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REVIEW ARTICLE
Year : 2006  |  Volume : 22  |  Issue : 2  |  Page : 105-112
 

Role of critical care in urological sepsis


Department of Surgical Intensive Care Unit, Christian Medial College, Vellore - 632 004, Tamil Nadu, India

Correspondence Address:
Nagamani Sen
Professor and Head, Surgical ICU, Christian Medical College, Vellore - 632 004, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-1591.26562

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   Abstract 

Infections arising from the urinary tract may either elicit a Systemic Inflammatory Response Syndrome or result in Sepsis. This may progress to severe sepsis with associated multi-organ dysfunction and perfusion abnormalities, including hypotension. The mortality associated with sepsis is high, reaching up to 46% in patients with septic shock. Infections arising from the urinary tract may arise either following a primary pathology in the urinary tract or may be acquired as a nosocomial infection. Most of these infections are caused by gram negative organisms, though occasionally gram positive organisms and fungi can infect the urinary tract under certain circumstances. Evaluation of a patient with sepsis should include establishing the diagnosis based on standard criteria, a search for the source and appropriate microbial cultures. Management of these patients requires aggressive fluid resuscitation to achieve well defined goals. This may need to be accompanied by the use of vasopressors and mechanical ventilation. Antimicrobial therapy based on the likely causative organism should be initiated, pending the culture results. Appropriate source control measures should also be taken. Prompt recognition, aggressive resuscitation and appropriate source control measures along with appropriate antimicrobial therapy will help to reduce the mortality in patients with urosepsis.


Keywords: Sepsis, urosepsis


How to cite this article:
Sen N, Matthias A, Raj JP. Role of critical care in urological sepsis. Indian J Urol 2006;22:105-12

How to cite this URL:
Sen N, Matthias A, Raj JP. Role of critical care in urological sepsis. Indian J Urol [serial online] 2006 [cited 2020 Oct 21];22:105-12. Available from: https://www.indianjurol.com/text.asp?2006/22/2/105/26562



   Introduction Top


Urinary tract infection (UTI) is the most common of all bacterial infections to affect persons throughout their life span, starting with an incidence of 1% in the neonatal age group. This increases to its peak during the reproductive age group. Females are more likely to be affected than males, except in the neonates, where the trend is reversed.[1] Infections of the urinary tract may be either the primary cause for admission to an ICU or acquired after instrumentation of the urinary tract and/or catheterisation in the ICU.

Infections of the urinary tract may present in a wide variety of ways. This ranges from asymptomatic bacteremia, to sepsis with multi-organ dysfunctions. Infections may arise from any part of the urinary tract such as the kidney as pyelonephritis, pyonephrosis, renal abscesses; the bladder as cystitis; the prostate as prostatitis and prostatic abscesses or the urethra as uretheritis. These presentations are by no way complete. UTI from whatever cause may fall into one of the following categories:

a. Complicated UTI associated with a variety of structural and functional abnormalities of the urinary tract and kidney. These include placement of stents, urine transport disturbances, instrumentation of urinary tract and the presence of calculi or tumours.

b. Uncomplicated UTI, without an anatomic or predisposing reason for infection.

c. Nosocomial UTI, which is generally catheter- associated.

d. Community acquired UTI.

Nosocomial infections of the urogenital tract are frequent and sometimes underestimated in the ICU.

Definitions

Bacteruria, in a non-catheterised patient is defined as the presence of more than 10 5 colony forming units (CFU) /ml of urine, with no more than two species of organisms isolated in culture.[2]

Nosocomial UTI is defined as the occurrence of a UTI, at least 48 hours after a hospital admission, with an isolation of at least 10 5 CFU/ml in culture. In cases of fungal isolates, a growth of more than 10[3] CFU /ml is considered diagnostic. The cut-off values commonly used for rapidly multiplying bacteria, cannot be applied to fungi or fastidious organisms to diagnose UTI.[3]

