1) SOLUBLE SALTS: Those plants containing only SOLUBLE oxalates (eg, rhubarb (raw leaf blades), star fruit ) do not produce irritation but may be eaten in sufficient quantities to produce systemic oxalate toxicity (eg, hypocalcemia) (Nelson et al, 2007). Soluble forms include oxalic acid and sodium, potassium, and ammonium oxalate.
2) INSOLUBLE SALTS: Those plants containing INSOLUBLE calcium oxalate crystals (eg, dieffenbachia, caladium) can produce local pain and irritation (ie, blistering) and edema in the oral cavity, but rarely result in systemic effects. Hoarseness, dysphonia and dysphagia may develop following oral exposure (Nelson et al, 2007).

a) In another case, a man tasted the root of the same plant and developed oral numbness, pain of the tongue and nausea about 2 hours after exposure. The throat appeared slightly inflamed. Morphine was given for pain. Approximately 7 hours after presentation, the patient left against medical advice still complaining of severe tongue pain (Moon et al, 2011).

a) SOLUBLE SALTS: Following large ingestions of soluble oxalates, oxalic acid is formed in the stomach and subsequently absorbed into the systemic circulation. There it binds with calcium, potentially resulting in hypocalcemia. This may rarely lead to weak, irregular pulse, bradycardia, hypotension and cardiac dysrhythmias (Tagwireyi & Ball, 2001). Rhythm disturbances, progressed to ventricular fibrillation, in a hypocalcemic (total calcium 6.3 mg/dL, ionized 2.3 mg/dL) patient (Farre et al, 1989).

a) INSOLUBLE SALTS: Respiratory distress, requiring endotracheal intubation, may occur if edema of the tongue and oropharynx is severe (Tagwireyi & Ball, 2001; McIntire et al, 1990).
b) ALOCASIA ODORA: A 43-year-old woman bit into the root stock of an A odora plant while inebriated and presented 2 hours after exposure. She was alert and oriented with complaint of oral numbness, dyspnea and throat discomfort. During endotracheal intubation, a swollen uvular and epiglottis were noted. Treatment included IV chlorpheniramine and methylprednisolone. Chest x-ray and laboratories studies were within normal limits with only mild leukocytosis. The patient was extubated 12 hours later with mild swelling of the arytenoids and epiglottis with no respiratory complaints. However, the patient continued to complain of oral numbness and tongue pain and was transferred to a local hospital for further pain control and nutritional support (Moon et al, 2011).

a) SOLUBLE SALTS: Dyspnea has been reported following toxicity due to soluble oxalate salts. Patients with preexisting renal failure are more prone to toxic effects (Chen et al, 2005; Chang et al, 2000). Respiratory depression requiring ventilation was noted in a comatose patient with acidosis and liver and kidney failure (Farre et al, 1989).

a) SOLUBLE SALTS: Pulmonary edema was seen in a fatality due to ingestion of Rumex crispus. Kidney failure was also present (Reig et al, 1990). Two cases of pulmonary edema complicating renal failure were reported following the ingestion of star fruit (Chen et al, 2001).

a) SOLUBLE SALTS: Ingestion of large quantities of plants containing sodium or potassium oxalates may produce hypocalcemic tetany secondary to complexation of ionized calcium with oxalic acid. About 600 mg of oxalic acid is equal to total blood calcium (Sanz & Reig, 1992).

a) SOLUBLE SALTS: Disturbance of consciousness, including coma, has been reported after the toxic ingestion of soluble oxalate salts. Patients who ingest this on an empty stomach or who are dehydrated or who have preexisting renal failure are more prone to the CNS depressant effects. Coma is common in patients with chronic renal failure who ingest star fruit (Tse et al, 2003; Tsai et al, 2005; Chen et al, 2005; Chang et al, 2002; Chang et al, 2000; Neto et al, 1998). In one case, deep coma was reported after ingestion of soluble oxalates; the patient had hypocalcemia and kidney and liver failure (Farre et al, 1989).
b) CASE REPORT: A 72-year-old diabetic dialysis patient developed nausea, vomiting, limb weakness, and disorientation after the ingestion of half a star fruit the day before. The next day, he was found unarousable with a GCS score of 3 of 15 with a positive Babinski's sign of the right foot, and intermittent hiccups. A brain CT scan did not show any specific abnormality except for mild brain atrophy; however, diffusion-weighted magnetic resonance imaging revealed hyperintense lesions in the left central regions. An EEG examination revealed found active focal sharp waves in the left central region that were compatible with nonconvulsive status epilepticus. Following anticonvulsant therapy and regular hemodialysis, he recovered and was discharged on the 20th day of hospitalization (Chang & Yeh, 2004).
c) CASE SERIES: In a study of 7 consecutive uraemic patients (5 patients were receiving peritoneal dialysis; 1 patient was on hemodialysis) each developed varying degrees of toxicity following star fruit ingestion. Symptoms included hiccup, confusion, vomiting, impaired consciousness, muscle twitching and hyperkalemia. The average onset of symptoms was 8 hours. Of the 7 patients, 5 required an increase in dialysis for several days with notable improvement in symptoms. All cases had high oxalate concentrations which likely led to oxalosis and the neurologic effects observed. No deaths were reported (Tse et al, 2003).

