Urinary Tract Infection

Keep in mind the possibility of UTI should be considered in any febrile child (temp >39)
Girls <24 months & boys < 6months are highest risk
Urine analysis is not reliable
False ve results (no pyuria <5WBCs/HPF) previous Antibiotics or obstructive lesions
False +ve results (pyuria > 5WBCs/HPF) contaminated sample specially the adhesive
plastic bag applied to the perineum
Urine culture is the only reliable test ( >10^5 colony forming units of single organism /ml)
or the presence of more than 1 organism
Older child > 6Years will be presented by
Fever vomiting Abdominal pain Dysuria Urgency Frequency Enuresis & Incontinence
Most common causes gram ve colonic bacteria (E.Coli 80%) Klebsiella Proteus (more
in males )
Note: Pseudomonas usually indicates structural anomaly as vesico-ureteric reflux
Further investigations for ( recurrent attack or prolonged fever > 48 hours with good
treatment )
Abdomino-pelvic US Abdominal X-ray Micturating cystourethrography to exclude
vesico-ureteric reflux
Medication ( Outpatient Antibiotics choice for 7-10days )
1-TMP-SFX 20mg/kg/day PO q12h
2-1st generation cephalosporins 50mg/kg/day PO q6h
Cephalexin or cephradine or cefadroxil
3-2nd generation cephalosporins 50mg/kg/day PO q8h
cefaclor

3-fluroquinolone cipro 20-30mg/kg/day PO q12h >18 years

Parental therapy ( Inpatient Antibiotics choice)
1-Ampicillin100-200mg/kg/day q12h I.V + Gentamicin 3mg/kg/day q12h IM Or Amikin
15mg/kg/day q12h IM
2-Ceftriaxone 50-100mg/kg/day q12-24h IV
Analgesics as acetaminophen & Ibuprofen
Analgesics to provide relief from burning , spasticity during voiding
Phenazopyridine like urisept 100mg tab (3LE)
6-12y : 1 tablet q8h after meal
>12y : 1-2 tablets q8h after meal
Alkalinizing agents to change the urine PH
As Epimag sachets / Xenomag sachets or Coliurinal eff. Orally twice daily
For recurrent attacks

Hematuria (Acute post streptococcal glomerulonephritis)

DDx
Ask about Dysuria,frequency and abdominal pain ( UTI)
History of trauma
Bruising (HSP)
Nose bleeding (Coagulation disorders)
Recent drugs (Aspirin)
Vigorous Exercise
Other DDx
1-Hemolytic uremic syndrome history of bloody diarrhea 2-7days before onset of renal
failure edema and petechiae pallor diagnosis made upon signs of ARF +
thrombocytopenia + Anaemia (stool culture E-coli)
2-IgA nephropathy
3-Hypercalciuria
4-SLE

5-Urolithiasis
6-Sickle cell haemoglobinopathies
7-Calculi
8-Wilm`s tumor
Acute post streptococcal glomerulonephritis
Clinical presentation of Acute post Streptococcal glomerulonephritis
1-Acute nephritic syndrome
Oliguria and hematuria usually improved by end of the 1st week
Low grade fever ,hedache
History of infection 2 weeks before onset of symptoms
Hypertension present in >70% cases (125/80)
Edema mild acute puffy eye lids & Lower limb edema
2-Hypertensive heart failure
3-Hypertensive encephalopathy
Renal biopsy is indicated only with persistent low C3 >3months or persistent hematuria
>6months
Home management in 95% of cases only hospitalization with severe hypertension or
severe oliguria
Management
Rest at least 1st week (during oliguria)
Diet salt & protein restriction
Fluids restrictions to 1L/day
Control of hypertension and edema (mild hypertension may persist for few weeks)
1-Furesmide is helpful in both and increase urine ouput (1mg/kg/day q12h)
12
2-If hypertension persists add CCBlockers as Hydralazine (1mg/kg/day q12h) PO
3-ACEIs effective but cause hyperkalemia
Penicillin (10 days oral course for eradication of any streptococcal infection
Furosemide :
1-Lasix 20,40mg ampule (2-4LE) 2-lasix 40mg tab (6LE) 3-Lafurex 20mg tab (4.5LE) 4-Lafurex
20mg ampule (1.5LE) 5-Diusex 20mg ampule (1.5LE)

