Paciente diabetes cirurgia oral
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    Paciente diabetes cirurgia oral Paciente diabetes cirurgia oral Document Transcript

    • ~i~, ¸¸ • • , iJ Oral Maxillofac Surg53:175-182, 1995 Management of the Diabetic Oral and Maxillofacial Surgery Patient EARL STEPHENSON JR, DDS,* RICHARD H. HAUG, DDS,t AND THOMAS A. MURPHY, MD:I: Diabetes mellitus is a complex syndrome of disor- Hyperglycemia leads to glycosuria, which can causedered metabolism and elevated blood glucose. It results severe dehydration by inducing an osmotic diuresis.from an absolute deficiency of insulin secretion (type Significant osmotic diuresis occurs whenever theI), or a combination of insulin resistance and inade- plasma glucose concentration exceeds the patients re-quate insulin secretion (type II). The etiology is not nal glucose threshold (approximately 180 to 250 rag/completely understood, but heredity plays an important dL). 2 This diuresis results in loss of sodium chloride,role in both types of diabetes. It affects over 15 million magnesium, and phosphate, as well as water. De-people in the United States, and the oral and maxillo- creased intravascular volume, with hypotension andfacial surgeon will frequently be required to treat pa- shock, may result. The ketone bodies, acetoacetic acidtients with this disease. ~ The purpose of this paper is and beta-hydroxybutyric acid, produce their effects byto review the pathophysiology, classification, clinical dissociation into hydrogen ions and anions, resultingsymptoms, diagnostic modalities, treatment regimens, in systemic acidosis. Ketoacidosis has multiple detri-and medical management considerations for the oral mental effects on cellular function, eventually inducingand maxillofacial surgery patient with diabetes mel- cardiovascular collapse. 2litus. Classification System Pathophysiology The most useful classification of diabetes is based Insulin is an anabolic hormone synthesized from on the clinical phenotype of the patient. 3 The classifi-proinsulin within the B cells of the pancreas. It stimu- cation of diabetes syndromes was developed by a spe-lates transmembrane transport of glucose and amino cial committee of National Diabetes Data Group andacids, glycogen formation in the liver and skeletal mus- is generally accepted today (Table 1). 4cles, glucose conversion to triglycerides, and nucleicacid and protein synthesis. In the absence of insulin, TYPE I DIABETES MELLITUSglucose cannot be effectively transported into muscleand adipose tissue. Insulin deficiency also leads to in- Type I diabetes mellitus, also called insulin-depen-creased hepatic glycogenolysis, gluconeogenesis and, dent diabetes mellitus (IDDM), is due to an absenceif the deficiency is severe enough, ketogenesis. The of insulin secondary to the destruction of B cells withinresult is hyperglycemia and metabolic acidosis (keto- the pancreas. 3-9 Environmental insult, genetic vulner-acidosis). ability, and autoimmunity all have been shown to lead to B-cell destruction (Fig 1). * Chief Resident, Department of Oral and Maxillofacial Surgery, Environmental insult has been linked to viral infec-Oklahoma Medical Center, Oklahoma City, OK. tions including mumps, measles, coxsackievirus B, cy- t Director, Division of Oral and Maxillofacial Surgery, Met-roHealth Medical Center, and Assistant Professor of Surgery, Case tomegalovirus, rubella, and infectious mononucleo-Western Reserve University School of Medicine, Cleveland, OH. sis. 579 Coxsackievirus and cytomegalovirus have been :~Director, Division of Endocrinology, MetroHealth Medical Cen- isolated from infected pancreases of diabetic patients inter; and Assistant Professor of Medicine, Case Western ReserveUniversity, Cleveland, OH. whom catastrophic catabolism has resulted in death. 79 Address correspondence and reprint requests to Dr Hang: Division There is an increased frequency of IDDM in patientsof Oral and Maxillofacial Surgery, MetroHealth Medical Center, with HLA gene alleles A1, A2, B8, B15, B18, CW3,2500 MetroHealth Dr, Cleveland, OH 44109-1998. DW3, and DW4. 79 These individuals may be vulner-© 1 9 9 5 A m e r i c a n A s s o c i a t i o n o f Oral a n d M a x i l l o f a c i a l S u r g e o n s able to virus-induced autoimmune attacks on their B0278-2391/95/5302-001253,00/0 cells. Autoimmunity involves both humoral and cell- 175
