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    Add as Frienddiabetes and infection

    by: ibrahim

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    1 : DIABETES AND INFECTION BY DR.IBRAHIM MOKHTAR CONSULTANT ENDOCRINOLOGY
    2 : 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.
    3 : 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 ?
    4 : 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 ?
    5 :
    6 : PREDISPOSING FACTORS FOR INFECTIONS IN DM Primary factors Granulocyte adherence , chemotaxis. and phagocytic dysfunction. Myloperoxidase deficiency. Complement pathway. Cytokine-mediated (e.g interleukin-1 and tumor necrosis factor ).
    7 : PREDISPOSING FACTORS FOR INFECTIONS IN DM Secondary 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.
    8 :
    9 : IMPACT OF INFECTION ON DM The stress of infection may worsen diabetic control due to : 1- Release of counter-regulatory hormones such as glucagon ,adrenaline and cortisol , which increases hepatic glucose release and causes hyperglycemia. 2-Release of cytokines such as IL1 and TNF that affects carbohydrate metabolism
    10 : IMPACT OF INFECTION ON DM The stress of infection may worsen diabetic control due to Release of counter-regulatory hormones such as glucagon ,adrenaline and cortisol , which increases hepatic glucose release and causes hyperglycemia 2-Release of cytokines such as IL1 and TNF that affects carbohydrate metabolism
    11 : 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
    12 : IMPACT OF INFECTION ON DM Infection is the most common predisposing cause for diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS ).
    13 : IMPACT OF INFECTION ON DM Poor food intake and vomiting that associate serious infections may predispose diabetic individuals to hypoglycemia .
    14 :
    15 : COMMON INFECTIONS IN PATIENTS WITH DM Urinary tract infection. Respiratory tract infections. Soft tissue infections.
    16 : URINARY TRACT INFECTIONS Asymptomatic bacteruria. Acute bacterial cystitis. Fungal cystitis. Acute pyelonephritis. Perinephric abscess.
    17 : URINARY TRACT INFECTIONS Predisposing 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.
    18 : URINARY TRACT INFECTIONS Clinical features Lower UTI. Upper UTI. Complicated UTI -Perinephric abscess -Papillary necrosis
    19 : URINARY TRACT INFECTIONS Diagnosis Urine microscopic exam., C/S. CBC. Blood C/S. KUB. Abdominal U/S ,CT. Retrograde pyelography.
    20 : URINARY TRACT INFECTIONS Treatment Uncomplicated UTI -Antibiotics. -Trimethoprim-sulphmethoxaxole potentiates the hypoglycemic effect of anti-hyperglycemic agents Complicated UTI. Fungal UTI. Bacteriological cure should be confirmed.
    21 :
    22 : 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.
    23 : RESPIRATORY TRACT INFECTIONS HOWEVER The incidence of bacteraemia ,delayed resolution ,and recurrence is higher following community-acquired pneumonia. Infection due to specific microorganisms clearly occurs with an increased frequency in diabetes ,including Staph.aureus ,Gram-negative bacteria ,Mycobacterium T.B and Mucor.
    24 : RESPIRATORY TRACT INFECTIONS An other group of infections are associated with increased morbidity and mortality ,including infections caused by Streptococci ,Legionella and Influenza. Individuals with DM have an increased incidence of T.B and more advanced disease at the time of diagnosis.
    25 :
    26 : SOFT TISSUE INFECTIONS Pyomyositis -Refer to infection of muscles without infection of contiguous tissue by Staph. aureus through haematogenous spread ,with abscess formation following minor trauma and haematoma formation. -Clinical features includes pain ,fever and swelling with pocket of pus formation. -CT or MRI may be needed to define the location and extent of the abscess.
    27 : INFECTIONS OCCURRING PREDOMINANTLY WITH DM Malignant /Invasive otitis externa. Rhinocerebral mucormycosis. Necrotizing fascitis. Fournier's gangrene. Emphysematous cholecystitis. Emphysematous pyelonephritis and cystitis. Renal papillary necrosis
    28 : 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 secondary to colonization of external ear canal by Aspergillus species.
    29 : MALIGNANT / INVASIVE OTITIS EXTERNA Clinical features Ear discharge ,severe pain and hearing impairment . Oedema ,intense cellulitis and polypoid tissue are seen in external ear canal. Crainial osteomylitis and intracranial spread of infection may occur. Facial nerve involvement may occur .
