Critical Care Medicine
Poisonous plants and animals
- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- 4. Specific Treatment
- 5. Disease monitoring, follow-up and disposition
Special considerations for nursing and allied health professionals.
What's the evidence?
Plant toxicity, Jamaican vomiting sickness, anticholinergic plant poisoning, green tobacco sickness, snake envenomation, hymenoptera envenomation, Africanized honeybee envenomation, scorpion sting, black widow spider envenomation, brown recluse spider envenomation
Cardiac glycoside poisoning, cyanide poisoning, anaphylactic shock
1. Description of the problem
Poisoning almost always occurs as a result of ingestion of plant parts or liquid extracts of plants.
Although serious poisoning is not common, a wide variety of plant toxins may produce life-threatening effects. Clinical effects vary depending on the specific species of plant ingested. Some plants produce an identifiable toxidrome but others do not.
Patients may be treated supportively based on presenting symptoms, but if possible, accurate identification of the plant may aid in predicting symptoms and targeting therapy.
Jimsonweed (Datura spp)
Angel's trumpet (Brugmansia spp)
Mandrake (Mandragora officinarum)
Deadly nightshade (Aropa belladona)
Henbane (Hyoscyamus niger)
Azalea, rhododendron (Rhododendron spp)
Christmas rose, hellebore (Helleborus niger)
Common oleander (Nerium oleander)
Death camas (Zigadenus spp)
False hellebore (Veratrum spp)
Foxglove (Digitalis spp)
Lily of the valley (Convallaria majalis)
Monkshood, wolfsbane (Aconitum spp)
Red squill (Urginea maritima)
Yellow oleander (Thevetia peruviana)
Yew (Taxus spp)
Hemlock water dropwort (Oenanthe crocata)
Strychnine (Strychnos nux vomica)
Water hemlock (Cicuta spp)
Chinaberry (Melia azedarach)
Nightshade (Solanum spp)
Pokeweed (Phytolacca americana)
Hawaiian baby woodrose (Argyreia nervosa)
Morning glory (Ipomoea violacea)
Nutmeg (Myristica fragrans)
Peyote (Lophophora williamsii)
Autumn crocus, meadow saffron (Colchicum spp)
Glory lily (Gloriosa superba)
Mayapple (Podophyllum peltatum)
Golden chain tree (Laburnum anagyroides)
Mescal bean bush, Texas mountain laurel (Sophora secundiflora)
Poison hemlock (Conium maculatum)
Tobacco (Nicotiana spp, Lobelia spp)
American mistletoe (Phoradendron spp)
Black locust (Robinia spp)
Castor bean (Ricinus communis)
Jequirity bean, rosary pea (Abrus precatorius)
Physic nut (Jatropha spp)
North American snake, spider, scorpion and hymenoptera species are capable of producing life-threatening envenomation in humans. Patients are not always able to report a bite or sting, so the clinician must be aware of endemic species and the clinical syndromes associated with envenomation by each.
Centruroides sculpturatus, also known as the Arizona bark scorpion, is the only dangerous native scorpion. It is found primarily in Arizona, although may occur in bordering regions of surrounding states (California, Utah, New Mexico).
Important venomous spiders in the U.S. include the black widow and the brown recluse. Black widow spiders include several Latrodectus spp (L mactans, L variolus, L hesperus) and are found throughout the country. The brown recluse (Loxosceles reclusa) resides in the midwest region of the country.
The vast majority of venomous snake bites that occur in the U.S. are due to native pit vipers. These include rattlesnakes, copperheads and cottonmouths. All species produce generally similar envenomation syndromes and are treated with the same Crotalidae Polyvalent Fab antivenom, making species identification unnecessary in determining appropriate treatment.
Coral snakes, members of the Elapidae family of snakes, are the only dangerous native non-viper species. Bites by the Eastern and Texas coral snakes (Micrurus spp) are associated with life-threatening neurotoxicity, while bites by the Sonoran coral snake (Micruroides spp) are considered harmless to humans.
Non-native venomous snake bites occur each year due to the practice of keeping exotic animals as pets. In these cases, every effort must be made to identify the species of snake and obtain the appropriate specific antivenom to treat symptoms.
Gila monsters (Heloderma suspectum) are the only species of venomous lizard found in the U.S. and are native to the southwest. These are shy animals that bite only if handled.
Hymenoptera include bees, wasps, yellow jackets, hornets and ants. Single stings may result in anaphylaxis in susceptible individuals. Africanized honeybees (Apis mellifera scutellata) now inhabit the southern U.S. and are known for their aggressiveness. They attack in swarms of hundreds to thousands, producing illness in the victim as a result of venom load rather than allergy to venom.
Clinical Features of Plant Poisoning
Most symptoms resulting from ingestion of plants occur within minutes to a few hours of ingestion. Clinical features vary widely depending on the particular plant toxins ingested. Emesis of plant material may be a clue to the diagnosis in some patients.
Severe vomiting begins within two hours following ingestion of unripe fruit. Severe hypoglycemia develops, with confusion, seizures, and coma. Death may result within 48 hours.
Patients often present with altered level of consciousness, ranging from mild delirium to severe agitation or CNS depression. Hallucinations may be present. A classic anticholinergic toxidrome may be seen, with typical antimuscarinic symptoms including tachycardia, mydriasis, flushed skin, dry axilla, hyperthermia, urinary retention, and diminished bowel sounds. Rhabdomyolysis is common.
In general, most cardiotoxic plants produce vomiting, paresthesias, and salivation in addition to bradycardia and hypotension. Cardiac arrhythmias and cardiogenic shock are less common with plants containing grayanotoxins, veratrum alkaloids, or aconitine, which function as sodium channel activators, and more common with cardiac glycoside containing plants. CNS depression may occur with all.
Cardiac glycoside plant toxins produce a clinical syndrome identical to digoxin toxicity, with severe acute ingestion also resulting in hyperkalemia. A large variety of cardiac arrhythmias may develop. Aconitine-containing plant ingestions are known for producing torsades de pointes. The yew plant contains a sodium channel antagonist which may lead to wide complex arrhythmias.
Ingestion of cicutoxin-containing plants (Cicuta spp, Oenanthe spp) leads to vomiting, typically within an hour of ingestion. Salivation, abdominal pain, weakness, and altered consciousness may also occur. Tachycardia is common. Symptoms progress quickly to grand mal seizures, which are often recurrent. Secondary effects include rhabdomyolysis, hyperthermia, and aspiration pneumonia. Status epilepticus can lead to respiratory failure, cardiac arrhythmias, cerebral edema, and death.
Strychnine ingestion produces severe muscle spasms, often referred to as convulsions, without true seizure activity. Patients are awake and may exhibit hypertension, tachycardia, anxiety, hyperreflexia and opisthotonos in response to the slightest stimulation. Convulsions may be frequent and severe enough to lead to respiratory failure, hyperthermia, and cardiac arrest.
