DIABETES AND INFECTION

BY/ Ahmed M.elmeligui House officer (Intern) at kasr elaini hospitals Internal medicine Department

INTRODUCTION  

Diabetes mellitus is a common worldwide health problem with significant morbidity and mortality. Infection is among the most serious complications of diabetes and is well recognized as causing significant morbidity and mortality in that patient population.

INTRODUCTION(CONT.)
The objective of this presentation is to try to answer the following questions :   

Why diabetics are more prone to infection ? What is the impact of infection on diabetes ? What are the common infections in patients with diabetes ?

INTRODUCTION(CONT.
)   

What are the infections occurring predominantly in patients with diabetes ? What are the principles of prevention and treatment of infections in diabetes ? How to manage DM during infection ?

and phagocytic dysfunction. chemotaxis. .g interleukin-1 and tumor necrosis factor ).  Complement pathway.  Cytokine-mediated (e.  Myloperoxidase deficiency.PREDISPOSING FACTORS FOR INFECTIONS IN DM Primary factors  Granulocyte adherence .

Gastroparesis . Loss of skin integrity.PREDISPOSING FACTORS FOR INFECTIONS IN DM Secondary factors     Ketoacidosis. Frequent hospitalization. Use of urinary catheters and I.    .V access lines . Chronic renal failure and dialysis.reflux and aspiration. Delayed wound healing.

adrenaline and cortisol .IMPACT OF INFECTION ON DM The stress of infection may worsen diabetic control due to  Release of counter-regulatory hormones such as glucagon . which increases hepatic glucose release and causes hyperglycemia  2-Release of cytokines such as IL1 and TNF that affects carbohydrate metabolism .

IMPACT OF INFECTION ON DM
The stress of infection may precipitate DM in individuals in the prediabetes stage or those at high risk to develop DM

IMPACT OF INFECTION ON DM
Infection is the most common predisposing cause for diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS ).

IMPACT OF INFECTION ON DM
Poor food intake and vomiting that associate serious infections may predispose diabetic individuals to hypoglycemia .

. Soft tissue infections. Respiratory tract infections.COMMON INFECTIONS IN PATIENTS WITH DM    Urinary tract infection.

. Fungal cystitis. Perinephric abscess.URINARY TRACT INFECTIONS      Asymptomatic bacteruria. Acute bacterial cystitis. Acute pyelonephritis.

 Other organisms include Klebsiela.URINARY TRACT INFECTIONS Predisposing factors  1-Frequent urinary catheterization.Pseudomonas .  vaginitis Common pathogens  E COLI is the commonest.and rarely Candida. Proteus . .  2-Autonomic neuropathy.

 Complicated UTI -Perinephric abscess -Papillary necrosis .URINARY TRACT INFECTIONS Clinical features  Lower UTI.  Upper UTI.

C/S.CT.  Blood C/S.URINARY TRACT INFECTIONS Diagnosis  Urine microscopic exam. .  Retrograde pyelography..  CBC.  KUB.  Abdominal U/S .

Bacteriological cure should be confirmed.  Fungal UTI.URINARY TRACT INFECTIONS Treatment  Uncomplicated UTI -Antibiotics. . -Trimethoprim-sulphmethoxaxole potentiates the hypoglycemic effect of anti-hyperglycemic agents  Complicated UTI.

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RESPIRATORY TRACT INFECTIONS  It is unclear whether diabetes constitutes an independent risk factor for an increased incidence or severity of common upper or lower respiratory tract infections. .

delayed resolution .Gramnegative bacteria .and recurrence is higher following community-acquired pneumonia.B and Mucor.Mycobacterium T.including Staph. Infection due to specific microorganisms clearly occurs with an increased frequency in diabetes .aureus . .RESPIRATORY TRACT INFECTIONS   The incidence of bacteraemia .

Individuals with DM have an increased incidence of T.Influenza. .B and more advanced disease at the time of diagnosis.including infections caused by Streptococci .Legionella and H.RESPIRATORY TRACT INFECTIONS   An other group of infections are associated with increased morbidity and mortality .

