Sphincterlike thoracoabdominal high pressure zone after esophagogastrectomy

Sphincterlike thoracoabdominal high pressure zone after esophagogastrectomy

GASTROENTEROLOGY 1993;105:1362-1369 Sphincterlike Thoracoabdominal High Pressure Zone After Esophagogastrectomy WALTER A. KLEIN, Departments of M...

940KB Sizes 10 Downloads 39 Views

GASTROENTEROLOGY

1993;105:1362-1369

Sphincterlike Thoracoabdominal High Pressure Zone After Esophagogastrectomy WALTER

A. KLEIN,

Departments

of Medicine and Surgery, Temple University School of Medicine, Philadelphia, Pennsylvania

HENRY

P. PARKMAN,

DANIEL

Background: The contribution of the crural diaphragm to the gastroesophageal high pressure zone (HPZ) may be important in prevention of gastroesophageal reflux. The purpose of this study was to investigate the manometric characteristics of the thoracoabdominal junction in patients after surgical removal of the lower esophageal sphincter. Methods: Ten patients with prior esophagogastrectomy were studied manometrically. Results: Esophageal manometry showed a HP2 and pressure inversion point distal to the anastomosis in 9 of 10 patients. Midrespiratory and end expiratory pressures were 14 + 7 and 6 f 4 mm Hg above intra-abdominal pressure, respectively. Breath holding caused inhibition of the phasic pressure component. This HP2 relaxed partially in response to deglutition (60% + 22%) and contracted in response to increased intraabdominal pressure induced by either leg lifts or abdominal compression (AHPZ/Aintra-abdominal pressure = 1.87 f 0.64 and 1.96 + 0.40, respectively). Conclusions: This study shows an HP2 at the thoracoabdominal junction after surgical removal of the lower esophageal sphincter. We suggest that this sphincterllke HP2 Is due to the crural diaphragm.

T

he high pressure geal junction

vention

zone (HPZ)

at the gastroesopha-

is an important

of gastroesophageal

barrier

reflux.’ This HP2 behaves

like a sphincter

in that it relaxes

mal stimulation

such as swallowing

of a bolus

the stomach,

sponse

into

to distal

stimulation

for the pre-

in response to permit

and it contracts to prevent

to proxipassage in re-

gastroesopha-

geal reflux.2 The HP2 has two components: a tonic pressure due to the lower esophageal sphincter (LES) with superimposed phasic pressure oscillations.3’4 Although studies recording diaphragrnatic electromyographic activity in humans and cats suggest that the phasic contractions are due to the crural diaphragm,L5 the sphincterlike properties of the gastroesophageal junction have been largely attributed to the smooth muscle LES.6 The contribution of the crural diaphragm to the adaptive sphincterlike manometric properties at the gastroesophageal junction HP2 is not well understood. The purpose of this study was to investigate the

T. DEMPSEY,

manometric junction moval specific at the

and ROBERT

characteristics in patients

who

of the intrinsic

S. FISHER

of the thoracoabdominal had undergone

lower esophageal

aims were to determine thoracoabdominal

esophagogastrectomy

junction

surgical sphincter.

reThe

(1) if an HP2

exists

in patients

after

and (2) if this HP2

behaves

like

a sphincter.

Methods Patient Selection Patients were selected for this study from the outpatient records of the Gastroenterology Section and the inpatient records of Temple University Hospital. All discharges were screened for 1986-l 99 1 using diagnoses coded according to the International Classification of Diseases: Version 9 (ICD-9) CM relevant to esophagogastrectomy.7 Inpatient admissions were identified by the Medical Information System Computer (TDS Health Care Systems Corporation, Atlanta, GA). Patients were included in the study if they had undergone an esophagogastrectomy with surgical removal of the gastroesophageal junction. Patients were excluded if they were pregnant, unwilling or unable to undergo esophageal manometry, or deceased. Ten asymptomatic control subjects with normal anatomy were also recruited for esophageal manometry. The protocol for the study was approved by the Investigation Review Board at Temple University Hospital. All patients gave informed consent before undergoing endoscopy and esophageal manometry. A total of 30 patients who had undergone esophagogastrectomy were identified. Eleven patients had died before their potential inclusion in this study. Twelve patients agreed to participate in this study, but only 10 completed the protocol. In one patient, the esophageal manometry catheter could not be passed across a tortuous thoracoabdominal junction; and in one patient persistent coughing prevented esophageal manometry.

