The concept of improved inpatient diabetes control has been gaining attention in hospitals nationwide as a mechanism for improving patient outcomes, decreasing readmission rates, reducing cost of care, and shortening hospital length of stay.14 The growing recognition that glycemic control is a critical element of inpatient care has prompted several national agencies, including the National Quality Forum (NQF), University Health System Consortium (UHC), Centers for Medicare and Medicaid Services (CMS), and the Joint Commission (JC) to make inpatient diabetes control a focus of quality improvement efforts and outcomes tracking.1 There is a national trend toward the use of intravenous insulin infusion for tight glycemic control of stress‐induced hyperglycemia in postoperative intensive care unit (ICU) and medical ICU patients.5, 6 Consequently, there is a need for the development of a standardized approach for performance evaluation of subcutaneous and intravenous insulin protocols, while ensuring patient safety issues. The analysis of glucose outcomes is based on the systematic analysis of blood glucose (BG) performance metrics known as glucometrics.7, 8 This has provided a means to measure the success of hospital quality improvement programs over time.

The 2008 American Diabetes Association (ADA) Clinical Practice Recommendations endorse BG goals for the critically ill to be maintained as close as possible to 110 mg/dL (6.1 mmol/L) and generally <140 mg/dL (7.8 mmol/L).2 The American Association of Clinical Endocrinologists/The American College of Endocrinology guidelines recommend for ICU care BG in the range of 80110 mg/dL.1, 4 Regarding the non‐critically ill patients, the ADA recommends targets for fasting BG of <126 mg/dL (7.0 mmol/L) and all random BG 180200 mg/dL (1011.1 mmol/L).2 A limitation for these BG goals is hypoglycemia; the ADA endorses that hospitals try to achieve these lower BG values through quality improvement initiatives devised to systematically and safely reduce the BG targets.2

Materials and Methods

The Medical University of South Carolina (MUSC) is a 709‐bed tertiary‐care medical/surgical center located in Charleston, South Carolina. The medical center consists of 6 adult ICUs: medical intensive care unit, coronary care unit, cardiothoracic intensive care unit, neurosurgical intensive care unit, neurosurgical trauma intensive care unit, and surgical trauma intensive care unit. Overall, 14% of patients are in the ICUs, and 86% of patients are on the wards. MUSC has an extensive referral network including neighboring hospitals, rehabilitation centers, outpatient specialty treatment and imaging centers, and doctors' offices.

Intravenous Insulin Protocol

The HDTF initially reviewed 15 evidence‐based protocols and identified 5 desirable protocol characteristics. These characteristics included easy physician ordering (requiring only a signature), ability to quickly reach and maintain a BG target range, minimal risk for hypoglycemic events, adaptability for use anywhere in the hospital setting, and acceptance and implementation by nursing staff.16

The IV protocol, a web‐based calculator (Figure 1), was developed based on the concept of the multiplier by White et al.17 For this protocol, the IV infusion (IVI) rate is changed based on a formula that uses a multiplier (a surrogate for insulin sensitivity factor) and the difference between measured BG and target blood glucose (TBG). The calculator uses the following mathematical formula: rate of insulin infusion/hour = (current BG 60 mg/dL) 0.03.18, 19 Additionally, the protocol requires that enough insulin be infused to address severe hyperglycemia at initiation with a rapid reduction in the insulin infusion rate as BG normalizes. The protocol also permits an adjustment of the insulin rate by tenths of a unit per hour to maintain the BG in the center of the target range. The main variant of this protocol is the value of the starting multiplier. The web‐based calculator is currently being used in all 6 adult ICUs and on all of the adult medical‐surgical floors at MUSC.

Figure 1

In early 2006, all adult ICUs were using our in‐house, web‐based intravenous insulin infusion calculator (IVIIC), which prompted more BG readings with intensification of insulin drip use.19 Specifically, initial monitoring for the IVIIC included BG readings every 24 hours. To avoid hypoglycemic events from occurring with the intensification of BG readings for the IVIIC, the BG monitoring frequency was increased to every hour in July 2006. Initial treatment for hypoglycemia was D50% (12.525 g), which tended to overcorrect BG. In July 2006, we revised the protocol using aliquots of D50% specific to the BG reading.19 This action has resulted in decreasing the glycemic excursions observed due to overcorrection of hypoglycemia.

BG target ranges to match the level of care are as follows: intensive care unit (80110 mg/dL); labor and delivery (70110 mg/dL); adult medical/surgical floors (80140 mg/dL); diabetic ketoacidosis (DKA)/hyperosmolar nonketotic coma (HHNK) (150200 mg/dL); neurosurgery ICU (90120 mg/dL); and perioperative patients (140180 mg/dL).20 These BG targets were created to satisfy the clinical requests of specific departments at MUSC. We have restricted starting the multiplier for DKA/HHNK at 0.01, to affect a slower rate of change and the multiplier for all others is set at 0.03.

Results

The baseline demographic characteristics of the four study groups are shown in Table 3. The four groups were found to be similar for gender distribution, mean age, and racial distribution. There were significant differences observed among hospital stay characteristics, insulin drip use, history of diabetes, ventilator support, kidney failure, dialysis, total parenteral nutrition (TPN), and red blood cell (RBC) transfusions. Overall, insulin drip use tended to increase over time. The percentage of patients with diabetes on admission or diagnosed during admission tended to decrease over time. This was likely due to an increase in the diagnosis and treatment of stress/steroid‐induced hyperglycemia during the hospital stay.

A total of 11,715 patient‐days, consisting of 56,401 individual BG readings obtained from 2,215 unique patients, were distributed across the 4 years. Table 4 presents the year‐specific patient‐day analysis. While the prevalence of mild (BG 5069 mg/dL) hypoglycemia was found to increase over the years studied (P < 0.01), the percentage of patient‐days with a mean BG in the range of 70180 mg/dL increased over the period of study (P < 0.01). The total hypoglycemia events <60 mg/dL are presented as comparative data to other studies.7 The percent of patient days with at least one BG < 70 mg/dL (reported in Table 4 as mild events) ranged from 3.72 in 2005 to as high as 10.71 in 2007; however, approximately one‐half of the hypoglycemic events are attributable to readings from BG 6069 since the proportion of patient days with a BG < 60 mg/dL was approximately one‐half that for BG < 70 mg/dL (Table 4). The prevalence of patient days with at least one moderate (BG 4049 mg/dL) or severe (BG < 40 mg/dL) hypoglycemia event was not found to increase in a linear manner. There was a statistical trend for potentially nonlinear relationship of year with moderate hypoglycemia and hyperglycemia.

Immediately following the implementation (year 2005), post hoc comparisons suggested that the rate of moderate hypoglycemia was lowest relative to the 3 other years, but no other statistical differences were observed. The year 2005 also had the lowest proportion of patient days with at least 1 hyperglycemic event.

The individual BG readings for the 2215 unique patients were also individually analyzed according to the methods of Goldberg et al.7 Even though no statistical tests were performed at the ward level, the descriptive data presented in Table 5 are consistent with the analysis of the patient‐day data. Several important features of the data are illustrated by Table 5. Most notably, the glycemic control at the hospital level is improved. The percentage of BG readings in the range of 70180 mg/dL increased annually whereas the mean BG values, the coefficient of variation, and the interquartile range (IQR) decreased annually.

Conclusions

Collectively, we have shown that implementing standardized insulin order sets including hypoglycemia, SC insulin, IV insulin, and IV to SC insulin transition treatment protocols at MUSC may generate the expected benefits for patient safety for this population of patients. The primary hypothesis that the rate of hypoglycemia and hyperglycemia would be lower after the implementation of these protocols was supported by the data, because the overall blood glucose control was markedly improved as a result of the protocols. However, the effect was strongest in 2005 (immediately following the protocol's implementation) and appeared to diminish some with time.

There were several other quality improvement measures initiated at MUSC that likely contributed to the decreasing rates of hypoglycemia and hyperglycemia. For example, comparing June 2004 with June 2007, the number of patients tested increased from 434 to 683. This increase could be attributed, in part, to a trend on medical/surgical services toward an increased focus on glucose monitoring.

When intensive glycemic control programs are implemented, hospitals should have a standardized, nurse‐driven hypoglycemia protocol.11 The success of such a hypoglycemia treatment protocol is demonstrated by the improvement observed at MUSC since the protocol was first implemented in October 2004.22

There are limitations that warrant consideration. A key limitation is that other procedural changes may have occurred during the years of study. Because the initial focus of the HDTF was to reduce hypoglycemic and hyperglycemic events, a multipronged approach was used, beginning with the treatment protocol but followed by other changes. These changes, while unmeasured in the current study, could have influenced the rate of hypoglycemia and hyperglycemia. Therefore, although the protocol that we developed has sound theoretical underpinnings, the improvement in glycemic control at other hospitals may vary. Second, because this was initially regarded as a quality improvement project for hospitalized patients with hypoglycemia and hyperglycemia, we did not evaluate morbidity, mortality, or other clinical outcome data other than BG targets and incidences of hypoglycemia and hyperglycemia. Third, there was no concurrent control group established for this study, rather the study used a retrospective, nonrandomized design with a historical control. As previously mentioned, we cannot rule out the idea that other changes occurred between the preprotocol and postprotocol interval to influence our results. Finally, there are statistical limitations to the research.

One limitation regarding the analysis of the BG data was the potential for an increased type I error (ie, false‐positive result) due to clustering of BG values within a patient and increased monitoring frequencies when a hypoglycemic or hyperglycemic event was observed. The generalized estimating equations directly addressed the first concern. In particular, the effective sample size for each participant was a function of the number of patient‐days and the correlation of patient‐day summaries. Therefore, patients with several highly‐correlated outcomes would contribute less to the analysis than other patients with the same number of patient‐days that were correlated to a lesser extent. As for the second concern, the patient‐day frequencies alleviate this problem and avoid the length‐of‐stay bias associated with a patient‐level (or patient‐stay) analysis. Power was less than planned due in part to the use of the patient‐day analysis instead of the originally designed ward‐level analysis. The change in the statistical design was a response to emerging evidence in the literature.7

In conclusion, the hypothesis that MUSC patients benefit from the use of standardized insulin order sets, hypoglycemia, and hyperglycemia treatment protocols, is supported by the data collected in this study. Because it has been recommended that a hypoglycemia and hyperglycemia prevention protocol as well as a hypoglycemia and hyperglycemia treatment protocol be in place, the HDTF will be focusing on the actual prevention of the hypoglycemic and hyperglycemic incidents occurring in the first place.2, 25 This may result in further reductions of hypoglycemic and hyperglycemic events. We have recently implemented hypoglycemia and hyperglycemia prevention policies at MUSC.

The concept of improved inpatient diabetes control has been gaining attention in hospitals nationwide as a mechanism for improving patient outcomes, decreasing readmission rates, reducing cost of care, and shortening hospital length of stay.14 The growing recognition that glycemic control is a critical element of inpatient care has prompted several national agencies, including the National Quality Forum (NQF), University Health System Consortium (UHC), Centers for Medicare and Medicaid Services (CMS), and the Joint Commission (JC) to make inpatient diabetes control a focus of quality improvement efforts and outcomes tracking.1 There is a national trend toward the use of intravenous insulin infusion for tight glycemic control of stress‐induced hyperglycemia in postoperative intensive care unit (ICU) and medical ICU patients.5, 6 Consequently, there is a need for the development of a standardized approach for performance evaluation of subcutaneous and intravenous insulin protocols, while ensuring patient safety issues. The analysis of glucose outcomes is based on the systematic analysis of blood glucose (BG) performance metrics known as glucometrics.7, 8 This has provided a means to measure the success of hospital quality improvement programs over time.

The 2008 American Diabetes Association (ADA) Clinical Practice Recommendations endorse BG goals for the critically ill to be maintained as close as possible to 110 mg/dL (6.1 mmol/L) and generally <140 mg/dL (7.8 mmol/L).2 The American Association of Clinical Endocrinologists/The American College of Endocrinology guidelines recommend for ICU care BG in the range of 80110 mg/dL.1, 4 Regarding the non‐critically ill patients, the ADA recommends targets for fasting BG of <126 mg/dL (7.0 mmol/L) and all random BG 180200 mg/dL (1011.1 mmol/L).2 A limitation for these BG goals is hypoglycemia; the ADA endorses that hospitals try to achieve these lower BG values through quality improvement initiatives devised to systematically and safely reduce the BG targets.2

Materials and Methods

The Medical University of South Carolina (MUSC) is a 709‐bed tertiary‐care medical/surgical center located in Charleston, South Carolina. The medical center consists of 6 adult ICUs: medical intensive care unit, coronary care unit, cardiothoracic intensive care unit, neurosurgical intensive care unit, neurosurgical trauma intensive care unit, and surgical trauma intensive care unit. Overall, 14% of patients are in the ICUs, and 86% of patients are on the wards. MUSC has an extensive referral network including neighboring hospitals, rehabilitation centers, outpatient specialty treatment and imaging centers, and doctors' offices.

