Diabetes mellitus (DM)

Diagnosis (confirm with the same test on another day)

Symptoms of diabetes

·         Polyuria

·         Polydipsia

·         Weight loss

·         Nocturia

·         Polyphagia

·         Blurry vision

·         PLUS random plasma Glucose ε 11.1 mmol/L (200 mg/dL) OR FBS ε 7.0 mmol/L (126 mg/dL) OR plasma glucose value ε 11.1 mmol/L (200 mg/dL) during two hour OGTT

Diagnostic testing

• Fasting blood glucose (FBG): best drawn the morning after overnight fast

• Oral glucose tolerance test (OGTT): 75 g glucose ingested, then plasma glucose levels measured following 0 and 120 minutes

Classification of Diabetes mellitus

Diabetes Secondary to Specific Etiologies

1.       Genetic

• Down syndrome, Turner’s syndrome, Huntington’s disease, genetic defects in ß-cell function and insulin action

2.       Diseases of the endocrine/exocrine pancreas

• Pancreatitis, neoplasia, cystic fibrosis (CF), hemochromatosis (bronzed diabetes)

3.       Endocrinopathies

• acromegaly, Cushing’s syndrome, glucagonoma, hyperthyroidism

4.       Drug-induced

• ß-agonists, glucocorticoids, thiazides, phenytoin

5.       Infections

• Cytomegalovirus (CMV), congenital rubella

Gestational Diabetes (GDM)

Glucose intolerance that develops during pregnancy

Incidence

• 2-4% of all pregnancies

Risk factors

• Age > 25 • member of high-risk ethnic group

• Obesity

• Previous GDM

• 1º relative with DM

• Previous macrosomic baby (> 4 kg)

Screening and diagnosis

• Any pregnant woman should be screened between 24 and 28 weeks

• 50 g glucose challenge test, measuring glucose one hour later

• If abnormal (7.8 mmol/L; 140 mg/dL), then 75 g oral glucose tolerance test (OGTT) should be done

• If any two of the following three values are met or exceeded, a diagnosis of GDM is established

• Fasting glucose ε 5.3 mmol/L (95 mg/dL)

• 1 hr value ε 10.6 mmol/L (190 mg/dL)

• 2 hr ε 8.9 mmol/L (160 mg/dL)

Fetus

Maternal hyperglycemia induces hyperinsulinemia in fetus results in macrosomia (insulin acts as a growth factor)

GDM: prone to respiratory distress, neonatal hypoglycemia, hypocalcemia, hyperbilirubinemia, polycythemia, and prematurity

Preexisting DM: all of the above plus intrauterine growth restriction (IUGR), sacral agenesis, cardiac structural defects

Mother

 Increased risk of developing subsequent type 2 DM

Progression of diabetic retinopathy and nephropathy

Management

• Preconception care to normalize HbA1c (if preexisting DM)

• Tight glucose control (shown to decrease both fetal and maternal complications)

• Oral hypoglycemics contraindicated

• Insulin to maintain tight glycemic control if diet inadequate

• Fetus must be monitored carefully

Impaired Glucose Tolerance (IGT)

Diagnosis based on

• Fasting glucose 6.1-6.9 mmol/L (110-125 mg/dL)

• 2-hour OGTT 7.8-11.1 mmol/L (140-199 mg/dL)

1-5% per year develops DM

50-80% reverts to normal glucose tolerance

Weight loss may improve glucose tolerance

Associated with progressively greater risk of developing macrovascular complications

Complications of diabetes

The majority of complications involve the vascular system

Aggravating factors: poor glycemic control, inadequate control of hypertension and cholesterol, smoking, high fat diet

Macroangiopathy

accelerated atherosclerosis leading to coronary artery disease (CAD), stroke, pulmonary vascular disease (PVD) most common cause of death in type 2 DM

