Cases reported "Craniocerebral Trauma"

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1/109. Oral clonidine to control hypertension after head injury.

    clonidine, an alpha2 agonist, was administered through a nasogastric tube for the treatment of hypertension in a head-injury patient with elevated plasma catecholamines. Haemodynamic parameters were stabilized with a reduction in sympathetic nervous activity. The plasma clonidine concentration, measured by radioimmunoassay, rapidly increased following the administration. After cessation of oral administration of clonidine, mean arterial blood pressure gradually increased. So clonidine was again administered orally and good blood pressure control was achieved and no change in consciousness level was observed. Oral clonidine was useful and effective for hypertension in this head injury patient.
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2/109. Heading injury precipitating subdural hematoma associated with arachnoid cysts--two case reports.

    A 14-year-old boy and a 11-year-old boy presented with subdural hematomas as complications of preexisting arachnoid cysts in the middle cranial fossa, manifesting as symptoms of raised intracranial pressure. Both had a history of heading the ball in a soccer game about 7 weeks and 2 days before the symptom occurred. There was no other head trauma, so these cases could be described as "heading injury." arachnoid cysts in the middle cranial fossa are often associated with subdural hematomas. We emphasize that mild trauma such as heading of the ball in a soccer game may cause subdural hematomas in patients with arachnoid cysts.
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3/109. Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury.

    OBJECT: Early impairment of cerebral blood flow in patients with severe head injury correlates with poor brain tissue O2 delivery and may be an important cause of ischemic brain damage. The purpose of this study was to measure cerebral tissue PO2, lactate, and glucose in patients after severe head injury to determine the effect of increased tissue O2 achieved by increasing the fraction of inspired oxygen (FiO2). methods: In addition to standard monitoring of intracranial pressure and cerebral perfusion pressure, the authors continuously measured brain tissue PO2, PCO2, pH, and temperature in 22 patients with severe head injury. microdialysis was performed to analyze lactate and glucose levels. In one cohort of 12 patients, the PaO2 was increased to 441 /-88 mm Hg over a period of 6 hours by raising the FiO2 from 35 /-5% to 100% in two stages. The results were analyzed and compared with the findings in a control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136.4 /-22.1 mm Hg). The mean brain PO2 levels increased in the O2-treated patients up to 359 /-39% of the baseline level during the 6-hour FiO2 enhancement period, whereas the mean dialysate lactate levels decreased by 40% (p < 0.05). During this O2 enhancement period, glucose levels in brain tissue demonstrated a heterogeneous course. None of the monitored parameters in the control cohort showed significant variations during the entire observation period. CONCLUSIONS: Markedly elevated lactate levels in brain tissue are common after severe head injury. Increasing PaO2 to higher levels than necessary to saturate hemoglobin, as performed in the O2-treated cohort, appears to improve the O2 supply in brain tissue. During the early period after severe head injury, increased lactate levels in brain tissue were reduced by increasing FiO2. This may imply a shift to aerobic metabolism.
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4/109. The possible role of hypoxia in the formation of axonal bulbs.

    AIMS: To assess the possible role of hypoxia in the formation of axonal bulbs. methods: Study material comprised sections from 28 brains showing evidence of cerebral hypoxia with no history of head injury, four with a history of head trauma but no evidence of hypoxic change, eight with a history of head trauma and hypoxic change, and four from control brains originally described as "diffuse axonal injury." These were subjected to microwave antigen retrieval and immunohistochemistry using monoclonal antibodies to beta amyloid precursor protein (beta APP), glial fibrillary acid protein (GFAP), and CD68-PGM1. RESULTS: Positive staining for beta APP was seen in all four controls, all four cases of head injury only, seven of eight cases of head injury and hypoxic changes, and 12 of 28 cases of hypoxia without history of head injury; 22 of 25 cases who had been ventilated showed positive staining. The majority of cases showed evidence of cerebral swelling. CONCLUSIONS: Axonal bulbs staining positively for beta APP may occur in the presence of hypoxia and in the absence of head injury. The role of hypoxia, raised intracranial pressure, oedema, shift effects, and ventilatory support in the formation of axonal bulbs is discussed. The presence of axonal bulbs cannot necessarily be attributed to shearing forces alone.
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5/109. Induced hypertension after head injury.

