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Table of Contents    
Year : 2019  |  Volume : 67  |  Issue : 2  |  Page : 439-441

Acute cholecystitis in patients with stroke

Department of Neurosurgery, Tokyo Women's Medical University Medical Center East, Tokyo, Japan

Date of Web Publication13-May-2019

Correspondence Address:
Dr. Yasuhiro Kuroi
Department of Neurosurgery, Tokyo Women's Medical University Medical Center East, Tokyo
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.258055

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 » Abstract 

Background: Although acute cholecystitis after stroke is rare, an immediate diagnosis and treatment is required.
Material and Methods: In the past five years, we observed six patients with acute cholecystitis during the initial hospitalization for stroke.
Results: Three patients had cardiac embolism, two had subarachnoid hemorrhage, and one had intra-cerebral hemorrhage. Four had calculous cholecystitis and two had acalculous cholecystitis. One of the patients with acalculous cholecystitis had hemorrhagic cholecystitis. The most commonly presented symptom was fever (50%), whereas only one patient (17%) had abdominal pain. Three patients (50%) were completely asymptomatic.
Conclusions: Acute cholecystitis and stroke are closely associated, and anti-thromboembolic drugs may cause hemorrhagic cholecystitis. Stroke patients tend to have atherosclerotic risk factors resulting in ischemic injury of the gallbladder. Furthermore, severe hemiparesis, a fasting state, dehydration, or bacteremia, which are occasionally exhibited by stroke patients, are known risk factors for acalculous cholecystitis. Stroke patients, especially patients with aphasia and consciousness disturbance, require immediate abdominal examination, if acute cholecystitis is suspected.

Keywords: Complication of stroke, acute cholecystitis, stroke and inflammation
Key Message: Atherosclerotic ischemia of the gallbladder, severe hemiparesis, fasting state, dehydration, or bacteremia, exhibited by stroke patients, are known risk factors for acalculous cholecystitis.

How to cite this article:
Kuroi Y, Imazato D, Yamazaki K, Kasuya H. Acute cholecystitis in patients with stroke. Neurol India 2019;67:439-41

How to cite this URL:
Kuroi Y, Imazato D, Yamazaki K, Kasuya H. Acute cholecystitis in patients with stroke. Neurol India [serial online] 2019 [cited 2020 Jul 2];67:439-41. Available from:

There have been significant advances in treatments for patients with stroke, especially for acute ischemic stroke.[1],[2] However, there are still many problems, including those related to in-hospital care, associated with the implemention of preventive and treatment strategies for stroke.

Patients with stroke sometimes develop acute cholecystitis (AC) during their initial hospitalization. There are some reports of the relationship between stroke and AC, but the pathophysiology has not been fully examined. Here, we report AC patients with a literature review to clarify the clinical features of AC in patients with stroke.

 » Material and Methods Top

Among patients with stroke admitted to our hospital between January 2012 and December 2016, those who developed AC during their hospitalization were analyzed. The diagnostic criteria for AC used in this study were as follows: (1) patients with accompanying clinical symptoms such as fever and/or abdominal tenderness; and (2) ultrasonographic findings including (a) dilation of the gallbladder to more than 80 × 40 mm, or (b) the presence of wall thickening to more than 4 mm, and/or biliary sludge or biliary calculus.[3] Data regarding age, sex, the past history of cholecystitis, the presence of gallstones, the interval from admission to the onset of cholecystitis, the clinical type of stroke, the diet at onset, and the modified Rankin Scale (mRS) at 90 days were evaluated. This study was approved by our Ethical Committee [Tokyo Women's Medical University's Ethics Committee (approval number: 4421)], which waived the need for informed consent due to the retrospective design of the study.

