Acalculous Cholecystitis in Critically Ill Patients Thomas N. Long, MD, Seattle, Washington David M. Heimbach, MD, Seattle, Washington C. James Carrico, MD, Seattle, Washington
Acute acalculous cholecystitis is a treacherous and potentially lethal disease. It may occur in patients without known biliary tract disease who are severely compromised by trauma or gastrointestinal dysfunction and require prolonged intensive care. Its onset is insidious, the presenting symptoms are inconstant, and its neglect can lead to necrosis of the gallbladder with sepsis and death. Previous reports reflect experience with Vietnam evacuees after severe trauma [l-3], patients with pediatric disease [4], burned patients [5], and civilian populations of critically ill patients [6-121. The present study describes seventeen patients who developed acalculous cholecystitis during a period of intensive care after unrelated surgical operations, severe trauma, or burns. Despite the subtleties of the presenting signs and symptoms, awareness of the problem, recognition of predisposing factors, and a careful search for clinical signs can lead to an early diagnosis. When the diagnosis is made, drainage of the gallbladder by tube cholecystostomy can be successfully employed without the added risk of formal laparotomy. Material and Methods Harborview Medical Center is a major trauma and burn referral center, admitting approximately 5,000 traumatized patients and 300 burned patients annually. One hundred fifty traumatized patients and 100 burned patients are admitted to the intensive care units each year. During the three year period from July 1974 to July 1977, twelve patients with acalculous cholecystitis were identified from a pool of 750 critically ill patients, an incidence of 1.6 per cent. An additional five patients with acalculous cholecystitis were encountered on the surgical services at the four hospitals in the University of Washington system From the Department of Surgery, School of Medicine, University of Washington, Seattle, Washington. Reprint requests should be addressed to C. James Carrico, MD, Department of Surgery, Harborview Medical Center, 325 Ninth Avenue, Seattle, Washington 98104. Presented at the Forty-Ninth Annual Meeting of the Pacific Coast Surgical Association, Newport Beach, California, February 19-22, 1978.
Volume 138, July 1978
during this same time period. Four of these patients had undergone extensive surgical procedures and all had required int.ensive care but did not have trauma as a predisposing feature. To better identify specific “risk factors” and to serve as a control group, fifteen additional patients were reviewed. These were patients who had comparable injuries requiring prolonged intensive care but who did not develop acalculous cholecystitis.
Results
Of seventeen patients with acalculous cholecystitis, fourteen were male and three female. Mean age was forty-six years (range, 15 to 82 years). Four patients were burn victims, eight suffered multiple system trauma, four had undergone extensive unrelated surgical procedures, and one was being treated for massive drug overdose. The mean time from admission to diagnosis was three weeks, but the range was extremely large, from three days in the woman with a polydrug overdose to ninety days in the patient with an 85 per cent total body surface burn who died and was diagnosed at autopsy. The diagnosis was made during the first week in one patient, during the second week in five, during the third week in four, fourth week in two, and after the fourth week in five. The findings at the time of diagnosis are presented in Table I. A specific preoperative diagnosis of acalculous cholecyst.itis was made in eleven patients. Five patients were operated on with another preoperative diagnosis and acalculous cholecystitis was found at operation. (Table II.) One patient died with burn wound sepsis, and a necrotic gallbladder was found at autopsy. Sixteen patients underwent operation; fourteen cholecyst.ostomy and two cholecystectomy. In all cases the operative findings were consistent: a dense, thickened, edematous, severely inflamed gallbladder without stones but containing a thick, black,
31
Long, Heimbach, and Carrico
TABLE I
Flndings at Time of Diagnosis 68% 94% 65% 59% 53 % 24% 24 %
Fever WBC > 10,000 Bilirubin >2 mg/lOO ml RUQ tenderness RUQ pain RUQ mass NauseaIemesis Note: RUQ = right upper quadrant.
TABLE II
Five Patients Operated on with another Preoperative Diagnosis
Preoperative Diagnosis
Postoperative Diagnosis Acalculous cholecystitis Gangrenous gallbladder dome with colon adhesion Interloop abscess Acalculous cholecystitis, incidental Small bowel obstruction Acalculous cholecystitis, incidental Bleeding Curling’s ulcer Necrotic gallbladder, incidental
Appendicitis lschemic colitis lntraabdominal
abscess
Small bowel obstruction Bleeding Curling’s ulcer
TABLE III
Causes of In-Hospital Mortality Interval after Cholecystectomy
Age (yr)
Cause(s) of Death
44
Burn wound sepsis Perforated acalculous cholecystitis Bronchopneumonia (necropsy) lntraabdominal abscesses + septic death Herpes pneumonia Renal failure Prolonged respiratory insufficiency Terminal bronchopneumonia Sepsis from peripancreatic abscess secondary to splenectomy Acute renal failure Decreasing central nervous system function Burn wound sepsis Hepatorenal syndrome
45 51 81 50
42
TABLE IV
24 hr 18da 4mo
3 wk
30 da
Risk Factors Factor
Patients
Controls
Morphine >6 days Prolonged ileus/NPO Mechanical ventilation More than 1 recent operation Multiple blood transfusions (>lO) Open wound/abscess Hyperalimentation (>3 days) PEEP (>24 hr) Refeeding phenomenon
77% 71% 59% 53% 53% 47 % 47% 35% 24%
40% 73% 60% 40% 60% 33 % 33% 20% N/A
Note: NPO = nothing by mouth; PEEP = positive end-expiratory pressure.
32
“crankcase oil” bile. Severe inflammation was found on all histologic sections, and five patients had focal necrosis or overt gangrene of the gallbladder at operation. The two patients with gangrene underwent cholecystectomy. Bile cultures were positive in eight of fifteen patients. Predominant organisms in decreasing order of frequency were: Klebsiella pneumonia (4 patients); Pseudomonas aeruginosa (2); Clostridium novii (1); enterobacter species (1); and Escherichia coli (I). It is of interest that three patients with positive klebsiella cultures had simultaneous positive klebsiella cultures at distant sites. Six of the seventeen patients died during their hospitalization, attesting to the severity of their associated diseases. (Table III.) The patient with undiagnosed acalculous cholecystitis died with fulminating burn wound sepsis. The necrotic gallbladder may have contributed to his demise. Another patient died 24 hours after his cholecystostomy. This patient had had multiple intraabdominal abscesses and his acalculous cholecystitis was an incidental finding at the time of abscess drainage. He remained in septic shock and died 24 hours after surgery. It is unlikely that his acalculous cholecystitis was a primary cause of death. The remaining four deaths occurred more than two weeks postoperatively and all were due to underlying illnesses. It is unlikely that the cholecystitis contributed to any of these patients’ deaths. Both patients undergoing cholecystectomy did well after operation, with decreasing fever and gradual improvement of their underlying illness. Twelve of the fourteen patients treated with cholecystostomy rapidly improved after operation. There were two complications associated with cholecystostomy. One tube was accidently removed and required replacement and one patient remained febrile in the postoperative period due to a large pericholecystic phlegmon present at the time of operation. This slowly responded to antibiotics and nonoperative treatment. Nine patients underwent tube cholangiography in the postoperative period. Once the acute attack had subsided, the x-ray films revealed no gallbladder, cystic duct, or common duct disease. Oral cholecystography was done in three instances; in one there was nonvisualization of the gallbladder and in two no abnormalities were revealed. Only two patients have required cholecystectomy during the short follow-up period. One patient experienced mild recurrent abdominal pain and had a nonvisualized gallbladder on oral cholecystogram. The other patient with the pericholecystic phlegmon described above maintained persistent mild right upper quadrant tenderness and discomfort after discharge.
