Lori R. Roust, MD

Restrictive Procedures (Laparoscopic Adjustable Gastric Band and Sleeve Gastrectomy)

These procedures produce weight loss by reducing the size of the stomach or creating an obstruction in the proximal stomach, limiting the consumption of large quantities at one time. They produce early satiety, but patients may still consume a large volume of calorie‐dense liquids compromising weight loss.

Laparoscopic Adjustable Gastric Band

Laparoscopic adjustable gastric band (LAGB; Figure 1A) is the primary form of restrictive procedures with 2 Food and Drug Administration‐approved bands (Lap Band [Allergan, Inc; Irvine, CA] and REALIZE band [Ethicon Endo‐Surgery, Inc; Cincinnati, OH]). A cuff is inflated around the proximal stomach creating a gastric pouch approximately 15‐30 mL in size. A subcutaneous reservoir is attached to the cuff allowing adjustment to the degree of restriction.8 LAGB has replaced the vertical banded gastroplasty (VBG). It is less invasive, adjustable, and reversible (0.1% operative mortality rate). Weight loss is maintained with this procedure but is generally less, with a higher failure rate compared to the more common gastric bypass procedure (Table 1).3, 9 Complications may include band dysfunction (ie, slippage, erosion, infections), esophageal dilatation, balloon failure, and port malposition, with rates approaching 3%‐5% per year requiring removal or repair.10 Patients may also experience GERD symptoms, especially if the condition was present preoperatively. Progressive GERD symptoms should be investigated with an upper gastrointestinal (GI) series to ensure there is no band slippage, esophageal dilation, or dysfunction.

Figure 1

Table 1.Comparison of Outcomes for Various Procedures

	LAGB	Roux‐en‐Y Gastric Bypass	Biliopancreatic Diversion With and Without Duodenal Switch
NOTE: References: Buchwald et al.3; Kendrick and Dakin.9 Abbreviations: LAGB, laparoscopic adjustable gastric band.
Excess weight loss	48%	62%	70%
Resolution of diabetes	48%	84%	98%

Combination Procedures (Roux‐en‐Y Gastric Bypass and Biliopancreatic Diversion With and Without Duodenal Switch)

These procedures produce weight loss by decreasing caloric intake and altering digestion and absorption.

Gastrointestinal Complaints

One of the most common causes of hospital admission any time postoperatively is abdominal pain. A differential diagnosis of abdominal pain, nausea, and/or vomiting in the post‐bariatric surgery patient should include small bowel obstruction, hernias (internal or incisional), band complications, food intolerance, dietary noncompliance, ileus, mesenteric venous thrombosis, strictures (such as outlet obstruction or anastomotic stenosis), ulcers, esophagitis, cholelithiasis, dumping syndrome, and Roux stasis syndrome.20

A thorough history targeted at the relationship between symptoms and food intake, attention to the character and location of the pain, and a thorough physical exam (specifically the presence or absence of palpable tenderness, guarding, or rebound) is essential. The physical exam may be misleading in obese patients and, if radiographic studies cannot be performed secondary to patient size, surgical exploration may be needed soon after presentation. Therefore, even lacking an obvious surgical need, the bariatric surgeon should be notified of admission.

Improper food choice, and failure to slowly and adequately chew food, can result in emesis and digestive difficulty. Physical incompatibility with the small gastric pouch and gastric outlet obstructions can be caused by nondigestible foods (ie, breads, steak, raw vegetables). This highlights the importance of ordering the appropriate hospital diet.8 Specific gastric bypass hospital diets for all consistencies should reflect the mechanical limitations and carbohydrate/protein requirements of these patients.

Increased gallstone formation is observed in patients with rapid weight loss (1.5 kg/wk), especially following RYGB and less often after LAGB procedures (40% vs 20% over 3 years). Routine use of ursodiol during rapid weight loss (6 months after RYGB) reduces this complication to <5%.8

Stenosis or ulceration at the anastomotic site for RYGB can cause abdominal pain and vomiting. The incidence of stomal stenosis has been reported at 5%‐19% and typically occurs within the first 3 postoperative months.22 This problem is often amenable to endoscopic dilatation, unless a ring was used to reinforce the anastomosis. Ulceration has been reported in 1%‐16% of patients and is usually secondary to tobacco or non‐steroidal anti‐inflammatory drug (NSAID) use, H. pylori, fistula‐induced acid exposure, reaction to foreign material, or ischemia from tension and poor tissue perfusion.23, 24 Endoscopy can diagnose the presence of ulcers, with biopsies to rule out H. pylori infection. Cessation of NSAIDs and tobacco are critical. Medical management including proton pump inhibitors and/or sucralfate is sufficient for up to 95% of patients. Surgical revision is reserved for persistent ulcers associated with obstruction, pain, and/or bleeding.25

Dumping syndrome is a complex of post‐prandial symptoms occurring most commonly in the RYGB patients. As many as 44% of RYGB patients may experience this syndrome characterized by flushing, dizziness, abdominal distension, pain, nausea, vomiting, and/or diarrhea.26 Symptoms may result from the ingestion of large amounts of sugars which empty from the altered gastric pouch at an unregulated rate. This large osmotic load causes fluid shifts and surges in peptide hormone levels, resulting in symptoms which may reinforce adherence to the prescribed postoperative diet. It occurs shortly after a meal and resolves over hours. Dietary modifications, such as increased protein and fiber intake with decreased consumption of simple sugars, will ameliorate symptoms in many patients, with most seeing resolution after the first year.8, 27 Some patients experience hyperglycemia secondary to ingestion of simple carbohydrates, with hypoglycemia approximately 2 hours later (late dumping). In our experience, limiting carbohydrate intake to 30 grams at any meal usually alleviates post‐prandial hypoglycemia.

If the patient reports an absence of bowel movements and flatus, an ileus from chronic narcotic use or a mechanical small bowel obstruction secondary to internal hernias or adhesions (see Late Surgical Complications) must be investigated. Severe or prolonged pain, lasting longer than a few hours, is cause for alarm and should prompt aggressive evaluation and possibly exploratory surgery.

Excessive Weight Loss

In diagnosing postoperative excessive weight loss, it is important to understand average anticipated weight loss parameters. Compared to the values expected for RYGB, LAGB produces less weight loss and BPD with and without DS produces more (Table 227). Patients experiencing more rapid or prolonged weight loss should be investigated for bacterial overgrowth syndrome, short bowel syndrome, or other anatomic abnormalities.

Known risk factors for bacterial overgrowth, which are prominent in this population, include decreased gastric acidity and slowed intestinal transit time (ie, narcotic use). Patients may be asymptomatic or experience weight loss, abdominal bloating and/or pain, nausea, vomiting, and diarrhea. The diagnosis can be made with a hydrogen breath test or by obtaining quantitative cultures of jejunal secretions during endoscopy. Questions remain on how the normalized values of these tests are affected by the postoperative environment, and on how this syndrome may present or be treated if it affects the excluded intestine. Bacterial overgrowth may be an incidental finding and not the cause of the gastrointestinal complaints. Although data is limited, treatment typically consists of a 7‐10 day course of rifaximin 1200 mg/day (divided doses) and/or a trial of dietary modifications.20, 2831 These may include avoiding lactose and eating a high fat, low carbohydrate, low fiber diet, so nutrients are readily absorbed and not left for bacterial consumption.32

Short bowel syndrome (<100‐200 cm of intestinal tissue remaining and subsequent malabsorption) can occur after any extensive colonic resection or bypass of the intestine.33 This condition rarely results after an initial bariatric procedure; however, subsequent procedures for small bowel obstructions or intestinal ischemia may result in short bowel syndrome. Typical presentations include diarrhea, weight loss, and symptoms of vitamin and mineral deficiencies. Short bowel can also predispose patients to the development of bacterial overgrowth, further complicating weight loss. Management consists of nutritional supplementation, occasionally parenteral nutrition, and rarely reoperation to increase the length of the common channel.34 Avoidance of further bowel resection is crucial in preventing short bowel syndrome.33, 34 In the setting of carbohydrate malabsorption with concomitant bacterial overgrowth syndrome, production of d‐lactic acid causing a metabolic acidosis with encephalopathy has been reported.35

Once medical complications have been ruled out, it is prudent to evaluate for a psychological component such as anorexia nervosa. It is helpful to involve a qualified psychologist who is familiar with this population. Addictions to alcohol, gambling, and pain medications have been reported in the post‐bariatric surgery population as a substitute for food addiction.

Neurological Complications and Vitamin Deficiencies

Neurological complications develop months to years postoperatively, secondary to vitamin, mineral, and nutrient deficiencies that result from malabsorption or inadequate intake. An inpatient provider should be aware of the potential role these conditions may play in a hospitalized patient.

