Evidence is mounting for the use of bariatric surgery to treat type 2 diabetes mellitus in patients whose body mass index (BMI) is 35 kg/m² or higher. In obese patients who also have type 2 diabetes, bariatric surgery sends it into remission (defined as normoglycemic control without the need for diabetic medications) in more than three-fourths of cases, with higher rates with the Roux-en-Y gastric bypass procedure than with the laparoscopic adjustable gastric banding procedure.

However, data on the effects of this surgery on type 2 diabetes come primarily from observational studies that lacked appropriate control groups, and the relative benefit of bariatric surgery vs aggressive medical antidiabetic therapy is not yet known. Needed are randomized trials comparing the two types of therapy (and the various types of bariatric surgery) in diabetic patients with less-severe obesity.

Further, why would bariatric surgery help with diabetes, and why would one procedure do it better than another? To be honest, we are not sure, but evidence points not only to weight loss but also to better insulin sensitivity and to alterations in levels of hormones secreted by the gut that increase insulin secretion.

OBESITY PROMOTES DIABETES; WEIGHT LOSS COUNTERACTS IT

Type 2 diabetes mellitus is a complex metabolic disease characterized by insulin resistance and progressive failure of pancreatic beta cells, resulting in hyperglycemia.^1,2

Obesity, a potent risk factor for type 2 diabetes, contributes to its development by inducing insulin resistance and inflammation, which in turn impair glucose regulation.^3,4 Fat deposits in the abdomen, muscles, and liver contribute to elevations of circulating free fatty acids and adipocyte-derived cytokines that mediate insulin resistance and inflammatory pathways.⁵

In the Diabetes Prevention Program,⁶ modest weight loss (5% to 10% of body weight) through diet and exercise reduced the incidence of type 2 diabetes, and in the ongoing Action for Health in Diabetes (Look AHEAD) study of the National Institutes of Health, it improved glucose homeostasis.^7,8

The current medical approach to type 2 diabetes includes advising the patient to lose weight through lifestyle modification, and prescribing drugs that restore glycemic control by reducing insulin resistance (biguanides, glitazones) and improving insulin secretion (incretin mimetics and analogues and sulfonylureas). ^9,10

However, several factors make type 2 diabetes challenging to treat in obese people. Patients who lose weight via behavioral changes and weight-loss drugs tend to gain the weight back. Antidiabetic drugs pose the risk of hypoglycemia. Moreover, although many new classes of drugs have been developed to treat type 2 diabetes, most patients fail to achieve the American Diabetes Association goal for glycemic control, ie, a hemoglobin A_1c level lower than 7%.¹¹

BARIATRIC PROCEDURES AND THEIR EFFECT ON DIABETES CONTROL

After bariatric surgery, patients lose more weight than with traditional weight-loss methods—up to 25% of their total body weight. Furthermore, of those with type 2 diabetes, 87% achieve at least better glucose control and need fewer antidiabetic medications,¹² and an average of 78% achieve normal glycemic control without taking any antidiabetic medications at all.^12,13

But not all bariatric procedures have the same effect on weight and diabetes: certain procedures have a greater effect.

The two major types are classified as gastric restrictive procedures and intestinal bypass procedures. The classification was initially based on the presumed mechanism of weight loss.

Gastric restrictive procedures (laparoscopic adjustable gastric banding, sleeve gastrectomy, vertical gastroplasty) limit gastric volume and, hence, restrict the intake of calories by inducing satiety. Afterward, patients lose approximately 10% to 20% of their total body weight.

Furthermore, multiple studies, including a randomized controlled trial¹⁴ (more about this below), have shown remission of type 2 diabetes with laparoscopic adjustable gastric banding but not with conventional medical therapy. The effect is primarily mediated by weight loss and improved insulin sensitivity, both of which occur several months following surgery. Of note, however: in this trial,¹⁴ all the patients had diabetes of short duration, less than 2 years.

Hence, different procedures have different effects on diabetes.¹² The speed at which type 2 diabetes goes into remission differs with restrictive vs malabsorptive procedures. After Roux-en-Y gastric bypass and biliopancreatic diversion, diabetes remits within days, even before the patient has lost much weight.¹⁵ This does not happen after gastric restrictive procedures.^12,16

Several observational studies have evaluated the benefit of Roux-en-Y surgery for patients with type 2 diabetes mellitus.

Pories et al¹⁵ followed 608 severely obese patients, of whom 165 (27%) had type 2 diabetes or impaired glucose tolerance.

At a mean follow-up of 7.6 years after surgery, 83% of the diabetic patients were off their antidiabetic drugs, and 99% of those with impaired glucose tolerance were normoglycemic, with normal fasting glucose and hemoglobin A_1c levels. Marked improvements in hyperlipidemia, hypertension, fertility, osteoarthritis, and obstructive sleep apnea were also noted.

Schauer et al¹⁷ observed similar results in 1,160 morbidly obese patients, of whom 240 (21%) had type 2 diabetes or impaired fasting glucose.

After laparoscopic Roux-en-Y gastric bypass surgery, fasting glucose and hemoglobin A_1c levels returned to normal levels in 83% of cases and were markedly improved in the remaining 17%. Significantly (80%) fewer patients needed oral antidiabetic agents or insulin (79% fewer). Patients most likely to achieve complete remission of diabetes were those with the shortest duration of diabetes (< 5 years), the mildest severity of diabetes (diet-controlled), and the greatest weight loss after surgery. The rate of diabetes remission in patients who had been diabetic for 5 years or less was 95%, compared with 75% in those who had been diabetic for 6 to 10 years and 54% in those who had been diabetic for more than 10 years (P < .001).

The Swedish Obese Subjects (SOS) study¹⁸ prospectively followed 1,703 patients, of whom 118 had type 2 diabetes, for 10 years after various bariatric surgery procedures (primarily vertical gastroplasty). In a control group that received medical therapy, 77 patients had type 2 diabetes. Medical therapy was ill-defined with respect to aggressiveness and adherence to intervention with lifestyle and pharmacotherapy.

At 2 years, the surgical group had lost a mean of 28 kg, glycemic control had improved in the diabetic patients, and many of them had been able to stop taking oral hypoglycemic drugs or insulin. In contrast, the need for these agents increased in the medically treated patients. The proportion treated by diet alone rose from 59% to 73% in the surgical group, but declined from 55% to 34% in the nonsurgical group.¹³

In these studies, surgery also reduced the risk of progressing from impaired glucose tolerance to type 2 diabetes; the risk was 30 times lower in the study by Pories et al.¹⁵ In the SOS study,¹⁸ the frequency of diabetes was 30 times lower at 2 years and five times lower at 8 years after surgery.

Studies of biliopancreatic diversion

Data on the effects of biliopancreatic diversion, a primarily malabsorptive procedure, are limited to European studies.

Scopinaro et al^19,20 reported long-term follow-up data on 312 patients with type 2 diabetes who underwent biliopancreatic diversion; 310 patients (99%) achieved normal fasting glucose values by 1 year after surgery. At 10 years after surgery, 98% of the patients were still in complete remission of diabetes, defined as normal glucose values without the use of antidiabetic medications.

Others have noted similar findings.^21,22

Limitations of the studies

Although these data seem encouraging, these studies had major limitations.

The patients were mostly white women with severe obesity, ie, a BMI greater than 40 kg/m², which is not representative of patients with type 2 diabetes in the community. Only about 20% had glucose intolerance or overt type 2 diabetes mellitus. Would other groups benefit, particularly men and those with lesssevere obesity?

Moreover, these studies were observational, with no randomized control groups. Many reports consisted of large case series. It is not clear how specific bariatric procedures were chosen or what criteria were used for performing bariatric surgery. A lack of complete follow-up data is also a concern.

Needed are large randomized trials evaluating the effects of various bariatric procedures in a less obese cohort with type 2 diabetes, ie, typical patients seen in the community. Moreover, surgery has not been compared directly with more vigorous medical weight-loss strategies, such as those used in the Diabetes Prevention Project⁶ and the Look AHEAD trial.^7,8

A randomized controlled trial of gastric banding

The only randomized controlled trial to date that compared standard medical diabetes therapy with bariatric surgery was conducted by Dixon et al.¹⁴

Sixty patients with type 2 diabetes (duration < 2 years and mean hemoglobin A1c 7.7%) were randomized either to receive medical management as defined by the American Diabetes Association guidelines or to undergo laparoscopic adjustable gastric banding.

At 2 years, the rate of remission (defined as hemoglobin A_1c < 6.2% and a normal fasting glucose level) was 13% in the medical treatment group vs 73% in the surgery group (P < .001). Patients receiving medical treatment had lost a mean of 1.7% of their body weight, vs 20.7% in the surgical patients (P < .001). Weight loss was strongly associated with remission of type 2 diabetes after surgery.

This study was controversial in that the medical intervention in this trial was not as aggressive as in the Diabetes Prevention Project and Look AHEAD trials.

INDICATIONS FOR BARIATRIC SURGERY IN PATIENTS WITH DIABETES

According to guidelines from the National Institutes of Health,²³ the current indications for bariatric surgery include a BMI of 40 kg/m² or higher, or a BMI between 35 and 40 kg/m² with at least two obesity-related comorbidities. Diabetes is considered a key comorbidity that justifies the risk of surgery. The guidelines suggest that bariatric surgery be discussed with all severely obese patients (BMI > 35 kg/m²) with type 2 diabetes who have not been able to lose weight with other weight-control approaches.

Since type 2 diabetes mellitus is a progressive disease characterized by relentless deterioration of beta-cell function, many endocrinologists favor aggressive weight-loss approaches early in the course of the disease. We believe that bariatric surgery should be considered early, as it may help preserve pancreatic betacell function and slow the progression of microvascular and macrovascular complications.

HOW DOES BARIATRIC SURGERY IMPROVE TYPE 2 DIABETES?

Hypothesis 1: Weight loss increases insulin sensitivity

The enforced caloric restriction, negative energy balance, and weight loss after bariatric surgery reduce insulin resistance. Consequently, the beta cells can rest because they don’t need to produce as much insulin. These effects have been observed after both gastric restrictive procedures and gastric bypass procedures.

Hypothesis 2: Less lipotoxicity, inflammation

Another theory is that bariatric surgery lessens insulin resistance by reducing “lipotoxicity,” a condition related to dysregulated fatty acid flux, lipid metabolites in tissues, and direct and indirect effects of hormones secreted by adipocytes.

The strongest evidence for this theory comes from Bikman et al,²⁶ who found that insulin sensitivity increased after Roux-en-Y surgery more than expected from weight loss alone. One year after surgery, even though they remained anthropometrically obese (BMI > 30 kg/m²), the patients had insulin sensitivity levels similar to those in a control group of lean people (BMI < 25 kg/m²).

Insulin sensitivity begins to improve within 1 week of intestinal bypass procedures,^15,27 suggesting that these procedures are doing something more than simply forcing weight loss via caloric restriction, as gastric restrictive procedures do.

Hypothesis 3: An effect on gut hormones

The “hindgut hypothesis” raised by Cummings et al²⁴ suggests that accelerated transit of concentrated nutrients (particularly glucose) to the distal intestine results in increased production of insulinotropic and appetite-controlling substances, which account for the reversal of hyperglycemia and obesity.

In contrast, the “foregut hypothesis” raised by Rubino et al²⁸ suggests that nutrient interactions in the duodenum are diabetogenic and, hence, bypassing the duodenum would reverse this defect. Their conclusions come from experiments in rodents that underwent jejunoileal bypass and subsequent refeeding through the bypassed intestine.

GUT HORMONES AND OTHER PEPTIDES ALTERED BY BARIATRIC SURGERY

Incretin hormones: GLP-1, GIP

Gastrointestinal hormones that increase insulin release after a meal are known as incretins. Of interest, they have this effect only when glucose is ingested orally—not when it is infused intravenously.^29,30

Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) account for 50% to 60% of nutrient-related insulin secretion. In addition to stimulating insulin, GLP-1 suppresses glucagon and slows gastric emptying, which delays digestion and reduces postprandial glycemia. GLP-1 also acts on the hypothalamus to induce satiety.

Laferrère et al³¹ and others^32,33 documented robust increases in postprandial levels of GLP-1 within 4 weeks after Roux-en-Y surgery. GLP-1 levels did not increase with comparable weight loss induced by diet.

Rubino et al^28,34 documented similar findings that occurred prior to marked weight loss, suggesting that the benefit of Roux-en-Y surgery on remission of diabetes may not be completely attributable to reduced caloric intake and weight loss. Insulin secretion is generally reduced after gastric restrictive procedures (eg, laparoscopic adjustable gastric banding) and biliopancreatic diversion,³⁵ and is increased after Roux-en-Y gastric bypass.^32,33,36

Noninsulinotropic peptides: Ghrelin, peptide YY

Noninsulinotropic gut peptides that are altered after Roux-en-Y surgery include ghrelin and peptide YY.

Ghrelin, a hormone derived from the gastric fundus, stimulates appetite. Ghrelin concentrations are lower after Roux-en-Y surgery, indicating that suppression of hunger signals helps sustain weight loss. In contrast, ghrelin levels increase with diet-induced weight loss.³⁷ However, the data on ghrelin levels at various times after bariatric surgical procedures are not consistent.^33,38

Peptide YY, like GLP-1, is secreted by L cells of the distal small intestine and is responsible for increasing satiety and delaying gastric emptying after meals. Numerous studies have consistently documented increases in postprandial peptide YY and GLP-1 levels after gastric bypass.^{32,33,39–41}

ACUTE EFFECTS OF BARIATRIC SURGERY ON INSULIN SECRETION, SENSITIVITY

Bariatric surgery alters both insulin secretion and insulin sensitivity, thus improving glucose regulation.

The relationship between insulin secretion and sensitivity is a hyperbolic curve, so that any change in insulin sensitivity is balanced by a reciprocal and proportionate change in insulin secretion. The development of type 2 diabetes is characterized by a reduction in insulin secretion (decompensation) relative to the severity of insulin resistance.

In the first 6 weeks after Roux-en-Y gastric bypass or biliopancreatic diversion, insulin sensitivity improves while insulin secretion increases disproportionately, associated with a robust increase in GLP-1, and resulting in normal glucose homeostasis.^16,31,42

In contrast, patients who lose weight by dieting or undergoing gastric restrictive procedures show a modest increase in insulin sensitivity and a compensatory reduction in insulin secretion, termed “beta-cell rest.”^16,31,42

RISKS OF BARIATRIC SURGERY

Short-term risks

An important concern about using bariatric surgery to treat type 2 diabetes is the risk of morbidity and death associated with these procedures.

Buchwald et al¹³ performed a meta-analysis of 136 bariatric studies that included 22,094 patients. The 30-day operative death rates were 1.1% with biliopancreatic diversion, 0.5% with Roux-en-Y surgery, and 0.1% with restrictive procedures.

Laparoscopic adjustable gastric banding is considered the safest of the current bariatric procedures. It does not involve bowel anastomosis, and the risks of major hemorrhage, gastric perforation, and pulmonary embolism are less than 1%. Late complications requiring reoperation include band slippage or prolapse (5%–10%) and band erosion (1%–3%). The entire intestinal tract is left intact, so subsequent nutritional deficiencies are rare.⁴³

Roux-en-Y gastric bypass carries an overall risk of major complications of 10% to 15%. Anastomotic leak (1%–5%), pulmonary embolism (< 1%), and hemorrhage (1%–4%) can be life-threatening but are rare if the staff are experienced. Late complications such as ulcer or stricture formation at the gastrojejunostomy site occur in 5% to 10% of cases and are managed nonoperatively.

Nutritional deficiencies

Protein-calorie malnutrition is recognized by signs such as edema, hypoalbuminemia, anemia, and hair loss. To minimize this problem after Roux-en-Y surgery, we suggest that patients take in 60 to 80 g of protein and 700 to 800 kcal a day.

Vitamin deficiencies can lead to Wernicke encephalopathy (due to thiamine deficiency), peripheral neuropathy (due to vitamin B¹² deficiency),^45,46 and metabolic bone disease (due to long-term deficiencies of vitamin D and calcium). Often, vitamin deficiencies are present before surgery and require prompt supplementation to avoid exacerbation of these deficiencies afterward.

Biliopancreatic diversion procedures are performed at relatively few centers worldwide, largely because of the massive amounts of protein, fat, and carbohydrate malabsorption they cause. Long-term deficiencies of fat-soluble vitamins, iron, calcium, and vitamins B¹² and D have been reported in one-third to one-half of patients undergoing these procedures, and nutritional supplementation is mandatory.⁴³ Protein-calorie malnutrition occurs in 7% of cases, and 2% of patients require operative revision to lengthen the common channel.

In rare cases, severe hypoglycemia has been noted after Roux-en-Y surgery and is associated with prandial hyperinsulinemia related to elevated GLP-1 levels.^36,47 Neuroglycopenia and seizures have been reported in severe cases. Initial treatment of hypoglycemia involves dietary modification targeting carbohydrate restriction, the use of alpha glucosidase inhibitors such as acarbose (Precose), and referral to an endocrinologist for further management.

Long-term death rates

Death rates after bariatric surgery must be weighed against the long-term cardiovascular risks of continued obesity and type 2 diabetes.

Strong evidence now exists that bariatric surgery increases life expectancy⁴⁸ and that this is largely attributable to reduction in cardiovascular risk factors such as diabetes and cancer. Recent studies have found that the long-term death rate is 32% to 73% lower for patients undergoing bariatric surgery than in matched controls who do not undergo surgery.⁴⁹ A decrease in the death rate related to diabetes has played an important role in these results.
 

Acknowledgments: We acknowledge support from the National Institutes of Health, Multidisciplinary Clinical Research Career Development Programs Grant 5K12RR023264 (SRK), National Center for Research Resources, CTSA 1UL1RR024989, and research grants from Ethicon Endo-Surgery (PS,SRK).

