the call,” is changing its online visage. I hope that our intent will not be viewed as unclear.

Our mission is unchanged: to provide our readers with free access to credible, relevant, readable information, and the opportunity to earn free CME credit. So why change the website? Innovations in digital publishing, the ability to offer a broader landscape of medical information—and the chance to more effectively solicit advertising to pay for it all—prompted us to collaborate with another publisher, Frontline Medical Communications.

Frontline describes itself as health care’s largest medical communications company and as a leader in digital, print, and live events. You likely have encountered their products, which include Internal Medicine News, Cardiology News, and Clinical Endocrinology News, and CME courses such as Perspectives in Rheumatic Diseases, which I codirect. Our collaboration will allow us to offer you links to new and, we hope, interesting material. For example, our online readers will have access to MD-IQ, a popular interactive self-test, as well as brief reports and timely commentaries from specialty scientific meetings.

But even though www.ccjm.org has a new look, everything on it remains open to all and free of charge. You will still have easy access to other educational and clinical information offered by Cleveland Clinic, including information about Clinic authors. At your first visit to our revamped site you will be asked to register, but your subsequent visits will be unencumbered except for a request to sign in using your e-mail address if you log in from a different device. The e-mail address is used for identification purposes only, as site sponsors want to know the (depersonalized) demographics of our readership. You will receive occasional e-mails with links to clinical content that may interest you. If you do not wish to receive these e-mails, just follow the instructions to opt out of them. Our goal is to be unobtrusive.

Our free CME process is the same. Each CME article includes a link to the Cleveland Clinic Center for Continuing Education site with instructions on how to complete the activity. Plus, the CME pull-down menu at the top of our home page will provide easy access to all currently active journal CME offerings. We hope the transition glitches will be few and the benefits many. And the option remains for you to read, download, and print our articles in PDF format, just as you always have.

As we start the new year, we at the Journal wish you our readers a happy, healthy, peaceful, and educational 2015.

In his monthly podcast for The Journal of Community and Supportive Oncology, Dr David Henry discusses articles on the recent approval of ramucirumab for advanced gastric or GEJ adenocarcinoma in previously treated patients with disease progression and the “small victories” in honing new therapies for hard-to-treat cancers such as ovarian, melanoma, and pancreatic. Quality of care and patient quality of life are the basis for the 3 Original Reports that Dr Henry addresses: one study looks at the impact of patient navigation on diagnostic resolution in women with abnormal screenings for breast or cervical cancer; a second examines how the information and communication needs of Chinese American women with breast cancer can be channeled into improving quality of life after treatment for cancer; and a third reports on how dignity therapy as an intervention in patients with advanced colorectal cancer can positively affect the quality of end-of-life care, treatment choices, and cost efficiency.

In his monthly podcast for The Journal of Community and Supportive Oncology, Dr David Henry discusses articles on the recent approval of ramucirumab for advanced gastric or GEJ adenocarcinoma in previously treated patients with disease progression and the “small victories” in honing new therapies for hard-to-treat cancers such as ovarian, melanoma, and pancreatic. Quality of care and patient quality of life are the basis for the 3 Original Reports that Dr Henry addresses: one study looks at the impact of patient navigation on diagnostic resolution in women with abnormal screenings for breast or cervical cancer; a second examines how the information and communication needs of Chinese American women with breast cancer can be channeled into improving quality of life after treatment for cancer; and a third reports on how dignity therapy as an intervention in patients with advanced colorectal cancer can positively affect the quality of end-of-life care, treatment choices, and cost efficiency.

In his monthly podcast for The Journal of Community and Supportive Oncology, Dr David Henry discusses articles on the recent approval of ramucirumab for advanced gastric or GEJ adenocarcinoma in previously treated patients with disease progression and the “small victories” in honing new therapies for hard-to-treat cancers such as ovarian, melanoma, and pancreatic. Quality of care and patient quality of life are the basis for the 3 Original Reports that Dr Henry addresses: one study looks at the impact of patient navigation on diagnostic resolution in women with abnormal screenings for breast or cervical cancer; a second examines how the information and communication needs of Chinese American women with breast cancer can be channeled into improving quality of life after treatment for cancer; and a third reports on how dignity therapy as an intervention in patients with advanced colorectal cancer can positively affect the quality of end-of-life care, treatment choices, and cost efficiency.

