Minimally Hyperpigmented Plaque With Skin Thickening on the Neck

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Minimally Hyperpigmented Plaque With Skin Thickening on the Neck

The Diagnosis: Fiddler's Neck 

A thorough patient history revealed that the patient was retired and played violin regularly in the local orchestra. Fiddler's neck, or violin hickey, is an uncommon physical examination finding and often is considered a badge of honor by musicians who develop it. Fiddler's neck is a hobby-related callus seen in highly dedicated violin and viola players, and in some circles, it is known as a mark of greatness. In one instance, members of the public were asked to display a violin hickey before they were allowed to play a $3.5 million violin on public display in London, England.1 Fiddler's neck is a benign submandibular lesion caused by pressure and friction on the skin from extensive time spent playing the instrument. The primary cause is thought to be mechanical, but it is not fully understood why the lesion occurs in some musicians and not others, regardless of playing time.1 This submandibular fiddler's neck is distinct from a similarly named supraclavicular lesion, which represents an allergic contact dermatitis to the nickel bracket of the instrument's chin rest and presents with eczematous scale and/or vesicles.2,3 Submandibular fiddler's neck presents with some combination of erythema, edema, lichenification, and scarring just below the angle of the jaw. Occasionally, papules, pustules, and even cyst formation may be noted. Lesions are sometimes mistaken for malignancy or lymphedema. Therefore, a thorough history and clinical expertise are important, as surgical excision should be avoided.2  

Depending on presentation, the differential diagnosis also may include malignant melanoma due to irregular pigmentation, branchial cleft cyst or sialolithiasis due to location and texture, or a tumor of the salivary gland. 

Management of fiddler's neck may include topical steroids, neck or instrument padding, or decreased playing time. However, the lesion often is worn with pride, seen as a testament to the musician's dedication, and reassurance generally is most appropriate.1  

References
  1. Roberts C. How to prevent or even cure a violin hickey. Strings. February 1, 2011. https://stringsmagazine.com/how-to-prevent-or-even-cure-a-violin-hickey/. Accessed January 31, 2020. 
  2. Myint CW, Rutt AL, Sataloff RT. Fiddler's neck: a review. Ear Nose Throat J. 2017;96:76-79. 
  3. Jue MS, Kim YS, Ro YS. Fiddler's neck accompanied by allergic contact dermatitis to nickel in a viola player. Ann Dermatol. 2010;22:88-90. 
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The authors report no conflict of interest.

Correspondence: Henry Tomlinson, MD, 167 Ashley Ave, Charleston, SC 29425 (Tomlinson.henry@gmail.com).

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Dr. Tomlinson is from the Department of Anesthesia, Medical University of South Carolina, Charleston. Dr. Wilson is from the Department of Dermatology, University of Virginia, Charlottesville.

The authors report no conflict of interest.

Correspondence: Henry Tomlinson, MD, 167 Ashley Ave, Charleston, SC 29425 (Tomlinson.henry@gmail.com).

Author and Disclosure Information

Dr. Tomlinson is from the Department of Anesthesia, Medical University of South Carolina, Charleston. Dr. Wilson is from the Department of Dermatology, University of Virginia, Charlottesville.

The authors report no conflict of interest.

Correspondence: Henry Tomlinson, MD, 167 Ashley Ave, Charleston, SC 29425 (Tomlinson.henry@gmail.com).

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The Diagnosis: Fiddler's Neck 

A thorough patient history revealed that the patient was retired and played violin regularly in the local orchestra. Fiddler's neck, or violin hickey, is an uncommon physical examination finding and often is considered a badge of honor by musicians who develop it. Fiddler's neck is a hobby-related callus seen in highly dedicated violin and viola players, and in some circles, it is known as a mark of greatness. In one instance, members of the public were asked to display a violin hickey before they were allowed to play a $3.5 million violin on public display in London, England.1 Fiddler's neck is a benign submandibular lesion caused by pressure and friction on the skin from extensive time spent playing the instrument. The primary cause is thought to be mechanical, but it is not fully understood why the lesion occurs in some musicians and not others, regardless of playing time.1 This submandibular fiddler's neck is distinct from a similarly named supraclavicular lesion, which represents an allergic contact dermatitis to the nickel bracket of the instrument's chin rest and presents with eczematous scale and/or vesicles.2,3 Submandibular fiddler's neck presents with some combination of erythema, edema, lichenification, and scarring just below the angle of the jaw. Occasionally, papules, pustules, and even cyst formation may be noted. Lesions are sometimes mistaken for malignancy or lymphedema. Therefore, a thorough history and clinical expertise are important, as surgical excision should be avoided.2  

Depending on presentation, the differential diagnosis also may include malignant melanoma due to irregular pigmentation, branchial cleft cyst or sialolithiasis due to location and texture, or a tumor of the salivary gland. 

Management of fiddler's neck may include topical steroids, neck or instrument padding, or decreased playing time. However, the lesion often is worn with pride, seen as a testament to the musician's dedication, and reassurance generally is most appropriate.1  

The Diagnosis: Fiddler's Neck 

A thorough patient history revealed that the patient was retired and played violin regularly in the local orchestra. Fiddler's neck, or violin hickey, is an uncommon physical examination finding and often is considered a badge of honor by musicians who develop it. Fiddler's neck is a hobby-related callus seen in highly dedicated violin and viola players, and in some circles, it is known as a mark of greatness. In one instance, members of the public were asked to display a violin hickey before they were allowed to play a $3.5 million violin on public display in London, England.1 Fiddler's neck is a benign submandibular lesion caused by pressure and friction on the skin from extensive time spent playing the instrument. The primary cause is thought to be mechanical, but it is not fully understood why the lesion occurs in some musicians and not others, regardless of playing time.1 This submandibular fiddler's neck is distinct from a similarly named supraclavicular lesion, which represents an allergic contact dermatitis to the nickel bracket of the instrument's chin rest and presents with eczematous scale and/or vesicles.2,3 Submandibular fiddler's neck presents with some combination of erythema, edema, lichenification, and scarring just below the angle of the jaw. Occasionally, papules, pustules, and even cyst formation may be noted. Lesions are sometimes mistaken for malignancy or lymphedema. Therefore, a thorough history and clinical expertise are important, as surgical excision should be avoided.2  

Depending on presentation, the differential diagnosis also may include malignant melanoma due to irregular pigmentation, branchial cleft cyst or sialolithiasis due to location and texture, or a tumor of the salivary gland. 

Management of fiddler's neck may include topical steroids, neck or instrument padding, or decreased playing time. However, the lesion often is worn with pride, seen as a testament to the musician's dedication, and reassurance generally is most appropriate.1  

References
  1. Roberts C. How to prevent or even cure a violin hickey. Strings. February 1, 2011. https://stringsmagazine.com/how-to-prevent-or-even-cure-a-violin-hickey/. Accessed January 31, 2020. 
  2. Myint CW, Rutt AL, Sataloff RT. Fiddler's neck: a review. Ear Nose Throat J. 2017;96:76-79. 
  3. Jue MS, Kim YS, Ro YS. Fiddler's neck accompanied by allergic contact dermatitis to nickel in a viola player. Ann Dermatol. 2010;22:88-90. 
References
  1. Roberts C. How to prevent or even cure a violin hickey. Strings. February 1, 2011. https://stringsmagazine.com/how-to-prevent-or-even-cure-a-violin-hickey/. Accessed January 31, 2020. 
  2. Myint CW, Rutt AL, Sataloff RT. Fiddler's neck: a review. Ear Nose Throat J. 2017;96:76-79. 
  3. Jue MS, Kim YS, Ro YS. Fiddler's neck accompanied by allergic contact dermatitis to nickel in a viola player. Ann Dermatol. 2010;22:88-90. 
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A 74-year-old man with a history of melanoma and basal cell carcinoma presented for an annual skin examination and displayed asymptomatic stable thickening of skin on the left side of the neck below the jawline of several years' duration. Physical examination revealed a 4×2-cm minimally hyperpigmented plaque with skin thickening and a pebbly appearing surface on the left lateral neck just inferior to the angle of the mandible. 

