Postoperative Per-Ebbe J\l=o"\nsson,MD,
\l=A%o\keAndersson,
Acute Acalculous MD
\s=b\ Two patients with acute acalculous cholecystitis after major surgical operations (cystectomy ad modum Bricker because of carcinoma of the urinary bladder, and proctocolectomy because of ulcerative colitis) are described. Various possible causes of acalculous cholecystitis after operation or after trauma are discussed. Postoperative acute acalculous cholecystitis has a more fulminant course than ordinary calculous cholecystitis. Treatment consists of immediate cholecystectomy. (Arch Surg 111:1097-1101, 1976)
cholecystitis occurring after trauma or operation both is rare. Only a few single postoperative cases had been reported up to 1947,1 after which the complica¬ tion began to receive wider attention. It was not until later that acute cholecystitis after trauma was reported," and then particularly after multiple and widespread war inju¬ ries. The cause of postoperative cholecystitis and that of posttraumatic cholecystitis are probably identical. In most of the cases on record the patients with injuries had also been operated on.'"11 A cute
Ü
or
'
"
REPORT OF CASES Two cases of postoperative acute acalculous cholecystitis were treated at the Department of Surgery, Kristianstad, Sweden in 1974 and 1975, respectively, and are reported below. Cask l.-A 63-year-old man with carcinoma of the urinary bladder was operated on ad modum Bricker under meperidine (petidina) and halothane (Fluothane) plus nitrous oxide and oxygen anesthesia. His blood pressure fell transiently in the induction phase of the anesthesia. The operation, during which the patient received 4 units of blood, was otherwise uncomplicated. Parenteral nutrition was given exclusively until the sixth postop¬ erative day, after which nutrition per os was started. However,
Accepted
Cholecystitis
for publication June 7, 1976. From the Department of Surgery, Central Hospital, Kristianstad, Sweden. Reprint requests to Department of Surgery, Central Hospital, S-291, 85 Kristianstad, Sweden (Dr J\l=o"\nsson).
owing
to
postoperative
intestinal
paralysis, parenteral
nutrition
resumed on the ninth day after the operation. The first few days after the operation the patient was subfebrile. Wound infection was observed on the sixth day, and chest roentgenogram revealed bilateral small basal atelectasis. On the basis of the results of culture, which had given growth of Escherichìa coli and Enterobacteriaceae, and of antibiotic suscep¬ tibility tests, the patient was treated with tetracycline. His condition improved until the 14th day after the operation, when he complained of stabbing pain in the right side of the chest during deep inspiration. Chest roentgenogram showed an elevated dia¬ phragm on the right side and basal parenchymal changes suggest¬ ing pneumonia. Tetracycline therapy was replaced by penicillin V. His condition improved and he was sent home on the 40th day was
after the
operation.
During his stay in hospital the patient had had a mild transient
increase in serum bilirubin level and postoperative anemia. Three weeks after discharge from hospital he was again admitted because of abdominal pain and a body temperature of 39 C. During his stay at home he had almost continually experienced mild pain in the upper portion of the abdomen. Pyelitis was assumed and treatment with ampicillin was started, but the abdominal pain increased in intensity and the temperature continued to rise. The patient became severely jaundiced, the serum bilirubin level rose to 6.1 mg/100 ml, and liver function tests showed signs of biliary stasis. The patient was operated on because of assumed acute cholecystitis; this operation was performed 74 days after the first operation. The gallbladder was found to be severely infected and gangrenous, and the cystic duct was slender. The gallbladder contained viscous, dark green bile, but no demonstrable stone. Microscopic examination showed severe acute inflammation with necroses, hemorrhages, and intramural abscesses. The postoperative course was uneventful and the patient has since had no abdominal symptoms. This patient had never previously had any symptoms or signs of gallbladder disease. Case 2.—In 1975, a 57-year-old man who had for some 30 years had ulcerative colitis was admitted to the Department of Orthope¬ dics because of sciatica. For many years the colitis had been treated with salicylazosulphapyridine (Salazopyrin), and during the last three years with corticosteroids. In 1971, assumed liver cirrhosis had been confirmed by needle biopsy aspiration of the liver. Owing to an increase in the severity of the ulcerative colitis
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Table 1
.—Postoperative
Acute
Cholecystitis No. of Cases
Without Stones Men
Source, yr