Peripheral neuropathy can develop secondary to several deficiencies, including vitamin B₁₂, thiamine, vitamin E, and copper. Their sources, deficiencies, and replacement regimens are presented in Table 3.3642 Thiamine deficiency, manifesting as Wernicke's encephalopathy, is particularly important in the postoperative patient with excessive vomiting. For prevention, we recommend all patients readmitted with vomiting and dehydration receive a banana bag or rally pack (thiamine 100 mg, folic acid 1 mg, multivitamin with iron and magnesium 3 g in one liter of D5 normal saline) over 4‐8 hours. Additional deficiencies after gastric bypass include folate, selenium, zinc, vitamin B₆, and riboflavin. A multivitamin with minerals will meet the needs of most patients. Multiple fat‐soluble vitamin deficiencies can occur with small bowel bacterial overgrowth or BPD.

Anemia

Iron deficiency affects 6%‐33% of patients after 1 year.43 Iron is preferentially absorbed in the duodenum and proximal jejunum which are bypassed postoperatively. The absence of gastric acid prevents conversion of ferric (Fe²⁺) to the absorbable ferrous (Fe³⁺) iron, further decreasing absorption.44 Ferritin reflects iron stores but is also an acute phase reactant and, therefore, may mask an underlying deficiency in an acutely ill hospitalized patient. A multivitamin with iron is recommended for all patients, but additional supplementation may be required for menstruating women.43 Parenteral administration may be necessary if oral supplements are not tolerated or are inadequately absorbed.44

Fractures and Osteomalacia

Calcium and vitamin D deficiencies are a significant problem in the bariatric surgery population, with resultant osteoporosis or osteomalacia and associated fractures.38, 43 Calcium is preferentially absorbed in the duodenum and proximal jejunum. Vitamin D is absorbed in the ileum or produced in the skin in response to ultraviolet B (UVB) radiation.45 Deficiency of vitamin D exacerbates calcium malabsorption, thereby causing secondary hyperparathyroidism, increased bone turnover, and osteomalacia. Dramatic weight loss can lead to bone loss, increasing the risk for osteoporosis and fractures.38 Hypocalcemia or osteomalacia may cause generalized bone pain, muscular weakness, tetany, and chronic musculoskeletal pain.45

Fat‐soluble vitamin deficiencies are more common in those undergoing malabsorptive versus restrictive procedures and, in the case of BPD, may be related to the length of the common channel.43 It is important to ensure that calcium and vitamin D levels are sufficient prior to surgery, and prior to starting any osteoporotic treatment such as bisphosphonates.45 We recommend at least 1200 mg of calcium citrate and 1000‐2000 IU of Vitamin D daily. Up to 50,000 IU weekly or daily may be required to correct deficiency and maintain sufficiency in this population.46, 47 Vitamin D₂ (ergocalciferol) or D₃ (cholecalciferol) can be used for supplementation. Cholecalciferol is preferred if given through a feeding tube because it is less prone to clogging the tube.46 With severe malabsorption, phototherapy may be necessary, as intravenous doses are often inadequate and intramuscular preparations require special compounding.46 Calcium carbonate requires acid for proper absorption, therefore calcium citrate may be preferred due to achlorhydria from gastric exclusion.

Restrictive Procedures (Laparoscopic Adjustable Gastric Band and Sleeve Gastrectomy)

These procedures produce weight loss by reducing the size of the stomach or creating an obstruction in the proximal stomach, limiting the consumption of large quantities at one time. They produce early satiety, but patients may still consume a large volume of calorie‐dense liquids compromising weight loss.

Laparoscopic Adjustable Gastric Band

Laparoscopic adjustable gastric band (LAGB; Figure 1A) is the primary form of restrictive procedures with 2 Food and Drug Administration‐approved bands (Lap Band [Allergan, Inc; Irvine, CA] and REALIZE band [Ethicon Endo‐Surgery, Inc; Cincinnati, OH]). A cuff is inflated around the proximal stomach creating a gastric pouch approximately 15‐30 mL in size. A subcutaneous reservoir is attached to the cuff allowing adjustment to the degree of restriction.8 LAGB has replaced the vertical banded gastroplasty (VBG). It is less invasive, adjustable, and reversible (0.1% operative mortality rate). Weight loss is maintained with this procedure but is generally less, with a higher failure rate compared to the more common gastric bypass procedure (Table 1).3, 9 Complications may include band dysfunction (ie, slippage, erosion, infections), esophageal dilatation, balloon failure, and port malposition, with rates approaching 3%‐5% per year requiring removal or repair.10 Patients may also experience GERD symptoms, especially if the condition was present preoperatively. Progressive GERD symptoms should be investigated with an upper gastrointestinal (GI) series to ensure there is no band slippage, esophageal dilation, or dysfunction.

Figure 1

Table 1.Comparison of Outcomes for Various Procedures

	LAGB	Roux‐en‐Y Gastric Bypass	Biliopancreatic Diversion With and Without Duodenal Switch
NOTE: References: Buchwald et al.3; Kendrick and Dakin.9 Abbreviations: LAGB, laparoscopic adjustable gastric band.
Excess weight loss	48%	62%	70%
Resolution of diabetes	48%	84%	98%

Combination Procedures (Roux‐en‐Y Gastric Bypass and Biliopancreatic Diversion With and Without Duodenal Switch)

These procedures produce weight loss by decreasing caloric intake and altering digestion and absorption.

Gastrointestinal Complaints

One of the most common causes of hospital admission any time postoperatively is abdominal pain. A differential diagnosis of abdominal pain, nausea, and/or vomiting in the post‐bariatric surgery patient should include small bowel obstruction, hernias (internal or incisional), band complications, food intolerance, dietary noncompliance, ileus, mesenteric venous thrombosis, strictures (such as outlet obstruction or anastomotic stenosis), ulcers, esophagitis, cholelithiasis, dumping syndrome, and Roux stasis syndrome.20

A thorough history targeted at the relationship between symptoms and food intake, attention to the character and location of the pain, and a thorough physical exam (specifically the presence or absence of palpable tenderness, guarding, or rebound) is essential. The physical exam may be misleading in obese patients and, if radiographic studies cannot be performed secondary to patient size, surgical exploration may be needed soon after presentation. Therefore, even lacking an obvious surgical need, the bariatric surgeon should be notified of admission.

Improper food choice, and failure to slowly and adequately chew food, can result in emesis and digestive difficulty. Physical incompatibility with the small gastric pouch and gastric outlet obstructions can be caused by nondigestible foods (ie, breads, steak, raw vegetables). This highlights the importance of ordering the appropriate hospital diet.8 Specific gastric bypass hospital diets for all consistencies should reflect the mechanical limitations and carbohydrate/protein requirements of these patients.

Increased gallstone formation is observed in patients with rapid weight loss (1.5 kg/wk), especially following RYGB and less often after LAGB procedures (40% vs 20% over 3 years). Routine use of ursodiol during rapid weight loss (6 months after RYGB) reduces this complication to <5%.8

Stenosis or ulceration at the anastomotic site for RYGB can cause abdominal pain and vomiting. The incidence of stomal stenosis has been reported at 5%‐19% and typically occurs within the first 3 postoperative months.22 This problem is often amenable to endoscopic dilatation, unless a ring was used to reinforce the anastomosis. Ulceration has been reported in 1%‐16% of patients and is usually secondary to tobacco or non‐steroidal anti‐inflammatory drug (NSAID) use, H. pylori, fistula‐induced acid exposure, reaction to foreign material, or ischemia from tension and poor tissue perfusion.23, 24 Endoscopy can diagnose the presence of ulcers, with biopsies to rule out H. pylori infection. Cessation of NSAIDs and tobacco are critical. Medical management including proton pump inhibitors and/or sucralfate is sufficient for up to 95% of patients. Surgical revision is reserved for persistent ulcers associated with obstruction, pain, and/or bleeding.25

Dumping syndrome is a complex of post‐prandial symptoms occurring most commonly in the RYGB patients. As many as 44% of RYGB patients may experience this syndrome characterized by flushing, dizziness, abdominal distension, pain, nausea, vomiting, and/or diarrhea.26 Symptoms may result from the ingestion of large amounts of sugars which empty from the altered gastric pouch at an unregulated rate. This large osmotic load causes fluid shifts and surges in peptide hormone levels, resulting in symptoms which may reinforce adherence to the prescribed postoperative diet. It occurs shortly after a meal and resolves over hours. Dietary modifications, such as increased protein and fiber intake with decreased consumption of simple sugars, will ameliorate symptoms in many patients, with most seeing resolution after the first year.8, 27 Some patients experience hyperglycemia secondary to ingestion of simple carbohydrates, with hypoglycemia approximately 2 hours later (late dumping). In our experience, limiting carbohydrate intake to 30 grams at any meal usually alleviates post‐prandial hypoglycemia.

