Cerebral Lactate Correlates with Early Onset Pneumonia after Aneurysmal SAH

• Published in: Translational stroke research 2014-04, Vol.5 (2), p.278-285
• Main Authors: Radolf, S., Smoll, N., Drenckhahn, C., Dreier, J. P., Vajkoczy, P., Sarrafzadeh, A. S.
• Format: Article
• Language: English
• Subjects: Adult; Aged; Aneurysms; Aphasia; Biomedical and Life Sciences; Biomedicine; Brain - metabolism; Cardiology; Catheters; Extracellular Fluid - metabolism; Female; Glucose - metabolism; Glutamic Acid - metabolism; Hemorrhage; Humans; Immune system; Ischemia; Lactates - metabolism; Male; Medical imaging; Metabolism; Microdialysis; Middle Aged; Mortality; Multivariate analysis; Neurology; Neurosciences; Neurosurgery; Original Article; Patients; Pneumonia; Pneumonia - etiology; Pneumonia - metabolism; Prospective Studies; Pyruvic Acid - metabolism; Subarachnoid Hemorrhage - complications; Subarachnoid Hemorrhage - metabolism; Traumatic brain injury; Variance analysis; Vascular Surgery; Ventilators
• ISSN: 1868-4483; 1868-601X
• DOI: 10.1007/s12975-013-0292-z

Pneumonia is a significant medical complication following aneurysmal subarachnoid hemorrhage (aSAH). The aSAH may initiate immune interactions leading to depressed immunofunction, followed by an increased risk of infection. It remains unclear as to whether there is a possible association between cerebral metabolism and infections. Clinical and microdialysis data from aSAH patients prospectively included in the CoOperative Study on Brain Injury Depolarisations protocol Berlin were analyzed. Levels of glucose, lactate, pyruvate, and glutamate were measured hourly using microdialysis in the cerebral extracellular fluid. The occurrence of pneumonia (defined by positive microbiological cultures) and delayed ischemic neurological deficits (DIND) was documented prospectively. Eighteen aSAH patients (52.7 ± 10.7 years), classified according to the World Federation of Neurological Surgeons in low (I–III, n  = 9) and high (IV–V, n  = 9) grades, were studied. Eight patients (45 %) experienced DIND, 10 patients (56 %) pneumonia (mean onset day 2.6). Lactate was elevated at day 3 in infected patients ( n  = 9, median = 6.82 mmol/L) vs. patient without infections ( n  = 6, median = 2.90 mmol/L, p  = 0.036). The optimum cut-off point to predict pneumonia at day 3 was 3.57 mmol/L with a sensitivity of 0.77, and a specificity of 0.66 (area under curve was 0.833 with p  = 0.034). Lactate at day 7 was higher in DIND patients compared to no-DIND-patients ( p  = 0.016). Early elevated lactate correlated with occurrence of bacterial pneumonia, while late elevations with DIND after aSAH. Future investigations may elucidate the relationship between cerebral lactate and markers of immunocompetence and more detailed to identify patients with higher susceptibility for infections.