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Jungle Juice: Methanol poisoning

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  • Jungle Juice: Methanol poisoning

    Think of this the next time you're in Asia and you decide to drink one of the "house specials"

    A nurse was being treated for horrific injuries in an Australian hospital Wednesday, after she was flown home from Indonesia in a coma brought on by drinking a toxic cocktail that has killed at least four foreigners.

    Jamie Johnston, 25, of Newcastle, in New South Wales, is struggling to speak, can barely walk and her legs are severely burnt after drinking a cocktail called Jungle Juice at a cafe on the island of Lombok, west of Bali.

    "It burnt her from the inside out," said Lyn Tisdell, the mother of Johnston's boyfriend Dennis.
    "There needs to be more awareness out there about these drinks. Young people going there for [end of school celebrations], please be careful of what you drink."

    The nurse collapsed at Denpasar Airport in Bali two weeks ago suffering renal failure, a day after drinking Jungle Juice with her mom at Happy Cafe on the last night of their vacation. Her mother, a lawyer, was not affected by the drink.

    Johnston slipped into a coma and sustained brain scarring because of lack of oxygen. She spent two days at the hospital in Denpasar with no improvement before being medically evacuated to Darwin, in northern Australia, at a cost of $50,000.

    Boyfriend of three years Dennis Tisdell, 28, said doctors suspected the drink was laced with the chemical methanol, sometimes used in the local brew arak, a distilled palm wine.

    He said they were told Johnston's mother did not get sick because the methanol was in the tops of the jugs of Jungle Juice. Four foreigners were among 25 people killed by a tainted batch of arak in 2009.
    Experienced Community organizer. Yeah, let's choose him to run the free world. It will be historic. What could possibly go wrong...

    "You're just a jaded cynical mother****er...." Jeffpeg

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  • #2
    Methanol is metabolized by the enzyme alcohol dehydrogenase (ADH) in the liver, via formaldehyde to formic acid, the latter being responsible for the adverse effects seen in methanol poisoning. The toxicity evolves from a combination of the metabolic acidosis (H+ production) and an intrinsic toxicity from the formate anion itself. Treatment consists of buffer such as sodium bicarbonate to correct metabolic acidosis and antidote to inhibit metabolism of methanol to its toxic metabolite, formic acid. If necessary, haemodialysis is supplied to further correct the acidosis, and remove both methanol and formate. In addition, folinic acid may enhance the endogenous metabolism of formate. Methanol poisonings occur as isolated episodes caused by accidental or intentional ingestion, or epidemics. In the latter situation a large number of victims are often reported.

    The most common effects of methanol intoxication are visual and neurologic; among visual effects are optic nerve atrophy, temporal pallor of the optic nerve head, visual field defects, and loss of visual acuity (severe to deep blindness). Neurological deficits include polyneuropathy and encephalopathy (from light to severe), ataxic gait (unstable walking), Romberg test positive (meaning that they cannot stay upright with their eyes closed), or sensory loss on the distal part of the legs. The effects tend to be irreversible. People that present in coma after methanol ingestion have a poor prognosis.

    Despite efficient treatment, methanol poisoning has a high morbidity and mortality. Some patients with methanol poisoning will probably remain unknown in a large outbreak, either having lesser symptoms and never being examined, or dying without the diagnosis of methanol poisoning being suspected. The prognosis depends on the degree of metabolic acidosis. Different findings on admission has been suggested as poor prognostic factors, e.g. high S-methanol concentration, although others do not find this. Coma on admission is generally considered a poor prognostic sign, and recently, increased pCO2 in the severely acidotic patient (lack of compensatory hyperventilation) is suggested as a new marker. The most frequent sequelae found at discharge are visual disturbances and neurological impairment of some kind.
    Experienced Community organizer. Yeah, let's choose him to run the free world. It will be historic. What could possibly go wrong...

    "You're just a jaded cynical mother****er...." Jeffpeg

    (more comments in my User Profile)
    russbo.com


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    • #3
      Originally posted by doc View Post
      Methanol is metabolized by the enzyme alcohol dehydrogenase (ADH) in the liver, via formaldehyde to formic acid, the latter being responsible for the adverse effects seen in methanol poisoning. The toxicity evolves from a combination of the metabolic acidosis (H+ production) and an intrinsic toxicity from the formate anion itself. Treatment consists of buffer such as sodium bicarbonate to correct metabolic acidosis and antidote to inhibit metabolism of methanol to its toxic metabolite, formic acid. If necessary, haemodialysis is supplied to further correct the acidosis, and remove both methanol and formate. In addition, folinic acid may enhance the endogenous metabolism of formate. Methanol poisonings occur as isolated episodes caused by accidental or intentional ingestion, or epidemics. In the latter situation a large number of victims are often reported.

      The most common effects of methanol intoxication are visual and neurologic; among visual effects are optic nerve atrophy, temporal pallor of the optic nerve head, visual field defects, and loss of visual acuity (severe to deep blindness). Neurological deficits include polyneuropathy and encephalopathy (from light to severe), ataxic gait (unstable walking), Romberg test positive (meaning that they cannot stay upright with their eyes closed), or sensory loss on the distal part of the legs. The effects tend to be irreversible. People that present in coma after methanol ingestion have a poor prognosis.

      Despite efficient treatment, methanol poisoning has a high morbidity and mortality. Some patients with methanol poisoning will probably remain unknown in a large outbreak, either having lesser symptoms and never being examined, or dying without the diagnosis of methanol poisoning being suspected. The prognosis depends on the degree of metabolic acidosis. Different findings on admission has been suggested as poor prognostic factors, e.g. high S-methanol concentration, although others do not find this. Coma on admission is generally considered a poor prognostic sign, and recently, increased pCO2 in the severely acidotic patient (lack of compensatory hyperventilation) is suggested as a new marker. The most frequent sequelae found at discharge are visual disturbances and neurological impairment of some kind.
      Thanks for sharing but don't you think that such a lengthy and long posts make the reader bore. lolzzz
      Don't mind, I was just kidding. Oakland County gyms
      Take again for sharing. regards
      Last edited by Daniel89; 11-26-2011, 01:51 PM.

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