It has been calculated that the incidence of catheter-associated bacteriuria (CAB) parallels the number of days of catheterisation and that the risk of developing bacteriuria increases by 5% for each day.[4]

One of the common causes of sepsis and septic shock is UTI. The 1991 American college of chest physicians/society of critical care medicine consensus conference standardised the terminology for the septic process. These definitions continue to be used to define the septic process.[5]

Systemic inflammatory response syndrome (SIRS)

SIRS is caused by any physiological insult to the body and is manifested by the presence of two or more of the following criteria:

1. Core body temperature, either > 38oC or < 36oC.

2. Heart rate > 90 beats/min.

3. Respiratory rate > 20 breaths /min or PaCO -2 < 32 mmHg.

4. A white blood cell (WBC) count of > 12,000 cells mm -3 or < 4000 cells mm -3 or the presence of 10% band forms on the differential count.

Multiple organ dysfunction syndrome (MODS)

This is a result of SIRS where there is organ dysfunction and homeostasis cannot be maintained without intervention.

Sepsis

Sepsis is SIRS in the setting of an infection.

Severe sepsis and septic shock

Severe sepsis is defined as sepsis associated with organ dysfunction and perfusion abnormalities such as lactic acidosis, oliguria and mental changes.

Septic shock is defined as sepsis with persistent hypotension, despite adequate fluid resuscitation along with perfusion abnormalities.

Whatever may be the aetiology, the adoption of above mentioned terms have become necessary,[6] because the causative organisms from the urinary tract can release endotoxins into the blood stream and produce severe sepsis.

SIRS and all its subsequent sequlae are associated with significant mortality. The mortality associated with SIRS is 7-17%, increasing to 20% for severe sepsis. The mortality in septic shock is as high as 46%.[7]

What constitutes a UTI?

The current centres for disease control and prevention (CDC) definitions stratify nosocomial UTI into symptomatic, asymptomatic and other infections of urinary tract.[8] By this definition, symptomatic bacteriuria occurs when there is more than 10 5 CFU per millilitre of urine, with not more than two species of organisms grown, associated with systemic signs of fever and objective evidence of an active infection in the urine. This would include presence of leucocytes, a positive dipstick test for nitrite or leukocyte esterase.

In the absence of antibiotics, a single microorganism could multiply over time to reach 10 5 CFU/ml in the essential urinary tract.[3] Asymptomatic bacteriuria is said to occur when a patient has a positive urine culture as described above, which is associated with an indwelling bladder catheter that has been present for at least 7 days prior to the culture and there is no fever or associated systemic symptoms. Other infections of the urinary tract include infections in the kidney, perinephric area and the retroperitoneum in addition to the urinary tract. The diagnosis is made when there is a positive culture from tissue or fluid other than urine, associated with systemic manifestations of infection. This must be augmented with evidence from physical examination as well as radiological evidence.

There is considerable variation among laboratories and clinicians in reporting and diagnosing catheter- acquired UTI (CAUTI) on the basis of colony counts.

An international sepsis forum consensus conference on definitions, recently has made recommendations on the range of clinical and laboratory criteria to be used for the diagnosis of infection in the ICU.[9] According to this definition, the presence of >10 3 CFU/ml is sensitive for catheter- associated UTI.

Specific definitions exist for certain categories of patients, such as those with spinal injuries or patients who require long-term catheterisation. The National Institute of Disability and Rehabilitation Research recommends the use of the threshold value of 10 2 CFU/ml to diagnose UTI from catheter specimens, from individuals on intermittent catheterization and 10 4 CFU/ml for clean void specimens from catheter-free males, using clean intermittent self- catheterization.[10] According to their recommendations, any detectable growth of uropathogens from indwelling catheters or suprapubic aspirate is considered significant.[10]


   Epidemiology Top


Urinary tract infections are one of the leading causes of nosocomial infections in hospitals, worldwide. In a study conducted among the German hospitals, UTI constituted 42.1% of all nosocomial infections compared to 20.6% for lower respiratory tract infection and 15.8% for surgical site infections and primary sepsis accounted for 8.3%.[11]

