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A
relatively common problem, has a 5-15% lifetime riskworldwide, M: F, 3:1, most between ages 20-50, has a 50% recurrence rate within 5
years. The first episode in men tends to occur at an average age of 30 yo, where as women have a bimodal age of onset, with
episodes peaking at 35 and 55 years. Peak incidence is the early AM due to hyperconcentration and low urine output.55% have a FHx of stones. Kidney stones are solid deposits that form in the kidneys from substances excreted
in urine. Children under 16 years of age constitute ~ 7% of all cases of renal stones with a 1:1 sex distribution. ~80% of
pt’s with urolithiasis form calcium stones, most of which are composed primarily of calcium oxalate, and less often,
calcium phosphate.
PP:The precise cause of urinary stone formation is unknown. It requires three elements: supersaturation, lack
of inhibitors, and stasis. The process of stone formation depends on urinary volume; concentrations of calcium, phosphate,
oxalate, sodium, and uric acid ions; concentrations of natural calculus inhibitors (e.g., citrate, magnesium, Tamm-Horsfall
mucoproteins, bikunin); and urinary pH.4 High ion levels, low urinary volume, low pH, and low citrate levels favor
calculus formation. When waste materials in urine do not dissolve completely, microscopic particles begin to form and over
time grow into kidney stones.Supersaturation of urine --> crystallizes,
and then aggregates.May have dec amount of urinary stone inhibitors (primarily
citrate).Nanobacteria (small intracellular bacteria that from a Ca-phosphate
shell) were present in the central nidus of 97% of kidney stones in ones study, but this was never replicated by others, thus
likely was a contaminent (Kidney Int 1999;56:1893). A polymorphism of the vitamin D receptor gene (Fok-1) appears to be associated
with some aspects of calcium urolithiasis (OR = 2.15) (BJU Int 2007;99:1534-1538)(higher first-void morning urinary calcium
levels)...They were also significantly younger than the median age of 45 years at the onset of the first episode (OR = 3.23).
Risks:
Bowel disease (chronic diarrheal states) promotes low urine volume, acidic urine (depletes available citrate) and hyperoxaluria.
Excess dietary meat (including poultry) creates acidic urinary milieu, depletes available citrate; promotes hyperuricosuria.
Excess dietary oxalate promotes hyperoxaluria. Excess dietary sodium promotes hypercalciuria.Low urine volume allows stone constituents to supersaturate. Obesity may promote hypercalciuria; other results similar
to excess dietary meat. Primary hyperparathyroidism creates persistent hypercalciuria. Prolonged immobilization leads to bone
turnover, whick creates hypercalciuria. Renal tubular acidosis (type 1) give an alkaline urine promotes calcium phosphate
supersaturation; loss of citrate. FHx of stones (3-fold risk, J Am Soc Nephrol
1997;8:1568), prolonged immobilization, recurrent urinary infections, drugs (Indinavir, acetazolamide, triamterene,
ephedrine, felbamate, topiramate and zonisamide, guaifenesin, calcium + Vit-D, or sulfadiazine). Systemic illnesses
that may increase the risk for kidney stone formation or otherwise affect the clinical course include primary hyperparathyroidism,
renal tubular acidosis, cystinuria, gout, diabetes mellitus, inflammatory bowel disease, renal insufficiency, sarcoidosis,
and medullary sponge kidney. Insulin resistance leads to ammonia mishandling; alters pH of urine. Gout promotes hyperuricosuria.
Chronically sleeping on the side at risk of calculi formation
can be seen in pt’s with unilateral stone dz (J Urol 2001;165:1085), consider attaching a tennis ball to sleep ware
to break this habit.HTN in 32.8%
(Semin Nephrol 1995;5:519–525). Men who work in the steel industry and are exposed to high temperatures have an increased
risk of developing urinary lithiasis (Urology 2005:65:858-861) (related to dehydration and hypocitraturia).
Urine pH: Calcium oxalate
stones are not pH-dependent.Most people excrete an acid urine which favors uric
acid precipitation which may promote the formation of calcium stones. Calcium phosphate stones form in a relatively alkaline
urine.
ICD-9 Codes:
592.0
Calculus of kidney - Nephrolithiasis NOS
592.1
Calculus of ureter
592.9
Urinary calculus, unspecified
594.1
Other calculus in bladder - bladder stone
594.9
Calculus of lower urinary tract, unspecified
788.0
Renal colic
S/s:Renal colic: a misnomer, aching flank pain that is usually constant, sometimes waxes and wanes.No position of comfort (unlike Appy, diverticulosis, salpingitis/
peritoneal inflammation (makes pt want to lay still).Pain starts as a
colicky flank pain radiating to the groin / testicle or labia and can be accompanied by N/V and hematuria.Character of the pain changes as is passes down the ureter and may diminish even if stuck as transition
from a hyperperistaltic to an aperistaltic ureter.At renal calyces is a deep,
dull flank/back ache.At the renal pelvis it is a sharp pain radiating to the
ipsilateral abd quadrant.At the upper-mid ureter it is sharp, bandlike radiating
to the mid-low abd.At the distal ureter it is boring that radiates to the ipsilateral
groin.Urgency and frequency can occur if stone is close to bladder.In the bladder it may produce a suprapubic pain with stranguria, urgency, frequency and/or dysuria.Pain resolves with passage of stone, may persist temporarily from ureteral edema.
Lab:U/A, BUN or Cr.+CBC, lytes, Ca, P.Gross of microscopic hematuria in 90%.
X-ray:KUB:Best study if PMHx of stones. 90% contain
calcium and are radiopaque (yet only 30% seen in ER, up to 70% with IVP), if >2-3 mm
should see on KUB. (r/o calcified mesenteric lymph node, phlebolith, fecalith, renal calcification, barium), misses 10% as
uric acid, struvite calculi and cysteine are radiolucent or poorly
visualized on plain film radiography.
Spiral (helical) CT: without
contrast (unenhanced) now considered best overall study to establish dx (96% sensitive), takes < 5 minutes,
no risk of contrast reaction, detects all stone types, rules out other pathologic processes (r/o AAA if age
>55yo).Takes 0.5mm cuts from top of bladder to top of kidneys (nl abd CT
take 1cm cuts).Noncontrast helical CT consistently has outperformed IVP
in studies of pt’s with suspected ureteral stones. Because helical CT has other advantages in this setting (no use of
contrast material, visualization of other intra-abd causes of sx’s), it is becoming the imaging procedure of choice
for these pt’s (Ann Emerg Med 2002;40:280-6).An unenhanced low-dose abd
CT (LDCT) protocol should replace the initial abd plain film in pt's with a clinical suspicion of renal colic (Urology. 2006;67:64-68)
(sensitivity of 95-100% with a 2.1-mSv radiation dose to women and 1.6 mSv to men) (the mean effective dose [all testing done]
was 3.5 mSv in group 1 and 6.9 mSv in group 2).
IVP: Delayed images required if high-grade obstruction (delayed “blush” if obstructed).
Ultrasound: has a lower
sens/spec, but it is the preferred imaging modality in pregnant women.
Three places stones get caught:
ureteropelvic junction (UPJ), midureteral (at iliac vessels), ureterovesical junction.
Stone
Types seen in the USA:
Mixed Ca-oxalate
and Ca-phosphate@37%.
Calcium oxalate@26%.
Calcium phosphate@7%.
Uric acid@5%.
Struvite@22%.
Cystine@2%.
(Kelly's
Textbook of Medicine. New York, Lippincott Williams &
Wilkins, 2006, pp 1243-1248).
Tx:Link: Consult Indications & Surgical
Options |No urgent intervention needed
unless the upper urinary tract is obstructed and infected, the renal function is compromised, or there is intractable pain
or vomiting.Most pt's can be managed expectantly with analgesics...NSAIDs like
Motrin 600-800mg TID, adequeat hydration, strain urine, local heat with an electric blanket at lateral abd & lower back.Takes an average of 8 days to pass, if not passed by then or fever or increased pain
etc, need to monitor serum Cr. For acute pain IV Toradol better than morphine.Pt's
treated with NSAIDs for renal colic report better pain relief and are less likely to need further analgesia than those treated
with opioids (and less N/V) (BMJ 2004;328:1401-4), based on a pooled analysis of 10 trials. Hydration (no benefit to stone
passage), strain urine, NSAIDs, Abx if evidence of infection.Local heat with
an electric blanket at lateral abd & lower back (42 C)
decreases the pain, anxiety and nausea of renal colic (J Urol 2003;170:741-44). A combination of IV morphine 5mg + Ketorolac
15 mg (both repeated in 20min) was superior to either drug alone for tx of acute renal colic (Ann Emerg Med 2006;48:173-81).