Ingestion of kernels or seeds of amygdalin-containing fruits may produce a clinical syndrome identical to that produced by inhalation of cyanide gas. Symptom onset occurs at least 20-30 minutes following ingestion and severity depends on the dose ingested. Symptoms may include vomiting, headache, weakness, confusion, dyspnea and metabolic acidosis. Severe cases may progress to coma, hypotension, circulatory failure, seizures, and death.
Many plant species may produce mild gastrointestinal effects when ingested. Ingestion of pokeweed may cause severe vomiting and diarrhea, which in some cases may be associated with electrolyte disturbances and hypotension. Immature fruit of a large variety of Solanum spp may lead to gastroenteritis in addition to hallucinations and delirium.
Vomiting is a frequent early event after ingestion of nutmeg or peyote. Hallucinations may occur, and sympathomimetic effects, including tachycardia, agitation, and mydriasis may also develop. Morning glory and Hawaiian baby woodrose toxicity produces symptoms similar to poisoning with LSD, including distortions of perception and euphoria or panic.
Early features of poisoning include severe vomiting and diarrhea with leukocytosis. This progresses over hours to several days to multiorgan system dysfunction with encephalopathy, acidosis, respiratory failure, cardiac arrhythmias, and bone marrow suppression. Peripheral neuropathy is common. Colchicine toxicity is also associated with alopecia.
Vomiting is an early and common feature of poisoning. Other early symptoms include salivation, diarrhea, headache, abdominal pain, tachycardia, hypertension, dizziness, muscle fasciculations, miosis, and confusion. Seizures may occur. These symptoms are followed by bradycardia and hypotension, CNS depression, muscular weakness and paralysis progressing to respiratory failure, cardiac arrhythmias, and death.
Ingestion of whole, undamaged seeds containing ricin or abrin typically does not produce symptoms. Mastication damages the hard shell and releases toxin, which may result in severe, but typically self-limited, gastroenteritis. Severe cases may exhibit elevation in transaminases, renal dysfunction, and electrolyte abnormalities. Rarely, seizures, CNS depression, shock, and death have occurred.
Clinical Features of Animal Envenomation
With most envenomations, patients will experience immediate pain regardless of the type of animal responsible for the bite or sting. Brown recluse spider bites may be an exception to this, as they often occur at night during sleep. Further clinical features depend on the particular envenomation.
Stings produce immediate pain without skin lesion or swelling. Pain may be transient and resolve quickly or progress to painful paresthesias which persist for hours to days.
Grade 1 describes mild envenomations with symptoms limited to local pain. Grade 2 describes presence of paresthesias distal from the sting site. Moderate to severe envenomations (Grade 3 and 4) are characterized by neuromuscular agitation, with involuntary twisting of the torso and flailing of the extremities, dysconjugate roving eye movements, hypersalivation, and fasciculations.
Early symptoms include vomiting and sensation of throat swelling. In severe cases, stridor, pulmonary edema, and hypoxia may occur. Complications include respiratory failure, aspiration pneumonia, and rhabdomyolysis.
Grade 3 describes presence of cranial nerve findings or neuromuscular agitation while Grade 4 describes presence of both.
Early findings include visible fang marks surrounded by a ring of erythema in many, but not all, cases. Common symptoms include severe pain and hypertension. Chest, abdomen, and back pain are frequent and may be due to muscle spasm or rigidity. Other symptoms include diaphoresis, anxiety, urinary retention, and eyelid edema. Rare cases of priapism and acute cardiomyopathy have been described.
Viscerocutaneous loxoscelism is associated with development of a dermal lesion within 8 hours of the spider bite. The bite is often not felt, but the lesion itself may be painful. Erythema and edema expand over days and surround a central, violaceous, sunken wound. Wounds may become large and healing may take weeks to months.
Systemic loxoscelism is characterized by fever, arthralgias, hemolysis, and coagulopathy. Vomiting and diarrhea, as well as a diffuse rash may develop. Renal failure, disseminated intravascular coagulation, and death may result in rare cases.
Coral snake envenomation produces neurotoxicity. Puncture wounds might not be identifiable and symptom onset may be delayed many hours. Effects may include paresthesias, ptosis, diplopia, weakness, and respiratory failure.
Pain and swelling occur at the bite site. Systemic anaphylactoid reactions may result in hypotension and angioedema severe enough to cause complete airway obstruction.
Vomiting and pain are common early findings, and may be followed by hypotension, respiratory distress, generalized edema, diarrhea, and decreased consciousness. Systemic effects include hemolysis, thrombocytopenia, disseminated intravascular coagulation, rhabdomyolysis, renal failure and, rarely, death.
Findings depend on the particular species of snake responsible for the envenomation. In general, vipers produce tissue swelling and necrosis as well as coagulopathy and thrombocytopenia. Elapids, which include cobras, mambas, and kraits, produce neurotoxicity. Overlap exists however, with some vipers also producing neurotoxicity and some elapids producing coagulopathy and tissue damage. Severe hemorrhage, shock, and circulatory failure may occur following bites by a large variety of snakes.
The first signs of a bite include visible puncture wounds and pain. Envenomation usually results in swelling at the bite site, which progresses proximally and can become severe. Tense, painful swelling can be difficult to distinguish clinically from compartment syndrome. Erythema may develop along lymphatics as venom is absorbed. Ecchymosis and hemorrhagic bullae develop over hours to days, especially with bites to digits.
Systemic symptoms may include tachycardia, metallic taste, vomiting, diarrhea, and hypotension, and when present, may serve as early indicators of an anaphylactoid response to venom with pending airway-threatening angioedema.
Neurotoxic effects occur with some species, but are typically limited to paresthesias or fasciculations. Envenomations by the Mojave rattlesnake may progress to paralysis and respiratory failure.
Common venom-induced hematologic effects include thrombocytopenia and hypofibrinogenemia with elevated prothrombin time. Bleeding is uncommon.
Rare patients develop compartment syndrome, disseminated intravascular coagulation, and severe hemorrhage. Deep necrosis may occur following bites to digits and lead to amputation of the digit.
Plant Poisoning: key management points.
Clinically ill patients should have their airway protected if needed, an accucheck performed to rule out hypoglycemia, IV access established, and IV fluid boluses administered. Hypotension may require the use of vasopressors.
If plant parts were ingested within the past hour and the patient is able to protect his or her airway and drink voluntarily, administration of 1 g/kg activated charcoal without sorbitol is appropriate.
Supportive care includes administration of IV fluids, antiemetics if needed, benzodiazepines as first-line therapy for seizures, atropine for symptomatic bradycardia, and vasopressors for hypotension.
If an anticholinergic toxidrome is present, consider administration of 1-2 mg IV physostigmine to reverse symptoms if no contraindications are present.
Attempt to identify the species of plant ingested to determine if antidotal therapy may be helpful.