Intravenous Insulin Protocol

The HDTF initially reviewed 15 evidence‐based protocols and identified 5 desirable protocol characteristics. These characteristics included easy physician ordering (requiring only a signature), ability to quickly reach and maintain a BG target range, minimal risk for hypoglycemic events, adaptability for use anywhere in the hospital setting, and acceptance and implementation by nursing staff.16

The IV protocol, a web‐based calculator (Figure 1), was developed based on the concept of the multiplier by White et al.17 For this protocol, the IV infusion (IVI) rate is changed based on a formula that uses a multiplier (a surrogate for insulin sensitivity factor) and the difference between measured BG and target blood glucose (TBG). The calculator uses the following mathematical formula: rate of insulin infusion/hour = (current BG 60 mg/dL) 0.03.18, 19 Additionally, the protocol requires that enough insulin be infused to address severe hyperglycemia at initiation with a rapid reduction in the insulin infusion rate as BG normalizes. The protocol also permits an adjustment of the insulin rate by tenths of a unit per hour to maintain the BG in the center of the target range. The main variant of this protocol is the value of the starting multiplier. The web‐based calculator is currently being used in all 6 adult ICUs and on all of the adult medical‐surgical floors at MUSC.

Figure 1

In early 2006, all adult ICUs were using our in‐house, web‐based intravenous insulin infusion calculator (IVIIC), which prompted more BG readings with intensification of insulin drip use.19 Specifically, initial monitoring for the IVIIC included BG readings every 24 hours. To avoid hypoglycemic events from occurring with the intensification of BG readings for the IVIIC, the BG monitoring frequency was increased to every hour in July 2006. Initial treatment for hypoglycemia was D50% (12.525 g), which tended to overcorrect BG. In July 2006, we revised the protocol using aliquots of D50% specific to the BG reading.19 This action has resulted in decreasing the glycemic excursions observed due to overcorrection of hypoglycemia.

BG target ranges to match the level of care are as follows: intensive care unit (80110 mg/dL); labor and delivery (70110 mg/dL); adult medical/surgical floors (80140 mg/dL); diabetic ketoacidosis (DKA)/hyperosmolar nonketotic coma (HHNK) (150200 mg/dL); neurosurgery ICU (90120 mg/dL); and perioperative patients (140180 mg/dL).20 These BG targets were created to satisfy the clinical requests of specific departments at MUSC. We have restricted starting the multiplier for DKA/HHNK at 0.01, to affect a slower rate of change and the multiplier for all others is set at 0.03.

Results

The baseline demographic characteristics of the four study groups are shown in Table 3. The four groups were found to be similar for gender distribution, mean age, and racial distribution. There were significant differences observed among hospital stay characteristics, insulin drip use, history of diabetes, ventilator support, kidney failure, dialysis, total parenteral nutrition (TPN), and red blood cell (RBC) transfusions. Overall, insulin drip use tended to increase over time. The percentage of patients with diabetes on admission or diagnosed during admission tended to decrease over time. This was likely due to an increase in the diagnosis and treatment of stress/steroid‐induced hyperglycemia during the hospital stay.

A total of 11,715 patient‐days, consisting of 56,401 individual BG readings obtained from 2,215 unique patients, were distributed across the 4 years. Table 4 presents the year‐specific patient‐day analysis. While the prevalence of mild (BG 5069 mg/dL) hypoglycemia was found to increase over the years studied (P < 0.01), the percentage of patient‐days with a mean BG in the range of 70180 mg/dL increased over the period of study (P < 0.01). The total hypoglycemia events <60 mg/dL are presented as comparative data to other studies.7 The percent of patient days with at least one BG < 70 mg/dL (reported in Table 4 as mild events) ranged from 3.72 in 2005 to as high as 10.71 in 2007; however, approximately one‐half of the hypoglycemic events are attributable to readings from BG 6069 since the proportion of patient days with a BG < 60 mg/dL was approximately one‐half that for BG < 70 mg/dL (Table 4). The prevalence of patient days with at least one moderate (BG 4049 mg/dL) or severe (BG < 40 mg/dL) hypoglycemia event was not found to increase in a linear manner. There was a statistical trend for potentially nonlinear relationship of year with moderate hypoglycemia and hyperglycemia.

Immediately following the implementation (year 2005), post hoc comparisons suggested that the rate of moderate hypoglycemia was lowest relative to the 3 other years, but no other statistical differences were observed. The year 2005 also had the lowest proportion of patient days with at least 1 hyperglycemic event.

The individual BG readings for the 2215 unique patients were also individually analyzed according to the methods of Goldberg et al.7 Even though no statistical tests were performed at the ward level, the descriptive data presented in Table 5 are consistent with the analysis of the patient‐day data. Several important features of the data are illustrated by Table 5. Most notably, the glycemic control at the hospital level is improved. The percentage of BG readings in the range of 70180 mg/dL increased annually whereas the mean BG values, the coefficient of variation, and the interquartile range (IQR) decreased annually.

Conclusions

Collectively, we have shown that implementing standardized insulin order sets including hypoglycemia, SC insulin, IV insulin, and IV to SC insulin transition treatment protocols at MUSC may generate the expected benefits for patient safety for this population of patients. The primary hypothesis that the rate of hypoglycemia and hyperglycemia would be lower after the implementation of these protocols was supported by the data, because the overall blood glucose control was markedly improved as a result of the protocols. However, the effect was strongest in 2005 (immediately following the protocol's implementation) and appeared to diminish some with time.

There were several other quality improvement measures initiated at MUSC that likely contributed to the decreasing rates of hypoglycemia and hyperglycemia. For example, comparing June 2004 with June 2007, the number of patients tested increased from 434 to 683. This increase could be attributed, in part, to a trend on medical/surgical services toward an increased focus on glucose monitoring.

When intensive glycemic control programs are implemented, hospitals should have a standardized, nurse‐driven hypoglycemia protocol.11 The success of such a hypoglycemia treatment protocol is demonstrated by the improvement observed at MUSC since the protocol was first implemented in October 2004.22

There are limitations that warrant consideration. A key limitation is that other procedural changes may have occurred during the years of study. Because the initial focus of the HDTF was to reduce hypoglycemic and hyperglycemic events, a multipronged approach was used, beginning with the treatment protocol but followed by other changes. These changes, while unmeasured in the current study, could have influenced the rate of hypoglycemia and hyperglycemia. Therefore, although the protocol that we developed has sound theoretical underpinnings, the improvement in glycemic control at other hospitals may vary. Second, because this was initially regarded as a quality improvement project for hospitalized patients with hypoglycemia and hyperglycemia, we did not evaluate morbidity, mortality, or other clinical outcome data other than BG targets and incidences of hypoglycemia and hyperglycemia. Third, there was no concurrent control group established for this study, rather the study used a retrospective, nonrandomized design with a historical control. As previously mentioned, we cannot rule out the idea that other changes occurred between the preprotocol and postprotocol interval to influence our results. Finally, there are statistical limitations to the research.

One limitation regarding the analysis of the BG data was the potential for an increased type I error (ie, false‐positive result) due to clustering of BG values within a patient and increased monitoring frequencies when a hypoglycemic or hyperglycemic event was observed. The generalized estimating equations directly addressed the first concern. In particular, the effective sample size for each participant was a function of the number of patient‐days and the correlation of patient‐day summaries. Therefore, patients with several highly‐correlated outcomes would contribute less to the analysis than other patients with the same number of patient‐days that were correlated to a lesser extent. As for the second concern, the patient‐day frequencies alleviate this problem and avoid the length‐of‐stay bias associated with a patient‐level (or patient‐stay) analysis. Power was less than planned due in part to the use of the patient‐day analysis instead of the originally designed ward‐level analysis. The change in the statistical design was a response to emerging evidence in the literature.7

In conclusion, the hypothesis that MUSC patients benefit from the use of standardized insulin order sets, hypoglycemia, and hyperglycemia treatment protocols, is supported by the data collected in this study. Because it has been recommended that a hypoglycemia and hyperglycemia prevention protocol as well as a hypoglycemia and hyperglycemia treatment protocol be in place, the HDTF will be focusing on the actual prevention of the hypoglycemic and hyperglycemic incidents occurring in the first place.2, 25 This may result in further reductions of hypoglycemic and hyperglycemic events. We have recently implemented hypoglycemia and hyperglycemia prevention policies at MUSC.

The concept of improved inpatient diabetes control has been gaining attention in hospitals nationwide as a mechanism for improving patient outcomes, decreasing readmission rates, reducing cost of care, and shortening hospital length of stay.14 The growing recognition that glycemic control is a critical element of inpatient care has prompted several national agencies, including the National Quality Forum (NQF), University Health System Consortium (UHC), Centers for Medicare and Medicaid Services (CMS), and the Joint Commission (JC) to make inpatient diabetes control a focus of quality improvement efforts and outcomes tracking.1 There is a national trend toward the use of intravenous insulin infusion for tight glycemic control of stress‐induced hyperglycemia in postoperative intensive care unit (ICU) and medical ICU patients.5, 6 Consequently, there is a need for the development of a standardized approach for performance evaluation of subcutaneous and intravenous insulin protocols, while ensuring patient safety issues. The analysis of glucose outcomes is based on the systematic analysis of blood glucose (BG) performance metrics known as glucometrics.7, 8 This has provided a means to measure the success of hospital quality improvement programs over time.

The 2008 American Diabetes Association (ADA) Clinical Practice Recommendations endorse BG goals for the critically ill to be maintained as close as possible to 110 mg/dL (6.1 mmol/L) and generally <140 mg/dL (7.8 mmol/L).2 The American Association of Clinical Endocrinologists/The American College of Endocrinology guidelines recommend for ICU care BG in the range of 80110 mg/dL.1, 4 Regarding the non‐critically ill patients, the ADA recommends targets for fasting BG of <126 mg/dL (7.0 mmol/L) and all random BG 180200 mg/dL (1011.1 mmol/L).2 A limitation for these BG goals is hypoglycemia; the ADA endorses that hospitals try to achieve these lower BG values through quality improvement initiatives devised to systematically and safely reduce the BG targets.2

Materials and Methods

The Medical University of South Carolina (MUSC) is a 709‐bed tertiary‐care medical/surgical center located in Charleston, South Carolina. The medical center consists of 6 adult ICUs: medical intensive care unit, coronary care unit, cardiothoracic intensive care unit, neurosurgical intensive care unit, neurosurgical trauma intensive care unit, and surgical trauma intensive care unit. Overall, 14% of patients are in the ICUs, and 86% of patients are on the wards. MUSC has an extensive referral network including neighboring hospitals, rehabilitation centers, outpatient specialty treatment and imaging centers, and doctors' offices.

Intravenous Insulin Protocol

The HDTF initially reviewed 15 evidence‐based protocols and identified 5 desirable protocol characteristics. These characteristics included easy physician ordering (requiring only a signature), ability to quickly reach and maintain a BG target range, minimal risk for hypoglycemic events, adaptability for use anywhere in the hospital setting, and acceptance and implementation by nursing staff.16

The IV protocol, a web‐based calculator (Figure 1), was developed based on the concept of the multiplier by White et al.17 For this protocol, the IV infusion (IVI) rate is changed based on a formula that uses a multiplier (a surrogate for insulin sensitivity factor) and the difference between measured BG and target blood glucose (TBG). The calculator uses the following mathematical formula: rate of insulin infusion/hour = (current BG 60 mg/dL) 0.03.18, 19 Additionally, the protocol requires that enough insulin be infused to address severe hyperglycemia at initiation with a rapid reduction in the insulin infusion rate as BG normalizes. The protocol also permits an adjustment of the insulin rate by tenths of a unit per hour to maintain the BG in the center of the target range. The main variant of this protocol is the value of the starting multiplier. The web‐based calculator is currently being used in all 6 adult ICUs and on all of the adult medical‐surgical floors at MUSC.

Figure 1

In early 2006, all adult ICUs were using our in‐house, web‐based intravenous insulin infusion calculator (IVIIC), which prompted more BG readings with intensification of insulin drip use.19 Specifically, initial monitoring for the IVIIC included BG readings every 24 hours. To avoid hypoglycemic events from occurring with the intensification of BG readings for the IVIIC, the BG monitoring frequency was increased to every hour in July 2006. Initial treatment for hypoglycemia was D50% (12.525 g), which tended to overcorrect BG. In July 2006, we revised the protocol using aliquots of D50% specific to the BG reading.19 This action has resulted in decreasing the glycemic excursions observed due to overcorrection of hypoglycemia.

