f01ddiabrtes and Infection

8/6/2019 f01ddiabrtes and Infection

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DIABETES

AND

INFECTION

BY/ Ahmed M.elmeliguiHouse officer (Intern) at kasr elaini hospitals

Internal medicine Department


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The objective of this presentationisto try to answer the followingquestions:

Why diabetics are more prone toinfection ?

What is the impact of infection ondiabetes ?

What are the common infections in

patients with diabetes ?

INTRODUCTION(CONT.)


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INTRODUCTION(CONT.

) What are the infections occurring

predominantly in patients with diabetes

?

What are the principles of preventionand treatment of infections in diabetes

? How to manage DM during infection ?


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PREDISPOSING FACTORS

FOR INFECTIONS IN DMPrimary factors

Granulocyte adherence , chemotaxis.and phagocytic dysfunction.

Myloperoxidase deficiency.

Complement pathway. Cytokine-mediated (e.g interleukin-1

and tumor necrosis factor ).


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PREDISPOSING FACTORS

FOR INFECTIONS IN DMSecondary factors

Ketoacidosis.

Frequent hospitalization.

Gastroparesis ,reflux and aspiration.

Use of urinary catheters and I.V access

lines . Delayed wound healing.

Loss of skin integrity.

Chronic renal failure and dialysis.


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IMPACT OF INFECTION ON

DMThe stress of infection may worsen

diabetic control due to

Release of counter-regulatory hormonessuch as glucagon ,adrenaline andcortisol , which increases hepatic

glucose release and causeshyperglycemia

2-Release of cytokines such as IL1 andTNF that affects carbohydrate

metabolism


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DM

Infection is the mostcommon predisposing causefor diabetic ketoacidosis

(DKA) and hyperglycemichyperosmolar state (HHS ).


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DM

Poor food intake and

vomitingthatassociateseriousinfectionsmaypredispose diabetic

individualstohypoglycemia.


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COMMON INFECTIONS IN

PATIENTS WITH DM

Urinary tractinfection. Respiratory tractinfections.

Softtissue infections.


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URINARY TRACT

INFECTIONS

Asymptomatic bacteruria.

Acute bacterialcystitis. Fungalcystitis.

Acute pyelonephritis.

Perinephricabscess.


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URINARY TRACT

INFECTIONSPredisposing factors

1-Frequent urinary catheterization.

2-Autonomic neuropathy.

vaginitis

Common pathogens

E COLI is the commonest.

Other organisms include Klebsiela,Proteus ,Pseudomonas ,and rarely

Candida.


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URINARY TRACT

INFECTIONSClinical features

Lower UTI. Upper UTI.

Complicated UTI-Perinephric abscess-Papillary necrosis


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URINARY TRACT

INFECTIONSDiagnosis

Urine microscopic exam., C/S. CBC.

Blood C/S.

KUB.Abdominal U/S ,CT.

Retrograde pyelography.


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URINARY TRACT

INFECTIONSTreatment

Uncomplicated UTI-Antibiotics.-Trimethoprim-sulphmethoxaxolepotentiates the hypoglycemic effect ofanti-hyperglycemic agents

Complicated UTI.

Fungal UTI.

Bacteriological cure should be confirmed.


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RESPIRATORY TRACT

INFECTIONS

It is unclear whether diabetesconstitutes an independent risk factorfor an increased incidence or severity ofcommon upper or lower respiratorytract infections.


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RESPIRATORY TRACTINFECTIONS

The incidence of bacteraemia ,delayedresolution ,and recurrence is higherfollowing community-acquired

pneumonia. Infection due to specific

microorganisms clearly occurs with anincreased frequency in diabetes,including Staph.aureus ,Gram-negative bacteria ,Mycobacterium T.Band Mucor.


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RESPIRATORY TRACT

INFECTIONS

An other group of infections are

associated with increased morbidity andmortality ,including infections caused byStreptococci ,Legionella andH.Influenza.

Individuals with DM have an increasedincidence of T.B and more advanceddisease at the time of diagnosis.


