Applied Evidence

Mr. H, a 62-year-old with type 2 diabetes, hypertension, and hypercholesterolemia, arrives at the emergency department complaining of acute onset chest pain. An EKG shows no ischemic changes and his initial cardiac enzymes are normal, but Mr. H is admitted to telemetry for further monitoring and to rule out myocardial infarction. Mr. H normally takes metformin and glipizide to manage his diabetes; his most recent glycosylated hemoglobin (HbA1c) was 8.2. After admission, he is placed on a diabetic diet and switched to insulin.

As primary care physicians, we all care for patients like Mr. H, who are hospitalized because of cardiovascular or other symptoms and have diabetes—a comorbidity that affects an estimated 12% to 25% of inpatients.¹ We are also well aware of the elevated risks such patients face—for bacterial infection, impaired wound healing, and reduced tissue and organ perfusion,² among others. In one study, a single blood glucose reading >220 mg/dL was associated with a nearly 6-fold increase in nosocomial infection.² A number of recent studies have also found hyperglycemia to be an independent marker of overall inpatient mortality.^1,3-5

American Diabetes Association goals. In 2008, the ADA issued new glycemic control goals for inpatients with diabetes. For critically ill patients, the association recommends that blood glucose levels be maintained at <140 mg/dL—and as close to 110 mg/dL as possible. For patients who are hospitalized but are not critically ill, the ADA recommends fasting blood glucose levels of 90 to 130 mg/dL and postprandial levels <180 mg/dL.⁶

As the ADA recommendations make clear, it is imperative that we do everything possible to lower the blood glucose levels of our hospitalized patients. Ironically, though, fear of hypoglycemia has prevented many physicians from putting patients with diabetes on a basal/bolus insulin protocol¹—a dosing regimen that, according to at least one recent report, is more effective than the traditional sliding-scale insulin regimen.⁷ (See “No heightened hypoglycemia risk with basal/bolus regimen”) To help you achieve glycemic targets safely and confidently using the basal/bolus regimen, we’ve assembled this review of the latest evidence, complete with strategies for success.

Oral agents are no match for the hospital routine

The hospital environment interferes with the patterns and schedules that people with diabetes rely on to manage their condition. Thus, it is not unusual even for patients whose glucose levels were very well-controlled at home to have poor glycemic control as inpatients. Dietary change is one of the primary reasons.

Mealtimes typically deviate from the patient’s at-home schedule. In addition, patients are often put on a calorie-restricted, carefully enforced diabetic diet, which is quite different from their usual eating pattern. NPO orders are also common in preparation for diagnostic testing or other procedures. And some medications—particularly high doses of steroids—affect glucose levels. It is difficult to adjust oral hypoglycemic agents to accommodate such variations.

A look at Mr. H’s regimen. Mr. H’s physician knew that continuation of his oral medications—particularly glipizide—in combination with the hospital’s strict diabetic diet could result in hypoglycemia. Continuing to take metformin was also a concern, given that Mr. H was at risk for new cardiac symptoms—a contraindication to metformin use. So his physician switched him over to insulin, a safer alternative.

Finding the right insulin regimen

For years, a sliding-scale regimen was the most common approach to glycemic management of inpatients with diabetes. This concept, developed in 1934, originally used urine glucose testing to determine dosing, and its convenience and ease of treatment initiation led to widespread use. Although many variations have been introduced over the years, traditional sliding-scale regimens use short-acting analog or regular insulin in predetermined doses based on blood glucose readings at mealtimes and bedtime.

Despite the popularity of this method, however, there is little evidence to support it. Sliding-scale insulin as monotherapy has not been associated with effective glycemic control or improved outcomes.^8,9 By design, this traditional regimen makes hyperglycemia the threshold for action, rather than taking action to prevent it. The result: wide fluctuations in blood sugar levels and the potential for prolonged periods of hyperglycemia.

Basal/bolus: A better approach

Mr. H’s physician started him on a basal/ bolus insulin regimen, which is more aggressive than a sliding-scale protocol and, as such, has prompted some physicians to view it warily. This strategy, in which a basal dose of long-acting insulin—typically given at bedtime—is accompanied by boluses of short-acting insulin at mealtimes,^1,10-12 follows the normal physiological release of insulin (FIGURE 1). Basic metabolic insulin is required to cover endogenous hepatic glucose production, even among diabetes patients who are NPO, and prandial insulin requirements are determined by exogenous glucose intake, whether in the form of a meal, intravenous (IV) fluids, tube feeding, or total parenteral nutrition (TPN).

Dosing guidelines. For most patients with type 2 diabetes, the correct daily insulin dose is 0.5 to 0.7 U/kg,^1,13 but factors other than weight also need to be considered:

• Previous insulin use. A lower initial dose (0.4 U/kg/d) may be preferable for insulin-naive patients, whereas a higher dose (0.7 U/kg/d) may be necessary for those with a history of insulin resistance.^1,3
• Risk of hypoglycemia. To be on the safe side, start patients who are at high risk of hypoglycemia (eg, because they are very lean, have hepatic or renal failure, or are undergoing hemodialysis) with a very low dose (0.3 U/kg/d).
• Other drugs or TPN regimen. A higher dose (0.7 U/kg/d) is appropriate for patients on high doses of steroids.^1,3 Even smaller doses of oral or IV glucocorticoids increase the risk of hyperglycemia, particularly after a meal. Patients receiving TPN or other enteral feedings may also require higher doses of insulin.

Doing the math. To determine specific insulin requirements, calculate the total daily dose and divide it in half. The patient should receive half of the total as long-acting insulin for basal coverage, usually at bedtime. Divide the remaining half into 3 equal portions; administer each portion as a short-acting insulin bolus with each meal.^1,3,10,11

Mr. H’s insulin requirements. Mr. H weighs 100 kg (220 pounds), so he needs 60 units (0.6 U/kg) of insulin per day. His physician writes an order for 30 units (one half of 60 units) of a long-acting insulin (glargine or detemir) at bedtime, and 10 units (one third of the remaining 30 units) of a short-acting insulin (as-part, lispro, or glulisine) with each meal (FIGURE 2).¹⁴

FIGURE 1
Basal/bolus regimen mimics normal insulin profile

FIGURE 2
Insulin types and duration

More insulin needed? Figuring out how much

It’s not unusual for patients on a basal/bolus regimen—particularly those like Mr. H, who have never been on insulin—to need supplemental insulin.¹⁵ Short-acting insulin is always used for this purpose, whether it is administered before a meal or at bedtime.

If a patient is hyperglycemic (>150 mg/dL) before a meal, a correction scale (TABLE) can be used to determine how much additional insulin to give. The supplemental insulin should be given at the same time as the mealtime bolus.

If hyperglycemia is detected at bedtime, a more conservative approach is needed to prevent overnight hypoglycemia. Thus, additional insulin is recommended at bedtime only if the blood glucose reading is >200 mg/dL, and approximately half of the recommended mealtime correction dose should be given.¹⁶

TABLE
Insulin correction scale: Calculating the supplemental dose

Is it time to revise the dosing regimen?

Consistent use of a correction scale to adjust the dosage generally indicates that the patient’s baseline dosing regimen needs to be revised. Dynamic insulin coverage requires careful monitoring, with blood glucose levels recorded and reviewed for trends that suggest a change is needed.

Poor subcutaneous perfusion, for example, may lead to a decreased or erratic uptake of injected insulin. Also, stress-related hyperglycemia may decrease or increase over the course of a hospital stay. And changes in medication, such as a decreasing steroid taper, may change overall insulin demand.^15,17

With vigilant monitoring, the basal/bolus regimen may be adjusted upward to 110% of current dosing for a patient with frequent elevated blood glucose readings—provided the patient’s glucose levels have not fallen below 80 mg/dL. Conversely, the regimen may be adjusted downward to 80% for a patient who continues to be hypoglycemic. Unlike the supplemental dosing based on the correction scale, these revised regimens affect both the basal (long-acting) and bolus (short-acting) doses.

To ensure timely adjustments to your patient’s regimen, make sure that all your orders for insulin administration are accompanied by provisions for revising the dosing regimen when changes in patient status occur. (Protocols for managing both hypo- and hyperglycemia should, of course, be part of your orders as well.)

IV insulin’s role—and is it expanding?

IV insulin is the treatment of choice for patients in diabetic ketoacidosis, but recent research suggests that it may also be the preferred approach to diabetes management in other critically ill patients, as well as in those undergoing surgery.^18-20

In a study comparing outcomes of surgical ICU patients managed with IV insulin during the perioperative and postoperative periods with surgical patients on conventional diabetes management, Van den Berghe found a 45% reduction in mortality rates among those receiving insulin infusions (4.6% of those on IV insulin died, compared with 8% of those receiving subcutaneous insulin). The use of IV insulin therapy also decreased the time spent in intensive care, although it did not shorten the overall length of stay.¹⁹

Regular insulin is used most often for insulin infusions. Some trials with ultra–short-acting insulin have been done, but the findings were inconclusive.

Your patient is leaving: Ease the transition

For inpatients with diabetes, discharge planning includes a transition, from insulin to oral agents, perhaps, and from maintaining glucose control based on a hospital schedule to adjusting to the patterns of daily life at home. Particular care is required for patients who will be transitioned from IV to subcutaneous insulin. IV insulin has a half-life of only 10 minutes, so the initial subcutaneous dose should be administered about 1 hour prior to discontinuation of the infusion. Failure to plan accordingly may result in significant hyperglycemia and associated complications.^17,21

Research suggests that patients be switched to their outpatient diabetes management plan at least 24 hours before discharge, a protocol that was followed in Mr. H’s case. He remained in the hospital for 5 days. After myocardial infarction was ruled out, Mr. H underwent a nuclear medicine cardiac stress test for which he needed to be NPO. When testing was completed, Mr. H resumed a diabetic diet, and discharge planning began. Since his diabetes was not well controlled on admission and he required >20 units of insulin per day in the hospital, Mr. H’s physician opted to include long-acting insulin at bedtime in his outpatient regimen. On the day before Mr. H was scheduled to leave the hospital, the physician discontinued the short-acting mealtime insulin and restarted oral metformin twice daily, closely monitoring the patient’s glucose levels until discharge. The physician told Mr. H to schedule a follow-up visit within a week so that his new outpatient regimen could be reviewed.

Ideally, a diabetes nurse specialist will be available, not only to get involved in discharge planning, but also to provide patient education, care, and advice. Researchers found that hospital stays for patients with diabetes were shortened (8 days vs 11 days) when a diabetes nurse specialist was involved in their care. The patients were also more knowledgeable and satisfied.²²

Take advantage of bedside conversations. An inpatient stay offers physicians and patients the opportunity to work together to fine-tune components of the diabetic regimen.²³ Make the most of these opportunities. In addition, once the patient goes home, you’ll need to ensure close follow-up to reconcile the differences between home self-management and the controlled hospital environment.

Correspondence
Donald R. Woolever, MD, Family Medicine Residency Program, Central Maine Medical Center, 76 High Street, Lewiston, ME 04240; [email protected].

Mr. H, a 62-year-old with type 2 diabetes, hypertension, and hypercholesterolemia, arrives at the emergency department complaining of acute onset chest pain. An EKG shows no ischemic changes and his initial cardiac enzymes are normal, but Mr. H is admitted to telemetry for further monitoring and to rule out myocardial infarction. Mr. H normally takes metformin and glipizide to manage his diabetes; his most recent glycosylated hemoglobin (HbA1c) was 8.2. After admission, he is placed on a diabetic diet and switched to insulin.

As primary care physicians, we all care for patients like Mr. H, who are hospitalized because of cardiovascular or other symptoms and have diabetes—a comorbidity that affects an estimated 12% to 25% of inpatients.¹ We are also well aware of the elevated risks such patients face—for bacterial infection, impaired wound healing, and reduced tissue and organ perfusion,² among others. In one study, a single blood glucose reading >220 mg/dL was associated with a nearly 6-fold increase in nosocomial infection.² A number of recent studies have also found hyperglycemia to be an independent marker of overall inpatient mortality.^1,3-5

American Diabetes Association goals. In 2008, the ADA issued new glycemic control goals for inpatients with diabetes. For critically ill patients, the association recommends that blood glucose levels be maintained at <140 mg/dL—and as close to 110 mg/dL as possible. For patients who are hospitalized but are not critically ill, the ADA recommends fasting blood glucose levels of 90 to 130 mg/dL and postprandial levels <180 mg/dL.⁶

As the ADA recommendations make clear, it is imperative that we do everything possible to lower the blood glucose levels of our hospitalized patients. Ironically, though, fear of hypoglycemia has prevented many physicians from putting patients with diabetes on a basal/bolus insulin protocol¹—a dosing regimen that, according to at least one recent report, is more effective than the traditional sliding-scale insulin regimen.⁷ (See “No heightened hypoglycemia risk with basal/bolus regimen”) To help you achieve glycemic targets safely and confidently using the basal/bolus regimen, we’ve assembled this review of the latest evidence, complete with strategies for success.

Oral agents are no match for the hospital routine

The hospital environment interferes with the patterns and schedules that people with diabetes rely on to manage their condition. Thus, it is not unusual even for patients whose glucose levels were very well-controlled at home to have poor glycemic control as inpatients. Dietary change is one of the primary reasons.

Mealtimes typically deviate from the patient’s at-home schedule. In addition, patients are often put on a calorie-restricted, carefully enforced diabetic diet, which is quite different from their usual eating pattern. NPO orders are also common in preparation for diagnostic testing or other procedures. And some medications—particularly high doses of steroids—affect glucose levels. It is difficult to adjust oral hypoglycemic agents to accommodate such variations.

A look at Mr. H’s regimen. Mr. H’s physician knew that continuation of his oral medications—particularly glipizide—in combination with the hospital’s strict diabetic diet could result in hypoglycemia. Continuing to take metformin was also a concern, given that Mr. H was at risk for new cardiac symptoms—a contraindication to metformin use. So his physician switched him over to insulin, a safer alternative.

Finding the right insulin regimen

For years, a sliding-scale regimen was the most common approach to glycemic management of inpatients with diabetes. This concept, developed in 1934, originally used urine glucose testing to determine dosing, and its convenience and ease of treatment initiation led to widespread use. Although many variations have been introduced over the years, traditional sliding-scale regimens use short-acting analog or regular insulin in predetermined doses based on blood glucose readings at mealtimes and bedtime.

Despite the popularity of this method, however, there is little evidence to support it. Sliding-scale insulin as monotherapy has not been associated with effective glycemic control or improved outcomes.^8,9 By design, this traditional regimen makes hyperglycemia the threshold for action, rather than taking action to prevent it. The result: wide fluctuations in blood sugar levels and the potential for prolonged periods of hyperglycemia.

Basal/bolus: A better approach

Mr. H’s physician started him on a basal/ bolus insulin regimen, which is more aggressive than a sliding-scale protocol and, as such, has prompted some physicians to view it warily. This strategy, in which a basal dose of long-acting insulin—typically given at bedtime—is accompanied by boluses of short-acting insulin at mealtimes,^1,10-12 follows the normal physiological release of insulin (FIGURE 1). Basic metabolic insulin is required to cover endogenous hepatic glucose production, even among diabetes patients who are NPO, and prandial insulin requirements are determined by exogenous glucose intake, whether in the form of a meal, intravenous (IV) fluids, tube feeding, or total parenteral nutrition (TPN).

Dosing guidelines. For most patients with type 2 diabetes, the correct daily insulin dose is 0.5 to 0.7 U/kg,^1,13 but factors other than weight also need to be considered:

• Previous insulin use. A lower initial dose (0.4 U/kg/d) may be preferable for insulin-naive patients, whereas a higher dose (0.7 U/kg/d) may be necessary for those with a history of insulin resistance.^1,3
• Risk of hypoglycemia. To be on the safe side, start patients who are at high risk of hypoglycemia (eg, because they are very lean, have hepatic or renal failure, or are undergoing hemodialysis) with a very low dose (0.3 U/kg/d).
• Other drugs or TPN regimen. A higher dose (0.7 U/kg/d) is appropriate for patients on high doses of steroids.^1,3 Even smaller doses of oral or IV glucocorticoids increase the risk of hyperglycemia, particularly after a meal. Patients receiving TPN or other enteral feedings may also require higher doses of insulin.

Doing the math. To determine specific insulin requirements, calculate the total daily dose and divide it in half. The patient should receive half of the total as long-acting insulin for basal coverage, usually at bedtime. Divide the remaining half into 3 equal portions; administer each portion as a short-acting insulin bolus with each meal.^1,3,10,11

Mr. H’s insulin requirements. Mr. H weighs 100 kg (220 pounds), so he needs 60 units (0.6 U/kg) of insulin per day. His physician writes an order for 30 units (one half of 60 units) of a long-acting insulin (glargine or detemir) at bedtime, and 10 units (one third of the remaining 30 units) of a short-acting insulin (as-part, lispro, or glulisine) with each meal (FIGURE 2).¹⁴

FIGURE 1
Basal/bolus regimen mimics normal insulin profile

FIGURE 2
Insulin types and duration

More insulin needed? Figuring out how much

It’s not unusual for patients on a basal/bolus regimen—particularly those like Mr. H, who have never been on insulin—to need supplemental insulin.¹⁵ Short-acting insulin is always used for this purpose, whether it is administered before a meal or at bedtime.

If a patient is hyperglycemic (>150 mg/dL) before a meal, a correction scale (TABLE) can be used to determine how much additional insulin to give. The supplemental insulin should be given at the same time as the mealtime bolus.

If hyperglycemia is detected at bedtime, a more conservative approach is needed to prevent overnight hypoglycemia. Thus, additional insulin is recommended at bedtime only if the blood glucose reading is >200 mg/dL, and approximately half of the recommended mealtime correction dose should be given.¹⁶

TABLE
Insulin correction scale: Calculating the supplemental dose

Is it time to revise the dosing regimen?

Consistent use of a correction scale to adjust the dosage generally indicates that the patient’s baseline dosing regimen needs to be revised. Dynamic insulin coverage requires careful monitoring, with blood glucose levels recorded and reviewed for trends that suggest a change is needed.