If the patient reports an absence of bowel movements and flatus, an ileus from chronic narcotic use or a mechanical small bowel obstruction secondary to internal hernias or adhesions (see Late Surgical Complications) must be investigated. Severe or prolonged pain, lasting longer than a few hours, is cause for alarm and should prompt aggressive evaluation and possibly exploratory surgery.

Excessive Weight Loss

In diagnosing postoperative excessive weight loss, it is important to understand average anticipated weight loss parameters. Compared to the values expected for RYGB, LAGB produces less weight loss and BPD with and without DS produces more (Table 227). Patients experiencing more rapid or prolonged weight loss should be investigated for bacterial overgrowth syndrome, short bowel syndrome, or other anatomic abnormalities.

Known risk factors for bacterial overgrowth, which are prominent in this population, include decreased gastric acidity and slowed intestinal transit time (ie, narcotic use). Patients may be asymptomatic or experience weight loss, abdominal bloating and/or pain, nausea, vomiting, and diarrhea. The diagnosis can be made with a hydrogen breath test or by obtaining quantitative cultures of jejunal secretions during endoscopy. Questions remain on how the normalized values of these tests are affected by the postoperative environment, and on how this syndrome may present or be treated if it affects the excluded intestine. Bacterial overgrowth may be an incidental finding and not the cause of the gastrointestinal complaints. Although data is limited, treatment typically consists of a 7‐10 day course of rifaximin 1200 mg/day (divided doses) and/or a trial of dietary modifications.20, 2831 These may include avoiding lactose and eating a high fat, low carbohydrate, low fiber diet, so nutrients are readily absorbed and not left for bacterial consumption.32

Short bowel syndrome (<100‐200 cm of intestinal tissue remaining and subsequent malabsorption) can occur after any extensive colonic resection or bypass of the intestine.33 This condition rarely results after an initial bariatric procedure; however, subsequent procedures for small bowel obstructions or intestinal ischemia may result in short bowel syndrome. Typical presentations include diarrhea, weight loss, and symptoms of vitamin and mineral deficiencies. Short bowel can also predispose patients to the development of bacterial overgrowth, further complicating weight loss. Management consists of nutritional supplementation, occasionally parenteral nutrition, and rarely reoperation to increase the length of the common channel.34 Avoidance of further bowel resection is crucial in preventing short bowel syndrome.33, 34 In the setting of carbohydrate malabsorption with concomitant bacterial overgrowth syndrome, production of d‐lactic acid causing a metabolic acidosis with encephalopathy has been reported.35

Once medical complications have been ruled out, it is prudent to evaluate for a psychological component such as anorexia nervosa. It is helpful to involve a qualified psychologist who is familiar with this population. Addictions to alcohol, gambling, and pain medications have been reported in the post‐bariatric surgery population as a substitute for food addiction.

Neurological Complications and Vitamin Deficiencies

Neurological complications develop months to years postoperatively, secondary to vitamin, mineral, and nutrient deficiencies that result from malabsorption or inadequate intake. An inpatient provider should be aware of the potential role these conditions may play in a hospitalized patient.

Peripheral neuropathy can develop secondary to several deficiencies, including vitamin B₁₂, thiamine, vitamin E, and copper. Their sources, deficiencies, and replacement regimens are presented in Table 3.3642 Thiamine deficiency, manifesting as Wernicke's encephalopathy, is particularly important in the postoperative patient with excessive vomiting. For prevention, we recommend all patients readmitted with vomiting and dehydration receive a banana bag or rally pack (thiamine 100 mg, folic acid 1 mg, multivitamin with iron and magnesium 3 g in one liter of D5 normal saline) over 4‐8 hours. Additional deficiencies after gastric bypass include folate, selenium, zinc, vitamin B₆, and riboflavin. A multivitamin with minerals will meet the needs of most patients. Multiple fat‐soluble vitamin deficiencies can occur with small bowel bacterial overgrowth or BPD.

Anemia

Iron deficiency affects 6%‐33% of patients after 1 year.43 Iron is preferentially absorbed in the duodenum and proximal jejunum which are bypassed postoperatively. The absence of gastric acid prevents conversion of ferric (Fe²⁺) to the absorbable ferrous (Fe³⁺) iron, further decreasing absorption.44 Ferritin reflects iron stores but is also an acute phase reactant and, therefore, may mask an underlying deficiency in an acutely ill hospitalized patient. A multivitamin with iron is recommended for all patients, but additional supplementation may be required for menstruating women.43 Parenteral administration may be necessary if oral supplements are not tolerated or are inadequately absorbed.44

Fractures and Osteomalacia

Calcium and vitamin D deficiencies are a significant problem in the bariatric surgery population, with resultant osteoporosis or osteomalacia and associated fractures.38, 43 Calcium is preferentially absorbed in the duodenum and proximal jejunum. Vitamin D is absorbed in the ileum or produced in the skin in response to ultraviolet B (UVB) radiation.45 Deficiency of vitamin D exacerbates calcium malabsorption, thereby causing secondary hyperparathyroidism, increased bone turnover, and osteomalacia. Dramatic weight loss can lead to bone loss, increasing the risk for osteoporosis and fractures.38 Hypocalcemia or osteomalacia may cause generalized bone pain, muscular weakness, tetany, and chronic musculoskeletal pain.45

Fat‐soluble vitamin deficiencies are more common in those undergoing malabsorptive versus restrictive procedures and, in the case of BPD, may be related to the length of the common channel.43 It is important to ensure that calcium and vitamin D levels are sufficient prior to surgery, and prior to starting any osteoporotic treatment such as bisphosphonates.45 We recommend at least 1200 mg of calcium citrate and 1000‐2000 IU of Vitamin D daily. Up to 50,000 IU weekly or daily may be required to correct deficiency and maintain sufficiency in this population.46, 47 Vitamin D₂ (ergocalciferol) or D₃ (cholecalciferol) can be used for supplementation. Cholecalciferol is preferred if given through a feeding tube because it is less prone to clogging the tube.46 With severe malabsorption, phototherapy may be necessary, as intravenous doses are often inadequate and intramuscular preparations require special compounding.46 Calcium carbonate requires acid for proper absorption, therefore calcium citrate may be preferred due to achlorhydria from gastric exclusion.

Restrictive Procedures (Laparoscopic Adjustable Gastric Band and Sleeve Gastrectomy)

These procedures produce weight loss by reducing the size of the stomach or creating an obstruction in the proximal stomach, limiting the consumption of large quantities at one time. They produce early satiety, but patients may still consume a large volume of calorie‐dense liquids compromising weight loss.

Laparoscopic Adjustable Gastric Band

Laparoscopic adjustable gastric band (LAGB; Figure 1A) is the primary form of restrictive procedures with 2 Food and Drug Administration‐approved bands (Lap Band [Allergan, Inc; Irvine, CA] and REALIZE band [Ethicon Endo‐Surgery, Inc; Cincinnati, OH]). A cuff is inflated around the proximal stomach creating a gastric pouch approximately 15‐30 mL in size. A subcutaneous reservoir is attached to the cuff allowing adjustment to the degree of restriction.8 LAGB has replaced the vertical banded gastroplasty (VBG). It is less invasive, adjustable, and reversible (0.1% operative mortality rate). Weight loss is maintained with this procedure but is generally less, with a higher failure rate compared to the more common gastric bypass procedure (Table 1).3, 9 Complications may include band dysfunction (ie, slippage, erosion, infections), esophageal dilatation, balloon failure, and port malposition, with rates approaching 3%‐5% per year requiring removal or repair.10 Patients may also experience GERD symptoms, especially if the condition was present preoperatively. Progressive GERD symptoms should be investigated with an upper gastrointestinal (GI) series to ensure there is no band slippage, esophageal dilation, or dysfunction.

Figure 1

Table 1.Comparison of Outcomes for Various Procedures

	LAGB	Roux‐en‐Y Gastric Bypass	Biliopancreatic Diversion With and Without Duodenal Switch
NOTE: References: Buchwald et al.3; Kendrick and Dakin.9 Abbreviations: LAGB, laparoscopic adjustable gastric band.
Excess weight loss	48%	62%	70%
Resolution of diabetes	48%	84%	98%

Combination Procedures (Roux‐en‐Y Gastric Bypass and Biliopancreatic Diversion With and Without Duodenal Switch)

These procedures produce weight loss by decreasing caloric intake and altering digestion and absorption.

