Justin Moore, MD

To the Editor: We appreciated the thoughtful 1-Minute Consult by Drs. Dobri and Lansang, “How should we manage insulin therapy before surgery?”¹ We agree with them in regard to the benefits of perioperative control of blood glucose levels. However, we disagree in general with their assertion that the full dose of the patient’s home dose of basal insulin be administered while the patient is nil per os (NPO) before surgery, with a reduction to 75% of the home dose only if the patient has a history of hypoglycemia, a recommendation that did not differentiate between patients with type 1 and type 2 diabetes mellitus.

The RABBIT 2 Surgery trial,² which showed superiority of basal-bolus insulin over sliding scale insulin in surgical patients with type 2 diabetes mellitus, also showed a surprisingly high rate of hypoglycemia—24 (23.1%) of 104 patients had blood glucose levels lower than 70 mg/dL, compared with a similar trial in nonsurgical patients in which 2 (3.1%) of 65 patients had a blood glucose level less than 60 mg/dL.³ The authors of the two studies explained² that “differences in hypoglycemic events between the two trials could be in part explained by reduced nutritional intake in surgical patients…”

Although patients with well-controlled type 1 diabetes mellitus may tolerate their full dose of basal insulin while NPO, we contend that patients with type 2 diabetes mellitus should be prescribed a reduced dose of basal insulin while NPO, regardless of the dose distribution or the patient’s overall glycemic control. It is routine practice on our consult service to reduce the basal insulin dose in such patients by roughly half.

To the Editor: We appreciated the thoughtful 1-Minute Consult by Drs. Dobri and Lansang, “How should we manage insulin therapy before surgery?”¹ We agree with them in regard to the benefits of perioperative control of blood glucose levels. However, we disagree in general with their assertion that the full dose of the patient’s home dose of basal insulin be administered while the patient is nil per os (NPO) before surgery, with a reduction to 75% of the home dose only if the patient has a history of hypoglycemia, a recommendation that did not differentiate between patients with type 1 and type 2 diabetes mellitus.

The RABBIT 2 Surgery trial,² which showed superiority of basal-bolus insulin over sliding scale insulin in surgical patients with type 2 diabetes mellitus, also showed a surprisingly high rate of hypoglycemia—24 (23.1%) of 104 patients had blood glucose levels lower than 70 mg/dL, compared with a similar trial in nonsurgical patients in which 2 (3.1%) of 65 patients had a blood glucose level less than 60 mg/dL.³ The authors of the two studies explained² that “differences in hypoglycemic events between the two trials could be in part explained by reduced nutritional intake in surgical patients…”

Although patients with well-controlled type 1 diabetes mellitus may tolerate their full dose of basal insulin while NPO, we contend that patients with type 2 diabetes mellitus should be prescribed a reduced dose of basal insulin while NPO, regardless of the dose distribution or the patient’s overall glycemic control. It is routine practice on our consult service to reduce the basal insulin dose in such patients by roughly half.

To the Editor: We appreciated the thoughtful 1-Minute Consult by Drs. Dobri and Lansang, “How should we manage insulin therapy before surgery?”¹ We agree with them in regard to the benefits of perioperative control of blood glucose levels. However, we disagree in general with their assertion that the full dose of the patient’s home dose of basal insulin be administered while the patient is nil per os (NPO) before surgery, with a reduction to 75% of the home dose only if the patient has a history of hypoglycemia, a recommendation that did not differentiate between patients with type 1 and type 2 diabetes mellitus.

The RABBIT 2 Surgery trial,² which showed superiority of basal-bolus insulin over sliding scale insulin in surgical patients with type 2 diabetes mellitus, also showed a surprisingly high rate of hypoglycemia—24 (23.1%) of 104 patients had blood glucose levels lower than 70 mg/dL, compared with a similar trial in nonsurgical patients in which 2 (3.1%) of 65 patients had a blood glucose level less than 60 mg/dL.³ The authors of the two studies explained² that “differences in hypoglycemic events between the two trials could be in part explained by reduced nutritional intake in surgical patients…”

Although patients with well-controlled type 1 diabetes mellitus may tolerate their full dose of basal insulin while NPO, we contend that patients with type 2 diabetes mellitus should be prescribed a reduced dose of basal insulin while NPO, regardless of the dose distribution or the patient’s overall glycemic control. It is routine practice on our consult service to reduce the basal insulin dose in such patients by roughly half.

