Urinary tract infections

 

Terms Cystitis Pyelonephritis

 

Aetiology

Vesicoureteric reflux Male/ female

Any anatomical abnormality of the tract, eg tumour, scaring

Enlarged prostate Stasis

Catheters and instrumentation Stones - bacteria get into the stones

Glucosuria Start of sexual activity in women

Haematogenic infections are also possible

 

Common pathogens

Coliform infection - Escherichia coli, Streptococcus faecalis, Proteus, Pseudomonas

 

Diagnosis

Lower tract infection - detection of pus cells, detection of nitrite

Prevent contamination of MSU by preventing contact with adjacent tissues

EMU to look for TB MSU for C and S

IVP Ultrasound

Isotope studies Cystoscopy

 

Pathophysiology

Bacterial infection of the urothelial surface

Interstitial cystitis may develop in the bladder wall with clear cultures - mostly in middle aged

women

Asymptomatic bacteriuria occur in 5 - 10% of women and is probably caused by sex

 

Clinical features Blood and pus in urine

 

Cystitis frequency, dysuria, urgency

 

Acute Pyelonephritis loin pain, fever, malaise, usually bilateral

 

Chronic Pyelonephritis

The end result of chronic infection often from childhood

Small, distorted asymmetrical kidneys Loin pain and tenderness

Possible hypertension Question about intake of NSAIDs

Culture, antibiotics, creatinine clearance tests

 

Prevention

Adequate fluid intake Ensure bladder is fully emptied Empty bladder after sex

 

Pregnancy

UTIs are common in pregnancy May ascend to the kidneys leading to premature delivery

Should be screened for bacteria in urine at first prenatal visit and given antibiotics if indicated

 

In children

2% of boys and 8% of girls develop UTIs in childhood

Reflux may cause UTI

Vesicoureteric reflux present in 8 - 40% of cases

Renal scaring may develop

Always culture if any suspicion of UTI

Refer all children with UTI for investigations

 

Treatments

High fluid intake Antibiotics Prophylactic antibiotics Surgery

 

DEFINITION

UTI is defined by the presence of a pure growth of more than 105 colony forming units of bacteria per ml. Lower counts of bacteria may be clinically important, especially in boys and in specimens obtained by urinary catheter. Any growth of typical urinary pathogens is considered clinically important if obtained by suprapubic aspiration. In practice, three age ranges are usually considered on the basis of differential risk and different approaches to management: children under 1 year; young children (14, 5, or 7 years, depending on the information source); and older children (up to 1216 years). Recurrent UTI is defined as a further infection by a new organism. Relapsing UTI is defined as a further infection with the same organism.

 

PREVALENCE

Boys are more susceptible before the age of 3 months; thereafter the incidence is substantially higher in girls. Estimates of the true incidence of UTI depend on rates of diagnosis and investigation. At least 8% of girls and 2% of boys will have a UTI in childhood.

 

AETIOLOGY

The normal urinary tract is sterile. Contamination by bowel flora may result in urinary infection if a virulent organism is involved or if the child is immunosuppressed. In neonates, infection may originate from other sources. Escherichia coli accounts for about three quarters of all pathogens. Proteus is more common in boys (about 30% of infections). Obstructive anomalies are found in 04% and vesicoureteric reflux in 840% of children being investigated for their first UTI. Although vesicoureteric reflux is a major risk factor for adverse outcome, other as yet unidentified triggers may also need to be present.

 

PROGNOSIS After first infection, about half of girls have a further infection in the first year and three quarters within 2 years. We found no figures for boys, but a review suggests that recurrences are common under 1 year of age but rare subsequently. Renal scarring occurs in 515% of children within 12 years of their first UTI, although 3270% of these scars are noted at the time of initial assessment. The incidence of renal scarring rises with each episode of infection in childhood. An RCT comparing oral versus intravenous antibiotics found retrospectively that new renal scarring after a first UTI was more common in children with vesicoureteric reflux than in children without reflux (logistic regression model: AR of scarring 16/107 [15.0%] with reflux v 10/165 [6%] without reflux; RR 2.47, 95% CI 1.17 to 5.24). A study (287 children with severe vesicoureteral reflux treated either medically or surgically for any UTI) evaluated the risk of renal scarring with serial DMSA
scintigraphy over 5 years. It found that younger children (under 2 years) were at greater risk of renal scarring than older children regardless of treatment allocation for the infection (AR for deterioration in DMSA scan over 5 years 21/86 for younger children v 27/201 for older children; RR 1.82, 95% CI 1.09 to 3.03). Renal scarring is associated with future complications: poor renal growth; recurrent adult pyelonephritis; impaired glomerular function; early hypertension; and end stage renal failure. A combination of recurrent urinary infection, severe vesicoureteric reflux, and the presence of renal scarring at first presentation is associated with the worst prognosis.

