Patel_8-18.qxd

Diabetes Mellitus: Considerations for
Dentistry
Srividya Kidambi and Shailendra B. Patel
JADA 10.14219/jada.archive.2008.0364 The following resources related to this article are available online at
jada.ada.org (this information is current as of March 9, 2014):
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50 articles
reprints
of this article or about permission to reproduce this article in whole or in part can be found at: Copyright 2014 American Dental Association. All rights reserved. Reproduction or republication strictly prohibited without prior written permission of the American Dental Association. Diabetes mellitus
Considerations for dentistry
Srividya Kidambi, MD; Shailendra B. Patel, BM, ChB, DPhil
Diabetes mellitus (DM) is a
A B S T R A C T
Background. The connection between oral
health and systemic health is bidirectional; systemic illnesses, especially metabolic disor- ders, affect oral health, and it appears that oral health may affect systemic health.
Methods. In this review, the authors outline
2005.1 Although the definition, thepathophysiological basis and much of the basic principles behind diabetes mellitus (DM) and provide some tips to help dentists manage the care of patients Results. DM negatively affects all microvasculature beds, and
the soft tissues and bones supporting the teeth are susceptible.
There is also strong evidence that the presence of periodontal dis- ease is associated with increased cardiovascular morbidity in Conclusions. DM is a chronic, systemic metabolic disorder in
which the orosystemic connection is becoming more understood.
Clinical Implications. DM is a relatively common condition
and, thus, is one that practicing dentists may encounter Key Words. Diabetes; insulin; hypoglycemia; periodontal
disease.4 In addition to altering thecourse of periodontal disease, the dia- Dr. Kidambi is an assistant professor of medicine, Division of Endocrinology, Metabolism and Clinical Nutrition, Department of Medicine, Medical College of Wisconsin, Milwaukee.
sions. Osteoporosis increasingly is being Dr. Patel is a professor of medicine, Division of Endocrinology, Metabolism and Clinical Nutri- tion, Department of Medicine, Medical College of Wisconsin, Milwaukee, and a professor ofmedicine, Clement J. Zablocki VA Medical Center, Milwaukee. Address reprint requests to Dr.
Patel at Division of Endocrinology, Metabolism and Clinical Nutrition, Medical College of Wis- consin, 9200 W. Wisconsin Ave., Milwaukee, Wis., 53226, e-mail “[email protected]”.
Copyright 2008 American Dental Association. All rights reserved. ular and maxillary bones.5,6 Periodontal disease DM may have the disorder at least 10 years seems to be associated with atherosclerotic car- before it is diagnosed clinically.11 This idea is sup- diovascular disease,7-9 and having periodontal dis- ported, in part, by data showing that diabetic ease and DM increases cardiovascular disease complications, which generally take 10 years to risk. Physicians and dentists need to be aware of develop, can occur in as many as 30 percent of the relationship between DM and periodontal dis- patients who receive diagnoses. With an increase ease and take adequate steps to minimize nega- in screening, type 2 DM is being diagnosed in In this review, we provide practicing dentists Type 1 DM. There is an absolute insulin defi-
with an update on the principles of DM, as well as ciency in type 1 DM, with autoimmune destruc- its complications and treatment. Although several tion of pancreatic beta cells being the most types of DM have been described, a number of common cause, although any loss of pancreatic them are rare, so we mention them only briefly.
tissue can result in insulin dependence (such as Our review focuses on providing current informa- pancreatitis, surgical removal or gland destruc- tion about type 1 DM (absolute insulin defi- tion from cystic fibrosis). Insulin administration ciency), type 2 DM (obligatory insulin action is essential in a typical patient with type 1 DM. If resistance) and gestational DM (GDM) (typically patients do not receive insulin, they develop dehy- transient DM lasting during pregnancy).
