my dad

[Guest guest]

He got the results of the skin biopsy today. Unfortunately, it is

melanoma. We don't know the extent of what we're looking at yet. Thank

God that he listened to his granddaughter, since he wouldn't listen to

anyone else.

I'm still a little numb and waiting for more test results before panicing.

I know that if caught early, it is very easy to treat.

Would appreciate all prayers on his behalf. My kids still need him around.

(So do I.)

God bless,

Wenoka

[Guest guest]

Hi Pat,

Your daddy lives on in your heart, as well in heaven. Your memorial to him

is a living legacy, and his legacy to us is -- YOU! I thank your father for

your blessing us.

Hugs and blessings, Ann

[Guest guest]

Hi Sharon,

I'm so very sorry to hear about your Dad. I lost my Dad about 6 months ago,

so I share the pain you and your family must be feeling. It takes a lot of

time to heal. I am not quite there yet, but the love and closeness of my family

does help a great deal. My Mom has been gone for several years now.

You and the girls are in my thoughts and prayers in this difficult time, and

the times ahead. God Bless!

Love and Prayers,

Louise Mom to , 17 (NDS) and , 15 (DS)

[Guest guest]

Sharon,

My condolences to you and your family on your loss. My dad passed last fall.

It takes time to heal, but knowing he lived a long full life has helped all of

us learn to let go. I will keep you and your family in my thoughts and

prayers.

nancy, mom of Sheila

[Guest guest]

Sharon, I am so sorry to hear about the loss of your father. Much love to you

and your family.

Jackie, Mom to 16ds, 13, and Bradley 10

> Sharon,

>

> My condolences to you and your family on your loss. My dad passed last fall.

> It takes time to heal, but knowing he lived a long full life has helped all of

> us learn to let go. I will keep you and your family in my thoughts and

> prayers.

>

> nancy, mom of Sheila

>

>

>

[Guest guest]

So glad to hear the encouraging news!

my dad

a,

Thanks so much for asking. He is about the same...dialysis 3 times a week. So

weak some days he can barely get out of bed. But still HERE! The Dallas Morning

News ran a story about him in this past Sunday's paper (a column by Steve Blow

on the front page of the Metro section). The story also referenced our website

for him http://www.helpdonsmith.com

We have our fingers crossed...he may have a new door opening for him here in

Dallas...a good connection and they do many more multiple organ transplants than

either hospital in Houston. Our fingers are crossed!

Again, thank you so much for asking and for your thoughts and prayers.

nna

Texas Autism Advocacy

Unlocking Autism

www.UnlockingAutism.org

Autism-Awareness-Action

Worldwide internet group for parents who have a

child with AUTISM.

SeekingJoyinDisability - Prayer support for those touched by Disability:

SeekingJoyinDisability/

[Guest guest]

So glad to hear the encouraging news!

my dad

a,

Thanks so much for asking. He is about the same...dialysis 3 times a week. So

weak some days he can barely get out of bed. But still HERE! The Dallas Morning

News ran a story about him in this past Sunday's paper (a column by Steve Blow

on the front page of the Metro section). The story also referenced our website

for him http://www.helpdonsmith.com

We have our fingers crossed...he may have a new door opening for him here in

Dallas...a good connection and they do many more multiple organ transplants than

either hospital in Houston. Our fingers are crossed!

Again, thank you so much for asking and for your thoughts and prayers.

nna

Texas Autism Advocacy

Unlocking Autism

www.UnlockingAutism.org

Autism-Awareness-Action

Worldwide internet group for parents who have a

child with AUTISM.

SeekingJoyinDisability - Prayer support for those touched by Disability:

SeekingJoyinDisability/

[Guest guest]

I am new to this list but wanted to extend my support and best wishes

for your dad, mom, you and all the family. I went through this a few

years ago with my dad and know how hard it is on all concerned. Keep

the faith and know that you all are in my thoughts.

Cheryl

>

> > How is your dad doing?

>

> -- Ehrhardt

> Body & Soap

> ***coming soon***

> www.bodyandsoap.com

[Guest guest]

My name is Shelia and I would be glad to speak with you or your dad directly. Please call me at 812-288-9000 anytime.

[Guest guest]

Hi Nelly - first of all, welcome to you and your dad. Sorry that he

has A, it truly isn't much fun but this site is a tremendous resource

of information and support.

> He has sufferred with it for a few years now, he is very worried

> about having anything done as he keeps hearing things to put him

> off, and thinks that nothing will really cure him. He is on the

> tablets but they do not really do much for him.

** Unfortunately, there is no 'cure' but most of us have come up with

ways to manage our A and lead pretty normal lives. It is scary and

many doctors don't know much about it. The next time you post, let us

all know where your dad lives and we may be able to refer him to a

doctor who does know and has some experience with A. What tablets is

he on?

>

> He is now sick all the time, We

> are constantly trying to get him to have something done, but he is

> very worried about the lack of experience the medical profession

> seem to have with achlasia, and has also heard some horror stories

> about people who have had some treatment.

** Understandable that he is concerned but on this site you will find

that most of us have had surgery to help correct the problem with

good success rates. The MOST IMPORTANT thing to do is find a

doctor/surgeon who has had experience - we can probably help you

there or even go to the database link at the top of the site - there

are several lists of doctors there.

>

> Any advice for him, or any similar stories you could share with me

> so I can 'print them out to show him' (he has never even switched

on

> a computer) would be very helpful.

** Keep posting and reading - we run the gamut here, age, gender,

symptoms, treatments. I've had A for over 20 years and I'm still

learning tons of stuff here from everyone.

Good luck to him in finding some relief and good luck to you in your

quest to help him. Please tell him not to put off treatment, the

longer he waits - the more long term damage he will do. There are

treatments out there that will help - he has no reason to suffer.

Also, the longer he waits the harder it is to do any kind of surgery.

>

> Thanks very much

> Nelly

Best of Luck!

Happy Swallowing!

-michelle in VA.

[Guest guest]

Hi Nelly,

Welcome to you and your Dad. We are a large range of ages here so feel at

home! I want to emphasise what said that it is important for your

Dad to get treatment as soon as possible because the longer you wait the

more damage is done. Please tell us where he is and someone will refer you

to an experienced set of doctors. Experience and interest in Achalasia is

vitally important and in the USA there are several centres to choose from.

There is relief available and he does not need to suffer unnecessisarily.

Good wishes,

Joan

My Dad

>

>

> Hi Everyone

>

> My dad is suffering from achalasia, I came across this site and he

> has asked me to see if there are any advances with helping his

> condition.

>

> He has sufferred with it for a few years now, he is very worried

> about having anything done as he keeps hearing things to put him

> off, and thinks that nothing will really cure him. He is on the

> tablets but they do not really do much for him.

>

> He is now sick all the time, he cannot sleep in the horizontal

> position and has about 12 pillows allowing him to sleep in a more

> upright position. Although he finds it difficult to eat and sicks

> it up frequently he persists and has not yet lost any weight. We

> are constantly trying to get him to have something done, but he is

> very worried about the lack of experience the medical profession

> seem to have with achlasia, and has also heard some horror stories

> about people who have had some treatment.

>

> Any advice for him, or any similar stories you could share with me

> so I can 'print them out to show him' (he has never even switched on

> a computer) would be very helpful.

>

> Thanks very much

> Nelly

>

>

>

>

>

>

>

>

>

>

[Guest guest]

Hi

Thanks for all your responses. Im not sure if I have replied

correctly, but bear with me, am new to groups like this.

My Dad is 67 years old, lives in Birmingham, England, takes

Nifiditine which he has been taking for two years. He also takes

losec to neutralise the acid. He has seen a consultant who wants to

do key hole surgery, but my Dad is concerned about his experience as

the doctor has only ever performed operations for reflux disease but

not 'A', I dont know how different the two are.

I have told him what you said about more damage can be caused if it

is left and he was wondering what damage and if this was from

personal experience of leaving the A untreated, or have the doctors

told you?

Thanks again

Nelly

>

> Hi Nelly - first of all, welcome to you and your dad. Sorry that

he

> has A, it truly isn't much fun but this site is a tremendous

resource

> of information and support.

>

> > He has sufferred with it for a few years now, he is very worried

> > about having anything done as he keeps hearing things to put him

> > off, and thinks that nothing will really cure him. He is on the

> > tablets but they do not really do much for him.

> ** Unfortunately, there is no 'cure' but most of us have come up

with

> ways to manage our A and lead pretty normal lives. It is scary and

> many doctors don't know much about it. The next time you post, let

us

> all know where your dad lives and we may be able to refer him to a

> doctor who does know and has some experience with A. What tablets

is

> he on?

