Prophylaxis Versus Treatment Use of Laxative for Paralysis of Lower Gastrointestinal Tract in Critically Ill Patients.

GOALS: To evaluate the prevalence of lower gastrointestinal tract paralysis and to compare the success to achieve defecation between treatment and prophylaxis strategies. BACKGROUND: Laxatives use is commonly the first-level measure to achieve defecation in critically ill patients with lower gastrointestinal tract paralysis. Studies comparing prophylaxis versus treatment of lower gastrointestinal tract paralysis have not been performed yet. STUDY: We designed 3 sequential phases of 4 months each: observational phase, treatment phase, and prophylaxis phase. First-level measure was intermittent polyethylene glycol (PEG) 4000 by nasogastric tube. Second-level measures were enema, neostigmine, and continuous PEG. Primary endpoints were the prevalence of constipation for the observational phase and the number of patients that failed to achieve defecation with first-level measures for the treatment and prophylaxis phases. RESULTS: Paralysis of lower gastrointestinal tract in the observational phase was found in 57 of 63 patients (90.5%). Failure to achieve defecation with the first-level measure occurred in 16 of 64 patients (25%) in the treatment phase and in 6 of 70 patients (8.6%) in the prophylaxis phase (P=0.01). Eighteen measures of second level were applied in the treatment phase and 6 in the prophylaxis phase. CONCLUSIONS: Paralysis of the lower gastrointestinal tract in mechanically ventilated ICU patients is common. PEG given as prophylaxis on the first day after mechanical ventilation is associated with faster resolution of paralysis of gastrointestinal tract than PEG given as a treatment on day 4.

Potential effects of corticosteroids on physiological dead-space fraction in acute respiratory distress syndrome.

BACKGROUND: Increased dead-space fraction is common in patients with persistent acute respiratory distress syndrome (ARDS). We evaluated the changes in the oxygenation and dead-space fraction in patients with persistent ARDS after corticosteroid therapy. METHODS: This was a non-randomized non-placebo, controlled observational study including 19 patients with persistent ARDS treated with corticosteroids. We measured P(aO(2))/F(IO(2)) and dead-space fraction at days 0, 4, and 7 after corticosteroids treatment (methylprednisolone) initiation. Patients were classified in intermediate group when corticosteroids were initiated between days 8-14 after ARDS onset, and in late group when initiated after 14 days. RESULTS: Mean time from the diagnosis of the ARDS to methylprednisolone treatment was 11 ± 2 days in the intermediate group (10 patients) and 21 ± 8 days in the late group (9 patients). When comparing days 0, 4, and 7 after methylprednisolone treatment, we found an increase in the P(aO(2))/F(IO(2)) (145 ± 64 mm Hg, 190 ± 68 mm Hg, and 226 ± 84 mm Hg, respectively, P < .001) and a decrease in the physiological dead-space fraction (0.66 ± 0.10, 0.58 ± 0.12, and 0.53 ± 0.11, respectively, P < .001). No differences were found between the intermediate and late groups. CONCLUSIONS: In patients with persistent ARDS, the increase in oxygenation was accompanied by a decrease in the dead-space fraction after a few days of corticosteroid treatment. To confirm potential benefit of corticosteroids on physiological parameters and mortality will require a powered randomized placebo controlled trial.

Hypoxic hepatitis in critically ill patients: incidence, etiology and risk factors for mortality.

PURPOSE: Hypoxic hepatitis may be induced by hemodynamic instability or arterial hypoxemia in critically ill patients. We investigated the incidence, etiology, association with systemic ischemic injury and risk factors for mortality in this population. METHODS: Retrospective analysis of patients with hypoxic hepatitis admitted to a multidisciplinary intensive care unit (ICU) of a university hospital. Hypoxic hepatitis was defined as the existence of a compatible clinical setting (cardiocirculatory failure or arterial hypoxemia) and aminotransferase levels higher than 1000 IU/L. RESULTS: During the 8-year study period, 182 out of the 7674 patients admitted presented hypoxic hepatitis (2.4%). The most common cause was septic shock. The rate of in-hospital mortality in hypoxic hepatitis was 61.5% (112 patients), and was higher in patients with septic shock (83.3%) and cardiac arrest (77.7%). Ischemic pancreatitis (25.6%), rhabdomyolysis (41.2%) and renal failure (67.2%) were common in these patients. Risk factors of mortality were prolonged INR (p = 0.005), need for renal replacement therapy (p = 0.001) and septic shock (p = 0.005). CONCLUSIONS: Hypoxic hepatitis was not a rare condition, and was frequently accompanied by multiorgan injury, with high mortality. Risk factors for increased mortality were prolonged INR, need for renal replacement therapy, and septic shock.

