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IRUKANDJI SYNDROME

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Irukandji syndrome is a group of severe, systemic signs and symptoms that develop after an initially mild jellyfish sting. Onset is generally delayed for 5 to 50 minutes after a sting. Manifestations include severe pain (usually starting in the back and spreading to trunk and extremities), hypertension, nausea, vomiting, diaphoresis, headache, anxiety, restlessness, piloerection and pallor. In severe cases, pulmonary edema or hypotension develop. Death from intracerebral hemorrhage has been reported rarely.
    B) Irukandji syndrome is most commonly reported along the northern coast of Australia. Cases have been described from the southern coast of Australia, as well as Hawaii and Florida in the US. A probable case from Thailand has also been described.
    C) Irukandji syndrome has been reported following envenomation by the following jellyfish: Carukia barnesi; the cubozoan jellyfish Alatina nr mordens, Carybdea alata, Malo maxima, and Caybdea xaymacana and an as-yet unnamed 'fire jelly'.

Specific Substances

    1) Carukia barnesi
    2) Jellyfish
    3) Irukandji syndrome

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) DESCRIPTION: Irukandji syndrome is a group of severe, systemic signs and symptoms that develop after a jellyfish sting.
    B) TOXICOLOGY: Venom delivered via nematocysts results in excess catecholamine release. Research suggests that this massive catecholamine release (primarily epinephrine and norepinephrine) is due to changes in sodium channel modulation. As expected, increases in systemic vascular resistance, and increased inotropy and cardiac output are seen.
    C) EPIDEMIOLOGY: Irukandji syndrome is caused by a jellyfish sting and envenomation, most often by the Irukandji jellyfish (Carukia barnesi). Other cubozoan jellyfish have been associated with this syndrome much less often. Most exposures occur off the coast of northern Australia during the months of October through May, which is the summer wet season. Rare cases have been reported from southern Australia, Hawaii, Florida, Papua New Guinea, and Thailand. Envenomation is rarely fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Pain, warmth, and erythema at the site of envenomation are common. What initially appears to be a mild envenomation may progress to severe symptoms over the next hour.
    2) SEVERE TOXICITY: Severe effects typically begin 5 to 50 minutes post-envenomation and may resolve over several hours or persist for a day or two. The initial manifestation of more severe envenomation is pain, which may be severe, and typically starts in the lower back and may spread to the limbs, abdomen and chest. it may be accompanied by nausea, vomiting, diaphoresis, headache, and sometimes piloerection. Tachycardia, severe hypertension, hyperventilation, headache, restlessness, anxiety, a feeling of impending doom, and palpitations are reported. Hypotension is reported to commonly follow hypertensive crisis. In severe cases, pulmonary edema may develop due to dilated cardiomyopathy and left ventricular hypokineses. Elevations in serum troponin I are reported in these cases. Rhabdomyolysis develops in some patients. Dysrhythmias and priapism are rare complications. Intracranial hemorrhage is rare but has been reported and may be fatal.

Laboratory Monitoring

    A) Monitor vital signs closely with particular attention to the blood pressure.
    B) Obtain an ECG and institute continuous cardiac monitoring.
    C) For those with persistent pain, obtain serum electrolytes, creatine kinase, and cardiac enzymes.
    D) Patients with dyspnea or hypoxia should have a chest x-ray to evaluate for pulmonary edema.

