[Traumatic brain injury and asymmetry in pupillary size in severe head injury at the initial state: aetiology and value of the mydriasis].
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Biomedical subjects
Publications and source records attributed to F Artru.
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BACKGROUND: There are few published large series on civilian craniocerebral gunshot injuries in children. Traumatic intracranial aneurysms (TICAs) are rare and highly unstable lesions. They represent less than 1% of all aneurysms and can either rupture within minutes after formation or remain quiescent for several weeks or years, manifesting with delayed hemorrhage and neurologic deterioration. CASE HISTORY: We report the case of a 10-year-old girl who was referred for coma after high-velocity craniocerebral gunshot wound and neurological deterioration 7 days after the initial injury. A massive right posterior occipital hematoma caused by the rupture of an unsuspected right posterior cerebral artery TICA was discovered. TICA was treated by coil embolization, with a good neurological recovery at 6-month follow-up. DISCUSSION: We discuss the pathogenesis and the management of TICA in a child after civilian craniocerebral gunshot injuries. CONCLUSIONS: TICAs should be suspected in patients with civilian craniocerebral gunshot injuries, presenting with secondary neurological deterioration, to carry out emergent CT scan and angiographic exploration before contemplating definitive endovascular treatment. Endovascular management may be a prompt safe-to-use technique and a valuable option, especially when surgery is highly risky.
Sitting position during neurosurgery is discussed because the risk of venous air embolism and paradoxical air embolism is increased. Preoperative transoesophageal echocardiography is proposed to screen patients with patent foramen ovale to avoid them for the sitting position. This work reported 2 patients in conflict with this screening. It is discussed the physiological principles governing the paradoxical air embolism and the actual recommended monitoring for this position.
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OBJECTS: Two children were admitted to hospital for treatment of craniocerebral injury with transorbital penetration. METHODS: One child aged 6 years and 6 months had poked a chopstick in his orbit. There was no report of either a palpebral or an ocular wound. He had subsequently developed a meningeal syndrome with a cerebral abscess managed by needle aspiration biopsy and intravenous antibiotics. The other child, aged 4, had fallen onto a metal rod. He presented with a palpebral wound, motor disorders and coma, all due to a frontal intracerebral hematoma. There was an improvement in outcome without complications of an infectious nature or motor sequelae. CONCLUSIONS: Such head injuries are rare. Clinical, radiological and ophthalmological investigations must be performed, including computed tomography (CT) scan or cerebral magnetic resonance imaging (MRI) with antibiotic treatment for suspected microorganisms.
We report the case of a 2-year-old child who sustained a permanent diabetes insipidus following a third ventriculostomy for hydrocephalus from a Dandy-Walker syndrome. Ventriculostomy, used for therapy of non-communicating hydrocephalus, can cause complications such as diabetes insipidus. The latter has rarely been reported and is usually transient. Following ventriculostomy, a close postoperative surveillance is essential, especially in children.
Cerebral internal venous thrombosis are rare and diagnosis is difficult. We report three cases in male adults. Clinical data were headaches, vomiting, dizziness and coma, in relation with an intracranial hypertension, or in a case, cardiocirculatory arrest. Cerebral internal veinous thrombosis was diagnosed by a CT scan and cerebral angiography twenty four hours after the admission in neurosurgical intensive care. CT scan showed hemorrhagic and ischemic lesions of thalami in two cases, diffuse cerebral edema in two patients, early or delayed hydrocephaly in two cases. No patient survived despite intensive treatment including heparinotherapy, ventricular CSF drainage, osmotherapy, dehydration, barbiturate, other antiepileptic drugs and mechanical ventilation. In two cases, general or local illness was found, sickle cell disease or radiotherapy for pineal tumor, and in case 3 clinical signs evoked autoimmune disease, not demonstrated by biological samples.
In 16 head injured patients, the monitoring of brain tissue oxygen pressure (ti-pO2) show 22 episodes of low ti-pO2 (< or = 12 mmHg). Mean episode duration was 16 h. At time of the lowest ti-pO2 value, cerebral perfusion pressure (CPP), was < 60 mmHg in 5 cases, 4 of them with impending brain death. Oxygen saturation values of the jugular venous blood (svjO2) remained in the normal range (55-85 mmHg) in 12 cases and exceeded 85 mmHg in 3 cases, 2 of them with impending brain death. Lactate-oxygen index (LOI) was normal (< 0.08) in 7/10 cases and at very high level (> 0.60) in 3 cases including 2 cases of impending brain death. A first group of low ti-pO2 episodes was clearly related to an insufficient CPP level (n = 13), comprising 4 cases of parallel decrease in CPP and ti-pO2 until brain death, and 9 cases in which ti-pO2 was restored along with a significant increase in CPP (p < 0.001). In 5 patients, low ti-pO2 episodes were due to another cause: vasospasm (2 cases), hypoxemia, anemia and premature interruption of anesthesia. Appropriate treatments were effective in restoring ti-pO2 with no change in CPP. In 4 patients, the cause of low ti-pO2 was not identifiable and episodes resolved spontaneously. The results confirm the critical influence of CPP and ti-pO2. Patients in whom elevation of CPP improved ti-pO2 have normal range CPP during the episode. Optimal CPP should therefore be sometimes higher than recommended. ti-pO2 monitoring appears a good method to define the optimal CPP level in individual patient. The duration of the artefactual period after catheter placement is to clarify.
