POSTGRAD. MED. J. (1965), 41, 471

ACUTE PANCREATITIS AND RENAL

FAILURE

H. A. LEE, B.Sc., M.B., B.S., M.R.C.P.Lecturer in Medicine

*E. A. HILLS, M.B., M.R.C.P.Registrar

Department of Medicine, King's College Hospital Medical School, S.E.5.

ACUTE oliguric renal failure complicating acutepancreatitis is rare and many standard textsfail to mention it. Russell Taylor (1949) foundit only once in 110 such patients, and in 163examined post mortem Blumenthal and Prob-stein (1959) found only one case where a lowernephron nephrosis seemed to be related to post-operative haemorrhage and shock, althoughalbuminuria without evidence of further renaldamage is not infrequent in acute pancreatitis(Siler and Wulsin, 1951). However, Balslov,Jorgensen and Nielsen described thirteen ex-amples of renal failure in 1962 and reviewed27 others from the world literature. The aetiol-ogy is not well understood, but causes suchas shock (Beisel, Herndon, Myers and Stones,1959), dehydration (Ducrot and Slama, 1960),anoxia (Beisel and others, 1959), bouts offever (Edlund, 1950), fat emboli in glomerularcapillary tufts (Lynch, 1954) and thrombi inrenal vessels (Ducrot and Slama, 1960) havebeen suggested.

Ducrot and Slama (1960) found acute pan-creatitis as the cause of renal failure in sevenof 400 patients with acute renal failure andBalslov and others (1962) found thirteen intheir series of 300. Among 30 patients withacute pancreatitis admitted to the hospital overthe past ten years none had acute renal failure.Four recent examples are described here whodeveloped renal failure in the absence of anyof the known causative factors mentioned above,and which was not recognized in two instancesuntil late in the course of the patients' illness.The nature of the renal lesion is discussed.

Case ReportsCase No. 1

This 52-year-old male was admitted to hospitalon 5.9.64 some ten hours after injury in a motor-car

* Present Address:Medical Registrar, St. Mary's Hospital, Paddington,

London.

accident in which a van which he was driving washit in the rear. His abdomen struck the steeringwheel on impact. He had gone home following theaccident, feeling alright, though a little shaken. Onadmission he complained of lower abdominal painand had had difficulty in micturition for six hours.On examination B.P. 140/90 mm. Hg., pulse rate

60; scattered rhonchi were heard in the chest. Therewas lower abdominal tenderness but bowel soundgwere present. Urine: S.G. 1018, a trace of albumin,reaction acid. HRb 102%.

Operation. A few hours after admission his pulserate rose to 80 and he had a laparotomy to excludebleeding. A haematoma was found around thepancreas extending into the small bowel mesentery.There was a small tear in the body of the pancreas.The small bowel was in spasm with associatedpallor thought to be of autonomic origin. Hispost-operative course was satisfactory, though hehad a variable pulse between 100 and 120 and con-tinued to drain clear yellow fluid from a drain.Gastric suction and intravenous fluid therapy weremaintained. His 24 hour urine volumes over thenext eight days were 900, 700, 580, 300, 680, 1100,400 and 280 ml. On 8.9.64 his blood urea was130 mg./100 ml., plasma bicarbonate 25 mEq./1 andserum potassium 5.1 mEq./l.He was transferred to this Unit on 11.9.64 because

of a rapid deterioration in his clinical state andincreasing uraemia. Examination now showed anill, tired, dehydrated patient with a blood pressureof 170/85, pulse rate of 110 and bilateral coarsebasal crepitations with inspiratory rhonchi wide-spread over the chest. He was expectorating darkbrown purulent sputum. There was abdominal dis-tension with lateral tenderness: bowel sounds wbrepresent and clear yellow fluid was still draining.Bilateral bluish patches discoloured the flanks (Grey-Turner sign). Neither myoglobin nor haemoglobincould be found on spectroscopic examination of theurine. The urine urea was 300 mg. /100 ml. and theS.G. 1009. Serum sodium 121, potassium 6.7, plasmabicarbonate 14 mEq./l. blood urea 550 mg. /100 ml.Serum amylase 550 units/ml. H'b 96%, PCV 47%,WBC 17,300 (93% neutrophils). Serum calcium8.0 mg./100 ml., total serum protein 7.2 g./100 ml.He was given a five-hour haemodialysis on the

