Toxicology

1. ToxicologyToxicology
Dalhousie Critical Care Lecture SeriesDalhousie Critical Care Lecture Series

2. ICU
ObjectivesObjectives
1.1.Discuss findings of sympathomimetic, anti-cholinergic, cholinergic Discuss findings of sympathomimetic, anti-cholinergic, cholinergic
and narcotic toxidromesand narcotic toxidromes
2.2.Discuss the essential investigations of a potential drug overdose.Discuss the essential investigations of a potential drug overdose.
3.3.Demonstrate the ability to calculate an anion gap, serum Demonstrate the ability to calculate an anion gap, serum
osmolality and osmolar gap. What is the significance of an osmolality and osmolar gap. What is the significance of an
elevated AG or osmolar gap?elevated AG or osmolar gap?
4.4.Discuss the presentation and management of common overdoses Discuss the presentation and management of common overdoses
including:including:
1.1.Toxic AlcoholsToxic Alcohols
2.2.ASAASA
3.3.TylenolTylenol
4.4.TCAsTCAs
5.5.Neuroleptic Malignant Syndrome and Serotonin syndromeNeuroleptic Malignant Syndrome and Serotonin syndrome
5.5.Which overdoses require nephrology consults for consideration of Which overdoses require nephrology consults for consideration of
dialysis?dialysis?

3. ICU OverdoseOverdose
Requires high index of suspicionRequires high index of suspicion
Non-specific symptomsNon-specific symptoms
Tylenol O/DTylenol O/D
Presents as other issuesPresents as other issues
AMI in setting of CO overdoseAMI in setting of CO overdose

4. ICU OverdoseOverdose
Suspect in the setting of:Suspect in the setting of:
Altered LOC/comaAltered LOC/coma
TraumaTrauma
Life threatening arrythmiaLife threatening arrythmia
Unexpected clinical findingsUnexpected clinical findings

5. ICU Diagnosis - HistoryDiagnosis - History
May be unreliable or incompleteMay be unreliable or incomplete
Things to considerThings to consider
History of depression/prior overdoseHistory of depression/prior overdose
Time of ingestion/last seen wellTime of ingestion/last seen well
Pill bottles present at scenePill bottles present at scene
Time of last refillTime of last refill
Medications of family memebersMedications of family memebers

6. ICU Diagnosis - PEDiagnosis - PE
VitalsVitals
HR, BP, RR, Temp, O2 satHR, BP, RR, Temp, O2 sat
NeuroNeuro
LOC, pupilsLOC, pupils
CVSCVS
ArrythmiasArrythmias
SkinSkin

7. ICU
Increased Osmolal GapIncreased Osmolal Gap
Osmolarity = 2x[Na] + glc + ureaOsmolarity = 2x[Na] + glc + urea
Osmolar gap = measured – calculated Osmolar gap = measured – calculated
normal = between 270 -290normal = between 270 -290
Normal osmolar gap <10 Normal osmolar gap <10

8. ToxicologyToxicology
Critical Care Lecture SeriesCritical Care Lecture Series

9. ICU What is a toxidrome?What is a toxidrome?
A collection of symptoms and signs that
consistently occur after ingestion of a
particular toxin or drug class or agent
Often identified with a basic history &
physical examination
Rapid identification of the toxidrome saves
time in evaluating and managing a
poisoned patient

10. ICU AnticholinergicAnticholinergic
MydriasisMydriasis
Blurred visionBlurred vision
FeverFever
Flushed dry skinFlushed dry skin
Psycosis, comaPsycosis, coma
SeizuresSeizures
IleusIleus
Urinary retentionUrinary retention
HypertensionHypertension
TachycardiaTachycardia
•Eg. TCA, antihistamines, atropine, benztropine
•Blind as a bat, hot as a hare, dry as a bone, red as
a beet, mad as a hatter