Women
With Stones
Sex Not Mentioned
Men
Women
Sex Not Mentioned
Sex Not Mentioned
Glenn.' 1947
12
Sparkman,7' 1952 Schwegman and deMuth," 1953 Leon,20 1954 Glenn and Wantz," 1956
Levin," 1956 Detrie,36 1957 Yedinak," 1959 Levin," 1961
Lynch,» 1961 Jouanneau et
al," 1962
al," 1962 Knudson and Zuber," 1963 Stern,' 1964 Ruderman," 1964 Strode." 1966 Champeau & Bruchou.' 1966 Bronstein," 1968 Herbert et al,'' 1969
Thompson
Bell and
et
Holubitsky,77 Roy," 1969 Hepp," 1969
52
46
10
10
1969
Thomeret and Bronstein," 1970 Robertson, » 1970 Fourati et al,*0 1971 Laws and Elliott," 1971 Callaghan.·' 1972 Howard and Delaney, 1972 Weill & Weill-Monteil. 1972 Dichtl,- 1972 Pelissier & Fagneiz," 1973 Montero & Garcia Fabian" 1973 Meissner,'7 1974 Eide et al, 1975 Present series '
'
Total
67
10
42
76
with frequent blood-stained stools, the patient was given blood transfusions on repeated occasions. On Feb 28, 1974, the patient was jaundiced and the serum bilirubin level rose to a maximum of 9.0 mg/100 ml. The rise was ascribed to the many blood transfu¬ sions. The ulcerative colitis became worse, and on March 20, 1974, the patient underwent a proctocolectomy after one week's preparation with parenteral nutrition. On the second postoperative day his body temperature rose to 40 C. Sepsis was suspected and treat¬ ment with ampicillin and gentamicin sulfate was started. On March 24 wound infection supervened and culture showed typical colonie flora susceptible to the antibiotics the patient was receiv¬ ing. Nutrition per os was given from March 27 to April 2. The patient complained continually of diffuse abdominal pain. He was sent home on April 23. On May 5 the patient sought advice because of stabbing abdominal pain and was treated with dilation of the ileostomy. Owing to increasing severity of the diarrhea the patient was admitted to hospital again on May 12 and complete parenteral nutrition was started. The abdominal pain persisted and temper¬ ature peaks of up to 39 C were recorded. On June 7 he was operated on because of the abdominal pain and the assumed diagnosis of acute cholecystitis, with a serum bilirubin level of 6.2 mg/100 ml. The gallbladder was severely distended and infected. Peroperative cholangiography showed no passage of contrast medium to the
46
79
26
reason choledochotomy was done. The bile duct was not found to contain any stone, but only thick, viscous bile. Neither did the gallbladder contain any demon¬ strable stone. Histopathologic examination of the gallbladder revealed acute phlegmonous inflammation with severe discolora¬ tion of the mucosa. The patient's postoperative course was un¬ eventful.
duodenum, for which common
COMMENT
In only 5% to 10% of all cases of acute cholecystitis is the condition acalculous.1711 On the other hand, the frequency of the acalculous form (Tables 1 through 3) is higher among published cases of postoperative and posttraumatic chole¬ cystitis. Acalculous cholecystitis is more common (92%) among the posttraumatic cases than among the postopera¬ tive cases (47%). This difference may perhaps be explained by differences in the ages of the patients in the two groups. In the posttraumatic cases the lesions were mostly war injuries and the patients mostly young. Calculous cholecystitis after operation may be simply a coincidence and not have anything to do with the operation.17' Postoperative acute acalculous cholecystitis occurs at all Judging ages, but 75% of the patients are over 50 years.1
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""
Table 2—Posttraumatic and
Postoperative Acute Cholecystitis No. of Cases With Stones
Without Stones
Source, yr
Men
Women
Sex Not Mentioned
Men
Women
Biebl," 1939
Mandelbaum and Palmer,'' 1968 Lindberg et al,6 1970 Shaw, 1970 Weeder et al," 1970 Wilson,' 1970 Fackler & Brodhead," 1971 Winegarner & Jackson,'' 1971 Munster and Brown," 1967 Howard and Delaney," 1972 Allendorf,' 1971 Vorster & Böttcher," 1971 Blatt & Floman," 1972 Neidhart et al,35 1972 Golden and Sears," 1973 Shields,'" 1973 Monfort et al," 1973 Kitchen," 1973 Inglesakis et al," 1974 Grosbuis et al,'" 1974 Total
12
82
Table 3.—Sex and
Age Distribution
for Patients With and Without Stones
Without Stones
Postoperative acute cholecystitis Sex
Age, yr
With Stones
Men
Women
Ratio
Men
Women
Ratio
67 59
10 65
7:1
42 61
46 60
1:1
52
78
Posttraumatic and acute
postoperative cholecystitis
82
Sex
Age, yr
from the cases on record, the condition is much more common in men than in women.1 Ordinary acute cholecys¬ titis, on the other hand, is much more common among women, but the difference decreases with increasing age. This variation of frequency with age holds also for postop¬ erative calculous cholecystitis, while the ratio of men to women with acalculous cholecystitis is as high as 7:1 (Table '
3).
