Guidelines for the safe provision of anaesthesia in magnetic resonance units 2019: Guidelines from the Association of Anaesthetists and the Neuro Anaesthesia and Critical Care Society of Great Britain and Ireland.

There has been an increase in the number of units providing anaesthesia for magnetic resonance imaging and the strength of magnetic resonance scanners, as well as the number of interventions and operations performed within the magnetic resonance environment. More devices and implants are now magnetic resonance imaging conditional, allowing scans to be undertaken in patients for whom this was previously not possible. There has also been a revision in terminology relating to magnetic resonance safety of devices. These guidelines have been put together by organisations who are involved in the pathways for patients needing magnetic resonance imaging. They reinforce the safety aspects of providing anaesthesia in the magnetic resonance environment, from the multidisciplinary decision making process, the seniority of anaesthetist accompanying the patient, to training in the recognition of hazards of anaesthesia in the magnetic resonance environment. For many anaesthetists this is an unfamiliar site to give anaesthesia, often in a remote site. Hospitals should develop and audit governance procedures to ensure that anaesthetists of all grades are competent to deliver anaesthesia safely in this area.

The longitudinal profile of bilirubin and ferritin in the cerebrospinal fluid following a subarachnoid hemorrhage: diagnostic implications.

BACKGROUND: Cerebrospinal fluid (CSF) spectrophotometry for bilirubin is a highly sensitive test in the diagnostic work up of a suspected subarachnoid hemorrhage (SAH). CASES: We report two cases suffering from an aneurysmal SAH in which extraventricular drainage for acute hydrocephalus was required. Longitudinal analyses of the CSF samples demonstrated that CSF bilirubin was detectable in all cases during the first week, becoming undetectable in one case in the second week. Importantly, CSF ferritin levels rose substantially (>1,000 ng/ml) after 6 days, peaking around 3,000 ng/ml after 2 weeks (normal upper reference range 12 ng/ml). In both cases blood was visible on the initial CT brain scan, disappearing on a later scan. CONCLUSION: CSF ferritin levels may be an important additional laboratory test in the diagnostic work-up of patients with a suspected SAH. CSF ferritin levels may prove particularly helpful in cases with late presentation if the CT brain scan is normal and CSF bilirubin level is undetectable.

Management of subarachnoid haemorrhage in a non-neurosurgical centre.

Subarachnoid haemorrhage is a common neurological emergency, which carries a high morbidity and mortality. It is usually caused by rupture of an intracerebral aneurysm or, less commonly, an arteriovenous malformation. Although most patients present to a non-neurosurgical hospital, they often require urgent neurosurgical or neuroradiological intervention. Whilst awaiting transfer to a neurological centre, active management of the patient must be instituted. This should include confirmation of the diagnosis with CT imaging, lumbar puncture or both, and recognition of the complications of subarachnoid haemorrhage, which include hydrocephalus, further haemorrhage and cerebral vasospasm. Medical management is directed towards maintaining adequate cerebral perfusion pressure whilst avoiding large increases in arterial blood pressure. Nimodipine therapy must be started early in an attempt to prevent cerebral vasospasm. The treatment options available at the neurological centre include surgical treatment or endovascular obliteration of the aneurysm or arteriovenous malformation.

Lactate provocation of panic attacks. II. Biochemical and physiological findings.

Thirty-one of 43 patients with panic disorder or agoraphobia with panic attacks and none of 20 normal controls panicked in response to infusions of sodium lactate. Before receiving lactate, patients showed higher heart rates than controls and also signs of hyperventilation. During lactate infusion, patients who did not panic, nevertheless, developed higher lactate and pyruvate levels and greater ionized calcium and pH changes than controls. Lactate-induced panic attacks were regularly accompanied by biological changes consistent with hyperventilation and central noradrenergic activation and irregularly by elevation of plasma norepinephrine and cortisol levels. Panic attacks were not associated with changes in epinephrine or calcium levels or pH. Baseline arousal increased the likelihood of panic during lactate infusion. It is hypothesized that lactate-induced panic primarily involves central noradrenergic discharge with inconsistent peripheral manifestations.

Lactate provocation of panic attacks. I. Clinical and behavioral findings.

To assess the pharmacologic and phenomenologic comparability of lactate-induced and naturally occurring panic attacks, patients meeting DSM-III criteria for panic disorder or agoraphobia with panic attacks were infused with 0.5M racemic sodium lactate before and after successful drug treatment. Lactate-induced and naturally occurring panic attacks were symptomatically similar. Following treatment, the patients' response to lactate did not differ from that of normal controls, whereas the pretreatment panic rate was much higher. These data suggest that lactate acts, by as yet unidentified mechanisms, to trigger the same panic attacks as occur spontaneously in vulnerable persons.

Effect of acute beta-adrenergic blockade on lactate-induced panic.

Many clinical and theoretic attempts have been made to link anxiety disorders and the beta-adrenergic nervous system. Six patients with panic disorder, who had panic attacks produced by sodium lactate infusions, were given repeated lactate infusions that were immediately preceded by intravenous administration of propranolol hydrochloride. In all cases, propranolol pretreatment infusion failed to prevent panic attacks, anxiety, tachycardia, and increased systolic BP during the lactate infusion.