Stone size:The likelihood of spontaneous stone passage is directly related to the size of the stone and the time needed
for passage.
If stone <5 mm:98% of proximal and distal stones pass spontaneously (J Urol 1997;158:1915–1921)
(within 4 weeks, may take up to 40 days).
If 5-10mm: ~53% pass spontaneously.
Observation and periodic intervention for pt’s with newly diagnosed stones <10 mm in diameter and controlled sx’s, with drugs offered when necessary to facilitate
stone passage, is an appropriate tx option (AUA 2007 Annual Meeting: AUA/EAU Guidelines Update: Ureteral Stone Management.
Presented May 21, 2007).
>10mm:
~20% pass and thus pt will likely need an intervention.
Time: Takes an average of
8 days to pass if <2mm, 12 days if 2-4mm and 22 days if >4mm (Time to stone passage. J Urol 1999;162:688-91).If no stone movement has occurred after a 4-6 weeks, intervention is warranted
because the incidence of complications (renal deterioration, sepsis, ureteral stricture) is increased.
Medical
Expulsive Therapy (MET): Indicated in most pt’s with ureteral stones measuring <1 cm who are candidates for observation, especially those with stones in
the distal ureter.Medical tx costs just a fraction of the average cost of ureteroscopy
($2,645) or shock wave lithotripsy ($4,225). The estimated cost for medical tx ranges from $10 to $74 for a 28-day course
of Cardura (doxazosin) to $104 to $141 for a 42-day course of Flomax.The likelihood
of spontaneous urinary stone passage can be increased significantly by tx with calcium channel blockers or alpha-blockers,
according to meta-analysis of 9 RCT’s with nearly 700 pt’s with urinary calculi (Lancet 2006; 368:1171-79) (chance
of expulsion is 65% greater) (Risk Ratio:CCB or alpha blockers @ 1.65.Alpha blockers @ 1.54.CCB @ 1.51.CCB + steroids @ 1.90).There are large
numbers of alpha-1 adrenoceptors in the distal ureter, these blockers inhibit basal ureteral tone and peristaltic frequency
and decrease the intensity of ureteral contractions.
Tamsulosin (Flomax):0.4 mg qd x 5-7 days.Instead of
immediately performing cystoscopy or lithotripsy, new research suggests that pt’s with distal ureteral stones should
be given a trial of MET (J Urol 2005;174:167-172)....210 pt's were randomized to receive home tx with tamsulosin, phloroglucinol,
or nifedipine + oral corticosteroid + Abx prophylaxis. Injectable diclofenac was given on an as-needed basis.
All were encouraged to drink 2 L of water daily.The expulsion rate for tamsulosin was 97.1%, whereas phloroglucinol and nifedipine
had rates of 64.3% and 77.1%, respectively.Pt's treated with tamsulosin achieved
stone passage in a shorter period of time and were less likely to be hospitalized and has less renal colic than pt's treated
with the other agents.In another study, stone expulsion was noted in 80%, 85%,
and 43%, in the nifedipine, tamsulosin, and control groups, respectively.With
lower ureteral stones < 1cm in diameter, tx with nifedipine or tamsulosin increases the rate of ureteral stone expulsion
and decreases the need for analgesic therapy (J Urol 2004;172:568-571). Stone expulsion in 80% on nifedipine (ave 9.3 days)
and 85% with tamsulosin (ave 7.9 days) Vs 43% of controls (ave 12 days) after 4 weeks. The authors conclude that for lower
ureteral stones nearest to the bladder the most effective tx is tamsulosin with cortisone, Nifedipine plus cortisone is useful
for stones which are lower-ureteral but further away from the bladder (Nifedipine versus tamsulosin for the management of
lower ureteral stones. J Urol 2004;172:568-71). Adjunctive tx with tamsulosin after ureteroscopic laser lithotripsy for large
renal and ureteric calculi improves the stone-free rate as well as pt’s' quality of life (AUA annual meeting. Abstract
1707. May 26, 2006)(4.3% experienced ureteric colic episodes
VS 23.4% of controls and 94.6% were stone-free Vs 83.1%).
Calcium channel blockers (Nifedipine
SR 30mg qd = Procardia XL or Adalat CC):x 7-28 days, and oral steroids
can facilitate stone passage, both may inc the success rate & also dec the pain after ESWL (Urology 2002;59:835-38).Nifedipine 40mg qd + oral methylprednisolone 16 mg qd x 45 days lead to stone
passage in 87% of pt’s Vs 65% who received methylprednisolone alone. Stone passage occurred at 11.2 +7.5 days
in the pt’s treated with combo tx Vs 16.4 +11.0 days in pt’s treated with methylprednisolone alone (J Urol
1994;152:1095-98).A RCT with an oral corticosteroid and nifedipine compared with corticosteroid alone found an improved stone expulsion
rate (79% Vs 35%), faster expulsion time (7 Vs 20 days) as well as a decreased requirement for analgesia (Urology 2000; 56:579–583).
F/u: If fail to pass stone
in 5-7 days, fever, unrelenting pain, vomiting.Check radiograph of kidney
and upper bladder (KUB), UA and serum Cr.
Urine strainer:can use a coffee filter or place a small square cut from a pair of nylon panty hose (rinse &
re-use) over the urethra while voiding to catch the stone for analysis.Send
passed or removed stone for analysis.(Acute renal colic from ureteral calculus.
NEJM 2004;350:684-93)
Consult Urology:if stone >5-7 mm diameter, severe persistent pain, not passed spontaneously in 1-2 wks
(depending on size), an upcoming away trip from home, persistent hydronephrosis, infection/sepsis, staghorn calculus, solitary
or transplant kidney, occupation (pilot or bus driver), anuria or renal failure.Urgent intervention is indicated in a pt with an obstructed, infected upper urinary tract, impending renal deterioration,
intractable pain or vomiting, anuria, or high-grade obstruction of a solitary or transplanted kidney. Women who develop nephrolithiasis during pregnancy have nearly double the risk of preterm delivery as pregnant
women who do not (Obstet Gynecol 2007;109:1099-1104).
Tx Options for Urologist:
For treating urolithiasis, shock wave lithotripsy,
ureteroscopy, and percutaneous nephrolithotomy have replaced open surgery (BMJ. 2007;334:468-472).....Shock wave lithotripsy
is effective in approximately 80% to 85% of simple renal calculi. For complex renal calculi, percutaneous nephrolithotomy
is the tx of choice. Staghorn calculi should be treated, preferably with percutaneous nephrolithotomy in most pt’s.
For pt’s who are pregnant, morbidly obese, or have coagulopathy, ureteroscopy is the preferred tx.
1.Emergent Decompression:With either a nephrostomy tube (percutaneous
nephrolitholapaxy = PCNL) or ureteral stent. Septic pt’s with obstruction should have nephrostomy tube
placed (can be done with local anesthesia), drainage can be monitored as opposed to internal stent that might not be draining
properly.