cholecystitis can occur after any form of operation, irrespective of the anesthetic used,11'7" but it is most common after abdominal surgery, and then particu¬ larly after operation on the colon.17·7'1'77' When cholecystitis occurs after surgical intervention, it may do so from anywhere between a few days and several months after Acalculous
The symptoms of the disease may therefore make the diagnosis diffi¬ be trivial and initially cult,17' especially as the usual postoperative abdominal symptoms can mask symptoms of cholecystitis. In addition, the surgeon's attention is directed more to the possibility of complications directly related to the operation, ie, acute pancreatitis and suture insufficiency.71 The symptoms of postoperative acalculous cholecystitis do not differ appre¬ ciably from those of ordinary acute calculous cholecystithe
operation.20·21·23-28
21:1
tis.is·7'·71 Transient bilirubinemia, signs of biliary stasis, and pronounced leukocytosis may occur. Cholecystitis may cause pleural effusion, basal lung changes, and elevation of the diaphragm on the right side.18·" Postoperative acute acalculous cholecystitis may have a more fulminant course than the acute calculous type, with an early appearance of gangrene and perforation.'1··7'17" Cholecystectomy must therefore be performed in the acute stage. The content of the gallbladder may be thick, viscous, and dark green.1 Microscopic examination may show hemorrhages, necroses, and abscesses in the gallbladder wall.ls Postoperative acalculous cholecystitis may be due to biliary stasis with distention of the gallbladder and secon¬ dary chemical inflammation.7'1'-11 Glenn,' and Glenn and Wantz1" claim that biliary stasis is the most important precipitating factor. Several possibilities may be consid¬ ered as a cause of postoperative biliary stasis. Parenteral nutrition can disturb the hormonal regulation of the gallbladder.17 Increased absorption of water causes concen¬ tration of the bile, which, like the mucin from the gall¬ bladder wall, increases the viscosity of the bile. Fever and disturbed fluid balance can increase the concentration and the viscosity of the bile still more. An increased concentra-
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"7S
tion and
viscosity
of the bile may also be due to severe degradation of the blood after large transfusions in asso¬ ciation with the primary operation. Womack and Haffner71 have shown experimentally that marked concentration and high viscosity of the bile alone is sufficient to cause cholecystitis. A tendency of the sphincter Oddi to become spastic with biliary stasis may occur as a result of starva¬ tion, anesthesia, and administration of analgesics.1'''14'"1 Once the patient begins to eat after the operation, with consequent stimulation of contractions of the gallbladder by cholecystokinin, emptying difficulties may occur because of the high viscosity of the bile. Glenn,7 Schwegman and deMuth,7'1 Lindberg et al," and Howard and Delaney7' have reported a correlation between the onset of cholecystitis and the first meal per os after the
operation. The postoperative paralysis
of the digestive tract can increase the intra-abdominal pressure and disturb emp¬ tying of the gallbladder. Pancreatic juice can be forced up into the gallbladder and thereby contribute further to the
development
of cholecystitis. Ischemia of the gallbladder wall as a result of postoper¬ ative shock,7" for example, may weaken the resistance to chemical or bacterial agents and cause cholecystitis.'7 Animal experiments by Golden et al3" have shown that shock with pronounced hypotension can cause focal necrosis of the mucosa of the gallbladder wall. Local hypotension in the liver and gallbladder alone may be sufficient to give rise to these focal gallbladder necroses. According to Laws and Elliott,11' anomalies of the blood vessels supplying the gallbladder result in a decreased flow of blood through the gallbladder wall in association with surgery, especially operations on the colon. Thompson et al83 found thrombi in the blood vessels of the gallbladder and thought them to be a contributory cause of postopera¬ tive cholecystitis. Thrombosis of the cystic artery alone is not regarded as sufficient to cause cholecystitis.1'1"
According to Howard and Delaney,7 generalized hypoperfusion may perhaps be sufficient to cause ischemie injury to the gallbladder wall. This holds true particularly for elderly patients with impaired preoperative circulation. Anemia and decreased lung ventilation as a consequence of the operation can also impair the supply of oxygen to the gallbladder wall in elderly patients. This results in the gallbladder being invaded by bacteria. The temporary improvement often seen during antibiotic therapy is probably a manifestation of such invasion. In our two patients the cholecystitis occurred after a major surgical operation in elderly men. Factors capable of causing biliary stasis and possibly of impairing the blood circulation in the gallbladder wall were present in both. The findings in the gallbladder were typical, ie, no demon¬ strable stone in the gallbladder or bile ducts, dark colored viscous bile, and severe inflammation of the gallbladder wall. The diagnosis of acute acalculous cholecystitis was not confirmed before reexploration of the abdomen, and then a long time after the first operation. But both patients showed evidence suggesting that cholecystitis had begun much earlier, viz obstinate, continual, diffuse abdominal pain; persistent elevation of the body tempera¬ ture; basal lung changes; elevation of the diaphragm on the right side, and transient rise in the serum bilirubin level. It is quite possible that the antibiotic therapy had checked incipient cholecystitis and thereby made the diagnosis more difficult. Cholecystectomy must be regarded as the most suitable treatment of such severe cholecystitis as in our patients. Both patients made a quick recovery. '
Names and Trademarks of Drugs
Nonproprietary
Gentamicin sulfate-Garamj/ci'n. Salicylazosulfapyridine—Accucol, Azidfidine, Rorasul, S.A.S.-500, Sulcolon, W-T Sasp Oral.
