B. Vigué

Role of systemic inflammatory response syndrome and infection in the occurrence of early multiple organ dysfunction syndrome following severe trauma.

ObjectiveTo evaluate the role of infection and systemic inflammatory response syndrome (SIRS) on the occurrence of early posttraumatic MODS.DesignRetrospective study.SettingUniversity Teaching Hospital ICU.Patients163 consecutive patients hospitalized for more than 48 hours following severe trauma.Measurements and main resultsThe patients were classified into two groups in respect to the existence of MODS at day 2. There was 27 patients in the MODS group and 136 patients in the no MODS group. The two groups were similar with respect to age, sex ratio and Simplified Acute Physiology Score. The MODS group had a higher mortality (52 versus 7%), Injury Severity Score (45±14 versus 31±13), hypovolemic shock rate (74 versus 30%), massive volume replacement rate (59 versus 6%) and SIRS rate (81 versus 54%) than the no MODS group (p<0.05). The rate of infection was similarly low in the MODS and no MODS group (4 versus 6% respectively).ConclusionEarly MODS is often associated with hypotension and massive volume administration but very rarely with infection, despite the high rate of SIRS.

Bench-to-bedside review: Optimising emergency reversal of vitamin K antagonists in severe haemorrhage – from theory to practice

Critical care physicians are increasingly facing patients receiving oral anticoagulation for either cessation of major haemorrhage or to reverse the effects of vitamin K antagonists ahead of emergency surgery. Rapid reversal of anticoagulation is particularly essential in cases of life-threatening bleeding. In these situations, guidelines recommend the concomitant administration of prothrombin complex concentrates (PCCs) and oral or intravenous vitamin K for the fastest normalisation of the international normalised ratio (INR). Despite their universal recommendation, PCCs remain underused by many physicians who prefer to opt for fresh frozen plasma despite its limitations in anticoagulant reversal, including time to reverse INR and high risk of transfusion-related acute lung injury. In contrast, the lower volume required to normalise INR with PCCs and the room temperature storage facilitate faster preparation and administration time, thus increasing the speed at which haemorrhages can be treated. PCCs therefore allow faster, more reliable and complete reversal of vitamin K anticoagulation, especially when administered immediately following confirmation of haemorrhage. In the emergency setting, probabilistic dosing may be considered.

Relationship between intracranial pressure, mild hypothermia and temperature-corrected PaCO2 in patients with traumatic brain injury.

Objective: To study the effects of mild hypothermia and associated changes in temperature-corrected PaCO2 (cPaCO2) on intracranial pressure (ICP), mean velocity of the middle cerebral artery (Vm), and venous jugular saturation in O2 (SjvO2) in patients with severe traumatic brain injury (TBI).¶Design: Prospective, observational study.¶Setting: Intensive care unit.¶Patients: Severe TBI patients mechanically ventilated, sedated and paralyzed.¶Interventions: Twenty patients were subjected to four consecutive periods: (a) normocapnia-normothermia; (b) hypocapnia-normothermia, where hypocapnia was induced by an increase in minute volume; (c) hypocapnia-hypothermia, where hypocapnia was induced by hypothermia maintaining the ventilatory settings constant; (d) normocapnia-hypothermia, where normocapnia was achieved by a decrease in minute volume.¶Measurements and results: cPaCO2 was 41 ± 8 mmHg in periods 1 and 4, and 31 ± 7 mmHg in periods 2 and 3. Core temperature was 37.1 ± 0.8 °C in periods 1 and 2, and 34.1 ± 1.1 °C in periods 3 and 4. End-tidal CO2 and cPaCO2 values showed no difference between periods 1 and 4 and periods 2 and 3. ICP and Vm were dependent on cPaCO2 but independent of core temperature values. SjvO2 was related to cPaCO2 and was significantly higher during period 3 than during period 2 (P < 0.05).¶Conclusion: The decrease in ICP was similar when hypocapnia was induced by hyperventilation or as a result of hypothermia alone. The relationship between cPaCO2 and ICP might predict variations in ICP during changes in core temperature. Further studies are needed to confirm the cerebral metabolic effects of moderate hypothermia in TBI patients.

Early SjvO2 monitoring in patients with severe brain trauma.

Objective: To investigate early cerebral variables after minimal resuscitation and to compare the adequacy of a cerebral perfusion pressure (CPP) guideline above 70 mmHg, with jugular bulb venous oxygen saturation (SjvO2) monitoring in a patient with traumatic brain injury (TBI). Design: Prospective, observational study. Setting: Anesthesiological intensive care unit. Patients: 27 TBI patients with a postresuscitation Glasgow Coma Scale score less than 8. Intervention: After initial resuscitation, cerebral monitoring was performed and CPP increased to 70 mmHg by an increase in mean arterial pressure (MAP) with volume expansion and vasopressors as needed. Measurements and results: MAP, intracranial pressure (ICP), CPP, and simultaneous arterial and venous blood gases were measured at baseline and after treatment. Before treatment, 37 % of patients had an SjvO2 below 55 %, and SjvO2 was significantly correlated with CPP (r = 0.73, p < 0.0001). After treatment, we observed a significant increase (p < 0,0001) in CPP (78 ± 10 vs 53 ± 15 mmHg), MAP (103 ± 10 vs 79 ± 9 mmHg) and SvjO2 (72 ± 7 vs 56 ± 12), without a significant change in ICP (25 ± 14 vs 25 ± 11 mmHg). Conclusion: The present study shows that early cerebral monitoring with SjvO2 is critical to assess cerebral ischemic risk and that MAP monitoring alone is not sensitive enough to determine the state of oxygenation of the brain. SjvO2 monitoring permits the early identification of patients with low CPP and high risk of cerebral ischemia. In emergency situations it can be used alone when ICP monitoring is contraindicated or not readily available. However, ICP monitoring gives complementary information necessary to adapt treatment.