The American Journal of Surgery
Acalculous Cholecystitis
.jt operation a chronically inflamed gallbladder encased in dense scar was found. The remaining patients have remained asymptomatic and are being followed regularly. The charts of all patients have been analyzed for the presence of previously suggested risk factors. The results of t>his analysis are shown in Table IV.
Comments Eliology 4 review
of the literature reveals that any patient sustaining prolonged critical illness is at risk of deve:.oping severe stasis within the gallbladder, bile inspissation and eventual obstruction of the cystic duct, and acute cholecystitis. A number of specific “risk factors” have been suggested by various authors. Glenn and Wantz [13] in their initial description of acalculous cholecystitis suggested that prolonged fasting, anesthesia, analgesia, and dehydration with resultant bile concentration set the stage for induction of gallbladder contractions producing mechanical outflow obstruction at the gallbladder neck. The Vietnam experience [I--31 revealed several other characteristics unique to these patients. Approximately 90 per cent had open draining wounds and had received blood transfusions of more than 10 units. Lindberg, Grinnan, and Smith [I] suggested that the increased bile pigment load secondary to t,ransfusions might injure the gallbladder, but at the present time this remains unproven [14]. Only half our patients received more than 10 units of blood and a similar proportion of patients who did not develop cholecystitis underwent equivalent transfusions. Hyperalimentation has been suggested as a risk factor because it decreases stimulus to the biliary tract and allows concentration of the bile [12]. This ma.y be aggravated by narcotics, volume depletion, and nasogastric suction [5]. Eight of our patients unlderwent hyperalimentation for more than three days. Seventy-seven per cent of our patients received mere than 8 mg morphine sulfate daily for six days or more. Sixty per cent of our patients underwent prolonged ventilatory support, and more than half of them were on positive end-expiratory pressure (PEEP). Positive pressure ventilation can be shown to produce hyperbilirubinemia, decreased portal blood flow, and reduced flow through the choledochoduodenal junction in dogs [15,16]. The other series in the literature do not mention ventilatory support as a risk factor. However, the experimental evidence and the high association in our series suggest a possible etiologic role, especially when PEEP is required. It is likely, as suggested by Golden,
Vohne 136,July
1979
Sears, and Wangensteen [IO], that the disease is a mosaic of many features, all of which may produce bile stasis. Predisposing factors, such as volume depletion, prolonged gastrointestinal rest, hyperalimentation, ventilatory support, morphine administration, multiple transfusions, and presence of infected wounds may all increase the likelihood of inducing inspissated bile. In our series, the following risk factors appeared to be more prevalent in patients who developed acalculous cholecystitis than in those who did not: morphine administration; mechanical ventilation with PEEP; and possibly, hyperalimentation and open wounds. However, the comparative number of patients is too small to draw any firm conclusions. The presence of any or all of these predisposing factors should alert the clinician to think of the disease when a patient develops any symptom referable to the right upper quadrant.. Dlagnosis
Although fever and an elevated white blood cell count were the most consistent findings in our series, these findings are unfortunately nonspecific in a group of severely ill postoperative patients. On the other hand, persistent fever, without other explanation, was the stimulus to investigate the biliary tract in a significant number of our patients. The findings of mass, pain, or tenderness were important when present, but there was no combination of symptoms that was diagnostic in all patients. Signs of nausea or vomiting were present in only four patients. Approximately half the patients complained of right upper quadrant pain, and these patients usually had specific tenderness in the right upper quadrant. Despite markedly distended gallbladders, fewer than one fourth of the patients demonstrated a palpable right upper quadrant mass or fullness. An elevated bilirubin level was present in 65 per cent of the group but was also found in 64 per cent of the patients in the control group who had received more than 10 units of blood. This bilirubin elevation was probably related more to the number of transfusions and episodes of hypotension than to biliary tract disease [19]. The presenting findings in our series do not markedly differ from those in other series, and differences may in reality represent the stage of the disease at the time of diagnosis rather than any major differences among patients. In earlier series, before the disease was well described, the diagnosis appears to have been made late in the course of the disease. As clinicians have become more familiar with the disease and the potential hazards of prolonged intensive care, earlier diagnosis should be possible before classic findings of palpable masses occur.
33
Long, Heimbach, and Carrico
The severity of these patients’ underlying illness and the multiple life-support devices required by them make the usual diagnostic procedures for biliary tract disease inconvenient and even potentially hazardous. Intravenous cholangiography, in our hands, has generally been unrewarding in these patients, resulting in nonvisualization of the entire biliary tree even in patients without elevated bilirubin levels. On the other hand, with continually improving technology and increasing experience, ultrasonic examination of the gallbladder may be of value in the diagnosis of equivocal cases.
Treatment
Once the diagnosis is suspected, immediate operation is the treatment of choice, with either removal of the infected gallbladder or decompression of the biliary tract. Medical therapy is unlikely to be rewarding. Most of our patients were receiving treatment that would normally be accepted as conservative management of cholecystitis. For example, most were receiving antibiotics and their gastrointestinal tracts were at rest. If the diagnosis can be made preoperatively, a cholecystostomy tube can be placed under local anesthesia with minimal disruption of physiologic function. Our patients were all critically ill and many had undergone multiple operations, and an additional anesthetic with a formal exploration is not necessary for the treatment of cholecystitis without associated cholangitis. Athough the adequacy of cholecystostomy in the treatment of suppurative cholangitis is controversial, its use in the emergency treatment of cholecystitis is on firmer ground [17,18]. Ternberg and Keating [4] used cholecystostomy in all seven of their pediatric patients, with good results in six. In our series tube cholecystostomy resulted in prompt resolution of the acute process in twelve of fourteen patients. The one patient who died within 24 hours of operation died of overwhelming sepsis from multiple intraabdominal abscesses. The other patient, with a pericholecystic phlegmon, defervesced slowly and might have benefited more promptly from cholecystectomy if it could have been done safely. He, however, suffered from familial thrombocytopenia, and this made extensive dissection through acutely inflamed tissue inadvisable. We do not know the long-term outcome of cholecystostomy in our patients, but we know that seven of nine surviving patients with cholecystostomy have not required subsequent cholecystectomy. In the absence of lithogenic bile, stone formation may not be a problem, but only prolonged follow-up will answer this question.