References 1. Duncan J: Femoral hernia; gangraene of gallbladder; extravasation of bile; peritonitis; death. North J Med 2:151-153, 1844-1845. 2. Kocher T, Matti H: Ueber 100 Operationen an den Gallenwegen mit Ber\l=u"\cksichtigungder Dauerfolge. Arch Klin Chir 81:655, 1906. 3. Vest SA Jr: Gangrene of the gallbladder. Int Surg Digest 15:131:160, 1933. 4. Fisher WA, quoted by SA Vest Jr: Gangrene of the gallbladder. Int Surg Digest 15:131-160, 1933. 5. Glenn F: Acute cholecystitis following the surgical treatment of unrelated disease. Ann Surg 126:411-420, 1947. 6. Lindberg EF, Grinnan GLB, Smith L: Acalculous cholecystitis in Viet Nam casualties. Ann Surg 171:152-157, 1970. 7. Shaw RC: Posttraumatic acute acalculous cholecystitis in young males. Milit Med 135:210-214, 1970. 8. Wilson TH Jr: Acute acalculous cholecystitis after trauma and surgery. Med Ann DC 39:560-562, 1970. 9. Weeder RS, Bashant GH, Muir RW: Acute noncalculous cholecystitis associated with severe injury. Am J Surg 19:729-732, 1970. 10. Mandelbaum I, Palmer RM: Posttraumatic acalculous cholecystitis. Arch Surg 97:601-604, 1968. 11. Munster AM, Goodwin MN, Pruitt BA Jr: Acalculous cholecystitis in burned patients. Am J Surg 122:591-593, 1971. 12. Wolfson WL, Rothenberg RE: Acute noncalculous cholecystitis. JAMA 106:1978-1980, 1936. 13. Byrne JJ: Acute cholecystitis. Am J Surg 97:156-172, 1959. 14. Munster AM, Brown JR: Acalculous cholecystitis. Am J Surg 113:730\x=req-\ 734, 1967.
15. Thomeret G, Bronstein R: Les cholecystites aigus postoperatoires. Ann Chir 24:1111-1117, 1970. 16. Glenn G, Wantz GE: Acute cholecystitis following the surgical treatment of unrelated disease. Surg Gynecol Obstet 102:145-153, 1956. 17. Knudson RJ, Zuber WF: Acute cholecystitis in the postoperative period. N Engl J Med 269:289-292, 1963. 18. Robertson RD: Noncalculous acute cholecystitis following surgery, trauma and illness. Am Surg 36:610-614, 1970. 19. Ruderman RL: Postoperative acute cholecystitis. Can Med Assoc J 91:1019-1021, 1964. 20. Leon W: Acute cholecystitis following unrelated surgery. Am Surg 20:549-555, 1954. 21. Schwegman CW, deMuth WE Jr: Acute cholecystitis following operation for unrelated disease. Surg Gynecol Obstet 97:167-172, 1953. 22. Levin JF: Death due to gangrenous cholecystitis and peritonitis following unrelated surgery. JAMA 160:1040-1042, 1956. 23. Thompson JW, Ferris DO, Baggenstoss AH: Acute cholecystitis complicating operation for other diseases. Ann Surg 155:489-494, 1962. 24. Sparkman RS: Abdominal emergencies following unrelated surgical procedures. Ann Surg 135:863-874, 1952. 25. Howard RJ, Delaney JP: Postoperative cholecystitis. Ann J Dig Dis 17:213-218, 1972. 26. Lynch KM Jr: Gangrenous cholecystitis after prostatectomy or unrelated surgery and unrelated trauma. J SC Med Assoc 57:209-213, 1961. 27. Bell GA, Holubitsky IB: Acute cholecystitis following unrelated surgery. Can Med Assoc J 101:94-96, 1969. 28. Levin MN: Acute cholecystitis following surgery unrelated to the
Downloaded From: http://archsurg.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 06/01/2015
biliary tract. JAMA 177:120-122, 1961. 29. Wagner DE, Elliott DW, Endahl GL, et al: Specific pancreatic enzymes in the etiology of acute cholecystitis. Surgery 52:259-265, 1962. 30. Robinson TM, Dunphy JE: An experimental study of the effect of pancreatic juice on the gallbladder. Gastroenterology 42:36-47, 1962. 31. Gottfries A: Lysolecithin: A factor in the pathogenesis of acute cholecystitis? Acta Chir Scand 135:213-217, 1969. 32. Anderson DL: Acalculous cholecystitis\p=n-\a possible complication of parenteral hyperalimentation: Report of a case. Med Ann DC 41:448-450,