    • 176 MANAGEMENT OF DIABETIC ORAL SURGERYmediated responses, but it is the latter that is involved I HLA-linkedIr--genesin B-cell destruction. Lymphocytic infiltration of the Regulate Ipancreatic islets ("insulitis") is frequently observedin cases of recent onset. 5 At the time of IDDM diagno-sis, 65% to 90% of cases are positive for islet cell I Wus =n,ectionI [,d~,athic (Priman/)Iantibodies; but after 3 years of disease, only about 20% /,, [ Auloimmunity Jto 25% of patients have detectable antibody. 59 Type I diabetes mellitus most frequently occurs in per- Damage to / sons under the age of 40, who are thin and almost invari- 13cells / ,ably exhibit weight loss.3 They generally present with an k,, / / "x Xaccelerating history of glucosuric symptoms.3 These pa- x Immune response Immune responsetients require daily insulin and are prone to ketosis.5 against altered against nonTml 1?) 13cells 13cells TYPE II DIABETES MELLITUS Type II diabetes mellitus, also called non-insulin- "-.. jdependent diabetes mellitus (NIDDM), is not related cell damageTable 1. Classification of Diabetes Mellitus [ Associated Factors/Clinical Class Characteristics FIGURE 1. A simplified schema to show pathways of B cell de-Type 1 insulin- Multiple etiologies (genetic, struction leading to insulin-dependent (type I) diabetes mellims. (Re- dependent (IDDM) environmental, autoimmunity); thin; printed with permission. 5) ketotic without insulin; symptomatic; usually under age 40; to HLA haplotypes and/or autoimmune responses. The female to male ratio is 1.Type II non-insulin- Insulin resistance, relative insulin pathogenesis of NIDDM remains controversial 3 and it dependent (NIDDM) deficiency, and obesity are etiologic is thought to be secondary to insulin resistance and factors; obese; ketotic only with relative insulin deficiencyY -79-11The insulin resistance stress; asymptomatic; usually over may be attributed to postreceptor blocks in the insulin- age 40; strong family history; stimulated pathways of intracellular glucose metabo- female to male ratio is 1:3.Gestational diabetes Etiology secondary to complex lism. 351° This resistance may be aggravated by obe- metabolic and hormonal factors; sity. 3 Obesity is an important diabetogenic influence onset and recognition during and, not surprisingly, approximately 80% of NIDDM pregnancy; increased risk of patients are obese. 5 In NIDDM, insulin levels may be diabetes development after decreased, normal, or increased, relative to nondiabetic childbirth, associated with increased perinatal complications or normal weight persons. 9 However, when NIDDM and mortality. patients are compared with weight-matched nondiabet-Diabetes secondary to: ics, it becomes clear that their circulating insulin levels Pancreatic disease Pancreatectomy; pancreatitis; are reduced. Thus, NIDDM represents a state of rela- carcinoma; hemochromatosis, etc. tive insulin deficiency) Hormonal excess Cushings disease; acromegaly; Clinically, the age of onset is usually over 40 years. 11 pheochromocytoma; primary aldosteronism; glucagonoma, etc. Many patients give a history of rapid weight gain. 3 Drugs Diuretics; glucocorticoids; oral The appearance of symptoms is insidious, and many contraceptives; phenytoin; of the patients are first diagnosed during an unrelated phenothiazines; tricyclic illness. Patients often have a positive family history antidepressants, etc. for type II diabetes, especially among first-degree rela- Receptor availability With circulating autoantibodies (ie, Graves disease) or without tives. 3"6 These patients require weight loss, caloric re- circulating autoantibodies (ie, striction, and often sulfonylurea treatment to reduce Acanthosis nigricans). hyperglycemia. These patients do not exhibit spontane- Genetic syndromes Hyperlipemias; myotonic dystrophy; ous ketosis, a11 but may become temporarily ketotic lipoatrophy; liprechaunism; during acute or surgical stress. 3 Friedreichs ataxia; Prader-Willi syndrome. GESTATIONAL DIABETES Modified with permission from Diabetes 28:1039, 1979. Copy- Gestational diabetes is, by definition, a form of dia-right © 1979 by American Diabetes Association, Inc. 4 betes mellitus which appears de novo during pregnancy