34
Conclusions inciting (1) The presence of any circumstance sluggish bile flow should alert the clinician caring for critically ill patients to the possibility of acalculous cholecystitis. (2) The presence of unexplained fever or elevated white blood cell count, particularly with any symptoms relating to the right upper quadrant, requires prompt investigation of the biliary tract. (3) Effective treatment can be instituted promptly by performance of cholecystostomy under local anesthesia in most cases. (4) If treatment is prompt and appropriate, the disease subsides and the patient’s morbidity returns to that of his underlying illness. Summary Acute acalculous cholecystitis is a treacherous and potentially fatal complication of severe trauma and prolonged intensive care. The present study reviews seventeen patients seen between June 1974 and August 1977. Although specific causes have been suggested-transfusions, fractures with immobilization, central hyperalimentation, respirators, and “refeeding’‘-there was no common denominator among our patients. Refeeding was a feature in 30 per cent of our cases, 50 per cent received more than 10 units of blood, 65 per cent had prolonged gastric suction, and 60 per cent had mechanical ventilation. Thus, although all suggested causes were seen, no single factor was dominant. Clinical presentation in this civilian group resembles that of other reports, but differs in remarkable areas. Only 65 per cent of our group presented with one or more of the classic symptoms of cholecystitis-pain, tenderness, or mass. Sixty-five per cent of patients had elevated bilirubin levels. However, the same incidence of hyperbilirubinemia was seen in another group of traumatized patients who did not develop acalculous cholecystitis. The smoldering and nonclassic presentation frequently delayed diagnosis for several days. It was correctly made in 65 per cent, discovered at autopsy in one patient, and found at laparotomy for “sepsis” in the rest. The present report is unique because 88 per cent of the patients had cholecystostomy as initial therapy. Although five patients who underwent operation ultimately succumbed, cholecystitis could be implicated in only one. This patient died of sepsis at 24 hours but also had multiple unrelated intraabdominal abscesses at surgery. Clinical presentation is more complex than previously reported and simple cholecystostomy is an effective mode of therapy in these critically ill patients.
The American Journal of SWerY
Acalculous
References 1. Lindberg EF, Grinnan GLB, Smith L: Acalculous cholecystitis in Viet Nam casualties. Ann Surg 171: 153, 1970. 2. Weeder RS, Bashant GH, Muir RW: Acute noncalculous cholecystitis associated with severe injury. Am J Surg 119: 729, 1970. 3. Winegarner FG, Jackson GF: Post-traumatic acalculous cholecystitis: a highly lethal complication. J Trauma 11: 567, 1971. Ternberg JL, Keating JP: Acute acalculous cholecystitis. Arch Surg 110: 543, 1975. Munster AM, Goodwin MN, Pruitt BA: Acalculous cholecystitis in burn patients. AmJ Surg 122: 591, 1971. Mandelbaum I, Palmer RM: Post-traumatic acalculous cholecystitis. Arch Surg 97: 601, 1968. Skillman JJ, Bushnell LS, Goldman H, Silen W: Respiratory failure, hypotension, sepsis, and jaundice. Am J Surg 117: 523, 1969. 8. Munster AM, Brown JR: Acalculous cholecystitis. Am J Surg 113: 730, 1967. 9. Thompson JW, Ferris DO, Baggenstoss AH: Acute cholecystitis as a complication of other diseases. Ann Surg 155: 489, 1962. IO. Golden GT, Sears HF, Wangensteen SL: Post-traumatic cholecystitis. Am Surg 39: 276, 1973. 11. Howard RJ, Delaney JP: Post-traumatic cholecystitis. JAMA 218: 1006, 1971. 12. Anderson DL: Acalculous cholecystiiis: a possible complication of parenteral hyperalimentation. Med Ann Disfr Columbia 41: 448. 1972. 1:3. Glenn F, Wantz GE: Acute cholecystitis following the surgical treatment of unrelated disease. Surg Gynecol Obstet 102: 510, 1956. 14. lnglesakis JA, Lanfranchi JP, Migliori G, et al: Cholecystites Aigues non Lithiasuques Chez les Polytraumatises. Nouv Press Med3: 19, 1974. l!j. Johnson EE, Hedley-White J: Continuous positive pressure ventilation and portal flow in dogs with pulmonary edema. J Appl Physiol33: 365, 1972. 16. Johnson EE, Hedley-White J: Continuous positive pressure ventilation and choledochoduodenal flow resistance. J Appl Physio139: 937, 1975. I?. Gagic N, Frey CF: The results of cholecystostomy for the treatment of acute cholecystitis. Surg Gyneco/ Obstet 140: 255, 1975. 18. Gingrich RA, Awe WC, Boyden AM. Peterson CG: Cholecystostomy in acute cholecystitis. Am J Surg 116: 310, 1968. 19. Kantrowitz PA, Jones WA, Greenberger NJ, lsselbacher KJ: Severe postoperative hyperbilirubinemia simulating obstructive jaundice. N fngl J Mecf 276: 591, 1967.