    The use of induced hypertension in head injury patients is controversial. We present the case of a 19-year-old man admitted with severe head trauma after a road accident and describe the beneficial effects that increasing arterial blood pressure had on the cerebral perfusion pressure, cerebral blood flow and jugular bulb oxygen saturation in this patient.
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6/109. Correlation between jugular bulb oxygen saturation and partial pressure of brain tissue oxygen during CO2 and O2 reactivity tests in severely head-injured patients.

    PURPOSE: To correlate the jugular bulb oxygen saturation (SjvO2) and brain tissue oxygen pressure (PbtO2) during carbon dioxide (CO2) and oxygen (O2) reactivity tests in severely head-injured patients. methods AND RESULTS: In nine patients (7 men, 2 women, age: 26 /- 6.5 years, GCS of 6.5 /- 2.9), a polarographic microcatheter (Clark-type) was inserted into nonlesioned white matter (frontal lobe). PbtO2 and SjvO2 were monitored simultaneously and cerebral vasoreactivity to CO2 and O2 was tested on days three, five and seven after injury. Simultaneous measurements of vasoreactivity by transcranial Doppler (TCD) were undertaken. A total of twenty-one CO2 and O2 reactivity tests were performed. Critical values of PbtO2 (< 15 mm Hg) during induced hyperventilation could be observed four times in two patients. High PbtO2 values up to 80 mm Hg were observed during hyperoxygenation (FiO2 100%). CO2 vasoreactivity by means of PbtO2 was absent in four tests in which measurements by TCD showed intact responses. A stronger correlation between SjvO2 and PbtO2 during the O2 reactivity tests was observed (r = 0.6, p < 0.001), in comparison to values obtained during the CO2 reactivity tests (r = 0.33, p < 0.001). In addition, there was no statistically significant correlation (r = 0.22, p = 0.26) between CO2 reactivity values measured by TCD (4.5 /- 5.7%) and PbtO2 (3 /- 2.8%). CONCLUSIONS: Correlation between SjvO2 and PbtO2 during CO2 reactivity test is low, even if significant differences between normo- and hyperventilation values are present. In comparison to SjvO2, monitoring of PbtO2 might more accurately detect possible focal ischaemic events during rapidly induced hyperventilation in severely head-injured patients. The CO2 vasoreactivity by means of changes in Vm MCA seems to be higher in comparison to changes of PbtO2. These observations lead to the hypothesis that vasoreactivity measured by TCD overestimates the cerebrovascular response to CO2.
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7/109. Fatal secondary increase in serum S-100B protein after severe head injury. Report of three cases.

    The S-100B protein is a small cytosolic protein that is found in astroglial or schwann cells. It is highly specific for brain tissue and is increasingly being investigated as a diagnostic tool to assess the neurological damage after head injury, stroke, subarachnoid hemorrhage, and cardiopulmonary bypass. The authors report on three patients with severe head injury with otherwise normal cerebral perfusion pressure, SaO2, PaCO2, and controlled intracranial pressure (ICP), in whom a secondary excessive increase in serum S-100B was observed. In all cases, the S-100B increase was followed by an increase in ICP. All three patients died within 72 hours after the excessive increase in S-100B. These findings indicate that major secondary brain damage may occur at a cellular level without being identified by current neuromonitoring techniques.
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8/109. Sevoflurane mask anesthesia for urgent tracheostomy in an uncooperative trauma patient with a difficult airway.

    PURPOSE: Proper care of the trauma patient often includes tracheal intubation to insure adequate ventilation and oxygenation, protect the airway from aspiration, and facilitate surgery. airway management can be particularly complex when there are facial bone fractures, head injury and cervical spine instability. CLINICAL FEATURES: A 29-yr-old intoxicated woman suffered a motor vehicle accident. Injuries consisted of multiple abrasions to her head, forehead, and face, right temporal lobe hemorrhage, and complex mandibular fractures with displacement. mouth opening was <10 mm. blood pressure was 106/71 mm Hg, pulse 109, respirations 18, temperature 37.3 degrees C, SpO2 100%. Chest and pelvic radiographs were normal and the there was increased anterior angulation of C4-C5 on the cervical spine film. Drug screen was positive for cocaine and alcohol. The initial plan was to perform awake tracheostomy with local anesthesia. However, the patient was uncooperative despite sedation and infiltration of local anesthesia. Sevoflurane, 1%, inspired in oxygen 100%, was administered via face mask. The concentration of sevoflurane was gradually increased to 4%, and loss of consciousness occurred within one minute. The patient breathed spontaneously and required gentle chin lift and jaw thrust. A cuffed tracheostomy tube was surgically inserted without complication. Blood gas showed pH 7.40, PCO2 35 mm Hg, PO2 396 mm Hg, hematocrit 33.6%. Diagnostic peritoneal lavage was negative. Pulmonary aspiration did not occur. Oxygenation and ventilation were maintained throughout the procedure. CONCLUSION: Continuous mask ventilation with sevoflurane is an appropriate technique when confronted with an uncooperative trauma patient with a difficult airway.
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9/109. Head injury monitoring using cerebral microdialysis and Paratrend multiparameter sensors.