Experimental

Design

Patients and control subjects fasted overnight and avoided consuming medications, coffee, alcohol, or tobacco Abbreviations used in this paper: EEP, end expiratory pressure; HPZ, high pressure zone; PIP, pressure inversion point. 0 1993 by the American Gastroenterological Association 00 16-5085/93/$3.00

November

1993

for 8 hours before the test. Patients and control subjects also completed a questionnaire that reviewed symptoms, medications, and medical history. Detailed information was obtained regarding heartburn, chest pain, dysphagia, odynophagia, regurgitation, nausea, vomiting, coughing, or weight loss. Endoscopy was performed under midazolam (range, 2-7 mg, mean, 5 mg) and meperidine (range, O-100 mg, mean, 50 mg) sedation in each patient to measure the location of the surgical anastomosis in centimeters from the incisors. The thoracoabdominal junction and the gastric remnant or bowel interposition were inspected for the presence of strictures, recurrent tumor, or inflammation. Esophageal manometry was performed at least 1 hour after endoscopy with either a four-lumen polyvinyl perfusion catheter (Wilson-Cook Medical Inc., Winston-Salem, NC) or a modified catheter equipped with a Dent sleeve’ (Arndorfer Medical Specialties, Greendale, WI) using the station pull-through technique. Cetacaine spray was used to anesthetize the oropharynx. Oral intubation was used to place the manometry catheter into the intra-abdominal stomach. Although the original intention was to use the Dent sleeve catheter in all patients and control subjects, it could not be passed across the thoracoabdominal junction in 5 patients. Therefore, in those patients, a standard perfusion catheter was passed over an endoscopically placed guidewire under fluoroscopic guidance. Position of the manometry catheter in the intra-abdominal stomach was confirmed for all patients first by fluoroscopy and then manometrically by a rise in pressure during inspiration. Each manometric port was connected to an external pressure transducer (Gould Inc, Cleveland, OH) and continuously perfused at a rate of 0.6 mL/min, using a low-compliance pneumohydraulic pump (Arndorfer Medical Specialties, Greendale, WI). The transducer outputs were recorded on a multichannel rectilinear recorder (Sensormedics Corporation, Yorba Linda, CA). Swallowing was monitored with an external microphone positioned on the neck over the epiglottis. All subjects were studied in the supine position throughout the procedure. A high pressure zone (HPZ) was identified manometritally and studied. Transition of the perfusion port of the manometry catheter from the abdomen into the thoracic cavity was determined by the pressure inversion point (PIP). When used, the Dent sleeve catheter was positioned in the high pressure zone with standard side hole ports proximal and distal to the Dent sleeve in the intrathoracic and intraabdominal cavities, respectively. Responses to dry swallows and wet swallows of 5 mL water were studied. Breath holding was performed at end-expiration to abolish respiratory motion and minimize diaphragmatic contraction. The response of the high pressure zone to increased intra-abdominal pressure was studied by having patients perform bilateral leg lifts at 45 degrees for 15 second intervals”,” and by abdominal compression using an abdominal binder inflated to 100 mm Hg.“-”

HIGH PRESSURE

ZONE

AFTER

ESOPHAGOGASTRECTOMY

1363

Data Analysis The manometric tracings of patients and controls were read independently by three investigators (WAK, HPP, RSF). The results were averaged to calculate a mean value for each parameter. Evaluation of the HPZ included measurement of its length and distance from the incisors in centimeters. The pressure amplitude of the HP2 and regions proximal and distal to the HPZ were assessed before and during swallows. Pressures were recorded in mm Hg above intra-abdominal gastric pressure. Parameters included midrespiratory pressure, end expiratory pressure, oscillation amplitude, and frequency of phasic oscillation. The percent relaxation was calculated at end expiration, with complete relaxation to intra-abdominal gastric pressure regarded as 100%. Response to breath holding was characterized by calculating the effect on both phasic and tonic pressures. Responses to leg lifts and abdominal compression using an inflatable binder were evaluated by comparing the change in the HPZ pressure to changes in intraesophageal and intraabdominal pressures between the patient and control groups. Results are presented as mean ? SD. Statistical analyses were performed using Student’s t test. A P value of <0.05 was considered statistically significant.

Results Demographics The demographic participating tions

for surgery

group

was comprised

age,

59 years;

junction; tient

29-77).

diverticulum;

esophagus

after

meat

an esophagogastrostomy

lated manually

indications: strictures;

in 1 patient

in 1 patient impaction;

in 4

in 1 pa-

with a large

with a perforated

and in 1 patient

hernia.

Eight

patients

in 5 patients

by several

hiatus

as had

and 2 had interpositions. were performed

The diaphragmatic

cut in 4 patients.

