Marine Toxins

Dr Michelle Dodds


  • Distribution: Tropical Australian waters, majority of stings occur from October to June.
  • Clinical presentation: immediate severe pain that can last 8 hrs; Sting pattern – crosshatched, linear welts
  • Systemic envenomation: sudden collapse or death within a few minutes of the sting, with cardiovascular effects including hypertension, hypotension, tachycardia, impaired cardiac contraction and arrhythmias
  • Treatment
  • CPR and antivenom if arrest (6 ampoules undiluted box jellyfish antivenom can be given as a rapid IV push in cardiac arrest)
  • NO pressure immobilisation bandaging (causes venom release from nematocysts)
  • Vinegar to stings + removal of tentacles
  • In systemic envenoming: 3 ampoules antivenom in 100ml N/Saline over 20 minutes
  • Treat pain: opiate analgesia + 1 ampoule antivenom for pain refractory to IV opioids

IRUKANDJI SYNDROME –caused by Carukia barnesi + likely other unidentified jellyfish

  • Distribution: Tropical Australian waters, as far south as Fraser Island
  • Clinical presentation: initial sting not felt

Symptoms of catecholamine surge: sense of impending doom, agitation, dysphoria, vomiting, generalized sweating, severe pain in the back, limbs or abdomen, hypertension and tachycardia, pulmonary oedema

  • Treatment
  • Vinegar to all sting sites (inactivate undischarged nematocysts)
  • No pressure immobilization bandage
  • No antivenom available
  • Manage pain – IV opiates, refractory pain may respond to magnesium (conflicting evidence – use is controversial)
  • Manage potential early life threats (catecholamine storm)
    • Severe hypertension (GTN infusion titrated to achieve SBP <160)
    • Pulmonary oedema (may need intubation and ventilation)
  • Symptoms of envenomation usually settle within 12 hours


  • Distribution: all parts of the Australian coastline (+ South East Asia, and the Pacific)
  • Toxin (in saliva) – potent sodium channel blocking neurotoxin that affects neurons and skeletal muscle, but not cardiac muscle. This results in sensory and motor blockade. Identical to the tetrodotoxin of the puffer fish
  • Clinical presentation
  • Non painful bite with minimal local symptoms
  • Ptosis, blurred vision, diplopia, difficulty swallowing
  • Rapidly progressive descending flaccid paralysis, fixed dilated pupils and respiratory failure
  • Treatment
  • Pressure immobilisation bandage
  • ABC approach to management of descending paralysis and respiratory failure – may require mechanical ventilation + sedation (patients are paralysed but still aware)
  • No antivenom available
  • Remember to check closely for subtle early signs of paralysis


  • Clinical presentation: Sting causes immediate local intense pain, red linear dermal marks, may have mild systemic symptoms (nausea, vomiting, malaise)
  • Treatment: remove adherent tentacles, hot water (ideally around 45 degrees for 20 minutes) and simple analgesia. Pain usually resolves in around 2 hours


  • Distribution – northern Australian waters
  • Clinical presentation – injects venom with external pressure on dorsal spines à immediate severe pain + puncture wound.

Systemic envenomation is rare – nausea, vomiting, dizziness, dyspnea and CVS collapse

  • Treatment – hot water immersion of affected limb + pain management (opiates)

For severe refractory pain or systemic envenoming – antivenom (1 ampoule for every 2 spine puncture wounds to max 3 ampoules)


  • Venomous barb in tail
  • Clinical presentation – either direct trauma (penetrating chest/neck/abdo trauma) or and/or systemic envenomation with viscus penetration (nausea and vomiting, diarrhea, abdominal pain, respiratory depression, hypotension, arrhythmias and myocardial ischaemia)
  • Treatment – analgesia, management of wound (control haemorrhage, debridement, tetanus, consider antibiotics), emergency/surgical management of more severe penetrating wounds


