reconstruct

1. DIABETES MELLITUS AND
THE SURGEON
PRESENTER : DR. VIKAS KUMAR
(JR GENERAL SURGERY)
MODERATOR : DR. R.S. JHOBTA
(ASSOC.PROFF.)
IGMC, SHIMLA

2. INTRODUCTION
■ Diabetes mellitus (DM) refers to a group of common metabolic
disorders that share the phenotype of hyperglycemia.
■ Depending on the etiology of the DM, factors contributing to
hyperglycemia include reduced insulin secretion, decreased
glucose utilization, and increased glucose production.
■ DM is the leading cause of end-stage renal disease (ESRD),
nontraumatic lower extremity amputations, and adult blindness.

3. CRITERIA FOR THE DIAGNOSIS OF DIABETES MELLITUS
■ Symptoms of diabetes plus random blood glucose
concentration >200 mg/dL (11.1 mmol/L ) or
■ Fasting plasma glucose >126 mg/dL (7.0 mmol/L ) or
■ HbA1C > 6.5% or
■ Two-hour plasma glucose >200 mg/dL (11.1 mmol/L )
during an oral glucose tolerance test

4. ETIOLOGIC CLASSIFICATION OF DIABETES
MELLITUS
■ I. Type 1 diabetes (beta cell destruction, usually leading to absolute
insulin deficiency)
A. Immune-mediated
B. Idiopathic
■ II. Type 2 diabetes
(may range from predominantly insulin resistance with
relative insulin deficiency to a predominantly insulin secretory defect
with insulin resistance)

5. ■ III. Other specific types of diabetes
-A. Genetic defects of beta cell function characterized by
mutations in:
1. Hepatocyte nuclear transcription factor (HNF) 4 (MODY 1)
2. Glucokinase (MODY 2)
3. HNF-1 (MODY 3)
4. Insulin promoter factor-1 (IPF-1; MODY 4)
5. HNF-1 (MODY 5)
6. NeuroD1 (MODY 6)
7. Mitochondrial DNA
8. Subunits of ATP-sensitive potassium channel
9. Proinsulin or insulin

6. -B. Genetic defects in insulin action
1. Type A insulin resistance
2. Leprechaunism
3. Rabson-Mendenhall syndrome
4. Lipodystrophy syndromes
-C. Diseases of the exocrine pancreas —pancreatitis, pancreatectomy,
neoplasia, cystic fibrosis, hemochromatosis
-D. Endocrinopathies—acromegaly, Cushing's
syndrome,glucagonoma,
hyperthyroidism,
pheochromocytoma,

7. -E. Drug- or chemical-induced —glucocorticoids, beta-adrenergic
agonists, thiazide, protease inhibitors, antipsychotics
- F. Infections—congenital rubella, cytomegalovirus, coxsackievirus
-G. Uncommon forms of immune-mediated diabetes— "stiff-person"
syndrome, anti-insulin receptor antibodies
- H. Other genetic syndromes sometimes associated with diabetes
— Wolfram's syndrome, Down's syndrome, Klinefelter's
syndrome, Turner's syndrome,
IV. Gestational diabetes mellitus (GDM)

8. TYPE 1 DM
■ Type 1 DM is the result of interactions of genetic, environmental,
and immunologic factors that ultimately lead to the destruction of the
pancreatic beta cells and insulin deficiency.
GENETIC CONSIDERATIONS
■ Susceptibility to type 1 DM involves multiple genes.
■ The concordance of type 1 DM in identical twins ranges
between 40 and 60%
■ The major susceptibility gene for type 1 DM is located in
the HLA region on chromosome 6.

9. IMMUNOLOGIC MARKERS
■ Islet cell autoantibodies (ICAs) are a composite of several different
antibodies directed at pancreatic islet molecules such as GAD,
insulin, IA-2/ICA-512, and ZnT-8, and serve as a marker of the
autoimmune process of type 1 DM.
■ Assays for autoantibodies to GAD-65 are commercially available.
ENVIRONMENTAL FACTORS
■ Numerous environmental events have been proposed to trigger the
autoimmune process in genetically susceptible individuals
■ Putative environmental triggers include viruses (coxsackie, rubella,
enteroviruses most prominently), bovine milk proteins,etc

