This is the first in a series of 3 blog posts recapping our residency’s most recent asynchronous small group exercise. For these posts, we’ll start with a case vignette and then highlight some key aspects of the presentation and cover some key learning points. You can also take a listen to the accompanying podcast for a slightly more in depth look at the case.
It was a Dark and Stormy Night in the ED…
As you setting into your shift, your first patient pops up on the track board
74 yo M, CC: Back Pain, Lethargy
Nursing note: Patient arrives via EMS, complains of back pain. EMS states fever 104 today and confusion per family. ESRD, last HD 2 days ago.
Vitals: Temp 98.9, BP 89/77, Pulse 111, SpO2 97% RA
As you gather the history from the patient, you find that he is a 74 yo M with PMHx of ESRD (HD MWF), DMII, and BPH with the primary complaint of back pain. EMS states they picked him up from a local hotel as his apartment building caught fire the day before and he is now staying there with family assistance. He tells you that he has had back pain for almost a year now and is just “tired of it.” EMS, however, tells you that the family told them that he is not acting like himself and had a fever today of 104 before they called 911. He hasn’t had any history of trauma. And, though he does have a history of ESRD he does typically make urine but hasn’t been able to urinate over the past several days.
On your physical exam you find him to be sleepy but participative in the exam. He has an irregularly, irregular tachycardic heart rate and rhythm. His lungs are clear if not a bit diminished in the bases and abdomen is soft and nontender. As the case unfolds, the nurse is ultimately unable to obtain urine and the patient has significant pain with attempts to place a foley. Performing a rectal exam, you find the patient to ultimately have an enlarged, tender, and soft prostate. The patient’s labs are remarkable for an elevated white count (24.6), mild elevation of lactate (2.8), and renal failure consistent with the patient’s history. You ultimately diagnose the patient with sepsis secondary to prostatitis.
Acute Bacterial Prostatitis
Acute bacterial prostatitis most commonly presents as pelvic pain and/or urinary tract infection symptoms (dysuria, frequency, obstruction) in men with a peak incidence occurring in patients aged 20-40 years old and >70 years old. (1). The causative organisms are typically the same bacteria that tend to cause other urinary tract infections (E. Coli, Pseudomonas, Klebsiella, Enterobacter). However in sexually active patients, one should also consider Neisseria gonorrhoeae and Chlamydia trachomatis. Patients who have had recent transurethral procedures are at greater risk of multi-drug resistant organisms.
On physical exam, patients with prostatitis will typically have an enlarged, tender, and “boggy” prostate. Because aggressive or repeated manipulation of the prostate during digital rectal exam can lead to bacteremia and possibly sepsis, the digital rectal exam should be performed gently. (1)
The treatment of acute bacterial prostatitis should include antibiotics that are directed towards likely causative organisms with attention paid to local antibiograms as well as risk factors for multi-drug resistant organisms. Abscesses of the prostate can occur (2.7% of patients) and should be considered for patients who are not responding to appropriate antibiotic therapy, immunocompromised patients, patients who have had recent transurethral procedures, and those with chronic indwelling foley catheters. Approximately 13% of patients will have a recurrence of symptoms so outpatient follow up with a primary care physician is important to ensure resolution of the infection. (1)
Atrial Fibrillation with RVR in the setting of Sepsis
Atrial fibrillation with rapid ventricular response in the setting of sepsis or concurrent medical illness can be a bit of a chicken and egg situation. Is this a patient who has atrial fibrillation and is appropriately tachycardic as a response to their underlying illness? Or is this a patient who’s tachydysrhythmia is leading to hypotension? If you choose to treat the tachycardia are you taking away the body’s appropriate response to some insult? Or will you improve their perfusion and hemodynamics by allowing greater filling time for their LV?
Scheuermeyer and colleagues (2) in 2015 published a retrospective descriptive cohort of patients looking to explore the exact conundrum these patient’s present. The authors hypothesized that patients with A fib with RVR and a concurrent illness who were treated with rate or rhythm control would have poorer outcomes than those who did not have rate or rhythm control. The outcomes they were looking for were major adverse events (new hypotension requiring vasopressors, intubation or NIPPV, new bradycardia requiring intervention, confirmed stroke or thromboembolic event, chest compressions and death). The reviewed cohort include 416 patients, 105 who had rate control, 30 who had rhythm control, and 281 who had no specific rate or rhythm control. The rate/rhythm control group had an adverse event rate of 40.7% whereas the group without rate or rhythm control had an adverse event rate of 7.1%.
Walkey and colleagues (3) specifically looked at septic patients with atrial fibrillation. Theirs was also a retrospective cohort study where they used a propensity matched cohort to look at mortality differences for different treatment strategies employed in the study population. Using an administrative database, they identified 39,711 patients who were diagnosed with atrial fibrillation and sepsis who also received some form of IV therapy for the treatment of atrial fibrillation. Calcium channel blockers were used in 36% of cases, beta-blockers in 28%, digoxin in 20%, and amiodarone in 16%. The authors performed a number of analyses comparing beta-blockers to each of the other treatment modalities, using propensity matching to identify a comparable cohort for each analysis. Outcomes in the beta blocker groups were better in all analyses when compared to digoxin and for amiodarone. In comparison to calcium channel blockers, the outcomes in the beta-blocker groups were better in all groups excepting those with new-onset A fib, pre-existing A fib, and those not requiring vasopressors. When all beta-blocker patients were compared to all calcium channel blocker patients, outcomes were better in the beta-blocker group.
There are several possible takeaways from these articles. First both of these articles are retrospective reviews and therefore, treatment effects can be exaggerated. Ideally these findings would be reproduced with prospective studies. Second, if these results are to be believed, one should approach these patients by first treating their underlying illness (be it sepsis or otherwise). If you do get to a point where you want to treat the rate or rhythm of a patient with A fib and sepsis, beta blockers may be a better way to treat those patients.
Coker, T. & Dierfeldt, D. (2016) Acute Bacterial Prostatitis: Diagnosis and Management. 15;93(2):114-20.
Scheuermeyer F, Pourvali R, Rowe B, et al. (2015) Emergency Department Patients With Atrial Fibrillation or Flutter and an Acute Underlying Medical Illness May Not Benefit From Attempts to Control Rate or Rhythm. Annals of Emergency Medicine. 65(5):511–2.
Walkey A, Evans S, Winter M, Benjamin E. (2016) Practice Patterns and Outcomes of Treatments for Atrial Fibrillation During Sepsis. CHEST. 149(1):74–83.
Authored by Jeffery Hill, MD MEd