5/29/2014 No Disclosures DAMAGE CONTROL Rochelle A. Dicker, MD Associate Professor of Surgery and Anesthesia University of California, San Francisco Definition Outline Term used in the Merchant Marines and in Human Injury/Damage Navies for the emergency control of Compartment syndrome situations that may hazard the sinking of a Guidelines for Damage Control ship Algorithm for Damage Control Highlighting ICU Care The Open Abdomen and Complications Enteroatmospheric fistulae 1
5/29/2014 Consequences of Major Anatomic Defects Injury or Disease Anatomic Derangement of the Airway Holes in blood vessels Holes in solid organs causing hemorrhage anatomic defect Holes in hollow viscera causing leakage of physiologic defect intestinal contents and urine iatrogenic defect Contusions of the lung and heart causing organ dysfunction Disruption of the skeleton … a lethal cascade of events ... Intercranial Injury Physiologic Consequences of Consequences of Prolonged Prolonged Shock Shock Hypoperfusion Loss of integrity of cellular membranes Vasoconstriction Leakage of fluid into interstitium Metabolic Acidosis Leakage of sodium into cells Massive Release of catecholamines, Result: Requirement for Massive glucocorticoids, ADH, Aldosterone, Fluid Infusion to restore intravascular Cytokines volume and tissue perfusion 2
5/29/2014 Iatrogenic Consequences of Resuscitation The Lethal Triad Massive Edema metabolic acidosis Increased intra-abdominal, intra-thoracic, hypothermia intracranial and subfascial pressures: i.e. coagulopathy Compartment Syndrome Definition of the World Congress on Risk Factors for Compartment Abdominal Compartment Syndrome Syndrome Post-traumatic hemorrhage Persistent bladder pressure of >20mm Intraperitoneal bleeding mercury with new onset organ dysfunction Retroperitoneal bleeding Any vigorous fluid resuscitation Post-resuscitative visceral edema Lethal triad 3
5/29/2014 Physiologic Consequences of the Splanchnic hypoperfusion Abdominal Compartment Syndrome Pulmonary Hepatic ischemia Gut edema Cardiovascular Decreased Decreased VR Intra-abdominal Compliance hypertension Increased SVR Coagulopathy Free radicals Increased PIP Hypothermia organ damage Hypotension Acidosis Increased PA pressure Splanchnic Circulation Increased Vd/Vt Decreased splanchnic flow Increased Qs/Qt Decreased pHi Abdominal Abdominal bleeding compartment Decreased hepatic artery Cerebral Circulation syndrome and portal vein flow Increased ICP Decreased Renal blood flow, Decreased CPP GFR and Urine Output A cycle of ischemia producing intra-abdominal hypertension and the abdominal compartment syndrome ( from Michael Rotondo, MD) . Damage Control Guidelines for Initiating Damage In Surgical Care Control Maneuvers Stone in 1983- Abbreviated celiotomy and Acidosis packing pH < 7.2 Base Deficit ≥ -8 Lactate ≥ 4 Damage Control in the Trauma setting Hypothermia coined by Rotondo and Schwab in 1993 < 35 ° celcius 4
5/29/2014 More Guidelines for Damage More Damage Control Guidelines Control Ongoing Resuscitation Coagulopathy Persistent shock with systolic BP <90 PTT > 60 > 10 litres crystalloid INR >1.6 >10 units packed red blood cells Host Factors Defining Reserve Operative Time Age > 60-90 minutes with abdominal cavity open Underlying disease Physiologic reserve: TIME Malperfusion and ISS Indications for the Open Goals of Damage Control Abdomen Laparotomy Control of Hemorrhage Damage Control for Trauma Abdominal Compartment Syndrome Rapid Control of Intestinal Spillage Massive Resuscitation Rapid Temporary Abdominal Closure Burn Rapid Transfer to the ICU for continued Pancreatitis resuscitation and restoration of physiologic Severe Abdominal Infection homeostasis Acute Mesenteric Ischemia Delay of intestinal reconstruction until Necrotizing Infection of the Abdominal Wall repeat laparotomy 24-48 hours later 5
5/29/2014 Algorithm for Damage Control Algorithm for Damage Control Step One Step Two Initial ED assessment Initial trauma laparotomy Resuscitation Hemorrhage control Recognition and operative decisions Contamination control Intra-abdominal packing Temporary dressing 6
5/29/2014 Algorithm for Damage Control Step Three ICU 2 ° resuscitation Warming Correct coagulopathy Individualized ventilatory support Secondary survey and planning 7