10. TYPE 2 DM
■ Insulin resistance and abnormal insulin secretion
are central to the development of type 2 DM
GENETIC CONSIDERATIONS
■ Type 2 DM has a strong genetic component. The concordance of type 2 DM in
identical twins is between 70 and 90%.
■ The disease is polygenic and multifactorial. The genes that predispose to type 2 DM
are incompletely identified.
ENVIRONMENTAL FACTORS
■
■
■
obesity,
nutrition, and
physical activity

11. RISK FACTORS FOR TYPE 2 DIABETES MELLITUS
■ Family history of diabetes (i.e., parent or sibling with type 2 diabetes)
■ Obesity (BMI > 25 kg/m2)
■ Physical inactivity
■ Race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific
Islander)
■ Previously identified with IFG, IGT, or an A1C of 5.7–6.4%
■ History of GDM or delivery of baby >4 kg (9 lb)
■ Hypertension (blood pressure 140/90 mmHg)
■ HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250 mg/dL
(2.82 mmol/L)
■ Polycystic ovary syndrome or acanthosis nigricans
■ History of cardiovascular disease

12. COMPLICATIONS OF DM
I) ACUTE
Diabetic ketoacidosis (DKA) and
Hyperglycemic hyperosmolar state (HHS)
■
■
II) CHRONIC
A) Microvascular
Eye disease
Retinopathy (nonproliferative/proliferative)
Macular edema
Neuropathy
Sensory and motor (mono- and polyneuropathy)
Autonomic
Nephropathy
□
□
□

13. B) Macrovascular
□ Coronary heart disease
□ Peripheral arterial disease
□ Cerebrovascular disease
C) Others
□ Gastrointestinal (gastroparesis, diarrhea)
□ Genitourinary (uropathy/sexual dysfunction)
□ Dermatologic
□ Infectious
□ Cataracts
□ Glaucoma
□ Periodontal disease
□ Hearing loss

14. DM AND THE SURGEON
I) EMERGENCY
□Emphysematous infections
□DKA and HHS
II) ELECTIVE
□Perioperative mgmt
□Diabetic foot
□Surgical treatment

15. APPROACH TO THE PATIENT
HISTORY
In a patient with established DM, the initial assessment should include :
■
■
■
■
■
■
■
prior diabetes care,
the type of therapy,
prior A1C levels,
self-monitoring blood glucose results,
frequency of hypoglycemia,
presence of DM-specific complications, and
assessment of the patient's knowledge about diabetes, exercise,
and nutrition
presence of DM-related comorbidities should be sought
(cardiovascular disease, hypertension, dyslipidemia )
■

16. PHYSICAL EXAMINATION
In addition to a complete physical examination, special attention should
be given to DM-relevant aspects such as
■
■
■
■
■
■
■
■
Weight or BMI,
Retinal examination,
Orthostatic blood pressure,
Foot examination,
Peripheral pulses,
Insulin injection sites
Neurological examination
Cardiovascular examination (Blood pressure >130/80 mmHg is
considered hypertension in individuals with diabetes)
Teeth and gums
■

17. LABORATORY ASSESSMENT
■
■
■
■
■
■
■
■
■
CHG
FBS
RFT/e
LFT
HbA1C
URINE R/M and for microalbumin (30-300mg/24hr)
LIPID PROFILE
FUNDUS EXAM.
THYROID FXN
IMAGING STUDIES
■
■
CXR
ECHO

18. EMERGENCY CONDITIONS
SPECIFIC EMERGENCIES :
■ EMPHYSEMATOUS CHOLECYSTITIS
■ EMPHYSEMATOUS PYELONEPHRITIS
AND CYSTITIS
■ DIABETIC KETOACIDOSIS
■ HYPEROSMOLAR HYPERGLYCEMIA
SYNDROME

19. I) EMPHYSEMATOUS CHOLECYSTITIS
■ Emphysematous cholecystitis is an uncommon condition
characterized by infection of the gallbladder wall by gas-
forming bacteria, particularly anaerobes.
■ Pt. presents as acute cholecytitis
■ Gangrene and perforation commonly complicate the
course of emphysematous cholecystitis.

