Peritoneal ammonia levels in acute intra-abdominal disease

Peritoneal Ammonia

Levels in Acute

Intra-Abdominal

Disease*

A Reappraisal ARLIE

R. MANSBERGER,

JR., M.D.,

Fromthe Department of Surgery, University of Maryland Srhool of Medicine, Baltimore,Maryland. Supported by a grant in aid front the NationalInstitute of Health, U.S.P.H.S. (ROI-A M-0527504-GM).

M

testinal tract. These same authors showed that intraluminal pressures of from 260 to 280 mm. Hg for the small intestine and 350 mm. Hg for the colon were required to cause leakage through perforations made by a 20 gauge needle. On the other hand, Wangensteen [4] states that the highest intraluminal pressures which develop in obstructed segments of the human intestine are from 200 to 300 mm. Hz0 for the small bowel and from 300 to 500 mm. He0 for the large intestine. The value of abdominal paracentesis as an aid in the diagnosis of primary peritonitis, strangulation of bowel, acute pancreatitis, and intra-abdominal hemorrhage has been well documented. Emphasis has rightfully been placed not only on the appearance and odor of peritoneal fluid but also on a complete examination of the fluid to include pH determinations, amylase levels, red blood cell counts, white blood cell counts, differential counts, analysis for malignant cells, protein determinations, and examination for the presence or absence of bacteria. In recent years we have taken advantage of the unique role of ammonia metabolism in the gastrcintestinal and genitourinary tracts and have conducted clinical experiments relative to the level of peritoneal fluid ammonia in a variety of disease states [S-IO]. The purpose of this paper is to present our total experience to date regarding the usefulness and limitations of this test as an adjunctive diagnostic measure in acute intra-abdominal disease.

AND MORBIDITY in the management of patients with acute intra-abdominal disease depend in no small measure upon the accuracy of early diagnosis. Even though it is acknowledged by most surgeons that the gross characteristics of peritoneal fluid observed at the time of abdominal operation not infrequently suggest the nature of an acute intra-abdominal pathologic entity, far too few of us take advantage of this fact when trying to decide whether or not a laparotomy is indicated. Reticence to utilize abdominal tap as a diagnostic tool may stem from an understandable but unwarranted fear of inserting hypodermic needles of various sizes and gauges into the peritoneal cavity for fear of penetration of and subsequent leakage from segments of the small or large intestine. The safety of diagnostic abdominal tap has been emphasized by many authors [I-3]. Rloretz and Erickson [I?] have penetrated the abdominal wall of experimental animals with large numbers of needles of varying size and g-auges and have shown a low incidence of “intestinal penetration.” They also have observed no peritonitis, ascites, or other peritoneal complications in these or other animals at the time of subsequent exploration after purposeful bowel puncture was carried out in as many as 250 different points along gastroinORTALITY

* Presented

Baltimore, Muryhnd

at the Seventh Annual Meeting of the Society for Surgery of the Alimentary Chicago, Illinois, June 25 and 26, 1966.

Vol. 113, January 1967

37

Tract,

Mansberger

38

TABLE PERITONEAL

FLUID

AMMONIA

Type of Lesion

LEVELS

IN

X0. of Patients

Strangulation, obstruction and/or perforated large or small bowel Perforated ulcer Perforated appendix with generalized peritonitis Simple mechanical bowel obstruction Pancreatitis Intraperitoneal bleeding Urinary extravasation (suspected) Ascites (including cardiac failure, carcinomatosis, and cirrhosis) Tuberculous peritonitis Biliary peritonitis

I

PATIENTS

\VITH

INTRA-ABDOMINAL

Ammonia Levels in Peritoneal Fluid (r/ml.)

43 18

1.19-lli 0.89-33.Ai

8 26 21 10 7

1.57-52.5 0 40-2.60 0.33-2.60 0.58-2.20 1.94-22.88

23 3 1

0.09-10.74 1.20-2.12 2.28

DISEASE

No. of Patients with Levels below 3 -,/cc.