    30 : 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.
    31 : MALIGNANT / INVASIVE OTITIS EXTERNA
    32 : MALIGNANT / INVASIVE OTITIS EXTERNA
    33 : MALIGNANT / INVASIVE OTITIS EXTERNA Treatment Early referral to otolaryngologist is crucial. Repeated surgical debridment of necrotic tissue. Systemic antipseudomonal antibiotics. Adjunctive topical antibiotic or acetic acid drops. Duration of therapy is often 4-6 weeks or longer
    34 :
    35 : RHINOCEREBRAL MUCORMYCOSIS Caused by fungi of the Rhizopus and Mucor species, which are ubiquitous saprophytic organisms, not uncommonly infecting the immunocompromised host. These fungi have a predilection to invade blood vessels ,causing infarction and necrosis.
    36 : RHINOCEREBRAL MUCORMYCOSIS Five clinical forms of mucormycosis : Rhinocerebral ,pulmonary ,gastrointestinal , primary cutaneouse and disseminated. Rhinocerebral type has the highest frequency and mortality.
    37 : RHINOCEREBRAL MUCORMYCOSIS Rhizopus sp Mucor species
    38 : RHINOCEREBRAL MUCORMYCOSIS 50% of cases occur in patients with DM. Usually occurs during an episode of DKA , with disruption of host defense mechanisms ,thereby permitting growth of Rhizopus oryzae. Such growth is inhibited by correction of acidosis.
    39 : RHINOCEREBRAL MUCORMYCOSIS Clinical 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 : very characteristic
    40 : RHINOCEREBRAL MUCORMYCOSIS Complications Cavernous sinus thrombosis. Multiple cranial nerve palsies. Visual loss. Frontal lobe abscess. Carotid artery or jugular vein thrombosis causing hemiparesis.
    41 : RHINOCEREBRAL MUCORMYCOSIS
    42 : RHINOCEREBRAL MUCORMYCOSIS
    43 : RHINOCEREBRAL MUCORMYCOSIS
    44 : RHINOCEREBRAL MUCORMYCOSIS
    45 : RHINOCEREBRAL MUCORMYCOSIS Diagnosis Punch biopsy of the lesion followed by fungal stains and culture. Histological examination reveals the characteristic broad , branching hyphae of Rhizopus invading the tissue. CT or MRI of the head reveal air-fluid level in the sinuses and involvement of deep tissues
    46 : RHINOCEREBRAL MUCORMYCOSIS Treatment Aggressive surgical debridement and drainage of the infected sinuses. Systemic amphotericin –B. More recently , liposomal amphotercin-B has been used.
    47 :
    48 : NECROTIZING FASCIITIS Uncommon soft tissue infection that spreads along fascial planes with relatively initial sparing of skin and underlying muscles. However , as the infection progresses skin may be necrosed due to thrombosis of cutaneouse vessels
    49 : 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. Type 2 -Caused by group A B-hemolytic streptococci with or without staphylococci. Release of endogenous cytokines and bacterial toxins cause tissue damage and systemic toxicity
    50 : NECROTIZING FASCIITIS Clinical 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 ,spread from distant sites or a Barrtholin,s gland abscess .
    51 : NECROTIZING FASCIITIS 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 of involvement. Thrombosis leads to serous and hemorrhagic bullae ,gangrene and ulceration.
    52 : NECROTIZING FASCIITIS Clinical features Crepitus is palpable in approximately 50% of cases. Dishwater pus due to liquefactive necrosis. Lymphadenitis and lymphangitis are rare. Destruction of subcutaneous nerves leads to anaethesia.
    53 : NECROTIZING FASCIITIS Diagnosis A high index of suspicion. The ability to pass a probe easily along normally adherent fascial planes. Gram's stain and culture of sample from necrotic centre. Plain X- ray , U/S , CT and MRI.
    54 : 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 + aminpglycoside with clidamycin or metronidazole. -Then according to results of C/S.
    55 : NECROTIZING FASCIITIS
    56 : NECROTIZING FASCIITIS
    57 : NECROTIZING FASCIITIS MRI
    58 : FOURNIER,S 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 include alcoholism , steroid abuse ,cancer chemotherapy and AIDS.