Nephrotic Syndrome

It`s combination of edema, heavy proteinuria, hypoalbuminemia & hyperlipidema

With NO hypertension or gross hematuria
Investigations
Protein in 24 hours urine > 40mg/m2/hr
Serum albumin < 3gm%
Serum cholesterol > 300mg%
Note : Renal function test C3 & A.S.O.T all are normal
Management : exclude active infection or other contraindications before starting Steroids
therapy
induction of remission ( daily therapy )
Prednisone (2mg/kg/day, maximum 60mg) for 6 weeks maximum single daily dose or split
into 2 doses
Either Steroid responsive : urine become free of Albumin
Steroid resistant : no response after 1 month so renal biopsy indicated
maintenance of remission ( alternate day therapy ) for steroid responsive
Prednisone (1.5mg/kg/day, maximum 40mg) single daily dose on alternate days for 2-6
months better 6 months to decrease relapse by about 33%
relapses (recurrence of edema) treated as the initial attack but alternate day therapy is
continued for longer period (6-12 months)
1-Hostacortin 5mg tab (4LE) 2-Hostacortin-H 5mg tab (4LE) 3-Prednisolone tab (1LE) 4Predilon tab (2LE) 5-Deltacortil 5mg tab (1.5 LE) 6-Urbason 4mg-8mg tab (10LE) 7-Solupred
5mg-20mg tab (23-40LE)

Frequently relapsing

and

steroid dependant disease

2 or more replases within 6 months

2 or more relapses during tapering
4 or more relapses within 12 months
or within 14 days of stopping
steroids
Both are steroids sensitive
Cyclophosphamide e.g: Endoxan 50mg tab (38LE) Alkyloxan tab (62LE)
It decrease rate of relapse compared to treatment of prednisolone
Dose (2mg/kg/day) single dose for 12 weeks . alternate day therapy with prednisone is
continued during the course of cyclophosphamide therapy
Cyclophosphamide is discontinued if WBCs count falls below 5000/cmm
Note:
Diuretics (furosemide) may be of benefit in childrens with edema however hypovolaemic
shock occurs with aggressive treatment
Antihypertensive therapy may be used but not with Acute Renal Failure
Home monitor for daily weight gain urine protein level steroid dose

Enuresis

Repeated involuntary voiding in childrens > 4years (expected age of bladder control)
It`s either 1ry (chiled never attained bladder control) or 2ry (chiled attained bladder control
for at least 6 months)
It`s either Nocturnal (at night) in majority of cases with good prognosis or Diurnal (day &
night) with bad prognosis
Note: Urinalysis (the most important screening test in a child with enuresis) exclude U.T.I
In 2ry enuresis (5% of cases) you`ll search for a cause and manage
1-Diabetes Mellitus (do Random blood sugar) 2- Diabetes Insipidus (look for urine specific
gravity) 3-genitourinary anomaly ( do U/S) 4-decrease level of ADH (measure it) 5-known
patient with Sickle cell anaemia 6-chronic constipation press on urinary bladder
Management of 1ry enuresis: before age of 5 years no drug treatment only 1-simple
measures 3
Reassurance bladder control usually between 1-5 years
Avoid excessive fluid intake 2 hours before bedtime
No punishment
Let child urinate before sleep
Reward the baby for the dry nights
Proper training such as holding urine as much as possible
2-Alarm

therapy should be considered for every patient. It is

reported to improve bedwetting by increasing
nocturnal bladder capacity or by enhanced arousal; it
does not reduce nocturnal urine output.cure rate up
to 80% but relapse rate between 10-40% it gives
good results after 2 weeks but it may be used upto 3
months or 1 month after being dry. If failed it should
be used again once the child is older and more motivated

3-Drug therapy : it`s only indicated for children above 5 years with 1ry nocturnal enuresis
1-imipramine it`s tricyclic antidepressant increase release of Anti Diuretic Hormone (theory)
success rate about 60% but relapse >90%
1-Tofranil 25mg tab(2.5LE) 2-tofranil 10mg tab(1.5LE) 3-imipramine 25mg tab(4.5LE) 4toframine 25mg tab(4.5LE)

Dose: start with 1 tablet daily 1 hour before sleep for 2 weeks if no response give 2 tablets
(50mg) for another 2 weeks if no response stop the drug . if there`s response continue the
drug for 3 months then tapering it by giving the same dose (25mg or 50mg) once every
other day for 3 weeks then once every third night for 3 weeks
2
.