Microangiopathy             

_ Major chronic complication of type 1 and type 2 DM

_ Path gnomonic lesion is basement membrane thickening

_ Classically causes retinopathy, nephropathy and neuropathy

_ Can involve many other organs, including heart and skin

1. Retinopathy

Epidemiology

• Present in 50% of patients after 10 years with DM

• One of the leading causes of blindness in North America

Types

• Non-proliferative (background)

• Generally no symptoms but may affect macula and impair vision

• Microaneurysms, hard exudates, dot and blot hemorrhages

• Pre-proliferative

• 10-40% progress to proliferative within one year

• Macular edema, venous shunts and beading, nerve fiber layer micro infarcts (cotton wool spots)

Proliferative

• Great risk for loss of vision

• neovascularization, fibrous scarring, vitreal detachment, retinal detachment

Presentation

• Asymptomatic to complete loss of vision

Prevention and management

• Tight glycemic control

• Photocoagulation (eliminates neovascularization)

• vitrectomy

• Frequent follow-up visits with an ophthalmologist (immediate referral after diagnosis of type 2 DM; in type 1, only after 5 years of DM

2. Nephropathy

Epidemiology

• Diabetes-induced renal failure is the most common cause of renal failure in North America

• 20-40% of persons with type 1 DM (after 5-10 years) and 4-20% with type 2 DM have progressive nephropathy

Presentation

• Initial changes include microalbuminuria, increased glomerular filtration rate (GFR) (up to 140%), enlarged kidneys

• Over 15 years, progresses to cause hypertension, persistent proteinuria (macroalbuminuria), nephrotic syndrome, renal failure

Prevention and management

• Tight glucose control

• Tight blood pressure control – ACE inhibitors (Shown to reduce nephropathic complications) and calcium channel blockers (CCB)

• limit use of nephrotoxic drugs and dyes

• Protein restriction (controversial)

3. Neuropathy

Epidemiology

• Common in both type 1 and type 2 DM

Pathophysiology

• Metabolic defect thought to be due to increased sorbitol and/or decreased myoinositol (exact mechanisms not understood)

Types

• Distal symmetric “glove and stocking” polyneuropathy

• Autonomic dysfunction (e.g. gastroparesis)

• Mononeuropathy (e.g. carpal tunnel syndrome)

Presentation

• Paresthesias or neuropathic pain

• Motor or sensory deficits (including cranial nerves)

• Orthostatic hypotension

• Impotence

• voiding difficulties

• Foot ulcers

Prevention and management

• Tight glucose control

• Anti-depressants (e.g. amitriptyline), capsaicin, and anti-epileptics (e.g. Tegretol, Neurontin) for painful neuropathic syndromes

• Erythromycin and domperidone for gastroparesis

• foot care education

4. Other Complications

·         Skin disease

·         Bone and joint disease

·         Cataracts

Treatment of diabetes

Diabetes Control and Complications Trial (DCCT) (1993) demonstrated a 50-70% decrease in microvascular complications in type 1 DM in an intensively treated group as compared to a conventionally treated group

United Kingdom Prospective Diabetes Study (1998) demonstrated a

• Decrease in diabetes complications in intensively treated group compared to conventionally treated group

• marked decrease in vascular complications in those with

Well-controlled blood pressure

Diet

·         Energy intake to achieve and maintain desirable weight

·         Other recommendations as per Canada's Food Guide

Lifestyle

Regular physical exercise can improve insulin sensitivity and lower lipid concentrations and blood pressure

stop smoking and decrease alcohol consumption

Oral Hypoglycemic Agents

Mainly for type 2 DM

Clinical Pearl

·         Sulfonyureas and Meglitimides “squeeze” endogenous insulin from the pancreas.

·         Biguanides and Thiazolidinediones act primarily in peripheral tissues remote from the pancreas.

