RENAL

Urosepsis

from LIFL – https://litfl.com/urosepsis/

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
Gram negative bacteria (~75%+)Escherichia coli (~50%)
Proteus (~15%)
Klebsiella
Enterobacter
Pseudomonas aerogenosa (~5%)
Gram positive bacteria (<25%)Enterococcus
Staphylococcus saprophyticus
Streptococcus agalactiae (GBS)
Fungal infectionsMay occur in the immunosuppressed (e.g. Candida albicans and Candida glabrata)

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
    • 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

  • 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 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:

  • 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)

Leave a Reply

Your email address will not be published. Required fields are marked *

This site uses Akismet to reduce spam. Learn how your comment data is processed.