Gastrointestinal Complaints

One of the most common causes of hospital admission any time postoperatively is abdominal pain. A differential diagnosis of abdominal pain, nausea, and/or vomiting in the post‐bariatric surgery patient should include small bowel obstruction, hernias (internal or incisional), band complications, food intolerance, dietary noncompliance, ileus, mesenteric venous thrombosis, strictures (such as outlet obstruction or anastomotic stenosis), ulcers, esophagitis, cholelithiasis, dumping syndrome, and Roux stasis syndrome.20

A thorough history targeted at the relationship between symptoms and food intake, attention to the character and location of the pain, and a thorough physical exam (specifically the presence or absence of palpable tenderness, guarding, or rebound) is essential. The physical exam may be misleading in obese patients and, if radiographic studies cannot be performed secondary to patient size, surgical exploration may be needed soon after presentation. Therefore, even lacking an obvious surgical need, the bariatric surgeon should be notified of admission.

Improper food choice, and failure to slowly and adequately chew food, can result in emesis and digestive difficulty. Physical incompatibility with the small gastric pouch and gastric outlet obstructions can be caused by nondigestible foods (ie, breads, steak, raw vegetables). This highlights the importance of ordering the appropriate hospital diet.8 Specific gastric bypass hospital diets for all consistencies should reflect the mechanical limitations and carbohydrate/protein requirements of these patients.

Increased gallstone formation is observed in patients with rapid weight loss (1.5 kg/wk), especially following RYGB and less often after LAGB procedures (40% vs 20% over 3 years). Routine use of ursodiol during rapid weight loss (6 months after RYGB) reduces this complication to <5%.8

Stenosis or ulceration at the anastomotic site for RYGB can cause abdominal pain and vomiting. The incidence of stomal stenosis has been reported at 5%‐19% and typically occurs within the first 3 postoperative months.22 This problem is often amenable to endoscopic dilatation, unless a ring was used to reinforce the anastomosis. Ulceration has been reported in 1%‐16% of patients and is usually secondary to tobacco or non‐steroidal anti‐inflammatory drug (NSAID) use, H. pylori, fistula‐induced acid exposure, reaction to foreign material, or ischemia from tension and poor tissue perfusion.23, 24 Endoscopy can diagnose the presence of ulcers, with biopsies to rule out H. pylori infection. Cessation of NSAIDs and tobacco are critical. Medical management including proton pump inhibitors and/or sucralfate is sufficient for up to 95% of patients. Surgical revision is reserved for persistent ulcers associated with obstruction, pain, and/or bleeding.25

Dumping syndrome is a complex of post‐prandial symptoms occurring most commonly in the RYGB patients. As many as 44% of RYGB patients may experience this syndrome characterized by flushing, dizziness, abdominal distension, pain, nausea, vomiting, and/or diarrhea.26 Symptoms may result from the ingestion of large amounts of sugars which empty from the altered gastric pouch at an unregulated rate. This large osmotic load causes fluid shifts and surges in peptide hormone levels, resulting in symptoms which may reinforce adherence to the prescribed postoperative diet. It occurs shortly after a meal and resolves over hours. Dietary modifications, such as increased protein and fiber intake with decreased consumption of simple sugars, will ameliorate symptoms in many patients, with most seeing resolution after the first year.8, 27 Some patients experience hyperglycemia secondary to ingestion of simple carbohydrates, with hypoglycemia approximately 2 hours later (late dumping). In our experience, limiting carbohydrate intake to 30 grams at any meal usually alleviates post‐prandial hypoglycemia.

If the patient reports an absence of bowel movements and flatus, an ileus from chronic narcotic use or a mechanical small bowel obstruction secondary to internal hernias or adhesions (see Late Surgical Complications) must be investigated. Severe or prolonged pain, lasting longer than a few hours, is cause for alarm and should prompt aggressive evaluation and possibly exploratory surgery.

Excessive Weight Loss

In diagnosing postoperative excessive weight loss, it is important to understand average anticipated weight loss parameters. Compared to the values expected for RYGB, LAGB produces less weight loss and BPD with and without DS produces more (Table 227). Patients experiencing more rapid or prolonged weight loss should be investigated for bacterial overgrowth syndrome, short bowel syndrome, or other anatomic abnormalities.

Known risk factors for bacterial overgrowth, which are prominent in this population, include decreased gastric acidity and slowed intestinal transit time (ie, narcotic use). Patients may be asymptomatic or experience weight loss, abdominal bloating and/or pain, nausea, vomiting, and diarrhea. The diagnosis can be made with a hydrogen breath test or by obtaining quantitative cultures of jejunal secretions during endoscopy. Questions remain on how the normalized values of these tests are affected by the postoperative environment, and on how this syndrome may present or be treated if it affects the excluded intestine. Bacterial overgrowth may be an incidental finding and not the cause of the gastrointestinal complaints. Although data is limited, treatment typically consists of a 7‐10 day course of rifaximin 1200 mg/day (divided doses) and/or a trial of dietary modifications.20, 2831 These may include avoiding lactose and eating a high fat, low carbohydrate, low fiber diet, so nutrients are readily absorbed and not left for bacterial consumption.32

Short bowel syndrome (<100‐200 cm of intestinal tissue remaining and subsequent malabsorption) can occur after any extensive colonic resection or bypass of the intestine.33 This condition rarely results after an initial bariatric procedure; however, subsequent procedures for small bowel obstructions or intestinal ischemia may result in short bowel syndrome. Typical presentations include diarrhea, weight loss, and symptoms of vitamin and mineral deficiencies. Short bowel can also predispose patients to the development of bacterial overgrowth, further complicating weight loss. Management consists of nutritional supplementation, occasionally parenteral nutrition, and rarely reoperation to increase the length of the common channel.34 Avoidance of further bowel resection is crucial in preventing short bowel syndrome.33, 34 In the setting of carbohydrate malabsorption with concomitant bacterial overgrowth syndrome, production of d‐lactic acid causing a metabolic acidosis with encephalopathy has been reported.35

Once medical complications have been ruled out, it is prudent to evaluate for a psychological component such as anorexia nervosa. It is helpful to involve a qualified psychologist who is familiar with this population. Addictions to alcohol, gambling, and pain medications have been reported in the post‐bariatric surgery population as a substitute for food addiction.

Neurological Complications and Vitamin Deficiencies

Neurological complications develop months to years postoperatively, secondary to vitamin, mineral, and nutrient deficiencies that result from malabsorption or inadequate intake. An inpatient provider should be aware of the potential role these conditions may play in a hospitalized patient.

Peripheral neuropathy can develop secondary to several deficiencies, including vitamin B₁₂, thiamine, vitamin E, and copper. Their sources, deficiencies, and replacement regimens are presented in Table 3.3642 Thiamine deficiency, manifesting as Wernicke's encephalopathy, is particularly important in the postoperative patient with excessive vomiting. For prevention, we recommend all patients readmitted with vomiting and dehydration receive a banana bag or rally pack (thiamine 100 mg, folic acid 1 mg, multivitamin with iron and magnesium 3 g in one liter of D5 normal saline) over 4‐8 hours. Additional deficiencies after gastric bypass include folate, selenium, zinc, vitamin B₆, and riboflavin. A multivitamin with minerals will meet the needs of most patients. Multiple fat‐soluble vitamin deficiencies can occur with small bowel bacterial overgrowth or BPD.

Anemia

Iron deficiency affects 6%‐33% of patients after 1 year.43 Iron is preferentially absorbed in the duodenum and proximal jejunum which are bypassed postoperatively. The absence of gastric acid prevents conversion of ferric (Fe²⁺) to the absorbable ferrous (Fe³⁺) iron, further decreasing absorption.44 Ferritin reflects iron stores but is also an acute phase reactant and, therefore, may mask an underlying deficiency in an acutely ill hospitalized patient. A multivitamin with iron is recommended for all patients, but additional supplementation may be required for menstruating women.43 Parenteral administration may be necessary if oral supplements are not tolerated or are inadequately absorbed.44

Fractures and Osteomalacia

Calcium and vitamin D deficiencies are a significant problem in the bariatric surgery population, with resultant osteoporosis or osteomalacia and associated fractures.38, 43 Calcium is preferentially absorbed in the duodenum and proximal jejunum. Vitamin D is absorbed in the ileum or produced in the skin in response to ultraviolet B (UVB) radiation.45 Deficiency of vitamin D exacerbates calcium malabsorption, thereby causing secondary hyperparathyroidism, increased bone turnover, and osteomalacia. Dramatic weight loss can lead to bone loss, increasing the risk for osteoporosis and fractures.38 Hypocalcemia or osteomalacia may cause generalized bone pain, muscular weakness, tetany, and chronic musculoskeletal pain.45

Fat‐soluble vitamin deficiencies are more common in those undergoing malabsorptive versus restrictive procedures and, in the case of BPD, may be related to the length of the common channel.43 It is important to ensure that calcium and vitamin D levels are sufficient prior to surgery, and prior to starting any osteoporotic treatment such as bisphosphonates.45 We recommend at least 1200 mg of calcium citrate and 1000‐2000 IU of Vitamin D daily. Up to 50,000 IU weekly or daily may be required to correct deficiency and maintain sufficiency in this population.46, 47 Vitamin D₂ (ergocalciferol) or D₃ (cholecalciferol) can be used for supplementation. Cholecalciferol is preferred if given through a feeding tube because it is less prone to clogging the tube.46 With severe malabsorption, phototherapy may be necessary, as intravenous doses are often inadequate and intramuscular preparations require special compounding.46 Calcium carbonate requires acid for proper absorption, therefore calcium citrate may be preferred due to achlorhydria from gastric exclusion.

