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Diabetes Mellitus Jane DisaSmith, D.O. Dec. 13, 2005 Slides by Billie Hall, D.O.

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Presentation on theme: "Diabetes Mellitus Jane DisaSmith, D.O. Dec. 13, 2005 Slides by Billie Hall, D.O."— Presentation transcript:

1 Diabetes Mellitus Jane DisaSmith, D.O. Dec. 13, 2005 Slides by Billie Hall, D.O.

2 Classification Diabetes can be grouped into 4 major categories… –Type 1 (IDDM) – deficiency of insulin secretion –Type 2 (NIDDM) – resistance to action of insulin by target organs and tissues –Secondary causes – such as drugs (steroids), genetics (down syndrome) –Gestational DM

3 Epidemiology Estimated that 100 million people worldwide have DM – 85-90% are type II In the U.S. aprox 5.9 million do not know they have diabetes From 1990-98, prevalence of DM rose 33%, in part to the increase in population over 65, but also related to epidemic levels obesity

4 Risk Factors Type I –Genetic predisposition if father has type I (3x more likely than if mom) –Dietary factors such as exposure to cow’s milk proteins, bovine serum albumin at age less than 3 months –Viral infections such as Coxsackie B, CMV and mumps

5 Risk Factors Type II (table 212-2) –Hypertension (>140/90) –Dyslipidemia (HDL 250) –Diet (high fat, starch, low fiber) –Sedentary lifestyle –Obesity (BMI > 25kg/m 2

6 Pathophysiology Type I – destruction of insulin-producing pancreatic beta cells and absolute insulin deficiency. Type II – development of insulin resistance and increased insulin production

7 Pathophysiology Organs and tissues most affected by DM – retina, kidneys and nerves – all readily take up glucose. This leads to intracellular accumulation of metabolic end products (sorbitol)

8 Pathophysiology Sorbitol competitively inhibits myo-inositol formation which causes a decrease in the uptake of phosphoinositides into cell membranes, leading in turn to a decrease in Na + K + ATPase activity Ultimate effect – slowed nerve conduction leading to neuropathy, retinopathy and nephropathy

9 Clinical features Type I frequently presents as DKA, associated with an infection or other stressor in children and young adults Type II can be present for years before onset of clinical symptoms and sometimes is dx only with initial presentation of microvascular or infection complication of the disease

10 Clinical features Classic DM signs and symptoms may include polyuria, polydipsia, fatigue polyphagia, unexplained weight loss, poor wound healing, blurred vision, and certain infections such as candidal vaginitis and balanitis, and recurrent UTI’s

11 Clinical features Symptoms of poor glucose control include visual changes, neurologic symptoms (such as numbness, dizziness and weakness), GI symptoms, GU symptoms (overflow incontinence, changes in amt of urine, sexual dysfunction)

12 Physical Exam When a diabetic patient presents to ER, PE should be tailored to their complaint. But it should also include BP measurement, fundoscopy, good cardio exam (bruits in abdomen and carotids), extremity exam (esp. feet), and good neuro exam (looking for neuropathy)


14 Diagnosis Diagnosis of DM can be established in 3 ways, 2 of which may be feasible in the ER. (Table 212-4) 1. Symptoms of DM plus casual plasma glucose level >200mg/dL (casual defined as any time of day) 2. FPG >126 mg/dL (fasting at least 8 hrs) 3. Oral Glucose Tolerance Test

15 OGTT 75 grams of glucose dissolved in water, which patient drinks. 2 hours later, blood glucose level of 200 mg/dL or greater is a positive test

16 Acute Hyperglycemia Defined as BG >300 Can represent metabolic decompensation If chronic, can represent high risk for developing macro and microvascular complications

17 Clinical Features H&P should focus on finding source of hyperglycemia, such as any medications patient is on that could contribute (steroids) Look for source of infectious process (pneumonia, UTI) ACS or CNS assault can cause hyperglycemia