Blood or urine samples should be obtained to analyze for plant toxins, but are immediately helpful in very few situations.
Animal Envenomation: key management points
Clinically ill patients should have their airway protected if needed. Have a low threshold for intubation and mechanical ventilation of any patient with angioedema, evidence of anaphylaxis, or snake bite to the head or neck area.
Intravenous access should be obtained and IV fluid boluses given, as well as antiemetics as needed.
Anaphylaxis or anaphylactoid reactions to venom are treated with epinephrine, antihistamines, and steroids. Continuous infusions of epinephrine may be required to treat anaphylaxis or hypotension.
Any constrictive dressings placed in the field should be removed and tetanus updated.
Determine if patient meets criteria for treatment with antivenom if an appropriate antivenom is available.
2. Emergency Management
Patients who present within 60 min of ingestion of plant material and who are able to protect their airway may be given a 1.0 g/kg dose of activated charcoal.
Assess airway and breathing. Patients with respiratory depression or inability to protect their airway should be intubated and mechanically ventilated. Significant hypoxia resulting from aspiration may also require intubation.
Establish IV access. If the patient has been vomiting, is hypotensive, or is otherwise clinically ill, IV fluid boluses should be administered.
Assess blood sugar and provide dextrose if patient is hypoglycemic.
Provide vasopressors if hypotension is present.
If patient is hyperthermic initiate cooling. Consider performing lumbar puncture if hyperthermia is not clearly due to plant poisoning.
Obtain an electrocardiogram to assess rhythm and intervals. If abnormal, consider sending a digoxin level to evaluate for cardiac glycoside plant poisoning.
Obtain a chest radiograph to look for signs of aspiration and to confirm placement of endotracheal tube.
Obtain blood for a complete blood count, electrolytes, liver and renal function tests, a creatinine phosphokinase, as well as additional blood and urine specimens to test for specific plant toxins.
Further diagnostics and management are dependent on the plant ingested (Diagnosis and Specific Treatment section).
If the diagnosis is unclear continue work up for other etiologies while providing supportive care.
Consider CT of the head if patient has altered sensorium or coma.
Assess airway and breathing. If there is evidence of airway edema, respiratory depression, or inability to protect the airway due to CNS depression the patient should be intubated and mechanically ventilated. Any early signs of swelling following snake bites to the head and neck area should prompt intubation.
Establish an IV and administer a fluid bolus. Patients with snake bite or massive honeybee envenomation may require multiple fluid boluses.
Anaphylactic reactions are treated in the usual fashion, with IM epinephrine, IV steroids, and IV antihistamines.
Hypotension should be treated with a continuous IV epinephrine infusion (titrate starting at 2-4 mcg/min).
If patient is clinically unstable or has significant co-morbidities, such as history of cardiac disease, obtain electrocardiogram and chest radiograph.
Severe muscle spasm, myoclonus, or agitation associated with black widow bites or scorpion stings may be treated with IV benzodiazepines.
Pain is treated with IV analgesics. Fentanyl is ideal since it is less likely than other opioids to produce mast cell degranulation. This avoids confusion as to the source of any rash that may develop (the venom, opioid, or antivenom).
Necessary laboratory evaluations vary depending on the envenomation. All patients with snake bite should have blood drawn for measurement of platelets, prothrombin time, and fibrinogen. Patients with scorpion or spider envenomations may not require blood work in some situations. Patients with massive honeybee envenomation should have a complete blood count, electrolytes, liver and renal function tests, creatinine phosphokinase, prothrombin time and fibrinogen checked.
Patients with snake bite to an extremity should have the extremity elevated above the level of the heart. Provide basic wound care and update tetanus prophylaxis. Remove any retained stingers.
Diagnosis of plant poisoning is based largely on history. If a patient is symptomatic and the species of plant is unknown, efforts should be made to obtain a sample or photograph of the plant in question for identification by a botanist. If a patient is vomiting or a nasogastric tube has been placed, aspiration of gastric contents may also allow identification of the species or provide fluid for laboratory analysis for a specific plant toxin.
Often, plant samples are not available and clinical symptoms and laboratory findings must be relied upon for diagnosis of the general class of poisonous plant and to guide management. If there is any doubt regarding the diagnosis of plant poisoning, a full investigation for alternative diagnoses should be pursued. Serum and urine samples may be sent for testing for specific plant toxins that correspond to the clinical picture, if assays for those particular toxins are available.
In some situations, as with poisoning by cardiac glycoside-containing plants, testing of body fluids can provide rapid results that may aid in acute management of the patient. An electrocardiogram may also help narrow the diagnosis to a particular class of plant toxins.
History of ingestion of unripe or canned fruit followed by severe hypoglycemia suggests this diagnosis.
Hypoglycin or methylene cyclopropyl acetic acid (MCPA) in blood or urine will confirm exposure but are often not present due to rapid clearance. Elevated urine and serum carnitines and elevated urine dicarboxylic acids support the diagnosis.
Differential diagnosis includes medium chain acyl-coenzyme A dehydrogenase (MCAD) deficiency, type II glutaric aciduria, sulfonylurea or insulin poisoning.
The diagnosis is supported by a history of exposure to plant parts or extract containing tropane alkaloids and the presence of clinical findings consistent with anticholinergic syndrome. Atropine and hyoscyamine may be identified by GCMS analysis of urine. Reversal of symptoms with administration of physostigmine will support the diagnosis but not confirm plant poisoning as the etiology.
Differential diagnosis includes encephalopathy due to other drugs and CNS infection.
History of ingestion of a plant or substance containing cardiac glycosides, grayanotoxins, veratrum alkaloids, aconitine, or taxine supports the diagnosis, as do clinical findings of vomiting, weakness, paresthesias, bradycardia, and cardiac arrhythmias. EKG may reveal bradycardia or cardiac arrhythmias. A prolonged QRS interval on EKG suggests taxine (yew) poisoning. Hyperkalemia suggests cardiac glycoside poisoning. Torsades de pointes suggests aconitine poisoning.
Serum can be tested for cross reaction with a digoxin assay to confirm exposure to cardiac glycoside-containing plants. LC-MS-MS has been used to detect taxine, grayanotoxins, aconitine alkaloids, and veratrum alkaloids in biological samples but is not widely available.
Differential diagnosis includes digoxin poisoning, beta blocker or calcium channel antagonist toxicity, sick sinus syndrome, primary cardiac arrhythmia, ischemic heart disease.
History of ingestion of plants or substances containing cicutoxin, oenanthotoxin, or strychnine prior to onset of seizures or convulsions is supportive. Diagnosis of strychnine poisoning may be confirmed by detection of strychnine in urine by GCMS.
Differential diagnosis includes primary seizure disorder, CNS trauma, CNS infection, exposure to sympathomimetic or other drug that lowers seizure threshold (isoniazid), withdrawal seizure.