Setting

Our tertiary‐care academic teaching hospital is a 200‐bed facility in metropolitan Phoenix, Arizona. All adult general medical and surgical specialties are represented, including transplantation services; the hospital also has a level 2 trauma center and an inpatient rehabilitation unit. Care is provided by various types of practitioners, including postgraduate trainees, faculty, physician assistants, and nurse‐practitioners. An electronic medical record links outpatient and inpatient records with laboratory results and pharmacy orders. The core electronic health record system is the Centricity/LastWord platform, provided by GE/IDX. The ancillary core systems, including laboratory and pharmacy, are interfaced with the Centricity system and maintained by on‐site Mayo Clinic information technology professionals.

Case Selection

Patients discharged with an International Classification of Diseases, 9th Revision, Clinical Modification (ICD‐9‐CM) diagnosis code for diabetes (ICD‐9‐CM code 250.xx) or hyperglycemia (ICD‐9‐CM code 790.6) were identified in a search of the hospital's electronic billing records.24 Our facility does not provide obstetric or pediatric services; therefore, corresponding ICD‐9‐CM codes for those populations were not included. Both primary and nonprimary diagnostic fields were searched. Discharges were extracted for the period between January 1, 2001, and December 31, 2004. Data retrieved included patient age, ethnicity/race, length of stay (LOS), and type of hospital service with primary responsibility for the patient's care. For confidentiality reasons, individual patients were not identified, and the unit of analysis was the discharge.

Our analyses focused principally on the noncritically ill, defined as those patients who did not require a stay in our intensive or intermediate care units; critically ill patients were identified based on room location in the data set and excluded. The reasons this study assessed hyperglycemia management in the noncritically ill were 2‐fold. First, the critically ill may migrate in and out of intensive care depending on their health status and thus experience different intensities of glucose management. Second, in our facility the therapeutic approach to hyperglycemia management is different for the critically ill than for the noncritically ill; the critically ill may receive intravenous and/or subcutaneous insulin, whereas subcutaneous insulin therapy only is given to the noncritically ill. Thus, the noncritically ill represent a more clearly defined patient population whose therapies would be easier to evaluate. We also restricted the final analysis to patients who had a LOS of 3 days or less, so that differences in glucose control and insulin therapy between the first and last 24 hours of hospital stay could be assessed.

Data on 30 randomly chosen patients from different years was extracted from electronic records. A spreadsheet of the data was compared against data in our online electronic medical records. The online data were printed, and packets were made of the data for each patient selected for review. The patient demographic information was validated against our registration screen. Inpatient stay was validated to verify a patient was in intensive or intermediate care. The result of each glucose test performed while the patient was in the hospital was printed and the calculations validated. The insulin given while the patient was hospitalized was also printed and reviewed to verify the type of insulin and calculations for the amounts of insulin given.

Assessment of Glycemic Control

After extraction of hospital cases, data were linked via patient identifiers to our electronic laboratory database to retrieve information on glucose values. Glucose data included both blood and bedside measurements. In our institution, bedside glucose monitoring is performed with an instrument that scans and records patient identification, followed by direct downloading to our laboratory database. Commercial software (Medical Automation Systems, Charlottesville, VA) facilitates the interfacing of glucometer data with the electronic laboratory file.

Nearly all hospitalized patients had either bedside glucose (84%) or blood glucose (86%) data available for analysis. However, the mean number of bedside glucose measurements was 3.4 per day, whereas the average number of blood glucose measurements was only 1.0 per day. Because of the greater number of bedside measurements and because practitioners typically make therapeutic decisions about hyperglycemia management on the basis of daily bedside glucose results, these values were used to assess glycemic control of patients in the hospital discharge data.15

To assess glycemic control, we used methods similar to those previously published by ourselves and others.15, 23 We averaged each patient's available bedside glucose measurements to determine the composite average (BedGluc_avg). We also computed the average of bedside glucose measurements obtained during the first 24 hours after admission (F24BedGluc_avg) and during the last 24 hours before discharge (L24BedGluc_avg), then examined the distributions of BedGluc_avg, F24BedGluc_avg, and L24BedGluc_avg. The first 24‐hour period was calculated forward from the recorded time of admission, and the last 24‐hour period was calculated backward from the time of discharge. We calculated the frequency that each patient's bedside measurements showed hypoglycemia (bedside glucose < 70, < 60, < 50, or < 40 mg/dL) and showed hyperglycemia (bedside glucose >2 00, > 250, > 300, > 350, or > 400 mg/dL). Results were recorded as the number of values per 100 measurements per person; this method allowed adjustment for variation in the individual number of measurements and captured information on multiple episodes of hypo‐ or hyperglycemia of individual patients.15, 23

Hyperglycemia Therapy

Links to our inpatient pharmacy database enabled determination of types of pharmacotherapy actually administered to patients to treat hyperglycemia. Our electronic pharmacy records are designed so that intravenous medications (eg, intravenous insulin), scheduled oral and subcutaneous medications (eg, subcutaneous insulin), and medications administered on a one‐time or as‐needed basis (eg, sliding‐scale insulin) are documented electronically as separate categories. In our facility, intravenous insulin is administered only in the intensive care setting or as a component of total parenteral nutrition, and we excluded intravenous insulin use from this data. Thus, our analysis of insulin therapy focused only on elucidating patterns of subcutaneous treatment.

We classified hyperglycemia treatment as no therapy, oral agents only, oral agents plus insulin, and insulin only. Patients were regarded as having received an oral agent or insulin if they were administered the medication at any time during their inpatient stay. For management of hyperglycemia in noncritically ill patients, the use of a programmed basal‐bolus insulin program is advocated rather than the use of only a short‐acting bolus or sliding‐scale regimen.7, 8 Therefore, we further examined the insulin treatment strategies by classifying the type of regimen as basal only (if only an extended‐release preparation was used), as basal bolus (if the therapy consisted of a long‐acting plus a short‐acting formulation), or as bolus only (if the only insulin administered was a short‐acting preparation).

In addition to characterizing the general therapeutic approaches to hyperglycemia, we determined changes in the amount of insulin administered according to the severity of the hyperglycemia. Among patients who received insulin, we compared the average total units of insulin used during the last 24 hours before discharge with the amount administered during the first 24 hours of hospitalization. If more units were used during the last 24 hours than in the first 24 hours, the amount of insulin administered was categorized as having increased; if fewer units were provided during the last 24 hours, then the insulin amount was classified as having decreased; otherwise, no change was considered to have occurred. The BedGluc_avg values were divided into 3 intervals using tertile cut points, and the differences in the proportion of patients by each type of insulin treatment regimen and the categories of insulin change were compared across tertiles; differences in proportions were determined using the ² statistic.

Patient Characteristics

Between January 1, 2001, and December 31, 2004, a total of 7361 patients were discharged from our facility with either a diabetes or a hyperglycemia diagnosis (16% of all discharges); the percentage of discharges associated with these diagnoses increased from 14.9% in 2001 to 16.4% in 2004. Most patients with diabetes or hyperglycemia (5198 or 71%) received care outside the intensive‐ or intermediate‐care setting.

Among the noncritically ill patients whose LOS was at least 3 days (N = 2916), average age was 69 years, and average LOS was 5.7 days. Most of the discharged patients were men (57%), and 90% were white. Most patients were discharged from primary care (45%; general internal medicine or family medicine) or surgical services (34%), with the rest discharged from other specialties (eg, cardiology, transplant medicine). Compared to the noncritically ill, who had an LOS of at least 3 days, those noncritically patients whose LOS was less than 3 days (n = 2282) were slightly younger (mean age 68 versus 69 years, P < .001 by Mann‐Whitney testing) but were comparable in sex and race distribution (P > .07 for both by chi‐square testing).

