Open access peer-reviewed chapter

Acute Alitasic Cholecystitis

Written By

Giovanni Petracca, Francesco Zappia, Maccarone Giuseppe, Mazzeo Mariano, Mio Francesco, Fabrizio Silvaggio, Mileto Ivana, Plutino Francesco, Posterino Antonietta and Danilo Cafaro

Submitted: June 9th, 2021Reviewed: July 1st, 2021Published: September 24th, 2021

DOI: 10.5772/intechopen.99188

Chapter metrics overview

108 Chapter Downloads

View Full Metrics

Abstract

Acute acalculous cholecystitis (AAC) is the inflammatory disease of the gallbladder in the absence of gallstones. Typically affects critically ill patients. Diagnosis is not straightforward as Murphy’s sign is difficult to detect in critically ill and many imaging findings are numb or nonspecific. Acalculous cholecystitis is a life-threatening disorder that has a high risk of perforation and necrosis compared to the more typical calculous disease. Management involves a percutaneous cholecystostomy, a surgical cholecystectomy, or, more recently, a metal stent placed endoscopically through the gastrointestinal tract into the gallbladder. Acalculous cholecystitis is a serious illness that has high morbidity and mortality. The reported mortality of the condition varies from 30 to 50% depending on the age of the patient. Even those who survive have a long recovery that can take months.

Keywords

  • cholecystitis
  • gallbladder
  • alithiasic

1. Introduction

Acute alithiasic cholecystitis is defined as an inflammatory disease of the gallbladder in the absence of gallstones or obstruction of the cystic duct and it has a multifactorial pathogenesis [1].

It accounts for approximately 10% (range, 2% -15%) of all cases of acute cholecystitis. Acute alithisiac cholecystitis occurs in approximately 0.2% -0.4% of all critically ill patients. Duncan recognized it, for the first time, in 1844 when a fatal case of acute cholecystitis complicating an incarcerated hernia was reported [2]. Acute cholecystitis acalculous is associated with a morbidity more serious and a rate mortality more elevated compared to acute lithiasic cholecystitis [3].

The death rate depends primarily on the presentation already critical of the patient as the disease affects both medically and surgically compromised patients. Clinically, acute alithiasic cholecystitis is indistinguishable from acute lithiasic cholecystitis. Many patients with acute cholecystitis acalculous have the same symptoms of gallstone cholecystitis: pain in the quadrant abdominal upper right, fever, neutrophili leukocytosis, elevated liver enzymes (ALT, AST, Alkaline phosphatase) increased serum total bilirubinand fractional [4].

There are various risk factors that predispose to the formation of acute alithiasic cholecystitis which are listed in Table 1, as noted this pathology mainly affects patients in serious clinical conditions: severe trauma, patients with shock of any type on mechanical ventilation, with sepsis, burns or in total parenteral nutrition [6].

Risk factors commonly associated with acute alithiasic cholecystitisRisk factors rarely associated with acute alithiasic cholecystitis
Severe trauma leading to hospitalization; some factors particularly useful for the diagnosis of acute alithiasic cholecystitis are blood transfusions (over 12 units) and cardiac arrhythmias.Hypovolemia
Recent cardio-pulmonary surgeryCholangiopancreatography Endoscopic retrograde
Shock of any kindLonger of hospital stay
Severe burnsImmunodeficiency: acquired immunodeficiency syndrome, organ transplant
Bacterial or viral sepsisChronic disease: diabetes, hypertension, atherosclerotic disease, morbid obesity
Critical illness (any patient requiring mechanical ventilation in the ICU)Vasculitis: Churg- Strauss, giant cell arteritis, Henoch-Shonlein purpura, polyartereitis nodosa, lupus.
Total parenteral nutrition
Prolonged fasting

Table 1.

Descending order of risk factors associated with acute alithiasic cholecystitis.

Owen & Jain [5] table.

Advertisement

2. Pathophysiology

The etiology of acute cholecystitis acalculous is multifactorial, but is mainly formed by biliary stasis or organ wall ischemia. Biliary stasis can be caused by fasting, post-surgical total parenteral nutrition that leads to an increase in bile viscosity which irritates the mucous membrane of the gallbladder. Gallbladder wall ischemia occurs due to decreased blood flow due to fever, dehydration, or heart failure, which leads to the pathogenesis of acute cholecystitis [7].

It arises acutely when the walls of the gallbladder become inflamed for the reasons mentioned above [8].

