nelson essential volume 2 Flashcards
what are the most common causes of intrinsic acute kidney injury in children?
tubular injury
- can have low, normal or high u/o depending on severity of the injury
tubular injury can occur from what mechanisms:
- acute tubular necrosis - hypoxia/ischemia
- infection - sepsis
- nephrotoxic agents - medications, contrast, myoglobin
- inflammation - interstitial nephritis
glomerular and vascular intrinsic acute kidney injury, how might they present?
hematuria, edema, hypertension and oliguria
glomerular injury - primary GN, vascultiis, HUS
vascular - renal vein thrombosis, arterial emboli, malignant HTN
How to tell pre renal from other causes of acute kidney injury?
- normal UA with high specific gravity (reflects appropriate renal retention of water when there is renal hypo perfusion) I think number is >1.03 ish (see previous flash card)
- urine output will be low
- urine Na will be 500 in child (>350 in neonate)
- normal renal US
see table pg 562 baby Nelson
How to tell renal from pre renal when oliguria (i.e. pre renal from ATN?)
use the Fena and osmoses etc
in renal cause:
1. urine output can be either low, nomal or high
2. urinalysis with RBCs, WBCs, protein or casts
3. urine Na high (kidney is peeing it out) >40 in kids or >50 in neonate
4. Fena >2%
5. urine osmoles approx 300
6. renal US might show increased echogenecity, decreased corticomedullary differentiation
Post renal vs other causes
low or normal u/o, everything else variable, U/S will show hydronephrosis
Common lab problems in AKI
hyperkalemia, metabolic acidosis, hypocalcemia, hyperphosphate
anemia can be observed frequently
Causes of pre renal AKI
dehydration bleed septic shock burns heart failure cirrhosis
which has a worse prognosis, oliguric or non oliguric AKI?
oliguric is worse prognosis, non oliguric usually recover well
Indications for dialysis
- acute or chronic dialysis:
volume overload, metabolic acidosis, eletrolyte, uremia - acute: ingestions, hyperammonemia
- chronic: poor growth, stage 5 renal diseae
Common complications of chronic kidney disease
- poor growth - including delayed puberty also , resistance to growth hormone
- anemia - since they can’t make enough EPO as well as iron deficiency
- renal osteodystrophy/secondary hyperparathyroidism : because make less 1,25 OHD in the kidney , hypocalcemia and and hyper phosphate ->can lead to rickets/bone deformities if goes for a long time
- cardiovastular: hypertension and LVH
- electrolyte abnormalities: high K, low Na, metabolic acidosis
- impact on learning and school
How to treat the complications above (Pg 563 baby nelson)
- growth: increase calories, treat acidosis, treat ROD, GH **adequate nutrition very very important even if need supplements and tube feedings
- anemia: EPO, iron
- calcitriol (aka 1,25 OHD), calcium supplement, restrict phosphorus and give phosphate binders
- treat HTN, don’t volume overload
- lytes: low K diet, furosemie, sodium polystyrene, sodium supplement, give alkali (**what to do with sodium depends on the aetiology i.e. many congenital anomalies have sodium wasting, vs those with GN tend to retain salt)
most common cause of CKD in less than 10 year olds
congenital anomalies of kidney and urinary tract
in >10 year old - more likely focal segmental glomerulosclerosis and GN
true or false - restrict protein intake in CKD in kids?
not usually
GFR in different stages of CKD?
>90 stage 1 60-90 stage 2 30-59 stage 3 15-30 stage 4 2 year old (since GFR at adult levels at this age)
definition of hypertension
BP >95th percentil for age, gender and height on at least 3 occasions
(normal is 99th
what is hypertensive emergency
severe elevation in BP with target organ damage - encephalopathy, heart failure
most common cause of HTN in teens? in younger kids?
essential in teens
more likely secondary in younger kids, with more severe elevation ->renal disease most likely
hypertensive and neurofibromatosis (cafe au lait) what finding to rule out
renal artery stenosis
see differential of HTN pg 564
Management of Hypertension
- lifestyle changes - asymptomatic stage 1
- medication - stage 2 or if stage 1 no respond
- calcium channe blocker or ACEi most frequent 1st line, ARB, beta blocker/diuretics sometimes used
How to treat a hypertensive emergency?
hospitalize
labetalol, esmolol, nicardipine or sodium nitro
why is hypertension bad?
may increase risk of CV, CNS and renal morbidity in adults
true or false - most - most vesicoureteral reflex is from structural problems?
false - most are from congenital invompentance, minority have UV abnormalities which are structural and don’t resolve
true or false - VUR can be familial
true - 30-40% of kids with VUR can have VUR
associated findings with VUR?
renal dysplasia
duplication of the ureters (can obstruct upper collecting system)
neurogenic bladder
from increased pressure when bladder outlet is obstructed
when to do VCUG
if hydronephrosis/scaring etc on US after UTI
if two febrile UTIs
radionuclid cystogram - advantage and disadvantage
less radiation
might miss PUV in males
renal scars?