3 3 3
3
2-Desmopressin it`s synthetic vasopressin analogue salt retention urine concentrate
decrease urine volume it`s mainly used in ttt of Diabetes Insipidus but effective in enuresis it
has 50% success but relapse >94%
Dose: start with minirin melt 60mcg (30tabs) (155LE) for 2 weeks if no response may increase
dose upto minirin melt 120mcg (30tabs) (300LE) for another 2 weeks in case of response use
the drug for 2 months then gradual tapering for 4 weeks it`s very expensive drug
3-Anticholinergic drus the only benefit of these drugs it makes the bladder hold more urine
but it doesn`t decrease bed time dose of oxybutynin 5mg PO daily and increased gradually
up to 20mg/day at sleep time
1-uripan 5mg/5ml (7.5LE) 2-Detrusan 5mg/5ml (6.5LE) 3-Detronin 5mg/5ml (6.5LE)
Some doctors use : bellacid tab (2LE) it contains belladonna 10mg & phenobarbitone 20mg

for nocturnal enuresis 1/2 to 1 tablet before bed time but it`s used for spastic colon

Surgical conditions in pediatrics

You should know about it ? you will see it ? you`ll refere it

Testicular Disorders
undescended testis

The diagnosis of undescended testes is usually made by the parents or first examining
physician. The important point is the absolute necessity of distinguishing between retractile
testes and the true undescended testes. Testes that can be drawn to the scrotum, even if
they retract again, are retractile testes and not undescended, the squatting position may aid
in helping descend the testes for exam. Retractile testis needs no further surgical
management.
Time of operation ? Tell the parents that pediatrics surgeon wait until the baby reach 6
months there`s a good chance for testicular descent without surgery if this not occurred
surgery must be done.

Testicular swelling

Any case of testicular swelling should do Testicular Ultrasonography why ? because in

children it`s very difficult to differentiate Hydrocele from Inguinal hernia clinically. don`t rely
on testicular size , transillumination or the size of swelling over time . moreover there may be
both hernia and hydrocele together specially in preterm babies
Why you do U/S ? because hernia may be incarcerated and this is surgical emergency
associated with acute pain, swelling(hard-red-painful), pulling up legs and vomiting

Hydrocele

A hydrocele is a collection of fluid in the space surrounding the testicle between the layers
of the tunica vaginalis. Hydroceles can be scrotal, of the cord, abdominal, or a combination
of the above. A hydrocele of the cord is the fluid-filled remnant of the
processus vaginalis separated from the tunica vaginalis. A communicating
hydrocele is one that communicates with the peritoneal cavity by way of a narrow opening
into a hernial sac. Hydroceles are common in infants. Some are associated
with an inguinal hernia. They are often bilateral, and like hernias, are more common on the
right than the left. Most hydroceles will resolve spontaneously by 1-2
years of age. After this time, elective repair can be performed at any
time

Inguinal hernia

is the most common surgical problem of childhood. The infant or child with an inguinal hernia
generally presents with a bulge at the internal or external ring or within the scrotum. no pain
is associated with a simple inguinal hernia in an infant. The parents may perceive the bulge
as being painful when, in truth, it causes no discomfort to the patient. The bulge commonly
occurs after crying or straining and often resolves during the night while the baby is sleeping.
Inguinal hernias never go away without treatment. Furthermore, if the sac is left open, a loop
of bowel or other organ may become trapped or incarcerated (strangulated) in the sac.
Patients with an incarcerated hernia generally present with a tender firm mass in the inguinal

canal or scrotum. The child may be fussy, unwilling to

feed, and inconsolably crying. The skin overlying the
bulge
may
be
edematous,
erythematous,
and
discolored.there`s sometimes vomiting and the baby will
stop stooling This is a surgical emergency

