- Email: [email protected]
Management of the Diabetic Patient
Salurday, March 2, 1996 dergoing a nonvascular interventional treatment and for azotemic patients who are undergoing vascular stenting, vena cava filter placement, embolotherapy, or intervascular thrombolysis. Postoperative Therapy Dialysis should be considered if fluid and electrolyte balance is difficult to attain. Special care should be exercised to diagnose infection or hemorrhagic complications as early as possible. SWlDmary
Treatment of the azotemic patient is complex and requires teamwork involving the interventional radiologist, nephrologist, urologist, and, occasionally, the anesthesiologist. All members of this team must understand that the risks of the interventional procedure are significantly increased by the patient's disease and that certain precautions or treatment modifications by all team members will be necessary. The nephrologist will supply the expertise necessary to optimize fluid and electrolyte balance. However, if these efforts prove inadequate, dialysis should be used preoperatively and postoperatively. Vascular diagnostic procedures have traditionally involved the use of contrast material, a substance that is especially dangerous to the azotemic patient. MR angiography and transcutaneous US should be substituted for procedures that require the use of contrast material. If intravascular information is needed, the use of contrast material should be limited to a nonionic, low-osmolar agent. Additionally, the volume of contrast material used should be as little as possible, substituting injections of carbon dioxide, intra-arterial vascular US, and intravascular determination of pressure gradients for angiographic images whenever possible. The patient's azotemic state and its effect on the possible prolongation of therapeutic effect must be considered when prescribing medications before, during, or after the interventional procedure.
References 1. Bastl CP, Rudnick MR, Narins RG.
Assessment of renal function: characteristics of the functional and organic forms of acute renal failure. In: Seldin DW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1819-1836.
2. Blantz RC. Intrinsic renal failure: acute. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1863-1884. 3. Bricker NS, Shapiro MS, Levine MM, Makoff RK. Physiology and pathology of electrolyte metabolism in chronic renal disease. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1837-1862. 4. Lang GR, ]onasson O. Acute renal insufficiency complicating surgery and trauma. In: Hardy JO, ed. Complications in Surgery and Their Management. Philadelphia: WE Saunders, 1981; 8&-97. 5. Malhorta V. Anesthesia and renal and genitourinary systems. In: Miller RO, ed. Anesthesia. New York: Churchill Livingstone, 1994; 1947-1968. 6. Martin LG, Casarella WJ, Gaylord GM. Azotemia caused by renal artery stenosis: treatment by percutaneous angioplasty. AJR 1988; 150:839-844. 7. Morrison G, Geheb MA, Earley LE. Chronic renal failure. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1901-1943. 8. Moser M. Hypertension. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 263-280. 9. Saurina GR, Bonventre]V. Acute renal failure. In: Rakel RE, ed. Conn's Current Therapy. Philadelphia: WE Saunders, 1995; 635-642. 10. Smith MC, Dunn MJ. Chronic renal failure. In: Rakel RE, ed. Conn's Current Therapy. Philadelphia: WE Saunders, 1995; 642-648. 11. Thurau K, Mason J, Gstraunthaler G. Experimental acute renal failure. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1885-1899.
II
1:05 pm Management of the Diabetic Patient Irl B. Hirsch, MD Learning objective: To become familiar with the management of diabetes during interventional procedures. The type of diabetes a patient has must be determined before that patient undergoes an in-
79
Saturday, March 2, 1996
mDM (Type I Diabetes) 5-10 g/h glucose infusion "BASAL-B LUS" REGIMEN
continuous subcutaneous insulin infusion (CSIT) or ultralente regimen
TIME OF ROCEDURE
EarlY~teAM I I
continue normal basal insulin* *CBG < 200 mg%
Figure 1. Regimens for IDDM.