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. -CT or MRI may be needed to define the location and extent of the abscess. -Clinical features includes pain . aureus through haematogenous spread .with abscess formation following minor trauma and haematoma formation.SOFT TISSUE INFECTIONS  Pyomyositis -Refer to infection of muscles without infection of contiguous tissue by Staph.fever and swelling with pocket of pus formation.

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Emphysematous pyelonephritis and cystitis. Necrotizing fascitis. Fournier's gangrene. Renal papillary necrosis .INFECTIONS OCCURRING PREDOMINANTLY WITH DM        Malignant /Invasive otitis externa. Emphysematous cholecystitis. Rhinocerebral mucormycosis.

rarely secondary to colonization of external ear canal by Aspergillus species. The majority of cases are caused by Pseud. Potentially life-threatening infection.MALIGNANT/INVASIVE OTITIS EXTERNA    Occurs in elderly diabetics and involves external auditory canal and skull.aeruginosa . .

 Oedema .severe pain and hearing impairment . .intense cellulitis and polypoid tissue are seen in external ear canal.  Cranial osteomylitis and intracranial spread of infection may occur.MALIGNANT / INVASIVE OTITIS EXTERNA Clinical features  Ear discharge .  Facial nerve involvement may occur .

MALIGNANT / INVASIVE OTITIS EXTERNA Diagnosis  Gram's stain . .culture and biopsy of debrided necrotic tissue.  MRI may be needed to define soft tissue and bone involvement.  D.D :uncomplicated non-invasive otitis externa and epidermal carcinoma.

MALIGNANT / INVASIVE OTITIS EXTERNA .

MALIGNANT / INVASIVE OTITIS EXTERNA .

 Repeated surgical debridment of necrotic tissue.  Systemic antipseudomonal antibiotics.  Adjunctive topical antibiotic or acetic acid drops.MALIGNANT / INVASIVE OTITIS EXTERNA Treatment  Early referral to otolaryngologist is crucial.  Duration of therapy is often 4-6 weeks or longer .

which are saprophytic organisms. .RHINOCEREBRAL MUCORMYCOSIS (zygomycosis)   Caused by fungi of the Rhizopus and Mucor species. These fungi have a predilection to invade blood vessels .causing infarction and necrosis. not uncommonly infecting the immunocompromised host.

RHINOCEREBRAL MUCORMYCOSIS   Five clinical forms of mucormycosis : Rhinocerebral . .gastrointestinal . primary cutaneous and disseminated.pulmonary . Rhinocerebral type has the highest frequency and mortality.

RHINOCEREBRAL MUCORMYCOSIS Mucor species Rhizopus sp .

thereby permitting growth of Rhizopus oryzae. with disruption of host defense mechanisms . Such growth is inhibited by correction of acidosis. .RHINOCEREBRAL MUCORMYCOSIS   50% of cases occur in patients with DM. Usually occurs during an episode of DKA .

 Fever and confusion.RHINOCEREBRAL MUCORMYCOSIS Clinical features  Onset with nasal stuffiness .  Black necrotic eschar on the nasal turbinates or palate : very characteristic .epistaxis and facial pain.  Later .proptosis . chemosis and ophthalmoplegia.

 Visual loss.RHINOCEREBRAL MUCORMYCOSIS Complications  Cavernous sinus thrombosis.  Multiple cranial nerve palsies.  Carotid artery or jugular vein thrombosis causing hemiparesis. .  Frontal lobe abscess.

RHINOCEREBRAL MUCORMYCOSIS .

RHINOCEREBRAL MUCORMYCOSIS .

RHINOCEREBRAL MUCORMYCOSIS .

RHINOCEREBRAL MUCORMYCOSIS .

RHINOCEREBRAL MUCORMYCOSIS Diagnosis  Punch biopsy of the lesion followed by fungal stains and culture.  Histological examination reveals the characteristic broad .  CT or MRI of the head reveal air-fluid level in the sinuses and involvement of deep tissues . branching hyphae of Rhizopus invading the tissue.

 More recently . .  Systemic amphotericin B. liposomal amphotercinB has been used.RHINOCEREBRAL MUCORMYCOSIS Treatment  Aggressive surgical debridement and drainage of the infected sinuses.