(mean

for benign

of a large hiatal

ent surgeons.

patient

of the esophagogastric

esophagus;

procedures

1. The

and 5 females

for the following

in 2 patients

indica-

Esophagogastrectomy

for adenocarcinoma

epiphrenic

surgical

of the patients previous

in Table

of 5 males

range,

for Barrett’s

treatment

and their

are listed

had been performed patients

characteristics

in this study

The differ-

was simply

di-

and the crura was partially

The operative

note could not be re-

covered in 1 patient. Usually, there was no reattachment of structures to the crura (8 patients). In one patient, part of the stomach was sutured to the diaphragm. Plications were performed at the surgical anastomosis in 7 patients, not at the diaphragm. Three patients with malignancy had received postoperative chemotherapy, and two had received external radiation therapy. Each patient had some postoperative esophageal

1364

KLEIN ET AL.

Table

1.

Demographic

GASTROENTEROLOGY

of the Ten Patients

Characteristics

With Prior Esophagogastrectomy

Sex

Age Cvr)

Age at surgery Cvr)

1

M

66

65

Esophageal adenocarcinoma

2

F

58

57

Esophageal adenocarcinoma

3

F

58

47

Epiphrenic diverticulum

4

M

77

75

Esophageal adenocarcinoma

5

M

29

27

Esophageal perloration

6

F

57

56

Esophageal stricture

7

F

71

37

Hiatal hernia

8

M

46

45

Esophageal stricture

9

F

68

68

Esophageal adenocarcinoma

10

M

63

55

Barrett’s esophagus with severe dysplasia

Patient

Vol. 105, No. 5

Diagnosis

Procedure Esophagogastrectomy Esophagogastrostomy Pyloroplasty Esophagogastrectomy Esophagogastrostomy Esophagogastrectomy Jejunal interposition Esophagogastrectomy Esophagogastrostomy Pyloromyotomy Esophagogastrectomy Esophagogastrostomy Pyloromyotomy Esophagogastrectomy Esophagocecocolojejunostomy Esophagogastrectomy Esophagogastrostomy Esophagogastrectomy Esophagogastrostomy Pyloroplasty Esophagogastrectomy Esophagogastrostomy Pyloroplasty Esophagogastrectomy Esophagogastrostomy PVloromvotomv

symptoms.

Six patients

complained

of dysphagia

solids, and one patient reported odynophagia. patients reported regurgitation,

to

Seven

and four complained

vealed the presence of a definite HP2 in all 10 control subjects and 9 of 10 patients; definite

HPZ. The location

1 patient did not show a of the manometric

HP2

of heartburn. Six patients experienced nausea and vom-

distal to the incisors was similar between the patient

iting. Six patients

group (44.5 -t 6.7 cm) and control group (44.3 f 3.4

reported

weight loss, while 4 pa-

tients had stable weights.

cm; P = 0.948).

Four patients were being treated with omeprazole or an H, antagonist at the time of their evaluation. One

anastomosis

which corresponds

patient was being treated with cisapride.

port of the manometric

The control group included 6 males and 4 females (mean age, 32 years; range, 19-62)

who were asymp-

tomatic and had normal anatomy.

Upper Endoscopy Endoscopy was performed at the time of esophageal manometry in each patient. The surgical anastomosis was identified at 31.5 f 4.7 cm (range, 23-37 cm) from the incisors. Mild to moderate inflammation at the surgical anastomosis was present in six patients. No inflammation was seen in four patients. No strictures or intraluminal tumors were identified.

Esophageal Manometry General observations of the HP2 at the thoracoabdominal junction. Esophageal manometry re-

This HP2 was distal to the surgical

in each patient by 13.3 f 4.7 cm. The PIP, to the point at which the pressure catheter

moved from the ab-

dominal cavity into the thoracic cavity, was located in the proximal

portion of this HP2 in each patient and

was also identified

in the patient

without

a definite

HPZ. The length of the HP2 was similar in the patient group (2.4 f 0.8 cm) and control group (2.9 k 0.6 cm; P = 0.179). The HP2 consisted of a tonic pressure with superimposed phasic pressure in all 10 control subjects and 7 esophagogastrectomy patients (Figures 1 and 2). The remaining 2 patients with an HP2 showed only a phasic component. In those patients undergoing manometry with a conventional perfusion port manometry catheter, the perfusion ports at the same level but displaced by 60 degrees showed radial pressure asymmetry of the HP2 in the patient group. The average midrespiratory pressure was significantly lower in the

November

1993

HIGH PRESSURE ZONE AFTER ESOPHAGOGASTRECTOMY

1365

PRESSURE PERFUSION WRT (mm Ho)

