This is the reality of intensive care: at any point, we are as apt to harm as we are to healAtul Gawande
If you are reading this, probably you are, or you’ll be a surgeon… If this is true, take a couple of big breaths before going on. The things we are going to talk about are really far from purely surgical stuff.
In this post, we are going to explain how to keep a patient alive after major trauma.
Haven’t you thought surgery alone is going to save traumatized patients, have you?! If you thought so… Well, take some more breaths and clear your mind…
We have already explained how Damage Control Surgery (DCS) works, and which principles it follows. However, it doesn’t work at all, if some more principles are not applied… And these principles start in the Emergency Department, continue in the Operating Room, and endure in the Intensive Care Unit. Usually, they are followed by anesthetists and intensivists; however, you need to know them as well and make sure you’re collaborating with them.
Let’s start as always with a clinical scenario…
If you have any doubts about the initial assessment, see our previous posts.
A – Male, 24 yo
T – 00.43 (time of arrival 1.07)
M – Multiple stabs to the chest and abdomen
I – 2x stabs in the abdomen, 2x posterior thoracoabdominal region
S – BP 60/35 mmHg, HR 147 bpm, Temp 34.7°C, SatO2 94% in room air, 31 breaths per min, GCS 11/15
T – 2 large-bore peripheral lines, administered 500 mL normal saline, oxygen through face-mask, fentanyl 100 mcg
A – Patient tubed on arrival
B – SatO2 97% with FiO2 60%. No lung sounds on the left side 🡪 intercostal drain inserted (drained air and 650 mL of blood)
C – BP 75/45, HR 122 bpm, no external active bleeding, abdomen not assessable, 2 stabs on the left side, pelvis stable.
D – GCS 2/10T, PEARL, no lateralizing signs (as far as assessable)
E – 2 stabs on the left posterior thoracoabdominal region. Temp 34.4°C, active warming
E-FAST – small left pneumothorax and hemothorax, intraabdominal free fluid
CXR & PXR – small left pneumothorax and hemothorax, ICD in place
ABG – pH 7.23, HCO3– 11.4, pO2 196 mmHg, pCO2 37 mmHg, Hb 8.4 g/dL, Lac 17 mmol/L, BE -16.7 mmol/L, Ca2+ 0.96 mmol/L
The patient has been taken directly to the OR. The surgical procedure consisted of laparotomy, evacuation of ≈2.5 L of blood, splenectomy, gastric primary repair (x2), and transverse colon primary repair, abdomen left open with negative pressure wound therapy (NPWT)… Basic DCS.
During surgery, the patient was transfused with 2 units of packed red blood cells (PRBCs), and an additional 2 L of fluids were infused (1.5 L crystalloids, and 500 mL colloids).
At the end of the operation, the patient was transferred to the ICU with the following parameters:
- Status: tubed, open abdomen with NPWT
- Vitals: BP 85/55, HR 118, SatO2 99% with FiO2 60%, Temp 34.8°C, Urine Output ≈0.3 mL/kg/h
- Medications: norepinephrine at 0.8 mcg/kg/min, 3rd unit of PRBC running
- ABG: pH 7.21, HCO3– 11.2, pO2 224 mmHg, pCO2 36 mmHg, Hb 8.7 g/dL, Lac 24 mmol/L, BE -21.2, Ca2+ 0.91 mmol/L
- Labs: Hb 8.4 g/dL, Creatinine 1.47 mg/dL, INR 2.1
I think we all agree this patient is dying… rapidly…
Now, the question is: what is going to save this patient?
Surgery has done what it could do. At this point, resuscitation is the only way to save this patient… And the Damage Control Resuscitation (DCR) is the correct approach.
Be clear that not everything done in the previous case scenario is correct and follows the DCR protocol.
But what is DCR precisely?
Damage Control Resuscitation enrolls all the approaches to resuscitation aimed at preventing or minimizing all the metabolic derangements secondary to the primary insult in severely injured patients.
Now, stop for a sec… Before delving into DCR, let’s take a step back and focus on what DCR fights…
The Vicious Cycle (previously known as the Triad of Death)
Severely injured trauma patients are used to develop three conditions: acidosis (pH <7.35), hypothermia (core temperature <35°C), and coagulopathy (INR >1.5). These events, if not promptly corrected, precipitate patients’ conditions, leading eventually to death.
The appearance of these conditions is usually simultaneous, and they sustain one another. Therefore, you cannot heal your patients if not addressing all three of them.
