Damage Control Orthopaedics

Definition. Damage control orthopaedics (DCO) is a staged approach to the fractures of a polytrauma patient. The skeleton is stabilised temporarily, usually with an external fixator, and definitive surgery is delayed until the patient's physiology has normalised. It runs in three phases: temporary stabilisation, a period of ICU optimisation, and conversion to definitive fixation.

How it arose. Through the 1980s and 1990s the paradigm was Early Total Care (ETC), early definitive fixation of every fracture, and femoral nailing within 24 hours became standard. Some patients deteriorated after that early surgery. The explanation, the second hit phenomenon, was that the operation itself adds an inflammatory insult, and DCO was developed for the high-risk polytrauma patient in whom that insult is not affordable.

The rationale. Major trauma produces a systemic inflammatory response, and a further surgical insult amplifies the cascade and can precipitate ARDS, multi-organ failure and death. DCO keeps the surgical trauma to a minimum until the inflammation subsides.

The first hit is the injury. Damaged tissue releases damage-associated molecular patterns (DAMPs), which activate the innate immune system and drive the release of IL-1, IL-6 and TNF-alpha. The result is the systemic inflammatory response syndrome (SIRS), matched by a compensatory anti-inflammatory response (CARS).

The second hit is the operation. Surgery adds tissue damage and further cytokine release to a system already primed, and tips the balance toward hyperinflammation. End-organ damage follows, in the lungs (ARDS), the kidneys and the liver, and multi-organ failure (MOF).

Patient classification. Polytrauma patients fall into four categories, and the category chooses the strategy.

Damage control orthopaedics cannot be separated from damage control resuscitation (DCR); the two run in parallel. DCO controls the skeletal second hit, and DCR reverses the physiology that makes the patient unsafe to operate on.

The lethal triad. The thresholds that follow are unified by the trauma triad of death: hypothermia, acidosis and coagulopathy. Each worsens the others in a self-perpetuating cycle. Hypothermia and acidosis impair the clotting cascade and platelet function, bleeding worsens acidosis, and transfusion, cold fluids and exposure worsen hypothermia. Breaking that cycle is the whole point of damage control: do the minimum to stop bleeding and stabilise, then correct physiology before any definitive reconstruction.

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Permissive hypotension. Tolerate a lower blood pressure, a palpable radial pulse or a systolic of about 80-90 mmHg, until surgical haemorrhage control is achieved, to avoid "popping the clot" and dilutional coagulopathy. The exception is traumatic brain injury, where cerebral perfusion must be maintained and hypotension avoided.

Haemostatic resuscitation. Give blood products early in balanced ratios approximating whole blood, around 1:1:1 red cells to plasma to platelets, through a massive transfusion protocol, and minimise crystalloid, which dilutes clotting factors and worsens the triad. Give tranexamic acid early: CRASH-2 showed that TXA within 3 hours of injury reduces death due to bleeding in trauma haemorrhage, and that it is harmful if given late.

Goal-directed correction and endpoints. Rewarm aggressively, correct ionised calcium, and guide product use with point-of-care viscoelastic testing (ROTEM or TEG) where available. Adequate resuscitation, and readiness to escalate fracture care, is signalled by clearance of lactate and base deficit, not by blood pressure alone.

The primary survey. ATLS principles come first. Control haemorrhage with a pelvic binder or a tourniquet, resuscitate with blood products, and identify every injury; a tertiary survey is essential. Then classify the patient as stable, borderline, unstable or in extremis.

The ongoing assessment. The category is not fixed, so the physiological parameters are trended and the patient reassessed regularly; the question is whether they are improving or deteriorating. Response to resuscitation is the key decision point, status can change rapidly, and the decision is shared with the trauma team, anaesthesia and ICU.

The investigations are the ones that feed the physiological table in the Classification section. The blood gas is the one that is repeated.

The viva trap is treating DCO and ETC as a binary. They sit on a spectrum, with Early Appropriate Care (EAC) as the modern, resuscitation-led bridge, and the three need to be distinguished clearly.

The EAC criterion. Vallier's protocol recommends definitive fixation within 36 hours if lactate is less than 4.0 mmol/L, pH is at least 7.25, or base excess is at least -5.5 mmol/L: any one of the three, not all of them. In the EAC cohort complications were 16.3% in those fixed within 36 hours versus 33.3% in those delayed.

Fixed timing or physiology-led timing. The traditional teaching, avoid days 2-4 and convert on day 5-10, is being displaced by EAC, which fixes definitively as soon as the resuscitation endpoints are met. The day-count is a guide, not a rule.

Who is truly borderline. There is no universally validated cut-off. Lactate trajectory, base deficit, chest injury severity and response to resuscitation matter more than any single number.

Reaming in the chest-injured patient. The fat embolism and second hit concern around reaming is debated, and modern data suggest that adequate resuscitation matters more than reaming per se.

Head injury and timing. Avoiding hypotension and hypoxia for the injured brain can argue for prompt fixation, which complicates a simple "delay everything" approach.

The frame has its own complications. Beyond pin site infection, pins loosen, malunion follows if pins are placed incorrectly, a pin can injure a nerve, and pins sitting in the path of the future nail make the conversion harder.

After the frame. The patient goes to ICU for ongoing resuscitation with serial lactate monitoring, and is optimised through the inflammatory peak without further surgery. The physiological parameters are reviewed daily, because the goal is to convert to definitive fixation as soon as it is safely possible: prolonged external fixation increases infection risk and complicates the conversion.

After conversion. Once the definitive fixation is in, the patient follows standard fracture rehabilitation with early mobilisation.

What DCO is credited with. Reduced ARDS in patients with a femur and chest injury, lower mortality in borderline and unstable patients, and comparable long-term outcomes when it is used appropriately. Used in an unstable patient it improves survival; the whole difficulty is identifying the borderline patient, who may decompensate with definitive surgery.

Global Epidemiology

• Trauma is among the leading causes of death worldwide in people aged under 45, and the leading cause of years of life lost.
• Long-bone and pelvic fractures are common in major polytrauma; the femur-plus-chest pattern is the prototypical high-risk DCO group (Pape 1993).
• Most major-trauma deaths follow a trimodal distribution; the late peak (days to weeks) from sepsis and multi-organ failure is the window DCO seeks to influence by limiting the surgical "second hit".

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