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CASE PRESENTATION

DIABETIC FOOT ULCER

Compiled by:
Bimasena Arya Yudha
1102013060

Advisory Lecturer:
dr. Herry Setya Yudha Utama, Sp.B, M.H.Kes, FInaCS

Clinical Rotation in Department of Surgery


Arjawinangun Regional General Hospital
Faculty of Medicine YARSI University
2019
CHAPTER I
CASE PRESENTATION

I. IDENTITY

Date of hospital entry : July 22th, 2019


Name : Mr. B
Age : 52 years old
Gender : Male
Occupation : Coolie
Address : Panongan
Religion : Muslim
Marital Status : Married

II. ANAMNESIS
Main Complain
Patient complain of a wound in right foot about 2 weeks ago.

History of Disease
Mr. B were taken to the arjawinangun hospital with complaints of
right leg sores and festering since 1 week before hospitalized. He also
complained of pain in his legs. This happened after the patient's right
leg was hit by a nail 2 weeks before being admitted to the hospital.
Initially the patient's leg is injured with a small wound, then the wound
becomes festering and swollen. The wound is accompanied by an
unpleasant odor, red in color, and does not feel itchy.
The patient also complained of his body feeling weak since the last
6 months. Complaints of weakness accompanied by thirst that often
and often wake up at night because you want to urinate. Everyday
patients often drink sugary drinks, especially coffee and sweet tea,
smoke often, and sleep irregularly. The patient had checked himself
into the puskesmas but there was no change.
History of past disease
Mr. B said he never had experienced the same symptoms before. The
patient had no history of surgery.The patient did not has history of
diabetes and is not regularly taking the medicine. Patient said he never
had a history of hypertension or allergy.
History of family disease
According to patients there is no history of diabetes in his family .

III. PHYSICAL EXAMINATION

a. Present Status

Genereal Condition : Mild Pain

Awareness : Composmentis

Blood pressure : 130/80 mmHg

Pulse : 84x/ minute

Breathing : 20x/ minute

Temperature : 36 C

Head Form : Normocephale, symmetrical


Hair : Black, no hair fall
Eye : Anemic conjungtivas (-/-), icteric schleras
(-/-)
Ear : Normal form, cerumen (-), intact thympany
membrane
Nose : Normal form, septum deviation(-),
epitaxis(-/-)
Mouth : Normal
Neck : Enlargement of lymph nodes (-), trachea in the middle

Thorax
Lungs – pulmonary
Inspection : The chest is symmetrical both left and right
Palpation : Fremitus vocale and tactile are symmetrical,
crepitation (-), tenderness (-), rebound
tenderness (-)
Percussion : Resonance sound in both lung fields
Auscultation : Vesicular and bronchial sound in the entire
lung field, ronchi (-/-), wheezing (-/-)
Abdomen
Inspection : Flat, symmetrical, mass (-)
Palpation : Tenderness (-), rebound tenderness (-)
Percussion : Tympani sound in four quadrants
Auscultation : Intestine sound (+)

Extremities
Upper
Muscle Tone : normal
Movement : active / active
Mass :-/-
Strenght :5/5
Oedema :-/-
Lower
Muscle tone : normal
Movement : active / active
Mass :-/-
Strenght :5/5
Oedema : + /-

b. Localized Status
Region of Dorsalis Pedis Dextra
Inspection: wounds diameter about ± 5 cm x 10 cm, irregular
shape, ulcer (+), pus (+), edema (+), hyperemia (+).
The skin around the wound edges is uneven black, the
middle is hyperemic (+).
Palpation: tenderness (-)
c. Laboratory Examination

Test Result Unit

Full Blood

Hemoglobin 13.2 gr/dl

Hematocrit 38.7 %

Leukocyte 19.8 10e3/µL

Trombocyte 467 10e3/µL

Erythrocyte 4.73 mm3

Counts (DIFF)

Eosinophil 0.1 %

Basophil 0.8 %

Segmen 86.3 %

lymphocytes 8.3 %

monocytes 4.4 %

Luc 0 %

Coagulation

Clotting time 4’ Minute

Bleeding time 2’ Minute

Immunology

HBsAg 0,01
Anti HIV non reactive

Chemical clinics
Random Blood
Glucose 346 Mg/dl

IV. DIAGNOSIS
Diabetic ulcer in the right foot
Type 2 diabetes mellitus

V. DIFFERENTIAL DIAGNOSIS
Tropic Ulcer
Varicosum ulcer
Thrombophlebitis

VI. TREATMENT
Cefazolin IV 2 X 1 gr
Ketorolac IV 3 X30 mg
Metronidazol IV 3 X 500mg
Metformin tab 3x500 mg
Debridement
VII. PROGNOSIS
AdVitam : dubia ad bonam
AdSanationam : dubia ad bonam
AdFungsionam : dubia ad bonam
CHAPTER II
LITERATURE REVIEW

I. DEFINITION
Diabetic ulcer is an open wound on the surface of the skin due to
complications of macroangiopathy resulting in vascular insuficiensies and
neuropathy, caused further injuries that are often not felt by the patient, and
can develop into infections caused by aerobic or anaerobic bacteria.