dration resulting from severe hyperglycemia andketoacidosis, both of which when not treated can CLASSIFICATION AND PATHOGENESIS
OF DIABETES MELLITUS
Similar to other autoimmune diseases, type 1 Classification of DM is based on pathogenic DM has a strong genetic predisposition and a few processes that can lead to absolute or relative susceptible genes that are involved primarily in deficiency of insulin resulting in hyperglycemia immune function.12 Although the general popula- (Table 1).10 Eighty-five to 90 percent of patients tion prevalence of type 1 DM is approximately 0.3 with DM have type 2 DM, and 5 to 10 percent percent, it is higher among the first-degree rela- have type 1 DM. As a good first approximation, tives of patients with type 1 DM. The prevalence patients with type 1 DM initially develop it when among the offspring of patients with DM is 3.0 they are young, most receive a diagnosis before percent if the mother is affected and 6.0 percent if the end of their teenage years (hence, type 1 DM’s the father is affected. Monozygotic twins have a being referred to as juvenile diabetes), and they concordance rate of 30 to 50 percent, and di- typically are lean. Type 2 DM is considered an zygotic twins have a concordance rate of 6 to 10 adult disorder (as it usually develops in patients percent. Variations at the human leukocyte older than 40 years), and it frequently is asso- antigen locus account for 40 to 60 percent of ciated with overweight or obese phenotypes. All of genetic susceptibility, with some alleles these distinctions, however, are becoming increasing the risk and some being protective.13 blurred, as some young, overweight children Patients with type 1 DM are especially suscep- receive a diagnosis of type 2 DM and some older, tible to microvascular complications such as thinner adults have absolute insulin require- neuropathy, retinopathy and nephropathy, ments and receive a diagnosis of type 1 DM.
and although coronary artery disease and The symptoms that are common for type 1 and atherosclerosis can occur, they are less common type 2 DM include new-onset polyuria and noc- turia, accompanying thirst and polydipsia, unex- Type 2 DM. Insulin resistance frequently pre-
plained weight loss, blurred vision and tiredness.
cedes type 2 DM,14,15 and it is characterized by a These symptoms are a direct result of high, per- decreased response of the target tissues to the sistent and fluctuating blood glucose levels. Since normal levels of circulating insulin. These target there is an absolute deficiency of insulin in type 1DM, the disorder’s presentation typically is acute(less than one week) and accompanied by serious ABBREVIATION KEY. DM: Diabetes mellitus. GDM:
symptoms and signs related to acid-base alter- Gestational diabetes mellitus. HbA : Glycosylated
ations, whereas many patients with type 2 DM hemoglobin. MI: Myocardial infarction. MODY:
can be relatively asymptomatic for years. It has Maturity-onset diabetes of the young. NPH: Neutral
been estimated that many patients with type 2 protamine Hagedorn. OHA: Oral hypoglycemic agent.
JADA, Vol. 139 http://jada.ada.org October 2008 Copyright 2008 American Dental Association. All rights reserved. state of hyperinsulinemia.
The mechanistic basis for Abbreviated classification of DM* based on
pathophysiology.
been fully characterized,and multiple levels of ETIOLOGY
Autoimmune destruction of beta cells in pancreas, leading toabsolute insulin deficiency Constitutional insulin resistance with relative insulin deficiency Gestational DM
Secondary to insulin resistance (associated with placental hormones) and relative insulin deficiency during second one-half Monogenic DM
almost normoglycemia, aswell as relatively normal Specific gene defects in beta-cell function—for example, MODY† 1, MODY 2 fatty acid levels to over-come the insulin resis- Genetic defects in insulin action—for example, Type A insulin resistance Diseases of
Usually associated with exocrine pancreatic dysfunction Exocrine
Pancreas
teria for type 2 DM. Fortype 2 DM to develop, it is Endocrino-
Caused by excessive secretion of hormones that counteract insulin, thus creating relative insulin deficiency necessary to have a defectin both the action and the this metabolic pathway isdemonstrated in people at By a variety of actions, some chemicals and drugs increase the Chemical-
Induced DM
such as the American Dia-betes Association.10 Infections
or impaired glucose toler-ance who manifest blood Associated
With Other
Genetic
Syndromes
Rare Immune-
Mediated DM
† MODY: Maturity-onset diabetes of the young.
cose tolerance test (140-199mg/dL). As much as 10 to tissues require higher-than-normal levels of 15 percent of the U.S. population has prediabetes.