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What’s Eating You? The South African Fattail Scorpion Revisited

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Identification

The South African fattail scorpion (Parabuthus transvaalicus)(Figure) is one of the most poisonous scorpions in southern Africa.1 A member of the Buthidae scorpion family, it can grow as long as 15 cm and is dark brown-black with lighter red-brown pincers. Similar to other fattail scorpions, it has slender pincers (pedipalps) and a thick square tail (the telson). Parabuthus transvaalicus inhabits hot dry deserts, scrublands, and semiarid regions.1,2 It also is popular in exotic pet collections, the most common source of stings in the United States.

The South African fattail scorpion (Parabuthus transvaalicus).

Stings and Envenomation

Scorpions with thicker tails generally have more potent venom than those with slender tails and thick pincers. Venom is injected by a stinger at the tip of the telson1; P transvaalicus also can spray venom as far as 3 m.1,2 Venom is not known to cause toxicity through skin contact but could represent a hazard if sprayed in the eye.

Scorpion toxins are a group of complex neurotoxins that act on sodium channels, either retarding inactivation (α toxin) or enhancing activation (β toxin), causing massive depolarization of excitable cells.1,3 The toxin causes neurons to fire repetitively.4 Neurotransmitters—noradrenaline, adrenaline, and acetylcholine—cause the observed sympathetic, parasympathetic, and skeletal muscle effects.1

Incidence
Worldwide, more than 1.2 million individuals are stung by a scorpion annually, causing more than 3250 deaths a year.5 Adults are stung more often, but children experience more severe envenomation, are more likely to develop severe illness requiring intensive supportive care, and have a higher mortality.4



As many as one-third of patients stung by a Parabuthus scorpion develop neuromuscular toxicity, which can be life-threatening.6 In a study of 277 envenomations by P transvaalicus, 10% of patients developed severe symptoms and 5 died. Children younger than 10 years and adults older than 50 years are at greatest risk for adverse outcomes.6 Children have a case fatality rate as high as 10 times the adult fatality rate.7

Clinical Presentation
The clinical presentation of scorpion envenomation varies with the species involved, the amount of venom injected, and the victim’s weight and baseline health.1 Scorpion envenomation is divided into 4 grades based on the severity of a sting:

Grade I: pain and paresthesia at the envenomation site; usually, no local inflammation

Grade II: local symptoms as well as more remote pain and paresthesia; pain can radiate up the affected limb

Grade III: cranial nerve or somatic skeletal neuromuscular dysfunction; either presentation can have associated autonomic dysfunction

Grade IV: both cranial nerve and somatic skeletal neuromuscular dysfunction, with associated auto-nomic dysfunction

 

 

The initial symptom of a scorpion sting is intense burning pain. The sting site might be unimpressive, with only a mild local reaction. Symptoms usually progress to maximum severity within 5 hours.1 Muscle pain, cramps, and weakness are prominent. The patient might have difficulty walking and swallowing, with increased salivation and drooling, and visual disturbance with abnormal eye movements. Pulse, blood pressure, and temperature often are elevated. The patient might be hyperreflexic with clonus.1,6

Symptoms of increased sympathetic activity are hypertension, tachycardia, cardiac dysrhythmia, perspiration, hyperglycemia, and restlessness.1,2 Parasympathetic effects are increased salivation, hypotension, bradycardia, and gastric distension. Skeletal muscle effects include tremors and involuntary muscle movement, which can be severe. Cranial nerve dysfunction may manifest as dysphagia, drooling, abnormal eye movements, blurred vision, slurred speech, and tongue fasciculations. Subsequent development of muscle weakness, bulbar paralysis, and difficulty breathing may be caused by depletion of neurotransmitters after prolonged excessive neuronal activity.1

Distinctive Signs in Younger Patients
A child who is stung by a scorpion might have symptoms similar to those seen in an adult victim but can also experience an extreme form of restlessness that indicates severe envenomation characterized by inability to lay still, violent muscle twitching, and uncontrollable flailing of extremities. The child might have facial grimacing, with lip-smacking and chewing motions. In addition, bulbar paralysis and respiratory distress are more likely in children who have been stung than in adults.1,2

Management

Treatment of a P transvaalicus sting is directed at “scorpionism,” envenomation that is associated with systemic symptoms that can be life-threatening. Treatment comprises support of vital functions, symptomatic measures, and injection of antivenin.8

Support of Vital Functions
In adults, systemic symptoms can be delayed as long as 8 hours after the sting. However, most severe cases usually are evident within 60 minutes; infants can reach grade IV as quickly as 15 to 30 minutes.9,10 Loss of pharyngeal reflexes and development of respiratory distress are ominous warning signs requiring immediate respiratory support. Respiratory failure is the most common cause of death.1 An asymptomatic child should be admitted to a hospital for observation for a minimum of 12 hours if the species of scorpion was not identified.2

 

 

Pain Relief
Most patients cannot tolerate an ice pack because of severe hyperesthesia. Infiltration of the local sting site with an anesthetic generally is safe and can provide some local pain relief. Intravenous fentanyl has been used in closely monitored patients because the drug is not associated with histamine release. Medications that cause release of histamine, such as morphine, can exacerbate or confuse the clinical picture.

Antivenin
Scorpion antivenin contains purified IgG fragments; allergic reactions are now rare. The sooner antivenin is administered, the greater the benefit. When administered early, it can prevent many of the most serious complications.7 In a randomized, double-blind study of critically ill children with clinically significant signs of scorpion envenomation, intravenous administration of scorpion-specific fragment antigen-binding 2 (F[(ab’]2) antivenin resulted in resolution of clinical symptoms within 4 hours.11



When managing grade III or IV scorpion envenomation, all patients should be admitted to a medical facility equipped to provide intensive supportive care; consider consultation with a regional poison control center. The World Health Organization maintains an international poison control center (at https://www.who.int/ipcs/poisons/centre/en/) with regional telephone numbers; alternatively, in the United States, call the nationwide telephone number of the Poison Control Center (800-222-1222).

The World Health Organization has identified declining production of antivenin as a crisis.12

Resolution
Symptoms of envenomation typically resolve 9 to 30 hours after a sting in a patient with grade III or IV envenomation not treated with antivenin.4 However, pain and paresthesia occasionally last as long as 2 weeks. In rare cases, more long-term sequelae of burning paresthesia persist for months.4

Conclusion

It is important for dermatologists to be aware of the potential for life-threatening envenomation by certain scorpion species native to southern Africa. In the United States, stings of these species most often are seen in patients with a pet collection, but late sequelae also can be seen in travelers returning from an endemic region. The site of a sting often appears unimpressive initially, but severe hyperesthesia is common. Patients with cardiac, neurologic, or respiratory symptoms require intensive supportive care. Proper care can be lifesaving.