II. EPIDEMIOLOGY
The prevalence of ulcers in the population ranges from 2 - 10%, in
fact only a small part of the foot problem then continues until it requires
amputation of the lower limbs. Most can be compared with careful
management. Whereas in Indonesia, the prevalence of diabetic ulcers in the
population is rarely reported. In Jakarta, in a population survey in 1983
there was a 2.4% prevalence of ulcers /healed ulcers. In the Endocrine
Polyclinic of Dr Kariadi Hospital, Semarang, from data collected from
January 2001 to June 2002, 4% of diabetic patients referred to the endocrine
polyclinic of this hospital had macroangiopathic complications in the form
of diabetic ulcers.
Diabetes mellitus is a major cause of non-traumatic lower limb
amputations in the United States. Amputation of the feet due to diabetes
consist 50% of the total amputation in the United States. While in Cipto
Mangunkusumo Hospital in Jakarta, the amputation rate is still very high,
which is equal to 23%. The fate of patients who have experienced
amputation is not encouraging. Data from all hospitals in the State of
California show that 13% of those who have been amputated will need
another amputation within 1 year. It was also found that 30-50% of patients
who had been amputated would require amputation of their next leg within
1-3 years. The fate of amputee diabetic ulcer patients in RSUPN Cipto
Mangunkusumi is also not encouraging. Within 1 year after amputation
14.8% died and increased 37% at 3 years.

III. PATHOGENESIS
Diabetes often causes peripheral vascular disease that blocks blood
circulation. The condition of the diabetic ulcer comes from a combination of
several causes such as poor blood circulation and neuropathy. The basis of
the occurrence of diabetic ulcers is the presence of an abnormality in the
nerves, blood vessel abnormalities and then an infection. Of the three things,
the most important role is abnormalities in the nerves, while blood vessel
abnormalities play a more significant role in wound healing so that it
determines the fate of the legs. Another explanation is neuropathy and
angiopathy as endogenous factors, while trauma and infection are
exogenous factors.
Diabetic-ischemic angiopathy
In this explanation, diabetes makes a disorder or complication through
damage to blood vessels throughout the body called diabetic angiopathy.
Diabetic angiopathy is caused by several factors, namely genetic, metabolic
and other risk factors. High glucose levels (hyperglycemia) turned out to
have a broad negative impact not only on carbohydrate metabolism, but also
on protein and fat metabolism which can cause calcification and narrowing
of blood vessels (atherosclerosis), as a result of large blood vessel
circulation disorders (makroangiopati) and small (mikroangiopati).
People with prolonged hyperglycemia will cause pathological changes
in blood vessels. This can cause thickening of the intima "arterial basement
hyperplasia", arterial occlusion (blockage), and hyperkeragulability or
tromborsit abnormality, thus delivering adhesion (adhesion) and clotting
(aggregation).

In addition, hyperglycemia also causes DM lecocytes to be abnormal


so that the chemotoxic function at the site of inflammation is disrupted.
Similarly, the function of intracellular phagocytosis and bactericides
decreases so that if there is an infection of microorganisms (bacteria), it is
difficult to be destroyed by intracellular phagocytosis-bactericidal systems.
This will be obtained by not only arterial stiffness, but also by abnormal
blood. According to the literature, an increase in fibrinogen levels and
increased platelet reactivity, will cause high aggregation of red blood cells
so that blood circulation becomes slow, and facilitates the formation of
platelets on arterial walls that have become stiff until eventually circulatory
disorders occur.
In this condition, there is a narrowing around the arteries which often
causes a significant decrease in circulation in the lower limbs and legs.
Signs and symptoms due to a decrease in blood flow to the legs include
claudication, pain that occurs on the palm or forefoot at rest or at night, no
popliteal pulse or superior tibial pulse, thinning or shiny skin, atrophy of
subcutaneous fat tissue , there are no hairs on the legs and lower legs,
thickening of the nails, redness of the affected area when the legs are silent,
or dangling, and pale when the feet are lifted. Poor circulation contributes to
the emergence of diabetic ulcers by reducing the amount of oxygen and
nutrients supplied to the skin and other tissues, causing the wound not to
heal.

