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Toxicology > Resuscitation (Murray 1.1-1.9) > Flashcards

Resuscitation (Murray 1.1-1.9) Flashcards

1
Q

Describe the resuscitation protocol for patients with a tox ingestion.

A

Airway, Breathing, Circulation, Detect + Correct: seizures (benzos), hypoglycaemia (treat BSL <4) and hyper/hypothermia, Emergency antidote administration

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2
Q

What is the principal mechanism by which airway compromise may occur with acute poisoning? What agents are often the cause?

A

Corrosive injury to oropharynx. Alkalis, acids, glyphosate, paraquat.

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3
Q

What condition may cause respiratory failure in overdose?

A

Cholinergic crisis: carbamates, nerve agents, organophosphates

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4
Q

How would you counteract a cholinergic crisis?

A

Rapid administration of atropine by serial doubling of atropine dose to achieve dry respiratory secretions

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5
Q

What drug can cause significant hypoxaemia? Why?

A

Paraquat due to oxygen free radical-mediated cellular injury of type II pneumocytes

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6
Q

How does hydrofluoric acid cause VF?

A

By causing hypocalcaemia

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7
Q

How do you treat hydrofluoric acid burns?

A

IV calcium bolus (60-90 ml 10% calcium gluconate) every 2 minutes + defibrillation

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8
Q

What does hydrofluoric acid cause?

A

VF

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9
Q

What drugs can cause VT and why?

A

All drugs causing fast sodium channel blockade. Including: chloroquine, cocaine, flecainide, Las, procainamide, propranolol, quinine, TCAs

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10
Q

How do you manage a patient with suspected sodium channel blockade?

A

Intubate, hyperventilate, bolus IV sodium bicarb every 1-2 minutes. Consider lignocaine.

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11
Q

What drugs do you never give in patients with a suspected sodium channel blockade?

A

Amiodarone and type 1a anti-dysrhythmics

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12
Q

What drugs an cause severe ventricular tachycardia/ectopy?

A

Chloral hydrate, hydrocarbons, organochlorines. This is due to toxin-induced myocardial sensitisation to catecholamines

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13
Q

What is the treatment of chloral hydrate-induced ventricular ectopy/VT?

A

IV beta-blockers

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14
Q

What drugs should you consider high-dose insulin therapy for in the event of hypotension?

A

CCBs, propranolol, LA agents

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15
Q

With what drug-induced tachycardia are beta blockers contraindicated?

A

Amphetamines, cocaine. Use benzos instead

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16
Q

What drug can cause SVT? How?

A

Theophylline due to adenosine antagonism. Thus adenosine is ineffective for treatment.

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17
Q

How is the SVT associated with theophylline treated?

A

Not with adenosine, instead trial beta-blockers and if fails then urgent haemodialysis

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18
Q

What clinical syndrome and what is the treatment of digoxin-toxicity?

A

Na-K-ATPase pump inhibition; digoxin-specific antibodies

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19
Q

What is the management for calcium channel blockade causing a toxidrome?

A

Atropine/pacing likely not successful. Bolus IV calcium (60 ml 10% calcium gluconate) + high-dose insulin

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20
Q

What toxidrome can cause hyperkalaemia?

A

Digoxin. Do not give calcium salts.

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21
Q

How do you manage hypoglycaemia caused by sulfonylureas?

A

Dextrose + octreotide administration

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22
Q

What two drugs in overdose are known to cause seizures?

A

Isoniazid (inhibition of GABA) and theophylline (adenosine antagonism)

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23
Q

What is the treatment of isoniazid seizures?

A

IV pyridoxine 1 gram per gram of ingested isoniazid (up to 5 grams total)

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24
Q

What are the most common toxicological causes for seizures in Australia?

A

Venlafaxine, tramadol, amphetamines, bupropion. Withdrawal seizures with benzos or ETOH are also common.

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25
Q

What drug is absolutely contraindicated in the management of toxicological seizures?

A

Phenytoin; poor efficacy and potentially exaccerbates sodium channel blockade

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26
Q

List drugs associated with hypoglycaemia in overdose.

A

Insulin, sulfonylureas, beta-blockers, quinine, chloroquine, salicylates, valproic acid

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27
Q

What are the 5 key components of the risk assessment?

A

(a) Agents, (b) Doses, (c) Time since ingestion, (d) Clinical features + progress, (e) Patient factors (weight/co-morbidities)

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28
Q

What are the management steps for toxicological ingestions?

A

(a) Supportive care + monitoring, (b) Screening + specialised testing, (c) Decontamination, (d) Enhanced elimination, (e) Antidotes, (f) Disposition

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29
Q

You are asked to draw up a plan for an acute intoxication patient, what should be included?