insulin for an adequate response (for example, Genetic predisposition for type 2 DM is even glucose uptake in muscles or suppression of fatty stronger than for type 1 DM.19,20 Almost 40 per- acid release in fat) to occur, thereby creating a cent of patients who have type 2 DM have at least Copyright 2008 American Dental Association. All rights reserved. Diagnostic criteria* for diabetes mellitus.
for a first-degree relativeof a patient who has type 2 TEST CRITERIA
PREDIABETES
OVERT DIABETES
MELLITUS
Fasting† Plasma Glucose Test
(Milligrams per Deciliter)
and weight-matchedpatients without a family Plasma Glucose After 75 Grams Oral
Glucose Tolerance Test‡ (mg/dL)
history of DM. Amongmonozygotic twin pairs Random Plasma Glucose Test§ With
Symptoms of Hyperglycemia¶ (mg/dL)
with one affected twin,type 2 DM eventually * Modified with permission from the American Diabetes Association.10 Copyright 2008 American Diabetes † Fasting indicates no caloric intake for eight hours prior.
‡ Oral glucose tolerance test involves measurement of plasma glucose at two hours after consuming 75 grams of glucose dissolved in water (this is the typical interval used for diagnosis of type 2 diabetes mellitus).
§ Random plasma glucose test involves measurement of plasma glucose at any time of the day without any temporal association to caloric intake.
¶ Symptoms of hyperglycemia include polyuria, polyphagia, polydipsia and unexplained weight loss.
risk, including African-Americans, HispanicAmericans, Native Americans, Asian Americans delay, if not prevent, type 2 DM, and this makes the identification of this condition important.
GDM. GDM is characterized by glucose intoler-
ance that is first diagnosed during pregnancy in a achieve adequate glycemic control with lifestyle woman who has not had DM.21 True GDM resolves changes such as medical nutritional therapy (also during the postpartum period. However, as many known as dietary therapy), with exercise and as 50 percent of women who had GDM remain at weight loss or both, whereas others require treat- risk of developing type 2 DM, so GDM is thought ment with oral hypoglycemic agents (OHAs). A to be a harbinger of DM in later life.22,23 The patho- subgroup of patients eventually will need to physiology of GDM is identical to that of type 2 receive insulin for adequate glycemic control and DM with pancreatic beta-cell dysfunction that is to prevent ketoacidosis, even though their bodies unable to meet the increased demands associated still produce some insulin. Acute complications with insulin resistance during pregnancy. A such as diabetic ketoacidosis or the nonketotic minority of patients may develop type 1 DM for the first time during pregnancy, which empha- occur, requiring immediate hospitalization.
sizes the connection between pregnancy and Chronic hyperglycemia can result in increased autoimmune disease.23 Recognition of GDM is susceptibility to infections and impairment of important because it provides an opportunity to growth in children. In addition to general symp- initiate interventional strategies to prevent the toms and signs that are present in all types of development of type 2 DM and to prevent fetal DM, special markers can help in the differential abnormalities by helping the patient maintain tight glycemic control during pregnancy.24 Patients with type 1 DM generally are lean or have normal body weight and may have other DIAGNOSIS
coexisting autoimmune diseases such as hypothy- The American Diabetes Association criteria for the roidism or sprue. Serologic markers of autoim- diagnosis of DM are listed in Table 2.10 Type 1 DM mune processes involved in the development of usually is diagnosed after acute onset of symp- type 1 DM can be detected in the blood early in toms that become metabolically unstable and require immediate evaluation and treatment.
throughout life. These markers include antiglu- However, type 2 DM can differ in manifestation.
tamic acid decarboxylase antibodies, islet cell In prediabetes, a stage during which impaired antibodies and anti-insulin antibodies.10 Rou- fasting glucose or impaired glucose tolerance may tinely checking for antibodies, however, is not rec- occur without fulfilling the criteria for type 2 DM, making lifestyle modifications (exercise, weight Type 2 DM usually is diagnosed by means of loss and diet) has been shown to significantly routine laboratory assessments, after clinical JADA, Vol. 139 http://jada.ada.org October 2008 Copyright 2008 American Dental Association. All rights reserved. defined as affecting arteri-oles and smaller blood ves- Microvascular and macrovascular complications
of diabetes mellitus.