Diabetic neuropathy
The condition of neurological disorders can affect sensory nerves,
motor nerves, and autonomic nerves. In blood vessel disorders, the feet can
feel painful, if touched feels cold, if there is a wound it is difficult to recover
because the blood flow to that part has decreased. Examination of the pulse
in the foot is difficult to touch, the skin looks pale or bluish, then in the end
can become gangrene or rotten tissue, then infected and germs thrive, this
will endanger the patient because the infection can spread throughout the
body (sepsis).
In nerve vessel disorders called diabetic neuropathy. This diabetic
neuropathy is a motor, sensory and autonomic disorder, each of which plays
a role in the occurrence of foot injuries.
1. Sensory disturbance where it feels numb, tasteless, until numbness even
punctured by needles / nails or exposed to panaas objects. An unwitting
injury can cause callus which can turn into an ulcer which, when
accompanied by an infection develops into cellulitis and ends with
gangrene. Diabetic gangrene is a long-term effect of arteriosclerosis and
small thrombus embolism. Diabetic angiopathy almost always results in
peripheral neuropathy. If you have gangrene, your feet should be cut
over the decaying part.

2. Motor disorders where muscle weakness occurs, muscle cramps, easy


reduction (atrophy) of the interosseus muscles in the legs. As a result of
this condition, there is an imbalance in the leg muscles, deformities in
the legs such as cock up toes, shifting joints (lucations) in the forefoot
joint (metatarsofalangeal) and thinning of the fat pads below the base of
the toes (kaput metatarsal). This causes an expansion of the area that is
under pressure, especially under the head of the metatarsal. Paralysis of
the leg muscles causes a change in balance in the foot joint, changes in
the way of walking, and will cause a new pressure point on the soles of
the feet so that callus occurs in that place

3. Autonomic nerve disorders result in loss of skin secretion so that the


skin is dry and easily experiences injuries that are difficult to heal.
These infections and wounds are difficult to heal and easily experience
necrosis due to three factors. The first factor is arteriolar angiopathy
which causes poor perfusion of leg tissue so that the inflammation
mechanism becomes ineffective. The second factor is the fertile blood
sugar environment for the development of pathogenic bacteria. The
third factor is the opening of arterial-venous shortcuts in subcutaneous,
nutrient flow will bypass the infection site in the skin.

Infections
The infection itself is very rarely a single factor for the occurrence of
diabetic ulcers. Infection is more often a complication that accompanies
diabetic ulcer due to ischemia or neuropathy. From cases of diabetic ulcers
or gangrene, 50% of diabetic legs will develop an infection due to the
emergence of a fertile blood sugar environment for the development of
pathogenic bacteria. Because of the lack of oxygen supply, the bacteria that
will thrive are mainly anaerobic bacteria. The bacteria that cause infection in
diabetic ulcers are Staphylococcus or Streptococcus aerobic germs and
anaerobic germs namely Clostridium perfringens, Clostridium novy, and
Clostridium septic.

IV. CLINICAL MANIFESTATION


Clinical features are distinguished:
1. Neuropathic Foot which consists of: Neuropathic Ulcer, Neuropathic
arthropathy (Charcot arthropathy), Neuropathic Edema
2. Neuro-ischemic-foot

Neuropathic foot
a) Neuropathic Ulcer
Diabetic peripheral neuropathy can provide small fibreneuropathy
resulting in somatic and autonomic disorders. The manifestation is loss
of heat sensation and pain before palpation and fibrosis are disrupted.
Also the sympathetic nerves experience denervation that interferes with
blood flow due to excessive flow with the arteriovenous shunting
around the capillaries-and dilation of peripheral arteries. This food-poor
blood flow reduces the effectiveness of tissue perfusion which has
diminished. Besides this neuropathy damages the sensory nerve C
fibers so that nociceptors occur. So this diabetic foot ulcer is due to
ischemia, often a gas picture is seen. The cause can be due to
Clostridium, E coli, Streptococusanaerob, and Bacteroides sp. To
identify cases that are susceptible to ulcers, now a simple screening tool
is used, namely TCD (Tactile Circumferential Discriminator) in Hallux
which correlates using a filament and a high fibration threshold. In
assessing the ulcer it is necessary to ascertain the extent and extent of
the ulcer. Often we are fooled because we take it lightly, even though
these lesions are the tip of the iceberg.

