Time to Change ATLS Classifications of Hemorrhagic Shock

Dear Editor, Advanced trauma life support (ATLS) classification of hemorrhagic shock (HS) and its modifications[1] are hitherto used as reference. However, its scarce inapplicability on the field and its theoretical and practical uselessness have distracted concentrating on the physiology underneath the clinic and impaired opportunities for advancement on the topic. Its main liability lies in the wrong conceptual approach: relying on blood loss instead of remaining cardiac or cardiocirculatory reserve and capacity of compensation, which, varying among individuals, must be tailored on the patient’s current physiology. The addition of Glasgow Coma Scale (GCS) and negative base excess (NBE) levels does not add advantage to the raison d’être of a classification of a condition such a HS, which is timing of intervention. NBE is certainly the fastest parameter of hypoxemia in rising and its level correlates with the degree of hypoxemia, especially if compared to lactic acid. It is not the degree of tissue hypoxia that can determine the need and timing for intervention, but macrocirculation, i.e., the remaining cardiac or cardiocirculatory reserve and the capacity of compensation varying among individuals.[2] The evaluation of microcirculation and cellular response to hypoxemia and assessment of tissue perfusion are worthy mainly after the first 3–4 days when cryptic shock about to abut into MOD/F needs to be prevented, identified, buffered, or reversed.[3] GCS in traumatic brain injury (TBI) does not affect timing of intervention of HS, whereas hypotension and hypoxemia affect TBI outcomes. A new classification, the “Revised Physiological Classification” [Figures 1 and 2], has been developed and refined since 2010, based on the physiological response to progressing hemorrhage with stress, timing of management, and applicability at glance.[4,5]Figure 1: Classification of hemorrhagic shock.[ 4 , 5 ] HS: Hemorrhagic shock, TBV: Total blood volume, SAP=Systolic arterial pressureFigure 2: Overall management of hemorrhagic shock stages.[ 4 , 5 ] NOM: Nonoperative management, PRC: Packed red cells, CA: Cardiac arrest, St-y: Sternotomy, TACC: Thoracic aorta cross-clamping, ERT: Emergency resuscitative thoracotomy, ALT: Anterolateral thoracotomy, THR: Titrated hypotensive resuscitation, IHD: Ischemic heart damage, CVE: Cerebrovascular event, DCS: Damage Control surgery, AACC=Abdominal Aorta cross-clampingIt is based on two physiological bastions: testing the presence and degree of compensation[6] and identifying the situation of subtle feeble delicate equilibrium maintained by the lifesaving reflexes in the most advanced preterminal stages. Circulation is essentially a binary dual system with a quasi pit stop at the arterial gate system. The mechanisms for the spontaneous fading or stopping of hemorrhage, known since World War I, are spasm, retraction and hypotension for arteries, and clot formation perispace containment and hypotension for veins. Whereas a bleeding from medium or large-sized vessel not anatomically contained, without source control progresses unabated, an intraparenchymal bleeding can spontaneously stop or be slowed enough. This is due (i) to the autoregulation of perfusion by the single organs, whereas major vessel macrohemodynamics is not similarly autoregulated, (ii) to the periorgan compression working for veins but lacked in most of major arteries beds, and (iii) to the different rate of bleeding between small arteries and arterioles within the parenchymal organs and medium-large diameter arteries, according to Bernoulli’s law. If no hemodynamic changes are seen with a fluid test bolus/es, specifically normalization of systolic arterial pressure (SAP) and inverse trend of tachycardia, then the hemorrhage is driven by an extraparenchymal bleeding source or the compensation mechanism of the arteriolar gate system has failed due to the advanced shock. When a patient manifests signs indicating critical physiology and impending CA, the balance between life-saving reflexes is stretched to the maximum, and remaining insufficient perfusion (blood, oxygen, and substrates) stays in a liable and delicate equilibrium, susceptible to any minimal change or interfering variables. Any forcing, spoiling, interrupting, or breaking of this life-holding equilibrium would push the patient to irreversible shock and exitus. The recognition of this critical stage has two ominous clinical implications: the correct interpretation of the cause of a concomitant collapse and the most useful timing to do an emergency resuscitative thoracotomy (ERT) or any other lifesaving extracorporeal life support (ECLS). Collapse in healthy controls during HS usually occurs at systolic arterial pressure of ≤60 mmHg, mean arterial pressure of ≤45 mmHg, and diastolic arterial pressure of ≤40 mmHg.[7] Patients with congestive heart failure, left main stem coronary artery stenosis, acute right heart failure, or hypertension collapse at higher values. If a patient faints while in compensated Stage II HS, it means an overlapping cardiac or cerebrovascular event has occurred, or there are other causes of peripheral or “medical” faint further needing to be addressed and managed. The first picture is more frequent in elderly hypertensive with underlying chronic cardiac or cerebrovascular liability. In a not compensated unstable progressing HS Stage III not responding to fluid test, indicating gate-system failure in a parenchymal bleeding or an ominous extraparenchymal hemorrhage, any faint in the elderly must be interpreted as progression to critical shock with impending cardiac arrest Stage IV, caused by a cardiac or a cerebrovascular event of hypoxemic etiology.[8,9] Instead, the stage of pre-CA in young and healthy does not usually present with a cardiac or a cerebrovascular event, due to a lesser liability to cardiac and cerebrovascular events of hypoxemic etiology and the different age-related compensatory ability to hypotension. Young and healthy can sustain a period of total blood volume of 50%–60% and a variable but brief phase of imminent cardiac arrest before dying of exsanguination, characterized by the presence of life signs in the absence of a central arterial pulse (Pers. Obs.). Schober et al. have identified and described this foggy clinical scenario in young and healthy with imminent CA highlighting the critical role a portable POCUS can have at the scene in the identifying this borderline situation.[10] The distinction is diriment. To do an ERT i.e. anterolateral thoracotomy (ALT) and/or sternotomy (St-y) and thoracic aorta cross-clamping (TACC) or an equivalent emergency resuscitative laparotomy and abdominal aorta cross-clamping (ERL/AACC), whereas the patient destined to arrest has still life signs, will obviously yield more chances of survival. Other advantages are its fitting conceptually with timely implementation, with tactics such as titrated hypotensive response and iatrogenic vasoconstriction, and strategies such as titrated-to-response anesthesia and damage control surgery advised or mandatory in advanced stages. If the bleeding is extraparenchymal, from a big vessel, especially vein, multiple, or mixed, as often is in major trauma, source control must be rapid or immediate, or even stat on the spot, without a fluid load test, which would be redundant. Only imaging, echo, and artificial intelligence can tell ab initio the site/s of bleeding source/s of answer the question above, which is the question per antonomasia, whose answer saves thousands of lives. Until then, the “Revised Physiological Classification” of HS is the most useful, comprehensive, and applicable appraising tool. Research quality and ethics statement The author followed applicable EQUATOR Network (http://www.equator-network.org/) guidelines during the conduct of this report. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.