This document summarizes a presentation on the management of poisoning. It begins with an overview of general principles for evaluating and initially treating poisoning cases. These include assessing the airway, breathing, circulation, and administering glucose and thiamine if needed. Specific types of poisoning are then discussed, including organophosphate and carbamate poisoning. For these cases, signs and symptoms relate to excess cholinergic activity. Management involves supportive care, administration of atropine as an antidote, and consideration of intubation for severe cases.

1. P R E S E N T E R : M E L E S E K I F L E ( M E D I C A L
I N T E R N )
M O D E R A T O R : D R F E K A D U ( I N T E R N I S T )
SEMINAR ON MANAGEMENT
OF POISONING

2. Presentation outline
 Case presentation
 Introduction
 General principles of management of poisoning
 Management of specific selected poisoning

3.  Identification
name:sime w/giworgis
age:55 yrs
sex:male
address:shirka
Admission date:29/10/07
 c/c:2,4-D poisoning of 4 hrs duration

4.  HPI: this is 55 yrs old male patient came after taking
2,4-d poisoning of about two areque cup .one hour after
ingestion of poison he started to experience vomiting of
ingested matter ,drooling of saliva, incontinence for both
feces and flatus.referred from health center with
asssment of organophosphate poisoning +aspiration
pneumonia.
 The patient experienced suicidal attempt two times
previously.he was experience abnormal behavior 02
months back cxd by shouting over close relatives and
dpression and loss of hope for which he uses unknown
traditional medication.he didn’t seek medical advice.

5.  He has no abnormal body movement, no travel
history to malaria endemic area ,no contact hx with
chronic cougher,not from malaria endemic area.his
serostatus was negative .he has no self or family
history of DM ,HTN,cardiac,renal and liver disease.

6.  PE
GA:ASL,comatose
v/s:BP=unrecordable PR=not palpable (apical 64)regular RR=44
T=35C
HEENT:pink conjunctiva,NIS,dry buccal mucosa
bloody mixed oral secretion
malathion odour up on breathing
LGS: no LAP
RS: deep breathing in RD,I/C and S/C retraction
transmitted sound all over lung field
CVS: quiet precordium ,jvp not raised
s1 and s2 well heard
ABD: flat moves with respiration
no organomegally
no sign of fluid collection

7.  GUS
 INT:no rash
 MSK: no edema
 CNS:comatose with GCS 3/15(E=,V=,M=)
pupil pin point and not reactive bilaterally
difficult to elicit meningeal sign
motor 0/5 in all extremity
DRT:arreflexia in all exterimity
ASS’T:COMA 2 TO 2,4-D POISONING+HYPOVOLUMIC
SHOCK 2 TO GI LOSS
ASPIRATION PNEUMONIA

8.  DONE: put on 100% o2 with face mask
iv line secured and resuscitated with crystalloids
catheterized and NG tube inserted
coma care given
cimetidine 400 mg iv loading the 200mg iv TID
ceftriaxone 1gm iv BID
metronidazole 500mg TID
atropine 2 gm iv every 20’ until secretion stopped
followed by neurosign chart

9. Date time bp pr rr t Pupillary reflex UOP GCS RBS atropi
ne
input motor seizur
e
29/1
0/07
3:55
pm
unrecorda
ble
64 44 35 Pinpoint and
fixed
3/15 126 2gm iv NS NO
4:15
pm
140/80 126 40 AT
T
“ “ 2gm iv “ “
4:45
pm
90/50 134 40 - “ “ 2gm iv “ “
5:15
PM
90/60 130 44 36.
5
Dilated and
non reactive
“ “ “
5:40
PM
90/50 136 42 36 “ 900ml/2
hr
“ 2gmiv “ “
6:40
pm
90/60 130 48 35.
4
“ “
7:40
pm
90/50 126 44 35.
4
“ “
8:40
pm
90/50 130 46 36 “ “
9:40
pm
90/60 140 40 36.
1
“ “
10:4
0pm
80/50 128
feeb
le
48 36 “ 2000ml/
6hr
RL “

10.  At around 10:20pm the patient started to gasp and
final v/s was BP=80/50 PR=126 feeble rr=46 t=35
HEENT: frank red bloody vomiting,secreted
andsuctioned with syringe
RS: transmitted sound all over chest
msk:cold extremity
CNS:comatose GCS 3/15
pupil dilated and non reactive bilaterally
motor 0/15 in all extremity
The patient expired at 10:30pm with possible cause of
death being respiratory failure 2 to 2,4-d poisoning

11. Introduction
 Poisoning refers to the development of dose-related
adverse effects following exposure to chemicals,
drugs, or other xenobiotics.
 There is ,however ,substantial individual variability
in response to and disposition of a given dose.
 Some of this variability is genetic, and some is
acquired on basis of enzyme induction or inhibition,
or because of tolerance.