5/29/2014 ICU Resuscitation ICU Resuscitation Rewarming/Correct hypothermia Correct coagulopathy, acidosis, electrolyte imbalance CENTRAL LINE Measure CBC, coags, fibrinogen Infusion of warm fluids Bair hugger Correct K+, Mg+, Ca+ deficiencies Measure and use base deficit as guideline Prevent insensible losses PRN humidifier on vent set at 40 ° Consider effect of Normal Saline on base deficit ICU Resuscitation ICU Resuscitation Utilize central venous pressures to assist If PA Catheter is necessary in guiding resuscitation CI > 3L/min KNOW the pitfalls of interpretation End diastolic volume index 120-140ml SaO2 >95% SVO2 >65% Consider ECHO 8
5/29/2014 ICU Care ICU Care-Best Practices Head of Bed at 30 ° Medications Peptic ulcer prophylaxis Frequent suctioning and oral hygiene H2 blockers or proton pump inhibitors Functioning nasogastric tube DVT prophylaxis Functioning wound vac Low molecular weight heparin is superior Hourly urine output Insulin drip Maintain blood glucose 80-110 mg/dl Bladder pressure checks (if applicable) Drips for analgesia and sedation Pad pressure points Antibiotic therapy with open abdomen Revolution in the Management Algorithm for Damage Control of the Open Abdomen Step Four Preservation of the Peritoneal Space Reoperation: Typically 12-36 hours Progressive abdominal closure (prevention of lateral fascial retraction) Pack removal Vacuum-assisted wound management Definitive repairs Use of biologic dressings Decisions on closure Scott BG, Feanny MA, Hirshberg A. Early definitive closure of the open abdomen: A quiet Revolution. Scand J Surg2005;94:9-14. 9
5/29/2014 Options for Biologic Dressing of Complications of the Exposed Viscera Open Abdomen Skin Flaps Abdominal Wound infection Homologous split thickness skin Dehiscence Autologous split thickness skin Fasciitis/necrosis Acellular dermal matrix Intra-abdominal abscess Musculofascial advancement flaps Enteroatmospheric fistula Rotation skin and muscle flaps Risks increase with multiple operations and Free flaps multiple Surgeons Principles of Management Problem of “ Entero- Specific for “ Entero- atmospheric ” Fistula atmospheric ” Fistula Absence of overlying soft tissue with good blood supply precludes spontaneous PREVENTION Control fistula healing Protect exposed effluent abdominal viscera Exposed abdominal viscera predisposes Rotate flaps with during open abdomen management good blood supply to development of additional holes in the Limit access to the to cover fistula in wound to one or two GI tract selected cases SENIOR people Complex Wound difficult to manage Attempt to seal leak Resect well when first recognized established “ entero- Protect adjacent viscera atmospheric ” fistula with biologic dressings only when patient fit to avoid additional holes and infection free 10
5/29/2014 Principle 4 Principle 4 Control Fistula Effluent Control Fistula Effluent DO NOT INTUBATE A FISTULA in the Fixed Visceral Block middle of a fixed visceral block open Vacuum Assisted Wound Management abdomen System You won ’ t control the drainage Wound Drainage Bags You will make the hole bigger Requires expert enthusiastic nursing assistance Risk of additional holes 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;46:511-4. 2.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;108:2066-8 3.Alvarez AA, Maxwell GL, Rodriguez GC. Vacuum-assisted closure for cutaneous gastrointestinal Fistula management. Gynecol Oncol 2001;80:413-6. 4. Cro C, George KJ, Donnelly J, et al. Vacuum assisted closure in the management of enterocutaneous Fistulae. Postgrad Med J. 2002;78:364-5. Clinical Signs: Complications of the Veering off Trajectory Open Abdomen Systemic Inflammatory Response Extra-Abdominal Tachycardia Ventilator-associated pneumonia Tachypnea Aspiration pneumonitis Elevated WBC ARDS Fever Increased pain and aggitation Bloodstream infections Deep venous thrombosis/Pulmonary embolus Mental status changes Pressure ulcers Decreased urine output Multiple organ dysfunction syndrome Worsening base deficit Each observation is relative to the last 11
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