SAN FRANCISCO—New research indicates that extending anticoagulant therapy to 2 years can reduce the risk of recurrent venous thromboembolism (VTE) without increasing major bleeding, but this benefit only lasts while patients are receiving the therapy.

In the PADIS-PE study, patients with a first episode of symptomatic, unprovoked pulmonary embolism (PE) received 6 months of treatment with a vitamin K antagonist (VKA), followed by 18 months of warfarin or placebo.

Patients who received warfarin had a 77% reduction in the relative risk of recurrent VTE or major bleeding while they received treatment. But an additional 2 years of follow-up showed that this benefit was lost once patients stopped anticoagulation.

Francis Couturaud, MD, PhD, of the Brest University Hospital Center in Brest, France, presented these data at the 2014 ASH Annual Meeting as LBA-3.*

He and his colleagues randomized patients to receive warfarin (n=184) or placebo (n=187) for 18 months after their intial VKA treatment. Patients were followed for an additional 24 months after treatment ended.

Most baseline characteristics were similar between the treatment arms, although there was a significantly higher percentage of females in the warfarin arm.

“[Overall,] the mean age was below 60, [and] the mean BMI [body mass index] was below 30,” Dr Couturaud noted. “About 4% of patients had previous cancer [that had been] resolved for more than 2 years, 8% had previous distal DVT [deep vein thrombosis] or superficial venous thrombosis, a quarter of women were on estrogen-containing pills, and about one-third had an associated proximal DVT at the time of PE diagnosis.”

“Before the randomization, the mean duration of VKA [therapy] was 6 months, and the mean percentage of time within the therapeutic range was 70. At inclusion, about one-third of patients had residual perfusion defect, about 15% had residual DVT, the mean D-dimer level was below 500 μg/L, and about 27% had thrombophilia.”

Results

The study’s primary outcome was the composite of recurrent VTE or major bleeding during the 18-month treatment period. Significantly fewer patients met this endpoint in the warfarin arm than in the placebo arm—6 (3.3%) and 25 (13.5%), respectively (hazard ratio [HR]=0.23, P=0.0004).

Likewise, the number of patients with recurrent VTE at 18 months was significantly lower in the warfarin arm than in the placebo arm—3 (1.7%) and 25 (13.5%), respectively (HR=0.11, P<0.0001).

On the other hand, there was no significant difference in the rate of major bleeding between the treatment arms at 18 months. Four patients (2.2%) had major bleeding in the warfarin arm, as did 1 (0.5%) in the placebo arm (HR=4.07, P=0.18).

At 42 months, there was no significant difference between the treatment arms with regard to the composite outcome, the rate of recurrent VTE, or the rate of major bleeding.

The composite outcome occurred in 33 (20.8%) patients in the warfarin arm and 42 (24%) in the placebo arm (HR=0.74, P=0.19). Recurrent VTE occurred in 28 (17.9%) and 39 patients (22.1%), respectively (HR=0.67, P=0.10). And major bleeding occurred in 6 (3.5%) and 5 patients (3%), respectively (HR=1.12, P=0.71).

“[E]xtending anticoagulation for 18 additional months was associated with a major relative risk reduction of 77% of recurrent VTE or major bleeding during the treatment period,” Dr Couturaud said in summary. “However, this benefit was lost during a long-term follow-up of 2 years after stopping anticoagulation.”

“In addition, recurrent VTE occurred in 80% of cases as recurrent PE and in 90% of cases as unprovoked VTE. So additional investigations are needed to identify subgroups of patients at lower risk who may not need indefinite anticoagulation.”

This study was sponsored by Brest University Hospital. Investigators received research funding from Actelion Pharmaceuticals, GlaxoSmithKline, Bristol-Myers Squibb, Boehringer Ingelheim, Sanofi, LEO Pharma, and Bayer.

*Information in the abstract differs from that presented at the meeting.