The European prevalence of nosocomial infection in intensive care (EPIC) study revealed that nosocomial UTI accounted for 17.6% of all nosocomial infections, with 80% associated with indwelling catheters[12] (3). The incidence of nosocomial UTI is much less in Indian intensive care units. Agarwal et al reported an incidence of 1.5% in a respiratory intensive care unit.[13] This trend has been seen in other ICUs in India as well (Rosenthal V, Sen N, Raj JP et al , unpublished data). Genitourinary manipulations account for 5 to 10% of nosocomial UTI.[6] At least 15% of complicated UTI are febrile.[14]

Infections arising in the urinary tract in intensive care units may be divided into two broad categories

A. UTI associated with non-urologic conditions.

i. Diabetes mellitus.

ii. Renal insufficiency.

iii. Immunodeficiency or immunosuppression.

iv. Trauma patients.

B. UTI associated with urological procedures or complications.

i. Urinary calculi or foreign bodies in the urological tract.

ii. Obstructions of the urinary tract.

iii. Procedures involving the urogenital tract.

iv. Renal transplantation.

v. Neurogenic bladder dysfunction.

Identification of an UTI into one of the above two categories is convenient, in terms of management. When the infection is associated with a non-urological condition such as diabetes mellitus, treatment with antimicrobial therapy is generally sufficient. However, where there is a urological basis for the UTI such as nephrolithiasis or obstruction, the causative factors should be identified and treated along with appropriate antimicrobial therapy.


   Pathophysiology Top


Catheter acquired bacteriuria

Organisms invading the urinary tract via the urethra generally cause UTI. A very important mechanisms contributing to UTI is the formation of bio-films, associated with the increasing number of biomaterials used in medical practice.[15] A bio-film is formed when there is an accumulation of microrganisms and their extracellular products form a structured community on a surface. Bio-film infection develops not only around foreign bodies such as urinary catheters or stents, but also in urinary stones, scar or necrotic tissue.[16] Obstructive uropathies or even chronic bacterial prostatitis can also lead to formation of a bio-film. Antimicrobial treatment is effective when the bio-film is 'young' or less than 24 hours old.[15],[16]

During the acute febrile phase of a bio-film infection, antimicrobial therapy is essential and can be effective because the planktonic bacteria (free-floating bacteria) are responsible for the febrile reactions and not the bacteria covered in the bio-film.[15] To eradicate pathogens from bio-film, the bio-film itself has to be removed. This would include removing the causative agent such as a catheter or calculi.

Catheter-associated bacteruria may lead on to bacteremia. Bacteremia, secondary to catheter-acquired bacteruria (CAB) can develop as a result of mucosal trauma associated with insertion or withdrawal of the catheter. They may also develop several days after catheterisation, when mucosal ulcerations frequently encountered.[17] This may cause systemic involvement, resulting in urosepsis.

Obstructive uropathy

Any obstructive lesion including malformations, strictures, calculi or tumours can cause a urinary tract infection that leads on to urosepsis. This may enter the blood stream, causing a systemic illness that manifests as SIRS, which may ultimately lead on to multi-organ failure. Invasive procedures to decompress the obstructed system such as a percutaneous nephrostomy, may cause a bacteremia that triggers a systemic response.[18] The likelihood of developing SIRS in a study of 189 patients with hydronephrosis was 26%, with 4% progressing on to severe sepsis.[18]

Causative organisms

The causative pathogens of UTI are almost exclusively bacteria and yeast. Viral pathogens are only found in patients with severe immunosuppression, such as after bone marrow transplantation. In an acute uncomplicated UTI,  Escherichia More Details coli is the predominant organism causing the infection across all age groups. Other aerobic gram-negative rods such as Klebsiella species, Proteus species, Citrobacter species, Acinetobacter species, Morganella species and Pseudomonas aeruginosa are also frequently isolated. Gram-positive bacteria such as Enterococci and Staphylococcus aureus, as well as yeast are important pathogens in complicated UTI.[1]

In acute uncomplicated cystitis, the etiological agents are highly predictable. E. coli accounts for 75 to 90% of isolates. Staphylococcus saprophyticus accounts for 5 to 15% of the isolates, particularly in young women.[1] The remaining 5 to 10% of isolates include Klebsiella sp , Proteus sp and Enterococci sp .


