Urosepsis

Dr. Tameem Mohammed

Department of Anesthesia and Intensive Care
San Fernando General Hospital
Outline

 Introduction
 Definition
 Risk factors
 Pathogens
 Pathophysiology
 Diagnosis
 Treatment
 Introduction

 In approximately one-third of patients with sepsis, the source of infection is the urinary tract. The
management of sepsis has rapidly changed over the past two decades, and a review of
urosepsis management is paramount.

 It is estimated that in 30% of patients with severe sepsis and septic shock, the underlying reason
is a urinary tract infection (UTI).

 The prevalence of microbiologically proven urosepsis in urology departments has been

reported as 1.5%

 On a global level, it has been postulated that 5.4 million deaths occur due to sepsis. The main
causes of urosepsis are indwelling urinary catheters and urologic interventions

2016 European Association of Urology. Published by Elsevier B.V.

Surviving Sepsis 2017

 2017 Guidelines
 Sepsis:“life-threatening organ dysfunction caused by a dysregulated host response to infection.”
 End organ damage is identified as an acute change in total Sequential [Sepsis-related] Organ
Failure Assessment score (SOFA) ≥2. (Rhodes 2017)

 Septic shock: A subset of sepsis “in which circulatory, cellular, and metabolic abnormalities are
associated with a greater risk of mortality than with sepsis alone.” (Singer 2016)

 SIRS criteria
 No longer considered in defining sepsis and septic shock
Risk factors-Host related risk factors
Risk factors -Environment

 Consist of external factors that contribute to bacterial virulence, transmission of bacteria to

host and compromise of host defense. The most important external factors can be
summarized:

 Inappropriate and unnecessary antibiotic consumption

 Limited health care resources
 Lack of local surveillance programs
 Risk factors - Urologic interventions

 Trauma to the genitourinary tract in the presence of bacteria in urine is associated with
increased risk of UTI and sepsis .The literature on frequency of sepsis following urologic
interventions is not clear because of the incoherent definitions and diagnostic criteria used.

 Published urosepsis rates after interventions are :

 Radical prostatectomy: 0%
 Transurethral resection of prostate: 0–4%
 Transrectal prostate biopsies: 0.5–0.8%
 Shock wave lithotripsy: 1%
 Ureteroscopy for stone treatment: 9% SIRS and 3% severe sepsis
 Percutaneous kidney stone surgery: 23–27% SIRS, 1.4–7% sepsis

Grabe M, Bartoletti R, Bjerklund-Johansen TE, et al.

Pathogens

 Urosepsis-causative pathogens are primarily gram negative. This is different from sepsis
overall, which is dominated by gram-positive bacteria.

 The most frequent pathogen, Escherichia coli, is encountered in almost half of urosepsis
cases. Other frequent pathogens are Klebsiella spp, Pseudomonas aeruginosa,
Enterococcus, and Enterobacter spp.
Pathophysiology
Pathophysiology

 Effects on the immune system

 Infection activates the complement system and the native immune system , leading to a massive initial pro-inflammatory
response. Hematopoietic growth factors stimulate the generation of neutrophilic granulocytes, which release bactericidal
substances such as proteases and oxygen radicals. Lymphocytes, too, are stimulated to produce antibodies and to mount a cell-
mediated immune response. Endothelial cells are induced to make nitric oxide (NO), which, in turn, lowers vascular tone, causing
hypotension. Damaged endothelium is abnormally permeable, and edema ensues . This initial phase is followed by an opposing
anti-inflammatory (immune-suppressive) phase that is responsible for the high mortality of sepsis in its later course. Macrophages
and neutrophils may succumb to immune paralysis, and lymphocytes and dendritic cells display high rates of apoptosis .

 Effects on hemostasis
 The over-activated complement system is closely linked to the clotting system. Surface receptors on endothelial cells and
neutrophils are up-regulated, causing increased mutual adhesiveness. Moreover, the clotting system is activated by endothelially
synthesized plasminogen-activator inhibitor; this predisposes to thrombosis and to disseminated intravascular coagulation (DIC). A
low antithrombin III level, Quick value, and platelet count may be the first signs of DIC. At the same time, anticoagulant
substances such as protein C are inhibited, promoting systemic coagulation and leading to microcirculatory insufficiency and
tissue hypoxi
Diagnosis

 Sepsis can rapidly shift to a more severe level influencing outcomes; therefore, prompt
diagnosis of sepsis is imperative .