0 I

DISTANCE FROM INCISORS

30 SBC 44

(cm)

43

42

tttt

SWALLOWS

tt

t

t

t

41

t

Figure 1. Manometric demonstration of an HPZ at the thoracoabdominal junction in a patient after esophagogastrectomy using the station pull-through technique with a standard perfusion catheter. Both phasic and tonic pressure components to the HPZ are present. Peak phasic pressure occurred with inspiration. A tonic comoonent was observed at end expiration. Partial relaxation of this HPZ occurred with swallows recorded by the swallow detector.

group

patient

group

(13.7 + 6.9 mm Hg) than in the control

(23.5 + 4.6 mm Hg, P < 0.001)

difference

resulted

from

sure was significantly

(Figure

3). This

the fact that expiratory

lower in the patient

pres-

group (6.0 +

4.5 mm Hg) than

the control

group

0.007).

component

of the HPZ was similar

The phasic

in the patient group

group

(7.7 f

3.5 mm Hg) and control

(7.2 + 1.8 mm Hg; P = 0.710).

received

a partial

(16.3 f 4.4; P =

anastomotic

Patients

plication

who had above

the

thoracoabdominal 7.9 mm

junction

Hg,

mean

(n = 7; mean MRP,

end

expiratory

6.0 z!~4.8 mm Hg) had similar expiratory

pressures

plication EEP,

midrespiratory

at the HPZ

(n = 2; mean MRP, suggesting

of the HPZ

patients

studied

9.3 +- 6.2; EEP, port catheter

the Dent 16.6 f

Characterization if

it

without

a

and P = 0.290, plication and am-

(P > 0.10) in those sleeve

catheter

(MRP,

3.8 + 4.3 mm Hg) and the perfusion

(MRP,

were performed mine

to those

The presence

was similar

with

and end

that an anastomotic

was not the cause of the HPZ. plitude

13.1 f (EEP),

17.4 ?I 3.4 mm Hg, mean

8.8 -+ 0.9 mm Hg) (P = 0.695

respectively),

Hg).

pressure

6.0; EEP,

7.5 + 4.3 mm

of the HPZ. Several maneuvers

to characterize displayed

the HPZ and to deter-

properties

suggestive

of

a

sphincter. Breath holding. Breath of phasic

pressures

and control

within

subjects

tory pressure

without

(Figure

holding

caused

the HPZ a change

inhibition

in both

patients

in end expira-

4).

Swallow Detector 0

t

I

Control Subjects

20 set Figure 2. Relaxation of the HPZ at the thoracoabdominal junction with swallowing in a patient after esophagogastrectomy. The pressure tracing at the HPZ was recorded using a Dent sleeve. Peak phasic pressures occurred with inspiration. Relaxation of the HPZ occurred with swallowing.

Figure 3. Comparison of the HPZ in 10 control subjects and 10 patients after esophagogastrectomy. The patient group has significantly lower midrespiratory (0) and EEP (EI) pressures. The difference in midrespiratory pressure is due to the significant decrease in tonic EEP pressure in the patient group. The phasic component is similar in both groups. Data given as mean + SD. **P < 0.01.

1366

KLEIN ET AL.

GASTROENTEROLOGY Vol. 105, No. 5

abdominal groups

pressure

in both

(maximal

the patient

AHPZ/A

and

control

intra-abdominal

pres-

sure = 1.96 + 0.40 and 1.55 f 0.39, respectively). ratio of this change abdominal

pressure

abdominal

binder

in the HP2 to the change induced

by either

were significantly

between

the patient

P = 0.117,

au =s

absence

10

$2X

Ill=*p

still

0

gsE

Breath holding

of the lower

an

Breath holding

tomy

Figure 4. Response to breath holding of the thoracoabdominal junction HPZ in a patient after esophagogastrectomy. Breath holding resulted in cessation of phasic pressures.

