Gangren Diabetik dan

Hiperglikemik Hiperosmolar State

Presenter : Dr. A. H. Putri
Pendamping : Dr. Pipin Andriyani

Selasa, 18 November 2013

RSUD SULTAN SULAIMAN KABUPATEN
SERDANG BEDAGAI
 Pendahuluan

Kasus ini merupakan kasus asli di RSUD Sultan

Sulaiman Kab. Serdang Bedagai.
Menurut data WHO, Indonesia menempati urutan keenam di dunia
sebagai negara dengan jumlah penderita Diabetes Mellitusnya
terbanyak setelah India, China, Uni Sovyet, Jepang, dan Brasil.
(1995) jumlah penderita diabetes di Indonesia mencapai 5 juta
dengan peningkatan sebanyak 230.000 pasien diabetes / thn, tahun
2005 diperkirakan akan mencapai 12 juta penderita.
Gangren diabetik ditemukan pada sekita 4%-nya. Gangren diabetik
merupakan dampak jangka lama arteriosclerosis dan emboli
trombus kecil.
Diabetes Today: An Epidemic
Pasien DM mempunyai resiko terjadinya
komplikasi kronik yaitu :
PJK dan penyakit pembuluh darah otak 2 kali
lebih besar
50 kali lebih mudah menderita ulkus/gangrene
7 kali lebih mudah mengidap gagal ginjal terminal
25 kali lebih cenderung mengalami kebutaan
akibat kerusakan retina pada pasien non DM.
Complications of diabetes are a major cause
of mortality and morbidity (2002 statistics)
90% of patients with diabetes are treated by
primary care physicians
ADA National Diabetes Fact Sheet. Available at: http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2005.pdf. Accessed April 11, 2005; ADA
Diabetes Statistics. Available at http://www.diabetes.org/utils/printthispage.jsp?PageID=STATISTICS_233181. December 29, 2005.
 Tujuan
Tujuan persentasi ini adalah untuk membahas diagnosis
dan penatalaksanaan secara holistik pada kasus gangren
diabetik dan status hiperglikemik hiperosmolar.

Data Administrasi Pasien

Nama : Tn. S
Umur : 48 tahun
Jenis kelamin : Pria
No. Register : 03.48.
Data Demografis
Alamat : Sei Rampah
Agama : Islam
Suku : Jawa
Pekerjaan : Kuli bangunan
Warga negara : Indonesia

Data Biologik
Tinggi Badan : 160 cm
Berat badan : 50 kg
Habitus : Merokok (+)
Data Klinis
Anamnesis

Pasien datang dengan luka bernanah di lengan atas yang

pecah sejak 2 hari yang lalu SMRS. Os merasa tangannya
luka sejak 2 minggu yang lalu dan susah sembuh. Pus
(+), darah (+) jaringan hitam (+) tendon (+) bengkak
(+) merah (+) nyeri (+).
RPT: Hipertensi (-), PJK (-), DM (disangkal Os) riwayat
sering haus (+), riwayat sering BAK (+), riwayat
penurunan BB (+).
Pemeriksaan Fisik
Tanda Vital
TD : 110/70 mmHg
HR : 80x/i
RR : 20x/i
T : 37 oC

Status Lokalisata
Kepala : Mata : Anemis(+/+) minimal, Ikterik (-/-)
Thoraks : Tidak dijumpai kelainan
Abdomen : soepel, peristaltik (+) N
Ekstremitas atas: regio ante brachii : gangren (+) pus (+), darah (+),
bengkak (+) merah (+) nyeri (+).
Ekstremitas bawah : edema (-/-) luka (-)
Pemeriksaan Penunjang
Laboratorium :
Darah rutin: Hb 9,7 gr% Leukosit 7100, Trombosit 218.000,
Hematokrit 30,3%.
LFT / RFT : Ur 38, Cr 1,0 / SGOT 27 SGPT 38
KGD ad random: HI mg/dl.
Kultur pus : belum dilakukan

