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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2669_Библиотеки_им_академика_М_И_Перельмана
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Decontaminate
• Activated charcoal (1g/kg up to 50g PO/NG) within 2 hours
(or longer if enteric coated or bezoar)
• Can consider whole bowel irrigation (ask Poison control)
Enhanced Elimination
• Alkalinize the urine and blood
– Aim to have a blood pH 7.4-7.5, do not go above 7.55 and urine pH 7.5-8
– Give 1-2mEq/kg IV bicarb then start an infusion at 250ml/h
• Watch K, Na and Ca
– Correct hypokalemia before alkalinization
• In hypokalemia, the renal tubules will absorb K and excrete H+, preventing alkalinization
1. Chyka et al. Clin Toxicol (phila) 2005;43:61
2. Neuvonen et al. Eur J Clin Pharmacol 1978;13:213
3. Goldfrank’s Emergency 9
th
Edition
4. Jurlink et al. Annals of Emergency Medicine 2015
Salicylate Treatment
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Salicylate Treatment: Enhanced Elimination
• Dialysis indicated if patient has one of the following:
– Salicylate Levels >7.2mmol/L
– Hypoxemia requiring supplemental O
2
– A change in mental status
– Renal failure (and salicylate level >6.5mmol/L)
– Progressive deterioration of vital signs
– Severe acid –base or electrolyte imbalance despite
appropriate treatment (pH <7.2)
– Hepatic compromise with coagulopathy
– Volume overload preventing admin of sodium bicarb
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Acetaminophen Toxicity
Tox ic it y:
• Likely to occur with single ingestions > 250 mg/kg or over 12g in 12 hour period
• Severe liver toxicity occurs in doses greater than 350 mg/kg
(AST and ALT > 1000) unless appropriately treated
Signs and Symptoms:
• Stage I (0.5 0 24 hrs) – nausea, vomiting, diaphoresis, pallor, lethargy, malaise, or
asymptomatic
• Stage II (24-72 hrs) – RUQ pain, jaundice, oliguria, rise in ALT & AST
• Stage III (72 – 96 hrs) – jaundice, confusion (hepatic encephalopathy), marked
elevation in AST & ALT, prolonged INR/PTT, bili > 68, hypoglycemia, lactic acidosis,
hyperammonemia, bleeding diathesis, renal failure
• Stage IV (96 hrs – 14 days) – recovery phase where hepatic necrosis may develop
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Treatment
• Acetaminophen levels
should be drawn 4 hours
after ingestion ideally and
plotted on modified
Rumack-Matthew
nomogram
• Not applicable in repeated
supratherapeutic ingestion
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Assessing Risk of Hepatotoxicity
If ANY of the following occur:
• Ingestion of greater than 7.5 – 10 g in 24 hours
• Ingestion of greater than 4g in 24 hours AND increased risk of
susceptibility to hepatotoxicity (ie. Chronic ETOH use)
• Abdominal pain, liver tenderness, nausea, vomiting, jaundice
• Supratherapeutic serum acetaminophen concentrations
(> 130 mmol/L)
• Elevated ALT or AST (> 50 U/L) on presentation
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Treatment Principles
Gastrointestinal decontamination: activated charcoal
(1g/kg or 50g) in patients presenting within 4 hours of
potentially toxic ingestion (single dose > 7.5 g)
NAC protocol indications:
• Serum concentration above treatment line on RM nomogram
• Single ingestion > 7.5 g (150 mg/kg)
• Unknown time of ingestion + concentration > 66 umol/L
• History of ingestion + liver injury
• Delayed presentation (>24 h) with evidence of liver injury
• Consider in acute undifferentiated liver failure
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NAC Protocols
20 Hour: 150 mg/kg over 60
min; 50 mg/kg over 4 hrs; 100
mg/kg over 16 hrs.
72 Hour: 140 mg/kg PO
loading dose; 70 mg/kg q4h
for 17 doses.
