SURGERY
DIABETIC FOOT INFECTION
GENERAL DATA: Quijote, Isabelito Dacal Dacal ,
a 61 years old , male, married , Filipino , Catholic,
born on 02/14/1964 and staying in San Antonio,
Jagobiao, Mandaue City , Cebu .
Admitting for the first time in our institution.
CHIEF COMPLAINT : Dyspnea and
Chest Discomfort
HISTORY OF PRESENT ILLNESS :
2 Weeks prior to admission , patient noted to have small
wound on his Right foot which gradually increases the size
and no pus noted , no itching and no bleeding noted and
associated with intermittent, nonradiating pain with the pain
score of 3-4/10 .No fever , vomitings , cough noted. No
medications taken . No consult done.
Hours prior to admission, patient noted to have
dyspnea associated with chest discomfort and
bipedal edema . No medications taken . No consult done .
Persistence of symptoms prompted to consult our
institution. Thus this Admission.
PAST MEDICAL HISTORY:
1. Patient has Diabetes Mellitus for the past 10 years . So he is under medication of Metformin and Gliclazise for the pa
2. Hypertension: Since one year Patient was diagnosed with hypertension. Losartan was taken for management.
PERSONAL AND SOCIAL HISTORY: Has 4 members in the family.
His wife and 2 children. Patient Claims that his wife died of hypertension last Aug 2024 and she had the BP range of 16
He had 2 children a male and female and they both were married.
The patient is catholic.
The patient had studied only at his 15 year's of age.
His occupation is Carpenter. He has no pet animals in his home and
lives alone.
Family History
Patient Mother and Sister are Diabetic
Patient Mother are Hypertensive
Other Family Members don't have any other history of comorbidities
Review of Systems
General: (-) fever , (-) vomiting, (-) cough, (-) dizziness, (-) dsypnea
Skin: (-) Pallor, (-) Skin lesions, (-) lacerations, (-) Bruising (-) rashes
Head: (-) Injury
Eyes: (-) Pain, (-) acuity change
ENT: (-) Earache, (-) Nasal Discharge, (-) Sore throat
Nexk: (-) Tenderness, (-) Swelling, (-) Neck pain (-) Thyromegaly
CVS: (-) Chest pain, (-) Palpations, (-) Orthopnea, (-) Syncope
Lungs: (-) Cough, (-) SOB, (-) Sputum, (-) Wheezing, (-) Hemoptysis
GI: (-) Vomiting, (-) Nausea, (-) Diarrhea, (-) Hematochezia, (-) Melena
Review of Systems
GUT: (-) Dysuria, (-) Urgency, (-) Frequency, (-) Nocturia, (-) Flank Pain, (-)
Hematuria, (-) Abnormal Genital discharge, (-) Abnormal bleeding
Musculoskeletal: (+) Knee pain, (-) Back problems
Neurological: (-) Focal weakness, (-) Headache, (-) Seizure, (-) Dizziness,
(-) Numbness
Psychiatric: (-) Depression, (-) Anxiety, (-) Suicidal ideation, (-) Homicide,
(-) Paranoia
Hematopoietic: (-) Brusing, (-) Adenopathy
Endocrine: (-) Polyuria, (-) Polydipsia
Immunology: (-) Urticaria, (-) Hay fever
PHYSICAL EXAMINATION
S: (-) fever , (-) vomiting, (-) cough, (-) dizziness, (-) dsypnea
O: Awake, alert, NIRD
Skin: good turgor, warm to touch, (-) rashes, (-) pallor
HEENT: AS, PPC, no nasal or oral discharges, lymphadenopathy
C/L: clear breath sounds, equal chest expansion, (-) retractions
CVS: DHS, (-) murmurs
ABD: (-) tenderness, soft, flabby, NABS
EXT: (+) wound on right foot, (+) bipedal edema
Diagnostic
Tests
ULTRASONOGRAPHY IMPRESSION
1. Cholelithiases with no signs of cholecystitis. 2. Normal sized kidneys suggestively increased parenchymal
echogenicity which may represent normal variance, infection or early nonspecific medical renal disease.
3. Unremarkable sonographic study of the liver, biliary ducts, visualized pancreas and spleen.
4. Underfilled urinary bladder.
5. Normal sized prostate gland with no focal lesion seen.
6. Minimal ascites.
ARTERIAL LOWER DUPLEX SCAN
ATHEROSCLEROTIC LOWER EXTREMITY ARTERIAL DISEASE WITH NO EVIDENCE OF HEMODYNA
SIGNIFICAN
STENOSIS OF THE BILATERAL LOWER EXTREMITIES.
VENOUS LOWER DUPLEX SCAN
No evidence of acute deep vein thrombosis of the bilateral lower extremities.x
RIGHT: Deep vein valve reflux of the posterior tibial vein. Superficial vein valve reflux of the gre
saphenous vein.
LEFT: Deep vein valve reflux of the posterior tibial vein. Superficial vein valve reflux of the great
saphenous vein.
