Surgical aspects of dm
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Transcript of Surgical aspects of dm
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SURGICAL ASPECTS OF DIABETES MELLITUS
Dr.Prashanth.SJunior Resident
Dept. of General Surgery
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• Perioperative management of diabetes
• Diabetic foot
• Surgical infections
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Perioperative management
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• Between 2 - 2.5 per cent of the population are known to be diabetic and there may be an equal number of undiagnosed diabetic individuals.
• Diabetes affects about one in six patients over the age of 65 years, and one in four over the age of 85 years.
• The perioperative mortality of diabetic patients varies between 4 -13%.
• Management of the diabetic patient does not only depend on the careful assessment of the state of glycaemia, but requires attention to the other sites of end-organ disease.
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• Cardiovascular system:
• 1. Hypertension - seen in 30 and 60 per cent, and may be part of the so-called syndrome X.
• Many of these hypertensive patients will have an associated autonomic neuropathy; they are at increased risk of gastroparesis and consequent aspiration, as well as sudden cardiorespiratory arrest.
• During anaesthesia, the diabetic patient with hypertension may be prone to hypotension, especially if the blood pressure was poorly controlled before the operation.
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• The combination of preoperative hypertension and intraoperative hypotension is associated with an increased incidence of postoperative renal and cardiovascular complications.
• 2. Coronary arterial disease - most common cause of death in elderly diabetic patients.
• Because of the functional denervation of the cardiac sympathetic afferent fibres, many cases of infarction are ‘silent'.
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• 3. Cardiorespiratory autonomic neuropathy - occurs in over 50 per cent of patients.
• Apart from silent ischaemia, the neuropathy may lead to orthostatic hypotension and cardiovascular instability during anaesthesia.
• Deficiency of catecholamine release associated with the induction of anaesthesia and during tracheal intubation; this may result in significant hypotension and bradycardia, especially in the presence of large doses of opioid drugs such as fentanyl.
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• Another aspect of the cardiac neuropathy is
prolongation of the QT interval, and
associated QT dispersion
has been suggested as a useful, non-invasive marker for estimating the perioperative risk of cardiac arrhythmias and sudden cardiac death.
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• Respiratory system:
• Most diabetic patients will also have a mild pulmonary restrictive defect due to reduced elastic recoil and a reduced carbon monoxide pulmonary diffusing capacity.
• The residual effects of general anaesthesia combined with the effects of major abdominal surgery can result in major postoperative respiratory complications.
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• Renal system:
• During anaesthesia, metabolic decompensation leads to hyperglycaemia, an osmotic diuresis, and marked reduction in the intravascular volume.
• As a result, renal perfusion falls and this may lead to acute perioperative renal failure, especially if the alternating combination of hypotension and hypertension is present.
• Hypoproteinaemia (as a sequel to the microalbuminuria); this will lead to increased free-drug concentrations (and hence the propensity to adverse effects).
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• Gastrointestinal system
• Delayed gastric emptying occurs in 20 to 30 per cent of all diabetic patients,( autonomic neuropathy.)
• Prescription of metoclopramide preoperatively is indicated.
• Stiff joint syndrome – 30%
• It arises from the glycosylation of tissue proteins secondary to chronic hyperglycaemia and may affect many joints of the body.(limited mobility of the temperomandibular and atlanto-occipital joints.)
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• Metabolic response to surgery
• Surgery produces a glycaemic stress response, the magnitude of which is dependent on the site and duration of surgery; the severity of the underlying pathology; and the type of diabetes.
• The main catabolic effects - adrenaline (epinephrine), noradrenaline (norepinephrine), glucagon, and cortisol.
• The diabetic patient is very unlikely to develop intraoperative hypoglycaemia unless treated with large doses of insulin.
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• Acute hyperglycaemia during surgery may result in a number of undesirable sequelae
(a) altered host defence mechanisms
(b) extracellular dehydration and electrolyte imbalance,
(c) intracellular dehydration and
(d) impaired wound healing.
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• Elective surgery in the type-II diabetic patient
• The acceptable upper limit for the fasting blood glucose is 7.8 mmol/l.
