Proximal muscle and respiratory paralysis of the extremities
Introduction
Introduction Proximal Limb Muscles and Respiratory Paralysis: A group of syndromes in which muscles and respiratory paralysis of the cranial nerves are caused by proximal muscles of the extremities, III-VII and X by dysfunction of postsynaptic neuromuscular junctions. A neurotoxicity caused by severe organophosphorus poisoning. The condition may be associated with acute organophosphorus pesticide poisoning such as tearing, salivation, excessive sweating, muscle twitching, and dilated pupils, mainly for respiratory failure caused by respiratory muscle paralysis. The disease focuses on prevention, especially in special occupational groups exposed to organophosphorus such as chemical plant workers. It is necessary to strengthen protection and management.
Cause
Cause
A neurotoxicity caused by severe organophosphorus poisoning, it is currently believed that its pathogenesis and cholinesterase activity are inhibited for a long time, so that a large amount of acetylcholine accumulated in the synaptic cleft continues to act on the N2 on the postsynaptic membrane. Receptors cause desensitization, leading to transmission of disorders at the nerves and muscle junctions, and skeletal muscle paralysis.
Examine
an examination
Related inspection
Limb and joint movement
After the symptoms of poisoning improved significantly, the symptoms of acute organophosphorus pesticide poisoning such as tearing, runny, sweating, muscle fibrillation and dilated pupils suddenly appeared, but there was no brain numbness, and the effect of increasing the dosage of atropine was significant.
Clinical examination
(1) There are corresponding AOPP signs after system examination.
(2) Respiratory system examination has signs of pulmonary edema (double lungs covered with wet voice).
2. Laboratory examination
(1) Determination of cholinesterase activity: It is a specific marker enzyme for organophosphorus pesticide poisoning, but the degree of enzyme activity decline is not completely consistent with the disease and prognosis.
(2) Determination of creatine kinase (CK) and troponin (cTnI): the degree of myocardial damage in response to AOPP.
(3) Others: Early detection of blood, urine and gastric poisoning has guiding value for diagnosis and treatment.
Diagnosis
Differential diagnosis
The intermediate syndrome needs to be differentiated from "bounce" and atropine poisoning during the treatment of organophosphate poisoning. In the former, after the symptoms of poisoning improved significantly, the symptoms of acute organophosphorus pesticide poisoning such as tearing, runny, sweating, muscle fibrillation and pupil dilation suddenly appeared, but there was no brain numbness, and the effect of increasing the dosage of atropine was significant; the latter often After high-dose application of Atropine, there were symptoms such as convulsions, coma, respiration, and circulatory failure. The symptoms improved after the reduction or discontinuation of atropine. Secondly, it should be distinguished from central respiratory failure and delayed peripheral neuropathy. Acute organophosphorus poisoning occurs in central respiratory failure, often suggesting central nervous system damage, often coma and pathological reflex. Most of the intermediate syndromes occur in the awake state. After the rescue, the consciousness turns clear, but there is still no spontaneous breathing. All of them suggest that respiratory failure is peripheral, but sometimes it can be mixed due to cerebral edema. Delayed peripheral neuropathy occurs mostly after 2 to 3 weeks of poisoning, mainly involving the distal muscles of the limbs, not involving the cranial nerves and respiratory muscles. Although the performance of the intermediate syndrome is diverse, most of the muscles with innervation are weak, the flexor and the respiratory muscles are the main, and the respiratory muscle paralysis is the most serious manifestation and the main cause of death.
