PATHOGENESIS OF GASTRIC ULCERATION

974 extractions in

severely affected patients it

can

be

under general anaesthesia. The purpose of the trial was to determine the minimum treatment required for safety. Human A.H.G. made by the Blood Products Laboratory was the main therapeutic agent. The amount of treatment required was related to the number, position, and type of teeth removed. The effectiveness of treatment was related to the level of factor-vin activity assayed in the patient’s blood. From the experience gained it is possible to predict the amount of treatment required for safety in the majority of cases and the dosage and duration of treatment varies with the extent of the operative procedure. We are greatly indebted to the Oxford Regional Transfusion

predicted

that plasma treatment alone will usually prove inadequate.

From our results it is possible to outline a policy consistent with safety and reasonable economy in the use of therapeutic materials. All extractions of deciduous teeth and single extractions of adult teeth in severely affected patients can safely be carried out using plasma. The dose should be above 15 ml. per kg., but should seldom exceed 20 ml. per kg., except in children. Such amounts, given as single doses daily, have never led to circulatory overloading, even in elderly patients. The number of daily doses to be given will depend on circumService without whose constant and willing cooperation the treatstances. In children extractions of single deciduous teeth ment of hsemophilic patients would be impossible. The assays of seldom need more than one or two doses. More extensive factor-vin activity were carried out under the supervision of Mr. extractions may need more prolonged treatment. Single K. W. E. Denson by various members of the staff of the Blood extractions in adults are seldom healed in less than 7 days, Coagulation Research Unit. but beyond the 5th day after extraction the amount of REFERENCES E. R., Bidwell, (1959) Brit. J. Hœmat. 5, 379. blood lost is usually trivial; probably it would be Biggs, Eveling, J., Richards, G. (1955) ibid. 1, 20. reasonable to give treatment for 5 days in the first instance, Macfarlane, R. G. (1962) Human Blood Coagulation and Its Disorders. Oxford. and thereafter only if serious bleeding occurs. (1965) The Clinical Management of Hæmophilia and Other For extractions of two to nine teeth the present series of Coagulation Defects. To be published. Oxford. Kekwick, R. A., Walton, P. L. (1964) Personal communication. investigations seem to suggest that better results can be Wolf, P. (1957) Lancet, i, 647. W. D’A., Evans, S., Vallet, L., Combridge, B., Wolf, P., obtained from the use of H.A.H.G. than of plasma, but Maycock, MacGibbon, B. H., French, E. E., Wallett, L. H., Dacie, J. V., Biggs, the numbers are too small to be certain. In this category R., Handley, D., Macfarlane, R. G. (1963). Brit. J. Hœmat. 9, 215. McIntyre, H., Barrett, K. E., Israëls, M. C. G., Wilkinson, J. F. (1964) it might be reasonable to administer H.A.H.G. in high Lancet, i, 584. 2 and to this with treatment. for follow days plasma dosage For major extractions (of more than ten teeth) or for the removal of impacted lower third molars, H.A.H.G. should undoubtedly be used, and it would be unwise to underPATHOGENESIS OF GASTRIC take such extractions without this concentrate. The results have shown that the response of the patients ULCERATION to treatment varies considerably, and a dose adequate for D. J. DU PLESSIS one patient is inadequate for another. When the average Ch.M. W’srand, F.R.C.S. dosage figure for tables ll-vil is calculated, it can be seen PROFESSOR OF SURGERY, UNIVERSITY OF THE WITWATERSRAND, that there is no correlation between dosage and clinical JOHANNESBURG, SOUTH AFRICA effect. The dose that we recommend-13-15 units per THE absence of hypersecretion in gastric ulceration has kg.-is a compromise. With this dosage some patients led to the assumption that the ulcer is due to lowered will bleed, but our experience suggests that bleeding will mucosal resistance. This resistance depends partly on the not be serious and many patients will be free of abnormal barrier action and neutralising effect of the surface layer bleeding. of mucus and partly on the regenerative ability of the Consideration of table x leads to the conclusion that gastric mucosa (Fogelson 1931, Barrett 1946-7, Johnson absolute freedom from bleeding after the removal of more 1957, Milton et al. 1960). than ten teeth will not be achieved without treatment comHistological Examination of Resected Stomachs parable to that required for safe major surgery. For major MATERIAL AND METHOD surgery we have suggested (Biggs and Macfarlane 1965) that Mucosal strips of resected stomachs were rolled up like the plasma level of factor vm should not fall below 25 % of swiss-rolls " (Stein 1937), and transverse sections were normal at any time during the first 5 days of treatment. stained with hamotoxylin and eosin (du Plessis 1960). 75 To achieve this objective with certainty in all major stomachs resected for gastric ulceration and 18 resected for dental cases would require an appreciable increase in duodenal ulceration were examined. dosage and probably administration twice daily. On the RESULTS whole this does not seem to be reasonable or necessary. All the stomachs showed histological evidence of chronic With the present dosage, patients with fewer than twenty gastritis (Palmer 1954). teeth extracted will not usually bleed sufficiently to Gastric Ulceration require transfusion. Dental bleeding-controlled as it In 61 of the 75 stomachs resected for gastric ulceration has been in these patients-is not dangerous, in sharp there was severe chronic gastritis extending from the distinction to the major-surgery cases where blood-loss pylorus for a variable distance proximally, usually further internally can be exceedingly dangerous. It would seem along the lesser curve than in the rest of the stomach (du reasonable to carry out such major extractions using Plessis 1960) and more severe at the proximal part of the doses of 13-15 units of factor-vm activity per kg. and to affected area. Because of this distribution the pyloric continue the treatment for 10 days. If material at present gland area (P.G.A.) of the stomach was always extensively supplied by the Blood Products Laboratory is used, the affected (fig. 1), whereas the fundic gland area (F.G.A.) was amount required will be 4-6 ml. of concentrate per kg. variably (fig. 2) affected. Summary Duodenal Ulceration This report is based on the study of 43 sessions of In duodenal ulceration the chronic gastritis was not dental extraction in 38 hsemophilic patients from whom a nearly as extensive or as severe as in gastric ulceration rota] of four hundred and thirty-three teeth were removed (figs) 3 and 4). -

