Surgical Critical Care

The Art of Alchemy (or How to Trick the Dark Lady) – Part 3

He cried with a loud voice “Lazarus… come forth!”. And he who was dead came out…

John 11:43-44

Glad to see you back here…

This post will end our talking about Damage Control Resuscitation (DCR) [part 1 & part 2].

Remember that these few concepts we have tried to explain are detrimental to trauma patients’ outcomes.

We understand it’s not easy for a surgeon to open his/her mind to this, but once you have done it you can aspire to become a “Surgical Super Saiyan”.

Sweetening the Acid Blood

As reported earlier, trauma patients develop lactic metabolic acidosis because of the establishment of anaerobic metabolism. Most of the times this acidosis resolves along with the correction of hypoperfusion through the resuscitation process. However, sometimes it is so pronounced it needs targeted therapy.

Acidosis can be tolerated up to a pH of 7.1. Below this level it may impair organ functions:

  • Decreases responsiveness to catecholamines;
  • Decreases left ventricular contractility;
  • Induces arrhythmias;
  • Causes arterial vasodilation;
  • Reduces cardiac output, blood pressure, and tissue perfusion;
  • Decreases clearance of lactate by the liver.

Some actions may help to correct the acidosis, such as:

  • Mechanical Ventilation Settings: it helps to correct the metabolic acidosis and it should be the first step to take. The principle is to establish an iatrogenic respiratory alkalosis (or to correct an iatrogenic respiratory acidosis, if serum HCO3 >6 mEq/L). It can be done by reducing the EtCO2, meaning more CO2 has been expelled from the respiratory system, and, consequently, from the blood. To do so, you need to increase the Tidal Volume and/or the Respiratory Rate. No further interventions should be adopted if ventilations has not been optimized.
  • Sodium Bicarbonate (1-2 mEq/kg): IV administration should be reserved only for patients with pH <7.1 (pH <7.2 if severe acute kidney injury). It should not be used in patients with mild-to-moderate metabolic acidosis because it may cause intracellular acidification and a decrease in ionized calcium. The goal is to keep arterial pH >7.3. Remember the equation HCO3 + H+ = H2CO3 = CO2 + H2O. This means sodium bicarbonate creates CO2, which must be removed through the respiratory system. If this does not happen, it penetrates cell membranes and worsens intracellular acidosis (even if arterial pH increases).
  • Continuous Renal Replacement Therapy: continuous venovenous hemofiltration (CVVH) is the method of choice (and the last resort) in patients with severe refractory metabolic acidosis. It has to be preferred over the intermittent method because it has only a small impact on the hemodynamic status.
Hypothermia

Hypothermia is defined as core temperature <35°C, and it must be treated as soon as possible.

Remember that trauma patients have many possible causes contributing to the development of hypothermia: exposure to an external cold environment, blood loss, they are undressed on arrival, anesthetic drugs and mechanical ventilation may decrease body temperature, surgery increases heat loss, etc…

There are three ways to treat hypothermia:

  • Passive: warming blankets, increase emergency room and OR temperature (>24°C), forced-air warming (≈43°C);
  • Active: warm fluids/blood products (37-41°C), bladder irrigation with warmed fluids, warmed humidification applied to mechanical ventilation;
  • Invasive: peritoneal or pleural cavity lavage with warm fluids.
Calcium: The Player in the Shadows

It has been known for a long time that trauma patients are prone to be hypocalcemic (Ca2+ <1.12 mmol/L). There are two main reasons beyond this: trauma itself decreases ionized calcium levels (secondary to blood loss and calcium depletion during coagulation), and iatrogenic transfusion-related hypocalcemia (citrate chelates calcium in the blood).

Why do we care about calcium levels?

Calcium seems closely related to the lethal triad:

  • It is an important cofactor during coagulation; it binds phospholipids that appear after the activation of platelets and functions as a binding point for other coagulation factors. Therefore, the lower the calcium levels, the worse the acidosis;
  • Calcium lower levels are associated with lower pH, and increasing acidosis;
  • Hypothermia decreases liver function, slowing down citrate metabolism, thus further reducing ionized calcium levels;
  • Low Ca2+ levels impair cardiac myocytes function and, consequently, cardiac contractility.