References
  1. Müller GJ, Modler H, Wium CA, et al. Scorpion sting in southern Africa: diagnosis and management. Continuing Medical Education. 2012;30:356-361.
  2. Müller GJ. Scorpionism in South Africa. a report of 42 serious scorpion envenomations. S Afr Med J. 1993;83:405-411.
  3. Quintero-Hernández V, Jiménez-Vargas JM, Gurrola GB, et al. Scorpion venom components that affect ion-channels function. Toxicon. 2013;76:328-342.
  4. LoVecchio F, McBride C. Scorpion envenomations in young children in central Arizona. J Toxicol Clin Toxicol. 2003;41:937-940.
  5. Chippaux JP, Goyffon M. Epidemiology of scorpionism: a global appraisal. Acta Trop. 2008;107:71-79.
  6. Bergman NJ. Clinical description of Parabuthus transvaalicus scorpionism in Zimbabwe. Toxicon. 1997;35:759-771.
  7. Chippaux JP. Emerging options for the management of scorpion stings. Drug Des Devel Ther. 2012;6:165-173.
  8. Santos MS, Silva CG, Neto BS, et al. Clinical and epidemiological aspects of scorpionism in the world: a systematic review. Wilderness Environ Med. 2016;27:504-518.
  9. Amaral CF, Rezende NA. Both cardiogenic and non-cardiogenic factors are involved in the pathogenesis of pulmonary oedema after scorpion envenoming. Toxicon. 1997;35:997-998.
  10. Bergman NJ. Scorpion sting in Zimbabwe. S Afr Med J. 1997;87:163-167.
  11. Boyer LV, Theodorou AA, Berg RA, et al; Arizona Envenomation Investigators. antivenom for critically ill children with neurotoxicity from scorpion stings. N Engl J Med. 2009;360:2090-2098.
  12. Theakston RD, Warrell DA, Griffiths E. Report of a WHO workshop on the standardization and control of antivenoms. Toxicon. 2003;41:541-557.
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Identification

The South African fattail scorpion (Parabuthus transvaalicus)(Figure) is one of the most poisonous scorpions in southern Africa.1 A member of the Buthidae scorpion family, it can grow as long as 15 cm and is dark brown-black with lighter red-brown pincers. Similar to other fattail scorpions, it has slender pincers (pedipalps) and a thick square tail (the telson). Parabuthus transvaalicus inhabits hot dry deserts, scrublands, and semiarid regions.1,2 It also is popular in exotic pet collections, the most common source of stings in the United States.

The South African fattail scorpion (Parabuthus transvaalicus).

Stings and Envenomation

Scorpions with thicker tails generally have more potent venom than those with slender tails and thick pincers. Venom is injected by a stinger at the tip of the telson1; P transvaalicus also can spray venom as far as 3 m.1,2 Venom is not known to cause toxicity through skin contact but could represent a hazard if sprayed in the eye.

Scorpion toxins are a group of complex neurotoxins that act on sodium channels, either retarding inactivation (α toxin) or enhancing activation (β toxin), causing massive depolarization of excitable cells.1,3 The toxin causes neurons to fire repetitively.4 Neurotransmitters—noradrenaline, adrenaline, and acetylcholine—cause the observed sympathetic, parasympathetic, and skeletal muscle effects.1

Incidence
Worldwide, more than 1.2 million individuals are stung by a scorpion annually, causing more than 3250 deaths a year.5 Adults are stung more often, but children experience more severe envenomation, are more likely to develop severe illness requiring intensive supportive care, and have a higher mortality.4



As many as one-third of patients stung by a Parabuthus scorpion develop neuromuscular toxicity, which can be life-threatening.6 In a study of 277 envenomations by P transvaalicus, 10% of patients developed severe symptoms and 5 died. Children younger than 10 years and adults older than 50 years are at greatest risk for adverse outcomes.6 Children have a case fatality rate as high as 10 times the adult fatality rate.7

Clinical Presentation
The clinical presentation of scorpion envenomation varies with the species involved, the amount of venom injected, and the victim’s weight and baseline health.1 Scorpion envenomation is divided into 4 grades based on the severity of a sting:

Grade I: pain and paresthesia at the envenomation site; usually, no local inflammation

Grade II: local symptoms as well as more remote pain and paresthesia; pain can radiate up the affected limb

Grade III: cranial nerve or somatic skeletal neuromuscular dysfunction; either presentation can have associated autonomic dysfunction

Grade IV: both cranial nerve and somatic skeletal neuromuscular dysfunction, with associated auto-nomic dysfunction

 

 

The initial symptom of a scorpion sting is intense burning pain. The sting site might be unimpressive, with only a mild local reaction. Symptoms usually progress to maximum severity within 5 hours.1 Muscle pain, cramps, and weakness are prominent. The patient might have difficulty walking and swallowing, with increased salivation and drooling, and visual disturbance with abnormal eye movements. Pulse, blood pressure, and temperature often are elevated. The patient might be hyperreflexic with clonus.1,6

Symptoms of increased sympathetic activity are hypertension, tachycardia, cardiac dysrhythmia, perspiration, hyperglycemia, and restlessness.1,2 Parasympathetic effects are increased salivation, hypotension, bradycardia, and gastric distension. Skeletal muscle effects include tremors and involuntary muscle movement, which can be severe. Cranial nerve dysfunction may manifest as dysphagia, drooling, abnormal eye movements, blurred vision, slurred speech, and tongue fasciculations. Subsequent development of muscle weakness, bulbar paralysis, and difficulty breathing may be caused by depletion of neurotransmitters after prolonged excessive neuronal activity.1

Distinctive Signs in Younger Patients
A child who is stung by a scorpion might have symptoms similar to those seen in an adult victim but can also experience an extreme form of restlessness that indicates severe envenomation characterized by inability to lay still, violent muscle twitching, and uncontrollable flailing of extremities. The child might have facial grimacing, with lip-smacking and chewing motions. In addition, bulbar paralysis and respiratory distress are more likely in children who have been stung than in adults.1,2

Management

Treatment of a P transvaalicus sting is directed at “scorpionism,” envenomation that is associated with systemic symptoms that can be life-threatening. Treatment comprises support of vital functions, symptomatic measures, and injection of antivenin.8

Support of Vital Functions
In adults, systemic symptoms can be delayed as long as 8 hours after the sting. However, most severe cases usually are evident within 60 minutes; infants can reach grade IV as quickly as 15 to 30 minutes.9,10 Loss of pharyngeal reflexes and development of respiratory distress are ominous warning signs requiring immediate respiratory support. Respiratory failure is the most common cause of death.1 An asymptomatic child should be admitted to a hospital for observation for a minimum of 12 hours if the species of scorpion was not identified.2

 

 

Pain Relief
Most patients cannot tolerate an ice pack because of severe hyperesthesia. Infiltration of the local sting site with an anesthetic generally is safe and can provide some local pain relief. Intravenous fentanyl has been used in closely monitored patients because the drug is not associated with histamine release. Medications that cause release of histamine, such as morphine, can exacerbate or confuse the clinical picture.

Antivenin
Scorpion antivenin contains purified IgG fragments; allergic reactions are now rare. The sooner antivenin is administered, the greater the benefit. When administered early, it can prevent many of the most serious complications.7 In a randomized, double-blind study of critically ill children with clinically significant signs of scorpion envenomation, intravenous administration of scorpion-specific fragment antigen-binding 2 (F[(ab’]2) antivenin resulted in resolution of clinical symptoms within 4 hours.11



When managing grade III or IV scorpion envenomation, all patients should be admitted to a medical facility equipped to provide intensive supportive care; consider consultation with a regional poison control center. The World Health Organization maintains an international poison control center (at https://www.who.int/ipcs/poisons/centre/en/) with regional telephone numbers; alternatively, in the United States, call the nationwide telephone number of the Poison Control Center (800-222-1222).

The World Health Organization has identified declining production of antivenin as a crisis.12

Resolution
Symptoms of envenomation typically resolve 9 to 30 hours after a sting in a patient with grade III or IV envenomation not treated with antivenin.4 However, pain and paresthesia occasionally last as long as 2 weeks. In rare cases, more long-term sequelae of burning paresthesia persist for months.4

Conclusion

It is important for dermatologists to be aware of the potential for life-threatening envenomation by certain scorpion species native to southern Africa. In the United States, stings of these species most often are seen in patients with a pet collection, but late sequelae also can be seen in travelers returning from an endemic region. The site of a sting often appears unimpressive initially, but severe hyperesthesia is common. Patients with cardiac, neurologic, or respiratory symptoms require intensive supportive care. Proper care can be lifesaving.

