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As I was perusing the AMOS site--where I started the WLS journey--I

was intrigued by the mortality rate difference between men and women.

It seems that those getting any wls the number of women out# the men

by 8:1, yet the mortality is far heavier on the male side. Why is

this? Are they 1)heavier 2)unhealthier 3)older 4) do they ignore s/s

of serioius complications? It was a curious thing to me, something

that concerns me as well, because my hubby may be following me in

this journey. All the more--do I want to research and prepare for his

sake.

I go back to the AMOS site infrequently, only to update my profile

and seek out more DS info. It is heavily on the RNY side--and if it

hadn't of been for me stumbling onto a profile of someone from my

home state I would have never found out about the DS. It would

behoove AMOS to provide more info on DS. It seems very limited.

The discussions here border on debate sometimes--but the " critical

thinking " and discerning natures are positives that benefit all who

visit. As a nurse and staunch pt. advocate I push people to ask

questions---and more questions---the time to ask them is before

jumping headlong into something so life altering. So many worry about

getting the " insurance " to foot the bill at the expense of good

decision making on the choice of surgery and surgeon.

Some may dislike the discussions here--but they elicit a broader view

of what we think this surgery is all about--both risks and benefits.

Pammi

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As I was perusing the AMOS site--where I started the WLS journey--I

was intrigued by the mortality rate difference between men and women.

It seems that those getting any wls the number of women out# the men

by 8:1, yet the mortality is far heavier on the male side. Why is

this? Are they 1)heavier 2)unhealthier 3)older 4) do they ignore s/s

of serioius complications? It was a curious thing to me, something

that concerns me as well, because my hubby may be following me in

this journey. All the more--do I want to research and prepare for his

sake.

I go back to the AMOS site infrequently, only to update my profile

and seek out more DS info. It is heavily on the RNY side--and if it

hadn't of been for me stumbling onto a profile of someone from my

home state I would have never found out about the DS. It would

behoove AMOS to provide more info on DS. It seems very limited.

The discussions here border on debate sometimes--but the " critical

thinking " and discerning natures are positives that benefit all who

visit. As a nurse and staunch pt. advocate I push people to ask

questions---and more questions---the time to ask them is before

jumping headlong into something so life altering. So many worry about

getting the " insurance " to foot the bill at the expense of good

decision making on the choice of surgery and surgeon.

Some may dislike the discussions here--but they elicit a broader view

of what we think this surgery is all about--both risks and benefits.

Pammi

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Having all of the particulars, on all available treatments, is the

only way to make an intelligent decision. The facts need to be

applied to your own lifestyle, and habit, in order to make the best

decision. Can you tolerate the lifestyle post surgery, or will it

drive you to not comply, causing dangerous side effects? Without

different personal opinions, there would not be horse races! Good

luck! Sue .

> As I was perusing the AMOS site--where I started the WLS journey--I

> was intrigued by the mortality rate difference between men and

women.

>

> It seems that those getting any wls the number of women out# the men

> by 8:1, yet the mortality is far heavier on the male side. Why is

> this? Are they 1)heavier 2)unhealthier 3)older 4) do they ignore

s/s

> of serioius complications? It was a curious thing to me, something

> that concerns me as well, because my hubby may be following me in

> this journey. All the more--do I want to research and prepare for

his

> sake.

>

> I go back to the AMOS site infrequently, only to update my profile

> and seek out more DS info. It is heavily on the RNY side--and if it

> hadn't of been for me stumbling onto a profile of someone from my

> home state I would have never found out about the DS. It would

> behoove AMOS to provide more info on DS. It seems very limited.

>

> The discussions here border on debate sometimes--but the " critical

> thinking " and discerning natures are positives that benefit all who

> visit. As a nurse and staunch pt. advocate I push people to ask

> questions---and more questions---the time to ask them is before

> jumping headlong into something so life altering. So many worry

about

> getting the " insurance " to foot the bill at the expense of good

> decision making on the choice of surgery and surgeon.

>

> Some may dislike the discussions here--but they elicit a broader

view

> of what we think this surgery is all about--both risks and benefits.