History of ingestion of plant seeds or products containing amygdalin or other cyanogenic glycoside prior to symptom onset supports the diagnosis. Symptoms consistent with cyanide toxicity, including presence of a metabolic acidosis, that are reversed with administration of a cyanide antidote, is supportive. Diagnosis may be confirmed by detection of amygdalin in urine by GCMS. Elevated red blood cell cyanide concentrations will also support the diagnosis but will not be immediately available.
Differential diagnosis includes poisoning by hydrogen cyanide, hydrogen sulfide, or azide; poisoning by iron, metformin, isoniazid, or toxic alcohols; sepsis; cardiogenic shock; anaphylaxis.
History of ingestion of plant parts or extract prior to onset of symptoms, or emesis of plant material, supports the diagnosis. Purple stains on skin from handling berries may indicate exposure to pokeweed. A 'foamy' quality to diarrhea or presence of plasmacytosis also support the diagnosis of pokeweed poisoning.
Differential diagnosis includes other plant poisonings, including toxalbumins, inhibitors of mitosis, nicotinic plants, cardiotoxic plants, and convulsant plants. Infectious gastroenteritis, mushroom poisoning, acetaminophen toxicity, iron poisoning, caustic ingestion and poisoning by cholinergic agents should be considered.
History of ingestion of plants or products containing plant-derived hallucinogenic substances, preceeding symptom onset, supports the diagnosis. Lysergic acid amide (ergine) may be identified in urine or blood to confirm exposure to Hawaiian baby woodrose or morning glory seeds, but testing is not widely available. GCMS analysis of urine may detect metabolites of myristicin and elemicin following exposure to nutmeg, and mescaline following exposure to peyote.
Differential diagnosis includes psychosis, anticholinergic delirium and CNS infection.
History of ingestion of plant parts containing colchicine or podophyllotoxin prior to symptom onset supports the diagnosis. Gastroenteritis associated with early leukocytosis followed by pancytopenia is supportive of the diagnosis. Plasma colchicine levels may be obtained to confirm diagnosis.
Differential diagnosis includes gastroenteritis, septic shock, other drug-induced bone-marrow depression, cardiogenic shock.
History of exposure to plant parts or extracts containing nicotinic alkaloids along with symptoms consistent with stimulation of nicotinic receptors (such as vomiting, sweating, salivation, weakness) suggest the diagnosis. GCMS testing of urine or blood may identify nicotine and other alkaloids.
Differential diagnosis includes gastroenteritis, organophosphate poisoning, poisoning with succinylcholine or nondepolarizing neuromuscular blocking agents, snake venom neurotoxicity, botulism.
History of ingestion of plant parts or extracts containing ricin, abrin, or other toxalbumins prior to onset of symptoms consistent with poisoning, such as vomiting and diarrhea, support the diagnosis. Urine testing for ricinine, if available, may confirm exposure to ricin.
Differential diagnosis includes drug induced or infectious gastroenteritis.
History of a witnessed bite or sting followed by sudden onset of symptoms usually makes diagnosis of envenomation straight-forward. Diagnosis becomes more difficult when patients present unconscious or are too young to provide a history. It is important for physicians to be aware of clinical syndromes associated with bites or stings by endemic venomous species.
Envenomation may sometimes be difficult to distinguish clinically from anaphylactic shock, and in some circumstances both may be present simultaneously.
Diagnosis is most easily made with history of witnessed sting followed by symptoms consistent with envenomation. If scorpion or sting not witnessed, diagnosis is supported by sudden onset of pain or crying, followed by development over minutes to a few hours of a syndrome characterized by dysconjugate eye movements and neuromuscular agitation.
Resolution of symptoms following administration of antivenom against Centruroides scorpions strongly supports diagnosis. Venom levels are not widely available.
Differential diagnosis of bark scorpion envenomation includes meningitis, sympathomimetic poisoning, black widow envenomation and seizure.
History of a witnessed bite followed by symptoms consistent with latrodectism establish the diagnosis in most cases. If the bite was not witnessed, then sudden onset of local pain which progresses over minutes to hours to include symptoms such as diffuse pain, hypertension, and diaphoresis support this diagnosis. Presence of a small target lesion is also supportive.
Resolution of symptoms following administration of Latrodectus antivenom is highly supportive of this diagnosis. Venom levels are not widely available.
Differential diagnosis includes scorpion envenomation, sympathomimetic toxicity, surgical abdominal pathology.
Presence of a skin lesion, necrotic wound, or signs consistent with systemic loxoscelism (such as hemolysis) following a witnessed bite by a positively identified Loxosceles spider is diagnostic. If spider or bite not witnessed, this is a diagnosis of exclusion since loxoscelism is very rare and misdiagnosis is common. Venom levels are not currently available.
Differential diagnosis is very broad, with alternative diagnoses far more common than loxoscelism, and includes infection, neoplastic disease, vascular disease.
Development of neurotoxicity after a coral snake bite confirms diagnosis of envenomation. If bite was not witnessed but diagnosis is suspected, reversal of symptoms with antivenom supports the diagnosis, but failure of symptoms to reverse with antivenom does not rule out diagnosis. Venom levels are not widely available.
The differential diagnosis includes spinal cord hemorrhage or infarction, acute inflammatory demyelinating neuropathy, myasthenia gravis, poisoning by other neurotoxic snake species.
Gila monsters tend to hang on when they bite and can be very difficult to disengage. History of a bite followed by symptoms consistent with envenomation, such as angioedema or hypotension, confirm the diagnosis. Venom levels are not widely available.
History of bee swarming with presence of numerous puncture wounds confirms diagnosis. If patient unable to provide history diagnosis should be considered when retained stingers, numerous puncture wounds, and edema are present. This diagnosis is supported by laboratory findings of rhabdomyolysis, coagulopathy, thrombocytopenia, and renal injury.
The differential diagnosis of toxicity resulting from large venom load includes anaphylactic reaction to venom.
A history of bite by a captive exotic snake followed by swelling or systemic symptoms is usually necessary to confirm diagnosis of envenomation. If the patient is unconscious and history not available, non-native snake envenomation should be considered if systemic symptoms and a wound consistent with snake bite are present.
History of bite by rattlesnake, copperhead, or cottonmouth, with symptoms of swelling, hematologic, neurologic, or systemic toxicity confirms diagnosis. If snake not identified or history not available, then presence of puncture wounds and progressive swelling, thrombocytopenia, coagulopathy, or other signs consistent with envenomation all support the diagnosis. Reversal of hematologic toxicity following administration of Crotalidae antivenom very supportive of diagnosis.
Venom levels are not widely available.
4. Specific Treatment
Care is supportive (as described in Emergency Management section), although specific antidotes are available for some plant poisonings.
Hypoglycemia is managed with intravenous dextrose. Check blood glucose at least hourly and adjust continuous infusion of IV dextrose as needed to maintain euglycemia.
