Environmental

A 5 year old boy is in your ED after sustaining a witnessed bite by a Red back spider

(a) Describe your assessment (50%)

(b) Outline how you would administer antivenom if indicated.

(50%)

A 35 year old man arrives in your Emergency Department after ingesting an organophosphatepesticide. He is vomiting, anxious and restless.(a) Describe the mechanism of organophosphate toxicity and the resultant symptoms and signs.(b) How would you assess and treat this patient?

1. A 10 year old child has been sprayed with a potent organophosphate. He needs resuscitation by staff working in isolation in full protective suits. Outline the main problems encountered and their possible solutions.

A 42 year old female factory worker is brought to hospital with protracted vomiting following a chemical spill at a local petrochemical plant. Hazchem information provided by her employer identifies the substance involved as an organophosphate.a) Describe the management of this patient on arrival at your department. (80%)b) Briefly discuss the investigations indicated. (20%)

A patient runs to the triage desk in the Emergency Department where you are standing. The patient has a black snake attached to the index finger of his right hand. The snake promptly lets go of the finger and slithers to the floor in the waiting room, whilst simultaneously the patient collapses to the floor.Discuss the initial, then subsequent management.

A 32 year old farm hand presents to triage stating he has been bitten by a snake. He then collapses.Discuss your management of this patient.

A 5 year old boy is brought to your major referral emergency department by his mother, who states he has been bitten on his ankle by a snake while playing in their back yard one hour previously. He has a pressure immobilization bandage in place. He is currently asymptomatic with the following vital signs:● PR 90 per min● BP 95/55 mmHg● RR 20 per min● O2 Sat 99% room air

a. What features on assessment would indicate envenomation? (50%)

One hour later the child is asymptomatic. Initial investigations are normal. The pressure

immobilization bandage is still in place.b. List the criteria which need to be met for the child to be discharged. (50%)

A pregnant 17 year old girl has been brought to your ED after a hypoxic episode related to deliberately inhaling paint (chroming). She has had several similar episodes in the past. Her GCS is now 15. Discuss the management options.

A 45-year-aid man with a sore thruat drinks 5mL of syrup from a bottle out ifl the shed, believing it to be cough medicine. He then notices the bottle actually is Metasystox, an insecticide. An ambulance is called. En route to the hospital, the bottle is spilt, with insecticide going on the patienrs and arobujance officers clothing. On arrival in the ED, the patient has slurred speech, constricted pupils, is salivating and unable to walk.Outtine your management of this situation.

1. While on duty in a regional ED in Northern Australia, you receive a 17 yo male who was rescued from the water at the local beach.Witnesses say he was found in distress, and unconscious when delivered to shore. He has multiple red wheals on the right arm.Outline your assessment and management.

General approach

Box jellyfish envenomation unconscious with unprotected airway likely shock and cardio-respiratory depression May be additional injuries, near-drowning and trauma from surf Antivenom indicated immediately

Assessment

Assessment simultaneous with management along ALS/ELS guidelines Team approach in resus cubicle.

Hx

Focussed Hx taken by team-memberIncludes ambulance handover/bystander/family.

Allergies: previous Box jellyfish/antivenom exposure.MPhx seizures, diabetesL Events

Confirm sequence as above and time to arrival in ED.Known jellyfish exposure (but still possible out of season and not witnessed by victim or

bystander)First aid given including CPR, antivenom by lifeguards (IM), compression bandages, vinegar

or tentacle removal.Known or suspected trauma

Drug or alcohol intoxication.Possibility of further victims.

Examination, investigation and management

Supportive

Assess major pulse and commence BLS/ALS if pulseless.Full monitoring.

Airway and breathing

Examine for foreign material and airway adequacychest for APO or aspiration and adequacy of ventilation.

C-spine immobilisationSuction and jaw-thrust O2 via air viva with ventilatory support as needed.Modified RSI once IVA established

Ketamine 1-2 mg/kg if hypotensive, pre-load fluidIn-line immobilisation

Ventilate.

Circulation

Anticipate shock. Continuous NIBP/ECG monitoringX2 large bore access and fluid bolus 20 mg/kg N.Saline.

Assess response with BP/pulse with repeat dose PRN

Inotrope infusion if inadequate response or APO.

Take FBE, U&E, LFT, BSL and venous blood gasses on insertion of IV. Treat hypoglycaemia with 50% dextrose.

