CASE REPORT

T Y PE II
DIABETES MELLITUS
PATIENT IDENTITY

Name : Mr. M
Date of Birth : 04-08-1957 (60 years old)
Gender : Male
Date enter hospital : 10th May 2018
ANAMNESIS
Main complaint : Swelling on both legs

Swelling on both legs started 1 month ago, slowly, and also its painful. Patient also
complaint about the swelling in his scrotum. There is a wet lesion on the patient's leg
that started about 2 weeks ago. The lesion appeared out of nowhere. No itching. The
patient had no fever and headache. Patient complaint about nausea but no vomitting.
Sometimes, the patient coughing and have chest pain. Defecation is normal and urination
is decreasing. Patient have diabetes mellitus since 2 years ago. The patient never had any
treatment for his diabetes mellitus.
 PHYSICAL EXAMINATION
GENERAL CONDITION HEAD & NECK
• Mild Pain • Conjunctiva anemic
• BMI = 27,34 kg/m2 (Obese I)
• No Icteric
• Compos mentis (E4M6V5)
• Lips are not dry
• Blood pressure : 120/80 mmHg
• Heart rate : 88 x/min, regular, strong
• The tongue is not dirty
• Respiratory rate : 20 x/min, thoracoabdominal • There is no enlargement of the lymph
• Temperature : 37,10C glands
 PHYSICAL EXAMINATION
THORAX HEART
• Inspection • Inspection
Symmetrical left and right, good development Ictus cordis is not visible
• Palpation • Palpation
No crepitation, no mass, normal vocal Ictus cordis is palpable
fremitus, no tenderness
• Percussion
• Percussion
Normal heart borders
Sonor left and right
• Auscultation
• Auscultation
Normal S1/II heart sound, no additional sound
Vesicular breathing sound, no wheezing, no
ronchi
 PHYSICAL EXAMINATION
ABDOMEN EXTREMITY
• Inspection • Pretibial edema present
Flat, no distention • Ankle region ulcers
• Auscultation • PUS present
Peristaltic present, normal impression • Dorsalis pedis artery difficult to palpate
• Palpation
Mass is not palpable, no tenderness, GENITAL ORGAN
hepar-lien is not palpable
Scrotum edema present
• Percussion
Shifting dullness and Ascites present
LABORATORY TEST
10 MEI 2018 10 MEI 2018
Examination Results Examination Results
WBC 10.700 /uL GDS 185 mg/dl
RBC 2.560.000 /uL Ureum 33 mg/dl
HGB 9,3 gr/dl Kreatinin 1,04 mg/dl
HCT 27 % SGOT 25 U/L
MCV 105 fL SGPT 29 U/L
MCH 36 pg Protein Total 5,5 gr/dl
MCHC 34 gr/dl Albumin 2,5 gr/dl
PLT 275.000 /uL Natrium 126 mmol/L
PT/INR 9,9 detik / 0,91 Kalium 4,7 mmol/L
APTT 29,1 detik Chlorida 95 mmol/L
GDP 95 mg/dl
GD2PP 114 mg/dl
LABORATORY TEST
24 MEI 2018 24 MEI 2018
Examination Results Examination Results
WBC 8.300 /uL Ureum 32 mg/dl
HGB 10,3 gr/dl Kreatinin 0,96 mg/dl
HCT 30 % SGOT 26 U/L
MCV 96 fL SGPT 15 U/L
MCH 33 pg Protein Total 5,4 gr/dl
MCHC 34 gr/dl Albumin 2,9 gr/dl
PLT 248.000 /uL Globulin 2,5 gr/dl
NEUT 52,9 % Asam Urat 7,5 mg/dl
GDS 208 mg/dl Natrium 132 mmol/L
HbA1C 6,5 Kalium 4,2 mmol/L
Klorida 99 mmol/L
Abdominal USG Thorax AP Image
• Bilateral Pleural Effusion • Cardiomegaly with pulmonary edema
• Other intraabdominal organs present • Bilateral Pleural Effusion
within normal limits • Aortae Dilatation