2. Extracorporeal Shock Wave Lithotripsy
(ESWL): Usually under mild IV sedation although some machines require general or regional anesthesia Shock waves
break up the stone into small fragments that pass out on own.Best choice
for renal, proximal and mid ureteral stones <1-2 cm.85% overall success rate.Occasionally
a fragment can obstruct the ureter and require intervention.Repeat tx required
10-20%.Lower-pole stones have been consistently associated with decreased stone-free
rates following SWL when compared with upper and middle-pole stones.Cystine,
brushite and calcium oxalate monohydrate stones have demonstrated a high degree of resistance to fragmentation by SWL owing
to their high density, whereas less dense stones (calcium oxalate dihydrate, hydroxyapatite and uric acid) are more susceptible
to SWL (Prediction of shockwave failure in pt’s with urinary tract stones. Curr Opin Urol 2006;16:88-92).Can gait the shocks to the pt’s ECG (heart rate) such that arrhythmia potential is lowered…R-wave triggered mode,
where ESWL can trigger the atrial output pulse and the subsequent inhibition of the following ventricular pulse if pt has
a dual pacemakers to the VVI or VOO mode prior to ESWL to prevent this occurrence. The rate of clearance of renal stones after
ESWL is lower in elderly pt’s than in younger pt’s (BJU Int 2007;100:392-395)(stone-free rate after ESWL: in the
>60 year age group at 37.6% Vs in the 40-and-under at 54% and 41-60 at 43%)....suggest that "more endoscopic procedures
should be offered to the elderly population."
Pneumatic lithotripter:
Can generate contact pressures of up to 2.9 MPa at the tip of the probe. The device is powered by a carbon dioxide cartridge
that can deliver at least 80 shocks via a spring-loaded hammer that drives a projectile into contact with the probe. The "StoneBreaker"
is a rapid and effective means of fragmenting urinary stones (BJU Internat 2007;100:629-631)...Hand-held portable, appears
to offer much faster intracorporeal lithotripsy compared with other ballistic lithotripters.
3. Ureteroscopy / ureterorenoscopy (URS) Stone Removal:Stone fragments are removed using suction,
graspers, or basket extraction. Endoscopic
(laser) lithotripsy can be successful in up to 95% for distal stones.Tx of choice
for distal stones or proximal stones > 1-2cm. Indicated for ESWL failures.Ureteroscopy traditionally requires the placement of a stent in order to minimize
the risk of flank pain secondary to ureteric edema and facilitate the passage of residual fragments. The presence of a ureteric
stent, however, has been shown to reduce quality of life in up to 80% of pt’s and thus many authors have shown that
it is not necessary on a routine basis (The management of ureteric colic. Curr Opin Urol 2006;16:71-76)….risk factors
for complication included renal pelvic stone location, bilateral procedure, lithotripsy, history of urolithiasis, diabetes
mellitus, recurrent/recent infection, operative time of 45 min or more plus lithotripsy and operative time of 45 min or more
plus ureteral dilatation.
4. Percutaneous Lithotripsy:Best for large/staghorn renal calculi, can be followed by ESWL for residual fragments.
Conventional PCNL is recommended in this situation only when there is a significant stone burden or when external shock-wave
lithotripsy fails.Minimally invasive percutaneous nephrolithotomy (mPCNL) is
an effective and safe strategy for dealing with upper urinary tract calculi in transplanted kidneys (BJU International 2007;99:1467-1471)....should
be the initial approach for most cases of upper urinary tract stones in transplanted kidneys, except for simple and small
stones in the middle or lower calyx
Complications
of Urolithiasis:renal failure, ureteral stricture, infection/ sepsis, urine extravasation, perinephric abscess, xanthogranulomatous
pyelonephritis. Stone bulk, dilated pelvicalyceal systems, and previous UTI have
strong associations with UTI after kidney stone surgery, while infected stones, pelvic urine, and cloudy urine are predictors
of urosepsis after percutaneous nephrolithotomy (EAU 22nd Annual Congress: Abstract 876. Presented March 23, 2007).
Retained
Stones:likely no problems if in the renal pelvis.Consider annual KUB to monitor
for size changes.Non-obstructing ureteral stones need annual monitoring of renal
US.
Normalization of body weight (BMI) and cardiovascular risk factors, sufficient physical
activity, balanced nutrition and sufficient circadian fluid intake would be the appropriate measures to avoid new calculus
formation.Up to 85% of all stone pt’s could anticipate lower risk
of stone recurrence with basic changes in lifestyle and dietary habits, ~15% of pt’s require additional specific pharmacological
prevention (Curr Opin Urology. 2005;15:119–126).
Diet: A low urinary volume
increases urinary supersaturation, thus fluid therapy is safe, cheap and effective: Increased water (8-10 cups a day) will
dec recurrence by 55%.Try to maintain 2L urine output a day or try to maintain
a clear-colored urine rather than yellow urine. Lemon juice/ lemonade increases
citrate excretion, particularly in the hypocitraturic stone former (4
ounces a day in divided doses).Can add lemon juice or
diluted potassium citrate to just plain water. The type of fluid consumed may be important; grapefruit juice may enhance the
risk of stone formation (Ann Intern Med 1998;128:534), whereas pt’s who ingest one bottle of beer a day may reduce the
risk of stone formation by 40% (Am J Epidemiol 1999;150:187).Higher sucrose intake is associated with an increased risk of stone formation in younger and older women
(Arch Intern Med 2004; 164:885).
Calcium: A normal-calcium,
low animal protein and low-salt diet reduce the risk of recurrence (NEJM 2002;346:77-84).Avoid soft drinks (promotes natriuresis and hypercalcuria).Dietary calcium
and supplemental calcium are not associated with increased risk of kidney stones and may even be protective in younger (27-44
yo) women (Arch Intern Med 2004;164:885-891). Recommendation for calcium intake cannot be generalized since the effect of
calcium intake on stone formation depends on the type of stone, oxalate intake, presence of stones and the efficiency of calcium
absorption from the bowel.Calcium restriction recommended in pt’s who
have moderately to severely elevated intestinal calcium absorption and urinary calcium levels.Pt’s with calcium phosphate stones may need to carefully monitor their calcium dietary intake.Except for absorptive hypercalciuria, calcium restriction
in nephrolithiasis pt’s is not recommended (Curr
Opin Urology. 2005;15:119–126).
Phytates (myoinositol hexaphosphate):
High intake better.Found in cold cereal, dark bread, wheat fiber, bran, rice, nuts and beans.Dietary phytate (the most
abundant form of phosphate in plants) binds tightly to double charged ions such as calcium (and zinc, iron, magnesium and
manganese) in the GI tract to reduce absorption and enhance urinary excretion, which may reduce stone formation (37%) (Arch
Intern Med 2004;164:885-891).Calcium
oxalate crystal formation is strongly inhibited in vitro by phytate.
Avoid excess: Protein (restrict to 1g/kg/d or ~<52g/d), salt (restrict to 2-3g/d by avoiding processed foods), oxalates
(if have Ca-oxalate stones, particularly if have hyperoxaluria on testing – not the same as oxalate
stones), prevent recurrent infections.Obesity and weight gain increase the risk
of kidney stones (JAMA. 2005;293:455-462) as a larger body size may result in increased urinary excretion of calcium, oxalate,
and uric acid.
W/u:All pt’s should have
stone analysis.Detailed metabolic evaluation should be postponed until after the acute stone event
has resolved.
Limited evaluation if first stone:— Because the rate of recurrence is variable, most recommend only a limited
evaluation after a first stone. Ck routine blood chemistries, including multiple measurements of serum calcium (at least two
and more in pt’s with high-normal values to r/o hyperparathyroidism).A
low serum phosphorus warrants further eval as well.A low plasma bicarbonate
concentration is suggestive of type 1 renal tubular acidosis or chronic diarrhea.
Furthier eval indicated if Recurrent, multiple stones, younger, FHx or pt requests
eval.Pt’s with stones composed of cystine, uric acid, calcium phosphate or struvite.A 2-day food diary may be helpful.
24-hour urine
collections: urine volume, pH, and excretion of calcium, uric acid, citrate, oxalate, sodium, creatinine, urinary
supersaturation. 2 or 3 separate collections may required to obtain all of this information.
Normal values:
Calcium: For a pt with a history of renal stone formation, urinary calcium results will be more
meaningful if the pt’s usual diet is followed for 3 days before specimen collection. Do not stop medications.If the urine calcium test is done because of a metabolic disorder, the pt should eat a low-calcium diet
and calcium medications should be restricted for 1 to 3 days before specimen collection.
Normal diet:Men<300 (7.5 mmol/day).Women <250 (6.25 mmol/day).Child <4mg/kg.