-

-

-

"

-

975

Fig. 5-Situation

Fig. l-Extent of chronic atrophic gastritis in the pyloric-gland area in 61 cases of gastric ulceration.,

duodenal scar without radioevidence of obstruction, but the logical macroscopic of these cases was identical with histological appearance that described for gastric ulceration. was a

or

Site of the Gastric Ulcer The gastric ulcer was always situated in the area affected by atrophic gastritis. In some instances there were multiple ulcers; the distribution of 81 ulcers in 65 stomachs is shown in fig. 5. 27% were found in the F.G.A., and in these cases the atrophic gastritis always extended into the F.G.A. (du Plessis 1960). 33 ulcers were on the proximal margin of the P.G.A., and in 15 the atrophic gastritis was limited to the P.G.A. or affected only a very small area of the F.G.A. (fig. 6) so that the ulcer was in the zone of atrophic mucous membrane abutting on normal acid and pepsin secreting fundic mucosa.

Exceptions In 75 of

3-Extent of chronic atrophic gastritis in the area in 18 cases of duodenal ulceration.

Fig.

pyloric-gland

cases

gastric ul-

10 ceration stomachs did not exhibit this "typical" distribution chronic of gastritis. In these cases the factors

probably sponsible

re-

for the formation of the gastric were ulcers chronic hy-

pertrophic gastritis (1), long-continued cortisone administration

(2), left gastric-artery thrombosis Fig. 4-Extent of chronic atrophic gastritis in the fundic-gland area of the resected portion of stomach in 18

cases

gastric ulcers.

Fig. 2-Extent of chronic atrophic gastritis in the fundic-gland area of the resected portion of stomach in 61 cases of gastric ulceration.

Combined Gastric and Duodenal Ulceration In 4 instances there

of 81

of duodenal ulceration.

(1),

benign

tumours

of

the stomach (2), and pyloric obstruction (4). DISCUSSION

The extensive chronic gastritis demonstrated in this investigation could predispose to ulceration by decreasing or altering the secretion of mucus and impairing the ability of the mucous membrane to regenerate after injury. The association of chronic gastritis with gastric ulceration has been observed before (Magnus Fig. 6-Histological findings in a stomach with a gastric ulcer in the proximal 1937) but has usuof the pyloric-gland area. portion been regarded ally The stomach is represented as opened as the result of along the greater curvature with the pylorus the gastric ulcer. inferiorly. Black line indicates the junction This seems un- between the pyloric-gland area and the likely because the fundic-gland area. chronic gastritis not only is distributed around the ulcer but also affects the distal part of the stomach. Gastric ulceration occurs in the area affected by chronic gastritis; hence there is more chronic gastritis in gastric ulceration than in duodenal ulceration (Meyers 1948, Morson 1955), and the higher the ulcer in the stomach the greater the extent of the chronic gastritis (Ball and