   Evaluation Top


Diagnosis

Clinical examination

A thorough clinical examination which includes a good medical history and physical examination, should be carried out. This would include measurement of the pulse rate and temperature. Elevation of both may be a pointer to infection. A widened pulse pressure with warm extremities is an indication of a vasodilatory state and points towards sepsis. Examination of the abdomen should include palpation of costophrenic area, lower abdomen, the pubic region, the inguinal lymphnodes, the genitalia, as well as digital transvaginal or transrectal examination.

Radiology

Radiological investigations include plain X-ray of the abdomen delineating the kidney, ureter and bladder. In an ICU setting, this may not be a good investigation, as portable X-rays frequently taken in the ICU do not penetrate well. The ultrasound is an important diagnostic device and its use should be frequently considered, both for diagnosis as well as for placing guided drains into infected collections. A CT scan of the abdomen may give better delineation of the pathological process, particularly if combined with an intravenous contrast. In a patient admitted in the ICU, this necessitates a trip to the radiology suite and is not without risk in an unstable patient. These patients may also have altered renal function, with increased risk of developing contrast-induced nephropathy. These factors should be taken into account while deciding on what radiological procedure is appropriate. Radionuclide scans and duplex ultrasound may be of importance to assess the perfusion and function of the kidney in patients who have had a renal transplant.

Urinary examination

Urine specimens from ICU patients are almost exclusively collected from catheters. Because urine from catheters has to be collected into a closed system, the urine specimen should be taken by a puncture of the catheter after aseptic precautions. This ensures that the system is not opened. Urinary catheters with aspiration ports for sampling are now available and these should be used if available.

Laboratory examination of the urine specimen

Dipstick test

This test is done with undiluted urine and investigates the following infection related parameters.

pH : An alkaline urine (pH > 8.0) is indicative of urease- producing organisms, particularly Proteus species . Other urease- producing organisms include E. coli, Klebsiella and Pseudomonas. Urease hydrolyzes urea (urea splitting), yielding ammonia, bicarbonate and carbonate, leading to a more alkaline urine, which allows crystal formation from the super saturation of carbonate apatite and struvite.

Nitrite : Most enterobacteriae have nitrate reductase, an enzyme that reduces nitrate to nitrite. Some common uropathogens such as Enterococcus and Staphylococcus lack nitrate. Detection of nitrites indicates presence of infection. This test is quite specific, with ranges from 82 to 98%.[19]

Leukocyte esterase : This is a test that detects presence of leukocyte esterase, an enzyme that indicates the presence of leukocytes. In catheterised patients, presence of leukocytes and erythrocytes may not be significant markers for infection.

Serum lab tests

Patterns that may be seen, include renal insufficiency with anaemia and hyperchloraemic metabolic acidosis with or without hyperkalemia. There may be high urea and creatinine or findings may mimic prerenal azotemia early on, with low urinary sodium and a fractional excretion of sodium less than 1%. Alternatively, the laboratory values may be completely normal.

Microbiology

Culture of the urine is the most important investigation, as it is diagnostic and the sensitivity pattern of the cultured organism guides the clinician as to what antibiotic would be appropriate. In the diagnosis of UTI, it is important to differentiate contamination from significant bacteriuria. Hence culture of microorgansims should be quantitative. The microbial count has to be interpreted in relation to the urinary dilution. These are usually reported as number of colony forming units (CFU) per millilitre of urine.

Organisms

Most of the organisms commonly causing UTI are found in the gut flora. Therefore, these organisms are said to be endogenous. Where there has been contamination from other sources, the organism is said to be exogenous.