> >

> > He is now sick all the time, We

> > are constantly trying to get him to have something done, but he

is

> > very worried about the lack of experience the medical profession

> > seem to have with achlasia, and has also heard some horror

stories

> > about people who have had some treatment.

>

> ** Understandable that he is concerned but on this site you will

find

> that most of us have had surgery to help correct the problem with

> good success rates. The MOST IMPORTANT thing to do is find a

> doctor/surgeon who has had experience - we can probably help you

> there or even go to the database link at the top of the site -

there

> are several lists of doctors there.

> >

> > Any advice for him, or any similar stories you could share with

me

> > so I can 'print them out to show him' (he has never even

switched

> on

> > a computer) would be very helpful.

>

> ** Keep posting and reading - we run the gamut here, age, gender,

> symptoms, treatments. I've had A for over 20 years and I'm still

> learning tons of stuff here from everyone.

> Good luck to him in finding some relief and good luck to you in

your

> quest to help him. Please tell him not to put off treatment, the

> longer he waits - the more long term damage he will do. There are

> treatments out there that will help - he has no reason to suffer.

> Also, the longer he waits the harder it is to do any kind of

surgery.

> >

> > Thanks very much

> > Nelly

>

> Best of Luck!

> Happy Swallowing!

> -michelle in VA.

[Guest guest]

Nellie, if you go to the group site and in the left hand side

click on database, and the the list of doctor referrals, you

will find several doctors listed there. Maybe that will help

you and your dad pick a more experienced surgeon.

Maggie

Alabama

[Guest guest]

I also live in England for the time being. I am going to see Doctor Maynard in Oxford in Feb.

[Guest guest]

Hi Nelly,

There are other people with Achalasia who live in England. I think there is

a mother with a young son in London and another () in Ireland. However,

look in the data base they may have posted the names of their doctors. Try

phoning the University Hospital in your area and speaking to the head of the

gastroenterology department. You might have waiting list problems so it is a

good idea to get into some place where your Dad can be seen eventually.

Also in the database there are links to information about achalasia. I will

try and attach a paper which is very good and covers most things about A - a

a bit technical. It is not just my experience but comes form several

doctors. My experience has been that I was diagnosed too late and my

oesophagus was already very distended when they tried to do the myotomy - it

did not work so well and I had to have a dilatation, which worked to about

50% and now I face an oesophagectomy ( removal of the oesophagus), because

it is too dilated and flabby to do anything with !

Sorry this is a bit long !

Good wishes,

Joan

Practice Guidelines

December 1999

Volume 94, Number 12

Pages 3406-3412

--------------------------------------------------------------------------

Diagnosis and Management of Achalasia

F. Vaezi, M.D., Ph.D.,a and E. Richter, M.D.,a for the

American College of Gastroenterology Practice Parameter Committee*

--------------------------------------------------------------------------

aCenter for Swallowing and Esophageal Disorders, Department of

Gastroenterology, The Cleveland Clinic Foundation, Cleveland, Ohio

--------------------------------------------------------------------------

Preamble

Guidelines for clinical practice are intended to suggest preferable

approaches to particular medical problems as established by interpretation

and collation of scientifically valid research, derived from extensive

review of the published literature. When data are not available that will

withstand objective scrutiny, a recommendation may be made based on a

consensus of experts. Guidelines are intended to apply to the clinical

situation for all physicians without regard to specialty. Guidelines are

intended to be flexible, not necessarily indicating the only acceptable

approach, and should be distinguished from standards of care that are

inflexible and rarely violated. Given the wide range of choices in any

health care problem, the physician should select the course best suited to

the individual patient and the clinical situation presented. These

guidelines are developed under the auspices of the American College of

Gastroenterology and its Practice Parameters Committee. These guidelines are

also approved by the governing boards of the American Gastroenterological

Association and the American Society for Gastrointestinal Endoscopy. Expert

opinion is solicited from the outset for the document. Guidelines are

reviewed in depth by the committee, with participation from experienced

clinicians and others in related fields. The final recommendations are based

on the data available at the time of the production of the document and may

be updated with pertinent scientific developments at a later time. The

following guidelines are intended for adults and not for pediatric patients.

Definition

Achalasia is a primary esophageal motor disorder of unknown etiology

characterized manometrically by insufficient lower esophageal sphincter

(LES) relaxation and loss of esophageal peristalsis, and radiographically by

aperistalsis, esophageal dilation, minimal LES opening with a " bird-beak "

appearance, and poor esophageal emptying of barium.

Achalasia is a well-recognized primary esophageal motor disorder of

unknown etiology. Available data suggest hereditary, degenerative,

autoimmune, and infectious factors as possible causes for achalasia, the

latter two being the most commonly accepted possible etiologies (1, 2).

Pathological changes found at autopsy or from myotomy specimens are in the

esophageal myenteric (Auerbach's) plexus with a prominent but patchy

inflammatory response consisting of T-lymphocytes and variable numbers of

eosinophils and mast cells, loss of ganglion cells, and some degree of

myenteric neural fibrosis (3). The end result of these inflammatory changes

is the selective loss of postganglionic inhibitory neurons, which contain

both nitric oxide and vasoactive intestinal polypeptide. The postganglionic

cholinergic neurons of the myenteric plexus are spared leading to unopposed

cholinergic stimulation (4). This produces high basal LES pressures, and the

loss of inhibitory input results in insufficient LES relaxation.

Aperistalsis is related to the loss of the latency gradient along the

esophageal body—a process mediated by nitric oxide.

Diagnosis

The diagnosis of achalasia should be suspected in anyone complaining

of dysphagia for solids and liquids with regurgitation of food and saliva.

The clinical suspicion should be confirmed by a barium esophagram showing

smooth tapering of the lower esophagus leading to the closed LES, resembling

a " bird's beak. " Esophageal manometry establishes the diagnosis showing

esophageal aperistalsis and insufficient LES relaxation. All patients should

undergo upper endoscopy to exclude pseudoachalasia arising from a tumor at

the gastroesophageal junction.

Most achalasia patients are symptomatic for years before seeking

medical attention. The most common symptoms are dysphagia for solids and

liquids, regurgitation, and chest pain. Although the dysphagia may initially

be for solids only, as many as 70-97% of patients with achalasia have

dysphagia for both solids and liquids at presentation (2). This contrasts

with patients having strictures or ring whose dysphagia is limited to

solids. Achalasia patients localize their dysphagia to the cervical or

xiphoid areas. Over the years, patients learn to accommodate to their

problem by using various maneuvers, including lifting the neck or drinking

carbonated beverages to help empty the esophagus. Regurgitation becomes a

problem with progression of the disease, especially when the esophagus

begins to dilate. Regurgitation of bland, undigested, retained food, or

accumulated saliva occurs in about 75% of achalasia patients (5). It occurs

most commonly in the recumbent position, awaking the patient from sleep

because of coughing and choking. Chest pain or discomfort, located in the

xiphoid area, is experienced by nearly 40% of patients with achalasia (5).

It may mimic angina by location and character, but differs in not being

aggravated by exercise or relieved by rest. About 60% of achalasia patients

may have some degree of weight loss at presentation because of poor

esophageal emptying and decreased or modified food intake (6). However,

weight loss is usually minimal, and some patients are obese. Surprisingly,

heartburn is reported by nearly 40% of achalasia patients. However, it is

not related to the reflux of acidic gastric contents, but most likely to

production of lactic acid from retained food or exogenous ingested acidic

materials such as carbonated drinks.

When the diagnosis of achalasia is suspected, a barium esophagram with

fluoroscopy is the single best diagnostic study. This test will reveal loss

of primary peristalsis in the distal two-thirds of the esophagus with

to-and-fro movement in the supine position. In the upright position, there

will be poor emptying with retained food and saliva often producing a

heterogeneous air-fluid level at the top of the barium column. Early in the

disease, the esophagus may be minimally dilated, but more chronic disease is

associated with sigmoid-like tortuosity and sometimes massive dilation of

the esophageal body. There is a smooth tapering of the lower esophagus

leading to the closed LES, resembling a " bird's beak. " When the esophagus is

minimally dilated, this may be misinterpreted as a peptic stricture. The

presence of an epiphrenic diverticulum suggests the diagnosis of achalasia

(7). Hiatal hernias are infrequent findings in patients with achalasia with

reported prevalence of 1-14% compared with 20-50% found in the general

population (8). The presence of a hiatal hernia on barium esophagram may

make the diagnosis of achalasia less likely, but it does not rule it out,

and does not change the management of these patients.