Evidence is mounting for the use of bariatric surgery to treat type 2 diabetes mellitus in patients whose body mass index (BMI) is 35 kg/m² or higher. In obese patients who also have type 2 diabetes, bariatric surgery sends it into remission (defined as normoglycemic control without the need for diabetic medications) in more than three-fourths of cases, with higher rates with the Roux-en-Y gastric bypass procedure than with the laparoscopic adjustable gastric banding procedure.

However, data on the effects of this surgery on type 2 diabetes come primarily from observational studies that lacked appropriate control groups, and the relative benefit of bariatric surgery vs aggressive medical antidiabetic therapy is not yet known. Needed are randomized trials comparing the two types of therapy (and the various types of bariatric surgery) in diabetic patients with less-severe obesity.

Further, why would bariatric surgery help with diabetes, and why would one procedure do it better than another? To be honest, we are not sure, but evidence points not only to weight loss but also to better insulin sensitivity and to alterations in levels of hormones secreted by the gut that increase insulin secretion.

OBESITY PROMOTES DIABETES; WEIGHT LOSS COUNTERACTS IT

Type 2 diabetes mellitus is a complex metabolic disease characterized by insulin resistance and progressive failure of pancreatic beta cells, resulting in hyperglycemia.^1,2

Obesity, a potent risk factor for type 2 diabetes, contributes to its development by inducing insulin resistance and inflammation, which in turn impair glucose regulation.^3,4 Fat deposits in the abdomen, muscles, and liver contribute to elevations of circulating free fatty acids and adipocyte-derived cytokines that mediate insulin resistance and inflammatory pathways.⁵

In the Diabetes Prevention Program,⁶ modest weight loss (5% to 10% of body weight) through diet and exercise reduced the incidence of type 2 diabetes, and in the ongoing Action for Health in Diabetes (Look AHEAD) study of the National Institutes of Health, it improved glucose homeostasis.^7,8

The current medical approach to type 2 diabetes includes advising the patient to lose weight through lifestyle modification, and prescribing drugs that restore glycemic control by reducing insulin resistance (biguanides, glitazones) and improving insulin secretion (incretin mimetics and analogues and sulfonylureas). ^9,10

However, several factors make type 2 diabetes challenging to treat in obese people. Patients who lose weight via behavioral changes and weight-loss drugs tend to gain the weight back. Antidiabetic drugs pose the risk of hypoglycemia. Moreover, although many new classes of drugs have been developed to treat type 2 diabetes, most patients fail to achieve the American Diabetes Association goal for glycemic control, ie, a hemoglobin A_1c level lower than 7%.¹¹

BARIATRIC PROCEDURES AND THEIR EFFECT ON DIABETES CONTROL

After bariatric surgery, patients lose more weight than with traditional weight-loss methods—up to 25% of their total body weight. Furthermore, of those with type 2 diabetes, 87% achieve at least better glucose control and need fewer antidiabetic medications,¹² and an average of 78% achieve normal glycemic control without taking any antidiabetic medications at all.^12,13

But not all bariatric procedures have the same effect on weight and diabetes: certain procedures have a greater effect.

The two major types are classified as gastric restrictive procedures and intestinal bypass procedures. The classification was initially based on the presumed mechanism of weight loss.

Gastric restrictive procedures (laparoscopic adjustable gastric banding, sleeve gastrectomy, vertical gastroplasty) limit gastric volume and, hence, restrict the intake of calories by inducing satiety. Afterward, patients lose approximately 10% to 20% of their total body weight.

Furthermore, multiple studies, including a randomized controlled trial¹⁴ (more about this below), have shown remission of type 2 diabetes with laparoscopic adjustable gastric banding but not with conventional medical therapy. The effect is primarily mediated by weight loss and improved insulin sensitivity, both of which occur several months following surgery. Of note, however: in this trial,¹⁴ all the patients had diabetes of short duration, less than 2 years.

Hence, different procedures have different effects on diabetes.¹² The speed at which type 2 diabetes goes into remission differs with restrictive vs malabsorptive procedures. After Roux-en-Y gastric bypass and biliopancreatic diversion, diabetes remits within days, even before the patient has lost much weight.¹⁵ This does not happen after gastric restrictive procedures.^12,16

Several observational studies have evaluated the benefit of Roux-en-Y surgery for patients with type 2 diabetes mellitus.

Pories et al¹⁵ followed 608 severely obese patients, of whom 165 (27%) had type 2 diabetes or impaired glucose tolerance.

At a mean follow-up of 7.6 years after surgery, 83% of the diabetic patients were off their antidiabetic drugs, and 99% of those with impaired glucose tolerance were normoglycemic, with normal fasting glucose and hemoglobin A_1c levels. Marked improvements in hyperlipidemia, hypertension, fertility, osteoarthritis, and obstructive sleep apnea were also noted.

Schauer et al¹⁷ observed similar results in 1,160 morbidly obese patients, of whom 240 (21%) had type 2 diabetes or impaired fasting glucose.

After laparoscopic Roux-en-Y gastric bypass surgery, fasting glucose and hemoglobin A_1c levels returned to normal levels in 83% of cases and were markedly improved in the remaining 17%. Significantly (80%) fewer patients needed oral antidiabetic agents or insulin (79% fewer). Patients most likely to achieve complete remission of diabetes were those with the shortest duration of diabetes (< 5 years), the mildest severity of diabetes (diet-controlled), and the greatest weight loss after surgery. The rate of diabetes remission in patients who had been diabetic for 5 years or less was 95%, compared with 75% in those who had been diabetic for 6 to 10 years and 54% in those who had been diabetic for more than 10 years (P < .001).

The Swedish Obese Subjects (SOS) study¹⁸ prospectively followed 1,703 patients, of whom 118 had type 2 diabetes, for 10 years after various bariatric surgery procedures (primarily vertical gastroplasty). In a control group that received medical therapy, 77 patients had type 2 diabetes. Medical therapy was ill-defined with respect to aggressiveness and adherence to intervention with lifestyle and pharmacotherapy.

At 2 years, the surgical group had lost a mean of 28 kg, glycemic control had improved in the diabetic patients, and many of them had been able to stop taking oral hypoglycemic drugs or insulin. In contrast, the need for these agents increased in the medically treated patients. The proportion treated by diet alone rose from 59% to 73% in the surgical group, but declined from 55% to 34% in the nonsurgical group.¹³

In these studies, surgery also reduced the risk of progressing from impaired glucose tolerance to type 2 diabetes; the risk was 30 times lower in the study by Pories et al.¹⁵ In the SOS study,¹⁸ the frequency of diabetes was 30 times lower at 2 years and five times lower at 8 years after surgery.

Studies of biliopancreatic diversion

Data on the effects of biliopancreatic diversion, a primarily malabsorptive procedure, are limited to European studies.

Scopinaro et al^19,20 reported long-term follow-up data on 312 patients with type 2 diabetes who underwent biliopancreatic diversion; 310 patients (99%) achieved normal fasting glucose values by 1 year after surgery. At 10 years after surgery, 98% of the patients were still in complete remission of diabetes, defined as normal glucose values without the use of antidiabetic medications.

Others have noted similar findings.^21,22

Limitations of the studies

Although these data seem encouraging, these studies had major limitations.

The patients were mostly white women with severe obesity, ie, a BMI greater than 40 kg/m², which is not representative of patients with type 2 diabetes in the community. Only about 20% had glucose intolerance or overt type 2 diabetes mellitus. Would other groups benefit, particularly men and those with lesssevere obesity?

Moreover, these studies were observational, with no randomized control groups. Many reports consisted of large case series. It is not clear how specific bariatric procedures were chosen or what criteria were used for performing bariatric surgery. A lack of complete follow-up data is also a concern.

Needed are large randomized trials evaluating the effects of various bariatric procedures in a less obese cohort with type 2 diabetes, ie, typical patients seen in the community. Moreover, surgery has not been compared directly with more vigorous medical weight-loss strategies, such as those used in the Diabetes Prevention Project⁶ and the Look AHEAD trial.^7,8

A randomized controlled trial of gastric banding

The only randomized controlled trial to date that compared standard medical diabetes therapy with bariatric surgery was conducted by Dixon et al.¹⁴

Sixty patients with type 2 diabetes (duration < 2 years and mean hemoglobin A1c 7.7%) were randomized either to receive medical management as defined by the American Diabetes Association guidelines or to undergo laparoscopic adjustable gastric banding.

At 2 years, the rate of remission (defined as hemoglobin A_1c < 6.2% and a normal fasting glucose level) was 13% in the medical treatment group vs 73% in the surgery group (P < .001). Patients receiving medical treatment had lost a mean of 1.7% of their body weight, vs 20.7% in the surgical patients (P < .001). Weight loss was strongly associated with remission of type 2 diabetes after surgery.

This study was controversial in that the medical intervention in this trial was not as aggressive as in the Diabetes Prevention Project and Look AHEAD trials.

INDICATIONS FOR BARIATRIC SURGERY IN PATIENTS WITH DIABETES

According to guidelines from the National Institutes of Health,²³ the current indications for bariatric surgery include a BMI of 40 kg/m² or higher, or a BMI between 35 and 40 kg/m² with at least two obesity-related comorbidities. Diabetes is considered a key comorbidity that justifies the risk of surgery. The guidelines suggest that bariatric surgery be discussed with all severely obese patients (BMI > 35 kg/m²) with type 2 diabetes who have not been able to lose weight with other weight-control approaches.

Since type 2 diabetes mellitus is a progressive disease characterized by relentless deterioration of beta-cell function, many endocrinologists favor aggressive weight-loss approaches early in the course of the disease. We believe that bariatric surgery should be considered early, as it may help preserve pancreatic betacell function and slow the progression of microvascular and macrovascular complications.

HOW DOES BARIATRIC SURGERY IMPROVE TYPE 2 DIABETES?

Hypothesis 1: Weight loss increases insulin sensitivity

The enforced caloric restriction, negative energy balance, and weight loss after bariatric surgery reduce insulin resistance. Consequently, the beta cells can rest because they don’t need to produce as much insulin. These effects have been observed after both gastric restrictive procedures and gastric bypass procedures.

Hypothesis 2: Less lipotoxicity, inflammation

Another theory is that bariatric surgery lessens insulin resistance by reducing “lipotoxicity,” a condition related to dysregulated fatty acid flux, lipid metabolites in tissues, and direct and indirect effects of hormones secreted by adipocytes.

The strongest evidence for this theory comes from Bikman et al,²⁶ who found that insulin sensitivity increased after Roux-en-Y surgery more than expected from weight loss alone. One year after surgery, even though they remained anthropometrically obese (BMI > 30 kg/m²), the patients had insulin sensitivity levels similar to those in a control group of lean people (BMI < 25 kg/m²).

Insulin sensitivity begins to improve within 1 week of intestinal bypass procedures,^15,27 suggesting that these procedures are doing something more than simply forcing weight loss via caloric restriction, as gastric restrictive procedures do.

Hypothesis 3: An effect on gut hormones

The “hindgut hypothesis” raised by Cummings et al²⁴ suggests that accelerated transit of concentrated nutrients (particularly glucose) to the distal intestine results in increased production of insulinotropic and appetite-controlling substances, which account for the reversal of hyperglycemia and obesity.

In contrast, the “foregut hypothesis” raised by Rubino et al²⁸ suggests that nutrient interactions in the duodenum are diabetogenic and, hence, bypassing the duodenum would reverse this defect. Their conclusions come from experiments in rodents that underwent jejunoileal bypass and subsequent refeeding through the bypassed intestine.

GUT HORMONES AND OTHER PEPTIDES ALTERED BY BARIATRIC SURGERY

Incretin hormones: GLP-1, GIP

Gastrointestinal hormones that increase insulin release after a meal are known as incretins. Of interest, they have this effect only when glucose is ingested orally—not when it is infused intravenously.^29,30

Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) account for 50% to 60% of nutrient-related insulin secretion. In addition to stimulating insulin, GLP-1 suppresses glucagon and slows gastric emptying, which delays digestion and reduces postprandial glycemia. GLP-1 also acts on the hypothalamus to induce satiety.

Laferrère et al³¹ and others^32,33 documented robust increases in postprandial levels of GLP-1 within 4 weeks after Roux-en-Y surgery. GLP-1 levels did not increase with comparable weight loss induced by diet.

Rubino et al^28,34 documented similar findings that occurred prior to marked weight loss, suggesting that the benefit of Roux-en-Y surgery on remission of diabetes may not be completely attributable to reduced caloric intake and weight loss. Insulin secretion is generally reduced after gastric restrictive procedures (eg, laparoscopic adjustable gastric banding) and biliopancreatic diversion,³⁵ and is increased after Roux-en-Y gastric bypass.^32,33,36

Noninsulinotropic peptides: Ghrelin, peptide YY

Noninsulinotropic gut peptides that are altered after Roux-en-Y surgery include ghrelin and peptide YY.

Ghrelin, a hormone derived from the gastric fundus, stimulates appetite. Ghrelin concentrations are lower after Roux-en-Y surgery, indicating that suppression of hunger signals helps sustain weight loss. In contrast, ghrelin levels increase with diet-induced weight loss.³⁷ However, the data on ghrelin levels at various times after bariatric surgical procedures are not consistent.^33,38

Peptide YY, like GLP-1, is secreted by L cells of the distal small intestine and is responsible for increasing satiety and delaying gastric emptying after meals. Numerous studies have consistently documented increases in postprandial peptide YY and GLP-1 levels after gastric bypass.^{32,33,39–41}

ACUTE EFFECTS OF BARIATRIC SURGERY ON INSULIN SECRETION, SENSITIVITY

Bariatric surgery alters both insulin secretion and insulin sensitivity, thus improving glucose regulation.

The relationship between insulin secretion and sensitivity is a hyperbolic curve, so that any change in insulin sensitivity is balanced by a reciprocal and proportionate change in insulin secretion. The development of type 2 diabetes is characterized by a reduction in insulin secretion (decompensation) relative to the severity of insulin resistance.

In the first 6 weeks after Roux-en-Y gastric bypass or biliopancreatic diversion, insulin sensitivity improves while insulin secretion increases disproportionately, associated with a robust increase in GLP-1, and resulting in normal glucose homeostasis.^16,31,42

In contrast, patients who lose weight by dieting or undergoing gastric restrictive procedures show a modest increase in insulin sensitivity and a compensatory reduction in insulin secretion, termed “beta-cell rest.”^16,31,42

RISKS OF BARIATRIC SURGERY

Short-term risks

An important concern about using bariatric surgery to treat type 2 diabetes is the risk of morbidity and death associated with these procedures.

Buchwald et al¹³ performed a meta-analysis of 136 bariatric studies that included 22,094 patients. The 30-day operative death rates were 1.1% with biliopancreatic diversion, 0.5% with Roux-en-Y surgery, and 0.1% with restrictive procedures.

Laparoscopic adjustable gastric banding is considered the safest of the current bariatric procedures. It does not involve bowel anastomosis, and the risks of major hemorrhage, gastric perforation, and pulmonary embolism are less than 1%. Late complications requiring reoperation include band slippage or prolapse (5%–10%) and band erosion (1%–3%). The entire intestinal tract is left intact, so subsequent nutritional deficiencies are rare.⁴³

Roux-en-Y gastric bypass carries an overall risk of major complications of 10% to 15%. Anastomotic leak (1%–5%), pulmonary embolism (< 1%), and hemorrhage (1%–4%) can be life-threatening but are rare if the staff are experienced. Late complications such as ulcer or stricture formation at the gastrojejunostomy site occur in 5% to 10% of cases and are managed nonoperatively.

Nutritional deficiencies

Protein-calorie malnutrition is recognized by signs such as edema, hypoalbuminemia, anemia, and hair loss. To minimize this problem after Roux-en-Y surgery, we suggest that patients take in 60 to 80 g of protein and 700 to 800 kcal a day.

Vitamin deficiencies can lead to Wernicke encephalopathy (due to thiamine deficiency), peripheral neuropathy (due to vitamin B¹² deficiency),^45,46 and metabolic bone disease (due to long-term deficiencies of vitamin D and calcium). Often, vitamin deficiencies are present before surgery and require prompt supplementation to avoid exacerbation of these deficiencies afterward.

Biliopancreatic diversion procedures are performed at relatively few centers worldwide, largely because of the massive amounts of protein, fat, and carbohydrate malabsorption they cause. Long-term deficiencies of fat-soluble vitamins, iron, calcium, and vitamins B¹² and D have been reported in one-third to one-half of patients undergoing these procedures, and nutritional supplementation is mandatory.⁴³ Protein-calorie malnutrition occurs in 7% of cases, and 2% of patients require operative revision to lengthen the common channel.

In rare cases, severe hypoglycemia has been noted after Roux-en-Y surgery and is associated with prandial hyperinsulinemia related to elevated GLP-1 levels.^36,47 Neuroglycopenia and seizures have been reported in severe cases. Initial treatment of hypoglycemia involves dietary modification targeting carbohydrate restriction, the use of alpha glucosidase inhibitors such as acarbose (Precose), and referral to an endocrinologist for further management.

Long-term death rates

Death rates after bariatric surgery must be weighed against the long-term cardiovascular risks of continued obesity and type 2 diabetes.

Strong evidence now exists that bariatric surgery increases life expectancy⁴⁸ and that this is largely attributable to reduction in cardiovascular risk factors such as diabetes and cancer. Recent studies have found that the long-term death rate is 32% to 73% lower for patients undergoing bariatric surgery than in matched controls who do not undergo surgery.⁴⁹ A decrease in the death rate related to diabetes has played an important role in these results.
 

Acknowledgments: We acknowledge support from the National Institutes of Health, Multidisciplinary Clinical Research Career Development Programs Grant 5K12RR023264 (SRK), National Center for Research Resources, CTSA 1UL1RR024989, and research grants from Ethicon Endo-Surgery (PS,SRK).

Evidence is mounting for the use of bariatric surgery to treat type 2 diabetes mellitus in patients whose body mass index (BMI) is 35 kg/m² or higher. In obese patients who also have type 2 diabetes, bariatric surgery sends it into remission (defined as normoglycemic control without the need for diabetic medications) in more than three-fourths of cases, with higher rates with the Roux-en-Y gastric bypass procedure than with the laparoscopic adjustable gastric banding procedure.

