Professional Documents
Culture Documents
Case
Lisa M.
Rich, MD; Marc R. Caine, MD; James W. Findling, MD; Joseph L. Shaker, MD
\s=b\ Clinically significant hypoglycemia is an unusual complication of anorexia nervosa. We describe a 44-year-old woman with a
5-year history of anorexia nervosa who presented with hypoglycemic coma and eventually experienced sudden death. Biochemical studies showed suppressed levels of insulin, C peptide, and proinsulin during hypoglycemia; appropriate elevations of growth hormone and cortisol levels were observed,
suggesting that the hypoglycemia was related to severe malnutrition. Nine previously reported cases of severe hypoglycemia in
anorexia nervosa are reviewed (six of the patients involved also
died). The presence of severe hypoglycemia in anorexia nervosa
implies a grave prognosis and mandates aggressive medical and
nutritional therapy to improve the chance of survival.
(Arch Intern Med. 1990;150:894-895)
thighs.
The electrocardiogram revealed sinus bradycardia, low voltage,
and nonspecific T-wave changes. Routine laboratory studies revealed
the following values: sodium, 133 mmol/L; potassium, 3.8 mmol/L;
chloride, 93 mmol/L; carbon dioxide content, 27 mmol/L; creatinine,
44.2 pmol/L; albumin, 22 g/L; aspartate transaminase, 143 U/L (nor
mal, <45 U/L); alanine transaminase, 73 U/L (normal, <45 U/L);
alkaline phosphatase, 150 U/L (normal range, 50 to 136 U/L) ; biliru
bin, 24 pmol/L (normal, <26 pmol/L); prothrombin time, 13.6 sec-
COMMENT
Source, y
Elias and Gwinup,31982
Patient No./Age, y/
Age at Onset, y/Sex/Weight, kg
Outcome
Glucose,
mmol/L
1/23/18/F/38.0
Death: respiratory
arrest
0.8
2/60/30/F/25.0
Death:
Death:
pneumonia
pneumonia
0.8
3/32/30/F/24.0
6/18/16/F/29.5
Survived:
1.4
Albumin,
g/L
Cortisol,
nmol/L
Insulin,
pmol/L
29
"Low"
1020
30
770
<30
<1.0
35
>1340
Undetectable
<1.0
24
>1340
Undetectable
1.2
24
1.0
20
pneumonia,
congestive heart
failure
Present case
7/27/24/M/38.5
Death: pulmonary
edema
4/57/27/F/22.5
Death: miliary
tuberculosis
5/27/23/F/26.5
Survived:
8/28/14/F/19.0
Survived:
9/26/13/F/31.4
Death:
0.8
28
Death: sudden
1.1
22
10/44/39/F/39.0
sepsis
pneumonia
pneumonia
vosa.1518
0.4
740
30
References
1. Hadden DR, Belf MD. Glucose, free fatty acids and insulin interrelations
in kwashiorkor and marasmus. Lancet. 1967;2:589-592.
2. Wharton B. Hypoglycemia in children with kwashiorkor. Lancet.
1970;1:171-173.
in adults. N
Engl
J Med.
1976;294:766-772.
8. Schwabe AD, Lippe BM, Chang RJ, Pops MA, Yager J. Anorexia nervosa. Ann Intern Med. 1981;94:371-381.
9. Gold PW, Gwirtsman H, Avgerinos PC, et al. Abnormal hypothalamic\x=req-\
pituitary-adrenal function in anorexia nervosa. N Engl J Med. 1986;314:1335\x=req-\
1342.
10.
1983;143:282-287.
19. Vara E, Tamarit-Rodriguez J. Glucose stimulation of insulin secretion in
islets of fed and starved rats and its dependence on lipid metabolism. Metabolism. 1986;35:266-271.
20. Blickle JF, Reville P, Stephan F, Meyer P, Demangeat C, Sapin R. The
role of insulin, glucagon, and growth hormone in the regulation of plasma
glucose and free fatty acid levels in anorexia nervosa. Horm Metab Res.
1984;16:336-340.
21. Brodows RG. Starvation enhances the ability of insulin to inhibit its own
secretion. Metabolism. 1985;34:53-56.
22. Slone D, Taitz LS, Gilchrist GS. Aspects of carbohydrate metabolism in
kwashiorkor. Br MedJ. 1961;1:32-34.
