CASE REPORT

FOOT DIABETIK
Devision Endocrine and metabolisme Subdivision
Department of Internal Medicine
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Group 3 :
Sucitra C014172049
Nurul Fuadi Yusuf C014172142
Adi Ahdiat C014172126
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Patient Identity :
Name : Ny. N
Age : 67 yo
Medical record : 841686
Sex : Women
Date of birth : 12 December 1950
Address : Baji Ateka Timur Street
Occupation : Housewife
Hospital : RSWS / L1BB
Date enter hospital : 1 May 2018
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History Taking
Main complaint: wound on the right foot
Patient came to hospital with complaint of wound on the right foot since 3
weeks ago. Patient also complaint fatigue, fever, chest pain, defecation
smooth with dark stool, nausea and vomiting (+)
History : patient have been amputation on digiti II dextra of foot finger in
Bhayankara Hospital since 2 weeks ago. History of Diabetes Mellitus (+),
hypertension (). Patient referenced transfusion from Siloam Hospital 4 RBC
pack from Hb 6,0 g/dl into 9,0 g/dl
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Physical Examination
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GENERAL DESCRIPTION HEAD TO NECK

Head : normocephal, strong and straight black
General condition : Severe illness
hair
BMI : 26,31 kg/m2 (Obes I) Face : normal
Awareness : E4M5V6 Eyes : Pupils isocor (d : 3,3 mm), normal light
Blood pressure : 120/70 mmHg reflex, conjungtiva pale, no subconjungtiva bleeding,
no icteric, no palpebra udema
Heart rate : 104 x/min, regular, strong Nose : No abnormalities, epistaxis (-)
Respiratory rate : 20 x/min, Lips : No abnormalities, cyanosis (-)
thoracoabdominal
Oral cavity : No abnormalities, gingiva hypertrophy (-)
Temperature : 36,7 C (axilla) Throat : No abnormalities, Pharyngeal hyperemia
(-), T1-T2 quiet
Neck : No lymphadenopathy, no enlargement of
thyroid gland, no deviation of the trachea

Physical Examinationc
THORAX
I : symmetry left and right
P : normal vocal fremitus ,
tenderness (-)
P : sonor left and right
A : vesicular breath sound, no
wheezing, no rhonki
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HEART
I : Ictus cordis not visible
P : thrill not palpable
P : normal heart borders
A : normal SI/II heart sound,
additional sound (-)
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Pemeriksaan Fisis
ABDOMEN EKSTREMITAS
I : Distention (-) Inspeksi :
A : normal peristaltic sound Limit of movement

P : mass (-), tenderness (-), Pitting edema (+)

hepatomegaly (-), splenomegaly
(-)
P : tympani, ascites (-)
Warm palpable
post amputatum Digiti II pedis
dextra
Diabetic Wound with gangren digiti I
pedis dextra grade 4 based on
Wagner classification
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Albumin : 2,6 g/dl

SGOT : 14 U/L
SGPT : 6 U/L
Ureum : 40 mg/dl
LABORATOR Kreatinin : 0,56 mg/dl
Y FINDING WBC : 18.800
PLT : 302.000
(5/5/2018) GDS : 220 mg/dl
Kolestrol total : 104 mg/dl
Kolestrol HDL : 19 mg/dl
Kolestrol LDL : 62 mg/dl
Trigliserida : 120 mg/dl
Laboratory finding
May 5th, 2018
Albumin 2,6 gr/dl 3,5-5 gr/dl
Kolestrol total 104 mg/dl 200 mg/dl
Kolestrol LDL 29 mg/dl L(>55); P(>65) mg/dl
Kolestrol HDL 62 mg/dl <130 mg/dl
Trigliserida 120 mg/dl 200 mg/dl
Natrium 148 mmol/l 136-145 mmol/l
Kalium 3.3 mmol/l 3,5-5,1 mmol/l
Klorida 110 mmol/l 97-111 mmol/l
May 7th, 2018
GDS 203 mg/dl 140 mg/dl
HbA1C 7% 4-6 %
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RADIOLOGY X-RAY : BRONCOPHENEUMONIA