    • STEPHENSON, HAUG, AND MURPHY 177and usually disappears when the pregnancy is termi- in diabetics aged 18 to 74 years was 26% in mennated. 3 The occurrence is most often in the second and 34% in women, while in age-matched nondiabeticand especially the third trimester. This is a time when males and females it was 13.7% and 19.5%, respec-resistance to insulin normally develops and carbohy- tively. ~2 The risk of cardiovascular death in a diabeticdrate tolerance declines, secondary to secretion of large person is roughly doubled by the coexistence of hyper-amounts of insulin antagonistic hormones, including tension. ~~3 Patients may have manifestations of sys-human chorionic somatomammatropin, estrogen, and tolic or diastolic hypertension, or both.progesterone. Up to 50% of gestational diabetics may Neuropathy may be the presenting symptom of dia-expect to become diabetic in a nonpregnant state within betes mellitus, 6"7 and is generally seen in poorly con-10 years. 3 Gestational diabetes is associated with peri- trolled diabetics.~ Peripheral neuropathy results in de-natal risks and fetal mortality. 23 creased conduction velocity of nerve impulses. This usually involves the lower extremities. It sometimes SECONDARY DIABETES affects motor function, but most often affects sensory nerves. Clinically, this results in a "stocking-glove" Secondary diabetes defines a class of patients in distribution of numbness and paresthesia, with musclewhom hyperglycemia is associated with another sys- wasting leading to foot deformity. Trauma due to di-temic disease. The clinical phenotype reflects the un- minished sensation may lead to deterioration of jointsderlying disorder. 3 Diabetes secondary to pancreatic (Charcots joint) and feet, with the ultimate productiondisease is type I in characteristics, while diabetes sec- of diabetic foot ulcers. 6v Mononeuropathy occurs sec-ondary to hormonal excess (ie, Cushings disease, ac- ondary to infarcts of a single nerve (simplex) or multi-romegaly, or glucagonoma) is type II in characteristics. ple single nerves (multiplex). The onset is rapid, withDrugs such as thiazide diuretics are also associated loss of motor and sensory function. Pain is severe alongwith diminished insulin secretion, while drugs such as the distribution of the nerve. Involvement can includeglucocorticoids or oral contraceptives lead to increased cranial nerves, producing Bells palsy and extraocularinsulin resistance. Finally, a number of diverse genetic muscle palsies. 6syndromes include diabetes mellitus among their mani- Cutaneous manifestations of diabetes include skinfestations, as illustrated in Table 1. infections, xanthoma diabeticorum, and necrobiosis li- poidica diabeticorum. Clinically, xanthoma appears as Clinical Findings a firm, nontender, yellowish nodules that contain lipid- filled macrophages. Necrobiosis lipoidica diabet- Polyuria, a common clinical finding, is secondary icorum manifests as a focal necrotic area within theto hyperglycemia and glycosuria. The increased urine dermis and subcutaneous tissues anywhere on theosmolarity induces an osmotic diuresis. This occurs at body. Dermatologic infections are the most commonthe patients renal glucose threshold of approximately of the cutaneous manifestations.180 to 250 md/dL. 2 Obligatory water loss combinedwith hyperosmolarity tends to deplete intracellular wa- Diagnostic Modalitiester and stimulate osmoreceptors in the brains thirstcenter, which manifests as polydipsia. URINE DIPSTICK Visual disturbances in diabetics may take the formof retinopathy, cataract formation, or glaucoma. 5 Traditionally, urine glucose testing has been used asBlindness is 10 times more common in the diabetic an index of prevailing serum glucose concentrations,population than in the nondiabetic population. 6 Reti- but the relationship between serum and urine glucosenopathy is the most common form of disturbance and concentrations is indirect. The presence of glucose inis divided into two categories: background and prolif- the urine occurs because the tubular resorptive capacityerative. Clinically, background retinopathy produces of glucose has been exceeded. Urine glucose measure-retinal hemorrhages, retinal exudates, edema, venous ments correlate poorly with plasma glucose levels be-dilations, microaneurysms, and thickening of retinal cause several physiologic factors affect renal thresholdcapillaries (microangiopathy). In proliferative retinop- and, subsequently, urine glucose concentrations. Suchathy, neovascularization is the hallmark clinical find- physiologic factors include high or low glomerular fil-ing. Proliferative retinopathy is more likely to produce tration and increased or decreased tubular resorption.blindness; 25% of diabetics with proliferative changes These factors contribute to inadequate reflection of se-are blind. 6 rum glucose concentration by urine testing. The urine Hypertension is well documented to be increased in dipstick may have some usefulness in stable, type IIdiabetics compared with nondiabetics. At the Joslin diabetics in whom physiologic variables have been ac-Clinic, in Boston, MA, the prevalence of hypertension counted for or eliminated, and in school-aged children