>

> Pammi

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One reason for the higher mortality of males with surgery is that

men are more likely to have central obesity and post op abdominal

compartment syndrome.

in Seattle

It seems that those getting any wls the number of women out# the men

> by 8:1, yet the mortality is far heavier on the male side. Why is

> this?

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One reason for the higher mortality of males with surgery is that

men are more likely to have central obesity and post op abdominal

compartment syndrome.

in Seattle

It seems that those getting any wls the number of women out# the men

> by 8:1, yet the mortality is far heavier on the male side. Why is

> this?

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,

Wonderful !!!! I am an 'apple', too ... ugh ...

What on earth is 'abdominal compartment syndrome' ??? Doesn't sound good

:-)

Bye,

Donna

marym@...

To: duodenalswitch

08/13/2001 cc:

09:36 AM Subject: Re: WLS

Mortality

Please respond

to

duodenalswitch

One reason for the higher mortality of males with surgery is that

men are more likely to have central obesity and post op abdominal

compartment syndrome.

in Seattle

It seems that those getting any wls the number of women out# the men

> by 8:1, yet the mortality is far heavier on the male side. Why is

> this?

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

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,

Wonderful !!!! I am an 'apple', too ... ugh ...

What on earth is 'abdominal compartment syndrome' ??? Doesn't sound good

:-)

Bye,

Donna

marym@...

To: duodenalswitch

08/13/2001 cc:

09:36 AM Subject: Re: WLS

Mortality

Please respond

to

duodenalswitch

One reason for the higher mortality of males with surgery is that

men are more likely to have central obesity and post op abdominal

compartment syndrome.

in Seattle

It seems that those getting any wls the number of women out# the men

> by 8:1, yet the mortality is far heavier on the male side. Why is

> this?

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

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The way it was explained to me is that men tend to have most of their fat

concentrated in their abdomen making it more difficult to conduct this surgery.

Joe Frost spoke of the role that " Abdominal Compartment Syndrome " played in his

surgical complications. He did not say whether it was more prevalent in men,

but given the above information, I could see the relationship...

from NE Philly, age 39

Open DS 6/27/01 - Dr. Pomp/Mt. Sinai/NYC - BMI 63

6 1/2 weeks out - 30+lbs down

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The way it was explained to me is that men tend to have most of their fat

concentrated in their abdomen making it more difficult to conduct this surgery.

Joe Frost spoke of the role that " Abdominal Compartment Syndrome " played in his

surgical complications. He did not say whether it was more prevalent in men,

but given the above information, I could see the relationship...

from NE Philly, age 39

Open DS 6/27/01 - Dr. Pomp/Mt. Sinai/NYC - BMI 63

6 1/2 weeks out - 30+lbs down

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At 9:55 AM -0400 8/13/01, Donna Joostema wrote:

>,

>

>Wonderful !!!! I am an 'apple', too ... ugh ...

>What on earth is 'abdominal compartment syndrome' ??? Doesn't sound good

>:-)

>

Rao Ivatury, MD, of the Medical College of Virginia reviewed the

pathophysiology and diagnosis of intra-abdominal hypertension and

intra-abdominal compartment syndrome which, he

pointed out, are not synonymous terms.[2] Elevated intra-abdominal

pressure with systemic signs and symptoms of that pressure results in

ACS. IAH is the measurement of the pressure.

The elevated pressure measurement, along with the associated clinical

changes, constitutes ACS. Because these patients are repeatedly

resuscitated they enter a cycle of ischemia/reperfusion,

which is known to be deadly to organs; systemic inflammatory response

syndrome appears initially, progressing to multiple organ dysfunction

syndrome and finally death.

Abdominal compartment syndrome was first described in the 1890s. Only

over the last several years, however, have surgeons begun to clearly

define the constellation of disorders

associated with an excess of pressure in the abdominal cavity. ACS is

likely to develop after any event that leads to an acute increase in

the volume of abdominal contents sufficient to cause

pressure-related organ dysfunction. As such, ACS can result from

either blunt or penetrating trauma and surgery, as well as numerous

medical conditions. It normally develops 12 to 24

hours after the first operation, especially after damage control.