However, data on the effects of this surgery on type 2 diabetes come primarily from observational studies that lacked appropriate control groups, and the relative benefit of bariatric surgery vs aggressive medical antidiabetic therapy is not yet known. Needed are randomized trials comparing the two types of therapy (and the various types of bariatric surgery) in diabetic patients with less-severe obesity.

Further, why would bariatric surgery help with diabetes, and why would one procedure do it better than another? To be honest, we are not sure, but evidence points not only to weight loss but also to better insulin sensitivity and to alterations in levels of hormones secreted by the gut that increase insulin secretion.

OBESITY PROMOTES DIABETES; WEIGHT LOSS COUNTERACTS IT

Type 2 diabetes mellitus is a complex metabolic disease characterized by insulin resistance and progressive failure of pancreatic beta cells, resulting in hyperglycemia.^1,2

Obesity, a potent risk factor for type 2 diabetes, contributes to its development by inducing insulin resistance and inflammation, which in turn impair glucose regulation.^3,4 Fat deposits in the abdomen, muscles, and liver contribute to elevations of circulating free fatty acids and adipocyte-derived cytokines that mediate insulin resistance and inflammatory pathways.⁵

In the Diabetes Prevention Program,⁶ modest weight loss (5% to 10% of body weight) through diet and exercise reduced the incidence of type 2 diabetes, and in the ongoing Action for Health in Diabetes (Look AHEAD) study of the National Institutes of Health, it improved glucose homeostasis.^7,8

The current medical approach to type 2 diabetes includes advising the patient to lose weight through lifestyle modification, and prescribing drugs that restore glycemic control by reducing insulin resistance (biguanides, glitazones) and improving insulin secretion (incretin mimetics and analogues and sulfonylureas). ^9,10

However, several factors make type 2 diabetes challenging to treat in obese people. Patients who lose weight via behavioral changes and weight-loss drugs tend to gain the weight back. Antidiabetic drugs pose the risk of hypoglycemia. Moreover, although many new classes of drugs have been developed to treat type 2 diabetes, most patients fail to achieve the American Diabetes Association goal for glycemic control, ie, a hemoglobin A_1c level lower than 7%.¹¹

BARIATRIC PROCEDURES AND THEIR EFFECT ON DIABETES CONTROL

After bariatric surgery, patients lose more weight than with traditional weight-loss methods—up to 25% of their total body weight. Furthermore, of those with type 2 diabetes, 87% achieve at least better glucose control and need fewer antidiabetic medications,¹² and an average of 78% achieve normal glycemic control without taking any antidiabetic medications at all.^12,13

But not all bariatric procedures have the same effect on weight and diabetes: certain procedures have a greater effect.

The two major types are classified as gastric restrictive procedures and intestinal bypass procedures. The classification was initially based on the presumed mechanism of weight loss.

Gastric restrictive procedures (laparoscopic adjustable gastric banding, sleeve gastrectomy, vertical gastroplasty) limit gastric volume and, hence, restrict the intake of calories by inducing satiety. Afterward, patients lose approximately 10% to 20% of their total body weight.

Furthermore, multiple studies, including a randomized controlled trial¹⁴ (more about this below), have shown remission of type 2 diabetes with laparoscopic adjustable gastric banding but not with conventional medical therapy. The effect is primarily mediated by weight loss and improved insulin sensitivity, both of which occur several months following surgery. Of note, however: in this trial,¹⁴ all the patients had diabetes of short duration, less than 2 years.

Hence, different procedures have different effects on diabetes.¹² The speed at which type 2 diabetes goes into remission differs with restrictive vs malabsorptive procedures. After Roux-en-Y gastric bypass and biliopancreatic diversion, diabetes remits within days, even before the patient has lost much weight.¹⁵ This does not happen after gastric restrictive procedures.^12,16

Several observational studies have evaluated the benefit of Roux-en-Y surgery for patients with type 2 diabetes mellitus.

Pories et al¹⁵ followed 608 severely obese patients, of whom 165 (27%) had type 2 diabetes or impaired glucose tolerance.

At a mean follow-up of 7.6 years after surgery, 83% of the diabetic patients were off their antidiabetic drugs, and 99% of those with impaired glucose tolerance were normoglycemic, with normal fasting glucose and hemoglobin A_1c levels. Marked improvements in hyperlipidemia, hypertension, fertility, osteoarthritis, and obstructive sleep apnea were also noted.

Schauer et al¹⁷ observed similar results in 1,160 morbidly obese patients, of whom 240 (21%) had type 2 diabetes or impaired fasting glucose.

After laparoscopic Roux-en-Y gastric bypass surgery, fasting glucose and hemoglobin A_1c levels returned to normal levels in 83% of cases and were markedly improved in the remaining 17%. Significantly (80%) fewer patients needed oral antidiabetic agents or insulin (79% fewer). Patients most likely to achieve complete remission of diabetes were those with the shortest duration of diabetes (< 5 years), the mildest severity of diabetes (diet-controlled), and the greatest weight loss after surgery. The rate of diabetes remission in patients who had been diabetic for 5 years or less was 95%, compared with 75% in those who had been diabetic for 6 to 10 years and 54% in those who had been diabetic for more than 10 years (P < .001).

The Swedish Obese Subjects (SOS) study¹⁸ prospectively followed 1,703 patients, of whom 118 had type 2 diabetes, for 10 years after various bariatric surgery procedures (primarily vertical gastroplasty). In a control group that received medical therapy, 77 patients had type 2 diabetes. Medical therapy was ill-defined with respect to aggressiveness and adherence to intervention with lifestyle and pharmacotherapy.

At 2 years, the surgical group had lost a mean of 28 kg, glycemic control had improved in the diabetic patients, and many of them had been able to stop taking oral hypoglycemic drugs or insulin. In contrast, the need for these agents increased in the medically treated patients. The proportion treated by diet alone rose from 59% to 73% in the surgical group, but declined from 55% to 34% in the nonsurgical group.¹³

In these studies, surgery also reduced the risk of progressing from impaired glucose tolerance to type 2 diabetes; the risk was 30 times lower in the study by Pories et al.¹⁵ In the SOS study,¹⁸ the frequency of diabetes was 30 times lower at 2 years and five times lower at 8 years after surgery.

Studies of biliopancreatic diversion

Data on the effects of biliopancreatic diversion, a primarily malabsorptive procedure, are limited to European studies.

Scopinaro et al^19,20 reported long-term follow-up data on 312 patients with type 2 diabetes who underwent biliopancreatic diversion; 310 patients (99%) achieved normal fasting glucose values by 1 year after surgery. At 10 years after surgery, 98% of the patients were still in complete remission of diabetes, defined as normal glucose values without the use of antidiabetic medications.

Others have noted similar findings.^21,22

Limitations of the studies

Although these data seem encouraging, these studies had major limitations.

The patients were mostly white women with severe obesity, ie, a BMI greater than 40 kg/m², which is not representative of patients with type 2 diabetes in the community. Only about 20% had glucose intolerance or overt type 2 diabetes mellitus. Would other groups benefit, particularly men and those with lesssevere obesity?

Moreover, these studies were observational, with no randomized control groups. Many reports consisted of large case series. It is not clear how specific bariatric procedures were chosen or what criteria were used for performing bariatric surgery. A lack of complete follow-up data is also a concern.

Needed are large randomized trials evaluating the effects of various bariatric procedures in a less obese cohort with type 2 diabetes, ie, typical patients seen in the community. Moreover, surgery has not been compared directly with more vigorous medical weight-loss strategies, such as those used in the Diabetes Prevention Project⁶ and the Look AHEAD trial.^7,8

A randomized controlled trial of gastric banding

The only randomized controlled trial to date that compared standard medical diabetes therapy with bariatric surgery was conducted by Dixon et al.¹⁴

Sixty patients with type 2 diabetes (duration < 2 years and mean hemoglobin A1c 7.7%) were randomized either to receive medical management as defined by the American Diabetes Association guidelines or to undergo laparoscopic adjustable gastric banding.

At 2 years, the rate of remission (defined as hemoglobin A_1c < 6.2% and a normal fasting glucose level) was 13% in the medical treatment group vs 73% in the surgery group (P < .001). Patients receiving medical treatment had lost a mean of 1.7% of their body weight, vs 20.7% in the surgical patients (P < .001). Weight loss was strongly associated with remission of type 2 diabetes after surgery.

This study was controversial in that the medical intervention in this trial was not as aggressive as in the Diabetes Prevention Project and Look AHEAD trials.

INDICATIONS FOR BARIATRIC SURGERY IN PATIENTS WITH DIABETES

According to guidelines from the National Institutes of Health,²³ the current indications for bariatric surgery include a BMI of 40 kg/m² or higher, or a BMI between 35 and 40 kg/m² with at least two obesity-related comorbidities. Diabetes is considered a key comorbidity that justifies the risk of surgery. The guidelines suggest that bariatric surgery be discussed with all severely obese patients (BMI > 35 kg/m²) with type 2 diabetes who have not been able to lose weight with other weight-control approaches.

Since type 2 diabetes mellitus is a progressive disease characterized by relentless deterioration of beta-cell function, many endocrinologists favor aggressive weight-loss approaches early in the course of the disease. We believe that bariatric surgery should be considered early, as it may help preserve pancreatic betacell function and slow the progression of microvascular and macrovascular complications.

HOW DOES BARIATRIC SURGERY IMPROVE TYPE 2 DIABETES?

Hypothesis 1: Weight loss increases insulin sensitivity

The enforced caloric restriction, negative energy balance, and weight loss after bariatric surgery reduce insulin resistance. Consequently, the beta cells can rest because they don’t need to produce as much insulin. These effects have been observed after both gastric restrictive procedures and gastric bypass procedures.

Hypothesis 2: Less lipotoxicity, inflammation

Another theory is that bariatric surgery lessens insulin resistance by reducing “lipotoxicity,” a condition related to dysregulated fatty acid flux, lipid metabolites in tissues, and direct and indirect effects of hormones secreted by adipocytes.

The strongest evidence for this theory comes from Bikman et al,²⁶ who found that insulin sensitivity increased after Roux-en-Y surgery more than expected from weight loss alone. One year after surgery, even though they remained anthropometrically obese (BMI > 30 kg/m²), the patients had insulin sensitivity levels similar to those in a control group of lean people (BMI < 25 kg/m²).

Insulin sensitivity begins to improve within 1 week of intestinal bypass procedures,^15,27 suggesting that these procedures are doing something more than simply forcing weight loss via caloric restriction, as gastric restrictive procedures do.

Hypothesis 3: An effect on gut hormones

The “hindgut hypothesis” raised by Cummings et al²⁴ suggests that accelerated transit of concentrated nutrients (particularly glucose) to the distal intestine results in increased production of insulinotropic and appetite-controlling substances, which account for the reversal of hyperglycemia and obesity.

In contrast, the “foregut hypothesis” raised by Rubino et al²⁸ suggests that nutrient interactions in the duodenum are diabetogenic and, hence, bypassing the duodenum would reverse this defect. Their conclusions come from experiments in rodents that underwent jejunoileal bypass and subsequent refeeding through the bypassed intestine.

GUT HORMONES AND OTHER PEPTIDES ALTERED BY BARIATRIC SURGERY

Incretin hormones: GLP-1, GIP

Gastrointestinal hormones that increase insulin release after a meal are known as incretins. Of interest, they have this effect only when glucose is ingested orally—not when it is infused intravenously.^29,30

Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) account for 50% to 60% of nutrient-related insulin secretion. In addition to stimulating insulin, GLP-1 suppresses glucagon and slows gastric emptying, which delays digestion and reduces postprandial glycemia. GLP-1 also acts on the hypothalamus to induce satiety.

Laferrère et al³¹ and others^32,33 documented robust increases in postprandial levels of GLP-1 within 4 weeks after Roux-en-Y surgery. GLP-1 levels did not increase with comparable weight loss induced by diet.

Rubino et al^28,34 documented similar findings that occurred prior to marked weight loss, suggesting that the benefit of Roux-en-Y surgery on remission of diabetes may not be completely attributable to reduced caloric intake and weight loss. Insulin secretion is generally reduced after gastric restrictive procedures (eg, laparoscopic adjustable gastric banding) and biliopancreatic diversion,³⁵ and is increased after Roux-en-Y gastric bypass.^32,33,36

Noninsulinotropic peptides: Ghrelin, peptide YY

Noninsulinotropic gut peptides that are altered after Roux-en-Y surgery include ghrelin and peptide YY.

Ghrelin, a hormone derived from the gastric fundus, stimulates appetite. Ghrelin concentrations are lower after Roux-en-Y surgery, indicating that suppression of hunger signals helps sustain weight loss. In contrast, ghrelin levels increase with diet-induced weight loss.³⁷ However, the data on ghrelin levels at various times after bariatric surgical procedures are not consistent.^33,38

Peptide YY, like GLP-1, is secreted by L cells of the distal small intestine and is responsible for increasing satiety and delaying gastric emptying after meals. Numerous studies have consistently documented increases in postprandial peptide YY and GLP-1 levels after gastric bypass.^{32,33,39–41}

ACUTE EFFECTS OF BARIATRIC SURGERY ON INSULIN SECRETION, SENSITIVITY

Bariatric surgery alters both insulin secretion and insulin sensitivity, thus improving glucose regulation.

The relationship between insulin secretion and sensitivity is a hyperbolic curve, so that any change in insulin sensitivity is balanced by a reciprocal and proportionate change in insulin secretion. The development of type 2 diabetes is characterized by a reduction in insulin secretion (decompensation) relative to the severity of insulin resistance.

In the first 6 weeks after Roux-en-Y gastric bypass or biliopancreatic diversion, insulin sensitivity improves while insulin secretion increases disproportionately, associated with a robust increase in GLP-1, and resulting in normal glucose homeostasis.^16,31,42

In contrast, patients who lose weight by dieting or undergoing gastric restrictive procedures show a modest increase in insulin sensitivity and a compensatory reduction in insulin secretion, termed “beta-cell rest.”^16,31,42

RISKS OF BARIATRIC SURGERY

Short-term risks

An important concern about using bariatric surgery to treat type 2 diabetes is the risk of morbidity and death associated with these procedures.

Buchwald et al¹³ performed a meta-analysis of 136 bariatric studies that included 22,094 patients. The 30-day operative death rates were 1.1% with biliopancreatic diversion, 0.5% with Roux-en-Y surgery, and 0.1% with restrictive procedures.

Laparoscopic adjustable gastric banding is considered the safest of the current bariatric procedures. It does not involve bowel anastomosis, and the risks of major hemorrhage, gastric perforation, and pulmonary embolism are less than 1%. Late complications requiring reoperation include band slippage or prolapse (5%–10%) and band erosion (1%–3%). The entire intestinal tract is left intact, so subsequent nutritional deficiencies are rare.⁴³

Roux-en-Y gastric bypass carries an overall risk of major complications of 10% to 15%. Anastomotic leak (1%–5%), pulmonary embolism (< 1%), and hemorrhage (1%–4%) can be life-threatening but are rare if the staff are experienced. Late complications such as ulcer or stricture formation at the gastrojejunostomy site occur in 5% to 10% of cases and are managed nonoperatively.

Nutritional deficiencies

Protein-calorie malnutrition is recognized by signs such as edema, hypoalbuminemia, anemia, and hair loss. To minimize this problem after Roux-en-Y surgery, we suggest that patients take in 60 to 80 g of protein and 700 to 800 kcal a day.

Vitamin deficiencies can lead to Wernicke encephalopathy (due to thiamine deficiency), peripheral neuropathy (due to vitamin B¹² deficiency),^45,46 and metabolic bone disease (due to long-term deficiencies of vitamin D and calcium). Often, vitamin deficiencies are present before surgery and require prompt supplementation to avoid exacerbation of these deficiencies afterward.

Biliopancreatic diversion procedures are performed at relatively few centers worldwide, largely because of the massive amounts of protein, fat, and carbohydrate malabsorption they cause. Long-term deficiencies of fat-soluble vitamins, iron, calcium, and vitamins B¹² and D have been reported in one-third to one-half of patients undergoing these procedures, and nutritional supplementation is mandatory.⁴³ Protein-calorie malnutrition occurs in 7% of cases, and 2% of patients require operative revision to lengthen the common channel.

In rare cases, severe hypoglycemia has been noted after Roux-en-Y surgery and is associated with prandial hyperinsulinemia related to elevated GLP-1 levels.^36,47 Neuroglycopenia and seizures have been reported in severe cases. Initial treatment of hypoglycemia involves dietary modification targeting carbohydrate restriction, the use of alpha glucosidase inhibitors such as acarbose (Precose), and referral to an endocrinologist for further management.

Long-term death rates

Death rates after bariatric surgery must be weighed against the long-term cardiovascular risks of continued obesity and type 2 diabetes.

Strong evidence now exists that bariatric surgery increases life expectancy⁴⁸ and that this is largely attributable to reduction in cardiovascular risk factors such as diabetes and cancer. Recent studies have found that the long-term death rate is 32% to 73% lower for patients undergoing bariatric surgery than in matched controls who do not undergo surgery.⁴⁹ A decrease in the death rate related to diabetes has played an important role in these results.
 

Acknowledgments: We acknowledge support from the National Institutes of Health, Multidisciplinary Clinical Research Career Development Programs Grant 5K12RR023264 (SRK), National Center for Research Resources, CTSA 1UL1RR024989, and research grants from Ethicon Endo-Surgery (PS,SRK).

The rush to adopt the electronic medical record (EMR) has accelerated since the signing of the Health Information Technology for Economic and Clinical Health (HITECH) Act, part of the American Recovery and Reinvestment (ie, the Stimulus) Act of 2009. The HITECH Act provides incentives for physicians to adopt EMRs. However, I fear that our mad rush to complete adoption of the hodgepodge of currently available EMR systems may have unforeseen and unintended consequences. A skeptical look at several unresolved issues is warranted.

