Irukandji (Carukia barnesi )
Irukandji is now the generic name given to at least 5
(probably more) small species and 2+ species of larger carybdeids
(box jellyfish with one tentacle in each corner) that cause the
Irukandji syndrome. The only one PROVEN to cause the Irukandji syndrome
is Carukia barnesi a tiny transparent jellyfish with a maximum bell
diameter of just 12-20mm that has only been caught to date, on and
around the Cairns beaches in North Queensland.
Larger species that probably cause a severe Irukandji syndrome was
discovered recently on the outer Great Barrier Reef [Gershwin, Seymour
unpublished information 2000-2001]). They are larger with bell sizes
of up to 70mm.
All species of Irukandji, small or large, are box jellyfish (carybdeids)
with 4 tentacles, one in each corner that may be a few cms long
when contracted, but extend out up to 10 times this length when
extended. They are transparent and practically impossible to see
in the water. These jellyfish, all currently grouped together under
the name "Irukandji", all may cause the severe syndrome called the
Irukandji occur in tropical waters from possibly
Bundaberg, certainly from Agnes Water, central Queensland and follow
a similar distribution to Chironex, northwards through Queensland,
across the Northern Territory and then south to Exmouth, Western
Australia. They occur in the summer months.
History of investigation into Irukandji
Dr Ronald Southcott was stationed with the Australian
Army in 1944 in the Cairns area. He noticed and described 2 types
of stings (Southcott 1959): `Type A' stings were minor with a small
and insignificant skin mark. However they were followed some time
later (usually between 20 to 30 minutes) by a number of severe systemic
symptoms that often caused prostration, even in the fittest of troops.
`Type B' stings had extreme skin pain with obvious wheal marks visible
on the stung area. Although many victims became somewhat sick and
lethargic, there were no deaths in this group during the study.
In 1956 in north Queensland, as a result of brilliant
field work by Dr Hugo Flecker, Southcott was given a specimen of
a chirodropid. He was then able to identify the jellyfish causing
Type `B' stings, naming it, aptly, Chironex fleckeri (Southcott
1956); and in 1967, following similar brilliant field work by Dr
Jack Barnes, he identified the jellyfish causing the Type `A' stings,
naming it Carukia barnesi (Southcott 1967).
Dr Hugo Flecker was a Radiologist in Cairns, north
Queensland in 1932. On January 20th 1955, when a 5-year-old boy
died after being stung in shallow water at Cardwell, north Queensland,
Flecker suggested that the police net the area. Three types of jellyfish
were caught, one of which was an unidentified, box-shaped jellyfish
with groups of tentacles arising from each corner.
Flecker sent it to Dr Ronald Southcott in Adelaide,
and on December 29th 1955 Southcott published his article introducing
it as a new Genus and species of lethal box jellyfish. He named
it Chironex fleckeri, the name being derived from the Greek `cheiro'
meaning `hand', and the Latin `nex' meaning `murderer', and `fleckeri'
in honour of its discoverer.
Flecker was also interested in the Type `A' stinging
and published his article in the Medical Journal of Australia in
1952 naming it the `Irukandji syndrome' after the "Irukandji" tribe
of Aboriginals who lived in the Palm Cove area where the stings
were frequently reported (Flecker 1952b). Flecker died in 1957 without
finding the jellyfish responsible for the syndrome.*
Flecker's field and experiment notebook, containing
almost certainly valuable information ahead of its time, disappeared
with his death. Rediscovery of this notebook would be a major historical
and possibly research advance.
Dr. Jack Barnes was a Cairns General Practitioner
who then took over the quest for the "Irukandji". He surmised that
the organism had to be a very small jellyfish that swam very quickly,
and probably close to the surface. After calculating the most likely
time and place to catch the animal Barnes lay on the bottom of the
seabed in shallow water wearing his SCUBA gear.
