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.