Clinically Silent Presentation of Acalculous Gangrenous Cholecystitis: A Case Report

A 43-year-old male presented to the emergency department with a five-day history of high-grade fever, chills, and generalized weakness. His medical history was significant for a recent intracerebral hemorrhage approximately one month prior to admission, complicated by residual right-sided hemiplegia. He had been discharged from a tertiary care hospital two weeks before the current presentation following neurological stabilization. Additional comorbidities included type 2 diabetes mellitus. On presentation, the patient appeared acutely ill. Initial vital signs demonstrated a temperature of 39.5°C, blood pressure of 120/80 mmHg, heart rate of 115 beats/min, respiratory rate of 18 breaths/min, and oxygen saturation of 98% on room air. Neurological examination demonstrated residual right-sided hemiplegia consistent with recent cerebrovascular injury. Initial abdominal examination revealed a soft abdomen without significant right upper quadrant tenderness, guarding, rebound tenderness, or other overt peritoneal signs. Murphy’s sign was not clearly elicited. Initial laboratory evaluation demonstrated marked systemic inflammation with leukocytosis, neutrophilia, and elevated C-reactive protein (CRP) (Table 1 ). Additional laboratory findings demonstrated a mixed hepatocellular-cholestatic pattern of liver dysfunction, with a predominance of cholestatic abnormalities (Table 2 ). Serum lactate and procalcitonin levels remained within normal limits (Table 1 ). AST: aspartate aminotransferase; ALT: alanine aminotransferase; GGT: gamma-glutamyl transferase; TBIL: total bilirubin Empiric intravenous antimicrobial therapy with cefepime and amikacin was initiated. During the subsequent 24-48 h, the patient demonstrated progressive clinical deterioration despite antimicrobial therapy and supportive management. CRP increased to 406 mg/L (Figure 1 ). Blood cultures yielded no growth. As part of the differential diagnostic evaluation for a potential urinary source of infection, a urine culture was obtained and grew drug-resistant  Klebsiella pneumoniae extensively despite an unremarkable urinalysis and the absence of findings suggestive of active urinary tract infection. The isolate remained susceptible only to amikacin and colistin. Given the absence of urinary symptoms, negative urinalysis findings, and the patient's recent history of hospitalization with prolonged urinary catheterization, this finding was interpreted as asymptomatic bacteriuria, with the extensively drug-resistant phenotype suggesting healthcare-associated acquisition and catheter-associated colonization. Abdominal ultrasonography demonstrated diffuse gallbladder wall thickening with intraluminal sludge and surrounding inflammatory changes without evidence of gallstones. Given the cholestatic liver enzyme abnormalities and concern for occult biliary obstruction or cholangitis, magnetic resonance cholangiopancreatography (MRCP) was performed, which demonstrated marked gallbladder wall thickening and pericholecystic inflammatory infiltration, without evidence of choledocholithiasis (Figures 2A - 2D ). Imaging findings raised suspicion for acalculous cholecystitis; however, definitive radiologic evidence of gangrenous transformation was not identified preoperatively. (A, C) Coronal, (B) axial, and (D) sagittal images. Pericholecystic fluid collections (red arrows), likely representing inflammatory exudate/infiltrate. Diffuse gallbladder wall thickening (green arrows). Intraluminal sludge within the gallbladder and cystic duct (blue arrows). (C) Fold/kinking at the gallbladder neck (yellow arrow). MRCP: magnetic resonance cholangiopancreatography; TRUFI: True Fast Imaging with Steady-State Free Precession Due to persistent systemic toxicity, progressive inflammatory response, and increasing concern for occult complicated biliary infection refractory to medical therapy, urgent laparoscopic exploration was undertaken. Laparoscopic cholecystectomy was successfully performed, along with extensive