BG target ranges to match the level of care are as follows: intensive care unit (80110 mg/dL); labor and delivery (70110 mg/dL); adult medical/surgical floors (80140 mg/dL); diabetic ketoacidosis (DKA)/hyperosmolar nonketotic coma (HHNK) (150200 mg/dL); neurosurgery ICU (90120 mg/dL); and perioperative patients (140180 mg/dL).20 These BG targets were created to satisfy the clinical requests of specific departments at MUSC. We have restricted starting the multiplier for DKA/HHNK at 0.01, to affect a slower rate of change and the multiplier for all others is set at 0.03.

Results

The baseline demographic characteristics of the four study groups are shown in Table 3. The four groups were found to be similar for gender distribution, mean age, and racial distribution. There were significant differences observed among hospital stay characteristics, insulin drip use, history of diabetes, ventilator support, kidney failure, dialysis, total parenteral nutrition (TPN), and red blood cell (RBC) transfusions. Overall, insulin drip use tended to increase over time. The percentage of patients with diabetes on admission or diagnosed during admission tended to decrease over time. This was likely due to an increase in the diagnosis and treatment of stress/steroid‐induced hyperglycemia during the hospital stay.

A total of 11,715 patient‐days, consisting of 56,401 individual BG readings obtained from 2,215 unique patients, were distributed across the 4 years. Table 4 presents the year‐specific patient‐day analysis. While the prevalence of mild (BG 5069 mg/dL) hypoglycemia was found to increase over the years studied (P < 0.01), the percentage of patient‐days with a mean BG in the range of 70180 mg/dL increased over the period of study (P < 0.01). The total hypoglycemia events <60 mg/dL are presented as comparative data to other studies.7 The percent of patient days with at least one BG < 70 mg/dL (reported in Table 4 as mild events) ranged from 3.72 in 2005 to as high as 10.71 in 2007; however, approximately one‐half of the hypoglycemic events are attributable to readings from BG 6069 since the proportion of patient days with a BG < 60 mg/dL was approximately one‐half that for BG < 70 mg/dL (Table 4). The prevalence of patient days with at least one moderate (BG 4049 mg/dL) or severe (BG < 40 mg/dL) hypoglycemia event was not found to increase in a linear manner. There was a statistical trend for potentially nonlinear relationship of year with moderate hypoglycemia and hyperglycemia.

Immediately following the implementation (year 2005), post hoc comparisons suggested that the rate of moderate hypoglycemia was lowest relative to the 3 other years, but no other statistical differences were observed. The year 2005 also had the lowest proportion of patient days with at least 1 hyperglycemic event.

The individual BG readings for the 2215 unique patients were also individually analyzed according to the methods of Goldberg et al.7 Even though no statistical tests were performed at the ward level, the descriptive data presented in Table 5 are consistent with the analysis of the patient‐day data. Several important features of the data are illustrated by Table 5. Most notably, the glycemic control at the hospital level is improved. The percentage of BG readings in the range of 70180 mg/dL increased annually whereas the mean BG values, the coefficient of variation, and the interquartile range (IQR) decreased annually.

Conclusions

Collectively, we have shown that implementing standardized insulin order sets including hypoglycemia, SC insulin, IV insulin, and IV to SC insulin transition treatment protocols at MUSC may generate the expected benefits for patient safety for this population of patients. The primary hypothesis that the rate of hypoglycemia and hyperglycemia would be lower after the implementation of these protocols was supported by the data, because the overall blood glucose control was markedly improved as a result of the protocols. However, the effect was strongest in 2005 (immediately following the protocol's implementation) and appeared to diminish some with time.

There were several other quality improvement measures initiated at MUSC that likely contributed to the decreasing rates of hypoglycemia and hyperglycemia. For example, comparing June 2004 with June 2007, the number of patients tested increased from 434 to 683. This increase could be attributed, in part, to a trend on medical/surgical services toward an increased focus on glucose monitoring.

When intensive glycemic control programs are implemented, hospitals should have a standardized, nurse‐driven hypoglycemia protocol.11 The success of such a hypoglycemia treatment protocol is demonstrated by the improvement observed at MUSC since the protocol was first implemented in October 2004.22

There are limitations that warrant consideration. A key limitation is that other procedural changes may have occurred during the years of study. Because the initial focus of the HDTF was to reduce hypoglycemic and hyperglycemic events, a multipronged approach was used, beginning with the treatment protocol but followed by other changes. These changes, while unmeasured in the current study, could have influenced the rate of hypoglycemia and hyperglycemia. Therefore, although the protocol that we developed has sound theoretical underpinnings, the improvement in glycemic control at other hospitals may vary. Second, because this was initially regarded as a quality improvement project for hospitalized patients with hypoglycemia and hyperglycemia, we did not evaluate morbidity, mortality, or other clinical outcome data other than BG targets and incidences of hypoglycemia and hyperglycemia. Third, there was no concurrent control group established for this study, rather the study used a retrospective, nonrandomized design with a historical control. As previously mentioned, we cannot rule out the idea that other changes occurred between the preprotocol and postprotocol interval to influence our results. Finally, there are statistical limitations to the research.

One limitation regarding the analysis of the BG data was the potential for an increased type I error (ie, false‐positive result) due to clustering of BG values within a patient and increased monitoring frequencies when a hypoglycemic or hyperglycemic event was observed. The generalized estimating equations directly addressed the first concern. In particular, the effective sample size for each participant was a function of the number of patient‐days and the correlation of patient‐day summaries. Therefore, patients with several highly‐correlated outcomes would contribute less to the analysis than other patients with the same number of patient‐days that were correlated to a lesser extent. As for the second concern, the patient‐day frequencies alleviate this problem and avoid the length‐of‐stay bias associated with a patient‐level (or patient‐stay) analysis. Power was less than planned due in part to the use of the patient‐day analysis instead of the originally designed ward‐level analysis. The change in the statistical design was a response to emerging evidence in the literature.7

In conclusion, the hypothesis that MUSC patients benefit from the use of standardized insulin order sets, hypoglycemia, and hyperglycemia treatment protocols, is supported by the data collected in this study. Because it has been recommended that a hypoglycemia and hyperglycemia prevention protocol as well as a hypoglycemia and hyperglycemia treatment protocol be in place, the HDTF will be focusing on the actual prevention of the hypoglycemic and hyperglycemic incidents occurring in the first place.2, 25 This may result in further reductions of hypoglycemic and hyperglycemic events. We have recently implemented hypoglycemia and hyperglycemia prevention policies at MUSC.

A 38‐year‐old Hispanic man was admitted to the telemetry floor with diagnosis of pericarditis. Blood cultures revealed methicillin‐sensitive Staphylococcus aureus and the patient was started on nafcillin. Despite appropriate antibiotic therapy, the patient remained febrile. Transesophageal echocardiogram (TEE) was performed to evaluate for endocarditis. An hour after the TEE, patient started to desaturate and complained of shortness of breath. At this point, the patient was afebrile, with a pulse rate of 110 beats/minute and blood pressure of 97/63 mm Hg. Oxygen saturation by pulse oximetry of 82% on room air progressively declined even with administration of supplemental oxygen to 77%, necessitating intubation. Despite mechanical ventilation with 100% oxygen delivery, the patient remained cyanotic, with pulse oximetry reading of 69%, and with the arterial blood obtained from the patient at this time for laboratory analysis appearing brown in color.

Based on the temporal correlation of benzocaine spray used during TEE and the symptomscyanosis, hypoxia despite 100% fraction of inspired oxygen (FiO₂), and chocolate‐brown arterial blooda diagnosis of methemoglobinemia was made. The patient's methemoglobin level was reported at 41% (normal range, 0‐3%). The patient received methylene blue, recovered rapidly, and was extubated the next day. Subsequent methemoglobin level obtained less than 24 hours later was reduced to 0.8%. Two days later the patient was discharged to home.

Discussion

Methemoglobin is the state in which ferrous (Fe²⁺) ions of heme are oxidized to the ferric state (Fe³⁺). Because red blood cells are continuously exposed to various oxidative stresses, a methemoglobinemia level of approximately 1% is present in normal individuals at baseline. This low level is maintained through reduction by enzyme systems within the erythrocyte. The most important is the reduced nicotinamide adenine dinucleotide (NADH)‐cytochrome‐b5 reductase system.1 Others, functioning mainly as reserve systems, are ascorbic acid, reduced glutathione, and reduced nicotinamide adenine dinucleotide phosphate (NADPH)‐methemoglobin reductase. The latter requires a natural cofactor or an autooxidizable dye such as methylene blue for activity.

Methemoglobinemia can be congenital or acquired. Congenital methemoglobinemia is very rare and is due to a cytochrome‐b5 reductase deficiency or presence of an abnormal hemoglobin M molecule.2 Acquired methemoglobinemia, the more common type, results from exposure to chemicals that cause more rapid accumulation of methemoglobin than the rate at which methemoglobin can be reduced. Many chemical and environmental agents can cause acquired methemoglobinemia (Table 1). Local anesthetics are the most common hospital‐based pharmacologic agents to cause methemoglobinemia. Prilocaine has been implicated most frequently, especially in newborns. Prilocaine‐induced methemoglobinemia is dose‐dependent and occurs when doses used exceed 600 mg in a 24‐hour period. Lidocaine is a rare cause of methemoglobinemia, but comorbidities like renal failure and use of other local anesthetics like benzocaine will increase the chances of methemoglobinemia. Benzocaine has been reported to cause methemoglobinemia after its use as a lubricant on endotracheal, bronchoscopic, and nasogastric or orogastric tubes, but more commonly after its use as a spray. Benzocaine is lipophilic and may continue to enter the bloodstream from adipose tissue after methylene blue concentrations are no longer therapeutic.

Clinical presentation varies based on methemoglobin levels. Early symptoms of methemoglobinemia, when the blood contains 15% to 50% methemoglobin, include nonspecific headache, fatigues, dyspnea, and lethargy. As the amount of methemoglobin in the blood exceeds 50%, the patients develop more serious neurological symptoms, ranging from confusion to seizures, respiratory depression, and death (Table 2). Clinical interpretation of methemoglobin levels must take into account the total hemoglobin value because anemic patients will have proportionately less functional hemoglobin.3 Methemoglobinemia that develops rapidly will be clinically more severe than a similar degree that develops gradually. The acute accumulation of 30% methemoglobinemia is usually well tolerated in the nonanemic patient.

The suspicion for methemoglobinemia should be raised in the presence of dark or chocolate‐brown arterial blood that does not become red with exposure to air.4 Dark‐colored blood from patients with hypoxia should redden with exposure to air; blood darkened by methemoglobin does not. The suspicion for methemoglobinemia should also be raised in the presence of a saturation gap, when the measured oxygen saturation of blood by pulse oximetry is less than the oxygen saturation calculated by routine blood gas analysis by more than 5%.5 The oxygen saturation on arterial blood gas is calculated from partial pressure of arterial oxygen (PaO₂) and pH. Since PaO₂ is within normal limits in methemoglobinemia, it leads to a normal, though inaccurate, calculated oxygen saturation. Multiple‐wavelength cooximetry is the accepted standard for confirming and quantifying methemoglobinemia.6 This assay involves measuring methemoglobin at its peak absorbance of 630 nm and requires the addition of cyanide to convert methemoglobin to cyanomethemoglobin, which absorbs at shorter wavelengths, resulting in an absorbance decrease at 630 nm due to the disappearance of methemoglobin. Hyperlipidemia and intravenous administration of methylene blue or other dyes may interfere with cooximetry measurements.

In asymptomatic patients with acute methemoglobinemia, discontinuation of the offending drug and proper monitoring is sufficient. In patients who are symptomatic, in addition to supplemental oxygen, methylene blue should be used to enhance the reducing capacity of erythrocytes. Methylene blue, given intravenously in a dose of 1 mg/kg over 5 minutes, acts as an electron acceptor, enhances the NADPH pathway, and rapidly reduces methemoglobin to hemoglobin.7 However, methylene blue should not be used in patients with glucose‐6‐phosphate dehydrogenase deficiency as it can cause life‐threatening hemolysis. In these patients, ascorbic acid should be used. Hyperbaric oxygen or exchange transfusion can also be used. In patients who are in shock secondary to the methemoglobinemia, blood transfusion or exchange transfusion is helpful.

Summary

Agents that inflict large oxidative stress, such as topical anesthetics, can cause methemoglobinemia. A frequently‐used topical anesthetic agent like benzocaine is a common cause of methemoglobinemia. The most characteristic findings of methemoglobinemia are blue‐gray or brown‐gray cyanosis of the skin, lips, and nail beds, dark brown color of the blood, and saturation gap. Symptomatic patients should be given methylene blue intravenously.