23. Kanis JA, Brown P, Fitzpatrick K, et al. Anorexia nervosa: a clinical
psychiatric and laboratory study. Q J Med. 1974;43:321-338.
blog.mycology.cornell.edu
http://blog.mycology.cornell.edu/2006/11/22/i-survived-the-destroying-angel/
vomiting reflex was strong. The pressure of the strong contractions forced stuff out both ends of the GI tract,
uncontrollably. I had a severe case of vomiting and diarrhea. At that point, deep down I knew I had made the big
mistake: I HAD EATEN AMANITA VIROSA, AKA, THE DESTROYING ANGEL. 1
For the next three hours, I was making trips constantly from my bed to the
bathroom. I was still in denial. My housemate asked me the first time I was
up Are you OK? I said Yes, I was just sick. By the time 7:30 had rolled
around, I had talked to my girlfriend, called in sick to work and still had not
mentioned that I thought it was Amanita poisoning. Finally, my housemate
again asked me what was going on. I responded saying I think I
accidentally poisoned myself with some bad mushrooms last night.
He said Maybe you should go get checked out at the local Convenient
Care Center.
I silently thought to myself, Yeah, If I go there, Ill be sitting and waiting and
by the time someones sees me, Ill be dead.
I found my mushroom book and looked up the symptoms for Amanita
poisoning: vomiting and diarrhea or severe constipation 6-8 hrs after
consumption.2 Oh, and by the way, its now destroying your liver and 50 to
80 percent of the people who ingest Amanita DO NOT SURVIVE! At that
point, I knew I was in deep, deep doo doo and in for the biggest fight of my
life, for my life.
I called the Poison Control Center 800-222-1222.
They suggested I go back to the area where I had picked the mushrooms
and get one to take with me for identification, then get myself to the local
emergency room. I went back to the area and picked the one mushroom I
had left because I thought it was Amanita. I also took a piece of stem I had
thrown into the garbage the night before.
At this point, as long as I didnt eat or drink anything I could get around. I
had pretty much eliminated everything from my GI tract.
I got in my car to drive myself to the emergency room. Three thoughts went
through my head as I prepared to leave:
1. Should I go back into the house and say goodbye to my cats? My response: No you idiot, you dont have time
for that!
2. If I didnt have health insurance, would I go to the emergency room knowing I was just about to wipe out my
cash reserve? Luckily I didnt have to ponder that question as I had insurance and felt very fortunate. But what
about someone who didnt? Would they deny their symptoms and just consider it food poisoning? What would
have been the end result? They probably would just start to feel better and then keel over from liver failure.
Amanita will fool you that way.
3. My last thought was Take one last look around you, because you may never be back here again. I did, and
left without telling anyone where I was going.
to the receptionist. She was on the phone with someone. She obviously was in a discussion with someone about
some problem and it wasnt going to be anytime soon that she could get off the phone. I waited patiently thinking, I
dont want to make a scene. Nevertheless, I didnt understand why she couldnt put the person on hold while she
addressed a new emergency room client.Finally, around 9:30, she got off the phone and asked What can I do for
you? I explained to her that I felt I had accidentally poisoned myself with some poisonous mushrooms. She asked
whether my records were at the hospital. I said yes. She checked my name and found I indeed was registered and
my insurance information was current. She asked me to be seated and informed me that someone would be with me
shortly.
I expected that someone would be out to see me within a minute or so since I had informed them that I suspected
mushroom poisoning. Instead, time dragged on. I kept thinking, just stay calm and collected. Finally, after waiting
another 20 minutes, someone came to get me.
Its amazing to me. Most people when they know they are dying think of what they didnt do or what they should have
done. In this case, all I could do was watch and monitor time like a hawk. My concern was I needed help NOW!
ASAP! But, I also knew I needed to stay calm so as not to create a panic situation.
I dont remember much once I was admitted other than them taking vital signs and getting the info they needed
regarding the poisoning and making sure that I was the only one involved. They kept me comfortable while someone
took the mushroom to Cornell for identification. They started an IV to replenish my fluids.
While waiting, I finally took the time to write down some phone numbers for people to call in case I didnt make it. I
also made a few more trips to the restroom.
The Emergency room staff came back saying a Cornell Mycologist (Kathie Hodge) had identified it. It was definitely
Amanita virosa mushroom poisoning.1
The first thing they did was make me drink a milk shake size container of charcoal. Have you ever seen a charcoal
drink? It is as black as you can imagine. I often practice the Bates palming eye improvement exercise. During this
exercise you rub your palms together, then place them over your eyes, and imagine the blackest black you can
imagine. This was the blackest black I had ever seen! It was really hard to get past the thought and just drink it. It had
a chalky flavor.
About a half hour later. The ER staff informed me they had called Bangs Ambulance and they were present, waiting to
transport me to Strong Memorial Hospital in Rochester, New York.
