Cerebral arterial air embolism after computed tomography-guided hook-wire localization of a pulmonary nodule: A case report.

RATIONALE: Cranial arterial air embolism is a rare but potentially fatal complication after computed tomography (CT)-guided pulmonary interventions. PATIENT CONCERNS: A 64-year-old man was diagnosed with a pulmonary nodule (diameter: approximately 1 cm) in the right lower lobe. The patient developed convulsions after CT-guided hook-wire localization. DIAGNOSIS: Cranial CT revealed arborizing/linearly distributed gas in the territory of the right middle cerebral artery. INTERVENTIONS: The patient was administered hyperbaric oxygen, antiplatelet aggregation therapy, and dehydration treatment. OUTCOMES: Clinical death occurred 55 hours after air embolism. LESSONS: Systemic air embolism is a serious complication of lung puncture. Clinicians should improve their understanding of this complication and remain vigilant against air embolism.

Atherosclerotic intracranial arterial stenosis: risk factors, diagnosis, and treatment.

Intracranial atherosclerosis is one of the most common causes of stroke worldwide and is associated with a high risk of recurrent stroke. New therapeutic approaches to treat this high-risk disease include dual antiplatelet treatment, intensive management of risk factors, and endovascular therapy. Early data from randomised trials indicate that aggressive medical therapy is better than stenting for prevention of recurrent stroke in high-risk patients with atherosclerotic stenosis of a major intracranial artery. Nevertheless, there are subgroups of patients who remain at high risk of stroke despite aggressive medical therapy. Further research is needed to identify these high-risk subgroups and to develop more effective treatments. Non-invasive vascular imaging methods that could be used to identify high-risk patients include fractional flow on magnetic resonance angiography (MRA), quantitative MRA, and high-resolution MRI of the atherosclerotic plaque. Alternative therapies to consider for future clinical trials include angioplasty alone, indirect surgical bypass procedures, ischaemic preconditioning, and new anticoagulants (direct thrombin or Xa inhibitors).

Factors associated with favorable response to hyperbaric oxygen therapy among patients presenting with iatrogenic cerebral arterial gas embolism.

BACKGROUND: Iatrogenic cerebral arterial gas embolism (CAGE) is an uncommon but potentially a fatal condition. Hyperbaric oxygen (HBO2) therapy is the only definitive treatment for patients with CAGE presenting with acute neurologic deficits. METHODS: We reviewed medical records and neuroimaging of consecutive CAGE patients treated with HBO2 at a state referral hyperbaric facility over a 22-year period. We analyzed the effect of demographics, source of intra-arterial gas, signs and symptoms, results of imaging studies, time between event and HBO2 treatment, and response to HBO2 treatment in 36 consecutive patients. Favorable outcome was defined by complete resolution or improvement of CAGE signs and symptoms at 24 h after HBO2 treatment. Unfavorable outcome was defined by unchanged or worsened neurologic signs and symptoms or in hospital death. RESULTS: A total of 26 (72%) of the 36 patients had favorable outcome. Patients with favorable outcome were younger compared to those with unfavorable outcome (mean age [years, SD] 44.7 ± 17.8 vs. 58.1 ± 24.1, p = 0.08). Cardiopulmonary symptoms were significantly more common in CAGE related to venous source of gas compared to arterial source (p = 0.024) but did not influence the rate of favorable outcomes. Adjusted multivariate analysis demonstrated that time from event to HBO2 ≤ 6 h (positively) and the presence of infarct/edema on head computerized tomography (CT)/magnetic resonance imaging (MRI) before HBO2 (negatively) were independent predictors of favorable outcome at 24 h after HBO2 treatment [odds ratio (OR) 9.08 confidence interval (CI) (1.13-72.69), p = 0.0376, and (OR) 0.034 (CI) (0.002-0.58), p = 0.0200, respectively]. Two of the 36 patients were treated with thrombolytics because of acute focal deficits and suspected ischemia-one with intravenous and the second with intra-arterial thrombolysis. The latter patient developed fatal intracerebral hemorrhage. CONCLUSIONS: A high proportion of CAGE patients treated with HBO2 had favorable outcomes. Time-to-HBO2 ≤ 6 h increased the odds of favorable outcome, whereas the presence of infarct/edema on CT/MRI scan before HBO2 reduced the odds of a favorable outcome. Timely diagnosis and differentiation from thrombo-embolic ischemic events appears to be an important determinant of successful HBO2 treatment.