Discussion George F. Sheldon (San Francisco, CA): I congratulate the authors on calling to our attention the insidious presentation and lethal consequence of acalculous cholecystitis. Moreover, their low mortality rate attests to the awareness their unit has of this pernicious disease. The disease was diagnosed preoperatively in eleven of seventeen patients; only one undiagnosed case is reported in their series. During the past two years we have seen more than twenty patients with acalculous cholecystitis and in recent months have noted five patients without dehydration or sepsis who are receiving long-term parenteral nutrition. Although we can only speculate as to the potential cause of this illness, it is clearly associated with critical and
Volume 136, July 1978
Cholecystitis
prolonged illness and bowel rest. Moreover, it is possible that the lack of fat stimulus to the secretion of bile may have an etiologic relationship to the development of this illness which occurs in patients deprived of oral feeding. We currently treat patients by intermittent administration of butter or some other fat source down the nasogastric tube to stimulate the gallbladder to contract and prevent it from remaining in a state of stasis. In addition, we have been very pleased with the diagnostic ac’curacy of sonography. Many of our patients on long-term parenteral feeding are routinely followed with ultrasound examination of their gallbladder to determine the potential development of biliary distention and bile sludge. Have you any diagnostic methods that are helpful other than those noted which were nonspecific? Although the results of the bacteriologic study of the bile cultures were reported, I would be interested in knowing the results of cultures of the gallbladder wall. We have found that cholecystostomy is often a good method for treating this illness; if the gallbladder is totally necrotic, however, one wonders if cholecystostomy is the optimal rnethod of treatment. Newlin Hastings (Los Angeles, CA): I would like to complement this presentation of adult pathology with a few observations based on pediatric pathology. There may be some clues for common denominators: stasis and infection. Acute acalculous cholecystitis is relatively more common in infanc,y and early childhood than in adulthood. In the youngest neonate and infant acute cholecystitis characteristically has factors for gallbladder stasis such as congenital stenosis of the duct or malformations like diverticuli or choledochal cyst. With stasis there is a milieu which is excellent for the growth of bacteria in bile. In older children characteristically there are infections either antecedent to or associated with respiratory or enteric infections. Often the enteric infection does not have a specific organism as salmonella; it may be associated with mesenteri.c adenitis. With all these infections small infants and children are often dehydrated, contributing to the development of the stasis which, with bacterial growth, leads to the development of cholecystitis. Specific organisms may be found: staphylococcus; streptococcus; or salmonella (much more common in previous years than recently). In some environments there is still a significant incidence of acalculous cholecystitis with salmonella in adult patients. The incidence of acute acalculous cholecystitis was much higher in infancy and childhood in the preantibiotic era; perhaps our use of drugs has cut down on this frequency. The ratio of bile salts and cholesterol and the solubility may be upset, of course, with the dehydration and stasis, increasing the favorable circumstances for cholecystitis. Acute obstruction may also create this situation. The late J. Norton Nichols, a member of this Society, had a patient for whom he performed a simple cholecystostomy for traumatic injury. William F. Pollock (Santa Monica, CA): Dr. Sheldon indicated the use of sonography to demonstrate sludging
35
Long, Heimbach, and Carrico
in the gallbladder. There is a form of ultrasound now available which demonstrates real time action and is used by obstetricians to show the function or site of the actual fetal parts. It might be a wonderful adaptation to this particular problem because this is real ultrasonography, SO that instead of a picture one sees a “fluoroscopic image.” Edward Passaro Jr (Los Angeles, CA): I have three brief comments First, a colleague of mine, Dr. Donald Wagner, as a resident made the same observation that the authors have made with regard to this clinical situation. It was his observation that the bile of these patients contained trypsin, presumably from reflux of pancreatic juice into the biliary system. He produced this black, machinery-oil bile by introducing trypsin into the bile of dogs. This might offer a way to investigate the cause; specimens could be examined for trypsin content. The second point concerns diagnostic technics. In attempting to do liver biopsies at our hospital, we occasionally introduce the needle into the gallbladder. It may be possible, therefore, to percutaneously and transhepatically aspirate some of this material from the gallbladder. Cultures and contrast studies for stones could be done, and if indicated, the hypothesis of trypsin reflux could be investigated. Last but not least, inasmuch as this may be iatrogenically produced, we should seek methods to correct this. Cholecystokinin will cause contraction of the gallbladder. In patients who are critically ill and who will be hospitalized for a long time, should we consider the use of cholecystokinin to periodically flush the gallbladder? Leon Morgenstern (Los Angeles, CA): In acalculous cholecystitis we should not necessarily infer the absence of common duct stones, because we have encountered a number of ductal stones in patients with this condition. Accurate radiographic evaluation of the common duct is imperative during the procedure (for example, cholecystocholangiography) or as soon as feasible after the procedure, by whatever radiographic maneuver is feasible. (Slide) This is a gallbladder from a patient operated on just last week. She was bedridden, had thrombophlebitis, was receiving steroids for rheumatoid arthritis, and was dehydrated. (Slide) The cholecystitis here is mild. Operative cholangiography shows several stones in the common duct. Choledochotomy showed much more sludge and soft calcareous material in the duct. In summary, it should be axiomatic in all cases of acalculous cholecystitis to remember the trap posed by the calculus-containing common duct. Charles J. Carrico (closing): Dr. Sheldon asked three questions. The first question involved cultures of the bile and of the gallbladder wall. The bile of fifteen patients was cultured, and eight cultures were positive. The gallbladder wall was not cultured in all fifteen, but two thirds of those that were cultured were positive. The organisms were the same when both were cultured.
36
One other comment about cultures which may say something about etiology is that in three of the patients the same organism, klebsiella, was grown from the bile and from a distant wound. In terms of ultrasound diagnostic technics, we do not have portable ultrasound capabilities. We are hopeful that, when available, it will become a very useful diagnostic aid. Dr. Sheldon also asked about when to do cholecystectomy. In our series cholecystectomies were done in the two patients who had grossly necrotic gallbladders. There were several patients treated by cholecystostomies who had small areas of focal gallbladder necrosis, and cholecystostomy provided adequate management of those patients. The real advantage of cholecystostomy in these very critically ill patients is that one can avoid general anesthesia, avoid formal laparotomy, do a fairly simple procedure using field block or local anesthesia, and treat this disease without a major physiologic insult. If the patient has undergone general anesthesia and laparotomy, then the question of whether to do cholecystectomy or cholecystostomy is a little more difficult. In general we still prefer cholecystostomy unless the gallbladder is grossly gangrenous. The question of cholangiography at the time of the procedure has been raised. Again, our intent and thought is to do something effective and to keep the patient on the operating table for as short a period of time as adequate. Therefore, we usually defer cholangiography for a later time. In the small number of patients with common duct problems (none in our series), cholecystostomy should provide adequate decompression of the common duct. If cholangiography shows abnormalities in the common duct or the patient does not defervesce rapidly, then we have to decide. But we would only do more extensive procedures on those patients who required that type of procedure. One of the previous series shown was Dr. Ternberg’s, which was of acute acalculous cholecystitis in children. All of them were treated by cholecystostomy, and six of the seven did very well. Dr. Passaro, we have not done chemical analyses on the bile. The presence of trypsin is interesting. A question we might ask ourselves is whether this represents pancreatic reflux. I do not know if this means that pancreatic juice with trypsinogen has gotten up into the qiliary tree and become activated. Dr. Passaro also mentioned the possibility of percutaneous aspiration of the gallbladder. My concern about purposeful aspiration of the gallbladder is safety, in particular the possibility of bile leak and bile peritonitis. The question of preventing this disease, as raised by Dr. Passaro, is crucial. As Dr. Sheldon has already mentioned, he intermittently feeds his patients butter to get the gallbladder to contract. That seems to be a fairly direct method. It is probably equally as effective as intermittent administration of cholecystokinin and certainly less expensive. Before we accept such maneuvers as common practice we would need to prospectively determine that they reduce the incidence of this complication in this series of patients. The American Journal of Surgery
Acute acalculous cholecystitis is a treacherous and potentially lethal disease. It may occur in patients without known biliary tract disease who are severely compromised by trauma or gastrointestinal dysfunction and require prolonged intensive care. Its onset is insidious, the presenting symptoms are inconstant, and its neglect can lead to necrosis of the gallbladder with sepsis and death. Previous reports reflect experience with Vietnam evacuees after severe trauma [l-3], patients with pediatric disease [4], burned patients [5], and civilian populations of critically ill patients [6-121. The present study describes seventeen patients who developed acalculous cholecystitis during a period of intensive care after unrelated surgical operations, severe trauma, or burns. Despite the subtleties of the presenting signs and symptoms, awareness of the problem, recognition of predisposing factors, and a careful search for clinical signs can lead to an early diagnosis. When the diagnosis is made, drainage of the gallbladder by tube cholecystostomy can be successfully employed without the added risk of formal laparotomy. Material and Methods Harborview Medical Center is a major trauma and burn referral center, admitting approximately 5,000 traumatized patients and 300 burned patients annually. One hundred fifty traumatized patients and 100 burned patients are admitted to the intensive care units each year. During the three year period from July 1974 to July 1977, twelve patients with acalculous cholecystitis were identified from a pool of 750 critically ill patients, an incidence of 1.6 per cent. An additional five patients with acalculous cholecystitis were encountered on the surgical services at the four hospitals in the University of Washington system From the Department of Surgery, School of Medicine, University of Washington, Seattle, Washington. Reprint requests should be addressed to C. James Carrico, MD, Department of Surgery, Harborview Medical Center, 325 Ninth Avenue, Seattle, Washington 98104. Presented at the Forty-Ninth Annual Meeting of the Pacific Coast Surgical Association, Newport Beach, California, February 19-22, 1978.