11. ICU
Anticholinergic Toxidrome - Anticholinergic Toxidrome -
ManagementManagement
ABC, supportive care, consider GI decontamination
Benzodiazepines
Physostigmine – specific antidote. – specific antidote.
May be used ifMay be used if
Severe agitation or psychosis unresponsive to other therapySevere agitation or psychosis unresponsive to other therapy
Sever peripheral and central anticholinergic featuresSever peripheral and central anticholinergic features
NO history of seizures history of seizures
Normal ECG especially QRS duration ECG especially QRS duration
NO co-ingestion of drugs altering intraventricular conduction co-ingestion of drugs altering intraventricular conduction
E.g. TCA’sE.g. TCA’s
Cardio-respiratory monitoring and resus facilities in placeCardio-respiratory monitoring and resus facilities in place

12. ICU CholinergicCholinergic
Eg. organophosphates, nerve agentsEg. organophosphates, nerve agents
DUMBELSDUMBELS
D-diaphoresis, diarrhea, decreased BPD-diaphoresis, diarrhea, decreased BP
U-urinationU-urination
M-miosisM-miosis
B-bronchorrhea, bronchospasm, bradyB-bronchorrhea, bronchospasm, brady
E-emesis, excitiation of skeletal muscleE-emesis, excitiation of skeletal muscle
L-lacrimationL-lacrimation
S-salivation, seizuresS-salivation, seizures

13. ICU
Cholinergic Toxidrome - Cholinergic Toxidrome -
ManagementManagement
ABC, supportive care
Decontamination procedures
Atropine
ACh antagonistACh antagonist
AntimuscarinicAntimuscarinic
Pralidoxime (2-PAM)
Regenerates AcetylcholinesteraseRegenerates Acetylcholinesterase
Removes phosphoryl group from enzymeRemoves phosphoryl group from enzyme
Must be given early before phosphorylation becomes Must be given early before phosphorylation becomes
irreversible (“aging”)irreversible (“aging”)

14. ICU
Sympathomimetic Sympathomimetic
(adrenergic) toxidrome(adrenergic) toxidrome
Increased tempIncreased temp
TachycardiaTachycardia
HypertensionHypertension
Dilated pupilsDilated pupils
CNS excitiationCNS excitiation
SeizuresSeizures
Nausea/vomitingNausea/vomiting
DiaphoresisDiaphoresis
Cocaine, MDMA (“ecstasy”), Amphetamines, Phencyclidine Cocaine, MDMA (“ecstasy”), Amphetamines, Phencyclidine
(PCP), Theophylline, Decongestants ((PCP), Theophylline, Decongestants (Ephedrine Pseudoephedrine
Phenylpropanolamine), Caffeine (very large doses)Caffeine (very large doses)

15. ICU
Adrenergic Toxidrome - Adrenergic Toxidrome -
ManagementManagement
ABC, supportive care, consider GI decontamination
Investigations
Screen for other drugs & treatable toxins (eg, acetaminophen, salicylate)Screen for other drugs & treatable toxins (eg, acetaminophen, salicylate)
Electrolytes (esp. sodium), urea, creatinine, blood sugar, anion gap. Electrolytes (esp. sodium), urea, creatinine, blood sugar, anion gap.
CK levels to check for rhabdomyolysisCK levels to check for rhabdomyolysis
Consider cranial CTConsider cranial CT
EKG & Cardiac biomarkers (eg, CPK-MB, troponin)EKG & Cardiac biomarkers (eg, CPK-MB, troponin)
Sedation – treats majority of effects – treats majority of effects
BenzodiazepinesBenzodiazepines
Temperature control
Treat hypertension unresponsive to benzodiazepines unresponsive to benzodiazepines
NitroprussideNitroprusside
NitroglycerineNitroglycerine
Labetalol (avoid isolated Labetalol (avoid isolated -blockade in mixed adrenergic agonist toxicity)-blockade in mixed adrenergic agonist toxicity)