2-D Echo
Concentric left ventricular hypertrophy with normal wall motion, contractility, and systolic function but with
Doppler evidence of grade 1 diastolic dysfunction.
Mitral sclerosis.
Aortic sclerosis.
Mild mitral regurgitation.
Moderate tricuspid regurgitation.
Mild pulmonary hypertension with pulmonic regurgitation.
Compared with previous study, present study showed no significant change except for the moderate tricuspid
regurgitation, mild pulmonary hypertension and minimal pericardial effusion.
IMPRESSION
NON-HEALING WOUND RIGHT FOOT
Uncomplicated wounds heal within 4 to 6 weeks. If they continue to remain
nonhealing beyond this time, they are termed chronic. Several local and systemic
factors affect the inflammatory phase of wound healing directly. These include
pressure, tissue hypoxia, infection, tissue contamination, desiccation, and
maceration. Systemic factors include age, stress, and comorbid conditions such as
diabetes, vascular insufficiency, immunocompromise, malnourishment, obesity, and
smoking.
In all nonhealing chronic wounds is the persistence of proinflammatory conditions.
These specific tissue deficits result in a chronic cycle of chronically migrating
inflammatory cells (PMNs, macrophages) that scavenge early healing tissue, degrade
the newly formed matrix proteins, and then cyclically recover only to restart the
inflammatory phase. This cycle leads to a chronically unstable wound that is unable to
progress to the next phases of healing: cell proliferation, tissue remodeling, and
resolution.
DIFFERENTIAL DIAGNOSIS
DIFFERENTIAL DIAGNODIS RULE IN RULE OUT
presence of ulcer on foot
reduced sensation
1. Diabetic foot ulcer disease Not applicable
poor glycemic control
diabetic retinopathy
Total lymphocyte count is
2. osteomylitis presence of chronic wound
not raised
history of hypertension
duplex studies didnt show
3. Peripheral arterial disease raised total cholesterol
arterial stenosis
decrease pulses in lower extremities
FINAL DIAGNOSIS
Non healing wound right foot; Diabetes
mellitus type 2 -uncontrolled; T/C Diabetic
Nephropathy
MANAGEMENT
1. Insulin 70/30- 18 u SC before breakfast
2. Linaglitin 5 mg - take one tab orally once a day
* Type of infection; likely bacteria; Antibiotic
cholea
1. Mild; Gram positive coil- eg: staph aureus;
Cephalexin I, clindamycin
2. Moderat; Gram positive, Gram nnegative-
anaerobic; Ampicillin- salbutamol
3. Severe; MRSA pseudomonas- anaerobes;
MEDS AS FOLLOWS
1. Telmisartan 80mg- take 1 tab orally once a day
2. Aclepromiol 100mg/tab- take 1 tab daily once a day
3. Sodium bicarbonate 650mg- take 2 tab twice a day
4. silver sulfadiazonecream- apply it 2 times a day in affected area
5. Daily wound dressing.
DISCUSSION
INTRODUCTION
DM is the leading cause of nontraumatic lower extremity amputation
in the United States. Foot ulcers and infections are also a major
source of morbidity in individuals with DM. The reasons for the
increased incidence of these disorders in DM involve the interaction
of several pathogenic factors which allows the patient to sustain
major or repeated minor trauma to the foot, often without
knowledge of the injury. More than 60% of nontraumatic lower
extremity amputations occur in diabetics. The age-adjusted lower
extremity amputation rate in diabetics (5.0 per 1000 diabetics) was
approximately 28 times that of people without diabetes (0.2 per
1000 people)
PATHOPHYSIOLOGY
The pathophysiology of primary diabetic lower limb complications has three main components:
(a) peripheral neuropathy (motor, sensory, and autonomic),
(b) peripheral vascular disease
(c) immunodeficiency
Altered foot biomechanics and gait caused by painless collapse of ligamentous support, foot
joints, foot arches change weight-bearing patterns. Blunted pain allows cutaneous ulceration to
begin.With breakdown of the skin barrier function, polymicrobial infections become established.
Bacterial invasion is often fostered by poor blood supply due to peripheral vascular disease
coupled with microangiopathy. Finally, local host defenses may be less effective in resisting
bacteria because of poor blood supply and impaired cellular function. Cutaneous ulcerations
may progress painlessly to involve deeper soft tissues and bone. The ultimate endpoint of this
process is such severe tissue damage that extremity amputation is the only treatment
remaining.
RISK FACTOR
Risk factors for diabetic foot infection are
(1) peripheral motor, sensory, and autonomic neuropathy
(2) neuro-osteoarthropathic deformities
(3) arterial insufficiency
(4) uncontrolled hyperglycemia
(5) disabilities such as reduced vision
(6) maladaptive behavior.