Glycemic Control

The median duration between admission and time of first bedside glucose measurement was 3.0 hours. Patients had an average of 19 bedside glucose measurements; the overall mean number of bedside measurements was 3.4 per day, 3.7 during the first 24‐hour period, and 3.4 during the last 24 hours of hospitalization. Nearly 25% of patients were hyperglycemic (bedside glucose > 200 mg/dL) during the first 24 hours of hospitalization (Fig. 1A), 20% had persistent hyperglycemia throughout the entire hospitalization (Fig. 1B), and 21% were hyperglycemic during the 24 hours before discharge (Fig. 1C), with some patients discharged with an average bedside glucose of at least 300 mg/dL during the 24 hours before discharge.

Figure 1

The incidence of hypoglycemic episodes was lower than that of hyperglycemic episodes: 21% of patients had at least 1 bedside glucose value less than 70 mg/dL, but 68% had at least 1 value greater than 200 mg/dL. The frequency of hypoglycemic measurements was low (Fig. 2A) compared with the frequency of hyperglycemic episodes (Fig. 2B).

Figure 2

Hyperglycemia Therapy

Most patients (72%) received subcutaneous insulin at some point during their hospital stay; 19% had no therapy, 9% had oral agents only, 26% had oral agents plus insulin, and 46% had insulin only. The proportion receiving no therapy decreased from 32% among patients whose BedGluc_avg was in the first tertile to 2% in the third tertile; the percentage of patients taking oral agents only decreased from 18% to 1%; the proportion taking oral agents plus insulin was 17% in the first tertile and 30% in the third; and the proportion of those taking insulin only was 32% in the first tertile and 66% in the third (Fig. 3). Thus, nearly all patients whose BedGluc_avg value was in the third tertile received insulin, either as monotherapy or in combination with oral agents.

Figure 3

Among insulin users, 58% received bolus‐only, 42% received basal‐bolus, and 1% received basal‐only injections. Because of the small proportion of basal‐only patients, we conducted analyses only of patients whose insulin treatment fell into 1 of the first 2 categories. The use of a basal‐bolus insulin program increased from 34% in patients whose BedGluc_avg was in the first tertile to 54% for those who had BedGluc_avg in the third tertile (P < .001; Fig. 4, left). Thus, although there was a greater transition to a more intensive insulin regimen with worsening hyperglycemia, a substantial number of patients (46%) whose BedGluc_avg was in the third tertile still did not have their insulin regimen intensified to a basal‐bolus program.

Figure 4

Fifty‐four percent of subcutaneous insulin users (N = 1680) had an increase in the amount of insulin administered between the first and last 24 hours of hospitalization (average increase, 17 U), 39% had a decrease (average decrease, 12 U), and 7% had no change. With rising hyperglycemia, more patients had their insulin increased by the time of discharge; 41% of persons who had BedGluc_avg values in the first tertile were on more insulin by the time of discharge, whereas 65% of those who had average glucose values in the third tertile had insulin increased (Fig. 4, right). However, the pattern of changes in the amount of administered insulin was heterogeneous, with increases, decreases, and no change occurring in all tertiles of BedGluc_avg (Fig. 3, right). Nearly 31% of patients whose BedGluc_avg values were in the third tertile actually had a decrease in insulin. This decrease occurred despite evidence of a low frequency of hypoglycemia (only 1.2 values < 70 mg/dL per 100 measurements per person) and a high frequency of hyperglycemia (55.4 values > 200 mg/dL per person per 100 measurements).

Setting

Our tertiary‐care academic teaching hospital is a 200‐bed facility in metropolitan Phoenix, Arizona. All adult general medical and surgical specialties are represented, including transplantation services; the hospital also has a level 2 trauma center and an inpatient rehabilitation unit. Care is provided by various types of practitioners, including postgraduate trainees, faculty, physician assistants, and nurse‐practitioners. An electronic medical record links outpatient and inpatient records with laboratory results and pharmacy orders. The core electronic health record system is the Centricity/LastWord platform, provided by GE/IDX. The ancillary core systems, including laboratory and pharmacy, are interfaced with the Centricity system and maintained by on‐site Mayo Clinic information technology professionals.

Case Selection

Patients discharged with an International Classification of Diseases, 9th Revision, Clinical Modification (ICD‐9‐CM) diagnosis code for diabetes (ICD‐9‐CM code 250.xx) or hyperglycemia (ICD‐9‐CM code 790.6) were identified in a search of the hospital's electronic billing records.24 Our facility does not provide obstetric or pediatric services; therefore, corresponding ICD‐9‐CM codes for those populations were not included. Both primary and nonprimary diagnostic fields were searched. Discharges were extracted for the period between January 1, 2001, and December 31, 2004. Data retrieved included patient age, ethnicity/race, length of stay (LOS), and type of hospital service with primary responsibility for the patient's care. For confidentiality reasons, individual patients were not identified, and the unit of analysis was the discharge.

Our analyses focused principally on the noncritically ill, defined as those patients who did not require a stay in our intensive or intermediate care units; critically ill patients were identified based on room location in the data set and excluded. The reasons this study assessed hyperglycemia management in the noncritically ill were 2‐fold. First, the critically ill may migrate in and out of intensive care depending on their health status and thus experience different intensities of glucose management. Second, in our facility the therapeutic approach to hyperglycemia management is different for the critically ill than for the noncritically ill; the critically ill may receive intravenous and/or subcutaneous insulin, whereas subcutaneous insulin therapy only is given to the noncritically ill. Thus, the noncritically ill represent a more clearly defined patient population whose therapies would be easier to evaluate. We also restricted the final analysis to patients who had a LOS of 3 days or less, so that differences in glucose control and insulin therapy between the first and last 24 hours of hospital stay could be assessed.

Data on 30 randomly chosen patients from different years was extracted from electronic records. A spreadsheet of the data was compared against data in our online electronic medical records. The online data were printed, and packets were made of the data for each patient selected for review. The patient demographic information was validated against our registration screen. Inpatient stay was validated to verify a patient was in intensive or intermediate care. The result of each glucose test performed while the patient was in the hospital was printed and the calculations validated. The insulin given while the patient was hospitalized was also printed and reviewed to verify the type of insulin and calculations for the amounts of insulin given.

Assessment of Glycemic Control

After extraction of hospital cases, data were linked via patient identifiers to our electronic laboratory database to retrieve information on glucose values. Glucose data included both blood and bedside measurements. In our institution, bedside glucose monitoring is performed with an instrument that scans and records patient identification, followed by direct downloading to our laboratory database. Commercial software (Medical Automation Systems, Charlottesville, VA) facilitates the interfacing of glucometer data with the electronic laboratory file.

Nearly all hospitalized patients had either bedside glucose (84%) or blood glucose (86%) data available for analysis. However, the mean number of bedside glucose measurements was 3.4 per day, whereas the average number of blood glucose measurements was only 1.0 per day. Because of the greater number of bedside measurements and because practitioners typically make therapeutic decisions about hyperglycemia management on the basis of daily bedside glucose results, these values were used to assess glycemic control of patients in the hospital discharge data.15

To assess glycemic control, we used methods similar to those previously published by ourselves and others.15, 23 We averaged each patient's available bedside glucose measurements to determine the composite average (BedGluc_avg). We also computed the average of bedside glucose measurements obtained during the first 24 hours after admission (F24BedGluc_avg) and during the last 24 hours before discharge (L24BedGluc_avg), then examined the distributions of BedGluc_avg, F24BedGluc_avg, and L24BedGluc_avg. The first 24‐hour period was calculated forward from the recorded time of admission, and the last 24‐hour period was calculated backward from the time of discharge. We calculated the frequency that each patient's bedside measurements showed hypoglycemia (bedside glucose < 70, < 60, < 50, or < 40 mg/dL) and showed hyperglycemia (bedside glucose >2 00, > 250, > 300, > 350, or > 400 mg/dL). Results were recorded as the number of values per 100 measurements per person; this method allowed adjustment for variation in the individual number of measurements and captured information on multiple episodes of hypo‐ or hyperglycemia of individual patients.15, 23

Hyperglycemia Therapy

Links to our inpatient pharmacy database enabled determination of types of pharmacotherapy actually administered to patients to treat hyperglycemia. Our electronic pharmacy records are designed so that intravenous medications (eg, intravenous insulin), scheduled oral and subcutaneous medications (eg, subcutaneous insulin), and medications administered on a one‐time or as‐needed basis (eg, sliding‐scale insulin) are documented electronically as separate categories. In our facility, intravenous insulin is administered only in the intensive care setting or as a component of total parenteral nutrition, and we excluded intravenous insulin use from this data. Thus, our analysis of insulin therapy focused only on elucidating patterns of subcutaneous treatment.