16. ICU NarcoticNarcotic
HypothermiaHypothermia
BradycardiaBradycardia
HypotensionHypotension
Respiratory depressionRespiratory depression
Constricted pupilsConstricted pupils
CNS depressionCNS depression

17. ICU
Opioid-Narcotic Toxidrome - Opioid-Narcotic Toxidrome -
ManagementManagement
ABC, supportive care
GI decontamination for oral ingestion
Naloxone
Specific antagonistSpecific antagonist
High doses may be needed for methadone & High doses may be needed for methadone &
pentazocinepentazocine
Short half-life compared to opioidsShort half-life compared to opioids
Infusion may be requiredInfusion may be required
Pulmonary edema and seizures have been reportedPulmonary edema and seizures have been reported

18. ICU
Serotoninergic ToxidromeSerotoninergic Toxidrome
Diarrhoea, trismus, myoclonus, tremor, rhabdoOther
Normal/decreased (SIADH possible)Urination
IncreasedBowel sounds
IncreasedReflexes
Normal/flushed/sweatingSkin
NormalMucous membranes
Normal/unreactivePupils
Agitated/irritableMental status
Physical examination
Normal/decreasedBlood pressure
IncreasedTemperature
IncreasedHeart rate
Normal/increasedRespiratory rate
Vital Signs
Eg. SSRI’s, MAOI’s, ecstasyEg. SSRI’s, MAOI’s, ecstasy

19. ICU
Serotoninergic Toxidrome - Serotoninergic Toxidrome -
FeaturesFeatures
Mental status changes
• Confusion (51%)Confusion (51%)
• Agitation (34%)Agitation (34%)
• Hypomania (21%)Hypomania (21%)
• Anxiety (15%)Anxiety (15%)
• Coma (29%)Coma (29%)
Cardiovascular
• Sinus tachycardia (36%)Sinus tachycardia (36%)
• Hypertension (35%)Hypertension (35%)
• Hypotension (15%)Hypotension (15%)
Gastrointestinal
• Nausea (23%)Nausea (23%)
• Diarrhea (8%)Diarrhea (8%)
• Abdominal pain (4%)Abdominal pain (4%)
• Salivation (2%)Salivation (2%)
Motor Abnormalities
• Myoclonus (58%)Myoclonus (58%)
• Hyperreflexia (52%)Hyperreflexia (52%)
• Muscle rigidity (51%)Muscle rigidity (51%)
• Restlessness (48%)Restlessness (48%)
• Tremor (43%)Tremor (43%)
• Ataxia/incoordination (40%)Ataxia/incoordination (40%)
• Shivering (26%)Shivering (26%)
• Nystagmus (15%)Nystagmus (15%)
• Seizures (12%)Seizures (12%)
Other
• Diaphoresis (45%)Diaphoresis (45%)
• Unreactive pupils (20%)Unreactive pupils (20%)
• Tachypnea (26%)Tachypnea (26%)
• Hyperpyrexia (45%)Hyperpyrexia (45%)
Sternbach H. The serotonin syndrome. Am J Psychiatry 1991;148:705-
13
Mills KC. Serotonin syndrome. Am Fam Physician 1995;52:1475-82

20. ICU
Serotoninergic Toxidrome - Serotoninergic Toxidrome -
ManagementManagement
Stop intake of causative agentStop intake of causative agent
ABC, supportive careABC, supportive care
AbsorptionAbsorption
Gastric lavage in early acute ingestion (1hr)
Activated charcoal
BenzodiazepinesBenzodiazepines
OthersOthers
Chlorpromazine
Diphenhydramine
? Serotonin antagonists e.g. cyproheptadine

21. ICU Diagnosis - InvestigationDiagnosis - Investigation
Essential labsEssential labs
CBC, lytes, BUN, Cr, BS CBC, lytes, BUN, Cr, BS
Ptt, INR, LFTsPtt, INR, LFTs
ABG (calculate AG)ABG (calculate AG)
Serum osmo (calculate osmo gap)Serum osmo (calculate osmo gap)
ASAASA
AcetaminophenAcetaminophen
OtherOther
Drug levelsDrug levels
UrineUrine