NlDDM (Type II Diabetes)
Late AM r Early PM 1/2 morning dose of intermediate-acting insulin *5~10 U safe for most; insulin resistant pts may require more
supplemental regular insulin if CBG> 200 mg/dL*
Figure 2. Insulin management for patients with insulin-treated NIDDM based on the time of the interventional procedure.
terventional procedure. The difference between being insulin-dependent and requiring insulin must be understood. Most patients with insulin-dependent (IDDM) or non-insulin-dependent (NIDDM) diabetes need 5-10 g of glucose per hour. The patient with IDDM may be on a basal-bolus regimen or an NPH/Lente regimen (Fig 1). The patient with NIDDM may be on a physiologic or nonphysiologic regimen. For all patients, the insulin regimens are easier to follow if the interventional procedure is scheduled early in the morning (Fig 2). If the patient with IDDM
80
or insulin-treated NIDDM is expected not to take anything orally for > 24 hours, the insulin regimen can be managed by using an intravenous insulin infusion. Although exceptions exist (in case of pregnancy or pancreas transplant), blood glucose levels should be maintained between 120-200 mg/dL. With non-insulin treated NIDDM, sulfonylureas should be withheld in most cases until after the procedure. For contrast studies, metformin should be discontinued 2-3 days before the procedure. Acarbose should only be administered with meals (Fig 3).
Saturday, March 2, 1996
II
NlDDM (Type II Diabetes)
•
INON-INSULIN-TREATED I
[
•
STOP METFORMIN 2-3 days prior to procedure if contrast study
•
withhold slilfonylurea or acarbose (or metformin if not already discontinued)
.
if fasting CBG > 200 and no ketonuria, consider failure to oral agent, stress of illness (e.g., MI), and need for oral agent or regular insulin at 0.075-0.1 U/kg Figure 3. Drug management for patients with non-insulin treated NIDDM who are to undergo an interventional procedure.
References 1. Binder C, Lauritzen T, Faber 0, Pramming S. Insulin pharmacokinetics. Diabetes Care 1984; 7:188-199. 2. Dimitriadis GD, Gerich JE. Importance of timing of premeal subcutaneous insulin administration in the management of diabetes mellitus. Diabetes Care 1983; 6: 374-377. 3. Galloway JA. Treatment of NIDDM with insulin agonists or substitutes. Diabetes Care 1990; 13:1011-1020. 4. Genuth S. Insulin use in NIDDM. Diabetes Care 1990; 13:1240-1264. 5. Hirsch IB, McGill JB, Cryer PE, White PF. Review: perioperative management of surgical patients with diabetes mellitus. Anesthesiology 1991; 74:346-359. 6. Hirsch IB, McGill JB. Role of insulin in management of surgical patients with diabetes mellitus. Diabetes Care 1990; 13:980-991. 7. Hirsch IB, Paauw DS, Brunzell J. Inpatient management of adults with diabetes. Diabetes Care 1995; 18:87Q-878. 8. Hirsch lB. Implementation of intensive diabetes therapy in IDDM. Diabetes Rev 1995; 3:288-307. 9. Skyler JS. Insulin pharmacology. Med Clin North Am 1988; 72. 10. Surwit RS, Schneider MS, Feinglos MN. Stress and diabetes. Diabetes Care 1992; 15:1413-1421.
11. Tumer RC, Holman RR. Insulin use in NIDDM: rationale based on pathophysiology of disease. Diabetes Care 1990; 13:10111020. 12. Vora JA, Burch A, Peters JR, Owens DR. Relationship between absorption of radiolabeled soluble insulin, subcutaneous blood flow, and anthropometry. Diabetes Care 1992; 15:1484-1493. 13. Watts NB, Gebhart SP, Clark RV, Phillips LS. Perioperative management of diabetes mellitus: steady state glucose control with bedside algorithm for insulin adjustment. Diabetes Care 1987; 10:722-728. 2:15 pm Overview of Conscious Sedation Elvira V. Lang, MD
Learning objectives: 0) To describe the indications for conscious sedation. (2) To discuss the methods of conscious sedation.