However . as the infection progresses skin may be necrosed due to thrombosis of cutaneouse vessels .NECROTIZING FASCIITIS   Uncommon soft tissue infection that spreads along fascial planes with relatively initial sparing of skin and underlying muscles.

 Type 2 -Caused by group A .NECROTIZING FASCIITIS Two bacteriological types  Type 1 -Caused by a combination of at least one anaerobe and one or more facultative anaerobe such as streptococci or enterococci.  Release of endogenous cytokines and bacterial toxins cause tissue damage and systemic toxicity . B-hemolytic streptococci with or without staphylococci.

minor trauma .  The source of introduction of the pathogen may be unknown or may follow surgery .spread from distant sites or a Barrtholin s gland abscess . perineum and extremities are the most common sites.NECROTIZING FASCIITIS Clinical features  Abdominal wall . .

 Thrombosis leads to serous and hemorrhagic bullae .  Rapid spread of infection along unseen fascial planes to involve contiguous areas away from the original site of involvement. .gangrene and ulceration.NECROTIZING FASCIITIS Clinical features  Early :Severe local pain with few local signs.  Fever and marked toxicity.

 Lymphadenitis and lymphangitis are rare.  Destruction of subcutaneous nerves leads to anaethesia. .  Dishwater pus due to liquefactive necrosis.NECROTIZING FASCIITIS Clinical features  Crepitus is palpable in approximately 50% of cases.

U/S . .ray .  Gram's stain and culture of sample from necrotic centre.NECROTIZING FASCIITIS Diagnosis  A high index of suspicion.  Plain X. CT and MRI.  The ability to pass a probe easily along normally adherent fascial planes.

-Then according to results of C/S. .NECROTIZING FASCIITIS Treatment  Early and adequate surgical debridement and fasciotomy play a key role in reducing mortality.  Systemic combination antibiotics : -Start with penicillin or cephalosporin + aminoglycoside with clidamycin or metronidazole.

NECROTIZING FASCIITIS .

NECROTIZING FASCIITIS .

NECROTIZING FASCIITIS MRI .

scrotum and penis.necrotizing fascitis of the perineum . steroid abuse . Other predisposing factors include alcoholism . 30 60% 0f cases have underlying DM. .cancer chemotherapy and AIDS. polymicrobial .FOURNIER S GANGRENE     First described by the French venereologist Fournier in 1882. A syndrome of synergistic .

 Proper systemic antibiotics and supportive care.FOURNIER S GANGRENE Diagnosis  Predominantly clinical.extensive disease . deranged renal function . Prognosis  High mortality rate specially with advanced age .sepsis and shock . Treatment  Surgical emergency with extensive surgery.

FOURNIER.S GANGRENE .

FOURNIER.S GANGRENE .

EMPHYSEMATOUS CHOLECYSTITIS    Rare variant of acute cholecystitis caused by ischemia of the gall bladder wall and infection with gas -producing organisms. 35. Thought to result from acalculous cystic duct obstruction .55% of cases have DM. with inflammatory oedema causing cystic artery occlusion followed by infection with gas-forming organisms .

 Gangrene and perforation of GB is more common  Toxicity is marked  Gall stones are present in only 50% . less than 4%) .EMPHYSEMATOUS CHOLECYSTITIS Clinical features  Clinically similar to acute cholecystitis However  Male predominance.  Mortality is higher ( 15 % vs.

EMPHYSEMATOUS CHOLECYSTITIS Diagnosis  plain x-ray is diagnostic.  CT scan is more sensitive. .  Abdominal U/S reveals high. -Gaseous ring appears in the lumen or within the lumen of GB 1-2 days after the onset of symptoms.level echoes outlying GB wall.

EMPHYSEMATOUS CHOLECYSTITIS Treatment  Early cholecystectomy is crucial.  Proper antibiotics and supportive care .

EMPHYSEMATOUS CHOLECYSTITIS .

