Diabetes Mellitus

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 cows 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/m2

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 NaKATPase 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
  UTIs

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)

13
Optic Exam

• TESTING OF VISUAL ACUITY MAY REVEAL PATIENTS
  INABILITY TO MEASURE A SELF-ADMINISTERED INSULIN
  DOSE

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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

• HP 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
  MIs (painless MIs)

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
• ACEIs 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

• ACEIs 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 DTRs
• Loss of these put the patient at high risk of
  foot ulcers

38
Neuropathy

• Drugs used to tx include TCAs (amitriptyline) as
  well as neurontin and phenytoin
• Avoid narcotics (abuse potential) and NSAIDs for
  possible nephrotoxic effects

39
Neuropathy

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

40
Neuropathy

• Treatments
• GERD H2 blockers and PPIs
• Gastroparesis Reglan
• Constipation Fiber
• Neurogenic bladder bethanechol
• Erectile dysfunction sildenafil (avoid in pts
  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 3rd 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 diabetics 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

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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 dont have to worry
  about supplementing K. T or F

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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

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Questions

• 5. If a diabetic presents to the ER with
  non-foot related complaints, then you dont 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