So. of Patients with Levels above 3 r/cc.

39

4*

13

5t 2* 26* 21* 10 2* 20* 3 1

3 0 0

* See text for more detailed discussion. t See Table III for explanation. MATERIAL

AND

METHODS

Fluid-yielding diagnostic paracentesis has been carried out in 190 instances on 160 patients since the initiation of this study. The volume of fluid obtained varied between 1 ml. and a quantity more than adequate to carry out any and all necessary diagnostic procedures. When paracentesis yielded sufficient fluid for only one determination, ammonia levels were determined as a preference. When possible (as was true in the majority of instances) all determinations were carried out in duplicate. Twenty-three of the patients in this series who had abdominal paracentesis (thirty-seven taps) did not have acute disease and were studied to gain some insight into the ammonia metabolism of patients with pathologic entities resulting in chronic ascitic fluid accumulations. TABLE AMMONIA

LEVELS* HUNDRED

Ammonia

IN

TABLE LEVELS TONEAL

GASTRIC

THIRTY-FIVE

90

JUICE

ONE

Patient

PATIENTS

No. of Patients 17 21 22 11 14 9 7 6 4 24

to 297 y ml.

IN

OF

AMMONIA

FLUID

IN

IN TEN

III

GASTRIC

Gastric Ammonia

Peritoneal Ammonia

(pg./ml.)

(pg./ml.)

149.2

3.38

R. F.

269.1

1.88

J. M.

48.0

3.06

P. F.

41.8

4.61

48.0 156.0 8.2 122.4 9.9 68.0

8.26 31.01 1.62

H. B. R. G. L. W.

WITH

AND

IN

PERI-

PERFORATED

ULCER

M. C.

A. B. L. H. B. H.

JUICE

PATIENTS

DUODENAL

II

FASTING

level r/ml.

* Range 1.8 r/ml.

Of the patients with acute intra-abdominal disease three were subjected to two diagnostic taps, two had three taps, and needle paracentesis was performed on one patient with pancreatitis on four separate occasions. Where there was any question regarding intraenteric penetration of the needle tip, a small quantity of water soluble radiopaque material was introduced through the probing needle and portable roentgenograms obtained. This was necessary in five instances. Ammonia determinations on blood and peritoneal fluid were carried out using a modification of the method of Seligson and Seligson [II]. Amylase

32.6i

0.89 10.57

Remarks

Ulcer sealed at operation Ulcer sealed at operation Early sealing at operation Partial sealing at operation Free perforation Free perforation Free perforation Free perforation Free perforation Free perforation

Peritoneal levels

weri

determined by

Ammonia

Levels in Intra-Abdominal

Disease

39

routine lahoratorv

methods. RESULTS

The clinical results of this study are shown in Tables I, II, and III and are graphically illustrated in Figures 1 and 2. Certain categories of disease require further elaboration. Strungulated and/or Perforated Bowel. It is of interest that of the forty-eight patients in this category all except four had peritoneal fluid ammonia levels above 3 pg./ml. These four patients deserve further comment. One, a seventy-two year old man from a mental institution, had signs and symptoms of peritonitis with a massive amount of free air under the diaphragm. The preoperative level of peritoneal fluid ammonia was 1.19 pg./ml. At operation three hours later the fluid ammonia level had risen to 3.1 wg./ml. There was some exudate in the right lateral gutter, but the free perforation could not be located. Apparently a small “pin point” type perforation had occurred which had sealed spontaneously. Whether or not the perforation was due to a small swallowed foreign body could not be proved. There was evidence of neither obstructive neoplasm nor of diverticulitis. Cecostomy and drainage d the right lateral gutter resuhed in recovery. ;\ light growth of Escherichia coli and alpha streptococcus was recovered in culture of the peritoneal fluid. The second and third cases were similar. Both patients were female and had loops of gangrenous ileum in the pelvis, partially walled off by omentum. Peritoneal fluid obtained preoperatively from the right lateral gutter revealed an ammonia level of only 2.4 and 2.9 pg./ml. Fluid obtained from the pelvis adjacent to the gangrenous loop at operation revealed ammonia levels of 48 pg./ml. and lS.6 gg./ml., respectively. Had the peritoneal fluid been obtained by cul de sac puncture, fluid with significant levels of ammonia would undoubtedly have been aspirated. The fourth patient had mesenteric thrombosis with gangrenous changes in the small intestine extending from the ligament of Trietz to the ileocecal valve. In this patient the aspirated peritoneal fluid had an ammonia level of only 1.9 pg./ml. This ammonia level was verified when determined on an aliquot of fluid obtained at operation. The probable explanation of this false-negative findin,g with respect to a lack of I.01. 113, January

