Multiple Episodes of Severe Bronchospasm During General Anesthesia: A Case Report.

Bronchospasm is the clinical component of exacerbated underlying airway hyper-reactivity or as part of a more severe underlying pathology such as anaphylaxis. This article reports multiple episodes of bronchospasm after general anesthesia induction for elective surgery of laparoscopic cholecystectomy. Bronchospasm is a joint event during the intubation period, especially in patients with respiratory disease, but in most cases resolves without further complications. It was manifested in isolation in this patient, with no cardiovascular compromise, no skin signs. This case report reviews the literature and the algorithm taken to manage this adverse event and guarantees patient care and successful outcome.

Carbon monoxide-releasing molecule-2 enhances coagulation and diminishes fibrinolytic vulnerability in diluted plasma in vitro.

BACKGROUND: A carbon monoxide-releasing molecule (tricarbonyldichlororuthenium (II) dimer; CORM-2) enhances coagulation and attenuates vulnerability to fibrinolysis in normal and hemophiliac human plasma. We tested the hypothesis that plasma diluted with resuscitative fluids would demonstrate improved coagulation and decreased fibrinolytic vulnerability after exposure to CORM-2. METHODS: Normal, platelet-poor plasma was diluted 0%, 20%, 30%, 40%, or 50% with 0.9% NaCl (NS) or low-molecular-weight hydroxyethyl starch (VOL) and, subsequently, exposed to 0 µmol/L or 100 µmol/L CORM-2 before activation with tissue factor (n = 4 per condition). Additional plasma samples diluted with NS or VOL (0% or 30%) were exposed to 0 µmol/L or 100 µmol/L CORM-2 and 0 U/mL or 100 U/mL tissue-type plasminogen activator to assess fibrinolytic vulnerability (n = 8 per condition). Thrombelastographic data were collected until either clot strength stabilized or clot lysis occurred, as appropriate. RESULTS: CORM-2 exposure maintained normal to supranormal velocity of clot formation and strength in plasma diluted up to 40% with NS. In contrast, although CORM-2 exposure improved coagulation kinetics, dilution with VOL markedly degraded thrombus formation kinetics. Similarly, fibrinolytic vulnerability to tissue-type plasminogen activator was markedly improved by CORM-2 exposure in samples diluted with NS, whereas VOL-diluted thrombi were still abnormally weak and easily lysed compared with undiluted samples despite CORM-2 exposure. CONCLUSIONS: CORM-2 exposure attenuated the decrease in coagulation kinetics and enhancement of fibrinolytic vulnerability associated with hemodilution. Extensive preclinical investigation remains to be performed to determine the route of administration, safety, and efficacy of CORM-2 and other CORMs to treat trauma-associated bleeding.

Carbon monoxide releasing molecule-2 enhances coagulation and diminishes fibrinolytic vulnerability in plasma exposed to heparin or argatroban.

BACKGROUND: It has been recently demonstrated that a carbon monoxide releasing molecule (tricarbonyldichlororuthenium [II] dimer; CORM-2) enhances coagulation and attenuates vulnerability to fibrinolysis in normal and hemophiliac human plasma. We tested the hypothesis that plasma anticoagulated with heparin or argatroban would demonstrate improved coagulation and decreased fibrinolytic vulnerability after exposure to CORM-2. METHODS: Normal plasma was anticoagulated with 0 to 0.1 U/mL unfractionated heparin or 0 to 1 µg/mL argatroban. Samples were subsequently exposed to 0 or 100 µM CORM-2 and activated with tissue factor. Additional samples with the same anticoagulant and CORM-2 exposure schema were incubated with 100 U/mL tissue-type plasminogen activator (tPA) to assess fibrinolytic vulnerability. Thrombelastographic data were collected until either clot strength stabilized or clot lysis occurred as appropriate. RESULTS: In the absence of tPA, CORM-2 significantly increased the velocity of clot growth in heparin (75%) and argatroban-exposed (40%) samples. Clot strength was also significantly increased in heparin (69%) and argatroban-exposed (72%) samples. In the presence of tPA, CORM-2-treated samples had even greater (94%-731%) increases in velocity of growth and strength after exposure to either anticoagulant and significantly increased clot lysis time (103%-200%). CONCLUSIONS: CORM-2 exposure resulted in faster-growing, stronger, longer-lived thrombi after anticoagulation with heparin or argatroban. Additional preclinical investigation is warranted to determine whether CORM-2 administration will be useful in attenuating bleeding complications associated with thromboprophylaxis.

