Compare home pulse pressure components collected directly from home
Case presentation OP.pptx
1. Case Presentation on
Organophosphate Poisoning
Presenter: Dr Shambel (EMCCR1)
Moderator: Dr Abdullaziz (EMCCR3)
Advisor: Dr Yonathan (ECCP)
8/18/2023 1
3. Case Discussion
Emergency Triage:-
• Patient name : XXX
• Age: 17yrs
• Sex: F
• Arrival date- 02/11/15 EC
• Arrival time: 05:30 PM
• Card NO-678767
• Address: Konbolcha
• Mode of arrival- by Ambulance
C/C- Pesticide Ingestion of 3hrs.
V/S
• BP- 64/41
• PR -64
• RR -32
• T- ….
• spo2- 78-82% on atm o2
-92% on FM/10L/Min/
Disposition:
• Red Zone
8/18/2023 3
4. Primary survey
A:
• Airway is patent is patent and protected by the patient
• There is excessive secretion which sucked out frequently with suction machine
• No foreign body & lost teeth
• Cx- collar not indicated
B:
• Midline trachea
• RR -32bpm ( deep,fast & regular)
• SPO2-78-82% on atms.O2 ;92% with FM.
• Diffuse coarse crepitation all over lungfield
8/18/2023 4
5. Cont…
C:
• Bp:68/56, PR:62 (regular ,feeble volume),
• Cold extremity ,capillary refill less than 3 sec
• Focus -Significant multiple B lines bilaterally
• Bilateral IV lines secured & put on N/S
D:
• GCS : 11/15 ( E 4 + V 3 + M 4) ,
• Pupil -pinpoint bilatarally.
• RBS -125mg/dl
E:
• T.????
• Feacal matter & urinary sacked cloth
8/18/2023 5
6. Cont…
HPI
◦ This is a 17yrs female patient who was relatively health before 3hrs at w/c time she
ingested pesticide intentionally due to feeling angry to her family.
In association to this :
◦ She has urine & feacal incontinence,excessive sweeting,SOB,change in mentation &
non billous non projectile ingested matter voming of multiple episodes.
8/18/2023 6
7. Cont…
Otherwise:
◦ No abnormal body mov”t
◦ No allergy & medication Hx
◦ No diagnosed chronic illness
◦ Her last meal is 3hrs prior the event
8/18/2023 7
8. Cont…
PE
◦ G/A- ASL
◦ Other systems: /listed in primary survey/
Ass- Acute Moderate Organophosphoste Poisoning
8/18/2023 8
9. Cont…
Plane
◦ Put on FM.oxygenation
◦ Secured bilateral IV line
◦ Resuscitate with 20ml/kg of N/S.
◦ Start atropine 2mg IV every 5minutes-256mg/atropanization
achieved/
◦ Frequent suctioning
8/18/2023 9
10. Cont…
◦ Wetted clothes remove & changed,well dressed
◦ Meanwhile communicate ICU side for fear of detoriation
◦ To do CBC,UA,OFT,SE,Coagulation profile
◦ Follow wth atropine challenge follow chart
8/18/2023 10
11. Cont…
•Atropanization achieved at 256mg of atropine & plan to descalate
•But in meanwhile the patient become arrested suddenly
•Ventilation with aboubage started & meanwhile the ptn.intubated with RSI
•ICU team arrived & the patient transferred for mechanical ventilation to HICU
&Putted on MV-AC/VC-mode
8/18/2023 11
12. Progress notes on 03/11/15
P1.1st PID for respiratory arrest 2nd org.poisoning
Currently
◦ F-NPO on MV.