Interventional radiologic procedures are usually performed on awake patients and can last for hours. Pain can be due to procedural stimuli, injection of radiographic contrast media, immobilization for extended periods, or preexisting conditions. Anxiety and fear of pain can make patients apprehensive 0,2). Thus, the stage is set for a potentially self-reinforcing spiral of increasing pain and anxiety, which can increase muscle tension, heart rate, blood pressure, and
81
Treatment of the azotemic patient is complex and requires teamwork involving the interventional radiologist, nephrologist, urologist, and, occasionally, the anesthesiologist. All members of this team must understand that the risks of the interventional procedure are significantly increased by the patient's disease and that certain precautions or treatment modifications by all team members will be necessary. The nephrologist will supply the expertise necessary to optimize fluid and electrolyte balance. However, if these efforts prove inadequate, dialysis should be used preoperatively and postoperatively. Vascular diagnostic procedures have traditionally involved the use of contrast material, a substance that is especially dangerous to the azotemic patient. MR angiography and transcutaneous US should be substituted for procedures that require the use of contrast material. If intravascular information is needed, the use of contrast material should be limited to a nonionic, low-osmolar agent. Additionally, the volume of contrast material used should be as little as possible, substituting injections of carbon dioxide, intra-arterial vascular US, and intravascular determination of pressure gradients for angiographic images whenever possible. The patient's azotemic state and its effect on the possible prolongation of therapeutic effect must be considered when prescribing medications before, during, or after the interventional procedure.
References 1. Bastl CP, Rudnick MR, Narins RG.
Assessment of renal function: characteristics of the functional and organic forms of acute renal failure. In: Seldin DW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1819-1836.
2. Blantz RC. Intrinsic renal failure: acute. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1863-1884. 3. Bricker NS, Shapiro MS, Levine MM, Makoff RK. Physiology and pathology of electrolyte metabolism in chronic renal disease. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1837-1862. 4. Lang GR, ]onasson O. Acute renal insufficiency complicating surgery and trauma. In: Hardy JO, ed. Complications in Surgery and Their Management. Philadelphia: WE Saunders, 1981; 8&-97. 5. Malhorta V. Anesthesia and renal and genitourinary systems. In: Miller RO, ed. Anesthesia. New York: Churchill Livingstone, 1994; 1947-1968. 6. Martin LG, Casarella WJ, Gaylord GM. Azotemia caused by renal artery stenosis: treatment by percutaneous angioplasty. AJR 1988; 150:839-844. 7. Morrison G, Geheb MA, Earley LE. Chronic renal failure. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1901-1943. 8. Moser M. Hypertension. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 263-280. 9. Saurina GR, Bonventre]V. Acute renal failure. In: Rakel RE, ed. Conn's Current Therapy. Philadelphia: WE Saunders, 1995; 635-642. 10. Smith MC, Dunn MJ. Chronic renal failure. In: Rakel RE, ed. Conn's Current Therapy. Philadelphia: WE Saunders, 1995; 642-648. 11. Thurau K, Mason J, Gstraunthaler G. Experimental acute renal failure. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1885-1899.
II
1:05 pm Management of the Diabetic Patient Irl B. Hirsch, MD Learning objective: To become familiar with the management of diabetes during interventional procedures. The type of diabetes a patient has must be determined before that patient undergoes an in-
79
Saturday, March 2, 1996
mDM (Type I Diabetes) 5-10 g/h glucose infusion "BASAL-B LUS" REGIMEN
continuous subcutaneous insulin infusion (CSIT) or ultralente regimen
TIME OF ROCEDURE
EarlY~teAM I I
continue normal basal insulin* *CBG < 200 mg%
Figure 1. Regimens for IDDM.