A 38‐year‐old Hispanic man was admitted to the telemetry floor with diagnosis of pericarditis. Blood cultures revealed methicillin‐sensitive Staphylococcus aureus and the patient was started on nafcillin. Despite appropriate antibiotic therapy, the patient remained febrile. Transesophageal echocardiogram (TEE) was performed to evaluate for endocarditis. An hour after the TEE, patient started to desaturate and complained of shortness of breath. At this point, the patient was afebrile, with a pulse rate of 110 beats/minute and blood pressure of 97/63 mm Hg. Oxygen saturation by pulse oximetry of 82% on room air progressively declined even with administration of supplemental oxygen to 77%, necessitating intubation. Despite mechanical ventilation with 100% oxygen delivery, the patient remained cyanotic, with pulse oximetry reading of 69%, and with the arterial blood obtained from the patient at this time for laboratory analysis appearing brown in color.

Based on the temporal correlation of benzocaine spray used during TEE and the symptomscyanosis, hypoxia despite 100% fraction of inspired oxygen (FiO₂), and chocolate‐brown arterial blooda diagnosis of methemoglobinemia was made. The patient's methemoglobin level was reported at 41% (normal range, 0‐3%). The patient received methylene blue, recovered rapidly, and was extubated the next day. Subsequent methemoglobin level obtained less than 24 hours later was reduced to 0.8%. Two days later the patient was discharged to home.

Discussion

Methemoglobin is the state in which ferrous (Fe²⁺) ions of heme are oxidized to the ferric state (Fe³⁺). Because red blood cells are continuously exposed to various oxidative stresses, a methemoglobinemia level of approximately 1% is present in normal individuals at baseline. This low level is maintained through reduction by enzyme systems within the erythrocyte. The most important is the reduced nicotinamide adenine dinucleotide (NADH)‐cytochrome‐b5 reductase system.1 Others, functioning mainly as reserve systems, are ascorbic acid, reduced glutathione, and reduced nicotinamide adenine dinucleotide phosphate (NADPH)‐methemoglobin reductase. The latter requires a natural cofactor or an autooxidizable dye such as methylene blue for activity.

Methemoglobinemia can be congenital or acquired. Congenital methemoglobinemia is very rare and is due to a cytochrome‐b5 reductase deficiency or presence of an abnormal hemoglobin M molecule.2 Acquired methemoglobinemia, the more common type, results from exposure to chemicals that cause more rapid accumulation of methemoglobin than the rate at which methemoglobin can be reduced. Many chemical and environmental agents can cause acquired methemoglobinemia (Table 1). Local anesthetics are the most common hospital‐based pharmacologic agents to cause methemoglobinemia. Prilocaine has been implicated most frequently, especially in newborns. Prilocaine‐induced methemoglobinemia is dose‐dependent and occurs when doses used exceed 600 mg in a 24‐hour period. Lidocaine is a rare cause of methemoglobinemia, but comorbidities like renal failure and use of other local anesthetics like benzocaine will increase the chances of methemoglobinemia. Benzocaine has been reported to cause methemoglobinemia after its use as a lubricant on endotracheal, bronchoscopic, and nasogastric or orogastric tubes, but more commonly after its use as a spray. Benzocaine is lipophilic and may continue to enter the bloodstream from adipose tissue after methylene blue concentrations are no longer therapeutic.

Clinical presentation varies based on methemoglobin levels. Early symptoms of methemoglobinemia, when the blood contains 15% to 50% methemoglobin, include nonspecific headache, fatigues, dyspnea, and lethargy. As the amount of methemoglobin in the blood exceeds 50%, the patients develop more serious neurological symptoms, ranging from confusion to seizures, respiratory depression, and death (Table 2). Clinical interpretation of methemoglobin levels must take into account the total hemoglobin value because anemic patients will have proportionately less functional hemoglobin.3 Methemoglobinemia that develops rapidly will be clinically more severe than a similar degree that develops gradually. The acute accumulation of 30% methemoglobinemia is usually well tolerated in the nonanemic patient.

The suspicion for methemoglobinemia should be raised in the presence of dark or chocolate‐brown arterial blood that does not become red with exposure to air.4 Dark‐colored blood from patients with hypoxia should redden with exposure to air; blood darkened by methemoglobin does not. The suspicion for methemoglobinemia should also be raised in the presence of a saturation gap, when the measured oxygen saturation of blood by pulse oximetry is less than the oxygen saturation calculated by routine blood gas analysis by more than 5%.5 The oxygen saturation on arterial blood gas is calculated from partial pressure of arterial oxygen (PaO₂) and pH. Since PaO₂ is within normal limits in methemoglobinemia, it leads to a normal, though inaccurate, calculated oxygen saturation. Multiple‐wavelength cooximetry is the accepted standard for confirming and quantifying methemoglobinemia.6 This assay involves measuring methemoglobin at its peak absorbance of 630 nm and requires the addition of cyanide to convert methemoglobin to cyanomethemoglobin, which absorbs at shorter wavelengths, resulting in an absorbance decrease at 630 nm due to the disappearance of methemoglobin. Hyperlipidemia and intravenous administration of methylene blue or other dyes may interfere with cooximetry measurements.

In asymptomatic patients with acute methemoglobinemia, discontinuation of the offending drug and proper monitoring is sufficient. In patients who are symptomatic, in addition to supplemental oxygen, methylene blue should be used to enhance the reducing capacity of erythrocytes. Methylene blue, given intravenously in a dose of 1 mg/kg over 5 minutes, acts as an electron acceptor, enhances the NADPH pathway, and rapidly reduces methemoglobin to hemoglobin.7 However, methylene blue should not be used in patients with glucose‐6‐phosphate dehydrogenase deficiency as it can cause life‐threatening hemolysis. In these patients, ascorbic acid should be used. Hyperbaric oxygen or exchange transfusion can also be used. In patients who are in shock secondary to the methemoglobinemia, blood transfusion or exchange transfusion is helpful.

Summary

Agents that inflict large oxidative stress, such as topical anesthetics, can cause methemoglobinemia. A frequently‐used topical anesthetic agent like benzocaine is a common cause of methemoglobinemia. The most characteristic findings of methemoglobinemia are blue‐gray or brown‐gray cyanosis of the skin, lips, and nail beds, dark brown color of the blood, and saturation gap. Symptomatic patients should be given methylene blue intravenously.

A 38‐year‐old Hispanic man was admitted to the telemetry floor with diagnosis of pericarditis. Blood cultures revealed methicillin‐sensitive Staphylococcus aureus and the patient was started on nafcillin. Despite appropriate antibiotic therapy, the patient remained febrile. Transesophageal echocardiogram (TEE) was performed to evaluate for endocarditis. An hour after the TEE, patient started to desaturate and complained of shortness of breath. At this point, the patient was afebrile, with a pulse rate of 110 beats/minute and blood pressure of 97/63 mm Hg. Oxygen saturation by pulse oximetry of 82% on room air progressively declined even with administration of supplemental oxygen to 77%, necessitating intubation. Despite mechanical ventilation with 100% oxygen delivery, the patient remained cyanotic, with pulse oximetry reading of 69%, and with the arterial blood obtained from the patient at this time for laboratory analysis appearing brown in color.

Based on the temporal correlation of benzocaine spray used during TEE and the symptomscyanosis, hypoxia despite 100% fraction of inspired oxygen (FiO₂), and chocolate‐brown arterial blooda diagnosis of methemoglobinemia was made. The patient's methemoglobin level was reported at 41% (normal range, 0‐3%). The patient received methylene blue, recovered rapidly, and was extubated the next day. Subsequent methemoglobin level obtained less than 24 hours later was reduced to 0.8%. Two days later the patient was discharged to home.

Discussion

Methemoglobin is the state in which ferrous (Fe²⁺) ions of heme are oxidized to the ferric state (Fe³⁺). Because red blood cells are continuously exposed to various oxidative stresses, a methemoglobinemia level of approximately 1% is present in normal individuals at baseline. This low level is maintained through reduction by enzyme systems within the erythrocyte. The most important is the reduced nicotinamide adenine dinucleotide (NADH)‐cytochrome‐b5 reductase system.1 Others, functioning mainly as reserve systems, are ascorbic acid, reduced glutathione, and reduced nicotinamide adenine dinucleotide phosphate (NADPH)‐methemoglobin reductase. The latter requires a natural cofactor or an autooxidizable dye such as methylene blue for activity.

Methemoglobinemia can be congenital or acquired. Congenital methemoglobinemia is very rare and is due to a cytochrome‐b5 reductase deficiency or presence of an abnormal hemoglobin M molecule.2 Acquired methemoglobinemia, the more common type, results from exposure to chemicals that cause more rapid accumulation of methemoglobin than the rate at which methemoglobin can be reduced. Many chemical and environmental agents can cause acquired methemoglobinemia (Table 1). Local anesthetics are the most common hospital‐based pharmacologic agents to cause methemoglobinemia. Prilocaine has been implicated most frequently, especially in newborns. Prilocaine‐induced methemoglobinemia is dose‐dependent and occurs when doses used exceed 600 mg in a 24‐hour period. Lidocaine is a rare cause of methemoglobinemia, but comorbidities like renal failure and use of other local anesthetics like benzocaine will increase the chances of methemoglobinemia. Benzocaine has been reported to cause methemoglobinemia after its use as a lubricant on endotracheal, bronchoscopic, and nasogastric or orogastric tubes, but more commonly after its use as a spray. Benzocaine is lipophilic and may continue to enter the bloodstream from adipose tissue after methylene blue concentrations are no longer therapeutic.

Clinical presentation varies based on methemoglobin levels. Early symptoms of methemoglobinemia, when the blood contains 15% to 50% methemoglobin, include nonspecific headache, fatigues, dyspnea, and lethargy. As the amount of methemoglobin in the blood exceeds 50%, the patients develop more serious neurological symptoms, ranging from confusion to seizures, respiratory depression, and death (Table 2). Clinical interpretation of methemoglobin levels must take into account the total hemoglobin value because anemic patients will have proportionately less functional hemoglobin.3 Methemoglobinemia that develops rapidly will be clinically more severe than a similar degree that develops gradually. The acute accumulation of 30% methemoglobinemia is usually well tolerated in the nonanemic patient.

The suspicion for methemoglobinemia should be raised in the presence of dark or chocolate‐brown arterial blood that does not become red with exposure to air.4 Dark‐colored blood from patients with hypoxia should redden with exposure to air; blood darkened by methemoglobin does not. The suspicion for methemoglobinemia should also be raised in the presence of a saturation gap, when the measured oxygen saturation of blood by pulse oximetry is less than the oxygen saturation calculated by routine blood gas analysis by more than 5%.5 The oxygen saturation on arterial blood gas is calculated from partial pressure of arterial oxygen (PaO₂) and pH. Since PaO₂ is within normal limits in methemoglobinemia, it leads to a normal, though inaccurate, calculated oxygen saturation. Multiple‐wavelength cooximetry is the accepted standard for confirming and quantifying methemoglobinemia.6 This assay involves measuring methemoglobin at its peak absorbance of 630 nm and requires the addition of cyanide to convert methemoglobin to cyanomethemoglobin, which absorbs at shorter wavelengths, resulting in an absorbance decrease at 630 nm due to the disappearance of methemoglobin. Hyperlipidemia and intravenous administration of methylene blue or other dyes may interfere with cooximetry measurements.

In asymptomatic patients with acute methemoglobinemia, discontinuation of the offending drug and proper monitoring is sufficient. In patients who are symptomatic, in addition to supplemental oxygen, methylene blue should be used to enhance the reducing capacity of erythrocytes. Methylene blue, given intravenously in a dose of 1 mg/kg over 5 minutes, acts as an electron acceptor, enhances the NADPH pathway, and rapidly reduces methemoglobin to hemoglobin.7 However, methylene blue should not be used in patients with glucose‐6‐phosphate dehydrogenase deficiency as it can cause life‐threatening hemolysis. In these patients, ascorbic acid should be used. Hyperbaric oxygen or exchange transfusion can also be used. In patients who are in shock secondary to the methemoglobinemia, blood transfusion or exchange transfusion is helpful.

Summary

Agents that inflict large oxidative stress, such as topical anesthetics, can cause methemoglobinemia. A frequently‐used topical anesthetic agent like benzocaine is a common cause of methemoglobinemia. The most characteristic findings of methemoglobinemia are blue‐gray or brown‐gray cyanosis of the skin, lips, and nail beds, dark brown color of the blood, and saturation gap. Symptomatic patients should be given methylene blue intravenously.