◦ A-PCM 1g po QID
◦ S-Thiopental 150mg IV PRN
◦ T-UFH 7500IU SC IV BID
◦ H-head elevation to 30
◦ U-Omeprazole 20mg IV bid
◦ G-glycemic control/108mg/dl/
8/18/2023 12
13. CONT…
A-
◦ Airway patent & protected by ETT No.6.5 fixed at 21cm;oral airway in place
B-
◦ On MV-AC/VC-mode
◦ TV-298,RR-14-27,SPO2-96-98%
◦ Chest is clear with good air entery bilatelly
C-BP.104-131/63-86 ,PR-110-133 ,
D-
GCS-8T(E3,M5,Vt)
◦ Pupil- dilated & NR bilaterally
8/18/2023 13
14. Cont…
E-Not done
F-Total input 800ml,output 400ml- balance +400ml
G-OGT is in place
I-Listed on investigation summery
ASS= The same
plan
to do SE
update OFT
follow closely
8/18/2023 14
18. Progress note on 05/11/15
The patient is improving overall and they plan to:
◦ Revise CBC
◦ Started weaning with CPAP
◦ Check for feeding intermittently
◦ Start dexamethasone 6mg iv qid
◦ Plan to consult senior & consider extubation for next day
8/18/2023 18
26. Cont…
Strength
Early diagnosis & intervention
Early interdepartmental communication &
respond
Good emergency team coordination & co-
working
Availability of emergency drug/atropine/ in
our hospital at a time
Limitation & pitfall
Nonfunctionality of our machine/MV./
Absence of radient warmer at ED
No isolated decontamination area
Not linked to psychiatric dept.on discharge
Delayed investigation
No temperature record
8/18/2023 26
30. Epidemiology
Worldwide, an estimated 3,000,000 people are exposed to organophosphate
or carbamate agent each year.
Which accounts up to 300,000 fatalities.
8/18/2023 30
31. Pathophysiology
Organophosphorus pesticides work by persistently inhibiting
the enzyme acetylcholinesterase, the enzymatic deactivator of
the neurotransmitter acetylcholine.
Inhibition of cholinesterase results in the accumulation and
subsequent prolonged effect of acetylcholine at a variety of
neurotransmitter receptors
8/18/2023 31
32. Cont…
Organophosphate compound bind irreversibly to
acetylcholinestares
Thus inactivating the enzyme through the process of
phosphorylation.
Aging → permanent, irreversible binding of the organophosphate
compound to the cholinesterase.
8/18/2023 32
33. Clinical Features
•Onset and duration of AChE inhibition varies depending on the:-
Organophosphorous agent's rate of AChE inhibition,
The route of absorption,
Enzymatic conversion to active metabolites, and
The lipophilicity of the organophosphorous agent.
8/18/2023 33
34. Cont..
Lipophilic agents such as dichlofenthion, fenthion, and malathion
are associated with delayed onset of symptoms (up to five days)
and prolonged illness (greater than 30 days), which may be related
to rapid adipose fat uptake and delayed redistribution from the fat
stores.
8/18/2023 34
35. Cont…
For most agents, oral or respiratory exposures generally result in
signs or symptoms within three hours
Symptoms of toxicity from dermal absorption may be delayed up to
12 hours
8/18/2023 35
36. Acute toxicity
Acute toxicity from organophosphorous agents presents with manifestations of cholinergic
excess.
Primary toxic effects involve the autonomic nervous system, neuromuscular junction, and
central nervous system (CNS).
8/18/2023 36
37. Cont…
The muscarinic signs can be remembered by use of one of two
mnemonics:
SLUDGE/BBB - Salivation, Lacrimation, Urination, Defecation,
Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia
DUMBELS - Defecation, Urination, Miosis,
Bronchorrhea/Bronchospasm/Bradycardia, Emesis, Lacrimation,
Salivation.
8/18/2023 37
39. Cont…
The nicotinic effects include fasciculations, muscle weakness, and
paralysis via acetylcholine stimulation of receptors at the
neuromuscular junction.
This mechanism is analogous to the depolarizing effects of
succinylcholine in producing neuromuscular blockade.
Nicotinic and muscarinic receptors also have been identified in the
brain, and may contribute to central respiratory depression,
lethargy, excitability, seizures, and coma
8/18/2023 39
40. Cont…
Fatalities from acute organophosphorous agent poisoning
generally result from respiratory failure due to a combination of
depression of the CNS respiratory center, neuromuscular
weakness, excessive respiratory secretions, and
bronchoconstriction.
Fatalities also occur due to cardiovascular collapse; although the
mechanism of this dysfunction is not completely understood,
inappropriate vasodilation may play a role.
8/18/2023 40
41. Intermediate syndrome
10 to 40 percent of organophosphorous agent poisoned patients
develop a distinct neurologic disorder within 24 to 96 hours after
exposure.