Figure 1. Neuropathic Ulcer

Clinically it looks dilated in the legs and lower limbs in a lying


position. Legs have faster flow and more vascularity. If there is an
ulcer, it is necessary to pay attention to the germs that cause the
infection. Send samples for bacterial cultures.

b) Neuropathic arthropathy
Motor, sensory and autonomic fiber damage facilitates Charcot
atropathy. This condition is thought to be due to autonomic nerve
dysfunction which results in abnormal perfusion of the bones of the
foot, resulting in bone fragmentation and arch collapse. Charcot
atropathy or by another name "Rocker-bottom foot" is susceptible to
tissue damage and ulceration. Peripheral vascular disorders both as a
result of macrovascular (atherosclerosis) and because of microvascular
disorders that cause foot ischemia. This situation besides being a cause
of ulcers also complicates the healing process of foot ulcers.
Foot deformity often results in ulceration. Diabetics tend to have a
bent finger pressing on the finger, which is associated with thinning and
shifting fat deposits under the head of the first metatarsal. As a result
this area is prone to ulceration and infection. The extreme form of this
leg deformity is Charcot's foot . The cause of fracture and bone
reabsorption at Charcot's foot is not yet clear, but it is thought to be due
to autonomic neuropathy (due to failure of vascular tone will increase
blood flow, formation of arteriovenous shunts and recurrence despite
low bone density diabetics) and peripheral neuropathy (loss of feeling,
active patient walking and so on despite bone fractures). As a result
there is a fracture, collapse of the joint, and deformity of the foot.
Initially Charcot's legs were acute: hot, red, with a hard pulse, with or
without trauma (need to be in DD with cellulitis). In stage4 it is easy to
have ulcers and infections and gangrene which can result in amputation.

Figure 2. Locations where diabetic ulcers occur


c) Neuropathic Edema
It is a rare complication of diabetic foot, where there is edema
(pitting) of the legs and lower limbs associated with peripheral nerve
damage (put aside first because of cardial and renal). Sympathetic
nerve disorders result in abnormal edema and venous pooling, and
vasomotor reflexes are lost in standing.

Neuro ischemic foot


This leg picture is a combination of accelerated atherosclerosis in
diabetes and neuropathic foot. Intermittent claudication complaints, resting
leg pain, with ulceration and gangrene. Generally resting pain at night, and
reduced foot attitude that depends. To differentiate from neuropathic ulcers,
here the pain ulcer, one necrosis, circled the erythematous periphery and not
accompanied by a callus. Predilection in the thumb, medial edge of the
metatarsal I, or tepilateral V metatarsal, and heel.

V. CLASSIFICATION
Classification of diabetic ulcers is useful for generalizing language in
the description and condition of the ulcer, as well as for management or
therapy. There are several classification systems to assess the gradation of
lesions, one of which is widely used is the classification of diabetic ulcers
based on the University of Texas Classification System. This classification
system assesses lesions not only in the depth factor of the lesion, but also
assesses whether there are factors of infection and ischemia.
Tabel 1. Classification diabetic wound by University of Texas

Based on the depth of the wound, the degree of infection and the degree
of gangrene, the classification of the degree of lesions in the diabetic foot was
made according to Wagner.

Tabel 2.Wagner classification for diabetic foot


Stage Foot characteristics
Grade 0 There is no ulceration, but high risk even if there is none
ulcerations , to become diabetic foot. Patients in this group
needs special attention. Periodic observation, maintenance
good feet and counseling is important to prevent ulceration.
Grade 1 Superficial ulcers, without infection, are also called neuropathic
ulcers, bybecause it is more often found in many leg
areasexperience weight pressure which is in the area of the toes
andplantar. Kallus is often seen.
Grade 2 Deep ulcer, accompanied by cellulitis, without abscess or bone
abnormalities the presence of deep ulcers, often accompanied by
infection but withoutbone abnormalities.
Grade 3 Deep ulcer accompanied by skin abnormalities and extensive deep
abscesses.
Grade 4 Gangrene is limited to only the toes, heel causesthe main thing is
ischemia, therefore it is also called the ischemic ulcer limited to
certain areas
Grade 5 Whole leg gangrene usually due to blockage of large arteries,but
there are also disorders of neuropathy and infection

