2. SEPSIS
• MALIGNANT DYSREGULATORY MULTIORGAN SYSTEM
RESPONSE TO INFECTION
• THE RESPONSE TO INFECTION BECOMES
INAPPROPRIATELY GENERALIZED
• NORMAL TISSUES AND ORGANS BECOME INVOLVED
THAT ARE REMOTE FROM THE SITE OF INJURY
3. SEPSIS
• NORMAL HOST RESPONSE TO INFECTION IS
COMPLEX
• LOCALIZES AND CONTROLS INFECTION
• INITIATES REPAIR OF INJURED TISSUE
• ACTIVATION OF CIRCULATORY AND FIXED
PHAGOCYTES CELLS
• GENERATION OF PRO-INFLAMMATORY AND ANTI-
INFLAMMATORY MEDIATORS
4. TRANSITION TO SEPSIS
• SEPSIS OCCURS WHEN PROINFLAMMATORY
MEDIATORS EXCEED BOUNDARIES OF LOCAL
ENVIRONMENT
• LEADS TO A MORE GENERALIZED RESPONSE THAT
DOES NOTHING TO DEFEAT INFECTION
• SIRS SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME NO LONGER USED BUT USEFUL TO KNOW
5. SEPSIS
• MALIGNANT BECAUSE IT IS UNCONTROLLED,
UNREGULATED AND SELF SUSTAINING
• INTRAVASCULAR: BLOOD SPREADS MEDIATORS
USUALLY CONFINED TO CELL-TO-CELL INTERACTION
WITHIN THE INTERSTITIAL SPACE
• INFLAMMATORY BECAUSE ALL CHARACTERISTICS OF
THE SEPTIC RESPONSE ARE EXAGGERATIONS OF
NORMAL INFLAMMATORY RESPONSE IN ORGANS NOT
INVOLVED
6. SEPSIS SYNDROMES DEFINITIONS
• CONTINUUM OF SEVERITY FROM INFECTION AND
BACTEREMIA TO SEPSIS TO MULTIPLE ORGAN
DYSFUNCTION SYNDROME (MODS) TO DEATH
• SIRS NO LONGER USED (MORE ACCURATE TOOLS
AND ASSOCIATED WITH MANY CAUSES)
• SCCM, ESICM, ATS, SIS
7. EARLY SEPSIS
• NO FORMAL DEFINITION
• INFECTION: INVASION OF NORMALLY STERILE TISSUE
BY ORGANISMS RESULTING IN INFECTIOUS
PATHOLOGY
• BACTEREMIA: PRESENCE OF VIABLE BACTERIA IN THE
BLOOD
• INFECTION AND BACTEREMIA MAY BE EARLY FORMS
OF THE PROCESS THAT LEADS TO SEPSIS
8. IDENTIFICATION OF EARLY SEPSIS
• IF SEPSIS IDENTIFIED EARLY MAY DECREASE SEPSIS-
RELATED MORTALITY
• 2016 SCCM/EISCM TASKFORCE ASSESSMENT TOOL
OUTSIDE ICU
• IDENTIFY PATIENTS AT RISK OF DYING OF SEPSIS
• QUICK SOFA (qSOFA)
• MODIFICATION OF SOFA: SEQUENTIAL (SEPSIS-
RELATED) ORGAN FAILURE ASSESSMENT SCORE
9. SOFA: SEQUENTIAL (SEPSIS-
RELATED)ORGAN FAILURE ASSESSMENT
SCORE
• SOFA: RISK OF MORTALITY IN ICU
• USES SIMPLE MEASUREMENTS OF ORGAN FAILURE TO
CALCULATE A SEVERITY SCORE
• CLINCALC.COM/ICUMortality/SOFA.aspx
• RESPIRATORY TRACT (PaO2/Fi02), CVS AMOUNT OF
VASOACTIVE MEDICATION TO PREVENT HYPOTENSION,
BILIARY TRACT BILIRUBIN, COAGULATION SYSTEM
PLATELETS, NEUROLOGIC SYSTEM GLASGOW COMA
SCORE, RENAL SYSTEM CREATININE, URINARY OUTPUT
10. QUICK SOFA
• SCCM/ESICM 2016 IDENTIFIES PATIENTS WITH EARLY
SPESIS OUTSIDE ICU
• RESPIRATORY RATE GREATER THAN 22/MIN