Most (80-90%) of community-acquired UTI in females are caused by Escherichia coli . Staphylococcus saprophyticus is the second most common pathogen, but infection with this organism rarely leads to sepsis and ICU admission. In men,

E. coli is also the commonest organism, but Enterococcus species and other common enterobacteriae are more commonly encountered.

For men and women, the spectrum of pathogens changes when UTI is acquired in the hospital environment. E. coli (47%), Enterococcus species (13%), Klebsiella (11%), Pseudomonas aerogenosa (8%), Proteus mirabilis (9%), Enterobacter species (4%) and Citrobactor (3%), together accounted for 91% of hospital-acquired UTI in a worldwide study.[20]

To make a diagnosis of asymptomatic bacteriuria, the following criteria are required:[8]

a) An indwelling urinary catheter is present less than 7 days before the urine is cultured. There is no fever (>38oC), urgency, dysuria or suprapubic tenderness. The urine culture shows 10 5 organisms/ml urine, with no more than two species of organisms.

b) No indwelling urinary catheter is present within 7 days before the first of two urine cultures, with more than or equal to 10 5 organisms/ml urine of the same organism, with more than two species of organisms and patient has no fever (>38oC) urgency, frequency, dysuria or suprapubic tenderness.


   Therapy Top


General principles

Therapy should be started in patients with significant symptoms and morbidity and in conditions where asymptomatic bacteriuria may be deleterious. These include patients who have undergone a renal transplant, pregnancy, severe diabetes mellitus and patients who are immunosuppressed.

However, it must be remembered that in 20 to 30% of all septic patients in ICU, the initial infectious focus is in the urogenital tract. Prompt evaluation and treatment eliminates the infectious focus and improves the organ perfusion.

Adequate antibiotic therapy is the most essential part of the treatment. To have improved outcome from the septic shock, broad spectrum coverage combination therapy should be used [Table - 1].[21]

Management of sepsis and severe sepsis

The management of sepsis has for years, relied on treatment of the underlying infection, good resuscitation and appropriate organ support as necessary. The general approach to resuscitation follows the VIP rule proposed by Weil and Shubin 35 yrs ago: Ventilation, infusion and pump.[22] More recently, evidence-based guidelines developed by the Surviving Sepsis Campaign (SSC), help direct management of the patient with severe sepsis or septic shock.[23] These guidelines are goal-directed.

A. Initial resuscitation

During the first 6 hours, the goals of initial resuscitation of sepsis-induced hypoperfusion should include:

1. Central venous pressure (CVP): 8-12 mmHg

2. Mean arterial pressure (MAP): 65 mmHg

3. Urine output 0.5 ml kg -1 hr -1

4. Central venous (superior vena cava) or mixed venous oxygen saturation 70%.

These goals are better achieved by invasive monitoring with a centrally placed venous catheter, invasive pressure monitoring in addition to monitoring the urine output, the respiratory rate and the sensorium.

During the first 6 hours of resuscitation, if the central venous saturation or mixed venous oxygen saturation of 70% is not achieved despite fluid resuscitation to a CVP of 8-12 mmHg, then packed red cells have to be transfused to achieve a hematocrit of 30% and /or Dobutamine infusion (up to a maximum of 20 mg kg -1 min -1) has to be administered to achieve this goal. This protocol is associated with an improvement in survival.[24]

B. Diagnosis

Appropriate culture should always be obtained before antimicrobial therapy is initiated. At least two blood cultures should be obtained. Cultures of urine, wound, respiratory secretions or other body fluids should be obtained. Diagnostic studies should be performed as mentioned previously.

C. Antibiotic therapy

Intravenous antibiotic therapy should be started within the first hour of recognition of severe sepsis, after appropriate cultures have been obtained. Initial empirical anti-infective therapy should include one or more drugs that have activity against presumed pathogens like bacteria or fungi and that penetrate into the presumed source of sepsis.[25]

The antimicrobial regimen should always be reassessed after 48-72 hrs, on the basis of microbiological and clinical data. Duration of therapy should be 7-10 days and guided by the clinical response.