18 Clinical Features Also look for changes or non-compliance with insulin or oral hypoglycemic therapy Younger adults may present with polyuria or polydipsia as symptoms, whereas older diabetics may present severely volume depleted with acute mental status changes

19 Clinical Features Lab tests –Electrolytes, BUN/Cr, ABG (though Tintinalli feels this is not always necessary) –Blood glucose measurements every 1-2 hours

20 Therapy Volume repletion IV regular Insulin Correction of electrolyte imbalance Correction of any causes of the hyperglycemia (infections)

21 Therapy Most significant electrolyte disorder is hypokalemia. Total body deficit secondary to significant extracellular volume loss Initial metabolic acidosis, which can elevate potassium levels, can mask true potassium deficits

22 Hypokalemia Potassium replacement should be a priority if level is at or below 5.5 mEq/L, assuming normal renal function Even with compromised renal function, levels at 3.3 mEq/L represent a severe deficit and need supplementation to prevent lethal dysrhythmias

23 Long-term Therapy For Type I, insulin therapy is key. Motivated patients can monitor their blood glucose levels and can self administer insulin to keep levels normal or as near normal as possible. Can also rely on an insulin pump that delivers a basal rate, with pre- programmed or patient set boluses around meals.

24 Long-term Therapy Type II diabetics use a staged approach. –Stage 1 – diet control and weight mgt –Stage 2 – oral hypoglycemic meds –Stage 3 – addition of insulin if failing oral agent therapy

25 Long-term Therapy Generally medication adjustment is best left to the primary care doc as dosage changes require close monitoring But if not readily available, adjustment of insulin units should not be more than 10% increase or decrease in a single day Oral med dosages should not be more than 20% increase or decrease

26 Complications Cardiovascular –Leading cause of DM deaths, accounting for 40% in men and 32% in women –Diabetics have six times the risk of MI as opposed to non-diabetics

27 Cardiovascular Contributing Factors –Increased incidence of atherosclerosis on coronary vessels –Microvascular disease, contributing to “silent” MI’s (painless MI’s)

28 Cardiovascular Therapy to reduce CV events include aggressive BP control to 130/80 or less Reduction of serum cholesterol to less than 200mg/dL Anti-platelet therapy with Aspirin or Plavix ® if ASA allergy ACEI’s to reduce nephropathy and CV events

29 Retinopathy Diabetic retinopathy is leading cause of cases of new blindness in ages 25 to 74 in US Glaucoma and cataracts more common in diabetics

30 Retinopathy In the ED, any history of vision changes, blurriness should arouse suspicion for retinopathy Retinal exam might show microaneurysms, exudates, and vascular proliferation

31 Retinopathy Red and/or painful eye with a HA, OR unexplained HA in a diabetic should warrant an intraocular pressure measurement All of these should include prompt referral to an ophthalmologist

32 Nephropathy One of the leading causes of end stage renal disease is DM nephropathy Aprox 43% of new renal failure cases each year are DM nephropathy

33 Nephropathy Hyperglycemia leads to glomerular HTN and hyperfiltration, which in turn leads to deposition of protein in mesangium These protein deposits cause sclerosis of the glomerulus and then renal failure

34 Nephropathy Most useful clinical marker is microalbuminuria Excretion of 30mg/day are still at high risk for developing nephropathy Microalbuminuria has also been shown to be associated with increased risk of coronary ischemic events

35 Nephropathy ACEI’s have been shown to delay onset and progression of DM nephropathy Overall prevention of DM nephropathy involves glycemic control, tx of htn, restriction of dietary protein and avoidance of nephrotoxic drugs/dyes

36 Neuropathy Divided into peripheral and autonomic Peripheral involves loss of both myelinated and unmyelinated fibers Usually bilateral, can result in stocking or glove like distributions of numbness to a constant burning sensation

37 Neuropathy Exam may show decrease or loss of vibratory sense and DTR’s Loss of these put the patient at high risk of foot ulcers