For a contrasting view

SO FAR, ELECTRONIC SYSTEMS ARE NOT INTERCONNECTABLE

More than 300 EMR systems are available, but only about two dozen account for most systems in use.¹ So far, these systems are not interconnectable, ie, they are unable to share information, so patients seen by different physicians may still have a fragmented electronic record.

EMRs can also be inefficient to use. Many systems require logging on to a separate, password-protected system to view images. These problems are likely to go away over time with Internet-based solutions under development by Google and others, but the current lack of interconnectivity leaves much to be desired.

ELECTRONIC RECORDS ARE AT RISK

EMRs are at considerable security risk. About 13% of medical offices in the United States are using some form of EMR.² A 1995 Harris poll revealed that 70% of Americans were concerned about the security of EMR systems.³ In 2007, the New York Times reported that more than 250,000 patients each year are victims of medical identity theft.⁴ A New Zealand survey revealed that 73.3% of patients were “highly concerned” about security and privacy.⁵ Even more troubling to physicians is the reported 13% incidence of patients withholding medical information because of security concerns. Furthermore, multiple breaches of electronic records have already been reported, including an extensive breach of the Veterans Administration system.⁶

DO ELECTRONIC RECORDS IMPROVE OR WORSEN THE QUALITY OF CAR E?

Proponents have repeatedly touted that EMRs improve the quality of medical care, and these claims have been used to accelerate the adoption of the EMR. The contention that EMRs improve the accuracy of billing, coding, and administrative functions is supported by considerable data; however, the evidence of the effect of EMRs on quality of care is mixed, with some information suggesting quality may not improve.

In an analysis of 750,000 patient records for a 2-year period as part of the National Ambulatory Care Survey, Linder et al⁷ found that the EMR was superior in one quality area, worse in another area, and the same as paper-based records in 14 other areas. They pointed out that previous studies showing improved outcomes were mainly from large institutions with internally developed EMR systems, and that outcomes reported from these “benchmark” institutions may not be broadly applicable.⁷ Linder et al concluded that use of electronic records “was generally not associated with improved quality of ambulatory care,”⁷ and that increased use of EMRs does not imply an automatic improvement in quality of care.⁷

Crosson et al⁸ evaluated diabetes care in a cross-sectional analysis of 50 ambulatory care practices from 2003 and 2004 and reported that “after controlling for potential practice- and patient-level confounders and for the clustering of patients within practices, patients with diabetes in practices that did not have an EMR were significantly more likely to have received care that met the guidelines for processes of care, treatment, and intermediate outcomes.”⁸

The Palo Alto Medical Foundation reported on the sources and types of discrepancies between EMR-listed medications and actual patient medications and found that 79.8% of the time the errors were generated by the EMR system.⁹ And an outpatient study that videotaped medical encounters to evaluate the accuracy of EMR in an area in which accuracy would be expected (medication lists) found that fewer than one-fifth of exchanges “ended with clear conclusions by both parties regarding prescribed medication regimens.”¹⁰ Never mind the lingering questions regarding our ability to define quality: these data provide at least some cause for concern and caution in our rush to adopt innovation in health care without proper consideration of the possible unintended consequences.

WHAT EFFECT ON MEDICAL EDUCATION?

Almost no information is available on the effects of the EMR on the process of medical student education. One could postulate and hope that embedded diagnostic algorithms and drug interaction software would facilitate the education process.

In a paper in Academic Psychiatry, Keenan et al noted that research on EMRs for education is in its infancy.¹¹ A 2008 study of the effects of EMR on third-year medical students’ clinical experience found that students reported significant concerns about the potential impact of EMRs on their ability to conduct the doctor-patient encounter.¹² Furthermore, 48% reported spending less time with patients face to face because of the EMR, and 34% reported less time talking to patients.¹² In today’s world of off-site rotations and with nearly two dozen EMR systems in outpatient use alone, it is likely that a considerable amount of medical students’ time and effort is expended learning how to use different systems, which may detract from their actual medical experience.

Lastly, a survey of Canadian and US medical schools¹³ found that only 44% of schools had a policy regarding medical students’ documentation of progress notes in the EMR during ambulatory internal medicine clerkships. In an era when the medical student has been relegated to an observer in the education process, ¹⁴ the EMR has introduced yet another poorly understood variable in student education, which clearly begs for a thorough evaluation as the use of EMRs becomes more widespread. How can we maximize rather than dilute student education through the vehicle of electronic records?

ACCURACY VS COPYING AND PASTING

A recent Veterans Adminstration study found that 99% of progress notes in EMRs that were examined contained copied or duplicated text.¹⁵ Ten percent of 98,753 examined records contained an instance of what was considered “high-risk copying.” Weir et al¹⁶ manually reviewed a set of 60 inpatient charts at the Salt Lake City VA Health Care System and found an average of one factual error introduced into the electronic record per episode of copying.¹⁶ The clinical accuracy of the EMR is therefore questionable. Physicians pressed for time are more likely to introduce errors in the EMR, and the information put into the EMR is unlikely to be questioned—and may well be perpetuated by copy-and-paste methodology.

A THIRD PARTY IN THE EXAMINATION ROOM

Considerable information is available about the effect of the EMR on doctor-patient interaction. Margalit et al¹⁷ studied videotapes of physician encounters and noted that physicians spent an average of 25% (in some cases as much as 42%) of each visit gazing at the computer screen. They also noted that screengazing seemed to be particularly disruptive to psychological and emotional exchange.

Ventres et al¹⁸ reported that in the examination room the EMR is “much like a third party to a conversation”¹⁸ and contended that the widespread use of EMRs would have intended and unintended consquences on the cognitive and social dimensions of the physician-patient encounter. They concluded that these issues demand thoughtful consideration as the use of the EMR proliferates, “not only to forestall problems but to maximize the effectiveness of this burgeoning medical technology.”¹⁸

DEVOID OF REAL MEDICAL THOUGHT

Notwithstanding data errors and the cutting and pasting of prior notes in the EMR, we still know very little about how the EMR affects how doctors express their thoughts and communicate with one another. My particular concern is with menu-driven or templatedriven notes: they produce reams of important data, and they help ensure that coding requirements are met. But this way of writing notes about a patient is devoid of real medical thought. To describe a patient in templatedriven fashion as “an 88-year-old white male” pales next to a personalized description such as “an 88-year-old World War II B-17 bomber pilot shot down three times over Europe.”

A colleague of mine recently lamented, “I can no longer make use of my partners’ templated notes, as they convey no real information.” I do believe we should be concerned about the undesirable effects that such changes in record-keeping may produce.

LET’S CHECK THE WATER BEFORE DIVING IN

What should we do as we face these issues?

First, we should be aware that governmental and financial pressures and the availability of new technology are pushing us rapidly into new, poorly understood territory. This awareness is critical, as it at least permits a more open mind and allows the potential for honest dialogue, rather than just following directives from above.

Second, we should recognize the gaps in our understanding of the overall effects of the EMR on medicine as a profession and begin to more critically study these effects: ie, we need to be proactive rather than reactive. Denying that we lack answers to key questions about EMRs is clearly counterproductive.

We live in the electronic age. EMRs will continue to proliferate, and they have the potential to be cost-effective, care-enhancing, and time-saving. Obviously, there is no turning back the clock. However, the issues I have raised here—and other issues such as additional physician time,¹ potential “billing creep,” and the opportunity for outright fraud (rarely discussed in physician circles), not to mention cost—are deeply concerning and worthy of notice and careful consideration.

My thoughts here are meant to serve as a call to reassess the possible unintended consequences of the federally mandated rush toward an as-yet poorly integrated system of EMRs. Perhaps we should check the water first, lest we find we are diving into a shallow pool.

The rush to adopt the electronic medical record (EMR) has accelerated since the signing of the Health Information Technology for Economic and Clinical Health (HITECH) Act, part of the American Recovery and Reinvestment (ie, the Stimulus) Act of 2009. The HITECH Act provides incentives for physicians to adopt EMRs. However, I fear that our mad rush to complete adoption of the hodgepodge of currently available EMR systems may have unforeseen and unintended consequences. A skeptical look at several unresolved issues is warranted.

For a contrasting view

SO FAR, ELECTRONIC SYSTEMS ARE NOT INTERCONNECTABLE

More than 300 EMR systems are available, but only about two dozen account for most systems in use.¹ So far, these systems are not interconnectable, ie, they are unable to share information, so patients seen by different physicians may still have a fragmented electronic record.

EMRs can also be inefficient to use. Many systems require logging on to a separate, password-protected system to view images. These problems are likely to go away over time with Internet-based solutions under development by Google and others, but the current lack of interconnectivity leaves much to be desired.

ELECTRONIC RECORDS ARE AT RISK

EMRs are at considerable security risk. About 13% of medical offices in the United States are using some form of EMR.² A 1995 Harris poll revealed that 70% of Americans were concerned about the security of EMR systems.³ In 2007, the New York Times reported that more than 250,000 patients each year are victims of medical identity theft.⁴ A New Zealand survey revealed that 73.3% of patients were “highly concerned” about security and privacy.⁵ Even more troubling to physicians is the reported 13% incidence of patients withholding medical information because of security concerns. Furthermore, multiple breaches of electronic records have already been reported, including an extensive breach of the Veterans Administration system.⁶

DO ELECTRONIC RECORDS IMPROVE OR WORSEN THE QUALITY OF CAR E?

Proponents have repeatedly touted that EMRs improve the quality of medical care, and these claims have been used to accelerate the adoption of the EMR. The contention that EMRs improve the accuracy of billing, coding, and administrative functions is supported by considerable data; however, the evidence of the effect of EMRs on quality of care is mixed, with some information suggesting quality may not improve.

In an analysis of 750,000 patient records for a 2-year period as part of the National Ambulatory Care Survey, Linder et al⁷ found that the EMR was superior in one quality area, worse in another area, and the same as paper-based records in 14 other areas. They pointed out that previous studies showing improved outcomes were mainly from large institutions with internally developed EMR systems, and that outcomes reported from these “benchmark” institutions may not be broadly applicable.⁷ Linder et al concluded that use of electronic records “was generally not associated with improved quality of ambulatory care,”⁷ and that increased use of EMRs does not imply an automatic improvement in quality of care.⁷

Crosson et al⁸ evaluated diabetes care in a cross-sectional analysis of 50 ambulatory care practices from 2003 and 2004 and reported that “after controlling for potential practice- and patient-level confounders and for the clustering of patients within practices, patients with diabetes in practices that did not have an EMR were significantly more likely to have received care that met the guidelines for processes of care, treatment, and intermediate outcomes.”⁸

The Palo Alto Medical Foundation reported on the sources and types of discrepancies between EMR-listed medications and actual patient medications and found that 79.8% of the time the errors were generated by the EMR system.⁹ And an outpatient study that videotaped medical encounters to evaluate the accuracy of EMR in an area in which accuracy would be expected (medication lists) found that fewer than one-fifth of exchanges “ended with clear conclusions by both parties regarding prescribed medication regimens.”¹⁰ Never mind the lingering questions regarding our ability to define quality: these data provide at least some cause for concern and caution in our rush to adopt innovation in health care without proper consideration of the possible unintended consequences.

WHAT EFFECT ON MEDICAL EDUCATION?

Almost no information is available on the effects of the EMR on the process of medical student education. One could postulate and hope that embedded diagnostic algorithms and drug interaction software would facilitate the education process.

In a paper in Academic Psychiatry, Keenan et al noted that research on EMRs for education is in its infancy.¹¹ A 2008 study of the effects of EMR on third-year medical students’ clinical experience found that students reported significant concerns about the potential impact of EMRs on their ability to conduct the doctor-patient encounter.¹² Furthermore, 48% reported spending less time with patients face to face because of the EMR, and 34% reported less time talking to patients.¹² In today’s world of off-site rotations and with nearly two dozen EMR systems in outpatient use alone, it is likely that a considerable amount of medical students’ time and effort is expended learning how to use different systems, which may detract from their actual medical experience.

Lastly, a survey of Canadian and US medical schools¹³ found that only 44% of schools had a policy regarding medical students’ documentation of progress notes in the EMR during ambulatory internal medicine clerkships. In an era when the medical student has been relegated to an observer in the education process, ¹⁴ the EMR has introduced yet another poorly understood variable in student education, which clearly begs for a thorough evaluation as the use of EMRs becomes more widespread. How can we maximize rather than dilute student education through the vehicle of electronic records?

ACCURACY VS COPYING AND PASTING

A recent Veterans Adminstration study found that 99% of progress notes in EMRs that were examined contained copied or duplicated text.¹⁵ Ten percent of 98,753 examined records contained an instance of what was considered “high-risk copying.” Weir et al¹⁶ manually reviewed a set of 60 inpatient charts at the Salt Lake City VA Health Care System and found an average of one factual error introduced into the electronic record per episode of copying.¹⁶ The clinical accuracy of the EMR is therefore questionable. Physicians pressed for time are more likely to introduce errors in the EMR, and the information put into the EMR is unlikely to be questioned—and may well be perpetuated by copy-and-paste methodology.

A THIRD PARTY IN THE EXAMINATION ROOM

Considerable information is available about the effect of the EMR on doctor-patient interaction. Margalit et al¹⁷ studied videotapes of physician encounters and noted that physicians spent an average of 25% (in some cases as much as 42%) of each visit gazing at the computer screen. They also noted that screengazing seemed to be particularly disruptive to psychological and emotional exchange.

Ventres et al¹⁸ reported that in the examination room the EMR is “much like a third party to a conversation”¹⁸ and contended that the widespread use of EMRs would have intended and unintended consquences on the cognitive and social dimensions of the physician-patient encounter. They concluded that these issues demand thoughtful consideration as the use of the EMR proliferates, “not only to forestall problems but to maximize the effectiveness of this burgeoning medical technology.”¹⁸

DEVOID OF REAL MEDICAL THOUGHT

Notwithstanding data errors and the cutting and pasting of prior notes in the EMR, we still know very little about how the EMR affects how doctors express their thoughts and communicate with one another. My particular concern is with menu-driven or templatedriven notes: they produce reams of important data, and they help ensure that coding requirements are met. But this way of writing notes about a patient is devoid of real medical thought. To describe a patient in templatedriven fashion as “an 88-year-old white male” pales next to a personalized description such as “an 88-year-old World War II B-17 bomber pilot shot down three times over Europe.”

A colleague of mine recently lamented, “I can no longer make use of my partners’ templated notes, as they convey no real information.” I do believe we should be concerned about the undesirable effects that such changes in record-keeping may produce.

LET’S CHECK THE WATER BEFORE DIVING IN

What should we do as we face these issues?

First, we should be aware that governmental and financial pressures and the availability of new technology are pushing us rapidly into new, poorly understood territory. This awareness is critical, as it at least permits a more open mind and allows the potential for honest dialogue, rather than just following directives from above.

Second, we should recognize the gaps in our understanding of the overall effects of the EMR on medicine as a profession and begin to more critically study these effects: ie, we need to be proactive rather than reactive. Denying that we lack answers to key questions about EMRs is clearly counterproductive.

We live in the electronic age. EMRs will continue to proliferate, and they have the potential to be cost-effective, care-enhancing, and time-saving. Obviously, there is no turning back the clock. However, the issues I have raised here—and other issues such as additional physician time,¹ potential “billing creep,” and the opportunity for outright fraud (rarely discussed in physician circles), not to mention cost—are deeply concerning and worthy of notice and careful consideration.

My thoughts here are meant to serve as a call to reassess the possible unintended consequences of the federally mandated rush toward an as-yet poorly integrated system of EMRs. Perhaps we should check the water first, lest we find we are diving into a shallow pool.

The rush to adopt the electronic medical record (EMR) has accelerated since the signing of the Health Information Technology for Economic and Clinical Health (HITECH) Act, part of the American Recovery and Reinvestment (ie, the Stimulus) Act of 2009. The HITECH Act provides incentives for physicians to adopt EMRs. However, I fear that our mad rush to complete adoption of the hodgepodge of currently available EMR systems may have unforeseen and unintended consequences. A skeptical look at several unresolved issues is warranted.

For a contrasting view

SO FAR, ELECTRONIC SYSTEMS ARE NOT INTERCONNECTABLE

More than 300 EMR systems are available, but only about two dozen account for most systems in use.¹ So far, these systems are not interconnectable, ie, they are unable to share information, so patients seen by different physicians may still have a fragmented electronic record.

EMRs can also be inefficient to use. Many systems require logging on to a separate, password-protected system to view images. These problems are likely to go away over time with Internet-based solutions under development by Google and others, but the current lack of interconnectivity leaves much to be desired.

ELECTRONIC RECORDS ARE AT RISK

EMRs are at considerable security risk. About 13% of medical offices in the United States are using some form of EMR.² A 1995 Harris poll revealed that 70% of Americans were concerned about the security of EMR systems.³ In 2007, the New York Times reported that more than 250,000 patients each year are victims of medical identity theft.⁴ A New Zealand survey revealed that 73.3% of patients were “highly concerned” about security and privacy.⁵ Even more troubling to physicians is the reported 13% incidence of patients withholding medical information because of security concerns. Furthermore, multiple breaches of electronic records have already been reported, including an extensive breach of the Veterans Administration system.⁶

DO ELECTRONIC RECORDS IMPROVE OR WORSEN THE QUALITY OF CAR E?

Proponents have repeatedly touted that EMRs improve the quality of medical care, and these claims have been used to accelerate the adoption of the EMR. The contention that EMRs improve the accuracy of billing, coding, and administrative functions is supported by considerable data; however, the evidence of the effect of EMRs on quality of care is mixed, with some information suggesting quality may not improve.