    • ] 78 MANAGEMENT OF DIABETIC ORAL SURGERYwith diabetes who resist blood testing. ~4 The diagnosis Table 2. Oral Hypoglycemic Agentsof diabetes is not made by urine testing. A positive Duration Maximaltest for glycosuria must always be confirmed by an of Starting Daily Doseselevated plasma glucose before treatment is begun. 3 Action Dose Dosage per Hypoglycemic Agent (h) (mg) (mg) Day SERUM GLUCOSE First-generation agents: Tolbutamide 6-8 500 3,000 2-3 Home capillary glucose monitoring is the keystone Acetohexamide 8-12 250 1,500 1-2of modern diabetes care.14 Capillary glucose monitor- Tolazamide 12-18 100 1,000 1-2ing is recommended for all patients willing and able Chlorpropamide 24-72 100 500 1to perform it, but is mandatory for pregnant diabetics, Second-generationagents:patients on intensive insulin regimens (eg, insulin Glipizide 12-18 2.5 40 1-2 Glyburide 16-24 1.25 20 1-2pumps), patients with frequent hypoglycemia, and forthose in whom specific problems dictate a switch fromurine testing. 1415 The consensus is that blood glucosemonitoring is reasonably accurate when correctly per- erythrocyte is exposed] 7 Hemoglobin Alc reflects theformed. 14 The American Diabetes Association policy degree of hyperglycemia over the previous 8 to 12statement indicates that capillary glucose monitoring weeks. H Although normal values for this test varyis preferable to urine testing in any insulin-requiring among laboratories, less than 6.2% is usually consid-diabetic because it 1) facilitates the prevention of hy- ered normal.~ sperglycemia that cannot be detected by urine testing,and 2) facilitates prevention of hypoglycemia, espe- T r e a t m e n t Modalitiescially in episodes of insulin overload. ~5 Capillary glu- DIETcose levels can be estimated by visual readings of stripsor reflective meters to gauge the reagent strips colori- Diet remains the cornerstone in the management ofmetric reaction. diabetes mellitus. 1911 Special diets for patients with diabetes mellitus have been prescribed for over a cen- GLUCOSE TOLERANCE TEST tury and a half. 2° The goals of nutritional therapy in diabetes are to attain and maintain desirable body This diagnostic modality measures serum glucose weight in adults, maintain normal growth rate in chil-levels at 30 minutes, 1 hour, and 2 hours after the dren, normalize blood glucose levels to avoid acuteadministration of 75 g of glucose to adults (1.75 g&g complications and prevent or delay long-term compli-in children) in the morning after a fast of 10 to 16 cations, and provide optimum nutrition. 19-21The Amer-hours. The main deficiency of this test is a lack of ican Diabetes Association recommends a diet con-reproducibility. A review of 10 literature studies taining 55% to 60% of calories from carbohydrates,showed a mean difference of 26 mg/dL at 1 hour and 12% of calories from protein, and less than 30% of20 mg/dL at 2 hours. 316 On the basis of the glucose calories from fat. 1~19-21 Diet regimens with increasedtolerance test, diabetes is defined by the National Dia- fiber content have been shown over the last decade tobetes Data Group as when a 2-hour value and one be of therapeutic value in lowering insulin require-preceding value exceed 200 mg/dL, while impairment ments, increasing peripheral tissue insulin sensitivity,of glucose tolerance is defined by a fasting serum glu- and decreasing serum cholesterol and triglyceride val-cose of 140 mg/dL and one value exceeding 200 mg/ ues. 2122 A goal of up to 40 g of fiber per day shoulddL. One percent to 5% of patients with impaired glu- be achieved.cose tolerance will become diabetic each year. 16 The most important dietary goal for individuals with type I diabetes mellitus is the establishment of a regular GLYCOSYLATED HEMOGLOBIN meal pattern with consistent day-to-day caloric and carbohydrate intake. The most important dietary and The measurement of glycosylated hemoglobin in di- therapeutic goal in obese persons with type II diabetesabetic patients has been available since about 1976 and is weight loss. 22serves as a determinant of mean serum glucose overtime. Hemoglobin Ale is one of several minor adducts ORAL HYPOGLYCEMICSof hemoglobin A and is formed by the glycosolutionof the N-terminal valine of one or both of the B chains Oral hypoglycemic agents have been available forof hemoglobin A. Hemoglobin AIo is formed at a rate the treatment of patients with NIDDM since 195523dependent on the glucose concentration to which the (Table 2). A sulfonamide derivative, 1-butyl-3-sulfo-