DMSA scan to ID
complications of reflux nephropathy
hypetension
chronic kidney disease
What is Potter syndrome?
bilateral renal agensis
flat facies
clubfoot
pulmonary hypoplasia
who is more likely to have unilateral renal agencies
infants of diabetic mothers and african americans
normal or minimally reduced renal function
associated findings with unilateral renal agenesis
VUR genital tract, ear skeletal system and CV abnormalities Turner syndrome Poland syndrome VACTERL association
true or false - renal hypoplasia/dysplasia can often progress to CKD?
true, because they have less nephrons, can’t fully absorb Na nd water
true or false - bilateral multi cystic renal dysplasia is lethal
true, because there is minimal or no functioning renal tissue
what should you look for in contralateral kidney of multi cystic renal dysplasia
VUR in contraleteral kidney - associated with multi cystic renal dysplasia
MCD often involutes on its own
rarely associated with hypertension or recurrent UTI
Clinical manifestations of posterior urethral valves
most common bladder outlet obstruction males -
parents may note a poor urine stream
urethra bets dilated, might get VUR, and hypertrophied detrusor muscle
severe obstruction can lead to oligohydramnios and pulmonary hypoplasia
What is the most common cause of ascites in the newborn period?
intrauterine rupture of the renal pelvis
Polycystic kidney disease -
from polycystin defects
most common inherited kidney disease
1. Autosomal recessive: marked bilateral renal enlargement, hepatic fibrosis with portal HTN, bile duct ectasia/biliary dysgenesis
2. Autosomal dominant PKD: middle adulthood usually, can have hepatic cysts, cerebral aneurysms can develop
most common abdo mass in newborn?
renal
most common UPJ obstruction
differential of renal cysts
- polycystic kidneys
- von Hippel-Lindau
- Tuberous sclerosis
- Bardet-Biedl syndrome
Causes of bladder stones?
recurrent UTI
neurogenic bladder
bladder surgery
bladder augmentation
Causes of renal stones
obstructive abnormalities
Metabolic
Causes of Urinary tract stones
most stones are here
symptoms when they get stuck at the ureteropelvic function or the ureterovesical junction
Metabolic causes:
1. idiopathic familial hypercalciuria, hyperoxaluria, uric acid disorders, distal RTA, cystinuria, hypercalcemic hypercalciuria, primary hyperparathyroidism
Diagnosis of renal stones
US can miss UT stones, CT is good but can sometimes be obscured
urine studies for minerals/electrolytes helps figure out which type of stone it is
Treatment of stones
1 .hydration - 2x maintenance rates
- analgesia
- for infection related: treat the infection, remove the stone
- specific treatments:
- idiopathic familial hypercalciuria - normal calcium with low Na and low oxalate ; some need potassium citrate or thiazies, may need lithotripsy or surgery
dysfunctional voiding what investigations to do
urinalysis and urine culture - to r/o occult infection, renal disease, glucose (i.e. diabetes)
daytime incontinence - should do US r/o structural problems
urodynamic- only when suspect neurogenic bladder or known neuro cause
treatment of dysfunctional voiding
- bladder hyperactivity/sensory defects - timed voiding and anticholinergic meds; more complicated includes biofeedback, alpha blockers, intermittent catheterization
phimosis -
inability to retract the prepuce
at birth - physiologic
in 90% of boys who are not circumcized, fully retractable by 3 years old
if persistent - can try a steroid cream to the foreskin
if ballooning of foreskin during voiding or phimosis beyond 10 years old and steroids don’t work, circumize
What is paraphimosis
foreskin is retracted and get get it back - edna leads to pain, and it gets stuck ; lubricate and try to put back, may need emergency surgery
1.5 year old with undescended testicle, likely to descend?
nope - not likely to descent after 1 year of age
other possibilities for what you think is undescended testicle is retractile testes, absent tests, ectopic tests
cryptorchidism - what to ask in history
was it every in scrotum
maternal drug use - steroids
family history
true undescended testis - usually along the embryologic path of descent - with patent processes vaginalis
what can be associated with undescended testis
- inguinal hernia
- risk of torsion
- risk of infertility
- increased malignancy risk (i.e. germ cell malignancy) - more if untreated or corrected during of after puberty
more likely to have cryptorchidim in newborns than older children, more in pregms, bilateral in 10% of kids
most common cause of scrotal pain and swelling in older adolescents
epididymitis - diagnosis is aided by history of sex or HUTI, but should consider testicular torsion when severe pain
(meanwhile in boys <6 years, testicular torsion is the major cause of acute scrotum) - here testicle will be swollen and cremasteric reflex absent
cryptorchidm - when should testicles descend by
if they haven’t descended by 4 months, it will stay undescended
most common tumour in undescended testis in teen or adult
seminoma - orchiopexy reduces this risk
when should undescended testis be treated by
should be treated surgically by 9-15 months of age at the latest - surgical correction at 6 months is appropriate , since spontaneous descent will not happen after 4 months of age
if the testicle stays down, start to see histological changes (atrophy/dysplasia)
early surgical correction -better chance of fertility
infrequenty - hormones (HCG) can be used to help the testicle descend
Hydrocele
transillumination shows fluid
should palpate testicle - can develop with association with timor
most congenital hydroceles resolve by 12 months of age , and are non communicating, those that persist beyond 12-18 moths after communicating and should be repaired
GN with low complement
post strep
lupus
membranoproliferative
when would you repair a communicating hydrocele
communicating - fluid and you can push it around - most resolve by 2, so if not resolved by 2 then can do it (mainly so you can palpate the balls)
non communicating - two separate bags - if by one year they haven’t resolved
what do you worry about with varicocele in right side or <10 year old
worry about renal or retroperitoneal masses
what are exam findings in varicocele
bag of worms
valsalva will make it worse
usually on the left side
false positive gross hematuria on dipstick
- beets
- rifampin
- dyes
- menstruating
- alkaline urine (urine pH .9 can give you false positive)
- myoglobin in urine
false negative gross hematuria on dipstick
- formalin (used as a urine preservative)
2. increased urinary vitamin C
most common cause of gross hematuria in children
UTI
8 year old - gradual onset one ball pain with blue dot
appendeal tosion
resolve 7-10 days
surgery only if not resolve or not sure what is joing on
epidydimitis organism in teen
epidydimitis
in prepubescent
e. coli/urinary tract obstruction
