The patient details below are anonymized and shared for academic purposes for fellow clinicians
Mr. Rakesh, a 62-year-old man (98 kg), had been unwell for nearly five years with a troubling triad: recurrent urinary symptoms suggestive of infection, persistent low-grade fever (approximately 98.6–100°F), and difficulty in passing urine with a poor urinary stream. Over this period, he consulted multiple renowned specialists and prestigious institutions.
Repeated urine microscopy consistently showed marked pyuria—typically 100–150 pus cells per high-power field, and at times as high as ~500 per high-power field. Despite repeated evaluations and multiple courses of treatment, his fever and urinary symptoms persisted.
Over time, the patient became increasingly distressed—not only due to his symptoms, but also because he felt unheard. At several points he was told, in effect, that his findings were “not significant,” that low-grade fever under 100°F and pyuria in the 100–150 range could be “normal,” and that he might be “over-sensitive.” Whatever the intention behind those reassurances, their impact was predictable: he returned home feeling dismissed and hopeless, with no clear plan and no meaningful relief.
Because of persistent weak stream and features consistent with bladder outlet obstruction, he underwent urologic intervention including cystoscopy, removal of a bladder stone, and prostate surgery (performed for a clinically appropriate indication at his age). The procedures were reasonable from the standpoint of mechanical obstruction, but the overall problem did not resolve the way he—and his family—had hoped.
When symptoms continue after appropriate interventions, the patient’s emotional burden often intensifies. In this case, the absence of relief after procedures, coupled with ongoing urinary difficulty and fever, led to growing anxiety, low mood, and despair.
Alongside his urinary complaints, Mr. Rakesh also suffered from familial degenerative cerebellar ataxia with two siblings having died from complications of the same condition. Understandably, the neurological prognosis weighed heavily on him and his family. His physical disability had progressed to the point that he felt he could no longer function as an earning member, which further deepened his depression and sense of futility.
This context matters. When a patient is already facing a life-altering degenerative illness, persistent “minor” symptoms—especially when repeatedly invalidated—can become psychologically devastating.
When I first saw him, I approached the situation with two parallel goals:
1. Re-evaluate the medical problem from first principles (history, pattern recognition, and careful review of records).
2. Restore trust by acknowledging the reality of his suffering and committing to a structured plan.
Given the persistent pyuria over years and the chronicity of symptoms, I treated him initially in line with the available microbiology: based on urine culture sensitivity, I prescribed a full course of a broad-spectrum antibiotic. (Injection ertapenem complete course)
However, the clinical response was not convincing. His pyuria did not meaningfully improve, and his low-grade fever persisted.
At this stage, I leaned on a principle that becomes more—not less—important with experience: a report is not a diagnosis; it is a clue. Persistent pyuria over years with persistent symptoms, particularly when not responding as expected to antibiotics, should prompt the clinician to revisit the underlying etiology and ask: What are we missing?..
In his case, the overall pattern—chronicity, persistent pyuria, low-grade fever, and obstructive urinary symptoms not responding to the procedures —raised my suspicion for genitourinary tuberculosis as an underlying driver, including the possibility of inflammatory/fibrotic involvement contributing to functional obstruction.
Even when tests are not definitive, tuberculosis remains a clinically relevant possibility in many real-world settings. Importantly, the patient’s course had become prolonged and disabling. After carefully weighing the clinical picture and the limitations of prior work-ups, I initiated anti-tubercular therapy (ATT) based on my clinical judgment.
Because I expected that chronic inflammation and fibrosis could be playing a key role in his obstructive symptoms, I also used corticosteroids in tapering doses for the first six weeks as an adjunct to ATT.
The rationale was pragmatic: in tubular structures, chronic inflammatory disease can lead to scarring and narrowing. In selected cases, early anti-inflammatory treatment—along with disease-specific therapy—may reduce the risk of ongoing fibrotic progression and help relieve symptoms. As with all steroid use, this was done thoughtfully, with attention to safety and close follow-up.
The improvement was striking and clinically meaningful.
· His urinary outflow improved substantially; he and his family described a clear improvement in the force and ease of urination.
· With periodic urine monitoring, pus cells gradually declined.
· His fever pattern improved, though more slowly—possibly reflecting reduced baseline immunity and long-standing inflammatory burden. Over the following weeks, he became afebrile and felt better overall.
· His constitutional symptoms reduced, and, equally important, his confidence returned. He began to feel that “something is finally working.”
Once the urinary illness began to respond, it became clear that the next barrier to recovery was psychological—depression secondary to chronic illness and disability, amplified by fear of the degenerative neurological prognosis.
We involved a psychiatrist who approached the patient with energy, realism, and hope. That stance mattered. The patient’s mindset shifted from resignation to engagement. With structured psychiatric support, she began working actively against overthinking and persistent negative rumination, and he started exploring ways to remain productive through intellectual work even if physical capacity remained limited.
1) Never tell a patient they have “no problem” simply because we do not yet have an answer
When we label a suffering patient as “over-sensitive,” we inadvertently close doors. The patient stops reporting symptoms accurately, trust breaks down, and follow-up becomes fragmented. A far better message is:
“Your symptoms are real. We may not have the full answer yet, but we will keep working systematically.”
2) Clinical reasoning must integrate the whole story—not only the latest report
History, trajectory, family context, treatment response, and the patient’s lived experience often contain the diagnosis when tests do not. Persistent patterns (like long-standing pyuria with symptoms) should never be minimized simply because they are inconvenient to explain.
3) Tuberculosis can present subtly; absence of “positive proof” is not proof of absence
In a compatible clinical context, clinicians should keep TB on the differential—especially when the course is chronic and response to conventional treatment is poor. Where appropriate, we may need to treat based on probability, not perfection—while ensuring careful monitoring and readiness to reassess.
4) If you start a long course of therapy, your job includes protecting adherence
With prolonged regimens such as ATT, many patients (and families) will revisit doubts—especially if earlier work-ups were not definitive. We must anticipate this and provide:
· clear explanation of reasoning
· expected time course of improvement
· close follow-up
· consistent reinforcement that incomplete treatment can undo progress
5) Do not transmit hopelessness—especially in conditions with poor prognosis
Degenerative disorders can understandably weigh on clinicians too. But if we allow pessimism to dominate, it leaks through our tone and body language and becomes contagious. Patients need realism, yes—but they also need the clinician’s steady belief that something can still be done, even if cure is not possible.
6) Never be overawed by prior opinions—start fresh, respectfully
Even the best centers and clinicians have limitations: time constraints, incomplete follow-up, or a missing piece of history. Each physician owes the patient a fresh evaluation, a careful review of facts, and the courage to question assumptions when the patient’s course does not fit.
This case reinforced a simple truth: many “difficult” patients are not difficult because their symptoms are exaggerated—they are difficult because their suffering has outlasted the system’s patience. When we persist, listen deeply, and integrate clinical judgment with compassionate follow-through, we sometimes convert a seemingly “stuck” case into a turning point—not only medically, but humanly.