Responsetodeghtition. Deglutition-induced

was present

with a HP2 (Table piratory

decreased the HP2

two esophagogastrectomy was recorded

with

The average

percent

cantly

patients

21.7%)

than (Table

relaxation group

(6.9

each swallow relaxation

f

subjects

2). The

duration

1.5 seconds)

of the

was similar

Partial

patients (92.2%

f

(60.4%

6.0%; P <

the

in the patient control

The average

group percent

studied

with

(65.2%

pa-

the Dent

(48.5% f 15.2%) and the standard

port catheter

+

of swallow-induced

than

perre-

sponses of the HP2 to increased intra-abdominal pressure induced by leg lifts or abdominal compression with an abdominal binder inflated to 100 mm Hg are summarized in Table 3. Both the patient and control groups showed a greater increase in the HP2 pressure than in the increase in intra-abdominal pressure during bilateral leg lifts to 45 degrees (AHPQ’A intraabdominal pressure = 1.87 It_ 0.64 and 1.80 + 0.42, respectively). Figure 5 illustrates the response induced by leg lifts in an esophagogastrectomy patient. Abdominal compression with a binder around the abdomen inflated to 100 mm Hg pressure (Figure 6) also caused a greater mcrease in the HP2 pressure than in intra-

at

the

esophagogastrec-

to distal

the presence

junction

stimulation.’

the

resection

of

The HP2 was comprised

smooth

muscle

pressure

oscillations

pressure.

This HP2 behaves

of a HP2

in patients

sphincter.

after

lower

at the surgical

esophageal

primarily

superimposed

of phasic

on a smaller

tonic

functionally

as a sphincter

relaxed

in response

to swallowing

in response

to increased

intra-abdomi-

nal pressure.’ Prior

manometric

investigations

junction

after

surgical

esophagus

have been

HP2

deglutition-induced

with

antireflux shown

barrier

of the thoracoabreplacement

conflicting.

after colonic

of the

The presence relaxation

at the diaphragmatic replacement

of an

and a weak

hiatus

has been

of the lower esopha-

gus* 12,13Other studies, however, have reported an absence of a HP2 in children and rhesus monkeys after colonic Some hernias

interposition.14T15 manometric have shown

studies

of patients

the presence

with

hiatal

of two separate

pres-

sure areas that have been attributed to the intrinsic LES and crural diaphragm.‘6,‘7 This suggests that both the LES and crural

f 23.4%; P > 0.10).

Response to increased intra-abdominalpressure. The

This study shows thoracoabdominal

dominal

tracing.

in esophagogastrectomy

in patients

1 of

relaxation

in the HP2

shorter

P < 0.002). HP2

Figures record

of the HP2 was signifi-

was also significantly

sleeve catheter fusion

swallows.

patients.

in control

(8.8 t- 0.9 seconds; relaxation tients

with

was

Discussion

and contracted

and endex-

in the

there

mechanism

in the

that responded

that

sphincter

sphincterlike

1 (P

(P = 0.785 and

suggested

esophageal

than

and were similar

groups

This

junction

in that it partially

and patients

and swallowing

less in esophagogastrectomy

0.025)

HP2 re-

subjects

2). Both midrespiratory

pressures

and 2 illustrates

in all control

adaptive

thoracoabdominal

15 set

laxation

and control

respectively).

leg lifts or an

greater

= 0.021 and P = 0.017, respectively)

The

in intra-

the antireflux

Table 2.

diaphragm

barrieq5

may function

a concept

also

to form

supported

by

Response of the HPZ at the Thoracoabdominal Junction to Deglutition

Basal EEP (mm Hg) Nadir of EEP during deglutition (mm Hg) Percent relaxation Duration of relaxation (s)

Control

Patient

group

group

P value

16.4 + 4.2

6.0 + 4.5


1.3 + 0.9 92.2 t- 6.0 8.8 + 0.9

2.7 + 2.1 60.4 -+ 21 .78 6.9 -+ 1.5

NOTE. Results expressed as mean f SD aPercent relaxation in the patient group was calculated patients who had an EEP >O.

0.078 10.00 1 <0.002

with the 7

November

1993

HIGH PRESSURE ZONE AFTER ESOPHAGOGASTRECTONlY

Table 3. Response of the HPZ at the Thoracoabdominal

Junction to Increased Intra-abdominal

1367

Pressure

Control group

Patient group

46.7 f 32.3

32.4 f

25.7 f

18.4 i- 8.5

P Value

Leg lifts a HPZ (mm Hg) a Intra-abdominal

(mm W 3. HPZ/A Intra-abdominal pressure Abdominal compression A HPZ (mm /-fg) A Intra-abdominal

15.9

pressure 14.0

1.80 k 0.42

1.87 k 0.64

13.7 f 4.6

12.8 f 6.3

8.9 + 2.6

6.4 + 2.5

1.55 f 0.39

1.96 -+ 0.40

0.785

pressure

(mm H8) S HPZ/A Intra-abdominal pressure

0.117

NOTE. Results expressed as mean k SD.