FINDING EFUSI PLEURA BILATERAL
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Diagnose
Primer : Diabetic Foot Wagner 4 classification on digiti I pedis
dextra
Sekunder :
1. Hipoalbumninemia
2. Community Acquired Pneumonia
3. Melena et causa stress ulcer
4. Anemia ec Chronic Disease
5. Perifer Arteri Disease
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Treatment
Infus NaCl 0,9 % 20tpm
Injeksi ceftriaxon 2 gr/24 jam/intravena
Injeksi Levofloxaxin 750gr/24 jam/intravena
Injeksi metronidazole 500 mg/ 8 jam/ intravena
Nevorapid 4-4-4 IU
lantus 0-0-10 IU
Injeksi lansopraszole 6 gr/12 jam/intravena
Nutrisi NGT via sonde
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Examination Plan
1. Pus culture for antibiotic sensitivity test
2. Consul BTKV
3. Control EKG
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No ASSESSMENT PLANNING Dx PLANNING THERAPY
1 Primer : Diabetic foot Wagner 4 on digiti I pedis dextra 1. Pus culture to 1. Infus NaCl 0,9 % 20tpm
Sekunder : antibiotic 2. Injeksi ceftriaxon 2 gr/24
1. Hipoalbumninemia sensitivity jam/intravena
2. Community Acquired Pneumonia test 3. Injeksi Levofloxaxin
3. Melena et causa stress ulcer 2. Consul BTKV 750gr/24 jam/intravena
4. Perifer arteri Disease 3. Control EKG 4. Injeksi metronidazole 500
5. Anemia ec chronic disease mg/ 8 jam/ intravena
5. Nevorapid 4-4-4 IU
S: Pasien datang dengan keluhan utama luka pada kaki kanan 6. lantus 0-0-10 IU
sejak 3 minggu yang lalu. Pasien juga mengeluh merasa 7. Injeksi lansopraszole 6
lemas, demam, nyeri pada dada kiri, ada mual dan muntah gr/12 jam/intravena
buang air besar berwarna hitam. 8. Nutrisi NGT via sonde
Riwayat : pasien sudah dilakukan amputasi pada jari kaki digiti
II dextra di RS Bhayankara sejak 2 minggu yang lalu. Pasien
memiliki riwayat diabetes melitus Riwayat hipertensi tidak
ada. Pasien dirujuk tansfusi dari RS Siloam 4 kantong RBC
dengan Hb 6,0.
O : Pemeriksaan fisis :
konjungtiva tampak anemis, Ada kesulitan dalam melakukan
pergerakan, pedis dekstra digiti I mengalami luka diabetik
grade 4 berdasarkan klasifikasi Wagner

Albumin : 2,6 mg/dl

GDS : 203 mg/dl
HBA1c : 4,0%
X-RAY : BRONCOPHENEUMONIA
EFUSI PLEURA BILATERAL TERUTAMA DEXTRA
 DISCUSSION
“DIABETES MELITUS TYPE 2”
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Definition
Diabetes mellitus is a group of metabolic diseases characterized
by hyperglycemia resulting from defects in insulin secretion,
insulin action, or both.
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
Regulation of
blood glucose
insulin

1 When a person eats, blood
glucose rises.
2 High blood glucose
stimulates the pancreas to
release insulin.
3 Insulin stimulates the uptake
of glucose into cells and
storage as glycogen in the
liver and muscles. Insulin
also
stimulates the conversion
of excess glucose into fat
for storage.
Intestine
Blood vessel
1 4 4 As the body's cells use
glucose, blood levels
decline.
Insulin
2 5 5 Low blood glucose
Glucagon stimulates the pancreas to
release glucagon
into the bloodstream.
Pancreas
6 6 Glucagon stimulates
Liver liver cells to break down
glycogen and release glucose
3 into the blood. a
7 Blood glucose begins to rise.
7
Key:
Glucose
Insulin
3 Fat cell
Glucagon
Glycogen
Muscle a
The stress hormone
epinephrine and other
hormones also bring
glucose out of storage.
Pathophysiology
Main Pathophysiological Defects in T2DM
pancreatic
incretin insulin
effect secretion
pancreatic