Congenital Orthopedic Disorders in pediatrics

Clubfoot (Congenital Talipes equivarus)
It`s a congenital deformity of the foot that occurs in about 1 in 1,000
births. The affected foot tends to be smaller than normal, with the
heel pointing downward and the forefoot turning inward. The heel
cord [achilles tendon] is tight, causing the heel to be drawn up toward
the leg. This position is referred to as "equinus," and it is impossible to
lace the foot flat on the ground. Since the condition starts in the first
rimester of pregnancy, the deformity is often quite rigid at birth. The three
:ssic signs of clubfeet are

p
t
cla

Fixed plantar flexion (equinus) of the ankle, characterized by the drawn up position of the
heel and inability to bring to foot to a plantigrade (flat) standing position. This is caused by
a tight achilles tendon
Adduction (varus), or turning in of the heel or hindfoot
Adduction (turning under) of the forefoot and midfoot giving the foot a kidney-shaped
appearance
If left untreated, the deformity will not go away. It will continue to get worse over time so
immediate refer to orthopaedic surgeon is required

In-toeing Gait in Children

An in-toeing gait is very common in children, and is a frequent complaint

of many parents. In fact, an in-toeing gait (pigeon-toed) is the most
common rotational deformity seen in pediatric orthopaedics. In the
overwhelming majority of patients, the in-toeing will correct with growth
over time.
What causes an in-toeing gait in children? The three most common
causes of in-toeing in children are femoral anteversion (twisting of the
femur/thigh), internal/medial tibial torsion (twisted tibia/shin bone), and
metatarsus adductus (curved foot).

Femoral anteversion/torsion
is the most frequent cause of in-toeing in children between the ages of 310 years. Femoral anteversion is therefore a condition in which the
femoral neck leans forward with respect to the rest of the femur. This
causes the lower extremity on the affected side to rotate internally (the
knee and foot twists towards the midline of the body). The normal child is born with
approximately 40 degrees of femoral anteversion. This will gradually decrease to 10-15
degrees at adolescence and generally improves with further growth. Femoral anteversion is
more common in females, and is usually most noticeable between the ages of 4-6 years.

Parents will notice that when the child is standing with the feet forward, the patellae
(kneecaps) will point inwards. Frequently, parents will also describe the child's gait as
awkward or clumsy. The in-toeing will often appear worse with running and at the end of the
day when fatigued. Femoral anteversion will decrease naturally in 99% of cases.

Internal tibial torsion

It causes an in-toeing gait from a twisting of the tibia (shin bone). It is most often first noticed
when a child is first starting to walk, and is most common between the ages of 2-4 years. The
inward torsion is a variation of normal anatomy and is caused partially by the child's position
in the uterus. The toddler or young child presents to the orthopaedic clinic with complaints of
"bowing legs." Examining a child with internal tibial torsion with the patellae (kneecaps)
straight, Tibial torsion almost always improves without treatment, and usually before school
age. Splints, special shoes, and exercise programs do not help. Surgery to re-set the bone
may be done in a child who is at least 8 to10 years old and has a severe twist that causes
significant walking problems.

Note: Flat Foot

In the child before age 3 years, the normal longitudinal arch of the foot is present, but often
masked by the fat pad in the instep. Hence all young children before age 3 look flat-footed,
even though they are not. After age 3, the fat pad disappears, and the arch becomes more
evident.

Metatarsus Adductus /Varus/MTA

Metatarsus adductus (MTA) or varus is a condition that is
commonly seen in newborns and young infants, where the
forefoot is twisted inwards relative to the hindfoot (or heel). MTA
is very common in the newborn, and is usually due to the feet
being "packed" in the womb in that position. The forefoot
adduction at this stage is very flexible, and with freedom of
movement, this postural condition of MTA often improves over
the next 6 to 12 weeks.In about 15% of cases, the adducted
position of the forefoot does not improve. MTA that is diagnosed
at
birth does not require treatment. It is usually postural, and with
growth, the MTA
resolves spontaneously over a period of 6 to 12 weeks. X-rays
are usually not necessary
Severe cases of metatarsus adductus may partially resemble a clubfoot deformity.

