D-dimer is a biomarker of thrombosis and recently been considered to predict a poor outcome in patients with infectious diseases. Plasma D-dimer levels were measured in critically ill patients to examine their relationship with the poor outcome. The plasma D-dimer levels were markedly higher in the patients with various underlying disease especially venous thromboembolism in comparison to those without severe underlying diseases. The plasma D-dimer levels in non-survivors were significantly higher than those in survivors. In a receiver operating characteristic analysis, the area under the curve was high for the disseminated intravascular coagulation (DIC) score, the D-dimer value, and the prothrombin time-international normalize ratio (PT-INR). Adequate cut-off values for predicting the outcome were 3 as follows: DIC score, 3 points; D-dimer, 4.2 mg/L; and PT-INR, 1.08. D-dimer, which is a biomarker for thrombosis, is increased in various underlying diseases and predicts a poor outcome.
Disseminated intravascular coagulation (DIC) is induced by excess activation coagulation, and activated platelets are also involved in pathogenesis. Therefore, plasma levels of soluble C-type lectin-like receptor 2 (sCLEC-2), a new marker for platelet activation, can be expected as a marker of DIC in critically ill patients. Plasma levels of sCLEC-2 and D-dimer were measured using the STACIA system. Plasma sCLEC-2 and D-dimer levels were significantly higher in patients with underlying diseases of DIC than in those with unidentified clinical syndrome (UCS). Plasma sCLEC-2 levels were significantly higher in the patients with DIC and Pre-DIC than in those without DIC or Pre-DIC. Similarly, plasma D-dimer levels were also significantly higher in patients with DIC and Pre-DIC than in those without DIC or Pre-DIC. The plasma sCLEC-2 levels in all patients and those with a DIC score ≤ 4 were significantly higher in non-survivors than survivors. The plasma D-dimer levels in all patients, those with a DIC score ≥ 5 and those with a DIC score ≤ 4, were significantly higher in non-survivors than in survivors. The plasma sCLEC-2 is expected as a marker for DIC/Pre-DIC as well as the prognostic marker in critically ill patients.
The authors present three patients with trigeminal neuralgia due to compression by an artery that transfixed the sensory root of the fifth cranial nerve. These cases represented 0.8% of 384 patients with trigeminal neuralgia treated by microvascular decompression at the authors' clinic during the past 12 years. In the remaining 381 cases, the compressing vessels were successfully removed from the trigeminal nerve without much difficulty, for an initial cure rate of 94.3%. In the three cases reported, however, the compressing artery penetrating the nerve could not easily be maneuvered away from the nerve. In the first two cases, partial rhizotomy perpendicular to the axis of the nerve at the site of arterial transfixion made it possible to separate the artery from the nerve. However, these two patients developed postoperative facial sensory impairment. In the third case, rhizotomy was performed longitudinal to the axis of the nerve at the site of arterial transfixion, making it possible to reposition the artery peripherally beyond the root entry zone of the nerve without causing any postoperative sensory deficits of the face. No recurrent pain has developed in more than 2 1/2 years since surgery in any of these three cases. When performing microvascular decompression surgery on patients in whom the compressing artery penetrates the nerve, the technique used in our third patient is the procedure of choice.
We report three cases of the spontaneous resolution of a traumatic chronic epidural hematoma. The patients were young adults with only mild headache after trauma. All patients were treated conservatively because of the very mild symptoms and the time lapse of 1 to 2 weeks between trauma and our unexpected detection of the frontal epidural hematomas. Slow, spontaneous resolution of the hematoma occurred in all three cases.
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