In an analysis of 750,000 patient records for a 2-year period as part of the National Ambulatory Care Survey, Linder et al⁷ found that the EMR was superior in one quality area, worse in another area, and the same as paper-based records in 14 other areas. They pointed out that previous studies showing improved outcomes were mainly from large institutions with internally developed EMR systems, and that outcomes reported from these “benchmark” institutions may not be broadly applicable.⁷ Linder et al concluded that use of electronic records “was generally not associated with improved quality of ambulatory care,”⁷ and that increased use of EMRs does not imply an automatic improvement in quality of care.⁷

Crosson et al⁸ evaluated diabetes care in a cross-sectional analysis of 50 ambulatory care practices from 2003 and 2004 and reported that “after controlling for potential practice- and patient-level confounders and for the clustering of patients within practices, patients with diabetes in practices that did not have an EMR were significantly more likely to have received care that met the guidelines for processes of care, treatment, and intermediate outcomes.”⁸

The Palo Alto Medical Foundation reported on the sources and types of discrepancies between EMR-listed medications and actual patient medications and found that 79.8% of the time the errors were generated by the EMR system.⁹ And an outpatient study that videotaped medical encounters to evaluate the accuracy of EMR in an area in which accuracy would be expected (medication lists) found that fewer than one-fifth of exchanges “ended with clear conclusions by both parties regarding prescribed medication regimens.”¹⁰ Never mind the lingering questions regarding our ability to define quality: these data provide at least some cause for concern and caution in our rush to adopt innovation in health care without proper consideration of the possible unintended consequences.

WHAT EFFECT ON MEDICAL EDUCATION?

Almost no information is available on the effects of the EMR on the process of medical student education. One could postulate and hope that embedded diagnostic algorithms and drug interaction software would facilitate the education process.

In a paper in Academic Psychiatry, Keenan et al noted that research on EMRs for education is in its infancy.¹¹ A 2008 study of the effects of EMR on third-year medical students’ clinical experience found that students reported significant concerns about the potential impact of EMRs on their ability to conduct the doctor-patient encounter.¹² Furthermore, 48% reported spending less time with patients face to face because of the EMR, and 34% reported less time talking to patients.¹² In today’s world of off-site rotations and with nearly two dozen EMR systems in outpatient use alone, it is likely that a considerable amount of medical students’ time and effort is expended learning how to use different systems, which may detract from their actual medical experience.

Lastly, a survey of Canadian and US medical schools¹³ found that only 44% of schools had a policy regarding medical students’ documentation of progress notes in the EMR during ambulatory internal medicine clerkships. In an era when the medical student has been relegated to an observer in the education process, ¹⁴ the EMR has introduced yet another poorly understood variable in student education, which clearly begs for a thorough evaluation as the use of EMRs becomes more widespread. How can we maximize rather than dilute student education through the vehicle of electronic records?

ACCURACY VS COPYING AND PASTING

A recent Veterans Adminstration study found that 99% of progress notes in EMRs that were examined contained copied or duplicated text.¹⁵ Ten percent of 98,753 examined records contained an instance of what was considered “high-risk copying.” Weir et al¹⁶ manually reviewed a set of 60 inpatient charts at the Salt Lake City VA Health Care System and found an average of one factual error introduced into the electronic record per episode of copying.¹⁶ The clinical accuracy of the EMR is therefore questionable. Physicians pressed for time are more likely to introduce errors in the EMR, and the information put into the EMR is unlikely to be questioned—and may well be perpetuated by copy-and-paste methodology.

A THIRD PARTY IN THE EXAMINATION ROOM

Considerable information is available about the effect of the EMR on doctor-patient interaction. Margalit et al¹⁷ studied videotapes of physician encounters and noted that physicians spent an average of 25% (in some cases as much as 42%) of each visit gazing at the computer screen. They also noted that screengazing seemed to be particularly disruptive to psychological and emotional exchange.

Ventres et al¹⁸ reported that in the examination room the EMR is “much like a third party to a conversation”¹⁸ and contended that the widespread use of EMRs would have intended and unintended consquences on the cognitive and social dimensions of the physician-patient encounter. They concluded that these issues demand thoughtful consideration as the use of the EMR proliferates, “not only to forestall problems but to maximize the effectiveness of this burgeoning medical technology.”¹⁸

DEVOID OF REAL MEDICAL THOUGHT

Notwithstanding data errors and the cutting and pasting of prior notes in the EMR, we still know very little about how the EMR affects how doctors express their thoughts and communicate with one another. My particular concern is with menu-driven or templatedriven notes: they produce reams of important data, and they help ensure that coding requirements are met. But this way of writing notes about a patient is devoid of real medical thought. To describe a patient in templatedriven fashion as “an 88-year-old white male” pales next to a personalized description such as “an 88-year-old World War II B-17 bomber pilot shot down three times over Europe.”

A colleague of mine recently lamented, “I can no longer make use of my partners’ templated notes, as they convey no real information.” I do believe we should be concerned about the undesirable effects that such changes in record-keeping may produce.

LET’S CHECK THE WATER BEFORE DIVING IN

What should we do as we face these issues?

First, we should be aware that governmental and financial pressures and the availability of new technology are pushing us rapidly into new, poorly understood territory. This awareness is critical, as it at least permits a more open mind and allows the potential for honest dialogue, rather than just following directives from above.

Second, we should recognize the gaps in our understanding of the overall effects of the EMR on medicine as a profession and begin to more critically study these effects: ie, we need to be proactive rather than reactive. Denying that we lack answers to key questions about EMRs is clearly counterproductive.

We live in the electronic age. EMRs will continue to proliferate, and they have the potential to be cost-effective, care-enhancing, and time-saving. Obviously, there is no turning back the clock. However, the issues I have raised here—and other issues such as additional physician time,¹ potential “billing creep,” and the opportunity for outright fraud (rarely discussed in physician circles), not to mention cost—are deeply concerning and worthy of notice and careful consideration.

My thoughts here are meant to serve as a call to reassess the possible unintended consequences of the federally mandated rush toward an as-yet poorly integrated system of EMRs. Perhaps we should check the water first, lest we find we are diving into a shallow pool.

While waiting to cross a street, a 30-year-old woman was suddenly struck by an oncoming vehicle, which crushed her legs against a parked automobile. She sustained a life-threatening traumatic injury and nearly exsanguinated at the scene. Nearby pedestrians assisted her, including a man who applied his belt to the woman’s left thigh to prevent complete exsanguination following the crush. She was emergently transported to an adult regional trauma center and admitted to the ICU.

The patient was given multiple transfusions of packed red blood cells, platelets, and frozen plasma in attempts to restore hemostasis. She underwent emergent surgery for a complete washout, debridement, and compartment fasciotomy on the right leg. The left leg required an above-knee amputation. Following surgery, full-thickness and split-thickness wounds were present on both extremities.

Before the accident, the woman had a history of hypertension controlled with a single antihypertensive. She was obese, with a BMI of 31.9. She had no surgical history. She denied excessive alcohol consumption, illicit drug use, or smoking. She was unaware of having any food or drug allergies.

The woman was married and had a 6-month-old baby. Until her accident, she was employed full-time as an investment accountant. She expressed contentment regarding her home, family, work, and busy lifestyle.

Once the patient’s condition was stabilized and hemostasis achieved in the trauma ICU, the bilateral lower-extremity wounds were managed by application of foam dressings via negative-pressure therapy. The dressings were changed on the patient’s lower-extremity wounds three times per week for about three weeks. When the wounds’ depth decreased and granulation was achieved, split-thickness skin grafts (STSGs) harvested from the right anterior thigh were applied to the open wounds (see Figure 1) in the operating room.

Following application of the STSGs and hemostasis of the patient’s donor site, silver silicone foam dressings were applied directly over the right lower-extremity graft and the donor site in the operating room. The dressings remained in place for four days (see Figure 2). A nonadherent, petrolatum-based contact layer was then applied to the left lower-extremity amputation graft site, followed by a negative-pressure foam dressing.

The negative-pressure pump was programmed for 75 mm Hg continuous therapy for four days. The silver silicone foam and negative-pressure foam dressings were removed from the respective graft sites on the fourth postpostoperative day. The grafts were viable and intact (see Figures 3 and 4). The silver silicone foam was reapplied to the lower-extremity STSGs and donor site and changed every four days.

When a few pinpoint dehisced areas were noted on the grafts, a silver-coated absorbent antimicrobial dressing was applied. A nonadherent, petrolatum-based contact layer, followed by wide-mesh stretch gauze, was secured as an exterior dressing over the graft sites. Both lower-extremity dressings were layered with elastic wraps to prevent edema. The dressings were changed daily for two weeks.

On postoperative Day 4, the silver silicone foam was removed from the donor site. A nonadherent contact layer of bismuth tribromophenate petrolatum, followed by the silver silicone foam, was selected for placement over the donor site. Gauze and an elastic wrap were secured as an exterior dressing and removed three days later.

The donor site dressing was reduced to a layer of bismuth tribromophenate petrolatum and left open to air. As the edges of the nonadherent contact layer dried, they were trimmed with scissors (see Figure 5). A moisturizing cocoa butter–based lotion was applied daily to the exposed areas of the donor site.

During the patient’s third postoperative week at the trauma center, as she underwent a continuum of aggressive rehabilitation and wound care, the donor and STSG sites were pronounced healed (see Figures 6, 7, and 8). The donor site was left open to air, with daily use of cocoa butter lotion. Maintenance care of the graft sites included daily application of cocoa butter lotion, stretch gauze, and elastic wraps. The patient was discharged from the rehabilitation unit to home, where she awaited a prosthetic fitting.

Throughout the patient’s hospitalization and rehabilitation, surgical, medical, pain, and nutrition management were monitored on a continuum, as were laboratory values. Her vital signs remained within reasonable limits. The patient remained infection free and experienced neither medical nor surgical complications during the course of her hospital stay.

DISCUSSION
Traumatic injuries often result in bodily deformities, amputations, and death. They represent the leading cause of death among people in the US younger than 45.^1,2

Compartment syndrome develops when increased pressure within a bodily cavity minimizes capillary perfusion, resulting in decreased tissue viability.³ Edema and hemorrhage are also precipitating factors for this condition.³ When it goes unrelieved, compromised circulation can lead to muscle devitalization. Amputation of the affected appendage may be necessary unless circulation is restored.

Surgical fasciotomy can help alleviate pressure within the musculofascial compartment to improve circulation.⁴ Typically, such a procedure leaves large open wounds—a challenge for the clinician who cares for the affected patient. Once the wound is stabilized and the tissue becomes viable with granulation, application of an STSG can be considered.^5,6

STSGs provide effective closure for open wounds. The grafting procedure entails removing, processing, and placing a portion of skin, both epidermal and partial dermal layers, on an open wound. Successful grafting requires adequate circulation, but excess bacteria can impede graft viability.⁷ Graft sites must be kept clean and moist without edema.⁵ Immediate application of negative-pressure therapy directly on an STSG has been shown to result in an outstanding graft “take,” as compared with use of traditional dressings.^5,6,8

Nutritional status must be optimal for a successful graft take, with adequate intake of protein, calories, fluids, vitamins, and minerals.^9,10

Treatment
Since days of old when traumatic wounds were treated with goat dung and honey, an array of methods and products has been developed, including numerous agents for cutaneous injuries alone.⁴ Occlusive, semiocclusive, or bacteriostatic topical ointments, foam, silver, or a combination of products can be used to manage and heal surgical wounds, grafts (including STSGs), and donor sites.^11,12

Currently, negative pressure is also used in STSGs to accelerate healing.^7,11 When applied to a wound, negative-pressure therapy enhances granulation, removes excess exudate, and creates a moist environment for healing.^5,13

Silver-coated absorbent antimicrobial dressings appear to reduce bacteria on the surface of the wound surfaces and postoperative surgical sites without inducing bacterial resistance or adversely affecting healthy tissue.^12,14-16 Silver silicone foam reduces bacterial colonization on wound surfaces and absorbs exudate into the foam dressing.^17,18 Wounds with devitalized tissue and excessive drainage are at risk for infection, inflammation, and chronic duration.¹⁹

Nutrition
It has been reported that about half of all persons admitted to US hospitals are malnourished, with increased risk for morbidity and mortality.²⁰ After experiencing hemorrhage, even well-nourished patients require additional protein and iron for successful recovery.¹⁰ Obese patients appear more susceptible to infection and surgical wound dehiscence than are their thinner counterparts, but further research is needed to study the impact of wound development and healing in this population.¹⁴

Tissue regeneration is known to require the amino acids arginine and glutamine for the construction of protein; additional research is also needed to support the theory that supplemental glutamine promotes wound healing.^9,21 Surgical patients and patients with wounds benefit from protein-enhanced diets; zinc and vitamins A and C can also help improve wound healing and clinical outcomes.²² Monitoring protein and prealbumin levels is helpful in evaluating nutritional status, allowing the clinician to modify the medical nutrition plan and optimize the patient’s health and wellness.²²

Rehabilitation
Surgical amputations of the lower extremities impair balance and mobility, necessitating extensive physical therapy and rehabilitation for affected patients.^23,24 Aggressive rehabilitation typically is exhausting for patients. It is important to initiate a supportive team approach (including physical and occupational therapists) soon after surgery, continuing beyond the acute hospitalization into rehabilitation. Individualized, patient-centered goals are targeted and amended as necessary. Physical and occupational therapy increase in intensity and duration to optimize the patient’s functionality. Prosthetic fitting takes place after edema diminishes and the limb is fully healed.²⁴

Patient Outcome
An obese young woman who sustained traumatic lower-extremity injuries and amputation experienced an optimal clinical outcome after 54 days of management. Exceptional surgical and medical strategies were initiated in the adult regional trauma center’s ICU and concluded at the adjoining rehabilitation center.

Strategic selection of products and interventions—negative pressure, silver silicone foam, silver-coated absorbent antimicrobial dressings, nonadherent contact layers, stretch gauze, and elastic wraps—and constant monitoring, including that of the patient’s nutritional status, resulted in expedient resolution of her traumatic wounds, STSGs, and donor site.

CONCLUSION
Despite revolutionary advances and life-sustaining measures in the surgical, medical, and wound care arena, traumatic events remain potentially debilitating and life-threatening for young adults. Triage of the trauma patient for appropriate medical care and collaborative management involving a team of trauma specialists and clinicians of all disciplines can now provide life-sustaining opportunities for these patients.

While waiting to cross a street, a 30-year-old woman was suddenly struck by an oncoming vehicle, which crushed her legs against a parked automobile. She sustained a life-threatening traumatic injury and nearly exsanguinated at the scene. Nearby pedestrians assisted her, including a man who applied his belt to the woman’s left thigh to prevent complete exsanguination following the crush. She was emergently transported to an adult regional trauma center and admitted to the ICU.

The patient was given multiple transfusions of packed red blood cells, platelets, and frozen plasma in attempts to restore hemostasis. She underwent emergent surgery for a complete washout, debridement, and compartment fasciotomy on the right leg. The left leg required an above-knee amputation. Following surgery, full-thickness and split-thickness wounds were present on both extremities.

Before the accident, the woman had a history of hypertension controlled with a single antihypertensive. She was obese, with a BMI of 31.9. She had no surgical history. She denied excessive alcohol consumption, illicit drug use, or smoking. She was unaware of having any food or drug allergies.

The woman was married and had a 6-month-old baby. Until her accident, she was employed full-time as an investment accountant. She expressed contentment regarding her home, family, work, and busy lifestyle.

Once the patient’s condition was stabilized and hemostasis achieved in the trauma ICU, the bilateral lower-extremity wounds were managed by application of foam dressings via negative-pressure therapy. The dressings were changed on the patient’s lower-extremity wounds three times per week for about three weeks. When the wounds’ depth decreased and granulation was achieved, split-thickness skin grafts (STSGs) harvested from the right anterior thigh were applied to the open wounds (see Figure 1) in the operating room.

Following application of the STSGs and hemostasis of the patient’s donor site, silver silicone foam dressings were applied directly over the right lower-extremity graft and the donor site in the operating room. The dressings remained in place for four days (see Figure 2). A nonadherent, petrolatum-based contact layer was then applied to the left lower-extremity amputation graft site, followed by a negative-pressure foam dressing.

The negative-pressure pump was programmed for 75 mm Hg continuous therapy for four days. The silver silicone foam and negative-pressure foam dressings were removed from the respective graft sites on the fourth postpostoperative day. The grafts were viable and intact (see Figures 3 and 4). The silver silicone foam was reapplied to the lower-extremity STSGs and donor site and changed every four days.

When a few pinpoint dehisced areas were noted on the grafts, a silver-coated absorbent antimicrobial dressing was applied. A nonadherent, petrolatum-based contact layer, followed by wide-mesh stretch gauze, was secured as an exterior dressing over the graft sites. Both lower-extremity dressings were layered with elastic wraps to prevent edema. The dressings were changed daily for two weeks.

On postoperative Day 4, the silver silicone foam was removed from the donor site. A nonadherent contact layer of bismuth tribromophenate petrolatum, followed by the silver silicone foam, was selected for placement over the donor site. Gauze and an elastic wrap were secured as an exterior dressing and removed three days later.

The donor site dressing was reduced to a layer of bismuth tribromophenate petrolatum and left open to air. As the edges of the nonadherent contact layer dried, they were trimmed with scissors (see Figure 5). A moisturizing cocoa butter–based lotion was applied daily to the exposed areas of the donor site.

During the patient’s third postoperative week at the trauma center, as she underwent a continuum of aggressive rehabilitation and wound care, the donor and STSG sites were pronounced healed (see Figures 6, 7, and 8). The donor site was left open to air, with daily use of cocoa butter lotion. Maintenance care of the graft sites included daily application of cocoa butter lotion, stretch gauze, and elastic wraps. The patient was discharged from the rehabilitation unit to home, where she awaited a prosthetic fitting.

Throughout the patient’s hospitalization and rehabilitation, surgical, medical, pain, and nutrition management were monitored on a continuum, as were laboratory values. Her vital signs remained within reasonable limits. The patient remained infection free and experienced neither medical nor surgical complications during the course of her hospital stay.

DISCUSSION
Traumatic injuries often result in bodily deformities, amputations, and death. They represent the leading cause of death among people in the US younger than 45.^1,2

Compartment syndrome develops when increased pressure within a bodily cavity minimizes capillary perfusion, resulting in decreased tissue viability.³ Edema and hemorrhage are also precipitating factors for this condition.³ When it goes unrelieved, compromised circulation can lead to muscle devitalization. Amputation of the affected appendage may be necessary unless circulation is restored.