peritoneal lavage, drainage placement, and debridement of necrotic pericholecystic tissue. Intraoperative findings included approximately 400-500 mL of bilious-purulent fluid with extensive fibrinous deposits distributed throughout the pericholecystic space, right subphrenic region, right paracolic gutter, and pelvis. Dense adhesions were present between the greater omentum and the anterior abdominal wall, as well as between the gallbladder and the omentum. The gallbladder was markedly enlarged with a thickened, friable wall and scattered serosal petechial hemorrhages (Figures 3A , 3B ). Calot’s triangle was densely inflamed and edematous. Microbiological culture of peritoneal fluid subsequently yielded pan-sensitive Escherichia coli . (A) Laparoscopic view demonstrating a markedly inflamed gallbladder with petechial serosal hemorrhages; (B) gross specimen following cholecystectomy demonstrating wall thickening and extensive dark red-to-black discoloration. Histopathological examination confirmed acute acalculous gangrenous cholecystitis characterized by diffuse transmural necrosis, hemorrhagic destruction, severe acute inflammatory infiltration, and complete loss of normal gallbladder mucosal architecture (Figures 4A , 4B ). Histopathological examination demonstrates extensive gallbladder wall necrosis with marked architectural destruction, associated hemorrhage (yellow arrows), diffuse acute inflammatory infiltrates (blue arrows), and interstitial edema (green arrows). The patient demonstrated rapid postoperative clinical improvement following definitive surgical source control. Fever resolved shortly after surgery, and inflammatory markers declined markedly during the early postoperative period. CRP levels demonstrated a pronounced postoperative decrease immediately following laparoscopic cholecystectomy (Figure 1 ). The patient progressively resumed oral intake and maintained normal bowel function. He was discharged in stable condition on postoperative day eight.

Acute acalculous cholecystitis (AAC) is an acute necroinflammatory disease of the gallbladder occurring in the absence of gallstones and accounts for approximately 10% of all cases of acute cholecystitis [ 1 ]. Although less common than calculous cholecystitis, AAC is associated with substantially higher morbidity and mortality due to its frequent progression to gallbladder ischemia, gangrene, perforation, and generalized biliary peritonitis [ 1 , 2 ]. The disease demonstrates a marked male predominance and is particularly challenging to diagnose in patients with severe underlying medical or neurological conditions [ 2 , 3 ]. AAC typically presents with clinical manifestations similar to those observed in acute calculous cholecystitis (ACC), including fever, tachycardia, hypotension, and abdominal pain. Nevertheless, the presentation in critically ill patients may be atypical, with abdominal symptoms being minimal or entirely absent. In these cases, the underlying critical condition can obscure the signs of AAC, making early recognition and diagnosis particularly challenging [ 4 ]. Laboratory abnormalities, including leukocytosis and liver enzyme elevation, are neither sensitive nor specific, and imaging findings may initially be subtle or inconclusive. Consequently, diagnosis is often delayed until advanced complications such as gangrenous cholecystitis or perforation have already developed. Gangrenous cholecystitis represents one of the most severe complications of AAC and develops in approximately 50% of affected patients [ 1 ]. We report a case of clinically occult AAC complicated by purulent biliary peritonitis in a patient with recent hemorrhagic stroke and residual neurological deficits who presented predominantly with severe systemic inflammatory response and minimal abdominal findings. This case highlights the diagnostic difficulty of severe biliary pathology in patients with neurological deficits. It emphasizes the importance of careful abdominal reassessment and timely surgical source control despite deceptively nonspecific clinical and laboratory findings.