James 1961). Because the chronic gastritis extends from the pylorus the chronic gastritis may be limited to the P.G.A. of the stomach and gastric ulcer is commoner in the P.G.A. In this series the frequency of ulcers in the P.G.A. is less than that quoted by others (Karsner 1949, Marks and Shay 1959, Oi et al. 1959), presumably because with the swiss-roll technique the pseudopyloric metaplasia of

proximally,

976

in atrophic gastritis (du Plessis 1960) is less likely to be mistaken for the P.G.A. The extensive involvement of the P.G.A. by atrophic gastritis in gastric ulceration suggests that the P.G.A. may protect the mucous membrane against ulceration, which then only occurs if most of the P.G.A. is damaged. The following findings favour this suggestion: the

F.G.A. seen

1. Gastric ulceration

occurs on

the average

two

years after

partial gastrectomy, but twenty-three and a half years after gastrojejunostomy (du Plessis 1962, Small 1964). 2. In gastric ulceration after previous gastrojejunostomy the P.G.A. of the stomach shows extensive chronic gastritis (du Plessis 1963). 3. Jejunal ulcers occur early after gastrectomy but late after gastrojejunostomy (Nuboer 1961, Small 1964), and in the presence of jejunal ulceration after previous gastrojejunostomy the P.G.A. is extensively damaged by chronic gastritis (du Plessis 1963). Johnson (1957) suggested that in combined gastric and ’

aspirate is commoner in patients in healthy people.

with

a

gastric

ulcer than

Further confirmation of this view was sought by the degree of biliary reflux in a group of

measuring patients.

MATERIAL AND METHOD

After the patient had fasted overnight the resting juice in the stomach was aspirated through a nasogastric tube. The aspirated fluid was examined for bile-acid conjugates by means of paper chromatography (Sjovall 1952, 1954). This investigation was carried out on 13 patients without dyspepsia, 10 with radiologically negative dyspepsia, 14 with gastric ulcers, 22 with duodenal ulcers, and 6 after partial gastrectomy. RESULTS

The results (fig. 7) indicate low levels in patients without dyspepsia and with non-ulcer dyspepsia, and high levels

duodenal ulceration the duodenal ulcer produces gastric stasis which predisposes to the formation of a gastric ulcer. This does happen, but was not apparent in the present series, and in other studies stasis could only be demonstrated in a minority of the cases (Mangold 1958, Aagaard et al. 1959). Cause of Chronic Gastritis in Gastric Ulceration

The " typical " distribution of chronic gastritis extending from the pylorus proximally for a variable distance suggests that the gastritis is caused by reflux of duodenal contents through the pylorus (Spira 1956). Under experimental conditions duodenal reflux can produce chronic gastritis (Lawson 1964) and stomachs removed after previous gastric operations reveal chronic gastritis around the stoma, presumably due to trans-stomal reflux of jejunal contents because the symptoms produced by this gastritis can be relieved by converting the gastrectomy into a Roux-en-Y type with a 14-in. vertical limb which prevents such reflux (du Plessis 1962). Moreover, James and Pickering (1949) pointed out that bile staining of the gastric

8-Total acid output in one hour after maximum histamine stimulation related to extent of atrophic gastritis in the fundicgland area of stomachs resected for gastric ulceration.

Fig.

in patients with gastric ulcer, post-gastrectomy patients, and some patients with duodenal ulceration. The differences in concentration of bile-acid conjugates could not be attributed to dilution, because the volumes of fasting gastric juice were very similar-an average of 15.4 ml. in patients without dyspepsia, 18.1 ml. in nonulcer dyspepsia, 18.0 ml. in duodenal ulceration, 15.0 ml. in gastric ulceration, and 15.7 ml. in the post-gastrectomy cases.