 

Identification

The South African fattail scorpion (Parabuthus transvaalicus)(Figure) is one of the most poisonous scorpions in southern Africa.1 A member of the Buthidae scorpion family, it can grow as long as 15 cm and is dark brown-black with lighter red-brown pincers. Similar to other fattail scorpions, it has slender pincers (pedipalps) and a thick square tail (the telson). Parabuthus transvaalicus inhabits hot dry deserts, scrublands, and semiarid regions.1,2 It also is popular in exotic pet collections, the most common source of stings in the United States.

The South African fattail scorpion (Parabuthus transvaalicus).

Stings and Envenomation

Scorpions with thicker tails generally have more potent venom than those with slender tails and thick pincers. Venom is injected by a stinger at the tip of the telson1; P transvaalicus also can spray venom as far as 3 m.1,2 Venom is not known to cause toxicity through skin contact but could represent a hazard if sprayed in the eye.

Scorpion toxins are a group of complex neurotoxins that act on sodium channels, either retarding inactivation (α toxin) or enhancing activation (β toxin), causing massive depolarization of excitable cells.1,3 The toxin causes neurons to fire repetitively.4 Neurotransmitters—noradrenaline, adrenaline, and acetylcholine—cause the observed sympathetic, parasympathetic, and skeletal muscle effects.1

Incidence
Worldwide, more than 1.2 million individuals are stung by a scorpion annually, causing more than 3250 deaths a year.5 Adults are stung more often, but children experience more severe envenomation, are more likely to develop severe illness requiring intensive supportive care, and have a higher mortality.4



As many as one-third of patients stung by a Parabuthus scorpion develop neuromuscular toxicity, which can be life-threatening.6 In a study of 277 envenomations by P transvaalicus, 10% of patients developed severe symptoms and 5 died. Children younger than 10 years and adults older than 50 years are at greatest risk for adverse outcomes.6 Children have a case fatality rate as high as 10 times the adult fatality rate.7

Clinical Presentation
The clinical presentation of scorpion envenomation varies with the species involved, the amount of venom injected, and the victim’s weight and baseline health.1 Scorpion envenomation is divided into 4 grades based on the severity of a sting:

Grade I: pain and paresthesia at the envenomation site; usually, no local inflammation

Grade II: local symptoms as well as more remote pain and paresthesia; pain can radiate up the affected limb

Grade III: cranial nerve or somatic skeletal neuromuscular dysfunction; either presentation can have associated autonomic dysfunction

Grade IV: both cranial nerve and somatic skeletal neuromuscular dysfunction, with associated auto-nomic dysfunction

 

 

The initial symptom of a scorpion sting is intense burning pain. The sting site might be unimpressive, with only a mild local reaction. Symptoms usually progress to maximum severity within 5 hours.1 Muscle pain, cramps, and weakness are prominent. The patient might have difficulty walking and swallowing, with increased salivation and drooling, and visual disturbance with abnormal eye movements. Pulse, blood pressure, and temperature often are elevated. The patient might be hyperreflexic with clonus.1,6

Symptoms of increased sympathetic activity are hypertension, tachycardia, cardiac dysrhythmia, perspiration, hyperglycemia, and restlessness.1,2 Parasympathetic effects are increased salivation, hypotension, bradycardia, and gastric distension. Skeletal muscle effects include tremors and involuntary muscle movement, which can be severe. Cranial nerve dysfunction may manifest as dysphagia, drooling, abnormal eye movements, blurred vision, slurred speech, and tongue fasciculations. Subsequent development of muscle weakness, bulbar paralysis, and difficulty breathing may be caused by depletion of neurotransmitters after prolonged excessive neuronal activity.1

Distinctive Signs in Younger Patients
A child who is stung by a scorpion might have symptoms similar to those seen in an adult victim but can also experience an extreme form of restlessness that indicates severe envenomation characterized by inability to lay still, violent muscle twitching, and uncontrollable flailing of extremities. The child might have facial grimacing, with lip-smacking and chewing motions. In addition, bulbar paralysis and respiratory distress are more likely in children who have been stung than in adults.1,2

Management

Treatment of a P transvaalicus sting is directed at “scorpionism,” envenomation that is associated with systemic symptoms that can be life-threatening. Treatment comprises support of vital functions, symptomatic measures, and injection of antivenin.8

Support of Vital Functions
In adults, systemic symptoms can be delayed as long as 8 hours after the sting. However, most severe cases usually are evident within 60 minutes; infants can reach grade IV as quickly as 15 to 30 minutes.9,10 Loss of pharyngeal reflexes and development of respiratory distress are ominous warning signs requiring immediate respiratory support. Respiratory failure is the most common cause of death.1 An asymptomatic child should be admitted to a hospital for observation for a minimum of 12 hours if the species of scorpion was not identified.2

 

 

Pain Relief
Most patients cannot tolerate an ice pack because of severe hyperesthesia. Infiltration of the local sting site with an anesthetic generally is safe and can provide some local pain relief. Intravenous fentanyl has been used in closely monitored patients because the drug is not associated with histamine release. Medications that cause release of histamine, such as morphine, can exacerbate or confuse the clinical picture.

Antivenin
Scorpion antivenin contains purified IgG fragments; allergic reactions are now rare. The sooner antivenin is administered, the greater the benefit. When administered early, it can prevent many of the most serious complications.7 In a randomized, double-blind study of critically ill children with clinically significant signs of scorpion envenomation, intravenous administration of scorpion-specific fragment antigen-binding 2 (F[(ab’]2) antivenin resulted in resolution of clinical symptoms within 4 hours.11



When managing grade III or IV scorpion envenomation, all patients should be admitted to a medical facility equipped to provide intensive supportive care; consider consultation with a regional poison control center. The World Health Organization maintains an international poison control center (at https://www.who.int/ipcs/poisons/centre/en/) with regional telephone numbers; alternatively, in the United States, call the nationwide telephone number of the Poison Control Center (800-222-1222).

The World Health Organization has identified declining production of antivenin as a crisis.12

Resolution
Symptoms of envenomation typically resolve 9 to 30 hours after a sting in a patient with grade III or IV envenomation not treated with antivenin.4 However, pain and paresthesia occasionally last as long as 2 weeks. In rare cases, more long-term sequelae of burning paresthesia persist for months.4

Conclusion

It is important for dermatologists to be aware of the potential for life-threatening envenomation by certain scorpion species native to southern Africa. In the United States, stings of these species most often are seen in patients with a pet collection, but late sequelae also can be seen in travelers returning from an endemic region. The site of a sting often appears unimpressive initially, but severe hyperesthesia is common. Patients with cardiac, neurologic, or respiratory symptoms require intensive supportive care. Proper care can be lifesaving.