Volume 138, July 1978
during this same time period. Four of these patients had undergone extensive surgical procedures and all had required int.ensive care but did not have trauma as a predisposing feature. To better identify specific “risk factors” and to serve as a control group, fifteen additional patients were reviewed. These were patients who had comparable injuries requiring prolonged intensive care but who did not develop acalculous cholecystitis.
Results
Of seventeen patients with acalculous cholecystitis, fourteen were male and three female. Mean age was forty-six years (range, 15 to 82 years). Four patients were burn victims, eight suffered multiple system trauma, four had undergone extensive unrelated surgical procedures, and one was being treated for massive drug overdose. The mean time from admission to diagnosis was three weeks, but the range was extremely large, from three days in the woman with a polydrug overdose to ninety days in the patient with an 85 per cent total body surface burn who died and was diagnosed at autopsy. The diagnosis was made during the first week in one patient, during the second week in five, during the third week in four, fourth week in two, and after the fourth week in five. The findings at the time of diagnosis are presented in Table I. A specific preoperative diagnosis of acalculous cholecyst.itis was made in eleven patients. Five patients were operated on with another preoperative diagnosis and acalculous cholecystitis was found at operation. (Table II.) One patient died with burn wound sepsis, and a necrotic gallbladder was found at autopsy. Sixteen patients underwent operation; fourteen cholecyst.ostomy and two cholecystectomy. In all cases the operative findings were consistent: a dense, thickened, edematous, severely inflamed gallbladder without stones but containing a thick, black,
31
Long, Heimbach, and Carrico
TABLE I
Flndings at Time of Diagnosis 68% 94% 65% 59% 53 % 24% 24 %
Fever WBC > 10,000 Bilirubin >2 mg/lOO ml RUQ tenderness RUQ pain RUQ mass NauseaIemesis Note: RUQ = right upper quadrant.
TABLE II
Five Patients Operated on with another Preoperative Diagnosis
Preoperative Diagnosis
Postoperative Diagnosis Acalculous cholecystitis Gangrenous gallbladder dome with colon adhesion Interloop abscess Acalculous cholecystitis, incidental Small bowel obstruction Acalculous cholecystitis, incidental Bleeding Curling’s ulcer Necrotic gallbladder, incidental
Appendicitis lschemic colitis lntraabdominal
abscess
Small bowel obstruction Bleeding Curling’s ulcer
TABLE III
Causes of In-Hospital Mortality Interval after Cholecystectomy
Age (yr)
Cause(s) of Death
44
Burn wound sepsis Perforated acalculous cholecystitis Bronchopneumonia (necropsy) lntraabdominal abscesses + septic death Herpes pneumonia Renal failure Prolonged respiratory insufficiency Terminal bronchopneumonia Sepsis from peripancreatic abscess secondary to splenectomy Acute renal failure Decreasing central nervous system function Burn wound sepsis Hepatorenal syndrome
45 51 81 50
42
TABLE IV
24 hr 18da 4mo
3 wk
30 da
Risk Factors Factor
Patients
Controls
Morphine >6 days Prolonged ileus/NPO Mechanical ventilation More than 1 recent operation Multiple blood transfusions (>lO) Open wound/abscess Hyperalimentation (>3 days) PEEP (>24 hr) Refeeding phenomenon
77% 71% 59% 53% 53% 47 % 47% 35% 24%
40% 73% 60% 40% 60% 33 % 33% 20% N/A
Note: NPO = nothing by mouth; PEEP = positive end-expiratory pressure.
32
“crankcase oil” bile. Severe inflammation was found on all histologic sections, and five patients had focal necrosis or overt gangrene of the gallbladder at operation. The two patients with gangrene underwent cholecystectomy. Bile cultures were positive in eight of fifteen patients. Predominant organisms in decreasing order of frequency were: Klebsiella pneumonia (4 patients); Pseudomonas aeruginosa (2); Clostridium novii (1); enterobacter species (1); and Escherichia coli (I). It is of interest that three patients with positive klebsiella cultures had simultaneous positive klebsiella cultures at distant sites. Six of the seventeen patients died during their hospitalization, attesting to the severity of their associated diseases. (Table III.) The patient with undiagnosed acalculous cholecystitis died with fulminating burn wound sepsis. The necrotic gallbladder may have contributed to his demise. Another patient died 24 hours after his cholecystostomy. This patient had had multiple intraabdominal abscesses and his acalculous cholecystitis was an incidental finding at the time of abscess drainage. He remained in septic shock and died 24 hours after surgery. It is unlikely that his acalculous cholecystitis was a primary cause of death. The remaining four deaths occurred more than two weeks postoperatively and all were due to underlying illnesses. It is unlikely that the cholecystitis contributed to any of these patients’ deaths. Both patients undergoing cholecystectomy did well after operation, with decreasing fever and gradual improvement of their underlying illness. Twelve of the fourteen patients treated with cholecystostomy rapidly improved after operation. There were two complications associated with cholecystostomy. One tube was accidently removed and required replacement and one patient remained febrile in the postoperative period due to a large pericholecystic phlegmon present at the time of operation. This slowly responded to antibiotics and nonoperative treatment. Nine patients underwent tube cholangiography in the postoperative period. Once the acute attack had subsided, the x-ray films revealed no gallbladder, cystic duct, or common duct disease. Oral cholecystography was done in three instances; in one there was nonvisualization of the gallbladder and in two no abnormalities were revealed. Only two patients have required cholecystectomy during the short follow-up period. One patient experienced mild recurrent abdominal pain and had a nonvisualized gallbladder on oral cholecystogram. The other patient with the pericholecystic phlegmon described above maintained persistent mild right upper quadrant tenderness and discomfort after discharge.