    • STEPHENSON, HAUG, AND MURPHY "179nylurea (carbutamide), developed to treat pneumonia, produced by a chemical conversion from pork or byalso was found to cause hypoglycemia, and subse- the use of recombinant DNA in Escherichia coli] 5quently proved effective in treating some diabetic pa- In general, human insulin preparations have a shortertients. 24 Oral hypoglycemics promote the release of duration of action than animal preparationsSinsulin from the pancreas, increase the quantity of re- The insulin regimen must be designed to mimicceptors on peripheral cell membranes, and correct he- physiologic insulin availability. Physiologic insulinpatic insulin resistanceY -26 Oral hypoglycemic agents regimens have components of insulin action designedare rapidly absorbed from the gastrointestinal tract to coincide with each major meal and a componentafter oral administration and can be measured in the designed to provide sustained insulin availability dur-plasma 1 hour after ingestion. 262s Food does not seem ing the basal state overnight] 5 The initial insulin dos-to significantly affect bioavailability or onset of action, age is 1 to 2 U per kg per day in children 4 and 0.5 towith the exception of glipizide, which may have de- 1.5 U per kg per day in adults. 4a9 Regimens may varylayed absorption. 26 Sulfonylureas are tightly bound to to meet a patients individual needs, but usually twoplasma albumin (90% to 99%). 24,26All oral hypoglyce- thirds of the total dose can be given in the morningmics undergo hepatic metabolism and are eliminated and one third in the evening. 429 The morning doseas metabolites or unchanged parent compounds via is divided into one third short-acting and two thirdthe kidneys. 24 Oral hypoglycemics are categorized into intermediate-acting insulin. One half of the eveningfirst and second generation compounds (Table 2), dose is given as short-acting and one half as intermedi-based primarily on potency. Therapy is usually insti- ate-acting insulin before supper. 29 Absorption of insu-tuted after a trial of diet and exercise that has failed lin can be erratic via the subcutaneous route, and day-to achieve euglycemia (140 to 180 mg]dL). 1j28 Oral to-day variation of absorption has been shown to behypoglycemics have a spectrum of side effects includ- 25% in individual patients. 27Less variation occurs withing hypoglycemia, anorexia, heartburn, occasional short-acting preparations. Thus regimens containingvomiting, flatulence, abdominal fullness, rashes, syn- greater proportions of regular insulin allow greater pre-drome of inappropriate antidiuretic hormone, and dictability in insulinemia and glycemia. 27flushing, diaphoresis, and mild headache associated Regional injection sites for insulin are the thigh,with alcohol ingestion, depending on which oral hypo- buttocks, arm, and abdomen. The fastest absorption isglycemic is being u s e d . 23242628 with the abdomen, followed by the arm, buttocks, and thigh. 27 Random regional site rotation is not indicated. INSULIN Rather, the injection site should be rotated within the same area to achieve predictable glycemic control. To treat excessive hyperglycemia, the abdomen should be Insulin was first discovered in 19214,7 and is used in considered the preferred site when supplemental regu-specific therapies to normalize plasma glucose levels. lar insulin is administered.Insulin is initiated in patients with type I diabetes, ortype II diabetics who have not responded to diet, exer- Medical M a n a g e m e n t of the Surgical Patientcise, and oral hypoglycemics. Insulin is available inthree species types (human, beef, and pork) and is Surgery elicits a response of stress-adaptive hor-classified according to its duration of action and ab- mones (catecholamines, cortisol, growth hormone, andsorption characteristics 27 (Table 3). Human insulin is glucagon), which elevates plasma glucose and de- creases tissue sensitivity to insulin. Therefore, preoper- ative management of the diabetic patient should beTable 3. Comparative Action of Different directed toward euglycemia and avoiding hypogly-Insulin Preparations cemia. Insulin Onset (h) Peak (h) Duration (h) Accurate physical assessment of complications re- lated to diabetes is necessary preoperativelyfl° In-Animal: creased mortality and morbidity in diabetics undergo- Regular 0.5-2.0 3-4 6-8 ing surgery are related mainly to cardiovascular NPH 4-6 8-14 20-24 complications, infection, and reduced rates of wound Lente 4-6 8-14 20-24 Ultralente 8-14 Minimal 24-36 healing. 