a) SOLUBLE SALTS: Seizures were seen in a pediatric patient experiencing renal impairment and electrolyte imbalance after rhubarb leaf ingestion (Kalliala & Kauste, 1964). Star fruit, a soluble oxalate, is reported to contain an unknown neurotoxin; in toxic doses, or in patients compromised with renal dysfunction, seizures have been reported (Chen et al, 2010; Yap et al, 2002; Chang et al, 2000).
b) CASE REPORT: A 67-year-old woman with diabetes mellitus and moderate renal insufficiency developed altered mental status including coma and seizures one day after ingesting a star fruit. A MRI showed a reversible focal cerebral lesion over the left occipital area. She was treated symptomatically and was started on hemodialysis and gradually regained consciousness. A repeat MRI approximately 2 weeks after exposure showed resolution of the lesion. No permanent sequelae developed (Chen et al, 2010).
c) CASE REPORT: A 52-year-old man with hypertension and chronic renal polycystic disease receiving hemodialysis developed a sudden onset of hiccoughs, an increase in blood pressure, seizures and confusion approximately 12 hours after ingesting a large amount of star fruit. A neurologic exam revealed severe ataxia, tetraparesis, loss of a gag reflex and bilateral ophthalmoparesis. A head CT was negative for a brain hemorrhage. Laboratory abnormalities included a plasma serum creatinine of 10.8 mg/dL, urea 209 mg/dL and metabolic acidosis (pH 6.84 and bicarbonate 6 mmol/L). The patient was placed on immediate hemodialysis for 18 hours and his neurologic function improved. A follow-up MRI showed no evidence of an acute cerebral ischemic event (Alessio-Alves et al, 2012).
d) CASE REPORT: A 72-year-old diabetic dialysis patient developed nausea, vomiting, limb weakness, and disorientation after the ingestion of half a star fruit the day before. The next day, he was found unarousable with a GCS score of 3 of 15 with a positive Babinski's sign of the right foot, and intermittent hiccups. A brain CT scan did not show any specific abnormality except for mild brain atrophy; however diffusion-weighted magnetic resonance imaging revealed hyperintense lesions in the left central regions. An EEG examination revealed found active focal sharp waves in the left central region and that were compatible with nonconvulsive status epilepticus. Following anticonvulsant therapy and regular hemodialysis, he recovered and was discharged on the 20th day of hospitalization (Chang & Yeh, 2004).
e) STATUS EPILEPTICUS: Refractory status epilepticus was reported in two elderly patients with chronic renal insufficiency, not dialysis dependent, (an 84-year-old woman and a 74-year-old man) after consuming 2 to 3 star fruit. Despite performing emergent hemodialysis, both patients died on day 23 and on day 7, respectively, of hospital admission (Tsai et al, 2005).
f) DIOSCOREA QUINQUELOBA: A 51-year-old healthy man ingested about 400 mL of the juice of raw tubers (D. quinqueloba) for general health and the following day he developed nausea and continuous vomiting. His wife drank a small amount of the juice and developed similar symptoms but the effects were milder and resolved a short time later. Upon admission his vital signs and laboratory studies were within normal limits. By the following day, his serum creatinine (Cr) was 2.9 mg/dL with a BUN of 42.7 mg/dL. On day 3, he was febrile (39 degrees Celsius) and developed a tonic-clonic seizure and a decreased level of consciousness. An EEG showed evidence of nonspecific and diffuse cerebral dysfunction and high anion gap metabolic acidosis was present. The patient was intubated and sedated and emergency hemodialysis was begun. By day 5, his BUN was 88.8 mg/dL and Cr was 8.6 mg/dL. He was then placed on continuous venovenous hemodiafiltration (CVVHDF) and his kidney function gradually improved. On day 12, CVVHDF was stopped and he was successfully extubated due to improved consciousness. He continued to receive supportive care and was discharged to home on day 26 with a BUN of 8.4 mg/dL and a Cr of 1.2 mg/dL (Kang & Heo, 2015).