The main risk involved in severe intracranial hypertension is, the occurrence of cerebral ischaemia, either locally during herniation or globally as a consequence of reduced cerebral perfusion pressure (CPP). Neurological features of ischaemia occur at a late stage. A continuous monitoring of brain function with EEG or evoked potential techniques, while largely used in the operating room have not been so far fully evaluated in the intensive care setting. Therefore, ischaemic criteria based on the registration of haemodynamic or metabolic data are gaining importance in management of increased intracranial pressure (ICP). Transcranial Doppler of middle cerebral arteries allows at any time the detection of a decrease in brain perfusion. An increased pulsatility index has been repeatedly demonstrated to correlate with decreased CPP. From these reports, the lower limit of autoregulation in brain injured patients appears to be much higher (70 mmHg) than previously estimated (40 mmHg). However, therapies with a cerebral vasoconstrictor impact and associated vasospasm are to be considered for a correct interpretation of Doppler data. Moreover, as a reduced cerebral blood flow is not necessarily insufficient to meet metabolic requirements, a routine insight in cerebral oxygenation and lactate production must be available. Continuous monitoring of jugular blood oxyhaemoglobin saturation (SjO2) measures the reserve of oxygen extraction and a decrease in SjO2 below 50% is considered as to indicate an impending cerebral ischaemia. Indeed, critically reduced CPP under a 70 mmHg limit is reflected by venous desaturation episodes. Increased cerebral lactate production, routinely appraisable by serial measurements of [(a-v) lactate], may afford confirmation of an existing ischaemia. ICP and CPP monitoring remains the basis for intensive care surveillance during the phase of intracranial hypertension, with alarming settled at admitted critical values (ICP = 30 mmHg; CPP = 70 mmHg). As ischaemic threshold for cerebral blood flow may be different in patients and in normal experimental animals, the reliability of these critical values of ICP and CPP is uncertain. Therefore, transcranial Doppler, jugular metabolic monitoring and, as recently available, cortical tissue PO2 monitoring are mandatory for early detection and assessment of ischaemia.
Cerebrovascular disorders are frequently associated with sickle cell disease, mainly in homozygous children. We report the case a 25-old-patient with known sickle cell disease who presented with coma inaugurated by manifestations of intracranial hypertension. CT revealed bilateral thalamic infarcts and angiography confirmed the thrombosis of internal cerebral veins. Treatment included heparin and blood transfusion. Severe cerebral oedema resulted in the lethal outcome three days later.
The use of intraparenchymatous ICP sensor is becoming increasingly popular at the expense of the traditional intraventricular catheter method, in spite of the impossibility, with the former technic, to correct a possible zero drift. The decision to initiate or discontinue ICP monitoring is essentially based upon whether suggestive aspects of raised ICP are or not present on CT-scan. The degree of basal cisterns effacement is particularly informative. The same data from successive CT-scans are used to check the validity of the monitoring. Predefining critical levels of ICP and cerebral perfusion pressure (CPP) allows to establish practical guide-lines for treatment. Cerebral ischemia is considered very likely when ICP rises above 30 mmHg. Regarding CPP, the therapeutical goal is to avoid its reduction under the critical level of 60-80 mmHg. As these thresholds vary with the patients age and the type of lesion, a parallel evaluation of cerebral ischemia by other methods is mandatory. Transcranial doppler allows an easy detection of critical reduction of arterial flow. However, in case of flow hypervelocity, interpretation needs measurement of absolute cerebral blood flow values. Cerebral venous oxygen saturation monitoring, at the level of the jugular golf, shows desaturation episodes indicative of cerebral ischemia. Blood sampling for determination of arterial and jugular venous lactate concentrations allows calculation of the lactate oxygen index, a practical correlate of the degree of cerebral ischemia. ICP measurement alone is of limited value to understand the cerebral hemodynamical and metabolical situation in severe brain injury. Preceding the rise of ICP, there exists a compensation phase during which a progressive decrease of intracranial compliance is the important event. Even more earlier, posttraumatic cellular metabolic dysfunctions are to-day objectives for a neurochemical monitoring. Therefore a special technical and human environment has became mandatory to take a real benefit from ICP monitoring.
The authors have reviewed the main effects of anaesthetic agents on sensory evoked potentials (EPs) in the auditory, somatosensory and visual modalities. Knowledge of EP changes induced by anesthetic drugs is important to avoid false alarms when monitoring neural structures at risk during surgery. Intraoperative EP monitoring is all the more efficient as the following points are taken into account: 1) whatever the sensory modality considered, EPs are more attenuated by volatile halogenated agents than by intravenous drugs; 2) the cortical components of EPs are more sensitive to anesthetic drugs than the brainstem components; 3) in each modality, the first component of the "primary cortical complex" is less attenuated by anaesthetic agents than the following cortical waves; 4) continuous administration of anaesthetic agents rather than acute administration (bolus) is preferred during EP monitoring. EPs also represent an objective means to assess the depth of surgical anaesthesia, since they may provide a reliable index of cortical depression. Amplitude changes of middle-latency auditory responses (Pa/Nb) seem to be a good marker for estimating depth of anaesthesia with the aid of EPs.