3°-33 Consequently, the diabetic patient spendsHuman: 30% to 50% more time in the hospital than the nondia- Regular 0.5-1.0 2-3 4-6 betic patient following minor surgery, even if the sur- NPH 2-4 4-10 14-18 gery proceeds without incident. 32 Adept management Lente 3-4 4-12 16-20 for this group of patients by the oral and maxillofacial Ultralente 6-10 12-16 20-30 surgeon is as important as the development of an effec-
    • "180 MANAGEMENT OF DIABETIC ORAL SURGERYtive liaison between the primary care physician and T a b l e 4. G u i d e l i n e s for Use of an I n s u l i n Dripanesthesiologist. Insulin MINOR [NTRAORAL PROCEDURES Blood Glucose (mg/dL) (U/h) (mL/h) Minor surgical procedures, including simple extrac- <80 0.0 0.0tions, biopsies, and placement of implants with local 81-100 0.5 5.0anesthesia alone or with nitrous oxide analgesia, may 141-180 1.5 15 181-220 2.0 20be performed in the office for well-controlled diabetics 221-260 2.5 25regardless of whether they are diet-controlled, on an 261-300 3.0 30oral hypoglycemic, or using insulin. However, if the 301-340 4.0 40diabetic patient is symptomatic and/or has fasting >341 5.0 50blood glucose greater than 140 mg/dL, it is best to Modified with permission.3vdelay elective procedures until the metabolic conditionis optimum. Management of the diet-controlled, oralhypoglycemic, and insulin-using patient includes must be performed under a general anesthetic. Gener-morning food consumption and the usual dose of oral ally, preoperative assessment should include serumhypoglycemic or insulin. measurements of glucose, sodium, potassium, chloride, bicarbonate, urea nitrogen, creatinine, and ketones, as MODERATE INTRAORAL PROCEDURES well as a complete blood count. 18.35.36Electrocardiogra- Moderate surgical procedures, such as removal of phy should be done on all diabetic patients preopera-impacted teeth, requiring intravenous sedation or am- tively and postoperatively for comparison, especiallybulatory general anesthesia are not as benign as might if any unusual surgical stress occurs, because painlessbe assumed in the diabetic patient. Some agents used to myocardial infarctions may occur during surgery. 1836produce anesthesia can alter carbohydrate metabolismand, when combined with surgical stress, anesthesia Diet-Controlled Diabeticshas a definite hyperglycemic effect. 34 There is no agent Well-controlled, diet-treated diabetics do not requirespecifically contraindicated and none specifically bene- any special treatment before and during surgery. 35 Ifficial in a diabetic patient. Autonomic neuropathy can the fasting plasma glucose is lower than 140 mg/dL,predispose the patient to orthostatic hypotension, high these patients can be treated initially with close obser-arrhythmia risk, urinary retention, and gastroparesis. vation. 3435 Plasma glucose levels should be measuredRenal complications may manifest as electrolyte and hourly intraoperatively. If blood glucose levels in-fluid disturbances, including hypokalemia. Such hypo- crease rapidly during or after surgery, it may be neces-kalemia during the induction of anesthesia may be a sary to give insulin] 4 The regimen of exogenous insu-major factor responsible for the development of cardiac lin given to type I or type II diabetics is appropriatearrhythmias. 34 The surgical and physiologic needs may for diet-controlled diabetics.be difficult for the surgeon to manage simultaneously.Consideration should be given to managing the insulin- Oral Antihyperglycemic-Controlled Diabeticsrequiring diabetic patient in the operating room as fora major procedure. The oral antihyperglycemic-con- Ideally, to achieve metabolic control, it is best totrolled patient should discontinue oral hypoglycemic admit the patient to the hospital the day before surgery.therapy the day before surgery. Fasting plasma glucose The patient should have oral hypoglycemic therapyconcentrations should be lower than 140 mg/dL. If discontinued the day before surgery. If the patient isfasting plasma glucose levels are above 140 mg/dL, taking long-acting agents (glyburide and chlorpro-and intravenous insulin infusion should be considered pamide), it is important to convert them to short-actingin an operating room setting. Intraoperative fluids agents (glipizide and tolbutomide) several days beforeshould consist of 5 % dextrose in normal saline. Postop- admission. 