D

Rapid assessment of GCS, pupils and for obvious focal signs prior to induction

E

Dry and avoid hypothermia. Tropical water and short exposure means this less likely

IDC/ N-G tubeCXR to check position of tube, possibility of APO.CT head if signs trauma

Secondary survey once stabilized including trauma injuries.Monitor urine output.

Specific therapy

Give antivenom immediately once available. Multiple vials IV stat in arrest orIV dose diluted in N.Saline. repeat ampoules titrated to responsePremedication not indicated but observe for anaphylaxis

Tentacle site

Pick off tentacles with tweezers. (Staff awareness of risks of exposure.)Vinegar over siteNo role for compression once antivenom available

Disposition

ICU. Likely need for fixed wing transfer.Ensure documentation/equipment/staff prepared.

Other

keep relatives informed and reassure as appropriate

Late

Unit needs to warn patient of serum sickness symptoms prior to dischargeDebrief and R/V protocolsinform lifeguards +/- media to raise awareness and for prevention.Education/ case studyCoroner’s case if dies.

Heavy Metals

Discuss the use of antidotes in patients who present with the following toxic ingestions:(a) Cyanide(b) Heavy metal poisoning

A 25 year old man presents claiming to have taken an overdose of 25 iron tablets. He has a haematemesis on arrival.Outline your

a) assessment (50%) and b) management (50%)-5~~-

A 4 year old child presents with haematemesis following ingestion of a bottle of iron tablets. Outline your assessment and managementHaematemesis in Iron Poisoning implies life-threatening iron toxicity that is likely in the multi-organ failure stage 4 – 12 hours post ingestion.

ASSESSMENTHistoryHistory of overdose – when/why found, which preparation of iron (determines amount of elemental iron), how many missing, any potential co-ingestants, any induced emesisPMHxNeonatal historyImmunisations

Growth and DevelopmentHousehold/Family structureSCAN – previous ED presentations, previous DOCS notifications, history of siblingsReview of systems particularly – bruising, urine output,

ExaminationNormal vital signs for this age group: HR 100 RR ~20 BP systolic 99+/- 20Specifically: assess haemodynames, signs of coagulopathyOther signs of injury or neglect – interaction with parents, bruising, level of hygiene

InvestigationsBedsideBSL, MSU, Urine drug screenABG – looking for metabolic acidosisBloodsLFTs – baseline, deranged LFTs may develop latterCoags – may develop a coagulopathy (early and late forms)FBC – baselineUrea/Cr- ATN, Acute renal failureFe levels – determines initiation and length of treatment

RadiologyRadio-opaque tablets on AXR – can assess success of WBI

MANAGEMENTResuscitationAirway – support, monitor Breathing – high flow oxygenCirculationNormal vital signs for this age group: HR 100 RR ~20 BP systolic 99+/- 20Commence initial resus with 20ml/kg of warm N/Saline Blood products if still hypotensive after 40ml/kgFFP/Cryo if coagulopathic and bleeding

DecontaminationCharcoal – will not bind Iron, may be useful if any co- ingestantsWhole Bowel Irrigation with Polyethyleneglycol if – tablets on x-ray, – <4hrs from ingestion, – SR prep

Specific TreatmentDesferrioxamineIndications: Iron level 60 – 90microg/l and symptomatic with acidosis, haematemesis or hypotension OR>90microg/l 3 hours post ingestion regardless of symptomsDose:15mg/kg body weight/hour intravenously, reduce dose by 50% if ARFuntil iron levels below 60microg/L and urine no longer (if it changed colour) back to normal colour

Supportive cares20ml/kg N/Saline while receiving desferrioxaminewill need close monitoring with IABP, CVL, HDUTreat haemorrhage – packed cells 20ml/kg, FFP, Cryo as neededSupport parents and siblingsConsider any SCAN issues and notify if reasonable suspicion

Ensure safety of siblingsWatch for APO, May develop after 24hrs of desferrioxamineMay need upper GI scope in longer term re: pyloric scarring

DisposalBed in Paediatric HDUConsults – Toxicologist, Paediatrician, Intensive Care, SCAN Paediatrician

A 22 month old presents to the ED with is mother 30 minutes after she found him playing with an open bottle of iron tablets. There are 4 tablets unaccounted for. (Ferrogradumet tablets 325 mg).

Outline your management of this patient in the ED.

This child has presented following possible ingestion of 4 iron tablets. Iron is a drug with significant side effects in overdose, and this patient must be carefully assessed for potential toxicity. He has presented early and may therefore be asymptomatic despite potential toxicity.

Initial ED assessment would include monitoring in an acute area to allow close observation, and obtaining a baseline set of observations including HR, RR, SpO2 and NIBP.

