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)
- amoxicillin 2 g IV q6h + gentamicin 5-7 mg/kg IBW IV loading dose then maintenance dosing
- 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
- CCC — Sepsis definitions
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
- Australian Therapeutic Guidelines — Antibiotics, 2015 [requires subscription]
Critical Care
Compendium
Chris is an Intensivist and ECMO specialist at The Alfred ICU, where he is Deputy Director (Education). He is a Clinical Adjunct Associate Professor at Monash University, the Lead for the Clinician Educator Incubator programme, and a CICM First Part Examiner.
He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives. He was one of the founders of the FOAM movement (Free Open-Access Medical education) has been recognised for his contributions to education with awards from ANZICS, ANZAHPE, and ACEM.
His one great achievement is being the father of three amazing children.
On Bluesky, he is @precordialthump.bsky.social and on the site that Elon has screwed up, he is @precordialthump.
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