This disorder, referred to as the "intermediate syndrome," consists
of characteristic neurological findings including, decreased deep
tendon reflexes, cranial nerve abnormalities, proximal muscle
weakness, and respiratory insufficiency, neck flexion weakness.
8/18/2023 41
42. Delayed toxicity
Organophosphorous agent induced delayed neuropathy (OPIDN)
typically occurs one to three weeks after ingestion.
The mechanism may involve inhibition of neuropathy target
esterase (NTE), rather than alterations in RBC
acetylcholinesterase function .
This enzyme, which is found in the brain, peripheral nerves, and
lymphocytes, is responsible for the metabolism of various esters
within the cell.
8/18/2023 42
43. Cont…
Delayed neurotoxicity primarily affects distal muscle groups, but in
severe neurotoxicity, proximal muscles groups may also be
affected
Sensory disturbances are usually mild.
8/18/2023 43
45. DIAGNOSIS
The diagnosis of organophosphate or carbamate poisoning is
made on clinical grounds.
In the absence of a known ingestion or exposure, the clinical
features of cholinergic excess should indicate the possibility of
organophosphate poisoning.
Many organophosphorous agents have a characteristic petroleum
or garlic-like odor, which may be helpful in establishing the
diagnosis.
8/18/2023 45
46. Management
Treatment is directed toward four goals:
(1) Decontamination,
(2) Prevention of Absorption,
(3) Reversal of acetylcholine excess at muscarinic sites, and
(4) Reversal of toxin binding at active sites on the cholinesterase
molecule.
8/18/2023 46
47. 1) Decontamination
In cases of topical exposure with potential dermal absorption,
aggressive decontamination with complete removal of the patient's
clothes and vigorous irrigation of the affected areas should be
performed.
The patient's clothes and belongings should be discarded since
they absorb organophosphorous agents, and reexposure may
occur even after washing.
8/18/2023 47
48. (2) Prevention of Absorption
Do not induce vomiting
There is no published evidence demonstrating that gastric lavage
improves outcome following organophosphate ingestion.
Gastric lavage undertaken within 1 hour of a very large ingestion
(following airway protection via endotracheal intubation) may be
beneficial, but its performance should not delay timely administration of
antidotal therapy.
Activated charcoal is sometimes recommended because
organophosphates do bind in vitro, although there is no evidence that
single or multiple doses of activated charcoal improve patient outcome.
8/18/2023 48
49. (3) Reversal of acetylcholine excess at
muscarinic sites
Atropine competes with acetylcholine at muscarinic receptors,
preventing cholinergic activation. For moderate to severe
cholinergic toxicity, atropine should be administered beginning at a
dose of 2 to 5 mg IV for adults and 0.05 mg/kg IV for children.
If no effect is noted, the dose should be doubled every three to five
minutes until pulmonary muscarinic signs and symptoms are
alleviated.
8/18/2023 49
50. (4) Reversal of toxin binding at active sites
on the cholinesterase molecule
Since atropine does not bind to nicotinic receptors, it is ineffective
in treating neuromuscular dysfunction.
Pralidoxime (2-PAM) is cholinesterase reactivating agents that are
effective in treating both muscarinic and nicotinic symptoms.
8/18/2023 50
51. Cont…
Pralidoxime therapy be given to all patients with evidence of cholinergic
toxicity, patients with neuromuscular dysfunction, or patients with
exposures to organophosphorous agents known to cause delayed
neurotoxicity .
The current World Health Organization recommendation for IV bolus
therapy with pralidoxime is at least 30 mg/kg in adults, and 25 to 50
mg/kg for children, based upon the severity of symptoms
8/18/2023 51
56. Disposition
Minimal exposures may require only decontamination and
6 to 8 hours of observation in the ED to detect delayed effects.
Admission to the intensive care unit is necessary for significant poisonings.
8/18/2023 56
Once aging occurs, the enzymatic activity of cholinesterase is permanently destroyed and a new enzyme must be resynthesized over a period of weeks.
If doubt exists as to whether an organophosphate or carbamate has been ingested, a trial of 1 mg atropine in adults (or 0.01 to 0.02 mg/kg in children) may be employed.
Health care workers must take precautions to avoid accidental exposure, including providing treatment in a well-ventilated area.