22. ICU
General ManagementGeneral Management
ABCABC
Consider thiamine, dextrose, naloxone if depressed GCSConsider thiamine, dextrose, naloxone if depressed GCS
Prevent further absorptionPrevent further absorption
Decontaminate eyes, clothes, skin, hair if appropriate eyes, clothes, skin, hair if appropriate
Activated charcoal + sorbitol (if < 1 hour from ingestion) + sorbitol (if < 1 hour from ingestion)
Gastric lavage (if < 1 hour from ingestion and life-threatening drug or dose) (if < 1 hour from ingestion and life-threatening drug or dose)
In general not usedIn general not used
Whole bowel irrigation for “body packing” illicit drugs for “body packing” illicit drugs
In general not usedIn general not used
Enhance eliminationEnhance elimination
Forced diuresis and urinary alkalinisation (salicylates and barbiturates) (salicylates and barbiturates)
Multiple dose activated charcoal 0.5 g/kg every 2-4 hours 0.5 g/kg every 2-4 hours
binds toxin and interrupts enterohepatic recirculationbinds toxin and interrupts enterohepatic recirculation
mainly life-threatening ingestion of carbamazepine, dapsone, phenobarbital, quinine or theophyllinemainly life-threatening ingestion of carbamazepine, dapsone, phenobarbital, quinine or theophylline
Extracorporeal removal (for active metabolites, delayed toxicity or poor organ clearance) (for active metabolites, delayed toxicity or poor organ clearance)
HaemodialysisHaemodialysis - low MW (<500 d), soluble, low Vd (< 1L/kg) e.g. methanol, ethylene glycol, - low MW (<500 d), soluble, low Vd (< 1L/kg) e.g. methanol, ethylene glycol,
salicylates, lithiumsalicylates, lithium
HaemoperfusionHaemoperfusion - e.g theophylline, phenobarbital, phenytoin, carbamazepine, paraquat - e.g theophylline, phenobarbital, phenytoin, carbamazepine, paraquat
HaemofiltrationHaemofiltration for large Vd and extensive tissue bound toxins but removes virtually all drugs for large Vd and extensive tissue bound toxins but removes virtually all drugs
AntidotesAntidotes

23. ICU Activated CharcoalActivated Charcoal
Universal absorbentUniversal absorbent
Produced by the controlled burning of Produced by the controlled burning of
various organic products at >600C, washed various organic products at >600C, washed
with inorganic acids and driedwith inorganic acids and dried
Small particle with highly developed Small particle with highly developed
internal pore system internal pore system
surface area of 50 gm AC = 10 football surface area of 50 gm AC = 10 football
fieldsfields
Absorbs substances in varying degreesAbsorbs substances in varying degrees
If comes into contact with toxin in GI If comes into contact with toxin in GI
track prior to absorption, can bind and track prior to absorption, can bind and
decrease systemic toxicity decrease systemic toxicity

24. ICU General TreatmentGeneral Treatment
Activated charcoalActivated charcoal
Inert, non-toxic, non-specific adsorptionInert, non-toxic, non-specific adsorption
Risk of aspirationRisk of aspiration
Dose 1g/kg patients weightDose 1g/kg patients weight
Ineffective for alcohols or heavy metalsIneffective for alcohols or heavy metals
? Multi-dose charcoal ? Multi-dose charcoal
may cause GI dialysis for some drugsmay cause GI dialysis for some drugs
Check with poison control!!!Check with poison control!!!