Expression of toll-like receptors 2 and 4 is upregulated during hospital admission in traumatic patients: lack of correlation with blunted innate immune responses.

BACKGROUND: There are reports with conflicting results on the expression of toll-like receptors (TLRs) in trauma patients. In addition, these studies analyzed TLR expression only at patients' hospital admission but not later when complications usually arise. OBJECTIVES: To analyze the surface expression of TLR2 and TLR4 on circulating monocytes from trauma patients during the hospitalization period and to correlate this with cytokine production after stimulation with TLR2 and TLR4 agonists. The phagocytic capacity of monocytes was analyzed at the same time points of TLR expression analysis; to correlate these molecular findings with the presence or absence of infections. METHODS: Prospective and observational study from June 2005 to June 2007. In all analysis, a control group composed of healthy subjects was included. RESULTS: We studied 70 trauma patients admitted to the intensive care unit (ICU) of a tertiary hospital, and 30 healthy volunteers. Blood samples were collected at hospital admission, on day 7 and 14. Forty-four patients (63%) developed at least one episode of infection. Monocytes from trauma patients expressed higher levels of TLR2 and TLR4 than monocytes from control subjects at all time points. Expression of TLR2 and TLR4 in monocytes from those patients who developed any infection was significantly lower than in those patients without infection but still significantly higher than in control subjects. Cellular responses to TLR4 agonist were impaired. Monocytes from traumatic patients phagocytosized less efficiently than monocytes from control subjects. CONCLUSIONS: These results indicate that trauma patients present a dysregulation of the innate immune system that persists during the first 14 days after hospital admission.

Lack of effect of glutamine administration to boost the innate immune system response in trauma patients in the intensive care unit.

INTRODUCTION: The use of glutamine as a dietary supplement is associated with a reduced risk of infection. We hypothesized that the underlying mechanism could be an increase in the expression and/or functionality of Toll-like receptors (TLR), key receptors sensing infections. The objective of this study was to evaluate whether glutamine supplementation alters the expression and functionality of TLR2 and TLR4 in circulating monocytes of trauma patients admitted to the intensive care unit (ICU). METHODS: We designed a prospective, randomized and single-blind study. Twenty-three patients received parenteral nutrition (TPN) with a daily glutamine supplement of 0.35 g/kg. The control group (20 patients) received an isocaloric-isonitrogenated TPN. Blood samples were extracted before treatment, at 6 and 14 days. Expression of TLR2 and TLR4 was determined by flow cytometry. Monocytes were stimulated with TLR specific agonists and cytokines were measured in cell culture supernatants. Phagocytic ability of monocytes was also determined. RESULTS: Basal characteristics were similar in both groups. Monocytes from patients treated with glutamine expressed the same TLR2 levels as controls before treatment (4.9 ± 3.5 rmfi vs. 4.3 ± 1.9 rmfi, respectively; P = 0.9), at Day 6 (3.8 ± 2.3 rmfi vs. 4.0 ± 1.7 rmfi, respectively; P = 0.7) and at Day 14 (4.1 ± 2.1 rfim vs. 4.6 ± 1.9 rmfi, respectively; P = 0.08). TLR4 levels were not significantly different between the groups before treatment: (1.1 ± 1 rmfi vs 0.9 ± 0.1 rmfi respectively; P = 0.9), at Day 6 (1.1 ± 1 rmfi vs. 0.7 ± 0.4 rmfi respectively; P = 0.1) and at Day 14 (1.4 ± 1.9 rmfi vs. 1.0 ± 0.6 rmfi respectively; P = 0.8). No differences in cell responses to TLR agonists were found between groups. TLR functionality studied by phagocytosis did not vary between groups. CONCLUSIONS: In trauma patients in the intensive care unit, TPN supplemented with glutamine does not improve the expression or the functionality of TLRs in peripheral blood monocytes. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT01250080.

Prognostic value of the pulmonary dead-space fraction during the early and intermediate phases of acute respiratory distress syndrome.

