Nephrolithiasis: (Case Study)

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Nephrolithiasis is the process of forming kidney stones. Kidney stones are common and can cause pain, blood in the urine, and reduced kidney function. Risk factors include diet, genetics, medical conditions, and low fluid intake.

Risk factors for kidney stones include low fluid intake, family history, metabolic disorders, obesity, certain medications, and diets high in protein, salt, and oxalates.

Common methods for treating kidney stones include extracorporeal shock wave lithotripsy (ESWL), ureteroscopy, and percutaneous nephrolithotomy. ESWL uses shock waves to break up stones, ureteroscopy uses instruments to remove or break stones, and percutaneous nephrolithotomy involves direct access through the skin.

NEPHROLITHIASIS

(CASE STUDY)

SUBMITTED BY:
JENNYLYN DE CHAVEZ
(BSN-1V GRP. 11)

SUBMITTED TO:
MRS. MAYUGA
I. Introduction
A. Definition of the Disease
Nephrolithiasis, the process of forming a kidney stone, a stone in the kidney (or lower down in the urinary
tract). Kidney stones are a common cause of blood in the urine and pain in the abdomen, flank, or groin. Kidney
stones occur in 1 in 20 people at some time in their life. The development of the stones is related to decreased urine
volume or increased excretion of stone-forming components such as calcium, oxalate, urate, cystine, xanthine, and
phosphate. The stones form in the urine collecting area (the pelvis) of the kidney and may range in size from tiny to
staghorn stones the size of the renal pelvis itself. The process of stone formation, nephrolithiasis, is also called
urolithiasis.

"Nephrolithiasis" is derived from the Greek nephros- (kidney) lithos (stone) = kidney stone "Urolithiasis" is
from the French word "urine" which, in turn, stems from the Latin "urina" and the Greek "ouron" meaning urine =
urine stone. The stones themselves are also called renal caluli. The word "calculus" (plural: calculi) is the Latin
word for pebble.

Etiology

 Elevated urinary levels of calcium, oxalate, and uric acid in stone formation, as well as reduced urinary
citrate levels.
 Hypercalciuria is the most common metabolic abnormality. Some cases of hypercalciuria are related to
increased intestinal absorption of calcium (associated with excess dietary calcium and/or overactive
calcium absorption mechanisms), some are related to excess resorption of calcium from bone (ie,
hyperparathyroidism), and some are related to an inability of the renal tubules to properly reclaim calcium
in the glomerular filtrate (renal-leak hypercalciuria).
 Magnesium and especially citrate are important inhibitors of stone formation in the urinary tract. Decreased
levels of these in the urine predispose to stone formation.
 A low fluid intake, with a subsequent low volume of urine production, produces high concentrations of
stone-forming solutes in the urine. This is an important, if not the most important, environmental factor in
kidney stone formation.
 The exact nature of the tubular damage or dysfunction that leads to stone formation has not been
characterized.
 The most common findings on 24-hour urine studies include hypercalciuria, hyperoxaluria,
hyperuricosuria, hypocitraturia, and low urinary volume. Other factors, such as high urinary sodium and
low urinary magnesium concentrations, may also play a role. To identify these risk factors, a 24-hour urine
profile, including appropriate serum tests of renal function, uric acid, and calcium, is needed. Such testing
is available from various commercial laboratories. A finding of hypercalcemia should prompt follow-up
with an intact parathyroid hormone study to evaluate for primary and secondary hyperparathyroidism.
Anatomy and physiology

The kidneys are essentially regulatory organs which maintain the volume and composition of body fluid by filtration
of the blood and selective reabsorption or secretion of filtered solutes.

the kidneys are retroperitoneal organs (ie located behind the peritoneum) situated on the posterior wall of the
abdomen on each side of the vertebral column, at about the level of the twelfth rib. The left kidney is lightly higher
in the abdomen than the right, due to the presence of the liver pushing the right kidney down.

The kidneys take their blood supply directly from the aorta via the renal arteries; blood is returned to the inferior
vena cava via the renal veins. Urine (the filtered product containing waste materials and water) excreted from the
kidneys passes down the fibromuscular ureters and collects in the bladder. The bladder muscle (the detrusor
muscle) is capable of distending to accept urine without increasing the pressure inside; this means that large
volumes can be collected (700-1000ml) without high-pressure damage to the renal system occuring.
When urine is passed, the urethral sphincter at the base of the bladder relaxes, the detrusor contracts, and urine is
voided via the urethra.