I would concurrently obtain a history with specific attention being paid to access to the tablets, how the tablets were accounted for, timing of the ingestion, any other medicines in the house, as well as an assessment of the family/social situation and the safety of the child. Given that this child has presented early there is unlikely to be any clinical manifestation of toxicity at this stage but I would perform an initial examination with particular emphasis on abdominal examination.

Iron is a drug that does not bind to charcoal. Decontamination could be done by either endoscopy if there was a large mass of tablets in the stomach, or by whole bowel irrigation (WBI) with Golytely. Both of these methods are invasive and in general there would have to be concerns about significant potential for toxicity before they were undertaken. In general if < 20 mg/kg of elemental iron ingested then decontamination not necessary, if > 20mg/kg and certainly if > 60mg/kg then it should be considered. WBI usually carried out by inserting NGT and running at 15 ml/kg/hr until clear rectal effluent obtained.

Specific management of the iron ingestion will depend on the amount of elemental iron ingested.

This child has taken potentially 4 FeGradumet tablets which are ~ 35% elemental ironIe each 325 mg tablet contains approximately 100 mg elemental iron therefore total of 400 mg.At 22 months an approximate weight would be ~14 kg therefore he has taken ~ 30 mg/kg elemental iron.

Toxic dose of iron based on elemental iron:< 20 mg/kg/ - low risk for toxicity20 – 60 mg/kg - moderate risk> 60 mg/kg - high risk

Phases of toxicityPhase 1: 0-3 hours – GIT symptoms predominatePhase 2: 3-12 hours – relatively quiescentPhase 3: 12-48 hours – onset of systemic toxicityPhase 4: 2 weeks – scarring and stricture formation

Initial investigations I would perform would include:

FBC WCC > 15,000 correlates with toxicity

U&E glucose LFT glucose > 8 correlates with toxicitySerum Fe and iron studiesSerum Fe : if > TIBC (transferrin x 1.5) then systemic toxicity likely 60 micromol/L considered toxic 90 micromol/L high riskGroup and holdVenous gas will show metabolic acidosis with raised anion gapCoagulation studiesAXR looking for tablets in stomach

Iron has a specific antidote – Desferrioxamine which acts to chelate the iron.It is best given intravenously, with 2x IV access preferred as it can potentially cause hypotension. It should be considered in cases with either signs of toxicity or at high risk of toxicity, however would not be indicated in this patient.(Usual dose range is to start at 5 mg/kg/hr and increase up to 15 mg/kg/hour).

Co-ingestion would have been explored in the history, as well as assessment of any potential child safety concerns.

This child needs to be admitted and observed for any potential signs of toxicity, with repeat investigations in 4-6 hours depending on the initial investigations.

Other general points (not for answer but learning points)Iron is taken up in the duodenum and jejunum. A mucosal transport protein takes up the iron and stores it as ferritin. If a patient is Fe deficient the body produces transferrin which removes Fe from cells. Transferrin is the major mechanism for safe Fe transport throughout the body. TIBC measures the amount of serum transferrin. If the serum Fe is > than TIBC then the transferrin transport system is overwhelmed and toxicity ensues.

GIT effects predominate initially with vomiting, diarrhoea, abdominal pain, mucosal bleeding, ulceration and perforation.As the mucosal surface is injured, iron passes unimpeded into the blood stream, leading to systemic toxicity once the ability of transferrin to bind Fe is exhausted. Iron enters the cells where it inhibits oxidative phosphorylation leading to a metabolic acidosis, direct myocardial damage, coma, encephalopathy, coagulopathy.Late effects (if survive initial phase) are of scarring and stricture formation.

Remember other poisons that don’t bind to charcoal:o alcohols o irono lithiumo KClo Gold saltso Strong acids and alkaliso Organophosphateso Arsenic

Whole bowel irrigation:NG instilled Golytely or PEG at 15 ml/kg/hr (though there seems to be a variety of doses quoted, I saw 50-250 ml/kg/hr somewhere but that seems a huge volume).

Contraindications are absent BS or obstruction.Common indications are SR preparations, illicit drug packing and agents that do not adsorb to charcoal.

Metabolic acidosis:Anion gap = ([Na] + [K]) – ([Cl] + [HCo3])

Upper limit of normal is 18.

Raised anion gap metabolic acidosis:Methanol poisoning, metforminUraemiaDKAParaldehyde, phenforminIsoniazid, ironLactic acidosisETOH, ethylene glycolSalicyclates

CV

Compare and contrast acute and chronic Digoxin poisoning.