12.  The most commonly implicated poisoning exposures
were due to analgesics(10.6%) , cleaning
substances(9.5%) , cosmetics(9.2%),foreign
bodies(5.1%) plants(4.7%) , sedative-hypnotics and
antipsychotics(4.4%), and cough and cold
preparations(4.3%).
 Fatalities most commonly resulted from carbon
monoxide poisoning or the ingestion of analgesics,
sedative-hypnotics, antipsychotics, antidepressants,
street drugs, cardiovascular drugs, or alcohols .

13.  Acetaminophen is the pharmaceutical agent most
often implicated in fatal poisoning.
 Overall, carbon monoxide is the leading cause of
death from poisoning

14. INITIAL EVALUATION AND TREATMENT
 A brief initial screening examination should be
performed on all patients to identify immediate
measures required to stabilize and prevent
deterioration of the patient.
 Evaluation involves recognition that poisoning has
occurred, identification of agents involved,
assessment of severity, and prediction of toxicity.

15.  Go for ABC of life
 The airway should be assessed and endotracheal
intubation strongly considered if there is doubt
about the patient's ability to protect the airway and
avoid aspiration.
 Vital signs, mental status, and pupil size should be
rapidly assessed, and pulse oximetry, continuous
cardiac monitoring, and an electrocardiogram
performed.

16.  Intravenous access should be obtained, and in-line
cervical immobilization is required in patients with
suspected occult trauma.
 Advanced cardiac life support measures must be
provided as required.

17.  Altered consciousness requires the rapid intravenous
administration of 100 mg of thiamine and 25 g of
dextrose (as 50 mL of a 50 percent dextrose solution)
for possible Wernicke's encephalopathy and
hypoglycemia, respectively.
 Complete exposure and examination of the patient
and measurement of core temperature are essential.

18.  The correct diagnosis can usually be established by
the history, physical examination, routine and
toxicologic laboratory evaluations, and characteristic
clinical course.

19.  The history should include
 the time, route, duration, and circumstances
(location, surrounding events, and intent) of
exposure
 the name and amount of each drug, chemical, or
ingredient involved;
 the time of onset, nature, and severity of symptoms
 the time and type of first-aid measures provided and
 the medical and psychiatric history.

20.  The physical examination should focus
 initially on the vital signs, cardiopulmonary system, and
neurologic status.
 The neurologic examination should include
documentation of neuromuscular abnormalities such as
dyskinesia, dystonia, fasciculation's, myoclonus, rigidity,
and tremors.
 The evidence of trauma and underlying illnesses.
 Focal neurologic findings are uncommon in poison
 all orifices should be examined for the presence of
chemical burns and drug packets.
 The odor of breath or vomitus and the color of nails, skin,
or urine may provide important diagnostic clues

21.  Examination of
 the eyes (for nystagmus, pupil size and reactivity)
 abdomen (for bowel activity and bladder size), and
 skin (for burns, bullae, color, warmth, moisture,
pressure sores, and puncture marks)
 The mental status, vital signs, and pupillary
examination are the most useful elements and
allow classification of the patient into either a state
of physiologic excitation or depression .

22.  Physiologic excitation,
 manifested by central nervous system stimulation
and increased pulse, blood pressure, respiratory rate
and depth, and temperature, is most commonly
caused by anticholinergic, sympathomimetic, or
central hallucinogenic agents, or by drug withdrawal
states.

23.  Physiologic depression
 manifested by a depressed mental status, blood
pressure, pulse, respiratory rate and depth, and
temperature, is most commonly precipitated by
cholinergic (parasympathomimetic), sympatholytic,
opiate, or sedative-hypnotic agents, or alcohols.