1967

FIG. 1. Each bar representsthe peritoneal fluid ammonia level of a single patient with acute intra-abdominal disease. ml.

I’alues for ammonia are given in pg. per

significant increase in peritoneal fluid ammonia probably lies in the recently presented work of Winitz, Adams, Seedman, and Graff [12,1.3]. These investigators reported substantial decreases in stool quantity and types and quantities of intestinal microorganisms within a week of change from a diet consisting of standard institutional food to one containing only a simple sugar, a minimal amount of fat in the form of ethyl linoleate, all the pertinent salts, ten essential amino acids, eight nonessential amino acids, and a vitamin supplement. For example, in stool samples of one of the human volunteers, only three of the original ten types of microorganisms could be found. Esch. coli were reduced from 5,000,000 to 4,000 per gm. of wet feces and,ythe Bacteroides

FIG. 2. Each bar represents the peritoneal fluid amylase level of a single patient with acute intra-abdominal discase. Values for amylase are expressed in Somogyi units.

40

Mansberger

count was reduced from 200,000 to 8,000 per gm. of wet feces. Since the severe myocardial disease for which this last patient was admitted precluded the oral intake of anything but water and some minimal amounts of fruit juice for the five day period prior to the onset of an episode of mesenteric thrombosis, it is likely that the decreased amount of intralumenal protein and a reduction in quantitative and qualitative fecal flora were responsible for the low levels of ammonia in the peritoneal fluid. Unfortunately ammonia levels of intralumenal content were not obtained for this patient. The results mentioned in these patients are in contrast to our findings in patients with simple mechanical obstruction. (Table I.) Of twenty-six patients in this category none had peritoneal fluid with ammonia levels above 3 pg./ml. Perforated Ulcer. Of the eighteen patients with proved perforation of duodenal ulcer, thirteen had ammonia levels above 3 pg./ml. The finding of low ammonia levels in two of the first eight patients with this diagnostic entity stimulated us to study the ammonia levels in a series of hospitalized patients without gastroenteric disease or uremia. The findings presented in Table II indicate a wide range of fasting gastric ammonia levels in these patients. In addition the last ten consecutive patients with perforated duodenal ulcers have had simultaneous measurements of gastric ammonia levels and peritoneal fluid ammonia levels. (Table III.) Our current studies indicate that the level of ammonia in bile and pancreatic juice is relatively low when compared to average gastric levels. It would seem reasonable therefore that peritoneal fluid ammonia levels in patients with perforated ulcers would not be significantly elevated when the following obtain : (1) when the ulcer has sealed and chemical irritation of the peritoneum has resulted in sufficient dilution to lower ammonia values, (2) when edema has resulted in pyloric obstruction and gastric contents do not traverse the pylorus and duodenal perforation; (3) when the gastric level of ammonia is low at the time of perforation. Pancreatitis. It would seem significant that none of the twenty-one patients with pancreatitis had a peritoneal fluid ammonia level above 3 pg./ml. One of our patients had a pseudocyst of the pancreas which was drained