Surgical fasciotomy can help alleviate pressure within the musculofascial compartment to improve circulation.⁴ Typically, such a procedure leaves large open wounds—a challenge for the clinician who cares for the affected patient. Once the wound is stabilized and the tissue becomes viable with granulation, application of an STSG can be considered.^5,6

STSGs provide effective closure for open wounds. The grafting procedure entails removing, processing, and placing a portion of skin, both epidermal and partial dermal layers, on an open wound. Successful grafting requires adequate circulation, but excess bacteria can impede graft viability.⁷ Graft sites must be kept clean and moist without edema.⁵ Immediate application of negative-pressure therapy directly on an STSG has been shown to result in an outstanding graft “take,” as compared with use of traditional dressings.^5,6,8

Nutritional status must be optimal for a successful graft take, with adequate intake of protein, calories, fluids, vitamins, and minerals.^9,10

Treatment
Since days of old when traumatic wounds were treated with goat dung and honey, an array of methods and products has been developed, including numerous agents for cutaneous injuries alone.⁴ Occlusive, semiocclusive, or bacteriostatic topical ointments, foam, silver, or a combination of products can be used to manage and heal surgical wounds, grafts (including STSGs), and donor sites.^11,12

Currently, negative pressure is also used in STSGs to accelerate healing.^7,11 When applied to a wound, negative-pressure therapy enhances granulation, removes excess exudate, and creates a moist environment for healing.^5,13

Silver-coated absorbent antimicrobial dressings appear to reduce bacteria on the surface of the wound surfaces and postoperative surgical sites without inducing bacterial resistance or adversely affecting healthy tissue.^12,14-16 Silver silicone foam reduces bacterial colonization on wound surfaces and absorbs exudate into the foam dressing.^17,18 Wounds with devitalized tissue and excessive drainage are at risk for infection, inflammation, and chronic duration.¹⁹

Nutrition
It has been reported that about half of all persons admitted to US hospitals are malnourished, with increased risk for morbidity and mortality.²⁰ After experiencing hemorrhage, even well-nourished patients require additional protein and iron for successful recovery.¹⁰ Obese patients appear more susceptible to infection and surgical wound dehiscence than are their thinner counterparts, but further research is needed to study the impact of wound development and healing in this population.¹⁴

Tissue regeneration is known to require the amino acids arginine and glutamine for the construction of protein; additional research is also needed to support the theory that supplemental glutamine promotes wound healing.^9,21 Surgical patients and patients with wounds benefit from protein-enhanced diets; zinc and vitamins A and C can also help improve wound healing and clinical outcomes.²² Monitoring protein and prealbumin levels is helpful in evaluating nutritional status, allowing the clinician to modify the medical nutrition plan and optimize the patient’s health and wellness.²²

Rehabilitation
Surgical amputations of the lower extremities impair balance and mobility, necessitating extensive physical therapy and rehabilitation for affected patients.^23,24 Aggressive rehabilitation typically is exhausting for patients. It is important to initiate a supportive team approach (including physical and occupational therapists) soon after surgery, continuing beyond the acute hospitalization into rehabilitation. Individualized, patient-centered goals are targeted and amended as necessary. Physical and occupational therapy increase in intensity and duration to optimize the patient’s functionality. Prosthetic fitting takes place after edema diminishes and the limb is fully healed.²⁴

Patient Outcome
An obese young woman who sustained traumatic lower-extremity injuries and amputation experienced an optimal clinical outcome after 54 days of management. Exceptional surgical and medical strategies were initiated in the adult regional trauma center’s ICU and concluded at the adjoining rehabilitation center.

Strategic selection of products and interventions—negative pressure, silver silicone foam, silver-coated absorbent antimicrobial dressings, nonadherent contact layers, stretch gauze, and elastic wraps—and constant monitoring, including that of the patient’s nutritional status, resulted in expedient resolution of her traumatic wounds, STSGs, and donor site.

CONCLUSION
Despite revolutionary advances and life-sustaining measures in the surgical, medical, and wound care arena, traumatic events remain potentially debilitating and life-threatening for young adults. Triage of the trauma patient for appropriate medical care and collaborative management involving a team of trauma specialists and clinicians of all disciplines can now provide life-sustaining opportunities for these patients.

While waiting to cross a street, a 30-year-old woman was suddenly struck by an oncoming vehicle, which crushed her legs against a parked automobile. She sustained a life-threatening traumatic injury and nearly exsanguinated at the scene. Nearby pedestrians assisted her, including a man who applied his belt to the woman’s left thigh to prevent complete exsanguination following the crush. She was emergently transported to an adult regional trauma center and admitted to the ICU.

The patient was given multiple transfusions of packed red blood cells, platelets, and frozen plasma in attempts to restore hemostasis. She underwent emergent surgery for a complete washout, debridement, and compartment fasciotomy on the right leg. The left leg required an above-knee amputation. Following surgery, full-thickness and split-thickness wounds were present on both extremities.

Before the accident, the woman had a history of hypertension controlled with a single antihypertensive. She was obese, with a BMI of 31.9. She had no surgical history. She denied excessive alcohol consumption, illicit drug use, or smoking. She was unaware of having any food or drug allergies.

The woman was married and had a 6-month-old baby. Until her accident, she was employed full-time as an investment accountant. She expressed contentment regarding her home, family, work, and busy lifestyle.

Once the patient’s condition was stabilized and hemostasis achieved in the trauma ICU, the bilateral lower-extremity wounds were managed by application of foam dressings via negative-pressure therapy. The dressings were changed on the patient’s lower-extremity wounds three times per week for about three weeks. When the wounds’ depth decreased and granulation was achieved, split-thickness skin grafts (STSGs) harvested from the right anterior thigh were applied to the open wounds (see Figure 1) in the operating room.

Following application of the STSGs and hemostasis of the patient’s donor site, silver silicone foam dressings were applied directly over the right lower-extremity graft and the donor site in the operating room. The dressings remained in place for four days (see Figure 2). A nonadherent, petrolatum-based contact layer was then applied to the left lower-extremity amputation graft site, followed by a negative-pressure foam dressing.

The negative-pressure pump was programmed for 75 mm Hg continuous therapy for four days. The silver silicone foam and negative-pressure foam dressings were removed from the respective graft sites on the fourth postpostoperative day. The grafts were viable and intact (see Figures 3 and 4). The silver silicone foam was reapplied to the lower-extremity STSGs and donor site and changed every four days.

When a few pinpoint dehisced areas were noted on the grafts, a silver-coated absorbent antimicrobial dressing was applied. A nonadherent, petrolatum-based contact layer, followed by wide-mesh stretch gauze, was secured as an exterior dressing over the graft sites. Both lower-extremity dressings were layered with elastic wraps to prevent edema. The dressings were changed daily for two weeks.

On postoperative Day 4, the silver silicone foam was removed from the donor site. A nonadherent contact layer of bismuth tribromophenate petrolatum, followed by the silver silicone foam, was selected for placement over the donor site. Gauze and an elastic wrap were secured as an exterior dressing and removed three days later.

The donor site dressing was reduced to a layer of bismuth tribromophenate petrolatum and left open to air. As the edges of the nonadherent contact layer dried, they were trimmed with scissors (see Figure 5). A moisturizing cocoa butter–based lotion was applied daily to the exposed areas of the donor site.

During the patient’s third postoperative week at the trauma center, as she underwent a continuum of aggressive rehabilitation and wound care, the donor and STSG sites were pronounced healed (see Figures 6, 7, and 8). The donor site was left open to air, with daily use of cocoa butter lotion. Maintenance care of the graft sites included daily application of cocoa butter lotion, stretch gauze, and elastic wraps. The patient was discharged from the rehabilitation unit to home, where she awaited a prosthetic fitting.

Throughout the patient’s hospitalization and rehabilitation, surgical, medical, pain, and nutrition management were monitored on a continuum, as were laboratory values. Her vital signs remained within reasonable limits. The patient remained infection free and experienced neither medical nor surgical complications during the course of her hospital stay.

DISCUSSION
Traumatic injuries often result in bodily deformities, amputations, and death. They represent the leading cause of death among people in the US younger than 45.^1,2

Compartment syndrome develops when increased pressure within a bodily cavity minimizes capillary perfusion, resulting in decreased tissue viability.³ Edema and hemorrhage are also precipitating factors for this condition.³ When it goes unrelieved, compromised circulation can lead to muscle devitalization. Amputation of the affected appendage may be necessary unless circulation is restored.

Surgical fasciotomy can help alleviate pressure within the musculofascial compartment to improve circulation.⁴ Typically, such a procedure leaves large open wounds—a challenge for the clinician who cares for the affected patient. Once the wound is stabilized and the tissue becomes viable with granulation, application of an STSG can be considered.^5,6

STSGs provide effective closure for open wounds. The grafting procedure entails removing, processing, and placing a portion of skin, both epidermal and partial dermal layers, on an open wound. Successful grafting requires adequate circulation, but excess bacteria can impede graft viability.⁷ Graft sites must be kept clean and moist without edema.⁵ Immediate application of negative-pressure therapy directly on an STSG has been shown to result in an outstanding graft “take,” as compared with use of traditional dressings.^5,6,8

Nutritional status must be optimal for a successful graft take, with adequate intake of protein, calories, fluids, vitamins, and minerals.^9,10

Treatment
Since days of old when traumatic wounds were treated with goat dung and honey, an array of methods and products has been developed, including numerous agents for cutaneous injuries alone.⁴ Occlusive, semiocclusive, or bacteriostatic topical ointments, foam, silver, or a combination of products can be used to manage and heal surgical wounds, grafts (including STSGs), and donor sites.^11,12

Currently, negative pressure is also used in STSGs to accelerate healing.^7,11 When applied to a wound, negative-pressure therapy enhances granulation, removes excess exudate, and creates a moist environment for healing.^5,13

Silver-coated absorbent antimicrobial dressings appear to reduce bacteria on the surface of the wound surfaces and postoperative surgical sites without inducing bacterial resistance or adversely affecting healthy tissue.^12,14-16 Silver silicone foam reduces bacterial colonization on wound surfaces and absorbs exudate into the foam dressing.^17,18 Wounds with devitalized tissue and excessive drainage are at risk for infection, inflammation, and chronic duration.¹⁹

Nutrition
It has been reported that about half of all persons admitted to US hospitals are malnourished, with increased risk for morbidity and mortality.²⁰ After experiencing hemorrhage, even well-nourished patients require additional protein and iron for successful recovery.¹⁰ Obese patients appear more susceptible to infection and surgical wound dehiscence than are their thinner counterparts, but further research is needed to study the impact of wound development and healing in this population.¹⁴

Tissue regeneration is known to require the amino acids arginine and glutamine for the construction of protein; additional research is also needed to support the theory that supplemental glutamine promotes wound healing.^9,21 Surgical patients and patients with wounds benefit from protein-enhanced diets; zinc and vitamins A and C can also help improve wound healing and clinical outcomes.²² Monitoring protein and prealbumin levels is helpful in evaluating nutritional status, allowing the clinician to modify the medical nutrition plan and optimize the patient’s health and wellness.²²

Rehabilitation
Surgical amputations of the lower extremities impair balance and mobility, necessitating extensive physical therapy and rehabilitation for affected patients.^23,24 Aggressive rehabilitation typically is exhausting for patients. It is important to initiate a supportive team approach (including physical and occupational therapists) soon after surgery, continuing beyond the acute hospitalization into rehabilitation. Individualized, patient-centered goals are targeted and amended as necessary. Physical and occupational therapy increase in intensity and duration to optimize the patient’s functionality. Prosthetic fitting takes place after edema diminishes and the limb is fully healed.²⁴

Patient Outcome
An obese young woman who sustained traumatic lower-extremity injuries and amputation experienced an optimal clinical outcome after 54 days of management. Exceptional surgical and medical strategies were initiated in the adult regional trauma center’s ICU and concluded at the adjoining rehabilitation center.

Strategic selection of products and interventions—negative pressure, silver silicone foam, silver-coated absorbent antimicrobial dressings, nonadherent contact layers, stretch gauze, and elastic wraps—and constant monitoring, including that of the patient’s nutritional status, resulted in expedient resolution of her traumatic wounds, STSGs, and donor site.

CONCLUSION
Despite revolutionary advances and life-sustaining measures in the surgical, medical, and wound care arena, traumatic events remain potentially debilitating and life-threatening for young adults. Triage of the trauma patient for appropriate medical care and collaborative management involving a team of trauma specialists and clinicians of all disciplines can now provide life-sustaining opportunities for these patients.

Mrs. J, age 75, has moderate Alzheimer’s dementia and lives at home with her husband. Since her Alzheimer’s disease (AD) diagnosis 2 years ago, Mrs. J generally has been cooperative and not physically aggressive, but has experienced occasional depressive symptoms. However, Mr. J reports that recently his wife is becoming increasingly confused and agitated and wanders the house at night. His efforts to calm and coax her back to bed often lead to increased agitation and yelling. On 1 occasion Mrs. J pushed her husband. Mr. J is concerned that if these behaviors continue he may not be able to care for her at home. Mr. J read online that antipsychotics might reduce aggressive behavior, but is concerned about the increased risk of mortality and stroke with these medications.

Mrs. J receives donepezil, 10 mg/d, sertra-line, 50 mg/d, and extended-release oxybutynin, 10 mg/d. Her over-the-counter (OTC) medications include acetaminophen, 650 mg as needed for pain, ranitidine, 150 mg/d, and docusate sodium, 100 mg/d. Several nights last week, Mr. J gave his wife an unknown OTC sleep medication, hoping it would stop her nighttime wandering, but it did not help. Physical examination, laboratory testing, and urine culture are all normal.

Most dementia patients experience neuropsychiatric disturbances, especially at later stages, that often lead to caregiver distress and nursing home placement. Although these symptoms may signal progressing dementia, environmental factors, medical conditions, and medications may worsen functioning and should be considered in the assessment.¹

Mrs. J has no medical problems that were identified as possible triggers for her behavior. Mr. J’s interference with his wife’s wandering could have increased her agitation, but he is gentle toward her and she has become agitated with no apparent trigger. “Sundowning” and poor sleep also may be involved, as sleep deprivation can lead to delirium and worsen cognitive deficits and behavioral problems.¹ Depression also should be considered.¹ Finally, Mrs. J is taking several medications with anticholinergic properties—oxybutynin, ranitidine, and an unknown OTC sleep medication, which likely contains diphenhydramine or doxylamine—that might contribute to her agitation.

Patients with dementia are highly sensitive to the cognitive and psychiatric adverse effects of anticholinergic medications. In studies of patients with mild or moderate Alzheimer’s dementia who received the potent anticholinergic scopolamine, adverse effects included:

• memory impairment
• restlessness
• disjointed speech
• motor incoordination
• drowsiness
• euphoria
• agitation
• hallucinations
• hostility.

Many of these effects worsened with increasing doses.^2,3 Age-matched controls experienced less severe memory impairment and no behavioral symptoms, which suggests that dementia-related damage to the cholinergic system leads to increased sensitivity to anticholinergics.

A cross-sectional study of 230 patients with AD identified anticholinergic use as a risk factor for psychosis (odds ratio 2.13, 95% confidence interval, 1.03 to 4.43), after adjusting for age and cognition.⁴ Among patients receiving 2 or 3 anticholinergics, 69% had psychotic symptoms compared with 48% of those receiving 1 anticholinergic and 32% of those receiving no anticholinergics.⁴ Anticholinergic overdoses can cause psychotic symptoms and delirium. A subtle presentation of delirium from prescribed anticholinergics may be confused with worsening dementia.¹ The sum of the evidence suggests that drugs with anticholinergic effects can contribute to agitation and psychosis in dementia.

When to discontinue

When diagnosing dementia it is important to address other potential causes of cognitive impairment, including medications. Approximately one-third of patients with dementia receive anticholinergic drugs, which suggests that providers often do not recognize the potential for harm with these medications.⁵ After patients receive acetylcholinesterase inhibitors (AChEIs)—which are used to enhance cognition in dementia patients—increased anticholinergic use may follow, often to treat adverse effects of AChEIs.⁵ This may negate the benefits of AChEIs and pose risk of further harm from the anticholinergics.^1,5 Although any time is a good time to discontinue an inessential anticholinergic in a patient with dementia, providers might consider screening for these drugs at the initial diagnosis, after initiating a cholinesterase inhibitor or increasing a dose, or if the patient develops psychotic or behavioral symptoms.

For Mrs. J, ranitidine and oxybutynin likely were used to treat gastrointestinal complaints and urinary frequency, which are known adverse effects of AChEIs. Many OTC preparations for insomnia, respiratory symptoms, and allergies contain older, anticholinergic antihistamines. Advise caregivers of dementia patients about possible adverse effects of OTC medications to prevent anticholinergic exposure. The Table provides a partial list of medications thought to have clinically significant anticholinergic effects.

‘Pharmacologic debridement’ refers to tapering and discontinuing medications that are no longer necessary or appropriate. Prescribers often are hesitant to discontinue medications prescribed by other clinicians and may assume that a medication used long term has been tolerated and helpful. However, as patients age—particularly if they develop dementia—their ability to tolerate a medication can change. Patients with dementia also may have difficulty attributing adverse experiences to medications and communicating these effects to providers. Some medical providers may not recognize adverse psychiatric and cognitive effects of the nonpsychiatric medications they prescribe because they do not have sufficient dementia expertise. Consulting with these providers may help determine the risk-benefit considerations of these medications.

Generally, anticholinergics should be discontinued if they are not essential to a patient’s health or if safer non-anticholinergic alternatives are available.⁵ Tapering may be necessary to prevent adverse effects from cholinergic rebound if a potent anticholinergic has been used chronically.⁵ The first step in addressing Mrs. J’s agitation is to discontinue the anticholinergic medications and monitor her symptoms. This pharmacologic debridement may avert the use of antipsychotics, which carry serious risks for dementia patients.¹

Table
Drugs with clinically significant anticholinergic effects*

Related Resources

• Cancelli I, Beltrame M, D’Anna L, et al. Drugs with anticholinergic properties: a potential risk factor for psychosis onset in Alzheimer’s disease? Expert Opin Drug Saf. 2009;8(5):549-557.
• Meeks TW, Jeste DV. Beyond the black box: what is the role for antipsychotics in dementia? Current Psychiatry. 2008;7(6): 50-65.
• Centers for Education and Research on Therapeutics. Anticholinergic pocket reference card. www.chainonline.org/home/content_images/Anticholinergic%20Pocket%20Card%20CLR%203_12_10.pdf.

