Mr. C.E. is a 79-year-old man who presented with septic shock and was found unresponsive at home. He has a history of metastatic prostate cancer, for which he underwent radical prostatectomy and cystectomy with an ileal conduit placement. In the ICU, he was diagnosed with septicemia from both gram-positive and gram-negative bacteria, acute kidney injury, uremia, and metabolic acidosis. Testing showed obstruction of the ureter leading to infection. Though aggressive treatment was planned, after discussing his living will with family, all life-saving interventions were withdrawn and he was made comfort care only, passing away comfortably later that day.

1. John Martinelli
IM Geriatric Case #2: Prostate CA/Septic Shock SBMC 2/24/14
History of Presenting Illness:
Mr. C.E. is a 79-year-old gentleman who arrived by ambulance to the SBMC ED on the
morning of February 17, 2014 after being found unresponsive in his home. In the ED, it
was determined he was in septic shock for which he received aggressive IV fluid
resuscitation and immediate broad spectrum IV antibiotic infusion. Upon admission to
the ICU, vasopressors were started with progressive improvement of his hemodynamic
status; however, he remained obtunded with altered mental status. He was anuric with
labs revealing probable acute kidney injury and uremia. His past medical history is
significant for metastatic prostate cancer for which he underwent radical prostatectomy,
cystectomy, and bilateral renal ureter ileal conduit placement. He has also been treated
for COPD (emphysema), hyperlipidemia, and peripheral vascular disease.
Physical Examination:
Post-resuscitation efforts, vitals were T 99.2, BP 79/63, HR 101, RR 17, O2sat 97% on
2L NC. Mr. C.E. exhibited severe lethargy but did become minimally responsive to
verbal and tactile stimuli by opening his eyes, however, he did not follow verbal
commands. He occasionally mumbled unrecognizable words. A GCS score of 6 was
recorded. Cardiovascular examination revealed tachycardia with S1, S2, and no evidence
of murmurs, gallops, or rubs. Peripheral pulses were palpated. There was no peripheral
edema with adequate perfusion. Lung sounds were equal bilaterally and clear to
auscultation. Abdomen was soft, non-distended, with active bowel sounds. Bilateral IV
access was patent at each forearm. A foley catheter was present. The ileal conduit stoma
appeared clean and dry.
Laboratory Investigations:
Blood cultures were positive for both gram(+) cocci in clusters suggesting
staphylococcus and gram(-) rods confirmed as e. coli by PCR analysis. ABG showed pH
7.33, pCO2 19, pO2 93. Lactic acid 2.9. CBC indicated Hgb 13.6, Hct 40.3, WBC 18.5,
Platelets 136. BMP showed Na 141, K 4.3, Cl 109, HCO3 9, BUN 157, Cr 9.82. Noncontrast abdominal CT revealed right-sided ureteral obstruction, dilatation, and
associated renal pelvic fluid collections. There was no urine output present in the foley.
There was no evidence of gastrointestinal obstruction, perforation, or air-fluid levels.
Discussion/Assessment/Plan:
Mr. C.E.’s ICU assessment and laboratory evidence was consistent with the diagnosis of
septicemia, septic shock, renal failure, and uremia status-post radical prostatectomy,
cystectomy, and ileal conduit placement. Considering blood cultures growing both
gram(+) and gram(-) organisms, the source of infection is likely multifactorial. Gram(+)

2. staphylococcus entry via the external abdominal stoma surface and classic gram(-) fecaloral transmission. Additionally, persistent ureteral obstruction leading to chronic
pyelonephritis is a significant factor with respect to septic source.
Mr. C.E. experienced fever, neutrophilia, hypotension, acidosis, thrombocytopenia, and
tachycardia, which are septic shock hallmarks. The neutrophilia is representative of an
infectious process, however, it is also responsible for producing inflammatory
vasodilation leading to systemic hypotension, distributive shock, and tachycardia. An
anion gap metabolic acidosis was evident along with appropriate respiratory
compensation. In the setting of hypotension, hypoperfusion and tissue ischemia, lactic
acidosis is expected and was indeed elevated contributing to the gap. Uremia was an
additional contributor with a BUN/Cr ratio indicating renal hypoperfusion leading to prerenal azotemia and uremic acidemia. In addition, serum creatinine was also very elevated
which corresponds to acute or acute-on-chronic renal failure likely from pre-renal
hypoperfusion, possible ischemic acute tubular necrosis (ATN), septic ATN, combined
with post-renal obstruction and pyelonephritis. This degree of renal injury/failure also
contributes to elevated blood urea levels and uremic acidosis. Regarding the acidosis,
platelet function will be altered leading to the thrombocytopenia observed.
Considering the level of acidosis, exemplified by an ABG pH @ 7.33, eventually multisystem organ failure, immunosuppression, opportunistic infection, hemorrhage, as well as
CNS/neurologic dysfunction can ensue. Recall the acidosis is present in the background
of other septic pathophysiologic processes, all which require aggressive treatment before
death ensues.
With regards to Mr. C.E.’s septic state, volume status, hemodynamic stability, renal
function, and metabolic acidosis, continued treatment was to be maintained in ICU.
Immediate dialysis/CRRT with central line access was planned, vancomycin and
meropenem was to be continued, IV fluids were to be continued with tapering of pressers,
and nephrology was consulted regarding future revision of ileal conduit/ureteral
obstruction. After meeting with the family and reviewing Mr. C.E.’s Living Will, it was
found that he requested no artificial life-saving interventions including dialysis and was
therefore made DNR/DNI. All treatment was suspended other than comfort care
measures with IV morphine. Several hours after this decision, Mr. C.E. passed away
comfortably with his family at his side.