COMPLICATION
FEATURES
PREVENTION
and macrovascular diseasecontribute to complications, Retinopathy
but greater morbidity isascribed to damage Nephropathy
with hyperglycemia; thepoorer the control of DM is, Neuropathy
cardiovascular, gastrointestinal andgenitourinary systems and awareness Cardiovascular
evaluation and exclusion of common causes of ischemia. It is responsible for retinopathy, a transient hyperglycemia have taken place.
major cause of blindness in the developed world; Because there is a long preclinical phase during neuropathy, which is painful and involves the which blood glucose levels are not high enough to loss of the sensations of pain and touch, with cause symptoms but can cause pathological subsequent risk of developing Charcot joints changes in susceptible tissues, as many as 30 per- and ulcers as a result of unattended trauma; cent of patients have complications such as and nephropathy, which is a major cause of retinopathy, neuropathy and nephropathy at the renal failure and dialysis and is implicated in Macrovascular disease is responsible for ather- COMPLICATIONS OF DIABETES MELLITUS
osclerotic disease that affects all major arteries The characteristic abnormality in DM is the inad- (particularly the coronary arteries, carotid equate action of insulin on target tissues, arteries and lower limb vascular tree) and can resulting in abnormal carbohydrate, protein and lead to myocardial infarctions (MIs), stroke and fat metabolism. DM is a true metabolic disorder peripheral vascular disease. Atherosclerotic and, thus, affects every tissue in the body.
processes are made worse by the presence of other Insulin’s action on each target tissue is unique to conventional risk factors, such as smoking, hyper- that tissue, so the action of insulin in the liver is tension and dyslipidemia. Although atheroscle- different than that in muscle or fat. DM is the rotic cardiovascular death may account for less most common disorder in patients admitted to than 20 percent of all causes of death in patients hospitals for any cause and accounts for more with type 1 DM, more than 80 percent of patients than 30 percent of health care visits to primary with type 2 DM will die of cardiovascular causes care providers, although it affects less than 10 (heart disease and stroke) prematurely.28 The percent of the general population.25,26 In general, combination of DM with diffuse arterial tree dis- complications in type 1 DM are those that occur as ease at many different levels poses a major chal- a result of microvascular disease, which is loosely lenge in the management of any tissue ischemia Copyright 2008 American Dental Association. All rights reserved. (for example, chronic foot ulcers and poor wound is administered to produce a peak coinciding healing). Silent MI also is a cause of concern for with absorption of ingested carbohydrates.
In the past, insulin was derived from porcine Although the role of DM and oral complications and bovine sources. These sources have been is reviewed in another article in this supplement,29 replaced by recombinant human insulin. Many two other DM-related issues need to be high- types of insulin have been developed to produce lighted: DM’s effect on joint function (articular varying levels of onset of action, ranging from and nonarticular components) and bone density.30 rapid-acting (for example, analog insulins such as Increased stiffness and loss of flexibility (presum- aspart, lispro and glulisine) to intermediate- ably as a result of increased glycation of long-lived acting (for example, neutral protamine Hagedorn, proteins in tendons and extracellular matrices31,32) commonly referred to as NPH) to long-acting (for are common clinical findings in patients with DM.
example, glargine and detemir) (Table 4). Insulin At the extreme end of this spectrum is diabetic pump therapy, also known as continuous subcuta- cheiroarthropathy, which involves significant stiff- neous insulin infusion, is portable and provides ness of these extra-articular tissues, resulting in flexibility and the convenience of fewer injections, significant deformity and inflexibility of joints.
especially for patients with type 1 DM. The When asked, many patients with DM report expe- insulin pump consists of an external pump and a riencing joint stiffness.33 Temporomandibular joint needle inserted into the skin that are connected dysfunction has not been studied specifically in by tubing. The pump has a reservoir, which is patients with DM, but since DM is a metabolic filled with rapid- or short-acting insulin for con- disorder, all joints may be susceptible.