measuring in normal anatomy been

diaphragmatic

alteration

at the thoracoabdominal

used to show

crural

electromyographic

subjects4T5 Surgical

diaphragm

junction

the separate and intrinsic

activity

of the normal has also

contributions

of the

LES to the HPZ.‘8-20

intrinsic zone

junction

LES. The phasic corresponds

to

caused by contraction

in the absence

nature

and

and relaxation

the HP2 ment catheter

sleeve permitted

without

of the

potential

esophagus

during

catheter

continuous artifact

relative

respiration,

is probably

of the crural

phragm.3,4~2’ Use of a manometric with a Dent

of an

of this high pressure

respirations

created to the

swallowing,

dia-

equipped

recording

also support during

by move-

with

catheter

the presence

obtained

perfusion

of the catheter movement

from

pa-

port catheter

of an HPZ, but the relaxation

may be, in part, relative

affected

by axial

to the HP2 either by

or esophageal

longitudinal

contrac-

tion.22 Besides

the

other

potential

HP2

in patients The

esophageal

crural

diaphragm,

explanations

there

lower

ligament,

esophageal

no longer

length-tension

present

ence of an HP2

phreno-

esophagus,

as contributors

in normal in our

characteristics

the Law of LaPlace

patients.

of smooth

monkeys

and to the

subjects23-26

but

Changes muscle

have been used to explain

in rhesus

of an

and recon-

sphincter,

intra-abdominal HP2

several

for the presence

Angle of His have been proposed were

were

after esophagogastrectomy

thoracoabdominal or

8*9,22Data

a standard

swallowing

struction. of

manometric leg lifts,

compression.

studied

movement

The data from our study show that an HP2 exists at the thoracoabdominal

abdominal tients

in and

the pres-

after esophagogas-

trectomy15 Smooth

&--J

i,-h--d Leg Lift

and in humans after fundoplication.25 muscle from the gastric fundus can show tonic

LA_ Leg Lift

SWALLOW

DETECTOR H

15 set Figure 5. Response of the thoracoabdominal junction HPZ to increased intra-abdominal pressure by leg lifts in a patient after esophagogastrectomy. Bilateral leg lifts to 45 degrees resulted in a greater increase in pressure at the HPZ than in the intra-abdominal stomach. The initial delay in pressure increase at the HPZ is due to the slow response rate of the Dent sleeve device.

ABDOMINAL BINDER PRESSURE (mmH9)

Figure 6. Effect of abdominal compression on the thoracoabdominal junction in a patient after esophagogastrectomy. Abdominal compression was produced by inflating an abdominal binder gradually to 100 mm Hg. A greater increase in pressure occurred at the HPZ compared with intra-abdominal gastric pressure.

1368

contraction

and relax in response

this would HP2

GASTROENTEROLOGY Vol. 105. No. 5

KLEIN ET AL.

not explain

or its ability

increased

either

the phasic

to contract

intra-abdominal

has been

shown

tients was significantly In addition,

HP2

gogastric

junction

diaphragm patulous

explain

hiatus

during

the pressure

The

of the

creation

Tightening

surgery

recorded

excision

the absence

HPZ in one of our patients. matic

of the esopha-

partial

the hiatus.30

could

HPZ.

in the two patients

Resection

can require

to widen hiatus

in our pa-

to the observed

of a

of a definite the diaphrag-

could potentially

augment

at the thoracoabdominal

or gastroesophageal

seen by endoscopy

reflux,3’,32 but

it was not

in our patients.

The tonic component of the HPZ in normal subjects has been attributed to the smooth muscle LES4 Seven esophagogastrectomy

patients

pressure,

i.e., a high

possible

that the tonic stricture

seen during

endoscopy.

pressure

with

been

under

subjects. A decrease

pressure of the HPZ tion.‘0,34 Psychological an increase

myographic

with

has

in human EMG activ-

during

by leg raising

rapid eye Sustained

and abdomi-

to augment

the tonic

at the gastroesophageal juncstress has also been reported to

in tonic

activity

respira-

diaphragm

anesthesia.33

has been shown

suggested is a phasic

circumstances

has been shown

contraction

nal compression

ation.

coinciding of the crural

sleep or halothane

diaphragmatic

cause

to the HPZ

certain

It is

this was not

have

in tonic diaphragmatic

ity at end expiration movement

studies

component contraction

reported

however,

Prior

contraction

a tonic

may have been due to

formation;

the diaphragmatic

showed

at end expiration.

pressure

postsurgical

tion.3 Tonic

also

pressure

and

crural

diaphragm

impairment

Use of a manometric

catheter

electro-

of LES

relax-

equipped

with

electromyographic electrodes may have permitted better characterization of crural diaphragmatic activity to the phasic and tonic components in the patient and control

bition

of the crural

In conclusion, at the

properties.