Kolff Twin Coil with satisfactory electrolyte adjust-ment. During dialysis he complained of severecentral abdominal pain which was partly relievedby 'Trasylol'. In the early hours of the followingmorning his blood pressure fell and the fluid drainingwas now blood-stained. It was assumed he hadanother leak from the pancreas. Soon after hedeveloped pulmonary oedema and a tracheostomy

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became necessary. He improved immediately with abetter colour and his blood pressure rose to 140/90.But he died suddenly next day.Necropsy: The peritoneal cavity contained 10

ounces of blood-stained fluid and areas of fatnecrosis were scattered throughout the omentum andperitoneal fat tissues. The pancreas was intenselyinflamed and showed severe patchy necrosis. Thebody of the pancreas showed a 2" tear in its sub-stance. The small bowel mesentery showed a 2"area of recent bruising. No; gallstones were found.There was a moderate-sized area of internal lacerationof the spleen near its hilum. Histologically thekidneys showed changes of tubular necrosis. Nomicro-emboli were seen.

Case No. 2A 62-year-old housewife vomited and passed three

loose stools following a pork meal. One hour latershe developed severe right epigastric pain whichpersisted until she was admitted to hospital twodays later. There was no further vomiting ordiarrrhoea. She had suffered from post-prandialdistension for many years. She drank alcohol oc-casionally.On Examination she was a. pale, fat, dehydrated

woman with a temperature of 970'F. She was inpain and her respiratory rate, was increased. Theabdomen was distended with marked epigastrictenderness and guarding. Bowel sounds were heard.B.P. 130/80, Hb 90%, WBC 12,300 i(80% poly-morphs).

Operation. At laparotomy there was blood-stainedperitoneal fluid, areas of fat necrosis and firmenlargement of. the oedematous pancreas.She passed only -150 ml. of urine, S.G. 1011, during

the 32 hours 'after admission, and remained oliguricuntil the seventh day of .her. illness. On the dayfollowing laparotomy alie developed pulmonary andperipheral oedema, was cyanosed and dyspnoeic andbecame hypotensive. Her blood pressure was restoredby hydrocortisone and metaramerol, and maintainedat over 100 mm. systolic pressure. On the secondpost-operative day a tracheostomy was done forrespiratory distress. Her blood urea on this day was152 mg. /100 ml., and three days later was 350mg. /100 ml. Her serum amylase was 4,200 Somogyiunits %. Althought her urine output improved onthe seventh day, she died suddenly that day.Necropsy showed haemorrhage and necrosis in

the pancreas. There was a double left ureter and thekidneys and lungs were oedematous. Histology ofkidney tissue showed disorganisation of tubularepithelium, but it was not possible to say how muchof this was due to post-mortem change.

Case No. 3This 49-year-old Ceylonese woman had suffered

for many years from attacks of wheezing precipitatedby respiratory infections.!, On 10.8.64 she developedanother attack and three days later had right sidedpleuritic pain. She was imnproved by treatment withtetracycline but on 16.8.64 she had diarrhoea, epi-gastric discomfort and vomiting. The following dayshe had severe constant left upper abdominal painand was admitted to hospital for surgical observation.She was asymptomatic for two days and on 23.8.64was transferred to another hospital under medicalcare. nOn Examination, she was pale; pulse 120/min.

