Disrupted sympathetic innervation and unopposed parasympathetic activity after a cervical or high-thoracic SCI leads to cardiovascular abnormalities, which includes profound changes in arterial BP and HR particularly in the acute phase. However, these complications can be short-term (acute), long-term (chronic) or both. During the acute phase of SCI, patients typically present with neurogenic shock, which refers to a condition that is characterized by the simultaneous presence of bradycardia and arterial hypotension without any other determined etiology. Together these conditions are recognized as an acute complication occurring following SCI (Furlan & Fehlings 2008; Krassioukov 2009; Popa et al. 2010).
Neurogenic shock is thought to be a consequence of a sudden reduction of sympathetic activity and output peripherally after SCI, in particular higher-level SCIs. Eight studies were found which investigated the incidence of neurogenic shock during acute SCI. Most of the studies used the term “neurogenic shock” when defining outcome measures, while others explicitly stated neurogenic shock as being determined by the presence of hypotension and bradycardia or by the presence of hypotension alone.
Zipnick et al. (1993) retrospectively reviewed patients who were admitted to an emergency department and noted an incidence of 7% acute neurogenic shock at the time of hospital arrival. Mallek et al. (2012) reviewed patients admitted to a trauma center beginning from their time of admission and observed a neurogenic shock incidence of 8.8% (16/180 patients); of those who endured neurogenic shock, 62.5% (n=10) of these patients had cervical SCI whereas 25.0% (n=4) had thoracic SCI and the remaining 2 patients had multiple levels of injury. In a more recent study, Ruiz et al. (2018) found slightly higher rates of neurogenic shock for those with cervical SCI at 53.6%. Guly et al. (2008) reviewed patients at first presentation to the emergency department. The incidence of neurogenic shock was subdivided by level of injury; 19.3%, 7%, and 3% of cervical, thoracic, and lumbar SCI patients developed neurogenic shock, respectively. Nakao et al. (2012) reviewed cervical SCI patients at 1 month after sustaining injury to investigate the incidence of hypotension. The authors defined hypotension as systolic atrial pressure <90mmHg or requiring intravenous administration of crystaloids and vasopressive agents. Within this population, 45.3% of patients were hypotensive. In a study by Bilello et al. (2003), patients who had sustained a high cervical (C1-C5) injury were reviewed and compared to patients who had sustained a lower cervical (C6-C7) injury. Patients were studied during the initial 24 hours of their intensive care unit stay (ICU). Neurogenic shock developed in 31% and 24% of high cervical injury and low cervical injury patients, respectively, although there was no significant difference in frequency of occurrence between these groups (p=0.56). Grossman et al. (2012) sought to determine the incidence of various acute complications that arise following SCI. Acutely injured patients were included in the study beginning from the time of hospital admission. Cardiac complications accounted for 21% of the most frequent severe complications, of which 45% involved severe bradycardia. Ravensbergen et al. (2014) evaluated SCI patients where data was collected on 5 occasions: at the start of and 3 months into inpatient rehabilitation, at rehabilitation discharge, and at 1 and 5 years after discharge. At the start of inpatient rehabilitation, participants were on average 100 days post injury, and the incidence of hypotension and bradycardia were recorded individually. Within this population, 33% of patients had hypotension and 4.5% of patients had bradycardia at the start of rehabilitation. The authors noted that there was no significant change in the prevalence of these complications over time. Finally, Tuli et al. (2007) conducted a post-hoc analysis as part of a multicenter RCT in part to assess the incidence of neurogenic shock among cervical SCI patients. Patients were acutely injured and were assessed beginning at their time of arrival at the emergency department. Neurogenic shock developed in 13% of patients and was higher among AIS A (17%) and B (18%) patients compared to AIS C/D (7%) patients.