Approximately 3500 species of centipedes are found in the class Chilopoda, phylum Arthropoda. They are among the less well-studied arthropods. Centipedes are elongated multisegmented arthropods with a single pair of legs on each body segment. They are distributed widely, being present on every continent except Antarctica, and are especially common in warm temperate and tropical regions. Centipedes spend much of their time underground or in rock piles and usually come out at night to actively hunt their prey. They are capable of very fast movement when exposed. The most dangerous species belong to the genus Scolopendra, with the largest members (Scolopendra gigantea) reaching lengths of 26 cm. See the image below.
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Giant desert centipede. Photo by Michael Cardwell.
The venom delivery apparatus consists of a modified pair of front legs (ie, forcipules) just behind the mandibles. Venom is produced in a gland, generally located at the base of each forcipule, and is injected through ducts when the forcipules are driven into the victim's tissues.
Centipede venoms have not been studied as extensively as many spider and scorpion venoms, but they do contain a wide array of components, including 5-hydroxytryptamine (serotonin), histamine, metalloproteases, hyaluronidase, pore-forming toxins, CAP proteins, and ion channel modulators.[1, 2] In addition, some centipede venoms may cause endogenous release of histamine.
In addition to venom, some species exude defensive substances from glands found along the body segments. These secretions are usually nontoxic to humans, although at least one species of the genus Otostigmus secretes a vesicating substance.
While good data are sparse, in some regions of the world, centipede stings are not infrequent. Medeiros et al reported 98 such stings presenting to Hospital Vital Brazil, Butantan Institute, São Paulo, Brazil, between 1990 and 2007.[3]
Prognosis is excellent in the vast majority of cases of centipede envenomation. Most species are relatively innocuous.
Fatalities are extremely rare following centipede stings. A death was reported in a 7-year-old Filipino girl who was stung on the head by a centipede of the large species Scolopendra subspinipes, which may reach 23 cm in length.
A case of electrocardiographic (ECG) changes suggestive of ischemia has been reported in a 60-year-old man after a sting by a 12-cm centipede in Turkey.[4] While there was a slight associated elevation in serum CK-MB and myoglobin, troponin I, troponin T, and delayed exercise stress testing were all normal, and the ECG returned to normal a few hours later. Another 20-year-old man in Turkey presented to an ED with chest pain approximately 24 hours after a reported centipede sting.[5] His ECG revealed inferior ST-segment elevation, and he had a positive rise in his CK-MB and troponin T levels. His echocardiogram was normal, and he did well after conservative therapy (without thrombolysis or angioplasty). Delayed coronary angiography revealed normal coronary arteries. The patient was noted to be "completely symptom free" at 17 months. He was felt to have suffered a myocardial infarction, possibly related to coronary vasospasm, inflammatory changes, or multifactorial effects.
A 22-year-old man without cardiac risk factors suffered an apparent ST elevation myocardial infarction following a purported centipede sting in India.[6] The victim was stung on the finger, had immediate pain and swelling, and, 2 hours later, developed chest pain with nausea, vomiting, and diaphoresis. On presentation to the hospital 14 hours after the injury, his ECG was consistent with anterior ST elevation myocardial infarction. He was treated with nitrates and morphine. His creatine kinase MB level was elevated and his troponin-I was 13.2 µg/L. Echocardiography revealed anterior wall hypokinesis. Cardiac catheterization revealed normal coronary arteries. Three days later, his ECG and echocardiography returned to normal.
A 31-year-old man in Turkey was stung on the foot by a 10-12 cm golden-colored centipede.[7] He presented to an emergency department approximately 1 hour after the sting, complaining of foot pain and swelling. Shortly after arrival, he developed squeezing chest pain radiating to his left arm. While an electrocardiogram (ECG) was being obtained, he went into cardiac arrest. He was successfully resuscitated within 5 minutes and was treated with aspirin, heparin, and intravenous nitroglycerin. His ECG demonstrated inferior-posterior acute myocardial infarction, and an echocardiogram revealed akinesis in the inferior and posterior segments of his left ventricle, as well as hypokinesis of the lateral wall. As he continued to have chest pain and ST elevations despite conservative treatment, the decision was made to administer 100 mg of tissue plasminogen activator (t-PA). After 90 minutes, the patient’s symptoms resolved and his ECG normalized. His troponin I peaked at 7.23 ng/mL at 12 hours. He was transferred to a facility capable of performing a cardiac catheterization, which revealed normal coronaries. Follow-up echocardiogram demonstrated only slight hypokinesis of the inferior wall of the left ventricle and an ejection fraction of 65%. His only cardiac risk factor was a smoking history. The authors of this report suspect his myocardial infarction and arrest were due to venom-induced coronary vasospasm leading to an acute coronary thrombosis.
A case of rhabdomyolysis complicated by compartment syndrome and acute renal failure requiring temporary hemodialysis has been reported following the sting of the giant desert centipede, Scolopendra heros.[8] Prolonged, isolated proteinuria without any other evidence of renal dysfunction has also been reported in a young female following Scolopendra sting.
Langley reported 5 centipede-related deaths recorded in the National Center for Health Statistics[9] CDC Wonder database in the United States between 1991 and 2001, though he had no supporting documentation to confirm that these deaths were truly due to centipedes.
The history of a centipede sting is usually straightforward. The victim (frequently a gardener) typically sees the creature. Patients may note the following:
The following laboratory studies may be appropriate for centipede envenomation:
A bedside urine test for proteinuria is reasonable.[11] The same test can detect myoglobinuria secondary to rhabdomyolysis in patients with significant swelling and pain of the affected extremity.