Treatment Overview

    0.4.7) BITES/STINGS
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Patients typically do well and pain relief and local wound care are all that is required. Ice packs placed on the site of envenomation may aid in pain relief.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) The first step in care for a patient stung by an Irukandji jellyfish is removal of the patient from the water. If necessary, normal basic life support and advanced cardiac life support measures should be undertaken immediately. Apply vinegar soaked dressings to the affected skin for one minute to prevent the nematocysts, if still in the victim's skin, from discharging. Another focus of therapy is pain relief. Intravenous narcotics and benzodiazepines are usually needed to achieve pain relief for severe envenomations. Treat hypertension with short-acting, titratable antihypertensive agents (eg, nitroglycerin, phentolamine, magnesium, nicardipine). Administer oxygen and aggressively control hypertension if pulmonary edema develops. Bilevel positive airway pressure (BiPAP) or endotracheal intubation may be necessary. Treat hypotension with dobutamine, epinephrine, or dopamine. Tetanus prophylaxis is also indicated.
    C) DECONTAMINATION
    1) PREHOSPITAL: Removal or adherent tentacles is paramount. If possible, inactivate the nematocysts on adherent tentacles by applying a vinegar soaked dressing for one minute. After using vinegar, carefully remove the tentacles with forceps or gloved hand. If vinegar is not available, applying sand has been described as well, followed by very gentle scraping of the tentacles from the skin with a credit card edge or some other blunt-edged tool.
    2) HOSPITAL: Apply a vinegar soaked dressing to the area and leave in place for one minute. Vinegar inactivates the nematocysts of the principal jellyfish responsible for Irukandji syndrome, and prevents their discharge. Then gently remove the tentacles with a forceps or gloved hand.
    D) AIRWAY MANAGEMENT
    1) Perform early in patients when indicated with severe intoxication (seizures, dysrhythmias, severe delirium).
    E) ANTIDOTE
    1) There in no antivenom for Irukandji jellyfish envenomation.
    F) PAIN
    1) Intravenous narcotics are usually necessary especially in cases of severe envenomation. Large doses are often required. Benzodiazepines may also be useful.
    G) HYPERTENSION
    1) Treat severe hypertension as it may progress to acute left ventricular failure and pulmonary edema. Because hypertension may be followed by hypotension, a short acting, titratable agent is generally preferred. Nitroglycerin 5 mcg/min IV and titrate to effect, magnesium sulfate 2 to 4 mg IV then 1 to 2 g/hr IV, nicardipine start at 5 mg/hr and titrate to effect, max 15 mg/hr, phentolamine 5 mg IV repeated as needed.
    H) PULMONARY EDEMA
    1) In addition to control of hypertension (nitroglycerin in first-line), oxygen is an important component of therapy. High flow oxygen or BiPAP should be administered. Intubation with mechanical ventilation may be required. Right heart catheterization may serve as a useful adjunct to guide therapy.
    I) HYPOTENSION
    1) May develop secondary to acute myocarditis, cardiac dilatation and left ventricular failure. Treat with dobutamine (2 to 20 mcg/kg/min), epinephrine (ADULTS: Initially 1 mcg/min titrate to response, CHILDREN: 0.1 mcg/kg/min titrate to response) and/or dopamine (5 mcg/kg/min titrate to response).
    J) DELIRIUM
    1) Sedate patient with benzodiazepines as necessary; large doses may be required.
    K) ENHANCED ELIMINATION PROCEDURE
    1) There is no role for enhanced elimination.
    L) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients who do not develop systemic manifestations within one hour of envenomation, and in whom the tentacles have been removed can be managed at home as long as adequate pain control can be achieved, and the sting victim's vital signs are normal.
    2) OBSERVATION CRITERIA: Patients who develop any symptoms beyond local irritation should be referred to a healthcare facility for evaluation and management.
    3) ADMISSION CRITERIA: Patients with significant persistent pain despite adequate analgesia, hypertension, hypotension, or pulmonary edema require admission and close monitoring.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity.
    M) PITFALLS
    1) Hypotension can follow hypertensive crisis, thus the use of short-acting and titratable antihypertensive medications is preferred.
    N) PHARMACOKINETICS
    1) Onset of severe symptoms is generally within 1 hour of envenomation. The syndrome usually resolves over the first day.
    O) DIFFERENTIAL DIAGNOSIS
    1) Stings from other jellyfish such as box jellyfish, window spider envenomation, hypertensive crisis, acute myocardial infarction, pheochromocytoma, sympathomimetic toxicity.

Range Of Toxicity

    A) TOXICITY: A single sting from these jellyfish can cause Irukandji syndrome and severe signs and symptoms; however, not all stings from Carukia barnesi result in Irukandji syndrome.

