Short-term and long-term mortality following pediatric intensive care.

BACKGROUND: The aim of the present study was to examine short-term and long-term mortality following discharge from the pediatric intensive care unit (PICU). METHODS: This was a prospective observational study. Data collected consisted of demographics, severity scores, procedures, treatment, need for and duration of mechanical ventilation (MV), length of PICU and hospital stay, and mortality at PICU and hospital discharge, at 3 and 6 months and at 1 and 2 years. RESULTS: A total of 300 patients (196 boys and 104 girls), aged 54.26 ± 49.93 months, were included in the study. Median (interquartile range) Pediatric Risk of Mortality (PRISM III-24) score was 7 (3-11) and predicted mortality rate was 11.16%. MV rate was 67.3% (58.3% at admission) for 6.54 ± 14.15 days, and length of PICU and hospital stay was 8.85 ± 23.28 days and 20.69 ± 28.64 days, respectively. Mortality rate at discharge was 9.7% and cumulative mortality rate thereafter was 12.7%, 15.0%, 16.7%, 19.0%, and 19.0% at hospital discharge, 3 months, 6 months, 1 year and 2 years, respectively. Significant risk factors of PICU mortality were inotrope use, PRISM III-24 score >8, MV, arterial and central venous catheterization, nosocomial infection, complications, and cancer. Independent predictors of mortality at discharge were inotrope use and PRISM III-24 score, whereas predictors of mortality at 2 years were comorbidity and cancer. CONCLUSIONS: A 2 year follow-up period seems sufficient for a comprehensive mortality analysis of PICU patients. Severity of critical illness is the key factor of short-term mortality, whereas comorbidity is the major determinant of long-term mortality.

The efficacy of antithrombin administration in the acute phase of burn injury.

Severe burn injury is characterized by the activation of coagulation, decreased fibrinolytic activity and decreased natural anticoagulant activity. The aim of our study was to investigate the effect of antithrombin (AT) administration on coagulation status and on organ function in the early post-burn period. Thirty-one patients were admitted to the burn intensive care unit and were then randomised into two groups (AT-treated and non-AT-treated) for four consecutive days after thermal injury. The clinical data, coagulation and fibrinolysis parameters were compared and the adverse effects were monitored. Significant differences in the time course of coagulation markers (thrombin/AT complexes, tissue plasminogen activator, D-dimer) were observed between AT-treated and non-AT treated groups. According to the International Society on Thrombosis and Haemostasis criteria, disseminated intravascular coagulation (DIC) diagnosis was made in 28 of 31 patients. The presence of overt DIC was associated with mortality (p < 0.001). The Sequential Organ Failure Assessment (SOFA) score time trend differed significantly between the two investigation groups (decreased in the treated group and did not change in the non-AT-treated group). AT-treated patients had an absolute reduction in a 28-day mortality of 25% as compared to the non-AT-treated group (p = 0.004). No treatment related side effects were observed. Treatment with AT seems to affect the coagulation status and reduce multiple organ failure incidence and mortality in the early post-burn period.

Early coagulation disorders after severe burn injury: impact on mortality.

OBJECTIVE: To evaluate the time course of coagulation markers in the early postburn period and clarify the role of coagulation alterations in organ failure and in mortality prognosis. DESIGN AND SETTING: This prospective study was conducted in the burn ICU of a tertiary hospital. PATIENTS: 45 patients with severe thermal burn injury. MEASUREMENTS AND RESULTS: Clinical data and coagulation and fibrinolysis parameters were measured during the first postburn week. The ICU 28-day mortality rate was 33%. Significant differences in the time course of coagulation markers were observed between survivors and nonsurvivors. SOFA score distinguished between patients with overt and nonovert disseminated intravascular coagulation (DIC) during the overall investigation period. Presence of overt DIC was related to mortality (OR=0.1). Antithrombin, protein S, plasminogen activator inhibitor 1, and SOFA score on day 3, protein C on day 5, and thrombin/antithrombin complexes on day 7 revealed a good prognostic value for ICU mortality, according to the area under ROC curves. CONCLUSIONS: Severe thermal injury is associated with the early activation of coagulation cascade, presence of DIC, organ failure, and increased mortality.

Effects of pneumoperitoneum and LPS-induced endotoxemia on cerebral perfusion pressure in pigs.