VI. DIAGNOSIS
Patients with diabetes mellitus have classic complaints, namely
polyuri, polidipsi and polifagi. History of examinations that have been
done before the doctor and laboratory support the diagnosis. The existence
of a family history of pain like this can be found, and indeed this disease
tends to be hereditary.
Anamnesis that must be asked including daily activities, shoes used,
callus formation, foot deformity, complaints of neuropathy, limb pain
during activity or rest, duration of suffering from DM, comorbid disease,
habits (smoking, alcohol), medications being consumed, history suffered
from previous ulcer / amputation.
Irregular history of treatment affects the clinical condition and
prognosis of a patient, because even though treatment has been good but
the treatment of diabetes is irregular it will be in vain. Complaints of pain
in the foot are not felt immediately immediately aftertrauma. Disorders of
sensory neuropathy obscure symptoms if the wound or ulcer is still mild.
After the wound gets wider and deeper, the pain begins to be complained
of by the sufferer and causes the doctor to come to the doctor or hospital.
Many of all people with diabetes mellitus with ulcer complications or
other forms of infection, have already checked themselves in a condition
that is advanced, so the management is more complicated and the
prognosis is worse (for example amputation or sepsis).

Physical Examination
On a physical examination, a doctor will find the ulcer is a defect in
the skin partially or completely (superficial or deep) that is chronic,
infected and can be found pus, necrotic tissue or foreign matter. Shallow
ulcers have only dermal or fat / subcutaneous tissue lesions. Deep ulcer
depth to muscle and even bone. Ulcers are often accompanied by
hyperemia around it which shows the inflammation process.
An abscess is a collection of pus or pus in a cavity that was previously
absent. On physical examination, the skin appears swollen, palpable and
fluctuating. An abscess that is located very deep physically is difficult to
diagnose, except pus has sought a way out of the source.
Phlegmon or cellulitis has clinical features such as reddish edema,
nonpitting edema, palpable warmth of the surrounding skin, no
fluctuations and tenderness. This indicates that the infection /
inflammation process has reached soft tissue or soft tissue.
Gangrene is a tissue that dies because of the absence of blood
perfusion. Clinically appear black, can be accompanied by brownish
liquid, foul smell and feel cold. If there is crepitus under the skin, it is
called gas gangrene.
Assessing foot ulcers is very important because it is related to
decisions in therapy. Physical examination is directed at getting a
description of the character of the ulcer, determining whether there is an
infection, determining the background of ulcers (neuropathy, peripheral
obstruction, trauma or deformity), ulcer classification and perform a
neuromuscular examination to determine the presence / absence of
deformity, the presence of pulsed arterial limbs and pedisation.
Description of diabetic ulcer must at least include; size, depth, smell,
shape and location. This assessment is used to assess the progress of
therapy. On the ulcer against which the ulcer neuropathy is usually dry,
fissure, warm skin, callus, normal skin color and location usually in
plantar precisely around the head of the I-III metatarsals, lesions are often
in the form of punch outs. Whereas lesions due to ischemia are cyanotic,
gangrenous, cold skin and the most common location is on the fingers. The
shape of the ulcer needs to be described as; edge, base, no / no pus,
exudate, edema or cephalus. The depth of the ulcer needs to be assessed
with the help of a sterile probe. The probe can help to determine the
presence of sinuses, knowing the ulcer involves tendons, bones or joints.
Based on Reiber's research, the location of the most common ulcers is on
the surface of the dorsal and plantar fingers (52%), the plantar area
(metatarsal and heel 37%) and the dorsum pedis area (11%).
Whereas to determine the factor of neuropathy as the cause of the
ulcer can be used reflex examination of the foot joint, examination of the
sensory, examination with tuning fork, or by monofilament test. The
monofilament test is a very simple and sensitive enough examination to
diagnose patients who are at risk of getting ulcers because they have
experienced peripheral sensory neuropathy. The test results are said to be
abnormal if the patient cannot feel the touch of nylon monofilament. The
part that is examined by monofilament is on the plantar side (metatarsal
area, heel and between the metatarsal and heel) and dorsal side.
Autonomic nerve disorders cause clinical signs of dryness of the skin
between the fingers and cruris. In addition there are fissures and cracked
skin, making it easy to get injured and then get an infection.
Pulsation examination is the most important thing in vascular
examination in patients with arterial occlusion in the lower extremities.
Femoral arteries, popliteal arteries, dorsalis pedis, posterior tibialis must
be assessed and their strength is categorized as aneurysm, normal, weak or
lost. In general, if the posterior tibialis and dorsalis pedisteraba artery
pulses are normal, perfusion at this level represents normal axial patency.
Patients with intermittent claudicatio have superficial femoral artery
disorders, and therefore despite palpable pulses in the groin but no
pulsations in the dorsalis pedis artery and posterior tibialis are present.
Diabetic sufferers are more often found to suffer from infiltrateal disorders
and therefore although palpable pulses in the femoral artery and
popliteatapi do not get distal pulses.
Ankle brachial index (ABI) is a non-invasive examination to
determine the presence of peripheral vascular obstruction. Examination of
ABI is very cheap, easy to do and has good sensitivity as a marker of
arterial insufficiency. An ABI examination is performed just as we
measure blood pressure using a blood pressure cuff, then the pressure
coming from the arteries will be detected by a Doppler probe (substitute
for the stethoscope). Under normal circumstances the systolic pressure in
the lower leg (ankle) is equal to or slightly higher than the upper arm
(brachial) systolic blood pressure. In situations where arterial stenosis
occurs in the lower limbs there will be a decrease in pressure. ABI is
calculated based on the ratio of ankle systolic pressure divided by brachial
systolic pressure. Under normal conditions, the normal price of ABI is>
0.9, ABI 0.71-0.90 mild ischemia occurs, ABI 0.41-0.70 has moderate
vascular obstruction, ABI 0.00-0.40 obstruction has occurred severe
vascular.
Diabetes mellitus and hemodialysis patients who have lesions in the
lower leg arteries, (due to blood vessel calcification), the ABI shows more
than 1.2 so that the ABI number is not a clue to diagnosis. Patients with
ABI of less than 0.5 are advised to operate (e.g amputation) because of a
poor prognosis. If ABI> 0.6 can be expected to benefit from drug therapy
and exercise.