A 47 year old man with a history of hypertension and depression has presented to your emergency department following deliberate self poisoning approximately 3hrs ago with 20 x 240mg slow release verapamil tablets.

His initial vital signs are:GCS 15HR 50 /minBP 115 / 70RR 16 /minSaO2 99% room air

Describe your management of this patient. (100%)

A 3yo female presents 1 hr post-ingestion of an unknown quantity of her mother’s metoprolol tablets (50mg tabs). She is currently asymptomatic.

(a) Outline your assessment of this child (50%)(b) Outline your management of this child (50%

3yo female (estimated weight 14kg)1hr post ingestion – Metoprolol 50mg tablets – unknown quantityAsymptomatic

Issues:1. Potential for lethality2. General assessment / Assessment for toxicity3. Decontamination4. Management of toxicity a. Supportiveb. Specificc. Dispositiond. Safety issues – eg: medication access

Potential for lethality

• This may potentially result in a lethal overdose – serious beta-blocker toxicity can be resistant to all treatment• The carers should be made aware of the potential serious outcomes; and the current asymptomatic state of the child is not necessarily reassuring• Metoprolol should show signs of toxicity within 4hrs. Elimination T1/2 of 3-4hrs. And has moderate lipid solubility – regarding potential CNS effects. Loses B1/B2 specificity in overdose.

(a) ASSESSMENT

General assessment / assessment for toxicity• History:o Circumstances of ingestion – Time – 1hr ago (from question)

Evidence of ingestion eg. tablets/residue in mouth; missing tablets when found with them If possible estimate maximum possible dosage ingested – confer with poison index regarding potentially toxic doses on a per kg basis. Given strength of tablets – expect if even 1 tablet ingested that potentially toxic (standard dose 1-2mg/kg) Any potential co-ingestants Access to medications – safety issues; neglect?; evidence to suggest non-accidental injury?

o Presence of symptoms prior to presentation (GI symptoms)– has child vomited (any tablets noted)o Past history – current illnesses or conditions that may be compromised or complicated by beta blocker ingestion ie: asthma, cardiac conditiono Current medications – any interact adversely with beta-blockers?

• Examination:o Baseline vital signso Currently asymptomatic but focus on systems affected by beta-blocker ingestion – cardiovascular (HR, BP, peripheral perfusion etc); respiratory (wheeze in asthmatics); CNS(altered level of consciousness; seizures)

• Investigations:o ECG – assessing for bradycardias; AV blocko Nil else at this stage as asymptomatic

(b) MANAGEMENT

• Connect to comprehensive non-invasive monitoring• Allow carers to stay with / nurse child

Decontamination

• At 1hr post-ingestion and asymptomatic – activated charcoal most effective. Dose 1g/kg – 14g.• If can confirm potentially life threatening ingestion has occurred then consider elective intubation and gastric lavage at this early stage – however if by this time it is well beyond 1hr then any benefit of lavage would be lost.

Management following charcoal decontamination proceeds either of 2 paths:

Management of toxicity

o Asymptomatic path: If initial clinical assessment and ECG reveal no abnormalities then child should be continuously monitored for a period of 6hrs If the child remains asymptomatic over this time and a repeat ECG is unchanged at this time then the child may be discharged assuming appropriate/safe social circumstances The carers should be advised on appropriate storage of medicines etc if this was an issue

o Symptomatic path: If the child becomes symptomatic of beta blocker toxicity (clinical or ECG) then supportive and specific treatment should commence

Reassess for immediate life threats-• Airway/breathing:• Apply high flow O2 via non-re-breathing mask; If decreased LOC or persistent seizures compromises airway – intubate and ventilate• Circulation:o IV access (bloods for baseline biochemistry).o Initial fluid bolus for hypotension (SBP <80) if present – 20ml/kg – 300ml 0.9% saline.o Bradycardia (HR <80) or AV block resulting in hypotension (SBP < 80mmHg) requires iv

glucagon 100-150mcg/kg bolus followed by infusion at 10-50mcg/kg/hr. Consider options for additional support with inotropes (adrenaline); temporary pacing; high dose insulin-glucose infusion; temporary cardiopulmonary bypass.o Aim HR>80 and SBP>80• Disability:o CNS complications – decrease LOC; seizures. Treat seizures with benzodiazepines (0.1mg/kg IV) and phenytoin (18mg/kg IV)• Check BSL – hypoglycaemia is a complication. Treat with 10ml/kg 5% Dextrose if present. Disposition will be to Paediatric ICU. With follow up also to cover safety issues regarding access to medications etc.