Design of the stenting and aggressive medical management for preventing recurrent stroke in intracranial stenosis trial.

BACKGROUND: Patients with recent transient ischemic attack (TIA) or stroke caused by 70% to 99% stenosis of a major intracranial artery are at high risk of recurrent stroke on usual medical management, suggesting the need for alternative therapies for this disease. METHODS: The Stenting and Aggressive Medical Management for Preventing Recurrent stroke in Intracranial Stenosis trial is an ongoing, randomized, multicenter, 2-arm trial that will determine whether intracranial angioplasty and stenting adds benefit to aggressive medical management alone for preventing the primary endpoint (any stroke or death within 30 days after enrollment or after any revascularization procedure of the qualifying lesion during follow-up, or stroke in the territory of the symptomatic intracranial artery beyond 30 days) during a mean follow-up of 2 years in patients with recent TIA or stroke caused by 70% to 99% stenosis of a major intracranial artery. Aggressive medical management in both arms consists of aspirin 325 mg per day, clopidogrel 75 mg per day for 90 days after enrollment, intensive risk factor management primarily targeting systolic blood pressure <140 mm Hg (<130 mm Hg in diabetics) and low density cholesterol <70 mg/dL, and a lifestyle modification program. The sample size required to detect a 35% reduction in the rate of the primary endpoint from angioplasty and stenting based on the log-rank test with an alpha of 0.05, 80% power, and adjusting for a 2% loss to follow-up and 5% crossover from the medical to the stenting arm is 382 patients per group. RESULTS: Enrollment began in November 2008 and 451 patients have been enrolled as of March 31, 2011. CONCLUSIONS: This is the first randomized stroke prevention trial to compare angioplasty and stenting with medical therapy in patients with intracranial arterial stenosis and to incorporate intensive management of multiple risk factors and a lifestyle modification program in the study design. Hopefully, the results of the trial will lead to more effective therapy for this high-risk disease.

[Study on optimum stimulation parameter for Shuigou (GV 26) in Xingnao Kaiqiao needling method].

OBJECTIVE: to investigate the influence of acupuncture parameter on acupuncture effect and to probe the optimum stimulation parameter for Shuigou (GV 26) in Xingnao Kaiqiao needling method. METHODS: The rat model of middle cerebral artery obstruction (MCAO) was replicated and "Shuigou" (GV 26) was stimulated by 9 acupuncture parameters combined by two factors at 3 levels, i. e. frequency 1, 2, 3 times/second, and needling duration 5 s, 60 s, 180 s. The effects of acupuncture at "Shuigou" (GV 26) with the 9 different acupuncture parameters on cerebral blood flow (CBF) in the MCAO rat were investigated by orthogonal test, factor analysis and one-way ANOVA. RESULTS: Acupuncture effect was influenced by acupuncture frequency, acupuncture duration and their combination. Among them, the acupuncture duration was the most important factor. The best acupuncture effect could be attained by using as long acupuncture duration as possibly with the fastest acupuncture frequency. CONCLUSION: In the Xingnao Kaiqiao needling method, acupuncture at "Shuigou" (GV 26) with fastest frequency and enough long duration can get the best acupuncture effect, which are the optimum stimulation parameters for "Shuigou" (GV 26).

Reversible MR angiographic findings in a patient with autoimmune Graves disease.

A 45-year-old woman presented with subacute encephalopathy due to autoimmune Graves disease. MR angiography (MRA) demonstrated stenosis of the major intracerebral arteries. After high-dose methylprednisolone therapy and plasmapheresis, her neurologic status improved dramatically, and the MRA findings resolved after 3 months. The angiographic findings in Graves disease that resemble those in Moyamoya disease are temporary.

Pulmonary barotrauma-induced cerebral arterial gas embolism with spontaneous recovery: commentary on the rationale for therapeutic compression.