SAN FRANCISCO—New research indicates that extending anticoagulant therapy to 2 years can reduce the risk of recurrent venous thromboembolism (VTE) without increasing major bleeding, but this benefit only lasts while patients are receiving the therapy.

In the PADIS-PE study, patients with a first episode of symptomatic, unprovoked pulmonary embolism (PE) received 6 months of treatment with a vitamin K antagonist (VKA), followed by 18 months of warfarin or placebo.

Patients who received warfarin had a 77% reduction in the relative risk of recurrent VTE or major bleeding while they received treatment. But an additional 2 years of follow-up showed that this benefit was lost once patients stopped anticoagulation.

Francis Couturaud, MD, PhD, of the Brest University Hospital Center in Brest, France, presented these data at the 2014 ASH Annual Meeting as LBA-3.*

He and his colleagues randomized patients to receive warfarin (n=184) or placebo (n=187) for 18 months after their intial VKA treatment. Patients were followed for an additional 24 months after treatment ended.

Most baseline characteristics were similar between the treatment arms, although there was a significantly higher percentage of females in the warfarin arm.

“[Overall,] the mean age was below 60, [and] the mean BMI [body mass index] was below 30,” Dr Couturaud noted. “About 4% of patients had previous cancer [that had been] resolved for more than 2 years, 8% had previous distal DVT [deep vein thrombosis] or superficial venous thrombosis, a quarter of women were on estrogen-containing pills, and about one-third had an associated proximal DVT at the time of PE diagnosis.”

“Before the randomization, the mean duration of VKA [therapy] was 6 months, and the mean percentage of time within the therapeutic range was 70. At inclusion, about one-third of patients had residual perfusion defect, about 15% had residual DVT, the mean D-dimer level was below 500 μg/L, and about 27% had thrombophilia.”

Results

The study’s primary outcome was the composite of recurrent VTE or major bleeding during the 18-month treatment period. Significantly fewer patients met this endpoint in the warfarin arm than in the placebo arm—6 (3.3%) and 25 (13.5%), respectively (hazard ratio [HR]=0.23, P=0.0004).

Likewise, the number of patients with recurrent VTE at 18 months was significantly lower in the warfarin arm than in the placebo arm—3 (1.7%) and 25 (13.5%), respectively (HR=0.11, P<0.0001).

On the other hand, there was no significant difference in the rate of major bleeding between the treatment arms at 18 months. Four patients (2.2%) had major bleeding in the warfarin arm, as did 1 (0.5%) in the placebo arm (HR=4.07, P=0.18).

At 42 months, there was no significant difference between the treatment arms with regard to the composite outcome, the rate of recurrent VTE, or the rate of major bleeding.

The composite outcome occurred in 33 (20.8%) patients in the warfarin arm and 42 (24%) in the placebo arm (HR=0.74, P=0.19). Recurrent VTE occurred in 28 (17.9%) and 39 patients (22.1%), respectively (HR=0.67, P=0.10). And major bleeding occurred in 6 (3.5%) and 5 patients (3%), respectively (HR=1.12, P=0.71).

“[E]xtending anticoagulation for 18 additional months was associated with a major relative risk reduction of 77% of recurrent VTE or major bleeding during the treatment period,” Dr Couturaud said in summary. “However, this benefit was lost during a long-term follow-up of 2 years after stopping anticoagulation.”

“In addition, recurrent VTE occurred in 80% of cases as recurrent PE and in 90% of cases as unprovoked VTE. So additional investigations are needed to identify subgroups of patients at lower risk who may not need indefinite anticoagulation.”

This study was sponsored by Brest University Hospital. Investigators received research funding from Actelion Pharmaceuticals, GlaxoSmithKline, Bristol-Myers Squibb, Boehringer Ingelheim, Sanofi, LEO Pharma, and Bayer.

*Information in the abstract differs from that presented at the meeting.

SAN FRANCISCO—New research indicates that extending anticoagulant therapy to 2 years can reduce the risk of recurrent venous thromboembolism (VTE) without increasing major bleeding, but this benefit only lasts while patients are receiving the therapy.

In the PADIS-PE study, patients with a first episode of symptomatic, unprovoked pulmonary embolism (PE) received 6 months of treatment with a vitamin K antagonist (VKA), followed by 18 months of warfarin or placebo.