BACKGROUND: Little is known about the alveolar dead-space fraction after the first week of acute respiratory distress syndrome (ARDS). We measured the dead-space fraction in the early phase (first week) and the intermediate phase (second week) of ARDS, and evaluated the association of dead-space fraction with mortality. METHODS: We prospectively measured dead-space fraction and other variables in 80 intubated patients during the early phase of ARDS and in 49 patients during the intermediate phase. We used multiple logistic regression analysis to evaluate data. The primary outcome was in-hospital mortality. RESULTS: In the early and intermediate phases the dead-space fraction was higher in patients who died than among those who survived (dead-space fraction 0.64 +/- 0.09 vs 0.53 +/- 0.11, P < .001, and 0.62 +/- 0.09 vs 0.50 +/- 0.10, P < .001, respectively). In both the early and intermediate phases the dead-space fraction was independently associated with a greater risk of death. For every dead-space-fraction increase of 0.05 the odds of death increased by 59% in the early phase (odds ratio 1.59, 95% confidence interval 1.18-2.16, P = .003) and by 186% in the intermediate phase (odds ratio 2.87, 95% confidence interval 1.36-6.04, P = .005). Age and Sequential Organ Failure Assessment score were also independently associated with a greater risk of death in both phases. CONCLUSIONS: Increased alveolar dead-space fraction in the early and intermediate phases of ARDS is associated with a greater risk of death.

Incidence and outcome of ischemic hepatitis complicating septic shock.

AIM: The specific incidence of ischemic hepatitis in septic shock patients remains unknown. The aim of this study was to evaluate the incidence of ischemic hepatitis in septic shock and its relationship with mortality. METHODS: We retrospectively studied 181 patients with septic shock admitted to the intensive care unit (ICU). We defined ischemic hepatitis as having a value of serum aminotransferases equal to or higher than 1000 IU/L. We recorded the age, sex, comorbidity, site of infection, the Sequential Organ Failure Assessment (SOFA) score on admission to the ICU, maximum SOFA score and inadequate antibiotic therapy. RESULTS: Twenty-five (13.8%) patients developed ischemic hepatitis. In-hospital mortality was 57% (103 patients). In the ischemic hepatitis group, mortality increased up to 84.0% (21 patients) compared with 52.6% (82 patients) in patients without ischemic hepatitis (control group) (odds ratio [OR]: 4.7; 95% confidence interval [CI]: 1.6-14.4; P = 0.003). The development of ischemic hepatitis, age, maximum SOFA score and inadequate antibiotic therapy were independently associated with an increased risk of death. The odds of death increased by 247% in ischemic hepatitis (OR: 3.47; 95% CI: 1.02-11.8; P = 0.047). CONCLUSION: Ischemic hepatitis is a common complication in septic shock patients, associated with a high mortality.

Pentobarbital versus thiopental in the treatment of refractory intracranial hypertension in patients with traumatic brain injury: a randomized controlled trial.

INTRODUCTION: Experimental research has demonstrated that the level of neuroprotection conferred by the various barbiturates is not equal. Until now no controlled studies have been conducted to compare their effectiveness, even though the Brain Trauma Foundation Guidelines recommend that such studies be undertaken. The objectives of the present study were to assess the effectiveness of pentobarbital and thiopental in terms of controlling refractory intracranial hypertension in patients with severe traumatic brain injury, and to evaluate the adverse effects of treatment. METHODS: This was a prospective, randomized, cohort study comparing two treatments: pentobarbital and thiopental. Patients who had suffered a severe traumatic brain injury (Glasgow Coma Scale score after resuscitation < or = 8 points or neurological deterioration during the first week after trauma) and with refractory intracranial hypertension (intracranial pressure > 20 mmHg) first-tier measures, in accordance with the Brain Trauma Foundation Guidelines. RESULTS: A total of 44 patients (22 in each group) were included over a 5-year period. There were no statistically significant differences in ' baseline characteristics, except for admission computed cranial tomography characteristics, using the Traumatic Coma Data Bank classification. Uncontrollable intracranial pressure occurred in 11 patients (50%) in the thiopental treatment group and in 18 patients (82%) in the pentobarbital group (P = 0.03). Under logistic regression analysis--undertaken in an effort to adjust for the cranial tomography characteristics, which were unfavourable for pentobarbital--thiopental was more effective than pentobarbital in terms of controlling intracranial pressure (odds ratio = 5.1, 95% confidence interval 1.2 to 21.9; P = 0.027). There were no significant differences between the two groups with respect to the incidence of arterial hypotension or infection. CONCLUSIONS: Thiopental appeared to be more effective than pentobarbital in controlling intracranial hypertension refractory to first-tier measures. These findings should be interpreted with caution because of the imbalance in cranial tomography characteristics and the different dosages employed in the two arms of the study. The incidence of adverse effects was similar in both groups. TRIAL REGISTRATION: (Trial registration: US Clinical Trials registry NCT00622570.).