1972. 33. Womack NA, Haffner H: Cholesterolosis: Its significance in the badly damaged gallbladder. Ann Surg 119:391-410, 1944. 34. Elman R, MacMaster PD: Physiological variations in resistance to bile flow to intestine. J Exp Med 44:151-171, 1926. 35. Neidhart JH, Barbe C, Morin A, et al: Cholecystites aigues post\x=req-\ operatoires non lithiasigues. Lyon Chir 68:106-111, 1972. 36. Detrie P: Cholecystite aigue apres un acute operatoire sans rapport avec les voies biliaires. Presse Med 23:527, 1957. 37. Meissner K: Die Gallenblase als Shockorgan. Langenbecks Arch Chir 336:25-33, 1974. 38. Golden GT, Sears HF, Wangensteen SL: Posttraumatic cholecystitis. Am Surg 39:275-278, 1973. 39. Laws HL, Elliott RL: Postoperative acalculous gangrenous cholecystitis. Am Surg 37:371-374, 1971. 40. Sj\l=o"\dahlR, Wetterfors J: Acute cholecystitis with an occluding thrombus of cystic artery. Acta Chir Scand 140:77-81, 1974. 41. Yedinak PR: Acute cholecystitis following surgery for unrelated disease. Am Surg 25:962-970, 1959. 42. Jouanneau P, Laumonier R, Lecaeur PH: Cholecystites aigues necrosantes secondaires. Mem Acad Chir 1962, pp 593-598. 43. Stern W: Acute cholecystitis following unrelated surgery. Med J Australia 2:876-877, 1964. 44. Strode JE: Acute cholecystitis as a complication. Surgery 2:195-198, 1966. 45. Champeau M, Bruchou P: Cholecystite aigue non lithiasique post\x=req-\ operatoire. Rev Med Chir 41:167-180, 1966. 46. Bronstein R: Cholecystites aigues post-operatoires diagnostic et traitement chirurgical, thesis, Paris, 1968. 47. Herbert JJ, Foucher J, Chevillard R: Cholecystites aigues apres des operations de chirurgie orthopedique lourde. Mem Acad Chir, 1969, pp 653\x=req-\ 658. 48. Roy MB: Cholecystites aigues postoperatoires non lithiasiques. Mem
Acad Chir, 1969, pp 328-329. 49. Hepp M: Cholecystites aigues non lithiasiques postoperatoire: Discussion. Mem Acad Chir, 1969, p 327. 50. Fourati M, Roussel D, Fournial G: Les cholecystites post-operatiores non lithiasiques. Tunis Med 6:351-353, 1971. 51. Callaghan J: Acute cholecystitis following unrelated surgical operations. J Iowa Med Soc, 1972, pp 119-123. 52. Weill E, Weill-Monteil N: Cholecystie aigue non lithiasique apres cure d'un anevrisme rompu de l'aorte abdominale sous-renale. Chirurgie 98:206\x=req-\ 209, 1972. 53. Dichtl K: Akute cholezystitis als postoperative Komplekation. Z Exp Chir 97:1321-1323, 1972. 54. Pelissier E, Fagniez PL: Cholecystites aigue non lithiasique apres intervention orthopedique. Chirurgie 99:52-57, 1973. 55. Montero VF, Garcia Fabian AP: Coleceistis agudas postoperatorias. Rev Esp Enferm Apar Dig 40:107-110, 1973. 56. Eide J, Norbye B, Hartveit F: Fatal haemorrhage following a traumatic liver rupture secondary to post operative perforation of the gallbladder. Acta Chir Scand 141:316-318, 1975. 57. Biebl: Traumatische Cholecystitis. Zbl f Chir 39:2164-2165, 1939. 58. Fackler ML, Brodhead CL: Post-traumatic cholecystitis in evacuees from the Vietnam Conflict. Read Before the Fifth Conference on Surgery, Tokyo, 1971. 59. Winegarner FG, Jackson GF: Posttraumatic acalculous cholecystitis: A highly lethal complication. J Trauma 7:567-569, 1971. 60. Allendorf H: Phlegmonose Cholecystitis nach strumpfen Bauchtrauma. Monatsschr Unfallheilkd 74:385-388, 1971. 61. Vorster C, Bottcher G: Isolierte Gallenblasennekrose als unfallfolge. Chir Praxis 15:45-49, 1971. 62. Blatt JM, Floman Y: Posttraumatic acute acalculous cholecystitis. Int Surg 12:982-983, 1972. 63. Shields MA: Acute acalculous cholecystitis: An important complication of trauma. JR Coll Surg Edinb 18:83-86, 1973. 64. Monfort J, Le Neel JC, Lebotgne J, et al: Les cholecystites aigue non lithiasiques chez les polytraumatises. Ann Chir 27:157-161, 1973. 65. Kitchen PRB: Post-traumatic cholecystitis without gallstones. Med J Aust 2:595-596, 1973. 66. Inglesakis JA, Lanfranchi JP, Migliori G, et al: Cholecystites aigues non lithiasiques chez les polytraumatises. Nouv Presse Med 3:19-21, 1974. 67. Grosbuis S, Beaufils F, Schortgen G, et al: Les necroses vesiculaires aseptiques tartives des polytraumatises. Sem Hop Paris 28:1967-1972, 1974.