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SOFT TISSUE INFECTIONS Pyomyositis

-Refer to infection of muscleswithout infection ofcontiguous tissue by Staph.aureus throughhaematogenous spread ,withabscess formation followingminor trauma andhaematoma formation.-Clinical featuresincludespain ,fever and swelling withpocket of pus formation.-CTor MRI may be neededto define the location andextent of the abscess.


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INFECTIONS OCCURRING

PREDOMINANTLY WITH DM

Malignant /Invasive otitis externa.

Rhinocerebralmucormycosis.

Necrotizingfascitis.

Fournier'sgangrene.

Emphysematouscholecystitis. Emphysematouspyelonephritisandcystitis.

Renalpapillary necrosis


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MALIGNANT/INVASIVE

OTITIS EXTERNA Occurs in elderly diabetics and

involves external auditory canal and

skull.

Potentially life-threatening infection.

The majority of cases are caused by

Pseud.aeruginosa ,rarely secondaryto colonization of external ear canalby Aspergillus species.


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MALIGNANT / INVASIVE

OTITIS EXTERNAClinical features

Ear discharge ,severe painandhearing

impairment . Oedema ,intense cellulitisandpolypoid

tissue are seeninexternalearcanal.

Cranialosteomylitisandintracranialspreadofinfectionmayoccur.

Facial nerve involvementmayoccur .


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OTITIS EXTERNADiagnosis

Gram'sstain ,culture andbiopsyofdebridednecrotictissue.

MRI maybe needed todefine softtissue andbone involvement.

D.D:uncomplicatednon-invasive otitisexternaandepidermalcarcinoma.


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OTITIS EXTERNA


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OTITIS EXTERNA


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MALIGNANT / INVASIVE OTITISEXTERNA

Treatment

Early referral to otolaryngologist iscrucial.

Repeated surgical debridment ofnecrotic tissue.

Systemic antipseudomonalantibiotics.

Adjunctive topical antibiotic or aceticacid drops.

Duration of therapy is often 4-6

weeks or longer


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RHINOCEREBRAL

MUCORMYCOSIS Five clinical forms of mucormycosis :Rhinocerebral ,pulmonary

,gastrointestinal , primary cutaneousand disseminated.

Rhinocerebral type has the highest

frequency and mortality.


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RHINOCEREBRAL

MUCORMYCOSIS

RhizopusspMucorspecies


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RHINOCEREBRAL

MUCORMYCOSIS 50% of cases occur in patients with DM.

Usually occurs during an episode ofDKA , with disruption of host defensemechanisms ,thereby permitting growthofRhizopus oryzae. Such growth is

inhibited by correction of acidosis.


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RHINOCEREBRAL

MUCORMYCOSISClinical features

Onset with nasal stuffiness ,epistaxis

and facial pain. Later ,proptosis , chemosis and

ophthalmoplegia.

Fever and confusion. Black necrotic eschar on the nasal

turbinates or palate :verycharacteristic


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RHINOCEREBRAL

MUCORMYCOSISComplications

Cavernous sinus thrombosis.

Multiple cranial nerve palsies.

Visual loss.

Frontal lobe abscess. Carotid artery or jugular vein

thrombosis causing hemiparesis.


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RHINOCEREBRAL

MUCORMYCOSIS


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RHINOCEREBRAL

MUCORMYCOSIS


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RHINOCEREBRAL

MUCORMYCOSIS


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RHINOCEREBRAL

MUCORMYCOSIS


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RHINOCEREBRAL

MUCORMYCOSISDiagnosis

Punch biopsy of the lesion followed by

fungal stains and culture. Histological examination reveals the

characteristic broad , branching hyphae

ofRhizopus invading the tissue.

CT or MRI of the head reveal air-fluidlevel in the sinuses and involvement ofdeep tissues


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RHINOCEREBRAL

MUCORMYCOSISTreatment

Aggressive surgical debridement anddrainage of the infected sinuses.

Systemic amphotericin B.

More recently , liposomal amphotercin-B has been used.


