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ED Fellowship --> Toxicology > Principles > Flashcards

Principles Flashcards

1
Q

Discuss principles of CPR in tox arrest

A

Unlike cardiac arrest in the older population resuscitation following acute poisoning can have good neurological outcome even after prolonged CPR (hours). ECMO if available can offer a bridging therapy in selected cases of severe refractory shock or ARDS

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2
Q

Discuss the management of toxic seizures

A

Toxic seizures are generalised and can be controlled with IV benzos.

The most common agent that causes seizures in poisoned patient in australia are

  • venlafaxine
  • tramadol
  • amphetamines
  • bupropion
  • seizure related to ETOH and benzo withdrawal are also common

Presence of focal seizure should raise concern of underlying neurlogical condition

Barbiturates can be used as second line agents and b6 for intractable seizure secondary to isonazid

Do not use phenytoin poor efficacy and can exacerbate sodium channel blockade ( dont use any sodium channel blocking anticonvulsants)

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3
Q

Discuss temperature control in toxicology

A

Hyperthemia is a associated with a number of life threatening poisons- temperature of 38.5 is an indication for continous core-temperature monitoring
Greater than 39.5 is an emergency that requires promt coooling. – NMB, I&V reduces heat from muscles – cooling blanets

Hypothermia mimics or causes cardiac arrest. ECMO if available is the most effective method of heating, Alternaitve include pleural lavage with warmed fluid to 40-45 degrees.

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4
Q

Discuss airway compromise due to corrosive injury to oropharynx and agent likley to cause

A

Agents: alkalis, acids, glyphosate, paraquat

Patient present with stridor, dysphageia and dysphonia – indicate potential for iminent airway compromise. Early intubation +- surgical airway often required

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5
Q

Discuss intubation of patient with significant toxic acidaemia and implications for ventilation post

A

Agent: ethlylene glycol, methanol, salicylates

Until late in the course of these patient there is oftern appropriate respiratory compensation. If need for intuabtion arises standard setting will worsen acidaemia and lead to rapid decline

Avoid normo or hypoventilation- maintain hypervenilation to achieve compensation, can consider 1-2mmol/kg boluses of iv sodium bicard to avoid worsening of acideamia

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6
Q

Discuss approach and agents that can cause respiratory failure

A

Agents: carbamates, nerve agents, organophosphate

Rapid decotamination, administraiotn of atropine to dry respiratory secretion with serial doubling as needed to achieve.

Paradoxamine for organophosphates

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7
Q

Discuss agents that can cause hypocalcaemia and management of dysrrythmia secondary to same

A

Agents: hydrofluroic acid, extensive cutaneous burns, ethalyne glycol

Defibrilation is unlilkey to be successful
adminiser 60-90ml of 10% calcium gluconate. Repeat this every 2 minutes until defib is successful

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8
Q

Discuss general management of V-tach secondary to fast na channel blockade and agents that can cause the same

A

Agents: Chloroquine, cocaine, flecainde, local anaethetics, procainamide, propanolol, TCA

Early intubation based on risk assessment – hyperventilate to achieve PH 7.5
Bolus IV sodium bicard 1-2mg/kg every 2 minutes until resolution of ECG changes
Lignocaine is third line therapy if ROSC not achieved and PH 7.5

If lipid soluble cause of fast NA channel blockade consider use of intralipid

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9
Q

Discuss management of refractory hypotension secondary to B-blocker or CA blocker

A

HIET (high dose insulin euglycmic therapy)
Inotropes (adrenaline)
Intralipid if lipid soluble
calcium gluconate if CA

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10
Q

Discuss HIET protocol

A
  • Start: bolus 50ml 50% glucose with 1unit/kg of actrapid
  • Continuing: actrapid 0.5 unit/kg titrated to 5unit/kg with 25g/hr (50ml 50% glucose) infusion titrated to maintain euglycamia
  • Monitor glucose 20 minutely for the first hour and then hourly after that
  • Correct K only if <2.5 and a source of loss

End points

  • improved EF
  • iproved mentation
  • improved lactate
  • adequate heart rate
  • reversal of cardiac conduction abnormalities
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11
Q

Discuss mechanism of action of HIET

A
  • Increased glucose and lactate up take into cells
  • increased myocardial contractility without increase in o2 demand
  • increased pyruvate dehydrogenase activity
  • promotes excitation–contraction coupling and contractility because increased glucose availability results in:
  • —–increased sarcoplasmic reticulum-associated calcium ATPase activity
  • ——-increased cytoplasmic calcium concentrations
  • ——-enhanced calcium entrance into mitochondria and sarcolemma
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12
Q