• ALTERED MENTATION
• SYSTOLIC BLOOD PRESSURE LESS THAN 100 mmHg
• 2 OR MORE FEATURES = POOR OUTCOME
• ADDITIONAL PROSPECTIVE VALIDATION NEEDED BEFORE
SOC FOR PREDICTION OF DEATH
11. SEPSIS
• 2016 SCCM/EISCM TASK DEFINITION: LIFE-
THREATENING ORGAN DYSFUNCTION CAUSED BY A
DYSREGULATED HOST RESPONSE TO INFECTION
• ORGAN DYSFUNCTION (2016 SCCM/EISCM) INCREASE
IF 2 OR MORE POINTS IN SOFA (SEQUENTIAL SEPSIS-
RELATED ORGAN FAILURE ASSESSMENT SCORE)
• SOFA BETTER THAN SIRS IN PREDICTING IN HOSPITAL
MORTALITY, SAME AS LODS (LOGISTIC ORGAN
DYSFUNCTION SYSTEM) BUT EASIER
12. SEPTIC SHOCK
• TYPE OF VASODILATORY OR DISTRIBUTIVE SHOCK
• DEFINITION: SEPSIS THAT HAS CIRCULATORY,
CELLULAR, AND METABOLIC ABNORMALITIES THAT
ARE ASSOCIATED WITH A GREATER RISK OF
MORTALITY THANS SEPSIS ALONE
• CLINICALLY FULFILL CRITERIA FOR SEPSIS WHO
DESPITE ADEQUATE FLUID RESUSCITATION REQUIRE
VASOPRESSORS TO MAINTAIN MAP OF 65 mm Hg OR
MORE AND LACTATE GREATER THAN 2 mmol/L
13. MULTIPLE ORGAN DYSFUNCTION
SYNDROME
• DEFINITION: PROGRESSIVE ORGAN DYSFUNCTION IN
AND ACUTELY ILL PATIENT, SO THAT HOMEOSTASIS
CANNOT BE MAINTAINED WITHOUT INTERVENTION
• IT IS AT THE SEVERE END OF THE SEVERITY OF
ILLNESS
• PRIMARY DUE TO THE INSULT ITSELF (ARF
SECONDARY TO RHABDOMYOLYSIS)
• SECONDARY ORGAN FAILURE IS A CONSEQUENCE OF
HOST RESPONSE (ARDS SECONDARY TO SEPSIS)
14. CYTOKINES
• HORMONE LIKE PROTEINS
• ENABLE IMMUNE CELLS TO COMMUNICATE
• INTEGRAL ROLE IN INITIATION, PERPETUATION, AND DOWN REGULATION
• TNF MEMBRANE BOUND ALLOWING COMMUNICATION BETWEEN CELLS
DIRECTLY
• INTERLEUKIN SOLUBLE MEDIATORS ALLOWED TO EXERT INFLUENCE AT
A DISTANCE
• BIND AND ALTER FUNCTION
15. CYTOKINENS
• RECRUITMENT OF INFLAMMATORY CELLS (POSITIVE
FEEDBACK LOOP)
• STIMULATION OF T-CELLS AND B-CELLS
• INDUCE CELL MIGRATION
• PREVENT INFLAMMATORY RESPONSE FROM
OVERWHELMING AND HARMING HOST (TGF-BETA,
IL-10)
17. EFFECTS OF SEPSIS
• BACTERIAL WALL COMPONENTS (EG ENDOTOXIN)
• BACTERIAL PRODUCTS (TSST-1, M-PROTEIN, STAPH
ENTEROTOXIN B)
• CONTRIBUTE TO TRANSITION FROM A LOCAL INFECTION
TO SEPSIS
• ENDOTXIN DETECTABLE IN BLOOD OF SEPTIC PATIENTS
• ENDOTOXIN ASSOCIATED WITH SHOCK AND MODS
• INFUSED ENDOTOXIN MIMICS SEPSIS
18. SYSTEMIC EFFECTS OF SEPSIS
• WIDESPREAD CELLULAR INJURY WHEN IMMUNE
RESPONSE BECOMES GENERALIZED
• CELLULAR INJURY PRECURSOR TO ORGAN
DYSFUNCTION
• MECHANISMS INCLUDE: TISSUE ISCHEMIA, CELLULAR
INJURY, ALTERED RATE OF APOPTOSIS
19. CYTOPATHIC INJURY
• PROINFLAMMATORY MEDIATORS INDUCE
