[Does cerebral salt wasting syndrome exist?]. / Le syndrome de perte de sel d'origine cérébrale existe-t-il?

Increased natriuresis is a frequent situation after subarachnoid haemorrhage (SAH). It may be responsible for hyponatremia, which can be dangerous in case of severe hypo-osmolarity or hypovolemia. Inappropriate secretion of antidiuretic hormone or cerebral salt wasting syndrome (CSWS) have been incriminated for hyponatremia after SAH, but it remains difficult to distinguish between both syndromes. There are many explanations for increased natriuresis after SAH, depending on the level of blood pressure, the volemia, and the presence or not of natriuretic peptides. The cerebral insult and the treatments, which are done to fight against elevated intracranial pressure or vasospasm, can modify any of these parameters. So it appears that the word "cerebral" in CSWS is probably not a good term and it would be better to talk about appropriate or non-appropriate natriuretic response. Corticoïds or urea can be useful for controlling hypernatriuresis.

[Early diagnostic for vasospasm after aneurysmal subarachnoid haemorrhage]. / Comment faire le diagnostic précoce d'un vasospasme?

Vasospasm is the leading cause of sequelae or deaths after aneurysmal subarachnoid haemorrhage. Vasospasm occurs 2-10 days after haemorrhage and that justifies close monitoring during this period. Because clinical signs appear often to late to reverse ischaemia, paraclinic tools have been developed. Arteriography is the historical gold standard for diagnosis but no clear validated rules exist to measure vessel sections. Diagnosis of vasospasm is, thus, relatively subjective and only reflects one moment of arteries status. Transcranial doppler is a non-invasive and easily repeatable method but sensibility and specificity for vasospasm diagnosis are low compared to arteriography. However, day-to-day changes of arterial blood cells velocities can help to determine vasospasm risk and/or indicate time for arteriography. CT-scanner, PET-scan or IRM can help to evaluate ratio between perfusion and metabolism. Nevertheless, as arteriography, it is only a one-time measurement without control of treatment effects. Waiting for improvement of diagnosis techniques, arteriography stays the gold standard. To choose the right moment for invasive methods, intensivists need to use clinical and transcranial doppler data and start treatment as early as possible to be efficacious.

[Intracerebral monitoring of a patient with vasopasm]. / Monitorage intracérébral d'un patient ayant un vasospasme.

Delayed neurological deficit occurs among 30% of patients after aneurysmal subarachnoid haemorrhage, mainly related to cerebral vasospasm. The early detection of cerebral ischemia remains problematic. Conventional cerebral monitoring (as intracranial pressure and cerebral perfusion pressure) appears to be insufficient, because cerebral ischemia may occur without elevated intracranial pressure. Global cerebral monitoring as venous jugular oxygen saturation are useful for regional monitoring. Local monitoring as oxygen tissue partial pressure (PtiO2) and microdialysis are sensible for brain ischemia detection, but may also ignore episodes occurring in non-monitored brain area. For the detection of most episodes of brain ischemia, several monitoring system should be use performing a multimodal intracerebral monitoring. Brain microdialysis and oxygen tissue partial pressure are promising monitoring system.

Multimodal cerebral monitoring and decompressive surgery for the treatment of severe bacterial meningitis with increased intracranial pressure.

Bacterial meningitis is still associated with a high mortality, mainly because of cerebral herniation as a result of increased intracranial pressure. Published data stress the necessity of an early diagnosis and immediate start of antibiotic therapy. Nevertheless, there are only few reports in which therapeutic strategy was based on the monitoring and the reduction of intracranial pressure (ICP). We report one case of bacterial meningitis caused by Neisseria meningitidis with an initial ICP value of 60 mmHg, which was treated by large hemicraniectomy and ventriculostomy, leading to a favorable neurological long-term result. The surgical decision was accelerated by an accurate ICP evaluation based on cerebral monitoring [transcranial Doppler ultrasonography (TCD) and intracranial ICP-device]. In selected patients with bacterial meningitis and clinical and radiological evidence of elevated ICP, cerebral monitoring and aggressive reduction of ICP may be crucial to improve survival and neurological outcome. When maximal medical ICP treatment fails to reduce severe intracranial hypertension, decompressive craniectomy should be rapidly proposed.

In vivo selection of oxacillinase-mediated ceftazidime resistance in Pseudomonas aeruginosa.

Ceftazidime-susceptible and -resistant Pseudomonas aeruginosa strains were isolated from pulmonary specimens following a treatment with ceftazidime in a patient who developed a nosocomial pneumonia. The ceftazidime-susceptible and -resistant strains were clonally related and harbored a self-transferable approximately 155-kb plasmid. These isolates expressed two OXA-10-like oxacillinases, the narrow-spectrum OXA-35 and the expanded-spectrum OXA-19, respectively, differing by one amino acid substitution. This is the first example of in vivo selection of an extended-spectrum oxacillinase from a restricted-spectrum oxacillinase.

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.