Symptoms of kidney stones include:


 Colicky pain: "loin to groin". Often described as "the worst pain ever experienced". This can also occur in
the lowerback.
 Hematuria: blood in the urine, due to minor damage to inside wall of kidney, ureter and/or urethra.
 Pyuria: pus in the urine.
 Dysuria: burning on urination when passing stones (rare). More typical of infection.
 Oliguria: reduced urinary volume caused by obstruction of the bladder or urethra by stone, or extremely
rarely, simultaneous obstruction of both ureters by a stone.
 Nausea/vomiting: embryological link with intestine– stimulates the vomiting center.
 Hydronephrosis
 Postrenal azotemia: when kidney stone blocks ureter
 Localization of kidney stone pain

Medical Care

The first part of this section discusses emergency management of renal (ureteral) colic. The second part addresses
the issues of medical therapy for stone disease. Medical therapy for stone disease takes both short- and long-term
forms (the former to dissolve the stone [possible only with noncalcium stones] and the latter to prevent further stone
formation). Stone prevention should be considered most strongly in patients who have risk factors for increased
stone activity, including stone formation before age 30 years, family history of stones, multiple stones at
presentation, renal failure, and residual stones after surgical treatment.

 General guidelines for emergency management


o After diagnosing renal (ureteral) colic, determine the presence or absence of obstruction or
infection.
o Obstruction in the absence of infection can be initially managed with analgesics and with other
medical measures to facilitate passage of the stone. Infection in the absence of obstruction can be
initially managed with antimicrobial therapy. In either case, promptly refer the patient to a
urologist.
o If neither obstruction nor infection is present, analgesics and other medical measures to facilitate
passage of the stone (see below) can be initiated with the expectation that the stone will likely pass
from the upper urinary tract if its diameter is smaller than 5-6 mm (larger stones are more likely to
require surgical measures).
o If both obstruction and infection are present, emergent decompression of the upper urinary
collecting system is required (see Surgical Care). Immediately consult with a urologist for patients
whose pain fails to respond to ED management.
 Specific guidelines for emergency management
o Although the role of supranormal hydration in the management of renal (ureteral) colic is
controversial, patients who are dehydrated or ill need adequate restoration of circulating volume.
o The cornerstone of ureteral colic management is analgesia, which can be achieved most
expediently with parenteral narcotics or nonsteroidal anti-inflammatory drugs (NSAIDs).
 Morphine sulfate is the narcotic analgesic drug of choice for parenteral use.
 Ketorolac tromethamine is the only NSAID approved for parenteral use in the United
States, and it is often effective when used for renal colic.
 Antiemetic agents such as metoclopramide HCl and prochlorperazine may also be added
as needed.
 If oral intake is tolerated, the combination of oral narcotics (eg, codeine, oxycodone,
hydrocodone, usually in a combination form with acetaminophen), NSAIDs, and
antiemetics, as needed, is a potent outpatient management approach for renal (ureteral)
colic.
o The traditional outpatient treatment approach detailed above has recently been improved with the
application of active medical expulsive therapy (MET). Although NSAIDs have ureteral-relaxing
effects and, as such, can be considered a form of MET, patient outcomes have been significantly
improved only with the use of more potent (off-label) medications. Many randomized trials have
confirmed the efficacy of MET in reducing the pain of stone passage, increasing the frequency of
stone passage, and reducing the need for surgery.3,4,5,6,7,8,9,10 MET should be considered in any
patient with a reasonable probability of stone passage. Stones smaller than 3 mm are already
associated with an 85% chance of spontaneous passage, and, as such, MET is probably most
useful for stones 3-10 mm in size. Overall, MET is associated with a 65% greater likelihood of
stone passage.11
 The initially popularized regimens for MET included corticosteroids such as prednisone.
Although corticosteroids are effective, concerns about their side effects (admittedly not
supported by randomized data) limited the acceptance of MET. More recently,
randomized studies have demonstrated great efficacy of the individual agents below,
sparing the corticosteroid component.
 The calcium channel blocker nifedipine relaxes ureteral smooth muscle and enhances
stone passage.
 The alpha-blockers, such as terazosin, and the alpha-1 selective blockers, such as
tamsulosin, also relax musculature of the ureter and lower urinary tract, markedly
facilitating passage of ureteral stones. Some literature suggests that the alpha-blockers are
more effective in this setting than the calcium channel blockers.
 MET with calcium channel blockers and alpha-blockers also appear to improve the
results of extracorporeal shock-wave lithotripsy (ESWL; see Extracorporeal shockwave
lithotripsy) inasmuch as the stone fragments resulting from treatment appear to clear the
system more effectively.
o Analgesic therapy combined with MET dramatically improves the passage of stones, addresses
pain, and reduces the need for surgical treatment. A typical regimen for this aggressive
management is 1-2 oral narcotic/acetaminophen tablets every 4 hours as needed for pain, 600-800
mg ibuprofen every 8 hours, and MET with 30 mg nifedipine extended-release tablet once daily,
0.4 mg tamsulosin once daily, or 4 mg of terazosin once daily. Limit MET to a 10- to 14-day
course, as most stones that pass during this regimen do so in that time frame. If outpatient
treatment fails, promptly consult a urologist.
 Long-term medical treatment of calcium-containing urinary calculi
o Urinary calculi composed predominantly of calcium cannot be dissolved with current medical
therapy; however, medical therapy is important in the long-term chemoprophylaxis of further
calculus growth or formation.
o Prophylactic therapy might include limitation of dietary components, addition of stone-formation
inhibitors or intestinal calcium binders, and, most importantly, augmentation of fluid intake.
o Besides advising patients to avoid excessive salt and protein intake and to increase fluid intake,
base medical therapy for the chronic chemoprophylaxis of urinary calculi on the results of a 24-
hour urinalysis for chemical constituents.

