Damage Control Resuscitation

What is it, and what can we do?

By Suzi Hamilton, Emergency Physician

The idea originated in 1950s during the Korean war and really gained momentum in the 1990s when it was realised that multiple interventions and lengthy surgeries in the multi-trauma patient were of little benefit. The patients’ physiology needs to be corrected before any surgery can be of use. The idea is that damage control surgery finds the bleeding and stops the bleeding, allowing 24-48hours in ICU to correct the physiology, after which the patient can return to theatre for definitive surgery. Damage control resuscitation (DCR) is a more recent expansion of the idea to include the resus phase. Since its introduction survival rates in the multi-trauma patient have markedly improved, although it remains the number 3 cause of death worldwide. Military papers report mortality from severe trauma as low as 6% now, while rates in urban trauma centres are generally 8-10%. To keep that in perspective, STEMIs who reach hospital have an in-hospital mortality rate of around 5%.

The major cause of death at all 3 peaks is traumatic brain injury (TBI). Next commonest cause (especially the immediate and early deaths) is haemorrhage – this is where we need to focus, as we can actually do something about it. The 3rd peak are the ones who develop sepsis or respiratory complications in the following weeks.DCR is an evolving idea – this is a summary of the current research and understanding. Many blogs exist on this topic and I’d encourage you to read around to get a fully informed opinion.

Nothing said here should ever replace your Clinical Practice Guidelines.

Aim of DCR: minimise blood loss, maximise oxygenation, optimise outcome.

A lot of talk exists about traumas “lethal triad” of acidosis, hypothermia and coagulopathy. This is misleading, as it implies all three are equally bad. In fact coagulopathy is the killer – the other two simply contribute to that. Our main focus for the severe trauma patient needs to be about stopping the bleeding. For that reason, modern trauma courses now teach a flipped primary survey of CABC – sort out the Circulation, then the Airway, then the Breathing, before reassessing the Circulation. An early intubation is of no use if the patient has bled to death while you were tubing them. The military teach their primary survey as ‘MARCH’ ie Massive haemorrhage, Airway, Breathing, Circulation, Hypothermia, highlighting the importance of addressing blood loss as the top priority.

3 steps in DCR:

  1. Permissive hypotension (also called low volume resus)
  2. Haemostatic resuscitation
  3. Damage control surgery

1. Permissive hypotension

Only for penetrating trauma: whole idea is to keep BP low enough to avoid exsanguination but high enough to enable organ perfusion. It’s tricky the find the sweet spot! No evidence of benefit for blunt trauma, although there is some thought around that it may be of value – watch this space.

Caveat: have to be pretty certain there isn’t another immediate life-threatening cause of the hypotension eg tension pneumothorax, pericardial tamponade.

Controversial: no high-level evidence (mostly animal studies), no clear agreement on target BP, most accept SBP 80-90 or MAP 65mmHg.

BP not the best indicator of perfusion: if the patient has good pulses, warm peripheries and is perfusing their brain (ie not agitated or drowsy) then their perfusion is good, regardless of their BP. A young person may tolerate a systolic BP of 60mmHg, an old person may need 120mmHg to maintain perfusion due to stiff arteries and baseline hypertension, so look at the patient more than the numbers.

Contraindicated with head injury: even if hosing blood from elsewhere, a hypoxic brain injury will never recover – good evidence shows 1minute with a BP <80 doubles their mortality.  Patients with TBI need a higher BP to maintain brain perfusion, eg MAP >85. A multi-trauma patient with severe TBI is a huge challenge and unlikely to survive.

2. Haemostatic resuscitation

Find the bleeding, stop the bleeding: think SCALP: Scalp, Chest, Abdomen, Long bones, Pelvis. If all these have been addressed and you’ve not found bleeding, is it really bleeding causing the low BP? Is it neurogenic shock from a spinal injury? Anaphylactic shock from a drug they’ve had, or something they’re exposed to? It could be retroperitoneal bleeding eg a ruptured AAA, but little can be done for that pre-hospital. Look for the SCALP sites. Remember tourniquets, splints, pelvic binders, direct pressure on vessels – stick a finger on it with just one square of gauze for direct pressure as huge pads usually don’t work and just hide it for a little while.

Minimal crystalloid use: crystalloids (saline) dilute the blood hence dilutes clotting factors, which makes them bleed more. The haemodilution also depletes the oxygen-carrying capacity of blood. This worsens ischaemia, which worsens acidosis, which worsens coagulopathy, hence perpetuating the vicious cycle. There has to be a really good reason for starting saline in the trauma patient – try and avoid if possible.

Early use of blood: if O-neg blood is available this should be used ASAP. Balanced blood products are recommended to maintain balance of clothing factors – current recommendations based on military experience are 1:1:1 ie 1unit blood to 1unit FFP to 1unit platelets. We use the massive transfusion protocol in ED which ensures balanced blood products are given following a strict protocol.

Tranexamic acid: TXA prevents the breakdown of fibrin, which holds blood clots together. It has been used in surgery to reduce bleeding for years, but has only recently become part of trauma management. CRASH-2 showed TXA given within 3hours of injury reduced mortality by 30% and had few adverse effects (NNT 125). Trials currently underway to ascertain the optimal timing and dose should soon clarify it’s use, but at present we give 1g IV on arrival to ED with another 1g 1hour later, aiming to prevent coagulopathy.