We classified hyperglycemia treatment as no therapy, oral agents only, oral agents plus insulin, and insulin only. Patients were regarded as having received an oral agent or insulin if they were administered the medication at any time during their inpatient stay. For management of hyperglycemia in noncritically ill patients, the use of a programmed basal‐bolus insulin program is advocated rather than the use of only a short‐acting bolus or sliding‐scale regimen.7, 8 Therefore, we further examined the insulin treatment strategies by classifying the type of regimen as basal only (if only an extended‐release preparation was used), as basal bolus (if the therapy consisted of a long‐acting plus a short‐acting formulation), or as bolus only (if the only insulin administered was a short‐acting preparation).

In addition to characterizing the general therapeutic approaches to hyperglycemia, we determined changes in the amount of insulin administered according to the severity of the hyperglycemia. Among patients who received insulin, we compared the average total units of insulin used during the last 24 hours before discharge with the amount administered during the first 24 hours of hospitalization. If more units were used during the last 24 hours than in the first 24 hours, the amount of insulin administered was categorized as having increased; if fewer units were provided during the last 24 hours, then the insulin amount was classified as having decreased; otherwise, no change was considered to have occurred. The BedGluc_avg values were divided into 3 intervals using tertile cut points, and the differences in the proportion of patients by each type of insulin treatment regimen and the categories of insulin change were compared across tertiles; differences in proportions were determined using the ² statistic.

Patient Characteristics

Between January 1, 2001, and December 31, 2004, a total of 7361 patients were discharged from our facility with either a diabetes or a hyperglycemia diagnosis (16% of all discharges); the percentage of discharges associated with these diagnoses increased from 14.9% in 2001 to 16.4% in 2004. Most patients with diabetes or hyperglycemia (5198 or 71%) received care outside the intensive‐ or intermediate‐care setting.

Among the noncritically ill patients whose LOS was at least 3 days (N = 2916), average age was 69 years, and average LOS was 5.7 days. Most of the discharged patients were men (57%), and 90% were white. Most patients were discharged from primary care (45%; general internal medicine or family medicine) or surgical services (34%), with the rest discharged from other specialties (eg, cardiology, transplant medicine). Compared to the noncritically ill, who had an LOS of at least 3 days, those noncritically patients whose LOS was less than 3 days (n = 2282) were slightly younger (mean age 68 versus 69 years, P < .001 by Mann‐Whitney testing) but were comparable in sex and race distribution (P > .07 for both by chi‐square testing).

Glycemic Control

The median duration between admission and time of first bedside glucose measurement was 3.0 hours. Patients had an average of 19 bedside glucose measurements; the overall mean number of bedside measurements was 3.4 per day, 3.7 during the first 24‐hour period, and 3.4 during the last 24 hours of hospitalization. Nearly 25% of patients were hyperglycemic (bedside glucose > 200 mg/dL) during the first 24 hours of hospitalization (Fig. 1A), 20% had persistent hyperglycemia throughout the entire hospitalization (Fig. 1B), and 21% were hyperglycemic during the 24 hours before discharge (Fig. 1C), with some patients discharged with an average bedside glucose of at least 300 mg/dL during the 24 hours before discharge.

Figure 1

The incidence of hypoglycemic episodes was lower than that of hyperglycemic episodes: 21% of patients had at least 1 bedside glucose value less than 70 mg/dL, but 68% had at least 1 value greater than 200 mg/dL. The frequency of hypoglycemic measurements was low (Fig. 2A) compared with the frequency of hyperglycemic episodes (Fig. 2B).

Figure 2

Hyperglycemia Therapy

Most patients (72%) received subcutaneous insulin at some point during their hospital stay; 19% had no therapy, 9% had oral agents only, 26% had oral agents plus insulin, and 46% had insulin only. The proportion receiving no therapy decreased from 32% among patients whose BedGluc_avg was in the first tertile to 2% in the third tertile; the percentage of patients taking oral agents only decreased from 18% to 1%; the proportion taking oral agents plus insulin was 17% in the first tertile and 30% in the third; and the proportion of those taking insulin only was 32% in the first tertile and 66% in the third (Fig. 3). Thus, nearly all patients whose BedGluc_avg value was in the third tertile received insulin, either as monotherapy or in combination with oral agents.

Figure 3

Among insulin users, 58% received bolus‐only, 42% received basal‐bolus, and 1% received basal‐only injections. Because of the small proportion of basal‐only patients, we conducted analyses only of patients whose insulin treatment fell into 1 of the first 2 categories. The use of a basal‐bolus insulin program increased from 34% in patients whose BedGluc_avg was in the first tertile to 54% for those who had BedGluc_avg in the third tertile (P < .001; Fig. 4, left). Thus, although there was a greater transition to a more intensive insulin regimen with worsening hyperglycemia, a substantial number of patients (46%) whose BedGluc_avg was in the third tertile still did not have their insulin regimen intensified to a basal‐bolus program.

Figure 4

Fifty‐four percent of subcutaneous insulin users (N = 1680) had an increase in the amount of insulin administered between the first and last 24 hours of hospitalization (average increase, 17 U), 39% had a decrease (average decrease, 12 U), and 7% had no change. With rising hyperglycemia, more patients had their insulin increased by the time of discharge; 41% of persons who had BedGluc_avg values in the first tertile were on more insulin by the time of discharge, whereas 65% of those who had average glucose values in the third tertile had insulin increased (Fig. 4, right). However, the pattern of changes in the amount of administered insulin was heterogeneous, with increases, decreases, and no change occurring in all tertiles of BedGluc_avg (Fig. 3, right). Nearly 31% of patients whose BedGluc_avg values were in the third tertile actually had a decrease in insulin. This decrease occurred despite evidence of a low frequency of hypoglycemia (only 1.2 values < 70 mg/dL per 100 measurements per person) and a high frequency of hyperglycemia (55.4 values > 200 mg/dL per person per 100 measurements).

Setting

Our tertiary‐care academic teaching hospital is a 200‐bed facility in metropolitan Phoenix, Arizona. All adult general medical and surgical specialties are represented, including transplantation services; the hospital also has a level 2 trauma center and an inpatient rehabilitation unit. Care is provided by various types of practitioners, including postgraduate trainees, faculty, physician assistants, and nurse‐practitioners. An electronic medical record links outpatient and inpatient records with laboratory results and pharmacy orders. The core electronic health record system is the Centricity/LastWord platform, provided by GE/IDX. The ancillary core systems, including laboratory and pharmacy, are interfaced with the Centricity system and maintained by on‐site Mayo Clinic information technology professionals.

Case Selection

Patients discharged with an International Classification of Diseases, 9th Revision, Clinical Modification (ICD‐9‐CM) diagnosis code for diabetes (ICD‐9‐CM code 250.xx) or hyperglycemia (ICD‐9‐CM code 790.6) were identified in a search of the hospital's electronic billing records.24 Our facility does not provide obstetric or pediatric services; therefore, corresponding ICD‐9‐CM codes for those populations were not included. Both primary and nonprimary diagnostic fields were searched. Discharges were extracted for the period between January 1, 2001, and December 31, 2004. Data retrieved included patient age, ethnicity/race, length of stay (LOS), and type of hospital service with primary responsibility for the patient's care. For confidentiality reasons, individual patients were not identified, and the unit of analysis was the discharge.

Our analyses focused principally on the noncritically ill, defined as those patients who did not require a stay in our intensive or intermediate care units; critically ill patients were identified based on room location in the data set and excluded. The reasons this study assessed hyperglycemia management in the noncritically ill were 2‐fold. First, the critically ill may migrate in and out of intensive care depending on their health status and thus experience different intensities of glucose management. Second, in our facility the therapeutic approach to hyperglycemia management is different for the critically ill than for the noncritically ill; the critically ill may receive intravenous and/or subcutaneous insulin, whereas subcutaneous insulin therapy only is given to the noncritically ill. Thus, the noncritically ill represent a more clearly defined patient population whose therapies would be easier to evaluate. We also restricted the final analysis to patients who had a LOS of 3 days or less, so that differences in glucose control and insulin therapy between the first and last 24 hours of hospital stay could be assessed.

Data on 30 randomly chosen patients from different years was extracted from electronic records. A spreadsheet of the data was compared against data in our online electronic medical records. The online data were printed, and packets were made of the data for each patient selected for review. The patient demographic information was validated against our registration screen. Inpatient stay was validated to verify a patient was in intensive or intermediate care. The result of each glucose test performed while the patient was in the hospital was printed and the calculations validated. The insulin given while the patient was hospitalized was also printed and reviewed to verify the type of insulin and calculations for the amounts of insulin given.

