The intermediate syndrome (IMS) following organophosphorus (OP) insecticide 
poisoning was first described in the mid-1980s. The syndrome described comprised 
characteristic symptoms and signs occurring after apparent recovery from the 
acute cholinergic syndrome. As the syndrome occurred after the acute cholinergic 
syndrome but before organophosphate-induced delayed polyneuropathy, the syndrome 
was called 'intermediate syndrome'. The IMS occurs in approximately 20% of 
patients following oral exposure to OP pesticides, with no clear association 
between the particular OP pesticide involved and the development of the 
syndrome. It usually becomes established 2-4 days after exposure when the 
symptoms and signs of the acute cholinergic syndrome (e.g. muscle 
fasciculations, muscarinic signs) are no longer obvious. The characteristic 
features of the IMS are weakness of the muscles of respiration (diaphragm, 
intercostal muscles and accessory muscles including neck muscles) and of 
proximal limb muscles. Accompanying features often include weakness of muscles 
innervated by some cranial nerves. It is now emerging that the degree and extent 
of muscle weakness may vary following the onset of the IMS. Thus, some patients 
may only have weakness of neck muscles whilst others may have weakness of neck 
muscles and proximal limb muscles. These patients may not require ventilatory 
care but close observation and monitoring of respiratory function is mandatory. 
Management is essentially that of rapidly developing respiratory distress and 
respiratory failure. Delays in instituting ventilatory care will result in 
death. Initiation of ventilatory care and maintenance of ventilatory care often 
requires minimal doses of non-depolarising muscle relaxants. The use of 
depolarising muscle relaxants such as suxamethonium is contraindicated in OP 
poisoning. The duration of ventilatory care required by patients may differ 
considerably and it is usual for patients to need ventilatory support for 7-15 
days and even up to 21 days. Weaning from ventilatory care is best carried out 
in stages, with provision of continuous positive airway pressure prior to 
complete weaning. Continuous and close monitoring of respiratory function 
(arterial oxygen saturation, partial pressure of oxygen in arterial blood, 
partial pressure of carbon dioxide in arterial blood) and acid-base status are 
an absolute necessity. Prophylactic antibiotics are usually not required unless 
there has been evidence of aspiration of material into the lungs. Close 
monitoring of fluid and electrolyte balance is mandatory in view of the profuse 
offensive diarrhoea that most patients develop. Maintenance of nutrition, 
physiotherapy, prevention of bed sores and other routine measures to minimise 
discomfort during ventilatory care are necessary. Recovery from the intermediate 
syndrome is normally complete and without any sequelae. The usefulness of oximes 
during the IMS remains uncertain. In animal experiments, very early 
administration of oximes has prevented the occurrence of myopathy. There are 
reports from developed countries where administration of oximes at recommended 
doses and within 2 hours of ingestion of OP insecticide did not prevent the 
onset of the IMS. Controlled randomised clinical studies are necessary to 
evaluate the efficacy of oximes in combating the IMS. Electrophysiological 
studies following OP poisoning have revealed three characteristic phenomena: (i) 
repetitive firing following a single stimulus; (ii) gradual reduction in twitch 
height or compound muscle action potential followed by an increase with 
repetitive stimulation (the 'decrement-increment response'); and (iii) continued 
reduction in twitch height or compound muscle action potential with repetitive 
simulation ('decrementing response'). Of these, the decrementing response is the 
most frequent finding during the IMS, whilst repetitive firing is observed 
during the acute cholinergic syndrome. The distribution of the weakness in human 
cases of the IMS, in general, parallels the distribution of the myopathy 
observed in a number of studies in experimental animals. This has led to 
speculation that myopathy is involved in the causation of the IMS. However, 
while myopathy and the IMS have a common origin in acetylcholine accumulation, 
they are not causally related to one another.