ks-cgmh guideline for diabetes mellitus department of endocrinology & metabolism august 31 2003

KS-CGMH Guideline for Diabetes Mellitus

Department of Endocrinology & Metabolism

August 31 2003

Criteria for the Diagnosis of DM• Symptoms of diabetes plus random blood glucose

concentration >200 mg/dL or• Fasting plasma glucose >126 mg /dL @,*

or• 2-hour plasma glucose >200 mg/dL during 75-g

oral glucose tolerance test*

Normal <110 mg/dL, IFG (impaired fasting glucose) 110-125 mg/dLSymptoms as polyuria, polydyspsia, polyphagia, body weight loss@Fasting as no caloric intake for at least 8h *The criteria should be confirmed by repeat testing in a different day

Classification of DM• Type 1 DM (5-10%) : immune mediated, idiopathic• Type 2 DM (90-95%)• Other specific type of DM (1-2%) A. Genetic defects of ß-cell function B. Genetic defects in insulin action C. Diseases of the exocrine pancreas D. Endocrinopathies E. Drugs- or chemical-related F. Infections G. Uncommon forms of immune-mediated disorder H. Other genetic syndromes associated with diabetes• Gestational diabetes mellitus (3-5% of all pregnancy)

C-peptide in DM

A good marker of ß-cell function because of its equimolar secretion with insulin

Fasting plasma C-peptide < 0.35 ng/dL indicating insulin-dependent diabetes

Type 1 DM

Type 2 DM

Management of DM• Diet: 30 Kcal/Kg /day (IBW) Overweight: 25Kcal/Kg/day Underweight: 31-32Kcal/Kg/day 長期臥床 : 25Kcal/Kg/day, 輕度工作 : 30Kcal/Kg/day, 中度工作 : 35Kcal/Kg/day, 重度工作 : 40Kcal/Kg/day [M: IBW= (BH-80)x0.7, F: IBW=(BH-70)x0.6] [Content: carbohydrate 55%, protein 15%, fat 30%]• Exercise: blood sugar >300 or <75 is not suitable

• Medicine: insulin, oral anti-diabetes agents

Insulin Therapy

• 0.5–1.0 U/kg/day first• Indication -- Type 1 DM -- Type 2 DM with acute illness, operation, pregnancy, OHA failure, DKA, HHS -- Short-acting: Regular (Actrapid HM) -- Intermediate-acting: NPH (Monotard HM) -- Long-action: Ultralente (Ultratard HM) -- Combination: Mixtard (70/30)

Time of Action

Preparation Onset Peak Effective Maximum

Duration Duration

Regular 0.5-1.0 2-3 3-4 4-6

NPH 2-4 6-10 10-16 14-18

Ultralente 6-10 10-16 18-20 20-24

Mixtard 0.5-1.0 dual 10-16 14-18

(h)

Insulin Regimens

Insulin Regimens

How to Adjust The Dosage of Insulin Twice Daily

Insulin regimen Qid Bid• Total daily dosage, divided into 2:1, 2/3 dose in

the morning, 1/3 dose in the evening• The morning dose divided into 2/3 NPH+1/3 RI• The evening dose divided into 1/2 NPH+1/2 RI

Oral Anti-diabetes Agents

Class• Sulfonylurea

• Meglitinide• Biguanide• α-glucosidase inhibitor• Thiazolidinedione

Available Agents• Gliclazide (Diamicron),

Glipizide (Glidiab), Chlopropamide (Diabinese)

Glimepiride (Amaryl)

• Repaglinide (NovoNorm)

• Metformin (Glucophage)

• Acarbose (Glucobay)

• Pioglitazone (Actos)

Sulfonylureas Meglitinides Biguanides α-glucosidase inhibitor

Thiazolidine-diones

Hypoglycemia + ± BW gain + ± +GI upset + +Lactic acidosis +Hepatotoxicity +Increased plasma

volume +

Contraindication Significant

liver/kidney

dysfunction

Significant

liver

dysfunction

Cr (M) >1.5,

(F) >1.4 m/dl

Acidosis

CHF

Hypoxia

Radiocontrast

Gastroparesis

IBD

Active liver

disease orGPT >2.5 UNL

CHF

relative Short & rapid

onset

relative

Acute Complications of DM

• Diabetic ketoacidosis (DKA)

• Hyperglycemic hyperosmolar state (HHS)

• Hypoglycemia

DKA (Diabetic Ketoacidosis) & HHS (Hyperglycemic Hyperosmolar State)

• DKA resulted from insulin deficiency combined with counterregulatory hormone excess.

