m&p poisoning

M&P poisoningM&P poisoning

Prof. Dr. Saad S Al AniSenior Pediatric ConsultantHead of Pediatric departmentKhorfakkan HospitalSharjah ,[email protected]

2

MushroomMushroom Poisoning Poisoning

04/12/23M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

MushroomMushroom Poisoning Poisoning

• Mushrooms are a great source of nutrition• They are: - Low in calories - Fat free - High in protein Making them an ideal food except for the fact that some are highly toxic if ingested

M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital 04/12/23 3

Cont.Cont.

• The clinical syndromes produced by mushroom poisoning are divided according to the: - Rapidity of onset of symptoms - Predominant system involved.•The symptoms are due to the principal toxin present in the ingested mushrooms

M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

404/12/23

Cont.Cont.

• The eight major toxins produced by mushrooms are categorized as: 1. Cyclopeptides 2. Monomethylhydrazine 3. Muscarine 4. Hallucinogenic indoles 5. Isoxazole 6. Coprine (disulfiram-like reaction) 7. Orellanine 8. Gastrointestinal tract–specific irritantsM&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

504/12/23

Cont.Cont.

• The wild mushroom: -Tricholoma equestre has been associated with delayed rhabdomyolysis -Clitocybe amoenolens and Clitocybe acromelalgia have been reported to cause erythromelalgia.• The toxins responsible for these effects are unknown.


604/12/23

Gastrointestinal: Delayed Onset

Amanita Poisoning

•Poisonings by species of Amanita and Galerina account for 95% of the fatalities due to mushroom intoxication •The mortality rate for this group is 5-10%. •Cells with high turnover rates, such as those in the gastrointestinal mucosa, kidneys, and liver, are the most severely affected.


704/12/23

• Most species produce two classes of cyclopeptide toxins: (1)Phallotoxins, which are heptapeptides believed to be responsible for the early symptoms of Amanita poisoning (2) Amanitotoxin, an octapeptide that inhibits RNA polymerase and subsequent production of messenger RNA.

Cyclopeptide toxins


804/12/23

Pathogenesis

Amanita poisoning causes:• Cellular necrosis which may occur throughout the gastrointestinal tract, the most heavily exposed site. • Acute yellow atrophy of the liver • Necrosis of the proximal renal tubules are found in lethal cases.


904/12/23

The clinical course of poisoning

• The clinical course of poisoning with Amanita or Galerina species is biphasic.• Nausea, vomiting, and severe abdominal pain ensue 6-24 hr after ingestion.• Profuse watery diarrhea follows shortly thereafter and may last for 12-24 hr.• During this time, as much as 9 L of fluid may be lost.


1004/12/23

Cont.

• From 24-48 hr after poisoning, jaundice ,hypertransaminasemia (peaking at 72 to 96 h), renal failure, and coma occur.• Death occurs 4-7 days after the ingestion.• A prothrombin time less than 10% of control is a poor prognostic factor.


1104/12/23

Treatment

•Treatment for Amanita poisoning is both supportive and specific. •Fluid loss from severe diarrhea during the early course of the illness is profound, requiring aggressive therapy for correction of this loss.• In the late phase of the disease, management of renal and hepatic failure is also necessary.


1204/12/23

Cont.

• Specific therapy for Amanita poisoning is designed to remove the toxin rapidly and to block binding at its target site.• Oral activated charcoal and lactulose combined with fluid and electrolyte replacement are recommended as part of the initial treatment for children with Amanita poisoning.


1304/12/23

Cont.

• Forced diuresis should be avoided, since this increases renal exposure.• Intravenous penicillin G (400,000 U/kg/ 24 hr) administered as a continuous infusion • Silybin dihemisuccinate, the water-soluble isomer of the flavolignone silymarin (in an intravenous dosage of 20-50 mg/kg/24 hr


1404/12/23

Cont.

• Silybin dihemisuccinate, act synergistically to: 1.Inhibit binding of both toxins 2.Interrupt enterohepatic recirculation of amanitotoxin, 3.Protect from further hepatic injury from the toxins. .


1504/12/23

Monomethylhydrazine Intoxication

• Species of Gyromitra contain monomethylhydrazine (CH3NHNH2), which inhibits central nervous system (CNS) enzymatic production of γ-aminobutyric acid (GABA).• Monomethylhydrazine also oxidizes iron in hemoglobin, resulting in methemoglobinemia.


