La cascade ischémique cérébrale

The pathophysiology of ischaemia depends on the residual cerebral blood flow. As a result, it is different in global ischaemia, when compared with focal ischaemia, where the centre area is surrounded with an area called an ischaemic penumbra. Ischaemia results from a sudden failure in the oxygen and glucose supply. Oxidative phosphorylation fails, a major event that is responsible for all the other reactions. Anaerobic metabolism produces lactate and H⁺. Cell membrane ionic pumps are inactivated, which results in a breakdown of ionic homeostasis. Ca⁺⁺ and Na⁺ penetrate into the cells, as K⁺ is released. The energy failure causes an extracellular accumulation of excitatory amino-acids, thus eliciting a hyperstimulation of the NMDA receptors. These receptors are hyperactivated as a result of the deterioration in the control systems with, especially, the blockade of the NMDA receptor by Mg⁺⁺. As a consequence, there is a massive entry of Ca⁺⁺ into the cell, inducing a series of enzymatic reactions involving phospholipases, proteases and endonucleases. Reperfusion will cause toxic lesions by producing free radicals, due to the action of arachidonic acid, xanthine oxidase and nitric oxide. The decrease in cell energetic supplies, as well as the overactivation of enzymes and the production of free radicals, result in cell death.     

Hypothermie modérée et protection cérébrale

To define the part played by mild-to-moderate hypothermia in neuroprotection, it is necessary to take into account the thermoregulatory responses that occur in the normal human as the change in central temperature exceeds 0.2 °C. The mechanisms induced by cold are cutaneous vasoconstriction and shivering. They must be suppressed before starting controlled hypothermia. In these conditions, controlled moderate hypothermia between 32 and 35 °C dœs not seem to have deleterious side-effects, especially on coagulation. Caution is needed with the analysis of the numerous papers reporting experiments concerning the effects of moderate hypothermia in animals with induced cerebral ischaemia because of significant differences in the study designs. These differences concern mainly the time of onset of hypothermia, viz before or after ischaemia, the fact that the ischaemia is either global or focal, that it is caused by vascular occlusion posttraumatic or initiated by hypo or hyperglycemia. Some differences are also existing in the criteria used to appreciate the neuronal damage, as well as in the level of temperature and the site where it is measured. The mechanism of neuroprotectionfrom moderate hypothermia seems to be not only a decrease in cerebral metabolism, but also involves a specific action on some intra-cellular events such as the blocking of the release of glutamate and of lipid peroxydation in brain tissue. An indirect proof of the neuroprotective effect of moderate hypothermia is the increase in the neuronal damage induced by moderate hyperthermia. It is conceivable that moderate hypothermia could exert a better neuroprotective effect than the drugs having this reputation, such as barbiturates, isoflurane and propofol. The possible induction of hypothermia into experiments concerning barbiturate or isoflurane protection could even explain the protection observed, as this has been proven for anti NMDA, MK-801. The few clinical studies already published do not show obvious differences allowing to recommend moderate hypothermia as a standard technique among the therapeutic modalities used for cerebral protection for intracerebral vascular surgery or cerebral resuscitation after severe head trauma. However, the experimental results are strong enough to justify futur controlled clinical studies. The prevention of brain hyperthermia may also emerge as a major objective of resuscitative intervention.     

Le retour veineux sanguin cérébral

It is generally assumed that the jugular veins are the only significant path for cerebral venous drainage. Little attention has been given to the possible role of other venous paths for the cerebral venous outflow. In fact, the meningorachidian venous plexus acts as the major outflow tract of cerebral circulation in the upright position. This phenomenon is linked with postural variations in cerebrospinal fluid pressure. It is difficult to assess the significance of this posterior venous plexus under physiopathologic conditions, which probably depends on the extent of the anastomoses between the two systems.     

Protection cérébrale médicamenteuse : agents spécifiques

Dysfunctional sodium influx is the first step in the ischaemic cascade. It has been recently demonstrated that reducing ionic flux through voltage-gated Na channels shortens the NMDA receptor activity of cultured hippocampal slices in which oxidative phosphorylation and glycolysis have been blocked. The implication of this finding is that blocking initial events in the ischaemic cascade, events which do not directly cause neuronal damage, will reduce the damage done by downstream events. It also seems intuitively reasonable to suppose that truncating initial steps of the ischaemic cascade, as distinct from blocking glutamate receptors and scavening free radicals, will reduce the probability of interferring with endogenous mechanisms of repair. Clinically useful, substantive, prophylactic, pharmacological cerebral protection will come from drugs that work upstream. And for pharmacological protection that can only be initiated subsequent to an ischaemic event, the more we learn about endogenous repair, or genetic pharmacology, the closer we will come to maximizing the benefits and minimizing the costs of downstream intervention.     