• HHS resulted from hyperglycemia-induced an osmotic diuresis that leads to profound intravascular volume depletion, and the insulin deficiency is only relative and less severe.

• The precipitating events are infection, infarction, stroke, drugs, inadequate insulin administration, compromises water intake...

ADA Diagnostic Criteria of DKA & HHS

• DKA: blood glucose >250 mg/dl, arterial pH <7.3, bicarbonate <15 mEq/l, and moderate ketonuria or ketonemia.

• HHS: blood glucose >600 mg/dl, arterial pH >7.3, bicarbonate >15 mEq/l, mild ketonuria or ketonemia, and effective serum osmolality >320 mOsm/kg H2O.

Diabetic Ketoacidosis (DKA)

• Symptoms • Signs – nausea/vomiting – tachycardia – thirst/polyuria – dry mucous and/or – abdominal pain skin turgor – altered mental status – dehydration – SOB – tachypnea/Kussmaul respirations/distress – abdomen tenderness – fever – lethargy/coma

Hyperglycemic Hyperosmolar State (HHS)

• Symptoms • Signs

– polyuria – tachycardia

– orthostatic hypotension – dry mucous or/

– altered mental status and skin tugor

– (less) abdomen pain, – hypotension

nausea/vomiting,SOB – lethargy/coma

Hypoglycemia

• Definition

Plasma glucose level < 40-50 mg/dL• Whipple’s triad

A. symptoms consistent with hypoglycemia

(neuroglycopenic/autonomic)

B. a low plasma glucose concentration

C. relief of symptoms after the plasma glucose

level is raised

How to manage a patient with low blood sugar level

• Does it meet the Whipple’s triad?

• Identify the cause of low blood sugar at bedside

• Give appropriate treatment

• Do not hold next insulin injection unless clinically warranted.

Hypoglycemia

• Management 1. Oral treatment with glucose-containing material* (15g) if the patient is able to eat 2. Intravenous glucose (20g) followed by a constant infusion of 5 or 10% dextrose if indicated 3. Intramuscular glucacon (0.5-1.0 mg) * 方糖 2 至 4 塊 , 含糖果汁 1/2 瓶 (120cc) 等

Chronic Complications of DM• Microvascular 1. Retinopathy, macular edema, cataracts 2. Neuropathy (sensory, motor, autonomic) 3. Nephropathy• Macrovascular 1. Coronary artery disease 2. Peripheral vascular disease 3. Cerebrovascular disease• Others 1. GI dysfunction (gastroparesis, diarrhea) 2. GU dysfunction (uropathy, sexual dysfunction) 3. Dermatologic

DM Retinopathy

• Background (simple, non-proliferative)

-- retinal vascular microaneurysms, blot

hemorrhage, cotton wool spots• Proliferative

-- neovasculization• Treatment

-- prevention (intensive sugar control), regular eye

exam, laser photocoagulation

DM Neuropathy• The most common DM neuropathy is distal symmetric polyneuropathy• Autonomic: resting tachycardia, orthostatic hypotension, neurogenic bladder, anhydrosis, gastroparesis• Treatment -- less satisfactory, intensive glycemic control, NCV, avoidance neurotoxin, supplement with vitamins and anti-neuralgia/anti-depressant agent

DM Nephropathy

DM Nephropathy

• Effective

-- near normalization of glycemia

-- strict BP control (without proteinuria <130/80,

with proteinuria <120/80 )

-- ACEI, ARB (drug of choice)

-- restriction of protein intake: 0.8g/kg/d, 10% of

daily caloric intake

Dyslipidemia on DM

• Goal on dyslipidemia LDL HDL TG DM with or <100 >45(M) <150 without CVD >55(F)

(mg/dL)

• Dietary changes, life-style modification, drugs

Drugs Choice for Dyslipidemia

DM Foot• Factors which reduce the resistance of the tissues

to trauma– Macrovascular disease– Microvascular disease– Autonomic neuropathy

• Factors which increase the likelihood of trauma

– Motor neuropathy

– Sensory neuropathy

– Limited joint mobility

– Other

EVALUATION OF THE DIABETIC FOOT

DM Foot

ADA recommendation:

(1) Off-loading

(2) Debridement

(3) Wound dressing

(4) Appropriate use of antibiotics

(5) Revascularization

(6) Limited amputation

DM Foot• Wound culture: --wound swab, pus aspiration• Simple cellulitis --Streptococcus: ampicillin, PCN --Staphylococcus: oxacillin• Severe infection need debridement --cefazolin+clindamycin (+GM with toxic sign)• Change antibiotic according to culture results and

clinical features

Malignant External Otitis (MEO)

• A progressive, invasive, or necrotizing cellulitis of the external auditory canal, with granulation tissue formation

• Pseudomonas aerugenosa in almost all cases• Severe otalgia, purulent discharge• Cranial nerves impairment (CN VII, IX, X, XI)• Menigitis may resulted by more extension.• Treatment: pipril+GM for 4 to 6 weeks

Emphysematous Pyelonephritis (EP)

• Severe bacterial UTI may result in EP, which reveals the presence of gas within the renal parenchyma, and may enter the perinephric space.

• Typical urinary pathogens: E. coli, K. pneumoniae, P. mirabilis, and Enterobacter.

• Mortality rate: 10% to 40%

• Treatment: antibiotics

• Nephrectomy: severe obstruction, or failed to medical treatment

Other Complicated Urinary Tract Infections

• Renal papillary necrosis

• Renal abscess

• Perirenal abscess

• Emphysematous cystitis

Emphysematous Cholecystitis (EC)

• EC is a rare complication of acute cholecystitis in which air is found in the lumen and wall of gallbladder, with possible extension to the pericholecystic space.

• Perforation and gangrene are more common.• Typical pathogens: E. coli, Clostridium perfringens.• Higher mortality rate in patients younger than 60.• Treatment: antibiotics (for G(+) and G(-))• Expeditious cholecystectomy

• Mucormycosis may present as a rhinocerebral, pulmonary, cutaneous, GI, or disseminated form of the disease.

• The typical patient presents with DKA.

• The most common pathogen: Rhizopus spp.

• S/S: nasal discharge, headache, facial pain, proptosis, visual loss, deterioration of neurologic function, lethargy, fatal pneumonia, or extensive thrombosis

• Treatment: surgical debridement combined with amphotericin B

Mucormycosis

Liver Abscess • Liver abscess caused by K. pneumoniae is a new clinical

syndrome that has emerged as an important infectious complication in diabetic patients in Taiwan.

• Clinical manifestation -- chills and fever, anorexia, weight loss, nausea and vomiting, weakness and malaise, abdominal pain, but may be non-specific and less obvious -- hepatomegaly, RUQ tenderness, or jaundice • An elevated serum ALK-P is the single most reliable

abnormality for liver abscess, and other tests of liver function may be normal.

• Drainage and antibiotic therapy (GM 1.5 mg/kg + metronidazole 500 mg q 8h) are important dual treatments for liver abscess.

Necrotizing Fascitis

• It is any necrotizing soft tissue infection that spreads along fascial planes, either with or without overlying cellulitis.

• Type 1: mixed flora infection Type 2: group A Streptococcus alone or with Staphylococcus infection• It occurs anywhere, especially the legs.• Edema, warmth, and tenderness initially; and bullae,

gangrene, and ulceration later• Repeated surgical exploration with debridement and

antibiotic treatment are necessary.

How to Approach a Diabetic Patient with Infection

No matter of what kind of infection impressed

• Detailed history taking

• Complete physical examination

• focused examination, including RUQ tenderness, CV angle knocking pain, suprapubic tenderness, musculoskeletal tenderness, perineum, prostate tenderness

Treatment Goals in Diabetic patients

• A HbA1c <7 %

• B BP <130/80 mmHg

• C LDL-Cholesterol <100 mg%

HDL (male) >40 mg%,

(female) >50 mg%

TG <150 mg%

Long-Term Treatment of DM

• Self-monitoring of blood sugar (individual frequency)• HbA1C testing (2-4 times/year)• Patient education (annual)• Eye examination (annual)• Foot examination (daily by patient, annual by

physician)• Screening for nephropathy (annual)• Blood pressure measurement• Lipid profile (annual)

Approach New Patient on Ward

• Duration, recent treatment, average blood sugar level, 3P symptoms

• Family history• Co-morbidity• Vital sign (BP, HR, posture BP), Body weight• Physical examination (cardiovascular, neurologic) • CXR, EKG, CBC & D/C, SMA-12, U/R, S/R

Approach New Patient on Ward

• HbA1c, CCr, 24-h urine protein, HDL-electrophoresis

• Finger stick blood sugar monitoring • Consult dietitian• Eye-ground examination