1604/12/23

Cont.

•Children with Gyromitra poisoning experience: vomiting, diarrhea, hematochezia and abdominal pain within 6-24 hr of ingestion of the toxin.


1704/12/23

Cont.

• Symptoms of CNS depression and seizures develop later in the clinical course. •Hemolysis and methemoglobinemia are potential life-threatening complications of monomethylhydrazine poisoning.


1804/12/23

Treatment

•Hypovolemia due to gastrointestinal fluid losses and seizures requires supportive intervention. •Pyridoxal phosphate, the coenzyme that catalyzes the production of GABA, can reverse the effects of monomethylhydrazine when administered in high doses.


1904/12/23

Cont.

• Pyridoxine hydrochloride (25 mg/kg) is administered intravenously at a frequency dependent on clinical improvement.• Parenteral administration of methylene blue is indicated if the methemoglobin concentration exceeds 30%;


2004/12/23

Cont.

• Severe methemoglobinemia may require dialysis. •Blood transfusions may be required for significant hemolysis


2104/12/23

Renal: Delayed Onset

Orellanine Poisoning •Species of Cortinarius contain the heat- stable toxin bipyridyl orellanine, whichcauses severe non-glomerular renal injury characterized by interstitial fibrosis and acute tubular necrosis.

22M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

04/12/23

•The exact mechanism of injury is unknown.• Cortinarius poisoning is characterized by: nausea, vomiting, and diarrhea That manifest 36-48 hr after ingestion.

Orellanine Poisoning (Cont.)

23M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital04/12/23

Orellanine Poisoning (Cont.)

• Although the initial symptoms may be trivial, more serious renal toxicity occurs in several days.• Acute renal failure occurs in 30-50% of those affected, beginning with polyuria and progressing to renal failure


Treatment

• Treatment for orellanine poisoning is supportive.• Early presentation, within 4-6 hr after ingestion, can be treated with activated charcoal and gastric lavage


Treatment (Cont.)

• Hemodialysis may be needed in patients suffering from renal failure.• Most patients recover within 1 mo but chronic renal insufficiency develops in one third to one half of patients


Autonomic Nervous System: Rapid Onset

Muscarine Poisoning •Mushrooms of the genera Inocybe and, to a lesser degree, Clitocybe contain muscarine or muscarine-related compounds. •These quaternary ammonium derivatives bind to postsynaptic receptors, producing an exaggerated cholinergic response.


Cont.

• The onset of symptoms is rapid (30 min to 2 hr after consumption) and the disease spectrum is characterized by the following: -Hypercholinergic response diaphoresis - Excessive lacrimation - Salivation and vomiting - Miosis - Urinary and fecal incontinence 28M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

04/12/23

Cont.

• Respiratory distress caused by broncho- spasm and increased bronchopulmonary secretions is the most serious complication•The symptoms subside spontaneously within 6-24 hr.


Treatment

•Atropine sulfate, the specific antidote, is administered intravenously (0.01 mg/ kg; max 2 mg). •This is repeated until the pulmonary symptoms resolve or the patient becomes overtly tachycardic


Coprine Ingestion

• Coprinus atramentarius and Clitocybe clavipes contain coprine. •Like disulfiram ,coprine inhibits the metabolism of acetaldehyde after ethanol ingestion.• The clinical manifestations result from accumulation of acetaldehyde.


Cont.

• Coprine intoxication becomes apparent after ethanol ingestion and may occur up to 5 days after consumption of the mushroom. •Hyperemia of the face and trunk, tingling of the hands, metallic taste, tachycardia, and vomiting occur acutely. •Hypotension may result from intense peripheral vasodilation.


Cont.

• The syndrome typically is self-limited and lasts only several hours.• No specific antidote is available.• If hypotension is severe, vascular reexpansion with isotonic parenteral solutions may be required.• Small oral doses of propranolol have also been suggested.


Central Nervous System: Rapid Onset

Isoxazole Intoxication •Although Amanita muscaria and Amanita pantherina may contain muscarine, the toxins responsible for the CNS symptoms after ingestion of these mushrooms are muscimol and ibotenic acid, the heat-stable derivatives of the isoxazoles. •Muscimol, a hallucinogen, and ibotenic acid, an insecticide, have anticholinergic effects. 34M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

04/12/23

Cont.