NS

a. Outline the spectrum of possible emergency department presentations resulting frommetamphetamine use (30%)b. Outline your approach to the treatment of acute behavioural disturbance caused bymethamphetamine toxicity (70%)

1. Compare and contrast the clinical features of serotonin syndrome, neuroleptic

malignant syndrome, anti-cholinergic syndrome and malignant hyperthermia

(100%).

Compare and contrast becoming increasingly common.

Need to succinctly highlight similarities which show the examiner that you are aware why this

question was asked and why it presents a diagnostic dilemma in real life.

Need to show the important points of difference between the subjects, so the examiner knows

that you are an efficient clinician.

Often a table will be the best way to highlight these above points, is an efficient way to answer

the question in an exam, and will often help you remember points of interest under the stress of

exam conditions. But make sure that you are not answering a question in table form for the first

time on the day of the exam! It takes some practice.

Relatively easy to highlight similarities – this is why the question was asked – it poses a

diagnostic dilemma.

Harder is to be sure of the differences between the conditions.

Think about what headings you will use – clinical features will be the most important.

Refer to both history and examination.

Consider other headings such as prognosis, complications.

This specifically asked about clinical features – other examples may be more open in which case

if you are struggling for information to include consider other headings such as differences in

investigations and treatment.

It is not wrong to say that you would refer to a clinical toxicologist, especially for obscure

scenarios.

2. The overall pass rate for this question was 28/56 (50%).3. It was expected that answers would make clear the causative agents, time course and

classic clinical4. features of both syndromes. Better answers made clear both the useful differentiating

points and the5. common features. The management questions were expected to include both general

supportive6. measures such as IV fluids, cooling and prevention of muscle breakdown induced

renal impairment,7. as well as syndrome specific drug treatments. Failing management answers drew little

distinction8. between the two syndromes and were light on with respect to specific therapies such

as9. bromocriptine, cyproheptadine and chlorpromazine

a. What are the symptoms and signs of lithium toxicity?

(30%)

b. Describe the specific treatments for lithium toxicity including their indications.

(70%)

AnswerAnswer and Interpretation

FACEM SAQ Exam 2006.2 – Question 1← The overall pass rate for this question was 48/57

(84.2%).← Pass Criteria← The examiners felt that this was overall a very good

question which would be anticipated to be well answered by the majority of candidates.

← A number of candidates struggled to obtain high marks by failing to address the specifics of the question.

← Candidates who did not pass the question failed to differentiate acute from chronic toxicity and the differing symptoms and signs.

← Features of unsuccessful answers← Poor answers also proposed using activated charcoal

without mention of co-ingestants and had no specific indications for therapy.Of particular concern was candidates advocating

dialysis therapy based on specific serum levels in the absence of any clinical correlation.

SAQ 338

Outline your treatment strategy for a 15 year old female brought to the ED with a fluctuating LOC and intermittent vomiting. Initially rectal temperature is 38.7 HR 140 and BP 90/60. Muscular rigidity is apparent. Empty bottles of Fluoxetine, Paracetamol, Phenelzine and Amitryptiline have been found beside her.

Key issues in the treatment of this patient include:

• Initial resuscitation• Decontamination• Management of specific features of overdose– serotonin syndrome- TCA- Paracetamol• Assessment of coingestion and comorbidity• Psych evaluation• Disposition

I would manage this patient in a resuscitation area and initially obtain baseline vital signs HR (140) RR BP (90/60) temp (38.7) BSL SpO2 and GCS.

Needs full cardiac monitoring and oximetry.IV access x 2 with pathology sent for FBC, U&E, creat, LFT, CK, Paracetamol levelInitial bolus of 1 litre N Saline for hypotension.Also HCO3 for TCA related hypotension – will discuss later.

Due to fluctuating LOC and vomiting I would intubate this patient to protect the airway and to optimise further management.RSISux/Midazolam/FentanylCautious due to hypotension on presentation which is most likely due to TCA Amitriptyline – ensure has had fluid bolus and HCO3 prior to intubation

Once intubated needs ETCO2 monitoring/NGT/IDCCXR to check positionAim for ETCO2 30 – 35 mmHg – confirm with ABG – enhancing elimination of TCA

Due to propensity for arrhythmias with this combination of agents I would have the external pacer/defib nearby.

DecontaminationSince airway has been protected I would give a dose of Activated Charcoal via the NGT. TCA will delay gastric emptying via anticholinergic actions, so depending on collateral history and timeframe I would consider repeat dose activated charcoal. I would consider lavage though it would depend on timeframe.