Prolonged ischemia of the gallbladder walls leads to gangrene and then perforation. If the process occurs slowly, the formation of cholecystoduodenal (70%), cholecystocholic (10–20%), and the less common cholecystogastric fistula is possible. This will lead to sepsis and shock. These findings are referred to as acute cholecystitis. Chronic acalculous cholecystitis usually presents more insidiously. Symptoms are more prolonged and may be less severe. Symptoms may also be more intermittent and vague, although patients can present with signs of acute biliary colic [9].

Advertisement

3. Epidemiology

Acalculous cholecystitis has an incidence rate of 0.12% in the entire population.

Rates are increased in HIV and other immunosuppressed patients. These individuals are more susceptible to certain opportunistic infections such as microsporidia, cytomegalovirus (CMV), and Cryptosporidium, which can seed and flourish in bile within the gallbladder [10].

Carriers of G. lamblia, H. pylori, and S. typhiare also associated with increased risks to develop cholecystitis.

It can occur in all breeds. Acute alithiasic cholecystitis has a slight male predominance (80% of case), unlike acute lithiasic cholecystitis, which has a female predominance and occurs at any age with a criticality threshold between the fourth and eighth decade of life [11].

Advertisement

4. Prognosis

Acalculous cholecystitis is a serious illness that has high morbidity and mortality. The reported mortality of the condition varies from 30 to 50% depending on the age of the patient. Even those who survive have a long recovery that can take months [12].

Advertisement

5. Mortality/morbidity

The rates of the mortality and morbidity associated with acute cholecystitis can be high; the disease is frequently seen in patients with sepsis or other serious conditions. The reported mortality range is 10% - 50% for acute cholecystitis acalculous compared to 1% for acute cholecystitis lithiasic [13].

Advertisement

6. Complications

Perforations or gangrene of the gallbladder and exstrabiliary abscess formation in the acute alithiasic versus lithiasic gallbladder may occur [14].

Advertisement

7. History and physical Exam

Often these patients are very seriously admitted to intensive care in mechanical ventilation and cannot participate in an anamnestic interview and therefore communicate their symptoms. Physical examination may detect fever, tenderness on the upper abdominal quadrants of the right associated with laboratory abnormalities such as neutrophil leukocytosis and altered liver tests (high values for ALT, AST, alkaline phosphatase and direct bilirubin) [15].

Advertisement

8. Diagnosis

The diagnosis of acute cholecystitis acalculous is difficult because no clinical data (symptoms, examination goal, testing laboratory) establish it. Although no combination of clinical factors will lead to the diagnosis, there seems to be a consensus on the fact that a high clinical suspicion for acute cholecystitis acalculous is indicated in all critically ill patients for whom no etiology has been found. The final diagnosis of acute cholecystitis is mainly based on radiological and ultrasound findings [16, 17, 18].

Advertisement

9. Radiology

There is controversy about what is the best imaging modality and which to use in the diagnosis of cholecystitis acute acalculous. However, radiological criteria for the diagnosis of acute alithic cholecystitis have been developed for the use of ultrasound and computed tomography. MRI is not used because it is a lengthy procedure with no benefit compared to the other modalities [19]. CT offers few advantages over ultrasound abdominal, unless there are other intra-abdominal pathologies that cannot be studied with the ultrasound. Therefore, abdominal ultrasound was the first line for the diagnosis of acute alithiasic cholecystitis as it can be performed at the bedside and favors patients who are intrasportable [20]. The ultrasound criteria for diagnosing acute alithiasic cholecystitis are: the thickness of the gallbladder wall, dangerous cystic fluid, wall, edema intramural gas, desquamated mucosa, mud or hydrops. The thickness of the gallbladder wall (3.5–4 mm) has been considered a crucial component for the diagnosis of acute alithiasic cholecystitis. Therefore, abdominal ultrasound is a very useful tool for diagnosing acute alithiasic cholecystitis as many prospective studies have suggested and, also, it is easy to use, fast, portable and easily repeatable at the bedside [21, 22, 23].

CT is useful for diagnosing acute alithiasic cholecystitis and other abdominal diseases. it requires patient transport, which may not be feasible, and offers few advantages compared to abdominal ultrasound. However, with a normal ultrasound, CT can diagnose acute alithiasic cholecystitis and make a differential diagnosis (Table 2) [5, 24, 25].

