Komplikasi diabetes

(akut dan kronik)

LUH GEDE SRI YENNY

 Daftar pustaka
2

 Gardner D.G, Shoback D. (2007): Greenspan’s

Basic & Clinical Endocrinology 8th Edition. Mc
Graw Hill.
 Harrison’s Principles of Internal Medicine 17th Ed.;
McGraw Hill Medical: 2008

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 Tujuan
3

 Mengetahui patofisiologi, gejala dan tanda dari

hipoglikemia, KAD, HHS, dan lactic acidosis
 Mengetahui pemeriksaan fisik dan laboratorium
(penunjang) dari hipoglikemia, KAD, HHS, dan lactic
acidosis
 Mengetahui penatalaksanaan dari hipoglikemia, KAD,
HHS, dan lactic acidosis
 Mengetahui jenis-jenis komplikasi kronik DM
 Mengetahui patofisiologi terjadinya komplikasi kronik DM
 Mengetahui penatalaksanaan komplikasi kronik DM

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 Komplikasi diabetes
4

Akut Kronik

 Hipoglikemi  Mikrovaskular
 Hiperglikemia
 Makrovaskular
 Diabetic ketoacidosis
(KAD)
 Hiperglykemic
hyperosmolar
nonketotic state
(HHS)
 Lactic acidosis

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 Hipoglikemia…
6

 Definisi: BS < 70 gr/dl

 Etiologi:
 obat: Insulin, sulfonilurea
 Makan terlambat, aktifitas berlebihan

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 CLINICAL MANIFESTATION

Whipple’s triad
 Hypoglycemic symptom (+)
 Low PG (plasma glucose) concentration
 Sympt relief when PG raised
 SYMPTOMS OF HYPOGLYCEMIA
(common sympts of acute hypoglycemia in diabetic pts)

 Neurogenic / Autonomic  cathecolamine release

 Sweating
 Pounding heart
 Shaking (tremor)
 Hunger
 Neuroglycopenic
 Confusion
 Drawsiness
 Speech dificulty
 Incoordination
 Atypical behaviour
RISK FACTORS FOR SEVERE HYPOGLYCEMIA

 Insulin treatment regimen

 Intensified regimens and tight glycemic control
 High ins dosages
 Impaired awareness of hypoglycemia
 Long duration of diabetes
 Increasing age of pts
 Sleep
 Excessive alcohol consumption
 TREATMENT

 Pts conscious  oral glucose (20-30 gr) or

sucrose
 Pts unconscious  IV glucose 50% (30-50 ml),
glucagon 1 ml/SC or IM

Check BG after 15-20 min
Confirm recovery

No recovery  D5/D10 IV
Recovery  identify cause, re-educate, take
measures to avoid hypoglycemia
 Glucagon

 Dosis : 1 mg, SC or IM or IV or intra nasal (spray)

 Act within minuts (IV > SC)
 Primary actions : hepatic glycogenolysis
 SE : nausea, vomiting, head ache.
 PREVENTION

 Pts education
 Frequent SMBG (self monitoring blood glucose)
 Flexible insulin and other drug regimens
 Individualized glycemic goals
 Professional guidance and support.
 Diabetic ketoacidosis (KAD)
14

 Definisi: suatu status dimana terjadi katabolisme

yang tidak terkontrol yang dicetuskan akibat
defisiensi insulin baik absolut maupun relatif.
 Pencetus:
 Infeksi
 Infark myocard

 Stres emosional yang berat

 Trauma

 Obat-obatan  steroid

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

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 Gejala kinis…
16

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 diagnosis ….
17

• Hiperglikemia (BS) > 300 mg/dl

• Ketosis  keton (+) pada darah atau urine
• Asidosis metabolik (bicarbonat menurun)
• Anion gap > 13 mEql
• Hiperosmolaritas

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 Anion gap = (Na)-(Cl + HCO3) (mEq/L)).

 Osmolarity = 2(Na + K)+ (glucose /18) +

(BUN/2.8)
(normal 280-300 mosm/kg).
 Management…
19

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 Cont…..
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 Cont…

 Natrium bicarbonat
 Dipakai bila ph darah ≤ 7.0
 ADA  50 meq/l sodium bicarbonat dalam 200 cc 0.45% salin
pada 1 jam pertama (bila ph 6.9-7.0) atau 100 meq/l dalam 400 cc
0.45% salin selama 2 jam (bila ph < 6.9).
 Terapi pencetus : antibiotika
 Prognosis…
22

 Dengan manajement baik dan koreksi pencetus 

mortalitas < 5%.