20. ■ Pockets of gas are evident in the area of the gallbladder
fossa on plain abdominal films, ultrasonography, and
abdominal CT.
■ Emergency antibiotic therapy with anaerobic coverage
and early cholecystectomy are warranted because the
risk of gallbladder perforation is high

23. II) EMPHYSEMATOUS PYELONEPHRITIS AND
CYSTITIS
■ Emphysematous cystitis and pyelonephritis are acute
necrotizing infections characterized by gas formation in
the tissues.
■ Gas is localized to the bladder wall and lumen in cystitis
and in and around the kidney in pyelonephritis.

24. ■ Emphysematous pyelitis is a gas-forming infection
restricted to the collecting system; the renal parenchyma
is spared.
■ E. coli is most commonly identified. Klebsiella and
Proteus are less common.
■ Almost all patients display the classic triad of fever,
vomiting, and flank pain in pyelonephritis.
■ Pneumaturia and irritative lower tract voiding symptoms
in cystitis.

25. ■ The diagnosis is established radiographically.
■ Tissue gas that is distributed in the parenchyma may appear on
abdominal radiographs as mottled gas shadows over the involved
kidney
■ A crescentic collection of gas over the upper pole of the kidney is
more distinctive.
■
CT is the imaging procedure of choice

27. ■ Emphysematous pyelonephritis is a surgical emergency.
■ Currently, percutaneous drainage is the recommended
initial approach because it is reported to be associated
with lower mortality rates than is medical management
alone or emergency nephrectomy

28. III) DIABETIC KETOACIDOSIS AND HYPEROSMOLAR
HYPERGLYCEMIA SYNDROME
■ DKA results from relative or absolute insulin deficiency combined
with counterregulatory hormone excess (glucagon, catecholamines,
cortisol, and growth hormone).
■ Surgery should be delayed, whenever feasible, in patients with DKA,
so that the underlying acid-base disorder can be corrected or, at
least, ameliorated.
■ Patients with HHS are markedly dehydrated and should be restored
quickly to good volume and improved metabolic status before
surgery.

29. ■ Precipitating events
□
□
□
□
□
Inadequate insulin administration
Infection
Infarction
Drugs (cocaine)
Pregnancy

30. ■ Symptoms
□ Nausea/vomiting
□ Thirst/polyuria
□ Abdominal pain
□ Shortness of breath
■ Physical Findings
□ Tachycardia
□ Dehydration/hypotension
□ Tachypnea/Kussmaul respirations/respiratory distress
□ Abdominal tenderness (may resemble acute pancreatitis or
surgical abdomen)
□ Lethargy/obtundation/cerebral edema/possibly coma

31. ■ DKA is characterized by hyperglycemia, ketosis, and
metabolic acidosis (increased anion gap) along with a
number of secondary metabolic derangements.
Management of Diabetic Ketoacidosis
1. Confirm diagnosis ( plasma glucose, positive serum
ketones, metabolic acidosis).
2. Admit to hospital; intensive-care setting may be
necessary for frequent monitoring or if pH <7.00 or
unconscious.

32. 3. Assess:
Serum electrolytes (K+, Na+, Mg2+, Cl–, bicarbonate, phosphate)
Acid-base status—pH, HCO3–, PCO2, -hydroxybutyrate
■
■
■ Renal function (creatinine, urine output)
4. Replace fluids: 2–3 L of 0.9% saline over first 1–3 h (15–20 mL/kg
per hour); subsequently, 0.45% saline at 250–500 mL/h; change to
5% glucose and 0.45% saline at 150–250 mL/h when plasma
glucose reaches 200 mg/dL (11.2 mmol/L).

33. 5. Administer short-acting insulin: IV (0.1 units/kg), then 0.1 units/kg
per hour by continuous IV infusion; increase two- to threefold if no
response by 2–4 h.
6. If the initial serum potassium is <3.3 mmol/L (3.3 meq/L), do not
administer insulin until the potassium is corrected. If the initial
serum potassium is >5.2 mmol/L (5.2 meq/L), do not supplement
K+ until the potassium is corrected.

34. 7. Assess patient: What precipitated the episode
(noncompliance, infection, trauma, infarction, cocaine)?
Initiate appropriate workup for precipitating event
(cultures, CXR, ECG).
8. Measure capillary glucose every 1–2 h; measure
electrolytes (especially K+, bicarbonate, phosphate) and
anion gap every 4 h for first 24 h.
9. Monitor blood pressure, pulse, respirations, mental
status, fluid intake and output every 1–4 h.