  • Clinical presentation – usually painless bite

Systemic envenoming: symmetrical descending flaccid paralysis + rhabdomyolysis

  • Treatment – as per usual snake bite management – pressure immobilisation bandaging, manage potential early life threats (paralysis + respiratory failure), investigations as per snake bite (FBC, U+E, CK, coags including d-dimer, CK at presentation and intervals after), antivenom if signs of envenomation
  • Antivenom – 1 ampoule sea snake antivenom

If sea snake not available, can use 3 ampoules of tiger snake antivenom or 3 ampoules polyvalent antivenom


  • Ciguatera poisoning
    • From eating reef fish such as: barracuda, red snapper, grouper
    • Presentation: Vomiting and watery diarrhoea, ‘hot-cold reversal’ (cold allodynia), headache, paraesthesiae of the mouth and extremities, pruritis, myalgias, weakness; rarely seizures and respiratory arrest.
  • Scombroid poisoning
    • From eating tuna, mahi-mahi, bonito, mackerel
    • Presentation (histamine release) – Gastroenteritis, flushed skin, hypotension, urticaria, wheezing
  • Neurotoxic shellfish poisoning
    • From eating bivalve mollusks, whelks
    • Presentation: Gastroenteritis, paraesthesiae, ataxia, respiratory paralysis





Procedural Sedation

Safety in procedural sedation (PSA)

Dr Michelle Dodds


  • ACEM policy endorses ANZCA guidelines on sedation + analgesia
    • 2-hours – clear liquids, 4-hours – breast milk, 6-hours – solids
    • Consider aspiration more likely with inhalational anesthetics + manipulation of airway (less common in ED)
  • Vomiting in PSA in ED actually rare (0.5% in QLD study with propofol sedation)
  • ACEP guideline 2014
    • Do not delay PSA in adults based on fasting time
    • Fasting has not demonstrated reduction in the risk of emesis/aspiration

Monitoring including ETCO2

  • ACEM guidelines
    • Pulse oximetry, pulse rate, blood pressure
    • Consider ECG and capnography
  • ETCO2 monitoring 17.6 times more likely to detect respiratory depression than standard monitoring alone
Early recognition of possible hypoventilation – allows early patient re-evaluation, airway support, ventilation to correct it Capnographic abnormality may not be clinically relevant (i.e. not lead to hypoxia)
Minimally invasive and safe – doesn’t cause harm to patient
(unable to study change in outcomes – hypoxic brain injury, aspiration, death)
False positives – caused by patient movement, nasal cannula displacement, patient verbalisations or crying
Not affected by supplemental O2 delivery Unnecessary interventions due to false positives – multiple interruptions, delay or abandonment of procedure
Low cost + easy to use

Number of personnel present for PSA

  • ACEM guidelines
    • Minimum 3 appropriately trained staff
    • 1 PSA, 1 procedure, 1 to monitor patient (RN)
  • No strong evidence to support 2 vs 3 staff (rates of complications same)

 Complication rates for procedural sedation

  • Airway complications (range from hypoventilation > transient apnoea > brief desaturation) – overall ~ 20%, most respond to simple airway manouvres
  • Vomiting – rare 0.5 – 2% depending on agent (more with ketamine)
  • Hypotension – usually transient, or responding to fluid bolus ~20% (more with propofol)

 Depth of Sedation in the ED

Minimal sedation – Near baseline level of alertness (responds to verbal command)
– Ventilatory + CVS function unaffected
Moderate sedation – Depressed consciousness – responds to verbal command + tactile stimulation

– Airway/ventilation + CVS function usually maintained

– Event amnesia common

Deep sedation – Depressed consciousness – not easily aroused, but respond purposefully after repeated/painful stimuli

– May have impaired airway/ventilation

General anaesthesia – Unresponsive to all stimuli

– Impaired airway/ventilation requiring intervention

– CVS function may be impaired

  • Rates of complications increase with increasing depth of sedation and increased ASA score (more underlying medical comorbidities)
  • Study on patient controlled sedation from the RBWH: lower doses of propofol and lighter sedation depths still result in procedural success, with less adverse effects