MITOCHONDRIAL DYSFUNCTION
• MITOCHONDRIAL DYSFUNCTION LEADS TO
CYTOTOXICITY
• LACTATE, PYRUVATE ADP, GLUCOSE DO NOT
PRODUCE ENERGY
• EVEN IF PRESENT CELLS CANNOT USE OXYGEN SO
THEY UNDERGO INJURY AND DEATH DUE TO ANOXIA
20. ORGAN SPECIFIC EFFECTS OF SEPSIS
• CELLULAR INJURY PROGRESSES TO ORGAN
DYSFUNCTION
• NO ORGAN SYSTEM IS PROTECTED FROM SEPSIS
• MULTIPLE ORGAN DYSFUNCTION (MODS) IS COMMON
21. ORGAN SPECIFIC EFFECTS OF SEPSIS
CIRCULATION
• HYPOTENSION SECONDARY TO DIFFUSE
VASODILATION
• UNINTENDED CONSEQUENCE OF RELEASE OF
VASOACTIVE MEDIATORS (NO, PROSTACYCLIN)
• REDISTRIBUTION OF INTRAVASCULAR FLUID
SECONDARY TO INCREASED ENDOTHELIAL
PERMEABILITY ADN REDUCED VASCULAR TONE
22. 0RGAN SPECIFIC EFFECTS OF SEPSIS
CIRCULATION
• CENTRAL CIRCULATION - DECREASED SYSTOLIC AND
DIASTOLIC FUNCTION (MYOCARDIAL DEPRESSANT
SUBSTANCES)
• REGIONAL CIRCULATION - INABILITY TO
REDISTRIBUTE AMONG MAJOR ORGAN SYSTEMS
• MICROCIRCULATION - MOST IMPORTANT TARGET
INABILITY TO EXTRACT OXYGEN
• ENDOTHELIUM - DYSFUNCTION LEADING TO
WIDESPREAD EDEMA
23. LUNG (ARDS)
• BERLIN DEFINITION (2012)
• RESPIRATORY SYMPTOMS WITHIN ONE WEKK OF
INSULT
• IMAGING COMPATIBLE WITH PULMONARY EDEMA
• NO CARDIAC FAILURE OR FLUID OVERLOAD
• MODERATE TO SEVERE IMPAIRMENT OF
OXYGENATION (PaO2/FiO2 LEVEL)
24. OTHER ORGANS
• GI TRACT - NORMAL BARRIER FUNCTION DEPRESSED
• LIVER - UNABLE TO CLEAR ENDOTOXIN, BACTERIA OR
DERIVED PRODUCTS
• KIDNEY - ACUTE RENAL FAILURE
• NERVOUS SYSTEM - ALTERED SENSORIUM
(ENCEPHALOPATHY)
25. MODS
• NO UNIVERSALLY ACCEPTED CRITERIA
• PROGRESSIVE ABNORMALITIES IN MULTIPLE ORGAN SYSTEMS
• SPECIFIC PARAMETERS USED TO DX MODS ALSO USED IN
SOFA (SEQUENTIAL SEPSIS-RELATED ORGAN FAILURE
ASSESSMENT SCORE)
• RESPIRATORY - PaO2/FiO2 RATIO, BLOOD - PLATELETS, LIVER -
BILIRUBIN, RENAL - CREATININE, BRAIN - GLASGOW, CVS -
HYPOTENSION AND VASOPRESSOR REQUIREMENTS
26. SIGNS AND SYMPTOMS OF SEPSIS
• SPECIFIC TO AN INFECTIOUS SOURCE (COUGH - PNEUMONIA, PURULENT
EXUDATE - WOUND INFECTION)
• HYPOTENSION SBP LESS THAN 90 mmHg, MAP LESS THAN 70 mm Hg, SBP
DROP OF 40 mm Hg
• TEMPERATURE GEATER THAN 38.3C OR LESS THAN 36C
• HEART RATE GREATER THAN 90 BPM
• RESPIRATORY RATE GREATER THAN 20/MIN
• ALTERED MENTAL STATE
• ILEUS
• DECREASED CAPILLARY REFILL, CYANOSIS, MOTTLING
27. LABORATORY SIGNS OF SEPSIS
• NONSPECIFIC MAY BE ASSOCIATED WITH UNDERLYING
CAUSE, TISSUE HYPOPERFUSION, OR ORGAN
DYSFUNCTION
• LEUKOCYTOSIS ABOVE 12000 OR LEUKOPENIA BELOW 4000
