Urosepsis

Reviewed and revised 3 January 2016

OVERVIEW

  • Urosepsis is sepsis with a source localised to the urinary tract (or male genital tract, e.g. prostate)
  • Urosepsis is a severe infection, distinguishing it from other urinary tract infections including mild pyelonephritis and accounts for ~5% of severe sepsis; whereas UTIs account for ~40% of nosocomial infections

CAUSES

Causative organisms are usually gram negative bacteria (~75%+)

  • Escherichia coli (~50%)
  • Proteus (~15%)
  • Klebsiella
  • Enterobacter
  • Pseudomonas aerogenosa (~5%)

Be wary of bacteria that may be ESCAPPM or an ESBL (require a carbapenem or fourth generation cephalosporin due to inducible resistance)

Gram positive bacteria are less common causes of urosespsis  (<25%)

  • Enterococcus
  • Staphylococcus saprophyticus
  • Streptococcus agalactiae (GBS)

Fungal infections may occur in the immunosuppressed (e.g. Candida albicans and Candida glabrata)

Polymicrobial infections are more common in the elderly

RISK FACTORS

Urosepsis, as opposed to UTIs in general, are more likely to be complicated UTIs

  • obstruction
    • calculi
    • tumour
    • radiation
  • instrumentation
    • IDC
    • stent
    • nephrostomy tube
    • urological procedures
  • impaired voiding
    • neurogenic bladder
    • vesicoureteral reflux
    • cystocele
  • immunosuppression
    • post-transplant
    • neutropaenia
  •  metabolic
    • diabetes mellitus
    • uraemia
    • nephrocalcinosis

All UTIs are more common in females

CLINICAL FEATURES

Clinical assessment

  • dysuria, frequency, haematuria, pyuria (UTI)
  • flank pain and fever (pyelonephritis)
  • pain on sitting and defection, tender boggy swelling on digital rectal exam (prostatitis)
  • perform per vaginal examination females (e.g. bimanually palpate abscess)
  • ‘SIRS’ and septic shock
  • underlying risk factors
  • PMH of UTIs, antibiotics and resistance
  • complications

Complications

  • severe sepsis, septic shock and MODS
  • renal scarring and end stage renal failure
  • abscesses (e.g. renal, perinephric) and septic embolisation
  • emphysematous pyelonephritis gas formation in renal parenchyma, collecting ducts and perinephric space; usually in diabetics)
  • papillary necrosis, sloughing and obstruction

INVESTIGATIONS

Bedside

  • urine (dipstick, microscopy and culture)
  • blood gas

Laboratory

  • septic screen including blood cultures
  • evidence of SIRS and MODS

Imaging

  • renal tract ultrasound (e.g. exclude obstruction, kidney size, scars, emphysematous pyelonephritis, abscesses)
  • CTU (e.g. bacterial interstitial nephritis, renal micro-abscesses, renal papillary necrosis)

MANAGEMENT

Resuscitation

  • address life threats, such as septic shock

Antimicrobial therapy (antibiotic recommendations from Australian Therapeutic Guidelines)

  • early empiric antibiotics:
    • amoxicillin 2 g IV q6h + gentamicin 5-7 mg/kg IBW IV loading dose then maintenance dosing
      • use gentamicin alone if penicillin hypersensitive
      • gentamicin maintenance dosing based on renal function and therapeutic drug monitoring
    • if gentamicin contra-indicated , use ceftriaxone 1 g IV q24h (Q12h if critically ill) OR 1 cefotaxime 1 g IV q8h (q6h if critically ill)
      • however these are not effective against  Pseudomonas aeruginosa, enterococci or ESBLs
    • Urosepsis due to MDROs is an emerging problem (e.g. ESBLs), especially in patients who have travelled to South/ East Asia)
      • if suspected use meropenem 1g q8h IV
      • meropenem is also indicated if melioidosis is suspected (e.g. Indigenous Australians in tropical regions with prostatic abscess)
  • modify empirical antibiotic therapy based on the results of cultures and susceptibility testing and clinical response
    • early conversion to oral therapy if improving
    • if susceptibility results are not available by 72 hours and empirical IV therapy is still required, stop gentamicin  and use ceftriaxone or cefotaxime
    • total duration of therapy (IV + oral) is usually 10 to 14 days, extended to 21 days in patients with a delayed response
    • repeat urine cultures 1 to 2 weeks after treatment is completed
  • perform investigations to exclude an anatomical or functional abnormality of the urinary tract, particularly if the patient does not respond to initial therapy – ensure that patient is not obstructed (renal tract U/S or CTU)
  • fungal infections (usually Candida spp)
    • non-severe UTIs usually resolve with IDC removal
    • however septic patients should be treated with antifungals (e.g. fluconazole, or caspofungin if azole-resistant Candida glabrata)

Source control

  • ideally perform within 6 hours of identification of the underlying problem
  • initial low-level invasive treatment
    • e.g. insertion of an indwelling catheter (IDC), JJ-stent or percutaneous nephrostomy
  • as sepsis improves, follow with definitive urological procedures (e.g. nephrectomy)
  • removal of pre-existing in situ devices (e.g. IDC, JJ stent)
    • should not delay antibiotic administration
    • antibiotics may only be transiently effective unless a pre-existing catheter or ureteric stent is removed or replaced, because most antibiotics penetrate poorly into biofilms that form on foreign material
    • treatment without device removal may also lead to superinfection with more resistant organisms
    • exact timing is controversial and varies on a case-by-case basis (e.g. duration in situ, response to antibiotics, severity of illness, ease of removal/ reinsertion of needed)

Seek and treat complications

Supportive care and monitoring


References and links

LITFL

Journal articles

  • Kalra OP, Raizada A. Approach to a patient with urosepsis. Journal of global infectious diseases. 1(1):57-63. 2009. [pubmed] [free full text]
  • Wagenlehner FM, Lichtenstern C, Rolfes C. Diagnosis and management for urosepsis. International Journal of Urology. 20(10):963-70. 2013. [pubmed] [free full text]

FOAM and web resources


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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