Low-calcium
diet: 50–150 mg/24 h or 1.25–3.75 mmol/d.The bulk of calcium
excreted is eliminated in the stool. Increased calcium in urine results from an increase in intestinal calcium absorption,
a lack of renal tubule reabsorption of calcium, resorption or loss of calcium from bone, or a combination of these mechanisms.
Ddx increased urine Ca: Hyperparathyroidism
(30% to 50% of cases).Sarcoidosis.Primary
cancers of breast and bladder.Osteolytic bone metastases.Multiple myeloma.Paget’s disease.Renal tubular acidosis.Fanconi’s syndrome.Vit-D intoxication. Idiopathic hypercalcuria.Diabetes mellitus.Crohn’s disease and some cases of ulcerative colitis.Thyrotoxicosis.Increased urinary calcium almost always accompanies
increased blood calcium levels.Ca excretion levels > calcium intake levels
are always excessive; urine excretion values >450 mg/24 hours are reliably abnormal.Increased Ca excretion occurs whenever Ca is mobilized from the bone, as in metastatic cancer or prolonged skeletal
immobilization.When Ca is excreted in increasing amounts, the situation creates
the potential for nephrolithiasis or nephrocalcinosis, especially with high protein intake.
Falsely elevated Ca levels: drugs (calcitonin, vitamins A, K, and C, corticosteroids), meals high in Ca (milk), increased exposure to
sunlight, immobilization (especially in children).
Ddx decreased
urine Ca:Hypoparathyroidism.Familial hypocalciuria hypercalcemia. Vit-D def. Preeclampsia. Acute nephrosis, nephritis, renal failure. Renal osteodystrophy.
Vit D–resistant rickets.Metastatic carcinoma of prostate. Malabsorption
syndrome—celiac-sprue disease, steatorrhea. Urine calcium decreases in late normal pregnancy.
Falsely decreased
Ca levels: increased ingestion of phosphate, bicarbonate, antacids. Alkaline urine. Thiazide diuretics. Oral contraceptives,
estrogens. Lithium.
Oxalate: Men <45 (0.5 mmol/day).Women <45
(0.5 mmol/day).
Citrate:
normal is 320-1300mg for men and women.
Phosphorus
(360-1600mg).
Na
(52-380mEq).
Mg
(28-180mg/d).
Urinary Creatinine
excretion:permits assessment of the completeness of the 24-hour collection.
Low level suggest an incomplete collection (need repeat) except for older subjects or malnourished pt’s with decreased
muscle mass.
Normal in <50 yo: 20-25 mg/kg (177-221
µmol/kg) lean body weight in men and 15-20 mg/kg (133-177 µmol/kg) in women.
Normal in >50yo: 10-12 mg/kg/d for men. 8-10mg/kg/d in women.
If normal, calculate the ratio of “measured-to-estimated creatinine clearance”.If <0.75 then repeat as inaccurate.
If 0.75-0.9 the inaccurate, but still may be useful. If 0.9-1.1 then accurate urine collection.
If 1.1-1.25 then inaccurate, but still may be useful. If >1.25 then inaccurate, needs
repeat.
Sodium excretion:
increased sodium intake can contribute to hypercalciuria.
24hr Urine (commercial kits are available) initially while pt on a random diet.Evaluate for volume (>2L), pH (Ca-phos stones form if pH>7, may be due to distal RTA if low urinary citrate, vegetarian diet if high citrate.If pH >7.5 suspect infection.If pH <5.5 suspect uric
acid, cysteine, chronic diarrhea or strenuous physical exercise). Can repeat 24hr Ur
after modified diets (Ca restriction to see if hypercalcuria is dependent on dietary intake), acid load test or on meds.
Check serum for:Ca, P, uric
acid, creatinine, alkaline phosphatase, intact PTH.A recent study found no significant
association between stone recurrence and initial phosphate levels in serum or urine, thus may not be necessary to check (Scan
J Urol 2002;36:368-72).In pt's with first-time kidney stones, conservative
therapy (dietary modification only) is the most cost-effective strategy, but for pt's with recurrent kidney stones, empiric
therapy (dietary modification and potassium citrate) and a modified simple metabolic evaluation (a single 24-hour urine collection
for renal stone risk factors, with potassium citrate and HCTZ for pt's with hypercalciuria and potassium citrate alone for
pt’s with normocalciuria) are equally cost-effective (J Urol 2004;172(6
pt 1):2275-81).
UroRisk &
StoneRisk diagnostic profiles: measures 10 urine risk factors for stone formation (Calcium oxalate - Brushite - Sodium
urate - Uric acid). It offers a urine collection and preservation system and is recommended for initial and recurrent stone
formers who test positive for a UTI.Calculates the "relative supersaturation.Give a choice of three customized profiles.(800) 330-6565, ext. 7308
Urine pH: Uric acid and
cystine stones associated with acid urine.Renal tubular acidosis (type
I), and infection related stones associated with alkaline urine.Tx of uric acid
and cystine stones includes alkalinization of urine, limit proteins
(50%)
(>300mg/d in M, >250 in F), causes 45% of Ca
stones. Idiopathic hypercalciuria (IH) is the most common cause of calcium-containing kidney stones. IH is
defined as excessive urinary calcium excretion (hypercalciuria) in the setting of normocalcemia and in the absence of secondary
causes of hypercalciuria. Determining the specific etiology of hypercalciuria
with special diets often not that helpful since it makes little difference in tx. The
disorder is familial, was initially thought to exhibit an autosomal dominant pattern of inheritance, but may be polygenetic.
May be due to: IH consists
of a spectrum of these disorders, with considerable overlap among these potential mechanisms.
1. Absorptive hypercalciuria: Excessive
intestinal calcium absorption. Inc intestinal absorption causes inc serum Ca (high normal), which suppresses PTH, dec P.
2. Renal Hypercalciuria:
Decreased renal tubular calcium reabsorption. Defective resorption of Ca in kidney, have dec serum Ca and inc PTH, no change
with fasting state.Due to Ca leaking from distal tubules.
3. Primary Hyperparathyroidism: Enhanced
bone demineralization. Inc PTH --> inc bone resorption of Ca and inc 1,25(OH)2D to stimulate intestinal
absorption.More common in women.R/o if high-normal serum Ca.The intact hormone assay is the best
choice for proving subtle HPT. This need to be treated with Alendronate, Calcitonin of Mithramycin.
4. Unclassified Hypercalciuria:
normal PTH and serum Ca with inc urinary Ca and no change with fasting.
Other --> RTA, Addison’s, sarcoid, hyperthyroid, V-D intoxication, milk-alkali syndrome.Only 5% have associated dz (RTA or hyperparathyroidism).
Tx of Hypercalciuria: Limit
dietary protein, oxalate and Na (<2g/d).High calcium diet (low intake increases
the risk of stones).A low-sodium, low-protein diet in place of a traditional
low-calcium diet is best for hypercalciuric men who form calcium oxalate stone (NEJM 2002;346-84).
Thiazide
diuretic:Start HCTZ@25-50mg qd,
increase up to 50mg BID as dictated by 24hr urine. Adding K-citrate 20-30mEq BID will inc excretion of citrate (a stone inhibitor)
as well as prevent dec K. Can also add a K-sparing diuretic.1/3 of females with Ca stone have medullary sponge kidney.Inc risk of osteoporosis in hypercalciuria: thiazides are beneficial.Ca-citrate
is the preferred Ca supplement in postmenopausal females with stones. Can also use Bendroflumethiazide 2.5 mg BID, Trichlormethiazide
2-4mg qd, Na-cellulose phosphate 2.5-5g TID or Orthophosphate 500mg BID.A
high calcium diet, if not accompanied by higher intake of fluids, potassium, magnesium and phosphate, may increase the risk
for calcium oxalate stones, results of a metabolic investigation suggest, the risk is increased further if calcium is increased
by using supplements rather than by diet based on urinary Ca excretion (J Urol 2003;169:470-474).(J Urol 1997;158) (Am J Clin Nutr 1994;60).
