Download Urinary Tract Infections

471Genitourinary Problems in Children
Urinary Tract Infections
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An infection somewhere in the nephrological system
Most common infection in childhood after respiratory infection
Newborns: boys - 5X more often than girls
After newborn: girls 10X more often than boys
May result from anatomical obstruction/ vesicoureteral reflux/ or acquired obstructions
90% of UTI related to E. Coli
UTI - History
• Age/Gender
• Polycystic Kidney disease
• Diabetes
• Catheterization
• Voluntary withholding of urine
• Wiping back to front
• Chemical irritation from soaps/bubble bath
• Sexual activity/ STD
UTI Symptoms
• Infants: anorexia, lethargy, jaundice, diarrhea, vomiting, failure to thrive
• Fever (may or may not)
• Pain on urination
• Burning
• Frequency/Urgency
• Foul smelling urine
• Low back pain
• Nocturnal enuresis or daytime bedwetting*
• Urinalysis and culture mandatory (midstream/clean catch) > 100,000 colonies/mL
• Blood cultures in children suspected of pyelonephritis
• Children (particularly girls) who have their first UTI under 5 years of age should have a voiding
cystourethrogram
• Differentials: pinworms, upper UTI, STDs in teens, other causes of abd pain or fever
UTI - Plan
• Amox 40mg/kg/day divided into 2-3 doses for 10 days (choice should be double checked with culture
results)
• Repeat urine in 2 weeks
• Education re: voluntary withholding of urine, wiping, STDs, voiding after sexual activity, good fluid
intake
• Vesicoureteral reflux: antibiotic prophylaxis (trimethoprim-sulfamethoxazole 4mg/kg/day at HS)
Enuresis
Nocturnal Enuresis
•Primary: Child has never been dry for prolonged period
•Multiple factors play a role:
•Decreased arousal from sleep in response to a full bladder
•Small functional bladder capacity
•High nocturnal urine production
•Food sensitivities
•Constipation
•Other factors – ADD, stressors, sleep apnea
•Majority of children have normal exams
Tx:
•Supportive
•Double void before bed
•Decrease caffeine and carbonated drinks
•Provide praise and encouragement
•Keep calendar to follow progress
•Do a dummy run with alarm while awake
•DDAVP (desmopressin acetate) – a temporary fix (0.2mg) 1-3 tabs q HS
•Or nasal spray 20mcg @ HS in divided dose
•Ditropan (oxybutynin) – use with small bladder capacity (relaxes smooth muscle,
increases capacity, delays initial urge to void) 5mg/5ml
•Enuresis bed alarm – very effective
•Secondary:
Child has resumed wetting after at least 6 consecutive months of dryness (look for
infections, diabetes, encopresis, emotional upheaval)
•Common in especially in boys and first-born
•Strong family history
Undescended Testicles (Cryptorchism)
• Development of testes begins in abd and at 7th month of gestation, begin descent into scrotal sac
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(through inguinal canal and out external ring into scrotum)
May have true undescended or retractile testes
Incidence:3% of term males; 20% preterm
80% descend by 1 year of age
Family history is strong
Parents frequently may not notice that testis is undescended
Exam
• Make sure room/hand are warm
• Do exam from top down so as not to active the cremasteric reflex
• Infant in relaxed supine position (older child may squat or sit cross legged)
• May have to “milk” down a retractile testis
• Examine scrotum for “lived-in” look
• May need to do ultrasound to see if there is a testis
Hydrocele
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Scrotal swelling (unilateral or bilateral)
Increases with activity
Usually painless
May be associated with a hernia
Fluid reabsorbs usually within a year, if not surgery consult is indicated
Monitor size and ask parents about any fluctuation
Adhesions of Foreskin vs Phimosis
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Adhesion of foreskin: tissue growth between foreskin and glans that make it difficult to retract
foreskin (foreskin remains supple). Resolves by 6 yrs of age
Phimosis: scarring of foreskin and can no longer be retracted over the glans
Cause debated: forcible retractions, irritation from soiled diaper, recurrent infections, congenital
abnormalities, diabetes
Exam: look for infection of foreskin or glans (balantitis)
Treatment: circumcision
Hypospadias
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Common anomaly – 1 in 150 male births
Urethra varies from mild glanular hypospadias to severe perineal hypospadias
Form of hypospadias is by location
Ambiguous Genitalia
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Under-development of male genitalia or over-development of female genitalia r/t hormonal
influences in utero
Incidence: 1 in 2000
Increased risk: maternal/family history congenital adrenal cortical hyperplasia
Child has genetically identifiable sex –determination should be held until testing completed
 Abnormal chromosomal cause include Klinefelter syndrome (XXY) and Turner syndrome
Labial Adhesion
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Fusion of labia minora – seen in infants and young girls, not present at birth
Thin flat membrane partially covers area from clitoris to posterior vaginal opening
Highest incidence occurs around 2 years
May be symptoms of dysuria or UTI
On exam, gently spread labia majora and observe the labia minora
Resolves spontaneously in most children
Tx with topical estrogen cream if interference with urination or UTIs
Precocious puberty (condensed from Mayo Clinic information)
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Signs and symptoms of precocious puberty include development of before age 8 in girls and
before age 9 in boys.