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NECROTIZING FASCIITIS Uncommon soft tissue infection that

spreads along fascial planes with

relatively initial sparing of skin andunderlying muscles.

However , as the infection progresses

skin may be necrosed due tothrombosis of cutaneouse vessels


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NECROTIZING FASCIITIS

Two bacteriological types Type 1

-Caused by a combination of at least oneanaerobe and one or more facultative

anaerobe such as streptococci or enterococci. Type 2

-Caused by group A , B-hemolytic streptococciwith or without staphylococci.

Release of endogenous cytokines and bacterialtoxins cause tissue damage and systemictoxicity


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NECROTIZING FASCIITISClinical features

Abdominal wall , perineum and

extremities are the most common sites. The source of introduction of the

pathogen may be unknown or may

follow surgery , minor trauma ,spreadfrom distant sites or a Barrtholins glandabscess .


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Clinical features Early :Severe local pain with few local

signs.

Fever and marked toxicity. Rapid spread of infection along unseen

fascial planes to involve contiguous areas

away from the original site ofinvolvement.

Thrombosis leads to serous andhemorrhagic bullae ,gangrene and

ulceration.


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NECROTIZING FASCIITISClinical features

Crepitus is palpable inapproximately 50% of

cases. Dishwater pus due to

liquefactive necrosis.

Lymphadenitis andlymphangitis are rare.

Destruction ofsubcutaneous nervesleads to anaethesia.


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NECROTIZING FASCIITISDiagnosis

A high index of suspicion.

The ability to pass a probe easily alongnormally adherent fascial planes.

Gram's stain and culture of samplefrom necrotic centre.

Plain X- ray , U/S , CT and MRI.


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NECROTIZING FASCIITISTreatment

Early and adequate surgical debridement

and fasciotomy play a key role inreducing mortality.

Systemic combination antibiotics :-Start with penicillin or cephalosporin +

aminoglycoside with clidamycin ormetronidazole.-Then according to results of C/S.


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NECROTIZING FASCIITISM

RI


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FOURNIERS GANGRENE First described by the French venereologist

Fournier in 1882.

A syndrome of synergistic , polymicrobial,necrotizing fascitis of the perineum,scrotum and penis.

30 60%0f cases have underlying DM.

Other predisposing factors includealcoholism , steroid abuse ,cancerchemotherapy and AIDS.


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FOURNIERS GANGRENE

Diagnosis

Predominantly clinical.Treatment

Surgical emergency with extensive

surgery. Proper systemic antibiotics and

supportive care.

Prognosis

High mortality rate specially withadvanced age ,extensive disease ,deranged renal function ,sepsis and

shock


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FOURNIER,S GANGRENE


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FOURNIER,S GANGRENE


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EMPHYSEMATOUS

CHOLECY

STITIS Rare variant of acute cholecystitis

caused by ischemia of the gall bladder

wall and infection with gas -producingorganisms.

35- 55% of cases have DM.

Thought to result from acalculous cysticduct obstruction , with inflammatoryoedema causing cystic artery occlusionfollowed by infection with gas-forming

organisms

EMPHYSEMATOUS


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EMPHYSEMATOUSCHOLECYSTITIS

Clinical features Clinically similar to acute cholecystitis

However

Male predominance. Gangrene and perforation ofGB is

more common

Toxicity is marked Gall stones are present in only 50% .

Mortality is higher ( 15% vs. less than

4 % )


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EMPHYSEMATOUS

CHOLECY

STITIS

Treatment

Early cholecystectomy is crucial.

Proper antibiotics and supportive care


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EMPHYSEMATOUS

CHOLECY

STITIS

EMPHYSEMATOUS


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EMPHYSEMATOUSPYELONEPHRITIS

Rare necrotizing infection of the renalparenchyma and perirenal tissue thatis characterized by gas formation.

Over 90% of cases occur in diabeticcases.

The most common causativepathogens are E.coli ,Proteus mirabilis

and Klebsiella pneumoniae thatferment glucose, lactate ,andproducts from necrotic tissue tocarbon dioxide ,hydrogen ,nitrogen

and unknown gases .