Intra-abdominal hypertension can develop from increased amounts of

blood, other fluids, packing, and edematous bowel and

other organs in the free abdominal cavity. Consequences of this

increasing pressure appear gradually. Increased pressure leads to

reduced hepatic arterial blood flow, decreases cardiac

output, and can cause mucosal ischemia and acidosis, and eventually

mesenteric thrombosis. Furthermore, studies have demonstrated that

abdominal pressures of 15 to 20 mm Hg can

produce oliguria, and in some models pressures beyond 20 mm Hg may

lead to anuria.

Dr. Ivatury cited a study by Lawrence Diebel, MD, from Wayne State

University in Detroit, Mich, that demonstrated that a small elevation

in intra-abdominal pressure results in decreased

mesenteric artery flow and mucosal blood flow in the small intestine,

despite maintenance of cardiac output.[3] Significant hemodynamic

complications and compromises of intra-abdominal

hypertension can translate to complications such as sepsis,

multiorgan failure, and death. Once the pressure is brought down by

opening the abdomen, these physiologic changes can be

reversed.

Diagnosis

Classic signs of ACS are decreased PO2, very highly elevated PCO2,

high peak inspiratory pressure, lack of urinary output, and a

massively distended abdomen. A better way of diagnosing

this condition, however, is through continuous intra-abdominal

pressure monitoring in the intensive care unit (ICU) in all

critically ill patients at high risk for these complications. Those at

high risk for IAH and ACS include:

Burn patients

Patients with extensive abdominal trauma

Patients with extensive intra-abdominal bleeding

Patients with coagulopathies

Patients with bowel ischemia

Patients with packing

Patients with massive colloidal and crystalloid resuscitation

Patients with pancreatic abscesses

--

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At 9:55 AM -0400 8/13/01, Donna Joostema wrote:

>,

>

>Wonderful !!!! I am an 'apple', too ... ugh ...

>What on earth is 'abdominal compartment syndrome' ??? Doesn't sound good

>:-)

>

Rao Ivatury, MD, of the Medical College of Virginia reviewed the

pathophysiology and diagnosis of intra-abdominal hypertension and

intra-abdominal compartment syndrome which, he

pointed out, are not synonymous terms.[2] Elevated intra-abdominal

pressure with systemic signs and symptoms of that pressure results in

ACS. IAH is the measurement of the pressure.

The elevated pressure measurement, along with the associated clinical

changes, constitutes ACS. Because these patients are repeatedly

resuscitated they enter a cycle of ischemia/reperfusion,

which is known to be deadly to organs; systemic inflammatory response

syndrome appears initially, progressing to multiple organ dysfunction

syndrome and finally death.

Abdominal compartment syndrome was first described in the 1890s. Only

over the last several years, however, have surgeons begun to clearly

define the constellation of disorders

associated with an excess of pressure in the abdominal cavity. ACS is

likely to develop after any event that leads to an acute increase in

the volume of abdominal contents sufficient to cause

pressure-related organ dysfunction. As such, ACS can result from

either blunt or penetrating trauma and surgery, as well as numerous

medical conditions. It normally develops 12 to 24

hours after the first operation, especially after damage control.

Intra-abdominal hypertension can develop from increased amounts of

blood, other fluids, packing, and edematous bowel and

other organs in the free abdominal cavity. Consequences of this

increasing pressure appear gradually. Increased pressure leads to

reduced hepatic arterial blood flow, decreases cardiac

output, and can cause mucosal ischemia and acidosis, and eventually

mesenteric thrombosis. Furthermore, studies have demonstrated that

abdominal pressures of 15 to 20 mm Hg can

produce oliguria, and in some models pressures beyond 20 mm Hg may

lead to anuria.

Dr. Ivatury cited a study by Lawrence Diebel, MD, from Wayne State

University in Detroit, Mich, that demonstrated that a small elevation

in intra-abdominal pressure results in decreased

mesenteric artery flow and mucosal blood flow in the small intestine,

despite maintenance of cardiac output.[3] Significant hemodynamic

complications and compromises of intra-abdominal

hypertension can translate to complications such as sepsis,

multiorgan failure, and death. Once the pressure is brought down by

opening the abdomen, these physiologic changes can be

reversed.