  • Bell A, Treston G, McNabb C, Monypenny K, Cardwell R. Profiling adverse respiratory events and vomiting when using propofol for emergency department procedural sedation. Emerg Med Australas. 2007 Oct;19(5):405-10.
  • Waugh JB, Epps CA, Khodneva YA. Capnography enhances surveillance of respiratory events during procedural sedation: a meta-analysis. J Clin Anesth. 2011 May;23(3):189-96.
  • Harvey M, Cave G, Betham C. Contemporary sedation practice in a large New Zealand emergency department. N Z Med J. 2011 Oct 14;124(1344):36-45.
  • Bell A, Lipp T, Greenslade J, Chu K, Rothwell S, Duncan A. A randomized controlled trial comparing patient-controlled and physician-controlled sedation in the emergency department. Ann Emerg Med. 2010 Nov;56(5):502-8.




Dr Peter Snelling

Propofol – Practice Points

  • Advantages: short acting hypnotic, short half life, anti-emetic, euphoric
  • Disadvantages: no analgesia, cardiorespiratory depression, injection pain, allergy
  • Anaphylaxis?
    • Although formulated in lipid vehicle containing refined soya bean oil and purified egg phosphatide, these elements not shown to be allergenic
    • Food allergy/anaphylaxis not a good predictor of propofol anaphylaxis
  • Injection site pain
    • Using ACF vein instead of hand, single most effective intervention (RR 0.14)
    • Pretreatment with lignocaine with venous occlusion (RR 0.29), lignocaine-propofol admixture (RR 0.4), opioid pretreatment (RR 0.49)
  • Hypoventilation
    • Risk for patients at extremes of age, obese, underlying illness ?suitable for ED
    • Titrate pre-procedure opioid analgesia, rather than peri-procedure use given synergism of respiratory depression
    • Front load 0.5-1.0mg/kg then 10-20mg titrations every 1-2 mins
    • Smaller doses more slowly (3-5mins) in elderly (test dose 100mg – age)
    • If dosing by actual weight, obese tend to need less and thin need more

Ketofol – Best of both worlds?

  • Combination of propofol and ketamine physically compatible and chemically stable when mixed
  • Theoretical benefits?
    • Lower doses of each required for effect, less adverse events
    • Offset of adverse effects by other agent eg emesis, respiratory depression, hypotension, recovery agitation
  • Evidence?
    • 2012 RCT, Annals of Emergency Medicine: Propofol vs 1:1 ketofol
      • No significant reduction in adverse respiratory events, no serious outcomes for either
      • Induction time, efficacy and sedation time were similar
      • Sedation depth more consistent with ketofol?
    • 2015 RCT, Annals of Emergency Medicine: Propofol vs 1:1 & 1:4 ketofol
      • Similar adverse events between groups, no serious events
      • Recovery agitation greater in ketofol 1:1 group
      • No apparent benefit of ketofol mixtures over propofol alone



  • Mehta H, Chehade M. Safety of Propofol use in Patients with Food Allergies. Journal of Allergy and Clinical Immunology. 2014; 133(2):AB152
  • Bradley AED, Tober KES, Brown RE. Use of Propofol in Patients with Food Allergies. Anaesthesia. 2008; 63:433-445.
  • Tashkandi J. My Patient is Allergic to Eggs, Can I Use Propofol? A Case report and review. Saudi Journal of Anaesthesia. 2010; 4(3):207-208.
  • Jalota L et al. Prevention of Pain on Injection of Propofol: systematic review and meta-analysis. BMJ. 2011; 342:d1110
  • Green SM, Andolfatto G. Managing Propofol-Induced Hypoventilation. Annals of Emergency Medicine. 2015; 65(1):57-60
  • Adnolfatto G et al. Ketamine-Propofol Combination (Ketofol) versus propofol alone for Emergency Department Procedural Sedation and Analgesia: A Randomized Double-Blind Trial. Annals of Emergency Medicine. 2012;59(6):504-512.e2
  • Miner JR et al. Randominzed, Double-Blinded, Clinical Trial of Propofol, 1:1 Propofol/Ketamine, and 4:1 Propofol/Ketamine for Deep Procedural Sedation in the Emergency Department. Annals of Emergency Medicine. 2015;65(5):479-488.e2


