In the treatment of traumatic cardiac arrest (TCA) a paradigm shift occurred in recent decades, switching resuscitation in TCA from a merely futile attempt to a more promising intervention. Several reasons account for this, ranging from a better understanding of the pathophysiology of TCA, division into distinct TCA entities, separation from other causes of CA, refined guidelines, and also improved training on this formerly potentially neglected topic. In addition, technical advances in both diagnostics (e.g., point of care ultrasound, POCUS) and therapy further reshape the management of TCA. Thus, although overall mortality of TCA is still very high, outcomes in selected subgroups are improving.

Prospective high-quality studies, i.e., RCTs, on TCA to inform guideline development, are virtually absent, despite the large impact of the TCA population on the patient, health care, and society. Therefore, TCA treatment guidelines are often based on a mix of expert opinions (e.g., Delphi procedures), retrospective studies, or extrapolated from related medical fields. This mix of informing sources partly explains why guidelines for treatment of TCA of several organizations show considerable differences, e.g., when comparing national or international guidelines, e.g., between Advanced Trauma Life Support (ATLS) or European Resuscitation Council (ERC) and the European Trauma Course (ETC).

3. Potentially Reversible Causes of TCA

The focus of TCA treatment is to rapidly address the potentially reversible causes of TCA; however, so far there is no universally accepted approach to cover this. One memory aid is the acronym H.O.T.T., e.g., endorsed by the European Resuscitation Council (ERC): 

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Hypovolemia (Hemorrhage, until proven otherwise);

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Oxygenation impairment;

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Tension pneumothorax;

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Tamponade of the pericardium, i.e., ‘cardiac tamponade’.

Hypovolemia (H) in trauma is almost exclusively caused by hemorrhage and is the most common, potentially reversible cause of TCA. Impairment of oxygenation (O) often requires the creation of a patent airway and optimizing oxygen supply. A tension pneumothorax (T) may present in spontaneously breathing patients, but also rapidly develop after endotracheal intubation and mechanical ventilation. A pericardial tamponade (T) may both be caused by blunt or penetrating chest trauma. Addressing all H.O.T.T. items rapidly is a key concept in current TCA treatment. The acronym H.O.T.T. resembles a trauma-related subset from the ALS-memory-aid ‘4xH and 4xT’ for all common reversible causes of cardiac arrest (i.e., 4xH represent hypovolemia, hypoxemia, hyper/hypokalemia, hypothermia and 4xT represent thrombosis, toxins, tamponade and tension pneumothorax). The individual H.O.T.T. etiologies can occur in combination, and can aggravate each other.

TCA resuscitation may be initiated when there are no obvious signs of futility of resuscitation and, currently, there is no universal consensus under which criteria resuscitation in TCA should (not) be initiated. The following criteria to withhold TCA resuscitation are published in the literature; however, they are difficult to follow in practice, e.g., because of the notorious uncertainty of reported time points and other information. The American College of Surgeons and National Association of Emergency Physicians suggested to withhold resuscitation attempts in TCA when death is inevitable, but also in trauma cases with apnea, pulselessness and absence of an organized ECG. The ERC considers the following criteria to withhold or terminate resuscitation in TCA.

Withhold resuscitation, if

Consider terminating resuscitation, if

Prolonged resuscitation efforts in futile TCA cases unnecessarily increase risks for the direct care providers and bystanders for stick or cut-injuries, infections, psychological trauma, and drain-limited system resources (e.g., personnel, ER capacity, and blood products). In cases where the typical reversible causes of TCA have been ruled out, or addressed, termination of treatment may be considered directly. However, others suggest continuing with an additional period (e.g., 10 min) of conventional CPR as a reasonable, practical decision, although this period is not backed up by high-quality data. This extra period of CPR may be used to re-evaluate and summarize the diagnostic and therapeutic interventions performed and achieve the univocal team decision to terminate futile efforts. Depending on cultural and personal preferences, this period may also be used to invite family members (particularly parents of their arrested children, if not already present) to the trauma bay, allowing them to witness the resuscitation efforts and be part of the scene, when CPR is eventually terminated.