    INTRODUCTION: Following head injury complex pathophysiological changes occur in brain metabolism. The objective of the study was to monitor brain metabolism using the Paratrend multiparameter sensor and microdialysis catheters. patients, MATERIAL AND methods: Following approval by the Local ethics Committee and consent from the relatives, patients with severe head injury were studied using a triple bolt inserted into the frontal region, transmitting an intracranial pressure monitor, microdialysis (10 mm or 30 mm membrane; glucose, lactate, pyruvate, glutamate) catheter and Paratrend multiparameter (oxygen, carbon dioxide, pH and temperature) sensor. A Paratrend sensor was also inserted into the femoral artery for continuous blood gas analysis. RESULTS: 21 patients were studied with cerebral microdialysis for a total of 91 monitoring days (range 19 hours to 12 days). Of these, 14 patients were also studied with cerebral and arterial Paratrend sensors. The mean ( /- 95% confidence intervals) arterial and cerebral oxygen levels were 123 /- 10.9 mmHg and 27.9 /- 5.71 mmHg respectively. The arterial and cerebral carbon dioxide levels were 34.3 /- 2.35 mmHg and 45.3 /- 3.07 mmHg respectively. Episodes of systemic hypoxia and hypotension resulting in falls in cerebral oxygen and rises in cerebral carbon dioxide were rapidly detected by the arterial and cerebral Paratrend sensors. Systemic pyrexia was reflected in the brain with the cerebral Paratrend sensor reading 0.17 degree C (mean) higher than the arterial sensor. Elevations of cerebral glucose were detected, but the overall cerebral glucose was low (mean 1.57 /- 0.53 mM 10 mm membrane; mean 1.95 /- 0.68 mM 30 mm membrane) with periods of undetectable glucose in 6 patients. Lactate concentrations (mean 5.08 /- 0.73 mM 10 mm membrane; mean 8.27 /- 1.31 mM 30 mm membrane) were higher than glucose concentrations in all patients. The lactate/pyruvate ratio was 32.1 /- 5.16 for the 10 mm membrane and 30.6 /- 2.17 for the 30 mm membrane. Glutamate concentrations varied between patients (mean 15.0 /- 10.5 microM 10 mm membrane; mean 28.8 /- 17.8 microM 30 mm membrane). CONCLUSION: The combination of microdialysis catheters and Paratrend sensors enabling the monitoring of substrate delivery and brain metabolism, and the detection of secondary metabolic insults has the potential to assist in the management of head-injured patients.
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10/109. Chronic hydrocephalus presenting with bilateral ptosis after minor head injury: case report.

    OBJECTIVE AND IMPORTANCE: Some patients with hydrocephalus may exhibit various signs of oculomotor dysfunction. However, ptosis has not previously been described in chronic hydrocephalus patients. CLINICAL PRESENTATION: We report a 50-year-old woman who was diagnosed with chronic hydrocephalus based on an evaluation for bilateral ptosis after a minor head injury. She exhibited bilateral ptosis and upward gaze paralysis, but other oculomotor functions were normal. Neuroimages revealed chronic hydrocephalus with no traumatic abnormalities. INTERVENTION: The eyelid dysfunction resolved after placement of a right ventriculoperitoneal shunt with a programmable pressure valve. CONCLUSION: The resolution of eyelid dysfunction by cerebrospinal fluid diversion suggests that chronic hydrocephalus was involved in the development of ptosis after the minor head injury. A mild but sudden cerebrospinal fluid pressure change at the time of minor head injury might induce functional impairment at the level of vulnerable periaqueductal structures, which barely withstood the longstanding ventriculomegaly, resulting in the clinical features observed in our patient.
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