The American Journal of Surgery
Acalculous Cholecystitis
.jt operation a chronically inflamed gallbladder encased in dense scar was found. The remaining patients have remained asymptomatic and are being followed regularly. The charts of all patients have been analyzed for the presence of previously suggested risk factors. The results of t>his analysis are shown in Table IV.
Comments Eliology 4 review
of the literature reveals that any patient sustaining prolonged critical illness is at risk of deve:.oping severe stasis within the gallbladder, bile inspissation and eventual obstruction of the cystic duct, and acute cholecystitis. A number of specific “risk factors” have been suggested by various authors. Glenn and Wantz [13] in their initial description of acalculous cholecystitis suggested that prolonged fasting, anesthesia, analgesia, and dehydration with resultant bile concentration set the stage for induction of gallbladder contractions producing mechanical outflow obstruction at the gallbladder neck. The Vietnam experience [I--31 revealed several other characteristics unique to these patients. Approximately 90 per cent had open draining wounds and had received blood transfusions of more than 10 units. Lindberg, Grinnan, and Smith [I] suggested that the increased bile pigment load secondary to t,ransfusions might injure the gallbladder, but at the present time this remains unproven [14]. Only half our patients received more than 10 units of blood and a similar proportion of patients who did not develop cholecystitis underwent equivalent transfusions. Hyperalimentation has been suggested as a risk factor because it decreases stimulus to the biliary tract and allows concentration of the bile [12]. This ma.y be aggravated by narcotics, volume depletion, and nasogastric suction [5]. Eight of our patients unlderwent hyperalimentation for more than three days. Seventy-seven per cent of our patients received mere than 8 mg morphine sulfate daily for six days or more. Sixty per cent of our patients underwent prolonged ventilatory support, and more than half of them were on positive end-expiratory pressure (PEEP). Positive pressure ventilation can be shown to produce hyperbilirubinemia, decreased portal blood flow, and reduced flow through the choledochoduodenal junction in dogs [15,16]. The other series in the literature do not mention ventilatory support as a risk factor. However, the experimental evidence and the high association in our series suggest a possible etiologic role, especially when PEEP is required. It is likely, as suggested by Golden,
Vohne 136,July
1979
Sears, and Wangensteen [IO], that the disease is a mosaic of many features, all of which may produce bile stasis. Predisposing factors, such as volume depletion, prolonged gastrointestinal rest, hyperalimentation, ventilatory support, morphine administration, multiple transfusions, and presence of infected wounds may all increase the likelihood of inducing inspissated bile. In our series, the following risk factors appeared to be more prevalent in patients who developed acalculous cholecystitis than in those who did not: morphine administration; mechanical ventilation with PEEP; and possibly, hyperalimentation and open wounds. However, the comparative number of patients is too small to draw any firm conclusions. The presence of any or all of these predisposing factors should alert the clinician to think of the disease when a patient develops any symptom referable to the right upper quadrant.. Dlagnosis
Although fever and an elevated white blood cell count were the most consistent findings in our series, these findings are unfortunately nonspecific in a group of severely ill postoperative patients. On the other hand, persistent fever, without other explanation, was the stimulus to investigate the biliary tract in a significant number of our patients. The findings of mass, pain, or tenderness were important when present, but there was no combination of symptoms that was diagnostic in all patients. Signs of nausea or vomiting were present in only four patients. Approximately half the patients complained of right upper quadrant pain, and these patients usually had specific tenderness in the right upper quadrant. Despite markedly distended gallbladders, fewer than one fourth of the patients demonstrated a palpable right upper quadrant mass or fullness. An elevated bilirubin level was present in 65 per cent of the group but was also found in 64 per cent of the patients in the control group who had received more than 10 units of blood. This bilirubin elevation was probably related more to the number of transfusions and episodes of hypotension than to biliary tract disease [19]. The presenting findings in our series do not markedly differ from those in other series, and differences may in reality represent the stage of the disease at the time of diagnosis rather than any major differences among patients. In earlier series, before the disease was well described, the diagnosis appears to have been made late in the course of the disease. As clinicians have become more familiar with the disease and the potential hazards of prolonged intensive care, earlier diagnosis should be possible before classic findings of palpable masses occur.
33
Long, Heimbach, and Carrico
The severity of these patients’ underlying illness and the multiple life-support devices required by them make the usual diagnostic procedures for biliary tract disease inconvenient and even potentially hazardous. Intravenous cholangiography, in our hands, has generally been unrewarding in these patients, resulting in nonvisualization of the entire biliary tree even in patients without elevated bilirubin levels. On the other hand, with continually improving technology and increasing experience, ultrasonic examination of the gallbladder may be of value in the diagnosis of equivocal cases.
Treatment
Once the diagnosis is suspected, immediate operation is the treatment of choice, with either removal of the infected gallbladder or decompression of the biliary tract. Medical therapy is unlikely to be rewarding. Most of our patients were receiving treatment that would normally be accepted as conservative management of cholecystitis. For example, most were receiving antibiotics and their gastrointestinal tracts were at rest. If the diagnosis can be made preoperatively, a cholecystostomy tube can be placed under local anesthesia with minimal disruption of physiologic function. Our patients were all critically ill and many had undergone multiple operations, and an additional anesthetic with a formal exploration is not necessary for the treatment of cholecystitis without associated cholangitis. Athough the adequacy of cholecystostomy in the treatment of suppurative cholangitis is controversial, its use in the emergency treatment of cholecystitis is on firmer ground [17,18]. Ternberg and Keating [4] used cholecystostomy in all seven of their pediatric patients, with good results in six. In our series tube cholecystostomy resulted in prompt resolution of the acute process in twelve of fourteen patients. The one patient who died within 24 hours of operation died of overwhelming sepsis from multiple intraabdominal abscesses. The other patient, with a pericholecystic phlegmon, defervesced slowly and might have benefited more promptly from cholecystectomy if it could have been done safely. He, however, suffered from familial thrombocytopenia, and this made extensive dissection through acutely inflamed tissue inadvisable. We do not know the long-term outcome of cholecystostomy in our patients, but we know that seven of nine surviving patients with cholecystostomy have not required subsequent cholecystectomy. In the absence of lithogenic bile, stone formation may not be a problem, but only prolonged follow-up will answer this question.
