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Here we go :lol:

You are called to a UPS station for a man passed out.. When you arrive you observe a male approximately 25 lying supine next to his UPS Truck. He is awake but extremely lethargic and very slow to respond to questions.

You note a distinct odor of chemicals coming both from the patient's skin and from the back of the truck.

You send your partner to investigate the truck and he returns to tell you he has found a 5 gallon jug of chemicals broken in the back of the truck and it appears that the driver had tried to wipe the spill up with paper towels.

Your are unable to ID the bottle because it had fallen and shattered upon impact..

The patient's VS are as follows: B/P 60/P, P 52 R10 and shallow. His skin is moist and extremely pale. His lung sounds are diminished in all fields.

He has urinated on himself and you note the smell of feces.. He is drooling and seems unable to control his oral secretions. You look at his pupils and they are miotic and he has what appears to be tears coming from his eyes.

You question him and although he is slow to answer, you understand him. He tells you he rounded a corner in his truck and this container fell off the shelf. He stopped to try and clean it up but became dizzy and had trouble seeing. He said he just made it back to his station and began having trouble breathing and then fell out of the truck.

He c/o abdominal pain and you note hyperactive bowel sounds. You repeat the vs and his b/p remains at 60/p but his pulse had now dropped to 45bpm. He is losing consciouness and you start 2 IVs and put him on a NRB at 15 l/min

His 3 lead shows sinus brady at 42 and you note a prolonged pr interval.

You rapidly transport to the nearest facility. Enroute you call your medical control officer and you advise of pt. situation and it suddenly dawns on you. You know what this is and you know how to treat it.

Tell me what you think and how you would treat this guy..

PS :shock: :shock: This is a real call that I answered in Florida in 1985. The patient fully recovered and my crew was awarded a commendation for our alert and conscientious treament. (as I pat myself on the back):lol::D

Talk to me.

Much Love and Respect


8) 8) I tell you what, the first person to correctly ID this case and give the proper treatment and also tell me the pathophysiology behind this problem and the treatment will receive some educational CD's of my choosing.

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Organophosphate (OP) or carbamate insecticide poisoning would be most likely. That or this guy was exposed to a nerve gas like Sarin or one of the related compounds

Treatment: Atropine until secretions dry up, pralidoxime (2-PAM chloride) if your protocols allow it.

The pathophysiology behind all of this is the fact that that the agents I suspect block the action of the acetylcholinesterase (AChE) enzyme which normally breaks down acetylcholine (ACh). This inactivation happens by phosphorylating the serine hydroxyl group located at the active site of AChE.

Once AChE has been inactivated, ACh accumulates throughout the autonomic nervous system, the somatic nervous system, and the brain, resulting in overstimulation of the muscarinic and nicotinic receptors. The preganglionic and postganglionic neurons in the parasympathetic nervous system release ACh. Postganglionic ACh acts on muscarinic receptors on the heart, eyes, glands, GI tract, and respiratory system. Somatic motor axons emerge from the spinal cord and directly innervate muscle cells at the neuromuscular junction, releasing ACh on nicotinic receptors. The brain and spinal cord both contain muscarinic and nicotinic receptors. The brain is richer in muscarinic receptors, whereas the spinal cord has relatively more nicotinic receptors. Cholinergic pathways in the brain are associated with various behaviors and functions, including hunger, thirst, thermoregulation, respiration, aggression, and cognition.

Signs and symptoms of OP poisoning can be divided into 3 broad categories, including (1) muscarinic effects, (2) nicotinic effects, and (3) CNS effects.

Muscarinic effects by organ systems include the following:

Cardiovascular - Bradycardia, hypotension

Respiratory - Rhinorrhea, bronchospasm, bronchorrhea, cough

Gastrointestinal - Increased salivation, nausea and vomiting, abdominal pain, diarrhea, and fecal incontinence

Genitourinary - Urinary incontinence

Ocular - Blurred vision, miosis

Glands - Increased lacrimation, increased sweating

Mnemonic devices used to remember the muscarinic effects of OPs are SLUDGE (salivation, lacrimation, urination, diarrhea, GI upset, emesis) and DUMBELS (diaphoresis and diarrhea; urination; miosis; bradycardia, bronchospasm, bronchorrhea; emesis; lacrimation excess; salivation excess).

