Organophosphate (OP) Poisining

1
Organophosphate (OP) Poisining
2
Organophosphate (OP) Poisining

• Initial treatment goal should consist of
  optimizing oxygenation and controlling excessive
  airway secretions.
• Tachycardia is neither a contraindication nor an
  endpoint for atropine administration.
• Patients exposed to organophosphate (OP) should
  be observed for at least 12 hours in a high
  acuity setting.
• Because of the risk of respiratory depression or
  recurrent symptoms after resolution of an acute
  cholinergic crisis, hospitalizing all symptomatic
  patients for at least 48 hours following
  resolution of symptoms is recommended.
• The symptoms of OP poisoning can mimic other
  toxicities and disease processes. The clinician
  must keep in mind that misdiagnosis is a
  potential medicolegal pitfall.

3
Organophosphate (OP) Poisining

• Organophosphate (OP) compounds are a diverse
  group of chemicals used in both domestic and
  industrial settings.

4
ANTICHOLINESTERASE

• anticholinesterase Any substance that inhibits
  the enzyme cholinesterase, which is responsible
  for the breakdown of the neurotransmitter
  acetylcholine at nerve synapses.
  Anticholinesterases, which include certain drugs,
  nerve gases, and insecticides, cause a build-up
  of acetylcholine within the synapses, leading to
  disruption of nerve and muscle function. In
  vertebrates, these agents often cause death by
  paralysing the respiratory muscles.

5

• cholinesterase (acetylcholinesterase) An enzyme
  that hydrolyses the neurotransmitter
  acetylcholine to choline and acetate.
  Cholinesterase is secreted by nerve cells at
  synapses and by muscle cells at neuromuscular
  junctions. Organophosphorus insecticides
  (pesticide) act as anticholinesterases by
  inhibiting the action of cholinesterase.

6
Acetylecholie

• Acetylcholine (ACh) is one of the main
  neurotransmitters of the vertebrate nervous
  system. It is released at certain (cholinergic)
  nerve endings and may be excitatory or
  inhibitory it initiates muscular contraction at
  neuromuscular junctions. Acetylcholine receptors
  (cholinoceptors) fall into two main classes
  muscarinic and nicotinic receptors. Once
  acetylcholine has been released it has only a
  transitory effect because it is rapidly broken
  down by the enzyme cholinesterase.

7
Pathophysiology

• The primary mechanism of action of
  organophosphate pesticides is inhibition of
  acetylcholinesterase (AChE).
• AChE is an enzyme that degrades the
  neurotransmitter acetylcholine (ACh) into choline
  and acetic acid.
• ACh is found in the central and peripheral
  nervous system, neuromuscular junctions, and red
  blood cells (RBCs).
• Organophosphates inactivate AChE by
  phosphorelation.

8
Pathophysiology

• Once AChE has been inactivated, ACh accumulates
  throughout the nervous system, resulting in
  overstimulation of muscarinic and nicotinic
  receptors.
• Clinical effects are manifested via activation of
  the autonomic and central nervous systems and at
  nicotinic receptors on skeletal muscle.

9
Pathophysiology

• Organophosphates can be absorbed cutaneously,
  ingested, inhaled, or injected.
• Although most patients rapidly become
  symptomatic, the onset and severity of symptoms
  depend on the specific compound, amount, route of
  exposure, and rate of metabolic degradation.

10
(No Transcript)
11
Signs and symptoms of organophosphate poisoning

• Can be divided into 3 broad categories,
  including
• (1) muscarinic effects,
• (2) nicotinic effects, and
• (3) CNS effects.
• Mnemonic devices used to remember the muscarinic
  effects of organophosphates are SLUDGE
  (salivation, lacrimation, urination, diarrhea, GI
  upset, emesis) and DUMBELS (diaphoresis and
  diarrhea urination miosis bradycardia,
  bronchospasm, emesis excess lacrimation and
  salivation).

12
Signs and symptoms of organophosphate poisoning

• Muscarinic effects by organ systems include the
  following
• Cardiovascular - Bradycardia, hypotension
• Respiratory - Rhinorrhea, bronchorrhea,
  bronchospasm, cough, severe respiratory distress
• Gastrointestinal - Hypersalivation, nausea and
  vomiting, abdominal pain, diarrhea, fecal
  incontinence
• Genitourinary - Incontinence
• Ocular - Blurred vision, miosis
• Glands - Increased lacrimation, diaphoresis

13
Signs and symptoms of organophosphate poisoning

• Nicotinic signs and symptoms include muscle
  fasciculations, cramping, weakness, and
  diaphragmatic failure.
• Autonomic nicotinic effects include hypertension,
  tachycardia, mydriasis, and pallor.
• CNS effects include anxiety, emotional lability,
  restlessness, confusion, ataxia, tremors,
  seizures, and coma.

