KOMPLIKASI

KRONIK DM
-MIKROVASKULAR
-MAKROVASKULAR

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 Classifications of Diabetic
KOMPLIKASI Vascular Disease
KRONIK DM

In most patients with diabetes, a number of

pathologic changes occur at variable intervals
during the course of the disease. These
changes
involve the vascular system for the most part;
however, they also occur in the nerves, the
skin, and the lens.
Diabetic vascular disease is conveniently
divided into 2 main categories: microvascular
disease and macrovascular disease.

A. Microvascular disease
Disease of the smallest blood vessels,
the capillary and the precapillary arterioles, is
manifested mainly by thickening of the capillary
basement membrane. ALPINE SKI HOUSE 2
 Classifications of Diabetic
KOMPLIKASI Vascular Disease
KRONIK DM
B. Macrovascular disease

Penyakit ini mengenai pembuluh darah besar yg

secara cepat menyebabkan atersosklerosis.
- Faktor timbulnya infark miokard,stroke,dan gangren
perifer
the exact cause of accelerated atherosclerosis
in the diabetic popularion remains unclear.
Abnormalities in vessel walls, platelets and
other components of the cloning system, red
blood cells, and lipid metabolism have all been
postulated to play a role. In addition, there is
evidence that coexistent risk factors such as
cigarette smoking and hypertension may be
important in determining the course of the
disease.
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OPHTHALMOLOGIC
COMPLICATIONS
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 DIABETIC
RETINOPATHY
For early detection--> adolescent or adult
patients who have had type 1 diabetes for
more than 5 years and all patients with
type 2 diabetes should be referred to an
ophthalmologist for examination.
-kalau disertai dengan hipertensilebih
baik cepat diatasi karena bisa mempercepat
proses menuju retinopati diabetic
EPIDEMIOLOGI
- In patients with type 1 diabetes, after 1 0 to 1 5 years,
25% to 50% of patients show some signs of retinopathy.
-This prevalence increases to 75% to 95%
after 15 years and approaches 1 00% after 30 years of
diabetes.
-In patients with type 2 diabetes, 60% have non
proliferative retinopathy
after 16 years.
KLASIFIKASI+ MANIFESTASI KLINIS
Two main categories of diabetic retinopathy exist: nonproliferative and
proliferative. Diabetic macular edema can occur at any stage.
1. Nonproliferative (background) retinopathy-->
stage awal yg muncul dan melibatkan retina.
- characterized:
by such changes as microaneurysms, dot hemorrhages, exudates,
and retinal edema.
- Patogenesis: kapiler retina mengalami kebocoran protein
,lemak/eritrosit ke retina-->kalau terjadi di makula(makula edema)
bisa mengganggu tajam penglihatan-->penyebab sering visual
impairement di DM-2
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TATA LAKSANA
DIABETIC
RETINOPATHY
-Avoiding tobacco use and correction of
associated hypertension are important
therapeutic.
-proliferative retinopathy is associated with
recent vitreous hemorrhages or in which
extensive new vessels are located on or near
the optic disk-->Extensive scatter xenon or
argon photocoagulation and focal treatment of
new vessels reduce severe visual loss
-macular edema--> scatter therapy,Injection of
bevacizumab (Avastin), an antivascular
endothelial growth factor (anti-VEGF)
2. PROLIFERATIVE RETINOPHATY
EPIDEMIOLOGI
Proliferative retinopathy can occur in both types of diabetes but is
more common in type 1 , developing about 7 to 10 years after
onset of symptoms, with a prevalence of 25% after 1 5 years'
duration.
PATOGENESESIS
involves the growth of new capillaries
and fibrous tissue within the retina and into the vitreous chamber.
It is a consequence of small vessel occlusion, which causes retinal
hypoxia; this in turn stimulates new vessel growth.
New vessel formation may occur at the optic disc or elsewhere on
the retina .
a preproliferative phase often occurs in which arteriolar ischemia is
manifested as cotton-wool spots (small infarcted areas of retina).
Vision is usually normal until vitreous hemorrhage or retinal
detachment occurs
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 CATARACT PATOGENESIS
( 1 ) glycosylation of the lens protein,
Two types of cataracts occur in diabetic and
patients: subcapsular and senile.
(2) an excess of sorbitol, which is formed from the
1. Subcapsular cataract occurs predominantly
increased
in patients with type 1 diabetes, may come on quantities of glucose found in the insulin-independent
fairly rapidly, and has a significant correlation lens.
with the hyperglycemia of uncontrolled Accumulation of sorbitol leads to osmotic changes in the
diabetes. lens that ultimately result in fibrosis and cataract
formation.
This type of cataract has a flocculent or
snowflake appearance and develops j ust
2. below
Senile the lens capsule.
cataract represents a sclerotic change of the lens
nucleus. It is by far the most common type of cataract
found in either diabetic or nondiabetic adults and tends to
occur at a younger age in diabetic patients, particularly
when glycemic control is poor.
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 GLAUKOMA

- Closed-angle glaucoma can result from

neovascularization of the iris in diabetic
persons.
After cataract extraction when accelerated new
vessel growth involving the angle of the iris
obstructs outflow.