Anesthésie pour chirurgie vasculaire cérébrale anévrismale

The two major neurological complications of subarachnoid haemorrhage (SAH) due to an intracranial aneurysm are rebleeding and delayed cerebral ischaemia related to cerebral vasospasm. The best way to prevent rebleeding is early surgery. Even when surgery is performed within the first 72 hours posthaemorrhage, the risk of cerebral ischaemia due to vasospasm is high. Conventional medical treatment of cerebral vasospasm includes haemodilution, hypervolaemia and increase of arterial blood pressure. Haemodilution is of limited value as the patients suffering from SAH have usually a low haematocrit. The effectiveness of hypervolaemia is controversial and it may worsen cerebral and pulmonary oedema. Systemic hypertension is an effective therapy of vasospasm, but which can only be used once the aneurysm is controlled. Nimodipine and nicardipine, two calcium antagonists, have a beneficial effect on neurologic outcome following SAH. Today, it is still debated whether the beneficial effect of nimodipine results from the vascular effect of the drug or from a direct cerebral cytoprotective mechanism. Early surgery implies that surgeons operate on brains in acute inflammatory state. Thus, it is mandatory to use peroperative techniques improving cerebral exposure. These techniques include infusion of mannitol, lumbar cerebrospinal fluid (CSF) drainage, administration of anaesthetic agents known to decrease cerebral blood flow (CBF) and hypocapnia. Usually, the effect of CSF drainage is very effective and sufficient by itself. The second objective in the peroperative period is to avoid ischaemia. In areas with decreased flow distal to vasospasm, autoregulation is impaired and CBF is directly dependent on cerebral perfusion pressure. Furthemore, the safe practice of transient clipping of vessels supplying the aneurysm has dramatically reduced the indications of controlled hypotension. During temporary clipping, some authors recommend a pharmacological brain protection using barbiturates, etomidate or propofol, but this practice has not been validated by randomized studies. However, it is generally agreed that the arterial pressure should be increased during temporary clipping to improve collateral blood flow and to maintain it after the aneurysm has been secured. To conclude, together with lumbar CSF drainage and transient clipping, the anaesthetic management of the patients should include : maintenance of the arterial blood pressure close to its preoperative level, maintenance of Paco₂ between 30 and 35 mmHg and of normovolaemia through replacement of fluid and blood losses. After completion of surgery, recovery from anaesthesia should be rapid to allow fast diagnosis of neurological complications. The monitoring of the status of consciousness is the key of the diagnosis of early postoperative complications.     

Risques peropératoires lors de chirurgie cérébrale anévrismale

The perioperative complications associated with cerebral aneurysm surgery require a specific anaesthetic management. Four major perioperative accidents are discussed in this review. The anaesthetic and surgical management in case of rebleeding subsequent to the re-rupture of the aneurysm is mainly prophylactic. It includes haemodynamic stability assur-ance, maintenance of mean arterial pressure (MAP) between 80–90 mmHg during stimulation of the patient such as endo-tracheal intubation, application of the skull-pin head-holder, incision, and craniotomy. The aneurysmal transmural pressure should be adequately maintained by avoiding an aggressive decrease of intracranial pressure. Once the skull is open, the brain must be kept slack in order to decrease pressure under the retractors and avoid the risks of stretching and tearing of the adjacent vessels. If, despite these precautions, the aneurysm ruptures again. MAP should be decreased to 60 mmHg and the brain rendered more slack, in order to allow direct clipping of the aneurysm, or temporary clipping of the adjacent vessels. The optimal agents in this situation are isoflurane (which decreases CMRO₂), intravenous anaesthetic agents (inspite their negative inotropic effect, they may potentially protect the brain) and sodium nitroprusside. Vasospasm occurs usually between the 3rd and the 7th day after subarachnoid haemorrhage. It may be seen peroperatively. The optimal treatment, as well as prophylaxis, is moderate controlled hypertension (MAP > 100 mmHg), associated with hypervolaemia and haemodilution, the so-called triple H therapy, with strict control of the filling pressures. Other beneficial therapies are calcium antagonists (nimodipine and nicardipine), the removal of the blood accumulated around the brain and in the cisternae, and possibly local administration of papaverine. Abrupt MAP increases are controlled in order to maintain adequate aneurysmal transmural pressure. Beta-blockers, local anaesthetics administered locally or intravenously, a carefully titrated level of anaesthesia, a maintained volaemia play a protective role. Cerebral oedema is sometimes already present at the opening of the skull or may arise later, due to a high pressure under the retractors, to the surgical manipulations of the brain or to brain ischaemia subsequent to temporary clipping. Its treatment is aggressive, with intravenous agents, mannitol, deep hypocapnia and/or lumbar drainage. Prophylaxis, according to the “brain homeostasis concept”, is the preferred method to avoid these four peroperative accidents. It includes normal blood volume, normoglycaemia, moderate hypocapnia, normotension, soft manipulation of the brain and optimal brain relaxation.     