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Conclusions inciting (1) The presence of any circumstance sluggish bile flow should alert the clinician caring for critically ill patients to the possibility of acalculous cholecystitis. (2) The presence of unexplained fever or elevated white blood cell count, particularly with any symptoms relating to the right upper quadrant, requires prompt investigation of the biliary tract. (3) Effective treatment can be instituted promptly by performance of cholecystostomy under local anesthesia in most cases. (4) If treatment is prompt and appropriate, the disease subsides and the patient’s morbidity returns to that of his underlying illness. Summary Acute acalculous cholecystitis is a treacherous and potentially fatal complication of severe trauma and prolonged intensive care. The present study reviews seventeen patients seen between June 1974 and August 1977. Although specific causes have been suggested-transfusions, fractures with immobilization, central hyperalimentation, respirators, and “refeeding’‘-there was no common denominator among our patients. Refeeding was a feature in 30 per cent of our cases, 50 per cent received more than 10 units of blood, 65 per cent had prolonged gastric suction, and 60 per cent had mechanical ventilation. Thus, although all suggested causes were seen, no single factor was dominant. Clinical presentation in this civilian group resembles that of other reports, but differs in remarkable areas. Only 65 per cent of our group presented with one or more of the classic symptoms of cholecystitis-pain, tenderness, or mass. Sixty-five per cent of patients had elevated bilirubin levels. However, the same incidence of hyperbilirubinemia was seen in another group of traumatized patients who did not develop acalculous cholecystitis. The smoldering and nonclassic presentation frequently delayed diagnosis for several days. It was correctly made in 65 per cent, discovered at autopsy in one patient, and found at laparotomy for “sepsis” in the rest. The present report is unique because 88 per cent of the patients had cholecystostomy as initial therapy. Although five patients who underwent operation ultimately succumbed, cholecystitis could be implicated in only one. This patient died of sepsis at 24 hours but also had multiple unrelated intraabdominal abscesses at surgery. Clinical presentation is more complex than previously reported and simple cholecystostomy is an effective mode of therapy in these critically ill patients.
The American Journal of SWerY
Acalculous
References 1. Lindberg EF, Grinnan GLB, Smith L: Acalculous cholecystitis in Viet Nam casualties. Ann Surg 171: 153, 1970. 2. Weeder RS, Bashant GH, Muir RW: Acute noncalculous cholecystitis associated with severe injury. Am J Surg 119: 729, 1970. 3. Winegarner FG, Jackson GF: Post-traumatic acalculous cholecystitis: a highly lethal complication. J Trauma 11: 567, 1971. Ternberg JL, Keating JP: Acute acalculous cholecystitis. Arch Surg 110: 543, 1975. Munster AM, Goodwin MN, Pruitt BA: Acalculous cholecystitis in burn patients. AmJ Surg 122: 591, 1971. Mandelbaum I, Palmer RM: Post-traumatic acalculous cholecystitis. Arch Surg 97: 601, 1968. Skillman JJ, Bushnell LS, Goldman H, Silen W: Respiratory failure, hypotension, sepsis, and jaundice. Am J Surg 117: 523, 1969. 8. Munster AM, Brown JR: Acalculous cholecystitis. Am J Surg 113: 730, 1967. 9. Thompson JW, Ferris DO, Baggenstoss AH: Acute cholecystitis as a complication of other diseases. Ann Surg 155: 489, 1962. IO. Golden GT, Sears HF, Wangensteen SL: Post-traumatic cholecystitis. Am Surg 39: 276, 1973. 11. Howard RJ, Delaney JP: Post-traumatic cholecystitis. JAMA 218: 1006, 1971. 12. Anderson DL: Acalculous cholecystiiis: a possible complication of parenteral hyperalimentation. Med Ann Disfr Columbia 41: 448. 1972. 1:3. Glenn F, Wantz GE: Acute cholecystitis following the surgical treatment of unrelated disease. Surg Gynecol Obstet 102: 510, 1956. 14. lnglesakis JA, Lanfranchi JP, Migliori G, et al: Cholecystites Aigues non Lithiasuques Chez les Polytraumatises. Nouv Press Med3: 19, 1974. l!j. Johnson EE, Hedley-White J: Continuous positive pressure ventilation and portal flow in dogs with pulmonary edema. J Appl Physiol33: 365, 1972. 16. Johnson EE, Hedley-White J: Continuous positive pressure ventilation and choledochoduodenal flow resistance. J Appl Physio139: 937, 1975. I?. Gagic N, Frey CF: The results of cholecystostomy for the treatment of acute cholecystitis. Surg Gyneco/ Obstet 140: 255, 1975. 18. Gingrich RA, Awe WC, Boyden AM. Peterson CG: Cholecystostomy in acute cholecystitis. Am J Surg 116: 310, 1968. 19. Kantrowitz PA, Jones WA, Greenberger NJ, lsselbacher KJ: Severe postoperative hyperbilirubinemia simulating obstructive jaundice. N fngl J Mecf 276: 591, 1967.