Assessment of Glycemic Control

After extraction of hospital cases, data were linked via patient identifiers to our electronic laboratory database to retrieve information on glucose values. Glucose data included both blood and bedside measurements. In our institution, bedside glucose monitoring is performed with an instrument that scans and records patient identification, followed by direct downloading to our laboratory database. Commercial software (Medical Automation Systems, Charlottesville, VA) facilitates the interfacing of glucometer data with the electronic laboratory file.

Nearly all hospitalized patients had either bedside glucose (84%) or blood glucose (86%) data available for analysis. However, the mean number of bedside glucose measurements was 3.4 per day, whereas the average number of blood glucose measurements was only 1.0 per day. Because of the greater number of bedside measurements and because practitioners typically make therapeutic decisions about hyperglycemia management on the basis of daily bedside glucose results, these values were used to assess glycemic control of patients in the hospital discharge data.15

To assess glycemic control, we used methods similar to those previously published by ourselves and others.15, 23 We averaged each patient's available bedside glucose measurements to determine the composite average (BedGluc_avg). We also computed the average of bedside glucose measurements obtained during the first 24 hours after admission (F24BedGluc_avg) and during the last 24 hours before discharge (L24BedGluc_avg), then examined the distributions of BedGluc_avg, F24BedGluc_avg, and L24BedGluc_avg. The first 24‐hour period was calculated forward from the recorded time of admission, and the last 24‐hour period was calculated backward from the time of discharge. We calculated the frequency that each patient's bedside measurements showed hypoglycemia (bedside glucose < 70, < 60, < 50, or < 40 mg/dL) and showed hyperglycemia (bedside glucose >2 00, > 250, > 300, > 350, or > 400 mg/dL). Results were recorded as the number of values per 100 measurements per person; this method allowed adjustment for variation in the individual number of measurements and captured information on multiple episodes of hypo‐ or hyperglycemia of individual patients.15, 23

Hyperglycemia Therapy

Links to our inpatient pharmacy database enabled determination of types of pharmacotherapy actually administered to patients to treat hyperglycemia. Our electronic pharmacy records are designed so that intravenous medications (eg, intravenous insulin), scheduled oral and subcutaneous medications (eg, subcutaneous insulin), and medications administered on a one‐time or as‐needed basis (eg, sliding‐scale insulin) are documented electronically as separate categories. In our facility, intravenous insulin is administered only in the intensive care setting or as a component of total parenteral nutrition, and we excluded intravenous insulin use from this data. Thus, our analysis of insulin therapy focused only on elucidating patterns of subcutaneous treatment.

We classified hyperglycemia treatment as no therapy, oral agents only, oral agents plus insulin, and insulin only. Patients were regarded as having received an oral agent or insulin if they were administered the medication at any time during their inpatient stay. For management of hyperglycemia in noncritically ill patients, the use of a programmed basal‐bolus insulin program is advocated rather than the use of only a short‐acting bolus or sliding‐scale regimen.7, 8 Therefore, we further examined the insulin treatment strategies by classifying the type of regimen as basal only (if only an extended‐release preparation was used), as basal bolus (if the therapy consisted of a long‐acting plus a short‐acting formulation), or as bolus only (if the only insulin administered was a short‐acting preparation).

In addition to characterizing the general therapeutic approaches to hyperglycemia, we determined changes in the amount of insulin administered according to the severity of the hyperglycemia. Among patients who received insulin, we compared the average total units of insulin used during the last 24 hours before discharge with the amount administered during the first 24 hours of hospitalization. If more units were used during the last 24 hours than in the first 24 hours, the amount of insulin administered was categorized as having increased; if fewer units were provided during the last 24 hours, then the insulin amount was classified as having decreased; otherwise, no change was considered to have occurred. The BedGluc_avg values were divided into 3 intervals using tertile cut points, and the differences in the proportion of patients by each type of insulin treatment regimen and the categories of insulin change were compared across tertiles; differences in proportions were determined using the ² statistic.

Patient Characteristics

Between January 1, 2001, and December 31, 2004, a total of 7361 patients were discharged from our facility with either a diabetes or a hyperglycemia diagnosis (16% of all discharges); the percentage of discharges associated with these diagnoses increased from 14.9% in 2001 to 16.4% in 2004. Most patients with diabetes or hyperglycemia (5198 or 71%) received care outside the intensive‐ or intermediate‐care setting.

Among the noncritically ill patients whose LOS was at least 3 days (N = 2916), average age was 69 years, and average LOS was 5.7 days. Most of the discharged patients were men (57%), and 90% were white. Most patients were discharged from primary care (45%; general internal medicine or family medicine) or surgical services (34%), with the rest discharged from other specialties (eg, cardiology, transplant medicine). Compared to the noncritically ill, who had an LOS of at least 3 days, those noncritically patients whose LOS was less than 3 days (n = 2282) were slightly younger (mean age 68 versus 69 years, P < .001 by Mann‐Whitney testing) but were comparable in sex and race distribution (P > .07 for both by chi‐square testing).

Glycemic Control

The median duration between admission and time of first bedside glucose measurement was 3.0 hours. Patients had an average of 19 bedside glucose measurements; the overall mean number of bedside measurements was 3.4 per day, 3.7 during the first 24‐hour period, and 3.4 during the last 24 hours of hospitalization. Nearly 25% of patients were hyperglycemic (bedside glucose > 200 mg/dL) during the first 24 hours of hospitalization (Fig. 1A), 20% had persistent hyperglycemia throughout the entire hospitalization (Fig. 1B), and 21% were hyperglycemic during the 24 hours before discharge (Fig. 1C), with some patients discharged with an average bedside glucose of at least 300 mg/dL during the 24 hours before discharge.

Figure 1

The incidence of hypoglycemic episodes was lower than that of hyperglycemic episodes: 21% of patients had at least 1 bedside glucose value less than 70 mg/dL, but 68% had at least 1 value greater than 200 mg/dL. The frequency of hypoglycemic measurements was low (Fig. 2A) compared with the frequency of hyperglycemic episodes (Fig. 2B).

Figure 2

Hyperglycemia Therapy

Most patients (72%) received subcutaneous insulin at some point during their hospital stay; 19% had no therapy, 9% had oral agents only, 26% had oral agents plus insulin, and 46% had insulin only. The proportion receiving no therapy decreased from 32% among patients whose BedGluc_avg was in the first tertile to 2% in the third tertile; the percentage of patients taking oral agents only decreased from 18% to 1%; the proportion taking oral agents plus insulin was 17% in the first tertile and 30% in the third; and the proportion of those taking insulin only was 32% in the first tertile and 66% in the third (Fig. 3). Thus, nearly all patients whose BedGluc_avg value was in the third tertile received insulin, either as monotherapy or in combination with oral agents.

Figure 3

Among insulin users, 58% received bolus‐only, 42% received basal‐bolus, and 1% received basal‐only injections. Because of the small proportion of basal‐only patients, we conducted analyses only of patients whose insulin treatment fell into 1 of the first 2 categories. The use of a basal‐bolus insulin program increased from 34% in patients whose BedGluc_avg was in the first tertile to 54% for those who had BedGluc_avg in the third tertile (P < .001; Fig. 4, left). Thus, although there was a greater transition to a more intensive insulin regimen with worsening hyperglycemia, a substantial number of patients (46%) whose BedGluc_avg was in the third tertile still did not have their insulin regimen intensified to a basal‐bolus program.

Figure 4

Fifty‐four percent of subcutaneous insulin users (N = 1680) had an increase in the amount of insulin administered between the first and last 24 hours of hospitalization (average increase, 17 U), 39% had a decrease (average decrease, 12 U), and 7% had no change. With rising hyperglycemia, more patients had their insulin increased by the time of discharge; 41% of persons who had BedGluc_avg values in the first tertile were on more insulin by the time of discharge, whereas 65% of those who had average glucose values in the third tertile had insulin increased (Fig. 4, right). However, the pattern of changes in the amount of administered insulin was heterogeneous, with increases, decreases, and no change occurring in all tertiles of BedGluc_avg (Fig. 3, right). Nearly 31% of patients whose BedGluc_avg values were in the third tertile actually had a decrease in insulin. This decrease occurred despite evidence of a low frequency of hypoglycemia (only 1.2 values < 70 mg/dL per 100 measurements per person) and a high frequency of hyperglycemia (55.4 values > 200 mg/dL per person per 100 measurements).