Administer antiemetics as needed for nausea and vomiting.
Seizures that persist after correction of hypoglycemia may be managed with benzodiazepines.
Agitation may be treated with benzodiazepines.
Delirium and/or agitation can be reversed with physostigmine. If there are no contraindications, adults may be treated with 1-2 mg IV physostigmine infused over 5 minutes. Children may receive 0.02 mg/kg IV.
If severe hyperthermia and agitation are present, intubate, sedate, and paralyze the patient, and provide cooling measures.
Urinary retention may necessitate Insertion of Foley catheter.
Hypovolemia resulting from vomiting and diarrhea should be treated with IV fluids.
Electrolyte abnormalities should be corrected.
If less than one hour since ingestion, patients who are able to drink and protect their airway may be given an oral dose of activated charcoal.
Digoxin-specific antibody fragments may reverse cardiac glycoside-associated arrhythmias and hyperkalemia. The ideal dose is unknown, may vary depending on the particular cardiac glycoside ingested, and is higher than that required to treat digoxin poisoning. A dose of 1200 mg (about 30 vials) was effective in reversing poisoning by yellow oleander in an RCT.
Bradyarrhythmias may be treated with atropine, followed by beta-adrenergic agents, and cardiac pacing if necessary.
Tachyarrhythmias may be treated with lidocaine.
Sodium Channel Toxins
Atropine may be administered to treat bradyarrhythmias. Beta-adrenergic agents may be used to increase heart rate. If these measures fail, temporary pacing may be necessary.
Hypotension is treated with IV fluids and beta-adrenergic agents.
Tachyarrhythmias may be treated with amiodarone, flecainide, or lidocaine.
Yew poisoning (Taxus spp) is associated with wide-complex arrhythmias that are resistant to traditional therapies, including anti-arrhythmic medications and sodium bicarbonate. Success has been reported following use of extracorporeal membrane oxygenation in the setting of life-threatening toxicity.
Benzodiazepines (diazepam or lorazepam) are first-line therapy to treat seizures. If seizures continue despite benzodiazepines, phenobarbital 20 mg/kg IV should be given. If there is any question of continued seizure activity, continuous EEG monitoring should be performed and additional benzodiazepines or barbiturates administered.
Intubation and mechanical ventilation is necessary for patients with persistent seizures, hyperthermia, or inability to protect their airway. Hyperthermia should also be treated immediately.
Hypotension should be treated initially with IV fluids followed by vasopressors.
Rhabdomyolysis may be managed with urinary alkalinization and IV fluid hydration.
Treatment is identical to that of cyanide poisoning. Cyanide antidotes include sodium nitrite followed by sodium thiosulfate or administration of hydroxocobalamin alone. Thiosulfate and hydroxocobalamin have also been used in combination.
The dose of sodium nitrite in adults is 300 mg IV (10 ml of a 3% solution) and the dose in children is 10 mg/kg (0.33 ml/kg of a 3% solution). This is followed by 12.5 g IV sodium thiosulfate in adults or 7 g/m2in children. These may be repeated at half the initial dose.
The adult dose of hydroxocobalamin is 5 g IV. This may be repeated one time. Pediatric dosing has not been studied in the United States, but doses of 70 mg/kg IV are given to children in other countries.
Care is entirely supportive, with administration of intravenous fluids, antiemetics, and correction of electrolyte abnormalities as needed.
Agitation or sympathomimetic symptoms may be treated with benzodiazepines as needed.
IV fluids and antiemetics may be used to treat nausea and vomiting.
Gastric decontamination measures include both gastric lavage, if the patient presents within an hour of plant ingestion, and activated charcoal. Use of multiple doses of activated charcoal may be considered in the absence of ileus since colchicine undergoes enterohepatic recirculation.
Antiemetics are given to treat nausea and vomiting and to improve tolerance of activated charcoal.
Care is supportive with IV fluid resuscitation and correction of electrolyte abnormalities. Hypotension may require treatment with vasopressors.
Monitor closely for cardiac arrhythmias, electrolyte disturbances, and bone marrow depression. Leukopenia may be treated with granulocyte colony stimulating factor.
Supportive care may include intubation and mechanical ventilation, hemodialysis for treatment of renal failure, blood transfusions, and/or antibiotics for treatment of secondary infections, depending on the clinical situation.
Care is supportive, with administration of IV fluids and antiemetics as needed to treat nausea and vomiting, and correction of electrolyte abnormalities.
Hypotension not responsive to IV fluids should be treated with vasopressors, such as norepinephrine.
Atropine may be given to reverse bradycardia.
Seizures may be treated initially with benzodiazepines. Persistent seizures are treated with phenobarbital.
Activated charcoal may be given to patients who present within an hour of ingestion of toxalbumin-containing plant parts.
Care is supportive, with use of IV fluids and antiemetics to treat nausea, vomiting, and diarrhea, and correction of electrolyte abnormalities.
Supportive care for envenomations includes early intubation and airway protection if there is evidence of airway obstruction or compromise, IV fluid resuscitation, management of hypotension with epinephrine, and pain control. Patients who present with evidence of anaphylaxis should be treated with IV antihistamines and steroids, as well as IV, IM, or SQ epinephrine, as needed.
Grade 1 and 2 envenomations, characterized by pain and paresthesias, may be treated with oral or parenteral analgesics, as needed.
Patients with low oxygen saturation, stridor, or other signs of respiratory compromise may require intubation and mechanical ventilation.
First-line treatment of agitation includes use of benzodiazepines, such as lorazepam or midazolam, and opioids, such as fentanyl or morphine. Typical weight-based doses of benzodiazepines may be used initially, but are often ineffective and should be titrated up to achieve effect.
IV fluid boluses may be given to treat dehydration related to increased motor activity and vomiting.
Grade 3 and 4 envenomations, characterized by neuromuscular agitation, hypersalivation, and sometimes respiratory distress, may be treated with anti-Centruroides antivenom (Anascorp®) if it is available.
Pain control may require use of IV opioid analgesics.
Anxiety and muscle spasm may be treated with IV benzodiazepines, such as diazepam or lorazepam.
IV fluids and antiemetics are given as needed.
Patients with continued severe pain or other signs of envenomation unresponsive to opioids and benzodiazepines are candidates for treatment with Antivenin Latrodectus mactans (Merck). This antivenom is a whole immunoglobulin product, with the potential to produce life-threatening anaphylactoid reactions. Since black widow envenomation is almost never life-threatening, a careful risk-benefit analysis should be done prior to use. It should be given in a closely monitored setting. The dose is one vial diluted in 50 ml saline solution and given as a slow infusion.
A Fab2 black widow spider antivenom is currently undergoing Phase 3 clinical trial.
Wounds related to the brown recluse spider bite typically do not require immediate intervention. Wound cleansing and tetanus prophylaxis as needed are appropriate. Prophylactic antibiotics are not indicated.