HPZ

tireflux Further crural

of the LES. These

investigation

pathogenesis and esophageal

subjects,

the crural

barrier

in addition

diaphragmatic

observations

is needed

diaphragm

to provide

to study

dysfunction

may reflux,

for

sphincterlike

to the intrinsic

of gastroesophageal motility

in patients

may be responsible

and may itself display

as an extrinsic

mechanism

a sphincterlike

junction

diaphragm

In normal

may function

inhi-

diaphragrn3’

removal

the crural

this residual

by marked

this study documents

thoracoabdominal

after surgical suggest

are accompanied

an anLES.4,5

the role that play

in

the

dysphagia,

disorders.

HPZ.

Postoperative stricture formation can occur because of recurrent tumor, scarring, anastomotic stapling devices,

sient LES relaxations

HPZ

pressure.28T29 How-

an HPZ was identified

who did not have a plication.

to

Fundoplication

anastomosis

proximal

of the

in response

pressure.

of the surgical

but

nature

further

to increase

ever, plication

to deglutition,”

groups.

Partial relaxation of the HPZ occurred with swallows in our esophagogastrectomy patient group. Electrical and mechanical inhibition of the crural diaphragm during swallows and balloon distention has been shown in anesthetized animal models.36 In awake humans with normal anatomy, swallow-induced LES relaxation is associated with minimal inhibition of the crural diaphragmatic electrical activity, while tran-

References 1. Richter JE, Caste11 DO. Gastroesophageal

reflux. Pathogenesis, diagnosis, and therapy. Ann Intern Med 1982;97:93103. 2. Boyle JT, Cohen S. Does intrinsic LES tone increase as an adaptive response to increased intraabdominal pressure? Dig Dis Sci 1984;29:760-76 1. 3. Boyle JT, Altschuler SM, Nixon TE, Tuchman DN, Pack Al, Cohen S. Role of the diaphragm in the genesis of lower esophageal sphincter pressure in the cat. Gastroenterology 1985;88:723730. 4. Mittal RK, Rochester DF, McCallum RW. Electrical and mechanical activity in the human lower esophageal sphincter during diaphragmatic contraction. J Clin Invest 1988;81: 1182- 1 189. 5. Mittal RK, Rochester DF, McCallum RW. Sphincteric action of the diaphragm during a relaxed lower esophageal sphincter in humans. Am J Physiol 1989;256:G 139-G 144. 6. Cohen S, Harris LD. Does hiatus hernia affect competence of the gastroesophageal sphincter? N Engl J Med 1971;284: 10531056. 7. Public Health Service-Health Care Financing Administration: The International Classification of Diseases 9th Revision Clinical Modification. 2nd ed. Washington D.C.: US Department of Health and Human Services, 1980. DHHS Publication Number (PHS) 801260. 8. Dent J. A new technique for continuous sphincter pressure measurement. Gastroenterology 1976;7 1:263-267. 9. Dodds WJ, Hogan WJ, Miller WN, Stef JJ, Arndorfer RC, Lydon SB. Effect of increased intraabdominal pressure on lower esophageal sphincter pressure. Dig Dis 1975;20:298-308. 10. Mittal RK, Fisher M, McCallum RW, Rochester DF, Dent J, Sluss J. Human lower esophageal sphincter pressure response to increased intra-abdominal pressure. Am J Physiol 1990;258: G624-G630. 11. Janisch HD, Weihrauch TR, Hampel KE. Is abdominal compression a useful stimulation test for analysis of lower esophageal sphincter function? Dig Dis Sci 1984;29:689-695. 12. Clark J, Moraldi A, Moossa AR, Hall AW, DeMeester TR, Skinner DB. Functional evaluation of the interposed colon as an esophageal substitute. Ann Surg 1976; 183:93- 100. 13. Moossa AR, Hall W, Wood RAB, Cooley GR, Skinner DB. Effect of pentagastrin infusion on gastroesophageal manometry and reflux status before and after esophagogastrectomy. Am J Sung 1977: 133:23-28. 14. Jones EL, Booth DJ, Cameron JL, Zuidema GD, Skinner DB. Functional evaluation of esophageal reconstructions. Ann Thorac Surg 197 1: 12:33 l-346. 15. Sieber AM, Sieber WK. Colon transplants as esophageal replace-

November

16.

17. 18.

19.

20.