• NORMAL WBC WITH GREATER THAN 10% BANDS
• HYPERGLYCEMIA GREATER THAN 140
• C-REACTIVE PROTEIN GREATER THAN 2 SD ABOVE NORMAL
• PROCALCITONIN GREATER THAN 2 SD ABOVE NORMAL
28. LABORATORY SIGNS OF SEPSIS
• ARTERIAL HYPOXEMIA PaO2/FiO2 LESS THAN 300
• OLIGURIA LESS THAN 0.5 ml/Kg/HR FOR 2 HRS DESPITE FLUID
RESUSCITATION
• RISE IN CREATININE OF MORE THAN 0.5 MG/DL
• COAGULATION ABNORMALITIES INR MORE THAN 1.5, PTT MORE
THAN 60, TCP BELOW 100,000
• BILIRUBIN ABOVE 4
• HYPERLACTATEMIA
• ABNORMAL ADRENAL FUNCTION (HYPONATREMIA, HYPERKALEMIA)
29. MICROBIOLOGY OF SEPSIS
• IDENTIFICATION OF ORGANISM IN CULTURE IN
PATIENT WHO DEFINES SPESIS IS HIGHLY SUPPORTIVE
BUT NOT NECESSARY
• ORGANISM NOT IDENTIFIED IN 50% WITH SEPSIS
• POSITIVE CULTURES NOT REQUIRED REGARDING
TREATMENT WITH EMPIRIC ANTIBIOTICS
30. SEPSIS SIX
• EASY TO APPLY WHILE MULTIDISCIPLINARY TEAM ASSEMBLED
IN UNIT NOT PREPARED FOR SEPSIS
• HIGH FLOW OXYGEN
• BLOOD AND OTHER CULTURES AND GRAM STAINS
• BROAD SPECTRUM ANTIBIOTICS
• MEASURE LACTATE
• START IV RESUSCITATE WITH CRYSTALLOIDS
• ACCURATE URINE OUTPUT
31. EARLY GOAL DIRECTED THERAPY
• BLOOD CULTURES BEFORE ANTIBIOTIC
ADMINISTRATION
• MEASURE BLOOD LACTATE
• BROAD SPECTRUM ANTIBIOTICS STARTED WITHIN
ONE HOUR
• PLACEMENT OF CVP AND ARTERIAL CATHETERS
• 500 CC BOLUS EVERY 30 MINUTES TO ACHIEVE CVP
OF 8-12 mmHg
32. EARLY GOAL DIRECTED THERAPY
• IF MEAN ARTERIAL PRESSURE UNDER 65,
VASOPRESSOR
• IF MEAN ARTERIAL PRESSURE MORE THAN 95,
VASODILATORS
• IF ScvO2 UNDER 70% RBC TRANSFUSION TO ACHIEVE
Hct OF 30%
• MAINTAIN URINE OUTPUT OF 0.5 mL/Kg/H
33. MATERNAL AND PERINATAL
COMPLICATIONS OF SEPSIS AND SEPTIC
SHOCK (BARTON AND SIBAI)
• ADMISSION OT ICU
• PULMONARY EDEMA
• ARDS
• ACUTE RENAL FAILURE
• SHOCK LIVER
• SEPTIC EMBOLI TO OTHER ORGANS
• MYOCARDIAL ISCHEMIA
• DIC
• DEATH
34. FETAL COMPLICATIONS OF SEPSIS
• PRETERM DELIVERY
• NEONATAL SEPSIS
• PERINATAL HYPOXIA OR ACIDOSIS
• FETAL OR NEONATAL DEATH
35. PROGNOSTIC INDICATORS OF POOR
OUTCOME IN SEPTIC SHOCK
• DELAY IN INITIAL DIAGNOSIS
• PRE-EXISTING DEBILITATING DISEASE(S)
• POOR RESPONSE TO FLUID RESUSCITATION
• DEPRESSED CARDIAC OUTPUT
• REDUCED OXYGEN EXTRACTION
• HIGH SERUM LACTATE (MORE THAN 4 mmol/L)
• MODS
36. SEPTIC SHOCK MANAGEMENT - FIRST 6
HOURS
INITIAL RESUSCITATION
• BLOOD CULTURES WITHIN ONE HOUR
• EMPIRIC ANTIBIOTICS WITHIN ONE HOUR
• CENTRAL LINE WITHIN 4 HOURS
• CVP 8 mm Hg OR HIGHER WITHIN 6 HOURS
• NOREPINEPHRINE IF MAP LESS THAN 65 AFTER
RESUSCITATION
• RBCs IF Hb LESS THAN 6 g/dl