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\l=A%o\keAndersson,
Acute Acalculous MD
\s=b\ Two patients with acute acalculous cholecystitis after major surgical operations (cystectomy ad modum Bricker because of carcinoma of the urinary bladder, and proctocolectomy because of ulcerative colitis) are described. Various possible causes of acalculous cholecystitis after operation or after trauma are discussed. Postoperative acute acalculous cholecystitis has a more fulminant course than ordinary calculous cholecystitis. Treatment consists of immediate cholecystectomy. (Arch Surg 111:1097-1101, 1976)
cholecystitis occurring after trauma or operation both is rare. Only a few single postoperative cases had been reported up to 1947,1 after which the complica¬ tion began to receive wider attention. It was not until later that acute cholecystitis after trauma was reported," and then particularly after multiple and widespread war inju¬ ries. The cause of postoperative cholecystitis and that of posttraumatic cholecystitis are probably identical. In most of the cases on record the patients with injuries had also been operated on.'"11 A cute
Ü
or
'
"
REPORT OF CASES Two cases of postoperative acute acalculous cholecystitis were treated at the Department of Surgery, Kristianstad, Sweden in 1974 and 1975, respectively, and are reported below. Cask l.-A 63-year-old man with carcinoma of the urinary bladder was operated on ad modum Bricker under meperidine (petidina) and halothane (Fluothane) plus nitrous oxide and oxygen anesthesia. His blood pressure fell transiently in the induction phase of the anesthesia. The operation, during which the patient received 4 units of blood, was otherwise uncomplicated. Parenteral nutrition was given exclusively until the sixth postop¬ erative day, after which nutrition per os was started. However,
Accepted
Cholecystitis
for publication June 7, 1976. From the Department of Surgery, Central Hospital, Kristianstad, Sweden. Reprint requests to Department of Surgery, Central Hospital, S-291, 85 Kristianstad, Sweden (Dr J\l=o"\nsson).
owing
to
postoperative
intestinal
paralysis, parenteral
nutrition
resumed on the ninth day after the operation. The first few days after the operation the patient was subfebrile. Wound infection was observed on the sixth day, and chest roentgenogram revealed bilateral small basal atelectasis. On the basis of the results of culture, which had given growth of Escherichìa coli and Enterobacteriaceae, and of antibiotic suscep¬ tibility tests, the patient was treated with tetracycline. His condition improved until the 14th day after the operation, when he complained of stabbing pain in the right side of the chest during deep inspiration. Chest roentgenogram showed an elevated dia¬ phragm on the right side and basal parenchymal changes suggest¬ ing pneumonia. Tetracycline therapy was replaced by penicillin V. His condition improved and he was sent home on the 40th day was
after the
operation.
During his stay in hospital the patient had had a mild transient
increase in serum bilirubin level and postoperative anemia. Three weeks after discharge from hospital he was again admitted because of abdominal pain and a body temperature of 39 C. During his stay at home he had almost continually experienced mild pain in the upper portion of the abdomen. Pyelitis was assumed and treatment with ampicillin was started, but the abdominal pain increased in intensity and the temperature continued to rise. The patient became severely jaundiced, the serum bilirubin level rose to 6.1 mg/100 ml, and liver function tests showed signs of biliary stasis. The patient was operated on because of assumed acute cholecystitis; this operation was performed 74 days after the first operation. The gallbladder was found to be severely infected and gangrenous, and the cystic duct was slender. The gallbladder contained viscous, dark green bile, but no demonstrable stone. Microscopic examination showed severe acute inflammation with necroses, hemorrhages, and intramural abscesses. The postoperative course was uneventful and the patient has since had no abdominal symptoms. This patient had never previously had any symptoms or signs of gallbladder disease. Case 2.—In 1975, a 57-year-old man who had for some 30 years had ulcerative colitis was admitted to the Department of Orthope¬ dics because of sciatica. For many years the colitis had been treated with salicylazosulphapyridine (Salazopyrin), and during the last three years with corticosteroids. In 1971, assumed liver cirrhosis had been confirmed by needle biopsy aspiration of the liver. Owing to an increase in the severity of the ulcerative colitis
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Table 1
.—Postoperative
Acute
Cholecystitis No. of Cases
Without Stones Men