Diagnosis

Classic signs of ACS are decreased PO2, very highly elevated PCO2,

high peak inspiratory pressure, lack of urinary output, and a

massively distended abdomen. A better way of diagnosing

this condition, however, is through continuous intra-abdominal

pressure monitoring in the intensive care unit (ICU) in all

critically ill patients at high risk for these complications. Those at

high risk for IAH and ACS include:

Burn patients

Patients with extensive abdominal trauma

Patients with extensive intra-abdominal bleeding

Patients with coagulopathies

Patients with bowel ischemia

Patients with packing

Patients with massive colloidal and crystalloid resuscitation

Patients with pancreatic abscesses

--

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From what I read, or what I could understand of what I read :-), it doesn't

really seem that this should be a

huge concern of mine. Maybe I should borrow trouble elsewhere, but thanks

for the information .... this was

a new one for me !!

Bye,

Donna

Steve Goldstein

<steve-goldstein@c To:

duodenalswitch

ox.rr.com> cc:

duodenalswitch , " Donna Joostema "

08/13/2001 11:00 Subject: Re:

Re: WLS Mortality

AM

Please respond to

duodenalswitch

At 9:55 AM -0400 8/13/01, Donna Joostema wrote:

>,

>

>Wonderful !!!! I am an 'apple', too ... ugh ...

>What on earth is 'abdominal compartment syndrome' ??? Doesn't sound good

>:-)

>

Rao Ivatury, MD, of the Medical College of Virginia reviewed the

pathophysiology and diagnosis of intra-abdominal hypertension and

intra-abdominal compartment syndrome which, he

pointed out, are not synonymous terms.[2] Elevated intra-abdominal

pressure with systemic signs and symptoms of that pressure results in

ACS. IAH is the measurement of the pressure.

The elevated pressure measurement, along with the associated clinical

changes, constitutes ACS. Because these patients are repeatedly

resuscitated they enter a cycle of ischemia/reperfusion,

which is known to be deadly to organs; systemic inflammatory response

syndrome appears initially, progressing to multiple organ dysfunction

syndrome and finally death.

Abdominal compartment syndrome was first described in the 1890s. Only

over the last several years, however, have surgeons begun to clearly

define the constellation of disorders

associated with an excess of pressure in the abdominal cavity. ACS is

likely to develop after any event that leads to an acute increase in

the volume of abdominal contents sufficient to cause

pressure-related organ dysfunction. As such, ACS can result from

either blunt or penetrating trauma and surgery, as well as numerous

medical conditions. It normally develops 12 to 24

hours after the first operation, especially after damage control.

Intra-abdominal hypertension can develop from increased amounts of

blood, other fluids, packing, and edematous bowel and

other organs in the free abdominal cavity. Consequences of this

increasing pressure appear gradually. Increased pressure leads to

reduced hepatic arterial blood flow, decreases cardiac

output, and can cause mucosal ischemia and acidosis, and eventually

mesenteric thrombosis. Furthermore, studies have demonstrated that

abdominal pressures of 15 to 20 mm Hg can

produce oliguria, and in some models pressures beyond 20 mm Hg may

lead to anuria.

Dr. Ivatury cited a study by Lawrence Diebel, MD, from Wayne State

University in Detroit, Mich, that demonstrated that a small elevation

in intra-abdominal pressure results in decreased

mesenteric artery flow and mucosal blood flow in the small intestine,

despite maintenance of cardiac output.[3] Significant hemodynamic

complications and compromises of intra-abdominal

hypertension can translate to complications such as sepsis,

multiorgan failure, and death. Once the pressure is brought down by

opening the abdomen, these physiologic changes can be

reversed.

Diagnosis

Classic signs of ACS are decreased PO2, very highly elevated PCO2,

high peak inspiratory pressure, lack of urinary output, and a

massively distended abdomen. A better way of diagnosing

this condition, however, is through continuous intra-abdominal

pressure monitoring in the intensive care unit (ICU) in all

critically ill patients at high risk for these complications. Those at

high risk for IAH and ACS include:

Burn patients

Patients with extensive abdominal trauma

Patients with extensive intra-abdominal bleeding

Patients with coagulopathies

Patients with bowel ischemia

Patients with packing

Patients with massive colloidal and crystalloid resuscitation

Patients with pancreatic abscesses

--

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

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Share on other sites

From what I read, or what I could understand of what I read :-), it doesn't

really seem that this should be a

huge concern of mine. Maybe I should borrow trouble elsewhere, but thanks

for the information .... this was

a new one for me !!