(15%
of stones)(>800mg/d M, >750mg F) Uric-acid stones are more difficult to diagnose than other types of kidney calculi
because they are radiolucent and therefore don't show up on standard abdominal x-rays. Can be seen in chronic diarrheal states
that cause loss of water and bicarb., hypermetabolic states, myeloproliferative d/o’s, medications such as thiazides.Uric acid can serve as a nidus for Ca-oxalate stones (12% of pt’s).Uric acid stones may be suspected on the basis of a history of uric acid stones or of gout (present in
~20% of pt’s with uric acid stones). The typical pt has normal amounts of uric acid in an acidic urine; this condition
increases the likelihood of uric acid crystallization. Pure uric acid calculi are radiolucent on plain imaging
but visible on U/S or CT. Other radiolucent stones that should be considered in appropriate clinical settings include matrix
stones (which are made of organic material and are occasionally seen in pt’s with urease-producing bacteria) and indinavir
stones. Pure uric acid stones primarily occur in pt’s in whom a persistently acid urine (pH <5.5) promotes uric acid
precipitation.That the incidence of nephrolithiasis is increasing, both
in the US and worldwide, particularly
for those composed of uric acid (Am J Kidney Dis 2006;48:897-904)....HTN, obesity and diabetes are significantly associated
with a dx of urate nephrolithiasis (OR = 1.22). Hyperoxaluria is often seen in pt’s with kidney stones who have undergone
bariatric surgery using currently accepted methods (J Urol 2007;177:565-569). Pt’s with elements of metabolic syndrome
are more likely to develop highly acidic urine, increasing their risk of forming uric-acid kidney stones (Clin j Am Soc Nephrol
2007;2:883-888).
Tx:Uric acid stones are unique in that they can be managed medically. Increase fluid intake.Avoid Purine rich foods, restrict animal protein to 5-7oz of meat/ fish per day) + Allopurinol (Zyloprim)
@100-300mg/d to dec uric acid production(especially if hyperuricemia) .Alkalinizing the urine (inc Ur
pH) with bicarb or potassium citrate 10-30 mEq (~20 mmol) TID to inc solubility of uric acid and dissolves pure uric acid
stones (goal is pH of 6.5-7, pt can measure with Nitrazine
paper, higher than 7 may cause CaP to precipitate). At a urinary pH below 5.5, uric acid is poorly soluble; solubility increases
at a pH above 6.5.Can dissolve them at a rate of 1cm/mo, imaging can be
repeated at one month to determine whether dissolution has occurred. Unless a stone is pure uric acid, however, oral dissolution
therapy is not possible. If oral dissolution therapy fails, tx should proceed as for a radiopaque stone.
(15%)(>40mg/d
of oxalate). Hyperoxaluria which may be present in up to 40% of male and 15% of female stone formers and is typically only
slightly elevated; in comparison, marked hyperoxaluria is usually associated with inflammatory bowel disease and/or malabsorption
or primary hyperoxaluria.75% of all stones are composed of some
CaOxalate, Mixed Ca-Oxalate-P in 34%. 15%
is related to dietary consumption of oxalate or inc Vit-C.Also seen in Crohn’s,
chronic pancreatitis, celiac sprue, Ca restriction, primary hyperoxaluria or other ileal dz because of inc absorption as Ca
is bound to free fatty acids.Recurrence rate for untreated Ca-Oxalate stones
--> 10% at 1 year, 35% in 5yr, 50% recur in 10yr.If inc urine output
to >2L/d will cut in ½ the recurrence rate.If serum Ca>10.3
--> check PTH.
Tx: avoid excess oxalates
(spinach/ leafy dark greens, nuts, rhubarb, instant coffee, tea, chocolate, berries, purple grapes, Tofu, wheat germ), Ca
or Mg-oxide 200-400mg BID supplements + Pyridoxine 25-100 mg qd (as many deficient) with
meals to bind oxalates in the gut.
K-Mg-Citrate: for recurrent
Ca-Oxalate stones, less GI SE’s than K-citrate (10-30 mEq qd).Dose of
42mEq K + 21mEq Mg + 63mEq citrate qd (J Uro 1997:158).Other less efficacious:
Cholestyramine 4g TID, Mg-citrate 10 mEq BID.Probiotics with Oxalobacter formigenes
may reduce the ocalate exretion (J Urol 2001;166:1487-91).
Moderately high: beans, all types of berries, carrots,
cashews, celery, coffee, concord grapes, okra, green onions, oranges, green peppers, sweet potatoes, tomatoes. Strawberries,
cranberries, raspberries, plums, and apples. This is somewhat confusing, however, because several of these have been shown
to decrease incidence of kidney stones even though they contain significant amounts of oxalate! In addition, some studies
have shown that eating oxalate- and calcium-containing foods together may actually decrease stone risk (The influence of diet
on kidney stone disease. J Urol 1996;155:432–440). A large cohort study of more than 85,000 women showed that those
who consumed black tea had an 8% decreased risk of developing kidney stones (Arch Intern Med 1998;128:534–540).
(20%)(<450-600mg/d
M, <650-800 in F) citrate is a stone inhibitor.Hypocitraturia can be marked in pt’s
with chronic metabolic acidosis; however, mild hypocitraturia occurs in a significant proportion of stone formers in the absence
of academia.
Tx: K-citrate (Urocit-K)
[5, 10 mEq tab] start @ 5mEq BID with food, titrate to 10-20 mEq TID-QID (0.5-1mEq/kg/d). Contra: hyperkalemia or renal insufficiency is present, monitor serum K and Cr.Avoid Na-citrate unless K-citrate not tolerated. The dosage should be adjusted to maintain a urine pH 6.5-7,
it usually needs to be continued indefinitely.
Causes: Often idiopathic,
may be RTA, met acidosis, high protein/ salt diet, dec K or Mg, UTI, carbonic anhydrase inhibitors, renal insufficiency, dehydration,
thiazides, diarrhea.People
subject to recurrent calcium renal stones tend to excrete low amounts of citrate in their urine (Am J Kidney Dis 2006;48:546-554)…..Their
analysis showed that hypocitraturia is associated with urinary potassium level, and may reflect low levels of potassium in
the diet, the chief source of which is fruit.
(8%): (Mg-P-NH3). Also known as infection or triple-phosphate stones, consist
of magnesium, ammonium, and calcium phosphate. Infection of the urinary tract with organisms that secrete the ectoenzyme urease
can greatly increase the urinary ammonia concentration and pH. From urea splitting organisms (Proteus, Pseudomonas, Providencia,
U. urealyticum). Struvite stones only form in pt’s with a chronic UTI due to a urease producing organism such as
Proteus or Klebsiella. Affected pt’s often have multiple magnesium ammonium phosphate crystals in the urine sediment.
The stone may grow rapidly over a period of weeks to mo’s and, if not adequately treated, can develop into a staghorn
or branched calculus involving the entire renal collecting system. They occur more often in women than in men and are the
leading cause of staghorn calculi.
Tx:
removal of entire stone. If the pt is febrile or presents with signs of systemic infection, surgical manipulation should be
delayed until Abx tx has been administered and the pt has been afebrile for at least 48 hours. After surgical intervention,
medical therapy should focus on preventing recurrent UTIs. Retained residual fragments increase the risk of recurrent UTI
and future calculi. Acetohydroxamic acid (Lithostat, 250mg TID) is an irreversible inhibitor of urease and can prevent the
crystallization of struvite stones, however, because of side effects (including deep venous thrombosis), it generally is reserved
for use in pt’s who cannot tolerate surgical intervention. Consider Amoxicillin suppressive therapy 250mg PO qd.
(3%):
consists of two cystine molecules linked with a disulfide bond.Cystinuria is
an autosomal recessive d/o in which excessive urinary excretion of the dicarboxylic amino acids (cystine, ornithine, lysine,
and arginine) results from impaired transport.Cystine stones develop in pt’s
with cystinuria due to the insolubility of cystine in the urine. Only homozygote
pt’s form cystine calculi and often present with stones during childhood.
Dx: The normal rate of cystine
excretion is 30 mg/day (1.3 mmol/day). In contrast, pt’s with cystinuria excrete >400 mg/day and sometimes up to
3,600 mg/day. The dx of cystinuria is made by identification of the pathognomonic
hexagonal cystine crystals on urinalysis (which can be seen in the initial urinalysis in about 25% of pt’), and by measurement
of urinary cystine excretion of >250 mg/liter.