externally through a polyethylene tube inserted into the pancreatic duct via a transduodenal approach. Levels of ammonia were obtained twice daily on the cyst drainage for a ten-day period and the highest ammonia level noted was 2.2 pg./ml. Urinary Extravasation. The small but interesting group of patients with suspected urinary extravasation has been reported in detail in another communication [9]. In this series of patients ammonia levels in fluid from the peritoneal cavity or retroperitoneal space helped identify urinary extravasation in a patient with spontaneous rupture of the bladder, in another with a surgically injured ureter, and in a third with recurrent ileus due to a partially disrupted ileal ureteral anastomosis. Operation on a fourth patient with known metastatic transitional cell carcinoma who had had a right ureteral ligation was avoided because the ammonia content of the aspirated fluid was low, indicating that the fluid was not urine. A fifth patient, transferred from another hospital subsequent to an iatrogenic bladder perforation, was operated upon and spontaneous sealing of the perforation had occurred. The fluid ammonia level was 1.4 lg./ml. Because the peritoneal fluid was clear, it is assumed that the abscess cavity adjacent to the sealed perforation had not been aspirated. Experience with this last patient as well as our experience in patients with perforated appendixes (Table I) and perforated ulcers suggests that ammonia disappears rapidly from the peritoneal fluid once sealing or abscess formation has occurred and that significant levels of ammonia will be found only if the abscess cavity is aspirated. Chronic Ascites. Of this group which includes patients with cardiac failure, carcinomatosis, and cirrhosis, elevated peritoneal fluid ammonia levels were found only in the patients with cirrhosis and hepatic failure. The extremely high level found in one patient from this group (Table I) was obtained via a tap performed immediately after death from hepatic failure. COMMENTS

That peripheral serum and peritoneal fluid amylase levels must be interpreted with caution is an established fact. Amerson, Howard, and Vowles [14], for example, in reporting serum and peritoneal fluid amylase concentrations in American

Journal

ofSurgery

Peritoneal

Ammonia

Levels in Intra-Abdominal

with acute gastroduodenal perforations, found elevations in twenty of twenty-six llatients. In seventeen of their patients the conrentrstion was above 200 Somogyi units and in three patients it wa< higher than 1,500 units. They concluded that the analysis of peritoneal fluid for amylase content is not a reliable means of differentiating between acute pancreatitis and acute perforation of gastric or duodenal ulcer. Gray and hXIChJr [IS] reported a case of acute mesenteric venous occlusion simulating acute pancreatitis in which peritoneal fluid amylase levels gradually elevated from 0 to 1,690 units. These authors cite Karlan and Zollinger as having observed elevated peritoneal fluid amylase levels from 800 to 2,000 units in four of six patients with venous mesenter ic thrombosis. They also quote Ellison to the effect that any amylase level above 1,000 units is strongly suggestive of the presence of necrotic intestine rather than of pancreatitis. They suggest further that a gram stain of the peritoneal fluid is probably the best method of differentiating pancreatitis from infarction of the gastrointestinal tract. Ammonia in the animal body is derived from many sources. Oxidative and hydrolytic enzymes in liver, kidney, muscle, brain, heart, and blood enter into reactions capable of liberating free ammonia. There is little doubt, however, that the bulk of ammonia formation in the body occurs in the gastrointestinal tract by putrefactive processes involving the fecal flora, and by the action of intestinal urease, which is bacterial in origin [16]. Damodaran and Narayanan [17] in 1X38 demonstrated that the liberation of ammonia by proteolytic activity was too small to account for the relatively vast amounts of ammonia entering the portal system It is also well known that the levels of ammonia in venous tributaries to the portal vein are highest in the cecal region and decrease as the duodenum is approached. The experimental work of Terroine and Lauresco [18] suggests that the longer dietary protein is retained in the gastrointestinal tract (under the influence of the normal intestinal flora). the greater is the conversion of aminonitrogen into ammonia. Blood entering the liver via the portal vein is cleared of most of its ammonia content by urea synthesis in a single passage of portal blood through the liver. An acute block to the venous drainage in

