DAMAGE CONTROL SURGERY
| DAMAGE CONTROL SURGERY: THE NEW PARADIGM —Joseph F. Rappold, MD, CDR/MC/USN, Director, Surgical Intensive Care Unit, Department of Surgery, Naval Medical Center, San Diego |
| Historical perspective: study—Feliciano looked at 300 consecutive abdominal gunshot wounds (GSWs); definitive repair achieved in majority of cases and overall survival ≈90%; if patient sustained abdominal GSW with hollow viscus or solid organ injury and vascular injury, survival drops to ≈60%; survival drops further if patient had multiple visceral injuries and vascular injury; survival in these patients inhibited if acidosis, hypothermia, and coagulopathy occur (≈85% of deaths attributed to these 3 factors); weaponry change in 1980s led to patients with multiple penetrating injuries from large-caliber and high-velocity weapons; large-caliber weaponry associated with marked increase in energy transfer, leading to massive tissue destruction and disruption; patients require massive amounts of crystalloid and blood products to prevent hypovolemic shock and hypothermia that may lead to cardiac dysrhythmia, platelet dysfunction, depletion coagulopathy, and nonsurgical bleeding; shock occurs at cellular level and results in inadequate tissue perfusion, leading to metabolic acidosis; difficult to reverse acidosis, hypothermia, and coagulopathy |
| Potential solutions: Stone described rapidly terminating laparotomy with abdominal packing after onset of coagulopathy, followed by hemodynamic stabilization of patient in surgical intensive care unit (SICU), then return to operating room (OR) at some defined point to correct major injuries; resuscitation performed in ICU rather than OR; Rotondo and Schwab described 3 distinct phases (control of hemorrhage and contamination with temporary abdominal closure; core rewarming, correction of coagulopathy, ventilatory support, identification of associated injuries, and maximization of hemodynamic values; at defined point, reexploration and definitive surgical repair); retrospective study of 46 patients with penetrating abdominal trauma requiring laparotomy and massive transfusion (eg, >10 units packed red blood cells [RBCs]); survival advantage to damage control surgery in subset of 22 patients with concomitant major vascular injury and hollow viscus or solid organ injury; survival rate in patients undergoing damage control surgery 77% and in patients undergoing definitive repair 11%; 3 phases—in OR, control hemorrhage and contamination (staple off injured segment of bowel, leaving it discontinuous with gastrointestinal [GI] tract) and perform temporary closure; in SICU and ICU, perform core rewarming, correction of coagulopathy with blood products, maximization of hemodynamics, ventilatory support, identification of additional injuries, and planning of next operative procedure; in OR, reestablish intestinal continuity, perform abdominal lavage, remove packs, and examine operative site |
| Patient selection: consider in patients with high-energy blunt torso trauma, who have injuries occurring from high-caliber weaponry or high-speed sport utility vehicle (SUV) collisons, or with multiple torso penetrations; consider in hemodynamically unstable patients and patients presenting with coagulopathy or hypothermia; injury patterns and complexes involve major abdominal vascular injury with multiple visceral injuries, multifocal or multicavitary exsanguination with concomitant injuries in abdomen, and multiregional injuries with competing priorities; look for metabolic acidosis (pH <7.3), hypothermia (<35°C), resuscitation, and operative time >90 min, coagulopathy from nonsurgical bleeding, and massive transfusion requirements |
| Postoperative management: ongoing resuscitation—achieve adequate O2 delivery with crystalloid and blood product transfusions (obtain hematocrit of 23%-30%); monitor response by observing heart rate, systolic blood pressure (BP), urine output, pH, and serum lactate, and correct coagulopathy; achievement of supernormal O2 delivery and consumption indicates adequate resuscitation (failure to achieve associated with poor prognosis); consider placing Swan-Ganz catheter for inotropic support in nonresponsive patients; pulmonary function—aim for 90% to 92% saturation with fraction of inspired O2 (FiO2 ) ≤0.6; may require switching to pressure-control ventilation or reversing inspiratory/expiratory (I/E) ratio to support pulmonary status; pressure-control ventilation achieves oxygenation and ventilation goals with reduced airway pressure; hemostasis—evaluate patient for abdominal compartment syndrome; thrombocytopenia most common cause of coagulopathy after massive transfusion (large volume of crystalloid and blood products reduces coagulation proteins; judiciously use fresh frozen plasma and platelets); surgical bleeding most common cause of persistent coagulopathy; normalize temperature; perform thorough tertiary survey and identify additional injuries not identified during initial resuscitation and operative procedure |