A

(1) Expected clinical course, (2) Potential complications according to individualised assessment, (3) Type of observation/monitoring required, (4) End points that must result in further review, (5) Management plans for agitation/delirium, (6) Criteria for changing management, (7) Provisional psychosocial risk + contingency plan should the patient attempt to abscond prior to psychosocial assessment

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30
Q

Describe the features of the ECG that should be noted in acute poisonings.

A

Rate, rhythm, PR interval, QRS interval, QT interval, dominant R wave in aVR

31
Q

What are the three screening tox tests?

A

ECG, BSL and serum PCM level

32
Q

How common is deliberate PCM poisoning?

A

Occurs in 15% of toxic ingestions

33
Q

What does a non-detectable PCM level at >1 hour post-ingestion indicate?

A

Non-significant ingestion of paracetamol

34
Q

List the drug levels that can be requested.

A

Carbamazapine, digoxin, ethanol, ethylene glycol, iron, lithium, methanol, methotrexate, paracetamol, phenobarbitone, salicylate, theophylline, valproic acid

35
Q

List the methods of GI decontamination.

A

(a) Induced emesis (syrup of ipecac), (b) Gastric lavage, (c) Activated charcoal, (d) Whole bowel irrigation

36
Q

Describe the GI decontamination triangle.

A

Risk assessment: (a) Given current clinical status, what are the potential adverse effects of lavage and (b) What are the potential benefits to outcome

37
Q

List the potential risks associated with GI decontamination.

A

Pulmonary aspiration, GI complications (bowel obstruction, perforation), Distraction of staff from other supportive care priorities/resuscitation, Diversion of departmental recources for performaance of procedure

38
Q

What is the timeframe (for most agents) where drug absorption is virtually complete?

A

Within 1 hour

39
Q

How soon does syrup of ipecac work?

A

Within 18 minutes

40
Q

What are contraindications for the use of syrup of ipecac?

A

Nontoxic ingestion, dose is know to be sub-toxic, seizures/ALOC, potential for seizures, activated charcoal available within 1 hour and known to bind agent, infants <12 months old, corrosive ingestion, hydrocarbon ingestion

41
Q

What are the potential complications of syrup of ipecac?

A

Prolonged vomiting (10-20%), diarrhoea (20-30%), aspiration, injuries secondary to vomiting (Mallory-Weiss tears, pneumomediastinum, gastric perforation)

42
Q

Describe the procedure of gastric lavage.

A

Left decubitus position with head 20 degrees down and in a resus bay. Measure external length and then pass a large bore 36-40 G lubricated tube down the oesophagus. Confirm position. Administer 200 ml warm water/normal saline into the stomach via the funnel and drain the fluid. Repeat then give activated charcoal 50 grams.

43
Q

What are the contraindications of gastric lavage?

A

Initial resuscitation incomplete, risk assessment suggests will not change outcome, unprotected airway, small children, corrosive or hydrocarbon ingestion

44
Q

What are the potential complications of gastric lavage?

A

Aspiration, hypoxia, laryngospasm, mechanical injury to GI tract, water intoxication (in children), hypothermia, distraction of staff from other priorities

45
Q

What is activated charcoal? How does it work?

A

Super-heating of distilled wood pulp resulting in a find porous particle solution suspended in water/sorbitol. Works by enormous surface area for binding.

46
Q

How long can activated charcoal be effective for?

A

Up to 4 hours after ingestion but most effective when given immediately after ingestion

47
Q

What are the potential complications of activated charcoal?

A

Mess, pulmonary aspiration, direct administration into the lung due to misplaced NGT (= fatal), impaired absorption of antidotes subsequently administered, corneal abrasions, distraction of staff

48
Q

What are the contraindications for giving activated charcoal?

A

Initial resuscitation incomplete, non-toxic ingestion, sub-toxic dose, uncoperative, decreased LOC, delirium, imminent seizures, agent not bound to activated charcoal

49
Q

List the drugs not bound to activated charcoal.

A

Hydrocarbons/alcohols (ethanol, isopropyl alcohol, ethyelene glycol, methanol), Metals (lithium, iron, potassium, lead, arsenic, mercury), Corrosives (acids, alkalis)

50
Q

What is the dose of activated charcoal?

A

50 grams (adults), 1 gram/kg in children

51
Q

Describe when whole bowel irrigation may be indicated.

A

(1) Iron overdose > 60 mg/kg, (2) Slow-release KCl ingestion > 2.5 mmol/kg, (3) Life-threatening SR verapamil/diltiazem ingestions, (4) Symptomatic arsenic trioxide ingestion, (5) Lead ingestion, (6) Body packers

52
Q

What fluid is used in whole bowel irrigation?