Discuss management of tachyadria and hypertension due to central and peripheral sympathomimetic respons

A
  • Beta blocker contrainidcated – due to unopposed alpha action
  • manage with benzo

-If further therapy required use titratetable infusion - GTN, sodium nitroprusside

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13
Q

Discuss risk assessment of tox patients

A

5 main question

1: agent
2: dose
3: time of ingestion
4: clinical features and progress
5: patient factors (weight, co-morbidities)

If patient unable to communicate information from ambulance and worst case scenerio

Stated dose and agent + time of ingestion should match with clinical condition

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14
Q

Discuss in general supportive measures that may be need in a tox patient

A

A: intubation
B: supplemental oxygen and ventilation
C: IV fluids, inotropes, control of HTN, ECMO
-Sedation and/or seizure control: benzo
-Metabolic: normoglycaemia and control of PH
-Fluids and electrolyte balance
-Renal: hydration +-HD
-General: nutrition, respiratory toilet, bladder acre, prevention of pressure sores, VTE prophylaxisis

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15
Q

Investigations to be performed for all tox patient

A

ECG, BSL, Paracetamol level

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16
Q

Discuss decontamination

A

Not routine
reserved for those in whom risk assessment predicts severe or life threatening toxicity. Supportive care and antidote alone should not be enough to ensure satisfactory outcome. Reasonable ground to believe significant amount of agent is unabsorbed and is amenable to removal

Never done in a patient with an altered GCS if airway is not secured first

17
Q

Discuss risk beneift of gastric decontamination

A

Benefits

  • improved clinical outcome
  • less severe clinical course
  • Reduced need for other potentially hazardous intervention (ETT)
  • reduced hospital length of stay

Risks:

  • Pulmonary aspiration
  • GIT complications (bowel obstruction, perf)
  • Distraction of staff
  • Diversion of departmental resources for performance of procedure
18
Q

Discuss single dose activated charcoal

A

Made by super heating distilled wood pulp and suspenced in water or sorbital provide an enormous surface area to reversibly adsorb most ingested toxins reducing fruther absorption

Some affect up to 4 hours but more effective closer to ingestion

Potential complications

  • mess
  • aspiration
  • direct administration into lung space via misplaced NG
  • Impaired absorption of subsequently administered oral antidotes or therapies
  • corneal abrasions

Contraindicatiosn

  • initial resus incomplete
  • non toxic dose
  • unco-operative patient
  • Risk assessment with good outcome with antidote and supportive care
  • risk assessment for imminenet onset of siezure or decrease in GCS
  • agent not bound
  • Corrosives

Give 50 grams or 1g/kg as a single dose - mix with icecream for kids

19
Q

List agents that are poorly bound to activated charcoal

A

Metals

  • lithium
  • iron
  • potassium
  • lead
  • arsenic
  • mercurary

Alcohols and hydrocarbons

  • ethanol
  • isoproyl alcohol
  • ehtylene glycol
  • methanol

Corrosives

  • Acids
  • alkalis
20
Q

Discuss whole bowel irrigation

A

Attempts to cleanse the entire bowel with large volumes of osmotically balanced polyethylene glycol electrolyte solutions.

Rarely used as risk-benifit analysis reserves this intervention for life threatening sustained release or enteric coated prepations or where agents will not bind to activated charcoal.

Technique

  • place NG and confirm on CXR
  • Administer PEG solution via NG tube at 2L/hour by continous infusion
  • Administer metoclopramide to reduce nausea and vomiting
  • Position patient on commode if possible
  • Continue irrigation until the effluent is clear may take up to 6 hours
  • Cease if distension or loss of bowel sounds

Complications

  • nasuea, vomiting, and abdominal bloating
  • NAGMA
  • Pulmonary aspiaration
  • Distraction from resus
  • Delayed retrieval

Contraindications

  • Risk assessment not appropirate
  • unco-operative patient
  • inability to place NG
  • uncontrolled vomiting
  • ileus or intestinal obstruction
  • intubated and ventilated patient
21
Q

Discuss potential indications for whole bowel irrigation

A

ABC Kil

  • Iron overdose (60mg/kg)
  • Slow release potassium chloride ingestion >2.5mmol/kg
  • Life threatening slow release verapamil or diltiazem ingestion
  • Symptomatic arsenic trioxide ingestion
  • lead ingestion
  • body packers
22
Q

Discuss enhanced elimination

A

Techniques employed to increase the rate of elimiantion of toxins.