Large necrotic wounds that have fully demarcated may require grafting and should be referred to a plastic surgeon.
Treatment of systemic loxoscelism is mainly supportive and includes IV fluids and blood products as needed. Some experts recommend use of systemic corticosteroids for 5-10 days if significant hemolysis present.
Asymptomatic patients should be monitored for 24 hours for development of symptoms of neurotoxicity.
Signs of envenomation should prompt immediate treatment with North American Coral Snake Antivenin, if available. A typical starting dose is 3-5vials. If this antivenom can not be obtained, care is entirely supportive, with intubation and mechanical ventilation for any evidence of respiratory compromise.
Provide local wound care, including removal of any foreign bodies and devitalized tissue. Update tetanus prophylaxis if needed.
Adequate pain control may require IV opioid analgesics.
If systemic symptoms are present, administer IV fluid boluses.
Symptoms of anaphylactoid reaction to venom, such as hypotension and angioedema, are treated with epinephrine, antihistamines, and corticosteroids. A continuous infusion of epinephrine may be needed.
Severe angioedema may necessitate intubation. Be prepared to perform cricothyrotomy if necessary.
Stabilize airway if indicated and establish IV.
Anaphylaxis is treated in the standard fashion, with systemic antihistamines, corticosteroids, and epinephrine.
IV fluid boluses and antiemetics are given to patients with nausea, vomiting, and diarrhea.
Steroids and antihistamines may be given to patients with severe symptoms after a large number of stings.
Hypotension not responsive to IV fluid boluses should be treated with a continuous epinephrine infusion. Epinephrine is not required for patients who are not experiencing allergic symptoms and who are not hypotensive.
Stingers should be removed as soon as possible after the patient has been stabilized.
Care is otherwise supportive, addressing rhabdomyolysis, hemolysis, disseminated intravascular coagulation, and other complications as they occur.
Stabilize the airway as needed and establish an IV. Provide continuous cardiac monitoring.
Determine the exact species of snake responsible and attempt to locate specific antivenom if it exists. Resources for locating exotic antivenoms include local zoos, reptile exhibits, the local poison control center, and the Antivenom Index maintained by the University of Arizona College of Pharmacy.
If the patient is symptomatic and specific antivenom is available administer as per package insert.
If the patient is symptomatic and specific antivenom is not available, supportive care includes airway protection as needed, administration of IV fluids, administration of epinephrine to treat hypotension or angioedema, blood products to replace losses from hemorrhage, maintaining adequate urine flow, pain control.
It is recommended that the local poison control center be contacted regarding all patients with snake envenomation and cases be discussed with a medical toxicologist experienced in the management of snake bite.
Any constrictive dressings placed in the field should be removed. Ice should not be applied to the wound.
If asymptomatic, patients should be observed for at least 8 hours for signs of envenomation, such as swelling, thrombocytopenia, or coagulopathy.
Mild swelling at the bite site should be observed for progression. If progressing, antivenom is indicated. The initial dose for stable patients is 4-6 vials of Crotalidae Polyvalent Immune Fab in 250 ml saline to infuse over one hour. Further doses may be needed to control swelling. See PUBMED:21291549 for a treatment algorithm.
The envenomed extremity should be elevated above the level of the heart. Monitor progression of swelling every hour until no longer progressing and then monitor swelling every 4 hours for first 18-24 hours after control of swelling has been established with antivenom.
Thrombocytopenia, hypofibrinogenemia, and increased prothrombin time are also indications for treatment with antivenom. Even very low platelet counts may be treated with antivenom alone in the absence of bleeding and will usually rise quickly following antivenom. Patients with severe bleeding may require treatment with blood products in addition to antivenom.
Neurotoxicity is also an indication for antivenom administration.
Patients who present with angioedema, anaphylaxis, or bites near the head or neck may require emergent intubation. If severe shock or hemorrhage is present administer IV fluid boluses and provide antivenom. An initial dose of 8-12 vials of Crotalidae Polyvalent Immune Fab may be given over one hour to unstable patients. See PUBMED:21291549. Hypotension is treated with IV fluid boluses and epinephrine infusions.
Compartment syndrome is rare following pit viper envenomation but may occur. If suspected, determine intracompartmental pressures. Do not perform empiric fasciotomy, as typical findings following envenomation can mimic compartment syndrome. Mildly elevated compartment pressures may respond to antivenom. Highly elevated pressures will necessitate fasciotomy.
Some patients may benefit from maintenance doses of antivenom following initial control of the envenomation. Contact the poison control center (1-800-222-1222) to learn local practices and recommendations.
Hemorrhagic bullae may develop over the first 12 to 48 hours following the bite. Unroofing bullae may provide some pain relief and allow assessment of underlying tissue. If tissue underlying bullae is necrotic in appearance patient may benefit from referral to hand surgeon for debridement and follow-up, as some patients will have progressive necrosis and subsequent digit amputation.
Patients with significant rhabdomyolysis should have adequate urine output maintained.
Following control of envenomation with antivenom, some patients develop recurrent swelling or hematologic toxicity. Swelling may recur within the first 24 hours following antivenom. If this swelling is not dependent in nature and improved with elevation of the extremity, the patient should receive additional antivenom.
Recurrence or late onset of thrombocytopenia and coagulopathy may develop as late as a week or more following treatment with antivenom and may be severe, necessitating retreatment with antivenom. For this reason, all patients treated with Crotalidae Polyvalent Immune Fab require measurement of platelet counts and fibrinogen within 2-3 days after last antivenom and again between 5-7 days after last antivenom.
5. Disease monitoring, follow-up and disposition
Expected response to treatment
With aggressive supportive care prior to development of any hypoxic injury to the brain, most patients should recover following plant poisonings. Complications such as rhabdomyolysis and aspiration pneumonia may require continued supportive care after resolution of the direct effects of the plant toxin.
Most patients who suffer an envenomation have a good prognosis for complete recovery, although permanent disability may result from some envenomations. Aggressive supportive care, as well as early antivenom administration when available and indicated, provide the best opportunity for full recovery for all types of envenomation.
With supportive care, patients with Grade 3 or 4 envenomations typically recover over 24 hours. Some patients will experience residual effects of sedative-hypnotic drugs after the envenomation has resolved.
For patients treated with antivenom, symptoms are expected to resolve within 1-2 hours.
Some patients describe paresthesias lasting for weeks following a sting.
Symptoms of envenomation typically resolve within 24-72 hours on their own and with supportive care, although some patients may have symptoms for up to a week following the bite. Rapid recovery within minutes to hours is described following treatment with antivenom.
Rare patients will develop large necrotic wounds that may take many months to heal or require surgical debridement and grafting.
Patients who develop paralysis prior to administration of antivenom may require ventilator management for many weeks. Following resolution of neurotoxicity, long term effects are not expected.
No long-term effects are expected following resolution of acute signs of envenomation.