Pulmonary barotrauma-induced cerebral arterial gas embolism (CAGE) continues to complicate compressed gas diving activities. Inadequate lung ventilation secondary to inadvertent breath holding or rapid buoyant ascent can quickly generate a critical state of lung over-pressure. Pulmonary over-pressurization may also occur as a consequence of acute and chronic pulmonary pathologies. Resulting barotrauma frequently causes structural failure within the terminal distal airway. Respiratory gases are then free to embolize the systemic circulation via the pulmonary vasculature and the left heart. The brain is a common target organ. Bubbles that enter the cerebral arteries coalesce to form columns of gas as the vascular network narrows. Small amounts of gas frequently pass directly through the cerebral circulation without occlusion. Larger columns of gas occlude regional brain blood flow, either transiently or permanently, producing a stroke-like clinical picture. In cases of spontaneous redistribution, a period of apparent recovery is frequently followed by relapse. The etiology of relapse appears to be multifactoral, and chiefly the consequence of a failure of reperfusion. Prediction of who will relapse is not possible, and any such relapse is of ominous prognostic significance. It is advisable, therefore, that CAGE patients who undergo spontaneous recovery be promptly recompressed while breathing oxygen. Therapeutic compression will serve to antagonize leukocyte-mediated ischemia-reperfusion injury; limit potential re-embolization of brain blood flow, secondary to further leakage from the original pulmonary lesion or recirculation of gas from the initial occlusive event; protect against embolic injury to other organs; aid in the resolution of component cerebral edema; reduce the likelihood of late brain infarction reported in patients who have undergone spontaneous clinical recovery; and prophylax against decompression sickness in high gas loading dives that precede accelerated ascents and omitted stage decompression.

Recommendations for hyperbaric oxygen therapy of cerebral air embolism based on a mathematical model of bubble absorption.

Transcranial doppler studies show that microscopic cerebral artery air emboli (CAAE) are present in virtually all patients undergoing cardiac surgery. Massive cerebral arterial air embolism is rare. If it occurs, hyperbaric oxygen therapy (HBO) is recommended as soon as surgery is completed. We used a mathematical model to predict the absorption time of CAAE, assuming that the volumes of clinically relevant CAAE vary from 10(-7) to at least 10(-1) mL. Absorption times are predicted to be at least 40 h during oxygenation using breathing gas mixtures of fraction of inspired oxygen approximately equal to 40%. When CAAE are large enough to be detected by computerized tomography, absorption times are calculated to be at least 15 h. Decreases in cerebral blood flow caused by the CAAE would make the absorption even slower. Our analysis suggests that if the diagnosis of massive CAAE is suspected, computerized tomography should be performed, and consideration should be given to HBO therapy if the CAAE are large enough to be visualized, even if patient transfer to a HBO facility will require several hours.

[Intravascular volume expansion and intravenous nimodipine in the treatment of cerebral vasospasm after surgical treatment of intracranial aneurysm]. / Remplissage vasculaire et nimodipine intraveineuse dans le traitement du vasospasme cérébral après cure chirurgicale d'un anévrysme intracranien.

The advantage of calcium antagonist on cerebral arterial spasm during the peri-operative period has been recently demonstrated. However, the role of volemia and cardiac output in the pathogenesis of arterial spasm seems predominant. The basal hemodynamic profile of 17 patients operated for an intracranial aneurysm was investigated. The hemodynamic and neurological modifications induced by treatment with nimodipine, modification of blood volume and the use of inotropic drug was subsequently analysed. In 8 patients there was a clearcut hypovolemia with diminished cardiac index whereas in 9 other patients there were low filling pressures with an unmodified cardiac index. As early as the 48th hour of treatment, there was an improvement of Hunt and Hess score in 12 patients whereas in 5 others the score remained unchanged. Two death occurred due to the extension of secondary ischemic lesions. This study seems to confirm the aggravating role of hypovolemia in the occurrence of vasospasm and the neurological improvement due to the association of a calcium antagonist, restoration of blood volume with or without a vasoconstrictor.

Cerebral arterial air embolism: I. Is there benefit in beginning HBO treatment at 6 bar?

A method for studying treatment of cerebral arterial gas embolism in dogs is described. The model produces severe cortical dysfunction and cerebral blood flow deficits. The efficacy of treatment was assessed using median nerve somatosensory cortical evoked potentials (CEP), [14C]iodoantipyrene autoradiographic cerebral blood flow studies, brain water content, and various physiological parameters. A direct comparison of modified U.S. Navy Treatment Tables 6 and 6A is reported. Complete recovery of CEP was not seen after 90 min of treatment. The maximum rate of CEP recovery occurred in the first 15 min of treatment. Recovery continued out to 60 min. Thereafter, some dogs on treatment 6A showed signs of deterioration. The cerebral blood flow studies were the same in both groups and showed no sign of pathologically low levels of flow. It appeared that there was no advantage in preceding 2.8-bar (60-ft) oxygen treatments with compression to 6 bar (165 ft) on air for the treatment of arterial air embolism in this model.

