The predictive value of catecholamines in assessing outcome in traumatic brain injury

Abstract

Because of the central role of the sympathetic nervous system in mediating the stress response, plasma norepinephrine (NE), epinephrine (E), and dopamine (DA) levels were measured in 61 traumatically brain-injured patients to determine whether catecholamine (CA) levels obtained within 48 hours after injury provide reliable prognostic markers of outcome. Patient outcome was determined at 1 week using the Glasgow Coma Scale (GCS) and at the time of discharge using the Glasgow Outcome Scale (GOS). Levels of NE, E, and DA correlated highly with the admission GCS score (NE: r = 0.58, p less than 0.0001; E: r = 0.46, p less than 0.0025; DA: r = 0.27, p less than 0.04). Moreover, in the 21 patients with GCS scores of 3 or 4 on admission, NE levels predicted outcome at 1 week. All six patients with NE levels less than 900 pg/ml (normal level less than 447 pg/ml) improved to GCS scores of greater than 11, while 12 of 15 with NE values greater than 900 pg/ml remained with GCS scores of 3 to 6 or died. Levels of E and DA were not as useful. Catecholamine levels also increased significantly as the GOS score worsened. Levels of NE and E were significantly higher in patients who died or remained persistently vegetative than in those with better outcomes. In the 54 patients who survived beyond 1 week, significant correlations were present between the length of hospitalization and NE (r = 0.71, p less than 0.0001) and E (r = 0.61, p less than 0.0001) levels. Concentrations of NE (r = 0.61, p less than 0.0004) and E (r = 0.48, p less than 0.01) were also highly correlated with the duration of ventilatory assistance. Analysis of the interactions of CA levels and GCS scores, duration of ventilatory assistance, and length of hospitalization revealed that the CA's either enhanced the reliability of the GCS score or were independent predictors of outcome. Thus, these findings indicate that alterations in circulating CA levels reflect the severity of the neurological insult and provide support for the use of CA measurements as a physiological marker of patient outcome in both the acute and chronic phases of traumatic brain injury.

Are Electrocardiographic Changes in Patients with Acute Subarachnoid Hemorrhage Associated with Takotsubo Cardiomyopathy?

“…It is suggested that these findings support the mechanism of catecholamine-mediated myocardial injury. A previous study indicated that serum levels of catecholamines also correlate with the severity of traumatic brain injury [41]. In our study, increased plasma levels of NE and 24-hour urine NE were not correlated with the severity of SAH.…”

Predictors of Neurocardiogenic Injury After Subarachnoid Hemorrhage

“…23,24 Previous studies indicate that serum levels of catecholamines correlate with the severity of neurological injury and neurological outcome. 18 However, animal models indicate that the direct release of toxic levels of catecholamines into the myocardium by the cardiac sympathetic nerve terminals is a more likely cause of neurocardiogenic injury than is adrenal release of catecholamines into the systemic circulation. 25 Higher HuntHess grades indicate greater neurological injury and thus may be associated with a greater degree of sympathetic outflow to the heart.…”

Traumatic Brain Injury Causes Endothelial Dysfunction in the Systemic Microcirculation through Arginase-1–Dependent Uncoupling of Endothelial Nitric Oxide Synthase

“…1 Survivors of TBI often experience profound catecholamine surges and additional systemic complications such as hypertension, pulmonary edema, and cardiomyopathy. [2][3][4][5][6][7][8][9] Notably, endothelial dysfunction secondary to systemic inflammation and shock is widely believed to contribute to systemic complications in severe trauma, 9,10 yet there have been no studies that directly measure endothelial function in systemic blood vessels after head trauma.…”