35. 10. Replace K+: 10 meq/h when plasma K+ < 5.0–5.2 meq/L (or 20–
30 meq/L of infusion fluid), administer 40–80 meq/h when plasma
K+ < 3.5 meq/L or if bicarbonate is given.
11. Continue above until patient is stable, glucose goal is 150–250
mg/dL, and acidosis is resolved. Insulin infusion may be
decreased to 0.05–0.1 units/kg per hour.
12. Administer long-acting insulin as soon as patient is eating. Allow
for overlap in insulin infusion and SC insulin injection.

36. ELECTIVE CONDITIONS
I) PERIOPERATIVE MGMT.
II) DIABETIC FOOT
III) SURGICAL TREATMENT

37. PERIOPERATIVE MGMT.
I) TYPE I DM
■ Insulin-treated patients undergoing major elective surgery
should preferably be admitted 2–3 days before surgery.
■ For elective procedures, the basal insulin should be given at
80% to 100% of the usual dose the evening before surgery, with
an insulin infusion initiated the morning of surgery.
■ Even with normal basal insulin the night before surgery, low
dose IV insulin will be required, and it is usually begun when the
blood glucose level rises above 130 mg/dL.

38. ■ Intravenous infusion of insulin, glucose, and potassium is
now standard therapy and has replaced subcutaneous
insulin therapy for the perioperative management of
diabetes.
■ Adequate fluids must be administered to maintain
intravascular volume.
■ The preferred fluids are normal saline and dextrose in
water.
■ Fluids containing lactate (i.e., Ringer’s lactate) cause
exacerbation of hyperglycemia.

39. ■ Insulin
-Two main methods of insulin delivery
have been used: either combining insulin with glucose
and potassium in the same bag (the GIK regimen) or
giving insulin separately as an infusion.
-Various regimens have been proposed for insulin
infusion.
-Regardless of whether separate or combined
infusions are given, close monitoring is required during
these infusion regimens.

40. Regimen for Separate Intravenous Insulin Infusion for
Perioperative Diabetes Management
■ Prepare a 0.1 unit/ml solution by adding 25 units regular insulin to 250 ml normal saline.
■ Flush 50 ml of insulin solution through infusion tubing to saturate nonspecific binding sites.
■ Set initial infusion rate (generally, 0.5-1.0 unit/h [5-10 ml/h]
■ Adjust infusion rate according to bedside blood glucose measurement as follows:
■ Blood Glucose (mg/dl)
<80
80–140
141–180
181–220
221–250
251–300
>300
Insulin Infusion Rate
Check glucose after 15 min
Decrease infusion by 0.4 unit/h(4ml/h)
No change
Increase infusion by 0.4 unit/h (4 ml/h)
Increase infusion by 0.6 unit/h (6 ml/h)
Increase infusion by 0.8 unit/h (8 ml/h)
Increase infusion by 1 unit/h (10 ml/h)

41. ■ Glucose
□Adequate glucose should be provided to
prevent catabolism, starvation ketosis, and
insulin-induced hypoglycemia.
□The physiological amount of glucose required
to prevent catabolism in an average
nondiabetic adult is ~120 g/day (or 5 g/h).

42. □ With preoperative fasting, surgical stress, and
ongoing insulin therapy, the caloric requirement in
most diabetic patients averages 5–10 g/h glucose.
□ This can be given as 5 or 10% dextrose. An infusion
rate of 100 ml/h with 5% dextrose delivers 5 g/h
glucose.
□ If fluid restriction is necessary, the more concentrated
10% dextrose can be used.

43. □ Many now prefer to give 10% dextrose at a starting
rate of ~100 ml/h.
□ The usual range of perioperative blood glucose that
clinicians are comfortable with is ~120–180 mg/dl.
□ The insulin and glucose infusion rates should be
adjusted accordingly if blood glucose monitoring
shows marked deviation from the acceptable range.

44. Potassium
□ The infusion of insulin and glucose induces an intracellular
translocation of potassium, resulting in a risk for hypokalemia.
□ In patients with initially normal serum potassium, potassium
chloride, 10 mEq, should be added routinely to each 500 ml of
dextrose to maintain normokalemia if renal function is normal.
□ Hyperkalemia and renal insufficiency are contraindications to
potassium infusion.

