Chpt 15 management of type 2 diabetes

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Diagnosis_and_Management_of_Type_2_DiabetesSteve V. Edelman, MD

R. Henry, MD

Microvascular Complications

Retinopathy, nephropathy, and neuropathy are the major microvascular

complications of Type 2 diabetes. Prevention, early detection, and

aggressive treatment are essential to reduce associated morbidity and

mortality. Good metabolic control has been clearly shown to prevent the

development and delay the progression of these complications in both types

of diabetes....

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Diabetic Retinopathy

The development and progression of retinopathy depend on the duration of

diabetes and the duration and severity of hyperglycemia. Because diabetic

retinopathy does not cause symptoms until it has reached an advanced stage,

early and frequent evaluation for vision problems is critical for patients

with diabetes. The following findings also support the importance of early

detection:

* Diabetes is the leading cause of all new cases of blindness (13%).

* Loss of vision associated with diabetic retinopathy and macular

edema can be reduced by at least 50% with laser photocoagulation if

identified in a timely manner.

Patients must be completely informed about the possible relationship between

hyperglycemia and retinopathy, stressing the importance of promptly

reporting any visual symptoms. They should be aware that hypertension can

worsen retinopathy and therefore be encouraged to take any antihypertensive

medications that have been prescribed. Most important, patients should

understand the potential visual complications associated with diabetic

retinopathy and how to prevent or reduce the severity of these problems.

The three categories of diabetic retinopathy that are part of a continuum

are:

* Nonproliferative or background

* Preproliferative

* Proliferative.

Nonproliferative:

Background changes are the earliest stage of retinopathy and are

characterized by microaneurysms and intraretinal " dot and blot " hemorrhages

(Figure 15.1). If serous fluid leaks into the area of the maculae (where

central vision originates), macular edema can occur and Macular edema cannot

be observed directly but is suggested by the presence of hard exudates lose

to the maculae. Any of these findings should prompt immediate referral to an

ophthalmologist.

FIGURE 15.1 -- Background Diabetic Retinopathy

Edelman_Fig15-1

Preproliferative

Advanced background retinopathy with certain lesions is considered the

preproliferative stage and indicates an increased risk of progression to

proliferative retinopathy. This stage is characterized by " beading " of the

retinal veins; soft exudates (also called " cotton-wool " spots that are

ischemic infarcts of the inner retinal layers) (Figure 15.2); and irregular,

dilated, and tortuous retinal capillaries or occasionally newly formed

intraretinal vessels. Any one of these signs suggests the need for further

evaluation by an ophthalmologist.

FIGURE 15.2 -- Preproliferative Retinopathy

Edelman_Fig15-2

Proliferative

Proliferative retinopathy is the final stage of this degenerative condition

and imparts the most serious threat to vision. Neovascularization typically

covers more than one third of the optic disk and may extend into the

posterior vitreous. These fragile new vessels, which are prone to bleeding,

probably develop in response to ischemia. Bleeding that occurs in the

vitreous or preretinal space can cause visual symptoms such as " floaters " or

" cobwebs " or retinal detachment that results from contraction of fibrous

tissue. Sudden and painless vision loss usually is related to a major

retinal hemorrhage.

Evaluation and Referral

Because visual acuity frequently changes in response to fluctuations in

glycemic control particularly extreme variations, eg, low-to-high and

high-to-low), the reason for any vision changes should be thoroughly

investigated. All patients with diabetes should have annual eye examinations

with complete visual history, visual acuity examinations, and careful

ophthalmoscopic examinations with dilated pupils. High-quality fundus

photographs can detect most clinically significant diabetic retinopathy.

Indications for referral to an ophthalmologist are shown in Table 15.8.

Patients with Type 1 diabetes should begin having annual eye examinations

after 5 years of diabetes. Patients with Type 2 diabetes should have annual

eye examinations starting at the time of diagnosis because of the

probability that glucose Intolerance was present for up to 4 to 7 years

before the diagnosis of diabetes.

TABLE 15.8 - Reasons to Refer Patients with Type 2 Diabetes Mellitus to an

Ophthalmologist

Edelman_Tab15-8

Treatment

Treatment of nonproliferative and preproliferative retinopathy typically

involves blood glucose control and blood pressure control. The only standard

treatment for background retinopathy, in addition to optimizing metabolic

control and blood pressure, is photocoagulation treatment. Results of the

Early Treatment Diabetic Retinopathy Study revealed the effectiveness of

argon laser photocoagulation applied focally (e.g., spot-welding the leaking

micro aneurysms) intreating macular edema and stabilizing vision.