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EMPHYSEMATOUS

PY

ELONEPHRITISClinical features

Chills ,fever ,flank pain ,dysuria ,nausea

and vomiting , lethargy and alteredsensorium, shock.

Crepitusif spread of infection to theperirenal space.

Bilateral involvement may occurinfrequently.


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EMPHYSEMATOUS

PY

ELONEPHRITISDiagnosis Failure of fever to resolve within 3-4 days

should raise the possibility of this infection. Leucocytosis and pyuria and +ve blood

culture Thrombocytopenia. Abdominal plain X ray and U/S diagnostic in

85%. Abdominal CT scan is diagnostic. Increased create level.


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EMPHYSEMATOUS

PY

ELONEPHRITISTreatment

Proper I.V antibiotics and vigoroushydration.

Surgery : nephrectomy vs.conservative approach with drainage of

the affected kidney with aggressivemedical treatment.


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EMPHYSEMATOUS

PY

ELONEPHRITIS

Complications

Acute renal failure. Renal papillary necrosis.

Septicemia.


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EMPHYSEMATOUS

PY

ELITIS This entity is distinct from

emphysematous pyelonephritis , as gas

is localized to the renal collectingsystem.

Radiography reveals gas following theoutlines of the renal pelvis.

I.V antibiotics and relieving theobstruction are sufficient therapy.

Mortality is lower.


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EMPHYSEMATOUS

CY

STITIS Associated with vesiccolic or vesicovaginal

fistula.

Characteristic features include pneumaturiaor may be haematuria.

Radiology shows air in the bladder wall,intramural air bubbles , or an air-fluid level in

the lumen. Antibiotics and relief of bladder outlet

obstruction are therapeutic.


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RENAL PAPILLARY

NECROSIS Necrosis and sloughing of the renal

papillae are five times more

prevalent in diabetic than in non-diabetic patients.

Clinical features

Persistent fever and flank paindespite being on antibiotics.

,


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RENAL PAPILLARY

NECROSISDiagnosis

Voided medullary tissue on urinalysis.

Retrograde pyelogram is diagnostic .a(ringsign) is present when a separatedpapilla is surrounded by contrastmedium. This may show calcification.

Treatment

Parenteral antibiotics.

Drainage to relieve obstruction.


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RENAL PAPILLARY

NECROSIS U/S


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PREVENTION OF

INFECTION IN DIABETICS Patients with well controlled diabetes

are no more susceptible to infection

than patients without diabetes. Good general and foot hygiene is

crucial.

Influenza and pneumoccal vaccination.


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USE OF ANTIBIOTICS IN

DM: SPECIALCONSIDERATIONS Particular caution is warranted to

avoid nephrotoxicity and eye toxicity. When administering oral antibiotics ,

the effects of gastropathy on oral

absorption should be considered. Effect of some antibiotics on glycemic

state should be cosidered.


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MANAGEMENT OF DM

DURING INFECTION

The challenge is to achievestrict near-normal glycemicstate , provide adequate

nutrition andminimize the risk ofhypoglycemia.

G O


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MANAGEMENT OF DM

DURING INFECTIONNear-normal glycemic state

For optimal wound healing and

phagocytic function BG should notexceed 150 mg/ dl.

Recent recommendation advise to keep

BG around 110 mg/dl to improvehealth outcome during critical illnessincluding serious infections

MANAGEMENT OF DM


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MANAGEMENT OF DM

DURING INFECTIONNear-normal glycemic state

To achieve these BG targets insulin is

usually needed. Common insulin regimen used during

acute illness include :-Basal- bolus regime.

-DEXTROSE-POTASIUM-INSULIN (DKI) -Separate I.V. infusion of dextrose andinsulin


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TAKE-HOME MESSAGE

Search for an occult infection ifDM is difficult to control.

Treat infection aggressively indiabetic individuals.

Monitor BG closelyduringinfection to ensure strictglycemic control and avoid

hypoglycemia. Early identify ,refer and treat

life- threatening infections indiabetic individuals


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