Poor subcutaneous perfusion, for example, may lead to a decreased or erratic uptake of injected insulin. Also, stress-related hyperglycemia may decrease or increase over the course of a hospital stay. And changes in medication, such as a decreasing steroid taper, may change overall insulin demand.^15,17

With vigilant monitoring, the basal/bolus regimen may be adjusted upward to 110% of current dosing for a patient with frequent elevated blood glucose readings—provided the patient’s glucose levels have not fallen below 80 mg/dL. Conversely, the regimen may be adjusted downward to 80% for a patient who continues to be hypoglycemic. Unlike the supplemental dosing based on the correction scale, these revised regimens affect both the basal (long-acting) and bolus (short-acting) doses.

To ensure timely adjustments to your patient’s regimen, make sure that all your orders for insulin administration are accompanied by provisions for revising the dosing regimen when changes in patient status occur. (Protocols for managing both hypo- and hyperglycemia should, of course, be part of your orders as well.)

IV insulin’s role—and is it expanding?

IV insulin is the treatment of choice for patients in diabetic ketoacidosis, but recent research suggests that it may also be the preferred approach to diabetes management in other critically ill patients, as well as in those undergoing surgery.^18-20

In a study comparing outcomes of surgical ICU patients managed with IV insulin during the perioperative and postoperative periods with surgical patients on conventional diabetes management, Van den Berghe found a 45% reduction in mortality rates among those receiving insulin infusions (4.6% of those on IV insulin died, compared with 8% of those receiving subcutaneous insulin). The use of IV insulin therapy also decreased the time spent in intensive care, although it did not shorten the overall length of stay.¹⁹

Regular insulin is used most often for insulin infusions. Some trials with ultra–short-acting insulin have been done, but the findings were inconclusive.

Your patient is leaving: Ease the transition

For inpatients with diabetes, discharge planning includes a transition, from insulin to oral agents, perhaps, and from maintaining glucose control based on a hospital schedule to adjusting to the patterns of daily life at home. Particular care is required for patients who will be transitioned from IV to subcutaneous insulin. IV insulin has a half-life of only 10 minutes, so the initial subcutaneous dose should be administered about 1 hour prior to discontinuation of the infusion. Failure to plan accordingly may result in significant hyperglycemia and associated complications.^17,21

Research suggests that patients be switched to their outpatient diabetes management plan at least 24 hours before discharge, a protocol that was followed in Mr. H’s case. He remained in the hospital for 5 days. After myocardial infarction was ruled out, Mr. H underwent a nuclear medicine cardiac stress test for which he needed to be NPO. When testing was completed, Mr. H resumed a diabetic diet, and discharge planning began. Since his diabetes was not well controlled on admission and he required >20 units of insulin per day in the hospital, Mr. H’s physician opted to include long-acting insulin at bedtime in his outpatient regimen. On the day before Mr. H was scheduled to leave the hospital, the physician discontinued the short-acting mealtime insulin and restarted oral metformin twice daily, closely monitoring the patient’s glucose levels until discharge. The physician told Mr. H to schedule a follow-up visit within a week so that his new outpatient regimen could be reviewed.

Ideally, a diabetes nurse specialist will be available, not only to get involved in discharge planning, but also to provide patient education, care, and advice. Researchers found that hospital stays for patients with diabetes were shortened (8 days vs 11 days) when a diabetes nurse specialist was involved in their care. The patients were also more knowledgeable and satisfied.²²

Take advantage of bedside conversations. An inpatient stay offers physicians and patients the opportunity to work together to fine-tune components of the diabetic regimen.²³ Make the most of these opportunities. In addition, once the patient goes home, you’ll need to ensure close follow-up to reconcile the differences between home self-management and the controlled hospital environment.

Correspondence
Donald R. Woolever, MD, Family Medicine Residency Program, Central Maine Medical Center, 76 High Street, Lewiston, ME 04240; [email protected].

Mr. H, a 62-year-old with type 2 diabetes, hypertension, and hypercholesterolemia, arrives at the emergency department complaining of acute onset chest pain. An EKG shows no ischemic changes and his initial cardiac enzymes are normal, but Mr. H is admitted to telemetry for further monitoring and to rule out myocardial infarction. Mr. H normally takes metformin and glipizide to manage his diabetes; his most recent glycosylated hemoglobin (HbA1c) was 8.2. After admission, he is placed on a diabetic diet and switched to insulin.

As primary care physicians, we all care for patients like Mr. H, who are hospitalized because of cardiovascular or other symptoms and have diabetes—a comorbidity that affects an estimated 12% to 25% of inpatients.¹ We are also well aware of the elevated risks such patients face—for bacterial infection, impaired wound healing, and reduced tissue and organ perfusion,² among others. In one study, a single blood glucose reading >220 mg/dL was associated with a nearly 6-fold increase in nosocomial infection.² A number of recent studies have also found hyperglycemia to be an independent marker of overall inpatient mortality.^1,3-5

American Diabetes Association goals. In 2008, the ADA issued new glycemic control goals for inpatients with diabetes. For critically ill patients, the association recommends that blood glucose levels be maintained at <140 mg/dL—and as close to 110 mg/dL as possible. For patients who are hospitalized but are not critically ill, the ADA recommends fasting blood glucose levels of 90 to 130 mg/dL and postprandial levels <180 mg/dL.⁶

As the ADA recommendations make clear, it is imperative that we do everything possible to lower the blood glucose levels of our hospitalized patients. Ironically, though, fear of hypoglycemia has prevented many physicians from putting patients with diabetes on a basal/bolus insulin protocol¹—a dosing regimen that, according to at least one recent report, is more effective than the traditional sliding-scale insulin regimen.⁷ (See “No heightened hypoglycemia risk with basal/bolus regimen”) To help you achieve glycemic targets safely and confidently using the basal/bolus regimen, we’ve assembled this review of the latest evidence, complete with strategies for success.

Oral agents are no match for the hospital routine

The hospital environment interferes with the patterns and schedules that people with diabetes rely on to manage their condition. Thus, it is not unusual even for patients whose glucose levels were very well-controlled at home to have poor glycemic control as inpatients. Dietary change is one of the primary reasons.

Mealtimes typically deviate from the patient’s at-home schedule. In addition, patients are often put on a calorie-restricted, carefully enforced diabetic diet, which is quite different from their usual eating pattern. NPO orders are also common in preparation for diagnostic testing or other procedures. And some medications—particularly high doses of steroids—affect glucose levels. It is difficult to adjust oral hypoglycemic agents to accommodate such variations.

A look at Mr. H’s regimen. Mr. H’s physician knew that continuation of his oral medications—particularly glipizide—in combination with the hospital’s strict diabetic diet could result in hypoglycemia. Continuing to take metformin was also a concern, given that Mr. H was at risk for new cardiac symptoms—a contraindication to metformin use. So his physician switched him over to insulin, a safer alternative.

Finding the right insulin regimen

For years, a sliding-scale regimen was the most common approach to glycemic management of inpatients with diabetes. This concept, developed in 1934, originally used urine glucose testing to determine dosing, and its convenience and ease of treatment initiation led to widespread use. Although many variations have been introduced over the years, traditional sliding-scale regimens use short-acting analog or regular insulin in predetermined doses based on blood glucose readings at mealtimes and bedtime.

Despite the popularity of this method, however, there is little evidence to support it. Sliding-scale insulin as monotherapy has not been associated with effective glycemic control or improved outcomes.^8,9 By design, this traditional regimen makes hyperglycemia the threshold for action, rather than taking action to prevent it. The result: wide fluctuations in blood sugar levels and the potential for prolonged periods of hyperglycemia.

Basal/bolus: A better approach

Mr. H’s physician started him on a basal/ bolus insulin regimen, which is more aggressive than a sliding-scale protocol and, as such, has prompted some physicians to view it warily. This strategy, in which a basal dose of long-acting insulin—typically given at bedtime—is accompanied by boluses of short-acting insulin at mealtimes,^1,10-12 follows the normal physiological release of insulin (FIGURE 1). Basic metabolic insulin is required to cover endogenous hepatic glucose production, even among diabetes patients who are NPO, and prandial insulin requirements are determined by exogenous glucose intake, whether in the form of a meal, intravenous (IV) fluids, tube feeding, or total parenteral nutrition (TPN).

Dosing guidelines. For most patients with type 2 diabetes, the correct daily insulin dose is 0.5 to 0.7 U/kg,^1,13 but factors other than weight also need to be considered:

• Previous insulin use. A lower initial dose (0.4 U/kg/d) may be preferable for insulin-naive patients, whereas a higher dose (0.7 U/kg/d) may be necessary for those with a history of insulin resistance.^1,3
• Risk of hypoglycemia. To be on the safe side, start patients who are at high risk of hypoglycemia (eg, because they are very lean, have hepatic or renal failure, or are undergoing hemodialysis) with a very low dose (0.3 U/kg/d).
• Other drugs or TPN regimen. A higher dose (0.7 U/kg/d) is appropriate for patients on high doses of steroids.^1,3 Even smaller doses of oral or IV glucocorticoids increase the risk of hyperglycemia, particularly after a meal. Patients receiving TPN or other enteral feedings may also require higher doses of insulin.

Doing the math. To determine specific insulin requirements, calculate the total daily dose and divide it in half. The patient should receive half of the total as long-acting insulin for basal coverage, usually at bedtime. Divide the remaining half into 3 equal portions; administer each portion as a short-acting insulin bolus with each meal.^1,3,10,11

Mr. H’s insulin requirements. Mr. H weighs 100 kg (220 pounds), so he needs 60 units (0.6 U/kg) of insulin per day. His physician writes an order for 30 units (one half of 60 units) of a long-acting insulin (glargine or detemir) at bedtime, and 10 units (one third of the remaining 30 units) of a short-acting insulin (as-part, lispro, or glulisine) with each meal (FIGURE 2).¹⁴

FIGURE 1
Basal/bolus regimen mimics normal insulin profile

FIGURE 2
Insulin types and duration

More insulin needed? Figuring out how much

It’s not unusual for patients on a basal/bolus regimen—particularly those like Mr. H, who have never been on insulin—to need supplemental insulin.¹⁵ Short-acting insulin is always used for this purpose, whether it is administered before a meal or at bedtime.

If a patient is hyperglycemic (>150 mg/dL) before a meal, a correction scale (TABLE) can be used to determine how much additional insulin to give. The supplemental insulin should be given at the same time as the mealtime bolus.

If hyperglycemia is detected at bedtime, a more conservative approach is needed to prevent overnight hypoglycemia. Thus, additional insulin is recommended at bedtime only if the blood glucose reading is >200 mg/dL, and approximately half of the recommended mealtime correction dose should be given.¹⁶

TABLE
Insulin correction scale: Calculating the supplemental dose

Is it time to revise the dosing regimen?

Consistent use of a correction scale to adjust the dosage generally indicates that the patient’s baseline dosing regimen needs to be revised. Dynamic insulin coverage requires careful monitoring, with blood glucose levels recorded and reviewed for trends that suggest a change is needed.

Poor subcutaneous perfusion, for example, may lead to a decreased or erratic uptake of injected insulin. Also, stress-related hyperglycemia may decrease or increase over the course of a hospital stay. And changes in medication, such as a decreasing steroid taper, may change overall insulin demand.^15,17

With vigilant monitoring, the basal/bolus regimen may be adjusted upward to 110% of current dosing for a patient with frequent elevated blood glucose readings—provided the patient’s glucose levels have not fallen below 80 mg/dL. Conversely, the regimen may be adjusted downward to 80% for a patient who continues to be hypoglycemic. Unlike the supplemental dosing based on the correction scale, these revised regimens affect both the basal (long-acting) and bolus (short-acting) doses.

To ensure timely adjustments to your patient’s regimen, make sure that all your orders for insulin administration are accompanied by provisions for revising the dosing regimen when changes in patient status occur. (Protocols for managing both hypo- and hyperglycemia should, of course, be part of your orders as well.)

IV insulin’s role—and is it expanding?

IV insulin is the treatment of choice for patients in diabetic ketoacidosis, but recent research suggests that it may also be the preferred approach to diabetes management in other critically ill patients, as well as in those undergoing surgery.^18-20

In a study comparing outcomes of surgical ICU patients managed with IV insulin during the perioperative and postoperative periods with surgical patients on conventional diabetes management, Van den Berghe found a 45% reduction in mortality rates among those receiving insulin infusions (4.6% of those on IV insulin died, compared with 8% of those receiving subcutaneous insulin). The use of IV insulin therapy also decreased the time spent in intensive care, although it did not shorten the overall length of stay.¹⁹

Regular insulin is used most often for insulin infusions. Some trials with ultra–short-acting insulin have been done, but the findings were inconclusive.

Your patient is leaving: Ease the transition

For inpatients with diabetes, discharge planning includes a transition, from insulin to oral agents, perhaps, and from maintaining glucose control based on a hospital schedule to adjusting to the patterns of daily life at home. Particular care is required for patients who will be transitioned from IV to subcutaneous insulin. IV insulin has a half-life of only 10 minutes, so the initial subcutaneous dose should be administered about 1 hour prior to discontinuation of the infusion. Failure to plan accordingly may result in significant hyperglycemia and associated complications.^17,21

Research suggests that patients be switched to their outpatient diabetes management plan at least 24 hours before discharge, a protocol that was followed in Mr. H’s case. He remained in the hospital for 5 days. After myocardial infarction was ruled out, Mr. H underwent a nuclear medicine cardiac stress test for which he needed to be NPO. When testing was completed, Mr. H resumed a diabetic diet, and discharge planning began. Since his diabetes was not well controlled on admission and he required >20 units of insulin per day in the hospital, Mr. H’s physician opted to include long-acting insulin at bedtime in his outpatient regimen. On the day before Mr. H was scheduled to leave the hospital, the physician discontinued the short-acting mealtime insulin and restarted oral metformin twice daily, closely monitoring the patient’s glucose levels until discharge. The physician told Mr. H to schedule a follow-up visit within a week so that his new outpatient regimen could be reviewed.

Ideally, a diabetes nurse specialist will be available, not only to get involved in discharge planning, but also to provide patient education, care, and advice. Researchers found that hospital stays for patients with diabetes were shortened (8 days vs 11 days) when a diabetes nurse specialist was involved in their care. The patients were also more knowledgeable and satisfied.²²

Take advantage of bedside conversations. An inpatient stay offers physicians and patients the opportunity to work together to fine-tune components of the diabetic regimen.²³ Make the most of these opportunities. In addition, once the patient goes home, you’ll need to ensure close follow-up to reconcile the differences between home self-management and the controlled hospital environment.

Correspondence
Donald R. Woolever, MD, Family Medicine Residency Program, Central Maine Medical Center, 76 High Street, Lewiston, ME 04240; [email protected].

Times are tough for primary care physicians—so tough that American Academy of Family Physicians’ President Jim King, MD, recently called for health care reform to ensure that coverage is affordable and that “physicians can continue to care for [patients] without fear of bankruptcy.”¹ Yet in virtually every family practice, opportunities to maximize reimbursements are missed. Undercoding, omitting modifiers, and submitting claims without the documentation needed to support them are everyday events.

The lost revenue is no small change. At the current Medicare reimbursement rate of $96.01 for a 99214 visit and $63.73 for a 99213 visit, a physician who undercodes just one level 4 visit per day could lose as much as $8,393 over the course of a year.²

Some family physicians undercode simply because they underestimate the value of the services they provide. Others deliberately take a conservative approach in hopes of avoiding a government audit—a misguided tactic that some coders believe is as likely as habitual overcoding to arouse suspicion.³ For still other physicians, the time it takes to document a level 4 visit is not worth the trouble. Brushing up on the requirements for higher-level visits (TABLES 1 AND 2)⁴ and using encounter templates to guide you through a review of systems, symptoms, and severity can help lighten the documentation load.

To provide additional help, we’ve developed 10 coding and billing tips based on our experiences in family practice. Each of these can help you to maximize reimbursement.

TABLE 1
Established patient visits: CPT codes and documentation requirements

TABLE 2
New patient visits: CPT codes and documentation requirements

1. Document and bill more 99214s

Centers for Medicare & Medicaid Services (CMS) data show that in 2006, family physicians billed 55.2% of their established outpatient visits as level 3s (99213) and 31.6% as level 4s (99214).² Evidence suggests that the percentage of 99214s could legitimately be higher. A study comparing family physicians’ choice of codes with those selected by expert coders revealed that the physicians undercoded one third of their established patient visits. In most cases, visits that warranted 99214 codes were instead coded as 99213s.⁵

To bill for a level 4 established patient visit, CPT (Current Procedural Terminology) guidelines require you to fulfill 2 out of 3 of the following components:

• a detailed history
• a detailed physical examination
• medical decision making of moderate complexity.⁴

When the history and medical decision making indicate a higher level of complexity, you can bill for a 99214 visit without having to count or document individual body systems or detailed exam elements. A new diagnosis with a prescription, an order for laboratory tests or X-rays, or a request for a specialty consult are all examples of moderately complex decision making. When it is necessary to show that you performed a comprehensive system review to justify a 99214 claim, history forms, filled out in the waiting room and subsequently reviewed with the patient, can be a valuable time-saver.

2. Avoid the 99203/99204 “complexity” pitfall

In 2006, CMS data showed that family physicians billed 43.9% of new patient visits as level 3s (99203) and just 28.5% as level 4s (99204).² In many cases, opportunities to bill for 99204s are missed.

Unlike a level 4 visit for an established patient, a 99204 code requires all 3 components—a detailed history, detailed physical examination, and moderately complex decision making (TABLE 2).⁴ Thorough data collection is crucial to justify the higher level code, which is appropriate whenever a new patient presents with a complex medical history warranting a new diagnosis, new medication, and tests or a specialty evaluation.