 » Results Top

We identified six of 1992 patients with stroke who met the criteria for AC. The overall incidence of AC among patients with stroke was 0.3%. The clinical features of these six patients are summarized in [Table 1]. The etiology of stroke in the six patients with accompanying AC included cardiac embolism in three, subarachnoid hemorrhage in two, and intracerebral hemorrhage in one patient. Gallstones were detected in four out of six patients, and they were diagnosed with calculous cholecystitis, whereas the two without gallstones were diagnosed with acalculous cholecystitis. The period from admission to the onset of AC ranged from 2 to 35 hospital days (mean 17 ± 14 days). The most commonly presented symptom was fever in 3/6 (50%) patients, and only one patient (17%) complained of abdominal pain. Three patients were completely asymptomatic, and none were receiving total parenteral nutrition. Three (50%) were bedridden at onset of their manifestations. The imaging of a representative patient is shown in the [Figure 1].
Table 1: Clinical features of the 6 cases of acute cholecystitis after stroke

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Figure 1: Patient 5. A 60-year old male patient with ruptured distal left anterior cerebral artery aneurysm (a). Initially, he was successfully treated with coil embolization (arrow) (b and c). A month after the onset of symptoms, he complained of abdominal pain after meals with inflammation and elevation of liver enzyme levels. Abdominal ultrasound and CT scan revealed no gallstones (d and e). He was first treated with an endoscopic nasobiliary drainage tube and his drained bile fluid contained fresh blood. He underwent cholecystectomy for possible malignancy. No tumor was found, and his final diagnosis was hemorrhagic cholecystitis

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 » Discussion Top

Among all cholecystitis patients, the frequency of acalculous cholecystitis was approximately 10%, and the majority of cases accompanied gallstones.[3] Operation, severe trauma, burns, and total parenteral nutrition are reported to be risk factors for acalculous cholecystitis. According to Tana et al., acalculous cholecystitis is a rare but a life-threatening disease because the mortality of acalculous cholecystitis is 30% and that of calculous cholecystitis is 1%.[4]

Among patients with stroke, the frequency of acalculous cholecystitis increases. It was reported that 1.2–2.4% of patients with stroke[5],[6] and 1.4% of patients with ischemic stroke[7] developed AC; 16 out of 24 (67%)[6] and 10 out of 12 (83%)[5] patients developed acalculous cholecystitis. Fukuoka et al., concluded that poor activities of daily living (ADL) due to severe hemiparesis and a long fasting state are the risk factors for cholecystitis.[7] On the other hand, Savoca et al., reported 47 patients with good ADL who developed acute acalculous cholecystitis in an outpatient clinic.[8] In our series, three of six patients were able to walk at onset, and none of our patients were in a fasting state. Therefore, the possibility of AC in patients with good ADL should be noted.

Symptoms are often non-specific to cholecystitis such as fever (70%), elevated C reactive protein (CRP) and white blood cells (WBC; 60%), elevation of transaminase (30%), and abdominal pain (20%).[5] In addition, it is difficult for some patients with stroke to complain of abdominal pain because they tend to have aphasia or a disturbance of consciousness. On abdominal ultrasound, not only the presence of gallstones but also the thickness of the gallbladder wall or biliary sludge should be carefully assessed. Acalculous cholecystitis, which has a high mortality rate compared with calculous cholecystitis, should not be misdiagnosed.

Glenn et al., previously reviewed the pathogenesis and risk factors of acalculous cholecystitis.[9] Occlusive disease of the bile duct, ischemic and reperfusion injury of the gallbladder wall, and cholestasis due to fasting are the main triggers of acalculous cholecystitis. Dehydration, bacteremia, and sedation may also cause acalculous cholecystitis. In the field of stroke treatment, patients tend to have atherosclerotic risk factors resulting in ischemic and reperfusion injury of the gallbladder wall. As dehydration, bacteremia, and sedation are occasionally exhibited by stroke patients, the preventable or treatable risk factors for AC should be addressed.

One patient had hemorrhagic cholecystitis. Hemorrhagic cholecystitis is a new entity of acalculous cholecystitis that is precipitated due to an increased use of anti-thromboembolic drugs. The contrast-enhanced CT scan demonstrated the spotty extravasation in the gallbladder. As ischemic and reperfusion injury cause hemorrhage in the submucosal layer of the gallbladder wall,[10] hemorrhagic cholecystitis needs to be considered during the treatment of stroke patients receiving anti-thromboembolic drugs.