A

PEG-ELS: osmotically balance polyethylene glycol electrolyte solution

53
Q

What are the potential complications of whole bowel irrigation?

A

Nausea/vomiting, bloating, NAGMA, pulmonary aspiration, distraction from resuscitation, delayed retrieval/commencement of definitive care

54
Q

What are contraindications for the use of whole bowel irrigation?

A

Uncooperative patient, inability to place NGT, uncontrolled vomiting, risk assessment suggests benefits do not outweigh risks, ileus/obstruction, intubated/ventilated patient (relative contraindication)

55
Q

What is the rate of administration of PEG in whole bowel irrigation?

A

2L/hour adults; 25ml/kg/hr in children

56
Q

What drug can be given in patients receiving whole bowel irrigation to assist?

A

Metoclopramide; assists gastric empyting and prevents vomiting

57
Q

In what toxic drug ingestions would you give multiple-dose activated charcoal?

A

Carbamazapine, dapsone, phenobarbitone, quinine, theophylline

58
Q

In what toxic drug ingestions would you give urinary alkalinisation?

A

Phenobarbitone, salicylate

59
Q

In what toxic drug ingestions would you do haemodialysis and haemofiltration?

A

Carbamazapine, lithium, meformin lactic acidosis, potassium, salicylate, theophylline, toxic alcohols, valproic acid

60
Q

In what toxic drug ingestions would you consider charcoal haemoperfusion?

A

Theophylline

61
Q

What are the characteristics of drugs that would benefit from enhanced elimination?

A

Severe toxicity syndrome, poor outcome despite good supportive care/antidote admin anticipated, slow endogenous rate of elimination, suitable pharmacokinetic properties

62
Q

What is the rationale for multiple-dose activated charcoal?

A

Progressively fills entire gut with charcoal enhancing drug elimintation in two ways: (a) interruption of enterohepatic circulation, (b) GI dialysis

63
Q

How does multiple-dose activated charcoal interrupt enterohepatic circulation?

A

Several types of drugs are excreted in the bile and then reabsorbed from the distal ileum. Charcoal in the SI prevents this reabsorption. Also relevant when a drug has a small volume of distribution.

64
Q

How does multiple-dose activated charcoal provide GI dialysis?

A

If the drug is bound to the activated charcoal in the lumen (low concentration), then the drug will naturally return into the gut lumen from the intravascular space down its concentration gradient

65
Q

What is the most common indication for MDAC?

A

Carbamazapine overdose

66
Q

What is the usual procedure with MDAC?

A

Initial dose of 50 grams charcoal (adults) or 1 gram/kg (children) PO. Repeat doses 25 grams (0.5 g/kg in children) every 2 hours. For a maximum of 6 total hours.

67
Q

How does urinary alkalinisation work?

A

Production of an alkaline urine pH promotes the ionisation of acidic drugs in the filtrate and prevents reabsorption across the renal tubular epithelium promoting urinary excretion.

68
Q

What are the drug properties that would make urinary alkalinisation work?

A

(a) Filtered at the glomerulus, (b) have a small volume of distribution, (c) weak acid

69
Q

How does urinary alkalinisation in salicylate overdose work?

A

Salicylates are normally eliminated by hepatic metabolism and thus not readily excreted in the urine. However, in overdose the metabolism is saturated and elimination half-life is prolonged. Alkalinsation greatly enhances eliminiation and is inidicated in any symptomatic patient.

70
Q

What are the contraindications for urinary alkalinisation?

A

Fluid overload

71
Q

What are the potential complications for urinary alkalinsation?

A

Alkalaemia (usually well tolerated) + fluid overload, hypokalaemia, hypocalcaemia (not usually clinically significant)

72
Q

Describe how to start urinary alkalinisation.

A

(1) Correct hypokalaemia, (2) Give 1-2 mmol/kg sodium biarb IV bolus, (3) Commence an infusion at 150 mmol sodium biarb in 850 ml 5% dextrose at 250 ml/hr, (4) 20 mmol of KCl may be added to the infusion to maintain normokalaemia, (5) Monitor serum bicarb/K + urine pH

73
Q

Why does hypokalaemia need to be reversed before urinary alkalinisation is started?

A

If there is hypokalaemia it is much harder to alkalinise the urine

74
Q

With salicylate toxicity, what are the two scenarios in which haemofiltration is indicated?

A

(1) Chronic intoxication with ALOC/mental status, (2) Late-presentation acute overdose with established toxicity

Toxicology (28 decks)

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