Surgical Care

 The primary indications for surgical treatment include pain, infection, and obstruction. Additionally, certain
occupational and health-related reasons exist.
 General contraindications to definitive stone manipulation include the following:
o Active, untreated urinary tract infection
o Uncorrected bleeding diathesis
o Pregnancy (a relative, but not absolute, contraindication)
 Specific contraindications may apply to a given treatment modality. For example, do not perform ESWL if
a ureteral obstruction is distal to the calculus or in pregnancy.
 For an obstructed and infected collecting system secondary to stone disease, virtually no contraindications
exist for emergency surgical relief either by ureteral stent placement (a small tube placed endoscopically
into the entire length of the ureter from the kidney to the bladder) or by percutaneous nephrostomy (a small
tube placed through the skin of the flank directly into the kidney). Urologists place ureteral stents in the
operating room while patients are under anesthesia; interventional radiologists or urologists perform
percutaneous nephrostomies in the clinic or radiology suite while patients are under local anesthesia.
o Many urologists prefer one or the other, but, in general, patients who are acutely ill, who have significant
medical comorbidities, or who harbor stones that probably cannot be bypassed with ureteral stents undergo
percutaneous nephrostomy, while others receive ureteral stent placement.
o Infection combined with urinary tract obstruction is an extremely dangerous situation, with significant risk
of urosepsis and death, and must be treated emergently in virtually all cases.
 The vast majority of symptomatic urinary tract calculi are now treated with noninvasive or minimally
invasive techniques, while open surgical excision of a stone from the urinary tract is now limited to isolated
atypical cases.
 In general, stones that are 4 mm in diameter or smaller will probably pass spontaneously, and stones that
are larger than 8 mm are unlikely to pass without surgical intervention. With MET, stones 5-8 mm in size
often pass, especially if located in the distal ureter. The larger the stone, the lower the possibility of
spontaneous passage, although many other factors determine what happens with a particular stone.
 Guidelines are now available to assist the urologist in selecting surgical treatments. The 2005 American
Urological Association staghorn calculus guidelines recommend percutaneous nephrostolithotomy as the
cornerstone of management.12 In the ureteral stone guidelines produced by a joint effort of the American
Urological Association and the European Association of Urology, ESWL and ureteroscopy are both
recognized as first-line treatments for ureteral stones.13
o Extracorporeal shockwave lithotripsy
 Most urinary tract calculi that require treatment are currently managed with this ESWL, which is the least
invasive of the surgical methods of stone removal. This modality was once believed to be a panacea.
Unfortunately, much of the literature has exposed the weaknesses of newer-generation lithotriptors. As a
result, ESWL success rates are not as good as they once were.
 The patient, under varying degrees of anesthesia (depending on the type of lithotriptor used), is placed on
a table or in a gantry that is then brought into contact with the shock head. The deeper the anesthesia
(general endotracheal), the better the results. In addition, evidence is mounting that slower shockwave
delivery (60-80 per minute) improves the results. New lithotriptors that have two shock heads, which