B.P. 170/105. There were coarse crepitations over theright lung base, dullness to percussion over thel right

hypochondrium and diffuse discomfort on palpationof the abdomen. Hb 75%, iblood urea 120 mg./100ml. A chest X-ray rhowed patchy pneumonic changesat both bases. Resolving pneumonia was diagnosed,and she was treated with penicillin, streptomycin,Phenergan and 'Amesec' for four days.The following day she had further severe abdominal

pain associated with generalised tenderness, maximalin the left iliac fossa and over the liver. Bouts ofabdominal pain with slight vomiting recurred andshe 'became confused and unco-operative. A variablepyrexia, a tachycardia, dyspnoea and increasing ab-dominal distension followed. By 23.8.64 she haddiminished 'breath sounds and crepitations over bothlung bases. On 25.8.64 she had deteriorated, wasstill dyspnoeic, and had'been constipated for 36 hours.A straight X-ray of the abdomen showed distendedbowel loops. Hb 59%, PCV 28%, blood urea 139mg./100 ml. Liver function tests were normal.Amoebic hepatitis was suspected and a trial ofemetine and chloroquine was started. Cloxacillinand tetracycline were given additionalTy on 27.8.64.As a result of continued vomiting she became severelydehydrated: gastric suction and intravenous fluidswere started with an intake of 5 litres per day.Marked 'positive fluid 'balance occurred and by28.8.64 she developed pulmonary oedema andanasarca. Chlorothiazide did not produce a diuresis.She was transferred to the Kidney Unit on 29.8.64.On Examination she was afebrile, pale, wasted,

anxious and very dyspnoeic with gross anasarca.Her pulse was regular, 140 per minute; B.P. 80/60,JVP raised to the angle of the jaw. Pericardialfriction was heard. She had signs of pulmonaryoedema and 'basal consolidation. The abdomen wasdistended, diffusely tender and bowel sounds werepresent. Hb 47°%, PCV 26%, WiBC 15,600 (96%neutrophils), 'blood urea 160 mg./100 ml., serumsodium 133, potassium 4.7, plasma bicarbonate 15mEq. /41., serum calcium 8.0, phosphate 6.5 mg. /100 ml., amylase 160 Somogyi units. Liver functiontests were normal and blood cultures sterile. Therewas verdiglobinuria and moderate albuminufia.UJrine osmolarity was 280 mOsm. /kg. and urine urea510 mg. /100 ml. Urine microscopy showed numerousred blood cells, a'few white 'blood cells, and a feworganisms. Coliforms were grown on culture. Achest X-ray showed moderate cardiac enlargement,and an X-ray of her abdomen was normal. Anelectrocardiogram showed generalised non-specificT wave inversion. Immediate dialysis was necessary.It proved difficult in view of the patient's circulatoryfailure but ultrafiltration was achieved. Post dialysisher jugular venous pressure was 3 cm. above thesternal angle and she was much less dyspnoeic. Sheremained hypotensive for 8 hours; Fluids wererestrig,ted to 500 ml. in 24 hours, and a high calorie,low salt diet given. Durabolin 50 mg. i.m. daily,cryst4line penicillin and codeine phosphate werealso;4iven. Her oedema lessened although her urineoutput was less than 1000 ml. daily (see Fig. 1).She had severe distressing diarrhoea which couldnot 'be measured because she was incontinent.Cystoscopy showed ulceration of the bladder, butretrograde 'pyelography was normal. She remainedvery ill and developed a severe oral monilial infection.An episode of atrial tachycardia with atrio-ventricularblock was attri'buted to digitalis intoxication and wassuccessfully treated with pronethalol.Apart from a post-cystoscopy fever, 'her tempera-

ture 'Was normal 'but leftocytosis became moremarked. (see Fig. 1).' On the eighth day after

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LEE and HILLS: Acute Pancreatitis and Renal Failure

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FiG. 1.-White cell count, blood urea, plasmabicarbonate and 24 hour urine volumes duringillness of patient No. 3.

