Analytical Profile of Coleus Forskohlii | Forskolin .pptx
poisoning.ppt
1. Poisoning
Ali Alhaboo Assisstant Professor of
Pediatrics
PICU consultant
Overview of pediatric
poisoning, diagnosis and
treatment
Summary of the most
encountered poisoning
2. Epidemiology
Most of the toxic exposures have
only minor or no effect on the child
85% - 90% of pediatric poisoning
occurs in < 5 yrs of age
(accidental) usually single agent
10% - 15% in older age, mainly
adolescents (intensional) usually
several agents
3-4% of PICU admission are
because of toxic exposures
3. ED referral recommendations
Serious exposures
Younger than 6 months
History of previous toxic ingestion
Questionable or unreliable history
5. Common agents Less common but
serious
Cosmetics and
personal care product
Cleaning substance:
flash is more serious than
Clorox because it melts the
esophagus and destroys it.
Plants
Analgesics: Paracetamol
is the commonest cause of
poisoning in children ( high
doses more than 200 mg/kg)
Fe supplements:
2nd most
common in
females.
Antidepressants
Anti-diabetics:
causing severe
hypoglycemia and
LOC.
Anti-
hypertensive.
Pesticides:
organophosphates.
Hydrocarbon
Note: OCPs are not harmful.
6. History
Identification of the toxic agent
Age of the child.
What has been done to the child.
The time elapsed and the dose taken (if it was
unknown consider it serious).
The route of exposure
Underlying medical problems
The clinical effect (with few exceptions rapidity of
symptoms progression correlates with severity of
poisoning.e.g., acetaminophen)
? Trauma in addition to ingestion (change in LOC).
7. Physical Exam
Weight (determine ? mg/kg ingested)
Vital signs
Check odors from the breath, skin, hair,
clothing
Thorough exam for any abnormal finding
24. Toxidromes of Common Pediatric
Poisonings
Toxin Signs or symptoms
Salicylates
Iron
Sympathomimetics
(amphetamines,
phenylpropanolamie
, ephedrine, caffeine,
cocaine,
aminophylline)
Fever, hyperpnea, vomiting,
tinnitus, acidosis, seizure,
lethargy, coma
Hyperglycemia, shock,
hemorrhagic diarrhea
Tachycardia, arrhythmias,
psychosis, hallucinations,
nausea, vomiting,
abdominal pain
25. Laboratory tests
Qualitative toxicology screening is rarely as helpful
as Hx and PE in determining the cause
Best done on urine and gastric aspirate samples
Quantitative serum level of known drug is indicated
when it can enable prediction of toxicity or
determination of treatment
ABGs with respiratory symptoms and to assess
acid-base balance
Blood glucose from 1st sample
Liver and kidney function (metabolism&excretion)
Serum electrolytes (anion gap, renal function)
Serum osmolar gap
CBC (anemia, hemolysis)
DIC panel when suspected
28. Radiography indications
If head trauma cannot be excluded
(skull and cervical spine film, head CT
if physical findings are suggestive)
If child abuse is suspected
(skeletal survey)
If patient is having respiratory distress
(CXRay)
If radiopaque substance is suspected
29. Common substances that are
radiopaque (CHIPES)
Chloral hydrate
Heavy metals
Iodine
Phenothiazine
Enteric coated and extended
release medication
Salt tablets
(in Fe ingestion, serial films indicate movement and elemination)
30. First you have to start with ABC, if hypotensive repeat ABCs.
Check the O2 saturation
Glucocheck for hypoglycemia. If hypoglycemic give 5-10%
dextrose (not higher than that because it might harm the
vessel). Dose: 2-5 ml/Kg.
Do toxicology screen.
LFT, U/E, RFT, coagulation profile (PT is the first to be affected,
if it was elevated give FFP or vitamin K) and albumin.
Give antidote as early as possible if available. (N-acetylcesteine
is the antidote for paracetamol. Desfuroxemine is the antidote
for iron.
Transfer the patient to the ICU, if there is no bed keep him in
the ER.
Steps of management
31. Treatment
Airway: patency and protective mechanisms (if
absent, use nonspecific antidote of D10W 2cc/kg
and Naloxone 0.1mg/kg; if no response intubate.
Breathing: clear secretions, give O2, continuous
O2 saturation, ABGs, CXRay, treat wheezing and
stridor, early controlled intubation prefered
Circulation: frequent VS, continuous CR monitor,
fluids for low BP, do baseline ECG, watch for
arrythmias, PALS guidelines
Neurologic status: frequent assessments, the
most common cause to admit intoxication to PICU,
use nonspecific antidotes, watch for seizures, rule
out metabolic causes of seizure
32. GI decontamination
Emesis-Syrup of Ipecac
Therapy Contraindications
Dosage in < 1 yr 10 ml
Young children 15 ml
Adolescents,
adults 30 ml
may repeat once
Petroleum distillates
Caustic agents
Impaired
consciousness,
seizures
Rapid coma-inducing
agents (e.g.,
propoxyphene, TCAs)
33. We use lavage when the patient presents
early and is stable.
If late presentation where the drug has
already passed to the duodenum use the
activated charcoal( through a NG tube)
where up to 1 million particles can adsorb
to the medication.
