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Old July 29th, 2005 #13
Jenab
Senior Goatly One
 
Join Date: Mar 2004
Location: Hillsboro, West Virginia
Posts: 1,302
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Quote:
Originally Posted by Kind Lampshade Maker
The deer's liver is obviously designed to take the abuse. But, I think you are confusíng the aftermath of other Muscaria variants. Indeed, that most dangerous white-colored variety requires a liver transplant for those Homosapiens who consume them.
You might be thinking of Amanita virosa, or A. verna, or A. phalloides, which are lighter in color than A. muscaria. The first two of those is actually white, while the third is white when young (the cap becomes pale yellow when older).

Quote:
Originally Posted by Kind Lampshade Maker
All in all, without a liver transplant, the eventual death is long and horrible. I think 20 days is the limit. At any rate, I wouldn't wish such a fate on anybody.
Here's what I found:

Quote:
Originally Posted by IPCS INCHEM
9.3 Course, prognosis, cause of death

The course of amanitin intoxication has 3 chronological 3 phases:

a) A latent phase of approximately 6 - 24 hours (mean 12.3
hours), rarely extending to 48 hours.

b) A gastrointestinal phase with abdominal pain, vomiting and
diarrhoea causing dehydration, hypovolaemia, electrolyte and
acid-base disorders. This phase usually lasts 2-3 days.

c) An hepatic phase which begins 36 - 48 hours after ingestion.
The pre-icteric phase can only be detected by an increase in
serum transaminases. Hepatitis becomes clinically evident with
the onset of jaundice on the 3rd -4th day after ingestion. In
severe intoxications, patients develop fulminant hepatitis with
hepatic coma, bleeding and anuria. When liver damage is
reversible, patients usually make a slow and steady recovery. In
fatal cases death occurs within 6 - 16 days (mean 8 days).

Prognosis: An analysis of the literature shows that the factors
most likely to indicate a poor prognosis in Amanita hepatitis are
peak prothrombin time > 100 sec; factor V < 10%; lactic
acidosis; gastrointestinal bleeding; and age < 12 years. Other
criteria, such as the duration of the latency period; the peak
serum concentration of aminotransferases; and amanitin analysis
are not useful for prognosis. Orthotopic liver transplantation
should be considered in patients with poor prognosis criteria.

In a study of 205 amanita intoxications, the gastrointestinal
syndrome was present in 199 patients and hepatitis in 198; 52
patients developed hepatic coma and the overall mortality was
22.4% (Floersheim et al, 1982)

9.4 Systematic description of clinical effects

9.4.1 Cardiovascular

In the gastrointestinal phase, vomiting and diarrhoea can
produce severe fluid losses resulting in hypovolaemic shock
with tachycardia and a fall in central venous pressure.
Functional reversible renal failure often accompanies
hypovolaemic shock secondary to gastrointestinal fluid loss.

When shock occurs in the hepatitic phase, it is mainly due
to haemorrhage secondary to severe coagulation disorders.
Cardiovascular collapse also accompanies severe hepatic
failure in the terminal phase.

9.4.2 Respiratory

Respiration is usually normal but hyperventilation
accompanies fulminant hepatitis. Respiratory failure with
hyperventilation or apnoea may occur in patients presenting
with hepatic coma and has a poor prognosis.


9.4.3 Neurological

9.4.3.1 CNS

Neurologic symptoms are related to hepatic
encephalopathy which usually occurs 5 - 6 days after
ingestion. Somnolence and confusion are the first
signs, and coma usually follows. Convulsions may be
observed in hepatic coma.

In severe hepatic failure, coma may also be due to
hypoglycaemia secondary to disordered glucose
metabolism.

9.4.3.2 Peripheral nervous system.

No data available.

9.4.3.3 Autonomic nervous system

No data available.

9.4.3.4 Skeletal and smooth muscle

No data available.

9.4.4 Gastrointestinal

Gastrointestinal symptoms appear after a latent period of 6
- 24 hours (mean 12.3 hours). In a study of 205 Amanita
intoxications, gastrointestinal symptoms were present in 199
patients (Floersheim et al, 1982).

a) Nausea, vomiting, colic.

There is a sudden onset of colicky abdominal pain rapidly
followed by nausea, frequent vomiting and diarrhoea.

b) Diarrhoea

In most cases, diarrhoea is severe, watery and cholera-like.
In the absence of fluid replacement, diarrhoea rapidly
induces dehydration, haemoconcentration and hypovolaemic
shock. Diarrhoea may persist for 2 - 4 days.

9.4.5 Hepatic

Clinical signs of hepatocellular damage usually develop on
the 3rd to 4th day after ingestion. Clinical presentation
may only include a mild jaundice and a mild hepatomegaly.

