Plus, the levels of plasma AChE do vary due to infection, pregnancy, and medical illness. Plasma AChE is not used as it is a liver acute-phase protein that circulates in the blood and has no correlation to symptoms. The red cell AChE correlates with neuronal AChE and can be used to determine response to therapy. The blood must be drawn before pralidoxime is administered. Today there is a portable test that can measure AChE in red blood cells within minutes. Some labs can directly measure red blood cell acetylcholinesterase activity, but these are often sent out to labs that are not available in a timely enough fashion to guide therapy. If symptoms resolve after atropine, this increases the likelihood of an acetylcholinesterase inhibitor poisoning. If organophosphate poisoning is on the differential but not confirmed, a trial of atropine may be employed. Some organophosphates have a distinct garlic or petroleum odor that may help in diagnosis. You must have a high clinical suspicion for organophosphate poisoning when no history of exposure or ingestion is known. Those who survive may also develop the following neuropsychiatric deficits:ĭiagnosis of acute or chronic organophosphate poisoning is strictly clinical. Most commonly this starts as stocking-glove paresthesia and progresses to symmetric polyneuropathy with flaccid weakness that starts in the lower extremities and progresses to include the upper extremities. Another later complication is neuropathy. This is linked to very specific organophosphate compounds that contain chlorpyrifos. With supportive care, these patients can have a complete return to normal neurologic function within 2 to 3 weeks. Symptoms include neck flexions, weakness, decreased deep tendon reflexes, cranial nerve abnormalities, proximal muscle weakness, and respiratory insufficiency. Intermediate neurologic symptoms typically occur 24 to 96 hours after exposure. If the patient survives the acute poisoning, there are other long-term complications. When death occurs, the most common reason is respiratory failure stemming from bronchoconstriction, bronchorrhea, central respiratory depression or weakness/paralysis of the respiratory muscles. This is a conformational change that renders the enzyme resistant to reactivation, making some treatment options useless.Īdditional symptoms can include anxiety, confusion, drowsiness, emotional lability, seizures, hallucinations, headaches, insomnia, memory loss, and circulatory or respiratory depression. At some point, which is different for each specific compound, the acetylcholinesterase-organophosphate compound undergoes a process called aging. The parasympathetic effects of organophosphate poisoning can be seen in multiple systems, including the heart, exocrine glands, and smooth muscles. Sweat glands within the sympathetic nervous system get overstimulated and cause large amounts of sweating. Muscarinic receptors are found in the parasympathetic and sympathetic nervous systems. These effects are usually slower than the nicotinic receptors because the effects occur via a G-protein-coupled receptor mechanism. Organophosphate poisoning also produces symptoms based on its action at muscarinic receptors. Nicotinic receptors also are found in the adrenal glands, which may cause hypertension, sweating, tachycardia, and leukocytosis with a left shift. This eventually leads to flaccid paralysis because of the depolarizing block. Overstimulation of nicotinic receptors found at neuromuscular junctions can lead to fasciculations and myoclonic jerks. This leads to an overabundance of acetylcholine within synapses and neuromuscular junctions. Once absorbed, the molecule binds to an acetylcholinesterase molecule in red blood cells, thus making the enzyme inactive. Organophosphate molecules can be absorbed via the skin, inhalation, or in the gastrointestinal tract.
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