34. GI decontamination
Lavage
Therapy Contraindications
Large bore orogastric hose (28 Fr
for young children, 36-40 Fr for
adolescents)
Left recumbent Trendelenburg’s
position to reduce the risk of
aspiration
Lavage with saline or 1/2 NS until
return is clear
Most successful for toxins that
delay gastric emptying (aspirin,
iron, anticholinergics) and for
those forming concretions (iron,
salicylates, meprobamate)
Corrosive
caustic agents
Controversial in
petroleum
distillates
ingestion
Stupor or coma
unless airway is
protected
35. GI decontamination
Activated Charcoal
Therapy Contraindications
Administer in all
cases after
emesis. It should
be only given for
conscious
patients.
Dosage:
- Children 1 g/kg
- Adults 50-100 g
Corrosive agents:
charcoal interfers
with GI endoscopy
Most feared complication
is aspiration leading to
severe pneumonitis and
ARDS
36. GI decontamination
Cathartics
Therapy Contraindications
MgSO4 250 mg/kg/dose
P.O.(max dose 30 g) in
10%-20% solution
Sorbitol magnesium
citrate
Repeat above
doses every 2-4 hrs
until passage of
charcoal stained stools
Avoid MgSO4 in
renal failure
37. Enhanced elimination
Forced diuresis by administering 2-3 times the
maintenance fluid to achieve U.O = 2-5 cc/kg/hr
(contraindicated in pulmonary or cerebral edema and
renal failure)
Urinary alkalinization to eleiminate weak
acids(salicylates, barbiturates and methotrexate), can
be achieved by adding NaHCO3 to the IV fluids, the goal
is urine pH of 7-8
Serum alkalinization in TCAs toxicity
Hemodialysis in low molecular weight substances
with low volume of distribution and low binding to
plasma proteins
Hemoperfusion, protein binding is not a limitation
38. Antidotal Therapy
Only a small proportion of
poisoned patients are amenable to
antidotal therapy
Only a few poisoning is antidotal
therapy urgent (e.g., CO, cyanide,
organophosphate and opioid
intoxication)
39. Specific Intoxications and Their Antidotes
Poison Antidote Indications
Acetaminophen N-Acetylcysteine
(Mucomyst)
Serum level in “probable”
hepatotoxic range
Anticholenergics Physostigmine SVT with hemodynamic
compromise
Beta blockers Glucagon Bradycardia
Isopreterenol,
dopamine,
epinephrine
Bradycardia
Benzodiazepines Flumazenil Symptomatic intoxication
Carbon monoxide O2 Level > 5-10%
Cyanide Amyl nitrite,
sodium nitrite,
sodium thiosulfate
Symptomatic intoxication
Digitalis Specific Fab
antibodies
40. Specific Intoxications and Their Antidotes
Poison Antidote Indications
Ethylene glycol Ethanol Osmolar gap and metabolic acidosis or
Serum level >20 mg/dl regardless of
symptomatology
Iron salts Desferoxamine Symptomatic patients
Serum iron > 350 g/ml or > TIBC
Positive deferoxamine challenge test
Isoniazid Pyridoxine
(vit B6)
Methanol Ethanol Metabolic acidosis and elevated
osmolar gap regardless of symptoms
Methemoglobinemi
a producing agents
Methylene blue Symptomatic poisoning
Methemoglobin level > 30-40 %
Narcotics Naloxane Symptomatic intoxication
Organophosphate
insecticides
Atropine
Pralidoxime
Cholenergic crisis
Fasciculation and weakness
Phenothiazines Diphenhydramine Symptomatic intoxication (oculogyric
crisis)
41. Acetaminophen
(paracetamol) poisoning
Nausea, vomiting and malaise for 24 hrs
Improvement for 24-48 hrs
Hepatic dysfunction after 72 hrs (AST is the
earliest and most sensitive)
Death may occur from fulminant hepatic failue
Toxicity likely with ingestion of > 150 mg/kg
Rumack-Matthew nomogram defines the risk of
hepatic damage in acute intoxication (level at 4
hrs post ingestion)
42. Acetaminophen (paracetamol)
poisoning management
GI decontamination
Activated charcoal within 4 hrs of ingestion
Antidote N-acetylcysteine is most effective if
given within 8 hrs of ingestion, total of 17
doses, P.O or IV (However, NAC should be
given even with > 24hrs presentation)
NAC should be given if serum acetaminophen
level is either in the “possible” or “probable”
hepatotoxic range
45. Prediction of acute salicylate
toxicity
Ingested dose can predict the severity
< 150 mg/kg toxicity not expected
(asymptomatic)
150-300 mg/kg toxicity mild to moderate
(mild to moderate hyperpnea,
lethargy or excitability)
300-500 mg/kg severe toxicity
(severe hyperpnea, coma
or semicoma, sometimes
with convulsions)
46. Management of salicylate toxicity
GI decontamination
Correct dehydration and force diuresis
Urine alkalinization and acidosis correction with
IV NaHCO3
Monitor electrolytes, glucose, calcium
Vit K for hemorrhagic diathesis
Decrease fever with external cooling
Hemodialysis for severe intoxication (Dome
nomogram), severe acidosis unresponsive to
NaHCO3, renal failure, pulmonary edema and
severe CNS manifestation