Peripherally inserted central catheters (PICCs) are being used with greater frequency than ever before for intravenous access in hospitals, and PICCs may offer advantages in safety over traditional central venous catheters (CVCs). Despite these potential advantages, a large number of CVCs are still being placed. In a recent 1‐day survey of 6 large urban teaching hospitals, 29% of all patients had a CVC in place (59.3% of intensive care unit [ICU] patients and 23.7% of non‐ICU patients).1 Most catheters were inserted in the subclavian (55%) or jugular (22%) veins, with femoral (6%) and peripheral (15%) sites less commonly used. Even in the non‐ICU setting, only 20% of all central catheters were PICCs.

PICCs may offer advantages over centrally‐inserted intravenous catheters, such as the reduced risks of pneumothorax,2 arterial puncture, uncontrolled bleeding of large central veins, central lineassociated bloodstream infections (CLAB),3, 4 and lower cost.5 In addition, central venous pressure monitoring can now be performed with the larger‐bore PICCs.6

The low risk of mechanical complications for PICC insertion has been well documented.7, 8 In contrast, femoral or retroperitoneal hematoma occurs in up to 1.3% of cases following femoral catheter insertion,9 and pneumothorax occurs in 1.5% to 2.3% of subclavian catheter insertions.10 However, there are only limited data to suggest that the risk of PICC‐related bacteremia is lower than that of centrally‐placed catheters.11, 12

The benefit of PICCs over centrally‐placed catheters in terms of venous thromboembolism (VTE) is also not as easy to show, and in fact the rate may be greater in PICCs. The reported incidence of PICC‐related VTE has been between 0.3% and 56.0%, and the wide variation in rates is likely related to the method of diagnosis.1315 It is likely that most patients with PICC‐related VTE are asymptomatic, and that its incidence is underestimated.16

In many hospitals PICCs are placed by a certified nurse, or by an interventional radiologist if the nurse is unsuccessful.17 There are few reports of PICCs being placed by nonradiology physicians. In one report of 894 patients referred to a critical care specialist for PICC insertion, venous access was achieved 100% of the time, there were no referrals to interventional radiology, and there were no incidents of pneumothorax or bleeding.8 In a university‐affiliated community hospital, we carried out a retrospective review of our experience with training hospital physicians to place PICCs.

Methods

In July 2006 our community hospital, which is affiliated with the University of Pittsburgh Medical Center, instituted a hospitalist program. Prior to the hospitalist program, 1 house physician was available to place PICCs in the antecubital vein without the aid of ultrasound, and there was no PICC‐certified nurse in the hospital. An interventional radiologist was available to place PICCs that could not be placed by the house physician. After July 2006 under the hospitalist service, 3 of the 5 physicians were trained to place PICCs in the deep veins of the arm with the use of ultrasound guidance.

Training included 1 day with the PICC training nurse at the tertiary hospital, followed by supervised placements in the community hospital until proficiency was obtained. Proficiency was relative and cumulative. Approximately 3 supervised procedures were necessary before the physician was able to place PICCs by him or herself. All PICCs were placed using 5 barrier precautions, with chlorhexidine cleansing, and with a time‐out prior to the procedure.

Retrospective hospital data for central catheter placement were examined for the 18 months prior to and following the start of the hospitalist program. These data were collected routinely by the hospital infection control nurse for purposes of quality improvement and patient safety. The data included central catheters placed by all physicians in the hospital; however, the vast majority of these were placed by the hospitalists. The catheters were placed throughout the hospital, both on the medical floors, cardiac step‐down unit, and the ICU. Information regarding the number of central catheters placed and the specific type of catheter (subclavian, jugular, femoral, or PICC) was available from July 2005 through December 2007. Also available from January 2005 were the numbers of femoral and nonfemoral catheter days (number of catheters multiplied by number of days in place) and the central catheterassociated bacteremia rates (number per 1000 catheter days) for femoral and nonfemoral catheters. The Centers for Disease Control and Prevention (CDC) definition of central lineassociated bacteremia was used, which is any documented bloodstream infection within 48 hours of the presence of a CVC in the absence of an alternate source of infection. Data for other complications such as pneumothorax and major bleeding were not consistently recorded.

Results

Figure 1 shows the number of internal jugular, subclavian, femoral, PICC, and total catheter placements from July 2005 through December 2007. The data are grouped into 3‐month increments for visual convenience. Comparing the periods before and after the inception of the hospitalist PICC service (Figure 1, dotted vertical line), the rate of PICC placements rose 4‐fold and the rate of total catheter placements approximately doubled. The rates of femoral and subclavian catheter placements decreased by approximately 50% and the rate of internal jugular catheter placement was roughly unchanged.

Figure 1

Figure 2 shows the numbers of femoral and nonfemoral catheter days by month for 2005 through 2007. The nonfemoral catheter days began to rise prior to the start of the hospitalist program and continued to rise afterward, showing an approximately 3‐fold increase by the end of the study period. The number of femoral catheters days was highly variable, but seemed to decrease by approximately 50%.

Figure 2

Figure 3 shows the rates of femoral and nonfemoral catheter‐associated bacteremia by month for 2005 through 2007. The absolute number of infections in both periods was low and is shown at the top of each bar in the figure.

Figure 3

To our knowledge, there were no episodes of pneumothorax or major bleeding with PICC placement. There were 3 inadvertent arterial punctures, each of which was easily controlled with local pressure. There was 1 incident of a coiled guidewire that could not be removed at the bedside and had to be removed in interventional radiology with no significant consequence to the patient.

Discussion

The complications associated with central catheter insertion continue to place the hospitalized patient at risk. PICCs may offer significant advantages over other types of central catheters in terms of decreased rates of mechanical and infectious complications. Despite this, hospital physicians have not traditionally been trained to place PICCs. We have shown in our small, university‐affiliated community hospital that training hospital physicians to place PICCs was associated with a decrease in the placement of centrally‐inserted venous catheters and a reduced rate of femoral catheter days. At the same time, the rate of central catheterrelated bacteremia remained low.

There are many limitations to our study. Since the analysis was retrospective and uncontrolled, it is not possible to attribute the decrease in femoral catheter days and the low infection rates solely to the use of PICCs. There may have been other factors, either related or unrelated to the transition to a hospitalist service, that influenced the results, such as improved hand hygiene, attention to the use of 5 barrier precautions, and the use of chlorhexidine cleansing. Also, since the study was descriptive and outcome measures were either not available or the numbers small, we cannot prove that there was benefit to the patients or that the changes in rates were statistically significant.

Training hospital physicians to place PICCs in our study was associated with a 2‐fold increase in the overall rate of catheter placements. The reason for this increase in the total number of catheter placements is not clear, but it is likely related to the ease of PICC placement and the increasing number of patients with difficult intravenous access. It is unclear if an equivalent number of traditional central catheters would have been placed were the hospitalists not trained in PICC placement. However, this increase in total number of catheters did not appear to result in an increase in catheter‐related bacteremia or in mechanical complications.

We observed no apparent decrease in the insertion rate of internal jugular catheters in our study, despite a decrease in the rates of subclavian and femoral catheter placements. Although the current CDC guideline recommends using the subclavian vein as the preferred site, the UK National Institute for Clinical Excellence (NICE) is now recommending the use of real‐time ultrasound with each placement,18 and we find that this is best done in the internal jugular vein. Also, the rate of placement of femoral catheters remained higher than that of subclavian cathetersmost likely because the femoral vein remained the site of choice for emergently‐placed cathetersas PICC, more so than subclavian, became the preferred site for elective catheters.

Training physicians to place PICCs was not a simple task. In our experience, the availability of trainers at the tertiary care hospital was limited and the distractions of other duties of the hospitalist complicated the learning process. Two of our 5 physicians could not schedule time with the training nurse and were not able to acquire the skill. However, after training, the 3 hospitalists found that there was such a demand for PICCs that with time it was easy to maintain and even refine this skill. Since we only had 3 of 5 hospitalists trained in PICC placement, we could not have a PICC‐trained hospitalist on site 24 hours a day and the remaining 2 physicians had to rely on centrally‐placed catheters for access or have 1 of the trained physicians come to the hospital from home.

In summary, PICCs may be a safe and easy alternative to centrally‐placed catheters for the hospital physician attempting to secure central intravenous access and may lead to a decrease in the need for more risky CVC insertions. More definitive, controlled investigation, with patient outcome data, will be required before this can be advocated as a universal recommendation.

Peripherally inserted central catheters (PICCs) are being used with greater frequency than ever before for intravenous access in hospitals, and PICCs may offer advantages in safety over traditional central venous catheters (CVCs). Despite these potential advantages, a large number of CVCs are still being placed. In a recent 1‐day survey of 6 large urban teaching hospitals, 29% of all patients had a CVC in place (59.3% of intensive care unit [ICU] patients and 23.7% of non‐ICU patients).1 Most catheters were inserted in the subclavian (55%) or jugular (22%) veins, with femoral (6%) and peripheral (15%) sites less commonly used. Even in the non‐ICU setting, only 20% of all central catheters were PICCs.

PICCs may offer advantages over centrally‐inserted intravenous catheters, such as the reduced risks of pneumothorax,2 arterial puncture, uncontrolled bleeding of large central veins, central lineassociated bloodstream infections (CLAB),3, 4 and lower cost.5 In addition, central venous pressure monitoring can now be performed with the larger‐bore PICCs.6

The low risk of mechanical complications for PICC insertion has been well documented.7, 8 In contrast, femoral or retroperitoneal hematoma occurs in up to 1.3% of cases following femoral catheter insertion,9 and pneumothorax occurs in 1.5% to 2.3% of subclavian catheter insertions.10 However, there are only limited data to suggest that the risk of PICC‐related bacteremia is lower than that of centrally‐placed catheters.11, 12

The benefit of PICCs over centrally‐placed catheters in terms of venous thromboembolism (VTE) is also not as easy to show, and in fact the rate may be greater in PICCs. The reported incidence of PICC‐related VTE has been between 0.3% and 56.0%, and the wide variation in rates is likely related to the method of diagnosis.1315 It is likely that most patients with PICC‐related VTE are asymptomatic, and that its incidence is underestimated.16

In many hospitals PICCs are placed by a certified nurse, or by an interventional radiologist if the nurse is unsuccessful.17 There are few reports of PICCs being placed by nonradiology physicians. In one report of 894 patients referred to a critical care specialist for PICC insertion, venous access was achieved 100% of the time, there were no referrals to interventional radiology, and there were no incidents of pneumothorax or bleeding.8 In a university‐affiliated community hospital, we carried out a retrospective review of our experience with training hospital physicians to place PICCs.

Methods

In July 2006 our community hospital, which is affiliated with the University of Pittsburgh Medical Center, instituted a hospitalist program. Prior to the hospitalist program, 1 house physician was available to place PICCs in the antecubital vein without the aid of ultrasound, and there was no PICC‐certified nurse in the hospital. An interventional radiologist was available to place PICCs that could not be placed by the house physician. After July 2006 under the hospitalist service, 3 of the 5 physicians were trained to place PICCs in the deep veins of the arm with the use of ultrasound guidance.

Training included 1 day with the PICC training nurse at the tertiary hospital, followed by supervised placements in the community hospital until proficiency was obtained. Proficiency was relative and cumulative. Approximately 3 supervised procedures were necessary before the physician was able to place PICCs by him or herself. All PICCs were placed using 5 barrier precautions, with chlorhexidine cleansing, and with a time‐out prior to the procedure.

Retrospective hospital data for central catheter placement were examined for the 18 months prior to and following the start of the hospitalist program. These data were collected routinely by the hospital infection control nurse for purposes of quality improvement and patient safety. The data included central catheters placed by all physicians in the hospital; however, the vast majority of these were placed by the hospitalists. The catheters were placed throughout the hospital, both on the medical floors, cardiac step‐down unit, and the ICU. Information regarding the number of central catheters placed and the specific type of catheter (subclavian, jugular, femoral, or PICC) was available from July 2005 through December 2007. Also available from January 2005 were the numbers of femoral and nonfemoral catheter days (number of catheters multiplied by number of days in place) and the central catheterassociated bacteremia rates (number per 1000 catheter days) for femoral and nonfemoral catheters. The Centers for Disease Control and Prevention (CDC) definition of central lineassociated bacteremia was used, which is any documented bloodstream infection within 48 hours of the presence of a CVC in the absence of an alternate source of infection. Data for other complications such as pneumothorax and major bleeding were not consistently recorded.

Results

Figure 1 shows the number of internal jugular, subclavian, femoral, PICC, and total catheter placements from July 2005 through December 2007. The data are grouped into 3‐month increments for visual convenience. Comparing the periods before and after the inception of the hospitalist PICC service (Figure 1, dotted vertical line), the rate of PICC placements rose 4‐fold and the rate of total catheter placements approximately doubled. The rates of femoral and subclavian catheter placements decreased by approximately 50% and the rate of internal jugular catheter placement was roughly unchanged.