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 Hiperglycemic hyperosmolar state (HHS)
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 Karakteristik:
 Hiperglikemia berat
 Hiperosmolaritas

 Dehidrasi

 Tanpa ketosis

 Sering terjadi pada usia tua/ pertengahan

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 Patogenesis ....
Relative insulin deficiency

Reduced thirst

Hyperglycaemia +++
Minimal/absent
ketogenesis

Dehydration
+++++ Hyperosmolality

24
 KAD or HHS ?
25

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 diagnosis…
26

Anamnesis Px fisik Penunjang

Lemas Takikardia •Hiperglikemia

Poliuri/polidipsi Hipotensi  syok •Hiperosmolaritas
Penurunan kesadaran Dehidrasi •Keton (-)
(koma) Somnolen-koma dalam •Asidosis (-)

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 Diagnostic criteria
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 Plasma glucose > 600mg/dl

 Plasma Osmolality > 320mOsm/Kg
 Urinary ketones usualy (-) or mild
 pH > 7.30 and HCO3 ≥15
 Management...
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 Hampir sama dengan KAD

 Rehidrasi  monitor terhadap status cairan!!
 Insulin
 Kalium
 Faktor pencetus

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 Prognosis
29

 Mortalitas  walaupun dengan penatalaksanaan

yang baik mortalitas lebih tinggi dibandingkan KAD

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 Lactic acidosis
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 Karakteristik:
 Pasien DM dengan penyakit berat
 Asidosis

 Anoin gap > 15 mEq/l

 Keton rendah/ tidak terdeteksi

 Laktat plasma > 5 mmol/l

 Pencetus

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 Asam laktat  merupakan produk akhir

metabolisme anaerob glukosa
 Normalnya:
 Asam laktat  piruvat  glukosa (di hepar)

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 Patogenesis…
32

Pasien sepsis/ sakit berat

Anoksia/ hipoksia jaringan

Asam laktat

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 Diagnosis…
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Anamnesis Px fisik Penunjang

Sesak Hiperventilasi •Gula darah dapat rendah,

Penurunan kesadaran  Tergantung pencetus normal, atau tinggi 
koma biasanya meningkat
Penyakit dasar/pencetus •Ph arteri dan bicarbonat
rendah
•Anoin gap meningkat
(normal 12-15 mEq/l)
•Keton (-) atau mnimal

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 Management….
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 Utama atasi faktor pencetus

 Hipotensi  cairan atau vasopresor
 Natrium bicarbonat  pertahankan ph
> 7.2

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 Klasifikasi..
36

 Vaskular

Mikrovaskular
Makrovaskular

 Non vaskular  gastroparesis, infeksi,

perubahan kulit

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patogenesis patogenesis
38

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 OPHTHALMOLOGIC COMPLICATIONS
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 Diabetic retinopathy
 Nonproliferative diabetic retinopathy
 usually
appears late in the first decade / early in the
second decade of the disease
 marked by retinal vascular microaneurysms, blot
hemorrhages, and cotton wool spots .
 proliferative diabetic retinopathy  appearance of
neovascularization in response to retinal hypoxia.

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 40

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 RENAL COMPLICATIONS
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 Diabetic nephropathy  the leading cause of

ESRD in the United States
 Proteinuria

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 Natural history…
42

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 NEUROPATHY
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 Diabetic neuropathy
 occurs in approximately 50% of individuals with
long-standing type 1 and type 2
 manifest as :
 Polyneuropathy
 Mononeuropathy
 and/or autonomic neuropathy.

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 GASTROINTESTINAL/GENITOURINARY
DYSFUNCTION
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 Gastrointestinal
 symptoms are delayedgastric emptying (gastroparesis)
and altered small- and largebowel motility (constipation
or diarrhea).
 Gastroparesis may presentwith symptoms of anorexia,
nausea, vomiting, early satiety, and abdominalbloating.

 Genitourinary systems.
 cystopathy, erectile dysfunction, and female sexual
dysfunction (reduced sexual desire, dyspareunia,
reduced vaginal lubrication).

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 CARDIOVASCULAR MORBIDITY AND MORTALITY
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 Cardiovascular disease  increased in individuals

with type 1 or type 2 DM.
 1-5 x in DM.
 Risk factors  dyslipidemia, hypertension,obesity,
reduced physical activity, and cigarette smoking.

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 LOWER EXTREMITY COMPLICATIONS
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 DM  the leading cause of nontraumatic lower extremity

amputation in the United States.
 Foot ulcers and infections

 Several pathogenic factors:

 Neuropathy

 abnormal foot biomechanics

 peripheral arterial disease

 poor wound healing.

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Diabetic foot

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 INFECTIONS
48

 Individuals with DM  have a greater frequency and

severity of infection.

 The reasons:
 incompletely defined abnormalities in cell-mediated
immunity and phagocyte function associated with
hyperglycemia
 diminished vascularization.

 Hyperglycemia  aids the colonization and growth of a

variety of organisms (Candida and other fungal species).

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 DERMATOLOGIC MANIFESTATIONS
49

 The most common skin manifestations 

protracted wound healing and skin ulcerations.
 Xerosis and pruritus

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Terima kasih…