• From 30 min to 3 hr after ingestion, CNS symptoms appear: obtundation, alternating lethargy and agitation, and, occasionally, seizures. •Nausea and vomiting are uncommon.• If large amounts of muscarine are contained in the mushroom, symptoms of cholinergic crisis also may occur.


Cont.

• Specific therapy must be carefully selected• If an exaggerated cholinergic response is observed, atropine should be administered.• Because ingestions of A. muscaria often are associated with anticholinergic findings the acetylcholinesterase inhibitor physostigmine is often used to reverse the delirium and coma.


Cont.

• Benzodiazepines also are used for the agitation and delirium.• Seizures can be controlled with diazepam•In most cases, however, early treatment with ipecac (if the patient is conscious) and close observation are all that is required.


Indole Intoxication

• Mushrooms belonging to the genus Psilocybe (“magic mushrooms”) contain psilocybin and psilocin, two psychotropic compounds.• Within 30 min after ingestion, patients experience euphoria and hallucinations, often accompanied by tachycardia and mydriasis.


Cont.

• Fever and seizures have also been observed in children with psilocybin poisoning.• These symptoms are short-lived, usually lasting for 6 hr after consumption of the mushroom. •Severely agitated patients may show response to diazepam.


Gastrointestinal: Rapid Onset• Many mushrooms from various genera produce local gastrointestinal manifestations. •The causative toxins are diverse and largely unknown.• Within 1 h of ingestion, patients experience acute abdominal pain, nausea, vomiting, and diarrhea. •Symptoms may last from hours to days depending on the species of mushroom


Treatment

• Treatment is mainly supportive.• Children with large fluid losses may require parenteral fluid therapy.• It is imperative to differentiate ingestion of mushrooms of this class from ingestion of Amanita and Galerina species containing cyclopeptide toxins.


42

PotatoPotato Poisoning Poisoning


Potato Poisoning

• Solanine is a mixture of several related toxins found in greened and sprouted potatoes. •Potatoes exposed to light and allowed to sprout produce a number of alkaloid glycosides containing the cholesterol derivative solanidine.


Solanine Poisoning

• Two of these glycosides, α- solanine and α- chaconine, are found in highest concentration in the peels of greened potatoes and in the sprouts. •Some solanine can be removed by boiling but not by baking.


Solanine Poisoning

•The major effect of α-solanine and α- chaconine is inhibition of cholinesterase•Cardiotoxic and teratogenic effects have also been reported.


Clinical manifestations of solanine and chaconine poisoning

•Intoxication occur within 7-19 hr after ingestion. •The most common symptoms are: vomiting, abdominal pain, and diarrhea • In more severe instances of poisoning neurologic symptoms, including: drowsiness, apathy, confusion, weakness, and vision disturbances, are rarely followed by coma or death.

04/12/23 46M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

Treatment of solanine poisoning

• Is largely supportive.• In the most severe cases, symptoms resolve within 11 days. •Atropine treatment has not been evaluated.

04/12/23 47M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

References

• Bedry R, Baudrimont I, Deffieux G, et al: Brief report: wild mushroom intoxication as a cause of rhabdomyolysis. N Engl J Med 2001; 345:798-804.•Diaz JH: Syndromic diagnosis and management of confirmed mushroom poisonings. Crit Care Med 2005; 33:427-436.•Berger KJ, Guss DA: Mycotoxins revisited: part II. J Emerg Med 2005; 28:175-183•Korpan YI, Nazarenko EA, Skryshevskaya IV, et al: Potato glycoalkaloids: true safety or false sense of security?. Trends Biotechnol 2004; 22:147-151.•Ruprich J, Rehurkova I, Boon PE, et al: Probabilistic modelling of exposure doses and implications for health risk characterization: glycoalkaloids from potatoes. Food Chem Toxicol 2009; 47:2899-2905.•http://www.crazyaboutmushrooms.com/mushroom_poisoning.html04/12/23 48M&P Poisoning Prof. Dr. Saad S Al Ani Khorfakkan Hospital

Thank You

m&p poisoning

Documents

ingestedmp poisoning

bymushroom poisoning

ingested mushroomsmp

mgkg24 hrmp poisoning

renal failure

galerina species

amanita poisoningis

severe diarrhea