Suxamethonium is contraindicated in the Guillain-Barré syndrome.
01 Nov 1991-Journal of Neurology, Neurosurgery, and Psychiatry (J Neurol Neurosurg Psychiatry)-Vol. 54, Iss: 11, pp 1018-1019
TL;DR: It is suggested that ischaemia resulting from arterial spasm may play a role in the visual failure associated with anterior communicating artery aneurysms as well as direct compression of the visual pathways.
Abstract: failure.2 Previous reports ofpermanent visual deterioration have all concerned large aneurysms of at least 12 x 15 mm.23 The mechanism of visual loss has always been attributed to compression of the optic pathways either by aneurysm or by an associated haematoma with the pattern of loss being determined by the position of the aneurysm in relation to the optic nerves and chiasm.4 In this case, almost complete and permanent visual failure occurred six days after the primary haemorrhage. There was no evidence of further haemorrhage or clot on CT scans and the aneurysm was of moderate size with no signs of compression being seen at the time of surgery. The visual failure could have been produced by ischaemic damage to the anterior visual pathways secondary to vasospasm. A reduction in the cerebral blood flow over the period ofonset of the visual failure was evident both clinically and by measurement. Vasospasm has been postulated as a cause for transient ischaemic amaurosis before,5 but this is the first time that such an ischaemic event has lead to permanent blindness and the vasospasm has been measured quantitatively during the evolution of the symptoms. We suggest that ischaemia resulting from arterial spasm may play a role in the visual failure associated with anterior communicating artery aneurysms as well as direct compression of the visual pathways. SIMON RUBEN FARHAD AFSHAR Department ofNeurosurgery, St Bartholomew's Hospital, West Smithfield, London, UK
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TL;DR: A clear diagnosis of the underlying disease and sufficient knowledge and understanding of the pathophysiology are of paramount importance to the practitioner and guide optimal perioperative management of affected patients.
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TL;DR: The anesthetic management for cesarean section and tubal ligation of a 23-year-old primipara with type II spinal muscular atrophy (benign Werdnig Hoffmann) is described.
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TL;DR: The pathogenesis of acute respiratory failure can be classified as neuromuscular in origin, secondary to acute and chronic obstructive airway diseases, alveolar processes such as cardiogenic and noncardiogenic pulmonary edema and pneumonia, and vascular diseases such as acute or chronic pulmonary embolism.
Abstract: Lung failure is the most common organ failure seen in the intensive care unit. The pathogenesis of acute respiratory failure (ARF) can be classified as (1) neuromuscular in origin, (2) secondary to acute and chronic obstructive airway diseases, (3) alveolar processes such as cardiogenic and noncardiogenic pulmonary edema and pneumonia, and (4) vascular diseases such as acute or chronic pulmonary embolism. This article reviews the more common causes of ARF from each group, including the pathological mechanisms and the principles of critical care management, focusing on the supportive, specific, and adjunctive therapies for each condition.
19 citations
TL;DR: A 7‐year‐old patient with possible SMA scheduled for a Grice‐arthrodesis is described, who was decided to use an epidural technique with sevoflurane sedation and spontaneous ventilation to avoid the use of muscle relaxants and systemic opioids and consequently admission to the intensive care unit.
Abstract: Spinal muscular atrophy (SMA) is a rare lower motor neurone disease in which anaesthetic management is often difficult as a result of muscle weakness and hypersensitivity to neuromuscular blocking agents. Neuraxial anaesthesia is controversial in these patients; however, some cases have been reported in which neuraxial anaesthesia has been used without neurological sequelae. We describe a 7-year-old patient with possible SMA scheduled for a Grice-arthrodesis. Because of previous prolonged postoperative drowsiness and poor oral intake, we decided to use an epidural technique with sevoflurane sedation and spontaneous ventilation to avoid the use of muscle relaxants and systemic opioids and consequently admission to the intensive care unit. After 3 days, the epidural analgesia was stopped and the patient regained her preoperative motor function within 5 h. Despite the controversy surrounding the use of neuraxial techniques in neuromuscular disease, we found no well-founded basis for this in patients with SMA in the literature.