DISCUSSION

These findings point to an excessive amount of duodenal reflux in gastric ulceration. Slight reflux is a normal finding, and this is presumably responsible for the chronic gastritis seen in all adults in the region of the pylorus. The increased amount of reflux in some of the patients with duodenal ulcers may be due to interference of the pyloric sphincter by the ulcer; this offers an explanation for the occurrence of gastric ulcers in the presence of duodenal ulcers (healed or unhealed) without duodenal obstruction. The very high concentration of bile-acid conjugates in the post-gastrectomy cases is not unexpected, and may be the cause of the chronic gastritis around the stoma, which in turn may be responsible for symptoms and even for serious complications (du Plessis 1962). on

Fig. 7-Concentration of bile-acid conjugates in the fasting gastric contents:

females o, males v

.

Effect of Atrophic Gastritis Secretory Function of the Stomach

Acid secretion is about normal if the ulcer is prepyloric, but is lower if it is elsewhere in the stomach (Marks and

977

Shay 1959) and decreases progressively the higher the position of the ulcer in the stomach (Ball 1961, Baron 1963). Acid output falls with increasing severity of gastritis (Bock et al. 1963), and the variation in acid secretion in gastric ulceration seems likely to be related of atrophic gastritis in the F.G.A.

to

the

extent

MATERIAL AND METHOD

augmented histamine test (Kay 1953) was performed in 21 patients with chronic gastric ulcers. After gastrectomy the resected portion of stomach was examined histologically, and the results of these two investigations were compared. The

RESULTS

The acid output is closely related to the extent of atrophic gastritis in the F.G.A. of the resected portion of stomach (fig. 8). The distance of the gastric ulcer from the pylorus also correldtes well with the extent of

atrophicc gastritis in the F.G.A. of the resected portion of stomach

(fig. 9). DISCUSSION

Fig. 9-Distance of the gastric ulcer from the pylorus related to extent of atrophic gastritis in the fundic-gland area of the resected portion of stomach.

These results support the view that the decrease of acid secretion with ulcers in the body of the stomach is

due to the atrophic gastritis in the F.G.A. It may be argued that the acid secretion drops with higher ulcers because the P.G.A. is larger, but Baron (1963) points out that the non-parietal component of gastric secretion also decreases if the ulcer is high in the stomach.

Conclusions. Gastric ulceration is preceded by chronic gastritis which lowers the resistance of the gastric mucous membrane by altering the mucus secretion and damaging the epithelial cells. Gastric ulceration is the end-stage of a widespread inflammation of the gastric mucous membrane. The P.G.A. must be significantly damaged before gastric ulceration takes place; the P.G.A. probably has a protective function and should not be resected needlessly. Chronic gastritis appears to be the result of reflux of duodenal contents through an abnormally functioning pylorus, or a pylorus which may have been damaged or

bypassed in previous surgery. Acid and pepsin are probably the final causes of the chronic gastritis. Reflux of the alkaline duodenal contents may act only by interfering with the protective layer of mucus and thus allow acid and pepsin to come into contact with the epithelium. This can explain why: 1. Postoperative gastric ulcers are common after operations for duodenal ulcer and are very much less common after operations for gastric ulcer (when acid secretion is very low). 2. Implantation of gastric mucous membrane into the gallbladder,(where there is no acid and pepsin) is not followed by gastritis (Byers and Jordon 1962). 3. Acid and pepsin produce gastritis if mucosal resistance is

impaired by cinchophen (Bollman

et

al.

1938).

4. After gastrojejunostomy vagotomy affords some protectiol of the gastric mucous membrane (Byers and Jordan 1962). 5. Postoperative gastric ulceiation is commoner after vago tomy and gastroenterostomy than after gastrectomy (when the acid is lower) (Sircus and Small 1964). 6. Atrophic gastritis is more severe, and ulcers are com. moner, on the proximal edge of the area affected by atrophi< gastritis which is closest to the source of acid and pepsin. It is not the amount of mucus but its protective qualities