a) SOLUBLE SALTS: Cerebral edema may occur (Arana, 1986).

a) Oral paresthesia, with severe pain and numbness in the perioral area and throat has been reported following ingestions of oxalate containing plants (Chan et al, 1995). Focal neurological defects are not usually present. The paresthesia is generally mild with resolution over 5 days.

a) Agitation, incoherent speech, insomnia and mental confusion have been reported after the ingestion of soluble oxalates, particularly star fruit (carambola) (Tsai et al, 2005; Chang et al, 2002; Yap et al, 2002; Neto et al, 1998).

a) SOLUBLE SALTS: Muscle weakness and extremity numbness have been reported following ingestions of star fruit. Patients with pre-existing renal failure are particularly susceptible to neurological effects of this plant (Chang et al, 2000).

a) Three patients experienced headache after ingesting plant material containing raphides (Watson et al, 2005).

a) RATS: Injections of an extract of star fruit provoked persistent tonic-clonic seizures in rats (Neto et al, 1998).

a) Nausea, vomiting, abdominal pain and diarrhea may occur with either type salt. Bloody emesis and diarrhea may occur with soluble salts. Vomiting may be profuse (Tsai et al, 2005; Chang & Yeh, 2004; Yap et al, 2002; Chang et al, 2002; Neto et al, 1998; Chan et al, 1995; Farre et al, 1989; Kalliala & Kauste, 1964; Streicher, 1964).

a) Contact with insoluble calcium oxalate crystals is not usually associated with the development of symptoms and rarely causes severe symptoms. Two large case series involving exposure to philodendrons and Dieffenbachias reported the incidence of minor symptoms to be 2.1% (Mrvos et al, 1991) to 15.5% (Krenzelok et al, 1996).
b) CASE SERIES: Lin et al (1998) described a case series of 25 patients who consumed a portion (1 to 2 mouthfuls) of the plant, alocasis macrorrhiza (giant elephant's ear). Onset of symptoms were almost immediate, with 18 patients developing throat irritation, 12 patients complained of numbness of the oral cavity, 6 patients had abdominal pain, 4 patients had difficulty speaking, 4 patients experienced excess salivation, 1 patient had dysphagia and 1 patient had swollen lips. All were described as mild poisonings, with symptoms resolving over one week (Lin et al, 1998).
c) CASE REPORT: After eating the root tuber of Alocasia macrorrhiza, a 29-year-old man presented with numbness, paresthesia and pain over his tongue, oral cavity and throat. Symptoms cleared within 5 days (Chan et al, 1995).

a) SOLUBLE SALTS: Intractable hiccups have commonly been reported following toxic ingestions of star fruit in patients with renal insufficiency (Alessio-Alves et al, 2012; Tsai et al, 2005; Chen et al, 2005; Chang & Yeh, 2004; Yap et al, 2002; Chang et al, 2002; Chang et al, 2000; Neto et al, 1998).

a) CASE REPORT: A 2-year-old boy with a history of pica, associated with iron deficiency anemia, developed an acute episode of sialorrhea, difficulty in speaking, dysphagia, and repeated swallowing movements after ingesting a leaf from a Colocasia esculenta (elephant's ear). Following 2 days of close observation, he recovered and was discharged home in good health (Mihailidou et al, 2002).

a) SOLUBLE SALTS: Centrilobular necrosis was seen in a fatality from R. crispus. The patient was an insulin-dependent diabetic and heavy smoker and drinker (Farre et al, 1989). A screen for other hepatotoxins was negative.
b) Liver enlargement and slight icterus were seen in a 4-year-old and 6-year-old who ate 20 to 100 g of stems and leaves of rhubarb (Streicher, 1964).