Patients who received warfarin had a 77% reduction in the relative risk of recurrent VTE or major bleeding while they received treatment. But an additional 2 years of follow-up showed that this benefit was lost once patients stopped anticoagulation.

Francis Couturaud, MD, PhD, of the Brest University Hospital Center in Brest, France, presented these data at the 2014 ASH Annual Meeting as LBA-3.*

He and his colleagues randomized patients to receive warfarin (n=184) or placebo (n=187) for 18 months after their intial VKA treatment. Patients were followed for an additional 24 months after treatment ended.

Most baseline characteristics were similar between the treatment arms, although there was a significantly higher percentage of females in the warfarin arm.

“[Overall,] the mean age was below 60, [and] the mean BMI [body mass index] was below 30,” Dr Couturaud noted. “About 4% of patients had previous cancer [that had been] resolved for more than 2 years, 8% had previous distal DVT [deep vein thrombosis] or superficial venous thrombosis, a quarter of women were on estrogen-containing pills, and about one-third had an associated proximal DVT at the time of PE diagnosis.”

“Before the randomization, the mean duration of VKA [therapy] was 6 months, and the mean percentage of time within the therapeutic range was 70. At inclusion, about one-third of patients had residual perfusion defect, about 15% had residual DVT, the mean D-dimer level was below 500 μg/L, and about 27% had thrombophilia.”

Results

The study’s primary outcome was the composite of recurrent VTE or major bleeding during the 18-month treatment period. Significantly fewer patients met this endpoint in the warfarin arm than in the placebo arm—6 (3.3%) and 25 (13.5%), respectively (hazard ratio [HR]=0.23, P=0.0004).

Likewise, the number of patients with recurrent VTE at 18 months was significantly lower in the warfarin arm than in the placebo arm—3 (1.7%) and 25 (13.5%), respectively (HR=0.11, P<0.0001).

On the other hand, there was no significant difference in the rate of major bleeding between the treatment arms at 18 months. Four patients (2.2%) had major bleeding in the warfarin arm, as did 1 (0.5%) in the placebo arm (HR=4.07, P=0.18).

At 42 months, there was no significant difference between the treatment arms with regard to the composite outcome, the rate of recurrent VTE, or the rate of major bleeding.

The composite outcome occurred in 33 (20.8%) patients in the warfarin arm and 42 (24%) in the placebo arm (HR=0.74, P=0.19). Recurrent VTE occurred in 28 (17.9%) and 39 patients (22.1%), respectively (HR=0.67, P=0.10). And major bleeding occurred in 6 (3.5%) and 5 patients (3%), respectively (HR=1.12, P=0.71).

“[E]xtending anticoagulation for 18 additional months was associated with a major relative risk reduction of 77% of recurrent VTE or major bleeding during the treatment period,” Dr Couturaud said in summary. “However, this benefit was lost during a long-term follow-up of 2 years after stopping anticoagulation.”

“In addition, recurrent VTE occurred in 80% of cases as recurrent PE and in 90% of cases as unprovoked VTE. So additional investigations are needed to identify subgroups of patients at lower risk who may not need indefinite anticoagulation.”

This study was sponsored by Brest University Hospital. Investigators received research funding from Actelion Pharmaceuticals, GlaxoSmithKline, Bristol-Myers Squibb, Boehringer Ingelheim, Sanofi, LEO Pharma, and Bayer.

*Information in the abstract differs from that presented at the meeting.

Credit: FDA

The US Food and Drug Administration (FDA) is alerting healthcare professionals not to use Wallcur, LLC, simulated intravenous (IV) products in human or animal patients, as the products are for training purposes only.

The FDA has become aware that some Wallcur training IV products have been distributed to healthcare facilities and administered to patients.

There have been reports of serious adverse events associated with some of these products, such as Practi IV Solution Bags.

Before administering IV solutions to patients, healthcare providers should carefully check the labels to ensure that products are not training products.

Wallcur’s training products, which may bear the words “for clinical simulation,” are not to be administered to patients.