Pencitraan : Tidak dilakukan

Diagnosa

Gangren diabetik o/t ante brachii +

status Hipeglikemik hiperosmolar

Ditegakkan berdasarkan anamnesis, pemerikasaan fisik dan hasil

laboratorium
Strategi penanganan masalah
Terapi

Oksigenasi
Rehidrasi dengan RL cor 1 Lt
Wound debridement
Antibiotik
Analgetik
Antipiretik jika demam
Insulin SC
Konsultasi dan Rujukan
Secara ranah kompetensi, kasus ini harus dikonsultasikan ke ahli
penyakit dalam untuk penanganan dan pemeriksaan
penunjang lanjutan.
 Penjelasan Pasien dan keluarga
Diagnosis
Bahwa pasien didiagnosis dengan gangren diabetik dan status
hiperglikemik hiperosmolar. Keadaan ini merupakan
komplikasi akut dan kronik pada penderita DM
Masalah dan resiko yang dihadapi
Menjelaskan bahwa penyakit DM tidak bisa disembuhkan
tapi dikontrol, resiko kecacatan dan gangguan metabolik
lainnya.
Jalan keluar
Penanganan dengan medikamentosa dan kontrol lebih lanjut
 Hal yang dapat dilakukan
Menjalani pengobatan secara teratur dan maksimal
Memberikan motivasi kepada pasien agar tidak khawatir
terhadap penyakitnya
Jika terjadi kondisi kegawatdaruatan, segera bawa pasien ke
Rumah Sakit
Diabetes Mellitus
Diabetes mellitus is characterized by chronic
hyperglycemia with disturbances of carbohydrate, fat,
and protein metabolism resulting from defects in insulin
secretion, insulin action, or both.
Chronic hyperglycaemia associated with long-term
damage to:
Eyes
Kidneys
Nerves
Heart and blood vessels
Insulin and glucose disposal
Gluconeogenesis
Glycogenolysis
Glycogen synthesis
Insulin

Blood glucose

Glycogen
synthesis Glucose uptake
Free fatty acid release
CLASSIFICATION OF DIABETES
MELLITUS

1. Type 1 diabetes (cell destruction, usually leading to

absolute insulin deficiency)
2. Type 2 diabetes (ranging from predominantly insulin
resistance with relative insulin deficiency to
predominantly an insulin secretory defect with insulin
resistance)
3. Other specific types of diabetes
4. Gestational diabetes mellitus (GDM)
Insulin deficiency in type 1 diabetes
Glucose uptake
Glycogenolysis
Gluconeogenesis (amino acids)
Ketone production (fatty acids)

Blood glucose

Glucose uptake
Protein degradation amino acids

Triglyceride degradation fatty acids

Type 2 Diabetes: Two Principal Defects

Genes Genes

b-cell dysfunction/
Insulin resistance
failure

Environment Environment

IGT IGT

Glucose Glucose
Type 2 diabetes
Toxicity Toxicity

Reaven GM. Physiol Rev. 1995;75:473-486

Reaven GM. Diabetes/Metabol Rev. 1993;9(Suppl 1):5S-12S;
Polonsky KS. Exp Clin Endocrinol Diabetes. 1999;107 Suppl 4:S124-S127.
 Insulin insensitivity in type 2 diabetes
Liver Fat tissues Muscles

Glycogenogenosis
Glycolysis Glycolysis
Gluconeogenesis Lipogenesis
Glycogenogenesis
Lipolysis

FFA
Glucose production Glucose Storage

Hyperglycaemia
 Insulin resistance and b-cell dysfunction
produce hyperglycaemia in type 2 diabetes
Pancreatic b-cell Insulin resistance
Increased
lipolysis

Elevated
Liver plasma FFA
+ - Elevated
Islet b-cell degranulation
Reduced insulin content TNF

Adipose tissue
Low plasma
Increased glucose output
insulin
Decreased glucose transport
& activity (expression) of GLUT-4
HYPERGLYCAEMIA

Modified from: Turner N, Clapham JC. Prog Drug Res 1998;51:3494

 Pathophysiology
Impaired entry of glucose into the cells
Accumulation of glucose in the blood

Inability of the cells Plasma osmolarity

utilize glucose

Urinary loss of glucose

Cellular starvation Loss of water and Na

Stimulating hunger
Dehydration of cells
Lipolysis and
proteolysis
Compensatory mechanism
Body weight Such as thirst
 Common Symptoms
Classic symptoms Others symptoms
fatigue
increased hunger
tingling or numbness in hands
increased thirst and feet
frequent urination recurring infections
gums, skin, lung, urinary
weight loss
bladder
slow healing
blurred vision
pruritus vulvae
erectile dysfunction
ADA definition of hyperglycaemic states
Criteria for the diagnosis of diabetes
Symptoms of diabetes plus casual plasma glucose 200 mg/dl (11.1 mmol/l)
or

FPG
< 100 mg/dl (5.6 mmol/l) normal fasting glucose
100125 mg/dl (5.66.9 mmol/l) impaired fasting glucose
126 mg/dl (7.0 mmol/l) diabetes

or
OGTT 2-h post-load glucose
< 140 mg/dl (7.8 mmol/l) normal glucose tolerance
140199 mg/dl (7.811.1 mmol/l) impaired glucose tolerance
200 mg/dl (11.1 mmol/l) diabetes

ADA = American Diabetes Association

Adapted from American Diabetes Association. Diabetes Care 2004; 27:S5S10.