Specific management of this patient:This patient presents with signs of serotonin syndrome – triad of altered mental state, autonomic dysfunction and abnormal neuromuscular activity due to increased CNS serotonin.

This has been precipitated by the combination of SSRI, MAOI and TCA.

• Treatment is largely supportive with anticipation of problems – maintain sedation with benzodiazepines – morphine and midazolam infusion +/- Valium 2.5 mg IV PRN.• Maintain paralysis• Watch for rhabdomyolysis – ensure good UO, baseline CK and monitor 6-12 hrly• Temperature control• Cyproheptadine 4-8 mg via NGT acts as a serotonin antagonist.• May have seizures – difficult to recognise in ED setting if paralysed/sedated – watch for

signs of increased HR and pupillary activity

ParacetamolManagement will depend on timing of ingestion if known and quantity of ingestion of known (ie if > 150 mg/kg).Likely that this collateral is not available at the outset –I would commence N acetyl cysteine empirically Regime IV 150 mg/kg IV over 15 minutes50 mg/kg IV over 4 hours100 mg/kg IV over 16 hours

Other issues to consider with Paracetamol are: comorbidity – ETOH abuse/malnutrition/glutathione depletion

I would take a baseline Paracetamol level and then a repeat level 4 hours later which would guide further Rx.

TCAMain issues are hypotension/arrhythmias and seizures.Triad of anticholinergic effects, CNS effects and CVS effects.This patient needs continuous cardiac monitoring which is in place.Hypotension would be treated with fluid loading and consider IV NaHCO3Mild hyperventilation to enhance elimination.

Patient needs full physical examination to ensure no other comorbidity – sepsis/aspiration etcCollateral history re – ingestion, previous medical history, drug history, psych history.

A 22 year old man is brought to your department by police. He was found wandering through heavy traffic and abusing drivers. He became increasingly aggressive in the police van and has been handcuffed. He has dilated pupils and is tachycardic. Describe your assessment.

a. How would you distinguish between neuroleptic malignant syndrome andserotonin syndrome?(50%)b. Outline your management of neuroleptic malignant syndrome. (25%)c. Outline your management of serotonin syndrome. (25%)

The overall pass rate for this question was 28/56 (50%).It was expected that answers would make clear the causative agents, time course and classic clinical features of both syndromes. Better answers made clear both the useful differentiating points and the common features. The management questions were expected to include both general supportive measures such as IV fluids, cooling and prevention of muscle breakdown induced renal impairment, as well as syndrome specific drug treatments. Failing management answers drew little distinction between the two syndromes and were light on with respect to specific therapies such as bromocriptine, cyproheptadine and chlorpromazine

Describe the management of acute alcohol withdrawal in the Emergency Department

A 17 year old female is brought to the Emergency Department by friends. They tell you she has taken an unidentified white tablet and alcohol at a party. She is tachycardic, agitated and confused and wants to leave the ED.Outline your assessment and management.

5.) A 62 year Vietnamese man is brought into your small community emergency department. Through family members you are told that he admits to taking 30 tablets of isoniazid approximately 1/24 ago. He was recently diagnosed with active pulmonary Th and discharged from your hospital only 10 days ago. His son tells you that he no longer wants to live and that he does not want to be treated.

a.) Outline your assessment (5 0%)b.) Outline your management (50%)

All Other

Discuss techniques used to enhance elimination of a drug after a toxic drug ingestion.

Describe the techniques available for enhanced elimination of potentially toxic drug ingestion (100%).

Options for enhanced elimination:• Repeat dose activated charcoal.• Urinary alkalinisation.• Haemodialysis.• Haemoperfusion.

(1) Repeat dose activated charcoal:• Enhances drug elimination by interrupting the enterohepatic circulation of a drug (gastrointestinal haemodialysis).• To be effective the drug in question must undergo significant enterohepatic circulation; be adsorbed by charcoal; have a slow endogenous elimination; a small Vd; and low protein binding.• Examples of drugs this technique is suitable for:i. Carbamazepineii. Phenobarbitoneiii. Phenytoin.iv. Salicylate.v. Theophylline.vi. Dapsone.• Method: Dose – 25-50g activated charcoal orally or NGT q4hr.(2) Urinary alkalinisation:• Enhances urinary excretion of unchanged drug.• To be effective the drug in question must be a weak acid; predominantly renally excreted in its unchanged form; have a low pKa; distributed mainly in the ECF; and with minimal protein binding.• By alkalinizing the urine the drug will be in an ionized state within the alkaline urine in the tubules and thus be unable to be resorbed.• Examples of drugs this technique is suitable for: salicylates, phenobarbitone.• Method: use NaHCO3 8.4%. Bolus 1-2mmol/kg – aim serum pH 7.5-7.55. Aim urine pH > 7.5. Maintain with iv infusion 10-100mmol/hr. Maintain normokalaemia with K+ supplementation.