Nicotinic signs and symptoms include muscle fasciculations, cramping, weakness, and diaphragmatic failure. Autonomic nicotinic effects include hypertension, tachycardia, pupillary dilation, and pallor.

CNS effects include anxiety, restlessness, confusion, ataxia, seizures, insomnia, dysarthria, tremors, and coma.


Vital signs

Depressed respiratory rate, bradycardia, and hypotension are common.

Hypothermia also can be observed.


Type I - Acute paralysis secondary to persistent depolarization at the neuromuscular junction

Type II (intermediate syndrome) - Intermediate syndrome was described in 1974, with an incidence from 8-49%. It develops 24-96 hours after resolution of acute cholinergic poisoning symptoms and manifests commonly as paralysis and respiratory distress. This syndrome involves proximal muscle groups, with relative sparing of distal muscle groups. Various degrees of cranial nerve palsies also are observed. Neuromuscular transmission defect and toxin-induced muscular instability play a role in intermediate syndrome. Intermediate syndrome persists for 4-18 days, can require intubation, and can be complicated by infections or cardiac arrhythmias.

Type III - Organophosphate-induced delayed polyneuropathy (OPIDP) occurs 2-3 weeks after exposure to large doses of certain OPs. Distal muscle weakness with relative sparing of the neck muscles, cranial nerves, and proximal muscle groups characterize OPIDP. Recovery can take up to 12 months.

Neuropsychiatric effects - Impaired memory, confusion, irritability, lethargy, psychosis, and chronic OP-induced neuropsychiatric disorder

Extrapyramidal effects - Dystonia, cogwheel rigidity

Other neurological and/or psychological effects - Guillain-Barrélike syndrome, isolated bilateral recurrent laryngeal nerve palsy

Ophthalmic effects - Optic neuropathy, retinal degeneration, defective vertical smooth pursuit, myopia, and miosis (due to direct ocular exposure to OPs)

Ears - Ototoxicity

Respiratory effects - Muscarinic, nicotinic, and central effects contribute to respiratory distress in acute and delayed OP toxicity.

Muscarinic effects, such as bronchospasm and laryngeal spasm, can lead to airway obstruction.

Nicotinic effects lead to weakness and paralysis of respiratory oropharyngeal muscles.

Central effects can lead to cessation of respiration.

Rhythm abnormalities - Sinus tachycardia, sinus bradycardia, extrasystoles, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation

Other cardiovascular effects - Hypotension, hypertension, and noncardiogenic pulmonary edema

GI manifestations such as nausea, vomiting, diarrhea, and abdominal pain are the first to occur after OP exposure.

Genitourinary and/or endocrine effects - Urinary incontinence, hypoglycemia or hyperglycemia

SOURCE: http://www.emedicine.com/med/topic1677.htm

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Exellcent job.. I am not sure why this jug was even in this truck unprotected. It was indeed Organophosphates.. We treated this guy with 15 mg Atropine in the ED and finally the spell was broken.. I believe that this guy would have been dead in a matter of minutes if the treatment was started when it was

At that time 2-pam was not being used. Now it is the standard of care.

pm with your e-mail address and I send you some software



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  • 3 months later...

Since this was in 1985 or so I'll give you the benefit of the doubt but my question that is screaming in my head is this

You smelled chemicals on this guy and you went in to the truck to investigate?????????? I would have removed the guy from the truck area and called HAZMAT to take care of the truck.

I know it was 1985 or so but the person who investigated the smell could have been the next patient.

On a sidebar, I had a call where the top hazmat guy in the county responded to a tanker truck crash and drove up to the scene and parked 10 feet from the ruptured tanker truck. Needless to say you can't buy good sense!!!

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