Drug Brand Names

• Amitriptyline • Elavil
• Atropine • Sal-Tropine
• Azelastine nasal spray • Astelin
• Belladonna alkaloids • Donnatal
• Benztropine • Cogentin
• Brompheniramine • Dimetane
• Carbamazepine • Carbatrol, Tegretol, others
• Carbinoxamine • Palgic
• Chlorpheniramine • Chlor-Trimeton
• Chlorpromazine • Thorazine
• Cimetidine • Tagamet
• Clemastine • Tavist
• Clidinium • Quarzan
• Clomipramine • Anafranil
• Clozapine • Clozaril
• Cyclobenzaprine • Flexeril
• Cyproheptadine • Periactin
• Darifenacin • Enablex
• Desipramine • Norpramin
• Dexbrompheniramine • Drixoral
• Dexchlorpheniramine • Polaramine
• Dicyclomine • Bentyl
• Dimenhydrinate • Dramamine
• Diphenhydramine • Benadryl, Sominex, others
• Docusate Sodium • Colace
• Donepezil • Aricept
• Doxepin • Adapin
• Doxylamine • Aldex, Unisom, others
• Flavoxate • Urispas
• Glycopyrrolate • Robinul
• Hydroxyzine • Atarax
• Hyoscyamine • Cystospaz, Levbid
• Imipramine • Tofranil
• Ipratropium • Atrovent
• Loxapine • Loxitane
• Meclizine • Antivert
• Meperidine • Demerol
• Mepyramine • Anthisan
• Methscopolamine • Pamine
• Molindone • Moban
• Nortriptyline • Aventyl
• Olanzapine • Zyprexa
• Olopatadine nasal spray • Patanase
• Orphenadrine • Norflex
• Oxybutynin extended-release • Ditropan XL
• Paroxetine • Paxil
• Phenyltoloxamine • Dologesic, Durayin, others
• Pimozide • Orap
• Prochlorperazine • Compazine
• Procyclidine • Kemadrin
• Promethazine • Phenergan
• Propanthelin • Pro-Banthine
• Protriptyline • Vivactil
• Quetiapine • Seroquel
• Ranitidine • Zantac
• Scopolamine • Scopace
• Sertraline • Zoloft
• Solifenacin • VESIcare
• Thioridazine • Mellaril
• Tiotropium • Spiriva
• Tolterodine • Detrol
• Trihexyphenidyl • Artane
• Trimethobenzamide • Tigan
• Trimipramine • Surmontil
• Triprolidine • Actifed
• Trospium • Sanctura

Acknowledgements

This work was supported by an Agency for Healthcare Research and Quality (AHRQ) Centers for Education and Research on Therapeutics cooperative agreement #5 U18 HSO16094.

Disclosure

Dr. Carnahan receives grant/research support from the Agency for Healthcare Research and Quality.

Mrs. J, age 75, has moderate Alzheimer’s dementia and lives at home with her husband. Since her Alzheimer’s disease (AD) diagnosis 2 years ago, Mrs. J generally has been cooperative and not physically aggressive, but has experienced occasional depressive symptoms. However, Mr. J reports that recently his wife is becoming increasingly confused and agitated and wanders the house at night. His efforts to calm and coax her back to bed often lead to increased agitation and yelling. On 1 occasion Mrs. J pushed her husband. Mr. J is concerned that if these behaviors continue he may not be able to care for her at home. Mr. J read online that antipsychotics might reduce aggressive behavior, but is concerned about the increased risk of mortality and stroke with these medications.

Mrs. J receives donepezil, 10 mg/d, sertra-line, 50 mg/d, and extended-release oxybutynin, 10 mg/d. Her over-the-counter (OTC) medications include acetaminophen, 650 mg as needed for pain, ranitidine, 150 mg/d, and docusate sodium, 100 mg/d. Several nights last week, Mr. J gave his wife an unknown OTC sleep medication, hoping it would stop her nighttime wandering, but it did not help. Physical examination, laboratory testing, and urine culture are all normal.

Most dementia patients experience neuropsychiatric disturbances, especially at later stages, that often lead to caregiver distress and nursing home placement. Although these symptoms may signal progressing dementia, environmental factors, medical conditions, and medications may worsen functioning and should be considered in the assessment.¹

Mrs. J has no medical problems that were identified as possible triggers for her behavior. Mr. J’s interference with his wife’s wandering could have increased her agitation, but he is gentle toward her and she has become agitated with no apparent trigger. “Sundowning” and poor sleep also may be involved, as sleep deprivation can lead to delirium and worsen cognitive deficits and behavioral problems.¹ Depression also should be considered.¹ Finally, Mrs. J is taking several medications with anticholinergic properties—oxybutynin, ranitidine, and an unknown OTC sleep medication, which likely contains diphenhydramine or doxylamine—that might contribute to her agitation.

Patients with dementia are highly sensitive to the cognitive and psychiatric adverse effects of anticholinergic medications. In studies of patients with mild or moderate Alzheimer’s dementia who received the potent anticholinergic scopolamine, adverse effects included:

• memory impairment
• restlessness
• disjointed speech
• motor incoordination
• drowsiness
• euphoria
• agitation
• hallucinations
• hostility.

Many of these effects worsened with increasing doses.^2,3 Age-matched controls experienced less severe memory impairment and no behavioral symptoms, which suggests that dementia-related damage to the cholinergic system leads to increased sensitivity to anticholinergics.

A cross-sectional study of 230 patients with AD identified anticholinergic use as a risk factor for psychosis (odds ratio 2.13, 95% confidence interval, 1.03 to 4.43), after adjusting for age and cognition.⁴ Among patients receiving 2 or 3 anticholinergics, 69% had psychotic symptoms compared with 48% of those receiving 1 anticholinergic and 32% of those receiving no anticholinergics.⁴ Anticholinergic overdoses can cause psychotic symptoms and delirium. A subtle presentation of delirium from prescribed anticholinergics may be confused with worsening dementia.¹ The sum of the evidence suggests that drugs with anticholinergic effects can contribute to agitation and psychosis in dementia.

When to discontinue

When diagnosing dementia it is important to address other potential causes of cognitive impairment, including medications. Approximately one-third of patients with dementia receive anticholinergic drugs, which suggests that providers often do not recognize the potential for harm with these medications.⁵ After patients receive acetylcholinesterase inhibitors (AChEIs)—which are used to enhance cognition in dementia patients—increased anticholinergic use may follow, often to treat adverse effects of AChEIs.⁵ This may negate the benefits of AChEIs and pose risk of further harm from the anticholinergics.^1,5 Although any time is a good time to discontinue an inessential anticholinergic in a patient with dementia, providers might consider screening for these drugs at the initial diagnosis, after initiating a cholinesterase inhibitor or increasing a dose, or if the patient develops psychotic or behavioral symptoms.

For Mrs. J, ranitidine and oxybutynin likely were used to treat gastrointestinal complaints and urinary frequency, which are known adverse effects of AChEIs. Many OTC preparations for insomnia, respiratory symptoms, and allergies contain older, anticholinergic antihistamines. Advise caregivers of dementia patients about possible adverse effects of OTC medications to prevent anticholinergic exposure. The Table provides a partial list of medications thought to have clinically significant anticholinergic effects.

‘Pharmacologic debridement’ refers to tapering and discontinuing medications that are no longer necessary or appropriate. Prescribers often are hesitant to discontinue medications prescribed by other clinicians and may assume that a medication used long term has been tolerated and helpful. However, as patients age—particularly if they develop dementia—their ability to tolerate a medication can change. Patients with dementia also may have difficulty attributing adverse experiences to medications and communicating these effects to providers. Some medical providers may not recognize adverse psychiatric and cognitive effects of the nonpsychiatric medications they prescribe because they do not have sufficient dementia expertise. Consulting with these providers may help determine the risk-benefit considerations of these medications.

Generally, anticholinergics should be discontinued if they are not essential to a patient’s health or if safer non-anticholinergic alternatives are available.⁵ Tapering may be necessary to prevent adverse effects from cholinergic rebound if a potent anticholinergic has been used chronically.⁵ The first step in addressing Mrs. J’s agitation is to discontinue the anticholinergic medications and monitor her symptoms. This pharmacologic debridement may avert the use of antipsychotics, which carry serious risks for dementia patients.¹

Table
Drugs with clinically significant anticholinergic effects*

Related Resources

• Cancelli I, Beltrame M, D’Anna L, et al. Drugs with anticholinergic properties: a potential risk factor for psychosis onset in Alzheimer’s disease? Expert Opin Drug Saf. 2009;8(5):549-557.
• Meeks TW, Jeste DV. Beyond the black box: what is the role for antipsychotics in dementia? Current Psychiatry. 2008;7(6): 50-65.
• Centers for Education and Research on Therapeutics. Anticholinergic pocket reference card. www.chainonline.org/home/content_images/Anticholinergic%20Pocket%20Card%20CLR%203_12_10.pdf.

Drug Brand Names

• Amitriptyline • Elavil
• Atropine • Sal-Tropine
• Azelastine nasal spray • Astelin
• Belladonna alkaloids • Donnatal
• Benztropine • Cogentin
• Brompheniramine • Dimetane
• Carbamazepine • Carbatrol, Tegretol, others
• Carbinoxamine • Palgic
• Chlorpheniramine • Chlor-Trimeton
• Chlorpromazine • Thorazine
• Cimetidine • Tagamet
• Clemastine • Tavist
• Clidinium • Quarzan
• Clomipramine • Anafranil
• Clozapine • Clozaril
• Cyclobenzaprine • Flexeril
• Cyproheptadine • Periactin
• Darifenacin • Enablex
• Desipramine • Norpramin
• Dexbrompheniramine • Drixoral
• Dexchlorpheniramine • Polaramine
• Dicyclomine • Bentyl
• Dimenhydrinate • Dramamine
• Diphenhydramine • Benadryl, Sominex, others
• Docusate Sodium • Colace
• Donepezil • Aricept
• Doxepin • Adapin
• Doxylamine • Aldex, Unisom, others
• Flavoxate • Urispas
• Glycopyrrolate • Robinul
• Hydroxyzine • Atarax
• Hyoscyamine • Cystospaz, Levbid
• Imipramine • Tofranil
• Ipratropium • Atrovent
• Loxapine • Loxitane
• Meclizine • Antivert
• Meperidine • Demerol
• Mepyramine • Anthisan
• Methscopolamine • Pamine
• Molindone • Moban
• Nortriptyline • Aventyl
• Olanzapine • Zyprexa
• Olopatadine nasal spray • Patanase
• Orphenadrine • Norflex
• Oxybutynin extended-release • Ditropan XL
• Paroxetine • Paxil
• Phenyltoloxamine • Dologesic, Durayin, others
• Pimozide • Orap
• Prochlorperazine • Compazine
• Procyclidine • Kemadrin
• Promethazine • Phenergan
• Propanthelin • Pro-Banthine
• Protriptyline • Vivactil
• Quetiapine • Seroquel
• Ranitidine • Zantac
• Scopolamine • Scopace
• Sertraline • Zoloft
• Solifenacin • VESIcare
• Thioridazine • Mellaril
• Tiotropium • Spiriva
• Tolterodine • Detrol
• Trihexyphenidyl • Artane
• Trimethobenzamide • Tigan
• Trimipramine • Surmontil
• Triprolidine • Actifed
• Trospium • Sanctura

Acknowledgements

This work was supported by an Agency for Healthcare Research and Quality (AHRQ) Centers for Education and Research on Therapeutics cooperative agreement #5 U18 HSO16094.

Disclosure

Dr. Carnahan receives grant/research support from the Agency for Healthcare Research and Quality.

Mrs. J, age 75, has moderate Alzheimer’s dementia and lives at home with her husband. Since her Alzheimer’s disease (AD) diagnosis 2 years ago, Mrs. J generally has been cooperative and not physically aggressive, but has experienced occasional depressive symptoms. However, Mr. J reports that recently his wife is becoming increasingly confused and agitated and wanders the house at night. His efforts to calm and coax her back to bed often lead to increased agitation and yelling. On 1 occasion Mrs. J pushed her husband. Mr. J is concerned that if these behaviors continue he may not be able to care for her at home. Mr. J read online that antipsychotics might reduce aggressive behavior, but is concerned about the increased risk of mortality and stroke with these medications.

Mrs. J receives donepezil, 10 mg/d, sertra-line, 50 mg/d, and extended-release oxybutynin, 10 mg/d. Her over-the-counter (OTC) medications include acetaminophen, 650 mg as needed for pain, ranitidine, 150 mg/d, and docusate sodium, 100 mg/d. Several nights last week, Mr. J gave his wife an unknown OTC sleep medication, hoping it would stop her nighttime wandering, but it did not help. Physical examination, laboratory testing, and urine culture are all normal.

Most dementia patients experience neuropsychiatric disturbances, especially at later stages, that often lead to caregiver distress and nursing home placement. Although these symptoms may signal progressing dementia, environmental factors, medical conditions, and medications may worsen functioning and should be considered in the assessment.¹

Mrs. J has no medical problems that were identified as possible triggers for her behavior. Mr. J’s interference with his wife’s wandering could have increased her agitation, but he is gentle toward her and she has become agitated with no apparent trigger. “Sundowning” and poor sleep also may be involved, as sleep deprivation can lead to delirium and worsen cognitive deficits and behavioral problems.¹ Depression also should be considered.¹ Finally, Mrs. J is taking several medications with anticholinergic properties—oxybutynin, ranitidine, and an unknown OTC sleep medication, which likely contains diphenhydramine or doxylamine—that might contribute to her agitation.

Patients with dementia are highly sensitive to the cognitive and psychiatric adverse effects of anticholinergic medications. In studies of patients with mild or moderate Alzheimer’s dementia who received the potent anticholinergic scopolamine, adverse effects included:

• memory impairment
• restlessness
• disjointed speech
• motor incoordination
• drowsiness
• euphoria
• agitation
• hallucinations
• hostility.

Many of these effects worsened with increasing doses.^2,3 Age-matched controls experienced less severe memory impairment and no behavioral symptoms, which suggests that dementia-related damage to the cholinergic system leads to increased sensitivity to anticholinergics.

A cross-sectional study of 230 patients with AD identified anticholinergic use as a risk factor for psychosis (odds ratio 2.13, 95% confidence interval, 1.03 to 4.43), after adjusting for age and cognition.⁴ Among patients receiving 2 or 3 anticholinergics, 69% had psychotic symptoms compared with 48% of those receiving 1 anticholinergic and 32% of those receiving no anticholinergics.⁴ Anticholinergic overdoses can cause psychotic symptoms and delirium. A subtle presentation of delirium from prescribed anticholinergics may be confused with worsening dementia.¹ The sum of the evidence suggests that drugs with anticholinergic effects can contribute to agitation and psychosis in dementia.

When to discontinue

When diagnosing dementia it is important to address other potential causes of cognitive impairment, including medications. Approximately one-third of patients with dementia receive anticholinergic drugs, which suggests that providers often do not recognize the potential for harm with these medications.⁵ After patients receive acetylcholinesterase inhibitors (AChEIs)—which are used to enhance cognition in dementia patients—increased anticholinergic use may follow, often to treat adverse effects of AChEIs.⁵ This may negate the benefits of AChEIs and pose risk of further harm from the anticholinergics.^1,5 Although any time is a good time to discontinue an inessential anticholinergic in a patient with dementia, providers might consider screening for these drugs at the initial diagnosis, after initiating a cholinesterase inhibitor or increasing a dose, or if the patient develops psychotic or behavioral symptoms.

For Mrs. J, ranitidine and oxybutynin likely were used to treat gastrointestinal complaints and urinary frequency, which are known adverse effects of AChEIs. Many OTC preparations for insomnia, respiratory symptoms, and allergies contain older, anticholinergic antihistamines. Advise caregivers of dementia patients about possible adverse effects of OTC medications to prevent anticholinergic exposure. The Table provides a partial list of medications thought to have clinically significant anticholinergic effects.

‘Pharmacologic debridement’ refers to tapering and discontinuing medications that are no longer necessary or appropriate. Prescribers often are hesitant to discontinue medications prescribed by other clinicians and may assume that a medication used long term has been tolerated and helpful. However, as patients age—particularly if they develop dementia—their ability to tolerate a medication can change. Patients with dementia also may have difficulty attributing adverse experiences to medications and communicating these effects to providers. Some medical providers may not recognize adverse psychiatric and cognitive effects of the nonpsychiatric medications they prescribe because they do not have sufficient dementia expertise. Consulting with these providers may help determine the risk-benefit considerations of these medications.

Generally, anticholinergics should be discontinued if they are not essential to a patient’s health or if safer non-anticholinergic alternatives are available.⁵ Tapering may be necessary to prevent adverse effects from cholinergic rebound if a potent anticholinergic has been used chronically.⁵ The first step in addressing Mrs. J’s agitation is to discontinue the anticholinergic medications and monitor her symptoms. This pharmacologic debridement may avert the use of antipsychotics, which carry serious risks for dementia patients.¹

Table
Drugs with clinically significant anticholinergic effects*

Related Resources

• Cancelli I, Beltrame M, D’Anna L, et al. Drugs with anticholinergic properties: a potential risk factor for psychosis onset in Alzheimer’s disease? Expert Opin Drug Saf. 2009;8(5):549-557.
• Meeks TW, Jeste DV. Beyond the black box: what is the role for antipsychotics in dementia? Current Psychiatry. 2008;7(6): 50-65.
• Centers for Education and Research on Therapeutics. Anticholinergic pocket reference card. www.chainonline.org/home/content_images/Anticholinergic%20Pocket%20Card%20CLR%203_12_10.pdf.