| Postoperative complications: can be caused by missed injuries; for temporary closure of abdomen, suture temporary prosthetic material to skin; vise fascia so available when closing abdomen; avoid closing under tension; fistula or infection may develop (multiple procedures result in high intra-abdominal infection rate); prefer enteral nutrition once intestinal continuity established; use prophylaxis to avoid deep vein thrombosis (DVT) and peptic ulcers; skin complications common; perform systematic and organized packing to avoid intra-abdominal hypertension (can occur during packing and definitive closure causing decreased venous return to heart, reduced abdominal wall blood flow, and splanchnic ischemia; also can lead to increased intracranial pressure); patient at risk for intra-abdominal hypertension if extensive abdominal injury leads to bowel edema with associated venous congestion or ischemia, or extensive contamination results in multiple intra-abdominal infectious processes, or fistula occurs |
| VASCULAR EMERGENCIES —Niren Angle, MD, Assistant Professor of Surgery In-Residence, University of California, San Diego, School of Medicine |
| Acute aortic dissection: pathophysiology—spontaneous or traumatic break in intima may lead to intramural hematoma that can progress to aortic dissection; break in intima leads to extravasation of blood between intima and media that progresses downstream; classification—Stanford type A equal to DeBakey types 1 and 2; Stanford type B equal to DeBakey type 3; Stanford type A dissection involves proximal aorta (ascending aorta or arch); Stanford type B dissection originates distal to left subclavian artery; untreated Stanford type A dissection associated mortality rate of ≈90% within 2 wk; type A dissection requires surgical management; initial treatment of type B dissection involves medical management; International Registry of Aortic Dissection (IRAD)—of 289 patients with type A dissections, 208 treated surgically and 81 treated medically; in-hospital mortality rate in patients treated surgically 26%, in patients treated medically 58%; Stanford type B dissection associated with surgical mortality of 31%, compared to medical mortality of 10%; clinical presentation—typical presentation involves middle-aged man presenting with acute or severe unrelenting lancinating pain in back, anterior chest, or torso; abnormal electrocardiography (ECG) not diagnostic of acute aortic dissection; Sanford type A dissections can dissect retrograde and involve coronary vessels, causing myocardial ischemia; can occur in children; diagnostic tools—use spiral computed tomography (CT) or transesophageal echocardiography (TEE); TEE useful in determining whether there is involvement of proximal arch, carotids or supra-aortic trunks; Stanford type B management—reduce hypertension with sustained control of BP using nitrates, nitroprusside, and β-blocker; reduce raw BP (dP/dt; ideally to ≈100 mm Hg); provide pain control; consider surgical management if patient has bowel or leg ischemia, frank rupture, or unrelenting pain despite adequate control of BP; requires long-term follow-up; dissected aorta can develop aneurysmal disease |
| Thoracoabdominal aortic aneurysms (TAA): Crawford classification—type I begins distal to subclavian artery and extends downward to renal arteries; type II (associated with highest operative risk) starts at subclavian artery and extends to iliac bifurcation (involves entire thoracoabdominal segment); type III starts at midthoracic aorta and goes down to iliac bifurcation; type IV involves total abdominal dissection (starts at diaphragm and extends to bifurcation); type V begins at midthoracic aorta and ends above renal arteries; complications of repair—myocardial infarction, bleeding, acute renal failure, visceral ischemia, and limb ischemia; paraplegia rate ranges from 6% to 8%; highest risk for paraplegia associated with type I and II TAA (repair requires interruption of blood flow to spinal cord via clamping that can lead to ischemia and paraplegia; reduction in paraplegia rate achieved by placing spinal drainage catheter before surgery and draining cerebrospinal