Beware of the tendency to code the visit based on the complexity of the diagnosis, rather than the extent of decision making involved. A new patient visit from a woman, age 57, who presents with congestion and a persistent cough occasionally accompanied by chest pain might warrant a 99204 if her medical history (eg, obesity, hypertension, and gastroesophageal reflux disease) and review of systems made it necessary to rule out acute myocardial infarction and congestive heart failure, among other serious conditions, before arriving at a diagnosis of bronchitis. If you’re unsure of whether you can use the higher code, review the coding and documentation requirements in TABLE 2.

3. Remember to use modifier -25 with the proper documentation

The Office of Inspector General notes that you can bill for an office procedure performed on the same day as you evaluate the patient, if the procedure “is significant, separately identifiable, and above and beyond the usual preoperative and postoperative care associated with the procedure….” To do so, though, it is necessary to attach modifier-25 to the evaluation and management (E/M) code, and to provide evidence that you performed 2 separate services.

Proper documentation is critical here. In 2002, Medicare approved some 29 million claims using modifier -25, then disallowed nearly 35% of them for failing to meet the documentation requirements.⁶ How can you avoid a similar fate?

While most third-party payers do not require physicians who bill for an E/M service and a procedural service for the same patient on the same day to submit 2 separate progress notes, the work performed for each must be clearly defined. If you saw a patient with diabetes for a medication check and she asked you to remove a wart, you would need to document the dimensions, depth, and location of the wart, along with details of your targeted evaluation and management.

4. Know when to bill for preventive and E/M services

We’re all familiar with the patient who comes in for a yearly health maintenance examination, then wants to discuss her depression or chronic back pain. In such a case, you may be justified in billing for both preventive services and an office visit—again, using modifier -25 to indicate that you provided significant, separate services.

The distinction can be harder to establish than when separating an E/M service and a procedure, however. If the acute or chronic problem that you evaluate is stable and closely related to the preventive examination—well-controlled asthma not requiring a change in medication, for example—submitting an E/M code is not warranted. But a new problem or an exacerbation of an existing problem requiring a significant history, physical examination, and treatment beyond what would typically be performed during a routine preventive visit would be a valid reason to bill for E/M services.

Management of 2 or more medically significant chronic problems requiring prescription refills and either laboratory or radiographic tests also justifies concomitant billing of an E/M code.

The best laid plans…. Even when billing for preventive and problem-oriented care is appropriate and the proper codes and documentation are submitted, you may not be reimbursed for both. Some third-party payers will pay a portion of each; others will deny the additional claim entirely. There are also some health plans that will require any patient who generates 2 charges on the same day to pay 2 separate copays.

5. Charge for patient counseling

When more than half the time you spend with a patient is devoted to counseling or coordination of care, “time may be considered the key or controlling factor to qualify for a particular level of E/M service,” according to CPT guidelines.⁴ That is, you may be able to justify the use of a higher level E/M code based solely on time, regardless of the complexity and detail of the medical history, physical examination, or medical decision making (TABLES 1 AND 2).

Medicare’s Documentation Guidelines for E/M Services direct physicians to document the total time of the patient encounter and to describe in detail the nature of the counseling or activities to coordinate care.⁷ That said, time spent before and after the face-to-face encounter—retrieving and reviewing records or test results in preparation for the visit and arranging referrals or communicating with other health care providers afterwards, for example—cannot be counted toward the total time of the patient encounter.

6. Watch your words when billing for derm procedures

To maximize your reimbursement of dermatologic procedures, you need to be especially mindful of the terminology you use and the descriptive details you record.

Start with terminology. A biopsy generally indicates that only a portion of a lesion was removed to obtain a histologic diagnosis, as in the case of a punch biopsy. When you remove an entire lesion, you use either a shave (horizontal partial-thickness cut that does not include the entire dermal layer) or an excision (a full-thickness removal of the lesion through the dermis to the adipose tissue). Using the correct terminology will ensure that you are properly reimbursed for the procedure you performed.

Focus on measurements. Size matters, too: The larger the lesion, the greater the reimbursement.

To bill for an excision, the size of the lesion must be documented and the excised area calculated by adding the lesion’s maximum diameter plus the sum of the narrowest margin.⁴ While margins are counted for excisions, that’s not the case with shaved lesions. The margins of a shaved lesion are not factored into the reimbursement formula, so document only the measurement of the lesion itself.

Location also dictates the scale of reimbursement, which is typically lower for procedures involving the trunk, arms, or legs than for those on the face or in the anogenital area. Malignant lesions also generate higher charges.

File multiple claims for multiple lesions. When multiple lesions are biopsied or removed during a single visit, file multiple claims, using modifier -59 for distinct (separate) procedural services.⁸ Be aware, however, that third-party payers may not provide full reimbursement for each lesion. For Medicare enrollees, routine excision of skin lesions is considered cosmetic and is not covered unless the lesions have malignant or potentially malignant, symptomatic, or functionally impairing features.

7. Use a template for the “Welcome to Medicare” exam

All new Medicare Part B beneficiaries are entitled to a “Welcome to Medicare” exam within their first 6 months of enrollment. It has 7 elements, all of which are required for full reimbursement. To appropriately conduct and bill for this exam, create a template listing all the requisite elements:

1. A comprehensive review of the patient’s medical, social, and family history
2. A review of risk factors for depression
3. A review of functional ability and level of safety
4. A focused physical exam (weight, height, blood pressure, and visual acuity are the only requirements)
5. An electrocardiogram, with interpretation
6. Brief education, counseling, and referral to address any issues discovered in the first 5 elements
7. Brief education, counseling, and referral, with a written plan for the patient regarding preventive services covered by Part B.⁹

To be reimbursed for the Welcome to Medicare exam, it is necessary to use 2 separate billing codes: G0344 for the physical examination (paid at a rate equal to a 99203 visit) and G0366 for the electrocardiogram.⁹ Although CMS does not provide coverage for a general preventive examination other than this initial “Welcome to Medicare” visit, many recommended preventive health services are covered by Medicare at specified intervals (TABLE 3).⁹

TABLE 3
Preventive services covered by Medicare

8. Code injections with care

Whether you are administering vaccines or analgesics, coding for injections presents multiple opportunities for error. Physicians often include the code for a vaccine, but forget the procedure code for its administration.

Omitting the dose indication is another common occurrence. (If you inject a 30-mg dose of ketorolac and submit a J1885 code, which covers a 15-mg dose, for example, it is necessary to indicate that you administered a double dose.) It’s also not unusual for physicians to fail to include all the required codes for patients who receive multiple vaccinations at a single visit.

If a 68-year-old man, an established patient, comes in for an annual flu shot and is given the pneumococcal vaccine during the same visit, the correct codes would be:

• 90658 (flu vaccine)
• G0008 (flu vaccine administration)
• 90732 (pneumococcal vaccine)
• G0009 (pneumococcal vaccine administration).

Omitting both procedure codes could cost you nearly $20—and could run into thousands of dollars a year if the error is a daily occurrence.

9. Prioritize diagnoses

Many patients present with multiple diagnoses to be addressed during a single routine office visit, each of which may be applicable for billing for services rendered. ICD-9 coding guidelines state that physicians should “list first the ICD-9-CM code for the diagnosis, condition, problem or other reason for the encounter/visit shown in the medical record to be chiefly responsible for the services provided, then list additional codes that describe any coexisting conditions.”¹⁰

Selecting the primary diagnosis for billing and coding, then listing the others in order of importance lets third-party payers know how you prioritized patient care—and helps ensure that you are reimbursed accordingly. (Be sure to list active and acute medical conditions discussed during the visit on the encounter form [eg, type 2 diabetes, hypertension] rather than those that are stable and not addressed that day—eg, seasonal allergies or migraine headaches.)

10. Bill extra for emergency services

From time to time, an unexpected office emergency arises that takes you away from the patient you are currently evaluating. In such cases, you can use CPT code 99058 to bill for services “provided on an emergency basis in the office, which disrupts other scheduled office services”—and bill for basic services provided to the patient, as well.⁴ Documentation, of course, must include the chief complaint, evaluation, diagnosis, and therapeutic plan and fully describe the emergent nature of the service to justify billing for the “emergency encounter.”

Be aware, however, that even when you code and document appropriately, you may not receive full reimbursement. Medicare and Medicaid often bundle emergency services with other services provided on the same day. Other third-party payers respond in different ways: Some pay the full fee; others pay only a small percentage. Depending on the payer’s policy, billing for a level 4 or 5 E/M visit may be preferable.

Disclosures
Dr. Heidelbaugh is a consultant for Takeda Pharmaceuticals North America, Inc. Dr. Riley and Ms. Habetler reported no potential conflict of interest relevant to this article.

Correspondence
Joel J. Heidelbaugh, MD, Ypsilanti Health Center, 200 Arnet, Suite 200 Ypsilanti, MI 48198; [email protected]

Times are tough for primary care physicians—so tough that American Academy of Family Physicians’ President Jim King, MD, recently called for health care reform to ensure that coverage is affordable and that “physicians can continue to care for [patients] without fear of bankruptcy.”¹ Yet in virtually every family practice, opportunities to maximize reimbursements are missed. Undercoding, omitting modifiers, and submitting claims without the documentation needed to support them are everyday events.

The lost revenue is no small change. At the current Medicare reimbursement rate of $96.01 for a 99214 visit and $63.73 for a 99213 visit, a physician who undercodes just one level 4 visit per day could lose as much as $8,393 over the course of a year.²

Some family physicians undercode simply because they underestimate the value of the services they provide. Others deliberately take a conservative approach in hopes of avoiding a government audit—a misguided tactic that some coders believe is as likely as habitual overcoding to arouse suspicion.³ For still other physicians, the time it takes to document a level 4 visit is not worth the trouble. Brushing up on the requirements for higher-level visits (TABLES 1 AND 2)⁴ and using encounter templates to guide you through a review of systems, symptoms, and severity can help lighten the documentation load.

To provide additional help, we’ve developed 10 coding and billing tips based on our experiences in family practice. Each of these can help you to maximize reimbursement.

TABLE 1
Established patient visits: CPT codes and documentation requirements

TABLE 2
New patient visits: CPT codes and documentation requirements

1. Document and bill more 99214s

Centers for Medicare & Medicaid Services (CMS) data show that in 2006, family physicians billed 55.2% of their established outpatient visits as level 3s (99213) and 31.6% as level 4s (99214).² Evidence suggests that the percentage of 99214s could legitimately be higher. A study comparing family physicians’ choice of codes with those selected by expert coders revealed that the physicians undercoded one third of their established patient visits. In most cases, visits that warranted 99214 codes were instead coded as 99213s.⁵

To bill for a level 4 established patient visit, CPT (Current Procedural Terminology) guidelines require you to fulfill 2 out of 3 of the following components:

• a detailed history
• a detailed physical examination
• medical decision making of moderate complexity.⁴

When the history and medical decision making indicate a higher level of complexity, you can bill for a 99214 visit without having to count or document individual body systems or detailed exam elements. A new diagnosis with a prescription, an order for laboratory tests or X-rays, or a request for a specialty consult are all examples of moderately complex decision making. When it is necessary to show that you performed a comprehensive system review to justify a 99214 claim, history forms, filled out in the waiting room and subsequently reviewed with the patient, can be a valuable time-saver.

2. Avoid the 99203/99204 “complexity” pitfall

In 2006, CMS data showed that family physicians billed 43.9% of new patient visits as level 3s (99203) and just 28.5% as level 4s (99204).² In many cases, opportunities to bill for 99204s are missed.

Unlike a level 4 visit for an established patient, a 99204 code requires all 3 components—a detailed history, detailed physical examination, and moderately complex decision making (TABLE 2).⁴ Thorough data collection is crucial to justify the higher level code, which is appropriate whenever a new patient presents with a complex medical history warranting a new diagnosis, new medication, and tests or a specialty evaluation.

Beware of the tendency to code the visit based on the complexity of the diagnosis, rather than the extent of decision making involved. A new patient visit from a woman, age 57, who presents with congestion and a persistent cough occasionally accompanied by chest pain might warrant a 99204 if her medical history (eg, obesity, hypertension, and gastroesophageal reflux disease) and review of systems made it necessary to rule out acute myocardial infarction and congestive heart failure, among other serious conditions, before arriving at a diagnosis of bronchitis. If you’re unsure of whether you can use the higher code, review the coding and documentation requirements in TABLE 2.

3. Remember to use modifier -25 with the proper documentation

The Office of Inspector General notes that you can bill for an office procedure performed on the same day as you evaluate the patient, if the procedure “is significant, separately identifiable, and above and beyond the usual preoperative and postoperative care associated with the procedure….” To do so, though, it is necessary to attach modifier-25 to the evaluation and management (E/M) code, and to provide evidence that you performed 2 separate services.

Proper documentation is critical here. In 2002, Medicare approved some 29 million claims using modifier -25, then disallowed nearly 35% of them for failing to meet the documentation requirements.⁶ How can you avoid a similar fate?

While most third-party payers do not require physicians who bill for an E/M service and a procedural service for the same patient on the same day to submit 2 separate progress notes, the work performed for each must be clearly defined. If you saw a patient with diabetes for a medication check and she asked you to remove a wart, you would need to document the dimensions, depth, and location of the wart, along with details of your targeted evaluation and management.

4. Know when to bill for preventive and E/M services

We’re all familiar with the patient who comes in for a yearly health maintenance examination, then wants to discuss her depression or chronic back pain. In such a case, you may be justified in billing for both preventive services and an office visit—again, using modifier -25 to indicate that you provided significant, separate services.

The distinction can be harder to establish than when separating an E/M service and a procedure, however. If the acute or chronic problem that you evaluate is stable and closely related to the preventive examination—well-controlled asthma not requiring a change in medication, for example—submitting an E/M code is not warranted. But a new problem or an exacerbation of an existing problem requiring a significant history, physical examination, and treatment beyond what would typically be performed during a routine preventive visit would be a valid reason to bill for E/M services.

Management of 2 or more medically significant chronic problems requiring prescription refills and either laboratory or radiographic tests also justifies concomitant billing of an E/M code.

The best laid plans…. Even when billing for preventive and problem-oriented care is appropriate and the proper codes and documentation are submitted, you may not be reimbursed for both. Some third-party payers will pay a portion of each; others will deny the additional claim entirely. There are also some health plans that will require any patient who generates 2 charges on the same day to pay 2 separate copays.

5. Charge for patient counseling

When more than half the time you spend with a patient is devoted to counseling or coordination of care, “time may be considered the key or controlling factor to qualify for a particular level of E/M service,” according to CPT guidelines.⁴ That is, you may be able to justify the use of a higher level E/M code based solely on time, regardless of the complexity and detail of the medical history, physical examination, or medical decision making (TABLES 1 AND 2).

Medicare’s Documentation Guidelines for E/M Services direct physicians to document the total time of the patient encounter and to describe in detail the nature of the counseling or activities to coordinate care.⁷ That said, time spent before and after the face-to-face encounter—retrieving and reviewing records or test results in preparation for the visit and arranging referrals or communicating with other health care providers afterwards, for example—cannot be counted toward the total time of the patient encounter.

6. Watch your words when billing for derm procedures

To maximize your reimbursement of dermatologic procedures, you need to be especially mindful of the terminology you use and the descriptive details you record.

Start with terminology. A biopsy generally indicates that only a portion of a lesion was removed to obtain a histologic diagnosis, as in the case of a punch biopsy. When you remove an entire lesion, you use either a shave (horizontal partial-thickness cut that does not include the entire dermal layer) or an excision (a full-thickness removal of the lesion through the dermis to the adipose tissue). Using the correct terminology will ensure that you are properly reimbursed for the procedure you performed.

Focus on measurements. Size matters, too: The larger the lesion, the greater the reimbursement.

To bill for an excision, the size of the lesion must be documented and the excised area calculated by adding the lesion’s maximum diameter plus the sum of the narrowest margin.⁴ While margins are counted for excisions, that’s not the case with shaved lesions. The margins of a shaved lesion are not factored into the reimbursement formula, so document only the measurement of the lesion itself.

Location also dictates the scale of reimbursement, which is typically lower for procedures involving the trunk, arms, or legs than for those on the face or in the anogenital area. Malignant lesions also generate higher charges.

File multiple claims for multiple lesions. When multiple lesions are biopsied or removed during a single visit, file multiple claims, using modifier -59 for distinct (separate) procedural services.⁸ Be aware, however, that third-party payers may not provide full reimbursement for each lesion. For Medicare enrollees, routine excision of skin lesions is considered cosmetic and is not covered unless the lesions have malignant or potentially malignant, symptomatic, or functionally impairing features.

7. Use a template for the “Welcome to Medicare” exam

All new Medicare Part B beneficiaries are entitled to a “Welcome to Medicare” exam within their first 6 months of enrollment. It has 7 elements, all of which are required for full reimbursement. To appropriately conduct and bill for this exam, create a template listing all the requisite elements:

1. A comprehensive review of the patient’s medical, social, and family history
2. A review of risk factors for depression
3. A review of functional ability and level of safety
4. A focused physical exam (weight, height, blood pressure, and visual acuity are the only requirements)
5. An electrocardiogram, with interpretation
6. Brief education, counseling, and referral to address any issues discovered in the first 5 elements
7. Brief education, counseling, and referral, with a written plan for the patient regarding preventive services covered by Part B.⁹

To be reimbursed for the Welcome to Medicare exam, it is necessary to use 2 separate billing codes: G0344 for the physical examination (paid at a rate equal to a 99203 visit) and G0366 for the electrocardiogram.⁹ Although CMS does not provide coverage for a general preventive examination other than this initial “Welcome to Medicare” visit, many recommended preventive health services are covered by Medicare at specified intervals (TABLE 3).⁹

TABLE 3
Preventive services covered by Medicare

8. Code injections with care

Whether you are administering vaccines or analgesics, coding for injections presents multiple opportunities for error. Physicians often include the code for a vaccine, but forget the procedure code for its administration.

Omitting the dose indication is another common occurrence. (If you inject a 30-mg dose of ketorolac and submit a J1885 code, which covers a 15-mg dose, for example, it is necessary to indicate that you administered a double dose.) It’s also not unusual for physicians to fail to include all the required codes for patients who receive multiple vaccinations at a single visit.