(3) Haemodialysis:

• Useful for drugs that have small Vd; slow endogenous clearance; small molecular weight.• Generally reserved for when other methods of decontamination / elimination / supportive care are failing and progressive end-organ damage is occurring.• Carried out in ICU setting.• Examples of drugs this technique is suitable for: i. Lithium.ii. Salicylates.iii. Theophylline.iv. Methanol.v. Ethylene glycol

(4) Haemoperfusion:• Perfuse blood through filters that will adsorb toxic drug.• Examples of filters – charcoal, fuller’s earth.• Carried out in ICU setting.• Drugs in question need to have small Vd; slow endogenous clearance; and adsorb / bind to substance within the filter.• Examples:i. Charcoal haemoperfusion – theophylline.ii. Fuller’s earth haemoperfusion

Discuss the methods of gastrointestinal decontamination in the management of acute drug overdose. Discuss the different methods of gastro-intestinal decontamination available in the treatment of poisoning, including where possible a discussion of the indications, contra-indications, efficacy and complications of each method.

Decontamination limits absorption and minimizes toxicity. Stomach is first receiving organ in ingestion therefore most treatment is directed at it.PositionL lat decubitus can decrease gastric emptying and systemic absorption by 2 hrs with paracetamolIpecacAdvantage use in home poisoning (especially paeds)Disadvantage only reduces absorption 30%Interferes with charcoal administrationInterferes with therapeutic and diagnostic measures necessary for well being of patientProlongs time in EDLavageAdvantage immediate recovery gastric contents (compared to 20min delay with ipecac)Control of lavage durationGiving charcoalDisadvantage Need secure airway, risk of aspirationEfficacy after 1-2 hrs questionable (except in severe OD)CharcoalAdvantage Very large SA 3000m2g. Activated has 3*SA of ordinary and whilelavage/ipecac can absorb 30%, it may absorb up to 50%Disadvantage MessyPatient complianceMay induce vomiting/aspirationCatharticsAdvantages Speed up GIT, shortening absorption timeDisadvantage Osmotically increased fluid loads may increase absorptionFrequent liquid stoolMay interfere with clinical/diagnostic/therapeutic measuresDehydration and ELFTs abnormality in paedsWhole Bowel IrrigationAdvantage Wash out of bowel for stuffers or SR medication (until clear poo)No significant change in ELFT/osm reported

Disadvantage complianceFrequent liquid stool

A 35-year-old man presents to your Emergency Department following an alleged overdose of aspirin tablets. His initial observations are:

GCS 15Temp 37.4HR 105 BP 100/40

His initial arterial blood gas is as follows: pH: 7.10 pCO2: 35 pO2: 110 HCO3: 14 BE: –10.5.

(a) Outline your assessment of this man. (50%)(b) Outline your management of this man. (50%)

Key issues:• Observations and results consistent with significant salicylate ingestion• Metabolic acidosis on ABG• Relatively normal PaCO2- suggestive of severe ingestion (respiratory depression), or co ingestants (eg benzodiazepines, narcotics, alcohol)

(a) Assessment:

History: (from patient and collateral)Circumstances of ingestion:• Time of ingestion• Formulation of aspirin tablets – strength, ?enteric coated or slow-release• Number taken – determine maximal possible dose ingested (>300mg/kg serious toxicity)• Any co-ingestants• Vomiting pre-hospital ?some tablets brought up

Symptoms of salicylate ingestion:• Nausea and vomiting• Tinnitus• SOB – from centrally stimulated tachypnoea or pulmonary oedema• Epigastric pain – gastric irritation

Past medical history:• Esp: asthma, PUD, renal disease – conditions that may potentially be exacerbated by salicylates

Past psychiatric history:• Previous overdoses• History of depression, psychotic illness, personality disorder etc