Bye,

Donna

Steve Goldstein

<steve-goldstein@c To:

duodenalswitch

ox.rr.com> cc:

duodenalswitch , " Donna Joostema "

08/13/2001 11:00 Subject: Re:

Re: WLS Mortality

AM

Please respond to

duodenalswitch

At 9:55 AM -0400 8/13/01, Donna Joostema wrote:

>,

>

>Wonderful !!!! I am an 'apple', too ... ugh ...

>What on earth is 'abdominal compartment syndrome' ??? Doesn't sound good

>:-)

>

Rao Ivatury, MD, of the Medical College of Virginia reviewed the

pathophysiology and diagnosis of intra-abdominal hypertension and

intra-abdominal compartment syndrome which, he

pointed out, are not synonymous terms.[2] Elevated intra-abdominal

pressure with systemic signs and symptoms of that pressure results in

ACS. IAH is the measurement of the pressure.

The elevated pressure measurement, along with the associated clinical

changes, constitutes ACS. Because these patients are repeatedly

resuscitated they enter a cycle of ischemia/reperfusion,

which is known to be deadly to organs; systemic inflammatory response

syndrome appears initially, progressing to multiple organ dysfunction

syndrome and finally death.

Abdominal compartment syndrome was first described in the 1890s. Only

over the last several years, however, have surgeons begun to clearly

define the constellation of disorders

associated with an excess of pressure in the abdominal cavity. ACS is

likely to develop after any event that leads to an acute increase in

the volume of abdominal contents sufficient to cause

pressure-related organ dysfunction. As such, ACS can result from

either blunt or penetrating trauma and surgery, as well as numerous

medical conditions. It normally develops 12 to 24

hours after the first operation, especially after damage control.

Intra-abdominal hypertension can develop from increased amounts of

blood, other fluids, packing, and edematous bowel and

other organs in the free abdominal cavity. Consequences of this

increasing pressure appear gradually. Increased pressure leads to

reduced hepatic arterial blood flow, decreases cardiac

output, and can cause mucosal ischemia and acidosis, and eventually

mesenteric thrombosis. Furthermore, studies have demonstrated that

abdominal pressures of 15 to 20 mm Hg can

produce oliguria, and in some models pressures beyond 20 mm Hg may

lead to anuria.

Dr. Ivatury cited a study by Lawrence Diebel, MD, from Wayne State

University in Detroit, Mich, that demonstrated that a small elevation

in intra-abdominal pressure results in decreased

mesenteric artery flow and mucosal blood flow in the small intestine,

despite maintenance of cardiac output.[3] Significant hemodynamic

complications and compromises of intra-abdominal

hypertension can translate to complications such as sepsis,

multiorgan failure, and death. Once the pressure is brought down by

opening the abdomen, these physiologic changes can be

reversed.

Diagnosis

Classic signs of ACS are decreased PO2, very highly elevated PCO2,

high peak inspiratory pressure, lack of urinary output, and a

massively distended abdomen. A better way of diagnosing

this condition, however, is through continuous intra-abdominal

pressure monitoring in the intensive care unit (ICU) in all

critically ill patients at high risk for these complications. Those at

high risk for IAH and ACS include:

Burn patients

Patients with extensive abdominal trauma

Patients with extensive intra-abdominal bleeding

Patients with coagulopathies

Patients with bowel ischemia

Patients with packing

Patients with massive colloidal and crystalloid resuscitation

Patients with pancreatic abscesses

--

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

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The following is a direct quote from Dr. Anthone's interview on

WebMD. (http://my.webmd.com/content/article/1700.50725)

Thanks, , for posting this link!!

" The medical contra-indications for obesity surgery are

difficult to define, but once a patient becomes so limited

so they can't even walk because of their obesity, the risk

for dying, either during or after surgery increases

dramatically. As a matter of fact, one patient out of 200

that has weight loss or obesity surgery dies. Now, that's

taking all morbidly obese patients as a group. And the

highest risk patient is one that cannot walk. They already

have cardiopulmonary failure. That's what that means.