Hypercapnia test as a predictor of success in spontaneous breathing trials and extubation.

BACKGROUND: The ventilatory capacity of the respiratory neuromuscular system can be studied with the hypercapnia test. OBJECTIVE: To determine whether decreased response to the hypercapnia test is associated with failure to pass a spontaneous breathing trial (SBT) or extubation failure. METHODS: We studied 103 intubated patients ready for SBT. We used a hypercapnia test in which we approximately doubled the dead space and thus caused re-inhalation of expired air. We calculated 3 ratios: the ratio of P(0.1) (airway occlusion pressure 0.1 s after the onset of inspiratory effort) during hypercapnia test to baseline P(0.1); the ratio of the change in minute volume [DeltaV(E)] to the change in P(aCO(2)) (we call this ratio the hypercapnic ventilatory response); and the ratio of the change in P(0.1) [DeltaP(0.1)] to the change P(aCO(2)) (we call this ratio the hypercapnic-respiratory-drive response). RESULTS: Thirty-six patients failed the SBT, and 11 patients failed extubation. The mean values for the SBT/extubation-success group, the extubation-failure group, and the SBT-failure group, respectively, were: ratio of hypercapnia-test P(0.1) to baseline P(0.1): 4.3 +/- 2.7, 3.7 +/- 1.3, and 3.0 +/- 1.8 (P = .03); hypercapnic ventilatory response: 0.60 +/- 0.35 L/min/mm Hg, 0.50 +/- 0.26 L/min/mm Hg, and 0.31 +/- 0.21 L/min/mm Hg (P < .001); hypercapnic respiratory-drive response: 0.48 +/- 0.24 cm H(2)O/mm Hg, 0.42 +/- 0.19 cm H(2)O/mm Hg, and 0.27 +/- 0.15 cm H(2)O/mm Hg (P < .001). For predicting SBT/extubation success, the sensitivities and specificities, respectively, were: ratio of hypercapnia-test P(0.1) to baseline P(0.1) 0.80 and 0.47; hypercapnic ventilatory response 0.86 and 0.53; hypercapnic respiratory-drive response 0.82 and 0.55. CONCLUSIONS: The SBT/extubation-failure patients had less response to the hypercapnia test than did the SBT/extubation-success patients, and the hypercapnia test was not useful in predicting SBT or extubation success.

Successful weaning from continuous renal replacement therapy. Associated risk factors.

PURPOSE: To identify risk factors of successful continuous renal replacement therapy (CRRT) weaning and to evaluate the effect of furosemide in the recovery of urine output after CRRT stop. MATERIALS AND METHODS: Retrospective, observational study of critical patients treated with CRRT. Weaning tests (WT) were classified in two groups: successful (urine output was recovered and CRRT was not required again) and failed (CRRT was required again). A multiple logistic regression model was used to identify risk factors of successful CRRT WT. The prediction ability was assessed with the area under the receiver operating characteristic curves (AUC-ROC). RESULTS: Eighty-six patients underwent 101 CRRT WT. The multivariate model identified that the risk factors of successful CRRT weaning were sex and 6h-urine output after CRRT stop. The AUC-ROC was 0.81 (0.72-0.90) for 6h-urine output before and 0.91 (0.84-0.96) for 6h-urine output after CRRT stop. The AUC-ROC for 6h-urine output after WT to predict successful CRRT weaning were 0.94 (0.88-1.0) in patients who received furosemide and 0.85 (0.72-0.99) in patients who did not. CONCLUSIONS: Urine output after CRRT stop was the main risk factor of successful CRRT weaning. Administration of furosemide increased the strength of this association.

