Autonomic neuropathy is an important and common complication of Guillain-Barre syndrome (GBS). Manifestations be present in cardiovascular, sudomotor, gastrointestinal and other systems involving both sympathetic and parasympathetic fibers. Some apparently selective acute autonomic neuropathies may be subvarieties of GBS. Experimental work in animal models, pathological studies of GBS patients, and autonomic function studies have provided some help in the understanding of this complication. In managing GBS patients with autonomic dysfunction there are important practical considerations that can improve their care. In this article we review the literature on autonomic neuropathy in GBS and propose a management scheme to accommodate it in the overall treatment of the neuropathy.

Autonomic involvement in Guillain-Barré syndrome : a review

Selective adrenoceptor agonists and antagonists have been used to analyse the effects of stimulation of individual types of adrenoceptor in various parts of the rabbit heart. The selective alpha 1- and alpha 2-adrenoceptor agonists used were St 587 and BHT 933 respectively, and the antagonists were prazosin (alpha 1) and WY 25309 (alpha 2). The selective beta 1- and beta 2-adrenoceptor antagonists were atenolol and ICI 118551, respectively. Pirbuterol was a highly selective beta 2-adrenoceptor agonist. The non-selective agonists noradrenaline, adrenaline and isoprenaline were also employed with various combinations of antagonists. Phenylephrine was found to stimulate beta- as well as alpha-adrenoceptors. Rimiterol was a beta-adrenoceptor agonist, partially selective for beta 2-adrenoceptors. In the sinus node beta 1-, but not beta 2-adrenoceptor stimulation increased the fast phase of depolarization (Vmax). Both beta 1- and beta 2-adrenoceptor stimulation increased the slope of slow diastolic depolarization, accelerated repolarization and increased maximum diastolic potential. After blockade of both beta 1- and beta 2-adrenoceptors alpha 1-adrenoceptor stimulation caused bradycardia, due exclusively to delayed repolarization. alpha 2-adrenoceptor stimulation had no effect. In Purkinje cells and papillary muscle both beta 1- and beta 2-adrenoceptor stimulation accelerated repolarization. Stimulation of alpha 2-adrenoceptors had no effect. Beta 1-, not beta 2-adrenoceptor stimulation augmented peak contractions 3-5-fold, and greatly increased rate of development of tension. After beta-blockade alpha 1-adrenoceptor stimulation moderately increased peak contractions (up to 47%), but increased time-to-peak and duration of contractions. These patterns of adrenoceptor-mediated effects were unchanged in animals pre-treated with sufficient 6-hydroxydopamine to eliminate responses to sympathetic nerve stimulation. The results would be consistent with beta 1-, and beta 2-adrenoceptor stimulation increasing inward calcium current, and with stimulation of alpha 1-adrenoceptors delaying its inactivation, rather than increasing its magnitude.

Effects of selective alpha 1-, alpha 2-, beta 1-and beta 2-adrenoceptor stimulation on potentials and contractions in the rabbit heart.

Severe life-threatening hyperkalaemia may occur following administration of suxamethonium during certain periods after burns, neurological injuries, and in certain other conditions. Although this response is well-known, there is disagreement about when it may occur. This review describes the normal hyperkalaemic response to suxamethonium, the factors affecting it, the conditions in which it may be exaggerated, and the periods of high risk.

Suxamethonium and Hyperkalaemia

Succinylcholine has long been the favored neuromuscular blocking agent for emergent airway management because of its rapid onset, dependable effect, and short duration. However, it has a plethora of undesirable side effects, ranging from the inconsequential to the catastrophic. When patients requiring tracheal intubation present with potential contraindications to succinylcholine use, the emergency physician will need to substitute a rapid-onset nondepolarizing neuromuscular blocking agent, such as rocuronium or mivacurium. An understanding of the pharmacology of these agents is essential.

Succinylcholine: Adverse effects and alternatives in emergency medicine

Synopsis: Fenoterol, the 4-hydroxyphenyl derivative of orciprenaline, is a resorcinol derivative with relatively high selectivity for β2-adrenoceptors. It is active in man after inhalation or oral administration and is indicated in the treatment of bronchospasm associated with asthma, bronchitis and other obstructive airway diseases.

Rimiterol: a review of its pharmacological properties and therapeutic efficacy in asthma.

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

https://www.bmj.com/content/bmj/282/6260/298.full.pdf

Suxamethonium is dangerous in polyneuropathy.

The bronchodilator and cardiac effects produced by aerosols of 0·5% salbutamol and 0·5% and 1% rimiterol administered for three minutes in 40% oxygen by intermittent positive-pressure ventilation (I.P.P.V.) were compared in 15 asthmatic patients. Salbutamol and both the concentrations of rimiterol were equipotent in peak bronchodilator effect, but salbutamol had a significantly longer duration of bronchodilator action. There was significantly less increase in heart rate after rimiterol than after salbutamol. Aerosols of 0·5% rimiterol, 0·5% salbutamol, and saline were administered by I.P.P.V. to 10 normal volunteers. There was no difference between the mean heart rates after 0·5% rimiterol and saline but a highly significant increase in mean heart rate was observed after 0·5% salbutamol. It was concluded that 0·5% rimiterol was an effective short-acting bronchodilator drug with little or no cardiac beta1-adrenergic activity when administered for three minutes by I.P.P.V. in 40% oxygen.

Response to rimiterol and salbutamol aerosols administered by intermittent positive-pressure ventilation.

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R. F. Willey

Papers

Suxamethonium is dangerous in polyneuropathy.

Response to rimiterol and salbutamol aerosols administered by intermittent positive-pressure ventilation.

Suxamethonium Is Dangerous in Polyneuropathy