Guideline-concordant administration of prothrombin complex concentrate and vitamin K is associated with decreased mortality in patients with severe bleeding under vitamin K antagonist treatment (EPAHK study)

IntroductionIn vitamin K antagonist (VKA)-treated patients with severe hemorrhage, guidelines recommend prompt VKA reversal with prothrombin complex concentrate (PCC) and vitamin K. The aim of this observational cohort study was to evaluate the impact of guideline concordant administration of PCC and vitamin K on seven-day mortality.MethodsData from consecutive patients treated with PCC were prospectively collected in 44 emergency departments. Type of hemorrhage, coagulation parameters, type of treatment and seven-day mortality mortality were recorded. Guideline-concordant administration of PCC and vitamin K (GC-PCC-K) were defined by at least 20 IU/kg factor IX equivalent PCC and at least 5 mg of vitamin K performed within a predefined time frame of eight hours after admission. Multivariate analysis was used to assess the effect of appropriate reversal on seven-day mortality in all patients and in those with intracranial hemorrhage (ICH).ResultsData from 822 VKA-treated patients with severe hemorrhage were collected over 14 months. Bleeding was gastrointestinal (32%), intracranial (32%), muscular (13%), and “other” (23%). In the whole cohort, seven-day mortality was 13% and 33% in patients with ICH. GC-PCC-K was performed in 38% of all patients and 44% of ICH patients. Multivariate analysis showed a two-fold decrease in seven-day mortality in patients with GC-PCC-K (odds ratio (OR) = 2.15 (1.20 to 3.88); P = 0.011); this mortality reduction was also observed when only ICH was considered (OR = 3.23 (1.53 to 6.79); P = 0.002).ConclusionsGuideline-concordant VKA reversal with PCC and vitamin K within eight hours after admission was associated with a significant decrease in seven-day mortality.

Transgastric, pulsed Doppler echocardiographic determination of cardiac output.

ObjectiveThe aim of this study was to evaluate the accuracy of cardiac output measurement with transesophageal echocardiography (TEE) using a transgastric, pulsed Doppler method in acutely ill patients.DesignCardiac output was simultaneously measured by thermodilution (TD) and a transgastric, pulsed Doppler method.SettingThe study was carried out in a surgical intensive care unit as part of the management protocol of the patients.PatientsThirty consecutive acutely ill patients with a Swan-Ganz catheter, mechanically ventilated, sedated and with a stable hemodynamic condition were included.MeasurementsPulsed Doppler TEE was performed using a transgastric approach in order to obtain a long axis view of the left ventricle. Cardiac output was calculated from the left ventricular outflow tract diameter, the velocity time integral of the blood flow profile and heart rate.ResultsOne patient was excluded because of the presence of aortic regurgitation and another, because of the impossibility of obtaining a transgastric view. Twenty-eight simultaneous measurements were performed in 28 patients. A clinically acceptable correlation and agreement were found between the two methods (Doppler cardiac output=0.889 thermodilution cardiac output +0.74l/min,r=0.975,p<0.0001).ConclusionTransgastric pulsed Doppler measurement across the left ventricular outflow tract with TEE is a very feasible and clinically acceptable method for cardiac output measurement in acutely ill patients.

Comparison of dopamine and norepinephrine after traumatic brain injury and hypoxic-hypotensive insult

After severe brain trauma, blood-brain barrier disruption and alteration of cerebral arteriolar vasoreactive properties may modify the cerebral response to catecholamines. Therefore, the goal of the present study was to compare the effects of dopamine and norepinephrine in a model of brain injury that consisted of a weight-drop model of injury complicated by a 15-min hypoxic-hypotensive insult (HH). Sprague-Dawley rats (n = 7 in each group) received, after brain injury, an infusion of either norepinephrine (TNE group) or dopamine (TDA group) in order to increase cerebral perfusion pressure (CPP) above 70 mm Hg. In addition, a control group (C group, no trauma) and a trauma group (T group, brain injury, no catecholamine infusion) were studied. Mean arterial pressure (MAP), intracranial pressure (ICP, intraparenchymal fiberoptic device), and local cerebral blood flow (LCBF, extradural laser-Doppler fiber) were measured throughout the protocol. In T group, brain injury and HH induced a decrease in CPP (by an increase of ICP and a decrease of MAP), and a decrease of LCBF. Both norepinephrine and dopamine failed to increase CPP, and ICP was significantly higher in TNE and TDA groups than in T group. Interestingly, norepinephrine was not able to alleviate the decrease in MAP. Neither norepinephrine or dopamine could induce an increase of MAP. LCBF decreased similarly in T, TNE and TDA groups. In conclusion, norepinephrine and dopamine are not able to restore values of CPP above 70 mm Hg in a model of severe brain trauma. Furthermore, their systemic vasopressor properties are altered.

