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FOURNIER GANGRENE

Dr KABERA Ren Family Physician RFMA

Introduction
First identified in 1883,by the French venereologist Jean Alfred Fournier. It is a polymicrobial necrotizing fasciitis of the perineal, perianal, or genital areas. This infectious process involves the superficial and deep fascial planes of the genitalia,often sparing the deep muscular structures and, to variable degrees, the overlying skin.

DR KABERA R

DR KABERA R

Mechanism/description
Inadequate hygiene leads to skin maceration and excoriation, providing bacteria access to the subcutaneous tissue Once the skin barrier is broken, polymicrobial flora spread along the fascial planes of the perineum Colles fascia fuses with the urogenital diaphragm, slowing propagation posteriorly and laterally Anteriorly, Buck and Scarpa fascia are continuous, allowing rapid extension to anterior abdominal wall and laterally along the fascia lata

DR KABERA R

Mechanism/description
The testes and urethra are usually spared Three anatomic origins account for most cases -40% lower urinary tract: urethral strictures, indwelling catheters -30% penile or scrotal: condom catheters, hydradenitis, and balanitis -30% anorectal: fistulas, perirectal infections, and hemorrhoids Rarely, intraabdominal sources such as perforating appendicitis, diverticulitis, or pancreatitis has produced Fournier's gangrene by dependent contiguous spread

DR KABERA R

Etiology
An infection by polymicrobial flora (mixed aerobic and anaerobic organisms) The mixed bacteria exert a synergistic tissue-destructive effect End arterial thrombosis in the subcutaneous tissues produces an anaerobic environment,promoting extension of the infection Bacterial toxins and tissue necrosis factors may contribute to the clinical presentation Risk factors include trauma, diabetes, alcoholism, other immunocompromised states, morbid obesity, and abdominal surgery
DR KABERA R

Pathophysiology
Infection of superficial perineal fascia (Colles fascia) may spread to the penis and scrotum via Buck and dartos fascia, or to the anterior abdominal wall via Scarpa fascia, or vice versa. Colles fascia is attached to the perineal body and urogenital diaphragm posteriorly and to the pubic rami laterally, thus limiting progression in these directions. Testicular involvement is rare, as the testicular arteries originate directly from the aorta and thus have a blood supply separate from the affected region.

DR KABERA R

Signs and symptoms


Clinical Presentation A rapidly progressive necrotizing infection of the perineum involving the subcutaneous and fascial tissues and often muscle layers; usually seen in diabetics or immunocompromised patients Nausea, vomiting, fever, chills, and complaints of pain Skin findings include bronze or violaceous discoloration of the skin, a thin brown watery discharge,ulceration, bullous vesicles, crepitance, subcutaneous air, frank necrosis, and eschar formation Early on, pain is out of proportion to the examination, but eventually the dead tissue becomes insensate Lethargy and an inappropriate indifference to the illness are common

DR KABERA R

Pediatric considerations
Though unusual in children, >50 cases in children have been described Most often are complications of burns, circumcision, balanitis, severe diaper rashes, or insect bites Organisms are more frequently Staphylococcus or Streptococcus Pediatric patients have more local disease and are less toxic

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Diagnosis
Essential workup Fournier's gangrene is a clinical diagnosis History and physical exam with special attention to the perineum, and evaluating for signs of sepsis Early surgical consultation for emergent debridement is essential Other workup directed toward the relevant comorbid factors such as diabetes or immunocompromised status

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Diagnosis
Laboratory Other than Gram stain of tissue and the associated drainage, there are no specific laboratory tests that are diagnostic of Fournier's gangrene Urinalysis FBC:Leukocytosis, anemia, electrolyte imbalances, acidosis, and renal failure are common Disseminated intravascular coagulation (DIC) may be present; PT, PTT, fibrin-split products, and fibrinogen levels help identify If patient is suspected of or known to have diabetes, glucose, electrolytes, and serum ketones to evaluate for diabetes and DKA Culture of blood, urine, and tissue (when available)

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Diagnosis
Radiology Plain films of the pelvis may reveal subcutaneous emphysema and an ileus CT scanning helps if an intraabdominal or ischiorectal source is suspected US may be useful in differentiating from other causes of acute scrotum Retrograde urethrography, anoscopy, proctosigmoidoscopy, and barium enemas may be helpful to localize anatomic sources of infection
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Differential diagnosis
Testicular torsion Scrotal cellulitis Epididymitis/orchitis Tinea cruris Scrotal abscess/inguinal abscess Perirectal infections Insect and human bites

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Treatment
Ed treatment Empiric broad-spectrum antibiotics Early emergent aggressive surgical debridement Hyperbaric oxygen therapy coordinated with surgical care Treat dehydration and correct electrolytes Blood products as needed for DIC or anemia; oxygen debt can be minimized by keeping the hematocrit >30% Tetanus prophylaxis as indicated

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Medications
Antibiotic regimens Multidrug regimen -Ampicillin: 2 g i.v. q6h (peds: 50 mg/kg) and -Clindamycin: 900 mg i.v. q8h (peds: 10 mg/kg) and -Gentamicin: 5 mg/kg daily load i.v. q8h Single-drug regimens (peds: safety not established) -Ampicillin/sulbactam: 3 g i.v. initial ED dose -Imipenem: 1 g i.v. initial ED dose -Piperacillin/tazobactam: 3.375 g i.v. initial ED dose -Ticarcillin/clavulanate: 3.1 g i.v. initial ED dose or
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Medications
Blood products as indicated Dopamine or dobutamine IV drips starting at 5 mcg/kg/min titrating to effect if hypotensive after aggressive hydration Insulin adjusted to control glucose and acidosis

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The end

Thank you

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