If you suspect that any Wallcur training IV products may have been administered to a patient, whether or not the incident has resulted in an adverse event, please report the incident to the FDA’s MedWatch Adverse Event Reporting Program.

The FDA said it will continue to investigate and monitor this issue. The agency is also working with the Centers for Disease Control and Prevention to inform healthcare professionals and state health departments.

Credit: FDA

The US Food and Drug Administration (FDA) is alerting healthcare professionals not to use Wallcur, LLC, simulated intravenous (IV) products in human or animal patients, as the products are for training purposes only.

The FDA has become aware that some Wallcur training IV products have been distributed to healthcare facilities and administered to patients.

There have been reports of serious adverse events associated with some of these products, such as Practi IV Solution Bags.

Before administering IV solutions to patients, healthcare providers should carefully check the labels to ensure that products are not training products.

Wallcur’s training products, which may bear the words “for clinical simulation,” are not to be administered to patients.

If you suspect that any Wallcur training IV products may have been administered to a patient, whether or not the incident has resulted in an adverse event, please report the incident to the FDA’s MedWatch Adverse Event Reporting Program.

The FDA said it will continue to investigate and monitor this issue. The agency is also working with the Centers for Disease Control and Prevention to inform healthcare professionals and state health departments.

Credit: FDA

The US Food and Drug Administration (FDA) is alerting healthcare professionals not to use Wallcur, LLC, simulated intravenous (IV) products in human or animal patients, as the products are for training purposes only.

The FDA has become aware that some Wallcur training IV products have been distributed to healthcare facilities and administered to patients.

There have been reports of serious adverse events associated with some of these products, such as Practi IV Solution Bags.

Before administering IV solutions to patients, healthcare providers should carefully check the labels to ensure that products are not training products.

Wallcur’s training products, which may bear the words “for clinical simulation,” are not to be administered to patients.

If you suspect that any Wallcur training IV products may have been administered to a patient, whether or not the incident has resulted in an adverse event, please report the incident to the FDA’s MedWatch Adverse Event Reporting Program.

The FDA said it will continue to investigate and monitor this issue. The agency is also working with the Centers for Disease Control and Prevention to inform healthcare professionals and state health departments.

Besides caring for these patients, many of us also have a parent, spouse, or a close relative with dementia. My 90-year-old mother has multi-infarct dementia from her diabetes and vascular disease, but is still able to live in an apartment with my 91-year-old father, with assistance from wonderful home aides. Despite her profound dementia, she can still play the piano and read music.

Menchola and Weiss are to be congratulated for their excellent, evidence-based review of the diagnosis, treatment, and prevention of Alzheimer’s disease (AD). (See "Addressing Alzheimer’s: A pragmatic approach.") They do not get caught up in unjustified enthusiasm for screening and drug treatment. Some of their important recommendations bear repeating here:

A look at the evidence on Alzheimer's disease should prompt us to use drugs sparingly and avoid treatments that do more harm than good. Do not routinely screen for AD. This may seem like heresy in these days of early detection and prevention. But for screening to be useful, there must be effective early interventions, and so far, early treatments for AD have been disappointing. Cholinesterase inhibitors and N-methyl-D-aspartate glutamate receptor blockers provide very small improvements in cognitive function and have significant adverse effects. Some behavioral interventions to delay onset of cognitive decline show promise—but are unproven.

Although routine screening is not recommended, “case finding” remains important. We need to be alert to signs and symptoms that suggest early dementia in our patients, and we need to evaluate these patients carefully or refer them for neurologic testing if the diagnosis is in doubt.

Use drugs sparingly, especially when treating behavioral problems. They have serious adverse effects, and behavioral interventions should always be used first. Encourage caregivers to seek out social support. My father attends an Alzheimer’s support group each month, and this has lifted some of the burden.

Address prognosis and end-of-life care, and avoid unnecessary and aggressive treatments that are likely to cause more harm than benefit. Hospice care is suitable and beneficial for those with late-stage Alzheimer’s, but feeding tubes are not.

With many new advances in research techniques, it is likely that investigators will develop better methods of diagnosis and treatment of AD. In the meantime, there is already much we can do to alleviate the suffering of these patients and support their caregivers. This knowledge will likely serve us at home, as well.

