Fever and thromboembolic disease in acute spinal cord injury.

Thromboembolic Disease (T.E.D.) is a major cause of morbidity and mortality in the first few months following spinal cord injury. The purpose of this three year retrospective study is to delineate the previously poorly described role of fever as both a common component of T.E.D. manifestation and, on occasion, the sole presenting sign of an otherwise occult T.E.D. process. We reviewed 148 consecutive admissions to the Southeastern Michigan Spinal Cord Injury System (1982-1985). Ten patients with documented T.E.D. were found and extensively reviewed; 3 had inadequate documentation of clinical manifestations and 1 patient was found from venography to have a non-acute thrombosis. Of the remaining 6 cases, all had fever as a sign, and 4 of these patients had fever as the sole presenting sign. Full fever work-ups were performed in each case and no other source for fever could be found. Fever spikes occurred most commonly at night, with a maximum temperature of 100.2 degrees F (oral) to a high in one case of 103.0 degrees F (oral). All fevers resolved within the first week of adequate anticoagulation therapy. These findings indicate that fever may be the earliest and, possibly, only clinical sign of an otherwise occult T.E.D. process.

Thromboxane and prostacyclin formation in patients with deep vein thrombosis.

The urinary excretion of 2,3-dinor-TxB2 and 2,3-dinor-6-keto-PGF1 alpha (the major urinary metabolites of thromboxane B2 and prostacyclin) was measured in ten patients with confirmed deep vein thrombosis, using specific methods based on gas chromatography - mass spectrometry with deuterium-labelled internal standards. Measurements of these major urinary metabolites makes it possible to monitor the in vivo formation of thromboxane A2 and prostacyclin. The results demonstrate an abnormally high and very variable excretion of 2,3-dinor-TxB2 and 2,3-dinor-6-keto-PGF1 alpha in patients with deep vein thrombosis. This indicate that both thromboxane A2 and prostacyclin are involved in the course of events associated with this disease.

Fibrinopeptide A in urine from patients with venous thromboembolism, disseminated intravascular coagulation and rheumatoid arthritis--evidence for dephosphorylation and carboxyterminal degradation of the peptide by the kidney.

Urinary fibrinopeptide A immunoreactivity was determined by radioimmunoassay using two anti-fibrinopeptide A sera with a different specificity in patients with venous thromboembolism, disseminated intravascular coagulation and rheumatoid arthritis. Elevated levels were frequently observed with both sera, and intravenous administration of heparin in patients with a thromboembolic disorder resulted in a decline of urinary fibrinopeptide A (FPA) concentrations to normal or nearly normal values. For both sera significant correlations with plasma levels were found although one of the sera reacted significantly better with the material in urine samples from these patients than the other (p less than 0.0001, n = 73). Analysis of urinary fibrinopeptide A immunoreactivity by high performance liquid chromatography (HPLC) provided evidence that A peptide material present in this body fluid was heterogeneous. In view of the characteristics of the antisera used in this study, data suggest that urinary FPA immunoreactivity consists to a large extent of carboxyterminally degraded FPA. Excretion of circulating FPA immunoreactive material through the kidneys apparently involves dephosphorylation and carboxyterminal breakdown of the A peptide. Since both synthetic and native phosphorylated or unphosphorylated fibrinopeptide A appeared to be stable in urine in vitro, an active role of the kidney in degrading the A peptide is likely.

Urinary excretion of thromboxane B2 in patients with venous thromboembolic disease.

Platelet activation occurs in the initial phase of venous thrombus formation. To determine if thromboxanes (Tx) are released during this process and if Tx measurements are useful in the diagnosis, urinary immunoreactive TxB2 was measured by a rapid, inexpensive assay in 100 consecutive patients with suspected thromboembolic disease. Urinary iTxB2 was not increased in patients who took aspirin, nor in patients studied several weeks after onset of symptoms. Of the remaining patients, iTxB2 was increased in 11 of 15 with confirmed deep vein thrombosis and in seven of ten with confirmed pulmonary emboli. Of the 54 patients in whom acute thrombosis was excluded, iTxB2 was increased in only four (7 percent). A second study evaluated 25 additional patients with nondiagnostic lung scans who required pulmonary angiography; iTxB2 was increased in seven of ten with positive angiograms and in 0 of 15 with negative angiograms. The three patients with negative iTxB2 and positive angiograms were receiving heparin when studied. These data suggest that, in the absence of aspirin, platelet Tx is released during thrombus formation. In combination with other noninvasive tests, urinary iTxB2 is a useful adjunct to diagnosing acute thromboembolic disease.