References
  1. Müller GJ, Modler H, Wium CA, et al. Scorpion sting in southern Africa: diagnosis and management. Continuing Medical Education. 2012;30:356-361.
  2. Müller GJ. Scorpionism in South Africa. a report of 42 serious scorpion envenomations. S Afr Med J. 1993;83:405-411.
  3. Quintero-Hernández V, Jiménez-Vargas JM, Gurrola GB, et al. Scorpion venom components that affect ion-channels function. Toxicon. 2013;76:328-342.
  4. LoVecchio F, McBride C. Scorpion envenomations in young children in central Arizona. J Toxicol Clin Toxicol. 2003;41:937-940.
  5. Chippaux JP, Goyffon M. Epidemiology of scorpionism: a global appraisal. Acta Trop. 2008;107:71-79.
  6. Bergman NJ. Clinical description of Parabuthus transvaalicus scorpionism in Zimbabwe. Toxicon. 1997;35:759-771.
  7. Chippaux JP. Emerging options for the management of scorpion stings. Drug Des Devel Ther. 2012;6:165-173.
  8. Santos MS, Silva CG, Neto BS, et al. Clinical and epidemiological aspects of scorpionism in the world: a systematic review. Wilderness Environ Med. 2016;27:504-518.
  9. Amaral CF, Rezende NA. Both cardiogenic and non-cardiogenic factors are involved in the pathogenesis of pulmonary oedema after scorpion envenoming. Toxicon. 1997;35:997-998.
  10. Bergman NJ. Scorpion sting in Zimbabwe. S Afr Med J. 1997;87:163-167.
  11. Boyer LV, Theodorou AA, Berg RA, et al; Arizona Envenomation Investigators. antivenom for critically ill children with neurotoxicity from scorpion stings. N Engl J Med. 2009;360:2090-2098.
  12. Theakston RD, Warrell DA, Griffiths E. Report of a WHO workshop on the standardization and control of antivenoms. Toxicon. 2003;41:541-557.
References
  1. Müller GJ, Modler H, Wium CA, et al. Scorpion sting in southern Africa: diagnosis and management. Continuing Medical Education. 2012;30:356-361.
  2. Müller GJ. Scorpionism in South Africa. a report of 42 serious scorpion envenomations. S Afr Med J. 1993;83:405-411.
  3. Quintero-Hernández V, Jiménez-Vargas JM, Gurrola GB, et al. Scorpion venom components that affect ion-channels function. Toxicon. 2013;76:328-342.
  4. LoVecchio F, McBride C. Scorpion envenomations in young children in central Arizona. J Toxicol Clin Toxicol. 2003;41:937-940.
  5. Chippaux JP, Goyffon M. Epidemiology of scorpionism: a global appraisal. Acta Trop. 2008;107:71-79.
  6. Bergman NJ. Clinical description of Parabuthus transvaalicus scorpionism in Zimbabwe. Toxicon. 1997;35:759-771.
  7. Chippaux JP. Emerging options for the management of scorpion stings. Drug Des Devel Ther. 2012;6:165-173.
  8. Santos MS, Silva CG, Neto BS, et al. Clinical and epidemiological aspects of scorpionism in the world: a systematic review. Wilderness Environ Med. 2016;27:504-518.
  9. Amaral CF, Rezende NA. Both cardiogenic and non-cardiogenic factors are involved in the pathogenesis of pulmonary oedema after scorpion envenoming. Toxicon. 1997;35:997-998.
  10. Bergman NJ. Scorpion sting in Zimbabwe. S Afr Med J. 1997;87:163-167.
  11. Boyer LV, Theodorou AA, Berg RA, et al; Arizona Envenomation Investigators. antivenom for critically ill children with neurotoxicity from scorpion stings. N Engl J Med. 2009;360:2090-2098.
  12. Theakston RD, Warrell DA, Griffiths E. Report of a WHO workshop on the standardization and control of antivenoms. Toxicon. 2003;41:541-557.
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Practice Points

  • Exotic and dangerous pets are becoming more popular. Scorpion stings cause potentially life-threatening neurotoxicity, with children particularly susceptible.
  • Fattail scorpions are particularly dangerous and physicians should be aware that their stings may be encountered worldwide.
  • Symptoms present 1 to 8 hours after envenomation, with severe cases showing hyperreflexia, clonus, difficulty swallowing, and respiratory distress. The sting site may be unimpressive.
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Aquatic Antagonists: Lionfish (Pterois volitans)

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Aquatic Antagonists: Lionfish (Pterois volitans)

The lionfish (Pterois volitans) is a member of the Scorpaenidae family of venomous fish.1-3 Lionfish are an invasive species originally from the Indian and Pacific oceans and the Red Sea that now are widely found throughout tropical and temperate oceans in both hemispheres. They are a popular aquarium fish and were inadvertently introduced in the Atlantic Ocean in South Florida during the late 1980s to early 1990s.2,4 Since then, lionfish have spread into reef systems throughout the Atlantic Ocean, Caribbean Sea, and Gulf of Mexico in rapidly growing numbers, and they are now fo und all along the southeastern coast of the United States.5

Characteristics

Lionfish are brightly colored with red or maroon and white stripes, tentacles above the eyes and mouth, fan-shaped pectoral fins, and spines that deliver an especially painful venomous sting that often results in edema (Figure 1). They have 12 dorsal spines, 2 pelvic spines, and 3 anal spines.

Figure1
Figure 1. Lionfish (Pterois volitans).

Symptoms of Envenomation

As lionfish continue to spread to popular areas of the southeast Atlantic Ocean and Caribbean Sea, the chances of human contact with lionfish have increased. Lionfish stings are now the second most common marine envenomation injury after those caused by stingrays.4 Lionfish stings usually occur on the hands, fingers, or forearms during handling of the fish in ocean waters or in maintenance of aquariums. The mechanism of the venom apparatus is similar for all venomous fish. The spines have surrounding integumentary sheaths containing venom that rupture and inject venom when they penetrate the skin.6 The venom is a heat-labile neuromuscular toxin that causes edema (Figure 2), plasma extravasation, and thrombotic skin lesions.7

Figure2
Figure 2. Edema of the right hand from a lionfish sting.

Wounds are classified into 3 categories: grade I consists of local erythema/ecchymosis, grade II involves vesicle or blister formation, and grade III denotes wounds that develop local necrosis.8 The sting causes immediate and severe throbbing pain, often described as excruciating or rated 10/10 on a basic pain scale, typically radiating up the affected limb. Puncture sites may bleed and often have associated redness and swelling. Pain may last up to 24 hours. Occasionally, foreign material may be left in the wound requiring removal. There also is a chance of secondary infection at the wound site, and severe envenomation can lead to local tissue necrosis.8 Systemic effects can occur in some cases, including nausea, vomiting, sweating, headache, dizziness, disorientation, palpitations, and even syncope.9 However, to our knowledge there are no documented cases of human death from a lionfish sting. Anaphylactic reactions are possible and require immediate treatment.6

A study conducted in the French West Indies evaluated 117 patients with lionfish envenomation and found that victims experienced severe pain and local edema (100%), paresthesia (90%), abdominal cramps (62%), extensive edema (53%), tachycardia (34%), skin rash (32%), gastrointestinal tract symptoms (28%), syncope (27%), transient weakness (24%), hypertension (21%), hypotension (18%), and hyperthermia (9%).9 Complications included local infection (18%) such as skin abscess (5%), skin necrosis (3%), and septic arthritis (2%). Twenty-two percent of patients were hospitalized and 8% required surgery. Local infectious complications were more frequent in those with multiple stings (19%). The study concluded that lionfish now represent a major health threat in the West Indies.9 As lionfish numbers have grown, health care providers are seeing increasing numbers of envenomation cases in areas of the coastal southeastern United States and Caribbean associated with considerable morbidity. Providers in nonendemic areas also may see envenomation injuries due to the lionfish popularity in home aquariums.9

 

 