For these reasons, some authors support the idea of a “Lethal Diamond” instead of the “Lethal Triad”. Regardless of the name you use, recognizing this concept means advocating the correction of ionized calcium levels. The protocol proposed consists of giving 1 g of calcium chloride (or gluconate) IV during or right after the first unit of PRBC, followed by 1 g every 4 more units. The goal is to keep Ca2+ >1.2 mmol/L.

Becoming Jesus

It’s 3.16 in the morning, and we are back to our Surgical Intensive Care Unit, receiving the patient from the OR.

Let’s look again with our “new eyes” to the patient’s characteristics:

  • 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
  • Fluids administered: 2000 mL crystalloids, 500 mL colloids, 2 units PRBC

We all agree the “vicious cycle” is running, and that the patient still needs extensive resuscitation…

Let’s analyze point-by-point what’s wrong and how to correct it:

  • Perfusion: the patient’s blood pressure is within the limits of permissive hypotension; however, he is on vasopressors on medium-high dosage. This means that if we stop the norepinephrine, his BP will drop significantly, and probably he will die. With this, we can conclude that his perfusion is not good enough. Two more signs are supporting this fact: the urine output is below 0.5 mL/kg/h, and the ABG shows he has a quite severe metabolic acidosis. Our plan should be to keep the BP as it is, reducing the need for vasopressor and improving perfusion. To do so, we must give him blood products. We must not infuse any more fluids!!! His shock index is 1.38 (way higher than the cut-off (i.e. 0.9)), and his ABC score was 3 before surgery. The MTP must be activated.
  • Metabolic status: as stated before, this patient is on severe lactic metabolic acidosis. The first step is to set up the ventilator settings in order to decrease the pCO2 (stay close to 30 mmHg). Moreover, the MTP will help to correct the acidosis as well. In this patient, there is no need for Bicarbonate infusion nor CVVH.
  • Temperature: our patient is hypothermic. Our first two ways to warm him up are to use a heating blanket and warm infusions (in this case warm blood products). If this is not enough, we can use the left ICD to infuse warm fluids inside the chest cavity.
  • Coagulation status: The infusion of FFP and Plt will help us to correct the ongoing coagulopathy. However, this could not be enough. What can we use? The correct approach should be to perform a TEG. In the meanwhile, since we are still within the first 3 h from the traumatic event, it’s not wrong to give the patient tranexamic acid (we can also wait for the TEG result). Additionally, the patient is hypocalcemic; therefore, we should administer calcium chloride/gluconate. Then, according to the TEG result, we may use additional FFP, Plt, cryoprecipitate, or fibrinogen. Additional TEGs should be repeated to monitor the patient’s changes in his coagulation status.

As you have seen, surgery alone can do little for patients who sustained severe injuries. The only way to save these patients is to work together with the intensivists… And to do so, you must know and understand DCR.

So-called surgeons who think they are God, able to save patients’ lives with their bare hands, are just huge assholes… and they are very dangerous… Keep away as far from them as possible!!!

Until next time: don’t be assholes, be acute care surgeons!!!

Cheers…

References
  1. Bogert JN, et al. Damage control resuscitation. Journal of Intensive Care Medicine 2014; DOI: 10.1177/0885066614558018.
  2. Pohlman TH, et al. Damage control resuscitation. Blood reviews 2015;29:251-62.
  3. 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.
  4. 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/].
  5. 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/].
  6. Wise R, et al. Strategies for intravenous fluid resuscitation in trauma patients. World J Surg 2017;41:1170-83.
  7. Cap AP, et al. Whole blood transfusion. Military Medicine 2018;183:45-51.
  8. Kraut JA, et al. Lactic acidosis. NEJM 2014;371:2309-19.
  9. Ditzel RM, et al. A review of transfusion- and trauma-induced hypocalcemia: is it time to change the lethal triad to the lethal diamond? J Trauma Acute Care Surg 2020;88:434-9.
How to Cite This Post

Bellio G, Marrano E. The Art of Alchemy – Part 3. Surgical Pizza. Published on November 21, 2020. Accessed on July 31, 2021. Available at [https://surgicalpizza.org/critical-care/the-art-of-alchemy-part-3/].

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