    59 : FOURNIER,S GANGRENE Diagnosis Predominantly clinical. Treatment Surgical emergency with extensive surgery. Proper systemic antibiotics and supportive care. Prognosis High mortality rate specially with advanced age ,extensive disease , deranged renal function ,sepsis and shock
    60 : FOURNIER,S GANGRENE
    61 : FOURNIER,S GANGRENE
    62 :
    63 : EMPHYSEMATOUS CHOLECYSTITIS Rare variant of acute cholecystitis caused by ischemia of the gall bladder wall and infection with gas -producing organisms. 35- 55% of cases have DM. Thought to result from acalculous cystic duct obstruction , with inflammatory oedema causing cystic artery occlusion followed by infection with gas-forming organisms
    64 : EMPHYSEMATOUS CHOLECYSTITIS Clinical features Clinically similar to acute cholecystitis However Male predominance. Gangrene and perforation of GB is more common Toxicity is marked Gall stones are present in only 50% . Mortality is higher ( 15 % vs. less than 4 % )
    65 : EMPHYSEMATOUS CHOLECYSTITIS Diagnosis plain x-ray is diagnostic. -Gaseous ring appears in the lumen or within the lumen of GB 1-2 days after the onset of symptoms. CT scan is more sensitive. Abdominal U/S reveals high- level echoes outlying GB wall.
    66 : EMPHYSEMATOUS CHOLECYSTITIS Treatment Early cholecystectomy is crucial. Proper antibiotics and supportive care
    67 : EMPHYSEMATOUS CHOLECYSTITIS
    68 : EMPHYSEMATOUS PYELONEPHRITIS Rare necrotizing infection of the renal parenchyma and perirenal tissue that is characterized by gas formation. Over 90% of cases occur in diabetic cases. The most common causative pathogens are E.coli ,Proteus mirabilis and Klebsiella pneumoniae that ferment glucose, lactate ,and products from necrotic tissue to carbon dioxide ,hydrogen ,nitrogen and unknown gases .
    69 : EMPHYSEMATOUS PYELONEPHRITIS Clinical features Chills ,fever ,flank pain ,dysuria ,nausea and vomiting , lethargy and altered sensorium. Crepitus if spread of infection to the perirenal space. Bilateral involvement may occur infrequently.
    70 : EMPHYSEMATOUS PYELONEPHRITIS Diagnosis Failure of fever to resolve within 3-4 days should raise the possibility of this infection. Leucocytosis and pyuria. Abdominal plain X ray and U/S diagnostic in 85 %. Abdominal CT scan is diagnostic.
    71 : EMPHYSEMATOUS PYELONEPHRITIS Treatment Proper I.V antibiotics and vigorous hydration. Surgery : nephrectomy vs. conservative approach with drainage of the affected kidney with aggressive medical treatment.
    72 : EMPHYSEMATOUS PYELONEPHRITIS Complications Acute renal failure. Renal papillary necrosis. Septicemia.
    73 : 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.V antibiotics and relieving the obstruction are sufficient therapy. Mortality is lower.
    74 : EMPHYSEMATOUS CYSTITIS Associated with vesiccolic or vesicovaginal fistula. Characteristic features include pneumaturia or mat 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.
    75 : 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 pain despite being on antibiotics. ,
    76 : RENAL PAPILLARY NECROSIS Diagnosis Voided medullary tissue on urinalysis. Retrograde pyelogram is diagnostic .a (ring sign) is present when a separated papilla is surrounded by contrast medium. This may show calcification. Treatment Parenteral antibiotics. Drainage to relieve obstruction.
    77 : RENAL PAPILLARY NECROSIS U/S
    78 :
    79 : 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.
    80 : USE OF ANTIBIOTICS IN DM: SPESIAL CONSIDERATIONS 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.
    81 : MANAGEMENT OF DM DURING INFECTION The challenge is to achieve strict near-normal glycemic state , provide adequate nutrition and minimize the risk of hypoglycemia.
    82 : 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
    83 : MANAGEMENT OF DM DURING INFECTION Near-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-INSULIM (DKI) -Separate I.V. infusion of dextrose and insulin
    84 : TAKE-HOME MESSAGE Search for an occult infection if DM is difficult to control. Treat infection aggressively in diabetic individuals. Monitor BG closely during infection to ensure strict glycemic control and avoid hypoglycemia. Early identify ,refer and treat life- threatening infections in diabetic individuals
    85 :
    86 : Thank You

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