24.  Mixed physiologic effects
 occur in polydrug overdoses or following exposure to
certain metabolic poisons (eg, hypoglycemic agents,
salicylates, cyanide), membrane-active agents (eg,
volatile inhalants, antiarrhythmic drugs, local
anesthetic agents), heavy metals (eg, iron, arsenic,
mercury, lead), or agents with multiple mechanisms
of action (eg, tricyclic antidepressants).

25. phase of poisoning and their management
 The preclinical phase: follows exposure but
precedes the development of signs and symptoms.
 Management is guided by the history and is aimed
at reducing or preventing the predicted toxicity .
 Decontamination is a priority

26.  The toxic phase: encompasses the period from the
onset to the peak of clinical or laboratory
manifestations of toxicity.
 The management objectives are to shorten the
duration and lessen the severity of toxicity.
 Treatment is guided largely by the physical
examination.
 The highest priorities in this phase are to stabilize
the patient's airway, breathing, and circulation, and
to administer antidote

27.  The resolution phase runs from peak toxicity to
recovery. Management is guided by clinical status,
and the major goal is to shorten the duration of
toxicity

28. Fundamentals of poisoning managment
 the provision of supportive care,
 prevention of poison absorption, and,
 when appropriate, the administration of antidotes
 enhancement of elimination of the poison.
 Prevention of reexposure

29.  Supportive care
 Airway protection
 Oxygenation/ventilation
 Treatment of arrhythmias
 Hemodynamic support

30.  Prevention of Further Poison Absorption
 Gastrointestinal decontamination
 Gastric lavage
 Activated charcoal
 Whole-bowel irrigation
 Dilution
 Endoscopic/surgical removal

31.  Administration of Anti-dotes
 Neutralization by antibodies
 Neutralization by chemical binding
Antidotes reduce or reverse poison effects by a variety
of means. They may- prevent absorption
-bind and neutralize poisons directly
- they inhibit conversion to more severe toxic
metabolite

32.  Enhancement of Poison Elimination
 Multiple-dose activated charcoal
 Alteration of urinary pH Chelation
 forced diuresis, urine ion trapping,
 hemodialysis, hemoperfusion, hemofiltration, and
exchange transfusion
 Prevention of Reexposure
 Adult education
 Child-proofing

33.  The presence of any of eight clinical criteria predicted a
complicated hospital course that could be best managed in an
ICU:
 PaCO2 >45 mmHg
 A need for emergency intubation
 The presence of postingestion seizures
 Unresponsiveness to verbal stimuli
 A non-sinus cardiac rhythm
 Second- or third-degree atrioventricular block
 Systolic blood pressure less than 80 mmHg
 QRS duration ≥0.12 seconds

34. MANAGEMENT OF SELECTED
POISONING
1) ORGANOPHOSPHATE and CARBAMATE
POISONING
 are potent cholinesterase inhibitors capable of
causing severe cholinergic toxicity following
cutaneous exposure, inhalation, or ingestion.
 Specific agents linked to human poisoning include
both carbamates (methomyl and aldicarb) and
organophosphate (parathion, fenthion, malathion,
diazinon, and dursban.)

35.  Organophosphate also inhibit plasma cholinestrase
and neuropathy target esterase
 Carbamate is transient cholinesterase inhibitors.
 They spontaneously hydrolyze from cholinesterase
enzymatic site within 48 hrs.
 Shorter duration of toxicity but mortality rate is
similar.

36. Clinical manifestation
 Onset and duration of AChE inhibition varies
depending on the organophosphorus agent's rate of
AChE inhibition, the route of absorption, enzymatic
conversion to active metabolites, and the
lipophilicity of the organophosphorus agent.
 Sign and symptoms may appear whithin three hrs
after oral and respiratory exposure but dermal
absorption may be delayed up to 12hrs.

37.  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.

38.  Acute toxicity -presents with manifestations of
cholinergic excess.
 Primary toxic effects involve the autonomic nervous
system, neuromuscular junction, and central nervous
system (CNS).
 The muscarinic signs are dominant features and can
be remembered by use of mnemonics:
 SLUDGE/BBB or DUMBELS– S alivation, L
acrimation, U rination, D efecation, G astric E
mesis, B ronchorrhea, B ronchospasm, B radycardia

39.  Nicotinic effects-fasciculation,muscle weakness,
paralysis
 cardiac arrhythmias, including heart block and QTc
prolongation, are occasionally observed
 Fatalities from acute organophosphorus 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.