D. Source control

After evaluating for the presence of a focus of infection, appropriate source control measures should be initiated. These include drainage of an abscess surgically or percutaneously, relieving obstruction, debridement of infected necrotic tissue or removal of infected or potentially infected devices.

E. Fluid therapy

After the initial resuscitation which is carried out within 6 hours of diagnosis, fluids should be continued to prevent further hypovolemia recurring. Fluid challenges may be given at a rate of 500-1000 ml of crystalloids or 300-500 ml of colloids over 30 minutes for hypotension and decreased urine output and repeated based on the response (an increase in MAP and urine output).

F. Vasopressors

When an appropriate fluid challenge fails to restore adequate blood pressure and oxygen perfusion, therapy with vasopressor agents should be started. Vasopressor therapy may also be required transiently to sustain life and maintain perfusion in the face of life- threatening hypotension.

The initial choice of a vasopressor agent is either noradrenaline or dopamine, administered through a central venous catheter. The drug dosage is titrated to get a MAP of 65 mm Hg. Low dose dopamine is not indicated for renal protection as part of the treatment of severe sepsis.[23]

G. Inotropic therapy

In patients with suspected or measured low cardiac output states, Dobutamine may be used to increase cardiac output. In the presence of low blood pressure, it should be combined with a vasopressor.

H. Steroids

Intravenous hydrocortisone 200-300 mg/day for 7 days in three or four divided doses or by continuous infusion, is recommended in patients with septic shock who despite adequate fluid replacement and require vasopressor therapy to maintain adequate blood pressure.[23]

I. Recombinant human activated protein C (rhAPC)

Recombinant human activated protein C, an endogenous anticoagulant with anti-inflammatory properties, has been shown to improve survival in patients with sepsis- induced organ dysfunction and is recommended in patients with sepsis who are at high risk of death. These include patients with an acute physiology and chronic health evaluation II (APACHE II) score > 25, sepsis induced organ failure, septic shock or sepsis-induced acute respiratory distress syndrome (ARDS) and with no absolute contraindication related to bleeding risk. [23]

J. Blood product administration

Red blood cell transfusion is indicated when there is hypotension with a drop in the haematocrit. In haemodynamically stable patients with sepsis, red cell transfusion is indicated only when the haemoglobin decreases to < 7.0 g/dL and is given to target 7.0-9.0 g/dL. [23]

K. Mechanical ventilation

High tidal volumes coupled with high plateau pressures should be avoided in patients with acute lung injury. The goal is a reduction in tidal volume over 1-2 hrs to 6 ml per kg of predicted body weight, with end-inspiratory plateau pressures < 30 cm H -2O.

Permissive hypercapnia (allowing Paco -2 to increase above normal) can be tolerated to minimise plateau pressures and tidal volumes.

L. Sedation, analgesia and neuromuscular blockade in sepsis

Protocol-based sedation and analgesia should be used as boluses or continuous infusion. Neuromuscular blockers should be avoided if at all possible.

M. Glucose control

After initial stabilisation of patients with severe sepsis, blood glucose should be maintained to <150 mg/dL. This should include monitoring of the blood glucose levels every 4 hours or earlier, if the sugars are labile. A continuous infusion of insulin ensures better glycemic control.

Other supportive therapy

a. Renal replacement therapy

b. Prophylaxis of deep vein thrombosis

c. Stress ulcer prophylaxis

Management of specific conditions that may require ICU admission, with or without sepsis and septic shock

Acute pyelonephritis:
Acute focal bacterial nephritis, renal abscess, emphysematous pyelonephritis and silent pyelonephritis is present in up to 33% of patients with clinical cystitis and may be latent for long periods. Subsequent deterioration should prompt a search for a urinary tract obstruction such as calculus or renal papillary necrosis or for an infective focus in or around the kidney. Such deterioration may also arise if the urinary pathogen is resistant to the chosen antimicrobial regimen. The renal function is assessed at the same time. Acute renal failure in this setting is usually due to acute tubular necrosis secondary to sepsis or due to drug toxicity.

