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νλ리λ μ¬(νν 2-PAMμΌλ‘ λΆλ¦Ό)μ μμνμμ **μ κΈ°μΈμ (OP)** μ€λ μ μΉλ£νλ λ° μ¬μ©λλ νΉμ΄μ ν΄λ μ μ λλ€. μ κΈ°μΈμ μ€λ κ³Ό κ΄λ ¨λ μ κ²½κ·Ό λ§λΉλ₯Ό ν볡μν€λ λ° μ¬μ©λ©λλ€. > **κ²½κ³ :** νλ리λ μ¬μ μμ μ¦μμ μ νμν€κ±°λ ν¨κ³Όκ° μμ μ μμΌλ―λ‘ μΉ΄λ°λ©μ΄νΈ μ€λ μλ μΌλ°μ μΌλ‘ κΈκΈ°μ λλ€. **μμ ν:** νλ리λ μ¬μ νμ‘λμ₯λ²½μ μ ν΅κ³Όνμ§ λͺ»νλ―λ‘ μ£Όλ‘ λ§μ΄ λμ½ν΄μ± μ¦μ(κ·Όμ‘ λ¨λ¦Ό, μ μ½, λ§λΉ)μ μννμ§λ§ μ€μΆμ κ²½κ³ μ¦μμλ ν¨κ³Όκ° μμ΅λλ€. μλͺ μ μννλ 무μ€μΉ΄λ¦°μ± μ¦μ(μλ§₯, κΈ°κ΄μ§ μμΆ λ° SLUDGE: μ μ°, λλ¬Ό, λ°°λ¨, λ°°λ³, μμ₯ μ₯μ , ꡬν )μ ν΄κ²°νλ **μνΈλ‘ν**κ³Ό νμ ν¨κ» μ¬μ©ν΄μΌ ν©λλ€. ν¨κ³Όλ₯Ό λ³΄λ €λ©΄ OP-ν¨μ 볡ν©μ²΄κ° 'λ Έν'(μꡬμ λΉκ°μμ κ²°ν©)λ₯Ό κ²ͺκΈ° μ (μΌλ°μ μΌλ‘ λ ΈμΆ ν 24~48μκ° μ΄λ΄)μ μ‘°κΈ° ν¬μ¬ν΄μΌ ν©λλ€.
μμ© κΈ°μ : Pralidoxime works by reactivating the **acetylcholinesterase (AChE)** enzyme that has been inactivated by organophosphate binding. It binds to the OP-AChE complex β cleaves the phosphate bond β releases the OP β restores the enzyme's ability to break down **acetylcholine** at the synaptic cleft. Additionally, it directly detoxifies certain unbound OP molecules through chemical inactivation and retards the 'aging' of phosphorylated cholinesterase into a non-reactive, permanently damaged form.
λλ¬Ό μ’ λ³ μ©λ
- Organophosphate toxicity Β· 10-20 mg/kg Β· IV/IM/SC Β· bid to tid Β· Until nicotinic signs resolve (usually 1-2 days) Β· Administer IV very slowly over 15-30 minutes. Can also be given as a continuous rate infusion (CRI). Must be given in conjunction with atropine.
- Organophosphate toxicity Β· 10-20 mg/kg Β· IV/IM/SC Β· bid to tid Β· Until nicotinic signs resolve (usually 1-2 days) Β· Administer IV very slowly over 15-30 minutes. Must be given in conjunction with atropine.
μ©λμ λ©΄ν μμ μ λ¬Έκ°λ₯Ό μν μμ μ°Έκ³ μλ£μ λλ€. νμ μ΅μ λΌλ²¨κ³Ό κ°λ³ νμμ λν΄ νμΈνμμμ€.
ν¬μ¬ κ²½λ‘
κΈκΈ°
- Carbamate toxicity (can exacerbate toxicity)
- Poisoning by non-anticholinesterase compounds
- Hypersensitivity to pralidoxime
μ΄μλ°μ
- Tachycardia
- Muscle rigidity
- Transient neuromuscular blockade (if given too rapidly IV)
- Hypertension
- Hyperventilation
μ½λ¬Ό μνΈμμ©
- Phenothiazines Β· May exacerbate organophosphate toxicity Β· major
- Succinylcholine Β· Prolonged neuromuscular blockade due to cholinesterase inhibition Β· major
- Morphine Β· May exacerbate respiratory depression in OP toxicity Β· moderate
- Aminophylline Β· May exacerbate toxicity Β· moderate
λͺ¨λν°λ§
- Heart rate and rhythm (ECG)
- Respiratory rate and effort
- Resolution of muscle fasciculations and weakness
- Blood pressure
- Renal function (urine output)
κ³Όμ©λ
Overdose can cause paradoxical neuromuscular blockade, muscle rigidity, tachycardia, and worsening of cholinergic signs. Treatment is supportive, including artificial ventilation if respiratory paralysis occurs.
VetSheet μ½λ¬Ό λ νΌλ°μ€λ λ©΄ν μμ μ λ¬Έκ°λ₯Ό μν μμ μμ¬κ²°μ 보쑰 λꡬμ΄λ©°, μ λ¬Έμ νλ¨μ΄λ μ μ‘°μ¬μ μ΅μ λΌλ²¨μ λμ νμ§ μμ΅λλ€.