which must be considered. Gastric mucus is affected b) the hydrogen-ion concentration, and acid precipitates mucus to form a protective coating on the mucous membrane ; but with a fall in acidity (as happens with reflux oj alkaline duodenal contents) the mucus becomes fluid, and this barrier is weakened (Ball and James 1961). Hence the amount of mucus aspirated from the stomach is not a criterion of the protective mucus layer, and excess mucus in the aspirate may in fact indicate the liquid nature of the mucus brought about by an unfavourable pH. This explains the high non-parietal component of gastric secretion in gastric ulceration (Hunt 1950, Baron 1963) and the neutrality of the night gastric content in the presence of chronic gastritis in the F.G.A. (Ball and James 1961). Whether this hypothesis of reflux as the cause of gastric ulceration can be reconciled with that of Dragstedt (Dragstedt 1962, Dragstedt et al. 1964) and Burge (1964), which favours stasis as the cause, needs consideration. Dragstedt suggests that gastric ulceration is the result of gastrin released by a poorly emptying stomach, either because of mechanical obstruction or because of gastric atony. Undoubtedly, obstruction produces gastric ulceration, but there is no clear evidence that stasis is a factor in the ordinary gastric ulcer. Stasis has been reported in ordinary cases of gastric ulceration (Dragstedt et al. 1964) but this has not yet been convincingly demonstrated. If stasis is shown to exist in the usual case, then reflux may still be complementary to the stasis which will allow the refluxing fluid more time to affect the gastric mucous membrane. This may explain why ulceration develops in only about 1 % of postoperative cases (Small 1964). Stasis will also permit longer action of acid and pepsin on the exposed mucuous membrane; this can explain why gastroenterostomy reduces the frequency of gastric ulceration in dogs on cinchophen (Bollman et al. 1938) and why gastric ulceration is commoner after gastrojejunostomy than after gastrectomy (Sircus and Small 1964). Although reflux gastritis creates suitable conditions for gastric ulceration, the exact site of gastric ulceration must be determined by other factors such as local peculiarities of blood-supply.

Summary Of 75 stomachs resected for gastric ulceration, 65 displayed chronic gastritis extending from the pylorus for a variable distance proximally. The chronic gastritis in these cases was much more extensive and severe than in 18 cases of duodenal ulceration. The gastric ulcer was always found in the area affected by chronic gastritis; this is thought to be the predisposing factor in these cases. Chronic gastritis may be due to reflux of duodenal contents through the pylorus. The concentration of bileacid conjugates in the fasting gastric aspirates of patients with gastric ulcers is abnormally high. Ulcers in the body of the stomach are associated with atrophic gastritis extending into the fundic-gland area. This lowers the acid secretion of the stomach. In some cases of duodenal ulceration duodenal reflux

978

is excessive: this may account for the gastric ulcers that follow duodenal ulceration without obstruction. The refluxing fluid probably acts by interfering with the protective layer of mucus and by allowing acid and pepsin free access to the mucous membrane. This explains why the ulcer is on the proximal edge of the

osmolarity of blood and urine tc assess concentrating power has the disadvantage of requiring osmometers (Hopkins et al. 1963). Molloy (1962) suggested that urinary urea levels should

affected mucosa. Duodenal reflux does not account for all gastric ulcers : in 10 cases other factors were responsible for the development of the ulcers.

be measured-a value of less than 1100 mg. per 100 ml. pointing to acute renal failure. This figure, however, fails to take into account the bloodPerlmutter et al. urea level. (1959) suggested that the urinary urea/blood-urea ratio was the best measure of renal concentrating power, a value of less than 14 in the presence of oliguria being indicative of renal impairment. This index has been used successfully by Barry and Malloy (1962) and by Luke et al. (1965), and presents no great problem to the laboratory even when large numbers of estimations are required. The value of the index is limited by its dependence on low urinary volume. We report here the use of an index based on both the urinary urea/blood-urea ratio and the 24-hour urine volume.

