Incidence and Natural Progression of Neurogenic Shock after Traumatic Spinal Cord Injury

Abstract

Neurogenic shock, a distributive type of circulatory shock after spinal cord injury (SCI), results in profound hypotension. The consequent hemodynamic instability complicates clinical management, delays surgical intervention, and impacts neurological outcome. Moreover, the reported incidence of this condition varies significantly. We establish the true incidence of neurogenic shock by comparing the most common clinical definitions used to diagnose the condition. Further, we characterize the acute progression and recovery of neurogenic shock. Daily blood pressure, heart rate, and fluid management as well as vasopressor therapy and neurologic status were collected over 30 days from 84 adults admitted to our tertiary trauma center after cervical (n = 56) and thoracic (n = 28) SCI. We found that the reported incidence of neurogenic shock varied greatly depending on which clinical definition was applied. By using a novel combination of hemodynamic and laboratory criteria to define neurogenic shock, the calculated incidence (29% cervical SCI) in our sample most appropriately reflects the true incidence, finding that hypovolemia was the primary factor responsible for the inconsistency in incidence reports between studies. In addition, we found a characteristic decline in blood pressure after the first week post-injury and that fluid management is not currently an integral aspect of clinical management (all persons were treated at a net fluid intake ≤ zero). The results demonstrate the need for accurate identification of neurogenic shock through consistent and appropriate criteria, which is not only important from a clinical point of view, but also in establishing accurate epidemiology to responsibly allocate resources to its management.

A porcine model for studying the cardiovascular consequences of high‐thoracic spinal cord injury

“…Instead, clinical studies have been typically limited to the earliest measures being documented at approximately 12-24 h after injury (e.g. Ruiz et al 2018), due in part to the time required to transport individuals from their site of injury to a specialist SCI centre. Nevertheless, that the findings at 4 h post-SCI in our T2-SCI model are similar to those reported at 12-24 h post-SCI in humans suggests that our T2-SCI model produces clinically relevant changes in basal haemodynamics.…”

Neurogenic Shock

“…Neurogenic shock is considered distributive in nature and refers to the loss of vasomotor tone and the instability that subsequently follows due to an imbalance in the autonomic nervous system (ANS) [3,4]. Loss of sympathetic tone leads to unopposed parasympathetic control, manifested by refractory hypotension and bradycardia [3].…”

“…Neurogenic shock most often occurs after an acute injury above T6, with a possible incidence of 29% in the cervical SCI population and 19% in the thoracic SCI population [4]. The onset may be variable in relation to the timing of the injury, but in SCI patients it most commonly manifests within 2 h of the trauma [7].…”

“…gray matter and ruling out other causes of shock is more challenging). Studies of incidence after SCI have been widely variable, ranging from 14 to 44% depending on the criteria used [4]. Extrapolating from a range of papers, criteria have ranged from systolic blood pressures (SBP) <70 mmHg up to <100 mmHg, and heart rates (HR) <50 beats per minute (BPM) up to ≤90 BPM in various combinations [12].…”

“…Extrapolating from a range of papers, criteria have ranged from systolic blood pressures (SBP) <70 mmHg up to <100 mmHg, and heart rates (HR) <50 beats per minute (BPM) up to ≤90 BPM in various combinations [12]. Examples include SBP <90 mmHG or HR <50 BPM as a cutoff, more recently others have used SBP <100 mmHG and HR <80 BPM, and still others simultaneous SBP <90 mmHg and HR <80 BPM with some variability in terms of whether or not lab values accounting for hypovolemia were examined as a confounder [4]. In one cohort of patients with isolated spinal cord injury (the majority of which were related to blunt trauma), defining neurogenic shock as SBP <100 mmHg, HR <80 BPM or both, out of 490 cases the incidence of hypotension was 25.8% and of classic neurogenic shock (hypotension and bradycardia) was only 19.3% [13].…”