45. II) TYPE II DM
■ Patients Treated With Oral Antidiabetic
Agents
□ Second-generation sulfonylureas should be discontinued 1 day
before surgery, with the exception of chlopropramide, which
should be stopped 2–3 days before surgery.
□ Other oral agents can be continued until the operative day.

46. □ These should be taken the evening before surgery
and omitted on the morning of surgery.
□ Metformin should be withhold 1–2 days before
surgery, especially in sick patients and those
undergoing procedures that increase the risks for
renal hypoperfusion, tissue hypoxia, and lactate
accumulation.

47. □ At a minimum, blood glucose should be monitored before and
immediately after surgery in all patients.
□ Those undergoing extensive procedures should have hourly
glucose monitoring during and immediately following surgery.

48. □ Bedside capillary blood glucose meters are adequate
for these monitoring requirements.
□ The recommended treatment for patients undergoing
major surgery and for those with poorly controlled
type 2 diabetes (i.e.>200 mg%) is intravenous insulin
infusion with glucose.

49. INTRAOPERATIVE
■ Insulin infusion regimen is continued
■ Look for complications :
□ Hypoglycemia
□ Arrythmias
□ Silent MI
□ Hypotension
□ Decrease urine output if nephropathy +

50. POSTOPERATIVE MANAGEMENT
■ The ideal time to transition from IV insulin to
subcutaneous insulin depends on several factors:
□ the presence of postoperative nausea and vomiting,
□ a planned subcutaneous regimen,
□ the meal schedule, and
□ discharge considerations.
■ For patients receiving an insulin infusion who were
previously well controlled on oral agents the oral
medication can be administered and 1 hour later the
insulin infusion can be discontinued.

51. ■ Of note, metformin should not be restarted until 48 hours after the
procedure and not until normal renal function has been confirmed
■ For patients receiving an insulin infusion who are not well controlled
on oral agents prior to admission or who are requiring more than
two to three units of insulin per hour, a transition to subcutaneous
insulin postoperatively is recommended.

52. ■ The total daily insulin requirement can be estimated by
taking the infusion rate for the preceding 4 to 8 hours
and extrapolating this dose to a 24-hour amount.
■ This should be reduced empirically by 40% to address
the acute stress of surgery and thus avoid hypoglycemia.

53. ■ If the plan is to use a long-acting analogue (eg. Glargine ) for basal
insulin and a rapid-acting analogue (eg. Lispro,aspart) for meals,
half of the total insulin requirement can be given as the long-acting
analogue, the remaining half being divided and given as a rapid-
acting analogue prior to each meal.
■ INSULIN BY SLIDING SCALE IS NOT RECOMMENDED

54. DIABETIC FOOT

55. INTRODUCTION
■ Of all the late complications of diabetes, foot problems
are probably the most preventable.
■ Foot ulceration is common and occurs in both T1DM
and T2DM.
■ Approximately 5% to 10% of diabetic patients have had
past or present foot ulceration, and 1% have undergone
amputation.

56. ■ Diabetes is the most common cause of nontraumatic
lower limb amputation.
■ Rates are 15 times greater than those in the nondiabetic
population.
■ The lifetime risk for development of a foot ulcer in a
diabetic patient is estimated to be as high as 25%.

57. RISK FACTORS
■ Diabetic Neuropathy
■ Peripheral Vascular Disease
■ Past Foot Ulceration or Foot Surgery
■ Retinopathy and renal dysfunction
■ Callus,
■ Deformity, and
■ High Foot Pressures

58. I) NEUROPATHY
■ Changes in the vasonervorum with resulting ischemia ? cause
□ Increased sorbitol in feeding vessels block flow and causes nerve
ischemia
Intraneural acculmulation of advanced products of glycosylation
□
■ Abnormalities of all three neurologic systems contribute to ulceration
A) Autonomic Neuropathy
□
□
Regulates sweating and perfusion to the limb
Loss of autonomic control inhibits thermoregulatory
function and sweating

59. ■ Result is dry, scaly and stiff skin that is prone to
cracking and allows a portal of entry for bacteria
B) Motor Neuropathy
□ Mostly affects forefoot ulceration
■ Intrinsic muscle wasting – claw toes
■ Equinous contracture