Needless to say, the charcoal drink did not stay down long. It would be at least another half hour before we left
because I had to first go to the restroom to honor the vomiting reflex. My body was still reacting to anything put into
my stomach and was rejecting the charcoal drink. Its probably a good thing I made the ambulance crew wait and
went to the bathroom when I did or I would have been upchucking in the ambulance all the way to Rochester.
Before leaving, I also made a few phone calls; to work, letting them know what was going on and that I probably
wasnt going to be available to work the weekend, to my housemate, and to my girlfriend Julie. Then I was strapped in
a gurney, loaded in the ambulance and on my to Rochester.
The trip to Rochester from Ithaca was uneventful. The attending ambulance technician comforted me all the way.
What I do remember the most was watching the clock above the rear doors. We left Ithaca around 3:00 p.m. in the
afternoon and arrived at Strong Memorial in Rochester around 5:37 p.m.
I was being sent to Strong Memorial because they had the only liver transplant unit in upstate New York. The
treatment of choice is often liver transplantation. With early diagnosis, another experimental treatment includes
massive doses of penicillin to stimulate the livers defenses. This was the treatment I would receive with the option to
transplant if my liver failed.
power cord glowing red was feeding power to keep it lit up. I was riding in a black limo and sparks flew from behind
the car as we drove over the power cord. The next thing I knew, I was next to my grandfathers grave. I was
wondering why I was there when I was awakened by the nurse for another blood sample.
When people ask me whether I had any near-death experiences, I usually relay my dream to them. I am here by the
grace of God! I feel so lucky and yet fortunate. I found out that of three people admitted in 2006 to Strong Memorial
with Amanita poisoning, I am the only one to have survived; 66% died.
Why did I live and the rest not live?
Was it the amount of toxin?
Was it that I knew what had happened to me and sought care and help quickly?
Was it my meditation/visualization and somatic self care/self help practice?
Was it the prayers of my friends and family and my faith?
Was it the doctors care? One of them said it was a miracle!
Simply said, I dont know that it was any individual thing, but a combination of everything.
Monday, July 24th was my birthday. I could not have received a better gift than the gift of life. Throughout my life, I
have been traumatized. I was born a blue baby, fell out of a silo at the age of 12, etc. I could go on, but the important
thing is, I am a survivor. I love catsmaybe I have nine lives!
How did I get in such a mess? In retrospect, I considered the possibility that I had subconsciously poisoned myself.
But in reality, the mistake I made was just not taking the time to positively identify the mushrooms I had picked
before ingesting them.
The Truth
Most victims of life-threatening mushroom poisoning in North America are people from Southeast Asia;
Laos, Cambodia, Thailand, Viet Nam. They apparently mistake Amanita for edible Paddy-Straw
(Volvariella volvacea) mushrooms. The two are similar in several ways; cap color, size, and the white
cup around the base of the stalk, but different in others (for example, the Paddy-Straw has a pink
spore print, the Amanita*, a white spore print; and the Amanita* has a partial veil). The Paddy Straw
mushroom occurs in tropical and temperate areas worldwide, and is especially common in Southeast
Asia; the Amanita, alas, does not occur in Southeast Asia, so folks from that part of the world are
unaware of the lethal look-alike.
Millions of North Americans pick and eat wild mushrooms every year, without as much as a belly ache.
Are they experts? Yes! At least, they are experts on the edible wild mushrooms they know. Either
their parents or grandparents taught them how to identify morels, or puffballs, or meadow mushrooms,
or they have a good field guide and they read it or both.
No one with a reasonable understanding of the importance of properly identifying mushrooms with a
serious awareness that some species are fatally toxic falls victim to the Destroying Angel*. The folks
who eat Destroying Angel* do not use field guides: they just pick the damned things and eat them. No
trip to the library. No reading. No spore prints. No idea what a partial veil is or what gill attachment
means.
So Is it really dangerous to eat wild mushrooms?
How dangerous is it to drive a car? If youre drunk or careless, it is VERY dangerous; if youre sensible
and pay attention, it is reasonably safe.
Consider this: Would you pick and eat an unfamiliar berry simply because it looked good? Of course
not. Finding, identifying, preparing, and eating wild mushrooms can be a delightful pastimeIF it is
done intelligently.
Otherwise, it is a terrible accident waiting to happen.
* I took the liberty of changing the name from deathcap to destroying angel or Amanita in the text
above. Its worth noting that Amanita phalloides most closely resembles the paddy-straw mushroom;
A. virosa less so.
Excerpted with permission from David Fischers American Mushrooms.