Over 90% of cases occur in diabetic cases.and products from necrotic tissue to carbon dioxide .coli .hydrogen . The most common causative pathogens are E. lactate .Proteus mirabilis and Klebsiella pneumoniae that ferment glucose. .nitrogen and unknown gases .EMPHYSEMATOUS PYELONEPHRITIS    Rare necrotizing infection of the renal parenchyma and perirenal tissue that is characterized by gas formation.

EMPHYSEMATOUS PYELONEPHRITIS Clinical features  Chills .nausea and vomiting .  Crepitus if spread of infection to the perirenal space. .fever .dysuria .flank pain . shock. lethargy and altered sensorium.  Bilateral involvement may occur infrequently.

 Abdominal plain X ray and U/S diagnostic in 85 %.  Abdominal CT scan is diagnostic.  Leucocytosis and pyuria and +ve blood culture  Thrombocytopenia.  Increased create level. .EMPHYSEMATOUS PYELONEPHRITIS Diagnosis  Failure of fever to resolve within 3-4 days should raise the possibility of this infection.

EMPHYSEMATOUS PYELONEPHRITIS .

V antibiotics and vigorous hydration. conservative approach with drainage of the affected kidney with aggressive medical treatment.EMPHYSEMATOUS PYELONEPHRITIS Treatment  Proper I. .  Surgery : nephrectomy vs.

EMPHYSEMATOUS PYELONEPHRITIS Complications  Acute renal failure.  Renal papillary necrosis.  Septicemia. .

EMPHYSEMATOUS PYELITIS     This entity is distinct from emphysematous pyelonephritis . as gas is localized to the renal collecting system. Radiography reveals gas following the outlines of the renal pelvis. I. Mortality is lower.V antibiotics and relieving the obstruction are sufficient therapy. .

Antibiotics and relief of bladder outlet obstruction are therapeutic.EMPHYSEMATOUS CYSTITIS     Associated with vesiccolic or vesicovaginal fistula. Radiology shows air in the bladder wall . Characteristic features include pneumaturia or may be haematuria. . or an air-fluid level in the lumen.intramural air bubbles .

RENAL PAPILLARY NECROSIS Necrosis and sloughing of the renal papillae are five times more prevalent in diabetic than in nondiabetic patients.  . Clinical features  Persistent fever and flank pain despite being on antibiotics. .

 Retrograde pyelogram is diagnostic .a (ring sign) is present when a separated papilla is surrounded by contrast medium. Treatment  Parenteral antibiotics.RENAL PAPILLARY NECROSIS Diagnosis  Voided medullary tissue on urinalysis. This may show calcification. .  Drainage to relieve obstruction.

RENAL PAPILLARY NECROSIS U/S .

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. Good general and foot hygiene is crucial.PREVENTION OF INFECTION IN DIABETICS    Patients with well controlled diabetes are no more susceptible to infection than patients without diabetes. Influenza and pneumoccal vaccination.

. When administering oral antibiotics . the effects of gastropathy on oral absorption should be considered.USE OF ANTIBIOTICS IN DM: SPECIAL CONSIDERATIONS    Particular caution is warranted to avoid nephrotoxicity and eye toxicity. Effect of some antibiotics on glycemic state should be cosidered.

provide adequate nutrition and minimize the risk of hypoglycemia.MANAGEMENT OF DM DURING INFECTION The challenge is to achieve strict near-normal glycemic state .  .

MANAGEMENT OF DM DURING INFECTION Near-normal glycemic state  For optimal wound healing and phagocytic function BG should not exceed 150 mg/ dl.  Recent recommendation advise to keep BG around 110 mg/dl to improve health outcome during critical illness including serious infections .

 Common insulin regimen used during acute illness include : -Basal. infusion of dextrose and insulin . -DEXTROSE-POTASIUM-INSULIN (DKI) Separate I.V.MANAGEMENT OF DM DURING INFECTION Near-normal glycemic state  To achieve these BG targets insulin is usually needed.bolus regime.

threatening infections in diabetic individuals . Early identify .refer and treat life. Treat infection aggressively in diabetic individuals.TAKE-HOME MESSAGE     Search for an occult infection if DM is difficult to control. Monitor BG closely during infection to ensure strict glycemic control and avoid hypoglycemia.