Many hours later his persistence was rewarded when
he saw a very small jellyfish swim in front of his mask. He managed
to catch this, and another when he saw a fish moving in an erratic
fashion which was seen to be caught in the tentacles of another
of these tiny jellyfish. To see if they caused the "Irukandji syndrome"
Barnes stung himself, his son Nick, and a lifesaver friend. After
the characteristic 30-minute delay all three developed the "Irukandji
syndrome" and had to be admitted to hospital with severe back pain,
muscle cramps, nausea, vomiting and headache (Barnes 1964).
These jellyfish specimens were also sent to Dr Ron
Southcott and in 1966 he described them as a new genus and species
of box jellyfish called Carukia barnesi. The `car' from Carybdea,
the type of single-tentacled box-jellyfish in whose Family it belonged,
and the `ruk' from "Irukandji"; `barnesi' named after its discoverer
Barnes - as the Medical Adviser to the Surf Life
Saving Association introduced `pantihose' as an effective protective
barrier preventing a serious Chironex sting. It was thick enough
to prevent penetration and consequent envenomation by the thread
tubes of the stinging cells of Chironex. It became a common site
in north Queensland to see Surf lifesavers wearing pantihose on
patrol. One pair was worn as usual on the lower half of the body
with the feet cut out and taped around the ankles, the other pair
had a small hole cut in the crutch and they were pulled over the
head with the arms put in the leg part, and the hands free. They
were able to safely enter the water to drag long mesh nets through
the shallows to see if Chironex were present, allow safer bathing
for the general public. The idea was not to rid the area of dangerous
jellyfish, but to detect their presence so the beach could be closed
to prevent envenomation.
The sting of an Irukandji jellyfish is usually a minor sting that
usually is usually hardly felt, although rarely it may be more painful.
The mark on the skin is usually the small imprint of the jellyfish
bell, making it very difficult, if not almost impossible to see;
less often, tentacle marks may be seen. A couple of moments after
the usual sting from the bell, the skin may develop a mild redness
and a `goose-pimple' effect which may last from 30 minutes or so
- in some cases this initial sting may be totally missed. The reddish
imprint, if visible, may sometimes last several days.
After a delay of usually 30 minutes (5-40 minutes)
severe systemic symptoms of the basic 'Irukandji syndrome' start with: -
· A severe 'boring' pain in the sacral (low back) area. Other symptoms
quickly develop with muscle pains or 'cramps' moving rapidly into
all four limbs and the abdominal and chest wall muscles. These pains
are severe, unbearable and come on in 'waves' (similar to labour
pains), although never fading completely. In the past these have
been confused for both appendicitis and, more commonly, for a heart
attack. Chest pain or 'tightness' occurs from spasm of the intercostal
muscles (those between the ribs) as well as probable heart muscle
pain in some severe cases.
Other symptoms include:
· Sweating - which may be localised to the area
of the sting, or even localized to a site well away from the stung
area! However, more commonly the sweating is generalised, profuse
· Severe nausea and vomiting may occur
· Localised (in the area of the sting) or generalised piloerection
- "hairs standing on end" or "goose pimples" occurs
· Anxiety and 'wretchedness' - the victim feels "terrible" and
often has "a feeling of impending doom" - a feeling that is often
shared by the treating first aider!
· They are very restless with the victim unable to stay still,
moving from sitting to lying to rolling around
· Severe frontal or global headache may occur, which may be incapacitating
· "Palpitations" - very fast heart rate with extra heart beats
· Increased respiratory (breathing) rate, often of a 'sighing
nature' or quite fast with short breaths
· The victim usually has a marked tremor and looks very pale;
they may have peripheral cyanosis (blue tinged nail beds and digits)
·Their urine output may be due to reduced kidney blood flow and
fluid loss from the sweating and/or vomiting
·High blood pressure
"Severe Irukandji Syndrome"
As above but with
· Life-threatening high blood pressure - usually
the top figure is over 230 - with levels as high as 280/180
mm. Hg, even in young fit people - the "normal blood pressure
is usually about 120/80 and a doctor will start someone
on tablets to reduce their blood pressure at about 150/100.
The higher the pressure, the more likely it will blow a
hole in the blood vessel - usually in the brain - and this
causes a stroke. This was the cause of death in the two
Irukandji deaths in January and March 2002.Toxic (poisonous)
effects on the heart causing it to swell up (dilate - proven
by echocardiography) and function inefficiently allowing:
· Later complications of fluid on the lungs - acute
pulmonary oedema, often starting some 10-18 hours
post- envenomation (occasionally less).