• In all patients, the oral hypoglycaemic agents should be discontinued on the morning of surgery and recommenced whenever possible the next day.
• The exceptions are those patients receiving chlorpropamide or metformin, where the longer half-lives of the drugs make it sensible for them to be discontinued on the day before surgery.
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• Most type-II diabetics have sufficient endogenous insulin secretion to carry them through minor surgery, so avoid the need for transient insulin therapy.
• For major surgery, exogenous insulin will usually be necessary to maintain glucose homeostasis.
• A threshold blood glucose of 11 mmol/l has been proposed as a suitable trigger for insulin therapy.
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• Elective surgery in the type-I diabetic patient
1. a ‘split-normal-dose' regimen where the patient receives 1/4 to 1/2 the usual morning dose of insulin plus 5 per cent dextrose solution at a rate between 100 and 200 ml/h;
2. the intensive Glucose–Insulin–Potassium regimen as described by Alberti and colleagues;
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• 3. the regular intravenous administration of boluses of insulin or an infusion of insulin with the simultaneous infusion of 5 per cent dextrose (with constant infusion of 100 ml/h of 5 per cent glucose, and adjustment of the rate of infusion of the insulin based on frequent blood glucose estimations).
• With all these methods of diabetic control, frequent blood glucose determinations are mandatory.
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• Fluid replacement should be given as normal saline.
• A higher blood glucose (and therefore higher insulin requirements) are found in patients receiving either 5 per cent dextrose or Hartmann's solution (Ringer's lactate), the latter being an important gluconeogenic precursor, especially in the starved or catabolic patient.
• The same regimen should be used for postoperative diabetic control.
• If a regimen of no insulin until the patient commences oral feeding is adopted, there is a high risk of them developing ketosis.
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• For patients undergoing surgery whilst receiving local anaesthesia alone (i.e., without sedation)
• For type I diabetes, most patients cope well if they receive between 50 to 60 per cent of their normal intermediate or long-acting insulin, if the blood glucose concentration exceeds 300 mg/dl (16.7 mmol/l).
• For type II patients, the best policy is to omit their oral medication before surgery, and then give it on return to the ward before they receive their normal diet.
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Diabetic foot
‘Diabetics should treat their Feet like they do their Face’
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Introduction
• Foot infections - among the most frequent and serious consequences of diabetes mellitus
• Responsible for more hospital days than any other complication of diabetes
• Dealing with this problem will require – Greater understanding of the pathophysiology of these infections
– Better systems for implementing proven effective measures
Lipsky BA, Berendt AR. Diabetes Metab Res Rev 2004; 20(Suppl 1): S56–S64.
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Definition
International Consensus on Diagnosing and Treating the Infected Diabetic Foot (2003)
Berendt T. Diabetic foot infection: what remains to be discovered?. FDA Anti-Infective Drugs Advisory Committee, October 2003. http://www.fda.gov/OHRMS/DOCKETS/ac/03/slides/3997S1_01_Berendt.ppt. Accessed on 24-7-06.
Any infection involving the foot in a person with diabetes originating in a chronic or acute injury to the soft tissues of the foot, with evidence of pre-
existing neuropathy and/or ischemia
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Typical Indian with diabetic foot
• First time presentation– Male with an average age of 56 yrs
– Type 2 diabetes with average duration of 12 yrs
– Most have some degree of neuropathy and few have peripheral Vascular Disease
– Common precipitating factors
Lack of footwear
Irregular foot care
Burns
Morbach S, Viswanathan . Diabet Med. 2004 Jan;21(1):91-5.
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Typical Indian with diabetic foot
• Patients requiring surgery– Majority of the patients had grade II and III ulcers (50% and
26.5%, respectively)
– Grade IV was seen in another 21.9%
• After surgery– The median healing time was 44 days
– Recurrence of infection occurred in 53%
More common in patients with neuropathy and peripheral vascular disease (PVD)
Vijay V, Narasimham DV. Diabet Med. 2000 Mar;17(3):215-8
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Pathogenesis of Diabetic foot
• Multi-factorial, Complex and still poorly understood– Neuropathy
– Vasculopathy
– Immune dysfunction
– Infection
• Prolonged Hyperglycemia contributes to all the above factors through different mechanisms
Lipsky BA. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S104-14.
