Discussion
CTRX, a third-generation cephalosporin antibiotic, is used worldwide to
treat infectious diseases, including lower respiratory tract infections,
bacterial meningitis, and skin and soft tissue infections, since it can
penetrate tissues. CTRX-associated pseudolithiasis is a known
complication, reported mainly in children. The mechanism is ascribed to
a high CTRX concentration in the gallbladder bile, which is 20- to
150-fold higher than that in the serum. When the CTRX concentration in
the gallbladder exceeds its threshold, CTRX can precipitate by binding
to calcium ions secreted along with bile acids. Since CTRX can
precipitate with calcium, CTRX-associated pseudocholelithiasis is
principally composed of calcium-CTRX complexes 3.
Subcutaneous, deep muscle, and retroperitoneal bleeding are predominant
bleeding sites in patients with AHA 1. However,
gallbladder hemorrhaging and rupture are extremely rare entities, with
only a few previously reported cases, even in patients using
anticoagulants or with bleeding disorders. According to reports,
mechanical irritation of the gallbladder wall due to preceding repeated
cholecystitis can result in hemorrhaging from the gallbladder and its
rupture 4,5. Yoshida et al. reported on the outcomes
with CTRX-associated pseudocholelithiasis. The median intervals from
CTRX administration to the diagnosis of CTRX-associated
pseudocholelithiasis and from CTRX cessation to pseudolithiasis
resolution were 10 days and 69 days, respectively. Events related to
pseudocholelithiasis occurred in 29% patients, but most of the cases
were improved with conservative treatment with CTRX cessation3. CTRX-associated pseudocholelithiasis can induce the
development of cholecystitis, but no cases with fatal outcomes,
including gallbladder hemorrhaging and rupture, have previously been
reported.
In our case, AHA was a predisposing factor, leading to gallbladder
hemorrhaging and rupture. The gallbladder is not structurally tolerant
of ischemia, since it is maintained by the cystic artery, which is a
terminal artery. Thus, high artery pressure due to a hematoma, boosted
by AHA and local ischemia from massive blood loss caused an ischemic
gallbladder wall, can trigger gallbladder rupture.
In conclusion, our case demonstrated that CTRX-associated
pseudocholelithiasis can unexpectedly induce gallbladder hemorrhaging
and rupture in a patient with a bleeding diathesis.
Clinicians should be alert for
CTRX-associated pseudocholelithiasis, which can cause a lethal outcome
in patients with a bleeding disorder, even if CTRX is ceased as soon as
pseudocholelithiasis is detected.