patients

Disease

11

one of the portal radicals results in venous strankwlation of the small bowel and the accumulation of hemorrhagic fluid within the peritoneal cavity. Hyaluronidase is present in significant quantities in strangulated obstructed loops of intestine and is of importance in increasing the permeability of the bowel wall [19]. Nemir and associates [20,21] have called attention to certain chemical and spectrophotometric changes in the intraluminal content of strangulated bowel. These same chemical and spectrophotometric changes were later demonstrated in the peritoneal fluid, indicating that certain intraluminal material could diffuse through the wall of the strangulated obstructed small bowel. The very origin of the fluid would suggest that its ammonia content should be elevated. It is also true that the ammonia content of peritoneal fluid should be elevated in any condition resulting in the transudation or spillage of intraluminal intestinal content into the peritoneal cavity. Thus the peritoneal fluid resulting from arterial strangulations or from perforations, traumatic puncture, or laceration of large or small intestine should result in elevated peritoneal fluid ammonia levels. Bidder and Schmidt first recognized anlmonia in the stomach contents [22]. Luck and Seth demonstrated that the ammonia content of the stomach was formed from urea by the action of urease present in the gastric wall and they suggested its possible significance as a protective mechanism against hyperacidity 123, 241. It is well known that the uremic patient usually has a low gastric acidity. The ammonia content of gastric juice is a result of urease activity on the specific substrate urea, the end products being ammonia and carbon dioxide. It becomes evident, therefore, that perforation of a gastric or duodenal ulcer may result in an elevation of peritoneal fluid ammonia content. The renal release of ammonia into the systemic circulation was first demonstrated by Nash and Benedict in 1921. Current evidence indicates that changes in urinary pH are important determinants of urinary ammonia excretion, lesser amounts appearing in alkaline than in acid urines [25]. Unless there is a rapid hydrogen ion secretion into the tubule, the resulting lower tubular pH increases the quantity of ammonia entering the urine. The

42

Mansberger TABLE

IV

RENALENZYMESYSTEMSCAPABLEOF

Enzyme

Glutamine Asparagine Most d-amino acids

L-amino

Most l-amino acids

Glycine oxidase Glutamic acid dehydrogenase Transaminase

Proline oxidase

Products

Substrate

Glutaminase Asparaginase D-amino acid oxidase acid oxidase

AMMONIAPRODUCTION*t

Glycine L-glutamic acid (1) I-aspartic acid plus ketoglutaric acid; (2) I-alanine plus ketoglutaric acid Proline

* Neither the transaminases nor the proline oxidase directly dehydrogenase, a net production of ammonia occurs. t From Madison, L. L. and Seldin, D. W. [.%I.

effect occurs when the urine becomes progressively inore alkaline. The epithelial cells of the last two thirds of the distal tubules are capable of synthesizing ammonia from glutamine or from amino acids. The bulk of ammonia formation in the kidney, however, results from the action of glutaminase or glutamine. Madison and Seldin [X] have identified the various enzymes which produce ammonia from amino acid in the human kidney. (Table IV.) Again it is evident that extravasation of urine into the peritoneum or into the retroperitoneal space should result in peritoneal or retroperitoneal fluid and a high ammonia content. In contrast to the foregoing situation, the fluid accumulating in the peritoneal cavity as a result of pancreatitis has a low ammonia content. This may well be due to the fact that pancreatitis is a sterile disease in most instances and therefore the substrates and enzymes necessary to produce ammonia in significant quantities are absent. The lack of peritoneal fluid ammonia elevations in several of the patients with lesions that require an early operative procedure only seems to emphasize that this laboratory test, or any current laboratory procedure, cannot be relied upon as a substitute for careful, judicious clinical observation. However, because ammonia levels are usually elevated in a group of acute intra-abdominal conditions which require operation and not in acute pancreatitis (which is usually managed without operation), the opposite