a) LIVER CONGESTION: Livestock animals poisoned with Alocasia macrorrhiza were found to have liver congestion (Morton, 1971).

a) SOLUBLE SALTS: Renal damage may be noted following ingestion of plants containing soluble oxalates (Reig et al, 1990; Tallqvist & Vaananen, 1960). Renal damage is uncommon but careful follow-up is indicated (Farre et al, 1989; Franceschi & Horner, 1980). These cases may require 2 to 48 hours before significant symptomatology begins.
b) HISTOLOGY: Renal lesions appear as small hemorrhages, congestion, cellular cloudy swelling, sclerosis and hyalin degeneration of the tubules, and lesions associated with interstitial tubular glomerulonephrosis (Bottarelli, 1968).

a) RUMEX ACETOSA/CASE REPORT: A 12-year-old boy ingested a large amount of sorrel (rumex acetosa) while playing in a field and developed acute tubulointerstitial nephritis. Although the amount was unknown, he continued to eat the plant until he felt full and developed mouth soreness. Initially, vomiting was the only reported symptom. Eighteen days later, he was admitted with polyuria. Laboratory studies were normal with the exception of hypophosphatemia and mildly elevated serum transaminase levels. Proteinuria and glucosuria were also present. A renal ultrasonography confirmed an increase echogenicity of both kidneys that was suggestive of proximal tubulopathy. Further urine testing was positive for oxalate (116 mg/1.73 m(2)/day; normal less than 45 mg/1.73 m(2)/day). Following oral rehydration and electrolyte replacement, the patient clinically improved and laboratory studies normalized within a few weeks. Although a renal biopsy would have been confirmatory, it was not performed due to the child's rapid clinical improvement with supportive therapy (Selcuk et al, 2015).

a) Nephritis is more common among people who use Colocasia and Xanthosoma species as a food crop (Kasilo, 1990).

a) SOLUBLE SALTS: Hematuria and oxaluria were seen several hours after a 16-year-old boy ingested 3 enormous helpings of red currants. Oxalate crystals were seen in the urine. No sequelae were seen (Vicary, 1977).

a) RATS: An acute oxalate nephropathy was induced by sour star fruit juice feedings in rats. The oxalate concentration in the juice was 2.46 g/dL; the rats received 4 mL/100 g body weight (or approximately 1 g oxalate/kg). Pathological examination of the kidney revealed extensive refractile oxalate crystals in some tubules (Fang et al, 2001).

a) SOLUBLE SALTS: METABOLIC ACIDOSIS was noted in a patient who died after ingesting 500 g of sorrel (Farre et al, 1989).
b) STAR FRUIT: A 52-year-old man with hypertension and chronic renal polycystic disease receiving hemodialysis developed a sudden onset of hiccoughs, an increase in blood pressure, seizures and confusion approximately 12 hours after ingesting a large amount of star fruit. A neurologic exam revealed severe ataxia, tetraparesis, loss of a gag reflex and bilateral ophthalmoparesis. A head CT was negative for a brain hemorrhage. Laboratory abnormalities included metabolic acidosis (pH 6.84 and bicarbonate 6 mmol/L), a plasma serum creatinine of 10.8 mg/dL and urea 209 mg/dL. The patient was placed on immediate hemodialysis for 18 hours and his neurologic function improved. A follow-up MRI showed no evidence of an acute cerebral ischemic event (Alessio-Alves et al, 2012).

a) SOLUBLE SALTS: Hypocalcemic tetany may occur following ingestion of plants containing soluble oxalates. The common gastrointestinal signs may be seen earlier.

a) SOLUBLE SALTS: Muscle cramps may result due to hypocalcemia following a toxic plant ingestion (Tagwireyi & Ball, 2001).

a) DILUTION: Remove all visible evidence of plant (eg, caladium, dieffenbachia, elephant's ear) debris from the oropharynx and administer milk or water to rinse out crystals and assist with oropharynx decontamination. Most ingestions are not large enough to result in severe toxicity; following a taste of the plant, demulcents (milk or water) to rinse the mouth and/or ice, may be all that is necessary (Tagwireyi & Ball, 2001).
b) ICE: Cold water or sucking on crushed ice will relieve oral pain. Popsicles are useful in children. Analgesic medication may be required for intense pain.

a) FLUID/ELECTROLYTES: Maintain adequate hydration with intravenous fluids if oral fluids cannot be tolerated.
b) HYPOCALCEMIA and tetany should be treated with intravenous calcium gluconate (Tagwireyi & Ball, 2001; Gosselin et al, 1984).

a) SOLUBLE SALTS: Seizures were seen in a pediatric patient experiencing renal impairment and electrolyte imbalance after rhubarb leaf ingestion (Kalliala & Kauste, 1964). Star fruit, a soluble oxalate, is reported to contain an unknown neurotoxin; in toxic doses, or in patients compromised with renal dysfunction, seizures have been reported (Alessio-Alves et al, 2012; Yap et al, 2002; Chang et al, 2000).