37. HEMODYNAMIC MANAGMENT
• CENTRAL LINE AND ARTERIAL PLACEMENT
• WARM CRYSTALLOID (SALINE OR LR)
• RAPID INFUSIONS OF 500 CC BOLUSES OVER 15 MIN
• 1 HOUR GOAL: 20 ml/Kg
• 3 hour goal: 30 ML/kG
• PHYSIOLOGIC PERFUSION ENDPOINTS: CVP 8-12 mm
Hg, MAP MORE THAN 65 mm Hg, UO 25 mm/HR
38. HEMODYNAMIC MANAGEMENT
CONTINUED
• VASOPRESSOR AGENTS IF MAP BELOW 65 mm Hg
AFTER FLUID RESUSCITATION (NOREPINEPHRINE)
• INOTROPIC AGENT IF ScvO2 REMAINS UNDER 70%
• INOTROPES USEFUL WITH REFRACTORY SHOCK AND
DIMINISHED CO
• SUPPLEMENT WITH O2, INTUBATE AND VENTILATE AS
NEEDED
39. ANTIBIOTIC THERAPY
• PROMPT CULTURES
• DO NOT DELAY THERAPY WHILE AWAITING CULTURE RESULTS
• SURVIVAL DIFFERENCES SEEN IN DELAY OF ANTIBIOTIC BY
ONLY ONE HOUR
• EMPIRIC THERAPY INITIALLY: PENICILLIN, GENTAMYCIN,
CLINDAMYCIN; VANCOMYCIN AND PIPERACILLIN AND
TAZOBACTUM, VANCOMYCIN AND PIPERACILLIN NAD
TAZOBACTUM
• CLINDAMYCIN REDUCES TOXIN PRODUCTION AND IS BETTER
CHOICE WHEN BACTERIA ARE IN STATIONARY PHASE (STILL
PRODUCE TOXINS)
40. MAINTENANCE PHASE
• INSULIN PROTOCOL IF INDICATED
• CORTICOSTEROID THERAPY FOR REFRACTORY SEPTIC SHOCK
(SBP UNDER 90) AFTER ADEQUATE FLUID RESUSCITATION AND
VASOPRESSOR NOT EFFECTIVE (HYDROCORTISONE 50 mg IV q6h)
• NUTRITION
• VTE PROPHYLAXIS
• REASSESS ANTIBIOTIC THERAPY AND NARROW SPECTRUM IF
APPROPRIATE
• TEMPERATURE CONTROL
41. TOXIC SHOCK SYNDROME
STAPHLOCOCCAL
• MUST BE CONSIDERED IN ANY PATIENT PRESENTING
IN SHOCK IN THE ABSENCE OF CLEAR ETIOLOGY
• TEMP MORE THAN 38.9C (102.0F)
• SBP 90 mm Hg OR LESS
• DIFFUSE MACULAR ERYTHRODERMIA
• 1-W WEEKS AFTER ONSET OF ILLNESS, PARTICULARLY
INVOLVING PALMS AND SOLES
42. TOXIC SHOCK SYNDROME
STAPHLOCOCCAL
• 3 OR MORE ORGANS SYSTEMS MUST BE INVOLVED
• GI: VOMITING OR DIARRHEA
• MUSCULAR: SEVERE MYALGIA OR CK MORE THAN 2 UPPER LIMIT OF NORMAL
• MUCOUS MEMBRANES: VAGINAL, OROPHARYNGEAL, OR CONJUNCTIVAL
HYPERMEIA
• RENAL: BUN OR CREATININE MOR THAN 2 TIMES NORMAL
• HEPATIC: BILIRUBIN OR TRANSAMINASES MORE THAN 2 TIMES NORMAL
• BLOOD: PLATELETS LESS THAN 100,000
• CNS: ENCEPHALOPATHY
43. TOXIC SHOCK SYNDROMES
STREPTOCOCCAL
• ISOLATION OF GAS FROM STERILE SITE
• HYPOTENSION SPB 90 mm Hg OR LESS
• RENAL DYSFUNCTION CREATININE 2 mg/dl OR GREATER
• COAGULOPATHY THROMBOCYTOPENIA, DIC
• LIVER DYSFUNCTION TRANSAMINASE OR BILIRUBIN MORE
THAN TWICE NORMAL
• ARDS
• SOFT TISSUE NECROSIS
44. NECROTIZING SOFT TISSUE
INFECTIONS
• CHARACTERIZED CLINICALLY BY FULMINANT TISSUE
DESTRUCTION, SYSTEMIC SIGNS OF TOXICITY, HIGH