Glutamic acid and ammonia Aspartic acid and ammonia Corresponding alpha keto acid plus ammonia Corresponding alpha keto acid plus ammonia Glyoxylic acid plus ammonia Ketoglutaric acid Alpha ketoglutaric acid plus ammonia (1) oxaloacetic acid plus glutamic acid; (2) pyruvic acid plus glutamic acid L-glutamic acid

produce

ammonia,

but if coupled

with glutamic

determination of ammonia in peritoneal fluid would seem to be a useful adjunct to our diagnostic methods when dealing with patients presenting with signs and symptoms of acute intra-abdominal disease. SUMMARY

AND CONCLUSIONS

1. In patients with acute abdominal disease elevations of ammonia levels above 3.0 pg./ml. in peritoneal fluid suggest the presence of strangulated, perforated, or lacerated small or large intestine, perforated gastric or duodenal ulcer, or urinary extravasation. 2. Peritoneal fluid ammonia levels were not elevated above 3.0 pg./ml. in any patients with pancreatitis evaluated in this study. 3. Amylase content of peritoneal fluid is of limited value in the differential diagnosis of acute intra-abdominal disease. In this study significant elevations were found in patients with pancreatitis, perforated duodenal ulcer, and strangulated small bowel with and without perforation. 4. The mechanisms by which ammonia appears in significant quantities in peritoneal fluid are discussed. 5. The mechanisms responsible for the falsenegatives observed in patients with perforated duodenal ulcers and in a few patients with gangrenous bowel are defined. REFERENCES 1. CHAPMAN, N. D., NYHUS, L. M., and HARKINS, H. N. Abdominalparacentesisasadiagnosticaid.

J.A.M.A.,

170: 1625, 1959. American Journal of Surgery

Peritoneal Ammonia Levels in Intra-Abdominal 3. MI JRETZ, W. H. and ERICKSON, W. G. Peritoneal I ap as an aid in tile diagnosis of acute abdominal clisease. _1~1. Szlrxfon, 20: 363, 1954. :$ MORETZ. W. H. and ERICKSON,W. G. The diagnostic peritoneal tap. .-lm. Surgeon, 22: 1095, 1956. 1. WANGESSTEEN. 0. H. Intestinal Obstruction, p. 37. Springfield, Illinois, 1955. Charles C Thomas. 5, KOPILSICK, M. and MANSBERGER, A. R., JR. .\mmonia determinations on peritoneal fluid value in differential diagnosis of acute abdominal disease. 1~~~clr_~land ilf.J., 12: 154, 1963. 6. MANSBERGER. A. R., JR.. CO~LEY, R. A., BESSMAN, S. P.. and BUXTON, R. W. The origin and utilization of ammonia in strangulation obstruction of the small bowel. .*lnn. Surg., 150: 880, 1959. 7. MANSBERGER, A. R., JR. and LANKFORD, P. The value of ammonia determinations on peritoneal fluid in the differential diagnosis of pathologic states resulting in hemorrhagic ascites. llrn. Surgeon, 26: 695. 1960. X. MANSBERGER. A. R., JR. The value of peritoneal fluid ammonia levels in the differential diagnosis of the acute abdomen. iInn. Surg., 155: 998, 1962. 9. MANSBERGER, A. R., JR. and YOUNG, J. D., JR. The value of alnmonia levels as an aid in the diagnosis of urinary extravasation. J. Ural., 94: 125, 1965. 10. TOLJNTAS, C. I’., TRAVASANO, F. J., JULES, A. J., WEATHERLY, L). W., and MANSBERGER, A. R.. JR. The value of anomia determinations in acute intra-abdominal disease. Maryland h{. J., 12: 147, 1963. 11. SELIGSOS. D. and SELIGSON, H. A microdiffusion method for the determination of nitrogen liberated as ammonia. J. Lab. Er’ C&n. Med., 38: 324, 1951. 12. WINITZ, M., ADAMS, R. F., SEEDMAN, D. A., and GRAFF, J. Regulation of intestinal flora with chemical diets. Fed. Proc. (abstr.), 25: 343, 1966. 13. WINITZ, M. Personal communication. 14. EMERSON, J. R., HOWARD, J. M. and VOWLES, K. D. J. The amylase concentration in serum and peritoneal fluid following perforation of gastroduodenal ulcers. Ann. Sury., 147: 245, 1958. 15. GRAY, E. B., JR. and AMADOR, E. Acute mesenteric venous thrombosis simulating acute pancreatitis. The value of peritoneal fluid analysis. J.A.hf.:l.