Medical Work Up
Investigation that can be done to make a definite diagnosis is to do a
complete examination of CBC (Complete Blood Count) examination,
blood sugar examination, kidney function, liver function, electrolytes.
To determine vascular patency several non-invasive examinations can
be used such as; (ankle brachial index / ABI) which has been explained on
a physical examination. Other tests are transcutaneous oxygen tension
(TcP02), ultrasound color Doppler or use a invasive examination such as;
digital subtraction angiography (DSA), magnetic resonance angiography
(MRA) or computed tomography angiography (CTA).
If the diagnosis of peripheral vascular obstruction is still in doubt, or if
revascularization is planned, digital subtraction angiography, CTA or
MRA examination needs to be done. The gold standard for the diagnosis
and evaluation of peripheral vascular obstruction is DSA. DSA
examination is necessary if endovascular intervention is a therapeutic
option.
Radiological plain photo examination on pedis is also important to
determine whether there are any complications of osteomyelitis. The photo
shows a picture of bone destruction and osteolytics.
Pus culture, knowing the type of germs on the wound and giving
antibiotics that are in accordance with the type of germs.

VII. DIFFERENTIAL DIAGNOSIS


a. Tropic Ulcer
Tropic ulcer is a rapidly developing and painful ulcer, usually in
the lower limbs. In the tropic ulcer there are several factors that
influence the occurrence of ulcers. Among other things, the existence of
trauma, poor hygiene, malnutrition and infection by Bacillus fusiformis.
In the slightest trauma greatly facilitates the entry of germs, especially
with poor nutritional status so that injuries due to small trauma can
develop into an ulcer.
It usually starts with a small wound, then forms a papule that
quickly expands into vesicles. The vesicles then rupture and small
ulcers form. After the ulcer is infected by germs, the ulcer extends to
the side and inward and gives a typical form of the tropic ulcer.

b. Varikosum ulcer
Varikosum ulcer is an ulcer caused by a disruption of venous
blood flow in the lower limbs. Disorders of venous flow can be caused
by abnormalities in the arteries such as venous abnormalities and
damages in the veins proximal to the lower limbs. The predilection area
is the area between the malleolus and calf, but tends to arise around the
medial malleolus. Can also extend to the upper limbs. Varicose veins
often occur in the lower limbs. Ulcers that have been going on for years
can change the edge of the ulcer to grow, and bump. A sign that is
typical of extremities with chronic venous insufficiency is edema.
Patients often complain of swelling in the feet which increases when
standing and is still, and will decrease when performed leg elevation.
Ulcers usually have irregular edges, varying size, and can be broad. At
the base of the ulcer, granulation tissue or fibrous material is seen. Can
also show a lot of exudate. The surrounding skin looks brownish red
due to hemosiderin.

VIII. TREATMENT
Management of diabetic ulcers is done comprehensively through
efforts; overcome comorbid diseases, eliminate or reduce load pressure
(offloading), keep the wound moist (moist), manage infections,
debridement, revascularization and elective, prophylactic, curative or
emergency surgical procedures.
DM involves a multi-organ system that affects wound healing.
Hypertension, hyperglycemia, hypercholesterolemia, cardiovascular
disorders (stroke, coronary heart disease), impaired kidney function, etc.
must be controlled.