Low-dose steroid therapy does not affect hemodynamic response in septic shock patients.

PURPOSE: Several studies showed that low-dose steroid therapy (LDST) in patients with septic shock leads to a significantly shorter duration of shock and a decreased mortality. However, these results have been criticized. Our purpose was to evaluate the effects of LDST on time to shock reversal and mortality in septic shock. MATERIALS AND METHODS: We retrospectively studied 203 patients with septic shock admitted to the intensive care unit of our tertiary hospital. A short corticotropin test was performed in all patients within 72 hours of septic shock onset. We performed a propensity score analysis through a logistic regression model with baseline relevant characteristics, and evaluated the influence of LDST on time to shock reversal and inhospital mortality. RESULTS: One hundred twenty-four patients were treated with LDST (steroid group) and 79 without LDST (control group). Patients treated with steroids presented higher Simplified Acute Physiology Score II and maximum Sepsis-Related Organ Failure Assessment scores. Both groups presented similar baseline and stimulated cortisol values. The hazard ratio of remaining on shock adjusted by severity of illness, inadequate antibiotic, and propensity score was 1.15 (95% confidence interval 0.71-1.86) for patients treated with steroids. Inhospital mortality was 62% in the steroid group and 52% in the control group (P = .84). Logistic regression analysis with propensity score neither showed differences between steroid and control group in the inhospital mortality. Predictors of inhospital mortality were age, maximum Sepsis-Related Organ Failure Assessment score, and inadequate antibiotics. CONCLUSION: In our study, treatment with low-dose steroid therapy was not associated to a reduction in time to shock reversal or mortality.

Relationship between plasma adrenocorticotropin hormone and intensive care unit survival in early traumatic brain injury.

BACKGROUND: Hypothalamic pituitary adrenal response has been recently evaluated in patients with traumatic brain injury (TBI) with different results. Our objective was to study this response and its relationship with outcome in the early stage after TBI. METHODS: We conducted a prospective observational clinical study in the intensive care unit of a tertiary level university hospital. The study included 50 consecutive patients who suffered isolated TBI. Intracranial pressure (ICP) was measured by an intraparenchymal probe. All patients were sedated and mechanically ventilated. Second-level measures were provided as per protocol, when needed. We measured plasma adrenocorticotropin hormone (ACTH) levels, as well as baseline and stimulated serum cortisol after a high-dose corticotrophin stimulation test, within 2 days after TBI for all patients. RESULTS: Mean age was 36 +/- 18 (range 16-77) years. Forty-four (88%) were male. Median Glasgow Coma Scale score was 7. Mean ACTH was 15.4 +/- 19.8 pg/mL. Mean baseline cortisol was 14.8 +/- 9.0 microg/dL and mean stimulated cortisol was 27.1 +/- 7.3 microg/dL and 30.5 +/- 7.2 microg/dL at 30 and 60 minutes, respectively. Baseline and stimulated cortisol were not correlated with mortality. Logistic regression analysis revealed that, either plasma ACTH levels <9 pg/mL or lack of indication to provide second-level measures to control ICP were significant independent predictors of survival. CONCLUSIONS: The presence of a low plasma ACTH concentration at an early stage of TBI and lack of indication to provide second-level measures to control ICP were associated with a higher intensive care unit survival.

Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD.