admission a -further haemodialysis was done pre-paratory to a laparotomy in order to exclude anabdominal source of infection. She died duringdialysis from pulmonary oedema.Necropsy: the lungs were congested and collapsed

and the pleural cavities contained straw-coloured fluid.There was a pericardial effusion and fibrinous exudateover the 'pericardial surfaces. There were 2 pints ofbile-stained fluid in the peritoneal cavity. There wererecent haemorrhagic adhesions between the left lobeof the liver and the anterior abdominal wall, alsoaround the second part of the duodenum. Theretroperitoneal tissues were oedematous and thepancreas was markedly swollen and haemorrhagic.Tne gallbladder and bile ducts were normal. Bothkidneys were enlarged and the capsules strippedwith difficulty to show coarse scarring. The cortices

were swollen and pale and the cortico-medullaryjunction poorly defined. Histology of the pancreasshowed extensive necrosis with acute inflammatoryexudate and congestion. The kidneys showedgeneralised tubular necrosis affecting the convolutedtubules and changes of chronic pyelonephritis withminimal arterial and arteriolar thickening.

Case No. 4A 62-year-old female was admitted to hospital on

21.1.65 with an 18-hour history of sudden onset ofsevere central abdominal pain and vomiting whichhad continued since.On examination she was grossly obese, in pain and

had a temperature of 100 F. (B'P 200/120, pulse94/min., regular, and there were bilateral basalcrepitations. Marked epigastric tenderness was presentwith guarding. Bowel sounds were present. Acutepancreatitis was diagnosed. Treatment by gastricsuction and intravenous fluids was begun.A plain X-ray of her abdomen was normal. Hb

96%, ESR 40 mm./hr., WBC 11,000/cu. mm. (77%neutrophils). Albumin, a few granular casts and whitecells were present in the urine. Urine culture wassterile. Serum amylase 64 units/ml., blood urea 25mg./100 ml. rising to 45 mg./100 ml. the next day.Over the next few days she continued to complam

of moderate to severe central abdominal pain some-times associated with vomiting. She remained verytender in the epigastrium with guarding. Her tachy-cardia continued though her pyrexia settled by 28.1.65.Severe epigastric and left hypochondrial tendernessand guarding were evident by 1.2.65 and the presenceof pseudopancreatic cyst questioned.

Operation. At laparotomy on 2.2.65 marked patchyfat necrosis of the omentum with free sero-sangumousfluid was found. The head of the pancreas was firmand swollen and there were many surroundingadhesions. A left sub-colonic drain was left in situ.Blood urea 325 mg. /100 ml., serum potassium 6.7,bicarbonate 10 mEq./l, WBC 15,000/cu. mm. (78%neutrophils). Her general condition deteriorated by4.2.65 when her blood urea was 330 mg./100 ml. and24-hour urine output 400 ml. and she was transferredto the Renal Unit.On Examination she was drowsy with acidotic

breathing, pulse 94/min., regular, BP 180/80, res-pirations 18/min., temperature normal. Straw-coloured fluid was draining,from the abdomen. Theabdomen was distended and there were no bowelsounds. Blood urea was 375 mg. /100 ml., serumsodium 135, potassium 6.7, plasma ibicarbonate 15mEq./l. Hib 60%, 'PCV 29%, WBC 13,750/cu. mm.The plasma and urine osmolalities were 297 and 312mOsm./kg. respectively. The urine urea was 950 mg./100 ml. with a urine/plasma ratio of 2.5. Serumamylase 264 units/ml. There was moderate albumin-uria but no glycosuria or haemoglobinuria. The urinewas sterile but there were a moderate number of puscells seen on microscopy.The patient was dialysed for six hours on the Kolff

Twin Coil with good electrolyte adjustment. Therewas an exacerbation of symptoms during dialysis.Gastric suction, intravenous fluids and 'Trasylol' weregiven. There was considerable improvement overthe next three days with recovery from the paralyticileus and start of the diuretic phase. The patientrelapsed on 10.2.65, once more developing paralyticileus although a good daily urine output of over alitre continued. She died on 11.2.65.Necropsy: There was complete autolysis of the

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pancreas, widespread fat necrosis in the abdomen andacute renal tubular necrosis.