Management

Individuals with lionfish stings should immerse the affected area in hot but not scalding water. Those with more serious injuries should seek medical attention. Home remedies that are generally contraindicated include application of topical papain or meat tenderizer.10 Data on ice packs are mixed, but because the toxin is heat labile, the most effective initial step in treatment is immersion of the affected area in water (temperature, 40°C to 45°C) for 30 to 90 minutes.6 The hot water inactivates the heat-labile toxin, leading to near-complete symptomatic relief in 80% of cases and moderate relief in an additional 14%. Immersion time more than 90 minutes considerably increases the risk for burns. Children should always be monitored to prevent burns. If a patient has received a nerve block for analgesia, the wound should not be immersed in hot water to avoid burns to the skin. The wound should be meticulously cleaned with saline irrigation, and radiography or ultrasonography should be performed as deemed necessary to look for any retained foreign bodies.8 Patients may require parenteral or oral analgesia as well as careful follow-up to ensure proper healing.9 Systemic symptoms require supportive care. Venomous fish wounds typically are small and superficial. Empiric antibiotic therapy is not advised for superficial wounds but may be required for clinically infected wounds.8 Tetanus prophylaxis should be given as appropriate to all affected patients. It has been noted that blister fluid contains high concentrations of lionfish venom, and when present, it increases the likelihood of converting the injury from a grade II to grade III wound with tissue necrosis; therefore, blisters should be drained or excised to decrease the chances of subsequent tissue necrosis.11,12 If secondary infection such as cellulitis develops, antibiotics should be chosen to cover likely pathogens including common skin flora such as staphylococci and marine organisms such as Vibrio species. Wounds showing signs of infection should be cultured, with antibiotics adjusted according to sensitivities.5 Deeper wounds should be left open (unsutured) with a proper dressing to heal. Any wounds that involve vascular or joint structures require specialty management. Wounds involving joints may on occasion require surgical exploration and debridement.

Public Health Concerns

In an attempt to slow the growth of their population, human consumption of the fish has been encouraged. The lionfish toxin is inactivated by cooking, and the fish is considered a delicacy; however, a study in the Virgin Islands found that in areas with endemic ciguatera poisoning, 12% of lionfish carried amounts of the toxin above the level considered safe for consumption. This toxin is not inactivated by cooking or freezing and can lead to ciguatera fish poisoning for which there is no antidote and can be associated with prolonged neurotoxicity.13

Conclusion

As lionfish numbers continue to increase, physicians across multiple specialties and regions may see an increase in envenomation injuries. It is important that physicians are aware of how to recognize and treat lionfish stings, as prompt and comprehensive treatment provides benefit to the patient.

References
  1. Pterois volitans. Integrated Taxonomic Information System website. https://www.itis.gov/servlet/SingleRpt/SingleRpt?search_topic=TSN&search_value=166883#null. Accessed September 6, 2018.
  2. Morris JA Jr, Whitfield PE. Biology, Ecology, Control and Management of the Invasive Indopacific Lionfish: An Updated Integrated Assessment. Beaufort, NC: National Oceanic and Atmospheric Administration; 2009. http://aquaticcommons.org/2847/1/NCCOS_TM_99.pdf. Accessed September 6, 2018.
  3. Pterois volitans/miles. US Geological Survey website. https://nas.er.usgs.gov/queries/FactSheet.aspx?speciesID=963. Revised April 18, 2018. Accessed September 6, 2018.
  4. Diaz JH. Invasive lionfish (Pterois volitans) pose public health threats [published online August 15, 2015]. J La State Med Soc. 2015;167:166-171.
  5. Diaz JH. Marine Scorpaenidae envenomation in travelers: epidemiology, management, and prevention. J Travel Med. 2015;22:251-258.
  6. Hobday D, Chadha P, Din AH, et al. Denaturing the lionfish. Eplasty. 2016;16:ic20.
  7. Sáenz A, Ortiz N, Lomonte B, et al. Comparison of biochemical and cytotoxic activities of extracts obtained from dorsal spines and caudal fin of adult and juvenile non-native Caribbean lionfish (Pterois volitans/miles). Toxicon. 2017;137:158-167.
  8. Schult RF, Acquisto NM, Stair CK, et al. A case of lionfish envenomation presenting to an inland emergency department [published online August 13, 2017]. Case Rep Emerg Med. 2017;2017:5893563.
  9. Resiere D, Cerland L, De Haro L, et al. Envenomation by the invasive Pterois volitans species (lionfish) in the French West Indies—a two-year prospective study in Martinique. Clin Toxicol (Phila). 2016;54:313-318.
  10. Auerbach PS. Envenomation by aquatic vertebrates. In: Auerback PS. Wilderness Medicine. 5th ed. Philadelphia, PA: Mosby Elsevier; 2007:1740-1741.
  11. Auerbach PS, McKinney HE, Rees RE, et al. Analysis of vesicle fluid following the sting of the lionfish, Pterois volitans. Toxicon. 1987;25:1350-1353.
  12. Patel MR, Wells S. Lionfish envenomation of the hand. J Hand Surg Am. 1993;18:523-525.
  13. Robertson A, Garcia AC, Quintana HA, et al. Invasive lionfish (Pterois volitans): a potential human health threat for Ciguatera fish poisoning in tropical waters. Marine Drugs. 2014;12:88-97.
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From the Department of Dermatology, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Henry Tomlinson, MD, 2194 Parkway Dr, Charleston, SC 29412 (tomlinson.henry@gmail.com).

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From the Department of Dermatology, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Henry Tomlinson, MD, 2194 Parkway Dr, Charleston, SC 29412 (tomlinson.henry@gmail.com).

Author and Disclosure Information

From the Department of Dermatology, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Henry Tomlinson, MD, 2194 Parkway Dr, Charleston, SC 29412 (tomlinson.henry@gmail.com).

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Related Articles

The lionfish (Pterois volitans) is a member of the Scorpaenidae family of venomous fish.1-3 Lionfish are an invasive species originally from the Indian and Pacific oceans and the Red Sea that now are widely found throughout tropical and temperate oceans in both hemispheres. They are a popular aquarium fish and were inadvertently introduced in the Atlantic Ocean in South Florida during the late 1980s to early 1990s.2,4 Since then, lionfish have spread into reef systems throughout the Atlantic Ocean, Caribbean Sea, and Gulf of Mexico in rapidly growing numbers, and they are now fo und all along the southeastern coast of the United States.5

Characteristics

Lionfish are brightly colored with red or maroon and white stripes, tentacles above the eyes and mouth, fan-shaped pectoral fins, and spines that deliver an especially painful venomous sting that often results in edema (Figure 1). They have 12 dorsal spines, 2 pelvic spines, and 3 anal spines.

Figure1
Figure 1. Lionfish (Pterois volitans).

Symptoms of Envenomation

As lionfish continue to spread to popular areas of the southeast Atlantic Ocean and Caribbean Sea, the chances of human contact with lionfish have increased. Lionfish stings are now the second most common marine envenomation injury after those caused by stingrays.4 Lionfish stings usually occur on the hands, fingers, or forearms during handling of the fish in ocean waters or in maintenance of aquariums. The mechanism of the venom apparatus is similar for all venomous fish. The spines have surrounding integumentary sheaths containing venom that rupture and inject venom when they penetrate the skin.6 The venom is a heat-labile neuromuscular toxin that causes edema (Figure 2), plasma extravasation, and thrombotic skin lesions.7

Figure2
Figure 2. Edema of the right hand from a lionfish sting.