MORTALITY
• MAY INCLUDE CELLULITIS, MYOSITIS, FASCIITIS
• WITHOUT SURGERY MORTALITY UP TO 50%
• HEIGHTENED SUSPICION AND WILLINGNESS TO TAKE
PROMPT ACTION ONLY ADVANTAGE WE HAVE IN
COMBATING THIS MONSTER
45. INCIDENCE AND EPIDEMIOLOGY NSTI
• TYPE I: POLYMICROBIAL, 70-80% OF CASES,
ANAEROBES AND AEROBES, USUALLY AFTER
SURGERY, BETTER PROGNOSIS
• TYPE II: GROUP A STEP OR STAPH, 20-30%, VERY
AGGRESSIVE, MARKED SYSTEMIC TOXICITY
• MORTALITY 9-73%, IN OBSTETRICS 33%
• PERINEUM NSTI TWICE AS LETHAL
• WILL NOT DISCUSS TYPE III OR IV (VIBRIO OR FUNGAL)
46. NECROTIZING SOFT TISSUE
INFECTION
• MOST OMINOUS FINDING ASSOC WITH MORTALITY IS DELAY IN
DIAGNOSIS AND PERFORMANCE OF RADICAL SURGICAL
DEBRIDEMENT
• DELAY BEYOND 48 HRS = 73% MORTALITY (STEPHENSEN AJOG
1992)
• EVEN DELAY BEYOND 24 HRS PORTENDS MORTALITY (MCHENRY
1993)
• EVEN WITH IDEAL CARE MORTALITY 12% (MORANTES 1195)
• COMORBID CONDITIONS (DIABETES, OBESITY,
IMMUNOSUPPRESSION ETC) ASSOC WITH INCREASED MORTALITY
47. NECROTIZING SOFT TISSUE INFECTION
PATHOPHYSIOLOGY
• MICROORGANISM GAINS ACCESS TO SOFT TISSUE,
PROLIFERATE, ELEASE TOXINS AND ENZYMES CAUSING
ISCHEMIA AND NECROSIS
• CYTOKINENS PRODUCTION INDUCED, CAUSING
SYSTEMIC TOXICITY, SEPSIS/SEPTIC SHOCK, MODS
• STREP A VIRULENCE FACTORS NUMEROUS: M1 M3
PROTEINS, STREPTOCOCCAL PYROGENIC EXOTOXINS A
B C (TSS)
• STAPH AUREUS: TOXIC SHOCK SYNDROME TOXIN (TSST),
STAPHYLOCOCCAL ENTEROTOXIN
48. NSTI CLINICAL PRESENTATION AND
MANAGEMENT
• NO KNOWN MARKERS THAT INDICATE WHICH
INFECTION WILL PROGRESS TO NSTI
• USUALLY PATIENTS HAVE A PREDISPOSING FACTOR
(TRAUMA, IMMUNOSUPPRESSION - DIABETES, CRF,
OBESITY)
• ANY PATIENT WHO HAS CELLULITIS THINK OF GAS
(ALTHOUGH RARE)
• MOST COMMON ERRORS: DELAY IN DIAGNOSIS AND
INADEQUATE SURGICAL DEBRIDEMENT
49. NSTI CLINICAL PRESENTATION AND
MANAGEMENT
• TYPICALLY SEVERE PAIN, MORE THAN EXPECTED
• ALWAYS ASSESS FOR CUTANEOUS ANESTHESIA
• SKIN DISCOLORATION LATE SIGN
• BROAD SPECTRUM ANTIBIOTICS AND TAKE TO
OPERATING ROOM
• DARK BROWN SATERY DISCHARGE TYPICAL BUT CAN
BE PURULENT
50. NSTI SIGNS AND SYMPTOMS
• ONCE DIAGNOSIS SUSPECTED - BROAD SPECTRUM
ANTIBIOTICS AND TKAE TO OPERATING ROOM
• DO NOT DELAY SURGICAL DEBRIDEMENT OF ALL NECROTIC
TISSUE
• FAILURE TO ADEQUATELY DEBRIDE RESULTS IN REPEATED
SURGERIES AND INCREASED MORTALITY
• SEND TISSUE FROM OPERATING ROOM FORM IMMEDIATE
PROCESSING FOR GRAM STAIN AND CULTURE
• DO NOT CLOSE WOUND, PACK WITH GAUZE AND 0.25%
ACETIC ACID AND REASSESS IN 6 HOURS