Figure 1

Figure 2 shows the numbers of femoral and nonfemoral catheter days by month for 2005 through 2007. The nonfemoral catheter days began to rise prior to the start of the hospitalist program and continued to rise afterward, showing an approximately 3‐fold increase by the end of the study period. The number of femoral catheters days was highly variable, but seemed to decrease by approximately 50%.

Figure 2

Figure 3 shows the rates of femoral and nonfemoral catheter‐associated bacteremia by month for 2005 through 2007. The absolute number of infections in both periods was low and is shown at the top of each bar in the figure.

Figure 3

To our knowledge, there were no episodes of pneumothorax or major bleeding with PICC placement. There were 3 inadvertent arterial punctures, each of which was easily controlled with local pressure. There was 1 incident of a coiled guidewire that could not be removed at the bedside and had to be removed in interventional radiology with no significant consequence to the patient.

Discussion

The complications associated with central catheter insertion continue to place the hospitalized patient at risk. PICCs may offer significant advantages over other types of central catheters in terms of decreased rates of mechanical and infectious complications. Despite this, hospital physicians have not traditionally been trained to place PICCs. We have shown in our small, university‐affiliated community hospital that training hospital physicians to place PICCs was associated with a decrease in the placement of centrally‐inserted venous catheters and a reduced rate of femoral catheter days. At the same time, the rate of central catheterrelated bacteremia remained low.

There are many limitations to our study. Since the analysis was retrospective and uncontrolled, it is not possible to attribute the decrease in femoral catheter days and the low infection rates solely to the use of PICCs. There may have been other factors, either related or unrelated to the transition to a hospitalist service, that influenced the results, such as improved hand hygiene, attention to the use of 5 barrier precautions, and the use of chlorhexidine cleansing. Also, since the study was descriptive and outcome measures were either not available or the numbers small, we cannot prove that there was benefit to the patients or that the changes in rates were statistically significant.

Training hospital physicians to place PICCs in our study was associated with a 2‐fold increase in the overall rate of catheter placements. The reason for this increase in the total number of catheter placements is not clear, but it is likely related to the ease of PICC placement and the increasing number of patients with difficult intravenous access. It is unclear if an equivalent number of traditional central catheters would have been placed were the hospitalists not trained in PICC placement. However, this increase in total number of catheters did not appear to result in an increase in catheter‐related bacteremia or in mechanical complications.

We observed no apparent decrease in the insertion rate of internal jugular catheters in our study, despite a decrease in the rates of subclavian and femoral catheter placements. Although the current CDC guideline recommends using the subclavian vein as the preferred site, the UK National Institute for Clinical Excellence (NICE) is now recommending the use of real‐time ultrasound with each placement,18 and we find that this is best done in the internal jugular vein. Also, the rate of placement of femoral catheters remained higher than that of subclavian cathetersmost likely because the femoral vein remained the site of choice for emergently‐placed cathetersas PICC, more so than subclavian, became the preferred site for elective catheters.

Training physicians to place PICCs was not a simple task. In our experience, the availability of trainers at the tertiary care hospital was limited and the distractions of other duties of the hospitalist complicated the learning process. Two of our 5 physicians could not schedule time with the training nurse and were not able to acquire the skill. However, after training, the 3 hospitalists found that there was such a demand for PICCs that with time it was easy to maintain and even refine this skill. Since we only had 3 of 5 hospitalists trained in PICC placement, we could not have a PICC‐trained hospitalist on site 24 hours a day and the remaining 2 physicians had to rely on centrally‐placed catheters for access or have 1 of the trained physicians come to the hospital from home.

In summary, PICCs may be a safe and easy alternative to centrally‐placed catheters for the hospital physician attempting to secure central intravenous access and may lead to a decrease in the need for more risky CVC insertions. More definitive, controlled investigation, with patient outcome data, will be required before this can be advocated as a universal recommendation.

Peripherally inserted central catheters (PICCs) are being used with greater frequency than ever before for intravenous access in hospitals, and PICCs may offer advantages in safety over traditional central venous catheters (CVCs). Despite these potential advantages, a large number of CVCs are still being placed. In a recent 1‐day survey of 6 large urban teaching hospitals, 29% of all patients had a CVC in place (59.3% of intensive care unit [ICU] patients and 23.7% of non‐ICU patients).1 Most catheters were inserted in the subclavian (55%) or jugular (22%) veins, with femoral (6%) and peripheral (15%) sites less commonly used. Even in the non‐ICU setting, only 20% of all central catheters were PICCs.

PICCs may offer advantages over centrally‐inserted intravenous catheters, such as the reduced risks of pneumothorax,2 arterial puncture, uncontrolled bleeding of large central veins, central lineassociated bloodstream infections (CLAB),3, 4 and lower cost.5 In addition, central venous pressure monitoring can now be performed with the larger‐bore PICCs.6

The low risk of mechanical complications for PICC insertion has been well documented.7, 8 In contrast, femoral or retroperitoneal hematoma occurs in up to 1.3% of cases following femoral catheter insertion,9 and pneumothorax occurs in 1.5% to 2.3% of subclavian catheter insertions.10 However, there are only limited data to suggest that the risk of PICC‐related bacteremia is lower than that of centrally‐placed catheters.11, 12

The benefit of PICCs over centrally‐placed catheters in terms of venous thromboembolism (VTE) is also not as easy to show, and in fact the rate may be greater in PICCs. The reported incidence of PICC‐related VTE has been between 0.3% and 56.0%, and the wide variation in rates is likely related to the method of diagnosis.1315 It is likely that most patients with PICC‐related VTE are asymptomatic, and that its incidence is underestimated.16

In many hospitals PICCs are placed by a certified nurse, or by an interventional radiologist if the nurse is unsuccessful.17 There are few reports of PICCs being placed by nonradiology physicians. In one report of 894 patients referred to a critical care specialist for PICC insertion, venous access was achieved 100% of the time, there were no referrals to interventional radiology, and there were no incidents of pneumothorax or bleeding.8 In a university‐affiliated community hospital, we carried out a retrospective review of our experience with training hospital physicians to place PICCs.

Methods

In July 2006 our community hospital, which is affiliated with the University of Pittsburgh Medical Center, instituted a hospitalist program. Prior to the hospitalist program, 1 house physician was available to place PICCs in the antecubital vein without the aid of ultrasound, and there was no PICC‐certified nurse in the hospital. An interventional radiologist was available to place PICCs that could not be placed by the house physician. After July 2006 under the hospitalist service, 3 of the 5 physicians were trained to place PICCs in the deep veins of the arm with the use of ultrasound guidance.

Training included 1 day with the PICC training nurse at the tertiary hospital, followed by supervised placements in the community hospital until proficiency was obtained. Proficiency was relative and cumulative. Approximately 3 supervised procedures were necessary before the physician was able to place PICCs by him or herself. All PICCs were placed using 5 barrier precautions, with chlorhexidine cleansing, and with a time‐out prior to the procedure.

Retrospective hospital data for central catheter placement were examined for the 18 months prior to and following the start of the hospitalist program. These data were collected routinely by the hospital infection control nurse for purposes of quality improvement and patient safety. The data included central catheters placed by all physicians in the hospital; however, the vast majority of these were placed by the hospitalists. The catheters were placed throughout the hospital, both on the medical floors, cardiac step‐down unit, and the ICU. Information regarding the number of central catheters placed and the specific type of catheter (subclavian, jugular, femoral, or PICC) was available from July 2005 through December 2007. Also available from January 2005 were the numbers of femoral and nonfemoral catheter days (number of catheters multiplied by number of days in place) and the central catheterassociated bacteremia rates (number per 1000 catheter days) for femoral and nonfemoral catheters. The Centers for Disease Control and Prevention (CDC) definition of central lineassociated bacteremia was used, which is any documented bloodstream infection within 48 hours of the presence of a CVC in the absence of an alternate source of infection. Data for other complications such as pneumothorax and major bleeding were not consistently recorded.

Results

Figure 1 shows the number of internal jugular, subclavian, femoral, PICC, and total catheter placements from July 2005 through December 2007. The data are grouped into 3‐month increments for visual convenience. Comparing the periods before and after the inception of the hospitalist PICC service (Figure 1, dotted vertical line), the rate of PICC placements rose 4‐fold and the rate of total catheter placements approximately doubled. The rates of femoral and subclavian catheter placements decreased by approximately 50% and the rate of internal jugular catheter placement was roughly unchanged.

Figure 1

Figure 2 shows the numbers of femoral and nonfemoral catheter days by month for 2005 through 2007. The nonfemoral catheter days began to rise prior to the start of the hospitalist program and continued to rise afterward, showing an approximately 3‐fold increase by the end of the study period. The number of femoral catheters days was highly variable, but seemed to decrease by approximately 50%.

Figure 2

Figure 3 shows the rates of femoral and nonfemoral catheter‐associated bacteremia by month for 2005 through 2007. The absolute number of infections in both periods was low and is shown at the top of each bar in the figure.

Figure 3

To our knowledge, there were no episodes of pneumothorax or major bleeding with PICC placement. There were 3 inadvertent arterial punctures, each of which was easily controlled with local pressure. There was 1 incident of a coiled guidewire that could not be removed at the bedside and had to be removed in interventional radiology with no significant consequence to the patient.

Discussion

The complications associated with central catheter insertion continue to place the hospitalized patient at risk. PICCs may offer significant advantages over other types of central catheters in terms of decreased rates of mechanical and infectious complications. Despite this, hospital physicians have not traditionally been trained to place PICCs. We have shown in our small, university‐affiliated community hospital that training hospital physicians to place PICCs was associated with a decrease in the placement of centrally‐inserted venous catheters and a reduced rate of femoral catheter days. At the same time, the rate of central catheterrelated bacteremia remained low.

There are many limitations to our study. Since the analysis was retrospective and uncontrolled, it is not possible to attribute the decrease in femoral catheter days and the low infection rates solely to the use of PICCs. There may have been other factors, either related or unrelated to the transition to a hospitalist service, that influenced the results, such as improved hand hygiene, attention to the use of 5 barrier precautions, and the use of chlorhexidine cleansing. Also, since the study was descriptive and outcome measures were either not available or the numbers small, we cannot prove that there was benefit to the patients or that the changes in rates were statistically significant.

Training hospital physicians to place PICCs in our study was associated with a 2‐fold increase in the overall rate of catheter placements. The reason for this increase in the total number of catheter placements is not clear, but it is likely related to the ease of PICC placement and the increasing number of patients with difficult intravenous access. It is unclear if an equivalent number of traditional central catheters would have been placed were the hospitalists not trained in PICC placement. However, this increase in total number of catheters did not appear to result in an increase in catheter‐related bacteremia or in mechanical complications.

We observed no apparent decrease in the insertion rate of internal jugular catheters in our study, despite a decrease in the rates of subclavian and femoral catheter placements. Although the current CDC guideline recommends using the subclavian vein as the preferred site, the UK National Institute for Clinical Excellence (NICE) is now recommending the use of real‐time ultrasound with each placement,18 and we find that this is best done in the internal jugular vein. Also, the rate of placement of femoral catheters remained higher than that of subclavian cathetersmost likely because the femoral vein remained the site of choice for emergently‐placed cathetersas PICC, more so than subclavian, became the preferred site for elective catheters.

Training physicians to place PICCs was not a simple task. In our experience, the availability of trainers at the tertiary care hospital was limited and the distractions of other duties of the hospitalist complicated the learning process. Two of our 5 physicians could not schedule time with the training nurse and were not able to acquire the skill. However, after training, the 3 hospitalists found that there was such a demand for PICCs that with time it was easy to maintain and even refine this skill. Since we only had 3 of 5 hospitalists trained in PICC placement, we could not have a PICC‐trained hospitalist on site 24 hours a day and the remaining 2 physicians had to rely on centrally‐placed catheters for access or have 1 of the trained physicians come to the hospital from home.

In summary, PICCs may be a safe and easy alternative to centrally‐placed catheters for the hospital physician attempting to secure central intravenous access and may lead to a decrease in the need for more risky CVC insertions. More definitive, controlled investigation, with patient outcome data, will be required before this can be advocated as a universal recommendation.

Since publication of the first randomized controlled trial of insulin infusion therapy in surgical intensive care unit (ICU) patients,1 most institutions have implemented insulin infusion protocols (IIP) for tight glycemic control in their ICUs.29 The major problem with tight glycemic control is the risk of hypoglycemia. In the randomized controlled trial involving medical ICU patients, 18.7% patients experienced at least 1 episode of blood glucose (BG) 40 mg/dL.10 Recently, a major insulin infusion trial involving patients with severe sepsis was stopped due to unacceptably high risk of hypoglycemia.11 Potential benefits of BG control may be offset by potential risks of hypoglycemia. While there can be multiple factors that could contribute to the risk of hypoglycemia, suboptimal protocol implementation is relatively amenable to correction.