Many of the signs and symptoms of the Irukandji syndrome
resemble those that occur when you have a fight - e.g. your "fight
or flight" mechanism caused by adrenaline. It is also similar to
the medical problem of an adrenal medullary tumour (phaeochromocytoma),
with excessive release of catecholamines into the bloodstream. The
symptoms are also very similar to the symptoms of the bite a Funnel-web
spider or a scorpion sting.
Recent work has shown that the venom is contains
a potent neuronal sodium channel agonist and that C. barnesi venom
powerfully stimulates noradrenaline (very similar to adrenaline)
release explaining, at least in part, the clinical features of the
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Vinegar is poured over the stung area and a vinegar-soaked
pad is placed on.
There is no actual other first aid treatment although
in the coming seasons a number of options will be tried to see if
they are effective and will include trials using either cold packs
(prevent or reduce venom being absorbed so more time to get to hospital)
or hot packs maybe denature (break-down) the venom.
Current research also includes a planned trial of
Nitrolingual spray to try reducing blood pressure to acceptable
It may also be possible to control the pain using
specialised ways of administering painkillers.
TREATMENT OF JELLYFISH STINGS WITH COLD PACKS
Cold packs or ice (wrapped in a cloth) are very effective,
applied to the area of a jellyfish sting to relieve local skin pain.
It is the first aid treatment of choice. They may be used if no
other treatment is available for Chironex Box Jellyfish stings,
but are less effective because of the severe pain, and deep tissue
remove any remaining adherent tentacles by washing with water.
that ice pack may be uncomfortable at first!
pack or ice in a wet cloth and apply directly over the sting
site for 10-20 minutes (apply only to stung area to avoid
hypothermia - especially small children).
pain and reapply cold pack or ice if necessary.
medical assessment if cold fails to relieve pain, or other
If a sting
covers a large area, particularly if the victim is cold or
wet, using a large number of cold packs, or packing the area
with ice may encourage hypothermia.
cases "ice massage" seems to help. A small block of ice is
held with a glove, or grasped with a cloth, and rubbed by
the first-aider all over the stung area for 10-20 minutes,
or until pain relief occurs. At the same time the rest of
the body can be kept warm with blankets or clothing.
simple treatment is not effective the patient is referred
to medical help.
Irukandji Envenomation - Protocol
(Fenner et al 1986b; Fenner et al 1988; Carney & Fenner
Table 1 - Primary hospital treatment
of Irukandji stings:
Accident and Emergency
the Irukandji syndrome: -
late onset symptoms after minor sting, back pain, sweating,
piloerection, hypertension, chest pain, limb cramps, headache,
vomiting, anxiety, restlessness
Fentanyl 0.5 µg every 5 mins,
morphine infusion with boluses 5 - 10mg (adult)
Catecholamine symptoms -
- phentolamine 5 - 10mg boluses (adult)
- IV GTN (50mg in 500ml 5% dextrose) commence at 3ml/hour
– administer oxygen to keep haemaglobin oxygen saturation
15 minutely (automatic machine – dynamap, if possible)
for nematocysts: -
- scrape a scalpel blade over stung area, place in saline
and centrifuge. Nematocysts are placed on a microscope slide
- put sticky tape onto skin of stung area. Inspect this under
cardiac enzymes - CK, CK:MB, cardiac troponin, serology for
jellyfish stings, catecholamines.
Time, Place, Winds, Temperature, Weather Conditions, Clothing?,
Stinger Suit?, T-shirt?, Sunsuit? Wet Suit?, Other people
in water?, Other people stung?, Tide, Time interval to onset
of symptoms, Jellyfish seen?, Tentacles/bell seen, Skin Marks,
Treatment?, Vinegar?, Fresh water exposure, ? other, site
of sting/pain/marks, name, age, sex, address, holidays, ?
stung before, activity when stung - ? swimming, surfing, ?
wading ? snorkelling, ? diving?, brief patient medical history.
high dependency ward
Table 2 - Possible ICU treatment
of Irukandji stings:
Dependency Medical Ward / ICU
- IV morphine infusion or fentanyl.