14
Physical

• Note that clinical presentation may vary,
  depending on the specific agent, exposure route,
  and amount.
• Symptoms are due to both muscarinic and nicotinic
  effects.
• Vital signs Depressed respirations, bradycardia,
  and hypotension are possible symptoms.
• Alternatively, tachypnea, hypertension, and
  tachycardia are possible.
• Hypoxia should be monitored for with continuous
  pulse oximetry.

15
TreatmentMedical Care

• Airway control and adequate oxygenation are
  paramount in organophosphate (OP) poisonings.
• Intubation may be necessary in cases of
  respiratory distress due to laryngospasm,
  bronchospasm, bronchorrhea, or seizures.
• Immediate aggressive use of atropine may
  eliminate the need for intubation.
• Succinylcholine should be avoided because it is
  degraded by acetylcholinesterase (AChE) and may
  result in prolonged paralysis.

16
Treatment/ Medical Care

• Continuous cardiac monitoring and pulse oximetry
  should be established an ECG should be
  performed.
• The use of intravenous magnesium sulfate has been
  reported as beneficial for organophosphate
  toxicity.
• The mechanism of action may involve acetylcholine
  antagonism or ventricular membrane stabilization.
• Remove all clothing and gently cleanse patients
  suspected of organophosphate exposure with soap
  and water because organophosphates are hydrolyzed
  readily in aqueous solutions with a high pH.
• Consider clothing as hazardous waste and discard
  accordingly.

17
TreatmentMedical Care

• Health care providers must avoid contaminating
  themselves while handling patients.
• Use personal protective equipment, such as
  neoprene gloves and gowns, when decontaminating
  patients because hydrocarbons can penetrate
  nonpolar substances such as latex and vinyl.
• Use charcoal cartridge masks for respiratory
  protection when decontaminating patients who are
  significantly contaminated.
• Irrigate the eyes of patients who have had ocular
  exposure using isotonic sodium chloride solution
  or lactated Ringer's solution.

18
Medication

• The mainstays of medical therapy in
  organophosphate (OP) poisoning include ATROPINE,
  pralidoxime , and diazepam
• Initial management must focus on adequate use of
  atropine. Optimizing oxygenation prior to the use
  of atropine is recommended to minimize the
  potential for dysrhythmias.

19
Medication

• Anticholinergic agents
• These agents act as competitive antagonists at
  the muscarinic cholinergic receptors in both the
  central and the peripheral nervous system.
• These agents do not affect nicotinic effects.

20
Atropine (Isopto, Atropair)

• Adult
• 1-2 mg IV bolus, repeat q1-5min prn for desire
  effects (drying of pulmonary secretions and
  adequate oxygenation)Strongly consider doubling
  each subsequent dose for rapid control of
  patients in severe respiratory distressAn
  atropine drip titrated to above endpoints can be
  initiated until patient's condition stabilized
• Pediatric
• 0.05 mg/kg IV, repeat q1-5min prn for control of
  airway secretionsStrongly consider doubling each
  subsequent dose to rapidly stabilize patients
  with severe respiratory distress

21
Complications

• Complications include respiratory failure,
  seizures, aspiration pneumonia, delayed
  neuropathy, and death.

22
Medicolegal Pitfalls

• Initial treatment goal should consist of
  optimizing oxygenation and controlling excessive
  airway secretions.
• Tachycardia is neither a contraindication nor an
  endpoint for atropine administration.
• Patients exposed to organophosphate (OP) should
  be observed for at least 12 hours in a high
  acuity setting. Toxicity after this is unlikely.
• Because of the risk of respiratory depression or
  recurrent symptoms after resolution of an acute
  cholinergic crisis, hospitalizing all symptomatic
  patients for at least 48 hours following
  resolution of symptoms is recommended.
• The symptoms of OP poisoning can mimic other
  toxicities and disease processes. The clinician
  must keep in mind that misdiagnosis is a
  potential medicolegal pitfall.