 Classic symptoms (+)

Fasting BG > 126 mg/dl Fasting BG < 126 mg/dl

.
(casual BG > 200) (casual BG <200)
Repeat BG

Fasting BG >126 or Fasting BG < 126 or

Casual BG > 200 Casual BG < 200

DIABETES MELLITUS OGTT

Diagnosis of type 2 Diabetes Mellitus

 Natural History of Type 2 Diabetes
Genetics
Environment Onset of
Complications
nutrition diabetes
obesity
exercise
Disability
Impaired
glucose Ongoing
tolerance hyperglycemia Death

Retinopathy Blindness
Insulin resistance
Nephropathy Renal failure
Hyperinsulinemia
Hypertension Neuropathy
Decreased HDL-C Coronary disease
Increased TG Atherosclerosis LE amputation
 Complications of Diabetes Mellitus
Chronic Complications of Acute Complications of
Diabetes Mellitus Diabetes Mellitus
Microvascular Hyperglycemia crisis
Retinopathy Diabetic ketoacidosis
(nonproliferative/proliferative) Hyperglycemia hyperosmolar
Nephropathy State
Neuropathy Lactic acidosis
Sensory and motor (mono- and Hypoglycemia
polyneuropathy)
Autonomic
Macrovascular
Coronary artery disease
Peripheral vascular disease
Cerebrovascular disease
 GANGRENE DIABETIK
Gangrene diabetik adalah gangren yang dijumpai pada penderita
DM. Gangrene adalah kematian jaringan oleh karena obstruksi
pembuluh darah yang memberikan makanan kepada jaringan
tersebut. Gangren diabetik ini dapat terjadi pada pasien bagian
tubuh yang terendah diujung terutama pada ekstremitas bawah.

Mikrobiologi penyebab
Kelompok I ( dinding abdomen dan perinium): polimikroba
(anaerob + anaerob fakultatif + batang gram negatif)
Kelompok II (ekstramitas) : stretococcus pyogenes stafilokokus
Kelompok III: infeksi vibrio marine
Atherothrombosis Has Multiple
Manifestations

Ischemic stroke Transient ischemic attack

Myocardial
infarction Angina:
Stable
Unstable

Peripheral arterial disease:

Intermittent claudication
Rest pain
Gangrene
Necrosis
Adapted from: Drouet L. Cerebrovasc Dis 2002;13(suppl 1):16
Diabetes and Macrovascular Disease

Libby and Plutsky. Circulation. 2002.

Diabetic foot disease
Approximately 15% of individuals with DM develop a foot ulcer, and a
significant subset will ultimately undergo amputation (14 to 24%risk
with that ulcer or subsequent ulceration).
Syndrome of diabetic foot disease
Peripheral neuropathy, peripheral vascular disease and tissue
infection
Risk factors for foot ulcers or amputation include:
male sex
diabetes 10 years duration
peripheral neuropathy
abnormal structure of foot (bony abnormalities,callus, thickened nails)
peripheral arterial disease
Smoking
history of previous ulcer or amputation
poor glycemic control.
Ulcers may be primarily neuropathic (no accompanying infection) or
may have surrounding cellulitis or osteomyelitis.
Pathophysiology of diabetic foot
Neuropathy

Motor Neuropathy Neuropathy Microvascular

dysfunction disease

Reduced pain
Sensation and
proprioception
Abnormal
Foot posture

Increased foot Dry, cracked

prssure Poor tissue
skin nutrition and
Cheiroarthropathy oxygenation

Arteriovenous
shunting
Callus

Ulcer
Mechanical,
Trauma thermal, Macrovascular
chemical Ischemia
disease
 Acute Complication of Diabetes
Mellitus

