Treatments and outcome, the point in head trauma.

When a severe traumatic brain-injured patient arrives to hospital, fear of failure and definite opinions about the outcome modify early care and provoke self-fulfilling prophecies. It is obvious that working on prognosis is not only useful to inform relatives but also permits to maintain a high level of care, key for a better outcome. Mortality is high (40-50%) if deaths in the first days are not excluded. Following guidelines in all cases will permit to decrease the number of preventable death and a decrease in morbidity. Well-defined networks of care leading to specialized centres with multimodal monitoring give best results. However, only 20% of living patients return to their previous life with mild handicap. These unsatisfactory results require intensifying research, notably in early rehabilitation in intensive care unit. Ethic issues should be discussed after few days of care and dialogue with relatives in a defined "window of opportunity". Ideally, we need to find strong and early indicators of outcome to limit fears on presumed handicap. A magnetic resonance imaging (MRI) sequence called diffusion tensor imaging (TDI) permits to visualise traumatic axonal injury. Studies with complex statistical methodology give a good estimated probability of bad outcome but must be confirmed by more validation studies. Progress will come from a better understanding of physiopathology. Focuses on processing chain, rapid multi-monitoring, biomarkers, and investigations in MRI and TDI will help to establish opportunities for treatments and to determine limits.

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). METHODS: Prospective, observational study of 18 severe TBI patients during pre-hospital medical care. TCD was performed to estimate cerebral perfusion in the field and upon arrival at the Level 1 trauma centre. Specific therapy (mannitol, noradrenaline) aimed at improving cerebral perfusion was initiated if the initial TCD was abnormal (defined by a pulsatility index >1.4 and low diastolic velocity). RESULTS: Nine patients had a normal initial TCD and nine an abnormal one, without a significant difference between groups in terms of the Glasgow Coma Scale or the mean arterial pressure. Among patients with an abnormal TCD, four presented with an initial areactive bilateral mydriasis. Therapy normalized TCD in five patients, with reversal of the initial mydriasis in two cases. Among these five patients for whom TCD was corrected, only two died within the first 48 h. All four patients for whom the TCD could not be corrected during transport died within 48 h. Only patients with an initial abnormal TCD required emergent neurosurgery (3/9). Mortality at 48 h was significantly higher for patients with an initial abnormal TCD. CONCLUSIONS: Our preliminary study suggests that TCD could be used in pre-hospital care to detect patients whose cerebral perfusion may be impaired.

[Transcranial doppler in neurosurgery]. / Le doppler transcrânien en neurochirurgie.

Transcranial doppler (TCD) is a noninvasive and easily repeatable method to measure the blood flow in basal cerebral arteries. Mean velocities of red blood cells in basal arteries are related to cerebral blood flow. Because of low peripheral resistance in cerebral arteries, diastolic velocity (V(d)) remains positive in cerebral circulation in physiological situations. The pulsativity index (PI; normal values for the middle cerebral artery=1.0+/-0.2) and end diastolic velocity (EDV; normal values for the middle cerebral artery=40+/-10 cm/s) give important information to evaluate the resistance status of small downstream arteries. A high PI (>1.4) with a low EDV (<20 cm/s) indicates a low blood flow with a high ischemic risk due to low cerebral perfusion pressure. TCD can also detect cerebral vasospasm after subarachnoid hemorrhage, but sensitivity and specificity for vasospasm diagnosis are low compared to angiography. However, a day-to-day increase in arterial blood cell velocities can help determine the vasospasm risk and/or indicate that angiography should be done.

[Therapeutic hypothermia]. / L'hypothermie thérapeutique.

The benefit of therapeutic hypothermia after severe head injury is highly controversial. However, hypothermia is still used and studied in this context for multiple reasons. Efficacy of hypothermia is demonstrated after cerebral ischemia in numerous animal studies and after cardiac arrest in human studies. Hyperthermia is a major independent factor of outcome after cerebral ischemic or traumatic brain injury. Moreover, ICP is related to core temperature, and hypothermia may be used to decrease intracranial hypertension. However, many questions are still unresolved and can explain discrepancies between clinical studies: direct measurement of cerebral temperature, relationship between ICP, temperature and PaCO(2), level and duration of hypothermia and precise methods for cooling and particularly for rewarming.

[Medical prehospital rescue in head injury]. / Prise en charge préhospitalière des traumatisés crâniens.