ModeCriteriaDiagnosis
Abdominal ultrasoundMajor: 3.5- to 4-mm (or more) thick wall (if at least 5-cm distended longitudinally with no ascites or hypoalbuminemia)
Pericholecystic fluid (halo)/subserosal edema
Intramural gas
Sloughed mucosal membrane
2 major or 1 major and 2 minor (most studies have favored the diagnostic triad—wall thickness, sludge, hydrops)
Minors: Echogenic bile (sludge)
Hydrops distension greater than 8-cm longitudinally or 5-cm transversely (with clear fluid)
TCMajor: 3- to 4-mm wall thickness
Pericholecystic fluid
Subserosal edema
Intramural gas
Sloughed mucosa
2 major or 1 major and 2 minor
Minors: Hyperdense bile (sludge)
Subjective distension (hydrops)

Table 2.

Imaging criteria.

Advertisement

10. Therapy

The two prevalent treatment options for acute alithiasic cholecystitis are cholecystostomy (gallbladder drainage) and/or cholecystectomy. Other methods such as ERCP using stents or tubes have been tried but unsuccessful. Cholecystectomy is generally considered the definitive therapy. Some authors propose cholecystostomy as the only treatment. Others claim that the cholecystostomy is just a bridge to the cholecystectomy more secure or just a treatment to see if the acute cholecystitis acalculous is resolved. Therefore, Boland et al. recommend the cholecystostomy prophylactic for all intensive care patients with abdominal sepsis who do not improve with medical therapy (high-dose antibiotic therapy) [26, 27]. The cholecystostomy is generrally plausible, quick and safe; it can be performed transperitoneally or transhepatically under ultrasound or CT guidance by interventional surgeons or radiologists. Therefore, cholecystostomy can provide time to optimize the patient’s condition for cholecystectomy surgery. There seems to be an unanimous tendency to favor the cholecystostomy before cholecystectomy, unless there is a strong evidence of an ischemic cholecystitis that the drainage alone does not alleviate.

Cholecystectomy is a definitive therapy when performed by open or laparoscopic surgery. Laparoscopic surgery has been favored in recent years because it can be both diagnostic and therapeutic, it is less invasive, and it has similar morbidity and mortality compared to open procedures [28, 29, 30, 31]. However, it should be noted that it may need to be converted to an open cholecystectomy and this should not be considered a failure of the surgeon on the contrary, when faced with situations in which it is not possible to distinguish, due to the inflammatory state of the gallbladder, the various structures anatomical, conversion to “open surgery” is preferable [32, 33, 34, 35].

11. Conclusions

When an acalculous acute cholecystitis is suspected, the cholecystostomy must be carried out immediately, because the patient can only improve with this technique. If the improvement occurs with the decompression and drainage through cholecystostomy, the tube can be removed after 3 weeks, and this is the only treatment needed [36, 37, 38, 39]. If there is no improvement, urgent cholecystectomy should be strongly considered as it can save the patient’s life and thus improve abdominal sepsis [40, 41, 42].