If a 68-year-old man, an established patient, comes in for an annual flu shot and is given the pneumococcal vaccine during the same visit, the correct codes would be:

• 90658 (flu vaccine)
• G0008 (flu vaccine administration)
• 90732 (pneumococcal vaccine)
• G0009 (pneumococcal vaccine administration).

Omitting both procedure codes could cost you nearly $20—and could run into thousands of dollars a year if the error is a daily occurrence.

9. Prioritize diagnoses

Many patients present with multiple diagnoses to be addressed during a single routine office visit, each of which may be applicable for billing for services rendered. ICD-9 coding guidelines state that physicians should “list first the ICD-9-CM code for the diagnosis, condition, problem or other reason for the encounter/visit shown in the medical record to be chiefly responsible for the services provided, then list additional codes that describe any coexisting conditions.”¹⁰

Selecting the primary diagnosis for billing and coding, then listing the others in order of importance lets third-party payers know how you prioritized patient care—and helps ensure that you are reimbursed accordingly. (Be sure to list active and acute medical conditions discussed during the visit on the encounter form [eg, type 2 diabetes, hypertension] rather than those that are stable and not addressed that day—eg, seasonal allergies or migraine headaches.)

10. Bill extra for emergency services

From time to time, an unexpected office emergency arises that takes you away from the patient you are currently evaluating. In such cases, you can use CPT code 99058 to bill for services “provided on an emergency basis in the office, which disrupts other scheduled office services”—and bill for basic services provided to the patient, as well.⁴ Documentation, of course, must include the chief complaint, evaluation, diagnosis, and therapeutic plan and fully describe the emergent nature of the service to justify billing for the “emergency encounter.”

Be aware, however, that even when you code and document appropriately, you may not receive full reimbursement. Medicare and Medicaid often bundle emergency services with other services provided on the same day. Other third-party payers respond in different ways: Some pay the full fee; others pay only a small percentage. Depending on the payer’s policy, billing for a level 4 or 5 E/M visit may be preferable.

Disclosures
Dr. Heidelbaugh is a consultant for Takeda Pharmaceuticals North America, Inc. Dr. Riley and Ms. Habetler reported no potential conflict of interest relevant to this article.

Correspondence
Joel J. Heidelbaugh, MD, Ypsilanti Health Center, 200 Arnet, Suite 200 Ypsilanti, MI 48198; [email protected]

Times are tough for primary care physicians—so tough that American Academy of Family Physicians’ President Jim King, MD, recently called for health care reform to ensure that coverage is affordable and that “physicians can continue to care for [patients] without fear of bankruptcy.”¹ Yet in virtually every family practice, opportunities to maximize reimbursements are missed. Undercoding, omitting modifiers, and submitting claims without the documentation needed to support them are everyday events.

The lost revenue is no small change. At the current Medicare reimbursement rate of $96.01 for a 99214 visit and $63.73 for a 99213 visit, a physician who undercodes just one level 4 visit per day could lose as much as $8,393 over the course of a year.²

Some family physicians undercode simply because they underestimate the value of the services they provide. Others deliberately take a conservative approach in hopes of avoiding a government audit—a misguided tactic that some coders believe is as likely as habitual overcoding to arouse suspicion.³ For still other physicians, the time it takes to document a level 4 visit is not worth the trouble. Brushing up on the requirements for higher-level visits (TABLES 1 AND 2)⁴ and using encounter templates to guide you through a review of systems, symptoms, and severity can help lighten the documentation load.

To provide additional help, we’ve developed 10 coding and billing tips based on our experiences in family practice. Each of these can help you to maximize reimbursement.

TABLE 1
Established patient visits: CPT codes and documentation requirements

TABLE 2
New patient visits: CPT codes and documentation requirements

1. Document and bill more 99214s

Centers for Medicare & Medicaid Services (CMS) data show that in 2006, family physicians billed 55.2% of their established outpatient visits as level 3s (99213) and 31.6% as level 4s (99214).² Evidence suggests that the percentage of 99214s could legitimately be higher. A study comparing family physicians’ choice of codes with those selected by expert coders revealed that the physicians undercoded one third of their established patient visits. In most cases, visits that warranted 99214 codes were instead coded as 99213s.⁵

To bill for a level 4 established patient visit, CPT (Current Procedural Terminology) guidelines require you to fulfill 2 out of 3 of the following components:

• a detailed history
• a detailed physical examination
• medical decision making of moderate complexity.⁴

When the history and medical decision making indicate a higher level of complexity, you can bill for a 99214 visit without having to count or document individual body systems or detailed exam elements. A new diagnosis with a prescription, an order for laboratory tests or X-rays, or a request for a specialty consult are all examples of moderately complex decision making. When it is necessary to show that you performed a comprehensive system review to justify a 99214 claim, history forms, filled out in the waiting room and subsequently reviewed with the patient, can be a valuable time-saver.

2. Avoid the 99203/99204 “complexity” pitfall

In 2006, CMS data showed that family physicians billed 43.9% of new patient visits as level 3s (99203) and just 28.5% as level 4s (99204).² In many cases, opportunities to bill for 99204s are missed.

Unlike a level 4 visit for an established patient, a 99204 code requires all 3 components—a detailed history, detailed physical examination, and moderately complex decision making (TABLE 2).⁴ Thorough data collection is crucial to justify the higher level code, which is appropriate whenever a new patient presents with a complex medical history warranting a new diagnosis, new medication, and tests or a specialty evaluation.

Beware of the tendency to code the visit based on the complexity of the diagnosis, rather than the extent of decision making involved. A new patient visit from a woman, age 57, who presents with congestion and a persistent cough occasionally accompanied by chest pain might warrant a 99204 if her medical history (eg, obesity, hypertension, and gastroesophageal reflux disease) and review of systems made it necessary to rule out acute myocardial infarction and congestive heart failure, among other serious conditions, before arriving at a diagnosis of bronchitis. If you’re unsure of whether you can use the higher code, review the coding and documentation requirements in TABLE 2.

3. Remember to use modifier -25 with the proper documentation

The Office of Inspector General notes that you can bill for an office procedure performed on the same day as you evaluate the patient, if the procedure “is significant, separately identifiable, and above and beyond the usual preoperative and postoperative care associated with the procedure….” To do so, though, it is necessary to attach modifier-25 to the evaluation and management (E/M) code, and to provide evidence that you performed 2 separate services.

Proper documentation is critical here. In 2002, Medicare approved some 29 million claims using modifier -25, then disallowed nearly 35% of them for failing to meet the documentation requirements.⁶ How can you avoid a similar fate?

While most third-party payers do not require physicians who bill for an E/M service and a procedural service for the same patient on the same day to submit 2 separate progress notes, the work performed for each must be clearly defined. If you saw a patient with diabetes for a medication check and she asked you to remove a wart, you would need to document the dimensions, depth, and location of the wart, along with details of your targeted evaluation and management.

4. Know when to bill for preventive and E/M services

We’re all familiar with the patient who comes in for a yearly health maintenance examination, then wants to discuss her depression or chronic back pain. In such a case, you may be justified in billing for both preventive services and an office visit—again, using modifier -25 to indicate that you provided significant, separate services.

The distinction can be harder to establish than when separating an E/M service and a procedure, however. If the acute or chronic problem that you evaluate is stable and closely related to the preventive examination—well-controlled asthma not requiring a change in medication, for example—submitting an E/M code is not warranted. But a new problem or an exacerbation of an existing problem requiring a significant history, physical examination, and treatment beyond what would typically be performed during a routine preventive visit would be a valid reason to bill for E/M services.

Management of 2 or more medically significant chronic problems requiring prescription refills and either laboratory or radiographic tests also justifies concomitant billing of an E/M code.

The best laid plans…. Even when billing for preventive and problem-oriented care is appropriate and the proper codes and documentation are submitted, you may not be reimbursed for both. Some third-party payers will pay a portion of each; others will deny the additional claim entirely. There are also some health plans that will require any patient who generates 2 charges on the same day to pay 2 separate copays.

5. Charge for patient counseling

When more than half the time you spend with a patient is devoted to counseling or coordination of care, “time may be considered the key or controlling factor to qualify for a particular level of E/M service,” according to CPT guidelines.⁴ That is, you may be able to justify the use of a higher level E/M code based solely on time, regardless of the complexity and detail of the medical history, physical examination, or medical decision making (TABLES 1 AND 2).

Medicare’s Documentation Guidelines for E/M Services direct physicians to document the total time of the patient encounter and to describe in detail the nature of the counseling or activities to coordinate care.⁷ That said, time spent before and after the face-to-face encounter—retrieving and reviewing records or test results in preparation for the visit and arranging referrals or communicating with other health care providers afterwards, for example—cannot be counted toward the total time of the patient encounter.

6. Watch your words when billing for derm procedures

To maximize your reimbursement of dermatologic procedures, you need to be especially mindful of the terminology you use and the descriptive details you record.

Start with terminology. A biopsy generally indicates that only a portion of a lesion was removed to obtain a histologic diagnosis, as in the case of a punch biopsy. When you remove an entire lesion, you use either a shave (horizontal partial-thickness cut that does not include the entire dermal layer) or an excision (a full-thickness removal of the lesion through the dermis to the adipose tissue). Using the correct terminology will ensure that you are properly reimbursed for the procedure you performed.

Focus on measurements. Size matters, too: The larger the lesion, the greater the reimbursement.

To bill for an excision, the size of the lesion must be documented and the excised area calculated by adding the lesion’s maximum diameter plus the sum of the narrowest margin.⁴ While margins are counted for excisions, that’s not the case with shaved lesions. The margins of a shaved lesion are not factored into the reimbursement formula, so document only the measurement of the lesion itself.

Location also dictates the scale of reimbursement, which is typically lower for procedures involving the trunk, arms, or legs than for those on the face or in the anogenital area. Malignant lesions also generate higher charges.

File multiple claims for multiple lesions. When multiple lesions are biopsied or removed during a single visit, file multiple claims, using modifier -59 for distinct (separate) procedural services.⁸ Be aware, however, that third-party payers may not provide full reimbursement for each lesion. For Medicare enrollees, routine excision of skin lesions is considered cosmetic and is not covered unless the lesions have malignant or potentially malignant, symptomatic, or functionally impairing features.

7. Use a template for the “Welcome to Medicare” exam

All new Medicare Part B beneficiaries are entitled to a “Welcome to Medicare” exam within their first 6 months of enrollment. It has 7 elements, all of which are required for full reimbursement. To appropriately conduct and bill for this exam, create a template listing all the requisite elements:

1. A comprehensive review of the patient’s medical, social, and family history
2. A review of risk factors for depression
3. A review of functional ability and level of safety
4. A focused physical exam (weight, height, blood pressure, and visual acuity are the only requirements)
5. An electrocardiogram, with interpretation
6. Brief education, counseling, and referral to address any issues discovered in the first 5 elements
7. Brief education, counseling, and referral, with a written plan for the patient regarding preventive services covered by Part B.⁹

To be reimbursed for the Welcome to Medicare exam, it is necessary to use 2 separate billing codes: G0344 for the physical examination (paid at a rate equal to a 99203 visit) and G0366 for the electrocardiogram.⁹ Although CMS does not provide coverage for a general preventive examination other than this initial “Welcome to Medicare” visit, many recommended preventive health services are covered by Medicare at specified intervals (TABLE 3).⁹

TABLE 3
Preventive services covered by Medicare

8. Code injections with care

Whether you are administering vaccines or analgesics, coding for injections presents multiple opportunities for error. Physicians often include the code for a vaccine, but forget the procedure code for its administration.

Omitting the dose indication is another common occurrence. (If you inject a 30-mg dose of ketorolac and submit a J1885 code, which covers a 15-mg dose, for example, it is necessary to indicate that you administered a double dose.) It’s also not unusual for physicians to fail to include all the required codes for patients who receive multiple vaccinations at a single visit.

If a 68-year-old man, an established patient, comes in for an annual flu shot and is given the pneumococcal vaccine during the same visit, the correct codes would be:

• 90658 (flu vaccine)
• G0008 (flu vaccine administration)
• 90732 (pneumococcal vaccine)
• G0009 (pneumococcal vaccine administration).

Omitting both procedure codes could cost you nearly $20—and could run into thousands of dollars a year if the error is a daily occurrence.

9. Prioritize diagnoses

Many patients present with multiple diagnoses to be addressed during a single routine office visit, each of which may be applicable for billing for services rendered. ICD-9 coding guidelines state that physicians should “list first the ICD-9-CM code for the diagnosis, condition, problem or other reason for the encounter/visit shown in the medical record to be chiefly responsible for the services provided, then list additional codes that describe any coexisting conditions.”¹⁰

Selecting the primary diagnosis for billing and coding, then listing the others in order of importance lets third-party payers know how you prioritized patient care—and helps ensure that you are reimbursed accordingly. (Be sure to list active and acute medical conditions discussed during the visit on the encounter form [eg, type 2 diabetes, hypertension] rather than those that are stable and not addressed that day—eg, seasonal allergies or migraine headaches.)

10. Bill extra for emergency services

From time to time, an unexpected office emergency arises that takes you away from the patient you are currently evaluating. In such cases, you can use CPT code 99058 to bill for services “provided on an emergency basis in the office, which disrupts other scheduled office services”—and bill for basic services provided to the patient, as well.⁴ Documentation, of course, must include the chief complaint, evaluation, diagnosis, and therapeutic plan and fully describe the emergent nature of the service to justify billing for the “emergency encounter.”

Be aware, however, that even when you code and document appropriately, you may not receive full reimbursement. Medicare and Medicaid often bundle emergency services with other services provided on the same day. Other third-party payers respond in different ways: Some pay the full fee; others pay only a small percentage. Depending on the payer’s policy, billing for a level 4 or 5 E/M visit may be preferable.

Disclosures
Dr. Heidelbaugh is a consultant for Takeda Pharmaceuticals North America, Inc. Dr. Riley and Ms. Habetler reported no potential conflict of interest relevant to this article.

Correspondence
Joel J. Heidelbaugh, MD, Ypsilanti Health Center, 200 Arnet, Suite 200 Ypsilanti, MI 48198; [email protected]

One of your patients, a 40-year-old woman, recently began an exercise program, and she now says she has persistent heel pain. Your first suspicion is “another plantar fasciitis case.” However, after asking a few questions and performing a brief examination, you realize the problem is not what you expected. The pain is in the wrong place for plantar fasciitis and the patient’s history is atypical. How should you proceed?

Knowing the precise location of maximum pain or tenderness (FIGURES 1A–1C) and pairing that with key findings from the exam and history (TABLE 1) can help you reach an accurate diagnosis and formulate proper treatment (TABLE 2).

Each of the 3 general areas of heel pain—posterior, plantar, and medial—introduces a unique differential. Bilateral symptoms or multiple joint involvement, of course, raises the possibility of associated systemic disease.

FIGURE 1
Common causes of heel pain by location

TABLE 1
A quick guide to narrowing your heel pain diagnosis

Posterior heel pain

The common causes of posterior heel pain are Achilles tendinopathy, retrocalcaneal bursitis, calcaneal apophysitis, posterior impingement (FIGURE 1A), and Achilles tendon strain or rupture. Rarer causes are sciatica, peroneal tendonitis, Haglund’s deformity, pump bump, and systemic disorders. The patient’s history and precise location of maximal tenderness¹ differentiates these problems.

Achilles tendinopathy (tendonitis): Is the patient an athlete?

Insertional and noninsertional Achilles tendinopathy are the most common causes of persistent posterior heel pain.^2,3 The inflammatory process occurs in the fatty tissue surrounding the Achilles tendon (the paratenon) rather than in the tendon itself. Patients tend to be highly active (often athletes) and may have recently increased their activity. Ask patients, too, whether they have recently taken a fluoroquinolone antibiotic. This drug class is known to increase the risk of both tendonitis and tendon rupture,⁴ and in July of this year the FDA directed drug manufacturers to add a black-box warning to that effect.⁵

Evaluation of noninsertional tendinopathy. Tenderness is usually located 2 to 6 cm above the Achilles insertion. Nodularity, swelling, or fluctuance of the tendon may be evident. Diagnosis generally can be made clinically. If confirmation is needed, consider ultrasonography or magnetic resonance imaging.

Treatment. Advise patients to decrease physical activity and do stretching exercises, undergo eccentric calf muscle training, use heel lifts, modify shoe fit, and use systemic or topical nonsteroidal anti-inflammatory drugs (NSAIDs) regularly for a few days, then as needed. Refractory cases may require surgery.⁶ New therapies that have proven effective include extracorporeal shock wave therapy (ESWT), prolotherapy (dextrose injections), and local application of nitroglycerin patches or gel.^7-18 ESWT can be expensive and is not widely available. Prolotherapy can be performed with minimal training, but is still relatively new. Topical nitroglycerin is affordable, but beware of such side effects as headache and hypotension.

Evaluation of insertional tendinopathy. Inflammation occurs at the tendon’s insertion to bone (enthesitis). Pain typically is at the midline and is reproduced by palpating the tendon insertion or by passively stretching the heel. The presentation may be difficult to distinguish from retrocalcaneal bursitis (discussed below).

Treatment is similar to that used for noninsertional tendinopathy. However, if insertional tendinopathy occurs in conjunction with a Haglund’s deformity (bony overgrowth of the calcaneus), surgery may be indicated, because noninvasive measures tend to fail.¹⁹

Use steroid injections with extreme caution due to the theoretical risk of tendon rupture.²⁰ Injections are effective when directed at concomitant inflammation of the retrocalcaneal bursa, but accurate positioning and careful postinjection care are paramount. After an injection, a patient may need absolute rest or even immobilization to protect from tendon rupture. Emphasize a careful return to activity or athletic training.

Retrocalcaneal bursitis: Look for subtle swelling

The retrocalcaneal bursa lies between the Achilles tendon and the calcaneus near the tendon’s insertion. This bursa may become inflamed with repetitive stress or with insertional Achilles tendinopathy.

Evaluation. Swelling is usually present but may be subtle. Pain is located just lateral to the midline of the posterior heel at the superior angle of the calcaneus, and it may also be medial to the tendon opposite the lateral location.