Tx: Stones can form rapidly increase fluids to 4-5L/d (round the clock).Alkalinize the uring to pH>7-7.5 with K-citrate 10-30mEq TID, Pyridoxine 50mg/d.If these measures are not effective, administration of cystine binders such as penicillamine (Cuprimine)
and tiopronin (Thiola) can help prevent cystine calculi.Bind sulfhydryl groups
to other molecules (chelation) by adding: D-Penicillamine 250mg QID, Captopril 50mg BID or Mercapto-propionylglycine 250mg
TID to interfere with disulfide bond formation.Dietary
manipulation with a low-methionine diet is difficult and rarely successful.
(7%):
often have an acidification disorder such as Distal RTA, giving an alkaline urine. Can also be due to primary hyperparathyroidism,
excessive alkalinization, and sarcoidosis. F>M. Same risks as Ca-Oxalate stones (other than hyperoxaluria and hyperuricosuria)… one
exception is that calcium phosphate stones are more typical of Type I (distal) renal tubular acidosis in which the urine pH
is persistently >5.3, even after an acid load.
Tx: K-citrate to increase
the inhibitor level to normal to correct the hypercalciuria.Care must be taken
to avoid excessive alkalinization, because high urinary pH can increase the urinary supersaturation of calcium phosphate salts.
If hypercalciuria persists, addition of a thiazide diuretic is indicated.
HypoMg-uria: <50mg/d
and no diarrhea d/o.Triamterene: found in diuretics and Indinavir.
Vesical
calculi affect men predominantly and account for 5% of urinary calculi in the Western world(Schwartz, 2000).Most occur in men older than 50 years and are often associated with bladder outlet obstruction.The majority of bladder calculi are struvite, but calcium oxalate and uric acid stones are also encountered.
Risk factors:bladder outlet obstruction; neurogenic bladder; chronic bacteriuria (urea-splitting organisms); foreign
bodies; bladder diverticula; and, rarely, upper tract stones.Children at risk
for ammonium urate bladder stones in underdeveloped nations where a low-protein, high-carbohydrate diet and chronic dehydration
predispose to endemic stones.
S/s: Bladder calculi are
often found incidentally during evaluation of pt’s with obstructive or irritative voiding sx’s. Recurrent UTIs
are common and are an identified risk factor.Bladder stones may be voided spontaneously,
with larger calculi precipitating acute urinary retention. Dysuria, gross hematuria, and suprapubic pain may occur. Interruption
of the urinary stream from impaction of the stone at the bladder neck or urethra is not uncommon.Bladder calculi are often radiolucent, may be single or multiple, and can be diagnosed as filling defects
on the cystogram phase of an IV urogram or as an incidental finding on CT scan. On U/S, a hyperechoic, mobile bladder mass
with shadowing is suspicious.
Tx: Cystoscopy
is essential to evaluate the bladder and the bladder outlet, both to determine the etiology of the stone and to plan the most
appropriate tx approach. Percutaneous suprapubic cystolithotripsy to remove bladder calculi can be safely accomplished under
local anesthesia (Urology 2006;68:38-41) (2% lignocaine (lidocaine) injected 3 to 4
cm above the symphysis pubis. Lignocaine gel was also used for urethral lubrication).
**Ref:(Campbell’s
Urology, 7th ed., 1998, WB Saunders) (Urologic Clin NA 1997;24:1, pp50-122) (NEJM 1992;327:1141-52)
(Prevention of recurrent nephrolithiasis. Am Fam Physician. 1999;60:2269-76) (Nephrolithiasis.
Semin Nephrol. 1999;19:381-8) (Urolithiasis.Uro Clin North Am
2000;27:2) (Acute Renal Colic from Ureteral Calculus. NEJM 2004;350:684-93)(An evidence-based literature
review of the management of urolithiasis. BMJ. 2007;334:468-472)
~12% to 16% of American children have developmental
or behavioral d/o’s (Developmental surveillance and screening of infants and young children. Pediatrics. 2001;108:192-196)….
but only 30% are identified before school entrance. The American Academy of Pediatrics (AAP) recommends that all infants and
young children be screened for developmental delays at every well-child visit, others recommend starting at the three year
well-child visit and annually thereafter….see Screening for Deveopmental Problems |Behavioral
changes or somatic complaints may be secondary to a variety of emotional problems; for example, abd pain may be the presenting
complaint for school avoidance, peer group issues, fear of pregnancy, or sexual abuse.
Info:
Children should not watch >2hr TV/d. The more time children spend watching
TV each day, the more likely they are to have behavioral problems (Arch Ped Adol Med 2002;156:910-4).A mother's good mental health apparently ameliorates the effects of poor paternal mental health on
children and in families with only the mother in poor mental health, the father's good profile significantly attenuated (but
did not eliminate) the children's behavioral and emotional problems (Arch Pediatr Adolesc Med 2004;158:721-9), thus, evaluate
the child in the context of the family.Sleep-disordered breathing (SDB), ranging
from snoring to obstructive sleep apnea, is associated with a higher prevalence of behavioral problems in children (Pediatrics
2004;114:1640-1648). Behavior problems in early life seem to precede the development of asthma sx's (Am J Respir Crit Care
Med 2005;171:323-327).
Divorce: Due to a 50% first marriage
and 60% 2nd marriage divorce rate in the US, <60% of children live with both parents, 25% live with their mothers
as a single parent.This may limit the child’s capacity for intimacy
and have significant affects on children’s moods and behaviors. Children should understand that they did not cause the
divorce and that they cannot bring their parent’s back together.
Open-ended questions: "How are you and
your partner managing xxxx's behavior?What do you do when you disagree?"
Common ICD-9 Codes:Axis I:
315 Specific delays in development
315.00Reading
d/o, unspecified
315.02Developmental
dyslexia
315.1 Specific arithmetical d/o - Dyscalculia
315.2 Other specific learning difficulties
315.31 Developmental language d/o
315.4 Coordination d/o - Clumsiness syndrome
315.5 Mixed development d/o
315.9 Unspecified delay in development = Learning
d/o NOS
312.0 Undersocialized conduct d/o, aggressive type
312.1 Undersocialized conduct d/o, unaggressive type
(stealing, tantrums, truancy)
312.9 Unspecified disturbance of conduct - Delinquency
(juvenile) = Disruptive Behavior d/o NOS
313.81Oppositional
d/o
313.82Identity
d/o
313.83Academic
underachievement d/o
313.3 Relationship problems - Sibling jealousy
313.8 Other or mixed emotional disturbances of childhood
or adolescence
313.2 Sensitivity, shyness, and social withdrawal
d/o
299.80 Pervasive Developmental Disorder, NOS
296.90 Mood d/o, NOS
307.6 Enuretic, nocturnal and diurnal.
313.81 Oppositional defiant d/o
314.01 ADHD, combined type.
Sources
for Parents:
http://www.parentsoup.com/
http://www.genesishealth.com/
www.healthyideas.com/children
Pediatric
sx checklist: Five questions forming the mnemonic PSYCH can be addressed to parents as a means of uncovering areas
of concern. The questions can be rephrased slightly and then directed to children as well.
1. Parent-child interaction: How are things going
with you and your child?
2. School: How are things going in school? (Academically
and behaviorally.)
3. Youth: How are things going with peer relationships?
4. Casa: How are things going at home? (Including
siblings, the marriage, and parents as individuals.)
5. Happiness: How would you describe your child's
mood? (Comfortable and happy versus tense and unhappy.) (Pediatr Clin N Am 1998;45:1037)
Evaluation:
It is useful to see both parents and the child first together, then the parents alone, and then the child alone. An attitude
of nonjudgmental inquiry can be communicated with supportive statements such as, “Let's see if we can figure out what
might be happening here and find some ways to make things better.”
When did it start?
Were there unusual stresses at that time?
How are the child's life and the family's functioning
affected?
What does the child say about the problem?
What attempts have been made to alleviate the problem?
Do the parents have any opinions about the cause
of the problem?