DiscussionThe diagnosis of pancreatitis may be difficult

to prove or even be overlooked until necropsyas in the third case described. But it is moreoften recognised than formerly, partly frommore frequent suspicion and partly because ofavailable tests such as the serum amylase.Unless the possibility of acute renal failurecomplicating pancreatitis is appreciated, thereis considerable risk of overtreatment by intra-venous therapy as in two of our patients.The value of serum amylase estimations in

diagnosing pancreatitis in the presence of acuterenal failure is difficult to evaluate. Elevatedserum amylase levels unassociated with pan-creatitis have been reported by Meroney,Lawson, Rubini and Carbone (1956) in acuterenal failure. However, Beisel and others (1959)and Varay (1957) have reported considerablefalls in the serum amylase level in acute pan-creatitis complicated by renal failure in spiteof continuing oliguria. It seems, therefore, thatserum amylase levels are worth measuring onat least two occasions. However, Albo, Silenand Goldman (1963) found that 36% of their133 cases uncomplicated by renal failure hada serum amylase level of less than 200 Somogyiunits.Whether pancreatitis or urnmia is the primary

disease in such combinations has beenquestioned (Merrill, 1955, and Ducrot andSlama, 1960) but in the patients reported herethere can be little doubt that pancreatitis wasthe primary disease. In all of them theabdominal disease preceded any renal failureand necropsy showed that the renal lesions wereacute. The poor prognosis of this combinationis well recognised. All five cases reported byBeisel and others (1959) died and Balslov andothers (1962) found a 78% mortality rate whenreviewing the world literature.The mechanism whereby renal failure comp-

licates pancreatitis is difficult to unravel. Thal,Kobold and Hollenberg (1963) have studiedvasoactive substances released into the cir-culation of patients with acute pancreatitis.They believe that when the pancreas is damaged,pancreatic enzymes are released and liberatepotent vasodilator substances from globulinprecursors in the plasma. These substances mayaffect capillary permeability but at all eventsa severe vasomotor collapse ensues and thehypotension is often sufficiently prolonged tocause renal failure. Our patients, however, did

not suffer from hypotension before the onsetof their renal failure. Hypercoagulability, whichhas been confirmed recently in acute pan-creatitis by Shinowara, Stutman, Walters andRuth (1962), does not seem to have played apart either in causing renal failure in thesepatients.Methaemalbuminaemia (Webb, 1963) and

haemoglobinuria (Gambill, Baggenstoss, VanPatter and Power, 1948) have been describedin association with acute hemorrhagic pan-creatitis and have been suggested as contributoryfactors in causing acute renal failure. Haemo-globinuria did not feature in the cases reportedbut methaemalbuminaemia was not looked for.Mirsky and Freis (1944) injected trypsin

solutions intraperitoneally into rats and rabbits,and intravenously into rabbits. All the animalsdeveloped a profound shock syndrome and died,but there were no control animals. The necropsystudies of the kidneys showed cloudy swellingand vascular congestion with degeneration ofcells in the convoluted and distal collectingtubules. There was massive deposition ofeosinophilic granular and fibrillar material inthe glomerular and tubular spaces with foci oflymphocytes around the distal collecting tubulesand arterioles. The urine contained red andwhite cells but no hemoglobin. However, itis not possi'ble to attribute these effects totrypsin per se because of the profound hypo-tension following these injections. Reid,Paulette, Challis and Hinton (1958) usingvarious pancreatic homogenates studied theeffects of these on the oxygen uptake of kidneyand other tissue homogenates. They found theoxygen uptake measured manometrically wasdepressed most markedly by the microsomefraction of the pancreatic homogenates. Purepancreatic secretion after vagal stimulation hada marked inhibitory effect which was destroyedby heating at 950 C for 15 minutes. This wouldnot destroy trypsin, suggesting that the inhibi±tory effect on oxygen uptake is due to someother agent. This unidentified agent may bean important factor in producing acute renalfailure by interfering with oxygen utilizationby renal tubules. This could, in turn, explainrenal failure occurring in patients with acutepancreatitis who have neither hypotension norevidence of obstruction in small renal vessels.