?
glucagon
secretion
gut
carbohydrate
delivery &
absorption
HYPERGLYCEMIA
Increase
glucose
reabsorption
+

peripheral
hepatic glucose
glucose uptake
production Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011 
 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 HbA1C FPG OGTT
RPG  200 mg/dl with classic symptom Diabetes 6,5  126 200
hyperglycemic. Prediabetes 5,7 – 6,4 100-125 140-199
OR Normal <5,7 <100 <140
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.
HIGH RISK FACTORS + WITHOUT CLASSIC SYMPTOM
Screenin
1. BMI  23 km/m2 + 1/> risk factor below :
g
a. Physical inactivity
b. First degree relative with diabetes
c. Members of high risk ethnic population
d. Women who delivered a baby weighing > 4 kg or were diagnosed with GDM
e. Hypertension (≥ 140/90 mmHg or on therapy for hypertension)
f. HDL cholesterol level < 35 mg/dl and/or triglyceride level > 250 mg/dl
g. Women with polycystic ovarian syndrome (PCOS)
h. Prediabetic history (IGT or IFG on previous testing)
i. Others clinical conditions associated with insulin resistance (severe obesity,
acanthosis nigricans
j. History of CVD

2. Age >45 yo + without risk factor above If high risk :

+ normal plasma glucose -> repeat every 3 year
+ prediabetes -> repeat every 1 year
TREATMENT
 AIM

LONG TERM :
SHORT TERM : Prevent complication
Eliminate symptoms Reduce morbidity and mortality
Maintain general well being (QoL)

STRATEGY:
Normalizing glucose, blood
pressure, body weight, lipd,
insulin level

ACTIVIITES :
Management with holistic
approach and self care principle
 1. Education
-To promote health life style
-education material : definition, compicate,
farmacologi and non farmacologi, interaction
with nutritional, exeracise, and OAD, observe
blood dan urin glucose by self care, foot care
education
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

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
 4. Farmacology
ORAL DIABETES AGENTS
Drug class Agent(s) Mechanism(s) of action Side effect
α-Glucosidase Acarbose, miglitol Delay carbohydrate absorption
Flatulen, soft stool
inhibitors

Biguanides Metformin Hepatic glucose production

Dispepsia, diarrhea, lactat acidosis
Insulin sensitivity in liver + muscle

Insulin secretion from pancreatic 

Sulfonylureas Glimepiride, Increase weight
cells
glipizide, glyburide Hipoglikemia

Insulin secretion from pancreatic  Increase weight

Meglitinides Nateglinide,
cells Hipoglikemia
repaglinide

Inhibit excess reabsorption glucose in

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

Sitagliptin, vildagliptin
DPP-IV inhibitors GLP-1 degradation; Glucose-
, Saxagliptin, vomit
dependent insulin secretion
Lanagliptin
Insulin sensitivity in fat cells +
Pioglitazone, Trujillo J. Formulary. 2006.
Tiazolidindion muscle edema
rosiglitazone Luna B, Feinglos MN. Am Fam Physician. 2001.
Smyth S, Heron A. Nat Med. 2006.
INSULIN
Insulin Indication : Side effect :

1. HbA1C >9% with metabolic -hipoglicemia

decompensation condition -allergic reaction
2. Weight loss within a short period of time
3. Severe hyperglycemia with ketotic
4. Hiperglycemia crisis
5. Failure OHO combination with optimal
dose
6. Severe stress (systemic infection. Major
surgery)
7 gestational diabetic
8. Renal or liver fungtional disturbance
9. Contraindication or allergic of OHO
10. Perioperative condition
5. Monitoring
Complication COMPLICATION
S

Acute Chronic

Microangiopathy Macroangiopathy

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

Depend on early diagnose or late diagnose, age, history, progressivity of disease.