13 citations
TL;DR: A 23-year-old woman developed weak arms and legs and diplopia during her second pregnancy and neuropathy relapsed over the next five years until she presented with deteriorating pulmonary function and an inability to cough due to muscle weakness, for which she required artificial ventilation.
Abstract: Case 1?A 23-year-old woman developed weak arms and legs and diplopia during her second pregnancy. On examination she had a mild peripheral sensory disturbance, definite distal muscle weakness, and absent tendon reflexes. Cerebrospinal fluid (CSF) protein was 20 g/1. The neuropathy relapsed over the next five years until she presented with deteriorating pulmonary function and an inability to cough due to muscle weakness, for which she required artificial ventilation. She was given atropine and thiopentone to induce anaesthesia and then paralysed with suxamethonium (succinylcholine) before in? tubation. During this procedure she developed a ventricular tachycardia, which returned promptly to sinus rhythm with intravenous lignocaine and DC cardioversion. Case 2?A 42-year-old man presented with paraesthesia in the hands and feet and left-sided facial weakness. Over the next seven months his arms and legs became progressively weak, extending proximally. He was almost completely paralysed in the arms, legs, and trunk and had a peripheral sensory dis? turbance and absent reflexes. CSF protein concentration was raised at 2-84 g/1. Because he could not cough effectively and his respiratory function was deteriorating he required artificial ventilation. He was given atropine 0-3 mg, thiopentone 200 mg, and suxamethonium 75 mg intravenously before intubation. His pulse was lost immediately, and ECG monitoring showed ventricular tachycardia, which progressed to ventricular fibrillation. He was given intravenous lignocaine and cardio verted on four occasions before returning to sinus rhythm. No further arrhythmias were noted. Case 3?A 75-year-old man was admitted with a five-month history of progressive weakness of the legs. On examination he had flaccid paralysis of all muscle groups with absent tendon reflexes. CSF protein concentration was 3-2 g/1. He developed purulent sputum and a chest radiograph showed consolidation in the right lower lobe. Because he was unable to cough and blood gas concentrations were falling he was intubated, artificial
5 citations
References
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TL;DR: Though SCh induces a small release of K+ in normal muscle, it produces a potentially lethal efflux in the presence of increased sensitivity and this K+-releasing action of SCh persists for 2 to 3 months in patients who have sustained burns or trauma, and perhaps 3 to 6 months in Patients with upper motor neuron lesions.
Abstract: SCh is unequivocally contraindicated in the management of patients who have sustainded thermal trauma or direct muscle trauma and those who have neurologic disorders involving motor deficits, including tetanus. The mechanism is clear in some, but not all, of these conditions, and is related to increased chemosensitivity of the muscle membrane due to the development of receptor sites in extrajunctional areas. Though SCh induces a small release of K+ in normal muscle, it produces a potentially lethal efflux in the presence of increased sensitivity. This K+-releasing action of SCh begins about 5 to 15 days after injury and persists for 2 to 3 months in patients who have sustained burns or trauma, and perhaps 3 to 6 months in patients with upper motor neuron lesions.
292 citations
TL;DR: A review of pathologic data obtained from the literature indicates that involvement of autonomic pathways in this condition is not uncommon and an approach to management that takes into account the autonomic status may lessen the mortality of this condition.
197 citations
TL;DR: The dangerously high levels of plasma potassium known to follow succinylcholine chloride administration in patients with burns or trauma have also been noted in Patients with paraplegia or hemiplegia, muscular dystrophy, and multiple sclerosis.
Abstract: The dangerously high levels of plasma potassium known to follow succinylcholine chloride administration in patients with burns or trauma have also been noted in patients with paraplegia or hemiplegia, muscular dystrophy, and multiple sclerosis. Of 40 patients with these neuromuscular diseases, 15 had increases in potassium levels between 1 and 6 mEq/liter after receiving succinylcholine chloride, 1 mg/kg of body weight. Most increases over 1 mEq/liter occurred in those patients who had been ill for less than six months or, if longer, who had disease of a progressive nature. The degree and extent of muscle paralysis seemed directly correlated with relaxant-induced hyperkalemia.
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