Pediatric Urolithiasis Treatment & Management
- Author: Sahar Fathallah-Shaykh, MD; Chief Editor: Craig B Langman, MD more...
The overall goals of care are as follows:
To prevent additional renal damage, which may lead to loss of renal parenchyma
To manage pain associated current stone(s)
To expedite passage or removal of any stones present
To prevent new stones from forming.
Management may include medical approaches, surgical interventions, and dietary modification.
Medical care largely depends on the type of presentation. Care may range from observation to emergency treatment. An obstructed infected portion of the urinary tract is a surgical emergency. (See Surgical Care, below.)
A child presenting with acute colic and gross hematuria can be managed with analgesics. Narcotics may be required, as well as enteral or parenteral hydration. When a stone is small and at the ureteropelvic or ureterovesical junction, it may pass spontaneously; a few days of observation for spontaneous passage may be indicated prior to more aggressive intervention.
A stone that completely obstructs the bladder outlet should be treated with catheterization using a Foley catheter. Once urine outflow has been established, the approach for removal vesicostomy versus cystoscopy versus lithotripsy is usually determined by the pediatric urologist. (See Surgical Care, below.)
Children with asymptomatic stones detected while screening for another problem should have blood and urine testing performed to identify underlying metabolic abnormalities.
Immobility may contribute to stone formation in some children. Generally, children with diseases and injuries should be mobilized as soon as possible. No activity restriction is necessary in urolithiasis.
The specific aims of surgical care include drainage of the urinary tract, removal of stones present in the urinary tract, and surgical correction of anatomic abnormalities, which may promote additional stone formation.
A child with an acute presentation indicative of an infected stone should be referred immediately to a pediatric urologist for drainage, antibiotic treatment, and supportive care.
Stones may need to be removed by a pediatric urologist. The removal technique used usually depends on the stone size and location. Surgical treatments may include ureteroscopic stone extraction, percutaneous nephrolithotomy, open stone surgery, and/or extracorporeal shockwave lithotripsy (ESWL). Alpha-1 adrenergic blocker agents, such as doxazosin, have been used as medical expulsive treatment in children with distal uretral stones.[13, 14]
The overall role of diet is to supply adequate quantities of material for growth and metabolism without a surplus of relatively insoluble material that requires urinary excretion. Most materials (eg, calcium, phosphate, oxylate, uric acid, cysteine) enter body fluids, and thus the urine, from one of the following 3 sources: dietary intake, de novo metabolic production, or normal turnover.
For example, calcium and phosphate are derived from dietary intake and normal turnover with bone remodeling. Oxalate is abundant in nature and enters body fluid via dietary intake and as an end product of de novo metabolism. Small quantities of uric acid are in the diet, but most uric acid is produced as an end product of purine metabolism. Purine largely comes from dietary intake. Cysteine is produced from dietary intake, normal metabolic cysteine turnover, and de novo production from methionine.
Dietary considerations depend on the type of stone. A high fluid intake leading to increased urine output is safe and generally beneficial for children with all types of stones, but stone analysis to identify the minerals present is critically important.
No randomized, prospective, double-blind studies describing the outcomes of groups of children with different metabolic stone-forming diseases that are controlled for diet alone are available. Because stone disease can cause considerable morbidity in some children, clinical trials may develop in the future.
Children with stones composed of calcium and who have excessive calcium intake or idiopathic gastrointestinal absorptive hypercalciuria may benefit from lowered dietary calcium intake. The author first restricts the calcium intake to the recommended daily allowance (RDA). The RDA was developed by estimating the daily need and then doubling. A dietitian is important in helping to develop this type of specialized diet. The goal is to lower urinary calcium such that no new stones are formed without producing calcium deficiency.
In some cases, diets containing calcium levels lower than the RDA may be required. If a diet with less than the RDA of calcium is considered, the parents and child should be included in discussion of risks versus benefits (ie, potential calcium deficiency versus decreased stone production).
In children with hypercalcinuria, restrict sodium to RDA for age. In an adult study in 2002, Borghi et al reported that sodium and animal protein restriction were more effective in reducing calcium stone formation than calcium restriction. To restrict children to the RDA for sodium and animal protein is probably not harmful and may be helpful with respect to stone formation.
Children with hyperuricosuria may benefit from avoiding purine-rich foods. Lowering purine intake to the RDA may lower serum uric acid and urinary uric acid excretion to the reference range. In the past, children receiving pancreatic enzymes ingested extra purine, which contributed to increased uric acid excretion. With newer enzyme preparations, excessive purine intake is no longer the case. In children with inborn errors of purine metabolism, lowering purine intake alone does not normalize urinary uric acid excretion.
Use caution; reduction of dietary components is intended to reduce urinary excretion, but be cautious not to develop a diet so restrictive that it produces nutritional deficiency.
Consultation with a pediatric dietitian, a pediatric nephrologist, and a pediatric urologist is usually appropriate. Generally, a pediatric nephrologist is most experienced with evaluation and management of renal stone disease in children. Consult a pediatric urologist for children who might need shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy, or open surgery.
The primary goals of inpatient care are to treat life-threatening infection, surgically remove stones, rehydrate a child with vomiting and dehydration, and manage severe pain. In the author’s experience, many children with kidney stones do not require inpatient care.
Effects of treatment should be monitored by measurement of urinary and plasma chemistries 1 month after initiating treatment and then every 2 months until a steady state is established. The blood and urine analytes measured depend on the type of stone, diet restrictions, and medication prescribed (vide infra).
Because of increased incidence of low bone density in children with hypercalciuria and nephrolithiasis, dual emission x-ray absorptiometry (DEXA) scanning should be performed at onset and then yearly in children aged 5 years and older. The test provides an absolute density measurement that can be monitored over time.
Patients should undergo annual imaging with renal ultrasonography to look for new or growing stones. New stone formation or growth in size suggests that therapy is ineffective and should be reevaluated.
Children with recurrent calculi who are on restrictive diets (eg, restricting calcium, purine derivatives) or medications that affect the excretion of these items should have their therapy assessed initially and reassessed periodically to determine in each case that treatment is beneficial and that the benefits outweigh the risks. Children on calcium restriction should have serum calcium, parathyroid hormone (PTH), and urine calcium excretion determined at onset, in 2 months, and then at 6-month intervals.
Children receiving thiazides should have serum electrolytes, cholesterol, uric acid, and urinary calcium excretion measured at onset, at 2 months, and then at 6-month intervals. Children receiving allopurinol should have a complete blood count (CBC), liver function tests, and urinary uric acid excretion tests performed every 2 months.
The medications listed above are used for both inpatient and outpatient care. Prevention of new stone formation requires a combination of medication, large fluid intake, and diet restriction described above.
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|Mechanism of Stone Formation||Drug||Primary Stone Composition|
|Crystallization of highly excreted, poorly soluble drug or metabolite causes stone formation.||Phenytoin, triamterene, sulfonamides, felbamate, ceftriaxone, indinavir, ciprofloxacin, guaifenesin/ephedrine||Drug or its metabolites|
|Drug may increase the concentration of stone-forming minerals.||1. Anti-cancer drugs
3. Allopurinol (if used in tumor lysis)
4. Loop diuretics
5. Calcium and vitamin D
|1. Uric acid
4. Calcium oxalate
|Drug inhibits activity of carbonic anhydrase enzymes in the kidney, causing metabolic acidosis, hypocitraturia, and elevated urine pH.||Topiramate, zonisamide, acetazolamide||Calcium phosphate|