TCA guidelines, e.g., the ERC TCA guidelines, de-prioritize the immediate initiation of chest compressions and adrenaline administration, as conventionally stressed in medical cases of CA. However, there are notable exceptions, where TCA treatment should follow the standard algorithm of ALS with immediate focus on high-quality CPR with chest compression and oxygenation/ventilation. Examples are TCA after cardiac contusions, asphyxiation (e.g., burial under sand or in a crowd crush), electricity injuries, and TCA after (isolated) traumatic brain injury, caused by ‘impact brain apnea’. Thus, although there is a reshuffling of priorities of resuscitation in TCA by strictly putting forward treatment of reversible causes, this should not delay chest compressions in patients who need it. In addition, numerous trauma patients in cardiac arrest primarily suffered from a medical cause of arrest, e.g., undergoing a myocardial infarction while driving a car, followed by a car crash. It is vital that a medical cardiac arrest is not misdiagnosed as a traumatic cardiac arrest and must be treated with the universal advanced life support (ALS) algorithm. Cardiac arrest or other causes of sudden loss of consciousness (e.g., arrhythmias, hypoglycemia, stroke, and seizures) may cause a secondary traumatic event. Some observational studies have reported that ~2.5% of non-traumatic out-of-hospital cardiac arrests (OHCAs) occur in cars. For a cardiac arrest to be traumatic, an adequate mechanism of injury is required, and secondary trauma after ‘medical’ cardiac arrest is frequently not adequate. Particularly for less experienced practitioners, or practitioners usually confronted merely with trauma cases, this may be challenging, because of either a biased expectation of the case, or the usually much more impressive presentation of the trauma aspect (e.g., with wounds and blood), than of the medical emergency. In addition, medical conditions and treatment hereof (e.g., usage of anticoagulants) may greatly affect treatment and outcome of the trauma patient.

Adrenaline is a potent vasoconstrictor, besides its cardiac effects, and thus theoretically supports vascular tone in hypovolemia. Adrenaline is the drug advocated most over the entire history of (ALS) resuscitation algorithms, and is still advocated in several current TCA algorithms (e.g., ATLS 10th edition). Although early administration of adrenaline in TCA is thus still widely taught and spread practice, the scientific foundation of its use in TCA is questionable. Retrospective studies, despite their limitations, hint towards improved survival in TCA patients given less, or no adrenaline. Thus, with regard to an intervention as controversial as adrenaline in TCA, one should balance the ‘economics of resuscitation’ and promote higher yield interventions that could be performed by the team instead, i.e., interventions addressing potentially reversible causes of TCA. There are exceptions in which adrenaline use may be more rational, e.g., traumatic (peri-)arrest caused by spinal injuries, as described below.

Hypovolemia in TCA is usually caused by traumatic blood loss, a prototypical form of absolute hypovolemia. In rare and thus frequently unexpected cases, relative hypovolemia may contribute to TCA. Relative hypovolemia is the condition in which the absolute blood volume may be normal, but misdistribution of blood, e.g., by vasoplegia, may cause life-threatening hypotension. In TCA, this distributive shock may be attributed to spinal cord injuries, in which sympathetic innervation of the vasculature fails (neurogenic shock). TCA by relative hypovolemia alone after spinal cord injury is exceptional, but as a complicating factor sympathetic innervation of the heart may also be impaired, aggravating the neurogenic shock to life-threatening levels, particularly in conjunction with other injuries. In contrast to absolute hypovolemia after hemorrhage, where refilling the vasculature with volume such as blood(-products) is appropriate, the vasoplegia causing relative hypovolemia (and bradycardia from cardiac denervation) may be treated with a catecholamine, e.g., adrenaline. Thus, this appears an appropriate indication for adrenaline in traumatic (peri-)arrest.