Large numbers of stings (usually > 1000) may lead to death, especially in patients at the extremes of age or with co-morbidities. Patients who survive have a good prognosis for full recovery. As the acute venom toxicity resolves, patient may require extended treatment of secondary effects, such as rhabdomyolysis, renal failure, or aspiration pneumonia.
Prognosis is dependent on the severity of the envenomation and varies widely. Patients with relatively minor envenomations are expected to have full recovery. Patients who present with cardiovascular collapse, massive hemorrhage, or intracranial bleeds related to the envenomation may have long-term disability or death. Patients with isolated neurotoxicity should have full recovery if they receive mechanical ventilation prior to sustaining hypoxic injury.
In general, patients with native pit viper envenomations have a good prognosis if they receive timely supportive care and antivenom. Some patients will experience long-term disability. Some patients experience severe envenomations with shock, hemorrhage, or airway compromise, and are at much greater risk of death or permanent disability.
If the patient does not stabilize with aggressive supportive care or improve following antidotal therapy (such as digoxin binding fragments given for cardiac glycoside plant poisoning or physostigmine for anticholinergic plant poisoning), alternative diagnoses should be sought.
Whenever a diagnosis of plant poisoning is uncertain, other life-threatening etiologies should be considered simultaneously and treated empirically if indicated. For example, if fever and delirium cannot be confidently attributed to an anticholinergic plant, work-up and treatment for meningitis should occur.
Alternative diagnoses should be considered for patients who do not follow the expected clinical course or respond to specific antivenom. For example, if a patient is suspected to have a bark scorpion envenomation but does not respond to antivenom, other diagnoses, including amphetamine poisoning, should be considered.
Plant poisoning should not result in long-term effects following resolution of acute toxicity. Patients who have experienced complications such as rhabdomyolysis, elevation of liver enzymes, renal insufficiency, or aspiration pneumonia should have continued follow up by their primary care physician until complete resolution of these complications is noted.
The need for follow-up after an acute envenomation varies depending on the specific envenomation. Most patients will require follow up only for any secondary complications that might have occurred, such as rhabdomyolysis.
Patients with necrotic wounds resulting from brown recluse envenomation should have frequent follow-up visits to assess healing and need for surgical referral.
Patients treated with Crotalidae Polyvalent Immune Fab antivenom for rattlesnake envenomation require careful follow up, ideally with a physician familiar with management of rattlesnake envenomation.
All patients, regardless of whether they exhibited thrombocytopenia or coagulopathy following the snake bite, should be screened for new or recurrent coagulopathy or thrombocytopenia 2-3 days following last antivenom administration, and again between 5-7 days following last antivenom administration. If present, need for retreatment with antivenom should be discussed with a medical toxicologist through the poison center (18002221222).
Most plants produce systemic toxicity after ingestion and gastrointestinal absorption of toxin. Toxicity may also occur following parenteral injection of some plant toxins. While dermal exposure to certain plants, such as Toxicodendron spp, may lead to contact dermatitis, significant dermal absorption of plant toxins leading to systemic toxicity is usually not a concern, although exceptions occur, such as with green tobacco sickness following dermal absorption of nicotine in tobacco workers.
Hypoglycin and its metabolite, methylene cyclopropyl acetic acid (MCPA), inhibit the carnitine-acyl CoA transferase system as well as other metabolic pathways, leading to impairment of beta oxidation of fatty acids and inhibition of gluconeogenesis. This leads to accumulation of fatty acids in blood and dicarboxylic acids in urine. Acidemia and aciduria result. Hypoglycemia and elevation in liver transaminases develop. Microvesicular steatosis has been noted on autopsy.
Belladonna alkaloids antagonize post-synaptic muscarinic acetylcholine receptors. This leads to anti-muscarinic effects, which include both central effects (altered sensorium, hallucinations, agitation) and peripheral effects (mydriasis, dry and flushed skin, tachycardia, decreased bowel motility, urinary retention, and fever).
Plant-derived cardiac glycosides act in an identical manner to that of digoxin, by inhibiting the Na+-K+-ATPase on the cardiac myocyte cell membrane. This produces a rise in intracellular sodium which then inhibits the Na+-Ca2+exchanger, leading to an increase in intracellular calcium. This rise in calcium leads to increased inotropy. If there is too much intracellular calcium, delayed after-depolarizations and a shortened refractory period occur, which may lead to arrhythmias. Cardiac glycosides also increase vagal tone. Hyperkalemia may occur with acute poisoning and is an indication for treatment with digoxin binding fragments.
Sodium Channel Activators
Aconitine alkaloids, grayanotoxins, and veratrum alkaloids act by binding to activated voltage-gated sodium channels and preventing or delaying their inactivation. This results primarily in cardiac toxicity but may also produce some neurotoxic effects. Bradycardia and hypotension are most common following poisoning with grayanotoxin and veratrum alkaloids, while aconitine is more likely to produce ventricular arrhythmias, including torsades de pointes.
Sodium Channel Blockers
Taxus spp contain taxine B, which has been shown to block both sodium and calcium channels, leading to wide QRS interval on electrocardiogram and ventricular arrhythmias.
Cicutoxin is thought to produce seizures through antagonism of the GABA A receptor.
After ingestion, hydrolysis of amygdalin within the gastrointestinal tract produces hydrogen cyanide. The resulting toxicity is identical to that produced through other means of exposure to cyanide, except for delayed onset and more prolonged toxicity
Cyanide inhibits multiple metabolic enzymes including cytochrome oxidase, which causes inhibition of electron transport and oxidative phosphorylation. Oxygen consumption is then decreased, leading to an increase in mixed venous oxygen content if cardiac output remains constant. Impairment of oxidative phosphorylation leads to development of metabolic acidosis with elevated lactate concentrations.
Pokeweed contains several toxic components, including phytolaccatoxin and phytolaccagenin, which are saponin glycosides that may cause severe gastrointestinal illness. Another active component is pokeweed mitogen, which, though not clinically important, may serve as a marker for ingestion by producing a plasmacytosis days after ingestion.
The major psychoactive component in nutmeg is myristicin, although other components likely contribute to clinical effects. The mechanism for toxicity is unclear, and undesirable effects, such as vomiting, tachycardia, dry mouth, and anxiety, are more common than the desired hallucinatory effects. When hallucinations do occur they are thought to result from action at serotonin receptors.
The peyote cactus contains mescaline as the psychoactive component. Mescaline produces hallucinogenic effects via action at serotonin receptors and its phenethylamine structure may also explain sympathomimetic effects that occur in patients intoxicated with this agent.
Lysergic acid amide (LSA) is the primary intoxicant found within the seeds of the morning glory (Ipomoea violacea) and Hawaiian baby woodrose (Argyreia nervosa) plants. LSA is a precursor to the synthetic hallucinogen LSD, and is thought to have similar effects on serotonin receptors, resulting in hallucinations.