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Motor Neuropathy
Sensory Neuropathy
AutonomicNeuropathy
Vasculopathy
Immune dysfunction
Complex interplay of factors
Ulbrecht JS, Cavanagh PR. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S73-82.
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Neuropathy
• Sensory– Loss of protective sensation
– Loss of position sense
• Motor– Muscle weakness
– Foot deformity
• Autonomic– Poor blood flow regulation
– Dry, stiff skin
Unaware of minor cuts/bruises
Poor weight distribution
Cracked skin allows easy entry of bacteria
Clawed toes
Prominent metatarsals
Ulbrecht JS, Cavanagh PR. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S73-82.
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Forefoot ulcer due to Neuropathy
Inappropriately high pressure distribution
Ulbrecht JS, Cavanagh PR. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S73-82.
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• Accelerated atherosclerosis
– Diabetes
– Hypertension
– Obesity
– Age
– Dyslipidemia
Decreased local blood flow
Poor wound healing
Poor antibiotic
penetration
Heel ulcer is typical of poor blood circulation due to vasculopathy
Vasculopathy
Watkins PJ. BMJ. 2003 May 3;326(7396):977-9.
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Immune dysfunction
• Impaired defenses against infection
1. Polymorphonuclear leukocyte migration
2. Phagocytosis
3. Intracellular killing
4. Chemotaxis
Geerlings SE, Hoepelman AI. FEMS Immunol Med Microbiol. 1999 Dec; 26(3-4):259-65
12
34
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Infection
– Foot infections in diabetic patients usually begin in a skin ulceration
– Most infections remain superficial, but 25% will spread contiguously from the skin to deeper subcutaneous tissues and/or bone.
– An infected foot ulcer precedes 60% of amputations, making infection perhaps the most important proximate cause of this tragic outcome.
– Because all skin wounds contain microorganisms, infection must be diagnosed clinically, that is, by the presence of systemic signs (e.g., fever, chills, and leukocytosis), purulent secretions (pus), or 2 local classical signs or symptoms of inflammation (warmth, redness, pain or tenderness, and induration).
– In chronic wounds, additional signs suggesting infection may include delayed healing, abnormal coloration, friability, or foul odor.
Lipsky BA. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S104-14.
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• Infection profile (n=775)– Polymicrobial
Average of 3.07 organisms isolated per case
71.09% aerobic
28.91% anaerobic
– Related to severity of disease
Staphylococcus and Streptococcus 50% in the first two Wagner grades and were reduced to less than one-fourth of the total organisms in the last two grades
Significant increase in the Gram-negative organisms and anaerobes in the last two grades
Pathare NA, Bal A. Indian J Pathol Microbiol. 1998 Oct;41(4):437-41.
Microbiology of Diabetic foot: India
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STAGES OF ULCER DEVELOPMENT
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STAGES OF ULCER DEVELOPMENT
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Classification
• Wagner’s Classification of diabetic ulcer
• Grade 0 — No ulcer in a high risk foot.
• Grade 1 — Superficial ulcer involving the full skin thickness but not underlying tissues
• Grade 2 — Deep ulcer, penetrating down to ligaments and muscle, but no bone involvement or abscess formation
• Grade 3 — Deep ulcer with cellulitis or abscess formation, often with osteomyelitis
• Grade 4 — Localized gangrene.
• Grade 5 — Extensive gangrene involving the whole foot.
Calhoun JH, Cantrell J. Foot Ankle. 1988 Dec;9(3):101-6.
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Examples of different grades
Hall J, Preventive foot care for diabetes patients in primary care. Pfizer. Data on file.