REFERENCES

Aagaard, P., Andreassen, M., Kurz, L. (1959) Lancet, i, 1111. Ball, P. A. J. (1961) ibid. i, 1363. James, A. H. (1961) ibid. p. 1365. Baron, J. H. (1963) Gut, 4, 243. Barrett, M. K. (1946-7) J. nat. Cancer Inst. 7, 127. Bock, O. H. A., Richards, W. C. D., Witts, L. J. (1963) Gut, 4, 112. Bollman, J. L., Stalker, L. K., Mann, F. C. (1938) Arch. intern. Med. 61, 119. Burge, H. (1964) Vagotomy. London. Byers, F. M., Jordan, P. H., Jr. (1962) Proc. Soc. exp. Biol., N.Y. 110, 864. Dragstedt, L. R. (1962) Ann. N.Y. Acad. Sci. 99, 190. Woodward, E. R., Linares, C. A., de la Rosa, C. (1964) Ann. Surg. 160, 497. du Plessis, D. J. (1960) S. Afr. med. J. 34, 101. (1962) ibid. 36, 471. (1963) S. Afr. J. Surg. 1, 3. Fogelson, S. J. (1931) J. Amer. med. Ass. 96, 673. Hunt, J. N. (1950) Lancet, ii, 397. James, A. H., Pickering, G. W. (1949) Clin. Sci. 8, 181. Johnson, H. D. (1957) Lancet, ii, 515. Karsner, H. T. (1949) Human Pathology. Philadelphia. Kay, A. W. (1953) Brit. med. J. ii, 77. Lawson, H. H. (1964) Lancet, i, 469. Magnus, H. A. (1937) St. Bart’s Hosp. J. 70, 314. Mangold, R. (1958) Brit. med. J. ii, 1193. Marks, I. N., Shay, H. (1959) Lancet, i, 1107. Meyers, W. C. (1948) Gastroenterology, 10, 923. Milton, G. W., Maxwell, G. A., Finckh, E. S. (1960) Brit. J. Surg. 67, 562. Morson, B. C. (1955) Lancet, ii, 1068. Nuboer, J. F. (1961) Ann. R. Coll. Surg. Engl. 28, 303. Oi, M., Oshida, K., Sugimura, S. (1959) Gastroenterology, 36, 45. Palmer, E. D. (1954) Medicine, 33, 199. Sircus, W., Small, W. P. (1964) Scot. med. J. 9, 453. Sjövall, J. (1952) Acta chem. scand. 6, 1552. (1954) ibid. 8, 15. Small, W. P. (1964) J. R. Coll. Surg. Edinb. 9, 255. Spira, J. J. (1956) Gastro-duodenal ulcer. London. Stein, H. B. (1937) S. Afr. J. med. Sci. 2, 117. -

—

-

-

—

ASSESSMENT OF POSTOPERATIVE RENAL FUNCTION

"Renal excretory index"

We set out to compare the accuracy of this method of detecting the onset of acute renal failure with that of urinary urea levels and of the urinary urea/blood-urea

ratio. Patients and Methods

R. M. LINDSAY MEDICAL STUDENT

A. L. LINTON * M.R.C.P.G., M.R.C.P.E.

M.B. Edin.,

REGISTRAR IN MEDICINE

C. J. LONGLAND M.V.O., M.S. Glasg., F.R.C.S. CONSULTANT SURGEON

From the

Royal Infirmary, Glasgow

TRANSIENT oliguria is common after surgery or anxsthesia and usually results from increased secretion of antidiuretic hormone, together with other less well-understood effects on electrolyte excretion (Hopkins et al. 1963). There are, in addition, two pathological causes of postoperative oliguria which are of more serious import; these are dehydration and acute renal failure. Dehydration can usually be detected by estimation of the packed-cell volume or of plasma-proteins, although in view of blood-loss at operation these values may be difficult to assess. The early detection of acute renal failure is of importance partly because of the need to regulate water and electrolyte .

intake, but also because of the possibility of reversal of

by intravenous mannitol (Barry and Malloy 1962,Luke et al. 1965). Detection of early acute renal failure by measurement of specific gravity of the urine is inaccurate, because of the effect of proteinuria (Molloy 1962), and measurement of the condition

*

Present address: Western

Infirmary, Glasgow, W.1.

Sixty patients undergoing operations ranging from haemorrhoidectomy to total colectomy in a general surgical unit were studied. The age-distribution of the patients was 14 to 92 years. Only four of the patients were operated on as an emergency, and no patient had serious electrolyte imbalance before operation. No patient had any preoperative evidence of renal impairment. At operation, blood-pressure, blood-loss, and excessive handling of organs were recorded. Urine collection was begun from the time of return to the ward, and 24-hour volumes were measured. 24 hours after operation, urinary urea and blood-urea levels were determined, and the " renal excretory index " was calculated. These estimations were repeated on each of the next 3 days. All urine samples for urea estimation were kept refrigerated until the estimation was performed. All urea estimations were carried out using a ’ Technicon’ autoanalyser. Results

Assuming that the lower limit of normal for the urinary-urea/blood-urea ratio is 14 as suggested by Perlmutter et al. (1959), and assuming that oliguria is present when the urinary volume falls below 600 ml. in 24 hours, then the lower limit of normal for the " renal excretory

600 84.

On this basis, fifty-five of the 10 sixty patients showed satisfactory renal function after operation. The remaining five patients developed acute renal failure; in each of them the diagnosis was proven either by subsequent clinical course or at necropsy. Of these five patients, three were found to have acute renal

index " is 14 x