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

a) Mild to moderate allergic reactions may be treated with antihistamines with or without inhaled beta adrenergic agonists, corticosteroids or epinephrine. Treatment of severe anaphylaxis also includes oxygen supplementation, aggressive airway management, epinephrine, ECG monitoring, and IV fluids.

a) ALBUTEROL

a) Consider systemic corticosteroids in patients with significant bronchospasm.
b) PREDNISONE: ADULT: 40 to 80 milligrams/day. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 to 2 divided doses divided twice daily (National Heart,Lung,and Blood Institute, 2007).

a) DIPHENHYDRAMINE

a) EPINEPHRINE: INJECTABLE SOLUTION: It should be administered early in patients by IM injection. Using a 1:1000 (1 mg/mL) solution of epinephrine. Initial Dose: 0.01 mg/kg intramuscularly with a maximum dose of 0.5 mg in adults and 0.3 mg in children. The dose may be repeated every 5 to 15 minutes, if no clinical improvement. Most patients respond to 1 or 2 doses (Nowak & Macias, 2014).

a) EPINEPHRINE

a) OXYGEN: 5 to 10 liters/minute via high flow mask.
b) INTUBATION: Perform early if any stridor or signs of airway obstruction.
c) CRICOTHYROTOMY: Use if unable to intubate with complete airway obstruction (Vanden Hoek,TL,et al).
d) BRONCHODILATORS are recommended for mild to severe bronchospasm.
e) ALBUTEROL: ADULT: 2.5 to 5 milligrams in 2 to 4.5 milliliters of normal saline delivered per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 2.5 to 10 mg every 1 to 4 hours as needed, or 10 to 15 mg/hr by continuous nebulization as needed (National Heart,Lung,and Blood Institute, 2007).
f) ALBUTEROL: CHILD: 0.15 milligram/kilogram (minimum 2.5 milligrams) per nebulizer every 20 minutes up to 3 doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulization (National Heart,Lung,and Blood Institute, 2007).

a) CARDIAC MONITOR: All complicated cases.
b) IV ACCESS: Routine in all complicated cases.

a) If hypotensive give 500 to 2000 milliliters crystalloid initially (20 milliliters/kilogram in children) and titrate to desired effect (stabilization of vital signs, mentation, urine output); adults may require up to 6 to 10 L/24 hours. Central venous or pulmonary artery pressure monitoring is recommended in patients with persistent hypotension.

a) SUMMARY: Antihistamines are second-line therapy and are used as supportive therapy and should not be used in place of epinephrine (Lieberman et al, 2010).
b) RANITIDINE: ADULT: 1 mg/kg parenterally; CHILD: 12.5 to 50 mg parenterally. If the intravenous route is used, ranitidine should be infused over 10 to 15 minutes or diluted in 5% dextrose to a volume of 20 mL and injected over 5 minutes (Lieberman et al, 2010).
c) Oral diphenhydramine, as well as other H1 antihistamines, can also be used as indicated (Lieberman et al, 2010).

a) Dysrhythmias and cardiac dysfunction may occur primarily or iatrogenically as a result of pharmacologic treatment (epinephrine) (Vanden Hoek,TL,et al). Monitor and correct serum electrolytes, oxygenation and tissue perfusion. Treat with antiarrhythmic agents as indicated.

a) There have been a few reports of patients with anaphylaxis, with or without cardiac arrest, that have responded to vasopressin therapy that did not respond to standard therapy. Although there are no randomized controlled trials, other alternative vasoactive therapies (ie, vasopressin, norepinephrine, methoxamine, and metaraminol) may be considered in patients in cardiac arrest secondary to anaphylaxis that do not respond to epinephrine (Vanden Hoek,TL,et al).