Hyperglycemia crisis
Diabetic ketoacidosis (DKA)
Hyperglycemic Hyperosmolar State (HHS)
Hypoglycemia
 Diabetic ketoacidosis
(DKA)
Hyperglycemic Hyperosmolar State
(HHS)
 Diabetic ketoacidosis
Hyperglycemia (>300 mg/dl) Ketonemi
a
osmotic Vomitin
Acidosis
diuresis g
dehydration
hypovolemia
impaired renal blood
flow
exacerbated hyperosmolality,
acidosis
CNS
depression
 Hyperglycemic, hyperosmolar,
nonketotic state
Hyperglycemia (>300 mg/dl)

osmotic
diuresis
dehydration
hypovolemia
impaired renal blood
flow
exacerbated hyperosmolality,
acidosis
CNS
depression
Pathophysiolgy of hyperglycemia crisis
 Diabetic ketoacidosis (DKA)
DKA was formerly considered a hallmark of type 1 DM
The symptoms and physical signs of DKA
Symptoms : Nausea/vomiting, Thirst/polyuria, Abdominal pain,
Shortness of breath
Physical findings : Tachycardia, Dry mucous membranes/reduced
skin turgor, Dehydration / hypotension, Tachypnea / Kussmaul,
respirations/respiratory distress, Abdominal tenderness (may
resemble acute pancreatitis or
surgical abdomen), Lethargy /obtundation / cerebral edema /
possibly coma
Precipitating factors
Inadequate insulin administration
Infection (pneumonia/UTI/
Gastroenteritis/sepsis
Infarction (cerebral, coronary, mesenteric, peripheral)
Drugs (cocaine)
Pregnancy
HHS: Differences from DKA
Patients usually older- typically 60 or more
Major pathophysiologic differences
longer uncompensated osmotic diuresis
greater volume depletion
Acidemia (pH > 7.3) and ketosis are mild
Higher mortality -
often 30-50%
primarily due to underlying vascular or infectious event
Occurs in Type 2 diabetics, often mild or unrecognized
Definition of HHS
Extreme hyperglycemia
Increased serum osmolality
Severe dehydration without significant ketosis or acidosis

Joslins Diabetes Mellitus, 13th ed

Clinical Findings of HHS
HHS should be suspect : elderly patient with or without the preexisting
diagnosis of diabetes who exhibits acute or subacute deterioration of
CNS function and severely dehydrated
Tachycardia
Low grade fever
Low or normal blood pressure
Dehydration dry mucous membrane, absent axillary sweat, poor skin
turgor.
Nausea, vomiting, distension, and pain-gastroparesis is due to
hypertonicity
Lethargy, hallucinations, and psychosis
Laboratory Findings
DKA HHS
Fluid Balance in Diabetic
Hyperosmolarity
ECF = 14 L ICF = 28 L

ECF ICF

H2O

Osmotic Diuresis ECF hyperosmolar from ICF autotransfusion

H2O

Osmotic Diuresis ECF and ICF both hyperosmolar

 Priority in the Treatment of
Hyperglycemia Crisis
Replacing volume deficits normal saline according to
BP, urine output and CVP value for old age, total deficits
around 6-9 liters.
Correcting hyperosmolarity to 300 milliosmoles/L
Managing any underlying illnesses
Insulin ; RI 0.15u/kg bolus then 0.1/kg/hr infusion until
blood sugar about 250mg/dl or osmo about 315
Clinical Uses of Insulin
Type 1 diabetes mellitus
Type 2 diabetes mellitus uncontrolled on maximal combination
therapy with oral agents
Gestational diabetes
Hyperglycemic emergencies
Total pancreatectomy patients
Acute or chronic hyperglycemia provoked by:
Infection or trauma
Steroid therapy
Endocrinopathies such as hyperthyroidism
Other types of secondary diabetes
Insulin Preparations
Ultra fast/ultra Lispro/aspart
short-acting
Short-acting regular

Plasma [Insulin]
Intermediate- NPH
acting
lente
Long-acting ultralente

Ultra long-acting glargine

0 4 8 12 16 20 24
Current Indonesian Society of Endocrinology
(Perkeni) treatment targets
HbA1c < 7%
Fasting BG < 100 mg/dl
Post prandial BG < 140 mg/dl
Blood pressure < 130/80 mmHg
LDL-cholesterol < 100 mg/dl (2.6 mmol/l)
HDL-cholesterol
Men > 40 mg/dl (1.1 mmol/l)
Women > 50 mg/dl (1.3 mmol/l)
Triglycerides < 150 mg/dl (1.7 mmol/l)
Konsensus PERKENI 2005