Spontaneous brachial plexus hemorrhage-case report.

BACKGROUND: Shoulder hemorrhage resulting in brachial plexus neuropathy is a rare occurrence most often seen in cases of traumatic injury or anticoagulation therapy. We report a unique case of spontaneous brachial plexus hemorrhage. CASE DESCRIPTION: This is the first report of a spontaneous shoulder hemorrhage in which a 48-year-old jackhammer operator presented to the emergency department with a sudden onset of right shoulder pain and upper extremity pain and numbness. Imaging studies revealed a hematoma in the right axilla and chest wall. Without evidence of active bleeding or worsening neurologic deficit, this patient was treated conservatively with pain control and observation and eventually experienced a full recovery. Had there been persistent neurologic deficit, however, surgical evacuation would have been indicated. CONCLUSIONS: Cases of nerve compression caused by a hematoma should be analyzed on the basis of the severity of the neurologic deficit and not on the underlying cause of bleeding. Conservative treatment may be indicated in cases of mild or improving neurologic deficit, but regardless of its etiology, a hematoma that results in severe or worsening neurologic symptoms must be surgically evacuated to prevent permanent nerve damage.

Studies on the comparative pharmacology and selective toxicity of tricaine methanesulfonate: metabolism as a basis of the selective toxicity in poikilotherms.

Tricaine methanesulfonate, administered at a dose of 150 mg/kg i.p., produced a flaccid paralysis and loss of the righting reflex in a number of poikilothermic species including the frog. Leopard frogs (Rana pipiens) given 150 mg/kg i.p. regained the righting reflex at 113 +/- 28 (S.D.) minutes after injection. A similar dose administered i.p. to mice produced no apparent pharmacological response. The biological half-life (T1/2) of tricaine in frogs (R. pipiens) was about 70 minutes at temperatures of 23 and 37.5 degrees C; at 7 degrees C the T1/2 was 309 minutes. In contrast, in the mouse the drug was metabolized so rapidly that 5 minutes after i.p. administration of 5 mg of tricaine methanesulfonate (250 mg/kg) none of the unchanged drug could be recovered from the animal. It was, however, recovered quantitatively as Bratton-Marshall reacting metabolites, including m-aminobenzoic acid. Incubations of tricaine with serum from bullfrogs, mice and humans indicated that the drug was metabolized to m-aminobenzoic acid with an apparent Km of 3 X 10(-3) M for the reaction. The Vmax for incubations of the drug with bullfrog and human serum was 40 nmol/min/ml of serum, whereas in mouse serum it was 93 nmol/min/ml of serum. In vitro studies with liver homogenates showed that mouse liver metabolized tricaine 39 times more rapidly than frog liver. We conclude, therefore, that the liver is the major site of tricaine hydrolysis in mammals and that the selective toxicity of tricaine for poikilotherms is a consequence of their slower rate of hepatic biotransformation of tricaine.

Influence of pH on the contractor effect of convulsant barbiturate on frog lung.

Pentobarbial, thiopental and the convulsant 5-ethyl-5-(2-cyclohexylideneëthyl) barbituric acid (CHEB) were tested for contractor effect on the isolated lung of the fullfrog at pH 7.0 (7% CO2 and 20 mM HCO3-) and pH 8.4 (0.3% CO2 and 20mM HCO3-). CHEB was a potent contractor, thiopental a feeble contractor, and pentobarbital lacked contractor effect. The contractor potencies of both CHEB and thiopental were greater at the more acid pH. The potencies of formally charged agonists such as acetylcholine and K+ were not altered by the pH differences employed in these experiments. The pKa of CHEB was found to be 8.18 at 15 degrees C and 8.03 at 27 degrees C. Calculation of concentration-effect relationships of ionized and nonionized CHEB showed that only the nonionized CHEB was responsible for the contractor effect.