Target INR < 1.3, ALT < 100
U/L, acetaminophen < 132)
before stopping.
Beware NAC infusion reactions.
Mild flushing/urticaria – continue infusion with
antihistamine/steroid.
Severe anaphylaxis or angioedema – stop and treat as in
allergy online slides
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After the Overdose…
Required Recovery Reading
Medication
Mechanism
Prescribing Notes
Naltrexone
Use for both:
Opioid Use Disorder
Alcohol Use Disorder
Competitive antagonist of Mu- receptor
Usual dose 50mg per day
With Opioid Use Disorder this is not first line,
consider if pt unable/unwilling to use others below.
Can improve retention in program and reduce
incarceration.
Must be OFF opioids 7-10d to avoid precipitated
withdrawal.
Can reduce frequency and amount of ETOH
Buprenorphine/Naloxone*
(SUBOXONE)
IM Buprenorphine
(SUBLOCADE) q28d
For Opioid Use Disorder
High affinity partial agonist at mu-receptor; at high
doses saturates receptor blocking effect of other
opioids.
*Naloxone orally = ++hepatic first pass effect, so no
significant systemic effect. BUT if Suboxone is
INJECTED however naloxone component will ppte
withdrawal.
Pt must be in withdrawal 12-24h opioid free to
initiate.
Standardized protocols using the Clinical Opioid
Withdrawal Scale (COWS) to titrate dosing exist.
Methadone
For Opioid Use Disorder
L-enantiomer binds mu-receptor, high intrinsic
activity ~ opioid, low affinity; S-enantiomer acts as
NMDA antagonist
Can start immediately
Need special license to prescribe
**QT prolonging**
+ Social Work, Addictions Medicine referral
+ Harm Reduction: Naloxone kits, safe injection practices/sites
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Methemoglobinemia Carbon Monoxide Cyanide Toxicity
Scenario Dizzy/confused after exposure to
dapsone/Septra/nitrates
Confused man w headache from his
cabin in the winter, AGMA Lactic acidosis
“Caught in industrial fire, now looks very
sick, coughing but sat is high”
Pathophysiology
Fe2+-Hgb is oxidized to Fe3+
Met-Hb can’t carry or release O2
Hb binds CO (CO-Hb) rather than O2;
HbO2 dissociation curve L shifted. CO
disrupts oxidative phosphorylation in
mitochondria. CO causes neuronal death
CN binds cytC-oxidase in mitochondria –
cannot do kreb’s cycle.
Anaerobic glycolysis = AGMA
Causes Many drugs – nitrates, sulfa… Carbon combustion w/ poor ventilation Combustion of plastic/wool/etc
Tox ic i ng es t ( bi tt er a lm on d, a pr i co t pi ts )
Signs/
Symptoms
Cyanosis
Chocolate brown blood
Cherry red skin
Headache, dizzy, “flu like”
Cardiac arrhythmias
Coma, Acidosis, Cardiac instability
CNS symptom, sz, coma
Severe lactic acidosis AGMA
Diagnosis ABG, MetHb
SpO2 80-85 w high PaO2
“PaO2-SpO2 mismatch” suggests
hemoglobinopathy
SpO2 high
AGMA with high lactate
Carboxy-Hb level (>10% abnormal,
Normal 1-2%, smokers 5-10%
VBG high venous sat
ABG high SaO2, AGMA
Antidotes Methylene Blue 1-2mg/kg 100% FiO2 Hydroxycobalamin 5g IV over 15. min
Other Rx Supportive Hyperbaric oxygen rarely (for severe
cases eg seizure/coma or pregnancy
related complications)
Sodium thiosulfate (enhances renal
excretion)
Nitrites (amyl nitrate/sodium nitrite) –
induce MetHb which has higher affinity
for CN than regular Hbg
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Carbon Monoxide poisoning
Sample scenario:
