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Ulf Schött

Publications and source records attributed to Ulf Schött.

5 recordsLinked to original sources

Acidosis impairs the coagulation: A thromboelastographic study.

BACKGROUND: Coagulopathy is a contributor to and predictor of death in bleeding patients. Acidosis is known to be a predictor of worse outcome in trauma patients and to be a coexisting factor in coagulopathic patients, but it has not been studied if it is a causal factor in the development of coagulopathy. METHODS: We have adjusted the pH level in blood samples from healthy volunteers to different levels between 7.4 and 6.8 by the use of hydrochloric acid. Thereafter we have studied the coagulation at the different pH levels by the use of thromboelastography. RESULTS: We found a strong correlation between pH levels and impairment of the coagulation, where the clot strength is increased much slower at pH levels below 7.4 even though the initiation of the clotting seems to be normal. The clot formation time was increased by 168% at pH 6.8 as compared with pH 7.4 (p < 0.00001, r = 0.89) whereas the clotting time was left unaffected. CONCLUSIONS: Acidosis causes a strong impairment of the coagulation as measured with thromboelastography. The impairment found when lowering pH from 7.4 to 7.15 was almost identical to the impairment seen in another study by Kettner et al. when the temperature was lowered from 36 degrees C to 32 degrees C.

Acidosis↗

Ethanol impairs coagulation and fibrinolysis in whole blood: a study performed with rotational thromboelastometry.

The objective was to study the effects of ethanol on coagulation and fibrinolysis in whole blood. Blood samples from healthy volunteers were analyzed before and after in-vitro addition of ethanol in order to achieve ethanol concentrations of 0, 1, 2 and 4 per thousand, respectively (0, 22, 44 and 88 mmol/l). Coagulation and fibrinolysis were then assessed using rotational thromboelastometry. We found that increasing ethanol levels increasingly impaired coagulation as evaluated with rotational thromboelastometry, with a maximum prolongation of the clot formation time of 118% at an ethanol level of 4 per thousand (P < 0.000001). We also found a very strong impairment of fibrinolysis already at an ethanol level of 1 per thousand. This is the first study assessing the effects of ethanol on coagulation and fibrinolysis in a whole blood model. The impairment of coagulation is similar in nature to the impairment found in patients suffering from hypothermia. The impairment is at a level that may be of clinical importance (e.g. in patients suffering from trauma). The inhibition of fibrinolysis is obvious already at an ethanol level of 1 per thousand and it may be a contributing factor to the increased amount of coronary and cerebrovascular ischemic events after binge drinking.

Alcohol Drinking↗

An in vitro evaluation of standard rotational thromboelastography in monitoring of effects of recombinant factor VIIa on coagulopathy induced by hydroxy ethyl starch.

BACKGROUND: Rotational thromboelastography (ROTEG) has been proposed as a monitoring tool that can be used to monitor treatment of hemophilia with recombinant factor VIIa (rFVIIa). In these studies special non-standard reagents were used as activators of the coagulation. The aim of this study was to evaluate if standard ROTEG analysis could be used for monitoring of effects of recombinant factor VIIa (rFVIIa) on Hydroxy Ethyl Starch-induced dilutional coagulopathy. METHODS: The study was performed in vitro on healthy volunteers. Prothrombin time (PT) and ROTEG analysis were performed after dilution with 33% hydroxy ethyl starch and also after addition of rFVIIa to the diluted blood. RESULTS: PT was impaired with INR changing from 0.9 before dilution to 1.2 after dilution while addition of rFVIIa to diluted blood lead to an overcorrection of the PT to an International Normalized Ratio (INR) value of 0.6 (p = 0.01). ROTEG activated with the contact activator ellagic acid was impaired by hemodilution (p = 0.01) while addition of rFVIIa had no further effects. ROTEG activated with tissue factor (TF) was also impaired by hemodilution (p = 0.01) while addition of rFVIIa lead to further impairment of the coagulation (p = 0.01). CONCLUSIONS: The parameters affected in the ROTEG analysis were Clot Formation Time and Amplitude after 15 minutes while the Clotting Time was unaffected. We believe these effects to be due to methodological problems when using standard activators of the coagulation in the ROTEG analysis in combination with rFVIIa.

Journal Article↗

Presentation of laboratory and sonoclot variables using principal component analysis: identification of hypo- and hypercoagulation in the HELLP syndrome.

The HELLP (Hemolysis, Elevated Liver enzyme, and Low Platelet) syndrome requires close monitoring of rapid changes in hemostasis. A bedside viscoelastic test--Sonoclot--was used together with coagulation, liver and hemolysis laboratory analyses in three parturients with the HELLP syndrome up to 10 days postpartum. Principal component analysis (PCA) was used to reduce the dimensionality of this multivariate problem and to visualize this process in a two-dimensional plot. It was possible to follow changes in these variables over time and to show how they changed in relation to 10 typical healthy parturients with normal laboratory and Sonoclot values as well as 20 simulated patients with hypo- or hypercoagubility. The effects of emergency delivery, correction of low plasma-antithrombin with plasma and antithrombin factor concentrate, plasma exchange and individualized dosages of low molecular weight heparin to counteract postpartum Sonoclot detected hypercoagulation were evaluated. The efficiency of each treatment strategy was visualized in the PCA plot by movement towards an area with normocoagulation. In conclusion, PCA of viscoelastic and laboratory coagulation analysis data facilitated the detection of both hypo- and hypercoagulative events and represents an alternative way to evaluate treatment strategies in patients with complex coagulative disorders, like the HELLP syndrome.

Adult↗