Insulin (see Table)

Doses adjusted for individual patient needs to meet target glycemic control

Administration

• Subcutaneous injections

• Continuous subcutaneous insulin infusion pump

• IV infusion (regular insulin only)

Preparations

• Ultra-rapid (Humalog)

• Rapid or regular (R or Toronto)

• Intermediate (N or NPH, L or Lente)

• Long-acting (U or Ultralente)

_ Multiple daily injections of different types of insulin usually necessary for optimal glucose control

_ Estimate of total daily insulin requirement when starting an adult type 1 diabetes patient on insulin = 0.5 - 0.6 units/kg

 Glucose Monitoring

_ Frequent self-monitoring and recording of blood glucose is now standard management

_ Hemoglobin A1c (HbA1c or glycosylated hemoglobin)

• Percentage indicates level of plasma glucose over past 3 months

• Extremely useful for monitoring patient’s long-term diabetes control

• Goal is to maintain HbA1c within 5-8% range (i.e. average blood glucose 5.0-11.0 mmol/L)

• HbA1c ε 10% indicates poor control

Variable Insulin Dose Schedule (“Sliding Scale”)

_ Patient takes fixed doses of intermediate-acting insulin (N) but varies doses of fast-acting insulin (R or H) based on blood glucose reading at time of dose

_ Use baseline R or H dose when in blood glucose target range; add or subtract units when above or below target

_ allows patient to make corrections to avoid long periods of hyper- or hypoglycemia

Insulin Pump Therapy

_ External, battery-operated pump continuously delivers basal dose of fast-acting insulin through small subcutaneous catheter

_ At meals, patient programs pump to deliver extra insulin bolus

_ Basal dose may be increased or decreased based on activity, sleep, etc.

_ Advantages: more flexible lifestyle (sleep in, eat / skip meals when desired), better glucose control

_ Disadvantages: very expensive, increased risk of DKA if pump inadvertently disconnected, frequent blood glucose testing required

Obesity

Definitions

·         20% or greater above ideal body weight (IBW) (Met. Life Ins. tables); 170% of IBW or BMI > 40 is morbid obesity

·         Most practical index is BMI (body mass index) = weight/height²(kg/m2 )

o   BMI < 20 or > 27 leads to increased health risk

Epidemiology

15-25% of North American adults

Possible Risk Factors

• Increasing age
• Genetic - variations in energy expenditure
• Behaviour/lifestyle - diet and exercise
• Secondary causes

o   Endocrine: e.g. Cushing’s syndrome, polycystic ovarian disease (PCOD)

o   Drugs: e.g. antidepressants, antiepileptics and antipsychotics

• Hypothalamic injury: trauma, surgical, lesions in ventromedial or paraventricular median nucleus

Pathophysiology- positive energy balance: energy input > energy output

Complications

Cardiovascular

• Hypertension, CAD, CHF, varicose veins, sudden death from arrhythmia

Respiratory

• dyspnea, sleep apnea, pulmonary embolus, infections

Gastrointestinal

• Gallbladder disease, gastroesophageal reflux disease (GERD), fatty liver

Musculoskeletal

• Osteoarthritis

Endocrine/metabolic

• impaired glucose tolerance (IGT) to type 2 DM, hyperuricemia, hyperlipidemia

• PCOD, hirsutism, irregular menses, infertility

Increased risk of neoplastic diseases

• Endometrial, post-menopausal breast, prostate, colorectal cancers

Treatment

General recommendations

• Treatment should be based on medical risk

• Safest and best therapy is a comprehensive approach including caloric restriction,increased physical activity and behaviour modification

Diet

• Caloric restriction with a balanced diet with reduced fat, sugar and alcohol

Exercise

Behavior modification

• Individual or group therapy

• Self-monitoring, stimulus control, stress management, cognitive change, crisis intervention

Drug therapy

• serotonergic-appetite suppressants fenfluramine-phentermine (Fen-Phen) were found to cause valvular heart disease and primary pulmonary hypertension (withdrawn)

• Pancreatic lipase inhibitor: orlistat (Xenical) found to be mildly to moderately effective 

Surgical therapy

• gastroplasty (“stomach stapling”) is treatment of last resort (controversial)

• Liposuction

• Weight loss is regained by fat accumulation at the same site or elsewhere

Hand signs to commiunicate with the dentist during proceedure?