Drug Brand Names

• Amitriptyline • Elavil
• Atropine • Sal-Tropine
• Azelastine nasal spray • Astelin
• Belladonna alkaloids • Donnatal
• Benztropine • Cogentin
• Brompheniramine • Dimetane
• Carbamazepine • Carbatrol, Tegretol, others
• Carbinoxamine • Palgic
• Chlorpheniramine • Chlor-Trimeton
• Chlorpromazine • Thorazine
• Cimetidine • Tagamet
• Clemastine • Tavist
• Clidinium • Quarzan
• Clomipramine • Anafranil
• Clozapine • Clozaril
• Cyclobenzaprine • Flexeril
• Cyproheptadine • Periactin
• Darifenacin • Enablex
• Desipramine • Norpramin
• Dexbrompheniramine • Drixoral
• Dexchlorpheniramine • Polaramine
• Dicyclomine • Bentyl
• Dimenhydrinate • Dramamine
• Diphenhydramine • Benadryl, Sominex, others
• Docusate Sodium • Colace
• Donepezil • Aricept
• Doxepin • Adapin
• Doxylamine • Aldex, Unisom, others
• Flavoxate • Urispas
• Glycopyrrolate • Robinul
• Hydroxyzine • Atarax
• Hyoscyamine • Cystospaz, Levbid
• Imipramine • Tofranil
• Ipratropium • Atrovent
• Loxapine • Loxitane
• Meclizine • Antivert
• Meperidine • Demerol
• Mepyramine • Anthisan
• Methscopolamine • Pamine
• Molindone • Moban
• Nortriptyline • Aventyl
• Olanzapine • Zyprexa
• Olopatadine nasal spray • Patanase
• Orphenadrine • Norflex
• Oxybutynin extended-release • Ditropan XL
• Paroxetine • Paxil
• Phenyltoloxamine • Dologesic, Durayin, others
• Pimozide • Orap
• Prochlorperazine • Compazine
• Procyclidine • Kemadrin
• Promethazine • Phenergan
• Propanthelin • Pro-Banthine
• Protriptyline • Vivactil
• Quetiapine • Seroquel
• Ranitidine • Zantac
• Scopolamine • Scopace
• Sertraline • Zoloft
• Solifenacin • VESIcare
• Thioridazine • Mellaril
• Tiotropium • Spiriva
• Tolterodine • Detrol
• Trihexyphenidyl • Artane
• Trimethobenzamide • Tigan
• Trimipramine • Surmontil
• Triprolidine • Actifed
• Trospium • Sanctura

Acknowledgements

This work was supported by an Agency for Healthcare Research and Quality (AHRQ) Centers for Education and Research on Therapeutics cooperative agreement #5 U18 HSO16094.

Disclosure

Dr. Carnahan receives grant/research support from the Agency for Healthcare Research and Quality.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/07/treating-insomnia-in-women.html#comments

Ms. A, age 44, reports a 3-month history of forgetfulness, difficulty concentrating, and insomnia. She says she can fall asleep but wakes up multiple times during the night and feels tired during the day. She has no history of a mood or anxiety disorder or medications that might be responsible for her symptoms.

Before her current insomnia began, Ms. A could sleep for 7 to 8 hours at night. Her husband suffers from obstructive sleep apnea (OSA), and his snoring occasionally would awaken her, but she slept well overall. Ms. A cannot identify anything that could be causing her sleep complaints. She states “The weird thing is that sometimes I am not sure if I’m cold or hot” and “I sometimes wake up drenched in sweat.” She also reports recent changes in the timing of her otherwise regular menstrual flow.

Ms. A attributes her memory problems to her poor sleep. A recent audit at her company held her responsible for several accounting errors, and Ms. A is worried that she might lose her job. She denies symptoms that would suggest major depression. You are unable to elicit a history of limb movements or excessive snoring.

Compared with men, women have a 1.3- to 1.8-fold greater risk for developing insomnia.^{Improve sleep with group CBT for insomnia,” Current Psychiatry, April 2009.) Pharmacotherapy during pregnancy and for breast-feeding mothers is guided by evaluating the risk/benefit ratio and safety considerations.}

Maintain a high index of suspicion for breathing-related sleep disorders, such as OSA,²¹ and RLS.²² Atypical presentations of OSA are common in pregnant or postpartum women; compared with men, women with OSA are more likely to report fatigue and less likely than to report sleepiness. Refer patients whom you think may have OSA for polysomnography.

If you suspect RLS, check for low ferritin and folate levels. Nutritional supplements may be necessary for women in high-risk groups, including those who are pregnant or have varicose veins, venous reflux, folate deficiency, uremia, diabetes, thyroid problems, peripheral neuropathy, Parkinson’s disease, or certain autoimmune disorders, such as Sjögren’s syndrome, celiac disease, and rheumatoid arthritis.²³ Advise these patients to avoid caffeine.

Although indicated for treating RLS, ropinirole and pramipexole are FDA Pregnancy Category C, which means animal studies have shown adverse effects on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite risks. Opioids, carbamazepine, or gabapentin may be safer for pregnant patients.²⁴

Insomnia during menopause

The prevalence of insomnia increases from 33% to 36% in premenopausal women to 44% to 61% in postmenopausal women.¹⁴ Hot flashes, comorbid mood disturbances, sleep-disordered breathing, and RLS contribute to increased insomnia risk in postmenopausal women (Table 3).^4,14,25,26

Treatment strategy. Always inquire about sleep in perimenopausal/postmenopausal women, even when her presenting complaint is related to menstrual cycle changes or vasomotor symptoms such as hot flashes.¹⁶ Assess patients for OSA, RLS, and mood, anxiety, and cognitive symptoms.²⁶ In addition to pharmacotherapy and behavioral therapy, treatment options include hormone replacement therapy (HRT) and herbal and dietary supplements (Table 4).^27-32

Table 3

Sleep difficulties during menopause: Differential diagnoses

Table 4

Treating insomnia in menopausal women

Comorbid psychiatric disorders

Women have a higher prevalence of psychiatric disorders such as major depressive disorder and anxiety disorders than men.¹ Women have a 10% to 25% lifetime risk of developing major depression. Three quarters of depressed patients experience insomnia.¹ Recent literature suggests insomnia is a risk factor for depression,³³ which emphasizes the need to screen women who present with sleep problems for depression and anxiety.

Five percent to 20% of women experience postpartum depression. Depression and insomnia are correlated to the rapid decline in estrogen and progesterone after delivery.³⁴

Treatment strategy. Insomnia is a common presenting symptom in patients with psychiatric conditions such as mood and anxiety disorders. Treating the underlying psychiatric disorder often alleviates sleeping difficulties. However, if the insomnia is disabling, treat the psychiatric disorder and insomnia concurrently.

CASE CONTINUED: Perimenopausal insomnia

Based on her history, you diagnose Ms. A with insomnia related to general medical condition (perimenopause). There are no indications to refer her for polysomnography. You educate Ms. A about sleep hygiene and recommend that she discuss her menstrual and physical complaints with her primary care physician or gynecologist. Ms. A is not interested in HRT because she has a strong family history of endometrial cancer. You reassure Ms. A and schedule a follow-up visit in 2 months to re-evaluate her insomnia.

Related resource

• Krahn LE. Perimenopausal depression? Ask how she’s sleeping. Current Psychiatry. 2005;4(6):39-53.

Drug brand names

• Carbamazepine • Carbatrol, Tegretol, others
• Escitalopram • Lexapro
• Eszopiclone • Lunesta
• Fluoxetine • Prozac
• Gabapentin • Neurontin, Gabarone
• Paroxetine • Paxil
• Pramipexole • Mirapex
• Ramelteon • Rozerem
• Ropinirole • Requip
• Sertraline • Zoloft
• Trazodone • Desyrel
• Zolpidem • Ambien

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgements

The authors thank Dr. Namita Dhiman and Darrel E. Willoughby for their assistance with this article.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/07/treating-insomnia-in-women.html#comments

Ms. A, age 44, reports a 3-month history of forgetfulness, difficulty concentrating, and insomnia. She says she can fall asleep but wakes up multiple times during the night and feels tired during the day. She has no history of a mood or anxiety disorder or medications that might be responsible for her symptoms.

Before her current insomnia began, Ms. A could sleep for 7 to 8 hours at night. Her husband suffers from obstructive sleep apnea (OSA), and his snoring occasionally would awaken her, but she slept well overall. Ms. A cannot identify anything that could be causing her sleep complaints. She states “The weird thing is that sometimes I am not sure if I’m cold or hot” and “I sometimes wake up drenched in sweat.” She also reports recent changes in the timing of her otherwise regular menstrual flow.

Ms. A attributes her memory problems to her poor sleep. A recent audit at her company held her responsible for several accounting errors, and Ms. A is worried that she might lose her job. She denies symptoms that would suggest major depression. You are unable to elicit a history of limb movements or excessive snoring.

Compared with men, women have a 1.3- to 1.8-fold greater risk for developing insomnia.^{Improve sleep with group CBT for insomnia,” Current Psychiatry, April 2009.) Pharmacotherapy during pregnancy and for breast-feeding mothers is guided by evaluating the risk/benefit ratio and safety considerations.}

Maintain a high index of suspicion for breathing-related sleep disorders, such as OSA,²¹ and RLS.²² Atypical presentations of OSA are common in pregnant or postpartum women; compared with men, women with OSA are more likely to report fatigue and less likely than to report sleepiness. Refer patients whom you think may have OSA for polysomnography.

If you suspect RLS, check for low ferritin and folate levels. Nutritional supplements may be necessary for women in high-risk groups, including those who are pregnant or have varicose veins, venous reflux, folate deficiency, uremia, diabetes, thyroid problems, peripheral neuropathy, Parkinson’s disease, or certain autoimmune disorders, such as Sjögren’s syndrome, celiac disease, and rheumatoid arthritis.²³ Advise these patients to avoid caffeine.

Although indicated for treating RLS, ropinirole and pramipexole are FDA Pregnancy Category C, which means animal studies have shown adverse effects on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite risks. Opioids, carbamazepine, or gabapentin may be safer for pregnant patients.²⁴

Insomnia during menopause

The prevalence of insomnia increases from 33% to 36% in premenopausal women to 44% to 61% in postmenopausal women.¹⁴ Hot flashes, comorbid mood disturbances, sleep-disordered breathing, and RLS contribute to increased insomnia risk in postmenopausal women (Table 3).^4,14,25,26

Treatment strategy. Always inquire about sleep in perimenopausal/postmenopausal women, even when her presenting complaint is related to menstrual cycle changes or vasomotor symptoms such as hot flashes.¹⁶ Assess patients for OSA, RLS, and mood, anxiety, and cognitive symptoms.²⁶ In addition to pharmacotherapy and behavioral therapy, treatment options include hormone replacement therapy (HRT) and herbal and dietary supplements (Table 4).^27-32

Table 3

Sleep difficulties during menopause: Differential diagnoses

Table 4

Treating insomnia in menopausal women

Comorbid psychiatric disorders

Women have a higher prevalence of psychiatric disorders such as major depressive disorder and anxiety disorders than men.¹ Women have a 10% to 25% lifetime risk of developing major depression. Three quarters of depressed patients experience insomnia.¹ Recent literature suggests insomnia is a risk factor for depression,³³ which emphasizes the need to screen women who present with sleep problems for depression and anxiety.

Five percent to 20% of women experience postpartum depression. Depression and insomnia are correlated to the rapid decline in estrogen and progesterone after delivery.³⁴

Treatment strategy. Insomnia is a common presenting symptom in patients with psychiatric conditions such as mood and anxiety disorders. Treating the underlying psychiatric disorder often alleviates sleeping difficulties. However, if the insomnia is disabling, treat the psychiatric disorder and insomnia concurrently.

CASE CONTINUED: Perimenopausal insomnia

Based on her history, you diagnose Ms. A with insomnia related to general medical condition (perimenopause). There are no indications to refer her for polysomnography. You educate Ms. A about sleep hygiene and recommend that she discuss her menstrual and physical complaints with her primary care physician or gynecologist. Ms. A is not interested in HRT because she has a strong family history of endometrial cancer. You reassure Ms. A and schedule a follow-up visit in 2 months to re-evaluate her insomnia.

Related resource

• Krahn LE. Perimenopausal depression? Ask how she’s sleeping. Current Psychiatry. 2005;4(6):39-53.

Drug brand names

• Carbamazepine • Carbatrol, Tegretol, others
• Escitalopram • Lexapro
• Eszopiclone • Lunesta
• Fluoxetine • Prozac
• Gabapentin • Neurontin, Gabarone
• Paroxetine • Paxil
• Pramipexole • Mirapex
• Ramelteon • Rozerem
• Ropinirole • Requip
• Sertraline • Zoloft
• Trazodone • Desyrel
• Zolpidem • Ambien

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgements

The authors thank Dr. Namita Dhiman and Darrel E. Willoughby for their assistance with this article.

Discuss this article at http://currentpsychiatry.blogspot.com/2010/07/treating-insomnia-in-women.html#comments

Ms. A, age 44, reports a 3-month history of forgetfulness, difficulty concentrating, and insomnia. She says she can fall asleep but wakes up multiple times during the night and feels tired during the day. She has no history of a mood or anxiety disorder or medications that might be responsible for her symptoms.

Before her current insomnia began, Ms. A could sleep for 7 to 8 hours at night. Her husband suffers from obstructive sleep apnea (OSA), and his snoring occasionally would awaken her, but she slept well overall. Ms. A cannot identify anything that could be causing her sleep complaints. She states “The weird thing is that sometimes I am not sure if I’m cold or hot” and “I sometimes wake up drenched in sweat.” She also reports recent changes in the timing of her otherwise regular menstrual flow.

Ms. A attributes her memory problems to her poor sleep. A recent audit at her company held her responsible for several accounting errors, and Ms. A is worried that she might lose her job. She denies symptoms that would suggest major depression. You are unable to elicit a history of limb movements or excessive snoring.

Compared with men, women have a 1.3- to 1.8-fold greater risk for developing insomnia.^{Improve sleep with group CBT for insomnia,” Current Psychiatry, April 2009.) Pharmacotherapy during pregnancy and for breast-feeding mothers is guided by evaluating the risk/benefit ratio and safety considerations.}

Maintain a high index of suspicion for breathing-related sleep disorders, such as OSA,²¹ and RLS.²² Atypical presentations of OSA are common in pregnant or postpartum women; compared with men, women with OSA are more likely to report fatigue and less likely than to report sleepiness. Refer patients whom you think may have OSA for polysomnography.

If you suspect RLS, check for low ferritin and folate levels. Nutritional supplements may be necessary for women in high-risk groups, including those who are pregnant or have varicose veins, venous reflux, folate deficiency, uremia, diabetes, thyroid problems, peripheral neuropathy, Parkinson’s disease, or certain autoimmune disorders, such as Sjögren’s syndrome, celiac disease, and rheumatoid arthritis.²³ Advise these patients to avoid caffeine.

Although indicated for treating RLS, ropinirole and pramipexole are FDA Pregnancy Category C, which means animal studies have shown adverse effects on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite risks. Opioids, carbamazepine, or gabapentin may be safer for pregnant patients.²⁴

Insomnia during menopause

The prevalence of insomnia increases from 33% to 36% in premenopausal women to 44% to 61% in postmenopausal women.¹⁴ Hot flashes, comorbid mood disturbances, sleep-disordered breathing, and RLS contribute to increased insomnia risk in postmenopausal women (Table 3).^4,14,25,26

Treatment strategy. Always inquire about sleep in perimenopausal/postmenopausal women, even when her presenting complaint is related to menstrual cycle changes or vasomotor symptoms such as hot flashes.¹⁶ Assess patients for OSA, RLS, and mood, anxiety, and cognitive symptoms.²⁶ In addition to pharmacotherapy and behavioral therapy, treatment options include hormone replacement therapy (HRT) and herbal and dietary supplements (Table 4).^27-32

Table 3

Sleep difficulties during menopause: Differential diagnoses

Table 4

Treating insomnia in menopausal women

Comorbid psychiatric disorders

Women have a higher prevalence of psychiatric disorders such as major depressive disorder and anxiety disorders than men.¹ Women have a 10% to 25% lifetime risk of developing major depression. Three quarters of depressed patients experience insomnia.¹ Recent literature suggests insomnia is a risk factor for depression,³³ which emphasizes the need to screen women who present with sleep problems for depression and anxiety.

Five percent to 20% of women experience postpartum depression. Depression and insomnia are correlated to the rapid decline in estrogen and progesterone after delivery.³⁴

Treatment strategy. Insomnia is a common presenting symptom in patients with psychiatric conditions such as mood and anxiety disorders. Treating the underlying psychiatric disorder often alleviates sleeping difficulties. However, if the insomnia is disabling, treat the psychiatric disorder and insomnia concurrently.

CASE CONTINUED: Perimenopausal insomnia

Based on her history, you diagnose Ms. A with insomnia related to general medical condition (perimenopause). There are no indications to refer her for polysomnography. You educate Ms. A about sleep hygiene and recommend that she discuss her menstrual and physical complaints with her primary care physician or gynecologist. Ms. A is not interested in HRT because she has a strong family history of endometrial cancer. You reassure Ms. A and schedule a follow-up visit in 2 months to re-evaluate her insomnia.

Related resource

• Krahn LE. Perimenopausal depression? Ask how she’s sleeping. Current Psychiatry. 2005;4(6):39-53.

Drug brand names

• Carbamazepine • Carbatrol, Tegretol, others
• Escitalopram • Lexapro
• Eszopiclone • Lunesta
• Fluoxetine • Prozac
• Gabapentin • Neurontin, Gabarone
• Paroxetine • Paxil
• Pramipexole • Mirapex
• Ramelteon • Rozerem
• Ropinirole • Requip
• Sertraline • Zoloft
• Trazodone • Desyrel
• Zolpidem • Ambien

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Acknowledgements

The authors thank Dr. Namita Dhiman and Darrel E. Willoughby for their assistance with this article.