167: 1734, 1958. 16. BESSMAN, S. P. Ammonia metabolism in animals. In: Inorganic Nitrogen Metabolism, p. 408. Edited by McElgry and Glass. Baltimore, 1956. The Johns Hopkins Press. 17. DAMODARAS, M. and ~YARAYANAN,E. K. Enzyme proteolysis. III. Asparagine peptides and anhydroglycyl-asparagine. Bioc-hem. J., 32: 2105, 1938.

Vol. Il.?. January

1967

Disease

19. ASI)ERSON. R. IS. and TANTZTRI.C. S. ltlcntitication of the toxin of clostridial organisms in c.xpcrimental intestinal obstruction. 1r( lr. .y~r,<. MI: 1x3. 1950. 20. SEMIR. P., JR., HA~VTHORNE,H. R., COHN. I.. JR.. and DRABKIN, D. L. Tile cause of death ill strangulation obstruction; an experimental study. I. Clinical course, chemical, hactcriologic and spectrophotometric studies. . I nn. .‘iur~_, 130: X57, 1949. 21. SEMIR. I’.. HA~~THORNE, H. R., and DIUHKIN. D. L. Further studies concerning the abnormal human pigment found in strangulation obstrurtion. S. Forum, 19.52. 22. CONWAY. E. J. The Biochemistry of Gastric Acid Secretion, p. 149. Springfield, Illinois. 195X. Charles C Thomas. 23. L~JCK, J. M. and SETH, T. N. Gastric urc’asc. Hio(-hem J., 18: 1227, lY24. 24. LUCK, J. M. and SETH, T. N. The physiology of gastric urease. Biochem. J., 19: 357, 1925. 25. OWEKS, E. E., TYOR, M. P., FLANAGAS, J, F.. and BERRY, J. ?j. The kidney as a source of blood ammonia in patients with liver disease: the effect of acctazolamide. J. C/in. Ino?.st. 39: 28X, 1960. 26. MADISON, L. L. and SELDIN, D. W. Ammonia escretion and renal enzymatic adaptation in human subjects as disclosed by administration of precursor amino acids. .I. Clin. Inw.sf., 7: 1613, 1958. DISCUSSION ARLIE

R.

MANSBERGER,

We have had five patients sidered ever,

to have the

shown

elevated

intraluminal

penetration

bility.

aspiration The

radiopaque luminal

Hypaque@

cognizant

Howdue

of the

of 10 cc. of a water

followed

will answer

was injected in whom

was suspected;

throughout contrast

were

to

soluble

by a portable the question

perpossi-

flat film of intra-

penetration.

of a patient tration

results.

values

as long as the physician

introduction

of the abdomen

Md.):

at the time of paracentesis.

remains

material,

(Baltimore,

false-positive

ammonia

This creates no problem forming

JR.

whose tests might be con-

the

diffusion

peritoneal

the intraluminal

terial may be equally penetration.

into the peritoneal

inadvertent

of contrast

cavity presence

obvious

cavity

intraluminal was

pene-

material

obvious.

of contrast

In ma-

and prove intraluminal