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