OBJECTIVE: To evaluate the effectiveness of prehospital medical care in head-injured patients. PATIENTS AND METHODS: All head-injured patients admitted in Bicêtre hospital from 1995 to 1999 were retrospectively studied. Glasgow Coma Scale (GCS) score, mean arterial pressure (MAP) and SpO(2) measured on the field were compared to GCS, MAP and SpO(2) on arrival in the hospital. All treatments given during transport and first data recorded in the hospital were noted. Each parameter was compared to outcome at 6 months. Then, significant parameters were compared with a multivariate analysis. RESULTS: Three hundred and four patients were included, 80% had a GCS

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.

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

OBJECTIVE: To 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. DESIGN: Randomized study. SETTING: Accredited animal laboratory. SUBJECTS: Adult Sprague Dawley rats. INTERVENTIONS: Anesthetized 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 microg/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 microg/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). CONCLUSIONS: Combination 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 alpha-1 adrenergic reactivity.

Comparison of the cerebral effects of dopamine and norepinephrine in severely head-injured patients.

OBJECTIVE: To compare the cerebral effects of dopamine and norepinephrine after severe head injury. DESIGN: Prospective, clinical study. SETTING: Surgical intensive care unit in a university hospital. PATIENTS: Nineteen patients with severe head-injuries already requiring vasopressor therapy. Group 1: patients receiving dopamine (n = 9); group 2: patients receiving norepinephrine (n = 10). INTERVENTION: Vasopressor therapy was switched from dopamine to norepinephrine in group 1 and from norepinephrine to dopamine in group 2, maintaining the same mean arterial pressure (MAP). MEASUREMENTS AND RESULTS: MAP, intracranial pressure (ICP), jugular venous oxygen saturation (SjvO2), transcranial Doppler mean velocity in the middle cerebral artery (Vm), and transoesophagal Doppler aortic output (AO) were evaluated under dopamine and norepinephrine. Means for each group were compared with the paired Student's t-test. For the same MAP, ICP was significantly higher with dopamine than norepinephrine in both groups (respectively, group 1: 26 +/- 11 vs 23 +/- 11 mmHg, P < 0.005; group 2: 39 +/- 13 vs 31 +/- 9 mmHg, P < 0.005). SjvO2, Vm, and AO did not change significantly between treatments. The ICP variation between treatments was not correlated with the variation of any other measured parameter. The ICP variation between treatments was significantly higher in group 2 than group 1, which could be explained by autoregulation mechanisms. CONCLUSIONS: For the same MAP, ICP was significantly higher with dopamine than norepinephrine with no argument supporting an increase of cerebral blood flow.

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 degrees C in periods 1 and 2, and 34.1 +/- 1.1 degrees 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.

Oxygen tolerance in patients with acute respiratory failure.

OBJECTIVE: To search for a threshold of pulmonary oxygen toxicity in patients with acute respiratory failure. DESIGN: Retrospective study over a 10-year period. SETTING: Three intensive care units of two university hospitals. PATIENTS AND PARTICIPANTS: Seventy-four patients with acute respiratory failure ventilated continuously with a FIO2 > or = 0.9 for at least 48 h were selected. INTERVENTIONS: Information regarding status, scoring, diagnosis and therapeutic interventions upon admission and ICU course were extracted from the patients' charts. MEASUREMENTS AND RESULTS: We found that total exposure [mean (standard error of the mean)] to a FIO2 of 0.9 (TE 90) or more was 5.6 (1.1) days in the 17 survivors (S) versus 5.9 (0.5) days in the 57 non-survivors (D) (NS). Total exposure time to a FIO2 more than 0.5 (TE 50) was 16.5 (2.6) days in S and 11.2 (1) days in D (p < 0.05). The PaO2/FIO2 ratio became significantly higher in S only 5 days after beginning FIO2 of 0.9 or more. Hypoxemia was not frequent at the time of death, whereas in 70% of the non-survivors there were at least three organ failures in the last 48 h. In univariate analysis, the duration of exposure to FIO2 of 0.9 or more was not different in survivors and non-survivors, and the average total duration of exposure to FIO2 of more than 0.5 was even longer in survivors. In multivariate analysis, exposure shorter than 10 days to FIO2 more than 0.5 and exposure longer than 4 days to a FIO2 of 0.9 or more were significantly associated with death. However, despite a larger exposure to a FIO2 of 0.9 or more during the last 5 years of the study, the trend moved towards a higher survival rate during this period compared with the first 5 years of the study. CONCLUSIONS: Thus, our data provide circumstantial evidence that the lungs of patients with acute respiratory failure might exhibit some relative resistance to prolonged oxygen exposure. Therefore, it might be worthwhile carrying out a prospective study of different FIO2 strategies in such patients.