Photocoagulation can slow the progression of vision loss in cases of macular

edema and reduce visual loss by >50% when used as a preventive measure to

limit neovascularization and vitreous hemorrhages. Pan retinal laser

treatment has been proven effective and is the treatment of choice for

patients with proliferative retinopathy and high-risk characteristics. A

scatter pattern of 1200 to 1600 burns is applied throughout the periphery of

the retina, avoiding the macular area.

Vitrectomy may be required to treat retinal detachment and large vitreous

hemorrhages. This procedure generally is reserved for patients with poor

vision in whom the benefits outweigh the risks.

Diabetic Nephropathy

Over 20% of adults who have had diabetes for >20 years have clinically

apparent nephropathy. This disease is progressive, takes years to develop,

and requires laboratory evaluation for early detection because it generally

is asymptomatic in the early stages.

Structural and functional changes in the kidneys occur early in the course

of poorly controlled diabetes but do not produce clinical symptoms. The

first sign of nephropathy is microalbuminuria (30 to 300 mg albumin/24

hours), which may be apparent at the time of diagnosis in patients with Type

2 diabetes. The presence of microalbuminuria is not only a predictable

marker of early diabetic nephropathy, but is also very strongly associated

with coronary artery disease in patients with Type 2 diabetes. In addition,

hypertiltration, indicated by an elevated CrCl, is also a finding in early

diabetic nephropathy. The important clinical point is that in this early

stage of nephropathy, aggressive management may reverse or completely

stabilize any abnormalities. Overt nephropathy is defined as urinary protein

excretion >0.5 g/24 hours and clinical proteinuria characterized by albumin

excretion rates >300 mg (0.3g)/24 hours, typically accompanied by

hypertension. The following conditions play a role in the development and

acceleration of renal insufficiency:

* Chronic uncontrolled hyperglycemia

* Hypertension (virtually all patients who develop nephropathy also

have hypertension [systolic blood pressure >135 mm Hg, diastolic blood

pressure >85mm Hg])

* Neurogenic bladder leading to hydronephrosis and infections

* Urinary tract infection (UTI) and obstruction

* Nephrotoxic drugs (nonsteroidal anti-inflammatory drugs, chronic

analgesic abuse, radiocon trast dyes [should be performed only when adequate

hydration and dieresis can be assured and if no other diagnostic

alternatives are available]).

Patients with diabetes often develop uremia at lower creatinine levels than

patients with renal insufficiency resulting from other causes. Second, even

with dialysis, the prognosis for patients with diabetes is worse than that

for nondiabetic patients. Patients with diabetes tend to start dialysis

earlier because they develop symptoms sooner than other patients with renal

disease. Therefore, a renal transplant is the preferred method of treatment,

if possible, at this stage.

Evaluation

A routine urinalysis should be done at the time of diagnosis and then

yearly. If the urinalysis is positive for protein (>300 mg of albumin or

macroalbuminuria), then a 24-hour quantitative measure along with a CrCl is

important to obtain. If the urinalysis is negative, a test for

microalbuminuria is indicated. The easiest method is the

albumin-to-creatinine ratio in a random spot collection. The gold standard

is a 24-hour collection and can be used to accurately follow the patient

over time and assess the success of therapy. If a UTI is present, it should

be treated promptly before determining the significance of proteinuria. A

positive result (>30 mg protein/24 hour) indicates the need for

pharmacologic therapy with an ACE inhibitor or an ARB.

Annual screening is important for patients who have negative results

(particularly those without microalbuminuria and hypertension), given that

certain factors can interfere transiently with this evaluation (e.g.,

exercise, infections, fever, uncontrolled diabetes, and hypertension). The

mean albumin excretion of three timed urine collections can be used to

establish a diagnosis of microalbuminuria if the values are equivocal.

It is important for physicians to inform patients with diabetes about the

relationship between high blood pressure and renal disease, and the benefits

of maintaining glycemic control. Patients should be encouraged to have their

blood pressure checked regularly (in addition to obtaining their own blood

pressure cuff to measure blood pressure at home), take antihypertensive

medications that have been prescribed, decrease their protein intake to

approximately 10% of daily calories, and monitor glucose levels frequently

with SMBG and take any other measures to improve glycemia. The importance of

reporting symptoms of UTI should be emphasized, along with following proper

treatment for this infection and avoiding nephrotoxic drugs.

Next Week: Treatment of Nephropathy and Diabetic Neuropathy

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