38 Neuropathy Drugs used to tx include TCA’s (amitriptyline) as well as neurontin and phenytoin Avoid narcotics (abuse potential) and NSAID’s for possible nephrotoxic effects

39 Neuropathy Autonomic neuropathy represent GI reflux, gastroparesis, neurogenic bladder, sexual dysfunction, and orthostatic hypertension

40 Neuropathy Treatments… –GERD – H 2 blockers and PPI’s –Gastroparesis – Reglan –Constipation – Fiber –Neurogenic bladder – bethanechol –Erectile dysfunction – sildenafil (avoid in pt’s taking nitrates) –Orthostatic hypotension – elastic stockings

41 Infections Diabetics have impaired PMN leukocytes, such as migration problems, phagocytosis and intracellular killing – all leading to intrinsic decrease in immunity Have a low threshold when deciding when to start IV Abx or when to admit a diabetic patient to the hospital for Abx therapy

42 Infections Fever without a clear source is a good enough reason to admit a diabetic patient to the hospital

43 Weird Infections Rhinocerbral Mucormycosis –Fungal infection of the nasal and paranasal sinuses –70% occur in patients in DKA –Patient presents with periorbital or perinasal pain, blood tinged nasal discharge, unilateral HA, decreased vision

44 Rhinocerebral mucorm… Physical signs include black eschar on nasal mucosa or hard palate due to ischemia Seizures can occur as well as brain abscesses Mortality is high - 50%, ENT consult is a must for debridement of necrotic tissue Drug of choice? – Amphotericin B

45 Malignant Otitis Externa Present with unilateral otalgia, decreased hearing, purulent discharge, fever Exam finds a tender inflamed external auditory canal Can progress to the mastoid, temporal bone or base of skull and meningitis

46 MOE Frequently due to Pseudomonas aeruginosa Abx for 4-6 weeks needed –Cipro, or 3 rd gen cephs and an antipseudomonal pen - ticarcillin

47 Cholecystitis Diabetics have higher incidence of gangrenous gallbladder that is more likely to perforate Unexplained fever, with or without abd pain should be evaluated with U/S for for stones Frequently due to Clostridium

48 Foot ulcers Account for nearly 60% of Lower Extremity amputations in US Neuropathy predisposes the foot to ulceration and infection A through exam of a diabetic’s feet should be performed during ER visits, even with unrelated complaints

49 Foot Ulcers Defined as non limb threatening, limb threatening and life threatening Non limb threatening defined as small (aprox 2 cm) of cellulitis or imflammation and does not involve deep structures or bone

50 Foot Ulcers Limb threatening is more than 2 cm of cellulitis with assoc ascending lymphangitis, deep ulcerations or abcess, large area of necrotic tissue, involvement of bone, gangrene and absence of palpable pulses

51 Foot ulcers Life threatening includes signs of sepsis such as fever, leukocytosis, hypotension, tachycardia, altered mental status and metabolic abnormalities such as DKA

52 Foot Ulcers Treatment depends on severity –Non limb threatening: (PO) Cephalexin, Clindamycin, Dicloxacillin, Augmentin –Limb threatening: (IV) Amp-sulbactam, Tic- clav, Cipro –Life threatening: Imipenem-cilastatin, Amp- sulbactam, Vanco

53 Admissions to Hospital Table 212-9 is a good lengthy table of disposition/admission guidelines

54 Questions 1. Type I diabetes is characterized by insulin resistance and an increase of insulin production T or F 2. If a patient is in DKA, and their initial BMP potassium is normal, you don’t have to worry about supplementing K. T or F

55 Questions 3. The organs and tissues most affected by diabetes – nerves, kidneys and retina – all readily take up glucose, hence causing all the problems. T or F 4. Glaucoma and cataracts are less common in diabetics than in the regular population T or F

56 Questions 5. If a diabetic presents to the ER with non-foot related complaints, then you don’t have to worry about doing a foot exam. T or F 1. F, that is type II 2. F, they are still at a total body deficit 3. T 4. F 5. F, You must still do a thorough exam

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