tinuous infusion. The pump can be programmedto deliver different basal and bolus rates and TREATMENT OF DIABETES MELLITUS
allows delivery of sophisticated regimens of Medical nutrition therapy (also known as dietary insulin that can be customized to each patient’s therapy) and lifestyle modification form the cen- lifestyle. The basis for any successful insulin terpiece of the management of DM, irrespective of therapy is the ability of patients to monitor their modality of therapy chosen. The goals of therapy own blood glucose levels by using glucometers, are to prevent complications of DM. Tight blood education that allows patients to adjust their glucose control prevents microvascular complica- insulin doses, diet and exercise to produce normo- tions in both type 1 and type 2 DM.11,34 Although glycemia and prevent hypoglycemia. Insulin glycemic control may not be as effective in therapy is associated with the risk of experi- reducing macrovascular complications, aggressive encing significant weight gain and developing therapies aimed at blood pressure levels, lipid levels and smoking cessation are effective in pre- Pramlintide. Since the secretion of amylin
from islets in patients with type 1 DM also is Insulin therapy. Insulin therapy is the
defective, amylin injections may help with glucose mainstay for patients with type 1 DM, and, in control. Amylin decreases postprandial glucagon most patients, frequent multiple dosing (basal release and delays gastric emptying (similar to actions of incretins), which may help prevent insulin delivery via pumps also is a fairly large excursions in glucose after meals. The com- common practice. All of these methods typically mercial preparation of amylin is pramlintide, involve subcutaneous injection, and a variety of which is approved by the U.S. Food and Drug insulin preparations can be used that allow the Administration for treatment of patients with physician and patient to select the best method both type 1 and type 2 DM. However, it has to be on the basis of cost and flexibility. Insulin injected before each meal. For glucose control in therapy should mimic the physiological release patients with type 1 DM, there are no orally of insulin, which is characterized by a con- tinuous basal secretion, to prevent fasting OHAs. These are the first-line agents used to
hyperglycemia, as well as prandial insulin treat patients with type 2 DM, and they either release to prevent postprandial hyperglycemia.
increase pancreatic insulin secretion or improve During fasting, long-acting basal insulin, which insulin action (the term “sensitizer” is used to has a flat profile without a peak, is used, and at describe them). Although debate continues about mealtime, a bolus injection of fast-acting insulin the merits of one kind over another, each class of JADA, Vol. 139 http://jada.ada.org October 2008 Copyright 2008 American Dental Association. All rights reserved. fonylurea receptors on betacells to release insulin.
Types of insulin and their profiles.
TYPE OF INSULIN
CHARACTERISTIC
Rapid-Acting
Insulin lispro
Insulin aspart
Insulin glulisine
gluconeogenesis andimproves muscles’ uptake of Used for continuous subcutaneous insulin infusion Short-Acting Insulin
Incretins. The newest
Intermediate-Acting
Neutral protamine
Hagedorn, commonly
referred to as NPH
(isophane suspension)
Long-Acting Insulin
Glargine
and delay gastric empty-ing.37-39 The incretin pathway OHA generally is as effective as the other. At first is attenuated in patients with type 2 DM,40 and approximation, most OHAs lead to an average 1.0 oral agents that specifically target the enzyme to 1.2 percent decrease in glycosylated hemoglobin dipeptidyl peptidase IV increase their half-lives in the bloodstream. Naturally occurring incretins The major classes of OHAs, their modes of in humans have a short half-life and are not action and adverse effects are shown in Table 5.
useful therapeutically. Exenatide is a synthetic Insulin secretagogues are those that stimulate analog of Gila monster incretin (exendin-4), and it insulin secretion from pancreatic beta cells. They targets the glucagon-like peptide-1 receptor. It is are of value only in patients in whom there is an injectable drug, however, and leads to weight some residual pancreatic function. Their advan- loss, unlike insulin, which causes weight gain.41-44 tage is that they mimic physiological insulin secre- Of all the approved agents used to treat DM, only tion. This class of agents includes sulfonylureas two (metformin and exenatide) consistently and meglitinides, both of which work through sul- reduce weight, as well as improve glycemic con- Copyright 2008 American Dental Association. All rights reserved. Oral hypoglycemic agent characteristics.
