Transient Septic Bacteremia in Burn and Necrotic Wound Debridement

TRANSIENT SEPTICBACTEREMIA IN BURNAND NECROTICWOUND DEBRIDEMENTBryan Tune CRNA, DNP

Objectives Identify patient populations that are athigh risk for Transient Septic Bacteremia Discuss Pathophysiology of SepticBacteremia Review the clinical signs and symptomsobserved during Transient SepticBacteremia. Discuss treatment and patientstabilization.

Transient Septic Bacteremia –AKA: Also referred to in the literature as: Transient Endotoxemia Sepsis Toxic Shock Syndrome TSS Shooter’s fever

What is Transient SepticBacteremia A septic “storm” or bacterial showerduring tissue manipulation of burn orwound debridement Classic sepsis presentation, however itoccurs in a matter of seconds. Cytokinemediated. Quick and effective treatment required

Brief Pathophysiology Proinflammatory response to infection Mediators• TNF Alpha, IL-1, IL-6• Complement system (C5 alpha)• Bacterial factors• Endotoxin, bacterial cell wall products, bacterialtoxins Immunosuppressive

TSB Pathophysiology Continued: TSB occurs as a result of a “BacterialShower” Bacterial colonies are released into thevascular system. Common: (Staph groupA and/or Clostridium) Endotoxins and cytokines are immediatelyreleased causing the classic sepsis picture TNF Histamine Bradykinin

Time-course of inflammatory response duringsepsis(modified from Management of Severe Sepsis and Septic Shock. Curr Opin Crit Care 2004;10:354-363)

Transient Septic BacteremiaBurns T.S.B. can occur during debridement ofburn wounds (usually not seen duringinitial burn debridement) Common in large deep 2 nd and 3 rd degreeburn tissue excision Burn tissue (non-viable) is a growthmedium for bacteria Early debridement and allografting? Debridement and antimicrobial dressings

TSB Also Found In: Large necrotic wound Necrotizing Fasciitis Necrotizing soft tissue wounds Fournier’s Gangrene Gastrointestinal surgical procedures Burns

Necrotizing Fasciitis

Necrotizing Fasciitis Soft tissue infection that primarily affectssuperficial fascia Commonly found in IVDA and “SkinPopping” Higher incidence in patients with poorlycontrolled diabetes Diagnosed by clinical exam, CT, and/ortissue biopsy

Necrotizing Fasciitis (NF) Type 1 A mixed infection caused by aerobic andanaerobic bacteria. These occur mostcommonly after surgery or in individuals withdiabetes and peripheral vascular disease. Type 2 A monomicrobial infection caused primarilyby group A streptococcus (GAS), although itis occasionally caused by communityassociatedmethicillin-resistantStaphylococcus aureus (MRSA)

Clinical Presentation of N.F. Diffuse swelling Erythema Extreme pain Frequently no drainage is observed Subcutaneous gas on C.T. and/or xray

Clinical signs and symptoms Acidosis Respiratory failure Low SVR High C/O Can progress to MODs Arrest

Necrotising Fasciitis of neckand chest as a result of IVDA

Risk Factors for NF Conditions associated with necrotizing vs.non-necrotizing infections Drug use Diabetes mellitus (present in up to 60% ofcases) Obesity Immunosuppresion Malnutrition HIV infection Alcoholism

Diagnosis of NF- Labs Interpretation of Risk Score > 6 should raise suspicion of NF > 8 is highly predictive of NF (75-80% in onestudy with NF had scores over 8)

Morbidity and Mortality Near 30% mortality with earlydetection/treatment Near 90% mortality with late intervention Repeated surgical debridement also greatlyincreases M/M Factors that increase mortality: Truncal involvement Diabetes Extremes of Age Anorectal Involvement

Causative Bacteria MRSA Group A Step Staph aureus Vibrio vulnificus Clostriduim

Fournier’s Gangrene Necrotizing Fasciitis of groin andperineum Found most common in patients withdiabetes and obesity Treatment is identical to necrotizingfasciitis in that extensive debridement andABX therapy is the only definitivetreatment

Fournier’s Gangrene

SepsisAll patients with severe sepsis require appropriateantimicrobial agents immediately and physiologicsupportive therapy.Antimicrobial therapy is often an empiric choicebecause of the time required for culture andsensitivity results. Larger spectrum, unless there is strong suspicion of theorganismMany patients do not have a pathogen identified.Empiric antifungal therapy is necessary in somecases.