BP - Phentolamine 5-10mg bolus, IV GTN 3ml/hour.
- ECG, oxygen saturation.
failure - high flow oxygen, CPAP, increase GTN, frusamide,
CVP line, inotropes.
necessary for control of the oedema and of hypoxia.
8 - 12 hours, 16 - 24 hours, 48 hours
- CK - CK:MB, cardiac troponin.
at 24 hours.
within first 24 hours.
for jellyfish stings on day of discharge.
Table 3 - Follow-up treatment
of Irukandji stings:
if first one abnormal.
CK, CK:MB, cardiac troponin.
CXR if any
abnormality on previous CXR in hospital.
Table 4 - Medical treatment of
stings involving arterial compromise:
involving arterial compromise
of local limb blood supply by keeping the patient warm takes
priority over concern for possible increase in systemic absorption
of the venom.
pulses over the involved extremity should be monitored by
direct physical examination and/or Doppler measurements and
circulatory compromise treated aggressively with: -
Intra-arterial urokinase (50, 000 i.u.) infused
over a period of 30 minutes and repeated if necessary (heparin,
cervical sympathectomy and tolazoline gave little apparent
Rehydration, maintenance of good fluid balance,
analgesia and oxygen (preferably 100%) are essential.
If necessary, anticoagulation and intravenous
infusion of lignocaine, vasodilators (such as papaverine),
prostaglandinE or antiplatelet aggregation agents (ie. prostacyclin)
should be tried.
Monitor for possible development of a compartment
intervention and/or hyperbaric oxygen therapy reserved for
unresponsive cases, but needs to be early when indicated.
in Williamson et al 1996, p.115)
Similar presentations (differential diagnosis)
1. Myocardial infarction
Cases with the initial chest pain of the
Irukandji syndrome, especially if pulmonary oedema (fluid
on the lungs) develops, have in the past been misdiagnosed
as an acute myocardial infarction with developing heart
failure.3 This may be reinforced by a history of swimming
(exertion) especially if the history of a mild sting is
not elicited, or is forgotten by the victim.
The situation is further confused if blood is taken for
cardiac enzymes. In the past enzymes used were the Creatinine
phosphokinase (CPK) level that was often raised well above
the normal levels. However when it was differentiated into
cardiac and general muscle factions (CK-MB) the cardiac
enzyme faction may be normal, whereas the general muscle
faction is elevated, often to very high levels - caused
by the intense muscle cramps experienced by the hapless
victim. However, some severe cases, usually with obvious
pulmonary oedema, may have a CK-MB well above the normal
range (<8), with an abnormal, and significant, ratio
These days' cardiac troponins are used as these are more
accurate and immediately give a clear indication of heart
involvement and damage if they are found to be high.
2. Decompression sickness (the "bends")
The Irukandji syndrome in a diver also resembles
decompression sickness, and may present a difficult differential
diagnostic problem. There have now been a number of cases
around the Great Barrier Reef who have phoned the DES (Diving
Emergency Services) number when, a short time after surfacing,
a diver suddenly develops severe low back pain, chest pain
(`trouble' breathing) and is distressed and restless.
A high index of suspicion and careful questioning is needed.
A history of a minor sting on the back of the neck when
surfacing, a small mark, often difficult to see, and/or
careful differentiation of the symptoms is necessary. All
this is conducted over a radiotelephone from a dive boat
on the reef to the DES phone Base in Adelaide - no easy
Case histories of 3 severe cases
Three cases of Irukandji envenomation occurred
in the Whitsunday's in north Queensland that developed severe
myocardial toxicity and pulmonary oedema. Two occurred in
March 1994, and the third in March 1996.