MODE OF ACTION
ADVERSE EFFECT
Insulin Secretagogues
Sulfonylureas (currently
third generation [glipizide,
glimepiride, etc.])
other and not produce thesame effects; for example, Duration of action and daily dosesvary by agent combining a sulfonylureawith a meglitinide may Meglitinides (repaglinide,
nateglinide)
onset of action, taken 15 minutesbefore meals to target Insulin Sensitizers
Biguanides (metformin)
of developing hypoglycemia whenused alone Transplantation.
Thiazolidinediones
(rosiglitazone, pioglitazone)
tation usually is per-formed in conjunction with α-Glucosidase Inhibitors
Acarbose
Miglitol
or reduce the need forintensive insulin therapy, which has been associatedwith severe hypoglycemia,to attain nearly normal glycemic control.45 Whole transplantation, obviating the high rates of pancreas transplantation can be performed alone, adverse effects resulting from the use of immuno- in combination with kidney transplantation or after kidney transplantation, and its success canbe limited by organ availability, graft failure and MONITORING THE COURSE OF DIABETES
MELLITUS
morbidity associated with immunosuppressivetherapy and surgical complications.46 Improve- The goal of therapy is to prevent complications.
ments in surgical techniques and immunosup- For both type 1 and type 2 DM, the prevention of pressive therapy regimens have helped reduce microvascular complications is achieved by morbidity and mortality, making this a viable improving glycemic control. Since macrovascular therapeutic alternative for the treatment of DM.47 disease is the major cause of premature death in The greatest promise of islet cell transplantation patients with type 2 DM, aggressive targeting of is the possibility of immunosuppression-free JADA, Vol. 139 http://jada.ada.org October 2008 Copyright 2008 American Dental Association. All rights reserved. For glycemic control, it is recommended that patients who have hypoglycemia. Patients who the HbA level (monitored every three months) be have DM and exhibit unusual behavior should maintained at less than 7 percent. If daily blood raise suspicion among staff members, and a glu- glucose monitoring is performed, fasting blood cometer should be used to test their blood glucose plasma levels should be less than 120 mg/dL and blood glucose levels two hours postprandial Every dental office should have a protocol for should be less than 150 mg/dL. For every 1 per- treating hypoglycemia in conscious and uncon- cent HbA level, there is an associated increase in scious patients (Box). It is prudent to have snack complication rates for both microvascular and foods or oral glucose gels or tablets available for macrovascular disease.48 In addition, poor such emergencies, especially in offices in which a glycemic control leads to poor wound healing and large number of minor surgical procedures are increased postoperative complications. Strict performed. Glucose gels are particularly helpful in glycemic control, especially when combined with treating children or adults who are uncooperative intensive insulin therapy, is desirable to prevent because the glucose begins to be absorbed when it long-term complications, but it is associated with is exposed to a mucosal surface. Patients taking immediate danger of extreme low blood glucose insulin are advised to carry their own glucometers levels.49 Recurrent hypoglycemia can result in with them, so asking them to check their own blunting of autonomic response,34,50 and the first blood glucose levels can be a simple remedy.
Patients who are at risk of developing hypo- without intervening autonomic symptoms.
glycemia are those who have received insulin therapy for a while, and screening for patients achieving a target lipid profile (total cholesterol who report taking insulin should alert staff mem- < 200 mg/dL, high-density lipoprotein cholesterol bers to this. Although patients who take OHAs are > 45 mg/dL in men and > 55 mg/dL in women, at a lower risk of developing hypoglycemia than low-density lipoprotein cholesterol < 100 mg/dL are those receiving insulin, the risk is increased and serum triglycerides < 150 mg/dL), and blood when the patient has renal or hepatic disease.
pressure should be less than 130/80 mm Hg Patients with DM who are diaphoretic should (lower if there is evidence of nephropathy). All have their blood glucose checked. For any pro- patients should exercise and aim to attain and cedure that requires sedation or systemic anes- maintain ideal body weight (typically a body mass thesia in the outpatient setting, blood glucose index of < 25). Medical surveillance includes fre- levels should be monitored before the procedure quent examination of patients’ feet to detect vas- and at hourly intervals if surgery is prolonged.
