A 33-year-old diabetic woman is transferred from an outside hospital with the diagnosis of obstructing ureteral stone and sepsis from pyelonephritis. She received 4 liters of saline and 2 gm of Cefepime while there.
She is alert but uncomfortable on arrival. Still mentating well enough to perceive and express pain.
Tachypnea to 34 with clear lungs. No impairment to inspiratory excursion or expiratory flow. Apparently not parenchymal in origin, the respiratory rate can represent an isolated pulmonary vascular problem, primary alkalosis, or response to a metabolic acidosis.
Tachycardic to 117 despite 4 liters of saline. With no evidence of heart failure, this could be from continued pain, but it is safer to presume she is venodilated and vasodilated, possibly with capillary leak. IVC collapses more than 50% with inspiration. Heart rate rises in attempts to maintain cardiac output during low venous return from peripheralization of volume.
Blood pressure 91/63 mm Hg. Her extremities are cool. Peripheral dermal and SQ vasoconstriction to try to maintain DBP in the setting of vasodilation of deeper vascular beds and suboptimal forward cardiac flow. These are not reassuring pressures.
RUQ exam. She is soft superficially atop the gallbladder fundus and running along the liver edge just below the inferior costal margin. Deep palpation, inferior and lateral to the right hepatic edge elicits involuntary guarding. This is either the hepatic flexure of the transverse colon or the right kidney.
Right CVA. Exquisite percussion tenderness. I move hand positions to confirm its severity: with one finger gently placed at her posterior axillary line inferior to the rib edge, and advanced slowly a centimeter, she grimaces and halts inspiration. This is the inferior renal pole. More tender than standard pyelonephritis. Purulence under pressure from a distal, completely obstructing ureteral stone? Renal abscess? Or something more?
WBC count returns greater than 20 and lactate more than 4. Practitioners attempt to ultrasound her right kidney to evaluate for hydronephrosis. It is mentioned to me that they cannot see the kidney. I wonder why for the moment, and then decide to check myself.
Shadows stream from the cortical margin peripherally. Ultrasound waves cannot penetrate it. This can represent a large staghorn calculus when emanating solely from the calyces. Similarly, emphysematous pyelitis with air restricted to the calyces and renal pelvis can reflect ultrasound waves. The outermost renal cortex should be visible in both cases. But her kidney is different; reflections start at the outer cortical margin of the kidney. All along its rim and from every angle, ultrasound cannot visualize parenchyma.
Diagnosis deconstructed: Emphysematous pyelonephritis. Air scattered throughout the entire cortex of the kidney because of a necrotizing infection consuming nephrons. We expedite CT, urology consult, and surgical ICU admission. Meropenem and amikacin are administered.
The CT scan confirms high-grade emphysematous pyelonephritis extending beyond Gerota's fascia and into the pararenal space. The native organ replaced by clouds of air with islands of morselized renal tissue floating in between. Unlike emphysematous pyelitis limited to the pelvicalyceal system and drainable from a well-placed nephrostomy tube, emphysematous pyelonephritis has devitalized the tubular cells and interstitium and does not always have a focal, drainable core.
Urology house staff mention their preference for conservative management with IV antibiotics and an attempt at nephrostomy drainage, an approach cited in recent literature based on multiple retrospective reviews, each with a small number of patients. Some reports describe increased mortality in emergency nephrectomy groups as compared with percutaneous drainage.
Sounds suspicious to me, and doesn't pass the common sense test for necrotic viscera with severe sepsis criteria. The reviews have no randomization of therapy. Their observations merely imply that patients who were sick and decompensated rapidly despite conservative measures required emergency surgery early in their course and generally did worse. Urologist decisions on when to operate and when to wait were not the pivotal mortality-makers here.
Similar to necrotizing soft--tissue infections (NSTI), the pathology, not the practitioner, determines urgency of intervention. Slowly percolating polymicrobial NSTIs have a muted systemic cascade, and can be debrided leisurely because of their less aggressive nature and lower mortality. But practitioner response cannot be the same for the rapidly advancing monomicrobial Streptococcus pyogenes NSTI whose SIRS is progressive and mandates early surgery to maximize an already-poor prognosis.
Shortly thereafter, our patient's pathology dictated her clinical course. Continued respiratory distress and vascular compromise required intubation, central access, and norepinephrine administration. She received an emergent nephrectomy at the demands of her devitalized kidney. Unlike many of the retrospectively assembled urgent operative cases in recent literature, she fared well.
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One in 15 FPs Spends Considerable Time in ED
About one of every 15 family physicians (FPs) spends at least 80 percent of his time in EDs or urgent care centers, according to researchers. The findings were published in the July/August issue of Journal of the American Board of Family Medicine.
The study also found that those who work in rural areas are seeing more patients than FPs in urban areas. The researchers used data from Maintenance of Certification for Family Physicians exam applications completed between 2008 and 2012, categorizing physicians according to the geographic setting in which they worked, ranging from urban to small rural to frontier.
Researchers also realized that FPs are most likely filling a gap in care because the ED often sees uninsured and underinsured women, children, and minorities, who face barriers to other sources of care, including primary care.