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Girls: Breast growth, First period (menstruation)
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Boys: Enlarged testicles and penis, Facial hair (usually grows first on the upper lip),
Deepening voice
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Both girls and boys: Pubic or underarm hair, Rapid growth, Acne, Adult body odor
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Causes: Often not found. Rarely, conditions such as infections, hormone disorders, tumors,
brain abnormalities or injuries may cause precocious puberty.
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Treatment typically includes medication to delay further development.
Causes
To understand what causes precocious puberty in some children, it's helpful to know what causes puberty
to begin. A complex process known as the hypothalamic-pituitary-gonadal (HPG) axis governs when
puberty occurs. This process involves the following steps:
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The hypothalamus makes gonadotropin-releasing hormone (Gn-RH).
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Gn-RH causes the pituitary gland to release two more hormones: luteinizing hormone (LH) and
follicle-stimulating hormone (FSH).
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LH and FSH cause the ovaries to produce hormones involved in the growth and development of
female sexual characteristics (estrogen) and the testicles to produce hormones responsible for
the growth and development of male sexual characteristics (testosterone). The adrenal glands
also begin to make estrogen and testosterone.
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The production of estrogen and testosterone causes the physical changes of puberty.
The reason this process begins early in some children depends on the type of precocious puberty they
have: central precocious puberty or peripheral precocious puberty.
Central precocious puberty
There's usually no identifiable cause for this type of precocious puberty.
In central precocious puberty, the entire HPG axis starts too soon. Although they begin earlier than they
should, the pattern and timing of the steps in the process are otherwise normal. For the majority of
children with this condition, there's no underlying medical problem and no identifiable reason for the HPG
axis to begin when it does.
In rare cases, the following may cause central precocious puberty:
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A tumor in the brain or spinal cord
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An infection, such as encephalitis or meningitis
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A defect in the brain present at birth, such as excess fluid buildup (hydrocephalus) or a
noncancerous tumor (hamartoma)
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Radiation to the brain or spinal cord
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Injury to the brain or spinal cord
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An obstruction of blood flow to the brain (ischemia)
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McCune-Albright syndrome — a genetic disease that affects bones and skin color and causes
hormonal problems
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Congenital adrenal hyperplasia — a group of inherited disorders involving abnormal hormone
production by the adrenal glands
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Hypothyroidism
Peripheral precocious puberty
Estrogen or testosterone in the child's body causes this type of precocious puberty.
Peripheral precocious puberty, which is less common than central precocious puberty, happens without
involvement of Gn-RH. Instead, the cause is release of estrogen or testosterone into the body because of
problems with the ovaries, testicles, adrenal glands or pituitary gland.
In both girls and boys, the following may lead to peripheral precocious puberty:
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A tumor in the adrenal glands or in the pituitary gland that secretes estrogen or testosterone
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McCune-Albright syndrome
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Exposure to external sources of estrogen or testosterone, such as creams or ointments
In girls, peripheral precocious puberty may also be associated with:
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Ovarian cysts
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Ovarian tumors
In boys, peripheral precocious puberty may also be caused by:
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A tumor in the cells that make sperm (germ cells) or in the cells that make testosterone (Leydig
cells)
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Gene mutation — a rare disorder called familial gonadotropin-independent sexual precocity,
which is caused by a defect in a gene, can result in the early production of testosterone in boys,
usually between ages 1 and 4.
Risk factors
Factors that increase a child's risk of precocious puberty include: female gender, African-American race,
obese children, being exposed to sex hormones (coming in contact with estrogen or testosterone cream,
dietary supplements), having other medical conditions (complication of McCune-Albright syndrome or
congenital adrenal hyperplasia)
Possible complications of precocious puberty include:
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Short height. Children with precocious puberty may grow quickly at first and be tall, compared
with their peers. But, because their bones mature more quickly than normal, they often stop
growing earlier than usual. This can cause them to be shorter than average as adults. Early
treatment of precocious puberty, especially when it occurs in very young children, can help them
attain more height than they would without treatment.
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Polycystic ovary syndrome. Girls who begin menstruating before the age of 8 are at increased
risk of developing this hormone disorder later on during puberty.