Let’s try to explain how a traumatic event activates this “Vicious Cycle”, and how it works:
- The index event (i.e. trauma) causes blood loss and, consequently, hypoperfusion and hypoxia, leading to activation of the anaerobic metabolism and to lactic metabolic acidosis;
- Hypoperfusion reduces the core temperature (the blood “distributes” the heat in our body);
- Hypothermia and acidosis reduce the clotting factors activity;
- Bleeding leads to clotting factors consumption;
- The shock status secondary to hemorrhage activates fibrinolysis, thus worsening the coagulopathy;
- Hypothermia reduces platelet aggregation and alters the enzymatic processes occurring during the clotting cascade, worsening the coagulopathy;
- Hypothermia causes a leftward shift of the oxygen-hemoglobin dissociation curve and reduces the myocardial contractility, both leading to reduced tissue oxygenation and, consequently, to metabolic acidosis through the activation of the anaerobic metabolism;
- Metabolic acidosis prolongs clot formation and increases fibrinolysis;
- Coagulopathy worsens the bleeding, reinforcing the “Vicious Cycle”.
And here is where DCR plays its major role… If DCR’s principles are not followed, our efforts to resuscitate the patient will definitely speed up the activation and progress of this cycle.
Consider just this:
- If large volumes of crystalloids are administered, they will cause hemodilution, reducing both clotting factors and hemoglobin concentration, exacerbating coagulopathy and metabolic acidosis;
- Crystalloids (mainly normal saline 0.9%) are acid, thus they may worsen the metabolic acidosis;
- If the fluids infused are not warm, they will aggravate hypothermia;
- PRBCs contain citrate to keep them fluid, and this may worsen the coagulopathy;
- Potassium may increase, thus increasing the risk of arrhythmias;
- If our aim is to keep the blood pressure close to normal (around 120/80 mmHg), this will exacerbate bleeding.
Now, we hope you have started to understand the importance of DCR and what we meant when we told you that in trauma patients you need to address physiology first. If you think as an elective surgeon, you will focus on anatomy, and the only thing you’re going to obtain is a perfectly done surgical operation on a dead patient…
The Damage Control Resuscitation’s Principles
Basically, DCR aims to prevent or treat all the factors supporting the Vicious Cycle. Its principles may be reported as follows:
- Minimize bleeding with early hemorrhage control measures (i.e. Stop the Bleed principles);
- Warm the patient: always use warming blankets and warm fluids;
- Permissive hypotension: target SBP of 50-70 mmHg in penetrating trauma, 80-90 mmHg in blunt trauma, and 100-110 mmHg / MAP >65 mmHg in traumatic brain injury;
- Prefer blood products to crystalloids: give crystalloids in small boluses (i.e. 250-500 mL), not exceeding 1.5 L;
- Massive transfusion protocol (MTP) activation: target a high ratio of plasma (FFP) and platelets (Plt) to red blood cells (i.e. PRBC:FFP:Plt 1:1:1 or 2:1:1 ratio);
- Correct the coagulopathy, targeting the treatment to the specific derangements: obtain functional laboratory measures of coagulation (e.g. TEG, ROTEM) to guide ongoing resuscitation, and administer pharmacological adjuncts as needed (e.g. fibrinogen, tranexamic acid, calcium…).
Applying these principles, the end points of DCR are:
- Status: no active bleeding; urine output >0.5 mL/kg/h
- Vitals: SBP >90 mmHg (MAP >65 mmHg); HR <100 bpm; Temp >35°C
- Blood gas: pH >7.3; BE >-3; Lactate < 2.5 mmol/L; Ca2+ >1.2 mmol/L; Hb >8 g/dL
- Coagulation: INR <1.5; Fibrinogen > 1 g/L; Thromboelastogram (TEG) within normal limits
Let’s finish here for now…
In the next posts, we are going to explain the basic DCR’s treatments… In the meanwhile, try to understand the complexity of physiologic changes occurring as a result of trauma. Once you have realized it, you can fully understand why trauma must be addressed by a team and must not be a one-man show…
- Bogert JN, et al. Damage control resuscitation. Journal of Intensive Care Medicine 2014; DOI: 10.1177/0885066614558018.
- Pohlman TH, et al. Damage control resuscitation. Blood reviews 2015;29:251-62.
- Chang R, et al. Advances in the understanding of trauma-induced coagulopathy. Blood 2016;128:1043-9.
- Cannon JW, et al. Damage control resuscitation in patients with severe traumatic hemorrhage: a practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg 2017;82:605-17.
- Nickson C. Damage Control Resuscitation. Life in the Fast Lane. Published on March 31, 2019. Accessed on August 6, 2020. Available at [https://litfl.com/damage-control-resuscitation/].
- Weingart S. EMCrit Podcast 30 – Hemorrhagic Shock Resuscitation. EMCrit Blog. Published on August 15, 2010. Accessed on August 6, 2020. Available at [https://emcrit.org/emcrit/trauma-resuscitation-dutton/].
How to Cite This Post
Bellio G, Marrano E. The Art of Alchemy – Part 1. Surgical Pizza. Published on October 24, 2020. Accessed on September 18, 2021. Available at [https://surgicalpizza.org/critical-care/the-art-of-alchemy-part-1/].