Cerebral arterial air embolism: II. Effect of pressure and time on cortical evoked potential recovery.

In a dog model of cerebral arterial gas embolism we studied the relative merits of several different treatments: air breathing at 2.8, 6, 8, and 10 bar (60, 165, 230, and 300 ft), and oxygen breathing at 2.8 bar. The study was confined to the recovery of cortical evoked potentials (CEP) while at pressure. It was confirmed that this was a very severe model; few dogs achieved full recovery and three failed to show any recovery. Injecting 0.4 ml of air into the right internal carotid artery was seen to be as effective in suppressing function in the left hemisphere as in the right. The level of recovery with compression treatment as a percentage of control was directly related to the level to which CEP was suppressed. No other physiological correlates were found with either the degree of CEP suppression or the degree of recovery. Nor was any improvement observed in the rate or maximum amount of recovery at any time out to 20 min as a result of pressures greater than 2.8 bar. Overall, no treatment surpassed oxygen at 2.8 bar.

Cerebral arterial air embolism: III. Cerebral blood flow after decompression from various pressure treatments.

The effect of various combinations of time between 2 and 20 min and between pressures of 2.8 and 10 bar (60 and 300 ft) breathing air or oxygen at 2.8 bar (60 ft), on the continued recovery of cortical evoked potentials (CEP), cerebral blood flow (CBF), and water content of the brain were studied in the dog cerebral arterial air embolism model. It was found that the compression-decompression cycle alone resulted in a rise in cerebrospinal fluid pressure sustained for at least 20 min. The CBF study at 30 min showed an increased flow in dived, nonembolized animals. Water content of the brain was also significantly increased in these animals. The data suggest that the clearance of air is probably independent of pressure once past a threshold of 2.8 bar and is certainly hastened by oxygen. A time of around 8 min is probably required to clear the embolism. The evidence of gas bubble redistribution with recurrence and development of new sites of vascular obstruction in dogs exposed to significant inert gas uptake, however, suggests that a second problem of the clearance of recirculating gas exists. An incidental observation suggests that recently dived dogs may have been more prone to secondary deterioration. The results of these studies again suggest that there may be advantages to confining the treatment of arterial gas embolism to 2.8 bar breathing oxygen.

Cerebral arterial air embolism: IV. Failure to recover with treatment, and secondary deterioration.

Cerebral arterial gas embolism was induced in 23 dogs that were then treated using one of six routines: no treatment; air at 2.8 bar (60 ft) for 2 min; air at 10 bar (300 ft) for 5 min; oxygen at 2.8 bar for 10 or 20 min; and air at 6 bar (165 ft) for 10 min. After decompression they were monitored for a total of 90 min after the time of embolization. The dogs then underwent an autoradiographic study of cerebral blood flow (CBF). A number of the air-treated dogs experienced a reduction in cortical evoked potential after decompression. Dogs in all groups, except the untreated group and the dog at 10 bar for 5 min, showed an improved CBF compared with their short-study counterparts. After compression treatment, CBF improved with time. Function in 7 dogs deteriorated to a variable small degree in the air-treated groups, while only 3 dogs in the group on oxygen for 10 min deteriorated by around 10%. The CBF of the oxygen groups was close to the undived control values, and their cerebrospinal fluid (CSF) pressures had returned to control levels. There was a dissociation between improving CBF and deteriorating function. It is evident that secondary deterioration is a random affair and therefore not easily studied. The results of the four-part series are summarized and discussed.

Reversibility of the chronic post-stroke state.

Forty patients with cerebral infarction associated with occlusion of the internal carotid artery (ICA) or the middle cerebral artery (MCA) were treated with hyperbaric oxygenation (HO). EEG analyses were performed regularly in order to assess the course of the cerebral lesion. Patients in an early post-stroke stage (III B) and patients in a chronic post-stroke stage (IV) had the changes in EEG analysis and neurological distributed evenly between these two groups.