Les perspectives thérapeutiques pharmacologiques du vasospasme cérébral

New therapies of cerebral vasospasm aim to prevent the effects of subarachnoid haemorrhage. These effects result in red blood cell haemolysis and release of oxyhaemoglobin, free radicals formation and lipid peroxidations, imbalance in endothelial modulation of vasomotor tone and activation of the complement system. Low doses of fibrinolytic agents administered intrathecally accelerate the fibrinolysis of the clot and reduce the oxyhaemoglobin release. The tissue-type plasminogen activator has proven to be effective in preventing vasospasm, but the modalities of this therapy remain to be defined. Free radical reactions may be inhibited by free radical scavengers and inhibitors of lipid peroxidations. Tirilazad is a potent inhibitor of lipid peroxidations, which improves the patients' outcome and has gone to Phase III human trials. Superoxide dismutase and tropolone derivatives are currently evaluated in animal models. Vasomotor tone can be modified in experimental models either by blocking endothelin receptors (BQ-123), or by facilitating the release and enhancing the effect of nitric oxide using protein kinase C inhibitors, drugs that increase intracellular calcium (cyclopiazonic acid, LP-805) and free radicals scavengers (superoxide dismutase). These possibilities are being investigated. Finally, preliminary studies have demonstrated the efficacy of FUT-175, an inhibitor of the complement system, in the prevention of vasospasm. In the next years, these new therapies have to be validated by prospective and randomized clinical trials to propose guidelines for the management of patients at risk of cerebral vasospasm after aneurysmal rupture.     

Effets du desflurane sur les vélocités sanguines cérébrales et la réactivité cérébrovasculaire au CO2 chez l'enfant

ObjectiveTo assess in children with a transcranial Doppler the effect on cerebral blood flow velocities of desflurane, whose cerebral vasodilator effects have been studied in animals and in adults with intracranial lesions.Study designProspective clinical study.PatientsTen healthy children, mean age: 3.4 yr, ASA physical class 1, undergoing minor urologie surgery, were included in this study.MethodInduction was obtained with atropine 10 μg·kg⁻¹, fentanyl 3 μg·kg⁻¹ and propofol 3 mg·kg⁻¹. Endotracheal intubation was facilitated by atracurium 0.3mg·kg⁻¹. Mechanical ventilation, with a 50% air/oxygen mixture was adjusted to achieve an end-tidal CO₂ (PETCO₂) level of 38 ± 2 mmHg. Monitoring included measurement of mean arterial blood pressure (MAP), heart rate, PETCO₂, SpO₂ and end-tidal desflurane concentrations (FETDes). Mean blood flow velocities (Vmean) were measured in the middle cerebral artery using a bi-directional 2 MHz TCD system (EME - TC 2000 S). A first TCD measurement followed intubation (11). Thereafter, desflurane was adjusted to 1 MAC. Six other TCDs were recorded each minute until FETDes reached the inspired fraction (T2-T7). Thereafter, CO₂ reactivity was assessed with a hypocapnia test, induced by hyperventilation. Measures were done at T8 (PETCO₂: 33 ± 1 mmHg), T9 (PETCO₂: 29 ± 1 mmHg), and T10 (initial PETCO₂: 38 ± 1 mmHg). All these measurements were made before starting surgery. Analysis of variance (ANOVA) was used to analyse the data (P < 0.05 was considered as significant).ResultsThe Vmean and heart rate increased significantly with increasing concentrations of desflurane (Vmean from 68 ± 27 to 106 ± 30 cm·s⁻¹ and heart rate from 109 ± 17 to 136 ± 15 b·min⁻¹ between T1 and T7). During hypocapnia, Vmean decreased to 68 ± 23 cm·s⁻¹ at T9, and returned to normal values with PETCO₂ at 38 mmHg at T10. SpO₂ remained unchanged. Mean arterial pressure was stable from T1 to T7, but decreased significantly at T9 and T10.ConclusionDesflurane elicits a dose-dependent increase in cerebral blood flow velocities and heart rate, but does not change mean arterial pressure, suggesting that its cerebrovascular action is independent of its systemic vascular action. CO₂ reactivity is maintained at one MAC. The results in children are similar to those seen in adults.     