References

  1. 1.Treinen C, Lomelin D, Krause C, Goede M, Oleynikov D.Colecistite acuta acuta nei malati critici: fattori di rischio e strategie chirurgiche.Langenbecks Arch Surg. 2015 maggio. 400 (4): 421-7. [Medline].
  2. 2.The Management of Gallstone Disease: A Practical and Evidence-Based Approach a cura di Michael R. Cox, Guy D. Eslick, Robert Padbury.
  3. 3.Tana M, Tana C, Cocco G, Iannetti G, Romano M, Schiavone C.Colecistite acuta acuta e malattie cardiovascolari: terra di confusione.J Ultrasound. 18 dicembre 2015 (4): 317-20. [Medline].
  4. 4.Theodorou P, Maurer CA, Spanholtz TA, et al. Colecistite acuta in pazienti gravemente ustionati: incidenza e fattori predisponenti.Ustioni. 2009 maggio. 35 (3): 405-11. [Medline].
  5. 5.Laurila J, Laurila PA, Saarnio J, et al. Organ system dysfunction following open cholecystectomy for acute acalculous cholecystitis in critically ill patients. Acta Anaesthesiol Scand 2006;50: 173-179.Laurila JJ, Ala-Kokko TI, Laurila PA, et al. Histopathology of acute acalculous cholecystitis in critically ill patients. Histopathology 2005;47:485-492.
  6. 6.Hamp T, Fridrich P, Mauritz W, Hamid L, Pelinka LE. Colecistite dopo un trauma.J Trauma. 2009 febbraio 66 (2): 400-6. [Medline].
  7. 7.Basar O, Kisacik B, Bozdogan E, et al. Una causa insolita di colecistite acuta durante la gravidanza: il virus dell'epatite A.Dig Dis Sci. 50 agosto 2005 (8): 1532. [Medline].
  8. 8.Fuoti M, Pinotti M, Miceli V, et al. [Colecistite acuta acuta come complicanza dell'epatite A: rapporto di 2 casi pediatrici] [Italiano].Pediatr Med Chir. 2008 marzo-aprile. 30 (2): 102-5. [Medline].
  9. 9.Inagaki FF, Hara Y, Kamei M, Tanaka M, Yasuno M. Colecistite acuta e cronica acuta associata a dissezione aortica.Rappresentante del caso J Surg. 2015 1 agosto 2015 (8): [Medline]. [Testo completo].
  10. 10.Gu MG, Kim TN, Song J, Nam YJ, Lee JY, Park JS. Fattori di rischio e risultati terapeutici della colecistite acuta acuta.Digestione. 2014. 90 (2): 75-80. [Medline].
  11. 11.Wood BE, Trautman J, Smith N, Putnis S. Caso clinico raro di colecistite acuta: torsione della cistifellea con conseguente rottura.SAGE Open Med Case Rep. 2019. 7: 2050313X18823385. [Medline]. [Testo completo].
  12. 12.Joseph T, Unver K, Hwang GL, et al. Colecistostomia percutanea per colecistite acuta: esperienza decennale.J Vasc Interv Radiol. 23 gennaio 2012 (1): 83-8.e1. [Medline].
  13. 13.Chung YH, Choi ER, Kim KM, et al. La colecistostomia percutanea può essere una gestione definitiva per la colecistite acuta acuta ?.J Clin Gastroenterol. 46 marzo 2012 (3): 216-9. [Medline].
  14. 14.Noh SY, Gwon DI, Ko GY, Yoon HK, Sung KB. Ruolo della colecistostomia percutanea per la colecistite acuta acuta: risultati clinici di 271 pazienti.Eur Radiol. 28 aprile 2018 (4): 1449-55. [Medline].
  15. 15.Soria Aledo V, Galindo Iniguez L, Flores Funes D, Carrasco Prats M, Aguayo Albasini JL. La colecistectomia è il trattamento di scelta per la colecistite acuta acuta? Una revisione sistematica della letteratura.Rev Esp Enferm Dig. 109 ottobre 2017 (10): 708-18. [Medline]. [Testo completo].
  16. 16.Kirkegard J, Horn T, Christensen SD, Larsen LP, Knudsen AR, Mortensen FV. La colecistostomia percutanea è un'opzione di trattamento definitivo efficace per la colecistite acuta acuta.Scand J Surg. 104 dicembre 2015 (4): 238-43. [Medline].
  17. 17.Irani S, Baron TH, Grimm IS, Khashab MA. Drenaggio della cistifellea guidato dall'EUS con uno stent metallico che appoggia il lume (con video).Gastrointest Endosc. 2015 dicembre 82 (6): 1110-5. [Medline].
  18. 18.Casillas RA, Yegiyants S, Collins JC. La colecistectomia laparoscopica precoce è la gestione preferita della colecistite acuta.Arch Surg. 2008 giugno 143 (6): 533-7. [Medline].
  19. 19.Schuld J, Glanemann M. Colecistite acuta.Viszeralmedizin. 31 giugno 2015 (3): 163-5. [Medline].
  20. 20.Anderson JE, Inui T, Talamini MA, Chang DC. La colecistostomia non offre alcun beneficio in termini di sopravvivenza nei pazienti con colecistite acuta acuta e sepsi e shock gravi.J Surg Res. 190 agosto 2014 (2): 517-21. [Medline].