Most of the patients seeking dental treatments might be having a problem of how to communicate with the dentist during the dental procedure. That is because our main source of communication is verble communication which will be affected during dental procedure.
Here are some hand signs which you can use to communicate with the dentist during dental procedure. Please use these hand signals to communicate with the dentist during your dental procedure.

Dear Dentists, You can display this poster in your clinic in the waiting room.

Sepsis and septic shock

Definitions

Systemic inflammatory response syndrome (SIRS)—Two or more of the following, due to either an infectious or a noninfectious etiology:

• Temperature >38⁰C or >36⁰C
• Respiratory rate >24 breaths/ min
• Heart rate >90 beats/ min
• WBC count >12,000/uL or <4000/uL, or >10% bands

Sepsis—SIRS witha proven or suspected microbial etiology

Severe sepsis—Sepsis withone or more signs of organ dysfunction

Septic shock—Sepsis witharterial blood pressure<90 mmHg or 40 mmHg below pt’s normal blood pressure for at least 1 hdespite fluid resuscitation

Etiology

• Blood cultures are positive in 20–40% of sepsis cases and in 40–70% of septic shock cases. Of cases with positive blood cultures,-40% are due to gram-positive bacteria, 35% to gram-negative bacteria, and 7% to fungi.

• Any class of microorganism can cause severe sepsis.

• A significant proportion of cases have negative microbiologic data.

Epidemiology and Risk Factors

The incidence of severe sepsis and septic shock is increasing in the United States, with >300,000 cases each year. Two-thirds of cases occur in pts hospitalized for other reasons. Sepsis is a contributing factor in >200,000 deaths eachyear in the United States.

The higher incidence of sepsis is due to the aging of the population, longer survival of pts withch ronic diseases, medical treatments (e.g., with steroids or antibiotics), and invasive procedures (e.g., catheter placement). Gram-negative sepsis is associated withunderlying diabetes mellitus, lymphoproliferative disorders, cirrhosis of the liver, burns, neutropenia, and indwelling urinary cathe ters. Gram-positive sepsis is associated withindwelling mechanical devices and intravascular catheters, IV drug use, and burns. Fungal sepsis is associated with neutropenia and broad-spectrum antimicrobial therapy.

Pathogenesis and Pathology

Local and Systemic Host Responses

• Recognition of microbial molecules by tissue phagocytes triggers production and release of cytokines and other mediators that increase blood flow to the infected site, enhance the permeability of local blood vessels, attract neutrophils to the infected site, and elicit pain.

• Through intravascular thrombosis (the hallmark of the local immune response), the body attempts to wall off invading microbes and prevent the spread of infection and inflammation. Key features of the systemic immune response include intravascular fibrin deposition, thrombosis, and DIC; the underlying mechanisms are the activation of intrinsic and extrinsic clotting pathways, impaired function of the protein C–protein S inhibitory pathway, depletion of antithrombin and protein C, and prevention of fibrinolysis by increased plasma levels of plasminogen activator inhibitor 1.

Organ Dysfunction and Shock

• Endothelial injury: Widespread endothelial injury is believed to be the major mechanism for multiorgan dysfunction.

• Septic shock: The hallmark is a decrease in peripheral vascular resistance despite increased levels of vasopressor catecholamines. Cardiac output and blood flow to peripheral tissues increase, and oxygen utilization by these tissues is greatly impaired.