In severe cases, hepatitis follows a fulminant course with
marked jaundice and hepatic coma and may be accompanied by
renal failure and cardiovascular collapse. In fatal cases,
death occurs within 6 - 16 days (mean 8 days).


9.4.6 Urinary

9.4.6.1 Renal

Two types of renal failure may be observed. During the
gastrointestinal phase a functional renal failure is
frequent. It is associated with hypovolaemia and is
secondary to fluid loss and to hypoperfusion of the
kidneys. It may improve if dehydration and
hypovolaemia are corrected aggressively.

Anuria and renal failure may occur during the third
phase of poisoning together with severe hepatitis,
hepatic coma and haemorrhage.

Serious kidney complications may be avoided by
administration of fluids (Constantino et al, 1978,
Vesconi et al, 1985). A direct nephrotoxic effect of
amatoxins has not been proven in human intoxication.

9.4.6.2 Others

No data available.

9.4.7 Endocrine and reproductive systems

No data available.

9.4.8 Dermatologic

Mild jaundice with icteric sclerae is present in the hepatic
phase.

9.4.9 Eyes, ear, nose, throat: local effects

Eyes:Scleral icterus occurs.

Nose:Nasal haemorrhage may occur in patients with
coagulation disorders secondary to severe
hepatocellular damage. If intubation is necessary, the
nasal route should be avoided because it may induce
severe local haemorrhage.

9.4.10 Haematological

Severe hepatocellular damage may result in severe
haemorrhage.

Usually the earliest indication of coagulopathy is
persistent bleeding from IV puncture sites (Bivins et al,
1985). Other bleeding, epistaxis and gastrointestinal
haemorrhage may occur.

These are due to marked coagulation defects secondary to
impaired synthesis of clotting factors. This indicates a

poor prognosis. (Floersheim, 1987).


9.4.11 Immunologic

No data available.

9.4.12 Metabolic

9.4.12.1 Acid based disturbances

In the gastrointestinal phase, metabolic acidosis may
occur as the result of bicarbonate loss in diarrhoea;
in later stages, acidosis may be due to hepatic
failure.

9.4.12.2 Fluid and electrolyte disturbances

Dehydration and hypovolaemia

The gastrointestinal syndrome often results in marked
dehydration and hypovolaemia with haemoconcentration
and functional renal failure.

Electrolyte disturbances

Hypokalaemia is particularly common in the
gastrointestinal phase.

9.4.12.3 Others

Glucose

Glucose metabolism is often disturbed in severe hepatic
failure. Spontaneous hypoglycaemia results from
impaired glycogenolysis and gluconeogenesis (Bivins et
al, 1985).

Hepatic enzymes

Elevated serum transaminase, LDH and serum bilirubin
are the first and best indicators of liver damage and
should be monitored throughout the course of the
illness. Hepatic enzymes usually reach a peak after 60
- 72 hours and then decrease. Enzyme levels may be
relatively low in massive liver necrosis (Bivins et al,
1985).

Coagulation parameters

Coagulation disorders indicate hepatic insufficiency.
Levels of clotting factors synthesized by the liver,
such as fibrinogen and prothrombin, may be decreased.
A prothrombin level below 10 per cent indicates a poor
prognosis (Floersheim 1987)


9.4.13 Allergic reactions

No data available.


9.4.14 Other clinical effects

Amatoxin does not affect temperature regulation directly but
temperature disorder may occur in severe hepatic failure
with encephalopathy.

9.4.15 Special risks: pregnancy, breast feeding, enzyme
deficiency

Pregnancy: Kauffmann et al, (1978) reported a Amanita
phalloides poisoning in a 25 year old woman at 9 weeks
gestation. The patient developed a toxic hepatitis
(transaminase 1800 U/l). After life threatening maternal
illness was overcome, a therapeutic abortion was carried out
at 12 weeks gestation. Histologic examination of the foetal
liver showed cellular damage related to amanitin toxicity.
Amatoxins therefore cross the placenta barrier in
concentrations sufficient to affect the foetus.

Breast-feeding: Because amatoxins are excreted in breast
milk, nursing mothers who have ingested Amanita, whether
they are symptomatic or not, should be told to stop nursing
until it is determined whether or not they have been
poisoned (Bivins et al, 1985).
The authors for the above were: A Jaeger , F Flesch, Ph Sauder, and J Kopferschmitt of Centre Anti-Poisons, Hospices Civils de Strasbourg, 67091 Strasbourg Cédex, France.

Quote:
Originally Posted by Kind Lampshade Maker
If the deer could filter out the nauseating effect of Anamita Muscaria consumption, I'm willing to go that route. But, the deer's gotta be female, or else, no dice
Shorter urethra to be defiled in, yeh.

Jerry Abbott