If blood glucose well controlled and stabile, obey on treatment and doing diet which it plan
by doctor, generally prognosis is good. 60% patient DM type 2 use insulin can survive like
normal healthy people. And other, can get the complication if uncontrolled like retinopaty,
chronic kidney disease, and fast death, and the patient with complication have bad
prognosiss

Ad vitam : dubia
Ad sanationam : dubia
Ad functionam : bonam (if blood glucose control)
 DISCUSSION
“DIABETIC FOOT”
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Introduction
Uncontrolled diabetes mellitus cause metabolic or long-term vascular

complications, which are macroangiopathy and microangiopathy. Diabetics also

susceptible to foot wound infections that can then develop into gangrene. Some of

severe diabetes mellitus do amputation of limbs, especially the extremities due to

wounds putrefaction.
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Etiology
◦The process of diabetic foot begins with angiopathy, neuropathy and
infection. Neuropathy causes a sensory disturbance that eliminates
or decreases the sensation of leg pain, so ulcers can occur unnoticed.
Motor disorders cause leg muscle atrophy thus altering the fulcrum
leading to foot ulceration. Angiopathy will disrupt blood flow to the
leg, the patient may feel leg pain after walking within a certain
distance. Infection is often a complication due to reduced blood flow
or neuropathy. Diabetic ulcers can be diabetic foot gangrene.
◦The cause of gangrene in patients with DM is anerob, bacterial, and
Clostridium sp. most common. This bacterium produces a gas called
gangrene
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Risk Factor
Patients with DM over 10 years, men, poor blood sugar
control, there are cardiovascular, retina and kidney
complications. Things that increase risk include peripheral
neuropathy with protective sensory loss, biomechanical
changes, increased pressure on the feet, peripheral vascular
disease (decreased dorsalis pedis pulsation), history of ulcers or
amputations and severe nail abnormalities.
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Pathophysiology
Diabetic foot ulcer is caused by three factors often called trias, namely: ischemia, neuropathy and
infection. Uncontrolled blood glucose levels will lead to chronic complications of peripheral
neuropathy in the form of sensory, motor and autoimmune neuropathy.
Sensoric neuropathy
It usually with severe symptom, so it can eliminate the sensation protection that is susceptible to
physical and thermal trauma, thus increasing the risk of foot ulcers. Proprioseption sensation is the
sensation of foot position is also lost.
Motoric Neuropati
Affects all muscles, resulting in abnormal protrusion of bone. Foot deformity raises the limited leg
plantar pressure and becomes an easy ulcer.
Autonomy Neuropathy
Characterized by dry skin, no sweating, and increased secondary capillary incision cause by short
of arteriovenosus skin. This triggers the onset of fissura, skin crusts so that the foot is vulnerable to
minimal trauma
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Classification
The Wagner-Meggit classification was developed in the 1970s, widely used to classify lesions in d

Table. Classification of diabetic feet based on Wagner-Meggit

Grade 0 symptom on foot like a pain

Grade 1 Superficial diabetic ulcer

Grade 2 Ulcer extension involving ligament, tendon,

joint capsule, or fascia with no abcess or
osteomyelitis
Grade 3 Deep ulcer with abcess or ostomyelitis