Only indicated if this will reduce mortality, length of stay, complications or need for other more invasive intervention

Suitable for only a few agents charactersied by

1) severe toxcitiy
2) poor outcome despite good supportive care, antidote
3) slow endogenous rates of elimiantion
4) suitable PK

23
Q

Discuss multiple dose activated Charcoal (MDAC)

A

Repeated administration of activated charcoal fills the gut lumen and enhances elimination in two ways

1) interruption of enterohepatic circulation – only works significantly if drus has small VD and undergoes enterohepatic circulation
2) GIT diaylsis - Drug passes across the gut mucosa from a relatively high intravscular concentration to a low conentration in the gut which is maintaned by continuing adsorption to charcoal

Contraindications

  • decreased LOC
  • bowel obstruction

Complications

  • vomiting
  • charcoal aspiration
  • constipation
  • charcoal bezoar
  • corneal abrasion
  • distractionn

Technique

  • given 50 g of AC
  • give repeated dose of 25 g every 2 hours
  • check for signifiacnt NG aspirates or loss of bowel sounds prior to admin of each dose
  • MDAC should rarely go longer than 6 hours
24
Q

Discuss indications for MDAC (these people drink charcoal quick)

A

Carbamezepine coma

  • most common reason
  • used with expectation that will reduce length of ICU stay
  • Phenobarb coma
  • rare
  • Dapsone overdose with methaemoglobinaemia
  • Quinine overdose
  • Theophylline overdose
25
Q

Discuss urinary alkalinisation

A

Production of alkaline urine promotes the ionisation of acidic drugs and prevents reabsorption across the renal tubular epithelium thus promoting drug excretion

Drug muse be filtered in the glomerulus, have a small VD and be a weak acid

Contraindicaitons
-fluid overload

Complications

  • alkalaemia
  • Hypokalaemia
  • Hypoclacaemia (usually not clinically significant)

Technique

  • correct K
  • Give 1-2mmol/kg of sodium bicarb IV Bolus
  • commenc infusion of 150mmol sodium bicarb in 850mls of 5% dextrose at 250mls.hour
  • 20mmol of K can be added to maintain K
  • Monitor serum hco3 and K every 4 hours
  • arim for uyrinary ph of 7.5
26
Q

Discuss indications for urinary alkalinisation

A

Only two drugs of signiciance

1) salicylate overdose
- normally eliminated by hepatic metabolism and are not readily excreted in acidic urine. In overdose metabolism is saturated and elimination half life greatly increased
- Urinary alkilinsation greatly increases elimination
- Severe established salicylate toxicity indicated immediate HD rather than a trial of urinary alkalinisation

2) phenobarb coma
- may attempted to reduce duration of coma and ICU lenght of stay
- MDAC superior to this for enhanced elinination

27
Q

Discuss Extracorporeal technique of elimination

A

Technique include

  • HD (continuous, intermittent)
  • Haemofilitration
  • Haemoperfusion
  • plasmapheresis
  • exchange transfusions

Effectively enhances elimination of any drug that is a small molecule has a small VD, rapid redistribution from tissue to plasma and a slow endogenous elimiantion

28
Q

Discuss indication fo extracorporeal techniques of elimination

A
  • Toxic alcohols (methanol, ethylene glycol)
  • Theophylline
  • Severe salicylate intoxication
  • Severe lithium intoxication
  • Phenobarbitone
  • metofrmin lactic acisdosis
  • massive valproate ocerdose
  • potassium salt overdose with life threatening hyperkalaemia
29
Q

Discuss retrieval of the poisoned patient

A

In most situation the primary receiving centre is well equipped to deal with the need of the presenting patient. If this is not the case retrieval needs to be organised early. Poisoning is unusual in that if retrieval needs to occur it is usually during the most severe phase of the illness

Resusciation: retrieval should not distact from initial resus attempts. Patient should be stabilised before transfer whenever possible

Stabilisation including intubation ventilation, control of seizure, maintenance of normothermia and normoglycaemia, resuscitation of hypothermia should eb attended to prior to transfer. If materials or skill not in place this should be communicated to the retrieval team

Planning is required to ensure that potential complications are thought of and managed proactively. Thus if coma is anticipated in the next few hours early intubation should be undertaken

Communications between referring centre, retirevalist and receiving centre needs to occur. If likely to need HD should be communicated

Pyschosocail factors should be taken into account

30
Q

List medications that if a child takes one of can be potentially fatal

A

Cant be that stupid cunt or take amphetamines

Ca channel blockade (verapamil, diltiazem) 
B-blocakd (propanalol, sotatalol) 
TCA
Sulfonylureas (gliclazide)
Chloroquines
Opiates
Theyophylline 
Amphetamine
31
Q

What constitutes a pack year of smoking

A

20 cig a day for a year = 1 pack year

ED Fellowship --> Toxicology (23 decks)

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