25. ICU Activated CharcoalActivated Charcoal
Binds most compounds; easier to Binds most compounds; easier to
remember what it doesn’t remember what it doesn’t

26. ICU Activated CharcoalActivated Charcoal
Big question in the use of AC is when Big question in the use of AC is when
to use itto use it
Effectiveness is time dependent – the Effectiveness is time dependent – the
longer the time from ingestion, the longer the time from ingestion, the
less effective AC isless effective AC is
Toxin already absorbed or past pylorisToxin already absorbed or past pyloris
Effectiveness is lost between 1 and 2 Effectiveness is lost between 1 and 2
hourshours

27. ICU AC: problemAC: problem
Patients with toxin ingestions will Patients with toxin ingestions will
present to the ED >3 hours after present to the ED >3 hours after
poisoningpoisoning
““should not be administered should not be administered
routinely”routinely”

28. ICU
Drugs and Extracorporeal Drugs and Extracorporeal
RemovalRemoval
Haemodialysis
• Methanolethanol
• Ethylene glycolEthylene glycol
• SalicylatesSalicylates
• LithiumLithium
Haemofiltration
•ProcainamideProcainamide
•MethotrexateMethotrexate
Haemoperfusion (Charcoal)
•TheophyllineTheophylline
•CarbamazepineCarbamazepine
•Amanita toxin (if early)Amanita toxin (if early)
•AminoglycosidesAminoglycosides
•ParaquatParaquat
•PhenobarbitalPhenobarbital
•PhenytoinPhenytoin
•SotalolSotalol

29. ICU
Urinary AlkalinisationUrinary Alkalinisation
FluorideFluoride
IsoniazidIsoniazid
Salicylic acidSalicylic acid
BarbituratesBarbiturates
MethotrexateMethotrexate

30. Specific IngestionsSpecific Ingestions

31. ICU AcetaminophenAcetaminophen
Peak plasma <1hr post ingestionPeak plasma <1hr post ingestion
Metabolized in liver d/t glucuronidationMetabolized in liver d/t glucuronidation
Toxic metabolite NAPQ1Toxic metabolite NAPQ1
NAPQ1 binds to hepatocytes and causes necrosisNAPQ1 binds to hepatocytes and causes necrosis
Detoxified by glutathione & eliminated by Detoxified by glutathione & eliminated by
kidneyskidneys
Toxic threshold adults - 7.5-10gToxic threshold adults - 7.5-10g

32. ICU AcetaminophenAcetaminophen
Phase I (<24 hrs):Phase I (<24 hrs):
Anorexia, malaise, N/V, Anorexia, malaise, N/V,
diaphoresisdiaphoresis
Phase II (24-48 hr):Phase II (24-48 hr):
RUQ pain, RUQ pain, LFTs, sx of LFTs, sx of
phase I resolvephase I resolve
Phase III (48-96 hr)Phase III (48-96 hr)
Severe liver failureSevere liver failure
Encephalopathy, Encephalopathy,
coagulopathy, coagulopathy, BSBS
PancreatitisPancreatitis
ARFARF
Phase IV (>4 days)Phase IV (>4 days)
Death/full Death/full
recovery/transplantrecovery/transplant

33. ICU AcetaminophenAcetaminophen
Limitations:Limitations:
Requires time of Requires time of
ingestioningestion
Very early or late Very early or late
ingestionsingestions
Chronic ingestionsChronic ingestions
Extended release Extended release
preparationspreparations
At risk populationsAt risk populations
ETOH abuseETOH abuse

34. ICU AcetaminophenAcetaminophen
TreatmentTreatment
Activated charcoalActivated charcoal
Given w/I 4-6 hrGiven w/I 4-6 hr
Reduced absorption Reduced absorption
by 50-90% by 50-90%
NACNAC
Replete glutathioneReplete glutathione
combines directly with combines directly with
NAPQ1NAPQ1
Antioxident propertiesAntioxident properties
vasodilatory propertiesvasodilatory properties
Treat:Treat:
Based on nomogramBased on nomogram
Level >5 w/o ingestion time Level >5 w/o ingestion time
knownknown
Evidence of hepatotoxicity or Evidence of hepatotoxicity or
level unknownlevel unknown