All patients with severe urosepsis should have immediate imaging of the urinary tract, preferably by computed tomography with contrast, because suppurative complications are common and require drainage as a priority. Abscesses and obstructed systems can be drained percutaneously under radiological guidance. Infected catheters or stents should be removed. Acute bacterial prostatitis can occasionally cause sepsis, requiring ICU admission.


   Prevention of infection from urinary catheters Top


One of the most important infection control measure is to limit the use of urinary catheters to carefully selected patients, where there is a definitive indication for catheterization. The use of a closed system will reduce the incidence of infection.

Catheter care measures such as aseptic catheter insertion, daily meatal cleansing and application of antimicrobial ointments may reduce micro organisms at the meatus from entering the bladder. Indwelling catheters should not be changed at arbitrarily fixed intervals.[26]

Urinary tract infection due to Candida infections

Disseminated invasive candidiasis may originate in the urinary tract or secondarily infect it. Neutropenia, loss of mucous membrane integrity due to chemotherapy, burns, use of steroids, diabetes mellitus, total parenteral nutrition and upper gastrointestinal surgery predispose to invasive candidiasis. Blood cultures are positive for Candida in only 50% of cases.[27]

Primary infection of the kidneys by Candida is generally associated with an indwelling urinary catheter, the use of broad-spectrum antibacterial agents and an obstructed urinary tract. The presence of unilateral or bilateral hydronephrosis should raise the suspicion of a fungal ball. Microscopic examination of the urinary sediment may show Candida casts. Careful evaluation is necessary for those patients who require early antifungal therapy.

In ICUs, patients with indwelling urinary catheters can have candiduria as a source of infection. The clinical course is relatively benign. The infection resolves spontaneously once the catheter is removed. Asymptomatic patients should only receive treatment if they are immunosuppressed, have undergone transplantation, are neutropenic or about to undergo invasive urologic procedures.

Infection control policies

Cross infection is likely to be responsible for the spread of all the nosocomial infections in the ICU. Therefore it is important that in the ICU, there is emphasis on hand washing and spatial separation of catheterized patients. It may also be necessary to separate infected patients from non-infected patients, reducing cross contamination and thus limiting infection.

In any case, microbiologic sampling (urine, blood, tissue culture) before the initiation of treatment is compulsory to tailor the initial empirical therapy according to laboratory results.

Summary of major recommendations for prevention of catheter-associated urinary tract infections:[26]

Category I: Strongly recommended for adoption

l Educate personnel in correct techniques of catheter- insertion and care.

l Catheterize only when necessary.

l Emphasize hand washing.

l Insert catheter using aseptic technique and sterile equipment.

l Maintain closed sterile drainage.

l Obtain urine samples aseptically.

l Maintain unobstructed urine flow.

Category II: Moderately recommended for adoption

l Use smallest suitable-bore catheter.

l Avoid irrigation unless needed to prevent or relieve obstruction.

l Refrain from daily meatal care.

l Do not change catheters at arbitrary fixed intervals.

Category III: Weakly recommended for adoption

l Consider alternative techniques of urinary drainage before using an indwelling urethral catheter.

l Replace the collecting system when sterile closed drainage has been violated.

l Avoid routine bacteriologic monitoring.

