Atlanto-occipital dislocation in a patient presenting with out-of-hospital cardiac arrest: a case report and literature review

Atlanto-occipital dislocation (AOD) is a ligamentous and/or osseous injury of the craniocervical junction (CCJ) [1]. It is associated with a high incidence of neurological complications and mortality [2].

AOD should be suspected in any high-energy trauma and is often associated with other severe injuries [3]. First described by Blackwood in 1908 [4], it was long believed to be a rare entity. Later studies, however, revealed an incidence of 6–10% in fatal cervical spine injuries from any mechanism [5, 6]. AOD is present in 1% of all cervical spine injuries but has been reported to be the most common cervical spine injury in motor vehicle accident (MVA) fatalities with an incidence of approximately 35% [7, 8]. The incidence is three times higher in children than in adults because of the laxity of the ligamentous structures and the relatively heavier head [9]. The prognosis of AOD has slightly improved [3, 8]. Three different mechanisms can lead to AOD: hyperextension, hyperflexion, and lateral flexion of the upper cervical spine. A combination of these mechanisms is a predictor of AOD [10‐12]. Predisposing conditions like rheumatoid arthritis, inflammation, and osteoporosis may increase the risk of AOD even in cases of relatively minor trauma [13].

Damage to the upper cervical spine may cause nervous injury by traction, compression, or ischemia due to cerebrovascular damage. Patients suffering from AOD can present with a wide range of symptoms, ranging from unilateral or bilateral weakness to tetraplegia. Up to 20% of patients complain of severe neck pain on examination only [14]. Because of the wide range of the symptoms, AOD should be suspected in any patient involved in a high-energy trauma presenting with neurological symptoms or neck pain.

If AOD is suspected, the application of a rigid cervical collar at the scene is mandatory [1] and cardiovascular and respiratory problems must be treated. In hospital, rapid imaging with computed tomography (CT) or magnetic resonance imaging (MRI) is necessary for timely diagnosis of AOD. There are different types of surgical strategies in different types of AOD, however, only early aggressive surgical stabilization is associated with improved outcomes and, in most cases, a posterior approach to the CCJ for decompression and stabilization is necessary [15‐20].

In the following, we present a case to demonstrate that this injury pattern may be part of complex clinical pictures and may therefore be challenging to diagnose. While it may seem deleterious on initial assessment, it can still be associated with good outcomes irrespective of initial prognostication.

We report a case of a patient who suffered from major trauma including AOD with OHCA and ROSC following a MVA.

This case’s key clinical question revolves around the cause and effect: Did cardiac arrest occur during the vehicle ride, leading to the crash and severe trauma including AOD due to a lack of muscular tension on impact? Or did polytrauma including AOD after the accident result in a secondary cardiac arrest due to inevitable apnea?

Some aspects of this case lead back to the first explanation: There were no signs of defense against the crash and no skid marks at the crash site. The mechanism was also somewhat atypical for AOD. Kluba et al. reported deceleration trauma in sleeping children as the “typical” scenario [22]. This may also be valid for sleeping adults or adults with cardiac arrest, due to a lack of muscular tension of the cervical spine while sleeping or cardiac arrest. However, cardiologists suspected VF after myocardial infarction as a cause of the accident. AOD is a severe life-threatening lesion with an estimated incidence of 25% of frontal crashes in children and the majority of patients die on the scene [23].

On the other hand, it seems relatively certain that this severe injury would have caused apnea. ECG alterations after CPR and the post-resuscitation syndromes as well as the found cardiomyopathy are common late effects.

The recurrent VF episode during neurological rehabilitation with one-shot life vest defibrillation does also support the hypothesis that the cause of the accident was a cardiac event.

Survivors of AOD often suffer from severe neurologic deficits such as paraplegia or tetraplegia. This patient developed critical illness myopathy and paresis of the hypoglossal nerve. All experts failed with their initial poor, in a strict sense, hopeless prognosis regarding our patient’s rehabilitation.

This underlines the value of MRI in the early treatment phase of severe trauma in select cases. The initial whole-body CT indicated complete destruction of the brainstem up to C5, whereas MRI demonstrated edema and hematoma only.

The conversation between the trauma leader and the emergency physician during the prehospital period was very important, so that the patient was not brought to a catheterization laboratory directly after ROSC. The common antiplatelet therapy during coronary angiography might have had negative effects on the outcome due to aggravation of bleeding.

In summary, AOD is an uncommon but increasingly recognized traumatic injury. This case demonstrates that good neurological outcome is possible even after multiple life-threatening injuries in combination with AOD. The cause of the cardiac arrest was probably myocardial infarction with VF. The impact of the car with the concrete dam and a lack of muscular tension of the cervical spine during cardiac arrest led to major AOD trauma in contrast to a relative minor trauma mechanism.