Haematuria

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16.2 Haematuria

1 In children haematuria usually originates from the kidneys.

2 Haematuria can be caused by urinary infection, glomerular disease, tumours, congenital abnormalities and coagulopathies.

3 All paediatric haematuria should be investigated.

4 All patients with haematuria require follow-up.

Introduction

Blood in the urine (haematuria) may be visible to the naked eye (macroscopic) or be detected only on dipstick testing and/or urine microscopy (microscopic). It may be found in isolation or associated with other urine abnormalities such as proteinuria, crystals and casts. It is essential to consider urinary tract infection (UTI) as a possible cause and, if confirmed, to manage accordingly (see Chapter 16.4).

Microscopic haematuria may be defined as >10 red blood cells (RBCs) per high-power field, or >50 RBCs mL^–1 of urine (confirmed on three separate occasions).

Note that small numbers of red cells are normally excreted in urine.

Macroscopic haematuria exists when visible to the naked eye and confirmed on testing as being blood.

Haematuria can originate at any site in the urinary tract but, in contrast to adults, lower tract haematuria is relatively uncommon in children (and therefore cystoscopy is rarely indicated).

Microscopic haematuria in the setting of an acute febrile illness can be normal. UTI should be excluded by urine culture and the urine tested again after the acute illness has passed.

Asymptomatic micro-haematuria in children without other signs of renal disease (hypertension, oedema, proteinuria, urinary casts, poor growth or renal impairment) is also relatively common.

Consider idiopathic thrombocytopenic purpura (ITP), Henoch–Schönlein purpura (HSP) and coagulation disorders.

Causes of glomerular haematuria include:

• glomerulonephritis (GN) (including nephritis in multisystem disorders, e.g. systemic lupus erythematosus (SLE));

• familial nephritis (Alport’s disease);

• thin basement membrane disease (‘benign’ familial haematuria);

• IgA nephropathy;

• polycystic kidney disease.

Causes for non-glomerular haematuria include:

• idiopathic hypercalciuria;

• anatomical abnormalities;

• sickle cell disease (in relevant ethnic groups).

History

As in all cases attending the emergency department (ED), a relevant and thorough general and specific history should be taken.

It is important to obtain a family history of renal tract disease in patients with isolated micro-haematuria. Considerations include the possibility of familial haematuria. Check for a family history of renal tract stones (suggesting hypercalciuria) or sensorineural deafness and nephritis (with Alport’s disease).

Ask about previous episodes of haematuria and/or features of HSP or SLE.

Historical features of upper tract haematuria include:

• brown urine;

• frothy urine, which may indicate proteinuria.

Features of lower tract haematuria include:

• pink or bright red colour;

• blood in the initial part of the urine stream suggests a urethral origin;

• blood towards the end of the urine stream suggests bladder origin.

Examination

Physical examination should seek to elicit signs of renal disease. A thorough general examination is essential, concentrating on the following in particular:

• cardiovascular status (pallor, BP, hypovolemia and/or fluid overload including gallop rhythm, pulmonary oedema, ascites, peripheral, scrotal/perineal oedema);

• abdominal examination (loin tenderness, ascites, petechiae or purpura);

• neurological status (anaemia, hypertensive encephalopathy, uraemia).

Investigations

In children presenting to the ED with haematuria, investigations should focus on identifying the anatomical source of the haematuria as well as its clinical significance.

Urine dipstick testing, microscopy and culture should always be performed as part of the initial evaluation of a child with haematuria.

Features suggestive of upper tract haematuria include the following:

• protein is often present;

• RBCs are often small and misshapen (dysmorphic);

• RBC casts and tubular casts may be seen.

Features suggestive of lower tract haematuria include:

• RBCs of normal shape (non-dysmorphic);

• no proteinuria.

NB. Urinary RBC morphology alone is an inaccurate method to determine the site of origin of haematuria and should not be relied upon in isolation.

The extent and type of other investigations done while in the ED will be determined by the clinical scenario. The following tests may be considered:

• urine calcium:creatinine ratio >0.7 mmol nmol^–1 (hypercalciuria);

• urine protein:creatinine ratio > 20 mg nmol^–1 (glomerulonephritides, chronic renal failure);

• plasma urea, creatinine + electrolytes (abnormal renal function);

• plasma calcium, PO_4, albumin (chronic renal failure);

• FBC, platelets, film (thrombocytopenia, anaemia);

• coagulation screen (coagulopathy);

• streptococcal serology (post-streptococcal GN);

• pharyngeal swab culture (post-streptococcal GN);

• complement C3, C4 (post-streptococcal GN, mesangiocapillary GN (MCGN), SLE);

• anti-nuclear antibody (ANA), (screening for SLE);

• abdominal X-ray (renal calculi, nephrocalcinosis);

• renal ultrasound (structural abnormalities, stones, etc.);

• sickle screen (sickle cell disease);

• schistosomiasis serology (schistosomiasis infection).

Differential diagnosis

It is important to remember that blood in urine may come from somewhere other than the urinary tract, e.g. vaginal haemorrhage, rectal fissure or contamination by the child or another person (such as in Münchausen syndrome by proxy).

Not everything staining the urine pink, brown or red is haematuria.

Urine dipstick tests for haematuria are very sensitive and will also be positive in the presence of haemaglobinuria and myoglobinuria. Dyes and foodstuffs (e.g. beetroot, blackberries) can colour the urine pink/red. Urates in the urine of neonates may also stain the nappy pink. Drugs (e.g. rifampicin, phenothiazines, phenolphthalein) and porphyria may also discolour the urine.

Treatment/disposition

• Treatment of patients presenting to ED with haematuria will obviously depend on clinical factors such as the presence or absence of hypertension, anaemia, problems of fluid balance and fluid distribution and pain or discomfort. Biochemical, haematological and imaging results may also be important.

• Whatever the ED management, all cases of haematuria should be followed up by the family doctor, a paediatrician or paediatric nephrologist (as appropriate).

Further reading

Andreoli S.P. Management of acute renal failure. In: Barratt T.M., Avner E.D., Harmon W.E., editors. Pediatric nephrology. 4th ed. Baltimore: Lippincott, Williams & Wilkins; 1999:1119-1134.

http://www.clinicalguidelines.scot.nhs.uk/Renal%20Unit%20Guidelines/Haematuria.pdf;. Renal Unit – Royal Hospital for Sick Children. Guidelines on the management and investigation of haematuria Glasgow, UK: Yorkhill Available at [accessed 21.10.10]

Leticia U.T., Fildes R.D. Hematuria and proteinuria. In: Barakat A.Y., editor. Renal disease in children – clinical evaluation & diagnosis. New York: Springer-Verlag; 1990:133-156.

. Royal Children’s Hospital – Melbourne Clinical Practice Guidelines – Haematuria. Available at http://www.rch.org.au/clinicalguide/cpg.cfm?doc_id=5208 [accessed 21.10.10]

Willis F.R., Geelhoed G.C. Haematuria. In: Management guidelines – Emergency Department. Perth, Western Australia: Princess Margaret Hospital for Children; 2002.

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Textbook of Paediatric Emergency Medicine