DAMAGE CONTROL. Outline. Definition 5/29/2014. No Disclosures

Transcription

1 DAMAGE CONTROL No Disclosures Rochelle A. Dicker, MD Associate Professor of Surgery and Anesthesia University of California, San Francisco Definition Term used in the Merchant Marines and in Navies for the emergency control of situations that may hazard the sinking of a ship Outline Human Injury/Damage Compartment syndrome Guidelines for Damage Control Algorithm for Damage Control Highlighting ICU Care The Open Abdomen and Complications Enteroatmospheric fistulae 1

2 Consequences of Major Injury or Disease anatomic defect physiologic defect iatrogenic defect a lethal cascade of events... Anatomic Defects Anatomic Derangement of the Airway Holes in blood vessels Holes in solid organs causing hemorrhage Holes in hollow viscera causing leakage of intestinal contents and urine Contusions of the lung and heart causing organ dysfunction Disruption of the skeleton Intercranial Injury Physiologic Consequences of Prolonged Shock Hypoperfusion Vasoconstriction Metabolic Acidosis Massive Release of catecholamines, glucocorticoids, ADH, Aldosterone, Cytokines Consequences of Prolonged Shock Loss of integrity of cellular membranes Leakage of fluid into interstitium Leakage of sodium into cells Result: Requirement for Massive Fluid Infusion to restore intravascular volume and tissue perfusion 2

3 The Lethal Triad metabolic acidosis hypothermia coagulopathy Iatrogenic Consequences of Resuscitation Massive Edema Increased intra-abdominal, intra-thoracic, intracranial and subfascial pressures: i.e. Compartment Syndrome Definition of the World Congress on Abdominal Compartment Syndrome Persistent bladder pressure of >20mm mercury with new onset organ dysfunction Risk Factors for Compartment Syndrome Post-traumatic hemorrhage Intraperitoneal bleeding Retroperitoneal bleeding Any vigorous fluid resuscitation Post-resuscitative visceral edema Lethal triad 3

4 Hepatic ischemia Coagulopathy Hypothermia Acidosis Abdominal bleeding Splanchnic hypoperfusion Intra-abdominal hypertension Abdominal compartment syndrome Gut edema Free radicals organ damage A cycle of ischemia producing intra-abdominal hypertension and the abdominal compartment syndrome ( from Michael Rotondo, MD). Physiologic Consequences of the Abdominal Compartment Syndrome Cardiovascular Decreased VR Increased SVR Hypotension Splanchnic Circulation Decreased splanchnic flow Decreased phi Decreased hepatic artery and portal vein flow Decreased Renal blood flow, GFR and Urine Output Pulmonary Decreased Compliance Increased PIP Increased PA pressure Increased Vd/Vt Increased Qs/Qt Cerebral Circulation Increased ICP Decreased CPP Damage Control In Surgical Care Stone in Abbreviated celiotomy and packing Damage Control in the Trauma setting coined by Rotondo and Schwab in 1993 Guidelines for Initiating Damage Control Maneuvers Acidosis ph < 7.2 Base Deficit -8 Lactate 4 Hypothermia < 35 celcius 4

5 More Guidelines for Damage Control Ongoing Resuscitation Persistent shock with systolic BP <90 > 10 litres crystalloid >10 units packed red blood cells Operative Time > minutes with abdominal cavity open More Damage Control Guidelines Coagulopathy PTT > 60 INR >1.6 Host Factors Defining Reserve Age Underlying disease Physiologic reserve: TIME Malperfusion and ISS Indications for the Open Abdomen Damage Control for Trauma Abdominal Compartment Syndrome Massive Resuscitation Burn Pancreatitis Severe Abdominal Infection Acute Mesenteric Ischemia Necrotizing Infection of the Abdominal Wall Goals of Damage Control Laparotomy Control of Hemorrhage Rapid Control of Intestinal Spillage Rapid Temporary Abdominal Closure Rapid Transfer to the ICU for continued resuscitation and restoration of physiologic homeostasis Delay of intestinal reconstruction until repeat laparotomy hours later 5

6 Algorithm for Damage Control Step One Initial ED assessment Resuscitation Recognition and operative decisions Algorithm for Damage Control Step Two Initial trauma laparotomy Hemorrhage control Contamination control Intra-abdominal packing Temporary dressing 6

7 Algorithm for Damage Control Step Three ICU 2 resuscitation Warming Correct coagulopathy Individualized ventilatory support Secondary survey and planning 7