Hypertension artérielle contrôlée et protection cérébrale

Among the techniques of cerebral protection, the use of controlled arterial hypertension is based on the following arguments : 1) Cerebral ischaemia is the final common pathway of any insult to the brain, particularly through secondary lesions. Causes of secondary cerebral lesions include pressure under the brain retractors, temporary clipping, arterial hypotension, hypoxaemia, anaemia and hypercapnia. 2) In the brain, the critical lower value for cerebral blood flow is around 25 mL · 100 g⁻¹ · min⁻¹, under which two types of ischaemic areas can be defined : the penlucida type where cerebral function is abolished, without permanent cerebral lesion and the penumbra type where cerebral tissue recovers only if flow is rapidly restored. In the latter case the duration of ischaemia is very important. 3) Cerebral blood flow is maintained stable within a large range of variations of mean arterial pressure through the autoregulation mechanisms, which is based on vasomotricity of the cerebral circulation, which implies major variations in cerebral blood volume. However, autoregulation needs several dozens of seconds to be achieved. Therefore, sudden variations in mean arterial pressure are associated with short lasting but major variations in cerebral blood volume. 4) In case of increased intracranial pressure, a decrease in cerebral perfusion pressure causes cerebral vasodilation through the autoregulation mechanism, with an increase in cerebral blood volume which will, in turn, increase intracranial pressure and thus decrease cerebral perfusion pressure, and so on. This is the vasodilatory cascade. The therapeutical increase in mean arterial pressure will correct this phenomenon and decrease intracranial pressure. This is called the vasoconstrictive cascade. 5) In case of vascular occlusion by vasospasm, extrinsic compression or during temporary clipping, cerebral protection may be based on the collateral vessels near the ischaemic area and also on vascular anastomoses inside the circle of Willis. Following Poiseuille's law, as vasodilation is already maximal distally to the stenosis, the major factor of vascular resistance is no longer the radius of the vessel, but its length. Accordingly, the increase in perfusion pressure will improve the local flow and participate in prevention or treatment of an ischaemic event. Indeed, the increase, although modest, of the local flow may be sufficient to switch from an ischaemia of penumbra type to a penlucida type. Finally, controlled arterial hypertension 1) implies to achieve the optimal cerebral perfusion pressure in order to create the vasoconstrictive cascade under cover of intracranial pressure monitoring and 2) helps to decrease the ischaemic risk secondary to vasospasm, for example by achieving a mean arterial pressure between 70 and 100 mmHg before clipping and between 100 and 120 mmHg after clipping. To obtain this level of pressure, phenylephrine, noradrenaline and dopamine are the agents of choice, as they are free of harmful effects on the cerebral circulation.     

Lambeaux osseux de revascularisation céphalique

Summary The authors have treated avascular necrosis of the femoral head by pedicle bone graft for 10 years. The necrotic tissue is excised and replaced by carcellous bone graft. We use an iliac crest graft vascularised by the deep circumflex ilias pedicle. This cloner site gives good carcellous bone and avoids a micro-anastomoses. The hip is approached via an extended Hueter incision without dislocation. 18 cases (16 patients) were followed up for an average of 4 years. There were 6 good results, 3 fair, 6 bad and 2 complete failors requiring revision to arthroplasty. In these young patients two thirds returned to work. These reults are disappointing but this technique is woth considering in view of the limited therapeutic options in this condition.