Newer technologies

The emergence of reduced infections with antibiotic or silver- coated intravenous lines has led this technology to be applied to urinary catheters as well. Novel urinary catheters impregnated with nitrofurazone or minocycline and rifampin or coated with a silver alloy-hydro gel exhibit anti-infective surface activity that significantly reduces the risk of catheter- acquired UTI for short-term catheterizations, not exceeding 2-3 weeks should be used.[28] In a recent double blinded trial in 850 patients, the silver-hydro gel catheter reduced the incidence of catheter associated UTI by 26% (25.7 vs. 15.4 per 100 catheters, RR 0.74 P = 0.04).[29]


   Conclusion Top


Sepsis can occur secondary to a wide variety of urological causes. Aggressive, goal-directed resuscitation, appropriate antimicrobial treatment and source control, will help in reducing the mortality of patients with urosepsis. Sepsis as a result of catheter-acquired UTI can be prevented to a large extent by following appropriate guidelines[30].

 
   References Top

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2.Leone M, Garnier F, Avidan M, Martin C. Catheter associated urinary tract infections in Intensive Care Units. Microbes Infect 2004;6:1026-32.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Stark RP, Maki DG. Bacteriuria in the catheterized patient. What quantitative level of bacteriuria is relevant? N Eng J Med 1984;311:560-4.  Back to cited text no. 3  [PUBMED]  
4.Garibaldi RT. Hospital acquired urinary tract infections. In : Prevention and Control of Nosocomial Infection: 2nd ed. Williams and Williams: Baltimore; 1993. p. 600-13.  Back to cited text no. 4    
5.American College of Chest physician / Society of Critical Care Medicine Consensus Conference Committee: Definitions for sepsis and organ failure and guidelines for the innovative therapies in sepsis. Crit Care Med 1992;20:864-7.  Back to cited text no. 5    
6.Warren JW. Nosocomial urinary tract infections. In Gehab C (editor): Principles and Practice of Medical Intensive Care. WB Saunders: Philadelphia; 1993.  Back to cited text no. 6    
7.Rangel-Frausto MS, Pittet D, Costigan M, Hwang T, Davis CS, Wenzel RP. The natural history of the systemic inflammatory response syndrome (SIRS). JAMA 1995;273:117-23.  Back to cited text no. 7  [PUBMED]  
8.Horan TC, Gaynes RP. Surveillance of nosocomial infections. In : Hospital Epidemiology and Infection Control, 3rd ed. Mayhall CG, editor. Lippincott Williams and Wilkins: Philadelphia; 2004. p. 1659-702.  Back to cited text no. 8    
9.CalandraT, Cohen J. The Internal Sepsis Forum Consensus Conference on Definitions of Infections in the Intensive Care Unit. Crit Care Med 2005;33:1538-48.  Back to cited text no. 9    
10.Biering-Sorensen F, Bagi P, Hoiby N. Urinary tract infection in patients with spinal cord lesion treatment and prevention. Drugs 2001:61:1275-87.  Back to cited text no. 10    
11.Gastmeier P, Kampf G, Wischnewski N, Hauer T, Schulgen G, Schumacher M, et al . Prevalence of nosocomial infections in representative German hospitals. J Hosp Infect 1998;38:37-49.  Back to cited text no. 11    
12.Vincent JL, Bihari DJ, Suter PM, Bruining HA, White J, Nicolas-Chanoin MH, et al . The prevalence of nosocomial infection in Intensive care units in Europe. JAMA 1995;274:639-44.  Back to cited text no. 12    
13.Agarwal R, Gupta D, Ray P, Aggarwal AN, Jindal SK. Epidemiology, risk factors and outcome of nosocomial infections in a Respiratory Intensive Care Unit in North India. J Infect. 2005 Dec 9;[Epub ahead of print]  Back to cited text no. 13    
14.Naber KG, Witte W, Bauernfeind A, Wiedemann B, Wagenlehner F, Klare I, et al . Clinical significance and spread of fluroquinoline resistant uropathogenesis in hospitalized urological patients. Infection 1994;22:S122-7.  Back to cited text no. 14    
15.Costerton JW. Introduction to biofilm. Int J Antimicrob Agents 1999;11:217-21.  Back to cited text no. 15  [PUBMED]  
16.Reid G. Biofilms in infectious disease and on medical devices. Int J Antimicrob Agents 1999;11:223-6.  Back to cited text no. 16  [PUBMED]  
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