Diabetes Management
Control of diseases in general include controlling blood sugar levels
with regular diet or drug administration from doctors, nutritional status,
blood pressure, cholesterol levels, and healthy lifestyle. Managing diabetes
mellitus, the step that must be taken is non-pharmacological management,
in the form of food planning and physical activities. Only later, if with
these steps the target of diabetes control determined has not been achieved,
followed by the next step, namely with the use of drugs or
pharmacological management. Food planning in patients with diabetes
mellitus is still the main treatment in the management of diabetes mellitus.
The means of controlling pharmacologically in diabetes mellitus can
be in the form of
a. Insulins
b. Oral Hypoglycemic Drugs (OHO), such as :
 Sulfonylurea.
 Biguanid.
 Alpha Glucosidase inhibitors.
 Insulin Sensitizing

Debridement
Debridement is an important therapy in cases of diabetic ulcers.
Debridement can be defined as an attempt to clean foreign matter and
necrotic tissue in the wound. Wounds will not heal if necrotic tissue,
debris, callus, fistula or cavity is obtained which allows the germ to
develop. After debridement, the wound must be irrigated with
physiological saline or other cleansers and dressings (compresses) are
carried out.
There are several choices in debridement actions, namely
o Mechanical debridement, enzymatic, autolytic, biological, surgical
debridement.
a) Mechanical debridement is carried out using physiological fluid
wound irrigation, ultrasonic laser, etc., in order to clean the
necrotic tissue.
b) Enzymatic debridement is carried out by topically administering
exogenous enzymes on the surface of the lesion. The enzyme will
destroy the residual protein residue. For example, collagenizing
provides collagen and elastin. Some types of debridement that are
often used are papine, DNAse and fibrinolisin.
c) Autolytic debridement occurs naturally when a person is injured.
This process involves endogenous macrophages and proteolytic
enzymes that naturally lyse necrotic tissue. Synthetically,
hydrogel and hydrocolloid preparations can create optimal
environmental conditions for the body's phagocytes and act as
agents that lyse necrotic tissue and stimulate the granulation
process. Sterilized maggots (Lucilla serricata) are often used for
biological debridement. Maggots produce enzymes that can
destroy necrotic tissue.
d) Surgical debridement is the most rapid and efficient type of
debridement. The aim of surgical debridement is to:
1. Evacuate contaminated bacteria,
2. Lifting necrotic tissue so that it can speed healing,
3. Eliminating callus tissue,
4. Reduce the risk of local infection.

Reducing Pressure Load (Off Loading)


When someone walks, the foot gets a big burden. In patients with DM
who experience plantar surface neuropathy, the foot is easily injured or the
wound becomes difficult to heal due to pressure from the body and chronic
irritation of the shoes used.
One thing that is very important but until now not getting attention in
diabetic foot care is reducing or eliminating the burden on the foot (off
loading). Efforts to off loading based on research have proven to accelerate
ulcer healing. Off loading methods that are often used are: reducing speed
when walking, resting (bed rest), wheelchairs, footwear, removable cast
walkers, total contact casts, walkers, ambulatory boots. Total contact cast
is the most effective off loading method compared to other methods. Based
on research Armstrong TCC can reduce the pressure on the wound
significantly and give cure between 73% -100%. TCC is designed
according to the shape of the feet and legs, and is designed so that the
plantar foot pressure is evenly distributed. The middle of the foot is
propped up with rubber so that it gives a flat surface with the sole and back
of the foot (heel).
Dressing techniques on Diabetic wounds
The latest dressing techniques on diabetic wounds emphasize the
moist wound healing method or keep the wound moist. Wounds will heal
quickly if the exudate can be controlled, keeping the wound moist, the
wound not sticky with compresses, avoiding infection and permeable to
gas. The dressing is an important component in accelerating the healing of
lesions. The principle of dressing is how to create an atmosphere in a
humid state so that it can minimize trauma and risk of surgery. There are
several factors that must be considered in choosing the dressing to be used,
namely the type of ulcer, the presence or absence of exudates, the absence
of infection, surrounding skin conditions and costs. There are several types
of dressings that are often used in wound care, such as: hydrocolloid,
hydrogel, calcium alginate, foam, anti-microbial compresses, and so on.
Ovington provides guidance in choosing the right dressing in maintaining
the moisture balance of wounds :
o The compress must be able to provide a moist wound environment
o Use clinical judgment in choosing compresses for certain wound
injuries to be treated
o The compresses used are able to keep the edges of the wound dry
while keeping the wound moist
o The compresses chosen can control the exudate and do not cause
maceration in the wound
o The selected compresses are easy to use and are not often replaced
o In using dressings, compresses can reach the wound cavity so as to
minimize bacterial invasion.
o All compresses used must be monitored appropriately