Status Epilepticus

May Loke – Advanced Trainee

Definitions : Neurocritical care guidelines 2012

5 minutes or more of clinical/EEG seizure activity OR two or more intermittent seizure activity without full recovery in between

Significant increase in morbidity and mortality with seizures lasting >30minutes – Mortality rates at 1hr 30-40% for generalised status epilepticus

Management points

A and B management is priority – will avoid complications
Early seizure termination
Avoid complications
Find underlying cause (– check glucose, toxins)

Complications with seizures

Hypermetabolic state
Hypoxia, hypercarbia, hypoglycaemia, hyperthermia, rhabdomyolysis, DIC

Evidence behind the treatment

1st line Tx – benzodiazepines

The only evidence based treatment
Based on three large trials and Cochrane review
NCC guidelines – lorazepam iv ideal benzo of choice (long acting 4-6h with less resp depression that diazepam)

  • Alldredge et al N Eng J Med 2001 A comparison of lorazepam, diazepam and placebo for treatment of out of hospital SE
  • Leppik Jama 1983 Double blind study of lorazepam and diazepam and status epilepticus
  • Treiman N Eng J Med 1998 a comparison of four treatments for generalised SE
  • Prasad 2005 Cochrane review anticonvulsant therapy for SE

2nd line treatment

Phenytoin, Valproate, Keppra
Phenytoin – our traditional second line treatment but now becoming more controversial due to side effect profile and newer drugs
Should we be using valproate/keppra instead?
Newer evidence shows equal if not improved efficacy in seizure termination and less side effects

Article from Seizure 2014 metanalysis of 27 studies
“the relative effectiveness of five anti epileptic drugs used in the treatment of benzodiazepine resistant status epilepticus” concluded phenytoin should not be used as first line treatment

Studies for valproate and Keppra mainly class 2 and 3 evidence – based on small studies and chart reviews.

Recently Journal of clinical neuroscience 2015
Levetiracetam vs phenytoin in the management of SE
Randomised trial of 44 patients – showed no difference between keppra and phenytoin

3rd line evidence : phenobarbitone, thiopentone, propofol, midazolam

Barbiturates falling out of favour due to high side effect profile
No evidence to show benefit of one third line treatment over other

4th/5th/6th line treatment Ketamine possible antiepileptic benefit… no evidence

Trauma Scoring Systems

Dr Kaushik Basu – Advanced Trainee

Trauma is a important cause of morbidity and mortality in the developed countries during the first four decades of life and the burden is even higher in the developing countries.

There is a need for the proper assessment of the trauma patient to have the best possible outcome.

The scoring system serves several purposes’ like proper triage and assessment of the patients, for prediction of the outcome ,for quality assurance and fro research purposes.

The scoring system is based on physiological parameters, anatomical description of the wounds and a combination of the two. Examples being : RTS, IIS,TRISS.

The GCS was developed 40 years back to assess the conscious level in the head injury patients.

Though it is being widely used in the evaluation of trauma patient but it has several shortcomings.

For example it was not originally intended to be converted into a single score ,its components’ are more important that the combined score. The same GCS will predict different TBI mortality depending on the components. Again there is a problem with the inter-rater reliability even between the experienced physicians. It does not take into account the brain stem reflexes.

Due to the shortcomings of the GCS several new scoring system has been developed like Simplified Motor Score which uses the motor component of the GCS ,The Full Outline of Unresponsiveness or the Four score .But all these scoring system have the same problem like GCS in terms of their complexities.

Due to widespread adoption GCS is still used for the assessment of TBI though it should be usesd cautiously because of its limitations and ongoing education in needed to make sure that it is applied correctly.