If evidence of rhabdomyolysis is present, serum electrolytes, CPK, and renal function studies should be obtained.
A complete blood cell count, if done, may reveal a neutrophilic leukocytosis.
An ECG should be obtained if the patient has a history of cardiac disease, chest pain, palpitations, or if there is any evidence of hemodynamic instability following centipede sting.
If the ECG is abnormal in the setting of chest pain following centipede sting, serum cardiac biomarkers (eg, troponins) should be checked.
If swelling of the affected extremity is severe and a compartment syndrome is suspected, intracompartmental pressures should be objectively assessed.
If a compartment syndrome is diagnosed, the limb should be elevated and plans should be made for fasciotomy. A brief trial of intravenous mannitol can be instituted in an effort to reduce pressures before surgery.
No specific first aid measures are available for centipede stings. Seek medical care if pain persists or systemic symptoms occur. Local application of ice may reduce some of the discomfort; however, others have anecdotally found that local heat application or immersion in hot (nonscalding) water is more comforting.[12, 13] This may reflect the thermolabile properties of a number of centipede venom constituents.
Management of centipede stings is entirely supportive.
Pain may be managed with systemic analgesics, as necessary. Pain may be managed with local injectable anesthetics (eg, lidocaine, bupivacaine). These can be injected locally or used in performing a regional nerve block. A standard text should be consulted regarding techniques of regional anesthesia.
Tetanus status should be updated as needed.
Prophylactic antibiotics are not necessary, but secondary infections should be cultured and treated with appropriate antibiotics (to cover gram-positive bacteria).
Antihistamines can be used for patients with significant pruritus.
Patients should be observed for approximately 4 hours for evidence of systemic toxicity.
Patients presenting with anaphylaxis should be managed in standard fashion (Anaphylaxis).
If soft tissue swelling is severe or rhabdomyolysis is evident after centipede envenomation, the patient should be admitted and observed for development of compartment syndrome and management of myoglobinuria as needed.
Most centipede stings are minor and do well with conservative management. In rare, more severe cases, consultation with a regional poison control center specialist may be helpful. Occasionally, a specialist will need to be involved, such as the following:
Surgeon: When there is concern for a possible developing compartment syndrome (for compartmental pressure testing and, if elevated, fasciotomy)
Cardiologist: If the patient has findings concerning for cardiac complications
Nephrologist: If rhabdomyolysis occurs and is complicated by acute renal injury
Clinical Context:
Acetaminophen is the drug of choice to treat pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.
Clinical Context:
This is indicated for the treatment of mild to moderate pain in adults. Codeine should be avoided in children because of variable metabolism and elevated risk of adverse effects, per a 2016 American Academy of Pediatrics Clinical Report.
Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who have sustained centipede envenomations.
Clinical Context:
This agent is used for symptomatic relief of allergic symptoms caused by histamines released in response to allergens. Diphenhydramine is effective and widely available.
Antihistamines prevent histamine response in sensory nerve endings and blood vessels; they are more effective in preventing a histamine response than in reversing it. H2 antihistamines are useful in the treatment of anaphylactic reactions when used concomitantly with H1 antagonists. Many H2 blockers are available.
Anesthetics are indicated for pain relief. They stabilize the neuronal membrane and prevent the initiation and transmission of nerve impulses, thereby producing local anesthetic action.
Clinical Context:
Ibuprofen is usually the drug of choice for the treatment of mild to moderate pain if no contraindications exist. It inhibits inflammatory reactions and pain, probably by decreasing prostaglandin synthesis.
Clinical Context:
Ketoprofen is used for the relief of mild to moderate pain and inflammation. Small dosages are initially indicated in small or elderly patients and in those with renal or liver disease. Doses greater than 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe the patient for response.
Clinical Context:
Flurbiprofen may inhibit cyclooxygenase, causing the inhibition of prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.
Clinical Context:
Naproxen is used for the relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.
Clinical Context:
Indomethacin is rapidly absorbed. Metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. It inhibits prostaglandin synthesis.
Clinical Context:
Piroxicam decreases the activity of cyclooxygenase, which, in turn, inhibits prostaglandin synthesis. These effects decrease the formation of inflammatory mediators.
NSAIDs are most commonly used to relieve mild to moderate pain. Although effects of NSAIDs in the treatment of pain tend to be patient specific, ibuprofen is usually the drug of choice for initial therapy. Other options include fenoprofen, flurbiprofen, mefenamic acid, ketoprofen, indomethacin, and piroxicam.
Clinical Context:
Mannitol is an osmotic diuretic. It inhibits tubular reabsorption of electrolytes by increasing the osmotic pressure of glomerular filtrate. It increases urinary output.
In the setting of documented compartment syndrome, osmotic diuretics such as mannitol may, when combined with elevation of the extremity, obviate the need for fasciotomy if pressures respond rapidly (within 1 h of administration).
Robert L Norris, MD, Professor Emeritus, Department of Emergency Medicine, Stanford University Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals
Disclosure: Nothing to disclose.
Gino A Farina, MD, FACEP, FAAEM, Professor of Emergency Medicine, Hofstra North Shore-LIJ School of Medicine at Hofstra University; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center
Disclosure: Nothing to disclose.
Chief Editor
Joe Alcock, MD, MS, Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center
Disclosure: Nothing to disclose.
Additional Contributors
Debra Slapper, MD, Physician, Southwest Washington Free Clinic System-Urgent Care; Former FEMA Physician and Military Contractor; Former Associate Professor, University of Miami, Leonard M Miller School of Medicine and University of South Florida Morsani College of Medicine
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