Esophageal manometry is the key test for establishing the diagnosis of

achalasia (9) (Table 1). Because achalasia involves the smooth muscle

portion of the esophagus, the manometric abnormalities are always confined

to the distal two-thirds of the esophagus. In the body of the esophagus,

aperistalsis is always present. This means that all wet or dry swallows are

followed by simultaneous contractions that are classically identical to each

other (isobaric or mirror images). The contraction amplitudes are typically

low (10-40 mm Hg) and may be repetitive (2). The term " vigorous achalasia "

is sometimes used when there is aperistalsis with normal or even high

amplitude contractions in the esophageal body (10). Patients with vigorous

achalasia usually have normal esophageal diameter on barium esophagram, but

otherwise do not differ from patients with classic achalasia. Some

manometric abnormality of the LES is always present in patients with

achalasia. The LES pressure is usually elevated but may be normal (10-45 mm

Hg) in up to 45% of patients; however, a low LES pressure is never seen in

patients with untreated achalasia. Abnormal LES relaxation is seen in all

achalasia patients. About 70-80% of patients with achalasia have absent or

incomplete LES relaxation with wet swallows. In the remaining 20-30%, the

relaxations are complete to the gastric baseline but are of short duration

(usually <6 s) and functionally inadequate as assessed by barium and nuclear

emptying studies (11).

--------------------------------------------------------------------------

Table 1. Radiographic and Manometric Features of Achalasia

--------------------------------------------------------------------

Barium esophagram

Essential features:

· " bird's beak " appearance of the LES with incomplete opening

· loss of primary peristalsis

· delayed esophageal emptying

Supportive features:

· dilated or sigmoid-like esophagus

· epiphrenic diverticula

Manometry

Essential features:

· aperistalsis in distal of the esophagus

· abnormal LES relaxation

Supportive features:

· hypertensive LES pressure

· low amplitude esophageal contractions

--------------------------------------------------------------------------

Pseudoachalasia results from a tumor at the esophagogastric junction

or in an adjacent area. These patients mimic classic achalasia clinically

and manometrically. The diagnosis should be suspected in patients with

advanced age, shorter duration of symptoms, and marked weight loss (5, 12).

However, the predictive accuracy of this triad of symptoms and signs is only

18% (13), possibly related to the low prevalence of the disease. Although

the gastric cardia may be assessed radiographically, its sensitivity is poor

in detecting tumors of the gastroesophageal junction causing

pseudoachalasia. Therefore, all patients with suspected achalasia should

undergo upper gastrointestinal endoscopy with close examination of the

cardia and gastroesophageal junction. At endoscopy, the esophageal body

usually appears dilated, atonic, and often tortuous with normal appearing

mucosa. Sometimes, the mucosa is reddened, friable, thickened, or even

superficially ulcerated secondary to chronic stasis, pills, or Candida

esophagitis. Retained secretions, usually saliva, liquids, or sometimes food

debris may be encountered. Patients with a markedly dilated esophagus may

need esophageal lavage or a clear liquid diet for several days before

endoscopy to avoid aspiration and to allow adequate visualization of the

esophagus. The LES region usually has a " rosette " appearance and remains

closed with air insufflation; however, the endoscope will easily traverse

this area with gentle pressure allowing examination of the stomach. If

excess pressure is required, the presence of pseudoachalasia should be

highly suspected, the gastroesophageal junction and cardia closely examined,

and biopsies taken. Tumors of the gastroesophageal junction may be missed

endoscopically in up to 60% of patients with pseudoachalasia (5, 14).

Endoscopic ultrasonography may prove useful in patients with a nondiagnostic

endoscopy and a high degree of clinical suspicion for pseudoachalasia, but

it is not recommended as a routine test in achalasia (15). The role of

computed tomography scans is limited in the diagnosis of pseudoachalasia

(14).

The Management of Patients With Achalasia

Although there is no cure for achalasia, the goal of treatment should

be relief of patient symptoms and improved esophageal emptying. The two most

effective treatment options are graded pneumatic dilation and surgical

myotomy. For patients who are at high risk for pneumatic dilation or

surgery, endoscopic injection of the LES with botulinum toxin or

pharmacological treatment with nitrates or calcium channel blockers may be

acceptable alternatives.

No treatment can restore the muscular activity to the denervated

achalasiac esophagus. Esophageal aperistalsis and impaired LES relaxation

are rarely, if ever, reversed by any mode of therapy. Therefore, all the

current treatment options for achalasia are limited to reducing the pressure

gradient across the LES, thus facilitating esophageal emptying by gravity.

This can be accomplished most effectively by pneumatic dilation and surgical

myotomy or less effectively by pharmacological agents injected

endoscopically into the LES (botulinum toxin) or taken orally (calcium

channel blockers and nitrates).

Pneumatic dilation is the most effective nonsurgical treatment option

for patients with achalasia. All patients considered for pneumatic dilation

should be surgical candidates, since esophageal perforation may result from

the procedure. Pneumatic dilation uses air pressure to intraluminally dilate

and disrupt the circular muscle fibers of the LES. A variety of dilators

were used in the past to treat patients with achalasia, including the

Rider-Moeller, Sippy, Mosher, and Brown-McHardy dilators (1). Today, the

most commonly used achalasia balloon dilators in the United States are the

nonradiopaque graded size polyethylene balloons (Microvasive Rigiflex

dilators). A less frequently used balloon is the over-the-endoscope Witzel

dilator. Table 2 lists the recommended technique for performing pneumatic

dilation using these graded balloons. Pneumatic dilation should always be

carried out with sedation and under fluoroscopy. These dilators come in

three different balloon diameters (3, 3.5, and 4 cm), and are positioned

over a guidewire usually placed at endoscopy. The most important aspect of

an effective pneumatic dilation is accurate positioning of the balloon

across the LES and effective obliteration of the balloon waist visualized

under fluoroscopy. The effectiveness of dilation does not depend on balloon

distention time so long as the balloon waist is appropriately positioned and

fully distended (17). After pneumatic dilation, all patients should undergo

a gastrograffin study followed by barium swallow to exclude esophageal

perforation (18). This procedure is usually performed as an outpatient with

patients observed postprocedure for 4-6 h for chest pain and fever.

--------------------------------------------------------------------------

Table 2. Recommended Technique for Pneumatic Dilation Using the Graded

Balloons*

--------------------------------------------------------------------

1.

Fasting for at least 12 h before procedure .

2.

Esophageal lavage with a large-bore tube (if needed).

3.

Sedation and endoscopy in RIGHT lateral position.

4.

Guidewire positioned in stomach and balloon passed over the

guidewire.

5.

Initial dilation with 3-cm diameter balloon; subsequent

progression to 3.5-cm and 4-cm balloons may be required at separate

sessions.

6.

Accurate placement of balloon across gastroesophageal junction

fluoroscopically.

7.

Balloon distention to obliterate the waist, which usually

requires 7-10 psi (this is the key to a successful dilation).

8.

Gastrograffin study followed by barium swallow to exclude

esophageal perforation.

9.

Observation for 4 h for chest pain and fever.

10.

Discharge with follow-up in 1 mo.

--------------------------------------------------------------------

*Before proceeding with pneumatic dilation, it is important to

ensure that a cardiothoracic surgeon is available in case of an esophageal

perforation.

--------------------------------------------------------------------------

Studies to date indicate that by using the graded dilators,

good-to-excellent relief of symptoms occurs in 50-93% of patients (Table 3)

(1). The clinical response improves in a graded fashion with increasing size

of the balloon diameter. Cumulatively, dilation with 3-, 3.5-, and 4-cm

balloon diameters results in good-to-excellent symptomatic relief in 74%,

86%, and 90% of 359 treated patients, respectively (19, 20, 21, 22, 23, 24,

25, 26, 27, 28, 29, 30, 31) with an average follow-up of 1.6 yr (range 0.1-6

yr). Additionally, studies show that the rate of perforation may be lower

with the serial balloon dilation approach (25); therefore, most experts

start with the smallest, 3-cm balloon, except in patients who have had prior

pneumatic dilations. The need for further dilation is based upon the

persistence of symptoms usually assessed 4 weeks postprocedure or the

recurrence of symptoms overtime.