-Glaucoma occurs in approximately 6% of persons

with diabetes

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NEFROPHATI
DIABETIKUM
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DEFINISI
-Diabetic nephropathy is initially manifested by
proteinuria;
subsequently, as kidney function declines, urea
and creatinine accumulate in the blood.
-Diabetic nephropathy is a clinical syndrome
characterized by the following [1] :
1.Persistent albuminuria (>300 mg/d or >200
μg/min) that is confirmed on at least 2 occasions
3-6 months apart
2. Progressive decline in the glomerular
filtration rate (GFR)
3. Elevated arterial blood pressure.
EPIDEMIOLOGI
4000 kasus end stage renal disease karena nefropati diabetik
terjadi .setiap tahun di antara pasien diabetes
-pasien DM-1 karena tidak diobati dengan terapi intensif
insulin--> 30-40% setelah 20 tahun pengobatan bisa terkena
komplikasi ini. sedangkan DM-2 hanya10-15%.
-tapi paling banyak tetap pada DM-type 2, karena DM-2 lebih
banyak terjadi dibanding dm-1
ETIOLOGI
The exact cause of diabetic nephropathy is unknown.
-hyperglycemia (causing hyperfiltration and renal injury), advanced
glycation products, and activation of cytokines.
-as an autoimun disorder-->role of innate immunity (toll-like receptors)
and regulatory T-cells (Treg).
-When there is insulin resistance, insulin cannot suppress hepatic
gluconeogenesis, which leads to hyperglycemia. Simultaneously, insulin
resistance in the adipose tissue and skeletal muscle leads to increased
lipolysis and reduction in disposal of glucose causing hyperlipidemia in
addition to hyperglycemia.
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 Pathophysiology
Three major histologic changes occur in the glomeruli of
persons with diabetic nephropathy.
- First, mesangial expansion is directly induced by
PATOGENESIS hyperglycemia, perhaps via increased matrix production or
glycation of matrix proteins.
- Second, thickening of the glomerular basement membrane
(GBM) occurs.
- Third, glomerular sclerosis is caused by intraglomerular
Thickening of capillary basement membranes hypertension (induced by dilatation of the afferent renal
and of the mesangium of renal glomeruli artery or from ischemic injury induced by hyaline narrowing
produces varying degrees of glomerulosclerosis of the vessels supplying the glomeruli).
and renal insufficiency.

-Diffuse glomerulosclerosis is more common than

nodular intercapillary glomerulosclerosis
(Kimmelstiel-Wilson lesions) ; both produce heavy
proteinuria.

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 PX FISIK:
Patients may have physical findings associated with long-
DIAGNOSIS standing diabetes mellitus, such as the following:
•Hypertension
•Peripheral vascular occlusive disease (decreased peripheral
pulses, carotid bruits)
•Evidence of diabetic neuropathy in the form of decreased fine
ANAMNESIS sensations and diminished tendon reflexes
•Evidence of fourth heart sound during cardiac auscultation
Diabetic nephropathy should be considered in patients •Nonhealing skin ulcers/osteomyelitis
who have diabetes mellitus (DM) and a history of one
or more of the following:
•Passing of foamy urine
•Otherwise unexplained proteinuria
•Diabetic retinopathy
•Fatigue and foot edema secondary to
hypoalbuminemia (if nephrotic syndrome is present)
•Other associated disorders such as peripheral vascular
occlusive disease, hypertension, or coronary artery
disease

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 DIAGNOSIS
(PX LAB)

-Typically, the urinalysis results from a patient with

established diabetic nephropathy show proteinuria
varying from 150 mg/dL to greater than 300 mg/dL,
glucosuria, and occasional hyaline casts.

Microalbuminuria is defined as albumin excretion of

more than 20 μg/min or an albumin-to-creatinine
ratio (µg/g) of greater than 30

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 PX LAB

Blood Tests
Blood tests, including calculation of GFR (by various
formulas, such as the MDRD formula), are helpful in
monitoring for the progression of kidney disease and in
assessing its stage.

Serum and Urinary Electrophoresis

Serum and urinary electrophoresis is performed mainly to
help exclude multiple myeloma (in the appropriate
setting) and to classify the proteinuria (which is
predominantly glomerular in diabetic nephropathy).

Renal Ultrasonography
Observe for kidney size, which is usually normal to increased in the
initial stages and, later, decreased or shrunken with chronic renal
disease. Rule out obstruction. Perform echogenicity studies for
chronic renal disease. ALPINE SKI HOUSE 14
 TATA LAKSANA
Hemodialysis has been of limited success in the
treatment of renal failure due to diabetic
nephropathy.

Growing experience with chronic ambulatory

peritoneal dialysis suggests that it may be a more
convenient method

Renal transplantation, especially from related

donors, is often successful.