To the Editor: In their article “The clinical picture: bilateral adrenal masses” in the December 2012 issue,¹ Drs. Saberi and Esfandiari provide excellent points about adrenal hemorrhage as a differential diagnosis for adrenal masses. However, there are two points worth emphasizing when mentioning this diagnosis, especially in the case they presented.

Drs. Saberi and Esfandiari cryptically mention this patient’s coagulopathy (with thrombocytopenia and a rise in creatinine) and anticoagulation as the probable causes of adrenal hemorrhage. We wonder if a diagnosis of antiphospholipid syndrome (APS) was overlooked. Even though overt Addison disease is reported in only 0.4% of patients with APS² and APS is diagnosed in fewer than 0.5% of all patients with Addison disease,³ we think that in this case, since the patient initially presented with an arterial thrombus in the abdominal aorta, screening for APS would have been warranted.

Second, though it is rare, bilateral adrenal hemorrhage with normal imaging on initial presentation has been described,^2,4 which raises this additional question: Should screening for adrenal insufficiency in a patient with possible APS or other coagulopathy be done early while waiting for repeat computed tomography to reveal hemorrhage? Occasionally, intraparenchymal microhemorrhages may not be recognized by sectional imaging but can nonetheless compromise adrenal function.⁴

To the Editor: In their article “The clinical picture: bilateral adrenal masses” in the December 2012 issue,¹ Drs. Saberi and Esfandiari provide excellent points about adrenal hemorrhage as a differential diagnosis for adrenal masses. However, there are two points worth emphasizing when mentioning this diagnosis, especially in the case they presented.

Drs. Saberi and Esfandiari cryptically mention this patient’s coagulopathy (with thrombocytopenia and a rise in creatinine) and anticoagulation as the probable causes of adrenal hemorrhage. We wonder if a diagnosis of antiphospholipid syndrome (APS) was overlooked. Even though overt Addison disease is reported in only 0.4% of patients with APS² and APS is diagnosed in fewer than 0.5% of all patients with Addison disease,³ we think that in this case, since the patient initially presented with an arterial thrombus in the abdominal aorta, screening for APS would have been warranted.

Second, though it is rare, bilateral adrenal hemorrhage with normal imaging on initial presentation has been described,^2,4 which raises this additional question: Should screening for adrenal insufficiency in a patient with possible APS or other coagulopathy be done early while waiting for repeat computed tomography to reveal hemorrhage? Occasionally, intraparenchymal microhemorrhages may not be recognized by sectional imaging but can nonetheless compromise adrenal function.⁴

To the Editor: In their article “The clinical picture: bilateral adrenal masses” in the December 2012 issue,¹ Drs. Saberi and Esfandiari provide excellent points about adrenal hemorrhage as a differential diagnosis for adrenal masses. However, there are two points worth emphasizing when mentioning this diagnosis, especially in the case they presented.

Drs. Saberi and Esfandiari cryptically mention this patient’s coagulopathy (with thrombocytopenia and a rise in creatinine) and anticoagulation as the probable causes of adrenal hemorrhage. We wonder if a diagnosis of antiphospholipid syndrome (APS) was overlooked. Even though overt Addison disease is reported in only 0.4% of patients with APS² and APS is diagnosed in fewer than 0.5% of all patients with Addison disease,³ we think that in this case, since the patient initially presented with an arterial thrombus in the abdominal aorta, screening for APS would have been warranted.

Second, though it is rare, bilateral adrenal hemorrhage with normal imaging on initial presentation has been described,^2,4 which raises this additional question: Should screening for adrenal insufficiency in a patient with possible APS or other coagulopathy be done early while waiting for repeat computed tomography to reveal hemorrhage? Occasionally, intraparenchymal microhemorrhages may not be recognized by sectional imaging but can nonetheless compromise adrenal function.⁴