237 Type II diabetics will probably requireeratively, these patients resume their oral hypoglyce- temporary use of exogenous insulin because these indi-mic. The diet-controlled diabetic requires no specific viduals have limited reserves of endogenous insulin,management considerations. and stress of surgery sometimes may push them into ketosis. 34 An insulin and glucose regimen should be MAJOR INTRAORAL/EXTRAORALPROCEDURES administered. This regimen can consist of subcutane- ous insulin with glucose infusion, combined insulin/ Major surgical procedures, such as trauma manage- glucose infusion, or separate insulin and glucose infu-ment, joint reconstruction, and infection management, sions, with hourly blood glucose assessments. Postop-
    • STEPHENSON, HAUG, AND MURPHY "18"1eratively, these patients are resumed on their oral Table 5. Combined Glucose-insulin Infusionhypoglycemic, but may require several days on a multi- Treatment Adjustmentple-dose insulin regimen to regain glycemic con-trol.3237 Diet, oral agent, Fasting blood glucose 120-180 mg/dL or insulin Add 10 U regular human insulin to 1,000 mL (<50 U/d) 5% dextrose plus 20 mEq potassium chlorideInsulin-Controlled Diabetics Insulin (>50 U/d) Fasting blood glucose 120-180 mg/dL Add 15 U regular human insulin to 1,000 mL All patients taking insulin, whether for type I or type 5% dextrose plus 20 mEq potassium chlorideII diabetes, should receive insulin therapy during the Infuse at a rate of 100 mL/hsurgical procedure. 32 Ideally, these patients should be Check blood glucose hourly:admitted the day before surgery to obtain metabolic If >180 mg/dL, increase insulin by 5 Ucontrol. The traditional method of management in- If <120 mg/dL, decrease insulin by 5 Uvolves subcutaneous injection of 30% to 50% of the Modified with permission?vusual morning dose of intermediate insulin NPH orLente on the morning o f s u r g e r y , 3234"373s combinedwith an intravenous infusion of dextrose (5%) in waterat a rate of 100 mL/h. This approach has several disad- and dosages adjusted as shown in Table 5. If serumvantages such as variable and unpredictable insulin glucose falls below 80 mg/dL, the same regimen isabsorption, extremes in glucose levels, and lack of followed as previously described. This method lacksability to modify effect. Postoperatively, management flexibility, but is acceptable when infusion pumps aretraditionally consists of supplemental schedules of reg- not available and/or when frequent variations in insulinular subcutaneous injections, 3438which results in a roll- needs are not anticipated. Twenty to 40 mEq of potas-ercoaster-like blood glucose profile. The newer man- sium chloride should be added to the maintenance flu-agement protocols are using intravenously controlled ids, based on serum potassium determinations.insulin/glucose infusion regimens, which is perhaps the The success of either of the insulin/glucose infusionpreferable method of managing type I diabetes during regimens is dependent on accurate hourly measure-surgery. 343vThis approach provides flexibility and can ments of blood glucose levels. 3239Postoperatively, thebe rapidly adjusted depending on the hourly variation infusion is continued until adequate dietary intake isin blood glucose. The infusions of insulin and glucose tolerated. Once food tolerance is established, the insu-can continue through the period of anesthesia and into lin-requiring diabetic is returned to the former dosagethe postoperative period. Usually 1 to 2 U of regular or a new basic regimen is established based on theinsulin and 5.0 to 7.5 g of glucose per hour given by previous days insulin requirement (25% breakfast,intravenous drip can maintain blood glucose levels in 25% lunch, and 25% dinner as regular insulin, andthe 120 mg/dL to 180 mg/dL range. 3239 25% at bedtime as N P H ) ] 2 The infusion is terminated Management with an insulin drip requires the mix- 30 minutes after first subcutaneous injection of short- acting insulin. 