--------------------------------------------------------------------------

Table 3. Cumulative Effectiveness of the Graded Pneumatic Dilators in

Achalasia

--------------------------------------------------------------------

Reference

Number of Patients

Study Design

Dilator (Size/cm)

Objective Assessments

% Sx Improvement

Follow-up (yr) Mean (Range)

Perforation (%)

--------------------------------------------------------------------

--------------------------------------------------------------------

%LES Pressure

Excellent/Good

--------------------------------------------------------------------

(19)

7

Prospective

3

86

0.8(0.5-1)

0

Gelfand (20)

24

Prospective

3, 4

60,68

70,93

0

Barkin (21)

50

Prospective

3.5

90

1.3(0.1-3.4)

0

Stark (22)

10

Prospective

3.5

74

0.5

0

Makela (23)

17

Retrospective

3, 3.5, 4

50,75,75

0.5

5.9

Levine (24)

62

Retrospective

3, 3.5

85,88

0

Kadakia (25)

29

Prospective

3, 3.5, 4

67

62,79,93

4(0.3-6)

0

Kim (26)

14

Prospective

3, 3.5

39

75

0.3

Lee (27)

28

Prospective

3, 3.5, 4

7

Abid (28)

36

Retrospective

3.5, 4

50,75,75

0.5

5.9

Levine (24)

62

Retrospective

3, 3.5

85,88

0

Kadakia (25)

29

Prospective

3, 3.5, 4

67

62,79,93

4(0.3-6)

0

Kim (26)

14

Prospective

3, 3.5

39

75

0.3

Lee (27)

28

Prospective

3, 3.5, 4

7

Abid (28)

36

Retrospective

3.5, 4

88,89

2.3(1-4)

6.6

Wehrmann (29)

40

Retrospective

3, 3.5

42

89

2-5

2.5

Lambroza (30)

27

Retrospective

3

67

1.8(0.1-4.8)

0

Bhatnagar (31)

15

Prospective

3, 3.5

73,93

1.2(0.3-3)

0

--------------------------------------------------------------------

Total

359

size 3

125/168=74%

1.6(0.1-6)yr

7/345=2%

size 3.5

184/214=86%

size 4

90/100=90%

--------------------------------------------------------------------------

Overall, studies find a 2% cumulative perforation rate using the

graded balloons, although some centers report higher perforation rates (1).

Patients with prompt recognition of perforation and surgical repair have

comparable outcomes to those undergoing elective surgery (16); however,

surgery for perforation is via an open thoracotomy approach. It is important

to note that the rate of perforation is variable and highly dependent on the

skill of the endoscopist. Physicians who do not perform pneumatic dilations

on a regular basis should consider referral to specialized centers with

expertise in performing this procedure. Other less prevalent complications

of pneumatic dilation include gastroesophageal reflux (0-9%), aspiration

pneumonia, gastrointestinal hemorrhage, and esophageal hematoma (32).

Patients with a dilated and tortuous esophagus, esophageal diverticula, or

previous surgery at the gastroesophageal junction may be at an increased

risk for esophageal perforation with balloon dilation and should be

considered for surgical myotomy as the first treatment option.

Traditionally, symptom improvement is used to assess the success of

pneumatic dilation. However, a recent study suggests that subjective and

objective parameters of improvement are discordant in about 30% of patients

postpneumatic dilation (33), suggesting that subjective improvement alone

may give a false sense of success in those with less than optimal relief of

their distal esophageal obstruction. Objective tests to better assess

improvement after pneumatic dilation include manometry (LES pressure <10 mm

Hg), esophageal scintigraphy, and the timed barium esophagram (34, 35, 36).

The adjunctive use of these tests may help to improve the long-term success

of pneumatic dilation, but this premise is still speculative.

Surgical myotomy for achalasia involves performing an anterior myotomy

across the LES (Heller's myotomy) usually associated with an antireflux

procedure (loose Nissen, incomplete Toupet, or Dor fundoplication). In the

past, the myotomy was done by an open procedure through a thoracic or

abdominal incision. The hospital stay was 7-10 days with a substantial

postoperative recovery period. The abdominal approach limits extension of

the myotomy proximally, with usually only a 1- to 2-cm distal myotomy onto

the stomach to decrease the frequency of postprocedure gastroesophageal

reflux. The transthoracic approach allows a longer proximal extension of the

myotomy to the level of the major pulmonary vessels, but the extension

distally onto the stomach may be limited. The results from published

studies, using either the abdominal or thoracic approaches, show

good-to-excellent symptom improvement in 83% of 2660 patients undergoing

myotomy through the abdominal approach and in 83% of 1210 patients who had a

transthoracic esophagomyotomy with a mean follow-up of ~7 yr (1). The main

late complication of a Heller's myotomy is gastroesophageal reflux disease.

The cumulative rates of heartburn and reflux disease reported in the studies

are 22% for the abdominal and 10% for the transthoracic approach (1). The

operative mortality for both procedures is very low (0.2% vs 1%), with most

studies reporting no deaths directly related to the operation.

The advent of minimally invasive surgery and laparoscopic myotomy has

resulted in shorter patient hospital stay (2 days), reduced morbidity, and

quicker return to daily activity, making the procedure an attractive initial

management option for healthy patients with achalasia. Studies show that

laparoscopic cardiomyotomy has a cumulative good-to-excellent clinical

response rate of 94% in 254 treated patients (Table 4) (37, 38, 39, 40, 41,

42, 43, 44, 45, 46, 47, 48). However, long-term outcome of patients

undergoing this procedure is unknown with current studies having a

cumulative mean follow-up time of only 1 yr (range 0.1-4 yr). Before

laparoscopic surgery, the most common indication for myotomy was the patient

with recurrent symptoms after graded pneumatic dilations. However,

laparoscopic surgery is increasingly performed as initial therapy for

healthy patients, if a skillful surgeon is available. The cumulative rate of

heartburn and reflux disease after laparoscopic myotomy is approximately 11%

(1). Patients with megaesophagus (esophageal diameter >8 cm) or those with

low LES pressure and persistent symptoms typically do not do well with

either pneumatic dilation or surgical myotomy and may require an

esophagectomy with a gastric pullup or colon interposition.

--------------------------------------------------------------------------

Table 4. Cumulative Effectiveness of the Laparoscopic Surgical Myotomy

in Achalasia

--------------------------------------------------------------------

Reference

Number of Patients

Study Design

Antireflux Procedure

Objective Assessments

% Sx Improvement

Follow-up (yr) Mean (Range)

% Complications

--------------------------------------------------------------------

--------------------------------------------------------------------

--------------------------------------------------------------------

%LES Pressure

Excellent/Good

GERD

Mortality

--------------------------------------------------------------------

ti (37)

25

Retrospective

yes

61

96

1(1-2)

0

Ancona (38)

17

Retrospective

yes

72

100

0.7

6

0

Esposito (39)

8

Retrospective

yes

100

0.9(0.8-1)

0

Raiser (40)

29

Prospective

yes

90

1.2(1-2)

27

0

Morino (41)

18

Prospective

yes

60

100

0.7(0.2-2)

6

0

Anselmino (42)

43

Prospective

yes

68

95

1(0.3-4)

6

0

Delgado (43)

12

Prospective

yes

42

83

0.3(0.1-1)

0

0

Slim (44)

8

Retrospective

yes

67

100

1

0

Bonovina (45)

33

Retrospective

yes

61

97

1(0.3-2)

on (46)

9

Retrospective

no

88

1.1(1-1.9)

13

0

Swanstrom (47)

12

Retrospective

yes

42

100

1.3

16

0

Hunter (48)

40

Retrospective

yes

90

1

0

--------------------------------------------------------------------

Total

254

59%

240/254 = 94%

1(0.1-4) yr

16/141=11%

0%

--------------------------------------------------------------------

GERD = gastroesophageal reflux disease.

--------------------------------------------------------------------------

Endoscopic injection of botulinum toxin, type A, into the LES is the

most recent treatment alternative for achalasia. Botulinum toxin acts by

inhibiting the calcium-dependent release of acetylcholine from nerve

terminals, thereby counterbalancing the effect of the selective loss of

inhibitory neurotransmitters in achalasia (49, 50). It is commercially

supplied as lyophilized powder (Oculinum; Allergan, Irvin, CA) in vials

containing 100 units each. The powder must be diluted with normal saline

(5-10 ml) and used within 4 h of reconstitution without agitation of the

solution because of the toxin's instability at room temperature. Botulinum

toxin is injected endoscopically via a 5-mm sclerotherapy needle into the

LES region as identified by a " puckered " appearance just above the

gastroesophageal junction. Aliquots equaling 20-25 units of the toxin are

injected into each of four quadrants for a total of 80-100 units.