DIABETIC FOOT CLASSIFICATION
WAGNER'S CLASSIFICATION
PEDIS CLASSIFICATION
TEXAS CLASSIFICATION
WAGNER'S CLASSIFICATION
Grade 0: No ulceration
Grade 1: Superficial ulceration
Grade 2: Deep ulceration exposing tendons and joints
Grade 3: Extensive ulceration involving bone
Grade 4: Gangrene
Grade 5: Extensive necrosis of foot
Classification of ulceration
Wagner grade 0 foot:
Diabetic foot without ulceration but with one or more risk factors such as bony deformities,
atrophic fat pad, plantar flexed metatarsals, PVD and Charcot joint disease.
Grade 1 foot:
Grade 1 ulceration implies presence of peripheral sensory neuropathy and at least one other
risk factor such as bony deformities, plantar flexed metatarsals with distally displaced fat pad,
limited joint mobility or ill fitting shoes.
It extends to the dermis but not beyo
nd.
Grade 2 foot:
Failure to adequately off-load grade 1 lesions lead to deepening ulcerations beyond the level
of dermis.
Deeper structures such as tendons or joint capsule may be involved.
Grade 3 foot:
Grade 2 ulceration that has not responded to local care or been neglected.
These ulceration involve bone and therefore require surgical debridement and
reconstructive su
rgery
Grade 4 foot:
Gangrenous change in lower extremity can occur in 2 ways:
When gangrene results from arterial insufficiency, revascularization should be performed.
DSA is used to assess the level of revascularization. Once revascularization has been
performed, an amputation at the most distal level should be performed.
Grade 5 foot:
Extensive necrosis of the foot
PEDIS CLASSIFICATION
Here's a breakdown of the PEDIS classification:
1. Perfusion (P): Assesses blood flow to the foot.
P0: Normal blood flow (e.g., palpable pulses).
P1: Mild ischemia (e.g., reduced or absent pulses).
P2: Moderate ischemia (e.g., cool foot, cyanosis).
P3: Severe ischemia (e.g., gangrene, non-healing ulcer).
2. Extent/Size (E): Measures the size of the ulcer.
E0: Ulcer less than 1 cm².
E1: Ulcer greater than 1 cm².
3. Depth/Tissue Loss (D): Determines how deep the ulcer penetrates.
D0: Superficial ulcer (confined to skin).
D1: Ulcer extending to tendon, capsule, or periosteum.
D2: Ulcer penetrating to bone or joint.
D3: Ulcer affecting bone or joint (osteomyelitis).
4. Infection (I): Evaluates the presence and severity of infection.
I0: No signs of infection.
I1: Mild infection (e.g., cellulitis).
I2: Moderate infection (e.g., abscess).
I3: Severe infection (e.g., osteomyelitis).
5. Sensation (S): Checks the patient's ability to feel sensation in the foot.
S0: Normal sensation.
S1: Mild loss of sensation (e.g., decreased sensation to touch or vibration).
S2: Moderate loss of sensation (e.g., unable to feel a 10-gram monofilament).
S3: Severe loss of sensation (e.g., absent sensation).
How to use the PEDIS score:
The overall PEDIS score is calculated by adding the individual scores for each category. A
higher score indicates a more severe ulcer, increasing the risk of non-healing, amputation, or
death. For example, a score of 7 or higher is considered a high-risk ulcer, indicating the need
for more aggressive treatment.
TEXAS CLASSIFICATION
Diabetic Foot Treatment
TREATMENT AND MANAGEMENT
1. Blood Sugar Control
Maintain strict blood glucose levels to promote healing.
2. Wound Care
Regular cleaning with saline.
Debridement (removal of dead tissue).
Moist wound dressing application.
3. Infection Management
Oral or IV antibiotics depending on severity.
Hospital admission if deep or spreading infection.
4. Offloading Pressure
Total contact casting, specialized footwear, or crutches to minimize pressure on ulcers.
5. Surgical Intervention
Drainage of abscesses.
Removal of necrotic tissue.
Vascular surgery if poor blood flow.
Amputation as a last resort.
RECONSTRUCTIVE OPTIONS FOR DIABETIC FOOT
Skin grafts might be indicated at times but cannot be expected
to provide durable coverage in weight-bearing or high-shear
areas. Local and regional flaps can be considered if the
extremity is free of significant occlusive peripheral vascular or
combined with vascular bypass. Microvascular free tissue
transfers are appropriate when defects are large or when local
flaps are not available. Combination lower extremity bypass
and free flap coverage has proved beneficial for the treatment
of the diabetic foot in terms of healing and reduction of
disease progression
Complications of Diabetic Foot
COMPLICATIONS
1. Foot Ulcers
Open sores that are slow to heal.
2. Infections
Cellulitis, abscess formation, osteomyelitis (bone infection).
3. Gangrene
Tissue death due to lack of blood flow and infection.
4. Amputation
Partial or complete removal of toes, foot, or leg if severe damage occurs.
5. Charcot Foot
Deformity and weakening of bones and joints due to nerve damage.
6. Poor Wound Healing
Delayed or non-healing wounds increase risk of serious infection.
7. Sepsis
Life-threatening infection spreading through the bloodstream.
Thank You