Infection Control
Giving antibiotics is based on the results of germ culture. But before
the results of the culture and sensitivity of the germs available antibiotics
must be given empirically to the infected diabetic foot. The antibiotics
recommended in diabetic feet are infected. In mild / moderate diabetic
ulcers the antibiotics given are focused on gram-positive pathogens. In
severe infected ulcers (limb or life threatening infection) more
polymicrobialgerms (including gram-positive bacteria in the form of
coccus, rod-shaped gram negative, and anaerobic bacteria) antibiotics must
be broadspectrum, given as an injection. Characteristics of anaerobic
bacterial skin infections cause swelling of the skin that is painful, painful,
reddish, open wounds (ulcers) with foul-smelling pus, severe skin
infections causing damage to the skin tissue (necrosis). Antibiotics that are
still sensitive to anaerobic bacteria include: chloramphenicol,
metronidazole and imipenem. Other antibiotics commonly used are
clindamycin or cefoxitin.
In severe infections that are limb threatening infections can be given
several alternative antibiotics such as: ampicillin / sulbactam, ticarcillin /
clavulanate, piperacillin / tazobactam, Cefotaxime or acftazidime +
clindamycin, fluoroquinolone + clindamycin. While for severe life
threatening infections, several antibiotic alternatives can be given as
follows: ampicillin / sulbactam + aztreonam, piperacillin / tazobactam +
vancomycin, vancomycin + metronbidazole + ceftazidime, imipenem /
cilastatin or fluoroquinolone + vancomycin + metronidazole. In severe
infections antibiotics are given for 2 weeks or more. When the ulcer is
accompanied by osteomyelitis the healing becomes longer and often
recurs. So osteomyelitis treatment in addition to antibiotics should also be
done surgical resection. Antibiotics are given empirically, through
parenterals for 6 weeks and then re-evaluated through radiological photos.
If the bone necrotic tissue has been resected until it is clean, antibiotics can
be shortened, usually requiring 2 weeks.
Empirical therapy is therapy that is carried out before the
identification of pathogenic bacteria that cause infection is known. In
general, empirical therapy uses broad-spectrum antibiotics that cover
gram-positive, gram-negative, and anaerobic bacteria.

Amputation Actions
The action of amputation is carried out when there is gas gangrene,
the infected tissue, to stop the expansion of the infection, remove the part
of the foot that has a recurrent ulcer. Severe complications of foot
infection in DM patients are necrotic fasciitis and gangrene gas. In such
circumstances emergency surgery is needed in the form of amputation.
Amputation aims to eliminate pathological conditions that interfere with
function, causes of disability or eliminate the cause.

IX. PROGNOSIS
Mortality in people with diabetes and foot ulcers is often the result
of associated large vessel arteriosclerotic disease involving the coronary or
renal arteries. Limb loss is a significant risk in patients with diabetic foot
ulcers, particularly if treatment has been delayed. Diabetes is the
predominant etiology for nontraumatic lower extremity amputations in the
United States. Half of all nontraumatic amputations are a result of diabetic
foot complications, and the 5-year risk of needing a contralateral
amputation is 50%.
In diabetic people with neuropathy, even if successful management
results in healing of the foot ulcer, the recurrence rate is 66% and the
amputation rate rises to 12%.
REFERENCES

 http://herryyudha.blogspot.com/2015/02/diagnosis-dan-penatalaksanaan-
ulkus.html
 https://emedicine.medscape.com/article/460282-overview
 Waspaji S. Kaki Diabetes. Dalam: Sudoyo A dkk, eds. Buku Ajar Ilmu
Penyakit Dalam jilid III edisi IV. Jakarta: FKUI press, 2007;1911.
 Konsensus PERKENI tahun 2011
 Suyono, Slamet. 1998. Masalah Diabetes di Indonesia dalam Buku Ajar
Ilmu Penyakit Dalam Jilid 1 edisi ketiga. Jakarta. Penerbit FKUI.
 Soegondo, Sidartawan Dr, dkk. 2011. Penatalaksaan Diabetes Mellitus
Terpadu,
 Pedoman penatalaksanaan kaki diabetic, oleh consensus PERKENI

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