Prevent acidosis: low blood pressure can result in low perfusion, which means cells aren’t getting enough oxygen so they switch to anaerobic respiration, which produces lactate. This is converted to lactic acid, which is responsible for the acidosis seen in hypovolaemic shock in trauma. How do you know if a patient is acidotic without a blood gas showing the pH? The resp rate: unless there’s a chest injury or infection, a high respiratory rate in a sick patient is often due to acidosis – they hyperventilate to blow off CO2 (an acid) to try and correct the pH. Once acidotic, blood clotting is impaired, hence worsening coagulopathy and bleeding. However studies have shown that when acidosis was treated with sodium bicarb, outcomes were worse, despite the pH being normalised. This suggests acidaemia may offer some protection against hypoxia, allowing cells to cling on to what little function they can. The take home point at this time is that while acidosis is bad it is simply a marker of the severity – we shouldn’t try and treat the acidosis per say, but fix the problems that are leading to it i.e. stop the bleeding.

Keep warm: hypothermia disrupts cellular function and clotting factors, which causes more bleeding, which causes more hypotension, which causes more acidosis, which causes more coagulopathy, which causes more bleeding… circling the drain. Using warm fluids, getting warm blankets on, removing wet clothes, getting patients out of the cold and the wind, are vital pre-hospital measures to prevent the lethal triad.

3. Damage control surgery

Scoop and run: address immediate life threats only. The longer the multi-trauma patient spends in the field getting cold, getting hypovolaemic, getting coagulopathic, the worse their outcome. They need warmed blood products, lab-guided resus and early surgery.

Damage control surgery: minimal intervention, just enough to stablise the patient to get them to ICU where their physiology can be addressed. Organs are partially resected, stapled, packed, decontaminated, covered with fibrin sealants and the abdomen is left open with a plan to return to theatre in 24-36hours time if the patient is stable.

 

Take home points

Lots of opinions on damage control resus around – it’s a tricky thing to get right and requires a whole team approach.

Pre-hospital measures definitely make a huge difference – simple things done early and done well. Keep them warm, stop the bleeding, avoid crystalloids, don’t worry about a low BP if they’re conscious and have pulses (with all the caveats mentioned above).

Don’t forget everyone’s welcome at the hospital trauma round 0730-0800 every Friday (unless it’s public holiday) in the Oncology lecture theatre – turn up to ED at 0720 and someone will be heading that way if you don’t know where it is.

As always, come and chat if you’ve any questions or feedback!

 

References:

  • Damage control: the modern paradigm. Brooks AJ et al. Trauma 2016;18(3):165-177
  • Ball CG. Damage control resuscitation: history, theory and technique. Can J Surg. 2014;57:(1)55-60.
  • Robertson LB. The transfusion of whole blood. BMJ 1916;2:384-386
  • Combat anaesthesia: the first 24hours. [book] Mahoney PF. 2016. ISBM 0160927536, 9780160927539
  • Beuran M, Lordache FM. Damage control surgery–new concept or reenacting of a classical idea? J Med Life. 2008 Jul-Sep;1(3):247-53.
  • Cirocchi R, Montedori A, Farinella E, Bonacini I, Tagliabue L, Abraha I. Damage control surgery for abdominal trauma. Cochrane Database Syst Rev. 2013 Mar 28;3:CD007438.
  • Blackbourne LH. Combat damage control surgery. Crit Care Med. 2008 Jul;36(7 Suppl):S304-10.
  • Midwinter MJ. Damage control surgery in the era of damage control resuscitation. J R Army Med Corps. 2009 Dec;155(4):323-6.
  • Parr MJ, Alabdi T. Damage control surgery and intensive care. Injury. 2004 Jul;35(7):713-22.
  • Rotondo MF, Schwab CW, McGonigal MD, et al. ‘Damage control’: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma. 1993;35:(3)375-82
  • Bickell WH, Wall MJ Jr, Pepe PE, Martin RR, Ginger VF, Allen MK, Mattox KL. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994 Oct 27;331(17):1105-9.
  • Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma. 2002 Jun;52(6):1141-6.
  • Bickell WH, Wall Jr MJ, et al. Immediate vs. Delayed Fluid Resuscitation for Hypotensive Patients with Penetrating Torso Injuries. N Engl J Med. 1994; 331:1105
  • Deakin CD, Low JL. Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study. BMJ. 2000 Sep 16;321(7262):673-4.
  • Duchesne JC, et al. Damage control resuscitation: from emergency department to the operating room. Am Surg 2011; 2:201-6.
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3 Comments Add yours

  1. Shane Lynch says:

    It was fantastic to have you along to our Coffee & Cases Suzi. Thank you so much for your input to our blog too, it’s great to see another thought process from someone so well respected in your field. Looking forward to seeing you along next year too.

    Like

  2. Tatsu Kuwasaki says:

    Such an easy read with normal language that makes sense even for this old paramedic. Thanks Suzi!

    Like

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