Available data indicate that botulinum toxin is effective in relieving

symptoms initially in about 85% of patients (1). However, symptoms recur in

more than 50% of patients within 6 months possibly because of regeneration

of the affected receptors (49). Older patients (>60 yr) and those with

vigorous achalasia, defined as esophageal amplitude >40 mm Hg, are more

likely to have a sustained response (up to 1.5 yr) to botulinum toxin

injection (51). In those responding to the first injection, 76% will respond

to a second botulinum toxin injection with decreasing response to further

injections, usually from antibody formation to this foreign protein. Less

than 20% of patients failing to respond to the first injection will respond

to a second injection of botulinum toxin. Studies have shown that botulinum

toxin is less effective than pneumatic dilation long term (52, 53).

Additionally, some reports indicate that cardiomyotomy may be more difficult

and less effective in patients who were previously treated with repeated

botulinum toxin injections, possibly because of submucosal scar formation in

the esophagus at the site of injection (54). Finally, the long-term safety

of repeated injections of botulinum toxin in achalasia patients is unknown.

Therefore, botulinum toxin injection should be reserved for elderly patients

or patients who are at high surgical risk or refuse pneumatic dilation and

surgical myotomy.

Calcium channel blockers and long-acting nitrates are effective in

reducing LES pressure and temporally relieving dysphagia, but do not improve

LES relaxation or improve peristalsis. Both agents are used sublingually by

opening the capsule and placing the contents under the tongue 15-45 min

before meals with doses ranging from 10-30 mg for nifedipine and 5-20 mg for

sublingual isosorbide dinitrate (55, 56). These drugs decrease LES pressure

by approximately 50% with the long-acting nitrates having a shorter time to

maximum effect (3-27 min) compared to sublingual nifedipine (30-120 min).

Overall, calcium channel blockers improve patient symptoms by 0-75%, whereas

sublingual nitrates result in symptom improvement in 53-87% of patients with

achalasia (1). The clinical response to these pharmacological agents is

short acting; they usually do not provide complete symptom relief, and

efficacy decreases with time. Side effects such as headache, hypotension,

and pedal edema are common limiting problems. Given these limitations,

calcium channel blockers and nitrates are recommended only for patients who

are very early in their disease with a nondilated esophagus, for symptomatic

patients who are not candidates for pneumatic dilation or surgical myotomy,

or for those who refuse invasive therapy and fail botulinum toxin

injections.

A suggested treatment algorithm for patients with achalasia is shown

in Figure 1. Symptomatic patients with achalasia who are good surgical

candidates should be given the option of either graded pneumatic dilation or

laparoscopic cardiomyotomy. The choice between the two procedures depends on

institutional preference and experience. In patients unresponsive to graded

pneumatic dilation, laparoscopic myotomy should be performed. In myotomy

failures, repeat pneumatic dilation can be attempted. In patients who are

poor candidates for surgery, initial treatment with botulinum toxin is

currently the preferred approach. Nifedipine or isordil may prove to be

beneficial in those unresponsive to botulinum toxin. Those with a

megaesophagus (sigmoid esophagus and diameter >8 cm), or those with low LES

pressure with persistent symptoms may require esophagectomy.

--------------------------------------------------------------------------

--------------------------------------------------------------------------

Figure 1. Suggested treatment algorithm for patients with achalasia.

*Initial dilation with a 3-cm balloon followed by 3.5-cm and then 4-cm

balloons in the nonresponders.

--------------------------------------------------------------------------

References

1. Vaezi MF, Richter JE. Current therapies for achalasia: Comparison

and efficacy. J Clin Gastroenterol 1998;27:21-35.

2. Birgisson S, Richter JE. Achalasia: What's new in diagnosis and

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3. Goldblum JR, Whyte RI, Orringer MB, et al. Achalasia: A morphologic

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4. Holloway RH, Dodds WJ, Helm JF, et al. Integrity of cholinergic

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5. Rozeman RW Jr, Achkar E. Features distinguishing secondary

achalasia from primary achalasia. Am J Gastroenterol 1990;85:1327-30.

6. Wong RKH, Maydonovitch CL. Achalasia. In: Castell DO, ed. The

esophagus, 2nd ed. New York: Little Brown, 1995:219-47.

7. Debas HT, Payne WS, Cameron AJ, et al. Physiopathology of the lower

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8. Ott DJ, Hodge RG, Chen MYM. Achalasia associated with hiatal

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9. Ergun GA, Kahrilas PJ. Clinical application of esophageal manometry

and pH monitoring. Am J Gastroenterol 1996;91:1077-89.

10. Goldenberg SP, Burrell M, Fette GG, et al. Classic and vigorous

achalasia: A comparison of manometric, radiographic, and clinical findings.

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11. Katz PO, Richter JE, Cowan R, et al. Apparent complete lower

esophageal sphincter relaxation in achalasia. Gastroenterology

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12. Tucker HJ, Snap WJ Jr, Cohen S. Achalasia secondary to carcinoma:

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13. Sandler RS, Bozymski EM, Orlando RC. Failure of clinical criteria

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14. Tracey JP, Traube M. Difficulties in the diagnosis of

pseudoachalasia. Am J Gastroenterol 1994;89:2014-8.

15. Van Dam J, Falk GW, Sivak MV, et al. Endosonographic evaluation of

the patient with achalasia: Appearance of the esophagus using the

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16. Schwartz HM, Cahow CE, Traube M. Outcome after perforation

sustained during pneumatic dilation for achalasia. Dig Dis Sci

1993;38:1409-13.

17. Khan AA, Shah WH, Alam A, et al. Pneumatic balloon dilation in

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18. Ott DJ, Richter JE, Wu WC, et al. Radiographic evaluation of the

achalasia esophagus immediately after pneumatic dilation. Gastrointest

Radiol 1987;32:962-7.

19. J, Buckton GK, JR. Balloon dilatation in achalasia: A

new dilator. Gut 1986;27:986-9.

20. Gelfand MD, Kozarek RA. An experience with polyethylene balloon

for pneumatic dilation for achalasia. Am J Gastroenterol 1989;84:924-7.

21. Barkin JS, Guelrud M, Reiner DK, et al. Forceful balloon dilation:

An outpatient procedure for achalasia. Gastrointest Endosc 1990;36:123-6.

22. Stark GA, Castell DO, Richter JE, et al. Prospective randomized

comparison of Brown-McHardy and Microvasive balloon dilators in treatment of

achalasia. Am J Gastroenterol 1990;85:1322-6.

23. Makela J, Kiviniemi H, Laitinen S. Heller's cardiomyotomy compared

with pneumatic dilation for the treatment of oesophageal achalasia. Eur J

Surg 1991;157:411-4.

24. Levine ML, Moskowitz GW, Dorf BS, et al. Pneumatic dilation in

patients with achalasia with a modified Gruntzig dilator (Levine) under

direct endoscopic control: Results after 5 years. Am J Gastroenterol

1991;86:1581-4.

25. Kadakia SC, Wong RKH. Graded pneumatic dilation using Rigiflex

achalasia dilators in patients with primary esophageal achalasia. Am J

Gastroenterol 1993;88:34-8.

26. Kim CH, Cameron AJ, Hsu JJ, et al. Achalasia: Prospective

evaluation of relationship between lower esophageal sphincter pressure,

esophageal transit, and esophageal diameter and symptoms in response to

pneumatic dilation. Mayo Clin Proc 1993;68:1067-73.

27. Lee JD, Cecil BD, Brown PE, et al. The Cohen test does not predict

outcome in achalasia after pneumatic dilation. Gastro[zhy]intest Endosc

1993;39:157-60.

28. Abid S, Champion G, Richter JE, et al. Treatment of achalasia: The

best of both worlds. Am J Gastroenterol 1994;89:979-85.

29. Wehrmann T, i V, Jung M, et al. Pneumatic dilation in

achalasia with a low-compliance balloon: Results of a 5-year prospective

evaluation. Gastrointest Endosc 1995;42:31-6.

30. Lambroza A, Schuman RW. Pneumatic dilation for achalasia without

fluoroscopic guidance: Safety and efficacy. Am J Gastroenterol

1995;90:1226-9.

31. Bhatnagar MS, Nanivadekar SA, Sawant P, et al. Achalasia cardia

dilatation using polyethylene balloon (Rigiflex) dilators. Indian J

Gastroenterol 1996;15:49-51.

32. Reynolds JC, Parkman HP. Achalasia. Gastroenterol Clin North Am

1989;18:223-55.

33. Vaezi MF, Baker ME, Richter JE. Assessment of esophageal emptying

post-pneumatic dilation: Use of timed-barium esophagram. Am J Gastroenterol

1999;94:1802-7.

34. Eckhardt VF, Aignherr C, Bernhard G. Predictors of outcome in

patients with achalasia treated by pneumatic dilation. Gastroenterology

1992;103:1732-8.