Tests and diagnosis: Hormone levels, x-rays of wrist/hand, referral to pediatric endocrinologist
Determining the type of precocious puberty
Once an initial diagnosis has been made, to find out which type of precocious puberty the child has,
injected with Gn-RH hormone. In children with central precocious puberty, a Gn-RH injection causes LH
and FSH hormone levels to rise. In children with peripheral precocious puberty, LH and FSH hormone
levels stay the same.
Proteinuria
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Found on dipstick in nearly 10% of all children between ages 8 and 15
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To be considered significant, the dipstick test should reveal a 1+ (30 mg/dL) or higher level of
proteinuria
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If very concentrated urine (SG > 1.015), may get false-positive for proteinuria. In this case, the
dipstick protein must be 2+ or higher to be significant
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Types and causes of proteinuria
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Transient (functional) proteinuria
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Temporary and clears when the inciting factor remits or is removed
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Can occur with fever, exercise, stress, or cold exposure
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May also be caused by hemodynamic alterations in glomerular blood flow as with
dehydration
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In cases of suspected exercise-induced proteinuria, obtain a urine sample and
compare it to one produced after 48 hours without heavy exercise to determine
whether protein is lower or absent. Up to 75% of children with proteinuria on the
first specimen have a normal urine result on the second specimen.
Orthostatic (postural) proteinuria
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60% of all cases of proteinuria; especially common in adolescents
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Normal protein excretion in a spot, first-morning urine sample after the child has
been supine for the entire night, but increased protein excretion (+ dipstick) at
least 4-6 hours after the child has been upright.
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Cause is not clear; however, the anatomic compression of the left renal vein has
been suggested
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Benign course; offer reassurance
Persistent proteinuria
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May be glomerular or tubulointerstitial in origin
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Can be primary (stemming from the renal tissue) or secondary (caused by
systemic diseases)
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When proteinuria is associated with hematuria, renal dysfunction, and
hypertension, significant renal disease may be present
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Common features of renal disease include growth failure, hypertension, and
edema (i.e., periorbital, presacral, genital, or ankle). Associated deafness or
visual impairment suggests hereditary nephritis.
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Glomerular diseases are more common than tubulointerstitial diseases
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Glomerular diseases
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Usually indicated by albumin and immunoglobulin G in the urine
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Examples of causes: systemic lupus erythematosus (SLE), diabetes
mellitus, infection (GABHS, hepatitis, mono, HIV), malignancies, mercury
toxin
Tubulointerstitial diseases
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Less common
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Tubular proteinuria rarely presents a diagnostic dilemma because the
underlying disease is usually detected before the proteinuria
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Examples of causes: acute tubular necrosis (due to NSAIDS,
radiocontrast media, aminoglycosides); acute tubulointerstitial nephritis
(due to NSAIDs, PCN, cephalosporins, quinolones, sulfonamides,
cimetidine, allopurinal); polycystic kidney disease; pyelonephritis; and
toxins (lead, copper, mercury)
Management
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The family can be reassured if the proteinuria is transient or orthostatic, and the child is
asymptomatic, has no associated hematuria, and has normal BP and GFR.
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Regular follow-up is important, however, as long as significant proteinuria persists.
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A child with persistent proteinuria should initially receive a physical examination, BP
measurement, urinalysis and blood tests for creatinine and urea nitrogen levels every 612 months. Once stable, follow-up can be annual.
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The treatment of persistent proteinuria should be directed at the underlying cause.
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Referral to a nephrologist or urologist is necessary for significant proteinuria, persistent
proteinuria, or for the presence of suspicious associated findings.
Hematuria
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Children may experience asymptomatic gross and microscopic hematuria
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Most common etiologic for microscopic hematuria: poststreptococcal glomerulonephritis,
hypercalciuria with or without renal calculi, and structural abnormalities such as a single kidney
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One study found no identifiable cause in most patients with microscopic hematuria
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UTI is a rare cause
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External vulvar irritation caused by soaps, bubble baths, Candida, and excoriations may
contribute to microscopic hematuria
Gross hematuria in children can be a grave concern, possibly signaling IgA nephropathy and
hypercalciuria (with or without calculi)
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Less commons causes: coagulopathies, UTIs, hydronephrosis, renal trauma, tumor,
epididymitis, strenuous exercise, some bacterial and viral illnesses
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Thorough urologic workup is warranted for pediatric gross hematuria
The presence of RBC casts or proteinuria suggests glomerular hematuria, a condition associated
with acute or chronic glomerulonephritis
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Order a urine C & S, consider ordering a renal ultrasound, and consider referral to an
urologist or nephrologist.
References:
Helming, M.B., (March 2009). Genitourinary disorders in children: A review of less common
presentations. Advance for Nurse Practitioners, 24-30.
Leung, A.K.C., & Wong, A.H.C. (September 15, 2010). Proteinuria in children. American Family
Physician, 82(6), 645-652.