Source, yr
Women
With Stones
Sex Not Mentioned
Men
Women
Sex Not Mentioned
Sex Not Mentioned
Glenn.' 1947
12
Sparkman,7' 1952 Schwegman and deMuth," 1953 Leon,20 1954 Glenn and Wantz," 1956
Levin," 1956 Detrie,36 1957 Yedinak," 1959 Levin," 1961
Lynch,» 1961 Jouanneau et
al," 1962
al," 1962 Knudson and Zuber," 1963 Stern,' 1964 Ruderman," 1964 Strode." 1966 Champeau & Bruchou.' 1966 Bronstein," 1968 Herbert et al,'' 1969
Thompson
Bell and
et
Holubitsky,77 Roy," 1969 Hepp," 1969
52
46
10
10
1969
Thomeret and Bronstein," 1970 Robertson, » 1970 Fourati et al,*0 1971 Laws and Elliott," 1971 Callaghan.·' 1972 Howard and Delaney, 1972 Weill & Weill-Monteil. 1972 Dichtl,- 1972 Pelissier & Fagneiz," 1973 Montero & Garcia Fabian" 1973 Meissner,'7 1974 Eide et al, 1975 Present series '
'
Total
67
10
42
76
with frequent blood-stained stools, the patient was given blood transfusions on repeated occasions. On Feb 28, 1974, the patient was jaundiced and the serum bilirubin level rose to a maximum of 9.0 mg/100 ml. The rise was ascribed to the many blood transfu¬ sions. The ulcerative colitis became worse, and on March 20, 1974, the patient underwent a proctocolectomy after one week's preparation with parenteral nutrition. On the second postoperative day his body temperature rose to 40 C. Sepsis was suspected and treat¬ ment with ampicillin and gentamicin sulfate was started. On March 24 wound infection supervened and culture showed typical colonie flora susceptible to the antibiotics the patient was receiv¬ ing. Nutrition per os was given from March 27 to April 2. The patient complained continually of diffuse abdominal pain. He was sent home on April 23. On May 5 the patient sought advice because of stabbing abdominal pain and was treated with dilation of the ileostomy. Owing to increasing severity of the diarrhea the patient was admitted to hospital again on May 12 and complete parenteral nutrition was started. The abdominal pain persisted and temper¬ ature peaks of up to 39 C were recorded. On June 7 he was operated on because of the abdominal pain and the assumed diagnosis of acute cholecystitis, with a serum bilirubin level of 6.2 mg/100 ml. The gallbladder was severely distended and infected. Peroperative cholangiography showed no passage of contrast medium to the
46
79
26
reason choledochotomy was done. The bile duct was not found to contain any stone, but only thick, viscous bile. Neither did the gallbladder contain any demon¬ strable stone. Histopathologic examination of the gallbladder revealed acute phlegmonous inflammation with severe discolora¬ tion of the mucosa. The patient's postoperative course was un¬ eventful.
duodenum, for which common
COMMENT
In only 5% to 10% of all cases of acute cholecystitis is the condition acalculous.1711 On the other hand, the frequency of the acalculous form (Tables 1 through 3) is higher among published cases of postoperative and posttraumatic chole¬ cystitis. Acalculous cholecystitis is more common (92%) among the posttraumatic cases than among the postopera¬ tive cases (47%). This difference may perhaps be explained by differences in the ages of the patients in the two groups. In the posttraumatic cases the lesions were mostly war injuries and the patients mostly young. Calculous cholecystitis after operation may be simply a coincidence and not have anything to do with the operation.17' Postoperative acute acalculous cholecystitis occurs at all Judging ages, but 75% of the patients are over 50 years.1
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""
Table 2—Posttraumatic and
Postoperative Acute Cholecystitis No. of Cases With Stones
Without Stones
Source, yr
Men
Women
Sex Not Mentioned
Men
Women
Biebl," 1939
Mandelbaum and Palmer,'' 1968 Lindberg et al,6 1970 Shaw, 1970 Weeder et al," 1970 Wilson,' 1970 Fackler & Brodhead," 1971 Winegarner & Jackson,'' 1971 Munster and Brown," 1967 Howard and Delaney," 1972 Allendorf,' 1971 Vorster & Böttcher," 1971 Blatt & Floman," 1972 Neidhart et al,35 1972 Golden and Sears," 1973 Shields,'" 1973 Monfort et al," 1973 Kitchen," 1973 Inglesakis et al," 1974 Grosbuis et al,'" 1974 Total
12
82
Table 3.—Sex and
Age Distribution
for Patients With and Without Stones
Without Stones
Postoperative acute cholecystitis Sex
Age, yr
With Stones
Men
Women
Ratio
Men
Women
Ratio
67 59
10 65
7:1
42 61
46 60
1:1
52
78
Posttraumatic and acute
postoperative cholecystitis
82
Sex
Age, yr
from the cases on record, the condition is much more common in men than in women.1 Ordinary acute cholecys¬ titis, on the other hand, is much more common among women, but the difference decreases with increasing age. This variation of frequency with age holds also for postop¬ erative calculous cholecystitis, while the ratio of men to women with acalculous cholecystitis is as high as 7:1 (Table '
3).