Clinical Effects

Summary Of Exposure

    A) DESCRIPTION: Irukandji syndrome is a group of severe, systemic signs and symptoms that develop after a jellyfish sting.
    B) TOXICOLOGY: Venom delivered via nematocysts results in excess catecholamine release. Research suggests that this massive catecholamine release (primarily epinephrine and norepinephrine) is due to changes in sodium channel modulation. As expected, increases in systemic vascular resistance, and increased inotropy and cardiac output are seen.
    C) EPIDEMIOLOGY: Irukandji syndrome is caused by a jellyfish sting and envenomation, most often by the Irukandji jellyfish (Carukia barnesi). Other cubozoan jellyfish have been associated with this syndrome much less often. Most exposures occur off the coast of northern Australia during the months of October through May, which is the summer wet season. Rare cases have been reported from southern Australia, Hawaii, Florida, Papua New Guinea, and Thailand. Envenomation is rarely fatal.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Pain, warmth, and erythema at the site of envenomation are common. What initially appears to be a mild envenomation may progress to severe symptoms over the next hour.
    2) SEVERE TOXICITY: Severe effects typically begin 5 to 50 minutes post-envenomation and may resolve over several hours or persist for a day or two. The initial manifestation of more severe envenomation is pain, which may be severe, and typically starts in the lower back and may spread to the limbs, abdomen and chest. it may be accompanied by nausea, vomiting, diaphoresis, headache, and sometimes piloerection. Tachycardia, severe hypertension, hyperventilation, headache, restlessness, anxiety, a feeling of impending doom, and palpitations are reported. Hypotension is reported to commonly follow hypertensive crisis. In severe cases, pulmonary edema may develop due to dilated cardiomyopathy and left ventricular hypokineses. Elevations in serum troponin I are reported in these cases. Rhabdomyolysis develops in some patients. Dysrhythmias and priapism are rare complications. Intracranial hemorrhage is rare but has been reported and may be fatal.

Vital Signs

    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Hypertension is very common in patients with Irukandji syndrome (Huynh et al, 2003). Hypertension may be quite severe. Diastolic pressures above 130 mmHg have been reported in previously healthy individuals (Fenner et al, 1986).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) Tachycardia is another common manifestation of Irukandji syndrome. Tachycardia is generally not severe enough to cause hemodynamic compromise.
    2) INCIDENCE: In a retrospective series of 88 patients with Irukandji syndrome, about half developed tachycardia (Macrokanis et al, 2004).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypertension is very common in patients with Irukandji syndrome (Tiong, 2009; Huynh et al, 2003). Hypertension may be quite severe. Diastolic pressures above 130 mmHg have been reported in previously healthy individuals (Fenner et al, 1986).
    b) INCIDENCE: In two retrospective series of patients with Irukandji syndrome presenting to Emergency Departments (one consisting of 88 and the other of 62 patients), 49% and 50%, respectively, developed hypertension (Macrokanis et al, 2004; Little & Mulcahy, 1998). In another series of 87 patients with Irukandji syndrome, of the 51 patients who had blood pressure recorded, 39 (76%) had hypertension(Nickson et al, 2009).
    B) SINUS TACHYCARDIA
    1) WITH POISONING/EXPOSURE
    a) Tachycardia is another common manifestation of Irukandji syndrome (Tiong, 2009; Macrokanis et al, 2004). Tachycardia is generally not severe enough to cause hemodynamic compromise.
    b) INCIDENCE: In a retrospective series of 88 patients with Irukandji syndrome, about half developed tachycardia (Macrokanis et al, 2004). In another series of 87 patients with Irukandji syndrome, 20 patients (23%) had tachycardia (Nickson et al, 2009).
    C) MYOCARDITIS
    1) WITH POISONING/EXPOSURE
    a) Toxic myocarditis develops in some patients, generally patients with persistent, severe pain. Manifestations can include elevated cardiac enzymes (serum troponin or CK-MB), non-specific ECG changes, and echocardiographic evidence of impaired wall motion with or without pulmonary edema.
    b) In a series of 116 patients with Irukandji syndrome, Troponin I concentration was measured in 103 patients with persistent severe pain after a single dose of parenteral opioid (Huynh et al, 2003). Troponin I was elevated in 25 (22%) of them. Eleven of these patients had non-specific ECG changes (mostly T wave inversion and ST depression). Echocardiograms were performed in 18 of the patients with elevated troponin I, and 6 of these were abnormal (mild to moderate impairment of systolic function, segmental hypokinesis, global myocardial dysfunction in one patient).
    c) Elevated troponin concentration persisted for at least 2 weeks in one patient, although she had a normal echocardiogram and only non-specific T wave flattening on ECG (McD-Taylor et al, 2002).
    D) LEFT HEART FAILURE
    1) WITH POISONING/EXPOSURE
    a) Echocardiograms in patients who develop pulmonary edema with Irukandji syndrome reveal global hypokinesis and decreased cardiac output (Little et al, 2003; Fenner et al, 1988).
    b) Depressed systolic function has been detected on echocardiography in patients with Irukandji syndrome with persistent, severe pain and elevated troponin I concentrations but without evidence of pulmonary edema (Huynh et al, 2003).
    c) Myocardial function has been found to return to normal in those patients who have had repeat echocardiograms (Huynh et al, 2003; Fenner et al, 1988).
    E) PULMONARY EDEMA
    1) WITH POISONING/EXPOSURE
    a) Pulmonary edema can occur in very severe envenomations. It is generally delayed 6 to 18 hours after the sting (Tibballs et al, 2012).
    b) ONSET: Onset is usually delayed. In a review of 12 cases of pulmonary edema associated with Irukandji syndrome, the mean time of onset was 14 hours, with a range of 1.5 to 18 hours post envenomation. Pulmonary edema developed in 10 hours or less in 60% of patients (Little et al, 2003).
    c) INCIDENCE: Two retrospective series of patients presenting to Emergency Departments with Irukandji syndrome have been published, one with 88 and the other with 62 patients. Two patients in each of these series developed pulmonary edema (Macrokanis et al, 2004; Little & Mulcahy, 1998).
    d) CASE REPORT: A 26-year-old man presented with symptoms of Irukandji syndrome, including pain, restlessness, agitation, palpitations, tachycardia, and hypertension 2 hours after a jellyfish sting (Carukia barnesi). Serial ECG results at 4.5 hours and 19 hours after envenomization showed persistent generalized hyperacute T waves. Laboratory results revealed elevated troponin with a peak troponin I of 5.5 mcg 14 hours later. At this time, mild degree of transient pulmonary edema was noted on his chest x-ray. He was treated with IV furosemide and glyceryl trinitrate infusion. Serial transthoracic echocardiograms revealed mid-ballooning stress cardiomyopathy with poor mid-regional wall motion. He was diagnosed with mid-ventricular stress cardiomyopathy with apical sparing and following supportive care, including repeated doses of morphine and intravenous magnesium sulfate, he was discharged 3 days later (Tiong, 2009).
    F) TAKOTSUBO CARDIOMYOPATHY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 26-year-old man presented with symptoms of Irukandji syndrome, including pain, restlessness, agitation, palpitations, tachycardia, and hypertension 2 hours after a jellyfish sting (Carukia barnesi). Serial ECG results at 4.5 hours and 19 hours after envenomization showed persistent generalized hyperacute T waves. Laboratory results revealed elevated troponin with a peak troponin I of 5.5 mcg 14 hours later. At this time, mild degree of transient pulmonary edema was noted on his chest x-ray. He was treated with IV furosemide and glyceryl trinitrate infusion. Serial transthoracic echocardiograms revealed mid-ballooning stress cardiomyopathy (takotsubo cardiomyopathy) with poor mid-regional wall motion. He was diagnosed with mid-ventricular stress cardiomyopathy with apical sparing and following supportive care, including repeated doses of morphine and intravenous magnesium sulfate, he was discharged 3 days later (Tiong, 2009).
    G) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Dysrhythmias are unusual but have been reported.
    b) A previously well 33-year-old man developed paroxysmal atrial fibrillation in conjunction with Irukandji syndrome (Huynh et al, 2003). It resolved spontaneously over several hours, and his echocardiogram was normal.
    c) A previously healthy 24-year-old woman developed atrial fibrillation with a ventricular response of about 120 beats/min in conjunction with Irukandji syndrome. She developed pulmonary edema about 18 hours after the sting, and echocardiography revealed global hypokinesis. She recovered with supportive care; repeat echocardiogram was normal (Martin & Audley, 1990a).
    d) A previously healthy 47-year-old man developed hypertension (190/105 mmHg), severe pain, and diaphoresis associated with Irukandji syndrome. He had multifocal ventricular premature contractions and one episode of nonsustained ventricular tachycardia. Seven hours after envenomation he developed pulmonary edema. He was treated with intensive supportive care and recovered over 5 days (Fenner et al, 1988; Fenner et al, 1988).
    e) In another series of 87 patients with Irukandji syndrome, one patient developed nonsustained ventricular tachycardia (Nickson et al, 2009).
    H) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension is unusual, but has been reported in patients with severe myocarditis with left ventricular failure and pulmonary edema (Little et al, 2003; Martin & Audley, 1990a).
    I) CHEST PAIN
    1) WITH POISONING/EXPOSURE
    a) Chest pain is a fairly common complaint. Chest tightness was reported in 16 of 62 (26%) patients who presented to an ED with Irukandji syndrome in one retrospective study, and in 31% in another study (n=88) (Macrokanis et al, 2004; Little & Mulcahy, 1998). In another series of 87 patients with Irukandji syndrome, 37 (43%) reported chest pain (Nickson et al, 2009).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache has been reported in some patients with Irukandji syndrome, perhaps related to sudden increases in blood pressure (Grady & Burnett, 2003; Little et al, 2001).
    b) INCIDENCE: In a series of 87 patients with Irukandji syndrome, 11 (13%) reported headache (Nickson et al, 2009).
    B) ANXIETY
    1) WITH POISONING/EXPOSURE
    a) Patients are often extremely anxious, restless and agitated (Tiong, 2009; Macrokanis et al, 2004; Grady & Burnett, 2003). Tremors and shaking have also been reported (Fenner et al, 1986). They may complain of a feeling of impending doom (Fenner et al, 1986).
    b) In a retrospective series of 88 patients presenting to an Emergency Department with Irukandji syndrome, 84% were judged to be in severe distress (Macrokanis et al, 2004).
    C) CEREBRAL HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) Two fatalities have been reported in patients who developed intracerebral hemorrhage associated with Irukandji syndrome (Huynh et al, 2003; Fenner & Hadok, 2002). Both patients developed severe hypertension (peak blood pressure 230/90 in one and 260/160 in the other). One of the patients was on coumadin with a supratherapeutic INR (4.9 on admission, 5.0 a week prior) (Fenner & Hadok, 2002).
    b) CASE REPORT: A 44-year-old man was stung on the chest, and rapidly developed severe pain, hypertension (230/90 mmHg), headache and dyspnea. He evacuated by helicopter and on arrival in the Emergency Department was incoherent and agitated with left hemiparesis, neck stiffness and a persistent right gaze. CT of the head revealed a right frontal intracerebral hemorrhage with blood in all the ventricles; angiogram was normal. A craniotomy was performed for evacuation of the clot and ICP was monitored. He developed intractable intracranial hypertension and was pronounced brain dead 13 days after the sting (Pereira et al, 2010).
    D) DELIRIUM
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 7-year-old boy presented with Irukandji syndrome, manifested by muscle pain, anxiety, sweating, agitation and progressing to pulmonary edema. He became confused and disoriented, developed periodic auditory and visual hallucinations, and eventually became unresponsive to commands. Blurring of the optic discs was noted on physical exam and cerebral edema was suspected but not confirmed. He was treated with intravenous mannitol, mental status improved within a few hours, and he recovered completely (Fenner & Heazlewood, 1997).