8 ICU Resuscitation Rewarming/Correct hypothermia CENTRAL LINE Infusion of warm fluids Bair hugger Prevent insensible losses PRN humidifier on vent set at 40 ICU Resuscitation Correct coagulopathy, acidosis, electrolyte imbalance Measure CBC, coags, fibrinogen Correct K+, Mg+, Ca+ deficiencies Measure and use base deficit as guideline Consider effect of Normal Saline on base deficit ICU Resuscitation Utilize central venous pressures to assist in guiding resuscitation KNOW the pitfalls of interpretation ICU Resuscitation If PA Catheter is necessary CI > 3L/min End diastolic volume index ml SaO2 >95% SVO2 >65% Consider ECHO 8

9 Medications ICU Care Peptic ulcer prophylaxis H2 blockers or proton pump inhibitors DVT prophylaxis Low molecular weight heparin is superior Insulin drip Maintain blood glucose mg/dl Drips for analgesia and sedation Antibiotic therapy with open abdomen ICU Care-Best Practices Head of Bed at 30 Frequent suctioning and oral hygiene Functioning nasogastric tube Functioning wound vac Hourly urine output Bladder pressure checks (if applicable) Pad pressure points Algorithm for Damage Control Step Four Reoperation: Typically hours Pack removal Definitive repairs Decisions on closure Revolution in the Management of the Open Abdomen Preservation of the Peritoneal Space Progressive abdominal closure (prevention of lateral fascial retraction) Vacuum-assisted wound management Use of biologic dressings Scott BG, Feanny MA, Hirshberg A. Early definitive closure of the open abdomen: A quiet Revolution. Scand J Surg2005;94:

10 Options for Biologic Dressing of Exposed Viscera Skin Flaps Homologous split thickness skin Autologous split thickness skin Acellular dermal matrix Musculofascial advancement flaps Rotation skin and muscle flaps Free flaps Abdominal Complications of the Open Abdomen Wound infection Dehiscence Fasciitis/necrosis Intra-abdominal abscess Enteroatmospheric fistula Risks increase with multiple operations and multiple Surgeons Problem of Enteroatmospheric Fistula Absence of overlying soft tissue with good blood supply precludes spontaneous healing Exposed abdominal viscera predisposes to development of additional holes in the GI tract Complex Wound difficult to manage Principles of Management Specific for Enteroatmospheric Fistula PREVENTION Protect exposed abdominal viscera during open abdomen management Limit access to the wound to one or two SENIOR people Attempt to seal leak when first recognized Protect adjacent viscera with biologic dressings to avoid additional holes Control fistula effluent Rotate flaps with good blood supply to cover fistula in selected cases Resect well established enteroatmospheric fistula only when patient fit and infection free 10

11 Principle 4 Control Fistula Effluent Fixed Visceral Block Vacuum Assisted Wound Management System Wound Drainage Bags Requires expert enthusiastic nursing assistance Creativity 1.Hyon SH, Martinez-Garbino JA, Benati ML, et al. Management of a high-output postoperative Enterocutaneous fistual with a vacuum sealing method and continuous enteral nutrition. ASAIO J. 2000;46: Erdmann D, Drye C, Heller L et al. Abdominal wall defect and enterocutaneous fistula treatment With Vacuum Assisted closure (V.A.C.) system. Plast Reconstr Surg 2001;108: Alvarez AA, Maxwell GL, Rodriguez GC. Vacuum-assisted closure for cutaneous gastrointestinal Fistula management. Gynecol Oncol 2001;80: Cro C, George KJ, Donnelly J, et al. Vacuum assisted closure in the management of enterocutaneous Fistulae. Postgrad Med J. 2002;78: Principle 4 Control Fistula Effluent DO NOT INTUBATE A FISTULA in the middle of a fixed visceral block open abdomen You won t control the drainage You will make the hole bigger Risk of additional holes Extra-Abdominal Complications of the Open Abdomen Ventilator-associated pneumonia Aspiration pneumonitis ARDS Bloodstream infections Deep venous thrombosis/pulmonary embolus Pressure ulcers Multiple organ dysfunction syndrome Clinical Signs: Veering off Trajectory Systemic Inflammatory Response Tachycardia Tachypnea Elevated WBC Fever Increased pain and aggitation Mental status changes Decreased urine output Worsening base deficit Each observation is relative to the last 11

12 Damage Control Long-Term Mortality Impact Now indisputable: Early studies from 53% survival to 90% survival Morbidity 76% readmission rate Sutton et al from Maryland Shock/Trauma Infection, hernia management and fistula management were reasons for readmission Survival of readmitted patients 100% Average ISS 33 12