Imaging in Trauma

Alexander Kochi – Advanced Trainee

Ultrasonography in the Trauma Room

Benefits of USS:

  • quick, accessible, portable, binary, non-invasive, repeatable, cheap
  • used for FAST, basic echo, detection of PTx, nerve blocks, fractures, foreign bodies, placement of devices such as lines / catheters

Evidence for USS:

  • ability of USS to identify need for laparotomy in unstable patients:

(133 patients / 3 studies1,2,3)

  • sensitivity 100%
  • specificity 96%
  • negative predictive value 100%
  • ability of USS to identify free fluid in abdominal cavity of all-comers (unstable plus stable) with blunt abdominal trauma:

(6,000+ patients / 18 studies4)

  • sensitivity 75%
  • specificity 98%
  • negative predictive value 94%
  • ability of USS to identify free fluid in abdominal cavity of stable patients with blunt abdominal trauma5:
    • sensitivity 40%
    • specificity 98%
    • negative predictive value 94%
  • ability of USS to detect pneumothorax in supine trauma patients compared to CXR6:
    • sensitivity 28-75% CXR vs 86-98% USS
    • specificity 100% CXR vs 97-100% USS

The Panscan:

Who gets a ‘panscan’?

  • decision based on:
    • clinical judgement, patient condition / compliance, mechanism of injury, physical examination findings (incl. cluster of injuries)
    • decision rules may help (NEXUS, Canadian head and C-spine, SCRAP – note there is no decision rule for the abdomen)
  • useful for identifying occult injuries (intracranial, retroperitoneal)
  • thought to change management and alter disposition
  • possibly used for clinician ‘peace of mind’

Risks of scanning:

  • radiation exposure:
    • a trauma series + panscan = ~ 30mSv of radiation7, ~1:300 chance (0.35% increased risk) of malignant cancer (tiny individual risk compared to 1:4 chance of dying of malignant cancer in all people regardless of exposure)
  • increased unnecessary interhospital transfers from places that don’t have access to CT / after hours CT
  • patient deterioration in the radiology department
  • risk of picking up and then treating ‘incidentaloma’ causing patient to become a victim of medical imaging and treatment (VOMIT)
  • contrast reactions and adverse effects
  • cost



  1. J Trauma. 1996 Nov;41(5):815-20: Hypotension after blunt abdominal trauma: the role of emergent abdominal sonography in surgical triage, Wherrett LJ, Boulanger BR, McLellan BA, Brenneman FD, Rizoli SB, Culhane J, Hamilton P
  2. Ann Surg. 1998 Oct; 228(4): 557–567: Surgeon-performed ultrasound for the assessment of truncal injuries: lessons learned from 1540 patients, G S Rozycki, R B Ballard, D V Feliciano, J A Schmidt, and S D Pennington
  3. J Trauma. 1994 Sep;37(3):439-41: Can ultrasound replace diagnostic peritoneal lavage in the assessment of blunt trauma?, McKenney M1, Lentz K, Nunez D, Sosa JL, Sleeman D, Axelrad A, Martin L, Kirton O, Oldham C
  4. Ng, Alexander., Trauma Ultrasonography: the FAST and Beyond, Dec 2001, available:
  5. 2010 Oct;148(4):695-700; discussion 700-1. doi: 10.1016/j.surg.2010.07.032. Epub 2010 Aug 30, FAST scan: is it worth doing in hemodynamically stable blunt trauma patients?, Natarajan B Gupta PK, Cemaj S, Sorensen M, Hatzoudis GI, Forse RA.
  6. Acad Emerg Med. 2010 Jan;17(1):11-7. doi: 10.1111/j.1553-2712.2009.00628.x,
Sensitivity of bedside ultrasound and supine anteroposterior chest radiographs for the identification of pneumothorax after blunt trauma, Wilkerson RG, Stone MB.
  7. X-Ray Risk Calculator, Available: