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Acute renal failure after a sea anemone sting
CASE REPORT
Acute Renal Failure After a Sea Anemone Sting Masashi Mizuno, MD, Kazuhiro Nishikawa, MD, Yukio Yuzawa, MD, Tami Kanie, MD, Hijiri Mori, MD, Yasutetsu Araki, Nigishi Hotta, MD, and Seiichi Matsuo, MD ● A 27-year-old man suffering from severe swelling and pain in his right arm was referred to our hospital. He showed signs of acute renal failure (ARF) with severe dermatitis of his right arm. Three days before being admitted, he accidentally touched some kind of marine organism with his right hand while snorkeling in the Sulu Sea around Cebu Island. Within a few minutes, he was experiencing severe pain in his right hand. Then his right hand gradually became swollen. The marine creature responsible for this injury was thought to have been a sea anemone, which is a type of coelenterate. Histologic findings of a renal biopsy indicated that acute tubular necrosis (ATN) had caused ARF in this patient’s case. Supportive therapies improved renal function of this patient, and steroid pulse therapy attenuated the severe skin discoloration. The ATN was thought to have been caused by the poison from a sea anemone because there were no other conceivable reasons for the patient’s condition. This is the first time that a marine envenomation case has been reported in which the sting of a sea anemone has caused ATN without the failure of any other organs. © 2000 by the National Kidney Foundation, Inc. INDEX WORDS: Acute renal failure (ARF); acute tubular necrosis (ATN); marine envenomation; sea anemone.
A
FEW MARINE creatures have evolved various ways of capturing their prey that, if targeted at humans, can result in discomfort, extreme pain, or even death. The stings of most coelenterates induce only mild dermatitis. Some species of coelenterates, especially those of jellyfish, induce severe dermatitis. Their poison sometimes can cause allergic shock but seldom leads victims to multiple organ failure. The sea anemone is also a kind of coelenterate. We have reported the first known case of acute renal failure (ARF) solely attributable to a sea anemone and without the presence of any other organ failures. CASE REPORT A 27-year-old Japanese man with severe swelling and pain in his right arm was admitted to our hospital in December of 1998. He was experiencing general fatigue. Two days before coming to our hospital, he had accidentally touched a marine organism with his right hand while snorkeling off Cebu Island in the Philippines. A few seconds after contact with the organism, he felt severe pain in the fingers of his right hand. The man then discovered clear, dark-brown tentacles stuck to his fingers. He rubbed them off, and later his right hand was rinsed with a solution of 70% ethyl alcohol to disinfect the wound. A few hours later, his right hand had become swollen, and he felt nauseous. Up until the time of his admission, the swelling continued to spread over his right arm, accompanied by increasing pain. During his childhood, the patient had suffered from a few epileptic seizures.
Physical Examination The patient weighed 68 kg and was 168.5 cm tall. His body temperature was 37.1°C, his blood pressure was 110/60
mm Hg, and his pulse was a regular 72 beats/min. Severe skin swelling was observed on his right hand, which had spread up his entire right arm (Fig 1A). Figure 1B shows some small ulcerations and some vesicles on the patient’s index finger and in between his index and middle fingers. The skin of his right arm had turned purple. Characteristic sting marks were observed, suggesting the injury had resulted from a sea anemone’s sting. He had no edema in his lower extremities nor in his left hand. Physical examination of other organs showed that the patient’s lungs, heart, and abdomen were normal. A neurologic examination also showed no abnormalities.
Laboratory Results On admission, the patient’s clinical laboratory data were as follows: his white blood cell count was 10,600 cells/mm3 (polymorphoneutrophils, 63.0%; lymphocytes, 28.0%; eosinophils, 3.0%; monocytes, 5.0%; basophils, 1.0%). His red blood cell count was 483 ⫻ 104/mm3, and his platelet count was 21.9 ⫻ 104/mm3. No fragmented red blood cells were noted. His blood urea nitrogen (BUN) was 54 mg/dL; creatinine, 4.6 mg/dL; uric acid, 10.8 mg/mL; Na, 137
From the The Third Department of Internal Medicine, Nagoya University School of Medicine, Nagoya, Japan; The Department of Dermatology, Nagoya University School of Medicine, Nagoya, Japan; and Okinawa Chuo Health Center, Naha, Okinawa, Japan. Received December 15, 1999; accepted in revised form April 14, 2000. Address reprint requests to Masashi Mizuno, MD, The Third Department of Internal Medicine, Nagoya University School of Medicine, Nagoya 466-8550, Japan. E-mail: [email protected] © 2000 by the National Kidney Foundation, Inc. 1523-6838/00/3602-0029$3.00/0 doi:10.1053/ajkd.2000.9006
American Journal of Kidney Diseases, Vol 36, No 2 (August), 2000: E10
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MIZUNO ET AL
Fig 1. The patient’s right hand on the day of his admission. Swelling of his right hand is severe. The wound is found on the patient’s index finger and between his index and middle fingers. The skin is purple and has vesicles. (A) Right hand. (B) Close-up of the area between the index and middle fingers of the right hand.
mEq/L; K, 4.5 mEq/L; Cl, 101 mEq/L; total protein, 6.8 g/mL; albumin, 4.4 g/dL; glutamic oxaloacetic transaminase, 16 U/L; glutamic pyruvic transaminase, 17 U/L; lactate dehydrogenase, 284 U/L; alkaline phosphatase, 150 U/L; ␥ glutamyl transpeptidase (␥GTP), 45 U/L; creatine kinase, 648 U/L; and C-reactive protein, 2.7 mg/mL. Serum levels of immunogloblin (Ig) A, IgM, IgE, C3, and C4 complement fractions, and CH50, were within the normal range. Neither anurine nor hypourine was found in the patient. Results of urinalysis were as follows: protein was at 30 mg/dL; sugar, 30 mg/dL; and occult blood, (⫹/⫺). Urine sediment showed no abnormal findings. Serum myoglobin was at 57.5 ng/mL, and urinary myogloblin levels were under detection (⬍10.0 ng/mL). Serum myoglobin was at its highest (94.6 ng/mL) on day 2, and it subsided to normal range on day 4. Findings of the patient’s chest radiograph and electrocardiograph were normal.
Clinical Course After his admission, supportive therapies including appropriate intravenous drip gradually improved the patient’s condition of ARF (Fig 2). A renal biopsy was performed on day 2 (Fig 3). The renal biopsy specimen included eight glomeruli. Not one glomerulus was collapsed. No apparent structural changes were observed in the glomeruli, except for mild ischemic changes in a few of them (Fig 3A). Tubular dilation or degeneration and detachment of tubular epithelial cells were prominent in the outer media (Fig 3B). No deposition of IgG, IgA, IgM, C3, C1q, C4, nor fibrinogen was found in the glomeruli as a result of direct immunofluorescent staining. The pathologic diagnosis was acute tubular necrosis (ATN). Both the BUN levels and serum creatinine levels had returned to normal (⬍1.1 mg/dL) by day 4. On day 2, steroid pulse therapy was administered (1 g/d methylprednisolone for 2 days) along with antibiotics (cefotiam HCl), because the right arm’s dermatitis was markedly severe and becoming worse. After treatment with methylprednisolone, swelling in the patient’s right arm decreased, and his skin coloration improved. The area that had been stung developed ulcerations. After pulse therapy, the only treatment was an ointment containing steroid. However, on day
11, the patient’s body temperature increased mildly. His CRP was elevated to 3.3 mg/dL, and his right arm’s swelling flared up once again. Therefore, the patient was given 3 mg/d betamethasone by mouth. Because his body temperature and CRP decreased on day 13, administration of betamethasone was decreased to 2 mg/d. On day 20, there was no swelling nor pain in the patient’s right hand, and his CRP was 0.0 mg/dL. The ulcerations on his fingers had developed into scars. On day 21, he was discharged from our hospital.
DISCUSSION
Our patient suffered severe dermatitis as a result of having been stung by a coelenterate in the Sulu Sea around Cebu Island. He consequently developed ARF. Our case showed ARF but no other major organ failures. In this case, histologic findings of the renal biopsy showed ATN. The causes of ATN usually include circulatory shock, myoglobinuria, drugs, poisons, and so on. Multiple bee stings, scorpion stings, and snakebites have been reported to induce ATN.1 In our case, neither shock, rabdomyolysis, nor drugs were the cause of our patient’s ATN, as seen from the course of his illness, results of his physical examination, and his laboratory data on admission. Poison from the sting of a coelenterate is believed to be responsible for causing ATN in this case. There are thousands of species of organisms in the seas and oceans of the world. It is known that just a few kinds of marine creatures have poison that enables them to protect themselves from their enemies or to hunt. Some kinds of coelenterates, such as sea urchins, jellyfish, and starfish, are poisonous to humans. The stings of most of these organisms induce only mild dermatitis,
MARINE ENVENOMATION AND ACUTE RENAL FAILURE
3
Fig 2. Clinical time course. CTM, cefotiam hydrochloride; MINO, minocycline hydrochloride.
which usually can be treated by either local steroid therapy or oral steroid administration combined with local steroid therapy.2,3 In this case, the patient’s dermatitis was very severe. Oral steroid administration after steroid pulse therapy was chosen to help the patient recover from his severe dermatitis. Of all coelenterate-
related injuries, those resulting from jellyfish are most frequently reported. For example, the notoriously deadly box-jellyfish, Chironex fleckeri, has been responsible for more than 80 documented deaths in northern Australian waters.4,5 Sea anemones are another kind of coelenterates, and most of them are harmless to humans or just
Fig 3. Light micrograph. (A) An ischemic change was found in glomeruli. No mesangial hypercellularity, nor matrix widening, nor depositions were found. (PAS stain; original magnification ⴛ400.) (B) In the tubules, cellular degeneration and necrosis can be found. Part of the tubular epithelial cells are detached. (Masson-Trichrome stain; original magnification ⴛ200.)
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MIZUNO ET AL
This report may be the first to discuss a marine envenomation case in which the sting of a sea anemone caused ATN without causing any other organ failures. We should realize that injuries from sea anemones can result in ATN. Steroid pulse therapy and oral steroid administration may be useful to alleviate severe dermatitis in the case of conspicuous skin discoloration caused by sea anemones. ACKNOWLEDGMENT Fig 4. Photograh of Phyllodiscus semoni. This is a photograph of the same type of sea anemone thought to have stung and caused ATN in our patient. P semoni is brown and known for its natural camouflage, mimicking a rock in an atoll. This photograph was taken in Okinawa, Japan.
induce mild dermatitis. Two kinds of sea anemones are known to induce severe dermatitis.2,3,6 However, systemic reactions to poison from sea anemones have seldom been reported. Only once has the sting of a sea anemone been reported to induce fulminant hepatitis in a patient.7 Severe injuries caused by marine envenomations may very easily lead to the victim’s death by drowning. This may explain why there are a small number of marine envenomation cases that lead to severe organ failures. In Okinawa (Japan), a kind of sea anemone called Phyllodiscus semoni (Fig 4) has a very potent poison.8,9 Severe dermatitis with swelling, local fever, and ulcerations are known symptoms of patients who have been stung by P semoni. In this case, the causative creature was thought to have been a harmful P semoni, because the wound on the patient’s right hand was characteristic of a sea anemone’s sting. As well, the patient described the marine organism he touched as looking like a brown rock and feeling like a sponge. This also resembles P semoni.2,3,6,8
The authors thank Dr S. Tomihara for his useful comments, M.S. Korcek for the English editing of this manuscript, and also the Okinawa Perfectural Institute of Health and Environment for the photograph of P. semoni.
REFERENCES 1. Solez K: Acute renal failure (Acute tublar necrosis, infarction, and cortical necrosis), in Heptinstall RH: Pathology of the Kidney (ed 4), chap 18. Boston, MA, Little, Brown and Company, 1992, pp 1238-1239 2. Hansen PA, Halstead BW: The venomous sea anemone actinodendron plumosum haddon of South Vietnam. Micronessica 7:124-136, 1971 3. Auerbach JF: Marine envenomations. N Engl J Med 325:486-493, 1991 4. Williamson J: Classification (with description and medical implications of seven venomous jellyfish), in some Australian marine stings, in Williamson J (ed): Envenomations and Poisonings. Brisbane, Surf Life Saving Foundation, 1981, pp 1-26 5. Fenner P: Medical frontiers in Australian seas, in Pearn J, Cobcroft M (eds): Fevers and Frontiers, chap 3. Brisbane, Australia Amphion, 1990, pp 73-84 6. McGoldrick J, Marix JA: Marine envenomations. Part 2: Invertebrates. J Emerg Med 10:71-77, 1992 7. Garcia PJ, Schein RM, Burnett JW: Fulminant hepatic failure from a sea anemone sting. Ann Intern Med 120:665666, 1994 8. Kwietniewski CR: Actiniaria von ambon und Thursday Island. Jena, Denkshriften der Medizich-und Naturwissenshaftliche Gesellschaft, 1897, pp 385-430 9. Nakamoto M, Uezato H: Stings of box-jellyfish and sea anemones. Clin Dermatol 52:29-33, 1998
Acute Renal Failure After a Sea Anemone Sting Masashi Mizuno, MD, Kazuhiro Nishikawa, MD, Yukio Yuzawa, MD, Tami Kanie, MD, Hijiri Mori, MD, Yasutetsu Araki, Nigishi Hotta, MD, and Seiichi Matsuo, MD ● A 27-year-old man suffering from severe swelling and pain in his right arm was referred to our hospital. He showed signs of acute renal failure (ARF) with severe dermatitis of his right arm. Three days before being admitted, he accidentally touched some kind of marine organism with his right hand while snorkeling in the Sulu Sea around Cebu Island. Within a few minutes, he was experiencing severe pain in his right hand. Then his right hand gradually became swollen. The marine creature responsible for this injury was thought to have been a sea anemone, which is a type of coelenterate. Histologic findings of a renal biopsy indicated that acute tubular necrosis (ATN) had caused ARF in this patient’s case. Supportive therapies improved renal function of this patient, and steroid pulse therapy attenuated the severe skin discoloration. The ATN was thought to have been caused by the poison from a sea anemone because there were no other conceivable reasons for the patient’s condition. This is the first time that a marine envenomation case has been reported in which the sting of a sea anemone has caused ATN without the failure of any other organs. © 2000 by the National Kidney Foundation, Inc. INDEX WORDS: Acute renal failure (ARF); acute tubular necrosis (ATN); marine envenomation; sea anemone.
A
FEW MARINE creatures have evolved various ways of capturing their prey that, if targeted at humans, can result in discomfort, extreme pain, or even death. The stings of most coelenterates induce only mild dermatitis. Some species of coelenterates, especially those of jellyfish, induce severe dermatitis. Their poison sometimes can cause allergic shock but seldom leads victims to multiple organ failure. The sea anemone is also a kind of coelenterate. We have reported the first known case of acute renal failure (ARF) solely attributable to a sea anemone and without the presence of any other organ failures. CASE REPORT A 27-year-old Japanese man with severe swelling and pain in his right arm was admitted to our hospital in December of 1998. He was experiencing general fatigue. Two days before coming to our hospital, he had accidentally touched a marine organism with his right hand while snorkeling off Cebu Island in the Philippines. A few seconds after contact with the organism, he felt severe pain in the fingers of his right hand. The man then discovered clear, dark-brown tentacles stuck to his fingers. He rubbed them off, and later his right hand was rinsed with a solution of 70% ethyl alcohol to disinfect the wound. A few hours later, his right hand had become swollen, and he felt nauseous. Up until the time of his admission, the swelling continued to spread over his right arm, accompanied by increasing pain. During his childhood, the patient had suffered from a few epileptic seizures.
Physical Examination The patient weighed 68 kg and was 168.5 cm tall. His body temperature was 37.1°C, his blood pressure was 110/60
mm Hg, and his pulse was a regular 72 beats/min. Severe skin swelling was observed on his right hand, which had spread up his entire right arm (Fig 1A). Figure 1B shows some small ulcerations and some vesicles on the patient’s index finger and in between his index and middle fingers. The skin of his right arm had turned purple. Characteristic sting marks were observed, suggesting the injury had resulted from a sea anemone’s sting. He had no edema in his lower extremities nor in his left hand. Physical examination of other organs showed that the patient’s lungs, heart, and abdomen were normal. A neurologic examination also showed no abnormalities.
Laboratory Results On admission, the patient’s clinical laboratory data were as follows: his white blood cell count was 10,600 cells/mm3 (polymorphoneutrophils, 63.0%; lymphocytes, 28.0%; eosinophils, 3.0%; monocytes, 5.0%; basophils, 1.0%). His red blood cell count was 483 ⫻ 104/mm3, and his platelet count was 21.9 ⫻ 104/mm3. No fragmented red blood cells were noted. His blood urea nitrogen (BUN) was 54 mg/dL; creatinine, 4.6 mg/dL; uric acid, 10.8 mg/mL; Na, 137
From the The Third Department of Internal Medicine, Nagoya University School of Medicine, Nagoya, Japan; The Department of Dermatology, Nagoya University School of Medicine, Nagoya, Japan; and Okinawa Chuo Health Center, Naha, Okinawa, Japan. Received December 15, 1999; accepted in revised form April 14, 2000. Address reprint requests to Masashi Mizuno, MD, The Third Department of Internal Medicine, Nagoya University School of Medicine, Nagoya 466-8550, Japan. E-mail: [email protected] © 2000 by the National Kidney Foundation, Inc. 1523-6838/00/3602-0029$3.00/0 doi:10.1053/ajkd.2000.9006
American Journal of Kidney Diseases, Vol 36, No 2 (August), 2000: E10
1
2
MIZUNO ET AL
Fig 1. The patient’s right hand on the day of his admission. Swelling of his right hand is severe. The wound is found on the patient’s index finger and between his index and middle fingers. The skin is purple and has vesicles. (A) Right hand. (B) Close-up of the area between the index and middle fingers of the right hand.
mEq/L; K, 4.5 mEq/L; Cl, 101 mEq/L; total protein, 6.8 g/mL; albumin, 4.4 g/dL; glutamic oxaloacetic transaminase, 16 U/L; glutamic pyruvic transaminase, 17 U/L; lactate dehydrogenase, 284 U/L; alkaline phosphatase, 150 U/L; ␥ glutamyl transpeptidase (␥GTP), 45 U/L; creatine kinase, 648 U/L; and C-reactive protein, 2.7 mg/mL. Serum levels of immunogloblin (Ig) A, IgM, IgE, C3, and C4 complement fractions, and CH50, were within the normal range. Neither anurine nor hypourine was found in the patient. Results of urinalysis were as follows: protein was at 30 mg/dL; sugar, 30 mg/dL; and occult blood, (⫹/⫺). Urine sediment showed no abnormal findings. Serum myoglobin was at 57.5 ng/mL, and urinary myogloblin levels were under detection (⬍10.0 ng/mL). Serum myoglobin was at its highest (94.6 ng/mL) on day 2, and it subsided to normal range on day 4. Findings of the patient’s chest radiograph and electrocardiograph were normal.
Clinical Course After his admission, supportive therapies including appropriate intravenous drip gradually improved the patient’s condition of ARF (Fig 2). A renal biopsy was performed on day 2 (Fig 3). The renal biopsy specimen included eight glomeruli. Not one glomerulus was collapsed. No apparent structural changes were observed in the glomeruli, except for mild ischemic changes in a few of them (Fig 3A). Tubular dilation or degeneration and detachment of tubular epithelial cells were prominent in the outer media (Fig 3B). No deposition of IgG, IgA, IgM, C3, C1q, C4, nor fibrinogen was found in the glomeruli as a result of direct immunofluorescent staining. The pathologic diagnosis was acute tubular necrosis (ATN). Both the BUN levels and serum creatinine levels had returned to normal (⬍1.1 mg/dL) by day 4. On day 2, steroid pulse therapy was administered (1 g/d methylprednisolone for 2 days) along with antibiotics (cefotiam HCl), because the right arm’s dermatitis was markedly severe and becoming worse. After treatment with methylprednisolone, swelling in the patient’s right arm decreased, and his skin coloration improved. The area that had been stung developed ulcerations. After pulse therapy, the only treatment was an ointment containing steroid. However, on day
11, the patient’s body temperature increased mildly. His CRP was elevated to 3.3 mg/dL, and his right arm’s swelling flared up once again. Therefore, the patient was given 3 mg/d betamethasone by mouth. Because his body temperature and CRP decreased on day 13, administration of betamethasone was decreased to 2 mg/d. On day 20, there was no swelling nor pain in the patient’s right hand, and his CRP was 0.0 mg/dL. The ulcerations on his fingers had developed into scars. On day 21, he was discharged from our hospital.
DISCUSSION
Our patient suffered severe dermatitis as a result of having been stung by a coelenterate in the Sulu Sea around Cebu Island. He consequently developed ARF. Our case showed ARF but no other major organ failures. In this case, histologic findings of the renal biopsy showed ATN. The causes of ATN usually include circulatory shock, myoglobinuria, drugs, poisons, and so on. Multiple bee stings, scorpion stings, and snakebites have been reported to induce ATN.1 In our case, neither shock, rabdomyolysis, nor drugs were the cause of our patient’s ATN, as seen from the course of his illness, results of his physical examination, and his laboratory data on admission. Poison from the sting of a coelenterate is believed to be responsible for causing ATN in this case. There are thousands of species of organisms in the seas and oceans of the world. It is known that just a few kinds of marine creatures have poison that enables them to protect themselves from their enemies or to hunt. Some kinds of coelenterates, such as sea urchins, jellyfish, and starfish, are poisonous to humans. The stings of most of these organisms induce only mild dermatitis,
MARINE ENVENOMATION AND ACUTE RENAL FAILURE
3
Fig 2. Clinical time course. CTM, cefotiam hydrochloride; MINO, minocycline hydrochloride.
which usually can be treated by either local steroid therapy or oral steroid administration combined with local steroid therapy.2,3 In this case, the patient’s dermatitis was very severe. Oral steroid administration after steroid pulse therapy was chosen to help the patient recover from his severe dermatitis. Of all coelenterate-
related injuries, those resulting from jellyfish are most frequently reported. For example, the notoriously deadly box-jellyfish, Chironex fleckeri, has been responsible for more than 80 documented deaths in northern Australian waters.4,5 Sea anemones are another kind of coelenterates, and most of them are harmless to humans or just
Fig 3. Light micrograph. (A) An ischemic change was found in glomeruli. No mesangial hypercellularity, nor matrix widening, nor depositions were found. (PAS stain; original magnification ⴛ400.) (B) In the tubules, cellular degeneration and necrosis can be found. Part of the tubular epithelial cells are detached. (Masson-Trichrome stain; original magnification ⴛ200.)
4
MIZUNO ET AL
This report may be the first to discuss a marine envenomation case in which the sting of a sea anemone caused ATN without causing any other organ failures. We should realize that injuries from sea anemones can result in ATN. Steroid pulse therapy and oral steroid administration may be useful to alleviate severe dermatitis in the case of conspicuous skin discoloration caused by sea anemones. ACKNOWLEDGMENT Fig 4. Photograh of Phyllodiscus semoni. This is a photograph of the same type of sea anemone thought to have stung and caused ATN in our patient. P semoni is brown and known for its natural camouflage, mimicking a rock in an atoll. This photograph was taken in Okinawa, Japan.
induce mild dermatitis. Two kinds of sea anemones are known to induce severe dermatitis.2,3,6 However, systemic reactions to poison from sea anemones have seldom been reported. Only once has the sting of a sea anemone been reported to induce fulminant hepatitis in a patient.7 Severe injuries caused by marine envenomations may very easily lead to the victim’s death by drowning. This may explain why there are a small number of marine envenomation cases that lead to severe organ failures. In Okinawa (Japan), a kind of sea anemone called Phyllodiscus semoni (Fig 4) has a very potent poison.8,9 Severe dermatitis with swelling, local fever, and ulcerations are known symptoms of patients who have been stung by P semoni. In this case, the causative creature was thought to have been a harmful P semoni, because the wound on the patient’s right hand was characteristic of a sea anemone’s sting. As well, the patient described the marine organism he touched as looking like a brown rock and feeling like a sponge. This also resembles P semoni.2,3,6,8
The authors thank Dr S. Tomihara for his useful comments, M.S. Korcek for the English editing of this manuscript, and also the Okinawa Perfectural Institute of Health and Environment for the photograph of P. semoni.
REFERENCES 1. Solez K: Acute renal failure (Acute tublar necrosis, infarction, and cortical necrosis), in Heptinstall RH: Pathology of the Kidney (ed 4), chap 18. Boston, MA, Little, Brown and Company, 1992, pp 1238-1239 2. Hansen PA, Halstead BW: The venomous sea anemone actinodendron plumosum haddon of South Vietnam. Micronessica 7:124-136, 1971 3. Auerbach JF: Marine envenomations. N Engl J Med 325:486-493, 1991 4. Williamson J: Classification (with description and medical implications of seven venomous jellyfish), in some Australian marine stings, in Williamson J (ed): Envenomations and Poisonings. Brisbane, Surf Life Saving Foundation, 1981, pp 1-26 5. Fenner P: Medical frontiers in Australian seas, in Pearn J, Cobcroft M (eds): Fevers and Frontiers, chap 3. Brisbane, Australia Amphion, 1990, pp 73-84 6. McGoldrick J, Marix JA: Marine envenomations. Part 2: Invertebrates. J Emerg Med 10:71-77, 1992 7. Garcia PJ, Schein RM, Burnett JW: Fulminant hepatic failure from a sea anemone sting. Ann Intern Med 120:665666, 1994 8. Kwietniewski CR: Actiniaria von ambon und Thursday Island. Jena, Denkshriften der Medizich-und Naturwissenshaftliche Gesellschaft, 1897, pp 385-430 9. Nakamoto M, Uezato H: Stings of box-jellyfish and sea anemones. Clin Dermatol 52:29-33, 1998