More than 90 % of cases are caused by amonomicrobial infection.Possible gram-negative pathogens include: Escherichia coli (40%) Klebsiella pnemoniae (7%) Pseudomonas species Proteus species Gram-positive organisms (e.g. streptococcus pneumoniae(15%)

Anaerobic microorganisms arefound in less than 5% of cases-RE: superficial colonization.Multiple isolates are found inless than 10%

Management Antibiotic therapy: Should be composed of triple therapy ifMRSA can not be ruled out:• Pen G• Vancomycin• Clindamycin

Antibiotic Therapy

Clinical Management:Preoperative metabolic status evaluationEvaluate preoperatively the need for Arterial BPmonitoring- Likely and central venous access.Need to anticipate potential for large volume bloodloss.Assure optimum venous access for fluid resuscitation Central line CVP monitoring Large fluid resuscitation requirements• Utilizing Early Directed Goal TherapyFoley Catheter

Clinical Management: Symptom and systems driven….*EARLY GOAL DIRECTED THERAPY* ABC’s Treat hypotension (fluids, blood products,vasopressors) Removal of contaminated tissue source bysurgeon. Debridement can result inmassive amounts of tissue excision beforehealthy tissue is reached

Intra-Operative ClinicalManagementLarge fluid resuscitation with crystalloid andcolloid• Can be 10-20 liters per day• Consider Plasma-lyte (lactate free) vs LREvaluate need for post-op ventilation with serialABG and metabolic panels during caseBase excess can be a useful predictor ofsuccessful fluid resuscitationKeep HCT at or above 24 to help optimizeintravascular drag coeffient and tissue perfusion.Identify coagulopothy- very likely (FFP and Cryo). ROTEM- Rotational Thromboelastometry??

Intra-operative ClinicalManagement-Vasopressors- Vasopressor therapy may be required for endorgan perfusion Consider Vasopressin: Evaluate appropriateness of Vasopressin infusionfor V2 receptor stimulation and splanchnicvascular contraction Does not affect coronary blood flow Can be used alone or with other catecholamines Infusion rate: 0.04 units per hour as a constant• Not titrated. First vasopressor on and last off.

Intra-operative ClinicalManagement:-Vasopressors- Norepinephrine (Levophed) infusion Improves and/or maintains MAP >60 Improves LVEDF Increases SVR Some recent data shows coronary arterydilation and increase myocardial perfusion Infusion dosing: 1-50 mcg/min. Titrated toSystolic and MAP.

Intraoperative TSB Management EpinephrineBacteremic storm can be so significant Epinephrinemay be required Mast cell stabilization Histamine response from histamine andbradykinin release from bacterial storm Emergency resuscitation for extremehypotension with ensuing bradycardia. 5-10 mcg bolus may be required, followedby an infusion of 1-20 mcg/min.

