Traumatic dental injury, Pip-Tazo and AKI, and Infected Nephrolithiasis
Hi Team,
Rapid-fire quick hits from last shift:
Traumatic Dental Injuries
We see plenty of "dental pain," but it's important to recognize the true dental emergencies:
Complicated dental fractures involving the pulp
Apply calcium hydroxide to exposed pulp (visible as pink tissue within the fractured tooth). See how to on this EMRAP video.
Arrange urgent dental follow-up.
Consider Panorex imaging for patients with significant dental trauma.
Do not prescribe oral antibiotics for isolated, closed dental fractures.
Tooth intrusion >3 mm (with or without an associated alveolar fracture)
Requires repositioning and stabilization in the ED.
Tooth avulsion
Reimplant the tooth in the ED whenever appropriate—time is tooth. The longer the tooth remains avulsed, the lower the likelihood of successful reintegration.
Do not attempt reimplantation for complicated crown fractures, root fractures, or injuries involving an alveolar fracture.
For a great review, read or listen to the EM Cases episode on traumatic dental emergencies.
2. Piperacillin-Tazobactam and AKI? Not So Fast.
The long-held belief that piperacillin-tazobactam is nephrotoxic took a hit with the ACORN Trial, a single-center randomized trial of 2,511 hospitalized adults with acute infection comparing cefepime and piperacillin-tazobactam.
Key findings:
No difference in AKI or death by Day 14.
No difference in major adverse kidney events.
No difference in 28-day mortality.
Cefepime was associated with more neurologic toxicity, including more delirium/coma and fewer days alive without neurologic dysfunction.
An important concept is the phenomenon of "pseudo-AKI." Piperacillin-tazobactam inhibits renal tubular creatinine secretion, leading to a rise in serum creatinine without a true reduction in GFR. Studies comparing creatinine with cystatin C support that this creatinine rise often reflects a laboratory artifact rather than genuine kidney injury.
One additional observational study suggested an association between piperacillin-tazobactam and increased 90-day mortality in sepsis, possibly related to disruption of anaerobic gut flora rather than nephrotoxicity. Whether causal or not, it's a good reminder to ask yourself: Does this patient actually need anaerobic coverage?
For an excellent summary, listen to the SIMKIT review of the ACORN trial.
3. Nephrolithiasis vs. Infected Obstructing Stone
A urinalysis cannot diagnose an infected obstructing stone by itself.
Stones frequently cause inflammation, so hematuria, mild pyuria, a few bacteria, and trace leukocyte esterase are common and do not necessarily indicate infection...hence the urology saying: "All stones are dirty."
However, findings that should increase your suspicion include:
Positive nitrites
Moderate-to-large leukocyte esterase
Marked pyuria
Numerous bacteria
These become much more meaningful when combined with:
Fever
Marked CVA tenderness
Leukocytosis or elevated inflammatory markers
Always interpret the urinalysis in the context of the patient's clinical picture. A febrile UTI with an obstructed stone on imaging is much more likely to need rapid decompression. Work with your urology team for these complicated cases and to ensure good follow-up!
For an excellent review of the evidence and diagnostic pitfalls, see High-Risk and Low-Prevalence Diseases: Infected Urolithiasis in the American Journal of Emergency Medicine.
Have a great weekend!
Dillon
