Fibrin degradation products in the cerebrospinal fluid of patients with pneumococcal meningitis.

Abstract

SUMMARY Raised levels of fibrin degradation products were found in the cerebrospinal fluid of nearly all of 35 patients with pneumococcal meningitis. The mean level was higher in patients who died subsequently than in those who survived. Cerebrospinal fluid from patients with pneumococcal meningitis showed increased fibrinolytic activity as assessed by clot lysis, suggesting local production of fibrin degradation products within the subarachnoid space.

Fibrinolytic Activity in Cerebrospinal Fluid of Dogs with Different Neurological Disorders

“…D‐dimers are specific degradation products of cross‐linked fibrin generated by the action of plasmin, thus any increase in CSF D‐dimer concentration should be a specific indicator of active intrathecal fibrinolysis. In fact, the D‐dimer test is being used as a sensitive marker of local fibrinolytic activity in humans and animals, and it is suggested that the fibrinolytic pathways are locally activated to avoid the detrimental effects of fibrin deposition in different body compartments , . Although the kinetics of D‐dimers in the CSF of humans and animals are unknown, due to the short half‐life of these products in serum and the fast turnover of CSF, a raised CSF D‐dimer concentration might be indicative of recent hypercoagulation and hyperfibrinolysis.…”

“…Although the origin of physiological and disease‐induced fibrinolysis in the central nervous system (CNS) remains controversial, the relationship among inflammation, coagulation, and fibrinolytic activity in CNS diseases is worth studying. CSF D‐dimer concentrations have been used to assess fibrinolytic activity in the CSF of humans with CNS infectious, neoplastic, traumatic, and vascular diseases . In addition, D‐dimers in the CSF have been proposed as markers of meningeal inflammation, and as a useful tool to differentiate between idiopathic subarachnoid hemorrhage and traumatic spinal tap .…”

Cerebrospinal fluid outflow resistance in rabbits with experimental meningitis. Alterations with penicillin and methylprednisolone.

“…Accumulation of leucocytes and eosinophilic debris has been identified in supracortical SAS in experimental meningitis (48) and has been confirmed in the rabbit model used in this study by light microscopy (personal observations). The increase in fibrin degradation products in the CSF of patients with pneumococcal meningitis (49) may reflect breakdown of plasm-a constituents in the SAS and levels of these products were higher in the fatal cases. This suggests that as inflanmmation increases, CSF absorption is curtailed by obstruction either in the supracortical SAS or at the arachnoid villus with subsequent elevations in ICP, neurological sequelae (e.g., hydrocephalus), raised fibrin-degradation product within the CSF and perhaps an increase in mortality rates.…”