Treatment. The bursitis often responds to icing and ice massage, shoe-fit adjustments, heel lifts, Achilles stretching programs, and systemic or topical NSAIDs.² Steroid injections are likely beneficial, but use them with caution and take care to avoid the Achilles tendon insertion.

Calcaneal apophysitis affects highly active kids

Calcaneal apophysitis (Sever’s disease) is a painful inflammation in the heels of skeletally immature children where the Achilles tendon inserts in the calcaneus apophysis.

Evaluation. Associated with peak growth rate and high activity level, this inflammatory process usually occurs in boys between the ages of 10 and 12 years, and in girls between the ages of 8 and 10 years.²¹ The process is similar to that occurring at other sites of traction apophysitis, such as Osgood-Schlatter disease at the tibial tuberosity. Children most susceptible are highly active, wear poorly fitting footwear, run frequently on hard surfaces, and have tight Achilles tendons. Clinical diagnosis usually suffices, although plain x-ray films can verify an active apophysis and rule out other sources of pain, such as tarsal coalition, calcaneal stress fractures, or infection.²²

Treatment. Calcaneal apophysitis is typically self-limiting, and the mainstay of treatment is rest. Heel lifts, stretching programs, icing, gel heel cups, and anti-inflammatory agents may also be used.²³

Posterior impingement: Pain with full plantar flexion

Posterior impingement at the ankle joint may be self-originating or arise as a consequence of an os trigonum, a posterior sesamoid bone of the talus that exists as a normal variant. In some cases, this bone creates a barrier to full plantar flexion at the ankle joint and creates pain at the posterior heel.

Evaluation. Pain with full plantar flexion is a critical distinguishing feature, because most other pathologies in the posterior heel cause pain with dorsiflexion at the ankle.^24,25 Patients often are involved in activities that require forced plantar flexion, such as gymnastics or dancing. Diagnosis is clinical for the most part, but plain x-ray films may confirm the presence of an os trigonum. Magnetic resonance imaging (MRI) is warranted for patients with persistent symptoms; it may reveal a hypertrophied synovial lining or other pathology (such as osteochondritis). MRI is also indicated before more invasive therapies, such as steroid injections or surgery.

Treatment. Advise rest with or without immobilization, NSAIDs, or local steroid injections. Severe impingement or recalcitrant cases may require surgical release of the posterior synovium or removal of an os trigonum.^24,25

Achilles strain and rupture: Middle-aged men are susceptible

The Achilles tendon is most susceptible to injury in middle-aged men who are active in sports requiring loading and sudden contraction of the calf muscles, such as basketball or football, although injuries may occur in a variety of other settings. A strain of the Achilles tendon should be carefully differentiated from a complete rupture. While strains can be treated similarly to Achilles tendinopathy, complete rupture is a much larger concern.

Evaluation. When the Achilles tendon ruptures, patients describe sudden pain and a pop that is often audible. Poor plantar flexion of the foot ensues.²⁶ Telltale signs on examination are a positive Thompson’s test (little or no plantar flexion with a calf squeeze) and a visible defect in the tendon. The rupture site is usually 1 to 2 inches proximal to its insertion on the calcaneus.

Treatment. Most of these patients should be seen by an orthopedic surgeon as soon as possible. For active and younger adults, treatment is almost always early surgical repair.²⁷ For some older individuals who are less active, nonsurgical management includes graduated casting, which progressively lessens plantar flexion over 6 to 10 weeks, followed by physical therapy.

3 less common causes of posterior heel pain

Haglund’s deformity is an overgrowth of the calcaneus at the insertion of the Achilles tendon.³ Caused by overuse and poorly fitted shoes, this condition commonly requires surgical intervention.

Pump bump is an inflamed superficial bursa commonly associated with a Haglund’s deformity, and it may respond to NSAIDs, shoe-fit modification, ice massage, or steroid injection.

Peroneal tendonitis is a tendinopathy of evertors and external rotators of the foot. The pain will follow the tendons posterior to the lateral malleolus and extend to the lateral midfoot. It is also treated with rest, NSAIDs, icing, and physical therapy.

Plantar-surface heel pain

The problems most likely to cause plantar-surface pain (FIGURE 1B) are plantar fasciitis, stress fracture of the calcaneus, and fat pad syndrome.

Plantar fasciitis: Pain is worst in the morning

This is by far the most common cause of heel pain primary care physicians will see. Rarely, infection and neoplasia will cause unilateral plantar heel pain.⁴

Evaluation. Tenderness localized to the plantar surface of the heel in adults usually indicates plantar fasciitis.

Pain is worst with the first step of the morning, and lessens with activity. The tender spot is the medial calcaneal tubercle, with pain radiating through the arch.^1,28-30

Treatment. The many therapeutic modalities—NSAIDs, stretching exercises, gel cups, arch supports, night splints, steroid injections, ESWT, and surgery—have been extensively reviewed elsewhere, including in a Cochrane review from 2005.^31-33

Calcaneal stress fracture: Suspect it in runners

Calcaneal stress fractures are relatively rare, but may occur in those who put significant stressors on their feet, such as avid runners or military recruits.

Evaluation. Most patients report a recent increase in frequency or intensity of activity, and runners can tell you when it is during their run that the pain begins. As the stress fracture worsens, the pain begins earlier in the activity and eventually is present with even minimal activity. A key distinction from plantar fasciitis, in which pain lessens with activity, is that the pain of a stress fracture typically worsens with activity and diminishes with rest.³⁴

Physical exam provides few clues except for the “squeeze test” (FIGURE 1A) Putting pressure on both the medial and lateral calcaneal tuberosities will cause discomfort. Pain will be absent in the posterior structures of the heel. Placing a vibrating 128-cps tuning fork on the calcaneus should also increase discomfort.

Plain x-ray films may be falsely negative, especially during the first 2 to 3 weeks of pain. Three-phase bone scans are nearly 100% sensitive for detecting stress fractures, with changes evident in as little as 1 to 2 days after injury. The specificity of MRI scans is superior to that of bone scans and can reveal alternate problems.³⁵

Treatment. Activity modification reduces trauma to the heel. Encourage patients to walk if they are pain free and to increase activity as comfort allows. Tell patients to stop activity if the fracture becomes symptomatic. Advanced fractures demand an absolute absence of weight bearing.

Pain can be controlled with NSAIDs TABLE 2 and ice. Lab and animal data have suggested that NSAIDs may impede fracture healing rates, but no similar data exist regarding their effect on stress fractures.³⁶ Symptoms abate within 2 or 3 weeks. Advise athletes to resume activity slowly in a stepwise progression, letting them know that a return to full activity is likely within 6 to 8 weeks. Have runners restart their routine at half their customary distance, increasing it by no more than 10% to 15% per week.

Any medical condition that weakens the bone may predispose a patient to stress fracture. To prevent primary and secondary stress fractures, correct the patient’s underlying medical problems. Evaluate young, thin women with a stress fracture for the “female athlete triad” (osteopenia, disordered eating, menstrual irregularity). The elderly are also at risk for stress fractures due to osteopenia or osteoporosis.

TABLE 2
Heel pain treatment options: A look at the evidence

Fat pad syndrome: More diffuse pain than plantar fasciitis

The plantar surface of the heel is protected by a thick fat pad. Those at risk of a thinned fat pad include the elderly (the pad thins with age), the obese (increased stress to the pad), and those who have previously received a corticosteroid injection in the pad. Cumulative or acute trauma to the heel can also cause contusion to the heel pad.

Evaluation. Pain typically is located more posteriorly than classic plantar fasciitis pain and is more diffuse. Pain from the fat pad should not radiate toward the arch and is not exacerbated by dorsiflexion of the foot.¹

Treatment. Recommend relative rest, gel heel cups, NSAIDs, and ice.³⁷

Less common causes of plantar-surface pain

Lateral plantar nerve entrapment may also cause neuropathic pain on the plantar surface. Patients who experience a painful pop in their heel associated with trauma may have ruptured their plantar fascia. A fallen arch may also be noted on exam. Treatment of both of these conditions is similar to that of plantar fasciitis.

Acute calcaneal fracture results from trauma, such as a fall from a height onto the soles of the feet. Look for localized pain and swelling around the calcaneus and evaluate the neurovascular status of the foot. Initial treatment includes elevating the foot, avoiding weight bearing, applying ice, controlling pain, and using a posterior splint. Many of these fractures require surgical fixation.

Medial heel pain

Posterior tibial tendonitis/dysfunction and tarsal tunnel syndrome are best classified as medial in location (FIGURE 1C). However, the pain is often more diffuse and may radiate to either the posterior or plantar heel.

Posterior tibial tendonitis/dysfunction are linked to obesity

Posterior tibial tendonitis (PTT) and posterior tibial tendon dysfunction (PTTD) are related diagnoses. PTTD refers to increased laxity of the tendon resulting in flat foot and increased heel varus. It is the most common cause of acquired flat foot in adults. PTT may exist separately or as part of PTTD.

Evaluation. Patients complain of pain at the posterior edge of the medial malleolus that may extend toward the arch of the foot.^38,39 Patients may also experience swelling or redness in the area. Both PTT and PTTD seem related to overuse and obesity. Young or nonobese patients with PTT or PTTD often have underlying systemic arthropathies.³⁵

Treatment. Early treatment is necessary to prevent progression of tendon incompetence. Interventions include weight loss, NSAIDs, icing, physical therapy,⁴⁰ and orthotics or bracing for arch and ankle support. You may also try immobilization in a short leg cast for 6 weeks.⁴¹ If conservative measures fail, surgery may be necessary for tendon repair, tendon transfer, calcaneal osteotomy, or tarsal bone fusion.^38,39

Tarsal tunnel syndrome: Pain can occur at night

Tarsal tunnel syndrome (TTS) is the most common compression neuropathy of the lower extremity. The tarsal tunnel is a fibro-osseous structure along the medial ankle that contains the tibial nerve, the posterior tibial artery, and the tendons of the tibialis posterior, flexor digitorum longus, and flexor hallucis longus. The posterior tibial nerve can become irritated as it runs through the tunnel. The inciting incident can be either a severe stretch to the nerve (from a medial ankle sprain) or from an anatomic compression. Pes planus foot or posterior tibial dysfunction have also been implicated as common causes.¹

Evaluation. Patients describe poorly localized pain with numbness and burning along the medial ankle, arch, or heel, with radiation proximally.^42,43 Symptoms are aggravated by exercise, and night pain is not uncommon. The tenderness of TTS is more diffuse than that from plantar fasciitis, and symptoms are evident directly over the tarsal tunnel itself.

The classic finding is a positive Tinel’s sign (reproduction of symptoms by tapping over the posterior tibial nerve as it passes through the tarsal tunnel). Placing the foot in dorsiflexion and eversion may also reproduce symptoms.¹

Imaging results are not always definitive, but can be helpful in determining the cause of the compression. Plain films and CT can detect fracture or bony deformity, while MRI is more helpful in evaluating soft-tissue structures, such as ganglions or varicosities. Abnormal nerve conduction studies can be suggestive of TTS, but a normal result does not rule out the diagnosis.

Treatment follows a stepped progression. Initially try activity modification, orthotics, and physical therapy. Physical therapy concentrates on medial arch strengthening, Achilles stretching, and ankle proprioception exercises.

NSAIDs and neuromodulatory drugs (tricyclic antidepressants and antiseizure medications) have shown some success. Steroid injections have been effective when given at the site of entrapment,⁴⁴ but care must be taken to avoid the posterior tibial tendon. If patients do not improve following these measures, they may require cast immobilization.⁴⁵

Surgery is a possibility when other options fail. The cause of the neural compression is identified in 60% to 80% of cases.^46,47 Success rates for various procedures of tarsal tunnel release and tibial nerve decompression range from 75% to 91%. If neural compression is absent, investigate other systemic causes of peripheral neuropathy, such as diabetes or alcoholism.⁴

Systemic diagnoses

Bilateral heel pain, multiple joint involvement, or fever suggests systemic disease. Common diseases affecting the heel include rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and inflammatory bowel disease.¹ Successful treatment of these disorders should relieve associated heel pain.

Correspondence
H. E. Woodall, MD, AnMed Health Family Medicine Residency, 2000 E Greenville Street, Suite 3600, Anderson, SC 29621; [email protected]

One of your patients, a 40-year-old woman, recently began an exercise program, and she now says she has persistent heel pain. Your first suspicion is “another plantar fasciitis case.” However, after asking a few questions and performing a brief examination, you realize the problem is not what you expected. The pain is in the wrong place for plantar fasciitis and the patient’s history is atypical. How should you proceed?

Knowing the precise location of maximum pain or tenderness (FIGURES 1A–1C) and pairing that with key findings from the exam and history (TABLE 1) can help you reach an accurate diagnosis and formulate proper treatment (TABLE 2).

Each of the 3 general areas of heel pain—posterior, plantar, and medial—introduces a unique differential. Bilateral symptoms or multiple joint involvement, of course, raises the possibility of associated systemic disease.

FIGURE 1
Common causes of heel pain by location

TABLE 1
A quick guide to narrowing your heel pain diagnosis

Posterior heel pain

The common causes of posterior heel pain are Achilles tendinopathy, retrocalcaneal bursitis, calcaneal apophysitis, posterior impingement (FIGURE 1A), and Achilles tendon strain or rupture. Rarer causes are sciatica, peroneal tendonitis, Haglund’s deformity, pump bump, and systemic disorders. The patient’s history and precise location of maximal tenderness¹ differentiates these problems.

Achilles tendinopathy (tendonitis): Is the patient an athlete?

Insertional and noninsertional Achilles tendinopathy are the most common causes of persistent posterior heel pain.^2,3 The inflammatory process occurs in the fatty tissue surrounding the Achilles tendon (the paratenon) rather than in the tendon itself. Patients tend to be highly active (often athletes) and may have recently increased their activity. Ask patients, too, whether they have recently taken a fluoroquinolone antibiotic. This drug class is known to increase the risk of both tendonitis and tendon rupture,⁴ and in July of this year the FDA directed drug manufacturers to add a black-box warning to that effect.⁵

Evaluation of noninsertional tendinopathy. Tenderness is usually located 2 to 6 cm above the Achilles insertion. Nodularity, swelling, or fluctuance of the tendon may be evident. Diagnosis generally can be made clinically. If confirmation is needed, consider ultrasonography or magnetic resonance imaging.

Treatment. Advise patients to decrease physical activity and do stretching exercises, undergo eccentric calf muscle training, use heel lifts, modify shoe fit, and use systemic or topical nonsteroidal anti-inflammatory drugs (NSAIDs) regularly for a few days, then as needed. Refractory cases may require surgery.⁶ New therapies that have proven effective include extracorporeal shock wave therapy (ESWT), prolotherapy (dextrose injections), and local application of nitroglycerin patches or gel.^7-18 ESWT can be expensive and is not widely available. Prolotherapy can be performed with minimal training, but is still relatively new. Topical nitroglycerin is affordable, but beware of such side effects as headache and hypotension.

Evaluation of insertional tendinopathy. Inflammation occurs at the tendon’s insertion to bone (enthesitis). Pain typically is at the midline and is reproduced by palpating the tendon insertion or by passively stretching the heel. The presentation may be difficult to distinguish from retrocalcaneal bursitis (discussed below).

Treatment is similar to that used for noninsertional tendinopathy. However, if insertional tendinopathy occurs in conjunction with a Haglund’s deformity (bony overgrowth of the calcaneus), surgery may be indicated, because noninvasive measures tend to fail.¹⁹

Use steroid injections with extreme caution due to the theoretical risk of tendon rupture.²⁰ Injections are effective when directed at concomitant inflammation of the retrocalcaneal bursa, but accurate positioning and careful postinjection care are paramount. After an injection, a patient may need absolute rest or even immobilization to protect from tendon rupture. Emphasize a careful return to activity or athletic training.

Retrocalcaneal bursitis: Look for subtle swelling

The retrocalcaneal bursa lies between the Achilles tendon and the calcaneus near the tendon’s insertion. This bursa may become inflamed with repetitive stress or with insertional Achilles tendinopathy.

Evaluation. Swelling is usually present but may be subtle. Pain is located just lateral to the midline of the posterior heel at the superior angle of the calcaneus, and it may also be medial to the tendon opposite the lateral location.

Treatment. The bursitis often responds to icing and ice massage, shoe-fit adjustments, heel lifts, Achilles stretching programs, and systemic or topical NSAIDs.² Steroid injections are likely beneficial, but use them with caution and take care to avoid the Achilles tendon insertion.

Calcaneal apophysitis affects highly active kids

Calcaneal apophysitis (Sever’s disease) is a painful inflammation in the heels of skeletally immature children where the Achilles tendon inserts in the calcaneus apophysis.

Evaluation. Associated with peak growth rate and high activity level, this inflammatory process usually occurs in boys between the ages of 10 and 12 years, and in girls between the ages of 8 and 10 years.²¹ The process is similar to that occurring at other sites of traction apophysitis, such as Osgood-Schlatter disease at the tibial tuberosity. Children most susceptible are highly active, wear poorly fitting footwear, run frequently on hard surfaces, and have tight Achilles tendons. Clinical diagnosis usually suffices, although plain x-ray films can verify an active apophysis and rule out other sources of pain, such as tarsal coalition, calcaneal stress fractures, or infection.²²

Treatment. Calcaneal apophysitis is typically self-limiting, and the mainstay of treatment is rest. Heel lifts, stretching programs, icing, gel heel cups, and anti-inflammatory agents may also be used.²³

Posterior impingement: Pain with full plantar flexion

Posterior impingement at the ankle joint may be self-originating or arise as a consequence of an os trigonum, a posterior sesamoid bone of the talus that exists as a normal variant. In some cases, this bone creates a barrier to full plantar flexion at the ankle joint and creates pain at the posterior heel.