Echocardiogram
• POOR ECHO WINDOW
• Left Ventricular systolic function decreases, EF 45% (BIPLANE)
• Hypokinesis of the Basal, Mild Inferoseptal, Anteroseptal
• Left Ventricular diastolic dysfunction; moderate degree
DIAGNOSIS
• Multiple Ulcer Pedis Bilateral et causa Soft Tissue Skin Infection
• Type II Diabetes Mellitus Obese
• Congestive Heart Failure NYHA II et causa Coronary Artery Disease
• Hypoalbuminemia
• Decubitus Ulcers Grade II
• Normochromic Normocytic Anemia
• Dysfonia Observation
THERAPY
• Diet DM 1500 kkal
• Gliklazid 60mg/24 jam/oral
• N-acetylcysteine 200mg/8 jam/oral
• Laxadine emulsi 10cc/24 jam/oral
• Furosemid 40mg/24 jam/oral
• Aspilet 80mg/24 jam/oral
• Fasorbid 10mg/24 jam/oral
• Valsartan 80mg/24 jam/oral
• Doksisiklin 100mg/12jam/oral
• Metronidazole 500mg/8 jam/intravena
• Human albumin 25% /24 jam/intravena
DISCUSSION
TYPE II DIABETES MELLITUS
DEFINITION
• Diabetes Mellitus is a group of metabolic diseases characterized by high blood
sugar (hyperglycemia) resulting caused by impaired insulin secretion and
insulin resistance or both.
• In type II diabetes mellitus, the pancreas can still make insulin, but the quality
of insulin produced is poor and can not function properly as the key to
entering glucose into cells. As a result glucose in the blood increases, and can
also occur because of body tissue cell in muscle patient are insensitive or
already insulin resistant.

(Haida Nurlaila, 2013. Hubungan Empat Pilar Pengendalian DM Tipe 2 dengan Rerata Kadar Gula Darah. Universitas Airlangga)
EPIDEMIOLOGY
• Based on IDF 2017, in the world there are 425 million adults have diabetes, 1
in 11 adults has diabetes, and 1 in 2 remains undiagnoses.
• WHO predicted increase DM prevalence in Indonesia form 8,4 million in
2000 become 21,3 million in 2013. the report show 2-3x frequent raise in
2035. International Diabetic Federation (IDF) predicted increase DM
prevalence in Indonesia form 9,1 million in 2014 become 14,1 million in 2035.
• DM type 2 is most common chronic and non communicable disease with high
morbidity & mortality. One of the leading cause of death by disease. DM
shortens life span by 15 years and it progressive if untreat. Prevalence DM
type 2 in Women more high than man
PATOPHYSIOLOGY
• In type II DM, insulin secretion in phase 1 or early peak occurring within the
first 3-10 minutes after eating is insulin secreted in this phase is insulin stored
in beta cells (ready to use) can not lower blood glucose so stimulate phase 2.
• Phase 2 is insulin secretion from 20 minutes after glucose stimulation to
produce more insulin, but can not increase insulin secretion as in normal
people.
PATOPHYSIOLOGY
• Disruption of beta cell secretion causes insulin secretion in phase 1
depressed, decreased blood insulin levels cause the production of glucose by
the liver increases, so fasting blood glucose level increases.
• Thus, type 2 DM begins with a phase 1 disorder that causes hyperglycemia
and phase 2 disorders in which hyperinsulinemia does not occur but is a beta
cell disorder.