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Differentiation of Ischaemic and Neuropathic Ulcer
Ischaemic ulcer Neuropathic ulcerSymptoms Claudication
Rest painUsually painless
Or painful neuropathy
Inspection Dependent ruborTrophic changes
Gangrenous digits
High arch + clawing of toes
No trophic changesSurrounded by callus
Palpation ColdPulseless
Warmpalpable pulses
Ulceration Painful At the distal and over
bony prominences
PainlessSites of pressures
(metatarsal heads, heels)
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Ischaemic ulcer Neuropathic ulcer
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Principles of Management
• Multidisciplinary approach– Medical
– Surgical
– Orthopedics
• Evaluation of the patient– Look for danger signs needing urgent intervention
• Good Blood glucose control
• Long term care after wound healing is complete– Education and preventive foot care
Watkins PJ. BMJ. 2003 May 3;326(7396):977-9.
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Evaluation of the patient
Check posterior tibial pulse
Check Dorsalis pedis pulse Sensory
examination
X-ray of the foot
Select patients• Doppler study• Angiography
Watkins PJ. BMJ. 2003 May 3;326(7396):977-9.
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Danger signs for urgent action
• Redness and swelling of a foot that even when neuropathic causes some discomfort and pain; this often indicates a developing abscess, and urgent surgery may be needed to save the leg
• Cellulitis, discoloration, and crepitus (gas in soft tissues)
• Pink, painful, pulseless foot even without gangrene indicates critical ischaemia that needs urgent arterial investigation followed by surgical intervention whenever possible
Watkins PJ. BMJ. 2003 May 3;326(7396):977-9.
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Cornerstones of treatment
• Surgical debridement– Drain pus and abscess cavities and to remove all necrotic and infected tissue
including devitalised and infected bone resulting from osteomyelitis
• Eradication of infection– Antibiotic choices should optimally be based on results of culture
If empirical therapy is necessary, it should cover S. aureus and anaerobes
Broader coverage should be considered based on the history & clinical judgment
• Adjuvant therapies– Utility remains controversial
• Reduction of weight bearing forces– Bed rest with foot raised
Lipsky BA, Berendt AR. Diab Metabol Res Rev 2004; 20: S56-S64. Ulbrecht JS, Cavanagh PR. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S73-82.
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Osteomyelitis in diabetic foot infections
• Dealing with osteomyelitis is perhaps the most difficult aspect in the management of diabetic foot infections
• Presence of osteomyelitis – Increases the likelihood of surgical intervention, including amputation
– Impairs healing of the overlying wound
– Acts as a focus for recurrent infection
– Increases the required duration of antibiotic therapy
• ESR of >40 mm/h was associated with almost a 12-fold increased likelihood of osteomyelitis
• Larger ( ulcer area > 2 cm) and deeper (depth > 3 mm) increases the likelihood of osteomyelitis
Lipsky BA, Berendt AB. Clinical Infectious Diseases 2004; 39:885–910 Lipsky BA. Clinical Infectious Diseases 1997;25:1318–
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Duration of antibiotic therapy
• The optimal duration of antibiotic therapy for diabetic foot infections is unknown.
• On the basis of available studies, – Mild to moderate infections, 1 to 2 weeks is usually effective
– Serious infections, 2 to 4 weeks is usually sufficient
• Longer duration may be needed for – Immunocompromised patients, poorly perfused, deep, large or necrotic wounds,
osteomyelitis, patients who cannot (or will not) undergo surgical resection, or who have an implanted foreign body at the infection site
• Adequate debridement, resection, or amputation of infected tissue can shorten the necessary duration of therapy.
• Antibiotic therapy can generally be discontinued when signs and symptoms of infection have resolved, even if the wound has not completely healed.
Lipsky BA, Berendt AR. Diabetes Metab Res Rev 2004; 20(Suppl 1): S56–S64.
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Adjuvant therapies are not universally accepted
• Several additional measures have been used to improve infection resolution, wound healing, and host response.
• Recombinant granulocyte-colony stimulating factor– Larger trials are needed to define whether, and for whom, these compounds can
be recommended.
• Hyperbaric oxygen– Expensive and limited resource that should remain reserved for severe cases
• Revascularization– An aggressive approach to revascularization in an ischemic infected foot can
result in 3-year limb-salvage rates of up to 98%
• Edema control– Simple interventions, such as leg elevation and compression stockings, are likely
to be beneficial l
Lipsky BA. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S104-14.