Grade 4 Gangrene to portion of forefoot

Grade 5 Extensive gangrene of foot

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Diagnostic Criteria
◦Examination of ulcers and the general state of the extremities
Diabetic ulcers tend to occur in the largest load-bearing areas, such as the heel, acute
metatarsal in the soles of the feet, prominent fingertips (first and second fingers). The ulcer
in malleolus occurs because it often gets traumatized. Other abnormalities can be found
such as hypertrophic callus, brittle / ruptured nails, dry skin, hammer toes, and fissura.
◦Assessment of risk of vascular insufficiency
Physical examination will get lost or decreased peripheral pulses. Other findings related to
atherosclerosis include iliac and femoral artery sounds, skin atrophy, loss of leg hair,
cyanosis of the toe, ulceration and ischemic necrosis, and capillary refill test over 2 seconds
◦Peripheral Neuropathy
Peripheral neuropathy signs include loss of sensation of vibration and position, loss of deep
tendon reflex, trophic ulceration, foot drop, muscle atrophy and hypertrophic callus
formation especially in heel suppressive areas.
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Treatment
◦Wound control
Adequate debridement will help reduce the necrotic tissue so it will reduce
pus / fluid from gangrene ulcers. Debridement can be done with several
methods, the most effective method is autolysis debridement
◦Microbiological Control
Generally obtained multiple bacterial infections, anaerobes and aerobes.
Antibiotics should always match the results of bacterial cultures and their
resistance. The first line of broad-spectrum antibiotics includes both gram-
negative and positive bacteria (eg cephalosporins), combined with
anaerobic germicides (eg, metronidazole)
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Prognosis
The prognosis of the diabetic foot depends on various factors
seen in the pathophysiology, complications, and accompanying
diseases. Holistic management is emphasized to reduce the
mortality and morbidity of diabetic feet.
 Correlation DM - PAD
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Risk factor
(genetic, Accumulation Obstruction
ciggeret smoke, Plaque perifer Decrease
lipid (LDL,TG) Blood flow
high cholesterol, atherosclerosi artery lumen
on artery
DM) s on limbs
Complication
chronic DM
Foot ischemia
(low oxygen supply)

Peripheral arterial disease (PAD) is

noncoronary arterial syndromes that are caused by Foot ulcer Necrosis /
narrowing the peripheral arteries which reducing gangren
blood flow to the limbs, arm, and head. Most
commonly in artery of the leg
infection
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Correlation DM-hipoalbuminemia
Hipoalbuminemia is a condition when serum albumin level below < 3,5 g/dl in blood vessel

Increase protein
excretion in urin
Fluid leaking from
hiperglychemia Decrease oncotic capillary to
hipoalbuminemia
pressure plasma interstitial tissue
Inflamation
vessel,
increase
permeability
capiler, capiler Edema tissue
leak
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Albumin function
a. Albumin as a binder and carrier

b. The effects of albumin anticoagulants

c. Albumin as an exposure

d. The antioxidant effects of albumin

Correlation DM and Melena ec
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gastropathy
Ulcus pepticum,
varices
Helicobacter esophageal
pylori infect
Epithel
NSAID
cell Ulcus, bleeding melena
medication
Gaster
mucosa
Stress
disturb Gastropathy is disturbance of the epithel
gastropathy
(excess Decrease healing cell gaster mucose and regeneration
gaster acid) without inflammatory process. It occur
because irritation by chemical substance
like NSAID and alcohol. Severe Irritation can
hiperglychemia
cause bleeding (melena)
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Correlation DM-anemia
Anemia is a condition which decrease total amount red blood cell
or hemoglobinto to carry inadequate oxygen to the body’s tissue,
with men <13 g/dl, women <12 g/dl.

Malnutrition
hiperglikemia
membrane plasm leak anemia
infection
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Correlation DM- Pneumonia HASANUDDIN

Pneumonia is inflammation on lung parencim caused by microorganism (bacteria, virus, fungi,

parasit)
Pneumonia classification :
-Community pneumonia
-nosocomial pneumonia : - Hospital acquired pneumonia (HAP)
- Health care associated pneumonia (HCAP)

Disturb neutrophil
and monosit
function, less
Decrease surfactan
hiperglychemia Lung
Immunity
infection
system
Disfunction epitel
napas and cilia
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