35. ICU AlcoholsAlcohols
Ethylene glycol, methanol, isopropanolEthylene glycol, methanol, isopropanol
Lab:Lab:
Anion gap MA, elevated osmolar gapAnion gap MA, elevated osmolar gap
Exceptions:Exceptions:
Normal AG Normal AG
Not yet formed metabolitesNot yet formed metabolites
Isopropanol ingestionIsopropanol ingestion
Sx may be delayed if co-ingested with ethanolSx may be delayed if co-ingested with ethanol

36. ICU Ethylene GlycolEthylene Glycol
Ethylene glycol
ETOH dehydrogenase
Oxalic acid
Oxalic acid Oxalic acid  Ca oxalate Ca oxalate  ARF ARF
HypocalcemiaHypocalcemia
Myocardial dysfunction (2Myocardial dysfunction (2
00
Ca)Ca)
100ml can be lethal100ml can be lethal

37. ICU Ethylene GlycolEthylene Glycol
Phase I (30min-12hr)Phase I (30min-12hr)
Inebriation, ataxia, seizures, AG-MA, OG, Inebriation, ataxia, seizures, AG-MA, OG,
hypocalcemia, crystalluria, cerebral hypocalcemia, crystalluria, cerebral
edemaedema
Phase II (12-24hr)Phase II (12-24hr)
Myocardial dysfunction, CHFMyocardial dysfunction, CHF
Phase III (2-3 days)Phase III (2-3 days)
ARFARF

38. ICU MethanolMethanol
150-240ml is lethal150-240ml is lethal
Presents with:Presents with:
Headache, inebriationHeadache, inebriation
Dizziness, ataxia, confusionDizziness, ataxia, confusion
Vision lossVision loss
PancreatitisPancreatitis
Methanol
ETOH dehydrogenase
Formic Acid

39. ICU TreatmentTreatment
Inhibit alcohol dehydrogenaseInhibit alcohol dehydrogenase
EthanolEthanol
FomepizoleFomepizole
Removal of alcohol & it’s metabolitesRemoval of alcohol & it’s metabolites
HemodialysisHemodialysis
Levels >50mg/dLLevels >50mg/dL
Significant MASignificant MA
Evidence of end-organ damageEvidence of end-organ damage

40. ICU IsopropanolIsopropanol
KetonuriaKetonuria
Absent AG or MAAbsent AG or MA
Hemorrhagic gastritisHemorrhagic gastritis
Generally just supportive careGenerally just supportive care
Hemodialysis if:Hemodialysis if:
Lethal ingestion (150-240ml)Lethal ingestion (150-240ml)
Refractory shock/prolonged comaRefractory shock/prolonged coma
Isopropanol
ETOH dehydrogenasez
Acetone

41. ICU Salicylate IntoxicationSalicylate Intoxication
Adult lethal dose - 10-30gAdult lethal dose - 10-30g
Sx include:Sx include:
TinnitusTinnitus
FeverFever
VertigoVertigo
Nausea/vomiting/diarrheaNausea/vomiting/diarrhea
AG MA & resp alkalosisAG MA & resp alkalosis
Altered LOC/comaAltered LOC/coma
ARDSARDS

42. ICU Salicylate TreatmentSalicylate Treatment
Level check q2h until 2 values decreased Level check q2h until 2 values decreased
from peakfrom peak
Activated charcoalActivated charcoal
?multiple dosing?multiple dosing
Supplemental glucoseSupplemental glucose
Alkalinization of serum & urineAlkalinization of serum & urine
Resp alkalosis not C/I to HCO3Resp alkalosis not C/I to HCO3
Urine pH = 8Urine pH = 8
DialysisDialysis

