3 Discussion
As a crucial component in cancer treatment, chemotherapy plays a vital
role in eliminating tumour cells. However, it also exerts a significant
cytotoxic effect on normal, rapidly dividing cells, particularly
haematopoietic cells. This often leads to chemotherapy-induced bone
marrow suppression, resulting in a reduced number of white blood cells
and platelets, which lowers the overall immune response in patients.
Tumour presence, chemotherapy, and compromised systemic immunity are
common predisposing factors for bacterial pyogenic liver abscess. In
China, Klebsiella pneumoniae is the predominant pathogen that causes
bacterial pyogenic liver abscess [13,14]. The primary route of
infection is through the intestines. As a normal inhabitant of the human
gastrointestinal tract, Klebsiella pneumoniae can translocate to the
portal vein or bile ducts, causing infection and resulting in Klebsiella
pneumoniae pyogenic liver abscess (KPPLA) when the immune defences in
the body are compromised. There is a high likelihood of KPPLA
haematogenous spread, which poses a risk of invasive infections in other
organs, especially with hypervirulent Klebsiella pneumoniae (hvKP)
[15,16]. The abundant capsule polysaccharides on the surface allow
the bacteria to evade phagocytosis by macrophages and neutrophils in the
bloodstream, as well as resist serum complement bactericidal activity.
In patients with chemotherapy-induced bone marrow suppression, the
significant decrease in white blood cells and neutrophils makes them
more susceptible to systemic dissemination of Klebsiella pneumoniae,
which can potentially penetrate the blood-ocular barrier and enter the
vitreous cavity. The vitreous, an avascular tissue rich in water and
proteins, provides an ideal environment for bacterial growth and
nutrition. Once infected, the vitreous is prone to the formation of
infectious foci, leading to the occurrence of EE. Currently,
chemotherapy-induced bone marrow suppression and KPPLA can be
successfully treated in most cases, but the prognosis for EE is
generally poor. EE can rapidly cause permanent irreversible visual
impairment [17], especially when associated with hvKP infection and
the optimal treatment window is missed. Indeed, hvKP infections can lead
to irreversible retinal photoreceptor cell damage within 48 hours of
ocular tissue infection. Reports indicate that 57.8% of eyes affected
by EE ultimately lose light perception, while 26.8% require removal to
eradicate the infection [18].
In clinical practice, patients often experience bone marrow suppression
after chemotherapy. The severity of bone marrow suppression ranges from
Grade 0 to Grade IV and is classified according to the Common
Terminology Criteria for Adverse Events (CTCAE) version 5.0 from the
National Cancer Institute (NCI). In this case, the patient underwent
three cycles of AC chemotherapy, resulting in Grade III bone marrow
suppression. KPPLA lesions are typically solitary and predominantly
located in the right lobe of the liver. They are possibly associated
with the large volume and rich blood supply of the right liver lobe.
Clinical manifestations primarily include fever and chills, and
diagnosis is typically based on blood tests and imaging examinations
such as colour ultrasound and CT. EE often affects a single eye, with
similar incidence rates in both the left and right eyes [11].
Initial symptoms of EE are mild and inconspicuous, and they are often
overlooked by physicians, who frequently misdiagnose EE as
iridocyclitis, acute necrotising retinitis, or panuveitis. However, the
condition progresses rapidly, leading to blurred vision accompanied by
ocular pain in the affected eye. Additionally, severe cases may exhibit
purulent discharge. Diagnosis is made according to the patient’s medical
history, symptoms, signs, ocular auxiliary examinations, microbial
bacterial cultures from intraocular specimens, and rapid identification
of bacterial species through PCR testing of aqueous humour and vitreous
samples.
Currently, there are no documented cases in the domestic or
international literature of chemotherapy-induced bone marrow suppression
combined with pyogenic liver abscess leading to EE. Since this article
represents the first report of such a case, there is no consensus
regarding the diagnosis and treatment of patients with similar
conditions. In clinical practice, treatment approaches predominantly
involve systemic and local interventions [20,21]. Systemic
treatments encompass both recovery therapy for bone marrow suppression
and anti-inflammatory measures. Febrile neutropenia (FN), which is the
most prevalent type of bone marrow suppression, is typically addressed
by stimulating bone marrow haematopoiesis using haematopoietic growth
factors. Additionally, granulocyte colony-stimulating factors (G-CSF)
are commonly employed in clinical settings, including short-acting
recombinant human G-CSF (rhG-CSF) and long-acting pegylated recombinant
human G-CSF (PEG-rhG-CSF). Both of these growth factors have been proven
to be effective in preventing FN [22]. In systemic anti-inflammatory
treatment, the initial step usually involves the empirical selection of
antibiotics that are sensitive to Klebsiella pneumoniae [23].