NlDDM (Type II Diabetes)
Late AM r Early PM 1/2 morning dose of intermediate-acting insulin *5~10 U safe for most; insulin resistant pts may require more
supplemental regular insulin if CBG> 200 mg/dL*
Figure 2. Insulin management for patients with insulin-treated NIDDM based on the time of the interventional procedure.
terventional procedure. The difference between being insulin-dependent and requiring insulin must be understood. Most patients with insulin-dependent (IDDM) or non-insulin-dependent (NIDDM) diabetes need 5-10 g of glucose per hour. The patient with IDDM may be on a basal-bolus regimen or an NPH/Lente regimen (Fig 1). The patient with NIDDM may be on a physiologic or nonphysiologic regimen. For all patients, the insulin regimens are easier to follow if the interventional procedure is scheduled early in the morning (Fig 2). If the patient with IDDM
80
or insulin-treated NIDDM is expected not to take anything orally for > 24 hours, the insulin regimen can be managed by using an intravenous insulin infusion. Although exceptions exist (in case of pregnancy or pancreas transplant), blood glucose levels should be maintained between 120-200 mg/dL. With non-insulin treated NIDDM, sulfonylureas should be withheld in most cases until after the procedure. For contrast studies, metformin should be discontinued 2-3 days before the procedure. Acarbose should only be administered with meals (Fig 3).
Saturday, March 2, 1996
II
NlDDM (Type II Diabetes)
•
INON-INSULIN-TREATED I
[
•
STOP METFORMIN 2-3 days prior to procedure if contrast study
•
withhold slilfonylurea or acarbose (or metformin if not already discontinued)
.
if fasting CBG > 200 and no ketonuria, consider failure to oral agent, stress of illness (e.g., MI), and need for oral agent or regular insulin at 0.075-0.1 U/kg Figure 3. Drug management for patients with non-insulin treated NIDDM who are to undergo an interventional procedure.
References 1. Binder C, Lauritzen T, Faber 0, Pramming S. Insulin pharmacokinetics. Diabetes Care 1984; 7:188-199. 2. Dimitriadis GD, Gerich JE. Importance of timing of premeal subcutaneous insulin administration in the management of diabetes mellitus. Diabetes Care 1983; 6: 374-377. 3. Galloway JA. Treatment of NIDDM with insulin agonists or substitutes. Diabetes Care 1990; 13:1011-1020. 4. Genuth S. Insulin use in NIDDM. Diabetes Care 1990; 13:1240-1264. 5. Hirsch IB, McGill JB, Cryer PE, White PF. Review: perioperative management of surgical patients with diabetes mellitus. Anesthesiology 1991; 74:346-359. 6. Hirsch IB, McGill JB. Role of insulin in management of surgical patients with diabetes mellitus. Diabetes Care 1990; 13:980-991. 7. Hirsch IB, Paauw DS, Brunzell J. Inpatient management of adults with diabetes. Diabetes Care 1995; 18:87Q-878. 8. Hirsch lB. Implementation of intensive diabetes therapy in IDDM. Diabetes Rev 1995; 3:288-307. 9. Skyler JS. Insulin pharmacology. Med Clin North Am 1988; 72. 10. Surwit RS, Schneider MS, Feinglos MN. Stress and diabetes. Diabetes Care 1992; 15:1413-1421.
11. Tumer RC, Holman RR. Insulin use in NIDDM: rationale based on pathophysiology of disease. Diabetes Care 1990; 13:10111020. 12. Vora JA, Burch A, Peters JR, Owens DR. Relationship between absorption of radiolabeled soluble insulin, subcutaneous blood flow, and anthropometry. Diabetes Care 1992; 15:1484-1493. 13. Watts NB, Gebhart SP, Clark RV, Phillips LS. Perioperative management of diabetes mellitus: steady state glucose control with bedside algorithm for insulin adjustment. Diabetes Care 1987; 10:722-728. 2:15 pm Overview of Conscious Sedation Elvira V. Lang, MD
Learning objectives: 0) To describe the indications for conscious sedation. (2) To discuss the methods of conscious sedation.
Interventional radiologic procedures are usually performed on awake patients and can last for hours. Pain can be due to procedural stimuli, injection of radiographic contrast media, immobilization for extended periods, or preexisting conditions. Anxiety and fear of pain can make patients apprehensive 0,2). Thus, the stage is set for a potentially self-reinforcing spiral of increasing pain and anxiety, which can increase muscle tension, heart rate, blood pressure, and
81