BACKGROUND: Hyperoxia-induced hypercapnia in subjects with COPD is mainly explained by alterations in the ventilation/perfusion ratio. However, it is unclear why respiratory drive does not prevent CO2 retention. Some authors have highlighted the importance of respiratory drive in CO2 increases during hyperoxia. The aim of the study was to examine the effects of hyperoxia on respiratory drive in subjects with COPD. METHODS: Fourteen intubated, ready-to-wean subjects with COPD were studied during normoxia and hyperoxia. A CO2 response test was then performed with the rebreathing method to measure the hypercapnic drive response, defined as the ratio of change in airway-occlusion pressure 0.1 s after the start of inspiratory flow (ΔP(0.1)) to change in P(aCO2) (ΔP(aCO2)), and the hypercapnic ventilatory response, defined as the ratio of change in minute volume (ΔV̇(E)) to ΔP(aCO2). RESULTS: Hyperoxia produced a significant increase in P(aCO2) (55 ± 9 vs 58 ± 10 mm Hg, P = .02) and a decrease in pH (7.41 ± 0.05 vs 7.38 ± 0.05, P = .01) compared with normoxia, with a non-significant decrease in V̇(E) (9.9 ± 2.9 vs 9.1 ± 2.3 L/min, P = .16) and no changes in P(0.1) (2.85 ± 1.40 vs 2.82 ± 1.16 cm H2O, P = .97) The correlation between hyperoxia-induced changes in V̇(E) and P(aCO2) was r(2) = 0.38 (P = .02). Median ΔP(0.1)/ΔP(aCO2) and ΔV̇(E)/ΔP(aCO2) did not show significant differences between normoxia and hyperoxia: 0.22 (0.12-0.49) cm H2O/mm Hg versus 0.25 (0.14-0.34) cm H2O/mm Hg (P = .30) and 0.37 (0.12-0.54) L/min/mm Hg versus 0.35 (0.12-0.96) L/min/mm Hg (P = .20), respectively. CONCLUSIONS: In ready-to-wean subjects with COPD exacerbations, hyperoxia is followed by an increase in P(aCO2), but it does not significantly modify the respiratory drive or the ventilatory response to hypercapnia.

Role of Elevated Aminotransferases in ICU Patients with Rhabdomyolysis.

To evaluate whether patients with rhabdomyolysis and serum alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST) higher than 1000 IU/L had higher mortality that patients with low aminotransferases. Retrospective analysis of intensive care unit patients with rhabdomyolysis [creatine kinase (CK) higher than 5000 IU/L]. Patients were classified in two groups: low aminotransferases group, when AST and ALT were equal or lower to 1000 IU/L, and elevated aminotransferases group, when AST or ALT was above 1000 IU/L. Forty-six out of 189 patients included in the analysis (24.3%) had elevated aminotransferases. The mortality of patients with rhabdomyolysis was 25.9 per cent, being higher in patients with elevated aminotransferases compared with patients with low aminotransferases (60.9% vs 14.7%; P < 0.001). Mortality stratified by quartiles of CK in patients with low aminotransferases was independent of the level of CK (P = 0.67). Logistic regression analysis showed that the independent variables associated with mortality were Simplified Acute Physiology Score II [1.11 (1.07-1.16) for each point of increase, P < 0.001], the international normalized ratio value [4.2 (1.6-10.7) for each point of increase, P = 0.003], and the need of renal replacement therapy [5.4 (1.7-17.2), P = 0.004]. Patients with rhabdomyolysis with elevated serum aminotransferases had higher mortality than patients with low serum aminotransferase levels.

Acute Hypothalamic-pituitary-adrenal response in traumatic brain injury with and without extracerebral trauma.

OBJECTIVE: Endocrine disturbances are common after traumatic brain injury (TBI). Hypothalamic-pituitary-adrenal (HPA) axis response in TBI patients may be related with hemodynamic status. However, its relationship with outcome is unclear. Our objective was to evaluate HPA axis response in the acute phase after TBI in patients with or without extracerebral trauma (ECT), and to investigate the impact of systemic injury and the mechanisms underlying HPA response. METHODS: We prospectively studied 165 patients with moderate to severe TBI. Between 24 and 48 h after TBI, blood samples were taken for plasma adrenocorticotrophin hormone (ACTH) and baseline cortisol measurements. Afterwards, a short corticotrophin hormone test (250 mug Synacthen) was performed and samples were obtained at 30 and 60 min. We compared HPA response in TBI patients presenting with and without ECT and investigate potential mechanisms underlying this response. RESULTS: One hundred and eight patients presented with isolated TBI, whereas 57 patients presented associated ECT. Both groups were comparable. Overall, 23.6% of patients fulfilled adrenal insufficiency (AI) criteria. Patients with plasma ACTH <9 pg/ml and patients presenting with hemorrhagic shock were more likely to present adrenal impairment. Variables associated with mortality were Injury Severity Score, Glasgow Coma Scale, Traumatic Coma Data Bank classification different than type II, need of second level measures to control intracranial pressure and plasma ACTH >9 pg/ml. CONCLUSION: Patients with TBI presenting with or without associated ECT present similar acute HPA response. AI is present in 23.6% of patients. Risk is increased in patients with low plasma ACTH levels and in patients with hemorrhagic shock. Both primary and secondary mechanisms of HPA failure were found. However, AI did not affect outcome.