43. ICU Salicylate TreatmentSalicylate Treatment
Hemodialysis IndicationsHemodialysis Indications
Altered LOCAltered LOC
Pulmonary or cerebral edemaPulmonary or cerebral edema
Renal failureRenal failure
Fluid overload that prevents HCO3Fluid overload that prevents HCO3
Plasma level >7.2Plasma level >7.2
Deterioration despite therapyDeterioration despite therapy

44. ICU TCA IntoxicationTCA Intoxication
Rapidly absorbed - peak dose 2-8hRapidly absorbed - peak dose 2-8h
T1/2 - 24-72hrT1/2 - 24-72hr
Enterohepatic recirculationEnterohepatic recirculation
Delayed absorption d/t anticholinergic Delayed absorption d/t anticholinergic
effects effects

45. ICUTCA - Clinical PresentationTCA - Clinical Presentation
CardiacCardiac
Inhibits fast Na channels - slowed depolarizationInhibits fast Na channels - slowed depolarization
QRS prolongationQRS prolongation
Reentry arrhythmias - V-tach, torsadeReentry arrhythmias - V-tach, torsade
Hypotension, Decreased COHypotension, Decreased CO
CNSCNS
Delerium, seizures, comaDelerium, seizures, coma
AnticholinergicAnticholinergic
temp, flushed, dilated pupils, ilieus, urinary temp, flushed, dilated pupils, ilieus, urinary
retention, sinus tach retention, sinus tach

46. ICU TCA - TreatmentTCA - Treatment
ABCsABCs
Activated charcoal - ?multidoseActivated charcoal - ?multidose
Gastric decontamination Gastric decontamination
NaHCO3 - most effective therapy!NaHCO3 - most effective therapy!
D/t raised pH and serum [Na]D/t raised pH and serum [Na]
Recommend for QRS >100msecRecommend for QRS >100msec
Push amps for arrhythmiasPush amps for arrhythmias
Do not give dilantin for seizures!Do not give dilantin for seizures!
No role for dialysis!!!!No role for dialysis!!!!

47. ICU B-Blocker OverdoseB-Blocker Overdose
Most are symptomatic within 4 hours of Most are symptomatic within 4 hours of
ingestioningestion
Asymptomatic pts with a normal EKG after 6hrs Asymptomatic pts with a normal EKG after 6hrs
generally don’t need ICUgenerally don’t need ICU
SX:SX:
HypotensionHypotension
Bradycardia/A-V blockBradycardia/A-V block
CHFCHF
BronchospasmBronchospasm
Decreased LOC, seizures, comaDecreased LOC, seizures, coma

48. ICU -blocker Treatment-blocker Treatment
ABCsABCs
Activated charcoalActivated charcoal
Temporary pacing/vasopressors prnTemporary pacing/vasopressors prn
GlucagonGlucagon
+ve inotropic and chronotropic effect d/t +ve inotropic and chronotropic effect d/t
increased AMP and intracell Caincreased AMP and intracell Ca
5-10mg bolus followed by 1-10mg/h gtt5-10mg bolus followed by 1-10mg/h gtt
High dose insulin/glucose dripHigh dose insulin/glucose drip
**Atenolol is dialyzable****Atenolol is dialyzable**

49. ICU Ca channel Blocker ODCa channel Blocker OD
Selectively inhibit the movement of Selectively inhibit the movement of
Ca through cardiac and vascular Ca through cardiac and vascular
smooth mmsmooth mm
Present withPresent with
HypotensionHypotension
Bradycardia/conduction delaysBradycardia/conduction delays
Confusion/ altered LOCConfusion/ altered LOC

50. ICU Ca Channel TreatmentCa Channel Treatment
ACBsACBs
Activated charcoalActivated charcoal
?Gastric lavage?Gastric lavage
Ca gluconateCa gluconate
GlucagonGlucagon
Insulin/glucose infusionInsulin/glucose infusion