60. C) SENSORY NEUROPATHY
□ Loss of protective sensation
□Starts distally and migrates proximally in
“stocking” distribution
□ Large fibre loss – light touch and
proprioception
□Small fibre loss – pain and temperature
□Usually a combination of the two

61. ■ Two mechanisms of Ulceration
□Unacceptable stress few times
■ rock in shoe, glass, burn
□Acceptable or moderate stress repeatedly
■ Improper shoe ware
■ deformity

62. II) VASCULAR DISEASE
■ 30 times more prevalent in diabetics
■ Diabetics get arthrosclerosis obliterans or “lead pipe
arteries”
■ Calcification of the media
■ Often increased blood flow with lack of elastic properties
of the arterioles
■ Not considered to be a primary cause of foot ulcers

63. ■ However, the common combination of vascular
disease with minor trauma can lead to
ulceration.
■ Minor injury and subsequent infection increase
the demand for blood supply beyond the
circulatory capacity, and ischemic ulceration and
risk of amputation develop.

64. RECOMMENDED EVALUATION OF A
DIABETIC FOOT
■ Describe the lesion (cellulitis, ulcer, etc.) and any drainage
(serous,purulent, etc.).
■ Enumerate the presence or absence and degree of various signs of
inflammation.
■ Define whether or not infection is present and attempt to determine
probable cause.
■ Examine the soft tissue for evidence of crepitus, abscesses, sinus
tracts, foreign bodies.

65. ■ Probe any skin breaks with sterile metal probe to see
whether bone is exposed or palpable.
■ Measure the wound (length * width; estimate depth);
consider taking photograph.
■ Palpate and record pedal pulses; use Doppler instrument
if necessary.
■ Evaluate neurological status: protective sensation, motor
and autonomic function.

66. ■ Cleanse and debride the wound; remove any foreign
material, eschar, or callus.
■ Culture the cleansed wound (preferably by curettage,
aspiration, rather than swab).
■ Order plain radiographs of the infected foot in most
cases; consider other imaging as needed.
■ Consider which consultants might need to see the
patient and how quickly.

67. CLASSIFICATION OF FOOT ULCERS
I) WAGNER DIABETIC FOOT ULCER CLASSIFICATION SYSTEM
Grade
0
Description
No ulcer, but high-risk foot (e.g., deformity,
callus, insensitivity)
1 Superficial full-thickness ulcer
2 Deeper ulcer, penetrating tendons, no bone
involvement
3 Deeper ulcer with bone involvement, osteitis
4 Partial gangrene (e.g., toes, forefoot)
5 Gangrene of whole foo

68. II) UNIVERSITY OF TEXAS WOUND CLASSIFICATION SYSTEM
Stage Grade 0 Grade 1 Grade 2 Grade 3
A Preulcer or Superficial ulcer Deep ulcer Wound
Postulcer lesion;
no skin break
to tendon or
capsule
penetrating
bone or joint
B + Infection + Infection + Infection +Infection
C + Ischemia + Ischemia + Ischemia +Ischemia
D + Infection and
ischemia
+ Infection and
ischemia
+Infection and
ischemia
+Infection and
ischemia

69. MANAGEMENT
■ ADA identified six interventions with
demonstrated efficacy in diabetic foot wounds:
(1) off-loading,
(2) debridement,
(3) wound dressings,
(4) appropriate use of antibiotics,
(5) revascularization, and
(6) limited amputation.

70. (1) OFF-LOADING
■ The TCC has long been recognized as the gold
standard for off-loading a foot wound.
■ TCCs are not usually recommended for management
of neuroischemic ulcers.
■ Removable cast walker (RCW) resulted in slower
healing than the TCC
■ Removable casts and pneumatic cast boots (Aircast)
may be used in cases without infection.

72. 2) DEBRIDEMENT
■ Almost all infected foot lesions (other than primary cellulitis)must be
debrided
■ Debridement is aimed at removing any eschar (full-thickness dead
skin), other necrotic tissue or foreign material, or surrounding callus.
■ Debridement is best done mechanically (i.e., with instruments)
rather than with enzymatic or chemical agents.

73. ■ Definitive debridement will often require more than one
session or need to be repeated at follow-up visits.
■ The presence of pus in an enclosed space requires
drainage.
■ Fulminant soft tissue infections, such as gas gangrene or
necrotizing fasciitis, require urgent debridement of
involved tissue.