Evaluation. Pain with full plantar flexion is a critical distinguishing feature, because most other pathologies in the posterior heel cause pain with dorsiflexion at the ankle.^24,25 Patients often are involved in activities that require forced plantar flexion, such as gymnastics or dancing. Diagnosis is clinical for the most part, but plain x-ray films may confirm the presence of an os trigonum. Magnetic resonance imaging (MRI) is warranted for patients with persistent symptoms; it may reveal a hypertrophied synovial lining or other pathology (such as osteochondritis). MRI is also indicated before more invasive therapies, such as steroid injections or surgery.

Treatment. Advise rest with or without immobilization, NSAIDs, or local steroid injections. Severe impingement or recalcitrant cases may require surgical release of the posterior synovium or removal of an os trigonum.^24,25

Achilles strain and rupture: Middle-aged men are susceptible

The Achilles tendon is most susceptible to injury in middle-aged men who are active in sports requiring loading and sudden contraction of the calf muscles, such as basketball or football, although injuries may occur in a variety of other settings. A strain of the Achilles tendon should be carefully differentiated from a complete rupture. While strains can be treated similarly to Achilles tendinopathy, complete rupture is a much larger concern.

Evaluation. When the Achilles tendon ruptures, patients describe sudden pain and a pop that is often audible. Poor plantar flexion of the foot ensues.²⁶ Telltale signs on examination are a positive Thompson’s test (little or no plantar flexion with a calf squeeze) and a visible defect in the tendon. The rupture site is usually 1 to 2 inches proximal to its insertion on the calcaneus.

Treatment. Most of these patients should be seen by an orthopedic surgeon as soon as possible. For active and younger adults, treatment is almost always early surgical repair.²⁷ For some older individuals who are less active, nonsurgical management includes graduated casting, which progressively lessens plantar flexion over 6 to 10 weeks, followed by physical therapy.

3 less common causes of posterior heel pain

Haglund’s deformity is an overgrowth of the calcaneus at the insertion of the Achilles tendon.³ Caused by overuse and poorly fitted shoes, this condition commonly requires surgical intervention.

Pump bump is an inflamed superficial bursa commonly associated with a Haglund’s deformity, and it may respond to NSAIDs, shoe-fit modification, ice massage, or steroid injection.

Peroneal tendonitis is a tendinopathy of evertors and external rotators of the foot. The pain will follow the tendons posterior to the lateral malleolus and extend to the lateral midfoot. It is also treated with rest, NSAIDs, icing, and physical therapy.

Plantar-surface heel pain

The problems most likely to cause plantar-surface pain (FIGURE 1B) are plantar fasciitis, stress fracture of the calcaneus, and fat pad syndrome.

Plantar fasciitis: Pain is worst in the morning

This is by far the most common cause of heel pain primary care physicians will see. Rarely, infection and neoplasia will cause unilateral plantar heel pain.⁴

Evaluation. Tenderness localized to the plantar surface of the heel in adults usually indicates plantar fasciitis.

Pain is worst with the first step of the morning, and lessens with activity. The tender spot is the medial calcaneal tubercle, with pain radiating through the arch.^1,28-30

Treatment. The many therapeutic modalities—NSAIDs, stretching exercises, gel cups, arch supports, night splints, steroid injections, ESWT, and surgery—have been extensively reviewed elsewhere, including in a Cochrane review from 2005.^31-33

Calcaneal stress fracture: Suspect it in runners

Calcaneal stress fractures are relatively rare, but may occur in those who put significant stressors on their feet, such as avid runners or military recruits.

Evaluation. Most patients report a recent increase in frequency or intensity of activity, and runners can tell you when it is during their run that the pain begins. As the stress fracture worsens, the pain begins earlier in the activity and eventually is present with even minimal activity. A key distinction from plantar fasciitis, in which pain lessens with activity, is that the pain of a stress fracture typically worsens with activity and diminishes with rest.³⁴

Physical exam provides few clues except for the “squeeze test” (FIGURE 1A) Putting pressure on both the medial and lateral calcaneal tuberosities will cause discomfort. Pain will be absent in the posterior structures of the heel. Placing a vibrating 128-cps tuning fork on the calcaneus should also increase discomfort.

Plain x-ray films may be falsely negative, especially during the first 2 to 3 weeks of pain. Three-phase bone scans are nearly 100% sensitive for detecting stress fractures, with changes evident in as little as 1 to 2 days after injury. The specificity of MRI scans is superior to that of bone scans and can reveal alternate problems.³⁵

Treatment. Activity modification reduces trauma to the heel. Encourage patients to walk if they are pain free and to increase activity as comfort allows. Tell patients to stop activity if the fracture becomes symptomatic. Advanced fractures demand an absolute absence of weight bearing.

Pain can be controlled with NSAIDs TABLE 2 and ice. Lab and animal data have suggested that NSAIDs may impede fracture healing rates, but no similar data exist regarding their effect on stress fractures.³⁶ Symptoms abate within 2 or 3 weeks. Advise athletes to resume activity slowly in a stepwise progression, letting them know that a return to full activity is likely within 6 to 8 weeks. Have runners restart their routine at half their customary distance, increasing it by no more than 10% to 15% per week.

Any medical condition that weakens the bone may predispose a patient to stress fracture. To prevent primary and secondary stress fractures, correct the patient’s underlying medical problems. Evaluate young, thin women with a stress fracture for the “female athlete triad” (osteopenia, disordered eating, menstrual irregularity). The elderly are also at risk for stress fractures due to osteopenia or osteoporosis.

TABLE 2
Heel pain treatment options: A look at the evidence

Fat pad syndrome: More diffuse pain than plantar fasciitis

The plantar surface of the heel is protected by a thick fat pad. Those at risk of a thinned fat pad include the elderly (the pad thins with age), the obese (increased stress to the pad), and those who have previously received a corticosteroid injection in the pad. Cumulative or acute trauma to the heel can also cause contusion to the heel pad.

Evaluation. Pain typically is located more posteriorly than classic plantar fasciitis pain and is more diffuse. Pain from the fat pad should not radiate toward the arch and is not exacerbated by dorsiflexion of the foot.¹

Treatment. Recommend relative rest, gel heel cups, NSAIDs, and ice.³⁷

Less common causes of plantar-surface pain

Lateral plantar nerve entrapment may also cause neuropathic pain on the plantar surface. Patients who experience a painful pop in their heel associated with trauma may have ruptured their plantar fascia. A fallen arch may also be noted on exam. Treatment of both of these conditions is similar to that of plantar fasciitis.

Acute calcaneal fracture results from trauma, such as a fall from a height onto the soles of the feet. Look for localized pain and swelling around the calcaneus and evaluate the neurovascular status of the foot. Initial treatment includes elevating the foot, avoiding weight bearing, applying ice, controlling pain, and using a posterior splint. Many of these fractures require surgical fixation.

Medial heel pain

Posterior tibial tendonitis/dysfunction and tarsal tunnel syndrome are best classified as medial in location (FIGURE 1C). However, the pain is often more diffuse and may radiate to either the posterior or plantar heel.

Posterior tibial tendonitis/dysfunction are linked to obesity

Posterior tibial tendonitis (PTT) and posterior tibial tendon dysfunction (PTTD) are related diagnoses. PTTD refers to increased laxity of the tendon resulting in flat foot and increased heel varus. It is the most common cause of acquired flat foot in adults. PTT may exist separately or as part of PTTD.

Evaluation. Patients complain of pain at the posterior edge of the medial malleolus that may extend toward the arch of the foot.^38,39 Patients may also experience swelling or redness in the area. Both PTT and PTTD seem related to overuse and obesity. Young or nonobese patients with PTT or PTTD often have underlying systemic arthropathies.³⁵

Treatment. Early treatment is necessary to prevent progression of tendon incompetence. Interventions include weight loss, NSAIDs, icing, physical therapy,⁴⁰ and orthotics or bracing for arch and ankle support. You may also try immobilization in a short leg cast for 6 weeks.⁴¹ If conservative measures fail, surgery may be necessary for tendon repair, tendon transfer, calcaneal osteotomy, or tarsal bone fusion.^38,39

Tarsal tunnel syndrome: Pain can occur at night

Tarsal tunnel syndrome (TTS) is the most common compression neuropathy of the lower extremity. The tarsal tunnel is a fibro-osseous structure along the medial ankle that contains the tibial nerve, the posterior tibial artery, and the tendons of the tibialis posterior, flexor digitorum longus, and flexor hallucis longus. The posterior tibial nerve can become irritated as it runs through the tunnel. The inciting incident can be either a severe stretch to the nerve (from a medial ankle sprain) or from an anatomic compression. Pes planus foot or posterior tibial dysfunction have also been implicated as common causes.¹

Evaluation. Patients describe poorly localized pain with numbness and burning along the medial ankle, arch, or heel, with radiation proximally.^42,43 Symptoms are aggravated by exercise, and night pain is not uncommon. The tenderness of TTS is more diffuse than that from plantar fasciitis, and symptoms are evident directly over the tarsal tunnel itself.

The classic finding is a positive Tinel’s sign (reproduction of symptoms by tapping over the posterior tibial nerve as it passes through the tarsal tunnel). Placing the foot in dorsiflexion and eversion may also reproduce symptoms.¹

Imaging results are not always definitive, but can be helpful in determining the cause of the compression. Plain films and CT can detect fracture or bony deformity, while MRI is more helpful in evaluating soft-tissue structures, such as ganglions or varicosities. Abnormal nerve conduction studies can be suggestive of TTS, but a normal result does not rule out the diagnosis.

Treatment follows a stepped progression. Initially try activity modification, orthotics, and physical therapy. Physical therapy concentrates on medial arch strengthening, Achilles stretching, and ankle proprioception exercises.

NSAIDs and neuromodulatory drugs (tricyclic antidepressants and antiseizure medications) have shown some success. Steroid injections have been effective when given at the site of entrapment,⁴⁴ but care must be taken to avoid the posterior tibial tendon. If patients do not improve following these measures, they may require cast immobilization.⁴⁵

Surgery is a possibility when other options fail. The cause of the neural compression is identified in 60% to 80% of cases.^46,47 Success rates for various procedures of tarsal tunnel release and tibial nerve decompression range from 75% to 91%. If neural compression is absent, investigate other systemic causes of peripheral neuropathy, such as diabetes or alcoholism.⁴

Systemic diagnoses

Bilateral heel pain, multiple joint involvement, or fever suggests systemic disease. Common diseases affecting the heel include rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and inflammatory bowel disease.¹ Successful treatment of these disorders should relieve associated heel pain.

Correspondence
H. E. Woodall, MD, AnMed Health Family Medicine Residency, 2000 E Greenville Street, Suite 3600, Anderson, SC 29621; [email protected]

One of your patients, a 40-year-old woman, recently began an exercise program, and she now says she has persistent heel pain. Your first suspicion is “another plantar fasciitis case.” However, after asking a few questions and performing a brief examination, you realize the problem is not what you expected. The pain is in the wrong place for plantar fasciitis and the patient’s history is atypical. How should you proceed?

Knowing the precise location of maximum pain or tenderness (FIGURES 1A–1C) and pairing that with key findings from the exam and history (TABLE 1) can help you reach an accurate diagnosis and formulate proper treatment (TABLE 2).

Each of the 3 general areas of heel pain—posterior, plantar, and medial—introduces a unique differential. Bilateral symptoms or multiple joint involvement, of course, raises the possibility of associated systemic disease.

FIGURE 1
Common causes of heel pain by location

TABLE 1
A quick guide to narrowing your heel pain diagnosis

Posterior heel pain

The common causes of posterior heel pain are Achilles tendinopathy, retrocalcaneal bursitis, calcaneal apophysitis, posterior impingement (FIGURE 1A), and Achilles tendon strain or rupture. Rarer causes are sciatica, peroneal tendonitis, Haglund’s deformity, pump bump, and systemic disorders. The patient’s history and precise location of maximal tenderness¹ differentiates these problems.

Achilles tendinopathy (tendonitis): Is the patient an athlete?

Insertional and noninsertional Achilles tendinopathy are the most common causes of persistent posterior heel pain.^2,3 The inflammatory process occurs in the fatty tissue surrounding the Achilles tendon (the paratenon) rather than in the tendon itself. Patients tend to be highly active (often athletes) and may have recently increased their activity. Ask patients, too, whether they have recently taken a fluoroquinolone antibiotic. This drug class is known to increase the risk of both tendonitis and tendon rupture,⁴ and in July of this year the FDA directed drug manufacturers to add a black-box warning to that effect.⁵

Evaluation of noninsertional tendinopathy. Tenderness is usually located 2 to 6 cm above the Achilles insertion. Nodularity, swelling, or fluctuance of the tendon may be evident. Diagnosis generally can be made clinically. If confirmation is needed, consider ultrasonography or magnetic resonance imaging.

Treatment. Advise patients to decrease physical activity and do stretching exercises, undergo eccentric calf muscle training, use heel lifts, modify shoe fit, and use systemic or topical nonsteroidal anti-inflammatory drugs (NSAIDs) regularly for a few days, then as needed. Refractory cases may require surgery.⁶ New therapies that have proven effective include extracorporeal shock wave therapy (ESWT), prolotherapy (dextrose injections), and local application of nitroglycerin patches or gel.^7-18 ESWT can be expensive and is not widely available. Prolotherapy can be performed with minimal training, but is still relatively new. Topical nitroglycerin is affordable, but beware of such side effects as headache and hypotension.

Evaluation of insertional tendinopathy. Inflammation occurs at the tendon’s insertion to bone (enthesitis). Pain typically is at the midline and is reproduced by palpating the tendon insertion or by passively stretching the heel. The presentation may be difficult to distinguish from retrocalcaneal bursitis (discussed below).

Treatment is similar to that used for noninsertional tendinopathy. However, if insertional tendinopathy occurs in conjunction with a Haglund’s deformity (bony overgrowth of the calcaneus), surgery may be indicated, because noninvasive measures tend to fail.¹⁹

Use steroid injections with extreme caution due to the theoretical risk of tendon rupture.²⁰ Injections are effective when directed at concomitant inflammation of the retrocalcaneal bursa, but accurate positioning and careful postinjection care are paramount. After an injection, a patient may need absolute rest or even immobilization to protect from tendon rupture. Emphasize a careful return to activity or athletic training.

Retrocalcaneal bursitis: Look for subtle swelling

The retrocalcaneal bursa lies between the Achilles tendon and the calcaneus near the tendon’s insertion. This bursa may become inflamed with repetitive stress or with insertional Achilles tendinopathy.

Evaluation. Swelling is usually present but may be subtle. Pain is located just lateral to the midline of the posterior heel at the superior angle of the calcaneus, and it may also be medial to the tendon opposite the lateral location.

Treatment. The bursitis often responds to icing and ice massage, shoe-fit adjustments, heel lifts, Achilles stretching programs, and systemic or topical NSAIDs.² Steroid injections are likely beneficial, but use them with caution and take care to avoid the Achilles tendon insertion.

Calcaneal apophysitis affects highly active kids

Calcaneal apophysitis (Sever’s disease) is a painful inflammation in the heels of skeletally immature children where the Achilles tendon inserts in the calcaneus apophysis.

Evaluation. Associated with peak growth rate and high activity level, this inflammatory process usually occurs in boys between the ages of 10 and 12 years, and in girls between the ages of 8 and 10 years.²¹ The process is similar to that occurring at other sites of traction apophysitis, such as Osgood-Schlatter disease at the tibial tuberosity. Children most susceptible are highly active, wear poorly fitting footwear, run frequently on hard surfaces, and have tight Achilles tendons. Clinical diagnosis usually suffices, although plain x-ray films can verify an active apophysis and rule out other sources of pain, such as tarsal coalition, calcaneal stress fractures, or infection.²²

Treatment. Calcaneal apophysitis is typically self-limiting, and the mainstay of treatment is rest. Heel lifts, stretching programs, icing, gel heel cups, and anti-inflammatory agents may also be used.²³

Posterior impingement: Pain with full plantar flexion

Posterior impingement at the ankle joint may be self-originating or arise as a consequence of an os trigonum, a posterior sesamoid bone of the talus that exists as a normal variant. In some cases, this bone creates a barrier to full plantar flexion at the ankle joint and creates pain at the posterior heel.

Evaluation. Pain with full plantar flexion is a critical distinguishing feature, because most other pathologies in the posterior heel cause pain with dorsiflexion at the ankle.^24,25 Patients often are involved in activities that require forced plantar flexion, such as gymnastics or dancing. Diagnosis is clinical for the most part, but plain x-ray films may confirm the presence of an os trigonum. Magnetic resonance imaging (MRI) is warranted for patients with persistent symptoms; it may reveal a hypertrophied synovial lining or other pathology (such as osteochondritis). MRI is also indicated before more invasive therapies, such as steroid injections or surgery.

Treatment. Advise rest with or without immobilization, NSAIDs, or local steroid injections. Severe impingement or recalcitrant cases may require surgical release of the posterior synovium or removal of an os trigonum.^24,25

Achilles strain and rupture: Middle-aged men are susceptible

The Achilles tendon is most susceptible to injury in middle-aged men who are active in sports requiring loading and sudden contraction of the calf muscles, such as basketball or football, although injuries may occur in a variety of other settings. A strain of the Achilles tendon should be carefully differentiated from a complete rupture. While strains can be treated similarly to Achilles tendinopathy, complete rupture is a much larger concern.

Evaluation. When the Achilles tendon ruptures, patients describe sudden pain and a pop that is often audible. Poor plantar flexion of the foot ensues.²⁶ Telltale signs on examination are a positive Thompson’s test (little or no plantar flexion with a calf squeeze) and a visible defect in the tendon. The rupture site is usually 1 to 2 inches proximal to its insertion on the calcaneus.

Treatment. Most of these patients should be seen by an orthopedic surgeon as soon as possible. For active and younger adults, treatment is almost always early surgical repair.²⁷ For some older individuals who are less active, nonsurgical management includes graduated casting, which progressively lessens plantar flexion over 6 to 10 weeks, followed by physical therapy.

3 less common causes of posterior heel pain

Haglund’s deformity is an overgrowth of the calcaneus at the insertion of the Achilles tendon.³ Caused by overuse and poorly fitted shoes, this condition commonly requires surgical intervention.