35. Levine ML, Dorf BS, Moskowitz GW, et al. Pneumatic dilation in

achalasia under endoscopic guidance: Correlation pre- and post-dilation by

radionuclide scintiscan. Am J Gastroenterol 1987;82:311-4.

36. de Oliveira JM, Birgisson S, Doinoff C, et al. Timed barium

swallow: A simple technique for evaluating esophageal emptying in patients

with achalasia. AJR 1997;169:473-9.

37. ti R, Fumagalli U, Bonavina L, et al. Laparoscopic approach to

esophageal achalasia. Am J Surg 1995;169:424-7.

38. Ancona E, Anselmino M, Zaninotto G, et al. Esophageal achalasia:

Laparoscopic versus conventional open Heller-Dor operation. Am J Surg

1995;170:265-70.

39. Esposito PS, Sosa JL, Sleeman D, et al. Laparoscopic management of

achalasia. Am Surgeon 1997;63:221-3.

40. Raiser F, Perdikis G, Hinder RA, et al. Heller myotomy via minimal

access surgery: An evaluation of anti-reflux procedures. Arch Surg

1996;131:593-8.

41. Morino M, Rebecchi F, Festa V, et al. Laparoscopic Heller

cardiomyotomy with intraoperative manometry in the management of oesophageal

achalasia. Int Surg 1995;80:332-5.

42. Anselmino M, Zaninotto G, Costantini M, et al. One-year follow-up

after laparoscopic Heller-Dor operation for esophageal achalasia. Surg

Endosc 1997;11:3-7.

43. Delgado F, Bolufer JM, ez-Abad M, et al. Laparoscopic

treatment of esophageal achalasia. Surg Lap Endosc 1996;2:83-90.

44. Slim K, Pezet D, Chipponi J, et al. Laparoscopic myotomy for

primary esophageal achalasia: Prospective evaluation.

Hepato-Gastroenterology 1997;44:11-5.

45. Bonovina L, ti R, Segalin A, et al. Laparoscopic Heller-Dor

operation for the treatment of oesophageal achalasia: Technique and early

results. Ann Chir Gynaecol 1995;84:165-8.

46. on GSM, Lloyd DM, Wicks ACB, et al. Laparoscopic Heller's

cardiomyotomy without an anti-reflux procedure. Br J Surg 1995;82:957-9.

47. Swanstrom LL, Pennings J. Laparoscopic esophagomyotomy for

achalasia. Surg Endosc 1995;9:286-92.

48. Hunter JG, Trus TL, Branum GD, et al. Laparoscopic Heller myotomy

and fundoplication for achalasia. Ann Surg 1997;225:655-65.

49. Tsui JKS. Botulinum toxin as a therapeutic agent. Pharmacol Ther

1996;72:13-24.

50. Pasricha PJ, Ravich WJ, Henrix TR, et al. Intrasphincteric

botulinum toxin for the treatment of achalasia. N Engl J Med 1995;322:774-8.

51. Pasricha PJ, Rai R, Ravich WJ, et al. Botulinum toxin for

achalasia: Long-term outcome and predictors of response. Gastroenterology

1996;110:1410-5.

52. Vaezi MF, Richter JE, Wilcox M, et al. Botulinum toxin versus

pneumatic dilation in the treatment of achalasia: A randomized trial. Gut

1999;44:231-9.

53. Prakash C, Freedland KE, Chan MF, et al. Botulinum toxin

injections for achalasia symptoms can approximate the short-term efficacy of

a single pneumatic dilation: A survival analysis approach. Am J

Gastroenterol 1999;94:328-33.

54. Gordon JMI, Eager ELY. Prospective study of esophageal botulinum

toxin injection in high-risk achalasia patients. Am J Gastroenterol

1997;92:1812-7.

55. Gelfond M, Rozen P, Gilat T. Isosorbide dinitrate and nifedipine

treatment of achalasia: A clinical, manometric and radionuclide evaluation.

Gastroenterology 1982;83:963-9.

56. Bortolotti M, Coccia G, Brunelli F, et al. Isosorbide dinitrate or

nifedipine: Which is preferable in the medical therapy of achalasia? Ital J

Gastroenterol 1994;26:379-82.

Appendix

Ad Hoc Committee on Practice Parameters:

Nimish Vakil, M.D., F.A.C.G., Chair

Freda L. Arlow, M.D., F.A.C.G.

Alan N. Barkun, M.D.

W. , Jr., M.D., F.A.C.G.

J. Caddick, M.D.

H. Caldwell, M.D.

D. Carey, M.D., F.A.C.G.

P. Cheney, M.D., F.A.C.G.

Sita S. Chokhavatia, M.D.

R. DeVault, M.D., F.A.C.G.

Francis A. Farraye, M.D., F.A.C.G.

Kris V. Kowdley, M.D.

Simon K. Lo, M.D., F.A.C.G.

S. Pratt, M.D.

Dawn Provenzale, M.D., F.A.C.G.

M. Simon, M.D., F.A.C.G.

Amy M. Tsuchida, M.D., F.A.C.G.

R. Viggiano, M.D., F.A.C.G.

J. Waring, M.D., F.A.C.G.

M. Wo, M.D.

Marc J. Zuckerman, M.D., F.A.C.G.

--------------------------------------------------------------------------

Reprint requests and correspondence: F. Vaezi, M.D., Ph.D.,

Center for Swallowing and Esophageal Disorders, Department of

Gastroenterology, The Cleveland Clinic Foundation, 9500 Euclid Avenue,

Cleveland, OH 44195.

Received Aug. 23, 1999; accepted Aug. 23, 1999.

--------------------------------------------------------------------------

Copyright ©1999 the American College of Gastroenterology

Published by Elsevier Science Inc.

Re: My Dad

>

>

> Hi

>

> Thanks for all your responses. Im not sure if I have replied

> correctly, but bear with me, am new to groups like this.

>

> My Dad is 67 years old, lives in Birmingham, England, takes

> Nifiditine which he has been taking for two years. He also takes

> losec to neutralise the acid. He has seen a consultant who wants to

> do key hole surgery, but my Dad is concerned about his experience as

> the doctor has only ever performed operations for reflux disease but

> not 'A', I dont know how different the two are.

>

> I have told him what you said about more damage can be caused if it

> is left and he was wondering what damage and if this was from

> personal experience of leaving the A untreated, or have the doctors

> told you?

>

> Thanks again

> Nelly

>

>

>

> >

> > Hi Nelly - first of all, welcome to you and your dad. Sorry that

> he

> > has A, it truly isn't much fun but this site is a tremendous

> resource

> > of information and support.

> >

> > > He has sufferred with it for a few years now, he is very worried

> > > about having anything done as he keeps hearing things to put him

> > > off, and thinks that nothing will really cure him. He is on the

> > > tablets but they do not really do much for him.

> > ** Unfortunately, there is no 'cure' but most of us have come up

> with

> > ways to manage our A and lead pretty normal lives. It is scary and

> > many doctors don't know much about it. The next time you post, let

> us

> > all know where your dad lives and we may be able to refer him to a

> > doctor who does know and has some experience with A. What tablets

> is

> > he on?

> > >

> > > He is now sick all the time, We

> > > are constantly trying to get him to have something done, but he

> is

> > > very worried about the lack of experience the medical profession

> > > seem to have with achlasia, and has also heard some horror

> stories

> > > about people who have had some treatment.

> >

> > ** Understandable that he is concerned but on this site you will

> find

> > that most of us have had surgery to help correct the problem with

> > good success rates. The MOST IMPORTANT thing to do is find a

> > doctor/surgeon who has had experience - we can probably help you

> > there or even go to the database link at the top of the site -

> there

> > are several lists of doctors there.

> > >

> > > Any advice for him, or any similar stories you could share with

> me

> > > so I can 'print them out to show him' (he has never even

> switched

> > on

> > > a computer) would be very helpful.

> >

> > ** Keep posting and reading - we run the gamut here, age, gender,

> > symptoms, treatments. I've had A for over 20 years and I'm still

> > learning tons of stuff here from everyone.

> > Good luck to him in finding some relief and good luck to you in

> your

> > quest to help him. Please tell him not to put off treatment, the

> > longer he waits - the more long term damage he will do. There are

> > treatments out there that will help - he has no reason to suffer.

> > Also, the longer he waits the harder it is to do any kind of

> surgery.

> > >

> > > Thanks very much

> > > Nelly

> >

> > Best of Luck!

> > Happy Swallowing!

> > -michelle in VA.