Epilogue
It was another week after leaving of the hospital before I felt comfortable eating and not being close to a bathroom. I
was back to work within two weeks of being released from the hospital. A month later, I was pretty much back to full
strength. My liver numbers normalized early, pretty much by the time I had left the hospital. It would be another month
and a half before my kidney numbers normalized.The liver is a remarkable organ. It is the only organ that can
regenerate itself. The kidneys are a different story. There is probably some permanent damage there but not sufficient
to require any long term care. People often donate and live with just one kidney.
I did have some strange thoughts during my recovery at home. Im assuming they were just lingering effects of the
toxins in my system. In general, Ive made a complete recovery and expect no long term effects. I am grateful to be
alive and feel very lucky. Im also grateful for my training in Hanna Somatic Education. It felt great to get back home
and in the routine of practicing my somatic exercises, exploring, and able to be comfortable in my body again. It was
like coming home to my body as well. I encourage everyone to get a copy of Thomas Hannas book: Somatics:
Reawakening the Minds Control of Movement, Flexibility, and Health or to visit the Hanna Somatics website.
Richard Eshelman can be contacted via phone at 607-280-6788, or by email at re16@cornell.edu or
upstatehse@aol.com.
A Special Thanks to Kathie Hodge for encouraging me to write this.
1. Editors Note: Amanita virosa and Amanita bisporigera are treated as two separate species by most
mycologists, but their appearance and effects are quite similar, and the names have sometimes been used
interchangeably. The Editor follows the authoritative example of Rod Tulloss and Zhu-liang Yang in treating
northeastern North American destroying angels as Amanita bisporigera, whereas Amanita virosa is a strictly
European species. There is some satisfaction in this, since A. bisporigera was described from the Ithaca area
exactly 100 years ago by my predecessor at Cornell, George F. Atkinson. This is a centennial poisoning!
2. Editors Note: For more on Amanita toxicity and recognition please see our Destroying Angels post.
3. Editors Note: Alpha-lipoleic acid, also known as thioctic acid, was advocated for treatment of Amanita
poisoning in the 1950s and 1960s, but subsequent studies failed to find a therapeutic effect, according to D.R.
Benjamin (1995, Mushrooms: Poisons and Panaceas. W.H. Freeman).
Photos: K.T. Hodge (young Amanita), and K.E. Loeffler (the mature Amanita that Richard brought with him to the
hospital for identification).
CASE STUDY
Roger S. Blumenthal, MD
HISTORY
Mrs. Gordon is a 35-year-old woman whose
mother died from heart disease at the age of 55.
She currently has 2 children and is planning a
pregnancy in the near future. On evaluation,
blood pressure is 130/80 mm Hg and body mass
index is 27.
LABORATORY RESULTS
Mrs. Gordons fasting lipid profile includes a total
cholesterol level of 300 mg/dL; the low-density
lipoprotein (LDL) level is 220 mg/dL, the high-density lipoprotein (HDL) level is 40 mg/dL, and the
triglyceride level is 200 mg/dL. Fasting blood glucose
level is 110 mg/dL. Liver enzyme assessment reveals an
alanine aminotransferase value of 25 U/L and an
aspartate aminotransferase value of 30 U/L.
INTERVENTION
Mrs. Gordons LDL level is more than double the
goal of 100 mg/dL recommended in the clinical
guidelines issued in May 2001 by the National
Cholesterol Education Program (NCEP) Adult
Treatment Panel (ATP III). The HDL level is low,
and below the cutpoint of 40 mg/dL. Moreover, her
family history of heart disease further increases her
own risk for coronary heart disease. Clearly, treatment for her hypercholesterolemia is warranted.
However, because Mrs. Gordon is considering
another pregnancy, the use of statins is contraindi-
167
CASE STUDY
168
Vol. 2, No. 5
March 2002
NOTES
169
Despite an absence of gastrointestinal complaints, colonoscopy, upper endoscopy, and video capsule endoscopy
were then performed, all of which were normal including random biopsies from the duodenum and colon. Fecal
A1AT clearance was found to be markedly abnormal at 299mg per 100ml (normal, <54mg per 100ml),
consistent with PLE. Fat malabsorption was also found to be present (29g/day; normal, 27g/day). Numerous
micronutrient deficiencies were identified including copper, zinc and selenium, and vitamins A and D. Given the
finding of PLE without a defined cause, an excisional lymph node biopsy was performed and revealed chronic
lymphocytic leukemia/small lymphocytic lymphoma. This was confirmed on a subsequent bone marrow
examination. He was subsequently treated with chemotherapy and his ascites and edema were gradually resolved.
At his last follow-up visit in May 2008, his ascites and edema were absent, albumin level was normal, previous
micronutrient deficiencies were resolved, and a repeat fecal fat collection was nearly normal at 10g/day. Fecal
A1AT clearance was not repeated.