1) In another case, a man tasted the root of the same plant and developed oral numbness, tongue pain and nausea about 2 hours after exposure. The throat appeared slightly inflamed. Morphine was given for pain. Approximately 7 hours after presentation, the patient left against medical advice still complaining of severe tongue pain (Moon et al, 2011).

1) Significant poisoning by rhubarb and sorrel has been reported only after ingestion in quantity, such as when used as a food.

1) SUMMARY: As little as half of a star fruit or approximately 25 mL of the juice can produce symptoms; however, the association between the amount ingested and symptoms is highly variable (Lee, 2012).
2) STAR FRUIT: Following an estimated ingestion of 13.1 and 9.2 g of oxalate (in star fruit juice) in a 77- and a 38-year-old men respectively, acute oxalate nephropathy developed. Both men drank the juice on an empty stomach and both were previously healthy. After hemodialysis, both recovered (Chen et al, 2001).
3) STAR FRUIT: A 72-year-old with dialysis dependent renal failure developed coma, hiccups, and nonconvulsive status epilepticus after ingesting half a star fruit (Chang & Yeh, 2004).
4) STAR FRUIT: One day after ingesting 3 star fruits (about 60 g per star fruit), a 60-year-old man with diabetes mellitus, hypertension, alcoholic cirrhosis, chronic renal failure developed chills, hiccups, tremor, irritability, hearing impairment, urinary retention, acute renal failure, acute respiratory failure, coma and hypothermia (30.4 degrees C). Following 2 sessions of hemodialysis and rewarming, his body temperature returned to normal, but he remained comatose. After a 6-hour session of charcoal hemoperfusion, his consciousness returned to normal within a day (Chen et al, 2005).
5) DIOSCOREA QUINQUELOBA: A 51-year-old healthy man ingested about 400 mL of the juice of raw tubers (D. quinqueloba) for general health and the following day he developed nausea and continuous vomiting. His wife drank a small amount of the juice and developed similar symptoms but the effects were milder and resolved a short time later. Upon admission his vital signs and laboratory studies were within normal limits. By the following day, his serum creatinine (Cr) was 2.9 mg/dL with a BUN of 42.7 mg/dL. On day 3, he was febrile (39 degrees Celsius) and developed a tonic-clonic seizure and a decreased level of consciousness. An EEG showed evidence of nonspecific and diffuse cerebral dysfunction and high anion gap metabolic acidosis was present. The patient was intubated and sedated and emergency hemodialysis was begun. By day 5, his BUN was 88.8 mg/dL and Cr was 8.6 mg/dL. He was then placed on continuous venovenous hemodiafiltration (CVVHDF) and his kidney function gradually improved. On day 12, CVVHDF was stopped and he was successfully extubated due to improved consciousness. He continued to receive supportive care and was discharged to home on day 26 with a BUN of 8.4 mg/dL and a Cr of 1.2 mg/dL (Kang & Heo, 2015).
6) DIOSCOREA QUNQUELOBA: A 68-year-old man started taking an extract containing D. quinqueloba for about a week for diabetes mellitus. Upon admission, he was oliguric with pitting edema of his lower extremities. His initial laboratory studies revealed a serum creatinine level of 4.6 mg/dL, creatinine kinase 66 Units/L (normal range, 35 to 172), sodium 133 mEq/L, potassium of 4.7 mEq/L and a BUN of 56.6 mg/dL. Urine sodium and creatinine were 50 mEq/L and 32.2 mg/dL, respectively. Hydration therapy was initiated. His creatinine gradually declined from 5.9 to 1.2 mg/dL. By day 6, he was discharged without permanent sequelae. In the second case, the 58 year-old brother of case 1 also developed pitting edema of his lower extremities, vomiting, diarrhea and polydipsia after taking the same D. quinqueloba extract for general well being. His serum creatinine level (5.8 mg/dL) and BUN (48.2 mg/dL) were both elevated. Similarly, he was diagnosed with intrinsic acute renal failure and treated with hydration therapy. His renal function gradually improved and his creatinine level decreased to 1.3 mg/dL approximately 10 days after admission (Kim et al, 2012).

a) Greater than 160 mL/kg -- fresh expressed juice (Fochtman et al, 1969)

1) Ongoing treatment is symptomatic and supportive.

1) SPECIFIC TOXIN