51. ICU CO poisoningCO poisoning
Seen with:Seen with:
 smoke inhalationsmoke inhalation
SA with car exhaust SA with car exhaust
poorly vented wood or gas stovespoorly vented wood or gas stoves
CO binds Hg 240X> then OCO binds Hg 240X> then O
22
Causes tissue hypoxiaCauses tissue hypoxia
Serum CO up to 5-10% in smokers or Serum CO up to 5-10% in smokers or
large citieslarge cities

52. ICU CO poisoningCO poisoning
PresentationPresentation
5-10% CO5-10% CO
H/A, mild dyspneaH/A, mild dyspnea
10-30%10-30%
H/A, dizziness, weakness, N/V, dyspnea, cardiac H/A, dizziness, weakness, N/V, dyspnea, cardiac
ischemiaischemia
>50%>50%
Coma, seizures, cardiovascular collapse, deathComa, seizures, cardiovascular collapse, death
10-30% survivors have delayed neuro deficits10-30% survivors have delayed neuro deficits

53. ICU CO poisoning - DiagnosisCO poisoning - Diagnosis
High index of suspicionHigh index of suspicion
Serum CO levelSerum CO level
Measured by co-oximeter of an ABGMeasured by co-oximeter of an ABG
Pulse oximetry can’t distinguish Pulse oximetry can’t distinguish
carboxyHg from oxyHgcarboxyHg from oxyHg
PO2 on ABG may be normal since it PO2 on ABG may be normal since it
represents dissolved oxygenrepresents dissolved oxygen
CT head may specifically demonstrate CT head may specifically demonstrate
globus pallidus abnormalitiesglobus pallidus abnormalities

54. ICUCO Poisoning - TreatmentCO Poisoning - Treatment
ABCsABCs
100% FiO2100% FiO2
T1/2 R/A - 5-6hrT1/2 R/A - 5-6hr
T1/2 100% - 40-90minT1/2 100% - 40-90min
Hyperbaric O2Hyperbaric O2
T1/2 - 15-30 minT1/2 - 15-30 min
If accessible, suggested for: If accessible, suggested for:
CO>25%CO>25%
Loss of consciousness, EKG changes, chest painLoss of consciousness, EKG changes, chest pain
pH<7.1pH<7.1

55. ICU
Antidotes
NaloxoneOpioids
Atropine, pralidoximeOrganophosphates
Methylene blueMethaemoglobinaemia
Ethanol/fomepizole, folateMethanol
PyridoxineIsoniazid
DeferoxamineIron
Dextrose, glucagon, ocreotideHypoglycaemic agents
Dimercaprol, EDTA, penicillamineArsenic, copper, gold, lead,
mercury
Ethanol/fomepizole, thiamine, pyridoxineEthylene Glycol
Digoxin-specific antibodiesDigoxin
Amyl nitrite/sodium nitrite/thiosulphate (Taylor Cyanide Antidote
Package) hydroxycobalamin
Cyanide
OxygenCarbon Monoxide
FlumazenilBenzodiazepines
AtropineAnticholinesterases
PhysostigmineAnticholinergics
N-acetylcysteineAcetaminophen
AntidoteToxin/effect

56. ICU SummarySummary
Familiarity with toxidromes will allow you to assess Familiarity with toxidromes will allow you to assess
and manage unconscious overdose/poisoning and manage unconscious overdose/poisoning
victimsvictims
Supportive care and decontamination is the Supportive care and decontamination is the
mainstay of most treatmentsmainstay of most treatments
Calculation of the anion gap and osmolar gap will Calculation of the anion gap and osmolar gap will
allow you to identify and treat toxic alcohol allow you to identify and treat toxic alcohol
ingestions prior to end organ damageingestions prior to end organ damage
In known overdoses and poisonings early In known overdoses and poisonings early
involvement of a toxicologist/poison control is very involvement of a toxicologist/poison control is very
helpful to direct specific antidote therapieshelpful to direct specific antidote therapies