Most IIPs are nurse driven. Nurses monitor BG levels every 30 to 60 minutes and make adjustments in insulin infusion rates. Each point of care testing and insulin dose adjustment takes about 5 minutes of nursing time.12 Given the numerous other nursing responsibilities for monitoring and documentation in very sick patients, nurses may not always be able check BGs at the recommended times. We investigated whether a delay in BG monitoring during insulin infusion therapy is associated with higher risk of hypoglycemia.

Methods

Data were collected for 50 consecutive patients treated with Brigham and Women's Hospital's insulin infusion protocol (BHIP) between September 27, 2006 and October 13, 2006. The investigation was part of the hospital's ongoing diabetes quality improvement program. Partners‐Health Human Research Committee approved the study. Patient demographics, history of diabetes mellitus, and glycosylated hemoglobin (A1C) were obtained from paper and electronic medical records. Point‐of‐care BG values were obtained from the bedside paper flow sheets. The exact times of individual BG measurements were ascertained from Point of Care Precision Web (QCM3.0; Abbott, Inc.).

Target BG range with BHIP is 80 to 110 mg/dL. BHIP requires BG testing every 60 minutes unless a BG value of 60 mg/dL is obtained; in which case, testing is required every 30 minutes. A time violation was assumed to have occurred if the BG was measured >70 minutes after a previous value of 60 mg/dL or >40 minutes after a previous BG value of 60 mg/dL (ie, >10 minutes after the recommended time for measurement). Although the choice of 10 minutes was arbitrary, we think it is a reasonable and practical time frame for getting a BG measurement. If a measurement was obtained earlier than the recommended time, it was not considered a time violation. However, measurements obtained within 30 minutes of a previous BG value (overwhelmingly drawn for confirmation of a previous BG value) were excluded from analysis.

BG values were divided into 2 categories: values following time violation and values following no time violation. The numbers of values in different BG ranges (80, 80110, >110 mg/dL) were compared in the 2 categories using a chi square test. Data are presented as mean standard deviation (SD), median and numbers with percentage. Statistical significance was set at P 0.05.

Results

Mean age of the 50 patients treated with BHIP was 64.0 13.6 years. There were 27 men and 23 women. Eighteen patients had preexisting diabetes (1 had type 1 and 17 had type 2 diabetes, mean A1C 7.1 1.7%) and 32 patients had no previous history of diabetes (mean A1C 5.9 0.9%). Mean serum creatinine was 1.34 1.0 mg/dL. Mean BG at the start of BHIP was 173 69.6 mg/dL; median 167.5 mg/dL. Mean BG during insulin infusion was 117.3 43.1 mg/dL; median 107 mg/dL. Mean BG during insulin infusion was higher in diabetic patients compared to nondiabetic patients (125.2 57.8 versus 113.4 38.8 mg/dL; P 0.01). Monitoring for BGs was done with similar frequency in all patients. Overall, 40.2% of the total 2,605 BG values were in a range of 80 to 110 mg/dL. A total of 1.5% of values were below 60 mg/dL; only 4 values were 40 mg/dL.

A total of 2,309 values could be studied for time violations. The remaining 296 values were either obtained within 30 minutes of the previous test or the exact time of measurement could not be ascertained. A total of 1,474 (63.9%) measurements had been obtained at the recommended time or earlier than the recommended time; 835 (36.1%) measurements had been obtained >10 minutes after the recommended time for measurement (time violation). The proportion of BG values below the target (80 mg/dL) was significantly higher following the time violation as compared to no time violation (Table 1). On the other hand, values >110 mg/dL were not more common following a time violation, compared to instances when no time violation occurred.

Frequency of time violation was similar in subgroups of patients divided according to gender, presence of diabetes and the type of ICU (Table 2). Comparison among subgroups of admission diagnoses was not possible due to the small number of patients. Overall, the proportion of low BG values was lower in diabetic patients compared to nondiabetic patients (11.9% versus 15.0%, P = 0.03). An increased rate of hypoglycemia following time violations was present in all subgroups except for the diabetic subgroup (Table 3).

Discussion

Our study shows that a delay in BG testing during BHIP is associated with higher chances of a low BG value. This effect was consistent in multiple subgroups. However, the effect was nonsignificant in diabetic patients, probably due to higher mean BG levels and less frequent low BG values. Over one‐third of all BG measurements were obtained after a time violation. Protocol violations in our study are no different from those reported by others.7, 13, 14 Our patient characteristics of severe hypoglycemic episodes and the overall BG control achieved with BHIP were also similar to those reported by others with similar protocols.5, 7, 1517 While the results of this study may still be specific to BHIP, we think they are applicable to other similar protocols.

Because a delay in testing by itself is unlikely to cause hypoglycemia, a more likely explanation for these results is that hypoglycemia occurred when insulin infusion adjustments were not made in a timely fashion due to prolonged BG monitoring intervals. Insulin infusions are the preferred treatment in rapidly changing clinical settings because changes in insulin doses can be made frequently. Most IIPs are designed with the assumption that insulin dose adjustments will be made regularly and frequently, based on BG measurements. Although there is no gold standard for the optimal BG test frequency, in most protocols BG testing is performed every hour in order to ensure safety as well as efficacy. Our results are consistent with the intuitive assumption that a timely measurement of the BG is important for successful implementation of an IIP.

It was somewhat surprising that high BG values were not more frequent following a time violation. We can only speculate as to the reason for this. It is possible that critically ill patients are near maximally insulin resistant and, once an effective insulin infusion rate is achieved, further increases are not as frequently required. On the other hand, insulin requirements may decrease rapidly as contributors to insulin resistance resolve. Another possibility is that there may be a limit to hepatic glucose production during acute illness making patients more prone to hypoglycemia. It is also possible that the nurses tend to test more promptly when the BG levels are running high. Thus, the insulin doses may be increased at proper times until BG levels are in the target range. However, when BG levels are in the target range, nurses may become less vigilant, leading to a delay in testing. As a result a decrease in insulin dose, when required, does not happen as promptly as an increase in dose.

In our study the absolute risk of hypoglycemia associated with time violation was 6%. Avoiding this hypoglycemia may have an impact on glycemic control in the ICU and may change clinical outcomes. Moreover, this is 1 of the few factors that are potentially amenable to correction. Therefore, measures to improve adherence to protocols, eg, prompts for BG testing and better nurse training regarding importance of timely testing, may reduce the risk of hypoglycemia.

Since publication of the first randomized controlled trial of insulin infusion therapy in surgical intensive care unit (ICU) patients,1 most institutions have implemented insulin infusion protocols (IIP) for tight glycemic control in their ICUs.29 The major problem with tight glycemic control is the risk of hypoglycemia. In the randomized controlled trial involving medical ICU patients, 18.7% patients experienced at least 1 episode of blood glucose (BG) 40 mg/dL.10 Recently, a major insulin infusion trial involving patients with severe sepsis was stopped due to unacceptably high risk of hypoglycemia.11 Potential benefits of BG control may be offset by potential risks of hypoglycemia. While there can be multiple factors that could contribute to the risk of hypoglycemia, suboptimal protocol implementation is relatively amenable to correction.

Most IIPs are nurse driven. Nurses monitor BG levels every 30 to 60 minutes and make adjustments in insulin infusion rates. Each point of care testing and insulin dose adjustment takes about 5 minutes of nursing time.12 Given the numerous other nursing responsibilities for monitoring and documentation in very sick patients, nurses may not always be able check BGs at the recommended times. We investigated whether a delay in BG monitoring during insulin infusion therapy is associated with higher risk of hypoglycemia.

Methods

Data were collected for 50 consecutive patients treated with Brigham and Women's Hospital's insulin infusion protocol (BHIP) between September 27, 2006 and October 13, 2006. The investigation was part of the hospital's ongoing diabetes quality improvement program. Partners‐Health Human Research Committee approved the study. Patient demographics, history of diabetes mellitus, and glycosylated hemoglobin (A1C) were obtained from paper and electronic medical records. Point‐of‐care BG values were obtained from the bedside paper flow sheets. The exact times of individual BG measurements were ascertained from Point of Care Precision Web (QCM3.0; Abbott, Inc.).

Target BG range with BHIP is 80 to 110 mg/dL. BHIP requires BG testing every 60 minutes unless a BG value of 60 mg/dL is obtained; in which case, testing is required every 30 minutes. A time violation was assumed to have occurred if the BG was measured >70 minutes after a previous value of 60 mg/dL or >40 minutes after a previous BG value of 60 mg/dL (ie, >10 minutes after the recommended time for measurement). Although the choice of 10 minutes was arbitrary, we think it is a reasonable and practical time frame for getting a BG measurement. If a measurement was obtained earlier than the recommended time, it was not considered a time violation. However, measurements obtained within 30 minutes of a previous BG value (overwhelmingly drawn for confirmation of a previous BG value) were excluded from analysis.

BG values were divided into 2 categories: values following time violation and values following no time violation. The numbers of values in different BG ranges (80, 80110, >110 mg/dL) were compared in the 2 categories using a chi square test. Data are presented as mean standard deviation (SD), median and numbers with percentage. Statistical significance was set at P 0.05.

Results

Mean age of the 50 patients treated with BHIP was 64.0 13.6 years. There were 27 men and 23 women. Eighteen patients had preexisting diabetes (1 had type 1 and 17 had type 2 diabetes, mean A1C 7.1 1.7%) and 32 patients had no previous history of diabetes (mean A1C 5.9 0.9%). Mean serum creatinine was 1.34 1.0 mg/dL. Mean BG at the start of BHIP was 173 69.6 mg/dL; median 167.5 mg/dL. Mean BG during insulin infusion was 117.3 43.1 mg/dL; median 107 mg/dL. Mean BG during insulin infusion was higher in diabetic patients compared to nondiabetic patients (125.2 57.8 versus 113.4 38.8 mg/dL; P 0.01). Monitoring for BGs was done with similar frequency in all patients. Overall, 40.2% of the total 2,605 BG values were in a range of 80 to 110 mg/dL. A total of 1.5% of values were below 60 mg/dL; only 4 values were 40 mg/dL.

A total of 2,309 values could be studied for time violations. The remaining 296 values were either obtained within 30 minutes of the previous test or the exact time of measurement could not be ascertained. A total of 1,474 (63.9%) measurements had been obtained at the recommended time or earlier than the recommended time; 835 (36.1%) measurements had been obtained >10 minutes after the recommended time for measurement (time violation). The proportion of BG values below the target (80 mg/dL) was significantly higher following the time violation as compared to no time violation (Table 1). On the other hand, values >110 mg/dL were not more common following a time violation, compared to instances when no time violation occurred.

Frequency of time violation was similar in subgroups of patients divided according to gender, presence of diabetes and the type of ICU (Table 2). Comparison among subgroups of admission diagnoses was not possible due to the small number of patients. Overall, the proportion of low BG values was lower in diabetic patients compared to nondiabetic patients (11.9% versus 15.0%, P = 0.03). An increased rate of hypoglycemia following time violations was present in all subgroups except for the diabetic subgroup (Table 3).

Discussion

Our study shows that a delay in BG testing during BHIP is associated with higher chances of a low BG value. This effect was consistent in multiple subgroups. However, the effect was nonsignificant in diabetic patients, probably due to higher mean BG levels and less frequent low BG values. Over one‐third of all BG measurements were obtained after a time violation. Protocol violations in our study are no different from those reported by others.7, 13, 14 Our patient characteristics of severe hypoglycemic episodes and the overall BG control achieved with BHIP were also similar to those reported by others with similar protocols.5, 7, 1517 While the results of this study may still be specific to BHIP, we think they are applicable to other similar protocols.

Because a delay in testing by itself is unlikely to cause hypoglycemia, a more likely explanation for these results is that hypoglycemia occurred when insulin infusion adjustments were not made in a timely fashion due to prolonged BG monitoring intervals. Insulin infusions are the preferred treatment in rapidly changing clinical settings because changes in insulin doses can be made frequently. Most IIPs are designed with the assumption that insulin dose adjustments will be made regularly and frequently, based on BG measurements. Although there is no gold standard for the optimal BG test frequency, in most protocols BG testing is performed every hour in order to ensure safety as well as efficacy. Our results are consistent with the intuitive assumption that a timely measurement of the BG is important for successful implementation of an IIP.