32ture of 25 U of regular insulin in 250 mL of normalsaline (1 U/10 mL). Perioperative fluids consisting of5% dextrose should be introduced at a rate of I00 ReferencesmL/h. Fifty mL of the solution is flushed through theintravenous line and the connection via piggyback to 1. Houston MC: Treatment of hypertension in diabetes. Am Heart J 118:819, 1989the system. Serum glucose should be monitored hourly 2. Schade DS: Surgery and diabetes. Med Clin North Am 72:1531,and dosages adjusted as shown in Table 4. If the serum 1988glucose falls below 80 mg/dL, the insulin is stopped 3. Genuth S: Classification and diagnosis of diabetes mellitus. Med Clin North Am 66:1191, 1982and an intravenous bolus of 50% dextrose in water (25 4. Guthrie RA: New approaches to diabetes control. Am Faro Phy-mL) is provided. Once the serum glucose is above sician Pract Ther 43:570, 199180 mg/dL, the infusion is restarted and the dosage 5. Robbins SL, Kumar V: Basic Pathology (ed 4). Philadelphia, PA, Saunders, 1987, pp 86-98modified. 6. Fishman MC, Hoffman AR, Thaler, MS: Medicine (ed 2). Phila- An alternate method is to combine insulin and main- delphia, PA, Lippincott, 1985, pp 239-252tenance fluids at a preestimated individualized concen- 7. Rose LF, Kaye D: Internal Medicine for Dentistry. St. Louis, MO, Mosby, 1983, pp 1259-1276tration. This is accomplished by the addition of 10 to 8. Cahill GF, McDevitt HO: Insulin-dependent diabetes mellitus: 15 U of regular insulin into 1,000 mL of normal saline The initial lesion. New Engl J Med 304:1454, 1981with 5% dextrose and 20 mEq potassium chloride. The 9. Albin J, Rifkin H: Etiologies of diabetes mellitus. Med Clin North Am 66:1209, 1982infusion is introduced at a rate of 100 mL/h (1.0 to 10. DeFronzo RA, Ferrannini E: The pathogenesis of non-insulin- 1.5 U/h). Serum glucose should be monitored hourly dependent diabetes. An update. Medicine 61:125, 1982
    • "182 MANAGEMENT OF DIABETIC ORAL SURGERY11. Reed RL, Mooradian AD: Treatment of diabetes in the elderly. 25. Skyler JS: Strategies in diabetes mellitus. Start of a new era. Am Faro Physician Pract Ther 44:915, 1991 Postgrad Med 89:45, 199112. Sowers JR, Felicetta JV: Systemic hypertension in diabetes mel- 26. Shank WA, Morrison AD: Oral sulfonylureas for the treatment litus. Am J Cardiol 61:34, 1988 of type II diabetes: An update. South Med J 79:337, 198613. Sowers JR, Levy J, Zemel MB: Hypertension and diabetes. Med 27. Hirsch IB, Herter CD: Intensive insulin therapy. Part I. Basic Clin North Am 72:1399, 1988 principles. Am Fam Physician 45:2141, 199214. McCall AL, Mullin CJ: Home blood glucose monitoring: Key- 28. Peters AL, Davidson MB: Use of sulfonylurea agents in older stone for modem diabetes care. Med Clin North Am 71:763, diabetic patients. Clin Geriatr Med 6:903, 1990 1987 29. Schiffrin A: Treatment of insulin-dependent diabetes with multi-15. Skyler JS: Self-monitoring of blood glucose. Med Clin North ple subcutaneous insulin injections. Med Clin North Am Am 66:1227, 1982 66:1251, 198216. Nelson RL: Subspecialty clinics: Endocrinology. Oral glucose 30. Kelly JU, Kelly TJ: Insulin-dependent diabetes. Its effect on the tolerance test: Indications and limitations. Mayo Clin Proc surgical patient. AORN J 54:61, 1991 63:263, 1988 31. Penn I: Diabetes mellitus and the surgeon. Curr Probl Surg 541,17. Jovanovic L, Peterson CM: The clinical utility of glycosylated 1987 hemoglobin. Am J Med 70:331, 1981 32. Gavin LA: Perioperative management of the diabetic patient.18. Butts DE: Perioperative care of the patient with diabetes melli- Endocrinol Metab Clin North Am 21:457, 1992 33. Shuman CR: Surgery in the diabetic patient. Diabetes 8:38, 1982 ms. Plast Surg Nurs 10:7, 1990 34. Podolsky S: Management of diabetes in the surgical patient.19. Anderson JW, Geil PB: New perspectives in nutritional manage- Med Clin North Am 66:1227, 1982 ment of diabetes mellitus. Am J Med 85:159, 1988 35. Hirsch IB, McGill JB, Cryer PE, et al: Perioperative manage-20. Kabadi UM: Nutritional therapy in diabetes. Rationale and rec- ment of surgical patients with diabetes mellitus. Anesthesiol- ommendations. Diabetes Ther 79:145, 1986 ogy 74:346, 199121. Silvis N: Nutritional recommendations for individuals with dia- 36. Reynolds C: Management of the diabetic surgical patient. Post- betes mellitus. S Afr Med J 81:162, 1992 grad Med 77:265, 198522. Bantle JP: The dietary treatment of diabetes mellitus. Med Clin 37. Gavin LA: Management of diabetes mellitus during surgery. North Am 72:1285, 1988 West J Med 151:525, 198923. Lebowitz HE: Oral hypoglycemic agents. Prim Care 15:353, 38. Edelson GW, Faehnie JD, Whitehouse FW: Perioperative Man- 1988 agement of Diabetes. Henry Ford Hosp Med J 38:262, 199024. Ferner RE: Oral hypoglycemic agents. Med Clin North Am 39. Watts NB: Perioperative glucose control in diabetic patients-- 72:1323, 1988 Strategies for the 1990s. West J Med 151:552, 1989