 

AIMS

To relieve acute symptoms; to eliminate infection; and to prevent recurrence, renal damage, and long term complications.

 

OUTCOMES

Short term: clinical symptoms and signs (dysuria, frequency, fever); urine culture; incidence of new renal scars. Long term: incidence of recurrent infection; prevalence of renal scarring; renal size and growth; renal function; prevalence of hypertension and renal failure.

 

 

 

 

UTIs in children

 

Aetiology

Vesicoureteric reflux is most common

Congenital obstructions

Bladder dysfunctions

Some forms of E. coli may adhere to the urinary endothelium so are not easily washed out

 

Presentation

Neonates

In neonates this is non-specific, e.g. poor feeding, vomiting, irratibility

May develop into sepsis with meningitis

 

Post neonatal

In young children presentation may include fever, irritability, diarrhoea, vomiting.

Features may look like a GI rather than a GU problem.

Frequency and dysuria are not reliable symptoms.

May or may not be suprapubic or loin tenderness.

 

School age children

More classical adult type presentation

Inflammatory features around the urethral orifice

 

Diagnosis

Microscopy and culture and sensitivity testing

Ward based tests for blood, protein, white cells and nitrite are indicative

Collect a clean specamine

Suprapubic samples being the most reliable, used under 1 year, best taken when the bladder is full

 

Management

In young children i.v. antibiotics to reduce the risk of disseminated infection

While waiting for sensitivity consider trimethoprim, cephalosporins, amoxicillin with clavulinic acid

Repeat C and S at the end of the antibiotic course to confirm resolution

Follow-up investigations of the urinary tract such isotope scanning, ultrasound scanning

Renal scaring (reflux nephropathy) is most likely in the first 5 years of life, the younger the child the more sensitive the kidneys

Scaring may lead to chronic renal insufficiency and hypertension

Over the age of 5 pre-existing renal scars may enlarge with repeated infection but new scars rarely occur.

Recurrent infections over the age of 5 do not cause renal scar formation

If there is vesicoureteric reflex put the child on prophylactic antibiotics for at least 2 years, probably more, consider trimethoprim or nitrofurantoin, once at night

Treat acute infections promptly

Surgical re implantation of the ureters may be considered in extreme cases

Vesicoureteric reflex usually resolves with a rate of about 10% per year

 

 

Other causes of UTI

Other causes of infection below the age of 5 years may also lead to renal scaring,

Therefore children must be well investigated after UTIs

 

Remember chronic pyelonephritis is a common indication of renal dialysis in later life and almost certainly has its origins before the age of 5 years.

 

Haemolytic uraemic syndrome (HUS)

 

 

Pathophysiology

Intravascular haemolysis with red cell fragmentation (microangiopathic haemolysis).

Thrombocytopenia.

Acute renal failure caused by thrombosis in small arteries and arterioles.

Microthrombi occlude small renal vessels.

Microthrombi may also occlude cerebral vessels leading to RICP with reduced GCS.

 

 

Aetiology

Usually Escherichia coli, usually 0157 which produce verocytotoxin.

 

 

Evolution

Usually starts with a febrile illness, often with gastroenteritis, known as diarrhoea associated HUS, (D+HUS).

HUS develops after the febrile episode.

Most patients recover renal function.

Acute mortality is 5%.

5% develop chronic renal failure.

30% exhibit long term renal damage with persistent proteinuria.

 

 

Management

Prevent cross infection.

Supportive therapy until renal function recovers.

Fluid end electrolyte balance, antihypertensive medication, nutritional support, probably dialysis.

If antibiotic or antimotility drugs are used to treat the diarrhoea there is a greater risk HUS and its complications.

Recurrent episodes have been described in the same individual.

 

 

Other forms of HUS

D-HUS HUS without diarrhoea may have a genetic aetiology and be a complement driven illness.

Sporadic cases may also present secondary to pregnancy or other disease processes.

Pneumococcus-assocaited HUS is a rare complication of Streptococcus pneumoniae infection.