>

>

>

>

>

>

>

>

[Guest guest]

Hi Nelly

I am so sorry to hear that your dad has achalasia. It is an awful condition for anyone to have. I have had it for 18 months now. I am 26 and live in Liverpool, UK. There are very few people in the group who live in the UK and I have found it very difficult to get advise on an experienced surgeon in the UK who is used to working with achalasia patients.

Because of this I have resorted to contacting a couple of Highly recommended surgeons in the USA. The database gives links to their websites. One is the Mt Sinai clinic NY nad the other is the Cleveland Clinic, Ohio. This is my first choice. I know that I will have to pay a hefty sum for treatment in the USA not including flights and accomodation but the surgeons here are really very experienced in dealing with achalasians.

I think that because the disease affects only 1 in every 100,000 people that it will be impossible to find an experienced surgeon in the UK given it's small population compared with the USA. If you do find one however, please let me know.

I have done a lot of research to make my decision about surgery and reached my conclusion to have it done outright. Quite a few people have told me that having dilation or botox prior to surgery can cause a build up of scar tissue. Should the patient eventually have surgery further down the line, there is a higher chance that it will be unsuccessful due to scar tissue than if it was the first option. I would seriously suggest that your dad has surgery if he is in a general good state of health. This is a condition that just worsens with time and he raelly should get it sorted. I would say, try the clinics in the USA. After all, you can't really put a price on someones health.

Best of luck and regards to your dad.

Charmainenellys121 <nellys121@...> wrote:

Hi EveryoneMy dad is suffering from achalasia, I came across this site and he has asked me to see if there are any advances with helping his condition.He has sufferred with it for a few years now, he is very worried about having anything done as he keeps hearing things to put him off, and thinks that nothing will really cure him. He is on the tablets but they do not really do much for him.He is now sick all the time, he cannot sleep in the horizontal position and has about 12 pillows allowing him to sleep in a more upright position. Although he finds it difficult to eat and sicks it up frequently he persists and has not yet lost any weight. We are constantly trying to get him to have something done, but he is very worried about the lack of experience the medical profession seem to have with

achlasia, and has also heard some horror stories about people who have had some treatment.Any advice for him, or any similar stories you could share with me so I can 'print them out to show him' (he has never even switched on a computer) would be very helpful.Thanks very muchNelly

ALL-NEW Messenger - all new features - even more fun!

[Guest guest]

Hello ,

You Dad did a great fight....and..the truth is he won

in our hearts and your continued fight means he left

something for all of us...My sympathy...

Rossana

--- heather wrote:

> I am sorry to say that Charlie Hall, my dad, passed

> away on Saturday, September 10th at 52 years-old. He has

> been battling small cell lung cancer since February 2003. We

> found out that it has spread to his brain in June 2004.

[Guest guest]

Dear ,

I am so sorry that your dad passed away at such a young age. I know

from your messages that the two of you were very close. I can relate

to your being in complete shock. I was 19 when my dad died of a

malignant brain tumor at age 58. His illness moved very rapidly also.

Like you, I couldn't believe it.

My heart goes out to you and your family.

heathermkay wrote:

> I am sorry to say that Charlie Hall, my dad, passed away on

> Saturday, September 10th at 52 years-old. He has been battling

> small cell lung cancer since February 2003. We found out that it

> has spread to his brain in June 2004. He seemed to be doing okay

> other than being weak and tired at times. We had lunch together on

> August 24th and he was fine. He even snatched the bill and ran to

> pay it before I could. On August 28th, he started having problems

> walking and his condition quickly deteoriated after that. We were

> not even able to leave him alone because he would try to get up and

> lose his balance and fall. I am in complete shock because I never

> thought he would go down hill so fast.

[Guest guest]

, I am so sorry for your loss. I do understand. I lost my Dad when I was

6 months pregnant in 2000.

Prayers to you and yours.

----- Original Message -----

From: heathermkay

My dad, passed away on Saturday, September 10th at 52 years-old.

[Guest guest]

Hi Anne,

Your dad is allowed to have his test results and they may make a small

charge if it's a lot of work......

His ferritin is important and made more so by the paper that I put up

few days back, concerning the effect of heme on the circadian rhythm,

mediated by the mitochondria.

If his ferritin is too low and that may be different, as between men

and women, he could have sleep disturbance, and endocrine disruption

from just that sleep disturbance (the cellular output of mRNA/proteins

that make up the circadian rhythm/body clock, also affects the output

of other proteins/enzymes which are, likewise, cyclic in their

production).

Other papers seem to indicate that fluorocarbon-based drugs might also

disrupt the circadian rhythm by interfering with the Krebs Cycle in

the mitochondria (the cell's power-houses ~ usually counted in their

millions per cell).

Now that would be doubly difficult to rectify if there was no account

taken of either factor in deciding the next treatment option.

I would make certain that your dad is accompanied to his next

appointment, if there's any doubt that he will understand what is said

to him or that the doctor won't understand the matters before him/her.

Low ferritin would imply that his adrenal function is adrift for the

reason mentioned above.......and a very strong argument for not

accepting a fluorinated drug for 'depression'.

Adding yet more thyroxine in these circumstances is counter-productive.

best wishes

Bob

>

> Hi there,

> Can any one please give me some advice that I can pass on to my Dad.

In November 2007 Dad saw an consultant physician because he was so

exhausted all the time, very forgetful and quite depressed. He

noticed that Dad's TSH was 6.8. (not sure of any other blood test

results) and started him on Thyroxine 25mcg. Initially Dad was ok.

But after a couple of weeks he started feeling anxious, had

palpitations and breathlessness. These were the worst symptoms. His

GP told him to up the Thyroxine to 50mcg and Dad felt worse and again

more and more tired. Dad went back again to the GP explained that he

needed his Ferritin level, FT4 and FT3 and to check the adrenal

situation with the spit test. His GP didn't know what he was talking

about ? Ferritin ? Adrenals. Anyway he ordered the blood tests. They

were done 6 weeks ago and Dad still hasn't got his Ferritin level as

the surgery will not give patients their results!! But Dad was

informed that he had to

> increase the Thyroxine again and he is now on 75mcg even though the

GP agrees that Dad is probably not converting T4 to T3. Dad was so

ill today with breathlessness, weakness and pains all over his body

that he is practically chair bound. His face is puffy and he doesn't

look his usual self.

> I'm intollerant of both Armour and T3 and Dr Peatfield has told me

not to take either. I feel Dad is the same. Please has anybody any

advice I am really worried for him. Thank you.

> Love Anne x

>

>

> ___________________________________________________________

> For Good helps you make a difference

>

> http://uk.promotions./forgood/

>

[Guest guest]

Hi Anne,

I can relate to your Dad's situation. I guess all that I can do is

tell you about my situation because it sounds a bit like your dads.

I cannot tolerate T3 (haven't tried Armour but that is next on the

cards because I'm not doing well on thyroxine either!) I'm running

out of ideas! When I commenced using thyroxine I started on 25mcg of

thyroxine because I also was getting palpitations and anxiety.

Neither was a problem prior to taking thyroid replacement hormones.

My doctor told me to stay at the low dose (25mcg) until the

palpitations eased up and then to step up to 50mcg. He ordered

regular TSH, T3, T4 and Reverse T3 tests to monitor what was going

on with my conversion of T4 to T3. I'm at 150mcg after a year, but

I still don't feel great & I have high RT3 levels and very low T3

levels. Next step is Armour because he is concerned about what is

going on with the thyroxine, but I'm not sure whether I'll tolerate

the T3 in it.

Just out of curiosity, you mentioned that you couldn't tolerate

Armour or T3. What happened to you when you used them???? I'd

really appreciate knowing since I'm thinking of using 'Armour' next

due to poor response to thyroxine alone.

Just a thought but I wonder whether your Dad's thyroxine dosage was

increased too quickly. It literally took me about 6 months to get

to a stage where I could even tolerate taking the stuff, but because

I knew I had to take SOMETHING I kept on going and putting up with

it.

I am not elderly, but my doctor increased my thyroxine levels based

on the regime that he uses with elderly people. He did that because

I was having problems with palpipations, etc. He increases the dose

very slowly and although it might take a bit longer for people to

increase their levels, he still thinks it is a better way to go. He

suggested that people may get ongoing palpitations and other adverse

symptoms if it is done too quickly. I still have palpitations, but

they are not as crazy as they used to be.

