Damage Control Surgery: Principles and Indications

Definition / Overview

Damage control surgery (DCS) is a staged operative strategy in which the initial operation is deliberately abbreviated to address only immediately life-threatening haemorrhage and contamination, followed by physiological resuscitation in the intensive care unit, with definitive anatomical reconstruction deferred to a planned re-look procedure once physiology has been restored.

• The concept emerged from management of severe hepatic and abdominal vascular trauma but has expanded to encompass thoracic, orthopaedic, and vascular injury patterns
• The fundamental premise is that physiological survival takes precedence over anatomical repair at the index operation
• DCS is not a strategy for every trauma patient, inappropriate application increases morbidity from complications of open abdomens, abdominal compartment syndrome, and unnecessarily deferred definitive care

Pathophysiology, The Lethal Triad

The physiological derangement driving the DCS decision is the lethal triad (also termed the "bloody vicious cycle"):

$$\text{Hypothermia} + \text{Acidosis} + \text{Coagulopathy}$$

Each element potentiates the other two, creating a self-reinforcing spiral toward death if uninterrupted by physiological rescue.

Hypothermia

• Core temperature $< 35^\circ\text{C}$ impairs enzymatic coagulation cascade function
• Temperatures $< 32^\circ\text{C}$ are associated with refractory coagulopathy and fatal arrhythmias
• Prolonged laparotomy with open body cavities, cold fluid resuscitation, and anaesthetic vasodilation all compound heat loss

Metabolic Acidosis

• Haemorrhagic shock produces lactic acidosis from tissue hypoperfusion ($\text{pH} < 7.2$ is a critical threshold)
• Acidosis reduces myocardial contractility and reduces the efficacy of vasopressors
• Coagulation enzyme activity falls sharply below $\text{pH}\,7.2$

Coagulopathy

• Dilutional coagulopathy from large-volume crystalloid resuscitation
• Consumptive coagulopathy from massive haemorrhage and release of tissue factor
• Fibrinolysis activation compounds the picture
• Recognised early as acute traumatic coagulopathy (ATC), which begins at the time of injury, not as a consequence of resuscitation alone

Indications for Damage Control Surgery

The decision to pursue DCS must be made early, ideally before the patient reaches physiological extremis. A combination of anatomical complexity, physiological deterioration, and resource context should inform the decision.

Physiological Triggers

Anatomical / Injury-Based Triggers

• Major vascular injury requiring complex reconstruction (aorta, IVC, mesenteric vessels)
• Multiple visceral injuries necessitating lengthy definitive repair at index operation
• Major hepatic injury requiring packing
• Combined thoracoabdominal injury
• Retroperitoneal haematoma with ongoing expansion after exploration
• Inability to achieve fascial closure due to visceral oedema or haemostatic packing

Resource and Contextual Triggers

• Operating at a centre without specialist vascular or hepatobiliary capabilities, temporising and transferring is a form of damage control
• Depletion of blood bank resources in an austere or mass-casualty environment
• Surgeon recognition that continuing the procedure exceeds current technical resources

The Three Phases of Damage Control Surgery

Phase I, Abbreviated Index Operation (Operative Damage Control)

The goal is to achieve haemorrhage control and limit contamination within 60-90 minutes. Anatomical restoration is explicitly not attempted.

Haemorrhage control techniques:

1. Manual compression and packing as the immediate first response on entering the abdomen
2. Perihepatic packing for liver injuries, packs placed to compress between the liver and the diaphragm/anterior abdominal wall
3. Aortic compression at the hiatus or supra-coeliac clamping for proximal haemorrhage control
4. Vessel ligation of non-critical vessels where technically feasible
5. Temporary intravascular shunting for major named vessels (iliac, femoral, SMA, popliteal) when reconstruction is deferred, shunts maintain distal perfusion for 12-48 hours
6. Topical haemostatic agents (oxidised cellulose, fibrin sealants) for diffuse ooze
7. Endovascular adjuncts: REBOA (Resuscitative Endovascular Balloon Occlusion of the Aorta) as a bridge to haemorrhage control in select centres

Contamination control techniques:

• Hollow viscus injuries stapled, tied, or rapidly oversewn without formal anastomosis
• Bowel ends left in discontinuity (not reconstructed at index operation)
• Gross contamination irrigated with warm saline
• Damaged or devascularised bowel resected but not anastomosed

Temporary abdominal closure (TAC):

• Fascial closure is frequently not possible or not safe
• Options include:
  • Bogotá bag (sterile IV bag sutured to skin)
  • Commercial negative pressure wound therapy (VAC) systems, preferred in most centres due to controlled effluent management and reduced fascial retraction
  • Wittmann patch (hook-and-loop system allowing sequential fascial approximation)
• Goal: protect viscera, allow decompression of intra-abdominal hypertension, facilitate re-look

Phase II, ICU Resuscitation

The most critical and often underappreciated phase. Surgical restraint is required, reoperation must be resisted until physiology is restored.

Targets for resuscitation before re-look:

• Core temperature $> 36^\circ\text{C}$
• $\text{pH} > 7.35$
• Lactate $< 2.5\,\text{mmol/L}$ or clearance $> 10\%$/hour
• INR $< 1.5$, fibrinogen $> 1.5\,\text{g/L}$, platelets $> 50 \times 10^9/\text{L}$
• Urine output $> 0.5\,\text{mL/kg/hr}$
• Vasopressor requirements trending down

Damage control resuscitation (DCR) principles in Phase II:

• Permissive hypotension until definitive haemorrhage control is achieved ($\text{SBP}\,80$-$90\,\text{mmHg}$ in haemorrhagic shock without TBI; target $\text{SBP}\geq 90$ if concurrent TBI)
• Minimise crystalloid, crystalloid exacerbates dilutional coagulopathy and visceral oedema
• Balanced blood product resuscitation: packed red cells: fresh frozen plasma: platelets in a 1:1:1 ratio
• Cryoprecipitate for fibrinogen replacement (target fibrinogen $> 1.5$-$2.0\,\text{g/L}$)
• Tranexamic acid $1\,\text{g}$ IV over 10 minutes then $1\,\text{g}$ over 8 hours, given within 3 hours of injury, reduces mortality from haemorrhage without increased thromboembolic risk in this window
• Massive transfusion protocol (MTP) activation, early and structured
• Warming: warm IV fluids, forced-air warming blankets, humidified ventilator circuits, warm irrigation at re-look
• Correct ionised calcium (calcium gluconate $10\,\text{mL of }10\%$ solution IV or calcium chloride $5$-$10\,\text{mL of }10\%$ IV), citrate in blood products chelates calcium

ICU monitoring:

• Intra-abdominal pressure monitoring via bladder catheter, target $< 20\,\text{mmHg}$; values $> 20\,\text{mmHg}$ with new organ dysfunction define abdominal compartment syndrome (ACS) requiring decompressive laparotomy
• Repeat lactate every 2-4 hours to guide resuscitation adequacy
• Thromboelastography (TEG) or rotational thromboelastometry (ROTEM) to guide targeted blood product therapy

Phase III, Planned Re-look and Definitive Repair

Typically undertaken at 24-72 hours after Phase I, once physiological targets are achieved. Premature return to theatre before normalisation of physiology will reproduce the lethal triad.

Re-look priorities:

1. Remove packs, reassess haemostasis and address any residual bleeding
2. Assess bowel viability, resect additional non-viable segments
3. Restore gastrointestinal continuity where safe (anastomosis or stoma formation)
4. Repair remaining visceral injuries (biliary, urological, diaphragmatic)
5. Vascular reconstruction, convert temporary shunts to definitive repair
6. Washout of peritoneal contamination
7. Achieve definitive fascial closure where possible, aim for primary fascial closure by 72 hours if feasible; rates of successful closure fall significantly beyond 7-10 days

Damage Control in Specific Anatomical Regions

Damage Control Orthopaedics (DCO)

• In polytrauma patients, early definitive fixation of long bone fractures (especially femur) can precipitate an immunological and inflammatory 'second hit' that drives ARDS and MODS
• DCO principle: apply external fixators rapidly to restore skeletal stability, avoid lengthy intramedullary nailing at the index presentation
• Definitive fixation deferred until the peritraumatic immunological storm has subsided (typically 3-7 days)
• Open fractures require early wound debridement, lavage, antibiotic cover, and temporary stabilisation regardless of DCO versus definitive approach