74. ■ Drain any areas of suspected infection, regardless of the patient’s
circulatory status.
■ Patients with systemic toxicity will not improve until the wound has
been adequately surgically debrided and thoroughly drained.
■ One form of debridement therapy that is used in some patients with
diabetic foot wounds is so-called larval (or maggot) biotherapy.

75. ■ This form of therapy is found to be safe and
effective.
■ One study even demonstrated that fewer days of
antibiotic therapy were required in patients who
were treated with maggot debridement.

79. 3) WOUND DRESSINGS

81. 4) ANTIBIOTICS
■ Antibiotics should usually be given intravenously
for patients who
□ are systemically ill,
□ have a severe infection,
□ are unable to tolerate oral agents, or
□ are known or suspected to have pathogens that are
not susceptible to available oral agents.

82. Suggested Antibiotic Regimens for Treating Diabetic Foot Infections
Severity of Infection Recommended Alternative
Mild/moderate Cephalexin (500 mg qid); or
Amoxiclav (875/125 mg bid);or
Levofloxacin (500 mg po qd) ±
clindamycin(300 mg po tid);or
Clindamycin (300 mg tid) TMP/SMX (2 DS po bid)
Moderate/severe Ampicillin/sulbactam (2g qid); or Ertapenem (1gm qd); or
Clindamycin (450 mg po qid) +
ciprofloxacin (750 mg bid)
Linezolid (600 mg bid)
±aztreonam (2 gm tid)
Life-threatening Imipenem/cilastatin (500 mg qid) Vancomycin (15 mg/kg bid) +
Clindamycin (900 IV mg tid) +
tobramycin (5.1 mg/kg/day) + ampicillin
ceftazidime(1 gm tid) +
metronidazole(7.5 mg/kg IV qid)
(50 mg/kg IV qid)

83. ■ The selected antibiotic regimen should almost always include an
agent that is active against staphylococci and streptococci
■ For mild to moderate infections, a 1- to 2-week course while for
more serious infections, treatment has usually been given for 2 to 4
weeks.
■ Treatment of osteomyelitis should usually be parenteral (at least
initially) and prolonged for at least 6 weeks.
■ If all of the infected bone is removed, a shorter course of antibiotic
therapy (e.g., 2 weeks) might be sufficient.

84. 5) REVASCULARIZATION
■ Lower-limb vascular procedures, including angioplasty and bypass
grafting, have been shown to be safe and effective for patients with
diabetic foot infections.
■ Feet with critical ischemia that once required amputation can now
often be saved with these techniques.
■ While initial debridement must be performed even in the face of
poor arterial circulation, revascularization is generally postponed
until sepsis is controlled.

85. ■ Waiting for more than a few days in hopes of sterilizing the wound is
inappropriate, however, and can result in further tissue loss.
■ Several studies suggest that early recognition and aggressive
surgical drainage of pedal sepsis followed by surgical
revascularization are critical to achieving maximal limb salvage.
■ Long-term follow-up studies have shown that the presence of
diabetes does not influence late mortality, graft patency, or limb
salvage rates after lower-limb arterial reconstruction

86. 6) LIMITED AMPUTATION
■ Amputation may range from ray amputation of a toe to transfemoral
amputation of a limb
■ A number of factors influence level selection:
□ amputation must be done proximal to an irreparably damaged or gangrenous
body part.
□ Tissue oxygen perfusion
□ Patients with uncontrolled psychosis or a history of major noncompliance with
foot care programs
□ Nicotine addiction and poor plasma glucose control.

89. FOOT CARE
■ 1. Take care of diabetes.
■ 2. Check feet every day
■ 3. Wash your feet every day.

90. ■ 4. Keep the skin soft and smooth.
■ 5. Smooth corns and calluses gently.
■ 6. Trim toenails straight across and file
the edges with nail file.

91. ■ 7. Wear shoes and socks at all times
■ 8. Protect feet from hot and cold.
■ 9. Don’t cross legs for long periods of time.
■ 10.Don’t smoke.

92. SURGICAL TREATMENT
1) GASTRIC BYPASS AND
BILIOPANCREATIC DIVERSION
2) PANCREATIC TRANSPLANTATION
3) ISLET CELL TRANSPLANTATION