cholecystitis can occur after any form of operation, irrespective of the anesthetic used,11'7" but it is most common after abdominal surgery, and then particu¬ larly after operation on the colon.17·7'1'77' When cholecystitis occurs after surgical intervention, it may do so from anywhere between a few days and several months after Acalculous
The symptoms of the disease may therefore make the diagnosis diffi¬ be trivial and initially cult,17' especially as the usual postoperative abdominal symptoms can mask symptoms of cholecystitis. In addition, the surgeon's attention is directed more to the possibility of complications directly related to the operation, ie, acute pancreatitis and suture insufficiency.71 The symptoms of postoperative acalculous cholecystitis do not differ appre¬ ciably from those of ordinary acute calculous cholecystithe
operation.20·21·23-28
21:1
tis.is·7'·71 Transient bilirubinemia, signs of biliary stasis, and pronounced leukocytosis may occur. Cholecystitis may cause pleural effusion, basal lung changes, and elevation of the diaphragm on the right side.18·" Postoperative acute acalculous cholecystitis may have a more fulminant course than the acute calculous type, with an early appearance of gangrene and perforation.'1··7'17" Cholecystectomy must therefore be performed in the acute stage. The content of the gallbladder may be thick, viscous, and dark green.1 Microscopic examination may show hemorrhages, necroses, and abscesses in the gallbladder wall.ls Postoperative acalculous cholecystitis may be due to biliary stasis with distention of the gallbladder and secon¬ dary chemical inflammation.7'1'-11 Glenn,' and Glenn and Wantz1" claim that biliary stasis is the most important precipitating factor. Several possibilities may be consid¬ ered as a cause of postoperative biliary stasis. Parenteral nutrition can disturb the hormonal regulation of the gallbladder.17 Increased absorption of water causes concen¬ tration of the bile, which, like the mucin from the gall¬ bladder wall, increases the viscosity of the bile. Fever and disturbed fluid balance can increase the concentration and the viscosity of the bile still more. An increased concentra-
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"7S
tion and
viscosity
of the bile may also be due to severe degradation of the blood after large transfusions in asso¬ ciation with the primary operation. Womack and Haffner71 have shown experimentally that marked concentration and high viscosity of the bile alone is sufficient to cause cholecystitis. A tendency of the sphincter Oddi to become spastic with biliary stasis may occur as a result of starva¬ tion, anesthesia, and administration of analgesics.1'''14'"1 Once the patient begins to eat after the operation, with consequent stimulation of contractions of the gallbladder by cholecystokinin, emptying difficulties may occur because of the high viscosity of the bile. Glenn,7 Schwegman and deMuth,7'1 Lindberg et al," and Howard and Delaney7' have reported a correlation between the onset of cholecystitis and the first meal per os after the
operation. The postoperative paralysis
of the digestive tract can increase the intra-abdominal pressure and disturb emp¬ tying of the gallbladder. Pancreatic juice can be forced up into the gallbladder and thereby contribute further to the
development
of cholecystitis. Ischemia of the gallbladder wall as a result of postoper¬ ative shock,7" for example, may weaken the resistance to chemical or bacterial agents and cause cholecystitis.'7 Animal experiments by Golden et al3" have shown that shock with pronounced hypotension can cause focal necrosis of the mucosa of the gallbladder wall. Local hypotension in the liver and gallbladder alone may be sufficient to give rise to these focal gallbladder necroses. According to Laws and Elliott,11' anomalies of the blood vessels supplying the gallbladder result in a decreased flow of blood through the gallbladder wall in association with surgery, especially operations on the colon. Thompson et al83 found thrombi in the blood vessels of the gallbladder and thought them to be a contributory cause of postopera¬ tive cholecystitis. Thrombosis of the cystic artery alone is not regarded as sufficient to cause cholecystitis.1'1"
According to Howard and Delaney,7 generalized hypoperfusion may perhaps be sufficient to cause ischemie injury to the gallbladder wall. This holds true particularly for elderly patients with impaired preoperative circulation. Anemia and decreased lung ventilation as a consequence of the operation can also impair the supply of oxygen to the gallbladder wall in elderly patients. This results in the gallbladder being invaded by bacteria. The temporary improvement often seen during antibiotic therapy is probably a manifestation of such invasion. In our two patients the cholecystitis occurred after a major surgical operation in elderly men. Factors capable of causing biliary stasis and possibly of impairing the blood circulation in the gallbladder wall were present in both. The findings in the gallbladder were typical, ie, no demon¬ strable stone in the gallbladder or bile ducts, dark colored viscous bile, and severe inflammation of the gallbladder wall. The diagnosis of acute acalculous cholecystitis was not confirmed before reexploration of the abdomen, and then a long time after the first operation. But both patients showed evidence suggesting that cholecystitis had begun much earlier, viz obstinate, continual, diffuse abdominal pain; persistent elevation of the body tempera¬ ture; basal lung changes; elevation of the diaphragm on the right side, and transient rise in the serum bilirubin level. It is quite possible that the antibiotic therapy had checked incipient cholecystitis and thereby made the diagnosis more difficult. Cholecystectomy must be regarded as the most suitable treatment of such severe cholecystitis as in our patients. Both patients made a quick recovery. '
Names and Trademarks of Drugs
Nonproprietary
Gentamicin sulfate-Garamj/ci'n. Salicylazosulfapyridine—Accucol, Azidfidine, Rorasul, S.A.S.-500, Sulcolon, W-T Sasp Oral.
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