Social circumstances – employment, social supports etcMedications / allergies

Examination:Vital signs Assess for any immediate life threats due to salicylate toxicity:• Airway and breathing:o Presume patent airway from question – GCS 15

o Adequate oxygenation from ABG pO2 110o Assess respiratory rate – note pCO2 35 would normally expect greater degree hypocarbia due to central stimulation and in compensation to metabolic acidosis• Circulation:o Tachycardic HR 105o BP borderline at SBP 100mmHgo Assess peripheral perfusion• Disability:o GCS 15 – no significant CNS involvement at this point. ?lethargy or agitation present (early finding)Systems examination – evidence of salicylate toxicity:• Respiratory – any evidence non-cardiogenic pulmonary oedema• GIT – epigastric tenderness / PR blood – to suggest upper GI bleed from erosions etc

Mental Health Examination:• Assess mental state• Assess risk for further self harm and potential to abscond• Determine need to make involuntary patient under Mental Health Act

Investigations:Bedside:• BSL• ECG – evidence of arrhythmiasLaboratory:• FBC – baseline – Hb (any occult GI bleeding)• Electrolytes – baseline – hypokalaemia common• Renal function – baseline – ARF may develop if rhabdomyolysis present• LFTs – may be deranged if chronic toxicity• Lipase – pancreatitis - uncommon• CK – evidence of rhabdomyolysis• Coagulation profile – prolonged PT -competitive inhibition of Vit K dependant factor synthesis (DIC is uncommon)• Paracetamol level at 4hrs to exclude as coingestant• Salicylate level – at 4hrs – limited clinical role; poor predictor of outcome. Serial levels may assist in determining that no further absorption taking place ie: slow release formulations

Radiology:• CXR – if indicated clinically for evidence of pulmonary oedema

(b) Management:

Place in monitored areaConnect to comprehensive non-invasive monitoringIV access x2 large bore

Treat any immediate life threats:• Apply supplemental O2 – maintain SaO2 >96%• IV fluid bolus 20ml/kg 0.9% saline – maintain BP >100mmHgDecontamination:• If <2hrs since ingestion 50g oral charcoal – though presence of metabolic acidosis at presentation suggests significant time has already elapsed Specific treatment:• Airway and breathing – may require intubation and ventilation if develops decrease level of consciousness or worsening gas exchange• Circulation – if develops hypotension resistant to further fluid challenges – will require CVL / IAL and use of inotropes (adrenaline)• Disability – potential for seizures / decrease level of consciousness. Provide airway protection (intubation) and iv midazolam 2mg aliquots until seizure controlled.• Enhanced elimination:o Urinary alkalinisation

Initial 1mmoll/kg 8.4% NaHCO3 IV bolus over 10min Then infusion – 50-100mmol/hr to maintain urinary pH>7.5 Monitor closely for fluid overload and hypokalaemia• Haemodialysis:o Indicated if deteriorating clinically, worsening acidosis, oliguric renal failure, pulmonary oedema and rising salicylate levels - despite decontamination, urinary alkalisation and other supportive measures.Supportive care:o Ongoing fluids – 0.9% saline – aim UO>1ml/kg/hr o Potassium replacement – aim K+ serum 4 – 5 mmol/Lo IDC q1hr UO measureso NGT if intubatedo Maintain normothermiaDisposition:o HDU / ICU if requiring ventilatory support, cardiac support / monitoring , or haemodialysiso Mental health review once stable

You are the Duty Consultant of a central tertiary hospital. You receive a call from a doctor in

a small regional hospital 2 hours by road from your ED, for advice regarding a three year old

patient who has ingested three suphonylurea tablets an hour earlier.

The child is currently alert with normal vital signs, and has a finger prick glucose reading of

2.6 mmol\L

(a) Outline your advice to the referring doctor (50%)

(b) Outline the arrangements you would make to transfer this child to your hospital.

Discuss the use of the Rumack-Matthew nomogram, including a discussion of its shortcomings.

It is a semi-logarithmic plot of serum paracetamol level verus time and estimation of risk of hepatotoxicity following a single acute ingestion.It determines the need for NAC using a single serum paracatamol level 4-24hrsBlood is preferably drawn at 4hrs and plottedIf above this line or large OD NAC startedIf ?time then longest possible time plottedThe lower 25% line allows for errorsReduce line 50% in chronic alcoholics/enzyme inducersGive whole course of NAC if initial level above line and all subsequent are belowShortcomings areChronic ODMultiple ODSustained release products (keep repeating levels)Only between 4-24 hrs. Levels outside these may not reflect clinical riskErrors in time of ingestion and error in lab measurement has lead to the 150 lineCheck lab units are same as nomogramCo-existing OD may delay gastric outflowPt died with levels 150-200 therefore use 150 lineDelay Rx waiting for levelMay not ID at risk pts initially and lower treatment line accordingly