Case History 1
A 25-year-old previously healthy female had
the typical onset of severe limb and abdominal pain followed
by nausea, vomiting and anxiety thirty minutes after being
stung by an unidentified jellyfish while swimming. Her BP
was 160/100mm Hg, within one hour of envenomation. Seven hours
after envenomation she was suffering severe muscle pains,
was tachycardic -112 beats per minute (bpm), normotensive
- BP 130/85, had piloerection over both arms but no erythema,
and had a clear chest with SaO2 of 92% on air. She was commenced
on a morphine infusion at 2mg/hour IV. Shortly after her Sa02
dropped to 88% on air and she had bilateral crepitations in
her lungs with a raised jugular venous pulse. Frusemide 40mg
was administered intravenously (IV), and oxygen via a mask
commenced. However she rapidly became sweaty, agitated and
had peripheral shut down.
An infusion of intravenous glyceryl trinitrate
(GTN) was commenced and titrated to keep the systolic blood
pressure in the range of 100-120mm Hg throughout the night.
The next morning a chest X-ray showed interstitial oedema
with a normal heart size. Her central venous pressure (CVP)
was 11cm H2O and CPAP of 5cm H2O via a facemask with Fi02
of 0.7 was given. The CK:MB was elevated (Table 6).
At 0530 on day two after admission the blood
pressure again fell to 82/52 mm Hg and fluid loading was attempted
while the GTN infusion was weaned and CPAP ceased. Urine output
fell to 24 ml/hour at 0700 that morning, and an infusion of
Dopamine was commenced and gradually increased to 3 mcg/kg/min.
The ECG showed a minor degree of ST depression in the inferior
leads; the chest was clinically clear, but a third heart sound
On the third morning after admission an echocardiogram
was performed, which showed severe, global left ventricular
hypokinesis (Table 5). An ECG showed a diminished R wave in
V3. Enalapril was commenced at a dose of 2.5 mg daily, which
was increased to 2.5mg bd the following day. She clinically
improved and was discharged on day six; a Swiss tourist, she
has unfortunately been lost to follow-up.
Case History 2
A 25-year-old previously well female was envenomated
at the same time as case 1 with findings: Initial BP 160/110mm
Hg, HR 120bpm, restless, sweaty and having several small patches
of erythema over the lower sternum and right arm; her chest
was clear. On admission to hospital, a morphine infusion of
1 - 2 mg/hour IV was commenced was commenced which eased her
muscle pains, but she was still sweating profusely, tachycardic
and had a severe tremor. At 1120 pm on the night of admission
eighty milligrams of propranolol was given orally in an attempt
to alleviate the tremor, anxiety and tachycardia.
At 0200 the patient was cold and clammy with
obvious peripheral shutdown and HR of 80pm. Her femoral and
carotid pulses were only just palpable, and she had a blood
pressure of 60/25mm Hg; despite the severe hypotension, the
patient was alert and communicative. A bolus of 500ml of haemaccel
was given with moderate effect (BP 63/47mm Hg). A femoral
artery catheter was inserted which revealed a dampened waveform
and a mean blood pressure of 60-mm Hg. The morphine infusion
was ceased temporarily at that point. An electrocardiograph
was grossly abnormal with a sinus rhythm of 78 bpm, a first-degree
heart block, broad complex QRS morphology, tall T waves and
poor R wave progression. At 0300 that the patients serum potassium
was to 8.5 (NR <5.5 mmol/litre), and CK 331 IU. The hyperkalaemia
was treated with 50 ml of 50% dextrose IV and short acting
insulin subcutaneously; the CVP was 20 cm H2O, and chest X-ray
was normal. An isoprenaline infusion was commenced at 0350;
electrolytes at this point showed K+ of 8.0 mmol/litre, HCO3
19 (NR 23-32 mmol/l) and Creatinine of was mildly elevated
at 0.122 (NR 0.04 -0.12 mmol/l). Five ml of 10% Calcium chloride
was given intravenously and a repeat ECG showed normal sinus
rhythm. The K+ was subsequently 6.5 with a pH of 7.28 and
a further 5 ml of 10% Calcium chloride was given. The isoprenaline
infusion was titrated against the blood pressure until 0630
when the BP was 112/79 with an infusion rate of 12 mcg/hour.