Intellectually
Gifted Child:
There is no typical gifted child. Each is unique
and displays special abilities in highly personal ways. Recognition of giftedness is contextual in nature and demands astute
observation from medical and education professionals to analyze the extent and exact nature of the ability.The estimate of intellectually gifted children ranges from 2% to 3% of the population. Discriminating between
giftedness and Asperger's syndrome is important.Misbehavior can stem from boredom
in a routine classroom that offers only tasks the student has already mastered. Without knowledge of these factors, such behavior
may lead to an improper dx of ADHD.
Presenting
characteristics: Child has acute awareness of physical surroundings.Child
has acute awareness of emotional surroundings. Child uses advanced vocabulary, sentence structure, or loves to play with words.Child asks questions about abstract ideas like love, feelings, relationships, or justice.
He or she insists that people be “fair” and complains when things are “unfair.”Child gives complex answers to questions( I am not choking. It's just that the birthday cake was stuck
for a moment on my epiglottis). Child explains ideas in complex and unusual ways. Child is very interested in clocks, calendars,
maps, or structures.Child has a long attention span for activities of interest.
Child moves around a lot, is very active, sometimes seems hyperactive, craves stimulation and activity, and rarely is content
to sit idly. Child reacts intensely to noise, light, smells, or touch but is able to function in a social setting.Child is extremely curious, asking why, how, and what if.Child
becomes so involved that he or she is not aware of anything else (“lost in own world”).Child has vivid imagination and may have trouble separating the real from the unreal.Child has an advanced sense of humor.
Child prefers playing with older children or being
with adults. Child becomes extremely frustrated when the body cannot do what the mind wants it to.
Dx:no uniform diagnostic categories of giftedness have been established.IQ tests remain the best way to pinpoint some degrees of advanced ability.
40 - 54 Severely challenged (Less than 1% of test
takers)
55 - 69Challenged
(2.3% of test takers)
70 - 84 Below average
85 - 114 Average (68% of test takers)
115 - 129 Above average
130 - 144 Gifted (2.3% of test takers)
145 - 159 Genius (Less than 1% of test takers)
160 - 175 Extraordinary genius
Pearls:
Unless parents ensure a proper educational match, a gifted child may develop poor self-esteem, patterns of underachievement,
or poor study skills, subsequently appearing less gifted. All children learn best when they are challenged moderately. If
schoolwork is too easy, they get bored, tune out, underachieve, and do not develop intellectual muscle. If the work is too
hard, they also tune out. Grade skipping may be a good choice if a child is socially mature and comfortable with older friends.
This decision is best made by a child study team of teachers, school psychologist, and parents. Other learning options include
cluster grouping in the classroom or placement in a multiage class, such as a Montessori group where students work at their
own paces and in fluid cohorts. Advanced curricula in a special, full-day, intensive, self-contained classroom also can be
advantageous. Mentors who share a child's interest, such as an architect or biologist, often can successfully motivate gifted
students. Grade skipping may not be a solution because the child may overtake older classmates quickly. Therefore, an analysis
of the curriculum over several years is important when parents request skipping. Grade skipping for an intellectually gifted
but socially or physically immature child may lead to a totally new variety of problems.
What
can the family provide to nurture the young child's intelligence:Parents
should seek out as many different exploratory experiences as possible. These can include visits to museums and parks, walks
in city neighborhoods, access to open space for running around or moving to music, listening to classical music, and reading
stories, nursery rhymes, and poetry. Manipulative toys that allow the imagination to flourish (eg, wooden blocks, tinker toys,
Lego or Capsela) are helpful. Children should have easy access to crayons, colored pencils, newsprint, old clothes for dress
up, puppets, and simple tools (eg, hammers, screwdrivers, nuts, and bolts). To ignore the significance of this drive to learn
could lead to a child being punished for restlessness, poor attention to the teacher, sloppy work, or diverting creative urges
into destructive mischief. Also important is an area for quiet and calm reflection. Such a place should have clean pillows
for snuggling, picture books, and some prints or photos, to avoid overstimulation. Parents should ask the school to conduct
an in-depth assessment of their child's strengths in specific areas. Proper dx of actual skills can help a family decide how
best to accommodate the gift. Out-of-level testing may be necessary for a school to learn the true “ceiling” of
a child's learning. Treating the needs of gifted children is not federally mandated, schools are not required to make any
curricular adjustments.Some schools have enrichment consultant specialists who
are helpful in guiding the decision of the child study team.
Further
Info:Hoagies Gifted Education Page @ http://www.ocsc.com/hoagies/gift.htm.www.jhu.edu/gifted. www.nagc.org. www.gifted.uconn.edu.
See Below for Coordinatino d/o | Speech Delay
| Learning Disability | See screening at Well Child Visits | Developmental Screening | Mental Retardation |
Developmental
Disability:when functional aspects of the child's development in one or
more domains (eg, motor, language, cognitive, social, emotional) are significantly delayed compared to the expected level
for age (eg, a discrepancy of >25% from the expected rate, or a discrepancy of 1.5 to 2 standard deviations from
the norm) (Primary Pediatric Care, 4th ed. Hoekelman, RA (Ed), Mosby, St. Louis 2001. p.274).
Surveillance
Process: A continuous process in which knowledgeable professionals perform
skilled observations of children during child health care visits that includes elicitation and attending to parental concerns,
identifying risk and protective factors (medical history, FHx, examination / observations, and evaluation of psychosocial
risks).Methods used informal checklist completed by the clinician / office staff
/ or parent or a standardized screening instrument such as the Denver-II.Simply
“waiting until the problem is obvious by clinical judgment alone” results in the detection of 30% fewer children
with developmental disabilities than reliance on formal developmental screening (J Pediatr 1987;111:651).
Referral
Early Intervention Programs: These programs provide evaluations of children
aged <3 yo for suspected developmental delay, a known developmental delay, or a medical condition associated with
a high probability of delay. There are benefits of early dx and tx for many conditions associated with developmental delay.
Federally funded early intervention services are available in all states. Refer for delayed speech, global delay, loss of
developmental milestones and parental concern about inappropriate development. Early intervention services result in significant
community cost saving through decreased need for special education services during the school years and increased income during
adulthood.
Clumsiness/
Coordination D/o:
M>F, 3-6% of children, onset age 2-6yo as infant
has trouble crawling, child repeatedly stumbles as tries to run or fumbles (shoelaces, zipper, buttons, tooth brushing) with
dressing self --> failure in sports, model building, penmanship.It
may be serious enough o interfere with academic performance and social integration.Typical coarse is that it becomes chronic, but less noticeable over the years due to compensation, but still have residual
clumsiness as adults.
Typical age of attainment of skills:
Age 4: buttoning and unbuttoning.
Age 4.5: dressing self (except shoelaces),
riding a bicycle with training wheels, cutting across a page with scissors, coloring within the lines.
Age 5: draws a square.Stands on foot for 15 sec.
Age 5.5:Tying shoelaces.Printing first and last name.Jumping down several steps.
Age 6: Riding a bicycle w/o training
wheels.Ability to spread butter with a dinner knife.Rhythmic skipping.
Age 7:Drawing a diagonal line.
Age 8: Finger gnosia (with eyes closed,
can you tell which finger you touch).8.8: alternating foot-hop in place.
Age 9: Sequential finger tapping at
high speed. Drawing a two-dimensional cross with same dimensions.
Age 10: Persistent tandem stance with
eyes closed for 10 sec.Absence of choreiform movements with arms extended.
Age 11: suppressing mirror movements
while doing sequential finger tapping.
Age 12: Drawing a 3-dimensional cube
with all sides angulated.
Ddx: MR, cerebral palsy, cerebellar
ataxia, Friedreich’s, hyperactivity.If any lost skills, consider mitochondrial
myopathies or degenerative d/o such as adrenoleukodystrophy.
Tx: remedial gym classes helpful. Encourage
them to participate in sports such as swimming and horseback riding to help them experience athletic success.Physical/ occupational therapy. Fatty acid supplementation (omega-3 and omega-6) may help children with
developmental coordination d/o (Pediatrics. 2005;115:1360-1366). (Pediatr Clin N Am 1999;46:905) (Evaluation of clumsiness
in children.Am Fam Phys 2002;66:1435-40)
Link:
Learning Disability |~2-3%
of children have a d/o of word production, 3-5% language expression.Can be isolated
or part of a more complex problem.