It was somewhat surprising that high BG values were not more frequent following a time violation. We can only speculate as to the reason for this. It is possible that critically ill patients are near maximally insulin resistant and, once an effective insulin infusion rate is achieved, further increases are not as frequently required. On the other hand, insulin requirements may decrease rapidly as contributors to insulin resistance resolve. Another possibility is that there may be a limit to hepatic glucose production during acute illness making patients more prone to hypoglycemia. It is also possible that the nurses tend to test more promptly when the BG levels are running high. Thus, the insulin doses may be increased at proper times until BG levels are in the target range. However, when BG levels are in the target range, nurses may become less vigilant, leading to a delay in testing. As a result a decrease in insulin dose, when required, does not happen as promptly as an increase in dose.

In our study the absolute risk of hypoglycemia associated with time violation was 6%. Avoiding this hypoglycemia may have an impact on glycemic control in the ICU and may change clinical outcomes. Moreover, this is 1 of the few factors that are potentially amenable to correction. Therefore, measures to improve adherence to protocols, eg, prompts for BG testing and better nurse training regarding importance of timely testing, may reduce the risk of hypoglycemia.

Since publication of the first randomized controlled trial of insulin infusion therapy in surgical intensive care unit (ICU) patients,1 most institutions have implemented insulin infusion protocols (IIP) for tight glycemic control in their ICUs.29 The major problem with tight glycemic control is the risk of hypoglycemia. In the randomized controlled trial involving medical ICU patients, 18.7% patients experienced at least 1 episode of blood glucose (BG) 40 mg/dL.10 Recently, a major insulin infusion trial involving patients with severe sepsis was stopped due to unacceptably high risk of hypoglycemia.11 Potential benefits of BG control may be offset by potential risks of hypoglycemia. While there can be multiple factors that could contribute to the risk of hypoglycemia, suboptimal protocol implementation is relatively amenable to correction.

Most IIPs are nurse driven. Nurses monitor BG levels every 30 to 60 minutes and make adjustments in insulin infusion rates. Each point of care testing and insulin dose adjustment takes about 5 minutes of nursing time.12 Given the numerous other nursing responsibilities for monitoring and documentation in very sick patients, nurses may not always be able check BGs at the recommended times. We investigated whether a delay in BG monitoring during insulin infusion therapy is associated with higher risk of hypoglycemia.

Methods

Data were collected for 50 consecutive patients treated with Brigham and Women's Hospital's insulin infusion protocol (BHIP) between September 27, 2006 and October 13, 2006. The investigation was part of the hospital's ongoing diabetes quality improvement program. Partners‐Health Human Research Committee approved the study. Patient demographics, history of diabetes mellitus, and glycosylated hemoglobin (A1C) were obtained from paper and electronic medical records. Point‐of‐care BG values were obtained from the bedside paper flow sheets. The exact times of individual BG measurements were ascertained from Point of Care Precision Web (QCM3.0; Abbott, Inc.).

Target BG range with BHIP is 80 to 110 mg/dL. BHIP requires BG testing every 60 minutes unless a BG value of 60 mg/dL is obtained; in which case, testing is required every 30 minutes. A time violation was assumed to have occurred if the BG was measured >70 minutes after a previous value of 60 mg/dL or >40 minutes after a previous BG value of 60 mg/dL (ie, >10 minutes after the recommended time for measurement). Although the choice of 10 minutes was arbitrary, we think it is a reasonable and practical time frame for getting a BG measurement. If a measurement was obtained earlier than the recommended time, it was not considered a time violation. However, measurements obtained within 30 minutes of a previous BG value (overwhelmingly drawn for confirmation of a previous BG value) were excluded from analysis.

BG values were divided into 2 categories: values following time violation and values following no time violation. The numbers of values in different BG ranges (80, 80110, >110 mg/dL) were compared in the 2 categories using a chi square test. Data are presented as mean standard deviation (SD), median and numbers with percentage. Statistical significance was set at P 0.05.

Results

Mean age of the 50 patients treated with BHIP was 64.0 13.6 years. There were 27 men and 23 women. Eighteen patients had preexisting diabetes (1 had type 1 and 17 had type 2 diabetes, mean A1C 7.1 1.7%) and 32 patients had no previous history of diabetes (mean A1C 5.9 0.9%). Mean serum creatinine was 1.34 1.0 mg/dL. Mean BG at the start of BHIP was 173 69.6 mg/dL; median 167.5 mg/dL. Mean BG during insulin infusion was 117.3 43.1 mg/dL; median 107 mg/dL. Mean BG during insulin infusion was higher in diabetic patients compared to nondiabetic patients (125.2 57.8 versus 113.4 38.8 mg/dL; P 0.01). Monitoring for BGs was done with similar frequency in all patients. Overall, 40.2% of the total 2,605 BG values were in a range of 80 to 110 mg/dL. A total of 1.5% of values were below 60 mg/dL; only 4 values were 40 mg/dL.

A total of 2,309 values could be studied for time violations. The remaining 296 values were either obtained within 30 minutes of the previous test or the exact time of measurement could not be ascertained. A total of 1,474 (63.9%) measurements had been obtained at the recommended time or earlier than the recommended time; 835 (36.1%) measurements had been obtained >10 minutes after the recommended time for measurement (time violation). The proportion of BG values below the target (80 mg/dL) was significantly higher following the time violation as compared to no time violation (Table 1). On the other hand, values >110 mg/dL were not more common following a time violation, compared to instances when no time violation occurred.

Frequency of time violation was similar in subgroups of patients divided according to gender, presence of diabetes and the type of ICU (Table 2). Comparison among subgroups of admission diagnoses was not possible due to the small number of patients. Overall, the proportion of low BG values was lower in diabetic patients compared to nondiabetic patients (11.9% versus 15.0%, P = 0.03). An increased rate of hypoglycemia following time violations was present in all subgroups except for the diabetic subgroup (Table 3).

Discussion

Our study shows that a delay in BG testing during BHIP is associated with higher chances of a low BG value. This effect was consistent in multiple subgroups. However, the effect was nonsignificant in diabetic patients, probably due to higher mean BG levels and less frequent low BG values. Over one‐third of all BG measurements were obtained after a time violation. Protocol violations in our study are no different from those reported by others.7, 13, 14 Our patient characteristics of severe hypoglycemic episodes and the overall BG control achieved with BHIP were also similar to those reported by others with similar protocols.5, 7, 1517 While the results of this study may still be specific to BHIP, we think they are applicable to other similar protocols.

Because a delay in testing by itself is unlikely to cause hypoglycemia, a more likely explanation for these results is that hypoglycemia occurred when insulin infusion adjustments were not made in a timely fashion due to prolonged BG monitoring intervals. Insulin infusions are the preferred treatment in rapidly changing clinical settings because changes in insulin doses can be made frequently. Most IIPs are designed with the assumption that insulin dose adjustments will be made regularly and frequently, based on BG measurements. Although there is no gold standard for the optimal BG test frequency, in most protocols BG testing is performed every hour in order to ensure safety as well as efficacy. Our results are consistent with the intuitive assumption that a timely measurement of the BG is important for successful implementation of an IIP.

It was somewhat surprising that high BG values were not more frequent following a time violation. We can only speculate as to the reason for this. It is possible that critically ill patients are near maximally insulin resistant and, once an effective insulin infusion rate is achieved, further increases are not as frequently required. On the other hand, insulin requirements may decrease rapidly as contributors to insulin resistance resolve. Another possibility is that there may be a limit to hepatic glucose production during acute illness making patients more prone to hypoglycemia. It is also possible that the nurses tend to test more promptly when the BG levels are running high. Thus, the insulin doses may be increased at proper times until BG levels are in the target range. However, when BG levels are in the target range, nurses may become less vigilant, leading to a delay in testing. As a result a decrease in insulin dose, when required, does not happen as promptly as an increase in dose.

In our study the absolute risk of hypoglycemia associated with time violation was 6%. Avoiding this hypoglycemia may have an impact on glycemic control in the ICU and may change clinical outcomes. Moreover, this is 1 of the few factors that are potentially amenable to correction. Therefore, measures to improve adherence to protocols, eg, prompts for BG testing and better nurse training regarding importance of timely testing, may reduce the risk of hypoglycemia.

Early diagnosis of peripheral neuropathies can lead to life‐saving or limb‐saving intervention. While infrequently a cause for concern in the hospital setting, peripheral neuropathies are commonoccurring in up to 10% of the general population.1 The hospitalist needs to expeditiously identify acute and life‐threatening or limb‐threatening causes among an immense set of differentials. Fortunately, with an informed and careful approach, most neuropathies in need of urgent intervention can be readily identified. A thorough history and examination, with the addition of electrodiagnostic testing, comprise the mainstays of this process. Inpatient neurology consultation should be sought for any rapidly progressing or acute onset neuropathy. The aim of this review is to equip the general hospitalist with a solid framework for efficiently evaluating peripheral neuropathies in urgent cases.

Literature Review

A General Approach for the Hospitalist

Pattern recognition and employing the essentials outlined above are key tools in the hospitalist's evaluation of peripheral neuropathy. Pattern recognition relies on a familiarity with the more common acute and severe neuropathies. For circumstances in which the diagnosis is not immediately recognizable, a systematic approach expedites evaluation. Figure 1 presents an algorithm for evaluating peripheral neuropathies in the acutely ill patient.

Figure 1

A Systematic Evaluation

When the etiology is not immediately evident, the essential questions identified in the review above are useful, and can be simplified for the hospitalist. First, understand the onset and timing of symptoms. Second, localize the symptoms to and within the peripheral nervous system (including classifying the distribution of nerve involvement). For acute, rapidly progressing or multifocal neuropathies urgent inpatient electrodiagnostic testing and neurology consultation should be obtained. Further testing, including laboratory testing, should be directed by these first steps.

Early diagnosis of peripheral neuropathies can lead to life‐saving or limb‐saving intervention. While infrequently a cause for concern in the hospital setting, peripheral neuropathies are commonoccurring in up to 10% of the general population.1 The hospitalist needs to expeditiously identify acute and life‐threatening or limb‐threatening causes among an immense set of differentials. Fortunately, with an informed and careful approach, most neuropathies in need of urgent intervention can be readily identified. A thorough history and examination, with the addition of electrodiagnostic testing, comprise the mainstays of this process. Inpatient neurology consultation should be sought for any rapidly progressing or acute onset neuropathy. The aim of this review is to equip the general hospitalist with a solid framework for efficiently evaluating peripheral neuropathies in urgent cases.

Literature Review

A General Approach for the Hospitalist

Pattern recognition and employing the essentials outlined above are key tools in the hospitalist's evaluation of peripheral neuropathy. Pattern recognition relies on a familiarity with the more common acute and severe neuropathies. For circumstances in which the diagnosis is not immediately recognizable, a systematic approach expedites evaluation. Figure 1 presents an algorithm for evaluating peripheral neuropathies in the acutely ill patient.

Figure 1

A Systematic Evaluation

When the etiology is not immediately evident, the essential questions identified in the review above are useful, and can be simplified for the hospitalist. First, understand the onset and timing of symptoms. Second, localize the symptoms to and within the peripheral nervous system (including classifying the distribution of nerve involvement). For acute, rapidly progressing or multifocal neuropathies urgent inpatient electrodiagnostic testing and neurology consultation should be obtained. Further testing, including laboratory testing, should be directed by these first steps.

Early diagnosis of peripheral neuropathies can lead to life‐saving or limb‐saving intervention. While infrequently a cause for concern in the hospital setting, peripheral neuropathies are commonoccurring in up to 10% of the general population.1 The hospitalist needs to expeditiously identify acute and life‐threatening or limb‐threatening causes among an immense set of differentials. Fortunately, with an informed and careful approach, most neuropathies in need of urgent intervention can be readily identified. A thorough history and examination, with the addition of electrodiagnostic testing, comprise the mainstays of this process. Inpatient neurology consultation should be sought for any rapidly progressing or acute onset neuropathy. The aim of this review is to equip the general hospitalist with a solid framework for efficiently evaluating peripheral neuropathies in urgent cases.

Literature Review

A General Approach for the Hospitalist

Pattern recognition and employing the essentials outlined above are key tools in the hospitalist's evaluation of peripheral neuropathy. Pattern recognition relies on a familiarity with the more common acute and severe neuropathies. For circumstances in which the diagnosis is not immediately recognizable, a systematic approach expedites evaluation. Figure 1 presents an algorithm for evaluating peripheral neuropathies in the acutely ill patient.

Figure 1

A Systematic Evaluation

When the etiology is not immediately evident, the essential questions identified in the review above are useful, and can be simplified for the hospitalist. First, understand the onset and timing of symptoms. Second, localize the symptoms to and within the peripheral nervous system (including classifying the distribution of nerve involvement). For acute, rapidly progressing or multifocal neuropathies urgent inpatient electrodiagnostic testing and neurology consultation should be obtained. Further testing, including laboratory testing, should be directed by these first steps.