Pump bump is an inflamed superficial bursa commonly associated with a Haglund’s deformity, and it may respond to NSAIDs, shoe-fit modification, ice massage, or steroid injection.

Peroneal tendonitis is a tendinopathy of evertors and external rotators of the foot. The pain will follow the tendons posterior to the lateral malleolus and extend to the lateral midfoot. It is also treated with rest, NSAIDs, icing, and physical therapy.

Plantar-surface heel pain

The problems most likely to cause plantar-surface pain (FIGURE 1B) are plantar fasciitis, stress fracture of the calcaneus, and fat pad syndrome.

Plantar fasciitis: Pain is worst in the morning

This is by far the most common cause of heel pain primary care physicians will see. Rarely, infection and neoplasia will cause unilateral plantar heel pain.⁴

Evaluation. Tenderness localized to the plantar surface of the heel in adults usually indicates plantar fasciitis.

Pain is worst with the first step of the morning, and lessens with activity. The tender spot is the medial calcaneal tubercle, with pain radiating through the arch.^1,28-30

Treatment. The many therapeutic modalities—NSAIDs, stretching exercises, gel cups, arch supports, night splints, steroid injections, ESWT, and surgery—have been extensively reviewed elsewhere, including in a Cochrane review from 2005.^31-33

Calcaneal stress fracture: Suspect it in runners

Calcaneal stress fractures are relatively rare, but may occur in those who put significant stressors on their feet, such as avid runners or military recruits.

Evaluation. Most patients report a recent increase in frequency or intensity of activity, and runners can tell you when it is during their run that the pain begins. As the stress fracture worsens, the pain begins earlier in the activity and eventually is present with even minimal activity. A key distinction from plantar fasciitis, in which pain lessens with activity, is that the pain of a stress fracture typically worsens with activity and diminishes with rest.³⁴

Physical exam provides few clues except for the “squeeze test” (FIGURE 1A) Putting pressure on both the medial and lateral calcaneal tuberosities will cause discomfort. Pain will be absent in the posterior structures of the heel. Placing a vibrating 128-cps tuning fork on the calcaneus should also increase discomfort.

Plain x-ray films may be falsely negative, especially during the first 2 to 3 weeks of pain. Three-phase bone scans are nearly 100% sensitive for detecting stress fractures, with changes evident in as little as 1 to 2 days after injury. The specificity of MRI scans is superior to that of bone scans and can reveal alternate problems.³⁵

Treatment. Activity modification reduces trauma to the heel. Encourage patients to walk if they are pain free and to increase activity as comfort allows. Tell patients to stop activity if the fracture becomes symptomatic. Advanced fractures demand an absolute absence of weight bearing.

Pain can be controlled with NSAIDs TABLE 2 and ice. Lab and animal data have suggested that NSAIDs may impede fracture healing rates, but no similar data exist regarding their effect on stress fractures.³⁶ Symptoms abate within 2 or 3 weeks. Advise athletes to resume activity slowly in a stepwise progression, letting them know that a return to full activity is likely within 6 to 8 weeks. Have runners restart their routine at half their customary distance, increasing it by no more than 10% to 15% per week.

Any medical condition that weakens the bone may predispose a patient to stress fracture. To prevent primary and secondary stress fractures, correct the patient’s underlying medical problems. Evaluate young, thin women with a stress fracture for the “female athlete triad” (osteopenia, disordered eating, menstrual irregularity). The elderly are also at risk for stress fractures due to osteopenia or osteoporosis.

TABLE 2
Heel pain treatment options: A look at the evidence

Fat pad syndrome: More diffuse pain than plantar fasciitis

The plantar surface of the heel is protected by a thick fat pad. Those at risk of a thinned fat pad include the elderly (the pad thins with age), the obese (increased stress to the pad), and those who have previously received a corticosteroid injection in the pad. Cumulative or acute trauma to the heel can also cause contusion to the heel pad.

Evaluation. Pain typically is located more posteriorly than classic plantar fasciitis pain and is more diffuse. Pain from the fat pad should not radiate toward the arch and is not exacerbated by dorsiflexion of the foot.¹

Treatment. Recommend relative rest, gel heel cups, NSAIDs, and ice.³⁷

Less common causes of plantar-surface pain

Lateral plantar nerve entrapment may also cause neuropathic pain on the plantar surface. Patients who experience a painful pop in their heel associated with trauma may have ruptured their plantar fascia. A fallen arch may also be noted on exam. Treatment of both of these conditions is similar to that of plantar fasciitis.

Acute calcaneal fracture results from trauma, such as a fall from a height onto the soles of the feet. Look for localized pain and swelling around the calcaneus and evaluate the neurovascular status of the foot. Initial treatment includes elevating the foot, avoiding weight bearing, applying ice, controlling pain, and using a posterior splint. Many of these fractures require surgical fixation.

Medial heel pain

Posterior tibial tendonitis/dysfunction and tarsal tunnel syndrome are best classified as medial in location (FIGURE 1C). However, the pain is often more diffuse and may radiate to either the posterior or plantar heel.

Posterior tibial tendonitis/dysfunction are linked to obesity

Posterior tibial tendonitis (PTT) and posterior tibial tendon dysfunction (PTTD) are related diagnoses. PTTD refers to increased laxity of the tendon resulting in flat foot and increased heel varus. It is the most common cause of acquired flat foot in adults. PTT may exist separately or as part of PTTD.

Evaluation. Patients complain of pain at the posterior edge of the medial malleolus that may extend toward the arch of the foot.^38,39 Patients may also experience swelling or redness in the area. Both PTT and PTTD seem related to overuse and obesity. Young or nonobese patients with PTT or PTTD often have underlying systemic arthropathies.³⁵

Treatment. Early treatment is necessary to prevent progression of tendon incompetence. Interventions include weight loss, NSAIDs, icing, physical therapy,⁴⁰ and orthotics or bracing for arch and ankle support. You may also try immobilization in a short leg cast for 6 weeks.⁴¹ If conservative measures fail, surgery may be necessary for tendon repair, tendon transfer, calcaneal osteotomy, or tarsal bone fusion.^38,39

Tarsal tunnel syndrome: Pain can occur at night

Tarsal tunnel syndrome (TTS) is the most common compression neuropathy of the lower extremity. The tarsal tunnel is a fibro-osseous structure along the medial ankle that contains the tibial nerve, the posterior tibial artery, and the tendons of the tibialis posterior, flexor digitorum longus, and flexor hallucis longus. The posterior tibial nerve can become irritated as it runs through the tunnel. The inciting incident can be either a severe stretch to the nerve (from a medial ankle sprain) or from an anatomic compression. Pes planus foot or posterior tibial dysfunction have also been implicated as common causes.¹

Evaluation. Patients describe poorly localized pain with numbness and burning along the medial ankle, arch, or heel, with radiation proximally.^42,43 Symptoms are aggravated by exercise, and night pain is not uncommon. The tenderness of TTS is more diffuse than that from plantar fasciitis, and symptoms are evident directly over the tarsal tunnel itself.

The classic finding is a positive Tinel’s sign (reproduction of symptoms by tapping over the posterior tibial nerve as it passes through the tarsal tunnel). Placing the foot in dorsiflexion and eversion may also reproduce symptoms.¹

Imaging results are not always definitive, but can be helpful in determining the cause of the compression. Plain films and CT can detect fracture or bony deformity, while MRI is more helpful in evaluating soft-tissue structures, such as ganglions or varicosities. Abnormal nerve conduction studies can be suggestive of TTS, but a normal result does not rule out the diagnosis.

Treatment follows a stepped progression. Initially try activity modification, orthotics, and physical therapy. Physical therapy concentrates on medial arch strengthening, Achilles stretching, and ankle proprioception exercises.

NSAIDs and neuromodulatory drugs (tricyclic antidepressants and antiseizure medications) have shown some success. Steroid injections have been effective when given at the site of entrapment,⁴⁴ but care must be taken to avoid the posterior tibial tendon. If patients do not improve following these measures, they may require cast immobilization.⁴⁵

Surgery is a possibility when other options fail. The cause of the neural compression is identified in 60% to 80% of cases.^46,47 Success rates for various procedures of tarsal tunnel release and tibial nerve decompression range from 75% to 91%. If neural compression is absent, investigate other systemic causes of peripheral neuropathy, such as diabetes or alcoholism.⁴

Systemic diagnoses

Bilateral heel pain, multiple joint involvement, or fever suggests systemic disease. Common diseases affecting the heel include rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and inflammatory bowel disease.¹ Successful treatment of these disorders should relieve associated heel pain.

Correspondence
H. E. Woodall, MD, AnMed Health Family Medicine Residency, 2000 E Greenville Street, Suite 3600, Anderson, SC 29621; [email protected]

Osteoarthritis (OA) and other rheumatic conditions account for as many office visits as cardiovascular disease or essential hypertension, according to national data, and most involve primary care physicians.¹ As the population ages, the prevalence of OA—estimated at 46.4 million in 2005 in the United States alone—will continue to rise.^2,3 So, too, will the number of patients needing treatment for pain and functional limitations related to OA of the hips and knees.

Physicians who treat these patients have a new tool at their disposal: the Osteoarthritis Research Society International (OARSI)’s evidence-based, expert consensus guidelines for the management of hip and knee OA. These recommendations, published in February 2008, are the first “internationally agreed and universally applicable guidelines for the management of these global disorders.”⁴

In caring for patients with OA of the hips or knees, family physicians should keep in mind 2 guiding principles at the heart of the OARSI recommendations:

• the importance of lifestyle modification, including regular exercise, in coping with this degenerative, potentially debilitating disease; and
• the need to incorporate both nonpharmacologic interventions and drug therapy to achieve optimal care.⁴

International team sifts through the evidence

To develop the guidelines, OARSI convened a committee of 16 physicians from 6 countries and 2 continents, with expertise in 4 disciplines: rheumatology, orthopedics, evidence-based medicine, and primary care. The team reviewed national and regional guidelines and studied systematic reviews; meta-analyses; randomized controlled trials (RCTs); controlled and uncontrolled trials; cohort, case-control, and cross-sectional studies; and economic evaluations from 1945 through 2001. The team also conducted a systematic review of evidence from January 2002 through January 2006.^4,5 To ensure the quality of evidence hierarchy, the team used internationally accepted research tools.

AP and tunnel images are key to OA diagnosis

A diagnosis of knee or hip osteoarthritis (OA) requires a medical history; physical examination; radiologic assessment, with standing X-rays of the lower extremities, including anterior-posterior and tunnel views for knee OA; and the exclusion of other conditions.30 The tunnel view shown here reveals bone-on-bone articulation in the medial compartment of the left knee, and demonstrates the importance of standing X-rays.

Differential diagnosis includes gout, pseudogout, rheumatoid arthritis, patella-femoral pain, pes anserine (knee) bursitis, iliotibial band pathology, meniscal tear, cruciate tears, and tumors. No blood tests are indicated unless an inflammatory process is suspected. Synovial fluid in an osteoarthritic knee has a white cell count of <2000/uL.³¹

The team used several criteria to rate the recommended strategies, including level of evidence, effect size for pain relief, level of consensus, and strength of recommendation (SOR). All of these criteria are included (and defined) in an at-a-glance summary of the OARSI recommendations ( TABLE ).

In particular, the SOR, which is used throughout this article, is an overall rating that reflects the opinions of the team members after consideration of the research evidence for efficacy, safety, and cost-effectiveness. It is based on a visual analog scale of 0 to 100 mm and is expressed as a percentage.

TABLE
OARSI guidelines rate the evidence for osteoarthritis treatment options

OARSI emphasizes patient education

Patient education about self-care and lifestyle modifications, such as weight loss, exercise, and pacing of activities to reduce the load on the affected joints, is OARSI’s strongest nonpharmacologic recommendation (SOR: 97%). The guidelines also call for the following interventions:

• correcting mechanical abnormalities of the skeleton;
• helping patients lose weight;
• assisting patients with smoking cessation efforts;⁶
• directing the use of nonprescription medications;
• prescribing assistive devices; and
• prescribing appropriate prescription drugs.

Nondrug options: Exercise that achy joint

To many patients, being told to exercise a joint in which movement is associated with stiffness and bone-on-bone pain seems counterintuitive. Referring to the findings of the OARSI panel may be helpful in explaining the importance of regular aerobic, muscle-strengthening, and range-of-motion exercises, all of which are strongly recommended (SOR: 96%). Exercise can be as simple as “regular aerobic walking” and home-based strengthening of the quadriceps.⁴ For patients with arthritic hips, water-based exercises are recommended.

Obesity can increase the risk of developing OA of the hips and knees, and excess weight puts extra stress on joints that are already arthritic. Thus, weight loss is both a risk modification factor (see “Is your patient at risk of OA? Take steps now” ) and a key OA management strategy (SOR: 96%). In a meta-regression analysis conducted by the committee, a reduction of >5% of body weight or a loss at a rate of >0.24% per week was associated with significant improvement in disability. One RCT had a number needed to treat (NNT) of 3 (95% confidence interval [CI], 2-9) to achieve improved pain and function scores after a 2-month low-energy diet.⁷

Don’t underestimate the power of a phone call

Other nonpharmacologic recommendations include referral to a physical therapist for evaluation and exercise instruction (SOR: 89%); instruction in the use of walking aids, such as a cane or crutch in the contralateral hand, to improve biomechanics (SOR: 90%); and the use of braces to support unstable knees, an unproven intervention that may increase proprioception and stability (SOR: 76%). Physicians should also recommend footwear with insoles or lateral wedges to decrease lateral thrust of the knee and medial compartment forces (SOR: 77%).

Regular telephone contact, possibly on a monthly basis, is a suggested strategy for promoting self-care, tested in patients with OA of the knee but recommended for those with arthritic hips solely on the basis of expert opinion. A number of other modalities, including thermal therapy (heat treatments with warm water or wax, or cold therapy with a 20-minute ice massage), transcutaneous electrical nerve stimulation (TENS), and acupuncture, are recommended for symptom relief.

Drug therapy: Start with acetaminophen

The OARSI guidelines cite acetaminophen as an “effective initial oral analgesic” for mild to moderate pain in patients with OA of the hips or knees (SOR: 92%).⁴ In analyses conducted by the committee, the NNT to achieve an improvement in pain ranged from 1 to 2 in an earlier systematic review⁸ to 4 to 16 in a subsequent meta-analysis.⁹

Prescribe NSAIDs for short-term relief. While acetaminophen is considered the preferred long-term oral treatment, the strongest pharmacologic recommendation for alleviating the pain and stiffness associated with OA of the hip or knee is for nonsteroidal anti-inflammatory drugs (NSAIDs) (SOR: 93%). The caveat, however, is that NSAIDs should be used in the lowest effective dose and are not considered a long-term option. Patients with increased gastrointestinal (GI) risk should use either a cyclooxygenase-2 (COX-2) agent or an NSAID with a proton pump inhibitor or misoprostol for GI protection.

For those with cardiovascular risks, both nonselective NSAIDs and COX-2 agents require caution; here, too, the lowest dose for the shortest possible duration is recommended.

The guidelines also call for the use of topical agents, such as topical NSAIDs and capsaicin, for relief of symptoms (SOR: 85%). The NNT for topical NSAIDs was 3 (95% CI, 2-4);⁴ capsaicin had an NNT of 4 (95% CI, 3-5) after 4 weeks of therapy.⁴ The recommendations also note that glucosamine and/or chondroitin sulfate may alleviate some symptoms of osteoarthritis of the knee, but should be discontinued if no benefit is observed after 6 months.

When something stronger is needed. For moderate to severe pain that has not responded to oral agents, intraarticular (IA) injections with corticosteroids are recommended, as are IA hyaluronate injections (SOR: 78% and 64%, respectively). Weak opioids/low-dose narcotics round out the recommendations for treating moderate pain, with stronger opioids reserved for patients whose pain is severe.

When to consider surgery

Joint replacement surgery is recommended for patients who do not achieve adequate pain relief and functional improvement from nonpharmacologic and pharmacologic modalities (SOR: 96%). A meta-analysis of 74 studies assessing quality of life 1 to 7 years after total hip and total knee replacement (THR and TKR) found substantial improvement in pain and function, but variable effects on mental health and social functioning. Risk factors for poor outcomes include older age; more (or more severe) preoperative pain; medical comorbidities; musculoskeletal comorbidities such as low back pain, with functional limitations; low mental health scores; and OA in the hip that was not replaced.^10,11

Unicompartmental knee replacement (UKR) had an SOR of 76%. Reviews that compared TKR to UKR found similar 5-year outcomes in knee pain and function. Those who underwent UKR had better range of motion, but prosthesis survival at 10 years was better in those with TKR (>90% vs 85% to 90%).¹²

In young adults, osteotomy and jointpreserving procedures are recommended for hip OA, especially when dysplasia is present. In young, active patients with unicompartment OA, high tibial osteotomies may delay TKR by as long as 10 years.¹³

Joint lavage and arthroscopic debridement in knee OA remain controversial, although they may provide short-term symptom relief (SOR: 60%). Joint fusion as a salvage procedure after failed TKR had an SOR of 69%.

Work as a team to improve outcomes

The inevitable increase in the number of patients with OA of the hips and knees underscores the importance of having a range of treatment strategies, often best delivered by a multidisciplinary team with the family physician at the helm. The OARSI guidelines, which are backed by both a thorough review of research findings and expert consensus, can help you convince patients to take an active role in managing this potentially debilitating condition. Patients’ commitment to lifestyle modifications and self-management, bolstered by your guidance and support, is the most effective way to keep patients with OA on the move.

Correspondence
Greg P. Gutierrez, MD, Associate Professor, University of Colorado Denver Health Sciences Center, Department of Family Medicine, Denver Health and Hospital, 660 Bannock St., Denver, CO 80218; [email protected].

Osteoarthritis (OA) and other rheumatic conditions account for as many office visits as cardiovascular disease or essential hypertension, according to national data, and most involve primary care physicians.¹ As the population ages, the prevalence of OA—estimated at 46.4 million in 2005 in the United States alone—will continue to rise.^2,3 So, too, will the number of patients needing treatment for pain and functional limitations related to OA of the hips and knees.