 Initial clinical signs and symptoms are usually nonspecific, and the overall clinical picture for
sepsis indicates a systemic illness.
 Symptoms include warm skin, increased respiratory rate (20 breaths/min), increased heart rate (90
beats/min), bounding pulse, and hyperdynamic state

 Identifying the source of sepsis is essential for appropriate management. Suspicion of sepsis
should be followed by identification of the source of infection as part of the diagnostic process;
however, this might not be straightforward because signs in septic patients may point to the
source of infection but also may be related to organ dysfunction.
Diagnosis

 A history of predisposing conditions will also contribute toward identifying whether the source is
the urinary tract.
 History of obstructive uropathies, recent urologic interventions, and stone disease should be sought

 Laboratory assessments prior to antibiotic administration must include urinalysis and blood and urine
culture

 Imaging studies should be carried out promptly to help confirm the source of infection. Rapid and
practical confirmation of the urinary tract as the source of infection can be done with ultrasonography.
Further imaging in urosepsis is helpful in identifying complicating factors within the urinary tract.

 Computed tomography (CT) is especially helpful in identifying urolithiasis and renal abscesses .
Treatment
Treatment

Effective treatment eliminates the infectious focus, and improves organ perfusion. Treatment
of urosepsis comprises three basic strategies:

a) Supportive therapy (stabilization and maintaining blood pressure)

b) Antimicrobial therapy in the first hour

c) Urosepsis source control

Supportive therapy

 Fluid Resuscitation
 Initial fluid resuscitation
 Unchanged from 2012 guidelines
 30ml/kg of IV crystalloid fluid within the first 3 hours of sepsis presentation. Patients may
require greater volumes of fluid as guided by frequent reassessment of volume
responsiveness.
 Static fluid status measurements (i.e. Central Venous Pressure) No longer
recommended as lone guiding principles as they carry limited value for measuring fluid
responsiveness. 2017 guidelines recommend the use of dynamic variables over static
variables to predict fluid responsiveness
 Vasopressors
 Useful in patients who remain hypotensive despite adequate fluid resuscitation. First line vasopressor: norepinephrine

 Steroids
 Indicated for patients with septic shock in which fluids and vasopressors fail to achieve hemodynamic stability
Supportive therapy

 Transfusion indicated in majority of patients only when hemoglobin <7.0g/dL

 Target glucose <180mg/dL

 Mechanical Ventilation
 Lung Protective Ventilation Strategy
 Target a tidal volume of 6mL/kg of ideal body weight
 Plateau pressure of <30cm H20
 PEEP: incresae with FiO2 as per ARDSnet protocol
 Recommend prone over supine position in patients with sepsis-induced ARDS and Pa/Fio2 ratio<150
Antimicrobial therapy

 Antibiotics

 First priority is source control and obtaining cultures. Cultures should be obtained prior to administration
of antibiotics when feasible

 Give antibiotics within 1 hour of identification of septic shock

Antimicrobial therapy
Urosepsis source control

 Actions to identify source should be started within the first hour of diagnosis

 It should be kept in mind that sepsis is a systemic illness, and infection source control management options
should be weighed according to their harms and benefits
 The least physiologic assaulting and most effective intervention should be selected
 Definitive management of the complicating factor can be carried out after the general condition of the
patient improves.

 Obstruction within the urinary tract is one of the most common underlying causes.
 Cause and level of obstruction are important to determine the most appropriate drainage technique
 Ureteral stent VS nephrostomy
 The principle of selecting the least physiologically assaulting intervention should be remembered; however, this
may not always be true. (eg, Fournier’s gangrene).
KEY POINTS

 Urosepsis is one of the most frequent sources of sepsis cases.

 Mortality in severe sepsis is still high nowadays.

 Early diagnosis and management is important.

 Antibiotic treatment in sepsis is always empiric and becomes more and more challenging
because of the worldwide increase of antibiotic resistance.

 It is important to study urosepsis as a specific sepsis entity, as many aspects in management

may be unique and different to other entities.
Thank you