Through the findings in the literature on the basis of 9 personal cases, we review the indications and value of decompressive hemicraniectomy with plasty of the dura mater in cases of medically uncontrolled and decompensated intracranial hypertension. Seven patients had a pseudo-tumoral brain infarction. Five patients survived and their functional recovery is consistent with an autonomous daily life. Another patient with acute traumatic sub-dural haemorrhage died. The ninth patient had presuppurative encephalitis and recovered with no disability. At the time of surgery, all the patients were comatose with herniation of the mesencephalon (n = 3), uncal transtentorial herniation which was either unilateral (n = 4) or bilateral (n = 2). ICP was between 25 and 60 mmHg before the operation. After flap removal, ICP decreased by 15% and, after opening of the dura, it fell a further 70%. In 6 patients we were able to carry out continued post-operative monitoring of ICP, which stayed below 50% of initial values. Decompressive hemicraniectomy is an effective means of treating ICH caused by carotid cerebrovascular accidents with a high degree of edema, where mortality rises to 70-85% when only medical treatment is administered. No haemorrhagic complications, which can occur during hemispherectomies, were observed during decompression.
A fiberoptic intracranial pressure transducer (Camino) was assessed prospectively in 100 patients. In all, 122 sensors were inserted intraparenchymally at the bedside, without the help of a neurosurgeon. Before the procedure, patients were given 2 to 4 mg of phenoperidine. The scalp was opened over a few millimeters in the frontal paramedian area. A burr holc was made with a 2 mm bit. The dura mater was opened and a hollow screw inserted in the diploë. When the zero of the transducer had been obtained, a 5 cm length was inserted within the screw. The transducer was then about 5 mm deep within cerebral parenchyma. The procedure took an average of about 15 min. An intracerebral haematoma around the transducer occurred five times. One had to be drained surgically. There were no infectious complications. The daily baseline drift was about 0.3 mmHg. The system seemed to be reliable: there was close agreement between the intracranial pressure (ICP), neurological status and CT scan findings. In trauma cases, there was also good correlation between mean ICP and the basal cistern obliteration score, finally, ICP became equivalent to mean arterial blood pressure in all brain dead patients. It is concluded that this system may be used in all cases where ICP requires to be monitored, even when the lateral ventricles are no longer visible, or when craniotomy has been performed. This will most probably result in a more extended use of ICP monitoring in neurosurgical intensive care.
Continuous monitoring of brainstem auditory evoked potentials (BAEPs) was carried out in 57 comatose patients for periods ranging from 5 hours to 13 days. In 53 cases intracranial pressure (ICP) was also simultaneously monitored. The study of relative changes of evoked potentials over time proved more relevant to prognosis than the mere consideration of "statistical normality" of waveforms; thus progressive degradation of the BAEPs was associated with a bad outcome even if the responses remained within normal limits. Contrary to previous reports, a normal BAEP obtained during the second week of coma did not necessarily indicate a good vital outcome; it could, however, do so in cases with a low probability of secondary insults. The simultaneous study of BAEPs and ICP showed that apparently significant (greater than 40 mm Hg) acute rises in ICP were not always followed by BAEP changes. The stability of BAEP's despite "significant" ICP rises was associated in our patients with a high probability of survival, while prolongation of central latency of BAEPs in response to ICP modifications was almost invariably followed by brain death. Continuous monitoring of brainstem responses provided a useful physiological counterpart to physical parameters such as ICP. Serial recording of cortical EPs should be added to BAEP monitoring to permit the early detection of rostrocaudal deterioration.
The authors studied the reliability and tolerance of a new intra-parenchymatous fiberoptic device for intracranial pressure monitoring in 20 neurosurgical children. The system proved to be reliable, and the measures were well correlated with clinical evolution, CT scan lesions, and the abolition of the cerebral perfusion pressure in the case of brain death. There was a minimal shift of the electric 0 after 15 days of monitoring. The tolerance was good and no hemorrhagic, infectious or epileptic complications were observed.
A case of unilateral hydrocephalus due to an abscess in the ipsilateral choroid plexuses, and revealed by intracranial hypertension is reported. Treatment with ceftriaxone, metronidazol and thiophenicol was clinically and radiographically successful, without surgery 3 weeks later. Management and mechanisms are discussed.
Central venous catheterization via the axillary vein was performed in 180 comatose patients with a success rate of 91%. The scarcity of serious nervous (none), thrombotic (6%), hemorrhagic (9.4%), infectious (1.8%), or thoracic (none) complications, the preservation of cerebral venous drainage, a longer distance between puncture site and tracheostomy or intubation tube make this safe and easy procedure perfectly convenient for comatose patients.