Wounds are classified into 3 categories: grade I consists of local erythema/ecchymosis, grade II involves vesicle or blister formation, and grade III denotes wounds that develop local necrosis.8 The sting causes immediate and severe throbbing pain, often described as excruciating or rated 10/10 on a basic pain scale, typically radiating up the affected limb. Puncture sites may bleed and often have associated redness and swelling. Pain may last up to 24 hours. Occasionally, foreign material may be left in the wound requiring removal. There also is a chance of secondary infection at the wound site, and severe envenomation can lead to local tissue necrosis.8 Systemic effects can occur in some cases, including nausea, vomiting, sweating, headache, dizziness, disorientation, palpitations, and even syncope.9 However, to our knowledge there are no documented cases of human death from a lionfish sting. Anaphylactic reactions are possible and require immediate treatment.6

A study conducted in the French West Indies evaluated 117 patients with lionfish envenomation and found that victims experienced severe pain and local edema (100%), paresthesia (90%), abdominal cramps (62%), extensive edema (53%), tachycardia (34%), skin rash (32%), gastrointestinal tract symptoms (28%), syncope (27%), transient weakness (24%), hypertension (21%), hypotension (18%), and hyperthermia (9%).9 Complications included local infection (18%) such as skin abscess (5%), skin necrosis (3%), and septic arthritis (2%). Twenty-two percent of patients were hospitalized and 8% required surgery. Local infectious complications were more frequent in those with multiple stings (19%). The study concluded that lionfish now represent a major health threat in the West Indies.9 As lionfish numbers have grown, health care providers are seeing increasing numbers of envenomation cases in areas of the coastal southeastern United States and Caribbean associated with considerable morbidity. Providers in nonendemic areas also may see envenomation injuries due to the lionfish popularity in home aquariums.9

 

 

Management

Individuals with lionfish stings should immerse the affected area in hot but not scalding water. Those with more serious injuries should seek medical attention. Home remedies that are generally contraindicated include application of topical papain or meat tenderizer.10 Data on ice packs are mixed, but because the toxin is heat labile, the most effective initial step in treatment is immersion of the affected area in water (temperature, 40°C to 45°C) for 30 to 90 minutes.6 The hot water inactivates the heat-labile toxin, leading to near-complete symptomatic relief in 80% of cases and moderate relief in an additional 14%. Immersion time more than 90 minutes considerably increases the risk for burns. Children should always be monitored to prevent burns. If a patient has received a nerve block for analgesia, the wound should not be immersed in hot water to avoid burns to the skin. The wound should be meticulously cleaned with saline irrigation, and radiography or ultrasonography should be performed as deemed necessary to look for any retained foreign bodies.8 Patients may require parenteral or oral analgesia as well as careful follow-up to ensure proper healing.9 Systemic symptoms require supportive care. Venomous fish wounds typically are small and superficial. Empiric antibiotic therapy is not advised for superficial wounds but may be required for clinically infected wounds.8 Tetanus prophylaxis should be given as appropriate to all affected patients. It has been noted that blister fluid contains high concentrations of lionfish venom, and when present, it increases the likelihood of converting the injury from a grade II to grade III wound with tissue necrosis; therefore, blisters should be drained or excised to decrease the chances of subsequent tissue necrosis.11,12 If secondary infection such as cellulitis develops, antibiotics should be chosen to cover likely pathogens including common skin flora such as staphylococci and marine organisms such as Vibrio species. Wounds showing signs of infection should be cultured, with antibiotics adjusted according to sensitivities.5 Deeper wounds should be left open (unsutured) with a proper dressing to heal. Any wounds that involve vascular or joint structures require specialty management. Wounds involving joints may on occasion require surgical exploration and debridement.

Public Health Concerns

In an attempt to slow the growth of their population, human consumption of the fish has been encouraged. The lionfish toxin is inactivated by cooking, and the fish is considered a delicacy; however, a study in the Virgin Islands found that in areas with endemic ciguatera poisoning, 12% of lionfish carried amounts of the toxin above the level considered safe for consumption. This toxin is not inactivated by cooking or freezing and can lead to ciguatera fish poisoning for which there is no antidote and can be associated with prolonged neurotoxicity.13

Conclusion

As lionfish numbers continue to increase, physicians across multiple specialties and regions may see an increase in envenomation injuries. It is important that physicians are aware of how to recognize and treat lionfish stings, as prompt and comprehensive treatment provides benefit to the patient.

The lionfish (Pterois volitans) is a member of the Scorpaenidae family of venomous fish.1-3 Lionfish are an invasive species originally from the Indian and Pacific oceans and the Red Sea that now are widely found throughout tropical and temperate oceans in both hemispheres. They are a popular aquarium fish and were inadvertently introduced in the Atlantic Ocean in South Florida during the late 1980s to early 1990s.2,4 Since then, lionfish have spread into reef systems throughout the Atlantic Ocean, Caribbean Sea, and Gulf of Mexico in rapidly growing numbers, and they are now fo und all along the southeastern coast of the United States.5

Characteristics

Lionfish are brightly colored with red or maroon and white stripes, tentacles above the eyes and mouth, fan-shaped pectoral fins, and spines that deliver an especially painful venomous sting that often results in edema (Figure 1). They have 12 dorsal spines, 2 pelvic spines, and 3 anal spines.

Figure1
Figure 1. Lionfish (Pterois volitans).

Symptoms of Envenomation

As lionfish continue to spread to popular areas of the southeast Atlantic Ocean and Caribbean Sea, the chances of human contact with lionfish have increased. Lionfish stings are now the second most common marine envenomation injury after those caused by stingrays.4 Lionfish stings usually occur on the hands, fingers, or forearms during handling of the fish in ocean waters or in maintenance of aquariums. The mechanism of the venom apparatus is similar for all venomous fish. The spines have surrounding integumentary sheaths containing venom that rupture and inject venom when they penetrate the skin.6 The venom is a heat-labile neuromuscular toxin that causes edema (Figure 2), plasma extravasation, and thrombotic skin lesions.7

Figure2
Figure 2. Edema of the right hand from a lionfish sting.

Wounds are classified into 3 categories: grade I consists of local erythema/ecchymosis, grade II involves vesicle or blister formation, and grade III denotes wounds that develop local necrosis.8 The sting causes immediate and severe throbbing pain, often described as excruciating or rated 10/10 on a basic pain scale, typically radiating up the affected limb. Puncture sites may bleed and often have associated redness and swelling. Pain may last up to 24 hours. Occasionally, foreign material may be left in the wound requiring removal. There also is a chance of secondary infection at the wound site, and severe envenomation can lead to local tissue necrosis.8 Systemic effects can occur in some cases, including nausea, vomiting, sweating, headache, dizziness, disorientation, palpitations, and even syncope.9 However, to our knowledge there are no documented cases of human death from a lionfish sting. Anaphylactic reactions are possible and require immediate treatment.6

A study conducted in the French West Indies evaluated 117 patients with lionfish envenomation and found that victims experienced severe pain and local edema (100%), paresthesia (90%), abdominal cramps (62%), extensive edema (53%), tachycardia (34%), skin rash (32%), gastrointestinal tract symptoms (28%), syncope (27%), transient weakness (24%), hypertension (21%), hypotension (18%), and hyperthermia (9%).9 Complications included local infection (18%) such as skin abscess (5%), skin necrosis (3%), and septic arthritis (2%). Twenty-two percent of patients were hospitalized and 8% required surgery. Local infectious complications were more frequent in those with multiple stings (19%). The study concluded that lionfish now represent a major health threat in the West Indies.9 As lionfish numbers have grown, health care providers are seeing increasing numbers of envenomation cases in areas of the coastal southeastern United States and Caribbean associated with considerable morbidity. Providers in nonendemic areas also may see envenomation injuries due to the lionfish popularity in home aquariums.9

 

 

Management

Individuals with lionfish stings should immerse the affected area in hot but not scalding water. Those with more serious injuries should seek medical attention. Home remedies that are generally contraindicated include application of topical papain or meat tenderizer.10 Data on ice packs are mixed, but because the toxin is heat labile, the most effective initial step in treatment is immersion of the affected area in water (temperature, 40°C to 45°C) for 30 to 90 minutes.6 The hot water inactivates the heat-labile toxin, leading to near-complete symptomatic relief in 80% of cases and moderate relief in an additional 14%. Immersion time more than 90 minutes considerably increases the risk for burns. Children should always be monitored to prevent burns. If a patient has received a nerve block for analgesia, the wound should not be immersed in hot water to avoid burns to the skin. The wound should be meticulously cleaned with saline irrigation, and radiography or ultrasonography should be performed as deemed necessary to look for any retained foreign bodies.8 Patients may require parenteral or oral analgesia as well as careful follow-up to ensure proper healing.9 Systemic symptoms require supportive care. Venomous fish wounds typically are small and superficial. Empiric antibiotic therapy is not advised for superficial wounds but may be required for clinically infected wounds.8 Tetanus prophylaxis should be given as appropriate to all affected patients. It has been noted that blister fluid contains high concentrations of lionfish venom, and when present, it increases the likelihood of converting the injury from a grade II to grade III wound with tissue necrosis; therefore, blisters should be drained or excised to decrease the chances of subsequent tissue necrosis.11,12 If secondary infection such as cellulitis develops, antibiotics should be chosen to cover likely pathogens including common skin flora such as staphylococci and marine organisms such as Vibrio species. Wounds showing signs of infection should be cultured, with antibiotics adjusted according to sensitivities.5 Deeper wounds should be left open (unsutured) with a proper dressing to heal. Any wounds that involve vascular or joint structures require specialty management. Wounds involving joints may on occasion require surgical exploration and debridement.