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NEUROPHATI
DIABETIKUM
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 DEFINISI
neuropati diabetika adalah adanya gejala dan /
atau tanda dari disfungsi saraf perifer dari
penderita diabetes tanpa ada penyebab lain
selain diabetes.
Apabila dalam jangka yang lama glukosa darah tidak berhasil
diturunkan menjadi normal maka akan melemahkan dan
merusak dinding pembuluh darah kapiler yang memberi makan
ke saraf sehingga terjadi kerusakan saraf yang disebut neuropati
diabetik

- Neuropati diabetik adalah adanya gejala dan

atau tanda dari disfungsi saraf penderita
diabetes tanpa ada penyebab lain selain
Diabetes Melitus (DM) (setelah dilakukan
eksklusi penyebab lainnya)

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 EPIDEMIOLOGI

berdasarkan observasi pada semua umur, 30% sampai 40% pasien dewasa dengan DM tipe 2 menderita
etnik, jenis kelamin dan tingkat pendidikan, Distal Peripheral Neuropathy (DPN). DPN berkaitan dengan
ditemukan angka yang cukup signifikan yang berbagai faktor resiko yang mencakup derajat hiperglikemia,
menunjukkan DM positif pada usia 30 – 39 indeks lipid, indeks tekanan darah, durasi menderita diabetes
tahun dan tingkat keparahan diabetes
- Neuropati diabetika terjadi hampir 50 % pada
pasien DM, dan pada DM tipe 1 dijumpai lebih
cepat sedangkan pada tipe 2 dijumpai lebih
lambat.

-Neuropati sensorimotor kronik merupakan

bentuk yang paling sering dari
polineuropati diabetik dan paling sering
didiagnosa pada diabetes tipe 2
sampai 10 %.
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FAKTOR RESIKO

a. Hiperglikemi
b. Lamanya menderita DM
c. Umur
d. Merokok
e. Konsumsi alkohol
f. Hipertensi
g. Hipokolestrolemia

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 Diabetic Neuropathy

Neuropati sensoris

• Parestesia
• Hiperalgesia
• hipestesia
Neuropati motoris

• Cepat lelah
• ↓ tenaga
Penumpulan saraf sensoris

• ↓pendengaran, pengecapan

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Diabetic Ulcer (Ulcus diabeticum)

• Patofisiologi :
• Angiopati
angiopati > sumbatan > gangren > gangren
kering.
- pulsasi arteri dorsalis pedis (-)
- sensibilitas (+)

• Neuropati
neuropati > disuse atropi > tekanan berlebih >
nekrosis > gangren basah.
- pulsasi arteri dorsalis pedis (+)
- sensibilitas (-)

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lanjutan
• Klasifikasi Wagner :
• Derajat 0 : tidak ada lesi terbuka, kulit masih utuh dengan kemungkinan
disertai kelainan bentuk kaki seperti “claw, callus”
• Derajat I : ulkus superficial terbatas pada kulit
• Derajat II : ulkus dalam menembus tendon dan tulang
• Derajat III : abses dalam dengan atau tanpa osteomyelitis
• Derajat IV : gangren jari kaki atau bagian distal kaki dengan atau tanpa
selulitis
• Derajat V : gangren seluruh kaki atau sebagian tungkai bawah

• Tindakan pengobatan :
• Derajat 0 : perawatan lokal secara khusus tidak ada
• Derajat I-IV : pengelolaan medik dan tindakan bedah minor
• Derajat V : tindakan bedah minor, bila gagal dilanjutkan bedah mayor
seperti amputasi di atas lutut atau dibawah lutut

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lanjutan

• Pada penderita DM sebaiknya pemasangan IVFD tidak di kaki karena end artery.

• Terapi DM dengan komplikasi ulcus adalah insulin > karena insulin adalah agen anabolik
sehingga baik untuk pembentukan jaringan, apalagi bila disertai underweight.

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Mengapa luka tak mudah sembuh?

• Imunitas ↓

• Penurunan fungsi leukosit :

• Fagositosis
• Kemotaksis
• Antibodi intrasel

• Kerentanan
• Ketidakstabilan kadar glukosa dalam darah
• Keton bodies

• mikro/makroangiopati : RBC, WBC, dan O2 sulit mencapai jaringan.

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 Terapi

• Sejauh ini, selain kendali glikemik yang ketat, belum ada bukti kuat suatu terapi dapat memperbaiki/mencegah neuropati
diabetik.

• Sedangkan untuk mengatasi keluhan nyeri pada neuropati diabetik dapat dianjurkan:
• NSAID (ibuprofen 600mg 4x/hari, sulindac 200mg 2x/hari)
• Antidepresan trisiklik (amitriptilin 50-150mg malam hari)
• Antikonvulsan (gabapentin 900mg 3x/hari)
• Antiaritmia (mexilletin 150-450mg/hari)
• Topikal : capsaicin 0,075% 4x/hari

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THANK
YOU
ZUFARISKY SAREL
+6287892314659

sarelrisky@gmail.com

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