Adrenal Insufficiency The incidence of adrenal insufficiency in sepsisapproximately 30-70% Defined as hypotension resistant to volumeresuscitation and dependent on vasopressors Annane, 2002 demonstrated that steroidsimprove mortality in patients with septic shockand adrenal insufficiency Mortality is more than double that of patientswith abnormal adrenal responsiveness hyponatremia, hyperkalemia, weakness, andhyperpigmentation not specific enough in ICUsetting

Cosyntropin Stim. Testing (ACTH) In the study by Annane, adrenalinsufficiency was defined as an increase intotal cortisol < 9 mcg/dL in response to a250 mcg Cosyntropin Stimulation Test This formed the basis for current practiceof treating patients with septic shock andadrenal insufficiency with stress dosesteroids

Steroid Dosing Stress dosing with hydrocortisone forpotential adrenal suppression (doses>300mg strongly discouraged in theliterature) Typical dosing of 50-100mg Bicarbonate Increase pH Improve vasopressor response in severeacidosis patient

Nutritional SupportFor clinicians caring for critically ill patients, thegoal of nutrition support has been to deliver 100%of nutrient requirements, calculated for the specificmetabolic condition, in the shortest time possible.Recently, clinical experts in intensive care medicineand nutrition and published studies in the medicalliterature have determined that for critically illpatients, administering nutrients at quantities lessthan a calculated metabolic expenditure maysignificantly improve outcomes.

Transient Septic BacteremiaCase Study 48 year old male- Scheduled for debridementand completion amputation of right leg. PMHX: IVDA, Hep-C, HTN, DM- poorlycontrolled, smoker, ETOH PSHX: Multiple abscess I&D’s, Left toeamputation, facial laceration repair, RightAKA. Social HX: Homeless, IVDA, Poor nutrition,limited resources, non-compliant with DMregimen. Admitted through ED with a-vascular leg with maggot infestation.

Preop: Case Study VS: BP- 91/40 HR: 138 Temp: 39.5 SpO2- 93% - 2 liters NC Diaphoretic Pertinent Lab Values: WBC- 68,000, HgB- 9.2, Lactate- 4, pH-7.22, Base Deficit- (-12).•OMG!

Case Study Preoperatively 2 liters of LR were rapidlyinfused prior to transport to OR. Consent: GETA Aline- (Placed preop under local) Central Line- Subclavian vs. IJ (placement afterGETA) Blood Products Postoperative Ventilation

Intraoperative: Induction: Midazolam 2mg Fentanyl 50mg Amidate 16mg (best choice???) Succinylcholine: 100mg Sevoflurane for maintance Fluid bolusing continued through inductionand during the course of the procedure.

Case Study: Intraoperative Surgical excision of necrotic tissue – pungentodor VSS with fluid bolusing in place at start ofprocedure. Within 10 minutes of surgical debridementand excision of right leg the patient began todecompensate quickly: HR- 150s BP- 79/40Neosynephrine bolus dosing at 100mcg everyminute needed to maintain blood pressure

Intraoperative: Vasopressin infusion initiated: 0.4 units permin Levophed Infusion initiated: 20mcg/min Despite aggressive and rapid initiation ofvasoactive drips and fluid bolusing thepatient continued to decompensate. BP continued to drop into the 50’s systolic HR- 160s Unresponsive to Neosynephrine doses 2 Amps of Bicarb administered Epinephrine 100mcg bolus x3

Intraoperative Bicarbonate infusion initiated Levophed increased to 40mcg/min 1 unit PRBC 3 Units FFP Albumin infusion Hydrocortisone 100mg IV

Case Study- Repeat labs sent after stabilization- Pt remained intubated and transported toPACU- Lab results: INR 2.1, HCT- 34, WBC-92,- ABG: pH: 7.21, CO2- 39, PO2- 160, BE- (-10)- *8 hours later nursing staff turned pt on side fordressing change and pt went into PEA. ACLSunsuccessful.

Transient Septic BacteremiaReviewCommon in burn wound debridement andnecrotic wound debridement (AKA’s, BKA,Arm amputations)Goal directed resuscitation(ventilation, fluids, blood, vasopressors,ABX)Minimally invasive C/O monitoring (vigileo?)-(pulse pressure variance).Post Op: Isolation, may require ventilatorsupport, sedation, vasopressors, andcontinued resuscitation in PACU/ICU

Lunch??Questions?