Public Health Concerns

In an attempt to slow the growth of their population, human consumption of the fish has been encouraged. The lionfish toxin is inactivated by cooking, and the fish is considered a delicacy; however, a study in the Virgin Islands found that in areas with endemic ciguatera poisoning, 12% of lionfish carried amounts of the toxin above the level considered safe for consumption. This toxin is not inactivated by cooking or freezing and can lead to ciguatera fish poisoning for which there is no antidote and can be associated with prolonged neurotoxicity.13

Conclusion

As lionfish numbers continue to increase, physicians across multiple specialties and regions may see an increase in envenomation injuries. It is important that physicians are aware of how to recognize and treat lionfish stings, as prompt and comprehensive treatment provides benefit to the patient.

References
  1. Pterois volitans. Integrated Taxonomic Information System website. https://www.itis.gov/servlet/SingleRpt/SingleRpt?search_topic=TSN&search_value=166883#null. Accessed September 6, 2018.
  2. Morris JA Jr, Whitfield PE. Biology, Ecology, Control and Management of the Invasive Indopacific Lionfish: An Updated Integrated Assessment. Beaufort, NC: National Oceanic and Atmospheric Administration; 2009. http://aquaticcommons.org/2847/1/NCCOS_TM_99.pdf. Accessed September 6, 2018.
  3. Pterois volitans/miles. US Geological Survey website. https://nas.er.usgs.gov/queries/FactSheet.aspx?speciesID=963. Revised April 18, 2018. Accessed September 6, 2018.
  4. Diaz JH. Invasive lionfish (Pterois volitans) pose public health threats [published online August 15, 2015]. J La State Med Soc. 2015;167:166-171.
  5. Diaz JH. Marine Scorpaenidae envenomation in travelers: epidemiology, management, and prevention. J Travel Med. 2015;22:251-258.
  6. Hobday D, Chadha P, Din AH, et al. Denaturing the lionfish. Eplasty. 2016;16:ic20.
  7. Sáenz A, Ortiz N, Lomonte B, et al. Comparison of biochemical and cytotoxic activities of extracts obtained from dorsal spines and caudal fin of adult and juvenile non-native Caribbean lionfish (Pterois volitans/miles). Toxicon. 2017;137:158-167.
  8. Schult RF, Acquisto NM, Stair CK, et al. A case of lionfish envenomation presenting to an inland emergency department [published online August 13, 2017]. Case Rep Emerg Med. 2017;2017:5893563.
  9. Resiere D, Cerland L, De Haro L, et al. Envenomation by the invasive Pterois volitans species (lionfish) in the French West Indies—a two-year prospective study in Martinique. Clin Toxicol (Phila). 2016;54:313-318.
  10. Auerbach PS. Envenomation by aquatic vertebrates. In: Auerback PS. Wilderness Medicine. 5th ed. Philadelphia, PA: Mosby Elsevier; 2007:1740-1741.
  11. Auerbach PS, McKinney HE, Rees RE, et al. Analysis of vesicle fluid following the sting of the lionfish, Pterois volitans. Toxicon. 1987;25:1350-1353.
  12. Patel MR, Wells S. Lionfish envenomation of the hand. J Hand Surg Am. 1993;18:523-525.
  13. Robertson A, Garcia AC, Quintana HA, et al. Invasive lionfish (Pterois volitans): a potential human health threat for Ciguatera fish poisoning in tropical waters. Marine Drugs. 2014;12:88-97.
References
  1. Pterois volitans. Integrated Taxonomic Information System website. https://www.itis.gov/servlet/SingleRpt/SingleRpt?search_topic=TSN&search_value=166883#null. Accessed September 6, 2018.
  2. Morris JA Jr, Whitfield PE. Biology, Ecology, Control and Management of the Invasive Indopacific Lionfish: An Updated Integrated Assessment. Beaufort, NC: National Oceanic and Atmospheric Administration; 2009. http://aquaticcommons.org/2847/1/NCCOS_TM_99.pdf. Accessed September 6, 2018.
  3. Pterois volitans/miles. US Geological Survey website. https://nas.er.usgs.gov/queries/FactSheet.aspx?speciesID=963. Revised April 18, 2018. Accessed September 6, 2018.
  4. Diaz JH. Invasive lionfish (Pterois volitans) pose public health threats [published online August 15, 2015]. J La State Med Soc. 2015;167:166-171.
  5. Diaz JH. Marine Scorpaenidae envenomation in travelers: epidemiology, management, and prevention. J Travel Med. 2015;22:251-258.
  6. Hobday D, Chadha P, Din AH, et al. Denaturing the lionfish. Eplasty. 2016;16:ic20.
  7. Sáenz A, Ortiz N, Lomonte B, et al. Comparison of biochemical and cytotoxic activities of extracts obtained from dorsal spines and caudal fin of adult and juvenile non-native Caribbean lionfish (Pterois volitans/miles). Toxicon. 2017;137:158-167.
  8. Schult RF, Acquisto NM, Stair CK, et al. A case of lionfish envenomation presenting to an inland emergency department [published online August 13, 2017]. Case Rep Emerg Med. 2017;2017:5893563.
  9. Resiere D, Cerland L, De Haro L, et al. Envenomation by the invasive Pterois volitans species (lionfish) in the French West Indies—a two-year prospective study in Martinique. Clin Toxicol (Phila). 2016;54:313-318.
  10. Auerbach PS. Envenomation by aquatic vertebrates. In: Auerback PS. Wilderness Medicine. 5th ed. Philadelphia, PA: Mosby Elsevier; 2007:1740-1741.
  11. Auerbach PS, McKinney HE, Rees RE, et al. Analysis of vesicle fluid following the sting of the lionfish, Pterois volitans. Toxicon. 1987;25:1350-1353.
  12. Patel MR, Wells S. Lionfish envenomation of the hand. J Hand Surg Am. 1993;18:523-525.
  13. Robertson A, Garcia AC, Quintana HA, et al. Invasive lionfish (Pterois volitans): a potential human health threat for Ciguatera fish poisoning in tropical waters. Marine Drugs. 2014;12:88-97.
Issue
Cutis - 102(4)
Issue
Cutis - 102(4)
Page Number
232-234
Page Number
232-234
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Aquatic Antagonists: Lionfish (Pterois volitans)
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Aquatic Antagonists: Lionfish (Pterois volitans)
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Practice Points

  • Lionfish are now found all along the southeastern coast of the United States. Physicians may see an increase in envenomation injuries.
  • Treat lionfish envenomation with immediate immersion in warm water (temperature, 40°C to 45°C) for 30 to 90 minutes to deactivate heat-labile toxin.
  • Infected wounds should be treated with antibiotics for common skin flora and marine organisms such as Vibrio species.
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