Klebsiella pneumoniae strains normally produce beta-lactamases and are
generally susceptible to third- and fourth-generation cephalosporins,
fluoroquinolones, aminoglycosides, and carbapenems. Antibiotic choices
should be guided by bacterial culture and sensitivity results, with
appropriate adjustments. Following infection control, a de-escalation
treatment strategy is necessary. The patient in this study initially
received ceftazidime but subsequently transitioned to the more sensitive
imipenem. After achieving improved infection control, she returned to
ceftazidime. It is crucial to note that for patients with a history of
diabetes, strict blood sugar control is essential during systemic
treatment. Elevated blood sugar levels may compromise the phagocytic
function of white blood cells [24], disrupt vascular permeability,
breach the blood-ocular barrier, facilitate bacterial dissemination in
the bloodstream, and aggravate symptoms of EE, potentially affecting
both eyes. Furthermore, attention should be directed towards digestive
symptoms such as nausea, vomiting, and diarrhoea, which are commonly
associated with chemotherapy. Ensuring the overall nutritional status of
the patient, correcting hypoalbuminaemia, anaemia, and electrolyte
imbalances, and enhancing the immune response of the body are essential
elements of care.
Local treatment mostly focuses on managing the KPPLA infection and
addressing the eye affected by EE. Since KPPLA is the primary source of
EE infection, local liver puncture drainage is a crucial intervention
for directly eliminating the cause and controlling the spread of
infection [25]. For infected lesions with a diameter greater than 3
cm and good liquefaction, percutaneous pyogenic liver abscess puncture
drainage under ultrasound or CT guidance is usually performed. Compared
to surgical treatment, puncture drainage is safer, more convenient, and
results in minimal trauma. As a result, it is more widely accepted by
patients. In cases with multiple abscess lesions, clinicians adopt a
sequential approach that addresses the larger abscesses before the
smaller ones. After puncture, imaging follow-ups are usually conducted
weekly to assess changes in abscess volume and identify new pyogenic
liver abscesses or liquefied lesions. If there are new abscesses, repeat
puncture may be necessary. In this study, the patient received a
follow-up abdominal CT one month after catheter placement. The scan
revealed a significant reduction in the pyogenic liver abscess cavity
with no new lesions, so the drainage tube was removed. Surgical
treatment should be considered in cases where puncture drainage proves
ineffective and there is a high risk of abscess rupture, or if rupture
has already occurred and has led to pleurisy, peritonitis, or concurrent
biliary tract diseases.
In the treatment of EE, the blood-ocular barrier limits the
effectiveness of intravenous antibiotic administration. It results in
low drug concentrations within the eye, making it difficult to achieve
positive therapeutic outcomes. Therefore, it is crucial to administer
local ocular treatment, which includes vitrectomy and intraocular drug
injection into the vitreous cavity. In contrast to subconjunctival
injection, topical eye drops, or systemic antibiotics, intraocular drug
injection effectively maximises drug concentrations within the vitreous
cavity. Clinically, antibiotics with favourable intraocular penetration
and a broad spectrum are commonly utilised, including vancomycin,
ceftazidime, amikacin, fluoroquinolones, and others, as well as
combinations of these drugs, as necessary. Ideally, drug injection
should be conducted within 48 hours of the onset of eye discomfort
symptoms. While intraocular drug injection effectively eliminates
pathogenic bacteria in the vitreous cavity, its impact on lesions under
the retina is limited. Hence, when deemed necessary, vitrectomy is
performed to thoroughly clear lesions under the retina, enhance the
intraocular environment, restore retinal function, reduce the risk of EE
recurrence, and prevent serious complications [26]. In our case,
given her compromised overall health, severe intraocular inflammation,
and elevated surgical risks, the patient declined surgical intervention
and opted solely for intraocular drug injection. Although the
intraocular infection was successfully controlled using this approach,
the patient experienced permanent vision loss in the affected eye.