“Confused elderly man comes with headache in
winter from remote cabin with normal BP and
unexplained AGMA lactic acidosis …”
Treatment
1. Remove source, move to well ventilated area
2. 100% FiO2 – HFNC or Intubate (i.e. Coma)
• COHb half lives
– Room air: 250-320 minutes
– 100% FiO2: 90 mins
– Increased atmospheric pressure (2.5ATA): 20 mins
1. Consider Hyperbaric O2
– Conflicting evidence – expert consensus
– Potential indications
• If within 6h of exposure is best
• CoHb > 25%
• Seizure or Coma
• Syncope
• Pregnant woman with >15% COHb or Fetal distress in
pregnancy
• If they are suffering CO poisoning after a smoke
inhalation, treat for concurrent cyanide poisoning
Pathophysiology
HYPOXIA
Hb binds CO (COHb) rather than O2
HbO2 dissociation curve L shifted
CO disrupts oxidative phosphorylation
CO causes neuronal death
Causes Carbon combustion + inadequate ventilation
• (eg) gas stoves
Others: Methylene chloride/bromide
Signs / Symptoms Early (<4hrs): H/A, dizziness, Nausea, ‘flu-like’
Continued exposure – end organ hypoxia
- CNS: Ataxia, syncope, coma
- Cardiac: arrhythmias, myocardial ischemia,
cardiomyopathy
- Resp: pulm edema (cardiogenic or ARDS), dyspnea
- Skin: Cherry red skin, skin bullae
- Metabolic: AGMA, lactic acidosis
- retinal hemorrhages
Delayed neurological sequelae
- Parkinsonism, dementia, psychosis, apraxia
Diagnosis Carboxyhemoglobin (COHb) level
- normal 1-2%
- smokers 5-10%
- >10% abnormal
SpO2 will over-estimate - i.e. will read 100%
CT/MRI – bilateral opacities in globus pallidus
Juurlink Br J Clin Phamacol 2023:89.942-945
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Cyanide (CN) Poisoning
Pathophysiology
HYPOXIA
CN blocks cytochrome oxidase function
Cells cannot use aerobic respiration (toxic to
mitochondria)
Anaerobic respiration = tissue hypoxia, lactic acidosis
Causes Inhalation of gases
- combustion of plastic, rubber, wool, silk, polyurethane
Ingestion: Casaver, apricot pits, bitter almonds
Intravenous: Nitroprusside
Signs / Symptoms 3 hallmarks: Coma, Acidosis, Cardiac instability
- ABRUPT onset (only delayed to hrs if ingestion)
- H/A, Nausea, Dizziness, Confusion
- Syncope, Seizure, Coma
- Severe lactic acidosis,
- Cardiac collapse, cardiac arrest, death
- VBG: Venous arterialisation – high venous sat
- ABG: High SaO2 (unlike CO toxicity), AGMA
- Smell of bitter almonds
- ECG: non-specific arrhythmias, blocks, brady, tachy
Diagnosis Diagnosis is purely clinical –
looks for hallmarks and high
mixed/central venous sat (>90%)
Cyanide levels
- Take too long to come back so not used in emergency
>2.4 coma. >3 death
Treatment
1. Supportive
• Control airway (intubate), 100% FiO2
• Crystalloids and vasopressors for shock
• Bicarb for acidosis
2. Hydroxycobalamin
• Binds CN forming cyanocobalamin -> Urine
• 5g IV over 15mins, repeat x1 if needed
• A/E:anaphylactoid reaction, HTN
3. Nitrites
• MetHb higher affinity for CN than Hb -> induce
methemobloginemia
• Pre-hospital: amyl nitrate
• Na nitrite 3% 10ml over 2-4mins IV
• A/E: Hypotension, hypoxia (don’t give if COHb)
4. Sodium thiosulfate
• Enhances renal excretion
• 150-200mg/kg over 10-20mins
• A/E: hypernatremia
1 and 2 are mainstay of management. 3 and 4 only
if hydroxycobalamin unavailable
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