Bowed Legs
Bowed legs in a toddler is very common. When a child with bowed legs stands with his or her
feet together, there is a distinct space between the lower legs and knees. This may be a
result of either one, or both, of the legs curving outward. Walking often exaggerates this
bowed appearance.
Adolescents occasionally have bowed legs. In many of these cases, the child is significantly
overweight.
Cause

Physiologic Genu Varum

In most children under 2 years old, bowing of the legs is simply a normal variation in leg
appearance. Doctors refer to this type of bowing as physiologic genu varum.
In children with physiologic genu varum, the bowing begins to slowly improve at
approximately 18 months of age and continues as the child grows. By ages 3 to 4, the bowing
has corrected and the legs typically have a normal appearance.

Blount's Disease

Left: Toddler with infantile Blount's disease involving the left

leg. Right: X-ray of the left knee shows the Blount's abnormality
along the top of the shinbone.
Blount's disease is a condition that can occur in toddlers, as
well as in adolescents. It results from an abnormality of the
growth
plate in the upper part of the shinbone (tibia). Growth plates
are located at the ends of a child's long bones. They help
determine the length and shape of the adult bone.
In a child under the age of 2 years, it may be impossible to
distinguish infantile Blount's disease from physiologic genu
varum. By the age of 3 years, however, the bowing will worsen and
an obvious problem can often be seen in an x-ray.

Rickets
Rickets is a bone disease in children that causes bowed legs and other bone deformities.
Children with rickets do not get enough calcium, phosphorus, or Vitamin D all of which are
important for healthy growing bones.
Nutritional rickets is unusual in developed countries because many foods, including milk
products, are fortified with Vitamin D. Rickets can also be caused by a genetic abnormality
that does not allow Vitamin D to be absorbed correctly. This form of rickets may be inherited
(discussed later).
Symptoms
Bowed legs are most evident when a child stands and walks. The most common symptom of
bowed legs is an awkward walking pattern.
Toddlers with bowed legs usually have normal coordination, and are not delayed in learning
how to walk. The amount of bowing can be significant, however, and can be quite alarming to
parents and family members.Turning in of the feet (intoeing) is also common in toddlers and
frequently occurs in combination with bowed legs.Bowed legs do not typically cause any pain.
During adolescence, however, persistent bowing can lead to discomfort in the hips, knees,
and/or ankles because of the abnormal stress that the curved legs have on these joints. In
addition, parents are often concerned that the child trips too frequently, particularly if
intoeing is also present.
Doctor Examination
Your doctor will begin your child's evaluation with a thorough physical examination.If your
child is under age 2, in good health, and has symmetrical bowing (the same amount of
bowing in both legs), then your doctor will most likely tell you that no further tests are
currently needed.However, if your doctor notes that one leg is more severely bowed than the
other, he or she may recommend an x-ray of the lower legs. An x-ray of your child's legs in
the standing position can show Blount's disease or rickets.If your child is older than 2 1/2 at
the first doctor's visit and has symmetrical bowing, your doctor will most likely recommend
an x-ray. The likelihood of your child having infantile Blount's disease or rickets is greater at
this age. If the x-ray shows signs of rickets, your doctor will order blood tests to confirm the
presence of this disorder.
Treatment
Natural Progession of Disease
Physiologic genu varum nearly always spontaneously corrects itself as the
child grows. This correction usually occurs by the age of 3 to 4 years.
An adolescent with Blount's disease.
Untreated infantile Blount's disease or untreated rickets results in progressive
worsening of the bowing in later childhood and adolescence. Ultimately, these
children have leg discomfort (especially the knees) due to the abnormal
stresses that occur on the joints. Adolescents with Blount's disease are most
likely to experience pain with the bowing.

 Congenital Torticollis
It`s shortening of the cervical muscles, most commonly the
sternocleidomastoid (SCM) muscle, and tilting of the head to the
opposite side. Management is conservative in most cases using
early physiotherapy exercises a mean duration of three months to
achieve full passive neck range of motion. Those children with
failed medical therapy should undergo surgical transection of the
SCM muscle. Consultation with orthopedic surgery is necessary

Thyroglossal Duct Cysts

Thyroglossal duct cyst (TDC) is the most common congenital
anterior midline neck mass usually (2/3 of cases) presenting before
the second decade of life. Symptoms appear at an average age of
four with the sudden appearance of a cystic mass at the angle of
neck level moving with tongue protrusion and swallowing. Management
is Sistrunk operation so immediate refer to general surgeon.