Multitrauma patients commonly develop abdominal compartment syndrome, which is defined as the end result of sustained, uncorrected, intra-abdominal hypertension. We aimed to assess the effects of increased intra-abdominal pressure (IAP) upon intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in the presence or absence of lipopolysacharide (LPS)-induced endotoxemia using an experimental porcine model of pneumoperitoneum. Experimental procedures were approved by the Animal Care Review Committee of the National Veterinary Institute. Sixteen female pigs weighing 20 to 25 kg, aged 3 to 4 months were used. The animal model of increased IAP employed in our studies was produced with intraperitoneal administration of helium at 25 mm Hg under general anesthesia. After induction of pneumoperitoneum, 16 animals were randomly divided into 2 groups of 8 pigs each. One group received LPS intravenously (endotoxin group) and the second group received saline (control group). ICP, CPP, and hemodynamic variables were continuously monitored and recorded. A significant reduction of the cardiac output and concurrent increases in systemic vascular resistance and central venous pressure were observed in both groups after induction of pneumoperitoneum. ICP increased whereas CPP decreased significantly compared with baseline values in both groups after elevation of IAP. After LPS administration (endotoxin group), the cardiac output and mean arterial pressure decreased significantly. The CPP decreased further in the endotoxin group after LPS administration, whereas ICP remained unchanged. IAP increases produce significant increases in the ICP and decreases in the CPP in this animal model. LPS-induced endotoxemia further decreased CPP.

Investigation of heart rate and blood pressure variability, baroreflex sensitivity, and approximate entropy in acute brain injury patients.

PURPOSE: The purpose of the study was to investigate longitudinally over time heart rate (HR) and blood pressure variability and baroreflex sensitivity in acute brain injury patients and relate them with the severity of neurologic dysfunction and outcome. METHODS: Data from 20 brain injured patients due to multiple causes and treated in the intensive care unit were used, with HR and blood pressure recorded from monitors and analyzed on a daily basis. We performed power spectral analysis estimating low frequencies (LF: 0.04-0.15 Hz), high frequencies (HF: 0.15-0.4 Hz), and their ratio and calculated the approximate entropy, which assesses periodicity within a signal and transfer function (TF), that estimates baroreflex sensitivity. Heart rate variance was considered as a measure of HR variability. RESULTS: Nonsurvivors (brain dead) had lower approximate entropy (0.65 +/- 0.24 vs 0.84 +/- 0.26, P < .05) and lower variance mean values (0.48 +/- 0.54 vs 1.29 +/- 0.42 ms(2)/Hz, P < .01), lower LF and HF minimum values (0.31 +/- 0.88 vs 1.11 +/- 0.46, P < .01; and 0.27 +/- 0.42 vs 0.86 +/- 0.30, P < .01, respectively), lower LF/HF (0.22 +/- 0.29 vs 0.62 +/- 0.28, P < .01), and lower TF mean values (0.43 +/- 0.29 vs 1.11 +/- 0.74, P < .05) during their whole stay in the intensive care unit in relation with survivors. The mean variance (P < .05), mean TF (P < .05), and mean LF/HF (P < .05) were significantly successful in separating survivors from nonsurvivors. CONCLUSIONS: We conclude that in acute brain injury patients, low variability, low baroreflex sensitivity, and sustained decrease in LF/HF of HR signals are linked with a high mortality rate.

Improvement of pain treatment after major abdominal surgery by intravenous S+-ketamine.

UNLABELLED: The use of intraoperative racemic ketamine for pain prevention after abdominal surgery is controversial. We compared one preincisional i.v. injection of S(+)-ketamine with its preincisional and repeated intraoperative use in 45 patients undergoing surgery with epidural and general anesthesia. S(+)-ketamine is a new drug formulation that contains the more potent S(+)-stereoisomer of ketamine. Patients were randomized to receive placebo, 0.5 mg/kg preincisional S(+)ketamine, or 0.5 mg/kg preincisional and 0.2 mg/kg intraoperative S(+)-ketamine repeated at 20-min intervals. In the postoperative period, epidural ropivacaine (2 mg/mL; 0.12 mL.kg(-1).h(-1)) was infused for pain therapy. Patients who received repeated S(+)-ketamine reported smaller pain scores than those who received placebo after awakening and 3 and 6 h later (P < or = 0.05). Fewer patients with repeated S(+)-ketamine required additional analgesics than those with placebo (P < or = 0.05). Cumulative consumption of additional diclofenac and dextropropoxyphene at 24 h was less after single (P < 0.05) and repeated (P < 0.05) S(+)-ketamine versus placebo. After awakening, patients who received repeated S(+)-ketamine reported being in a better mood than those in the other groups (P < 0.05). No psychotomimetic side effects were noted. In conclusion, preincisional and repeated intraoperative small-dose S(+)-ketamine added to general and epidural anesthesia causes better postoperative pain relief than general and epidural anesthesia alone. IMPLICATIONS: After major visceral surgery, preincisional and repeated intraoperative small-dose S(+)-ketamine added to general and epidural anesthesia causes better postoperative pain relief than general and epidural anesthesia alone.