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Abstract 151: GFAP Measurements for Rapid Prehospital Identification of Intracranial Hemorrhage in Patients With Acute Coma

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Background: Prehospital triage and treatment of patients with acute coma is challenging for rescue services, as the underlying pathogenetic conditions are highly heterogenous and difficult to assess. Glial fibrillary acidic protein (GFAP) has been recently identified as a biomarker of intracerebral hemorrhage. The aim of this study was to test the diagnostic value of a GFAP point-of-care(poc) device to rapidly differentiate intracranial hemorrhage from other causes of acute coma (including seizures, metabolic disorders, cardiovascular disorders, and intoxication) in the prehospital phase. Methods: Patients who were admitted to the emergency department due to acute coma (Glasgow Coma Scale scores between 3-8) were enrolled prospectively. Blood samples were collected already in the prehospital phase. Plasma GFAP measurements were performed on the i-STAT Alinity® (Abbott) device (duration of analysis 15 min). The primary endpoint was the final diagnosis at hospital discharge. Results: 95 patients were enrolled (mean age 64±20 years, 43% female). GFAP concentrations were strongly elevated in patients with a primary cerebral cause of coma compared to primary non-cerebral causes (p<0.001). The GFAP concentrations (mean±SD in pg/mL) according to final diagnosis were as follows: intracerebral hemorrhage 4840±4500 (n=15), subarachnoid hemorrhage 4858±4662 (n=11), subdural or epidural hematoma 3462±4005 (n=4), ischemic stroke 992±2857 (n=12), seizure 45±21 (n=11), cardiovascular or metabolic disorder 258±888 (n=29), intoxication 30±2 (n=6), psychogenic stupor 29±0 (n=2); n=5 patients had missing diagnoses. GFAP values over 1000 pg/ml indicated a primary cerebral cause of coma with 100% certainty (hereof, 86% had intracranial hemorrhage). Conclusion: Increased GFAP plasma values in patients with acute coma identify a primary cerebral cause of coma (mostly intracranial hemorrhage) with very high diagnostic accuracy. Patients with primary non-cerebral causes of coma showed overall low GFAP concentrations. Prehospital GFAP measurements on a poc platform may allow rapid stratification according to the underlying cause of coma by rescue services. This could have major impact on triage and management of these critically ill patients.
Title: Abstract 151: GFAP Measurements for Rapid Prehospital Identification of Intracranial Hemorrhage in Patients With Acute Coma
Description:
Background: Prehospital triage and treatment of patients with acute coma is challenging for rescue services, as the underlying pathogenetic conditions are highly heterogenous and difficult to assess.
Glial fibrillary acidic protein (GFAP) has been recently identified as a biomarker of intracerebral hemorrhage.
The aim of this study was to test the diagnostic value of a GFAP point-of-care(poc) device to rapidly differentiate intracranial hemorrhage from other causes of acute coma (including seizures, metabolic disorders, cardiovascular disorders, and intoxication) in the prehospital phase.
Methods: Patients who were admitted to the emergency department due to acute coma (Glasgow Coma Scale scores between 3-8) were enrolled prospectively.
Blood samples were collected already in the prehospital phase.
Plasma GFAP measurements were performed on the i-STAT Alinity® (Abbott) device (duration of analysis 15 min).
The primary endpoint was the final diagnosis at hospital discharge.
Results: 95 patients were enrolled (mean age 64±20 years, 43% female).
GFAP concentrations were strongly elevated in patients with a primary cerebral cause of coma compared to primary non-cerebral causes (p<0.
001).
The GFAP concentrations (mean±SD in pg/mL) according to final diagnosis were as follows: intracerebral hemorrhage 4840±4500 (n=15), subarachnoid hemorrhage 4858±4662 (n=11), subdural or epidural hematoma 3462±4005 (n=4), ischemic stroke 992±2857 (n=12), seizure 45±21 (n=11), cardiovascular or metabolic disorder 258±888 (n=29), intoxication 30±2 (n=6), psychogenic stupor 29±0 (n=2); n=5 patients had missing diagnoses.
GFAP values over 1000 pg/ml indicated a primary cerebral cause of coma with 100% certainty (hereof, 86% had intracranial hemorrhage).
Conclusion: Increased GFAP plasma values in patients with acute coma identify a primary cerebral cause of coma (mostly intracranial hemorrhage) with very high diagnostic accuracy.
Patients with primary non-cerebral causes of coma showed overall low GFAP concentrations.
Prehospital GFAP measurements on a poc platform may allow rapid stratification according to the underlying cause of coma by rescue services.
This could have major impact on triage and management of these critically ill patients.

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