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Lambeaux osseux de revascularisation céphalique

Résumé Le traitement des nécroses de la tête fémorale par greffe pédiculée a été proposé depuis près de 10 ans. Il consiste en une excision du tissu nécrosé et en son remplacement par une greffe d' os spongieux. Nous utilisons un greffon iliaque vascularisé par le pédicule circonflexe iliaque profond. L'avantage du site de prélèvement est double : le greffon est riche en os spongieux et sa proximité permet d'éviter une micro-anastomose. L'abord de la hanche se fait par une voie de Hueter élargie sans luxation de la hanche. Par une arthrotomie antérieure, on réalise une fenêtre dans le col qui permet d'exciser la nécrose et de réaliser la greffe. Notre série comporte 16 cas dont 2 bilatéraux. L'âge moyen des patients est de 36 ans. Il s'agit de nécrose stade II ou III. Le recul moyen est de 4 ans. Nous avons obtenu 6 bons et très bons résultats, 3 résultats passables, 6 résultats médiocres et mauvais, 2 échecs qui ont dû être repris par une arthroplastie. S'agissant de patients jeunes, deux tiers des opérés ont repris une activité professionnelle régulière. Les résultats obtenus sont assez décevants. Cependant, cette technique mérite d'être discutée en raison des possibilités thérapeutiques limitées dans cette affection.

     

Anesthésie pour cœliochirurgie en pédiatrie

The increasing use of laparoscopic surgery in children is associated with the enlargement of the spectrum of indications to appendicectomy, extramucosal pylorotomy and cure of œsophageal reflux. It is also linked with new problems, mainly due to physiologic modifications elicited by pneumoperitoneum and patient's posture. Although sufficient data are not yet available, the respiratory and cardiovascular modifications are probably similar to those occurring in adults, at least in children more than 4-month-old, as long as the intra-abdominal pressure remains under 15 mmHg. The use of higher intra-abdominal pressures has not been reported in children. In this case, the cardiovascular changes consist mainly in an increase in arterial pressure. In some children, non specific decreases in heart rate and in blood pressure can be observed. The latter can be elicited by a surgical complication, hypovolaemia, head-elevated position or deep anaesthesia. In the newborn and infant under 6 months, intra-abdominal pressures of 15 mmHg or more carry a risk of low cardiac output due to a decrease in contractility and compliance of the left ventricle. In this group of age it is therefore recommended to establish a pressure not higher than 6 mmHg. Moreover, in these very young children, the risk for reopening of the right-left shunts can result in heart insufficiency and systemic gas embolism. Peroperative respiratory changes include an increase in Petco₂ and more rarely a decrease in Sa_o2. The interpretation of the former depends on the site of gas sampling in the anaesthetic system. It is easily controlled by an increased minute ventilation. Various causes, such as bronchial intubation, inhalation of gastric contents or gas embolism, can decrease Sao₂. Contra-indications for laparoscopic surgery include hypovolaemia, heart diseases, increased intracranial pressure and alveolar distension. Therefore newborns are patients at high risk in so far as their foramen ovale or their ductus arteriosus is patent, the pulmonary arterial resistances remain increased and a bronchodysplasia is existing. In some cases a special disease is often associated. As an example recurrent bronchitis or asthma is associated with an œsophageal reflux and a sickle-cell disease in patients with cholelithiasis. These patients require special pre-, per- and postoperative care for prevention of complications. Anaesthesia for laparoscopic surgery does not require a major extension of the usual security regulations. Special attention must be paid to arterial pressure. Therefore end-expiratory concentration of the halogenated anaesthetic agent should not be kept higher than 1.5 times the MAC related to the age during maintenance of anaesthesia. A swift postanaesthetic recovery has to be planned when surgery of the abominal wall is not required at the end of the procedure. Up today the reported complications are related to surgery. However a risk for anaesthetic complications is existing. Their optimal prevention can be obtained by training anaesthetists in centres experienced in paediatric anaesthesia.     