Besides caring for these patients, many of us also have a parent, spouse, or a close relative with dementia. My 90-year-old mother has multi-infarct dementia from her diabetes and vascular disease, but is still able to live in an apartment with my 91-year-old father, with assistance from wonderful home aides. Despite her profound dementia, she can still play the piano and read music.

Menchola and Weiss are to be congratulated for their excellent, evidence-based review of the diagnosis, treatment, and prevention of Alzheimer’s disease (AD). (See "Addressing Alzheimer’s: A pragmatic approach.") They do not get caught up in unjustified enthusiasm for screening and drug treatment. Some of their important recommendations bear repeating here:

A look at the evidence on Alzheimer's disease should prompt us to use drugs sparingly and avoid treatments that do more harm than good. Do not routinely screen for AD. This may seem like heresy in these days of early detection and prevention. But for screening to be useful, there must be effective early interventions, and so far, early treatments for AD have been disappointing. Cholinesterase inhibitors and N-methyl-D-aspartate glutamate receptor blockers provide very small improvements in cognitive function and have significant adverse effects. Some behavioral interventions to delay onset of cognitive decline show promise—but are unproven.

Although routine screening is not recommended, “case finding” remains important. We need to be alert to signs and symptoms that suggest early dementia in our patients, and we need to evaluate these patients carefully or refer them for neurologic testing if the diagnosis is in doubt.

Use drugs sparingly, especially when treating behavioral problems. They have serious adverse effects, and behavioral interventions should always be used first. Encourage caregivers to seek out social support. My father attends an Alzheimer’s support group each month, and this has lifted some of the burden.

Address prognosis and end-of-life care, and avoid unnecessary and aggressive treatments that are likely to cause more harm than benefit. Hospice care is suitable and beneficial for those with late-stage Alzheimer’s, but feeding tubes are not.

With many new advances in research techniques, it is likely that investigators will develop better methods of diagnosis and treatment of AD. In the meantime, there is already much we can do to alleviate the suffering of these patients and support their caregivers. This knowledge will likely serve us at home, as well.

Besides caring for these patients, many of us also have a parent, spouse, or a close relative with dementia. My 90-year-old mother has multi-infarct dementia from her diabetes and vascular disease, but is still able to live in an apartment with my 91-year-old father, with assistance from wonderful home aides. Despite her profound dementia, she can still play the piano and read music.

Menchola and Weiss are to be congratulated for their excellent, evidence-based review of the diagnosis, treatment, and prevention of Alzheimer’s disease (AD). (See "Addressing Alzheimer’s: A pragmatic approach.") They do not get caught up in unjustified enthusiasm for screening and drug treatment. Some of their important recommendations bear repeating here:

A look at the evidence on Alzheimer's disease should prompt us to use drugs sparingly and avoid treatments that do more harm than good. Do not routinely screen for AD. This may seem like heresy in these days of early detection and prevention. But for screening to be useful, there must be effective early interventions, and so far, early treatments for AD have been disappointing. Cholinesterase inhibitors and N-methyl-D-aspartate glutamate receptor blockers provide very small improvements in cognitive function and have significant adverse effects. Some behavioral interventions to delay onset of cognitive decline show promise—but are unproven.

Although routine screening is not recommended, “case finding” remains important. We need to be alert to signs and symptoms that suggest early dementia in our patients, and we need to evaluate these patients carefully or refer them for neurologic testing if the diagnosis is in doubt.

Use drugs sparingly, especially when treating behavioral problems. They have serious adverse effects, and behavioral interventions should always be used first. Encourage caregivers to seek out social support. My father attends an Alzheimer’s support group each month, and this has lifted some of the burden.

Address prognosis and end-of-life care, and avoid unnecessary and aggressive treatments that are likely to cause more harm than benefit. Hospice care is suitable and beneficial for those with late-stage Alzheimer’s, but feeding tubes are not.

With many new advances in research techniques, it is likely that investigators will develop better methods of diagnosis and treatment of AD. In the meantime, there is already much we can do to alleviate the suffering of these patients and support their caregivers. This knowledge will likely serve us at home, as well.