Pancreatic homogenates have also been foundto reduce the oxygen uptake of heart muscle(Reid and others, 1958). de Jode and Howard,(1962), suggest that the ECG changes thatsometimes accompany acute pancreatitis mayreflect the effects of activated trypsin in the

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August, 1965 LEE and HILLS: Acute Pancreatitis and Renal Failure 475

circulation upon heart muscle. Pulmonaryoedema indicating myocardial embarrassmentis not an infrequent complication of acutepancreatitis and occurred in our patients. Caseno. 3 also developed a fibrinous pericarditiswhich seems to have been related to her acutepancreatitis.The evidence for implicating fat droplet

emboli as the cause for renal failure in pan-creatitis is poor. Lynch (1954) reported fivesuch cases, but these were all post mortemstudies and there was little supporting clinicalevidence for acute renal failure. Furthermore,if emboli were the cause then a patchy ratherthan uniform distribution of the renal lesionwould be expected, which is not the case.Circulatory enzymes and toxic tissue productswould be more likely to cause the uniformrenal lesions in the absence of hypotension.Another contributory factor in the aetiology

of renal failure complicating traumatic pan-creatitis without hypotension is suggested bythe laparotomy findings in case no. 1. Pallorand spasm of the small bowel had been foundan effect of sympathetic nerve over activity.Sympathetic fibres supplying the small boweland kidneys are intimately related at theirorigin in the coeliac plexus (Gray, 1954).Therefore in this case it is possible that intensesympathetic vasomotor activity was occurringin the kidneys at the same time as in the bowel,due to stimulation of the coeliac plexus follow-ing trauma. Such sympathetic vasomotoractivity may have been sufficient and prolongedenough to cause renal anoxia in the absenceof systemic hypotension.Danker and Herfitz (1951) studied the

creatinine clearances of patients with acutepancreatitis not complicated by any circulatorycollapse. In some they found a reduction increatinine clearance which was maximal at24-48 hours and associated with an abnormalpattern of amylase excretion. This againsuggests that some factor released from thepancreas or from plasma precursors maydirectly involve renal function in the absence ofhypotension. It also shows how easily renalfailure may be missed in these cases unlesscareful watch on urine volumes and specificgravities are kept.

Balslov and others (1962) pointed out thatanticoagulation required for hemodialysis didnot cause an exacerbation of hmmorrhagicpancreatitis or increased tendency to retro-peritoneal hmmatoma. Case no. 1, however,complained of severe abdominal pain duringhiemodialysis associated with blood staining of

the pancreatic fluid from the abdominal drain.It is felt, therefore, that regional heparinizationshould be used when dialysing such patients.From our experience and those. of others, it

seems that careful control of the acute renalfailure both by conservative management andhemodialysis does little to alter the prognosis,although such treatment is necessary if thepatient is to recover. Two of our patientssurvived for three weeks and one entered theearly diuretic phase but all died from theunderlying pancreatitis. Both increased enzymeactivity and increased enzyme production havebeen found to occur in acute pancreatitis andconventional treatment of continuous aspirationof gastric and duodenal contents is designed toinhibit such secretion. The an.atomy of thepancreas is such that it precludes pancreatec-tomy as a means of removing the source ofenzyme production. It may be, therefore, thatthe administration of a kallikrein-trypsininactivator (e.g. 'Trasylol') from the onset ofthe disease may improve the prognosis in thisgroup of patients. Many reports have alreadyappeared showing that the mortality rate inacute pancreatitis not complicated by renalfailure is reduced by using this inactivator.Though used in two of our patients, it wasgiven late in the course of the illness andsubmaximal doses were used and no conclusionscan be drawn with regard to its effectivenessin this situation.

SummaryFour patients are described who had acute

oliguric renal failure unrelated to hypotensionin the course of acute pancreatitis. Themechanism of such renal failure is discussed.The importance of appreciating the appearanceof renal failure in the absence of knownprecipitating causes is stressed.Our thanks are due to Dr. Clifford 'Hoyle, Director

of the Medical Unit, for his encouragement andhelpful criticisms in the preparation of this paper.