    E) DECREASED LEVEL OF CONSCIOUSNESS
    1) WITH POISONING/EXPOSURE
    a) Transient periods of decreased level of consciousness have been described (Fenner & Lippmann, 2009).
    b) INCIDENCE: In a series of 87 patients with Irukandji syndrome, 5 (6%) were described as drowsy (Nickson et al, 2009).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting are common manifestations. In two retrospective series of patients presenting to Emergency Departments with Irukandji syndrome (62 patients in one study, 88 in the other), the incidence of nausea and vomiting was 39% and 33%, respectively (Macrokanis et al, 2004; Little & Mulcahy, 1998). In another series of 87 patients with Irukandji syndrome, 41 (47%) developed nausea and/or vomiting (Nickson et al, 2009).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal pain and cramping is another common manifestation; pain may be quite severe. In two retrospective series of patients presenting to Emergency Departments with Irukandji syndrome (62 patients in one study, 88 in the other), the incidence of abdominal pain and cramping was 40% and 57%, respectively (Macrokanis et al, 2004; Little & Mulcahy, 1998). In another series of 87 patients with Irukandji syndrome, 46 (53%) reported abdominal pain (Nickson et al, 2009).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) PRIAPISM
    1) WITH POISONING/EXPOSURE
    a) Priapism is a rare effect, but it has been reported in several patients with Irukandji syndrome, one of whom had been treated with phentolamine, which could theoretically have been the cause of priapism (Fenner & Carney, 1999; Nickson et al, 2010).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) Diaphoresis is a common finding in Irukandji syndrome. It was reported in 22% of a series of 88 patients in one retrospective study (Macrokanis et al, 2004). In another series of 87 patients with Irukandji syndrome, 28 (32%) developed diaphoresis (Nickson et al, 2009).
    b) Diaphoresis may be generalized, or may be localized to the area of the sting (Fenner et al, 1986).
    B) PILOERECTION
    1) WITH POISONING/EXPOSURE
    a) Piloerection has been reported in association with Irukandji syndrome, but it is not a common manifestation (Fenner et al, 1986; Corkeron, 2003).
    b) INCIDENCE: In series of 87 patients with Irukandji syndrome, 9 (10%) developed piloerection (Nickson et al, 2009).
    C) ERYTHEMA
    1) WITH POISONING/EXPOSURE
    a) Erythema and edema may be noted at the site of the sting, although the involved area may be small (Grady & Burnett, 2003a).
    b) Generalized flushing is common. In a retrospective series of 88 patients presenting to an ED with Irukandji syndrome, 28% developed flushing (Macrokanis et al, 2004).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) PAIN
    1) WITH POISONING/EXPOSURE
    a) Severe, unrelenting pain is a hallmark of Irukandji syndrome. It generally starts as severe back pain, and may then spread to involve severe abdominal pain and cramping, chest tightness, and pain in the large muscles of the legs and arms.
    b) INCIDENCE: In a retrospective series of 88 patients who presented to the Emergency Department with Irukandji syndrome, 57% had abdominal cramps, 58% had back pain, 49% had leg cramps and 31% had chest tightness (Macrokanis et al, 2004). In another series of 62 patients with Irukandji syndrome, 40% had abdominal cramps, 39% had back pain, 34% had limb cramps, and 26% had chest tightness (Little & Mulcahy, 1998).
    c) SEVERITY - In a retrospective series of 88 patients who presented to an Emergency Department with Irukandji syndrome, 45% rated their pain 10 on a scale of 1 to 10 (Macrokanis et al, 2004). In another series of 87 patients with Irukandji syndrome 46 patients (65%) out of the 71 in whom a pain scale was recorded rated their pain as 10 out of 10 (Nickson et al, 2009).
    d) ONSET: In a series of 87 patients with Irukandji syndrome, the median time between the sting and the onset of pain was 9 minutes, and among the 63 patients in whom the onset of pain was recorded, 50 (79%) developed pain within 30 minutes of the sting (Nickson et al, 2009).
    e) DURATION: Severe pain may last from several hours to several days. Many patients have mild pain for days to weeks after the envenomation (Grady & Burnett, 2003; Fenner et al, 1986).
    B) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Mild to moderate rhabdomyolysis has been reported in a few patients with Irukandji syndrome (Fenner et al, 1986; Grady & Burnett, 2003; Hadok, 1997; Little et al, 2001). None of these patients have developed acute renal failure.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs closely with particular attention to the blood pressure.
    B) Obtain an ECG and institute continuous cardiac monitoring.
    C) For those with persistent pain, obtain serum electrolytes, creatine kinase, and cardiac enzymes.
    D) Patients with dyspnea or hypoxia should have a chest x-ray to evaluate for pulmonary edema.