Hypoglycaemia of 1.8 (NR 3.5-8.0 mmol/l) was
noted and 10 ml of 50% dextrose was infused. At 0900 there
were crepitations noted at the right lung base, and the SaO2
was 93 % while having FiO2 of 0.28
At 1300 the SaO2 was 92% on 12 litre/minute
of oxygen via a facial mask, BP 121/62, CVP 13 cm H2O, HR
92 bpm ; the isoprenaline infusion was weaned and ceased at
1430. At 1530 5 cm H2O of CPAP was commenced via a face mask
with an FiO2 of 0.6 yielding SaO2 of 92% ; an IV infusion
of GTN was commenced. At 1700 the patient complained of severe
pain in the lower limbs and profuse sweating and an intravenous
infusion of morphine was again commenced.
The CPAP was increased to 10 cm H2O with an
FiO2 of 0.6 giving an SaO2 of 95 %. At 2300 the FiO2 was increased
to 0.7. Despite a fever of 38.1oC blood cultures and a urine
specimen revealed no growth. The FiO2 and CPAP were gradually
weaned and on the third morning after admission only oxygen
via a face mask was needed at 35 % giving an SaO2 of 98 %.
The K+ was 4.0, and CK 285, and CK:MB 11 (ratio 4.7%). Echocardiography
was performed which showed a mild impairment on left ventricular
systolic function (Table 5) and enalapril 2.5mg per day was
commenced, and later increased to 5-mg bd. The patient clinically
improved and was discharged on day five and was lost to follow-up.
Case History 3
A 19-year-old previously-well woman was stung on
the left arm by a jellyfish while swimming in the Whitsunday's
at 1130 is on the 26/03/96. She developed severe back pain
and breathlessness 15 minutes later. She required 100 mg of
pethidine IVand 50 mg IM during transport for muscle pains.
The SaO2 during transfer was 96 % on oxygen.
On arrival in Proserpine Hospital she was treated
with a total of 15 mg of intravenous phentolamine for mild
hypertension (140/110), 5 mg of intravenous midazolam and
10 mg of intravenous diazepam for agitation; a pethidine infusion
was commenced at 30 mg/hour for severe pain.
At 0300 the following night she woke with cough
and a wheeze and became tachycardic with a heart rate of 130.
The SaO2 fell to 75 % on room air, and 85 % on 2 litres/minute
via the nasal prongs. Bilateral crepitations were noted, and
a chest xray showed bilateral hazy infiltrates suggestive
of pulmonary oedema. Nebulised salbutamol was given with no
significant effect, and then two 40 mg IV boluses of frusemide
were given. She started coughing pink frothy sputum at 0445.
The oxygen saturation was 85 % on 15 litres/minute of oxygen
via a non-rebreathing mask. The blood pressure did not rise
above 140/90 during the night.
Intravenous glyceryl trinitrate was commenced
at 0900 and she was transferred to the Mackay Base Hospital
at 1130. She was commenced on CPAP by mask at 7.5 cm H20 and
the SaO2s improved to 90 %. The CK was elevated at 330 (Table
6); subsequently the LDH rose to 255 two days after envenomation.
The FBC showed a neutrophil leukocytosis (PMN 21.7, WCC 24.1).
The UEC was normal, and LFT normal except AST 63. The ECG
showed sinus rhythm, right axis deviation, non-specific lateral
t-wave changes, and poor R-wave progression anteriorly.
In the ICU at 1230 the BP was 100/61, pulse
130 and SaO2 was 90 %. The intravenous GTN was weaned to 5
mcg/min. Pressure support ventilation of 10 cm H2O and CPAP
7.5 cm was commenced by mask and the SaO2 improved to 94 %.
She was alert, orientated but still had bilateral crepitations,
with an S3 gallop rhythm.
The first echocardiogram at 1630 showed severe
global left ventricular dysfunction (Table 5) with trivial
mitral regurgitation. A left radial intra-arterial line and
a left subclavian central venous line were inserted. The initial
CVP reading was 11 mm Hg.