They're usually seen in wheelchairs, or on little motor

scooters. Their ambulatory or walking status is so inhibited

because of their obesity that their heart and lungs can no

longer oxygenate the tissues enough to walk. So, if they

can't walk before surgery, they're sure not going to walk

after surgery. And, when a patient can't get up and walk

after surgery all kinds of complications take place. You

develop pneumonias or pressure sores or blood clots in the

legs that can dislodge and travel to the heart and cause the

heart not to pump blood to your lungs. Those are all real

indications for a patient dying after surgery. So, we have

to determine who can make it through surgery and who can't.

Unfortunately, bariatric surgeons, myself in particular

because I'm at a university, we get referred patients all

the time who are in that situation and their obesity is

already life threatening. And, I consider it almost too high

a risk to perform surgery, however, we do it sometimes. "

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The following is a direct quote from Dr. Anthone's interview on

WebMD. (http://my.webmd.com/content/article/1700.50725)

Thanks, , for posting this link!!

" The medical contra-indications for obesity surgery are

difficult to define, but once a patient becomes so limited

so they can't even walk because of their obesity, the risk

for dying, either during or after surgery increases

dramatically. As a matter of fact, one patient out of 200

that has weight loss or obesity surgery dies. Now, that's

taking all morbidly obese patients as a group. And the

highest risk patient is one that cannot walk. They already

have cardiopulmonary failure. That's what that means.

They're usually seen in wheelchairs, or on little motor

scooters. Their ambulatory or walking status is so inhibited

because of their obesity that their heart and lungs can no

longer oxygenate the tissues enough to walk. So, if they

can't walk before surgery, they're sure not going to walk

after surgery. And, when a patient can't get up and walk

after surgery all kinds of complications take place. You

develop pneumonias or pressure sores or blood clots in the

legs that can dislodge and travel to the heart and cause the

heart not to pump blood to your lungs. Those are all real

indications for a patient dying after surgery. So, we have

to determine who can make it through surgery and who can't.

Unfortunately, bariatric surgeons, myself in particular

because I'm at a university, we get referred patients all

the time who are in that situation and their obesity is

already life threatening. And, I consider it almost too high

a risk to perform surgery, however, we do it sometimes. "

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Wow Steve--where did you find this? Reading that against what Larry

was going through the days before with the decreased urinary output--

need I say any more?

Thanks so much for posting this--puts me on my toes!!

Pammi

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Wow Steve--where did you find this? Reading that against what Larry

was going through the days before with the decreased urinary output--

need I say any more?

Thanks so much for posting this--puts me on my toes!!

Pammi

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At 8:25 PM +0000 8/13/01, psbilyeu@... wrote:

>Wow Steve--where did you find this?

[abdominal compartment syndrome?]

http://www.medscape.com

>Reading that against what Larry

>was going through the days before with the decreased urinary output--

>need I say any more?

Scared the heck out of me when I read it, because my belly had been

greatly distended for several days post-op. Most likely in my case

it was because I had discontinued my diuretic. When I went back on,

the belly came down. Nopw, BTW, my PCP cut the dose of the diuretic

in half (HCTZ 50 -> 25 mg), and I have not lost weight in over a

week; in fact, I may have added a pound of fluid.

--Steve

--

Steve Goldstein, age 61

Lap BPD/DS on May 2, 2001

Dr. Elariny, INOVA Fairfax Hospital, Virginia

Starting (05/02/01) BMI = 51

BMI on 08/07 = 42

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Aha! I knew I didn't have to look further for that answer. Thanks again

Steve!

>

Rao Ivatury, MD, of the Medical College of Virginia reviewed the

pathophysiology and diagnosis of intra-abdominal hypertension and

intra-abdominal compartment syndrome which, he

pointed out, are not synonymous terms.[2] Elevated intra-abdominal

pressure with systemic signs and symptoms of that pressure results in

ACS. IAH is the measurement of the pressure.

The elevated pressure measurement, along with the associated clinical

changes, constitutes ACS. Because these patients are repeatedly

resuscitated they enter a cycle of ischemia/reperfusion,

which is known to be deadly to organs; systemic inflammatory response

syndrome appears initially, progressing to multiple organ dysfunction

syndrome and finally death.

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