REFERENCESALBO, R., SILEN, W., and GOLDMAN, L. (l%963): A

Critical Clinical Analysis of Acute Pancreatitis,Arch. Surg., 86, 1032.

BALSLOV, J. T., JORGENSEN, H. E., and NIELSEN, R.(1962): Acute Renal Failure Complicating SevereAcute Pancreatitis, Acta. chir. scand., 124, 348.

BEISEL, W. R., HERNDON, E. G., MYERS, J. E., andSTONES, L. i(1959): Acute Renal Failure as a

"Complication of Acute 'Pancreatitis, Arch. intem.AMed., 104, 539.

BLUMENTHAL, H. T., and PROBSTEIN, J. G. ((1959):Pancreatitis: A Clinical Pathologic Correlation,Springfield, Illinois: Charles C. Thomas.

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DAIKNER, A., and HERFITZ, C. J. ((1951): Inter-rehtionship of Blood and Urine Diastase ESuringTranssknt Acute Pancreatitis, Gastroenterology, 18,207.

DE JODE, L. R., and HOWARD, J. M. (1 963): TheManagement of Patients with Acute Pancreatitis,Surg. Clin. N. Amer., 42, 1489.

DUCROT, H., and SLAMA, R. (1960): Les InsuffisancesRenales Associ6es A une Pancreatite Aigue, Rev.med.-chir. Mal. Foie, 35, 199.

EDLUND, Y. (1950): Acute Necrosis of the Pancreas,Acta, chir. scand., 99, 497.

GAMBILL, E. E., BAGGENSToSS, A. H., VAN PATrER,W. G., and POWER, M. H. (1948): Acute Hamor-rhagic Pancreatitis: Study of Patient havingDessiminated Fat Necrosis, Hypocalcamia, Hypo-potassemia, Uremia, Diabetes Mellitus, Ascites andBilateral Hydrothorax, Gastroenterology, 11, 371.

GRAY'S ANATOMY (1954): Thirty-first edition, p. 1201,London: Longmans Green.

LYNCH, M. J. (1954): Nephrosis and Fat Embolismin Acute Hemorrhagic Pancreatitis, Arch. intern.Med., 94, 709.

MERONEY, W. H., LAWSON, N. L., RUBINI, M. E.,and CARBONE, J. V. (1956): Some Observations ofthe Behaviour of Amylase in Relation to AcuteRenal Insufficiency, New Engl. J. Med., 255, 315.

MERRILL, J. P. (1955): The Treatment of RenalFailure, New York: Grune and Stratton.

MIRSKY, I. A., and FREIs, E. D. (1944): Renal andHepatic Injury in Trypsin "Shock", Proc. Soc. exp.Biol. (N.Y.), 57, 278.

REID, L. C., PAULETTE, R. E., CHALLIS, T. W., andHINTON, J. W. (1958): The Mechanism of thePathogenesis of Pancreatic Necrosis and theTherapeutic Effect of Propylthiouracil, Surgery, 43,538.

RUSSELL TAYLOR (1949): The Aetiology, Pathology,Diagnosis and Treatment of Acute Pancreatitis,Annti. roy. Coll. Surg. Engl., 5, 213.

SHINOWARA, G. Y., STuTMAN, L. J., WALTERS, M. I.,and RuTH, M. E. (1963): Hypercoagulability inAcute Pancreatitis, Amer. J. Surg., 105, 714.

SILER, V. E., and WULSIN, J. H. (1951): Considerationof Lethal Factors in Acute Pancreatitis, Arch. Surg.,63, 496.

THAL, A. P., KOBOLD, E. E., and HOLLENBERG, M. J.(1963): The Release of Vasoactive Substances inAcutePancreatitis, Amer. J. Surg., 105, 708.

VARAY, A. (1957): Retentissement Renal des Pan-creatites Aigues, Acta gastro-ent. belg., 20, 865.

WEBB, A. J. (1963): Hypocalcmmic Tetany andMethaemalibuminwmia in Acute Fulminating Pan-creatitis, Postgrad. med. J., 39, 361.

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