Carbon monoxide releasing molecule-2 increases fibrinogen-dependent coagulation kinetics but does not enhance prothrombin activity.

We have previously determined that tricarbonyldichlororuthenium (II) dimer (CORM-2) increases plasma clot velocity of formation and strength by enhancing thrombin-fibrinogen interactions as determined by thrombelastography. The purpose of the present investigation was to further define the nature of CORM-2 interaction with prothrombin and fibrinogen by exposing purified proteins to CORM-2 or generating protein concentration-response curves in the absence or presence of CORM-2. Purified prothrombin was exposed to 0 or 100 micromol/l CORM-2 prior to being added to prothrombin-deficient plasma (n=7-8 per condition). Fibrinogen-deficient plasma had fibrinogen added for a final concentration of 100-800 mg/dl and was exposed to 0 or 100 micromol/l CORM-2 (n=4 per condition). Following tissue factor activation, thrombelastographic data were collected until clot strength stabilized. Exposure of prothrombin to CORM-2 did not significantly enhance coagulation kinetics. In sharp contrast, CORM-2 exposure enhanced fibrinogen coagulation kinetics in a concentration-dependent fashion, with peak effect seen at a fibrinogen concentration of 300 mg/dl that then progressively decreased throughout the range tested. Our data demonstrate that CORM-2 does not enhance plasma coagulation kinetics by modifying prothrombin; instead, the concept that CORM-2 modifies fibrinogen is the most likely explanation for the enhanced thrombin-fibrinogen interactions observed.

Carbon monoxide releasing molecule-2 enhances coagulation and diminishes fibrinolytic vulnerability in subjects exposed to warfarin.

INTRODUCTION: It has been recently demonstrated that a carbon monoxide releasing molecule (tricarbonyldichlororuthenium (II) dimer; CORM-2) enhances coagulation and attenuates vulnerability to fibrinolysis in normal and hemophiliac human plasma. We tested the hypothesis that plasma obtained from warfarin-treated subjects would demonstrate improved coagulation and decreased fibrinolytic vulnerability following exposure to CORM-2. MATERIALS AND METHODS: Anonymous donor plasma samples with international normalized ratios (INR) values ranging from 1.5-5.4 were exposed to 0 or 100 microM CORM-2 and activated with tissue factor (12 samples). Additional samples within the same INR range were exposed to 0 or 100 microM CORM-2 and 0 or 100 U/ml tissue-type plasminogen activator (tPA) to assess fibrinolytic vulnerability (8 samples). Thrombelastographic data were collected until either clot strength stabilized or clot lysis occurred as appropriate. RESULTS AND CONCLUSIONS: In the absence of tPA, all but one sample (INR=1.5) demonstrated a marked increase in the velocity of clot formation (40-577%) and strength (42-180%) following CORM-2 exposure. Of interest, in the presence of tPA, all samples (including the previously unresponsive sample) were noted to have an increase in the velocity of clot formation and strength, coupled with a prolonged onset to maximal rate of clot lysis (60-242%) and increased clot lysis time (74-149%). As with normal and hemophilic plasma, both enhancement of coagulation and attenuation of fibrinolysis occur following CORM-2 exposure in plasma from warfarin-treated subjects. Future investigation must determine if carbon monoxide releasing molecules could be used therapeutically to control bleeding in warfarin-treated patients.