Cerebral microdialysis monitoring: determination of normal

• Cerebral ischemia caused by local arterial vasospasm may complicate the condition and is esponsible for delayed neurological deterioration in 25 to 30% of patients with aneurysmal SAH;
• The time period extending from onset of the vascular insult to irreversible cell damage is eferred to as the therapeutic window and usually represents a period of only a few hours;
• If treatment is not initiated within this time frame, ischemic neurons will degenerate and cerebral infarction will occur;
• Cerebral microdialysis monitoring has been used extensively in basic research and has proved useful in the detection of metabolic perturbations of CNS tissue;
• The method allows for frequent sampling and nearly real-time estimates of CNS ECF concentrations of a wide variety of substances, including markers of energy metabolism (glucose, pyruvate, and lactate)4,6,9 and neuronal injury (glycerol and glutamate);
• The local ethics committee approved this study. Patients suffering from poor-grade (Fisher CT Grade 3 or 4 and/or Hunt and Hess Grade III or IV) acute SAH from a ruptured aneurysm located at the ICA, ACA, or MCA were included after informed consent had been obtained from either the patient or a family member
• General management of patients with SAH also included intraarterial injection of
  papaverine if symptoms of cerebral vasospasm were suspected and the vasospasm was verified by cerebral angiography;
• At the time of ventriculostomy (performed in patients with SAH-induced hydrocephalus or in those in whom intracranial pressure monitoring was necessary) or aneurysm surgery, a microdialysis electrode was implanted in the cortical territory of interest (the ACA or MCA at the site of the aneurysm);
• Of 46 patients monitored by microdialysis, two subgroups of patients are reported: 1) 14 patients without clinical signs of delayed cerebral ischemia following treatment,
  and 2) five patients who deteriorated neurologically and subsequently suffered brain death and, therefore, represented severe as well as complete cerebral ischemia ;
• Microdialysis monitoring is based on neurochemical analysis of a perfusate obtained after passive bidirectional diffusion through a thin dialyzing membrane implanted in CNS tissue;
• Low-molecular-weight substances in the CNS ECF will pass through the dialyzing membrane, and the concentration detected in the dialysate will reflect the corresponding concentration in the ECF;
• Cerebral microdialysis was performed using a microdialysis catheter (CMA 70; MA/Microdialysis, Solna, Sweden) with a membrane length of 10 mm. The probe
  was positioned intraparenchymally at a depth of approximately 1.2 to 1.5 cm below the surface of the cerebral cortex, and the catheter was connected to a perfusion pump
  (CMA 106; CMA/Microdialysis);
• Perfusion fluid (CMA T [CMA/Microdialysis], consisting of Na+ 147 mmol/L, K+ 4 mmol/L, Cl 156 mmol/L, pH 6, osmolality 290 mosm/kg) was pumped through the system at a flow rate of 0.3 l/minute;
• Samples were collected every hour during the first 2 days following aneurysm treatment andevery 2 hours for up to 7 days or until the patient was discharged from the ICU;
• Bedside microdialysis analyzing equipment (CMA 600; CMA/Microdialysis), based on enzymatic reagent and colorimetric measurements, was used for immediate neurochemical analysis of ECF glucose, pyruvate, lactate, glycerol, and glutamate concentrations;