1993

ment: cineradiographic and manometric evaluation in children. Ann Surg 1968; 168: 116- 122. Code CF, Kelley ML, Schlegel JF, Olsen AM. Detection of hiatal hernia during esophageal motility tests. Gastroenterology 1962;43:52 I-531. Habibulla KS. The diaphragm as an anti-reflux barrier. Thorax 1972;27:692-702. Mann CV, Ellis FH, Schlegel JF, Code CF. Abdominal displacement of the canine gastroesophageal sphincter. Surg Gynecol Obstet 1964;118:1009-1018. Lind JF, Cotton DJ, Blanchard R, Crispin JS, Dimopolos GE. Effect of thoracic displacement and vagotomy on the canine gastroesophageal junction. Gastroenterology 1969;56: 1078- 1085. Radmark T, Pettersson GB. The contribution of the diaphragm and an intrinsic sphincter to the gastroesophageal antireflux barrier. An experimental study in the dog. Stand J Gastroenterol

1989;24:85-94. 21. Welch RW, Gray JE. Influence of respiration on recordings of lower esophageal sphincter pressure in humans. Gastroenterology 1982;83:590-594. 22. Dodds WJ, Stewart ET, Hogan WJ, Stef JJ, Arndorfer RC. Effect of esophageal movement on intraluminal esophageal pressure recording. Gastroenterology 1974;67:592-600. 23. Bombeck CT, Dillard DH, Nyhus LM. Muscular anatomy of the gastroesophageal junction and role of phrenoesophageal ligament. Ann Surg 1966; 164:643-654. 24. DeMeester TR, Wernly JA, Bryant GH, Little AG, Skinner DB. Clinical and in vitro analysis of determinants of gastroesophageal competence. A study of the principles of antireflux surgery. Am J Surg 1979; 137:39-46. 25. O’Sullivan GC, DeMeester TR, Joelsson BE, Smith RB, Blough RR, Johnson LF, Skinner DB. Interaction of lower esophageal sphincter pressure and length of sphincter in the abdomen as determinants of gastroesophageal competence. Am J Surg 1982; 143:40-47. 26. Skinner, DB. Pathophysiology of gastroesophageal reflux. Ann Surg 1985;202:546-556. 27. Lind JF, Duthie HL, Schlegel JF, Code CF. Motility of the gastric fundus. Am J Physiol 196 1;20 1: 197-202.

HIGH PRESSURE ZONE AFTER ESOPHAGOGASTRECTOMY

1369

28.

Lipshutz WH, Eckert RJ, Gaskins RD, Blanton DE, Lukash WM. Normal lower-esophageal-sphincter function after surgical treatment of gastroesophageal reflux. N Engl J Med 1974;29 1: 1107-

29.

Ellis FH, El-Kurd MFA, Gibb SP. The effect of fundoplication on the lower esophageal sphincter. Surg Gynecol Obstet 1976; 143:1-5. Ellis FH, Gibb SP, Watkins E. Jr. Limited esophagogastrectomy for carcinoma of the cardia. Indications, technique, and results. Ann Surg 1988;208:354-36 1. Bender EM, Walbaum PR. Esophagogastrectomy for benign esophageal stricture. Fate of the esophagogastric anastomosis. Ann Surg 1987;205:385-388. Muehrcke DD, Donnelly RJ. Complications after esophagogastrectomy using stapling instruments. Ann Thorac Surg 1989;48: 257-262. Muller N, Volgyesi G, Becker L, Bryan MH, Bryan AC. Diaphragmatic muscle tone. J Appl Physiol 1979;47:279-284. Mittal RK, Rochester DF, McCallum RW. Effect of the diaphragmatic contraction on lower oesophageal sphincter pressure in man. Gut 1987;28: 1564- 1568. Mittal RK, Stewart WR, Ramahi M, Chen J, Farace E. Psychological stress increases tonic and phasic activity of the crural diaphragm and impairs relaxation of the lower esophageal sphincter. Gastroenterology 1992; 102:A487. Altschuler SM, Boyle JT, Nixon TE, Pack Al, Cohen S. Simultaneous reflex inhibition of lower esophageal sphincter and crural diaphragm in cats. Am J Physiol 1985;249:G586-G59 1. Mittal RK, Fisher MJ. Electrical and mechanical inhibition of the crural diaphragm during transient relaxation of the lower esophageal sphincter. Gastroenterology 1990;99: 1265- 1268.

1110.

30.

31.

32.

33. 34.

35.

36.

37.

Received August 10, 1992. Accepted March 29, 1993. Address requests for reprints to: Henry P. Parkman, M.D., Gastroenterology Section, Department of Medicine, Parkinson Pavilion, 8th Floor, Temple University School of Medicine, 3401 North Broad Street, Philadelphia, Pennsylvania 19140.