Low Cerebral Oxygenation Levels during Resuscitation in Out-of-hospital Cardiac Arrest Are Associated with Hyperfibrinolysis.

BACKGROUND: The authors investigated whether patients with out-of-hospital cardiac arrest with an initial low cerebral oxygen level during cardiopulmonary resuscitation are more prone to develop hyperfibrinolysis than patients with normal cerebral oxygenation levels and which part of the fibrinolytic system is involved in this response. METHODS: In 46 patients, hyperfibrinolysis was diagnosed immediately upon emergency department admission using rotational thromboelastometry and defined as a lysis more than 15%. Simultaneously, initial cerebral tissue oxygenation was measured using near-infrared spectroscopy, and oxygen desaturation was defined as a tissue oxygenation index (TOI) of 50% or less. Blood sample analysis included markers for hypoperfusion and fibrinolysis. RESULTS: There was no difference in prehospital cardiopulmonary resuscitation duration between patients with or without hyperfibrinolysis. An initial TOI of 50% or less was associated with more clot lysis (91% [17 to 100%; n = 16]) compared with patients with a normal TOI (6% [4 to 11%]; n = 30; P < 0.001), with lower levels of plasminogen (151.6 ± 61.0 vs. 225.3 ± 47.0 µg/ml; P < 0.001) and higher levels of tissue plasminogen activator (t-PA; 18.3 ± 7.4 vs. 7.9 ± 4.7 ng/ml; P < 0.001) and plasminogen activator inhibitor-1 (19.3 ± 8.9 vs. 12.1 ± 6.1 ng/ml; P = 0.013). There were no differences in (activated) protein C levels among groups. The initial TOI was negatively correlated with t-PA (r = -0.69; P < 0001). Mortality rates were highest in patients with hyperfibrinolysis. CONCLUSION: Activation of the fibrinolytic system is more common in out-of-hospital cardiac arrest patients with an initial cerebral tissue oxygenation value of 50% or less during resuscitation and is linked to increased levels of t-PA rather than involvement of protein C.

Acute and delayed mild coagulopathy are related to outcome in patients with isolated traumatic brain injury.

INTRODUCTION: The relationship between isolated traumatic brain injury (TBI) associated coagulopathy and patient prognosis frequently lacks information regarding the time course of coagulation disorders throughout the post-traumatic period. This study was conducted to assess the prevalence and time course of post-traumatic coagulopathy in patients with isolated TBI and the relationship of these hemostatic disorders with outcome. METHODS: The local Human Subjects Committee approved the study. We retrospectively studied the medical records of computed tomography (CT)-confirmed isolated TBI patients with an extracranial abbreviated injury scale (AIS) <3 who were primarily referred to a Level 1 trauma centre in Amsterdam (n = 107). Hemostatic parameters including activated partial thromboplastin time (aPTT), prothrombin time (PT), platelet count, hemoglobin, hematocrit, glucose, pH and lactate levels were recorded throughout a 72-hour period as part of a routine standardized follow-up of TBI. Coagulopathy was defined as a aPPT >40 seconds and/or a PTT in International Normalized Ratio (INR) >1.2 and/or a platelet count <120*109/l. RESULTS: Patients were mostly male, aged 48 ± 20 years with a median injury severity score of 25 (range 20 to 25). Early coagulopathy as diagnosed in the emergency department (ED) occurred in 24% of all patients. The occurrence of TBI-related coagulopathy increased to 54% in the first 24 hours post-trauma. In addition to an increased age and disturbed pupillary reflex, both coagulopathy upon ED arrival and during the first 24 hours post-trauma provided an independent prognostic factor for unfavorable outcome (odds ratio (OR) 3.75 (95% CI 1.07 to 12.51; P = 0.04) and OR 11.61 (2.79 to 48.34); P = 0.003). CONCLUSIONS: Our study confirms a high prevalence of early and delayed coagulopathy in patients with isolated TBI, which is strongly associated with an unfavorable outcome. These data support close monitoring of hemostasis after TBI and indicate that correction of coagulation disturbances might need to be considered.

Beat-to-beat hemodynamic monitoring during electroconvulsive therapy.

OBJECTIVES: Rapid parasympathetic and sympathetic hemodynamic effects during electroconvulsive therapy (ECT) may pose vulnerable patients to significant risk for cardiovascular complications. Here, we evaluated the clinical feasibility of noninvasive beat-to-beat arterial blood pressure (BP) measurements in patients undergoing ECT. METHODS: Beat-to-beat hemodynamic effects were measured with a noninvasive BP monitor in 24 individual patients undergoing ECT during general anesthesia. Heart rate, systolic (SBP), and diastolic BP (DBP) as well as cardiac output (CO) were measured continuously. A significant increase in pulse rate and/or BP was treated with intermittent administration of esmolol and ketanserin. Data are presented as mean ± SD. RESULTS: The ECT stimulus induced a transient drop in BP and pulse rate, followed by a sharp rise in both parameters. The parasympathetic phase lasted 17 ± 9 seconds and was characterized by a drop in heart rate from 89 ± 15 to 42 ± 24 beats per minute, in SBP from 143 ± 22 to 91 ± 31 mm Hg, in DBP from 82 ± 13 to 54 ± 22 mm Hg, and in CO from 5.7 ± 2.3 to 1.4 ± 1.0 L/min, respectively. During the subsequent sympathetic phase, the heart rate increased to 125 ± 26 beats per minute, the SBP to 192 ± 33 mm Hg, the DBP to 113 ± 21 mm Hg, and the CO to 7.4 ± 4.3 L/min. The time interval between the lowest and highest SBP was 60 ± 48 seconds. CONCLUSIONS: Noninvasive beat-to-beat BP measurements are feasible during ECT and may be used to guide rapid therapeutic interventions during ECT-induced hemodynamic effects.