Clinical Features

• Hyperventilation
• Encephalopathy (disorientation, confusion)
• Hypotension
• DIC, acrocyanosis, ischemic necrosis of peripheral tissues (e.g., digits)
• Skin: hemorrhagic lesions, bullae, cellulitis. Skin lesions may suggest specific pathogens—e.g., petechiae and purpura with Neisseria meningitidis, ecthyma gangrenosum in neutropenic pts with Pseudomonas aeruginosa.
• Gastrointestinal: nausea, vomiting, diarrhea, ileus, cholestatic jaundice
• Hypoxemia: ventilation-perfusion mismatchand increased alveolar capillary permeability withincreased pulmonary water content

Major Complications

• Cardiopulmonary manifestations:

Acute respiratory distress syndrome (progressive diffuse pulmonary infiltrates and arterial hypoxemia) develops in -50% of pts withsevere sepsis or septic shock.

Hypotension: Normal or increased cardiac output and decreased systemic vascular resistance distinguish septic shock from cardiogenic or hypovolemic shock.

Myocardial function is depressed withdecreased ejection fraction.

• Renal manifestations: oliguria, azotemia, proteinuria, renal failure due to acute tubular necrosis

• Coagulation: thrombocytopenia in 10–30% of pts. With DIC, platelet counts usually fall below 50,000/uL.

• Neurologic manifestations: polyneuropathy with distal motor weakness in prolonged sepsis

Laboratory Findings

• Leukocytosis with a left shift, thrombocytopenia

• Prolonged thrombin time, decreased fibrinogen, presence of D-dimers, suggestive of DIC

• Hyperbilirubinemia, increase in hepatic aminotransferases, azotemia, proteinuria

• Metabolic acidosis, elevated anion gap, elevated lactate levels, hypoxemia

Diagnosis

Definitive diagnosis requires isolation of the microorganism from blood or a local site of infection. Culture of infected cutaneous lesions may help establish the diagnosis. Lacking a microbiologic diagnosis, the diagnosis is made on clinical grounds.

Treatment

1. Antibiotic treatment

2. Removal or drainage of a focal source of infection

·         Remove indwelling intravascular catheters and send tips for quantitative culture; replace Foley and other drainage catheters.

·         Rule out sinusitis in pts withnasal intubation.

·         Perform CT or MRI to rule out occult disease or abscess.

3. Hemodynamic, respiratory, and metabolic support

    a. Maintain intravascular volume withIV fluids. Initiate treatment with 1–2 L of normal saline administered over 1–2 h, keeping pulmonary capillary wedge pressure at 12–16 mmHg or central venous pressure at 8–12 cmH2O, urine output at >0.5 mL/kg per hour, mean arterial blood pressure at >65 mmHg, and cardiac index at >4 (L/min)/m2. Add inotropic and vasopressor therapy if needed. Maintain central venous O2 saturation at _70%, using dobutamine if necessary.

    b. Maintain oxygenation withventilator support as indicated.

    c. Monitor for adrenal insufficiency or reduced adrenal reserve. Pts witha plasma cortisol response of <9 ug/dL to an ACTH challenge may have improved survival if hydrocortisone (50 mg q6h IV) and 9-alpha fludrocortisone (50 ug/d via nasogastric tube) are administered for 7 days.

4. Other treatments (investigational): Antiendotoxin, anti-inflammatory, and anticoagulant drugs are being studied in severe sepsis treatment. The anticoagulant recombinant activated protein C (aPC), given as a constant infusion of 24 ug/kg per hour for 96 h, has been approved for treatment of severe sepsis or septic shock in pts with APACHE II scores of >25 preceding aPC infusion and low risk of hemorrhagic complications. The long-term impact of aPC is uncertain, and long-term survival data are not yet available. Other agents have not improved outcome in clinical trials.

Shock Algorithm Guidelines  

Prognosis

In all, 20–35% of pts withsevere sepsis and 40–60% of pts with septic shock die within 30 days, and further deaths occur within the first 6 months. The severity of underlying disease most strongly influences the risk of dying.

Prevention

In the United States, most episodes of severe sepsis and septic shock are complications of nosocomial infections. Thus the incidence of sepsis would be affected by measures to reduce those infections (e.g., limiting the use and duration