fluid (CSF) to maintain CSF pressure ≤10 mm Hg (avoids swelling of spinal cord that can result from ischemia); arteria radicularis magna (ARM; also artery of Adamkewicz) main arterial feeder for lower region of spinal cord; ARM arises from segment between T8 and L1 in 75% of patients; intercostal arteries in this area important; requires intercostal patch and reimplantation rather than sacrifice; consider obtaining assistance from cardiac surgeon, depending on extent of operation; repair—partial left heart bypass allows sequential clamping; use Biomedics pump (heparin-bonded circuit); during proximal anastomosis, place clamp while perfusing viscera and spinal cord or intercostal arteries; move clamp down and do distal anastomosis; allows better control of BP and shorter ischemia time for visceral artery and intercostal arteries; cut out piece of aorta with button and sew it onto graft; perform full neurologic assessment after TAA and leave spinal drainage catheter in ≥48 hr to avoid delayed-onset paraplegia; spinal drainage catheters recommended for types I, II, and III TAA |
| Acute mesenteric ischemia: connections between superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and celiac trunk maintain blood flow to intestine; associated with mortality rate >60% because of nonrecognition; most common causes include embolization to SMA and thrombosis of preexisting lesion at origin of vessel; less common causes include nonocclusive mesenteric ischemia and mesenteric venous thrombosis; clinical presentation—patients present with pain out of proportion to clinical findings (eg, abdomen not tender); embolism occurs ≈10 cm downstream of origin of SMA (some proximal branches spared); patients present with precipitous pain; patients feel urgent need for bowel evacuation; peritoneal irritation not usually present; see increase in hematocrit and leukocytosis; treat with resuscitation, antibiotics, and heparin; identify acute mesenteric ischemia using arteriography or CT angiography; repair—find SMA at root of bowel, make transverse arteriotomy, remove clot, and close; come back 24 hr later to remove any ischemic bowel |
| Acute arterial and graft occlusion: acute limb ischemia —embolism or thrombosis of native artery or bypass graft; etiologic factors include arrythmias, (eg, atrial fibrillation), hypotension, thrombosis of graft, and aortoiliac disease; history and physical examination critical in determining appropriate therapy; patients present with sudden onset of pain in affected extremity; painful limb may mask signs of acute limb ischemia elsewhere; look for 5 Ps (pain, pallor, paresthesia, pulselessness, and paralysis); determine extent of sensation and motor function; give patient 100 units/kg of heparin if suspicion high for acute limb ischemia, unless patient has had stroke or has active bleeding; use vascular findings to determine therapy (eg, palpable pulses); if femoral pulse absent, take patient to surgery; if femoral and popliteal pulses present, use arteriography to get information about tibial vessels; treatment options—surgery (thromboembolectomy or bypass graft) or thrombolysis; contraindications to thrombolytic therapy include recent surgery, stroke in last 6 mo, GI bleeding, and patient’s inability to stay flat in bed for 72 hr; consider thrombolysis if patient has no significant deficits, small amount of numbness, but leg can be moved and foot looks normal; consider surgery if patient has severely diminished sensation and cannot move toes; thrombolysis—place sheath into contralateral femoral artery; infuse thrombolytic agents (eg, tissue plasminogen activator (tPA), urokinase, or reteplase [Retavase]); heparin infused in side port of sheath to prevent clot formation on sheath; infuse tPA for 48 to 72 hr; surgical therapy—consider embolectomy with balloon catheters or bypass if flow cannot be restored; severity of ischemia determines need for fasciotomy; paresthesias may manifest as sensory deficit; soft touch and proprioception lost before hypesthesia and anesthesia develop; look for swollen and tense compartment and compartment pressures >30 to 40 mm Hg in diagnosing compartment syndrome; avoid elevating compartment because it reduces arterial perfusion pressure; failure to recognize and treat can lead to irreversible neurologic deficits |
