Part 2 of a series.
My own self-appointed role as my father’s health care advocate during his prostate cancer battle was a natural consequence of my training as a medical researcher. After earning a PhD in medical science, I became the elected family health and wellness guru, offering insight into everything from hangnails to stem cells, with the ongoing disclaimer that “I’m not a doctor, I just play one on TV.” Though not versed in clinical care, my theoretical knowledge of the scientific literature, as well as years of training in critical assessment, evidence-based investigation, and emerging standards of care put me in a position to help my father and family navigate the disorienting and overwhelming experience of being a cancer patient. I had the emotional motivation and the time to meticulously pore over my father’s test results, comb through the medical literature and extend an ever-watchful eye over my father, noticing patterns of symptoms and potential gateways for intervention. After the devastating missed diagnosis of metastatic recurrence and the resulting small window of opportunity for treatment, I made it my mission to be a perpetual thorn in the side of my father’s medical team- an additional line of defense against mistakes. I can only imagine the rolling eyes and sighs that the repeated pleas of the interfering daughter provoked when they were mentioned at Grand Rounds. Despite my attempts to stay one step ahead in the game of chess that was my father’s deteriorating health, the missed opportunities for timely and adequate care accumulated.
Active surveillance: What is being monitored and how closely?
Active surveillance is a term used to describe the regular monitoring of a prostate cancer patient’s disease status in order to delay invasive interventions and their related risks and side effects, thereby maximizing the quality of life. Active surveillance typically involves twice yearly prostate-specific antigen (PSA) bloodwork, a digital rectal exam (DRE) and assessment of new symptoms, as well as regular prostate biopsies and diagnostic imaging as required. In men who have previously had their diseased prostate surgically removed, active surveillance excludes DREs and biopsies, emphasizing PSA blood work as a gauge of cancer recurrence. Since PSA is produced by prostate cells, a man without a prostate is expected to have a PSA blood level close to zero. A PSA rise in such men is presumed to be the result of cancer relapse.
Active surveillance is often recommended in older men who face additional health challenges, whose cancer is expected to grow slowly, based on a low Gleason Score (a clinical measure of aggressiveness), and whose cancer is small and confined to the prostate. At the time of diagnosis in 2011, my father’s PSA level was elevated, though not as high as typically seen in cases of aggressive, non-metastatic prostate cancer. Due to the aggressiveness of the cancer, he was not considered a candidate for active surveillance and was advised that if he “would like to see the sunrise” surgical removal of his prostate was his best chance for survival. The operation was deemed successful, and although pathology samples of the prostate confirmed the initial biopsy results of aggressive cancer, further treatment with radiation or chemotherapy was not considered necessary. Instead, my father became a candidate for post-operative active surveillance. Between 2011-2017, he attended his doctor’s appointments every six months without fail, each time receiving a clean bill of health after PSA blood work showed unchanged (near zero) levels of PSA. During this time, his urological oncologist did not order any diagnostic imaging, relying on PSA as the primary measure of disease-free status.
In 2016, my father’s medical history was complicated by a diagnosis of indolent lymphoma, a slow-growing cancer of the blood that often remains stable for years, even regressing spontaneously in some cases. At the time of diagnosis, my father’s hematologist ordered a routine full-body CT scan, the results of which did not show evidence of lymph node enlargement, either from the lymphoma or prostate cancer. His hematologist was confident that as long as my father was not exhibiting symptoms, he did not require treatment. He was now under active surveillance for two types of cancer.
In April 2017, my father received his first worrisome PSA results — the numbers were slightly elevated. Additional blood tests over the next year confirmed the trend, and he was told that his PSA had reached a high enough level that it indicated cancer relapse. During the multiple visits with his urological oncologist over the course of that year, we discussed additional tests and treatment options. Despite repeated requests for a CT scan or alternative diagnostic imaging to assess the extent of disease recurrence, we were told that there was no imaging available that would pick up the “pinhead cluster” of microscopic cells representative of such a low rise in PSA. We were advised that although my father’s PSA was elevated, it was still so low that there was minimal concern for metastatic spread. Given this, my father was counseled to consider localized pelvic radiation therapy, based on the assumption that the relapse was confined to the area where his prostate once was.
Meanwhile, the new and unexplained constipation, loss of appetite and weight loss that my father was experiencing caught the attention of his family physician, who sent him for an abdominal ultrasound in May 2018. This test showed numerous spots on his liver, suspicious for metastatic disease. My father presented these results to his urological oncologist, and our year-long plea for a CT scan was finally honored. The CT results showed extensive full-body lymph node enlargement in the pelvis, abdomen, chest and neck regions, in addition to innumerable tumors in the liver. A liver biopsy definitively ruled out lymphoma, demonstrating that the liver tumors were most likely prostate cancer. A week after the 2018 CT was taken, an addendum was surreptitiously added to the 2016 CT scan report, stating that upon further review, enlarged lymph nodes were, in fact, present in the abdomen and pelvis. The radiologist reading the CT scan in 2016 neglected to accurately interpret and report the findings. By the time he added this information to the report in 2018, it was too late — the prostate cancer had infiltrated my father’s liver and the lymph nodes throughout his body. Nobody from my father’s medical team informed us of — let alone took responsibility for, this appalling mistake. I discovered it while reviewing my father’s reports during the writing of this article, shocked to discover that he had at least a two-year window during which to receive timely and effective treatment.
Based on my father’s liver biopsy results, the malignant cells did not express much PSA receptor, which in retrospect was not surprising given that his cancer was a low PSA secretor, as some aggressive types of prostate cancer are. My father’s PSA levels were relatively low at the time of initial diagnosis and at the time of cancer recurrence, never accurately reflecting the extent of disease burden. The assumption that his rising (yet low) PSA during 2017-2018 represented a highly treatable, localized relapse was yet another tragic mistake. As my father’s case demonstrates, tracking PSA is not a reliable diagnostic tool on its own, particularly in patients who are being monitored for relapse following treatment of aggressive disease. For those rare patients who present outside of the statistical norm, the current protocols for active surveillance are insufficient. The limitations of the PSA test should be acknowledged and alternative practices for adequate and close monitoring, such as early and routine scans, should be implemented, particularly if there are signs of recurrence and regardless of the extent to which PSA values rise.
Had my father undergone routine diagnostic imaging during the years following his surgery, his urological oncologist may have discovered much earlier that the cancer had spread to the lymph nodes and that there was a conspicuous mass adjacent to the surgical clips in the area where surgeons had removed his prostate, which in retrospect was presumed to be the likely source of metastatic spread. Had my father’s repeated requests for diagnostic imaging been honored when his PSA first began to rise in April 2017, his urological oncologist would have discovered that his PSA level did not represent localized recurrence, but rather extensive metastatic spread. Had hormonal therapy been initiated at this point, before my father developed symptoms and his functional status began to decline, it may have made a significant difference to his short- and long-term prognosis, particularly since the final CT scan before he passed showed that the hormonal therapy he received two months earlier was working. Instead, my father’s family physician discovered metastatic disease on a simple abdominal ultrasound, while his urological oncologist, who was responsible for his ongoing care, glibly conceded “I guess I’m going to have to eat my hat.” Three months elapsed from the time we heard those words to the time my father passed. The small window of opportunity for treatment narrowed with each additional oversight during the multiple outpatient procedures and hospital admissions that followed.
Iris Kulbatski is a science writer.
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