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Suggested antibiotic regimens for treatment of diabetic foot infections*
• Mild/moderate (oral for entire course) – Clindamycin (300 mg t.i.d.) or Cephalexin (500 mg. q.i.d.) or Levofloxacin (750
mg q.d.) • Moderate/severe (iv until stable, then switch to oral equivalent)
– Clindamycin (450 mg q.i.d.) + ciprofloxacin (750 mg b.i.d.)– Clindamycin (600 t.i.d.) + ceftazidime (2 g t.i.d.)– Ampicillin/sulbactam (3.0 g q.i.d.)
• Life-threatening (prolonged iv) – Clindamycin (900 mg t.i.d.) + tobramycin (5.1 mg/kg./d) + ampicillin (50
mg/kg. q.i.d.)– Imipenem/cilastin (500 mg q.i.d.)– Vancomycin (15 mg/kg b.i.d.) + aztreonam (2.0 g t.i.d.) + metronidazole (7.5
mg/kg q.i.d.)
*Based on theoretical considerations and available clinical trials.A similar agent of the same class or generation may be substituted.
Lipsky BA. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S104-14.
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Prevention
• Regular foot exams and patient education can prevent 85% of amputations
• Four basic steps for preventive foot care – Early identification of the high risk diabetic foot
– Early diagnosis of foot problems
– Early intervention to prevent further deterioration that may lead to amputation
– Patient education for proper care of the the feet and footwear
Ulbrecht JS, Cavanagh PR. Clin Infect Dis. 2004 Aug 1;39 Suppl 2:S73-82.
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• Offloading is a precaution in wound care that required you to keep all weight off of the extremity that has the ulcer.
most effective is contact casting.
specialized offloading shoe (not designed for walking.)
• prescribe you a walker, crutches or a wheelchair if patient must be mobile.
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Educate Patients on Proper Foot Care – The “DO’s”
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Educate Patients on Proper Foot Care – The “DON’Ts”DO NOT …
Cut your own corns or callouses
Treat your own in-growing toenails or slivers with a razor or scissors. See your doctor or foot care specialistUse over-the-counter medications to treat corns and warts
Apply heat with a hot water bottle or electric blanket – may cause burns unknowingly
Soak your feet
Take very hot baths
Use lotion between your toes
Walk barefoot inside or outside
Wear tight socks, garter or elastics or knee highs
Wear over-the-counter insoles – may cause blisters if not right for your feet
Sit for long periods of time
Smoke
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Summary
• Foot ulceration, sepsis, and amputation are known and feared by almost every person who has diabetes
• Potentially, they are the most preventable of all diabetic complications by the simplest techniques of education and care
• The majority can also be cured by immediate and energetic treatment which includes appropriate antibiotic selection– Clindamycin (Dalacin C) is safe and effective as monotherapy or
in a combination regime and offers many advantages over alternative agents e.g., in patients with osteomyelitis
Watkins PJ, BMJ. 2003 May 3;326(7396):977-9. Klainer AS. Clindamycin in the treatment of diabetic foot infections. In: Zambrano D ed. Clindamycin in the treatment of human infections. Ch 11. Sec.11.1- 11.16.Diamantopoulos EJ ; Haritos D. Exp Clin Endocrinol Diabetes. 1998; 106(4):346-52
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Surgical infections
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• Suboptimal response to infection in a person with diabetes is caused by the presence of chronic complications, such as vascular disease and neuropathies, and by the presence of hyperglycemia and altered neutrophil function.
• Hyperglycemia and glycosuria may influence the growth of microorganisms and increase the severity of the infection.
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• Certain types of infections occur with increased frequency in people with diabetes:
• Respiratory s.pneumoniae
influenza
H1N1
tuberculosis
• Urinary tract asympomatic bactiruria
fungal cystitis
emphysematous cystitis
bacterial pyelonephritis and perinephric abscess
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• GIT H.pylori infection
oral and oesophageal candiasis
emphysematous cholecystitis
hepatitis C and B
enteroviruses
• Skin and soft tissue infections
carbuncle
necrotising fascitis and fournier’s gangrene
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• Head and neck
invasive otitis externa
rhinocerebral mucormycosis
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Thank you