cular and neuropathic changes, at least an Although no level of hyperglycemia is com- annual full eye examination (including the pletely safe, there are no specific guidelines retinas) and screening for early renal changes via regarding high blood glucose levels and how they random urinary microalbumin screening. A daily should be managed before or during a procedure.
aspirin regimen should be followed unless con- If blood glucose levels are elevated to the point traindicated (for example, in patients with hyper- that the patient has altered sensorium, it is pru- sensitivity or who are receiving warfarin therapy) dent to avoid performing any procedures in that patient. Having well-controlled blood glucoselevels is important for infection prevention and MANAGING THE DENTAL CARE OF
proper healing; however, a scheduled procedure PATIENTS WITH DIABETES MELLITUS
probably does not need to be postponed as long as Managing the care of patients with DM in the the patient is conscious and able to follow dental office should not pose a significant chal- instructions. Postoperative instructions should lenge. Hypoglycemia is the major issue that usu- emphasize the importance of blood glucose level ally confronts dental practitioners when they are control during the healing phase, and the treating patients with DM, especially if patients patient’s primary care physician should be kept are asked to fast before undergoing a procedure.
informed to help the patient maintain adequate Although patients with DM usually recognize hypoglycemia and take action before becoming Loss of pain associated with DM typically affects unconscious, occasionally they may not. Staff the distal extremities; central pain sensation is pre- members should be trained to recognize and treat served. Joint flexibility is impaired in patients with Copyright 2008 American Dental Association. All rights reserved. Identification and treatment of hypoglycemia
require allowing breaks for the patient tomove his or her stiff joints. There are no in the dental office.
published data to suggest that temporo-mandibular joint dysfunction is more SYMPTOMS OF HYPOGLYCEMIA
dental practitioners may need to payextra attention when procedures SIGNS OF HYPOGLYCEMIA
Altered consciousness (lethargy and obtundation or personality change)Blood glucose level of less than 60 milligrams per deciliter GENERAL PRINCIPLES
Treatment should be initiated as soon as possible, and staff members should not wait for laboratory results or for a response from a If the blood glucose levels are extremely low (for example, more than 40 mg/dL), blood should be drawn and sent to the laboratory for accurate blood glucose level measurement because the precision of glucometers is low at extremely low blood glucose levels.
CONSCIOUS HYPOGLYCEMIC PATIENT
preventive aspects of DM. They canaggressively screen and diagnose perio- Treat with 15 grams of simple carbohydrates: d4 ounces of regular fruit juice;d3 to 4 glucose tablets.
Repeat finger-stick glucose test in 15 minutes.
If the blood glucose level is more than 60 mg/dL, the patient should be asked to eat a meal if it is close to mealtime. If it is not close tomealtime, a mixed snack that includes carbohydrates, proteins and fat (for example, peanut butter and jelly sandwich or graham crackers with peanut butter or milk and crackers) should be given to maintain the patient’s blood glucose level. A pure carbohydratesnack will cause the patient to revert back to hypoglycemia quickly. Proteins and carbohydrates in the snack provide sus- If the blood glucose level then is less than 60 mg/dL, repeat treatment of 15 g of simple carbohydrates and check the blood glucose level CONCLUSIONS
in 15 minutes. Continue this protocol until the blood glucose levelis higher than 60 mg/dL and then follow with a mixed snack.
Ask the patient to discuss the hypoglycemia with his or her physician who is managing his or her diabetes mellitus.
UNCONSCIOUS HYPOGLYCEMIC PATIENT OR PATIENT UNABLE TO
CONSUME ORAL CARBOHYDRATE
With Intravenous Access
Administer 5 to 25 g of 50 percent dextrose immediately; it will be fol- Notify patient’s physician immediately.
can ask patients with DM how oftenthey check their blood glucose levels, if Without Intravenous Access
Apply glucose gel inside the mouth in a semiobtund patient or treat with 1 mg of glucagon intramuscularly or subcutaneously; the patient should regain consciousness in 15 to 20 minutes.
Repeat the blood glucose test in 15 minutes.
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