(Indriwasari, Wiwi, 2010. Hubungan Indeks Glikemik Asupan Makanan Dengan Kadar Glukosa Darah pada Pasien Rawat Jalan
Diabetes Mellitus Tipe 2. Makassar)
PATOPHYSIOLOGY

Type 2 Diabetes Mellitus

CLINICAL MANIFESTATION
Type 2 diabetes is often without symptoms in its early stages. That’s the reason
there are 40% of people with Type 2 diabetes are unaware of their disease. When
there are symptoms, they may occur gradually. If present, they usually are:

• Classic symptom :
Polyuria, polydipsia, polyphagia,Weight-loss unexplained
• Other symptom :
Feeling tired and weak, numbness feet, blurred eyesight, sexual disfungtion,
pruritus ,having frequent infections
DIAGNOSIS CRITERIA
FPG  126 mg/dl. Fasting is defined as no caloric intake for at least 8h.

OR
OGTT  200 mg/dl - 2h post-load glucose 75 g dissolved in 250 cc water.
OR
RPG  200 mg/dl with classic symptom hyperglycemic.

OR
HbA1C  6,5% mg/dl with classic symptom hyperglycemic. The test should
be performed in a laboratory using a method that is NGSP certified and
standardized to the DCCT assay.
TREATMENT
TREATMENT
1. Education
• To promote health life style
• Education material : definition, complicate, pharmacology and non pharmacologi, interaction with
nutritional, exeracise, and OAD, observe blood dan urin glucose by self care, foot care education
2. Nutritional management
• Recommendation nutritional compotition :
Carbohydrate 45-65% of TE, 3x/day
Lipid 20-25% of TE
Protein 10-20% of TE
Natrium <2300 mg/day
Fiber 20-35g/day
3. Exercise
Exercise :Aerobic Exercise (cycling, jogging, swimming)
10 min x 3 times a day = 30 min per day
3-5x/ week -> during 30-45 minute
PHARMACOLOGICAL THERAPY
Drug class Agent(s) Mechanism(s) of action Side effect
α-Glucosidase
Acarbose, miglitol Delay carbohydrate absorption Flatulen, soft stool
inhibitors
Liver glucose production
Biguanides Metformin Dispepsia, diarrhea, lactat acidosis
Insulin sensitivity in liver + muscle

Glimepiride, Increase weight

Sulfonylurea Insulin secretion from pancreatic  cells
glipizide, glyburide Hipoglikemia

Nateglinide, Increase weight

Meglitinides Insulin secretion from pancreatic  cells
repaglinide Hipoglikemia

Inhibit excess reabsorption glucose in distal

SGLT-2 Inhibitors Canagliflozin, empagliflozin Dehidration, ISK
tube kidney

Sitagliptin, vildagliptin , GLP-1 degradation

DPP-IV inhibitors Vomit
Saxagliptin, Lanagliptin Glucose-dependent insulin secretion

Pioglitazone,
Tiazolidindion Insulin sensitivity in fat cells + muscle Edema
rosiglitazone

Trujillo J. Formulary. 2006.

Luna B, Feinglos MN. Am Fam Physician. 2001.
Smyth S, Heron A. Nat Med. 2006.
 INSULIN THERAPY
Total daily Insulin
0.5 x BB

Total Prandial Insulin (TPI) Total Basal Insulin (TBI)

60% TDI 40% TDI

Morning Dose Day Dose Evening Dose Night Dose

1/3 x TPI 1/3 x TPI 1/3 x TPI (10.00)
100% TBI

Petunjuk Praktis Terapi Insulin pada Pasien Diabetes Mellitus (PB PAPDI)
INSULIN THERAPY
MONITORING
GOALS THERAPY
Good Borderline Evaluation
Glucose
fasting 80-100 100-125 >126
2 hour post-prandial 80-144 145-179 >180
A1c <6.5 6.5-8 >8

Setiati S, Sudoyo AW, Alwi I, Simadibrata M, Setiyohadi B, Syam FA. Buku Ajar Ilmu Penyakit Dalam. Edisi 6. Jakarta: Interna, 2014.
COMPLICATION
COMPLICATIONS

Acute Chronic

Microangiopathy Macroangiopathy

-Ketoacidosis -retinopathy
-Hiperosmolar non -CAD
-nephropathy
ketotic -PVD
-neuropathy
-Hipoglycemia -Stroke
THANK YOU