Acute acalculous cholecystitis (AAC) is an uncommon but severe inflammatory disease of the gallbladder associated with high morbidity and mortality. Although classically described in critically ill hospitalized patients, AAC may also occur in patients without ongoing critical illness, particularly in the presence of vascular comorbidities, diabetes mellitus, recent major systemic illness, prolonged immobilization, or prior hospitalization [ 1 ]. This patient had several important predisposing factors for AAC, including male sex, recent severe neurological illness, prolonged hospitalization, reduced mobility, diabetes mellitus, and possible periods of relative hypoperfusion during the preceding cerebrovascular event. In the present case, gallbladder sludge was demonstrated on imaging (Figure 2 ). Prolonged fasting and total parenteral nutrition, both commonly encountered during hospitalization for severe illness, impair gallbladder emptying and promote the formation of biliary sludge [ 5 ]. Although recent hospitalization and neurological illness may have contributed to gallbladder stasis and represent a plausible mechanism underlying sludge formation, this association remains speculative, as no prehospitalization abdominal imaging was available to establish the timing of sludge development. The pathogenesis of AAC is multifactorial and is believed to result primarily from gallbladder ischemia and cholestasis. The gallbladder is supplied by the cystic artery, a terminal artery particularly susceptible to hypoperfusion and ischemia [ 6 ]. Prolonged fasting and long-term total parenteral nutrition (TPN) in critically ill patients can lead to biliary stasis due to the absence of cholecystokinin (CCK) stimulation. Gallbladder stasis increases intraluminal pressure and causes distention, resulting in inflammation and thickening of the gallbladder wall. If the pressure is not relieved, impaired blood flow from the cystic artery can lead to ischemia [ 1 , 7 ]. This static condition increases the seeding and growth of enteric organisms, particularly Escherichia coli , Klebsiella, Bacteroides, Proteus, Pseudomonas, and Enterococcus faecalis , and may result in gangrenous transformation, perforation, and biliary peritonitis [ 7 ]. In the present case, it is conceivable that gallbladder ischemia may have originated during the patient’s earlier hospitalization for intracerebral hemorrhage, when immobility, altered nutritional intake, and potential episodes of impaired perfusion may have contributed to the development of acalculous gallbladder injury. Although this temporal association cannot be definitively established, it represents a plausible pathophysiological explanation linking the patient’s recent cerebrovascular event with subsequent development of AAC. The differential diagnosis initially included other potential infectious sources, including urinary tract infection, cholangitis, pancreatitis, and other causes of systemic inflammatory response [ 1 , 7 ]. Given the absence of clinical and laboratory evidence supporting urinary tract infection, the extensively drug-resistant (XDR) Klebsiella pneumoniae isolate was interpreted as catheter-associated asymptomatic bacteriuria, as prolonged urinary catheterization is associated with a daily bacteriuria acquisition rate of 3-7%, with nearly universal colonization after a month of catheterization [ 8 ]. Moreover, the isolate's extensive drug-resistance profile is consistent with a healthcare-associated origin. Although imaging is essential in diagnosing acute cholecystitis, no definitive gold standard exists for gangrenous cholecystitis. Ultrasound is typically the first-line modality due to its availability and bedside use, showing high sensitivity for acute cholecystitis, but limited specificity for gangrenous changes, as findings such as wall thickening and pericholecystic fluid are nonspecific. CT is commonly used as a second-line modality. It has good diagnostic performance for acute cholecystitis and is commonly performed to further evaluate disease severity and identify potential complications; however, its sensitivity for gangrenous transformation is limited. Magnetic resonance cholangiopancreatography (MRCP) provides superior soft-tissue contrast and enables better evaluation of inflammatory changes in the gallbladder wall [ 9 ]. MRCP is often helpful to exclude concurrent choledocholithiasis [ 4 , 10 ]. In this case, ultrasonography and MRCP demonstrated gallbladder wall thickening, sludge, and pericholecystic inflammatory changes without evidence of choledocholithiasis or major biliary obstruction. Although these findings were supportive, definitive diagnosis was ultimately achieved through surgical exploration and subsequent histopathological examination. Several limitations of this study should be acknowledged. First, the temporal relationship between the patient’s prior intracerebral hemorrhage and the imaging findings remains speculative, as no preillness abdominal imaging was available. Second, the exact onset of gallbladder ischemia cannot be definitively established, and a causal relationship between the identified risk factors and disease development cannot be proven. Third, colonization with multidrug-resistant Klebsiella pneumoniae in the context of prolonged urinary catheterization is a plausible explanation; however, definitive confirmation would have required precatheterization urine cultures, which were not available in this case.

This case highlights the diagnostic challenges of acute acalculous cholecystitis, particularly in patients with recent severe neurological illness, in whom abdominal symptoms may be absent or difficult to recognize. Clinicians should maintain a high index of suspicion for occult intra-abdominal pathology when systemic inflammation is disproportionate to physical examination findings. This case also underscores the importance of careful clinical correlation with microbiological findings. Although extensively drug-resistant Klebsiella pneumoniae was isolated from the urine, it was considered colonization rather than the primary source of infection and therefore did not warrant targeted antimicrobial therapy. Early diagnosis and timely surgical source control remain essential for favorable outcomes in complicated acalculous cholecystitis while helping to avoid unnecessary antibiotic use.