Physicians who treat these patients have a new tool at their disposal: the Osteoarthritis Research Society International (OARSI)’s evidence-based, expert consensus guidelines for the management of hip and knee OA. These recommendations, published in February 2008, are the first “internationally agreed and universally applicable guidelines for the management of these global disorders.”⁴

In caring for patients with OA of the hips or knees, family physicians should keep in mind 2 guiding principles at the heart of the OARSI recommendations:

• the importance of lifestyle modification, including regular exercise, in coping with this degenerative, potentially debilitating disease; and
• the need to incorporate both nonpharmacologic interventions and drug therapy to achieve optimal care.⁴

International team sifts through the evidence

To develop the guidelines, OARSI convened a committee of 16 physicians from 6 countries and 2 continents, with expertise in 4 disciplines: rheumatology, orthopedics, evidence-based medicine, and primary care. The team reviewed national and regional guidelines and studied systematic reviews; meta-analyses; randomized controlled trials (RCTs); controlled and uncontrolled trials; cohort, case-control, and cross-sectional studies; and economic evaluations from 1945 through 2001. The team also conducted a systematic review of evidence from January 2002 through January 2006.^4,5 To ensure the quality of evidence hierarchy, the team used internationally accepted research tools.

AP and tunnel images are key to OA diagnosis

A diagnosis of knee or hip osteoarthritis (OA) requires a medical history; physical examination; radiologic assessment, with standing X-rays of the lower extremities, including anterior-posterior and tunnel views for knee OA; and the exclusion of other conditions.30 The tunnel view shown here reveals bone-on-bone articulation in the medial compartment of the left knee, and demonstrates the importance of standing X-rays.

Differential diagnosis includes gout, pseudogout, rheumatoid arthritis, patella-femoral pain, pes anserine (knee) bursitis, iliotibial band pathology, meniscal tear, cruciate tears, and tumors. No blood tests are indicated unless an inflammatory process is suspected. Synovial fluid in an osteoarthritic knee has a white cell count of <2000/uL.³¹

The team used several criteria to rate the recommended strategies, including level of evidence, effect size for pain relief, level of consensus, and strength of recommendation (SOR). All of these criteria are included (and defined) in an at-a-glance summary of the OARSI recommendations ( TABLE ).

In particular, the SOR, which is used throughout this article, is an overall rating that reflects the opinions of the team members after consideration of the research evidence for efficacy, safety, and cost-effectiveness. It is based on a visual analog scale of 0 to 100 mm and is expressed as a percentage.

TABLE
OARSI guidelines rate the evidence for osteoarthritis treatment options

OARSI emphasizes patient education

Patient education about self-care and lifestyle modifications, such as weight loss, exercise, and pacing of activities to reduce the load on the affected joints, is OARSI’s strongest nonpharmacologic recommendation (SOR: 97%). The guidelines also call for the following interventions:

• correcting mechanical abnormalities of the skeleton;
• helping patients lose weight;
• assisting patients with smoking cessation efforts;⁶
• directing the use of nonprescription medications;
• prescribing assistive devices; and
• prescribing appropriate prescription drugs.

Nondrug options: Exercise that achy joint

To many patients, being told to exercise a joint in which movement is associated with stiffness and bone-on-bone pain seems counterintuitive. Referring to the findings of the OARSI panel may be helpful in explaining the importance of regular aerobic, muscle-strengthening, and range-of-motion exercises, all of which are strongly recommended (SOR: 96%). Exercise can be as simple as “regular aerobic walking” and home-based strengthening of the quadriceps.⁴ For patients with arthritic hips, water-based exercises are recommended.

Obesity can increase the risk of developing OA of the hips and knees, and excess weight puts extra stress on joints that are already arthritic. Thus, weight loss is both a risk modification factor (see “Is your patient at risk of OA? Take steps now” ) and a key OA management strategy (SOR: 96%). In a meta-regression analysis conducted by the committee, a reduction of >5% of body weight or a loss at a rate of >0.24% per week was associated with significant improvement in disability. One RCT had a number needed to treat (NNT) of 3 (95% confidence interval [CI], 2-9) to achieve improved pain and function scores after a 2-month low-energy diet.⁷

Don’t underestimate the power of a phone call

Other nonpharmacologic recommendations include referral to a physical therapist for evaluation and exercise instruction (SOR: 89%); instruction in the use of walking aids, such as a cane or crutch in the contralateral hand, to improve biomechanics (SOR: 90%); and the use of braces to support unstable knees, an unproven intervention that may increase proprioception and stability (SOR: 76%). Physicians should also recommend footwear with insoles or lateral wedges to decrease lateral thrust of the knee and medial compartment forces (SOR: 77%).

Regular telephone contact, possibly on a monthly basis, is a suggested strategy for promoting self-care, tested in patients with OA of the knee but recommended for those with arthritic hips solely on the basis of expert opinion. A number of other modalities, including thermal therapy (heat treatments with warm water or wax, or cold therapy with a 20-minute ice massage), transcutaneous electrical nerve stimulation (TENS), and acupuncture, are recommended for symptom relief.

Drug therapy: Start with acetaminophen

The OARSI guidelines cite acetaminophen as an “effective initial oral analgesic” for mild to moderate pain in patients with OA of the hips or knees (SOR: 92%).⁴ In analyses conducted by the committee, the NNT to achieve an improvement in pain ranged from 1 to 2 in an earlier systematic review⁸ to 4 to 16 in a subsequent meta-analysis.⁹

Prescribe NSAIDs for short-term relief. While acetaminophen is considered the preferred long-term oral treatment, the strongest pharmacologic recommendation for alleviating the pain and stiffness associated with OA of the hip or knee is for nonsteroidal anti-inflammatory drugs (NSAIDs) (SOR: 93%). The caveat, however, is that NSAIDs should be used in the lowest effective dose and are not considered a long-term option. Patients with increased gastrointestinal (GI) risk should use either a cyclooxygenase-2 (COX-2) agent or an NSAID with a proton pump inhibitor or misoprostol for GI protection.

For those with cardiovascular risks, both nonselective NSAIDs and COX-2 agents require caution; here, too, the lowest dose for the shortest possible duration is recommended.

The guidelines also call for the use of topical agents, such as topical NSAIDs and capsaicin, for relief of symptoms (SOR: 85%). The NNT for topical NSAIDs was 3 (95% CI, 2-4);⁴ capsaicin had an NNT of 4 (95% CI, 3-5) after 4 weeks of therapy.⁴ The recommendations also note that glucosamine and/or chondroitin sulfate may alleviate some symptoms of osteoarthritis of the knee, but should be discontinued if no benefit is observed after 6 months.

When something stronger is needed. For moderate to severe pain that has not responded to oral agents, intraarticular (IA) injections with corticosteroids are recommended, as are IA hyaluronate injections (SOR: 78% and 64%, respectively). Weak opioids/low-dose narcotics round out the recommendations for treating moderate pain, with stronger opioids reserved for patients whose pain is severe.

When to consider surgery

Joint replacement surgery is recommended for patients who do not achieve adequate pain relief and functional improvement from nonpharmacologic and pharmacologic modalities (SOR: 96%). A meta-analysis of 74 studies assessing quality of life 1 to 7 years after total hip and total knee replacement (THR and TKR) found substantial improvement in pain and function, but variable effects on mental health and social functioning. Risk factors for poor outcomes include older age; more (or more severe) preoperative pain; medical comorbidities; musculoskeletal comorbidities such as low back pain, with functional limitations; low mental health scores; and OA in the hip that was not replaced.^10,11

Unicompartmental knee replacement (UKR) had an SOR of 76%. Reviews that compared TKR to UKR found similar 5-year outcomes in knee pain and function. Those who underwent UKR had better range of motion, but prosthesis survival at 10 years was better in those with TKR (>90% vs 85% to 90%).¹²

In young adults, osteotomy and jointpreserving procedures are recommended for hip OA, especially when dysplasia is present. In young, active patients with unicompartment OA, high tibial osteotomies may delay TKR by as long as 10 years.¹³

Joint lavage and arthroscopic debridement in knee OA remain controversial, although they may provide short-term symptom relief (SOR: 60%). Joint fusion as a salvage procedure after failed TKR had an SOR of 69%.

Work as a team to improve outcomes

The inevitable increase in the number of patients with OA of the hips and knees underscores the importance of having a range of treatment strategies, often best delivered by a multidisciplinary team with the family physician at the helm. The OARSI guidelines, which are backed by both a thorough review of research findings and expert consensus, can help you convince patients to take an active role in managing this potentially debilitating condition. Patients’ commitment to lifestyle modifications and self-management, bolstered by your guidance and support, is the most effective way to keep patients with OA on the move.

Correspondence
Greg P. Gutierrez, MD, Associate Professor, University of Colorado Denver Health Sciences Center, Department of Family Medicine, Denver Health and Hospital, 660 Bannock St., Denver, CO 80218; [email protected].

Osteoarthritis (OA) and other rheumatic conditions account for as many office visits as cardiovascular disease or essential hypertension, according to national data, and most involve primary care physicians.¹ As the population ages, the prevalence of OA—estimated at 46.4 million in 2005 in the United States alone—will continue to rise.^2,3 So, too, will the number of patients needing treatment for pain and functional limitations related to OA of the hips and knees.

Physicians who treat these patients have a new tool at their disposal: the Osteoarthritis Research Society International (OARSI)’s evidence-based, expert consensus guidelines for the management of hip and knee OA. These recommendations, published in February 2008, are the first “internationally agreed and universally applicable guidelines for the management of these global disorders.”⁴

In caring for patients with OA of the hips or knees, family physicians should keep in mind 2 guiding principles at the heart of the OARSI recommendations:

• the importance of lifestyle modification, including regular exercise, in coping with this degenerative, potentially debilitating disease; and
• the need to incorporate both nonpharmacologic interventions and drug therapy to achieve optimal care.⁴

International team sifts through the evidence

To develop the guidelines, OARSI convened a committee of 16 physicians from 6 countries and 2 continents, with expertise in 4 disciplines: rheumatology, orthopedics, evidence-based medicine, and primary care. The team reviewed national and regional guidelines and studied systematic reviews; meta-analyses; randomized controlled trials (RCTs); controlled and uncontrolled trials; cohort, case-control, and cross-sectional studies; and economic evaluations from 1945 through 2001. The team also conducted a systematic review of evidence from January 2002 through January 2006.^4,5 To ensure the quality of evidence hierarchy, the team used internationally accepted research tools.

AP and tunnel images are key to OA diagnosis

A diagnosis of knee or hip osteoarthritis (OA) requires a medical history; physical examination; radiologic assessment, with standing X-rays of the lower extremities, including anterior-posterior and tunnel views for knee OA; and the exclusion of other conditions.30 The tunnel view shown here reveals bone-on-bone articulation in the medial compartment of the left knee, and demonstrates the importance of standing X-rays.

Differential diagnosis includes gout, pseudogout, rheumatoid arthritis, patella-femoral pain, pes anserine (knee) bursitis, iliotibial band pathology, meniscal tear, cruciate tears, and tumors. No blood tests are indicated unless an inflammatory process is suspected. Synovial fluid in an osteoarthritic knee has a white cell count of <2000/uL.³¹

The team used several criteria to rate the recommended strategies, including level of evidence, effect size for pain relief, level of consensus, and strength of recommendation (SOR). All of these criteria are included (and defined) in an at-a-glance summary of the OARSI recommendations ( TABLE ).

In particular, the SOR, which is used throughout this article, is an overall rating that reflects the opinions of the team members after consideration of the research evidence for efficacy, safety, and cost-effectiveness. It is based on a visual analog scale of 0 to 100 mm and is expressed as a percentage.

TABLE
OARSI guidelines rate the evidence for osteoarthritis treatment options

OARSI emphasizes patient education

Patient education about self-care and lifestyle modifications, such as weight loss, exercise, and pacing of activities to reduce the load on the affected joints, is OARSI’s strongest nonpharmacologic recommendation (SOR: 97%). The guidelines also call for the following interventions:

• correcting mechanical abnormalities of the skeleton;
• helping patients lose weight;
• assisting patients with smoking cessation efforts;⁶
• directing the use of nonprescription medications;
• prescribing assistive devices; and
• prescribing appropriate prescription drugs.

Nondrug options: Exercise that achy joint

To many patients, being told to exercise a joint in which movement is associated with stiffness and bone-on-bone pain seems counterintuitive. Referring to the findings of the OARSI panel may be helpful in explaining the importance of regular aerobic, muscle-strengthening, and range-of-motion exercises, all of which are strongly recommended (SOR: 96%). Exercise can be as simple as “regular aerobic walking” and home-based strengthening of the quadriceps.⁴ For patients with arthritic hips, water-based exercises are recommended.

Obesity can increase the risk of developing OA of the hips and knees, and excess weight puts extra stress on joints that are already arthritic. Thus, weight loss is both a risk modification factor (see “Is your patient at risk of OA? Take steps now” ) and a key OA management strategy (SOR: 96%). In a meta-regression analysis conducted by the committee, a reduction of >5% of body weight or a loss at a rate of >0.24% per week was associated with significant improvement in disability. One RCT had a number needed to treat (NNT) of 3 (95% confidence interval [CI], 2-9) to achieve improved pain and function scores after a 2-month low-energy diet.⁷

Don’t underestimate the power of a phone call

Other nonpharmacologic recommendations include referral to a physical therapist for evaluation and exercise instruction (SOR: 89%); instruction in the use of walking aids, such as a cane or crutch in the contralateral hand, to improve biomechanics (SOR: 90%); and the use of braces to support unstable knees, an unproven intervention that may increase proprioception and stability (SOR: 76%). Physicians should also recommend footwear with insoles or lateral wedges to decrease lateral thrust of the knee and medial compartment forces (SOR: 77%).

Regular telephone contact, possibly on a monthly basis, is a suggested strategy for promoting self-care, tested in patients with OA of the knee but recommended for those with arthritic hips solely on the basis of expert opinion. A number of other modalities, including thermal therapy (heat treatments with warm water or wax, or cold therapy with a 20-minute ice massage), transcutaneous electrical nerve stimulation (TENS), and acupuncture, are recommended for symptom relief.

Drug therapy: Start with acetaminophen

The OARSI guidelines cite acetaminophen as an “effective initial oral analgesic” for mild to moderate pain in patients with OA of the hips or knees (SOR: 92%).⁴ In analyses conducted by the committee, the NNT to achieve an improvement in pain ranged from 1 to 2 in an earlier systematic review⁸ to 4 to 16 in a subsequent meta-analysis.⁹

Prescribe NSAIDs for short-term relief. While acetaminophen is considered the preferred long-term oral treatment, the strongest pharmacologic recommendation for alleviating the pain and stiffness associated with OA of the hip or knee is for nonsteroidal anti-inflammatory drugs (NSAIDs) (SOR: 93%). The caveat, however, is that NSAIDs should be used in the lowest effective dose and are not considered a long-term option. Patients with increased gastrointestinal (GI) risk should use either a cyclooxygenase-2 (COX-2) agent or an NSAID with a proton pump inhibitor or misoprostol for GI protection.

For those with cardiovascular risks, both nonselective NSAIDs and COX-2 agents require caution; here, too, the lowest dose for the shortest possible duration is recommended.

The guidelines also call for the use of topical agents, such as topical NSAIDs and capsaicin, for relief of symptoms (SOR: 85%). The NNT for topical NSAIDs was 3 (95% CI, 2-4);⁴ capsaicin had an NNT of 4 (95% CI, 3-5) after 4 weeks of therapy.⁴ The recommendations also note that glucosamine and/or chondroitin sulfate may alleviate some symptoms of osteoarthritis of the knee, but should be discontinued if no benefit is observed after 6 months.

When something stronger is needed. For moderate to severe pain that has not responded to oral agents, intraarticular (IA) injections with corticosteroids are recommended, as are IA hyaluronate injections (SOR: 78% and 64%, respectively). Weak opioids/low-dose narcotics round out the recommendations for treating moderate pain, with stronger opioids reserved for patients whose pain is severe.

When to consider surgery

Joint replacement surgery is recommended for patients who do not achieve adequate pain relief and functional improvement from nonpharmacologic and pharmacologic modalities (SOR: 96%). A meta-analysis of 74 studies assessing quality of life 1 to 7 years after total hip and total knee replacement (THR and TKR) found substantial improvement in pain and function, but variable effects on mental health and social functioning. Risk factors for poor outcomes include older age; more (or more severe) preoperative pain; medical comorbidities; musculoskeletal comorbidities such as low back pain, with functional limitations; low mental health scores; and OA in the hip that was not replaced.^10,11

Unicompartmental knee replacement (UKR) had an SOR of 76%. Reviews that compared TKR to UKR found similar 5-year outcomes in knee pain and function. Those who underwent UKR had better range of motion, but prosthesis survival at 10 years was better in those with TKR (>90% vs 85% to 90%).¹²

In young adults, osteotomy and jointpreserving procedures are recommended for hip OA, especially when dysplasia is present. In young, active patients with unicompartment OA, high tibial osteotomies may delay TKR by as long as 10 years.¹³

Joint lavage and arthroscopic debridement in knee OA remain controversial, although they may provide short-term symptom relief (SOR: 60%). Joint fusion as a salvage procedure after failed TKR had an SOR of 69%.

Work as a team to improve outcomes

The inevitable increase in the number of patients with OA of the hips and knees underscores the importance of having a range of treatment strategies, often best delivered by a multidisciplinary team with the family physician at the helm. The OARSI guidelines, which are backed by both a thorough review of research findings and expert consensus, can help you convince patients to take an active role in managing this potentially debilitating condition. Patients’ commitment to lifestyle modifications and self-management, bolstered by your guidance and support, is the most effective way to keep patients with OA on the move.

Correspondence
Greg P. Gutierrez, MD, Associate Professor, University of Colorado Denver Health Sciences Center, Department of Family Medicine, Denver Health and Hospital, 660 Bannock St., Denver, CO 80218; [email protected].