Re your Dad's body pains and weakness. I use a thing called 'pic-

mins' that just about got rid of my joint & body pains. I used to

walk with a limp and couldn't walk more than 50m without taking a

rest. It hurt to roll over or get out of bed because of joint

pains. Prior to that I was reasonably active. My sister has the same

thyroid hassles as me and after seeing that I could walk better and

wasn't in so much pain, she started using pic-mins and for the first

time in a long time, she didn't need to take pain killers. It is

worth doing an internet search for it to see whether it might be

good for your dad or not. Remember to add the hyphen when you do the

search. Everyone is different, so it may or may not work for him

or suit him. Sounds like I'm selling the stuff, but I'm not. I

just think it is worth letting others know of things that have

helped others, so then you can do your own research and make a

decision about whether it will help your situation or not.

Hope this info helps a bit. I'm not a doctor though and I'm only

speaking from my own experience.

Good luck with it all.

P

>

> Hi there,

> Can any one please give me some advice that I can pass on to my

Dad. In November 2007 Dad saw an consultant physician because he

was so exhausted all the time, very forgetful and quite depressed.

He noticed that Dad's TSH was 6.8. (not sure of any other blood

test results) and started him on Thyroxine 25mcg. Initially Dad was

ok. But after a couple of weeks he started feeling anxious, had

palpitations and breathlessness. These were the worst symptoms.

His GP told him to up the Thyroxine to 50mcg and Dad felt worse and

again more and more tired. Dad went back again to the GP explained

that he needed his Ferritin level, FT4 and FT3 and to check the

adrenal situation with the spit test. His GP didn't know what he

was talking about ? Ferritin ? Adrenals. Anyway he ordered the

blood tests. They were done 6 weeks ago and Dad still hasn't got

his Ferritin level as the surgery will not give patients their

results!! But Dad was informed that he had to

> increase the Thyroxine again and he is now on 75mcg even though

the GP agrees that Dad is probably not converting T4 to T3. Dad was

so ill today with breathlessness, weakness and pains all over his

body that he is practically chair bound. His face is puffy and he

doesn't look his usual self.

> I'm intollerant of both Armour and T3 and Dr Peatfield has told me

not to take either. I feel Dad is the same. Please has anybody any

advice I am really worried for him. Thank you.

> Love Anne x

>

>

> ___________________________________________________________

> For Good helps you make a difference

>

> http://uk.promotions./forgood/

>

[Guest guest]

Hi Anne,

The surgery cannot not tell the patient the test results- Freedom of

information Act They can be awkward and charge for printed copies, but they

cannot withhold results.

If doc ‘can’t ‘

help and agrees on conversion problem then surely a referral is in order. Sheila

may be able to help with one near to your dad’s area.

Subject:

My Dad

Hi there,

They were done 6 weeks

ago and Dad still hasn't got his Ferritin level as the surgery will not give

patients their results!! But Dad was informed that he had to

increase the Thyroxine again and he is now on 75mcg even though the GP agrees

that Dad is probably not converting T4 to T3. Dad was so ill today with

breathlessness, weakness and pains all over his body that he is practically

chair bound. His face is puffy and he doesn't look his usual self.

I'm intollerant of both

Armour and T3 and Dr Peatfield has told me not to take either. I feel Dad

is the same. Please has anybody any advice I am really worried for

him. Thank you.

Love Anne x

Sent from .

More Ways to Keep in Touch.

[Guest guest]

Hi there Anne, your dad may well have adrenal problems, they need to be tested first, (24 hour salivary test) this is better done privately . if they are weak , he mostlikely will need to take some support for them before taking thyroid medication.as the thyroid medicine will not be able to do it`s job properly. angel. .

Sent from .

A Smarter Inbox.

[Guest guest]

You need to go to our website www.tpa-uk.org.uk and check our "Associated Conditions" under the heading "Hypothyroidism" in the Menu. Read everything about low Ferritin(stored iron), Candida Albicans and Adrenals, as any of these conditions can stop your thyroid hormone medication from working.

Do the Candida and Adrenal Questionnaires that you will find in the FILES on this Forum and see how you score. Having any of these conditions is often the reason why sufferers of hypothyroidism are unable to tolerate either Levothyroxine, Liothyronine or Armour and must be address first. Any of these conditions, you must stop taking thyroid hormone medication for at least (if possible) two weeks. Levothyroxine has a half life of 6 too 8 weeks to get completely out of your system, so you probably won't even miss it, but all the info about what to do and how to treat these conditions are on the website.

Many sufferers are unable (for one reason or another) to convert the inactive T4 into the active T3. T3 has to get into every cell in your body and brain to make them function. If you are unable to convert to T3, this is the reason many people get pain, brain fog, short term memory and continue to have all the symptoms of hypothyroidism. Read everything in the article about hypothyroidism in our website.

Luv - Sheila

Re: My Dad

Hi Anne,I can relate to your Dad's situation. I guess all that I can do is tell you about my situation because it sounds a bit like your dads. I cannot tolerate T3 (haven't tried Armour but that is next on the cards because I'm not doing well on thyroxine either!) I'm running out of ideas! When I commenced using thyroxine I started on 25mcg of thyroxine because I also was getting palpitations and anxiety. Neither was a problem prior to taking thyroid replacement hormones. My doctor told me to stay at the low dose (25mcg) until the palpitations eased up and then to step up to 50mcg. He ordered regular TSH, T3, T4 and Reverse T3 tests to monitor what was going on with my conversion of T4 to T3. I'm at 150mcg after a year, but I still don't feel great & I have high RT3 levels and very low T3 levels. Next step is Armour because he is concerned about what is going on with the thyroxine, but I'm not sure whether I'll tolerate the T3 in it. Just out of curiosity, you mentioned that you couldn't tolerate Armour or T3. What happened to you when you used them???? I'd really appreciate knowing since I'm thinking of using 'Armour' next due to poor response to thyroxine alone.Just a thought but I wonder whether your Dad's thyroxine dosage was increased too quickly. It literally took me about 6 months to get to a stage where I could even tolerate taking the stuff, but because I knew I had to take SOMETHING I kept on going and putting up with it.I am not elderly, but my doctor increased my thyroxine levels based on the regime that he uses with elderly people. He did that because I was having problems with palpipations, etc. He increases the dose very slowly and although it might take a bit longer for people to increase their levels, he still thinks it is a better way to go. He suggested that people may get ongoing palpitations and other adverse symptoms if it is done too quickly. I still have palpitations, but they are not as crazy as they used to be.Re your Dad's body pains and weakness. I use a thing called 'pic-mins' that just about got rid of my joint & body pains. I used to walk with a limp and couldn't walk more than 50m without taking a rest. It hurt to roll over or get out of bed because of joint pains. Prior to that I was reasonably active. My sister has the same thyroid hassles as me and after seeing that I could walk better and wasn't in so much pain, she started using pic-mins and for the first time in a long time, she didn't need to take pain killers. It is worth doing an internet search for it to see whether it might be good for your dad or not. Remember to add the hyphen when you do the search. Everyone is different, so it may or may not work for him or suit him. Sounds like I'm selling the stuff, but I'm not. I just think it is worth letting others know of things that have helped others, so then you can do your own research and make a decision about whether it will help your situation or not.Hope this info helps a bit. I'm not a doctor though and I'm only speaking from my own experience. Good luck with it all.P>> Hi there,> Can any one please give me some advice that I can pass on to my Dad. In November 2007 Dad saw an consultant physician because he was so exhausted all the time, very forgetful and quite depressed. He noticed that Dad's TSH was 6.8. (not sure of any other blood test results) and started him on Thyroxine 25mcg. Initially Dad was ok. But after a couple of weeks he started feeling anxious, had palpitations and breathlessness. These were the worst symptoms. His GP told him to up the Thyroxine to 50mcg and Dad felt worse and again more and more tired. Dad went back again to the GP explained that he needed his Ferritin level, FT4 and FT3 and to check the adrenal situation with the spit test. His GP didn't know what he was talking about ? Ferritin ? Adrenals. Anyway he ordered the blood tests. They were done 6 weeks ago and Dad still hasn't got his Ferritin level as the surgery will not give patients their results!! But Dad was informed that he had to> increase the Thyroxine again and he is now on 75mcg even though the GP agrees that Dad is probably not converting T4 to T3. Dad was so ill today with breathlessness, weakness and pains all over his body that he is practically chair bound. His face is puffy and he doesn't look his usual self.> I'm intollerant of both Armour and T3 and Dr Peatfield has told me not to take either. I feel Dad is the same. Please has anybody any advice I am really worried for him. Thank you.> Love Anne x> > > __________________________________________________________ > For Good helps you make a difference > > http://uk.promotions./forgood/>

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[Guest guest]

Gentle hugs Beth for you and your family. Please know you will be inour thoughts and prayers.

Donna**************Need a new ride? Check out the largest site for U.S. used car listings at AOL Autos. (http://autos.aol.com/used?NCID=aolcmp00300000002851)