deliver a synchronous or asynchronous pair of shocks (possibly increasing efficacy), have attracted great
interest.
 The shock head delivers shockwaves developed from an electrohydraulic, electromagnetic, or
piezoelectric source. The shockwaves are focused on the calculus, and the energy released as the
shockwave impacts the stone produces fragmentation. The resulting small fragments pass in the urine.
 ESWL is limited somewhat by the size and location of the calculus. A stone larger than 1.5 cm in
diameter or one located in the lower section of the kidney is treated less successfully. Fragmentation still
occurs, but the large volume of fragments or their location in a dependent section of the kidney precludes
complete passage. In addition, results may not be optimal in large patients, especially if the skin-to-stone
distance exceeds 10 cm.14
o Ureteroscopy
 Ureteroscopic manipulation of a stone, depicted in the image below, is the next most commonly applied
modality. A small endoscope, which may be rigid, semirigid, or flexible, is passed into the bladder and
up the ureter to directly visualize the stone.
 The typical patient has acute symptoms caused by a distal ureteral stone, usually measuring 5-8 mm. This
calculus can be rapidly addressed with miniaturized instruments. A stone can be either directly extracted
using a basket or grasper or broken into small pieces using various lithotrites (eg, laser, ultrasonic,
electrohydraulic, ballistic).
 Often, a ureteral stent must be placed following this procedure in order to prevent obstruction from
ureteral spasm and edema. A ureteral stent is often uncomfortable; consequently, many urologists eschew
stent placement following ureteroscopy in selected patients.
o Percutaneous nephrostolithotomy
 Percutaneous nephrostolithotomy allows fragmentation and removal of large calculi from the kidney and
ureter and is often used for the many ESWL failures. A needle, and then a wire, over which is passed a
hollow sheath, are inserted directly in the kidney through the skin of the flank.
 Percutaneous access to the kidney typically involves a sheath with a 1-cm lumen. Relatively large
endoscopes with powerful and effective lithotrites can be used to rapidly fragment and remove large
stone volumes.
 In some cases, a combination of ESWL and a percutaneous technique is necessary to completely remove
all stone material from a kidney. This technique, called sandwich therapy, is reserved for staghorn or
other complicated stone cases. In such cases, experience has shown that the final procedure should be
percutaneous nephrostolithotomy
PATHOPHYSIOLOGY

Non-modifiable Factors Modifiable Factors


 Age (over 20 to 40 y/o)  Faulty Diet
Low urinary
 Sex flow
(Male>Female 4:1)  Metabolic disorders, obesity
 Family history,  Excessive medications
Hereditary  Low fluid intake and excessive
 Race (Mostly Caucasian), intake of protein, salt and oxalate
influence with lifestyle,  Nature of work (occupation)
diet  Stimulation of Calcium
 Seasonal factors precursor
 Urinary tract  Weight Loss
malformation  Hypertension
 Hyperparathyroidism
 Diabetes Melitus

Supersaturation of urine Low urinary flow May produce excess amounts of


with increased calcium mucoprotein in the bladder

Allowing crystallites to be
deposited and trapped forming
calculi or stones

Urine (upon voiding) moves


tiny stones to the ureter

Large stones Tiny stones

Blocks the ureter Causes spasm Makes urine’s turbidity cloudy

Injures the wall of the ureter


Becomes nidus Low urine output
for bacteria
hematuria
Urinary Tract Infection
Painful urine
output ↓ Hgb count
Causes ↑ WBC
count

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