| Iatrogenic causes of vascular injury: include cardiac catheterization, diagnostic angiography, central venous catheterization, arterial catheter insertion, and intra-aortic balloon pump; dissection most common injury; pseudoaneurysm— use duplex ultrasonography (US) to diagnose; intervention indicated for expanding hematoma, pseudoaneurysm that compresses skin with potential to cause ischemia, unrelenting pain, and compression of vein that produces leg swelling; consider intervention in patient taking warfarin (Coumadin); consider US-guided compression (avoid if infection present, or in patient with critical limb ischemia, impending compartment syndrome, or if pseudoaneurysm above inguinal ligament); consider thrombin injection under US guidance; surgical treatment involves making small incision under spinal or general anesthesia to remove clot |
| Venous thrombosis: phlegmasia that can progress to venous gangrene, superficial thrombophlebitis manifest by palpable cord and erythema, and bland DVT exhibited by edema and local tenderness; treat with heparin, warfarin, or oral thrombin inhibitors; phlegmasia—phlegmasia alba dolens manifests as weak pulse and pallor; progresses to phlegmasia cerulea dolens (indicated by cyanosis and marked edema) and then to venous gangrene without intervention; phlegmasia caused by massive thrombosis of venous channels and compromised venous outflow; present in 20% to 40% of patients with polycystic kidney disease; thrombosis can involve only major deep venous channels with diminished venous return (phlegmasia alba dolens); thrombosis can extend into collateral veins, with massive fluid sequestration and bullae formation (phlegmasia cerulea dolens; reversible); to reverse, treat with prompt anticoagulation (>100 units/kg heparin), thrombolysis (inferior vena cava [IVC] and iliac veins do not require IVC filter), or surgical venous thrombectomy; arterial pulses may still be present in superficial venous gangrene; venous gangrene involving muscular compartment produces pulse deficit, leading to compartment syndrome; shock can occur from fluid sequestration |
Educational Objectives
| The goal of this program is to educate the listener about damage control surgery and vascular emergencies. After hearing and assimilating this program, the clinician will be better able to: |
 | 1. Discuss the evidence that damage control surgery can improve the survival rate in some patients with traumatic injuries. |
| 2. Identify which trauma patients may benefit from a staged surgical approach. |
| 3. Determine the postoperative management of a trauma patient who has been treated with a staged surgical approach. |
| 4. Identify the types of vascular emergencies that can occur. |
| 5. Describe the treatment methods for each type of emergency. |
Discussed on This Program
Heparin sodium injection
Reteplase, recombinant (recombinant tissue plasminogen activator) [Retavase]
Urokinase [Abbokinase, Abbokinase Open-Cath]
Warfarin sodium [Coumadin]
Suggested Reading
Bilkovski RN et al: Targeted resuscitation strategies afte.injury. Curr Opin Crit Care 10:529, 2004; Chuter TA et al: Management of abdominal aortic aneurysm: a decade of progress. J Endovasc Ther 11 Suppl 2:II82, 2004; Freeman AJ et al: Damage control surgery and angiography in cases of acute mesenteric ischaemia. ANZ J Surg 75:308, 2005; Greenberg R et al: Aortic dissections: new perspectives and treatment paradigms. Eur J Vasc Endovasc Surg 26:579, 2003; Hildebrand F et al: Damage control: extremities. Injury 35:678, 2004; Keel M et al: Pathophysiology of polytrauma. Injury 36:691, 2005; Loveland JA et al: Damage control in the abdomen and beyond. Br J Surg 91:1095, 2004; Montalvo JA et al: Surgical complications and causes of death in trauma patients that require temporary abdominal closure. Am Surg 71:219, 2005; Murray D et al: Staged open and endovascular repair of thoracoabdominal aneurysms using the common carotid artery. Ann Vasc Surg 19:103, 2005; Parr MJ et al: Damage control surgery and intensive care. Injury 35:713, 2004; Rotondo MF et al: Damage control surgery for thoracic injuries. Injury 35:649, 2004; Schwab CW: Introduction: damage control at the start of 21st century. Injury 35:639, 2004; Sugrue M et al: Damage control surgery and the abdomen. Injury 35:642, 2004; Swaroop M et al: Multiple laparotomies are a predictor of fascial dehiscence in the setting of severe trauma. Am Surg 71:402, 2005.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported nothing to disclose.
Drs. Angle and Rappold were recorded July 22-24, 2004, in San Diego, at Critical Care Summer Session, sponsored by the University of California, San Diego, School of Medicine. The Audio-Digest Foundation thanks the speakers and the sponsor for their cooperation in the production of this program.
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