http://www.postgradmed.com/issues/1999/09_99/debanto.htm
What could be causing chronic abdominal pain?
Anything from common peptic ulcers to uncommon pancreatic trauma
John R. DeBanto, MD; Gary W. Varilek, MD; Laurie Haas, MD
VOL 106 / NO 3 / SEPTEMBER 1999 / POSTGRADUATE MEDICINE
--------------------------------------------------------------------------------
CME learning objectives
To identify a possible cause and formulate a treatment plan in patients
who present with chronic abdominal pain
To understand embryologic origins of intestinal structures and use this
knowledge to conceive a diagnosis
To recognize signs of a serious problem and the need to refer to a
gastroenterologist
--------------------------------------------------------------------------------
Preview: Establishing a reasonable diagnosis and treatment plan in
patients with chronic abdominal pain can be difficult and frustrating.
Most cases involve a common and readily identified condition (eg,
gallbladder disease, GERD, irritable bowel syndrome). Other cases,
however, resist ready diagnosis because they offer no intra-abdominal
explanation. In this article, the authors summarize several diverse
possibilities as the source of the pain, and they describe how to
approach evaluation to avoid unnecessary testing.
DeBanto JR, Varilek GW, Haas L. What could be causing chronic abdominal
pain?: anything from common peptic ulcers to uncommon pancreatic trauma.
Postgrad Med 1999;106(3):141-6
Chronic abdominal pain is a common complaint of patients seeing a
primary care physician, and it is a leading reason for referral to a
gastroenterologist. The pain usually has persisted for 3 to 6 months and
is affecting the patient's activities of daily living. Diagnosis can be
perplexing, because it often requires piecing together a medical history
from a seemingly endless barrage of signs and symptoms.
History taking
Often, the diagnosis can be made through history taking. Physical
examination, laboratory testing, and other evaluations (eg, endoscopy)
should be considered complementary measures.
Patients often find their abdominal discomfort difficult to describe, so
providing example descriptors (eg, burning, dull, achy, sharp, stabbing,
crampy) may be helpful. Such prompting may elicit a more accurate
response from the patient and assist in diagnosis.
Location of the pain often suggests a source. This information can help
direct questioning to ascertain a possible diagnosis. Location is most
easily categorized on the basis of embryologic origin.
Pain located between the xiphoid process and the umbilicus originates in
the foregut, which includes the distal esophagus, stomach, proximal
duodenum, biliary tree, pancreas, and liver (although conditions of the
liver usually do not cause chronic abdominal pain).
Pain in the periumbilical region arises from viscera of the midgut (eg,
small intestine, appendix, ascending colon, proximal two thirds of the
transverse colon).
Pain between the umbilicus and the symphysis pubis emanates from hindgut
organs (eg, distal one third of the transverse colon, descending colon,
rectosigmoid region) (1).
Common causes
Evaluation of chronic abdominal pain typically begins with ruling out
common gastrointestinal causes (eg, peptic ulcer disease,
gastroesophageal reflux disease, biliary colic). Once this avenue of
investigation is exhausted, assessment is directed to uncommon causes.
Peptic ulcer
Typically, pain caused by a peptic ulcer is localized to the epigastrium
and is dull, achy, nonradiating, and altered with ingestion of food.
Nausea and vomiting may be reported. If an ulcer is suspected, workup
should include a stool guaiac test and hemoglobin measurement. In
patients over age 50, the addition of upper gastrointestinal tract
endoscopy is prudent. Esophagogastroduodenoscopy should be performed if
any warning features (eg, weight loss, anemia, hematemesis, melena,
hematochezia) are present that may represent a serious condition, such
as tumor.
Chronic pancreatitis
Pain caused by chronic pancreatitis is usually midepigastric, with
radiation to the lower thoracic or upper lumbar vertebral region. It is
described in various ways, often as dull and severe, and is commonly
accompanied by nausea and vomiting. Dehydration often ensues before
medical assistance is sought. Presentation also may include
malabsorption, diarrhea, weight loss, or diabetes. Patients often have
known alcoholic pancreatitis.
Amylase and lipase levels may be normal, especially with long-standing
disease that has resulted in greatly impaired pancreatic function.
Abdominal x-ray films often show pancreatic calcification. Patients with
chronic pancreatitis are at risk for endocrine and exocrine
insufficiency.
Usually, the pain of chronic pancreatitis is best treated with
narcotics, despite the strong predilection of alcoholic patients for
addiction. An alternative to narcotics is nerve-block therapy, in which
a sclerosing agent is injected under radiologic guidance into the celiac
plexus. Subtotal pancreatectomy or the Puestow procedure
(pancreaticojejunostomy, in which the pancreas is sliced open and the
pancreatic duct anastomosed to a loop of jejunum for drainage) is a last
resort. Despite these measures, many patients still experience pain.
Although they rarely alleviate discomfort, pancreatic enzymes should be
administered in patients with malabsorption.
Gastroesophageal reflux disease
Gastroesophageal reflux disease can cause epigastric pain, usually
described as a burning sensation, that is limited to the upper abdomen
or chest. Typically, a trial of histamine2 (H2) receptor antagonists or
proton pump inhibitors is sufficient to confirm the diagnosis. However,
if the patient reports dysphagia, odynophagia, weight loss, or signs of
anemia, immediate referral to a gastroenterologist is needed so
endoscopy can be performed to rule out a serious problem (eg, malignant
stricture).
Dyspepsia
A diagnosis of nonulcer dyspepsia, a nondescript sensation of epigastric
discomfort, is usually assigned to patients in whom other diagnoses have
been excluded. At present, there is no treatment recommendation for this
troublesome entity. At the University of Kentucky College of Medicine,
Lexington, we typically treat dyspepsia symptoms with H2 receptor
antagonists or proton pump inhibitors and have had mixed results.
Gallbladder disease
Chronic pain in the right upper quadrant usually originates in the
biliary tree or gallbladder; rarely, it emanates from the proximal
transverse colon. Biliary colic usually prompts a dull and achy
sensation. Alternatively, it may be described as sharp and episodic or
persistent, and it can be debilitating. It is often, but not always,
associated with ingestion of fatty foods. The pain is occasionally
accompanied by nausea and vomiting, and it often occurs in the middle of
the night.
Patients with right upper quadrant pain and an intact gallbladder should
undergo ultrasound evaluation. If abnormalities are revealed (eg,
stones, sludge), cholecystectomy is usually performed. Unfortunately,
many patients continue to have pain. Those with elevated liver enzyme
levels should be referred to a gastroenterologist for endoscopic
retrograde cholangiopancreatography to evaluate for biliary causes, such
as choledocholithiasis or biliary dyskinesia.
Irritable bowel syndrome
The abdominal pain of irritable bowel syndrome is typically nonspecific,
diffuse, crampy, and accompanied by bloating and occasionally by nausea.
It is usually relieved by bowel movements. In most patients,
constipation or diarrhea is the predominate symptom, and in some
patients the two symptoms alternate. Mucus may be present in the stool.
Symptoms are often aggravated by emotional stress. Therapy for irritable
bowel syndrome is guided by symptoms.
Inflammatory bowel disease
Chronic abdominal pain is more common in patients with Crohn's disease
than in those with ulcerative colitis. The pain is typically located in
the right lower quadrant, and a mass may be palpable. Patients may
describe mucus and blood in their stools. In contrast to irritable bowel
syndrome, in inflammatory bowel disease, symptoms and signs of
inflammation (eg, arthralgias, weight loss, fever, failure to thrive)
and markers of inflammation (ie, elevated C-reactive protein level and
sedimentation rate) are often present. Depending on the severity of the
disease, anemia and low serum levels of albumin and zinc also may be
found.
Uncommon causes
After common causes of chronic abdominal pain have been excluded, less
common causes should be considered. Abdominal wall pain is one of the
more frequently encountered but relatively uncommon sources of chronic
abdominal discomfort. In addition, pain may be referred from points of
origin that are outside the abdominal cavity, may present long after a
traumatic event, or may result from psychological or metabolic disorder.
Abdominal wall pain
Trauma or overexertion is often the initiating event in abdominal wall
pain. The pain also may arise from the peripheral nervous system,
similar to the sensory neuropathy of patients with diabetes. Other
sources of peripheral nervous system pain are neuroma, peripheral
neuralgia that follows the tract of a sensory nerve, and postherpetic
neuralgia (ie, occurring after an attack of herpes zoster).
Abdominal wall pain often has an insidious onset and may follow a
dermatomic pattern. Characteristically, it is sharp initially and
becomes dull over time, but in some cases, it remains sharp. Sneezing,
coughing, or lifting heavy objects may exacerbate the discomfort, and
changing positions or applying heat may relieve it.
The diagnosis is derived from history taking and physical examination,
which relies on palpation for Carnett's sign (2). In this evaluation,
the examiner first palpates the area of tenderness and applies enough
pressure to elicit maximal stimulation. Then, the patient is asked to
tense the abdominal muscles, usually with straight leg-raising, and the
examiner again applies pressure. The pain is intensified if it
originates in the abdominal wall and is unchanged if it originates in
viscera.
Several general treatment measures may be useful in abdominal wall pain.
The most effective is probably injections of bupivacaine hydrochloride
(Marcaine HCl, Sensorcaine) plus a corticosteroid into trigger points
(see box below). Stretching the involved area and spraying it with a
vapo-coolant (eg, ethyl chloride) is occasionally helpful. Heat and rest
may be beneficial. Other methods that have had some success include use
of amitriptyline hydrochloride (Elavil) or other antidepressants,
nonsteroidal anti-inflammatory drugs (NSAIDs), or muscle relaxants;
application of 0.025% capsaicin cream (Zostrix); and use of
low-intensity ultrasound.
Fibromyalgia: Patients with fibromyalgia often have multiple trigger
points over the entire body. They usually respond poorly to
trigger-point injections and require long-term follow-up. Myofascial
pain may be a manifestation of fibromyalgia, but it typically does not
involve the muscles of the abdominal wall.
Painful rib syndrome: Thoracic nerves VII through XII innervate the
anterior abdominal wall. Therefore, the chest or thoracic spine may be
the source of abdominal pain.
Painful rib syndrome results from increased mobility of the anterior
costal cartilage of the 8th through 11th ribs (3). Normally, fibrous
attachments bind the lower costal cartilages to one another. If these
attachments are loosened (eg, by trauma), the ribs may be able to slide
over one another, pinching the intercostal nerve. The outcome is severe,
sharp pain followed by a dull ache, usually localized to one area. The
pain, typically at the costal margin, may be elicited by hooking the
fingers over the lower edge of the ribs and applying gentle traction.
Treatment with trigger-point injection often brings some relief, but
pain may persist. NSAID therapy and rest may be helpful.
Tietze's syndrome: This well-established entity, also called costal
chondritis, can cause anterior chest wall discomfort and pain along the
costal margin or subxiphisternal region that mimics epigastric or upper
quadrant disease. NSAID therapy may be helpful in some patients.
Typically, Tietze's syndrome is recurrent, and reassurance may be the
most beneficial form of treatment.
Posttraumatic pain: Abdominal muscle strain, myofascial injury, and
rectus sheath hematoma are typical outcomes of trauma. They are
difficult to differentiate clinically, although localized fluid
collection represents hematoma. Most such injuries heal spontaneously
with use of conservative measures (eg, rest, NSAID therapy). However,
patients who have repeated trauma to the abdominal wall (eg,
construction workers, weight lifters, football players) often need
trigger-point injections and sustained rest. Long-term prognosis is
excellent, and minimal follow-up is required.
In some patients, postoperative pain develops along the scar from an
abdominal incision. It is not unusual that an extensive workup has
preceded diagnosis of this pain, which is relieved with trigger-point
injections.
Hernia: A ventral hernia usually occurs postoperatively when weakened
abdominal muscles do not heal properly or separate with strain. In
adults, umbilical hernias are caused by predisposing factors, such as
pregnancy or abdominal distention caused by ascites, abdominal mass, or
obesity. A hernia is usually easily recognized, especially when the
patient tenses the abdominal muscles on rising from a supine to a
sitting position. Palpating the hernia may elicit the pain. Expectant
therapy and reassurance are usually adequate, but surgical correction is
occasionally warranted.
Precordial catch syndrome
This syndrome usually occurs in young patients. It consists of a sudden,
stabbing chest pain that is so severe it causes patients to grab and
bend toward the affected area, often while wincing with pain (4). The
pain may cause a "catch" in breathing or force patients to take shallow
breaths. It lasts for only a few seconds and may be followed by a dull
ache. The pain of precordial catch syndrome may mimic biliary colic.
Diagnosis is suggested by a history of sudden, sharp pain without an
obvious inciting event. With conservative therapy, the discomfort
typically diminishes within a few days. The cause of this syndrome
remains unknown.
Thoracic disk herniation
The pain of thoracic disk herniation may closely resemble that of
chronic pancreatitis. It may be episodic and localize to the epigastrium
with radiation to the back (5). Alternatively, it may radiate to the
lumbar region or midline of the back near the affected disk or follow a
radicular pattern around the chest. Other signs and symptoms of disk
herniation include muscle weakness, sensory loss, and bowel or bladder
incontinence. Thorough history taking can usually eliminate the
diagnosis of chronic pancreatitis. When thoracic disk disease is
suspected, magnetic resonance imaging of the vertebral column and
referral to a neurosurgeon are indicated.
Spinal-muscle or vertebral-body disorder
Both visceral sympathetic and somatic nociceptive afferent nerves
converge in the same dorsal horn along the spinal cord. In addition,
visceral and somatic noxious stimuli may be conveyed along the same
spinothalamic tract that carries pain fibers. Thus, pain from the spinal
muscles or vertebral bodies may be interpreted as abdominal in origin.
Jorgensen and Fossgreen (6) com-pared 39 patients who had chronic upper
abdominal pain in the absence of any demonstrable organic
intra-abdominal cause with 28 healthy controls. They found that 28 (72%)
of the patients with abdominal pain also had back pain (versus 5 [17%]
of the controls) and that 21 (75%) of those patients who had back pain
had physical-examination findings pointing to a vertebral organic cause.
Most of the findings were localized in the lower thoracic or
thoracolumbar region, where innervation is shared with the upper
abdominal tract. Of the 39 patients with abdominal pain, about half had
symptoms of irritable bowel syndrome and about 40% had heartburn.
Pancreatic injury from blunt trauma
Acute pancreatitis is a well-recognized consequence of blunt trauma to
the abdomen (7), but chronic abdominal pain is not. Typically in such
cases, injury is to the tail of the pancreas, and patients recover
rapidly; however, months to years after the initial injury, they present
with persistent abdominal pain. In this setting, the serum amylase level
is usually normal, but on endoscopic retrograde
cholangiopancreatography, the distal duct is found to be obstructed. On
laparotomy, the head of the pancreas is often normal, but the tail is
fibrotic and the duct stenotic. After distal pancreatectomy, symptoms
usually abate. Therefore, during history taking, it can be useful to ask
patients with chronic abdominal pain about blunt trauma to the abdomen
within the past several months.
Psychological disorder
Psychological illnesses can manifest as pain. The pain is often
described as intense, constant, diffuse, and persisting for years, but
it is not consistent with abnormality of any anatomic structure.
Typically, these patients look well, and an organic cause is elusive.
They often have a history of depression, anxiety, childhood sexual
abuse, and somatoform disorders. Treatment is difficult, and the
assistance of a psychiatrist usually is warranted.
Metabolic disease
Rare metabolic conditions should be considered in differential diagnosis
in patients with unexplained chronic abdominal pain. Among the possible
causes are porphyria, chronic renal failure, and Addison's disease.
Conclusion
Careful and thorough assessment of patients with chronic abdominal pain,
including precise examination of historical and physical findings,
should result in an appropriate management strategy. This method avoids
unnecessary and expensive investigations that can further complicate the
initial presentation. In many patients, a treatable cause can be
identified. In others, the cause of ongoing abdominal pain remains
unknown. A critical element of care in these latter patients is
reassurance, for them and their significant others, that the pain is
real and not caused by serious illness. Treatment should focus on
improving quality of life and returning patients to a normal functional
existence. A multidisciplinary approach, including psychotherapy and
pain-relief programs, may be needed to accomplish these goals.
References
Yamada T, Alpers DH, Owyang C, et al. Textbook of gastroenterology. 2d
ed. Philadelphia: Lippincott-Raven, 1995:754-6
Christensen J, Summers RW. Puzzling abdominal pain. Gastro Dis Today
1994;3(3):1-7
Scott EM, Scott BB. Painful rib syndrome: a review of 76 cases. Gut
1993;34(7):1006-8
Sharpstone D, Colin-Jones DG. Chronic, non-visceral abdominal pain. Gut
1994;35(6):833-6
Whitcomb DC, Martin SP, Schoen RE, et al. Chronic abdominal pain caused
by thoracic disc herniation. Am J Gastroenterol 1995;90(5):835-7
Jorgensen LS, Fossgreen J. Back pain and spinal pathology in patients
with functional upper abdominal pain. Scand J Gastroenterol
1990;25(12):1235-41
Gholson CF, Sittig K, Favrot D, et al. Chronic abdominal pain as the
initial manifestation of pancreatic injury due to remote blunt trauma of
the abdomen. South Med J 1994;87(9):902-4
--------------------------------------------------------------------------------
Suggested procedure for trigger-point injections to relieve abdominal
wall pain
Cleanse the skin with povidone-iodine and alcohol. In a 20-mL syringe,
combine 5 mL of a 10 mg/mL solution of triamcinolone acetonide
(Kenalog-10) and 15 mL of 0.5% bupivacaine hydrochloride (Marcaine HCl,
Sensorcaine).
With the patient supine, insert the needle perpendicular to the plane of
the abdomen at the point of maximum tenderness (ie, trigger point).
Injections should be deep enough to traverse the subcutaneous tissue and
reach the fascial layer. The weight of the syringe usually ensures
adequate penetration but, occasionally, mild pressure is needed. When
the syringe comes to an abrupt halt, the fascial layer has been reached;
the patient often winces in pain. Inject about 5 mL of solution at each
trigger point. Apply a bandage if any bleeding occurs.
Pain relief is usually immediate. Occasionally, additional treatments at
intervals are necessary.
--------------------------------------------------------------------------------
Dr DeBanto is a fellow and Drs Varilek and Haas are assistant
professors, department of internal medicine, division of
gastroenterology, University of Kentucky College of Medicine, Lexington.
Correspondence: Gary W. Varilek, MD, Department of Internal Medicine,
Division of Gastroenterology, MN649, 800 Rose St, University of Kentucky
College of Medicine, Lexington, KY 40536-0084. E-mail:
var...@pop.uky.edu.
--------------------------------------------------------------------------------
Jean, it typically *does* involve the diaphragm. Which is really big...
Just a thought.
Deirdre ;-)
--
B-12 methylmalonuric acid (MMA) test links: References:
http://www.b12.com/page1i.htm
Doctors' letters and e-mail addy for enquiries:
http://www.b12.com/page1j.htm
.
> J Wootton wrote:
> >
> > N.B.
> > 1) This list is by no means complete.
> > 2) Myofascial pain may be a manifestation of fibromyalgia, but it
> > typically does not involve the muscles of the abdominal wall.
> > FWIW
> > J
>
> Jean, it typically *does* involve the diaphragm. Which is really big...
Deirdre,
If you have some urls, confirming and describing the pain, would be very helpful (for
me and/or lurkers).
Thanks,
J
http://www.google.com/search?q=diaphragm+anatomy
Searched the web for diaphragm anatomy. Results 1 - 10 of about
13,900. Search took 0.11 seconds.
Whew. That's *fast*.
Diaphragm Anatomy
EMG Homepage Quick-Anatomy Trunk Muscles. Diaphragm
Phrenic Nerve C3-C4-C5. ...
Not bad. Hard for me to see but gives a good idea of where the diaphragm
is and what part of it might be hurting and roughly where, also - maybe
- why. Worth a little close study. BTW I've looked for materials on the
diaphragm before and it's my observation that it's hard for anatomical
artists to depict. So one has to do a little thinking.
http://www.teleemg.com/Anatomy/Muscles/diaanat.htm
diaphragm (anatomy)
diaphragm. In mammals, a thin muscular sheet separating
the thorax from the abdomen. It is attached ...
http://ebooks.whsmithonline.co.uk/encyclopedia/51/M0029751.htm
I passed on the next two:
Shrew Talk
... Recipients: > 174 Contents of this Issue o Editorial o Research 1.
Diaphragm anatomy
in shrews 2. Venom in shrews 3. Skulls and 'noisy mice' 4. Blood samples
o ...
http://members.vienna.at/shrew/shrewtalk=1-04.html - 11k - Cached -
Similar pages
Untitled
... Inquiry by Jukka Savolainen, April 1997 jsavo...@joyl.joensuu.fi
Diaphragm anatomy in shrews: Whereas in mammals the diaphragm is
described to be a dome ...
http://members.vienna.at/shrew/oldinquiries.html - 14k - Cached -
Similar pages
This is not bad - has a well written description of anatomical
arrangement. Drawings not all that helpful to me unfortunately.
Diaphragm - A-to-Z Science - DiscoverySchool.com
... A-to-Z Science > Diaphragm Diaphragm, «DY uh fram,» the large muscle
attached to
the lower ribs, separates the chest from the abdomen. Only human beings
and ...
http://school.discovery.com/homeworkhelp/worldbook/atozscience/
d/157720.html
I passed on this one too. I would expect to spend the rest of my
afternoon peering.
Vesalius Image Archive: Diaphragm Development and CDH
... 2. diaL3002. Pleuroperitoneal canals. Narr: 3. diaL3003.
Diaphragm anatomy. Narr: 4. diaL3004. Bochdalek ...
http://www.vesalius.com/graphics/archive/archtn_diaph_devpmt.asp
This is a bit of a hoot - if you wish to memorize the names of various
anatomical structures - in contiguity - here are some memonics or
memorization devices. Boys will be boys... some people might be
offended.
Anatomy Mnemonics for CHA101L
... by references to male/female anatomy, please don't look at this
page! Spinal Cord and Vertebral Column. c3-4-5 keeps the diaphragm alive
(innervation of phrenic ...
http://cim.ucdavis.edu/users/grogo/cha101/mnemonics.shtml
Just in general, over the years, I have found that abdominal pain can be
ascribed to the diaphragm. It's big, extensive, and its attachment right
across the chest at the level of the syphoid cartilage right at the
lower end of the breastbone are particularly hardworking and I feel in
PWFMS liable to be quite spastic. Waistbands are unbearable - hipsters
forever. The band of the brassiere lands in an unbearably sensitive
place.
I haven't seen a mention of the diaphragm in any description of
costochondritis and yet of course much of the discomfort could be caused
by spastic contraction of the diaphragm. I suspect that what used to be
called a "stitch" or sharp pain in the side (which people try to reduce
by leaning sharply to that side) is caused by a spasm of an area of the
diaphragm.
Now I will go search for > phrnic nerve anatomy < and see what I can
catch.
Such fun...
Love from Deirdre ;-)
> []
> Gee, Jean - you really must be feeling kind of under the weather.
Yes, and a transition from @home to rogers (chaos for days now).
> []. I suspect that what used to be
> called a "stitch" or sharp pain in the side (which people try to reduce
> by leaning sharply to that side) is caused by a spasm of an area of the
> diaphragm.
That's the spleen/diaphragm, Deirdre. (or can be, if felt on the left side)
http://groups.google.com/groups?hl=en&threadm=5rtd73%24pp66%40news02.comp.pge.com&rnum=2&prev=/groups%3Fas_q%3Dspleen%2520stitch%26hl%3Den
Absolutely certain is, however, that a full stomach, cold air or running
downhill is increasing the probability of stitches.The inner organs are
hanging from several ligaments, which, in turn, are fixed to the diaphragm,
the muscular "plate" between chest and abdomen. Liver, spleen, stomach, small
intestine and colon form a weight of several kilograms, hanging from the
diaphragm like from a thin thread. <end snip>
See after a meal, the spleen engorges with blood (for unknown reasons, I suspect it's a
"sugar" rush, but forget now and can't remember where I filed that <g>), so is heavier for
about an hour. So too the stomach (full of food, epigastric emptying or something).
I was looking for connections ... fM, trigger point, diaphragm and descriptions of the
pains being experienced. (to rule in or out some of what I've been experiencing which they
tell me is GERD in combo with FM trigger point.
All very interesting about the diaphragm. (saved it).
Phrenic nerve sounds interesting. Maybe that's the sharp pain I get out my left upper
back? (rhetorical)
Thanks Deirdre, always interesting. :)
J
--
Ellen/Nelle
Duchess of the Ozarks
Royal Realm of W.H.I.N.E..
"J Wootton" <jwoo...@rogers.com> wrote in message
news:3C00CFB7...@rogers.com...
I don't think anyone's been all that forthcoming about abdominal pain -
we obviously have a lot of abdominal pain that's hard to identify, and
of course it's important to find out what it is. But there are a lot of
structures in the abdomen.
Phrenic nerve anatomy search:
http://www.google.com/search?hl=en&q=phrenic+nerve+anatomy
A fruitful search.
Here's one that might suggest at least part of what's going on when
people are having a panic attack. It might also suggest *why* I'm always
saying take yer B vitamins... and yer miny-ruls:
http://uscneurosurgery.com/glossary/p/phrenic%20nerve.htm
This one is from Baylor - excellent written description of both anatomy
and nerve function. None of these materials is definitive but taken
together they help build up a mental picture.
Review of Anatomy: The Neck
... Phrenic nerve - C3-5; Brachial ... related to recurrent laryngeal
nerve and parathyroid glands; Blood ... superimposed on superficial neck
anatomy): The neck can be ...
http://www.bcm.tmc.edu/oto/studs/anat/neck.html
This one from Virtual Hospital is of course stupendous. It's also slow
loading but everything is labelled. I can't see a lot of it though. I
need higher contrast than most images supply.
http://www.vh.org/Providers/Textbooks/HumanAnatomy/3Section/01.html
I can give you a first hand account of a recent experience during an
i.v. nutritional support injection. I received 2.5 g ascorbic acid and
magnesium sulfate (epsom salts) which for reasons unknown or unrevealed
to me at any rate amplifies the antioxidant effect of the vitamin C
(ascorbic acid).
The effect is of *heat* and this is real heat - hot heat.
Magnesium sulfate is used by many obstetricians to treat preeclampsia. I
did a little reading - this *is* interesting stuff. It's not known
whether it's really all that effective in preventing eclampsia or not. I
will say it definitely helps reduce pain of the chronic variety. I get
these treatments to help me in my battle to save my lower limbs but
they're generally beneficial and don't do my eyes any harm either. I
started these treatments in late summer 1998 to try to get my vision
back. I got back partial vision - a very satisfactory outcome.
Apparently everyone feels the effect of this infusion differently though
it's typically described as heat. Some people feel it in their head only
and nowhere else. Remarkable, truly. Others feel it in other areas. I
felt it mainly across my chest and I felt it was mainly active in the
areas of the diaphragm closest to the ribs. The effect is powerful. The
best description I can give is "heat". And it's definitely not cool or
gentle but *strong heat* (?!)
I would say I received my maximum dose. When I was being treated for my
cataracts originally I was receiving magnesium and came to a point at
which I felt I was "topped up". I do think there's a point at which
magnesium's special usefulness to PWFMS could be not just to the max but
actually exceeded.
I've had the same experience with oral magnesium supplementation. I
believe the patient should set the upper limits. An excessively high
dose can have a number of untoward effects.
I should imagine that thermography would prove very interesting in these
treatments. What is happening is the breakdown of oxides or oxidation
products so that they can be cleared in harmless forms. The magnesium
sulfate causes a drop in blood pressure, presumably by reducing vascular
spasm and permimtting improved perfusion by the blood.
Here's another link relating to the phrenic nerve - pretty interesting
stuff too. This is approach to hyperalgesia due to nerve damage
investigates the use of zinc.
http://anatomy.med.unsw.edu.au/tracey/tracey.htm
The photogaph of that truly deucedly handsome gentleman is far too dark
and that's a wrong use of a flash but... my, my, my...
I find hiccups *most* painful - I hiccup and say "ow" because it really
does hurt - and I absolutely hate ever having them. I put my attention
anywhere else - that's my method of dealing with them. I'm sure
solutions are quite individual.
Here's a page that explained to me what's hurting when I have hiccups.
Interesting:
http://www.madsci.org/posts/archives/dec96/837802597.An.r.html
Hope all this proves uplifting... heh heh... There's much, much more out
there. I've barely disturbed the surface - haven't even scratched it.
Love from Deirdre ;-)
Clue
Well ligaments seem to be attached to the diaphragm (Deirdre's theory) and
my further post.
A year or so ago, I posted an article that said this city had a very high
% of FM'ers.
Since disability no longer recognizes FM, and doctors continue to
attribute symptoms to FM and/or "out of shape", this does not bode well
for those on disability, at the time of their 2-year medical reviews.
Besides, personally I don't care what they call it, I'm just frustrated
because there's no apparent solution.
For instance, last week doc told me to do stretching exercises. He says
it's a combo of FM and GERD but the GERD pills don't fix/stop it.
It's exactly stretching (body, arms, upper torso)(and/or a "trigger
point" on my left rear thoracic protrusion which they all seem to think is
a swollen muscle..for 3 years???) that starts up these vicious
intermittent pains, so I have to stop moving and/or lie down (so my
muscles don't move) to stop the pains.
I'm frustrated and discouraged. Can you tell?
Best,
J
--
Ellen/Nelle
Duchess of the Ozarks
Royal Realm of W.H.I.N.E..
"J Wootton" <jwoo...@rogers.com> wrote in message
news:3C01C7B9...@rogers.com...
J Wootton <jwoo...@rogers.com> wrote in message
news:3C021525...@rogers.com...
Good to know, as they're next in my sights. Turns out when they dropped me
from LTD after 24 months, it WASN'T automatic as they'd claimed, but rather
based on their making an uncontested decision I was no longer qualified as
disabled... Took me a long time to find the document stating that, as I
moved three times since then and have been in a whirlwind of competing
crises. But now it's come to the point where I need the money and insurance
they should have been providing. Desperately...
"Michael Baugh" <baug...@bellsouth.net> wrote in message
news:fXoM7.58923$Lo5.7...@e3500-atl1.usenetserver.com...
"J Wootton" <jwoo...@rogers.com> wrote in message
news:3C00CFB7...@rogers.com...
> N.B.
> 1) This list is by no means complete.
> 2) Myofascial pain may be a manifestation of fibromyalgia, but it
> typically does not involve the muscles of the abdominal wall.
> FWIW
> J
>
><snip>
<pre>
Subject: endometriosis
Gynecol Obstet Invest 1998;46(1):58-60
Chemical assay of iron in ovarian cysts: a new diagnostic method to evaluate
endometriotic cysts.
Iizuka M, Igarashi M, Abe Y, Ibuki Y, Koyasu Y, Ikuma K
Department of Obstetrics and Gynecology, Gunma University School of
Medicine, Maebashi, Japan.
CA-125 is abundantly secreted from ovarian endometriotic cysts, but is
not specific to endometriosis. In order to develop a new, more
specific diagnostic marker for endometriosis, the iron concentrations
in various ovarian cysts were assayed. The ovarian cysts were
punctured and the contents aspirated laparoscopically,
laparotomically, or transvaginally. The iron concentration in the
ovarian cystic fluid was assayed using a spectrophotometer after
protein precipitations and chromogen treatment. The iron
concentrations in ovarian cysts were 69.5+/-10.4 micromol/l in serous
cystadenomas, 73.5+/-29.3 in mucinous cystadenomas, 65.4+/-12.4 in
dermoid cysts, and 92.5+/-18.2 micromol/l in adenocarcinomas. On the
other hand, high iron concentrations were demonstrated in
endometriotic cysts (1,749.6+/-41.5 micromol/l), a lutein cyst
(1,393.8), hemorrhagic corpus luteum (1,957.5) and endometrioid
adenocarcinomas (1,860.9+/-157.9 micromol/l). Cytological smear tests
of the contents as well as histological examination allowed
differential diagnosis between endometriosis and endometrioid
adenocarcinoma. In conclusion, assay of the ovarian cystic iron
concentration is a useful diagnostic tool for the evaluation of
ovarian endometriotic cysts.
_________________________________________________________________
Subject: endometriosis
Ultrastruct Pathol 1997 May-Jun;21(3):273-80
The lipofuscin-iron association in pigmentosis tubae.
Munichor M, Kerner H, Cohen H, Iancu TC
Department of Pathology, Rambam Medical Center, Haifa, Israel.
Pigmentosis tubae (PT) is a rare condition characterized by the
presence of numerous lipofuscin-laden macrophages in the lamina
propria of the fallopian tube. Two women, who also had endometriotic
ovarian cysts, showed polypoid pigmented tubal mucosae. In addition to
lipofuscin, occasional cells showed spotty positivity for iron.
Ultrastructural examination of the tubal mucosa showed the
lipofuscin-containing bodies, which were similar to
lipofuscin-containing lysosomes found in other pigmented conditions.
Cytoplasmatic ferritin and hemosiderin in siderosomes were observed in
macrophages and endothelial cells of the lamina propria. The present
study is the first to demonstrate the presence of iron-containing
particles and lipofuscin in the residual bodies of PT. The origin of
the excess iron is not clear, but erythrophagocytosis and an abnormal
tubal environment could play a role. Iron-promoted lipid peroxidation
may alter the lysosomal membranes and contribute to the excessive
accumulation of lipofuscin in these cells.
Comments:
* Comment in: Ultrastruct Pathol 1997 Nov-Dec;21(6):605
_________________________________________________________________
_________________________________________________________________
From The June 2000 Issue of Nutrition Science News
Feature
Too Much of a Good Thing
by Bill Sardi
fortified bread Recent studies reveal that blood donors exhibit lower
rates of many diseases and experience better than average health.
Additionally, the centuries-old practice of bloodletting is being
revived as a treatment for disorders such as heart disease, cancer and
Alzheimer's.1 Why would blood reduction improve health parameters? In
part, because blood removal helps to control circulating iron levels.
Iron is an essential component of hemoglobin in red blood cells, is
associated with strength, and is required for oxygen transport, DNA
synthesis and other processes. But it also has a destructive nature.
In its free form, unbound from hemoglobin or other binding proteins,
it accelerates oxidation or "rusting" of body tissues. Since
iron-induced oxidation worsens the course of virtually every disease,
iron control could be a universal approach to disease prevention and
therapy.2
Whereas poor iron intake, or impaired absorption, may lead to anemia,
too much iron--iron overload--is even more problematic.3 After full
growth is achieved, at about age 18 or so, excess iron accumulates in
the blood of all humans at the rate of 1 mg per day.2 About 80 percent
of the body's iron stores are in the blood. Women are less at risk for
iron buildup than men because of the blood they lose monthly during
menstruation. As a result, women have somewhere around half the
circulating iron levels as men. Their rates for heart disease, cancer
and diabetes are also about half those of males. Because men have no
direct outlet for iron, by age 40 their iron levels are similar to
those of a postmenopausal 70-year-old woman. This amount of iron can
lead to premature aging and diseases such as arthritis, cancer,
cataracts, diabetes, osteoporosis, and retinal, liver and brain
disorders.4 Postmenopausal women, or women who have undergone early
hysterectomy in their 20s, 30s and early 40s, may experience similar
problems.5
Recognizing the Problem
Iron overload hasn't gone completely unnoticed. There are a number of
books on the topic, but most are written for health professionals,
leaving the public largely unaware of the problem. Also, some
confusion exists regarding the role of iron in health and disease.
First, there is a mistaken idea that the majority of the people
affected by iron overload diseases have the genetic form, called
hemochromatosis, which affects only about 1 million of the estimated
275 million Americans. In fact, the potential threat of iron overload
is universal. It comes with advancing age and regardless of genetic
factors. Second, the emphasis on preventing anemia in children and
menstruating women has detracted attention from progressive iron
buildup in adult men and postmenopausal women.6
Upon closer inspection, many health-promoting practices inadvertently
control iron. For example, taking an aspirin a day to prevent heart
attacks and strokes causes blood loss via the digestive tract on the
order of about a tablespoon per day. This results in iron loss.7
Raymond Hohl, M.D., an assistant professor of internal medicine and
pharmacology at the University of Iowa in Iowa City, says even chronic
use of a baby aspirin may help to control iron and in some cases can
induce iron-deficiency anemia.8 Aspirin also appears to increase the
production of ferritin, an iron-binding protein that prevents iron
from inducing oxidation.9 By exercising, a person loses about 1 mg of
iron through sweat.10 Fasting and vegetarian diets, both of which
promote longevity in animals and humans, limit iron consumption
because red meat contains the highly absorbable heme iron. Whether or
not related to iron consumption, restricting red meat consumption has
been shown in various studies to reduce the risk of colon cancer.11
Normal Iron Regulation
In healthy individuals there is little if any unbound iron circulating
in the blood. In all disease states, however, unbound iron (also
called free iron) is released at sites of inflammation and can spark
uncontrolled oxidation.12 Fortunately, there are numerous automatic
mechanisms in the body that help to control iron, many by
chelation--compounds that bind to a toxic substance (such as iron) and
render it nontoxic or nonactive. Albumin, a simple protein found in
blood, acts as a chelator by loosely binding to iron.13 Ferritin,
produced in the liver, is another iron-binding protein.14 Transferrin
is a protein that chelates iron and totes it back to the liver, where
it is metabolized and excreted.15 The liver produces lactoferrin,
another iron chelator, when challenged by infectious agents.16 This is
important because pathogenic organisms such as viruses, bacteria and
fungi require iron for growth. Furthermore, as iron stores increase,
the gastric absorption of iron decreases. So the body employs numerous
mechanisms to control iron that are activated when threatened by
disease. However, these defensive mechanisms can be overwhelmed.
Blood tests for iron levels (i.e., hemoglobin and ferritin levels are
checked for transferrin saturation percentages) are often useful, but
the results of these tests are confounded in states of prolonged
inflammation or disease.17 A skilled hematologist is often the best
professional from whom to obtain personal information concerning blood
iron levels.
Differentiating between anemia and iron overload can be difficult
because both conditions cause fatigue. One study at the Department of
Medicine, University of Western Ontario in Canada, found that iron
overload can produce a wide range of symptoms, such as joint pain
(particularly hip), unexplained gastric pain, frequent infections,
skin bronzing, elevated liver enzymes, cessation of menstruation, hair
loss and heart flutters (fibrillation). Yet, of 410 iron-overload
patients, 27 percent experienced no symptoms whatsoever.18 Common
symptoms of iron-deficiency anemia are lowered resistance to
infections, fainting, breath holding, mental fatigue, sleepiness, cold
hands and feet, and cravings for ice, meat or tomatoes, all which are
more likely to occur among women.19
Dietary Iron Control
Various dietary practices can help control iron levels. In a
relatively short period of time, dietary changes can result in anemia,
iron overload or an ideal state of iron control. Anemia can be induced
in about 120 days, while symptoms of iron overload can come on in just
60 days.
Humans absorb only a fraction of the iron they consume, but there are
many controlling factors.20 Iron absorption rates from food vary
widely, from less than 1 percent to nearly 100 percent.21 Cooks who
use iron or stainless steel pots increase the amount of iron they
consume.22 Generally, iron in plant foods is not as well absorbed as
iron from meat: Only 5 percent of iron in plant foods is available,
vs. 30 to 50 percent of iron from meat.23 Olive oil and spices such as
anise, caraway, cumin, licorice and mint promote iron absorption,24
while antacids, eggs and soy reduce availability.25 Since dairy
products contain lactoferrin, milk also inhibits the absorption of
iron.26 Moderate alcohol consumption is unlikely to pose a problem
with iron absorption, but excessive amounts of alcohol is associated
with iron overload, particularly in adult males.27
Vitamin C also increases iron absorption.28 However, there is no
evidence that vitamin C leads to iron overload. Thus vitamin C should
not be avoided by meat-eaters for this reason, since studies show
high-dose vitamin C supplements are associated with a decreased risk
for heart disease, cancer, cataracts and other disorders.29 A
vegetarian diet does not generally cause iron-deficiency anemia
because there is more vitamin C in plant-food diets, which enhances
absorption.30
A 1982 human study was conducted to assess the effect of various
drinks on iron absorption. A subject ate a standard meal of a
hamburger, string beans, mashed potatoes and water. When green tea was
drunk instead of water, iron absorption was reduced by 62 percent.
Coffee reduced iron absorption by 35 percent, whereas orange juice (as
a source of vitamin C) increased absorption by 85 percent. Contrary to
other studies, milk and beer had no significant effect.31
Bioflavonoids (found in berries, coffee, green tea, pine bark,
quercetin and the rind of citrus fruits, particularly blueberry,
cranberry, elderberry and grape seed) and phytic acid (a component of
whole grains and seeds such as sesame) bind to iron and other minerals
in the gastric tract and help to limit iron availability. If
bioflavonoids and phytic acid haven't bound to minerals in the
digestive tract they will get into the bloodstream, where they can
bind to free iron, acting as blood-cleansing iron chelators.
Therefore, maximum iron chelation in the blood circulation is achieved
when these iron binders are consumed apart from meals.
Phytic acid--also called inositol hexaphosphate, or IP6--is comprised
of six phosphorus molecules and one molecule of inositol. It has been
mistakenly described for decades as an "anti-nutrient" because it
impairs mineral absorption. However, in the 1980s food biochemist
Ernst Graf, Ph.D., began to tout phytic acid for its beneficial
antioxidant properties achieved through mineral chelation.32
Phytic acid in foods or bran should be distinguished from supplemental
phytic acid, which is derived from rice bran extract. In foods, phytic
acid binds to iron and other minerals in the digestive tract and may
interfere with mineral absorption. As a purified extract of rice bran,
taken between meals so it will not bind to minerals in the digestive
tract, phytic acid is readily absorbed into the bloodstream, where it
acts as a potent mineral chelator.33 Phytic acid binds to any free
iron or other minerals (even heavy metals such as mercury, lead and
cadmium) in the blood, which are then eliminated through the kidneys.
Phytic acid removes only excess or unbound minerals, not mineral ions
already attached to proteins.
Phytic acid is such a potent--but safe--iron and mineral chelator that
it may someday replace intravenous chelation therapy such as the
mineral-chelator EDTA or iron-binding drugs such as desferrioxamine
(Desferal). Because of its ability to bind to iron and block
iron-driven hydroxyl radical generation (water-based) as well as
suppress lipid peroxidation (fat-based), phytic acid has been used
successfully as an antioxidant food preservative.34
Phytic acid supplements should not be taken during pregnancy since the
developing fetus requires minerals for proper development. Because
aspirin causes a small loss of blood and consequently helps to control
iron levels, the simultaneous use of phytic acid with a daily aspirin
tablet is not advised. A three-month course of phytic acid should
achieve adequate iron chelation, and prolonged daily supplementation
may lead to iron-deficiency anemia. Anemic individuals who take phytic
acid as a food supplement are likely to feel weak shortly after
consumption, whereas iron-overloaded individuals are likely to feel
increased energy.
For those at risk for iron overload, it may be wise to avoid iron in
multivitamins and shun fortified foods that provide more than 25
percent of the recommended daily intake for iron. No doctor should
prescribe iron tablets for patients who complain of fatigue without
blood tests and a thorough health history. Iron-rich foods such as red
meat and molasses may prevent anemia and build strength during the
growing years but in adulthood may lead to iron overload among men and
postmenopausal women. Those individuals who learn how to achieve iron
balance will maintain the most desirable state of health throughout
life.
Sidebars:
Why Fortify Foods?
Bill Sardi is a health journalist and consumer advocate in Diamond
Bar, Calif. He recently published
The Iron Time Bomb (Bill Sardi, 1999).
References
1.Bonkovsky HL, et al. Iron in liver diseases other than
hemochromatosis. Semin Liver Dis 1996;16:65-82.
2. Gutteridge JMC, Halliwell B. Antioxidants in nutrition, health and
disease. New York: Oxford University Press; 1994. p 24-39.
3. McCord JM. Iron, free radicals, and oxidative injury. Sem in Hem
1998;35:5-12.
4. Crawford RD. Proposed role for a combination of citric acid and
ascorbic acid in the production of dietary iron overload: a
fundamental cause of disease. Biochem Mol Med 1995;54:1-11.
5. Emery TF. Iron and your health. Boca Raton (FL): CRC Press; 1991. p
1-13.
6.Arthur CK, Isbister JP. Iron deficiency. Drugs 1987;33:171-82.
7. Rider JA, et al. Double-blind comparison of effects of aspirin and
namoxyrate on pH of gastric secretions, fecal blood loss, serum iron
and iron-binding capacity in normal volunteers. Curr Ther Res
1965;7:633-8.
8. Bankhead C. In assessing anemia, doctors must decipher role of iron
deficiency. Med Tribune Clin Focus 1997 Mar; 20:24.
9. Oberle S, et al. Aspirin increases ferritin synthesis in
endothelial cells: a novel antioxidant pathway. Circ Res
1998;82:1016-20.
10. Vellar OD. Studies on sweat losses of nutrients. Scand J Clin Lab
Invest 1968;21:157-67.
11. Kampman E, et al. Meat consumption, genetic susceptibility, and
colon cancer risk. Cancer Epid Biomarker Prev 1999;8:15-24.
12. Griffiths, E. Iron and infection. New York: John Wiley &
Sons;1987. p 1-25.
13. Goldwasser P, Feldman J. Association of serum albumin and
mortality risk. J Clin Epid 1997;50:693-703.
14. Aust SD. Ferritin as a source of iron and protection from
iron-induced toxicities. Toxicol Lett 1995;82:941-4.
15. Aisen P, Brown EB. The iron-binding function of transferrin in
iron metabolism. Sem Hematol 1977;14:31-46.
16. Baker EN, et al. Three-dimensional structure of lactoferrin. Adv
Exp Med Biol 1998;443:1-14.
17. Hulten L, et al. Iron absorption from the whole diet in men: how
effective is the regulation of iron absorption? Am J Clin Nut
1997;66:347-56.
18. Adams PC, et al. The relationship between iron overload, clinical
symptoms and age in 410 persons with genetic hemochromatosis.
Hepatology 1997;25:162-6.
19. Marinella MA. Tomatophagia and iron-deficiency anemia. N Eng J Med
1999;341:60-1.
20. Monsen ER. The ironies of iron. Am J Clin Nutr 1999;69:831-2.
21. Hurrell RF. Preventing iron deficiency through food fortification.
Nut Rev 1997;55:210-22.
22. Park J, Brittin HC. Increased iron content of food due to
stainless steel cookware. J Am Diet Assoc 1997;97:659-61.
23. U.S. Agricultural Research Service, USDA Bulletin. 1998 Dec 23.
24. El-Shobaki FA, et al. The effect of some beverage extracts on
intestinal iron absorption. Z Ernahrungswiss 1990;29:264-9.
25. Morris ER. An overview of current information on bioavailability
of dietary iron to humans. Fed Proc 1983;42:1716-20.
26. Davidsson L, et al. Influence of ascorbic acid on iron absorption
from an iron-fortified chocolate-flavored milk drink in Jamaican
children. Am J Clin Nut 1998:67:873-7.
27. Fletcher LM. Alcohol and iron: one glass of red or more? J Gastro
Hepatol 1996;11:1039-41.
28. Derman DP, et al. Importance of ascorbic acid in the absorption of
iron from infant foods. Scand J Haematol 1980;25: 193-201.
29. Gerster H. High-dose vitamin C: a risk for persons with high iron
stores? Int J Vitam Nutr Res 1999;69:67-82.
30. Craig WJ. Iron status of vegetarians. Am J Clin Nut 1994 May; 59(5
Suppl):12335-7.
31. Hallberg L, Rossander L. Effect of different drinks on the
absorption of non-heme iron from composite meals. Hum Nutr Appl Nutr
1982;36:116-23.
32. Graf E, et al. Phytic acid--a natural antioxidant. J Biol Chem
1987;262:11647-50.
33. [No authors listed] Phytic acid: new doors open for a chelator.
Lancet 1987 Sept 19:2;2(8560):664-6.
34. Lee BJ, Hendricks DG. Phytic acid protective effect against beef
round muscle lipid peroxidation. J Food Sci 1995;60:241-4.
Who loves ya.
Tom
--
Jesus was a Vegetarian! http://www.nucleus.com/watchman
Moses was a Mystic! http://www.nucleus.com/watchman/light.html
Actually smooth muscle is simply unstriated. It's fully innervated and
responsive to neurologically activating substances that both agonize and
antagonize kinesis of various kinds.
The muscles of the gut wall most certainly can be affected - they are
striated and not "smooth muscle".
The musculature of the gut is composite and complex. However the
intestinal lining has no nociception - that is, the layer that carries
mucus-producing structures. Beneath that layer the musculature is fully
innervated and nociception is *very* possible within the gut proper.
More...
>
> >"J Wootton" <jwoo...@rogers.com> wrote in message
> >news:3C00CFB7...@rogers.com...
> >N.B.
> >1) This list is by no means complete.
> >2) Myofascial pain may be a manifestation of fibromyalgia, but it
> >typically does not involve the muscles of the abdominal wall.
> >FWIW
> >J
I noticed that note in the article - I really question it. Doctors
should not believe that pain is impossible in the gut wall. I feel MPS
is absolutely possible in muscles supporting the abdomen.
For me, *chronic* pain that's ever present is from my *diaphragm*.
Another possible cause of chronic abdominal pain would affect sexually
active women who still have the uterus.
However none of these things is responsible for "shotgun" pain. To my
way of thinking that's not even "chronic". It's acute abdominal pain.
Deirdre ;-)
> >
> >
> >http://www.postgradmed.com/issues/1999/09_99/debanto.htm
> >What could be causing chronic abdominal pain?
> >Anything from common peptic ulcers to uncommon pancreatic trauma
> >
> >John R. DeBanto, MD; Gary W. Varilek, MD; Laurie Haas, MD
> >
> >VOL 106 / NO 3 / SEPTEMBER 1999 / POSTGRADUATE MEDICINE
> >
> >
> >
--
Might want to be aware of the amended version, at
http://graham.main.nc.us/~bhammel/INS/compl_ammend.html
And the website gives a massive commentary of the case
action, as well as a lot of other potentially helpful stuff, at
http://graham.main.nc.us/~bhammel/INS/judydoc.html
Randy <ra...@noname.net> wrote in message news:3c033...@news.vic.com...
I had been keeping up with her both personally and via her email list for a
while (years back), but my email box was just deluged with tons of very long
letters, legal documents, etc., and I eventually had to opt out.
I'll give it another look-see since it's coming closer to home for me now.
Thanks again.
"Michael Baugh" <baug...@bellsouth.net> wrote in message
news:cBYM7.2187$S93.1...@e3500-atl2.usenetserver.com...