Infections are a common cause of death and an even more common cause of morbidity in patients with a wide variety of neoplasms. Autopsy studies show that most deaths from acute leukemia and half of deaths from lymphoma are caused directly by infection. With more intensive chemotherapy, patients with solid tumors have also become more likely to die of infection. Fortunately, an evolving approach to prevention and treatment of infectious complications of cancer has decreased infection-associated mortality rates and will probably continue to do so. This accomplishment has resulted from three major steps:
The practice of using “early empirical” antibiotics reduced mortality rates among patients with leukemia and bacteremia from 84% in 1965 to 44% in 1972. Recent studies suggest that the mortality rate due to infection in febrile neutropenic patients dropped to <10% by 2013. This dramatic improvement is attributed to early intervention with appropriate antimicrobial therapy.
“Empirical” antifungal therapy has also lowered the incidence of disseminated fungal infection, with dramatic decreases in mortality rates. An antifungal agent is administered—on the basis of likely fungal infection—to neutropenic patients who, after 4–7 days of antibiotic therapy, remain febrile but have no positive cultures.
Use of antibiotics for afebrile neutropenic patients as broad-spectrum prophylaxis against infections has decreased both mortality and morbidity even further. The current approach to treatment of severely neutropenic patients (e.g., those receiving high-dose chemotherapy for leukemia or high-grade lymphoma) is based on initial prophylactic therapy at the onset of neutropenia, subsequent “empirical” antibacterial therapy targeting the organisms whose involvement is likely in light of physical findings (most often fever alone), and finally “empirical” antifungal therapy based on the known likelihood that fungal infection will become a serious issue after 4–7 days of broad-spectrum antibacterial therapy.
A physical predisposition to infection in patients with cancer (Table 30-1) can be a result of the neoplasm’s production of a break in the skin. For example, a squamous cell carcinoma may cause local invasion of the epidermis, which allows bacteria to gain access to subcutaneous tissue and permits the development of cellulitis. The artificial closing of a normally patent orifice can also predispose to infection; for example, obstruction of a ureter by a tumor can cause urinary tract infection, and obstruction of the bile duct can cause cholangitis. Part of the host’s normal defense against infection depends on the continuous emptying of a viscus; without emptying, a few bacteria that are present as a result of bacteremia or local transit can multiply and cause disease.
TABLE 30-1Disruption of Normal Barriers that May Predispose to Infections in Patients with Cancer |Favorite Table|Download (.pdf) TABLE 30-1 Disruption of Normal Barriers that May Predispose to Infections in Patients with Cancer
|Type of Defense ||Specific Lesion ||Cells Involved ||Organism ||Cancer Association ||Disease |
|Physical barrier ||Breaks in skin ||Skin epithelial cells ||Staphylococci, streptococci ||Head and neck, squamous cell carcinoma ||Cellulitis, extensive skin infection |
|Emptying of fluid collections ||Occlusion of orifices: ureters, bile duct, ...|