Pre-hospital transcranial Doppler in severe traumatic brain injury: a pilot study

Background: Investigation of the feasibility and usefulness of pre‐hospital transcranial Doppler (TCD) to guide early goal‐directed therapy following severe traumatic brain injury (TBI).

Hypoxia-hypotension decreases pressor responsiveness to exogenous catecholamines after severe traumatic brain injury in rats

ObjectiveTo quantify the phenylephrine pressor responsiveness after severe brain injury combined with hypoxia-hypotension, and to study the respective roles of brain injury and hypoxia-hypotension in the observed alteration. DesignRandomized study. SettingAccredited animal laboratory. SubjectsAdult Sprague Dawley rats. InterventionsAnesthetized animals were assigned to control, brain injury, hypoxia-hypotension, and brain injury combined with hypoxia-hypotension groups. Brain injury was induced with an impact-acceleration device. During the 15-min hypoxia-hypotension, arterial oxygen pressure was decreased to 40 torr (5.3 kPa) and mean arterial pressure to 30 mm Hg. Thirty-six of the 53 included rats were alive at the end of hypoxia-hypotension (nine animals per group). In an additional group (Hypo, n = 8), mean arterial pressure was lowered to the level observed in brain injury combined with hypoxia-hypotension with pentobarbital infusion. Sixty minutes after injuries (T60), animals received 0.1, 1, and 10 &mgr;g/kg phenylephrine in a random order. Pressor responsiveness to phenylephrine was defined as maximal postinjection minus preinjection mean arterial pressure. Measurements and Main Results During hypoxia-hypotension, mortality was higher and residual restored blood volume was lower (p < .01) in the animals with brain injury and hypoxia-hypotension compared with hypoxia-hypotension alone. At T60, mean arterial pressure (mm Hg) was lower (p < .01) in the brain injury group (83 ± 22) compared with controls (110 ± 10) and in brain injury combined with hypoxia-hypotension (76 ± 18) compared with controls and hypoxia-hypotension (107 ± 14). Pressor responsiveness (mm Hg) to 1 and 10 &mgr;g/kg phenylephrine was less (p < .05) in brain injury combined with hypoxia-hypotension (15 ± 6 and 44 ± 8) and hypoxia-hypotension (15 ± 3 and 44 ± 8) compared with controls (26 ± 2 and 57 ± 11). No significant difference was observed for phenylephrine pressor responsiveness between controls and the Hypo group (25 ± 5 and 66 ± 7). ConclusionsCombination of brain injury and hypoxia-hypotension induces a severe hemodynamic alteration associated with a decreased pressor responsiveness to phenylephrine. Transient hypoxia-hypotension is responsible for the depressed &agr;-1 adrenergic reactivity.

The Limits of Succinylcholine for Critically Ill Patients

BACKGROUND:Urgent tracheal intubations are common in intensive care units (ICU), and succinylcholine is one of the first-line neuromuscular blocking drugs used in these situations. Critically ill patients could be at high risk of hyperkalemia after receiving succinylcholine because one or more etiologic factors of nicotinic receptor upregulation can be present, but there are few data on its real risk. Our objectives in this study were to determine the factors associated with arterial potassium increase (&Dgr;K) and to assess the occurrence of acute hyperkalemia ≥6.5 mmol/L after succinylcholine injection for intubation in the ICU. METHODS:In a prospective, observational study, all critically ill patients intubated with succinylcholine in an ICU were screened. Only intubations with arterial blood gases and potassium measurements before and after (Kafter) a succinylcholine injection were studied. RESULTS:During 18 months, 131 critically ill patients were intubated after receiving succinylcholine with arterial potassium before and after intubation (Kafter) for a total of 153 intubations. After multivariate analysis, the only factor associated with &Dgr;K was the length of ICU stay before intubation (&rgr; = 0.561, P < 0.001). The factors associated with Kafter ≥6.5 mmol/L (n = 11) were the length of ICU stay (P < 0.001) and the presence of acute cerebral pathology (P = 0.047). The threshold of 16 days was found highly predictive of acute hyperkalemia ≥6.5 with 37% (95% confidence interval: 19%–58%) of Kafter ≥6.5 after the 16th day compared with only 1% (95% confidence interval: 0%–4%) of Kafter ≥6.5 when succinylcholine was injected during the first 16 days. CONCLUSIONS:This study shows that the risk of &Dgr;K after succinylcholine injection is strongly associated with the length of ICU stay. The risk of acute hyperkalemia ≥6.5 mmol/L is highly significant after 16 days.