Receptive D/o: Due to cognitive impairment
in language comprehension. Anatomical (visual or hearing impairment).
Expressive D/o: Voice d/o from abnormal
sound, pitch, or quality (vocal abuse, allergies, laryngeal nerve palsy). CN damage causing dysarthria.Fluency d/o such as stuttering.
Articulation
(Speech) Disorders: characterized by difficulty producing speech sounds in
comparison to what is expected at the child's chronologic age. The difficulty in production typically occurs with consonants,
although in severe cases, even vowel distortions can occur. When difficulties with articulation exist, the child may be forced
to compensate by producing sounds in an easier way. As a result, the speech may consist of speech sound omissions, sound substitutions,
or distortions. In addition, overall oral inactivity or slurring may be noted. As a result of these errors, the child's speech
may be difficult to understand or even unintelligible. Poor speech intelligibility is a primary characteristic of an articulation
disorder.
Phonology
disorder: speech sound substitutions, omissions, and distortions, making the speech difficult to understand.
Omissions:
if the child has so much difficulty with the motor requirements for speech that he leaves out sounds in words. “I
ri the bu to coo”. (I ride the bus to school).
Substitutions:when an incorrect sound is substituted for the correct one. “I eat tate and
tooties” (I eat cake and cookies).
Distortions:when the child is attempting to produce the sound correctly, but an incorrect articulatory
placement results in an altered sound.Causes include oral/motor dysfunction
and structural anomalies such as cleft palate or velopharyngeal dysfunction. Ankyloglossia (tongue-tie) usually does not interfere
with speech production. A common distortion occurs with the production of the /r/ sound. Many children have difficulty
with the motor requirements for producing this sound. If the tongue is not high enough or retracted enough, a distortion will
result. Other common distortions are lisps, which occur on sibilant or “teeth sounds” (s, z, sh, ch, j). An anterior
or frontal lisp is the result of the tongue articulating against or between the incisors during sibilant sound production.
This causes a distortion that sounds almost like a /th/ sound. A lateral lisp occurs when the tongue tip or dorsum of the
tongue articulates against the alveolar ridge or palate, stopping the anterior movement of the airstream. As a result, the
airstream is redirected laterally, causing a slushy type of sound. At times, saliva can be seen bubbling at the sides of the
mouth during speech.
Apraxia
of speech: Verbal apraxia is when the pt has difficulty with motor planning and sequencing of movements. Although he or
she may be able to move the oral structures normally for feeding and other nonspeech activities, difficulty in coordinating
movements required for speech is demonstrated. As a result, the speech is characterized by many inconsistent substitutions,
frequent sound omissions, sound and syllable reversals, and occasional struggle behaviors during speech production. Speech
is best when producing single sounds or words but breaks down when the child is combining the sounds and words to produce
the longer utterances of connected speech.
Morphology
problems: difficulty understanding and using the rules of words for appropriate
verb tense, plurals, possessives, prefixes and suffixes, and comparatives. Syntax refers to the structure of the sentences.
Children with syntax problems may have difficulty with word order and with the use of words that have little meaning but that
form the glue for the sentence. As a result, they may use improper sentence structures or omit the smaller words, such as
prepositions, articles, and conjunctions. This may cause the sentences to be somewhat telegraphic. They may also use improper
forms of words, such as the be verbs (is, am, are) or forms of do (do, did, does). Examples of problems with syntax and morphology
include the following: That a dog. Him go school. What her doing? Mommy Daddy go work. How him break that?
Pragmatic
/ Language Disorders: do not understand certain basic rules of conversation
such as:A conversation begins with a greeting. All of one's utterances must
relate to the topic at hand.The speaker needs to let the listener know if he
or she is changing the topic.All pronouns should be referenced before using
them.A conversation is based on what the listener knows.Conversation and responses should be appropriate for the situation. For example, the sentence “Could
you please pass the salt?” is actually a command and does not require an affirmative answer. Expressions or idioms,
such as “Two heads are better than one,” may be interpreted literally, with no understanding of the deeper meaning.
Causes of language disorders include hearing loss, mental retardation, environmental deprivation, or neurologic damage or
dysfunction.
Mild: Child <1yr who fails initial
early language milestone.Child age <2yo with 3-6mo delay in language development.
Mild stuttering (repetitions by a child unaware of any difficulty).
Moderate: Child >3yo who is difficult
to understand.Child 1-3yo who fails initial and repeat early language milestone
screening test. Moderate stuttering (prolongations and blockages, but no verbal inhibitions).
Severe: Child >5yo with delayed or
abnormal language development. Severe stuttering associated with fear and avoidance of speaking.Associated global impairment such as learning difficulties or neurological dz.
Hx: Hearing/ vision problems, when was
problem noted, any changes, progression/ static, familial.
S/s: Dysmorphic features, TM’s
scarred, malnutrition, social withdrawal, muscle control, behavior. Newborn screening picks up most cases.
Lab: Full Audiology eval. Speech pathologist/
dev peds/ psychology/ neuro.The
USPSTF state that evidence is insufficient to recommend for or against routine use of brief, formal screening instruments
in primary care to detect speech and language delay in children up to 5 years of age (Pediatrics 2006;117:497-501).
Speech Delay: milestones: random
vocalize @1mo, social smile @ 2mo, smile to speech @3mo, vocalize in response to social smile @4mo, mimic sounds @6mo, babble
@ 7mo, first words @ 10mo, name familiar objects @12mo, two word phrases @ 21mo.60%
of cases of speech delay in children <3yo resolve spontaneously (BJM 2004;328:272-76).
Refer if:
@18mo --> if no meaningful words,
no response to name when called, disinterest in communicating.
@24mo --> no two-word phrases, unintelligible
to parents, speaks but never communicates with intent, poor comprehension of two word commands.
@36mo --> if >50% unintelligible
speech, no sentences, echolalia, extreme preservation.
Hx: Sz’s, familial, medical, hearing,
social relatedness, home env stimulating, motor skills.Lab: MRI if have focal
neuro abn, Karyotype and Fragile X screen, LFT’s, urine organic acids, serum AA’s.
Screening:Listen to the child's spontaneous speech while he is talking to a parent or playing.Elicit communication by saying such things as the following: What do you want to be
when you grow up?...Why?What does a (fireman) do? Tell me how you make a peanut
butter and jelly sandwich. Explain the game of baseball to me.Do
you understand your child's speech all the time, most of the time, some of the time, or hardly at all?How well do strangers understand his or her speech? When your child is talking, how many words does he
or she put together at a time?Does your child leave out words in the sentence?Is your child talking as well as other children his age?
Etiology of Speech/ language delay:
Polygenic/ familial, single gene (AD --> neurofibromatosis,
deafness.X-linked --> fragile X, Duchenne’s), teratogenic (CMV,
toxo, rubella, ETOH, cocaine, Tob), perinatal ischemia/ hypoxia, postnatal infection (meningitis), traumatic head injury.
Tips
of Parents: Be pt. Wait for a response: especially with young children, adults tend to jump in too quickly to fill
the void. Provide incentives for use of clear communication..some suggest the "money method" by putting a jar in a central
location in your home and adding a penny for every good "s" you hear your child say.Converse with your child during most activities....maintain a conversational atmosphere rather than a mood of testing
and teaching such that you get spontaneous output or responses from indirect models rather than imitation.Use "expansion—add" to what your child says (child:"doggy" - parent: "Yes, that's a doggy.") (child:
"Look at the truck." parent: "That cement truck is backing up. I can hear it - beep,beep,beep."). Use real words. Baby talk
may be cute initially but doesn't age well and no one else will know what your family terminology means. Use new vocabulary
items with old to help establish meaning in a conversational context. e.g., "1 like your turquoise shoes. They're sort of
blue and sort of green - they're turquoise."Avoid routine to spark new language......use
objects or activities that are different from the usual or each other (an odd color, out-of-character action, a broken object)...A
child may be more likely to comment on the unusual rather than the routine. (Source: 101 Ways to Enhance Your Child's Communication
Skills. By Munson. 1994)
Elective/ Selective Mutism:
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