Discussion George F. Sheldon (San Francisco, CA): I congratulate the authors on calling to our attention the insidious presentation and lethal consequence of acalculous cholecystitis. Moreover, their low mortality rate attests to the awareness their unit has of this pernicious disease. The disease was diagnosed preoperatively in eleven of seventeen patients; only one undiagnosed case is reported in their series. During the past two years we have seen more than twenty patients with acalculous cholecystitis and in recent months have noted five patients without dehydration or sepsis who are receiving long-term parenteral nutrition. Although we can only speculate as to the potential cause of this illness, it is clearly associated with critical and
Volume 136, July 1978
Cholecystitis
prolonged illness and bowel rest. Moreover, it is possible that the lack of fat stimulus to the secretion of bile may have an etiologic relationship to the development of this illness which occurs in patients deprived of oral feeding. We currently treat patients by intermittent administration of butter or some other fat source down the nasogastric tube to stimulate the gallbladder to contract and prevent it from remaining in a state of stasis. In addition, we have been very pleased with the diagnostic ac’curacy of sonography. Many of our patients on long-term parenteral feeding are routinely followed with ultrasound examination of their gallbladder to determine the potential development of biliary distention and bile sludge. Have you any diagnostic methods that are helpful other than those noted which were nonspecific? Although the results of the bacteriologic study of the bile cultures were reported, I would be interested in knowing the results of cultures of the gallbladder wall. We have found that cholecystostomy is often a good method for treating this illness; if the gallbladder is totally necrotic, however, one wonders if cholecystostomy is the optimal rnethod of treatment. Newlin Hastings (Los Angeles, CA): I would like to complement this presentation of adult pathology with a few observations based on pediatric pathology. There may be some clues for common denominators: stasis and infection. Acute acalculous cholecystitis is relatively more common in infanc,y and early childhood than in adulthood. In the youngest neonate and infant acute cholecystitis characteristically has factors for gallbladder stasis such as congenital stenosis of the duct or malformations like diverticuli or choledochal cyst. With stasis there is a milieu which is excellent for the growth of bacteria in bile. In older children characteristically there are infections either antecedent to or associated with respiratory or enteric infections. Often the enteric infection does not have a specific organism as salmonella; it may be associated with mesenteri.c adenitis. With all these infections small infants and children are often dehydrated, contributing to the development of the stasis which, with bacterial growth, leads to the development of cholecystitis. Specific organisms may be found: staphylococcus; streptococcus; or salmonella (much more common in previous years than recently). In some environments there is still a significant incidence of acalculous cholecystitis with salmonella in adult patients. The incidence of acute acalculous cholecystitis was much higher in infancy and childhood in the preantibiotic era; perhaps our use of drugs has cut down on this frequency. The ratio of bile salts and cholesterol and the solubility may be upset, of course, with the dehydration and stasis, increasing the favorable circumstances for cholecystitis. Acute obstruction may also create this situation. The late J. Norton Nichols, a member of this Society, had a patient for whom he performed a simple cholecystostomy for traumatic injury. William F. Pollock (Santa Monica, CA): Dr. Sheldon indicated the use of sonography to demonstrate sludging
35
Long, Heimbach, and Carrico
in the gallbladder. There is a form of ultrasound now available which demonstrates real time action and is used by obstetricians to show the function or site of the actual fetal parts. It might be a wonderful adaptation to this particular problem because this is real ultrasonography, SO that instead of a picture one sees a “fluoroscopic image.” Edward Passaro Jr (Los Angeles, CA): I have three brief comments First, a colleague of mine, Dr. Donald Wagner, as a resident made the same observation that the authors have made with regard to this clinical situation. It was his observation that the bile of these patients contained trypsin, presumably from reflux of pancreatic juice into the biliary system. He produced this black, machinery-oil bile by introducing trypsin into the bile of dogs. This might offer a way to investigate the cause; specimens could be examined for trypsin content. The second point concerns diagnostic technics. In attempting to do liver biopsies at our hospital, we occasionally introduce the needle into the gallbladder. It may be possible, therefore, to percutaneously and transhepatically aspirate some of this material from the gallbladder. Cultures and contrast studies for stones could be done, and if indicated, the hypothesis of trypsin reflux could be investigated. Last but not least, inasmuch as this may be iatrogenically produced, we should seek methods to correct this. Cholecystokinin will cause contraction of the gallbladder. In patients who are critically ill and who will be hospitalized for a long time, should we consider the use of cholecystokinin to periodically flush the gallbladder? Leon Morgenstern (Los Angeles, CA): In acalculous cholecystitis we should not necessarily infer the absence of common duct stones, because we have encountered a number of ductal stones in patients with this condition. Accurate radiographic evaluation of the common duct is imperative during the procedure (for example, cholecystocholangiography) or as soon as feasible after the procedure, by whatever radiographic maneuver is feasible. (Slide) This is a gallbladder from a patient operated on just last week. She was bedridden, had thrombophlebitis, was receiving steroids for rheumatoid arthritis, and was dehydrated. (Slide) The cholecystitis here is mild. Operative cholangiography shows several stones in the common duct. Choledochotomy showed much more sludge and soft calcareous material in the duct. In summary, it should be axiomatic in all cases of acalculous cholecystitis to remember the trap posed by the calculus-containing common duct. Charles J. Carrico (closing): Dr. Sheldon asked three questions. The first question involved cultures of the bile and of the gallbladder wall. The bile of fifteen patients was cultured, and eight cultures were positive. The gallbladder wall was not cultured in all fifteen, but two thirds of those that were cultured were positive. The organisms were the same when both were cultured.
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One other comment about cultures which may say something about etiology is that in three of the patients the same organism, klebsiella, was grown from the bile and from a distant wound. In terms of ultrasound diagnostic technics, we do not have portable ultrasound capabilities. We are hopeful that, when available, it will become a very useful diagnostic aid. Dr. Sheldon also asked about when to do cholecystectomy. In our series cholecystectomies were done in the two patients who had grossly necrotic gallbladders. There were several patients treated by cholecystostomies who had small areas of focal gallbladder necrosis, and cholecystostomy provided adequate management of those patients. The real advantage of cholecystostomy in these very critically ill patients is that one can avoid general anesthesia, avoid formal laparotomy, do a fairly simple procedure using field block or local anesthesia, and treat this disease without a major physiologic insult. If the patient has undergone general anesthesia and laparotomy, then the question of whether to do cholecystectomy or cholecystostomy is a little more difficult. In general we still prefer cholecystostomy unless the gallbladder is grossly gangrenous. The question of cholangiography at the time of the procedure has been raised. Again, our intent and thought is to do something effective and to keep the patient on the operating table for as short a period of time as adequate. Therefore, we usually defer cholangiography for a later time. In the small number of patients with common duct problems (none in our series), cholecystostomy should provide adequate decompression of the common duct. If cholangiography shows abnormalities in the common duct or the patient does not defervesce rapidly, then we have to decide. But we would only do more extensive procedures on those patients who required that type of procedure. One of the previous series shown was Dr. Ternberg’s, which was of acute acalculous cholecystitis in children. All of them were treated by cholecystostomy, and six of the seven did very well. Dr. Passaro, we have not done chemical analyses on the bile. The presence of trypsin is interesting. A question we might ask ourselves is whether this represents pancreatic reflux. I do not know if this means that pancreatic juice with trypsinogen has gotten up into the qiliary tree and become activated. Dr. Passaro also mentioned the possibility of percutaneous aspiration of the gallbladder. My concern about purposeful aspiration of the gallbladder is safety, in particular the possibility of bile leak and bile peritonitis. The question of preventing this disease, as raised by Dr. Passaro, is crucial. As Dr. Sheldon has already mentioned, he intermittently feeds his patients butter to get the gallbladder to contract. That seems to be a fairly direct method. It is probably equally as effective as intermittent administration of cholecystokinin and certainly less expensive. Before we accept such maneuvers as common practice we would need to prospectively determine that they reduce the incidence of this complication in this series of patients. The American Journal of Surgery