The next morning (28/3) Lisinopril 2.5 mg mane
was commenced and frusemide 40 mg bd orally continued. The
blood pressure was 97/75 with pulse 130, SaO2 was 95 % on
FiO2 0.7 and PS 10/CPAP 7.5. The ventilation was ceased and
oxygen given via a non-rebreathing mask at 1200.
The following day (29/3) the BP fell to 82/54
and bilateral crepitations were still audible throughout both
lung fields. Dopamine was commenced at 4 mcg/kg/min with no
significant change in the blood pressure then Dobutamine was
substituted and increased to 12 mcg/kg/min and the BP improved
to 95/50. The urine output fell off during the day, and with
a CVP recording of 2-mm Hg a total of 500 ml of Haemaccell
was given in boluses and Dopamine recommenced at 5 mcg/kg/min,
with a substantial improvement in urine output and blood pressure
to 112/60. Hypokalaemia of 3.4 was treated oral potassium
The following day (30/3) the SaO2s were 94
% on room air, and the BP 109/50 and pulse 117 with a good
urine output. The Dobutamine was weaned and the Lisinopril
increased to 5 mg mane. An ECG showed sinus rhythm with a
right axis deviation and t wave inversion in leads V1 - V4
with a diminished R wave in V2.
The next day (31/3) the Dopamine was ceased.
A repeat echocardiogram showed an improvement in left ventricular
function (Table 5). She was discharged on the 2/4/96 on Lisinopril
5-mg mane. An echocardiogram on the 3/2/96 showed normal LV
function (Table 5).
Table 5 - Echocardiogram results
Table 6 - Clinical and Laboratory Parameters
Irukandji and vinegar
|Vinegar poured freely over the stung area
|Vinegar-soaked pad on top of sting
In 1988 after Dr Fenner caught two specimens
of Carukia barnesi (the Irukandji), vinegar, methylated spirits
and 20% w/v aluminium sulphate were applied to isolated tentacle
segments. The nematocysts of this carybdeid were completely
inhibited by the vinegar and 20% aluminium sulphate ("stingose"),
whereas methylated spirits resulted in mass discharge (Fenner
& Williamson 1987), similar to that reported in Chironex
(Hartwick et al 1980).
Due to the severity of the syndrome and Barnes
experience with self-stinging when his son, a friend and Barnes
himself ended up in hospital (Barnes 1964), no attempts were
made at the above stinging experiments to see if inhibition
or "failure to discharge" had occurred after the use of the
above chemicals. However, these experiments seem to continue
those proving to date, that vinegar is effective when used
for nematocysts inhibition on any cubozoan sting.
After envenomation with Carukia there has never
been a recorded case of tentacles remaining on the skin. However,
it has been shown that there are still remaining, unfired
(Fenner PJ, Williamson JA, Burnett JW, Colquhoun DM,
Godfrey S,Gunawardane K, Murtagh W. The "Irukandji syndrome"
and acute pulmonary oedema (Med J Aust 1988;149:150-156)
The stung area is scraped with a scalpel blade
in the manner first suggested by Barnes (1960). This technique
has since been modified by Currie & Wood (1995) who also
found that sticky tape was just as effective as it lifted
the remaining nematocysts off the skin. These could then be
observed under a microscope and as each nematocyst is different
and a "blueprint" of its species. This test can be used to
help identify the actual jellyfish responsible, as this is
not always certain; many stings occur from unseen, or unknown,
Because the systemic symptoms and effects are
so devastating for such a small total envenomation, the author
suggested to the lifesavers and lifeguards who treat these
stings, that further envenomation must be prevented.
Thus, treatment is vinegar poured on the stung
area for a minimum of 30 secs, similar to that suggested for
Chironex stings. Because of the time delay from the time of
envenomation to the time of onset of symptoms is usually some
30 minutes (from 5-40mins), there is a "window of opportunity"
for possible treatment. Experienced lifesavers and lifeguards
will be able to identify the small mark of envenomation with
its pinkish appearance, local sweating and piloerection. If
the first sting should be missed, they frequently come in
multiple stings and subsequent stings should be recognised
much earlier. Consequently a further suggested treatment was
that a vinegar-soaked pad be placed over the sting.