Page 2764 - Cote clinical veterinary advisor dogs and cats 4th

1438 Organophosphate and Carbamate Intoxication

Organophosphate and Carbamate Intoxication
VetBooks.ir Known or suspected exposure to organophosphate or carbamate insecticide or

other AChE-inhibiting agent

No clinical signs Clinical signs are present

Decontamination of patient
(assess patient risk) • Observe respirations and auscult lung fields
• Induce emesis • Assess for increased airway fluid sounds
• Activated charcoal

Monitor in hospital Lung sounds are
8 to 12 hours minimum reasonably clear, dry Airway fluid sounds are increased
for onset of expected signs (probably NOT an (from increased goblet cell mucus
(do not pretreat with atropine) AChE inhibitor) secretion)
• Physical exam Expect systemic muscarinic
Still no clinical signs: Clinical signs focus: lack of ‘‘overdrive’’ signs, or “SLUDDE” effect
• Discharge with instructions become apparent: systemic “SLUDDE” • Hyperactive parotid and lacrimal
for elimination of all possible • Proceed to signs glands, dyspnea, urinary bladder
sources of toxin to prevent manage as • Definitive confirmation and bowel incontinence, vomiting
re-exposure; activity indicated of presence or absence
restriction for 24 hours; of toxicosis
close monitoring for onset of
clinical signs for 24 hours; If still in question, consider the
and immediate recheck if “atropine test”
clinical signs occur • Use low (preanesthetic) dose
(0.02-0.03 mg/kg slow IV)

If there is no AChE inhibition, If AChE inhibition is in process,
the following should be apparent: this low atropine dose will
dry mouth, mydriasis, give minimal to no effect;
increased HR this is due to competitive
inhibition for ACh receptors

Definitive • Repeat the atropine, but use
• Continue confirmation higher dosage: 0.1-0.2 mg/kg
patient workup of presence or (half IV, half SQ; repeat prn)
• Pursue absence of • Reassess for the expected
differentials list
toxicosis atropine effect
An atropine effect should
now be apparent: dry mouth,
• Laboratory: submit chilled, whole mydriasis, increased HR
blood sample (EDTA [lavender top]
or heparin [green top] tube)
• Significant interspecies variation; • Presumptive evidence
specific reference range for normal • Suspect AChE inhibition
values is in process
• Significant evidence: 50% of • Pursue clinical management
normal AChE activity plus expected
muscarinic, nicotinic signs present

Atropine (higher dosage: Pralidoxime (Protopam Stabilize any CNS and Supportive care: Monitor:
0.1-0.2 mg/kg [half IV, HCl, “2-PAM”): nicotinic signs: • Ensure perfusion, hydration, • Endpoint muscarinic, nicotinic,
half SQ]) • Organophosphate • Diazepam or propofol prn oxygenation CNS signs
• Repeat dosing prn to intoxication only for seizures (0.2-1 mg/kg IV) • Normal body temperature • Remain stable without further
effect, based on lung (because cholinesterase • Methocarbamol prn for • Chemistry panel in severe need for drug intervention
field quality inhibition with nicotinic effects (100-150 cases (especially • 24- to 72-hour average
• Goal: dry lung field, carbamates is reversible) mg/kg IV; daily maximum pancreas, liver) hospital stay required
patient oxygenation • 10-20 mg/kg q 8-12h IM, 330 mg/kg)
SQ, IV
• Goal: reactivate ChE
ACh, Acetylcholine; AChE, acetylcholinesterase; CNS, central nervous system; HR, heart rate; IM; intramuscular;
IV, intravenous; prn, as needed; SLUDDE, salivation, lacrimation, urination, diarrhea, dyspnea, emesis; SQ, subcutaneous.
EDITED BY: Leah A. Cohn, DVM, PhD, DACVIM
ORIGINALLY WRITTEN BY: Michael W. Knight, DVM, DABVT, DABT
www.ExpertConsult.com