40.  Fatalities also occur due to cardiovascular collapse
 Survivors may have neurobehavioral deficits such as
decreased memory, abstraction, and Parkinsonism,
which may be permanent

41.  Intermediate syndrome — 10 to 40 percent of
patients develop a distinct neurologic disorder 24 to
96 hours after exposure.
 These include:- neck flexion weakness, decreased
deep tendon reflexes, cranial nerve abnormalities,
proximal muscle weakness, and respiratory
insufficiency

42. Delayed neurotoxicity — Organophosphorus
agent induced delayed neuropathy (OPIDN) typically
occurs one to three weeks after ingestion.
 Affected patients present with transient, painful
"stocking-glove" paresthesias followed by a
symmetrical motor polyneuropathy characterized by
flaccid weakness of the lower extremities, which
ascends to involve the upper extremities

43. Management
 Initial resuscitation — the severely poisoned
patients with markedly depressed mental status
require 100 percent oxygen and immediate
endotracheal intubation.
 patients with mild to moderate poisoning should
also be considered for early endotracheal intubation.

44.  Bradycardia and hypotension are usually
present in moderate to severe poisonings. Adequate
volume resuscitation with isotonic crystalloid (eg,
normal saline or lactated Ringer's solution) should
be performed

45.  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.

46.  Gastric lavage may be done in patients who
present less than one hour following ingestion of an
organophosphorus agent, after performing
endotracheal intubation and initiating therapy with
atropine and an oxime.
 Activated charcoal (AC) may be given to patients
presenting within one hour an organophosphorus
agent or carbamate ingestion.
 The standard dose is 1 g/kg (maximum dose 50
grams).

47.  Atropine — atropine should be administered
beginning at a dose of 2 to 5 mg IV for adults. If no
effect is noted, the dose should be doubled every
three to five minutes until pulmonary muscarinic
signs and symptoms are alleviated.
 Atropine dosing should be titrated to the
therapeutic end point of the clearing of respiratory
secretions and the cessation of bronchoconstriction

48.  Pralidoxime —Since atropine does not bind to
nicotinic receptors, it is ineffective in treating
neuromuscular dysfunction.
 Pralidoxime should be administered slowly over 30
minutes, since rapid administration has occasionally
been associated with cardiac arrest.
 The current World Health Organization
recommendation for IV bolus therapy with
pralidoxime is at least 30 mg/kg in adults

49.  Pralidoxime should NOT be administered without
concurrent atropine in order to prevent worsening
symptoms due to transient oxime-induced
acetylcholinesterase inhibition.

50.  Benzodiazepines — Organophosphorus agent-
induced seizures should be treated with a
benzodiazepine.
 Prophylactic diazepam has been shown to decrease
neurocognitive dysfunction after organophosphorus
agent poisoning.
 Phenytoin ?

51. 2)2,4 –dichlorophenoxy acetic acid
poisoning
 It is a common systematic herbicide used in control
of broad leaf weeds.
 Is a member of the phenoxy family of herbicides
 Ingestion of 2,4,D will result central nervous system
depressant and it is also respiratory system irritant
that can cause prolonged difficulty of breathing and
coughing .

52.  The primary target organ of this chemical are , eye,
thyroid, kidney , adrenals, ovaries, and testes
 Severe intoxication with 2,4,D has poor prognosis.
 They have been considered as carcinogenic to
humans.

53. 3)Hydrocarbon Poisoning
 These include kerosene, turpentine, lubricating oils,
tar
 They have greatest risk of aspiration and pulmonary
symptoms.
 They may result in complications like
pneumothorax,pleural effusion, secondary bacterial
infection and even respiratory failure.

54.  Gastric lavage is contra indicated.
 If gastric lavage is necessary a cuffed endotracheal
tube should be inserted in to patients air way before
lavage.

55. 4)Caustics poisoning
 Includes acid and base poisoning
 Examples of acid:-include metals,batteriers
 Examples of bases:- include dish washing detrgents,
liqiud plummer
 Burning of mucus may bee seen upon presentation,
difficulty of swallowing and drooling of the saliva.

56. managment
 Emesis and gastric lavage are contraindicated nor
should activated charcoal used.
 Endoscopy should be done in patients whose
history is suggestive of burns from caustic ingestion

57. REFERENCES
1)Harrison principles of internal medicine,18th edition
2)Uptodate 21.2
3)
4)