Damage Control for Vascular Trauma

• Temporary intraluminal shunts (e.g. Argyle or Javid shunts, or improvised with IV tubing) restore distal perfusion while definitive repair is deferred
• Allows transfer to a vascular-capable centre or return after physiological resuscitation
• Fasciotomy of the affected compartment should be performed prophylactically when ischaemia time exceeds 4-6 hours or there is significant soft tissue injury

Damage Control Thoracic Surgery

• Emergency thoracotomy (resuscitative or operative) follows similar principles
• Pulmonary tractotomy rather than formal lobectomy for penetrating lung injury
• Hilar clamping for uncontrolled pulmonary haemorrhage
• Cardiac injuries: digital occlusion, Foley catheter tamponade, or stapled repair as temporising measures before formal repair

Complications and Special Considerations

Open Abdomen Complications

• Enteroatmospheric fistula (EAF): the most feared complication; incidence increases with prolonged open abdomen; meticulous handling of bowel, avoidance of unnecessary bowel manipulation, and timely closure reduce risk
• Abdominal compartment syndrome: may develop even with open abdomen if packs excessive; monitor bladder pressure regularly
• Fascial loss: prolonged open abdomen leads to fascial retraction and loss; planned component separation or biological mesh may be required for delayed closure
• Septic complications: peritonitis, wound infection, anastomotic dehiscence at re-look if bowel anastomosis was undertaken prematurely

Avoiding Inappropriate Application of DCS

• DCS carries its own morbidity, open abdomen, multiple returns to theatre, ICU complications, fistula formation
• Stable patients with contained injuries should undergo definitive repair at index operation
• Avoid DCS purely for surgeon convenience or inexperience with complex repair
• Evidence suggests DCS has been over-applied; careful patient selection is essential

Coagulopathy Management, Targeted Therapy

• TEG/ROTEM-guided resuscitation allows targeted product use rather than empirical 1:1:1
• Clot amplitude (MA on TEG): low amplitude → platelet/fibrinogen deficiency → cryoprecipitate and platelet transfusion
• Clot formation rate (K and angle): impaired → fibrinogen deficiency → FFP and cryoprecipitate
• Fibrinolysis (LY30): elevated → antifibrinolytic therapy (tranexamic acid, if not already given)

Perioperative Management Considerations

Pre-operative Phase

• Activate MTP early, do not wait for laboratory confirmation of coagulopathy
• Communicate DCS intent clearly with anaesthetics team, scrub team, and ICU before incision
• Warm theatre environment, warm fluids, cell salvage where contamination is absent
• REBOA insertion (Zone I for abdominal haemorrhage, Zone III for pelvic haemorrhage) at centres with capability

Intraoperative Phase

• Assign a dedicated team member to monitor operative time, aim to complete Phase I within 60-90 minutes
• Regular communication with anaesthetist regarding temperature, pH, haemoglobin, and product use
• Avoid unnecessary dissection, control, pack, and close
• Do not attempt anastomoses or complex reconstructions if any element of the lethal triad is present

Postoperative / ICU Phase

• Daily reassessment of physiology before deciding timing of re-look
• Nutrition: early enteral nutrition via nasogastric/post-pyloric tube as tolerated with open abdomen, reduces gut mucosal breakdown and bacterial translocation
• DVT prophylaxis: mechanical (sequential compression devices) immediately; pharmacological (low molecular weight heparin) deferred until haemostasis is confirmed, typically 24-48 hours post-haemostasis
• Involve critical care, haematology, nephrology (for AKI), and respiratory teams early

Long-term Considerations

• Ventral hernia is the commonest long-term sequela of open abdomen management, counsel patient and plan elective repair at 6-12 months once physiological recovery and nutrition are optimised
• Psychological impact of ICU stay and prolonged recovery, early liaison psychiatry and rehabilitation input improves outcomes

Summary: Key Decision Points for the Viva

Sources

• ATLS (Advanced Trauma Life Support)
• RACS position statements & curriculum (Royal Australasian College of Surgeons)