Transcript foot plasma screen

Case Presentation
CC: “Can’t see out of right eye”
History of Present Illness
• 68 yo African American male presents with
sudden painless vision loss in right eye.
• Describes flashes of light in peripheral vision
before vision loss
• Then states that felt that a curtain was being
drawn down over his right eye.
• Notes that vision has been slowly getting
worse in both eyes “over the years.”
History
• Past Ocular Hx: myopia (near-sighted),
decrease in visual acuity over past several
years at near and distance, told has slight
cataracts, no ocular medications, no eye
surgeries or trauma, mother lost vision when
in her late 70’s
• Past Medical Hx: HTN, diabetes mellitus
• Past Surgical Hx: cholecystectomy at age 57
History
• Allergies: KNDA
• Social Hx: smokes 1 PPD, occasional alcohol,
no drugs
• Family Hx: mother with myopia, no family
history of any other ocular conditions, no
cancers run in family, hx of diabetes
• Review of systems: notes frequent nighttime
urination, burring in feet
Exam
• Vital Signs: T 98.6, HR 80, RR 16, BP 142/90
• General: No acute distress, alert and oriented x3,
obese
• Head, ear, nose, throat: atraumatic and normocephalic,
no rhinorrea or epistaxis, no pharyngeal erythema or
lesions
• Lymph: no swollen glands
• Cardiovascular: regular rate and rhythm, 2/6 systolic
murmur over left sternal boarder, 1+ lower extremity
edema
• Respiratory: clear to auscultation bilaterally, no
wheezes, rales, or rhonchi
• What is the differential for a patient with
sudden painless vision loss?
Differential Diagnosis of Painless
Sudden Vision Loss
•
•
•
•
•
Retinal detachment
Retinal artery occlusion
Retinal vein occlusion
Vitreous hemorrhage
Temporal Arteritis
• What other exams or tests should be done?
Tests/Imaging
• Dilated fundus exam
• B- scan ultrasonography
• Optical Coherence Tomography (OCT): able to
visualize the retina in cross-section
• Fluorescein angiography (if cause still
uncertain or to further evaluate retinal
vasculature)
Ophthalmic Exam
• Visual Acuity with correction
– RE: no light perception
– LE: 20/60
• External exam
– Pupils: relative afferent pupillary defect on right
– Intraocular pressure: normal (~15 mm hg) bilaterally
• Dilated fundus exam:
– RE: only able to get portion of retina in focus
– LE: a few small hemorrhages and hard exudates
present
Dilated Fundus Exam RE (Retinal
Detachment)
http://www.floridalionsfoundation.org/Retinal%20Detachment.htm
Dialated Fundus Exam LE (proliferative
diabetic retinopathy)
Increased
blood vessels
http://www.aao.org/theeyeshaveit/acquired/early-retinopathy.cfm
Diabetic Retinopathy
Normal Fundus Exams
Normal Right Eye
http://en.wikipedia.org/wiki/Fundus_photography
Normal Left Eye
http://www.geteyesmart.org/eyesmart/diseases/detached-torn-retina.cfm
Right Eye B-scan Ultrasonography
Total retinal detachment and vitreous hemorrhage
http://emedicine.medscape.com/article/1228865-overview#a30
Diagnosis
• Retinal detachment in RE
– Need to assess whether affects the macula. If the
macula is detached then the vision will not be able
to be restored.
• Diabetic Retinopathy (proliferative diabetic
retinopathy)
Type 2 Diabetes
• Presentation:
– Polyuria and polydipsia
– End organ damage (described latter)
– Hyperosmolar hyperglycemic state
• Plasma glucose often >600 mg/dL with dehydration but no ketonuria
– Asymptomatic and discovered with screening
• Closely linked to an increase in in weight
– Overweight: BMI ≥85th % and <95th %
– Obese: BMI ≥95th %
• Other risk factors: family hx, female gender, ethnicity (Native
American, Hispanic, Asian-American, and Pacific Islander), other
insulin resistant states (ex. Polycystic ovary syndrome)
• Much of damage from diabetes results from vascular complications
Pathogenesis of Type 2 DM
• Increased obesity leads to increased
peripheral resistance to insulin-mediated
glucose uptake. Initial beta cells of pancreas
can produce increased insulin to counteract
resistance. But can only up regulate
production so much. Eventually, the beta cells
burn out and insulin production falls leading
to even worse glucose control.
Diagnosing Type 2 Diabetes
• Fasting plasma glucose ≥126 mg/dL
• Symptoms of hyperglycemia and random plasma
glucose of ≥200 mg/dL
• Abnormal oral glucose tolerance test (OGTT): plasma
glucose ≥200 mg/dL measured 2 hours after glucose
load of 1.75 g/kg
• Hemoglobin A1C ≥6.5%
• Unless unequivocal hyperglycemia is present, the
diagnosis should be confirmed by repeat testing on a
subsequent day.
Small Vessel Damage
Accumulation of advanced glycosylation end products in the
plasma contributes to microvascular disease. Improved
glycemic control improves the risk of microvascular
complications.
• Nephropathy: microalbuminuria (30-300 mg/day) is earliest
stage. Screening for microalbuminuria with microalbuminto-creatinine ratio in random urine sample
• Retinopathy: ophthalmic screening at time of diagnosis of
type 2 DM. Subsequent follow-up by ophthalmologist
• Neuropathy: affects autonomic and peripheral nerves.
Screen for with yearly foot exams with a monofilament.
Large Vessel Damage
• Macrovascular complications
– Coronary artery disease
– Peripheral vascular disease
– Cerebral vascular disease
• Association between glycemic control and risk of
complications not as clearly established as with
microvascular complications. A large prospective
study (United Kingdom Prospective Diabetes
Study) did find a benefit from better control.
Comorbidities
• Hypertension
• Dyslipidemia
• Nonalcoholic fatty liver disease
Regulating Blood Sugars
Individualized A1C goals for patients, but a
value of <7% is often appropriate
• Non-pharmacologic:
– Dietary modification
– Weight loss
– Increased physical activity
Pharmacologic management
• Metformin: often initial pharmacologic choice
• Sulfonylureas (eg. glipizide): can cause hypoglycemia
• Thiazolidinediones “TZDs” (rosiglitazone and
pioglitazone): increase insulin sensitivity. Infrequently
used due to concerns over hepatotoxicity/MI
• Meglitinides (repanglinide and neteglinide)
• DPP-4 Inhibitors (sitagliptin and saxagliptin)
• Glucagon-like peptide 1 “GLP-1” agonists (exenatide
and liraglutide)
• Alpha-glucosidase inhibitors (acarbose and miglitol)
• Insulin
Management
• Macrovascular risk factor management
– Smoking cessation
– Aspirin
– Blood pressure control
– Reduction in serum lipids
– Diet/exercise