  21. 21.Jones MW, Ferguson T.Colecistite acuta.StatPearls [Internet]. 16 gennaio 2019. 2018: [Medline]. [Testo completo].
  22. 22.Barie PS, Eachempati SR. Acute acalculous cholecystitis. Curr Gastroenterol Rep 2003;5:302-309.
  23. 23.Owen CC, Jain R. Acute acalculous cholecystitis. Curr Treat Options Gastroenterol 2005;8:99-104.
  24. 24.Beckman I, Dash N, Sefczek RJ, et al. Ultrasonographic findings in acute acalculous cholecystitis. Gastrointest Radiol 1985;10 387-389.
  25. 25.Mariat G, Mahul P, Prev TN, et al. Contribution of ultrasonography and cholescintigraphy to the diagnosis of acute acalculous cholecystitis in intensive care unit patients. Intensive Care Med 2000;26:1658-1663.
  26. 26.Boland GW, Slater G, Lu DS, et al. Prevalence and significance of gallbladder abnormalities seen on sonography in intensive care unit patients.AJR Am J Roentgenol. 2000;174(4):973-7.
  27. 27.Ryu JK, Ryu KH, Kim KH. Clinical features of acute acalculous cholecystitis. J Clin Gastroenterol 2003;36:166-169.
  28. 28.Glenn F, Becker CG. Acute acalculous cholecystitis. An increasing entity. Ann Surg 1982;195:131-136.
  29. 29.Inoue T, Mishima Y. Postoperative acute cholecystitis: a collective review of 494 cases in Japan. Jpn J Surg 1988;18:35-42.
  30. 30.McChesney JA, Northup PG, Bickston SJ. Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoperfusion: a case series and review of pathophysiology. Dig Dis Sci 2003;48:1960-1967.Wang AJ, Wang TE, Lin CC, et al. Clinical predictors of severe gallbladder complications in acute acalculous cholecystitis. World J Gastroenterol 2003;9:2821-2823.
  31. 31.Kalliafas S, Ziegler DW, Flancbaum L, et al. Acute acalculous cholecystitis: incidence, risk factors, diagnosis, and outcome. Am Surg 1998;64:471-475.
  32. 32.Deitch EA, Engel JM. Ultrasonic detection of acute cholecystitis with pericholecystic abscesses. Am Surg 1981;47:211-214.
  33. 33.Yasuda H, Takada T, Kawarada Y, et al. Unusual cases of acute cholecystitis and cholangitis: Tokyo guidelines. J Hepatobiliary Pancreat 2007;14:98-113.
  34. 34.Westlake PJ, Hershfiled NB, Kelly JK, et al. Chronic right upper quadrant pain without gallstones: does HIDA scan predict outcome after cholecystectomy? Am J Gastroenterol 1990;85:986– 990.
  35. 35.Ziessman HA. Cholecystokinin cholescintigraphy: clinical indications and proper methodology. Update Nucl Med 2001;39:997-1006.Shuman WP, Rogers JV, Rudd TG, et al. Low sensitivity of sonography and cholescintigraphy in acalculous cholecystitis. AJR Am J Roentgenol 1984;142:531-534.
  36. 36.Taoka H. Experimental study on the pathogenesis of acute acalculous cholecystitis, with special reference to the roles of microcirculatory disturbances, free radicals and membrane-bound phospholipase A2. Gastroenterol Jpn 1991;26:633-644.
  37. 37.Sanda RB. Acute acalculous cholecystitis after trauma: the role of microcirculatory failure and cellular hypoxia. South Med J 2008;101:1087-1088.
  38. 38.Hakala T, Nuutinen PJ, Ruokonen ET, et al. Microangiopathy in acute acalculous cholecystitis. Br J Surg 1997;84:1249-1252.
  39. 39.Mirvis SE, Vainright JR, Nelson AW, et al. The diagnosis of acute acalculous cholecystitis: a comparison of sonography, scintigraphy, and CT. AJR Am J Roentgenol 1986;147:1171-1175.
  40. 40.Boland GWL, Slater G, Lu DSK, et al. Prevalence and significance of gallbladder abnormalities seen on sonography in intensive care unit patients. AJR Am J Roentgenol 2000;174:973-977.
  41. 41.Deitch EA, Engel JM. Acute acalculous cholecystitis. Ultrasonic diagnosis. Am J Surg 1981;142:290-292.
  42. 42.Deitch EJM. Ultrasound in elective biliary tract surgery. Am J Surg 1980;140:277-283.

Written By

Giovanni Petracca, Francesco Zappia, Maccarone Giuseppe, Mazzeo Mariano, Mio Francesco, Fabrizio Silvaggio, Mileto Ivana, Plutino Francesco, Posterino Antonietta and Danilo Cafaro

Submitted: June 9th, 2021Reviewed: July 1st, 2021Published: September 24th, 2021