Colchicine and podophyllotoxin bind to tubulin, preventing formation of microtubules and causing arrest of mitosis in metaphase.
Nicotinic alkaloids act as agonists at nicotinic acetylcholine receptors. Initially they stimulate the receptors, resulting in membrane depolarization and resultant stimulatory effects, such as tachycardia and hypertension. If the receptor stimulus is sustained however, this leads to receptor blockade, manifested by depressant effects, such as hypotension, bradycardia and respiratory depression.
Toxalbumins inhibit protein synthesis by binding to the 60S ribosomal subunit. Depending on the dose and route of absorption, cytotoxic effects can be limited to mild gastrointestinal symptoms or can result in multiorgan system failure and death.
Envenomation results when venom is injected into the victim via a bite or sting from a venomous animal. Topical exposure to venom may produce allergic or irritant effects, but is not expected to produce systemic envenoming. All venoms are complex, with many having multiple toxic components. The pathophysiology varies depending on the animal responsible for the envenomation.
The components of scorpion venom responsible for clinical toxicity in humans are neurotoxins that act by prolonging activation of neuronal sodium channels. This leads to increased release of neurotransmitters into the synapse and subsequent increase in binding of these neurotransmitters to their specific receptors.
The main toxic component in Latrodectus venom is alpha-latrotoxin. This toxin creates pores in presynaptic membranes through which calcium enters, resulting in release of neurotransmitters into the synaptic space.
The major venom component thought responsible for clinical effects in humans is sphingomyelinase D. Other enzymes, including hyaluronidase, may contribute to toxicity. Pathophysiologic mechanisms for development of dermonecrosis include direct damage to cell membranes, initiation of an inflammatory response, and neutrophil chemotaxis.
Venom contains both alpha and beta neurotoxins which produce progressive neurologic dysfunction.
Venom contains helothermine, which can produce an anaphylactoid reaction with significant angioedema and hypotension.
The major toxic components in venom are melittin and phospholipase A2. These, and other fractions in venom, lead to mast cell degranulation, cause release of inflammatory mediators, and damage cell membranes leading to cell lysis, myonecrosis, and hemolysis.
The pathophysiology of snake envenomation depends on the dose and composition of venom. All snake venoms consist of a large variety of proteins, and clinically important components may include metalloproteinases, phospholipases A2, serine proteases, c-type lectin-like proteins, vascular endothelial growth factors, and bradykinin-potentiating peptides.
Whether envenomation leads to cytotoxic, anticoagulant, pro-coagulant, platelet, or neurotoxic effects is dependent on the venom composition and the specific species responsible for the envenomation.
Crotalinae venom is extremely complex, containing multiple enzymes and peptides that act individually and in combination to produce the clinical effects seen following envenomation, including swelling, hypotension, dermatonecrosis, myonecrosis, neurotoxicity and hematolgoic toxicity. Clinical effects in any individual patient may vary depending on the dose of venom delivered as well as the venom composition of the particular snake.
Plants account for roughly 5% of exposures reported to poison centers each year. Most of these occur in children under 6 years of age and most do not result in serious harm. Severe poisoning and death are uncommon, but do occur, and typically result from ingestion of plant parts or teas made from plant parts. Poisonous plant ingestions occur when the plants are mistaken for edible species, when they are taken medicinally or recreationally, or when they are ingested with suicidal intent.
Envenomations are a relatively uncommon reason for presentation to a health care facility, but affect people of all ages and demographic groups. Even in areas with few native venomous creatures, the practice of keeping exotic venomous pets allows for encounters with a variety of types of envenomed patients regardless of geographical location.
Scorpion envenomations occur largely within the state of Arizona, although the bordering regions of surrounding states may also harbor bark scorpions. Though most sting victims are adults, the vast majority of victims with clinically important systemic envenomation are young children. Occasionally children over 10 years of age, or even adults, may require hospitalization for management of neurologic toxicity, but typically severe symptoms occur in children under four years of age.
Five species of widow spiders reside in the United States, with all capable of producing envenomation. Only Latrodectus mactans has the classic red hourglass shape on the abdomen, with the others having a variation in the color and shape of the marking. Spiders may enter dwellings but prefer isolated places, such as sheds or barns.
Several species of Loxosceles spiders are found throughout the United States. The most famous is L reclusa, and this is the only native species that has been implicated in systemic loxoscelism. Other Loxosceles species may also be responsible for dermonecrosis, but well-documented cases are rare.
The brown recluse is 'reclusive' and avoids human contact. Envenomations occur in the Midwest region of the U.S., where this species is endemic. Most people who are bitten by this spider do not develop significant effects. Dermonecrosis affects a small percentage of victims, while systemic effects, including hemolysis, are even less common, and primarily affect children.
Up to 100 coral snake bites are reported in the southeast United States each year, with most occurring in Florida. Clinically important species are the Eastern and Texas coral snakes (Micrurus fulvius and M tener). The Sonoran coral snake (Micruroides euryxanthus) does not produce significant envenomation. Young men are the most frequent victims.
In 1990, honeybees that had been introduced to Brazil from Africa began to move into the southern United States. Over the last 20 years, increasing southern populations of domestic honeybees have become 'Africanized', leading to more defensive and aggressive behavior. Hundreds to thousands of bees may attack an individual at once, seemingly without provocation, resulting in a massive venom load and in some cases life-threatening illness due to venom toxicity (as opposed to hypersensitivity).
Attacks may occur in urban or rural areas and affect people of all ages.
Victims of exotic snake bite tend to be adult men who have intentionally handled a pet snake. The type of snake implicated varies widely, with bites from nearly 80 species reported over a ten-year period.
There are more than 20 species and many subspecies of pit vipers (family Viperidae, subfamily Crotalinae) native to the United States. Pit vipers inhabit all states except Maine, Alaska, and Hawaii, and up to 8000 venomous bites are reported to poison centers each year.
Although bites to the lower extremities in persons who were unaware of the presence of a snake are common, the majority of victims are young adult men who have intentionally handled a pet or wild snake and are bitten on an upper extremity. Mortality from native snake envenomation is low, with generally fewer than ten deaths reported each year.
Special considerations for nursing and allied health professionals.
What's the evidence?
DESCRIPTION OF THE PROBLEM: POISONOUS PLANTS
DESCRIPTION OF THE PROBLEM: VENOMOUS ANIMALS
EMERGENCY MANAGEMENT: POISONOUS PLANTS
EMERGENCY MANAGEMENT: VENOMOUS ANIMALS
DIAGNOSIS: POISONOUS PLANTS
DIAGNOSIS: VENOMOUS ANIMALS
SPECIFIC TREATMENT: POISONOUS PLANTS
SPECIFIC TREATMENT: VENOMOUS ANIMALS
DISEASE MONITORING, FOLLOW UP AND DISPOSITION
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