Protection cérébrale : apport des agents anesthésiques intraveineux

The administration of an intravenous anaesthetic agent before experimental cerebral ischaemia in animals improves the functional and histological outcome. Cerebral ischaemia may be global or focal, complete or incomplete. Intravenous anaesthetic agents reduce the cerebral metabolic demand for oxygen (CMRO₂) and abolish electrophysiological activity. This reflects a discontinuation of the functionnal neuronal activity with maintenance of its basic metabolic activity. The oxygen spared by the decrease in consumption, while reducing the functional activity, might be used by the neurons to sustain longer periods of ischaemia. This protective effect is also observed after pretreatment with either lidocaine or volatile agents, but their potentially deleterious vasodilating effect must be considered. Ketamine has recently been shown to antagonize NMDA receptors. The protective effect of barbiturates was experimentally demonstrated more than 30 years ago. They are still used as a reference. They reduce CMRO₂, optimise the ratio between oxygen consumption and oxygen delivery and thus reduce cerebral blood flow and cerebral blood volume, as a result of the decrease of the metabolic demand. This might explain why a protective effect is seen in case of global or focal hypoxia with increased intracranial pressure, while no protection is documented in case of global cerebral ischaemia, such as after cardiac arrest, where EEG is immediately flat and ICP low. However, at doses required to obtain a protective effect, barbiturates induce deleterious side effects such as severe arterial hypotension, which limits their use. Cerebrovascular and cardiac surgery or surgery of the carotids are characterised by potentially ischaemic episodes which can be predicted. This allows proper application of protective measures, such as administration of intravenous anaesthetic agents. Not surprisingly, the only clinical documentation of a protective effect of barbiturates in man was achieved in patients undergoing cardiac surgery under extracorporeal circulation. The concept of pharmacological cerebral protection in case of cerebral ischaemia was investigated with other agents than barbiturates, such as etomidate, gamma-OH and propofol. Anaesthetic agents with their properties of reducing CMRO₂ might be of benefit if applied early, by « buying timein the very first phase of the ischaemic insult.     

Concept d'agression cérébrale secondaire d'origine systémique (ACSOS)

The prevention and treatment of secondary insults to the brain of systemic origin in severely head injured patients remain of utmost importance. Head injury remains the leading cause of traumatic death, being responsible for 50–60 % of fatalities. Head-injured patients not only suffer from the primary injury at the time of trauma, but also from the secondary, largely ischaemic, brain damage that occurs later. Some of these insults are of extracranial origin (or systemic), such as arterial hypotension, hypoxaemia, hypercarbia and anaemia. Their impact on mortality and morbidity is extremely high and requires greater efforts in improving the care of head-injured patients. Systemic insults occur either before the patient reaches hospital or during interfacilty transfer or, in a surprisingly large number of cases, within hospital during emergency procedures, intrahospital transport or during their stay in intensive care units. Hypoxaemia, although quite easy to treat, is still common. This calls for better and earlier protection of the airway, more systematic administration of oxygen to trauma patients and wider use of pulse oximetry. Arterial hypotension has even more dramatic consequences in severe head injury. Recent studies indicate that short episodes of hypotension may induce severe brain ischaemia, that will be present even after complete systemic haemodynamic restoration. The treatment of hypotensive episodes should be immediate and agressive. In some circumstances, restoration of an adequate cerebral perfusion pressure may not be obtained sufficiently rapidly with fluids alone and may require early use of vasopressors. Optimal haemodynamic resuscitation of the trauma patient with haemorrhagic hypotension and severe head injury remains a special challenge. Hypertonic saline, with or without additional colloids, could be beneficial, especially in the prehospital setting. Numerous experimental and a few recent clinical studies are promising but need further clinical investigations.     

Intérêt de l'IRM dans l'embolie graisseuse cérébrale

We report two clinical cases of cerebral fat embolism, thereby demonstrating the value of MRI.     

Agressions cérébrales secondaires d'origine systémique chez les enfants traumatisés craniocérébraux graves

ObjectiveTo assess incidence of secondary brain insults of systemic origin (SBISOs) such as arterial hypotension, hypoxaemia, hypercarbia, and anaemia in severely head injured children; to assess their impact on mortality and morbidity in the short- and long-term.Study designProspective, open study covering a 24month period.PatientsSeventy-one children, under 15 years of age, admitted to a trauma centre for severe brain injury.MethodAnalysis of SBISOs and outcome.ResultsTwenty-five children were admitted with SBI-SOs. The mortality rate was 37%. After hospitalization, 84% of the children with SBISOs vs 46% without SBISOs had severe disability (Glasgow outcome score = 1,2 and 3). After 1 year, 20 out of the 45 children still alive were contacted. One of the four with SBISOs communicated a bad recovery. Fifteen children without SBISOs presented good recovery: GOS = 4–5, paediatric overall performance category (POPC scale) = 1–2.ConclusionHypotension was associated with significant increase in mortality (x 3.6) in children with severe head injury. The consequences were worse when anaemia was associated.