There is a possibility that the frequency of 0.3% in our case series of AC is low compared with the previously published reports because our study may have lacked immediate and proper abdominal examination. Patient 3 developed AC even though he was eating normally and performing a good grade of ADL. Therefore, asymptomatic liver enzyme elevation should not be ignored in patients with stroke. Although the most common cause of liver enzymatic elevation is an adverse effect of the drugs administered, it may also be due to cholecystitis.

 » Conclusion Top

Stroke patients sometimes develop AC during the initial hospitalization. AC often develops asymptomatically or with non-specific symptoms in patients with stroke. There are several possible etiologies that must be considered, including ischemic and reperfusion injury of the gallbladder wall, dehydration, bacteremia, or adverse drug effects. Acalculous cholecystitis comprises the minority of all cholecystitis types, but its frequency increases in patients with stroke. As the morbidity of acalculous cholecystitis is higher than that of calculous cholecystitis, it must be kept in mind in case either an asymptomatic liver enymatic elevation or abdominal syptoms are detected in a patient with stroke.

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Conflicts of interest

There are no conflicts of interest.

 » References Top

Aaron S, Mani S, Prabhakar AT, Babu PS, Kumar S, Benjamin RN, et al. Sonothrombolysis for acute ischemic stroke-Break on through to the other side. Neurol India 2017;65:52-7.  Back to cited text no. 1
[PUBMED]  [Full text]  
Pan C, Liu N, Lian L, Xu F, Zhu S, Tang Z. Effects of endovascular therapy on acute ischemic stroke: An updated meta-analysis of randomized controlled trials. Neurol India 2016;64:1160-8.  Back to cited text no. 2
[PUBMED]  [Full text]  
Takada T, Strasberg SM, Solomkin JS, Pitt HA, Gomi H, Yoshida M, et al. TG: 13 Updated Tokyo guidelines for acute cholangitis and acute cholecystitis. J Hepatobiliary Pancreat Sci 2013;20:1-105.  Back to cited text no. 3
Tana M, Tana C, Cocco G, Romano M, Schiavone C. Acute acalculous cholecystitis and cardiovascular disease: A land of confusion. J Ultrasound 2015;18:317-20.  Back to cited text no. 4
Ushiyama M, Koike J, Zenisaka H, Seguchi K, Ikeda S, Yanagisawa N. Acute acalculous cholecystitis as a complication of cerebrovascular disease. Clin Neurol 1997;37:213-8.  Back to cited text no. 5
Koizumi K, Suzuki K, Akutsu T, Hoshino K, Hamada J, Sakai F. Acute acalculous cholecystitis in acute cerebrovascular disease. Kitasato Med J 2006;36:1-4.  Back to cited text no. 6
Fukuoka T, Hayashi T, Kato Y, Ohe Y, Deguchi I, Maruyama H, et al. Clinical review of 24 patients with acute cholecystitis after acute cerebral infarction. Intern Med 2014;53:1321-3.  Back to cited text no. 7
Savoca PE, Longo WE, Zucker KA, McMillen MM, Modlin IM. The increasing prevalence of acalculous cholecystitis in outpatients. Results of a 7-year study. Ann Surg 1990;211:433-7.  Back to cited text no. 8
Glenn F, Necker CG. Acute acalculous cholecystitis. An increasing entity. Ann Surg 1982;195:131-6.  Back to cited text no. 9
Yamanaka H, Kawanami H, Oiwa T, Watanabe N, Murata Y, Kawai S, et al. A case of ruptured pseudoaneurysm of the gallbladder involving gallbladder bleeding developed in acalculous cholecystitis during antiplatelet therapy after cerebral infarction. Japanese J Gastroenterol Surg 2013;46:431-4.  Back to cited text no. 10


  [Figure 1]

  [Table 1]


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