Transcript Diabetes Mellitus - Cleveland Clinic Hospital Locations

Diabetes Mellitus
Jane DisaSmith, D.O.
Dec. 13, 2005
Slides by Billie Hall, D.O.
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
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
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
Risk Factors
• Type II (table 212-2)
– Hypertension (>140/90)
– Dyslipidemia (HDL < 35 and or triglycerides >
250)
– Diet (high fat, starch, low fiber)
– Sedentary lifestyle
– Obesity (BMI > 25kg/m2
Pathophysiology
• Type I – destruction of insulin-producing
pancreatic beta cells and absolute insulin
deficiency.
• Type II – development of insulin resistance
and increased insulin production
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)
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
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
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
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)
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)
Optic Exam
• TESTING OF VISUAL ACUITY MAY
REVEAL PATIENT’S INABILITY TO
MEASURE A SELF-ADMINISTERED
INSULIN DOSE
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
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
Acute Hyperglycemia
• Defined as BG >300
• Can represent metabolic decompensation
• If chronic, can represent high risk for
developing macro and microvascular
complications
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
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
Clinical Features
• Lab tests
– Electrolytes, BUN/Cr, ABG (though Tintinalli
feels this is not always necessary)
– Blood glucose measurements every 1-2 hours
Therapy
•
•
•
•
Volume repletion
IV regular Insulin
Correction of electrolyte imbalance
Correction of any causes of the
hyperglycemia (infections)
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
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
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 preprogrammed or patient set boluses around
meals.
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
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
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
Cardiovascular
• Contributing Factors
– Increased incidence of atherosclerosis on
coronary vessels
– Microvascular disease, contributing to “silent”
MI’s (painless MI’s)
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
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
Retinopathy
• In the ED, any history of vision changes,
blurriness should arouse suspicion for
retinopathy
• Retinal exam might show
microaneurysms, exudates, and vascular
proliferation
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
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
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
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
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
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
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
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
Neuropathy
• Autonomic neuropathy represent GI reflux,
gastroparesis, neurogenic bladder, sexual
dysfunction, and orthostatic hypertension
Neuropathy
• Treatments…
– GERD – H2 blockers and PPI’s
– Gastroparesis – Reglan
– Constipation – Fiber
– Neurogenic bladder – bethanechol
– Erectile dysfunction – sildenafil (avoid in pt’s
taking nitrates)
– Orthostatic hypotension – elastic stockings
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
Infections
• Fever without a clear source is a good
enough reason to admit a diabetic
patient to the hospital
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
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
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
MOE
• Frequently due to Pseudomonas
aeruginosa
• Abx for 4-6 weeks needed
– Cipro, or 3rd gen cephs and an
antipseudomonal pen - ticarcillin
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
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
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
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
Foot ulcers
• Life threatening includes signs of sepsis
such as fever, leukocytosis, hypotension,
tachycardia, altered mental status and
metabolic abnormalities such as DKA
Foot Ulcers
• Treatment depends on severity
– Non limb threatening: (PO) Cephalexin,
Clindamycin, Dicloxacillin, Augmentin
– Limb threatening: (IV) Amp-sulbactam, Ticclav, Cipro
– Life threatening: Imipenem-cilastatin, Ampsulbactam, Vanco
Admissions to Hospital
• Table 212-9 is a good lengthy table of
disposition/admission guidelines
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
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
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.
2.
3.
4.
5.
F, that is type II
F, they are still at a total body deficit
T
F
F, You must still do a thorough exam