Radiographic Studies

    A) CT SCAN
    1) Perform a cranial CT scan in any patient with altered mental status. Intracerebral hemorrhage has been reported in two patients (Fenner & Hadok, 2002; Huynh et al, 2003), and cerebral edema was clinically suspected in another (Fenner & Heazlewood, 1997).

Methods

    A) Nematocyst Identification
    1) Nematocysts can be identified from skin scraping (Huynh et al, 2003a).
    2) The sting site can be scraped firmly with a sterile scalpel blade, place specimen in a sterile specimen container with 10% buffered formalin. Centrifuge the specimen at 5000 revolutions per minute for 10 minutes, stain with eosin and distribute onto a Kova slide for microscopic examination (Huynh et al, 2003a).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.6) DISPOSITION/BITE-STING EXPOSURE
    6.3.6.1) ADMISSION CRITERIA/BITE-STING
    A) SUMMARY: Patients with significant persistent pain despite adequate analgesia, hypertension, hypotension, or pulmonary edema require admission and close monitoring.
    B) Patients with persistent pain after 8 hours of treatment in the ED should be admitted to an observation unit or inpatient. Patients should not be discharged if they have required parenteral narcotics within the preceding 8 hours (Little & Mulcahy, 1998; Fenner & Carney, 1999).
    C) Patients with severe persistent pain should be admitted. Those with elevated cardiac markers (troponin or CK-MB) or ECG changes should be admitted to a telemetry unit or ICU. Those with evidence of pulmonary edema should be admitted to intensive care (Little & Mulcahy, 1998; Fenner & Carney, 1999).
    6.3.6.2) HOME CRITERIA/BITE-STING
    A) Patients who do not develop systemic manifestations within one hour of envenomation, and in whom the tentacles have been removed can be managed at home as long as adequate pain control can be achieved, and the sting victim's vital signs are normal.
    6.3.6.3) CONSULT CRITERIA/BITE-STING
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity.
    6.3.6.5) OBSERVATION CRITERIA/BITE-STING
    A) Patients who develop any symptoms beyond local irritation should be referred to a healthcare facility for evaluation and management.
    B) Patients should be observed in the ED for 2 hours, if no systemic symptoms develop during this time they may be discharged to return if symptoms develop (Little & Mulcahy, 1998; Fenner & Carney, 1999).

Monitoring

    A) Monitor vital signs closely with particular attention to the blood pressure.
    B) Obtain an ECG and institute continuous cardiac monitoring.
    C) For those with persistent pain, obtain serum electrolytes, creatine kinase, and cardiac enzymes.
    D) Patients with dyspnea or hypoxia should have a chest x-ray to evaluate for pulmonary edema.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) HOSPITAL: Apply a vinegar soaked dressing to the area and leave in place for one minute. Vinegar inactivates the nematocysts of the principal jellyfish responsible for Irukandji syndrome, and prevents their discharge. Then gently remove the tentacles with a forceps or gloved hand.

Range Of Toxicity

Summary

    A) TOXICITY: A single sting from these jellyfish can cause Irukandji syndrome and severe signs and symptoms; however, not all stings from Carukia barnesi result in Irukandji syndrome.

Maximum Tolerated Exposure

    A) A single sting can cause severe envenomation; however, not all stings by Carukia barnesi result in Irukandji syndrome. The clinical syndrome may be influenced by the thickness of the skin and presence of hair on the body part that is stung. The length of tentacle involved and duration of contact may also be important (Huynh et al, 2003).

Pharmacology Toxicology

Toxicologic Mechanism

    A) The hypertension and myocardial effects seen in Irukandji syndrome are suspected to be, at least in part, secondary to catecholamine release induced by the venom.
    B) ANIMAL TOXICOLOGY
    1) In piglets, crude extracts of the jellyfish Carukia barnesi induced a 200-fold increase in serum norepinephrine and a 100-fold increase in serum epinephrine, along with severe hypertension and mild pulmonary hypertension (Winkel et al, 2005; Tibballs et al, 2001).
    2) In rats, C barnesi venom induced hypertension that could be blocked by prazosin, an alpha-1 adrenoreceptor antagonist, suggesting that the hypertension is catecholamine mediated (Ramasamy et al, 2005).
    3) In rats, Alatina nr mordens venom increased plasma epinephrine and norepinephrine concentrations and induced a pressor response that could be mitigated by prior administration of prazosin, suggesting that the cardiovascular effects of envenomation are mediated in part by release of endogenous catecholamines (Winter et al, 2008).

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