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2007
Lithotripsy : benefits and unwanted side effects
Joseph Wendell Dieringer
The University of Toledo
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Dieringer, Joseph Wendell, "Lithotripsy : benefits and unwanted side effects" (2007). Master’s and Doctoral Projects. Paper 300.
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Lithotripsy: Benefits and unwanted side effects
Joseph Wendell Dieringer
University of Toledo
2007
2
Dedication
To my wife Brenda, and my daughters Kaitlyn and Ashleigh; thank you for all your patience and
understanding the past two years.
3
Acknowledgements
To my major advisor, Dr James Hampton, Ph.D., thank you for all your assistance and
guidance throughout the past year. To Jolene Miller, Scholarly Project Coordinator, thank you
for your help in my research and with the organization of my paper.
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Table of Contents
Introduction ......................................................................................................................................1
Lithotripsy ........................................................................................................................................2
Types of Stones ................................................................................................................................4
Side Effects ......................................................................................................................................6
Pancreatitis .....................................................................................................................................14
Diabetes Mellitus ...........................................................................................................................17
Linking Lithotripsy with Diabetes Mellitus...................................................................................21
References ......................................................................................................................................24
Abstract ..........................................................................................................................................32
1
Introduction
Shockwave lithotripsy (SWL) has been used in the United States since 1982 to
effectively treat nephrolithiasis. The procedure was thought to be relatively benign with few
complications other than bruising on the back where the shock wave entered and hematuria. One
complication, often viewed as minor, was the development of acute pancreatitis; however no
long term follow up studies had been done (Krysiewicz, 1992). In May 2006, The Journal of
Urology published a 19 year follow-up study on patients who received shockwave lithotripsy in
1985 at the Mayo Clinic. This study showed that patients who received SWL had an increased
risk of developing diabetes mellitus as compared to controls. When multivariate analysis was
used to take change in body mass index (BMI = wt (kg)/ ht(m2)) into consideration, the relative
risk increase was 3.75 (Krambeck et al., 2006). The development of diabetes is thought to be due
to pancreatitis (discussion to follow) which, as mentioned above, was thought to mostly be a
minor complication. (Krambeck et al.). If future studies uphold the results of Krambeck et al,
pancreatitis as a complication of SWL may have to be viewed as potentially having more serious
long term consequences.
2
Lithotripsy
The effect of shock waves on aircraft was being studied in the late 1960’s by Dornier
Systems in West Germany. Part of the study included the effects of the shock waves on humans.
Through tissue and animal studies, several important observations were made. These included: 1)
shock waves can travel through water and tissues without loss of energy; 2) the shock waves
traveling through water could be focused; 3) other than the lungs, tissues tolerated shock waves
without damaging effects; 4) brittle materials were fractured by the stress of the shock waves. In
1974, a grant was awarded to Egbert Schmiedt at the University of Munich where he began using
these principles to produce a safe and reproducible method of treating kidney stones. On
February 8, 1980, the first shock wave destruction of a kidney stone in a human patient took
place (deVere White, Ralph W. Palmer, & M., 1987).
The shock waves used to break the stone are generated in water. By placing a pair of
electrodes in the water and creating a spark between them, a small amount of water is vaporized.
The vapor expands and then as it cools it condenses and collapses onto itself. As it collapses it
creates an expanding shock wave. The energy of this shock wave is then focused, using a brass
bowl, to a point in space called F2. F2 is the point where the energy of the shock wave is at its
highest density (Chaussy et al., 1982; Marberger, Fitzpatrick, Jenkins, & Pak, 1991). Focusing of
the shock wave onto the stone is done through the use of two x-rays. The patient is positioned
using the x-rays as a guide to assure that the stone is aligned with the focal point (F2) of the
shock wave (Fuchs, Rassweiler, & Eisenberger, 1985). To prevent possible interference with the
electric conduction system of the heart, and possible development of arrhythmias, the shock
waves need to be transmitted during the refractory phase of the cardiac cycle. This is done by
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initiating the transmission during the R wave of the patients EKG (Chaussy et al.; Marberger, et
al.).
The first lithotripters used a pair of electrodes in water to create the shock wave. With
these lithotripters the patient was submerged in a water bath, because water was needed to
conduct the shock wave. The patient also had to be under general anesthesia due to the pain
caused by the shock wave (Marberger, et al., 1991). Newer model lithotripters employ water
filled units that contain the shock wave generator. This unit is then placed directly on the patient
using ultrasound jelly as a conduction medium and eliminating the need for submerging the
patient in a water bath. The method of shock wave generation has also changed. Electromagnetic
generators create high energy sound waves that are focused and used to shatter the stone (Sheir,
Madbouly, & Elsobky, 2003). These newer innovations have decreased discomfort for the
patient and general anesthesia has been replaced with mild sedation during the treatment.
However the effectiveness of stone disintegration has also decreased and the rate of repeat
treatment has increased (Gerber, Studer, & Danuser, 2005).
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Types of Stones
There are three main types of nephrolithiasis: calcium oxalate stones, uric acid stones,
and struvite stones. Calcium oxalate stones make up the majority of nephrolithiasis, about 77%.
Uric acid stones make up about 11% of all kidney stones. Struvite stones make up about 8%
(Grases, Costa-Bauza, & Prieto, 2006). Calcium oxalate stones are caused by four main factors:
hypercalciuria, hyperuricosuria, hyperoxaluria, and hypocitraturia. Hypercalciuria is due to either
the increased absorption of calcium in the small intestines, hyperparathyroidism which leads to
increased reabsorption of bone, or to the inability of the renal tubual to reabsorb filtered calcium.
Hyperuricosuria is due to dietary excess of uric acid. Hyperoxaluria is due to the increased
absorption of oxalate by the small intestines. Citrate is able to bind to calcium in solution and
prevent it from forming stones. For this reason hypocitraturia can lead to calcium stone
formation (Stoller & Carroll, 2006).
Diet modifications can help to prevent calcium oxalate stones. By decreasing the amount
of oxalate containing foods consumed, the amount of oxalate available for stone formation is
reduced. Foods such nuts, spinach, chocolate, green tea, and those containing soybean seeds are
all high in oxalate. Increasing foods such as legumes and cereal brans increase the amount of
phytate in the body, which in turn can inhibit calcium salt crystallization. An increase in the
amount of citrate consumed, commonly done through potassium citrate supplements, can also
inhibit the formation of calcium containing stones. Increasing fluid intake, particularly water, can
decrease the concentrations of calcium and oxalate in the urine and inhibit stone formation
(Grases, et al. 2006).
Uric acid nephrolithiasis are typically found in urine with a pH less than 5.5. By
increasing the pH of the urine above 6.5 many large uric acid stones can be dissolved. This is
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most commonly done by supplementing the diet with potassium citrate. Other contributing
factors can include rapid weight loss, medications and malignancy. The medication allopurinol
can be used to reduce the amount of stone formation if hyperuricemia is present (Tierney,
McPhee, & Papadakis, 2006).
Struvite stones are common in women with recurrent urinary tract infections that are
intractable to appropriate antibiotics. The stones are due to the urease produced by the infecting
bacterium. These include proteus, pseudomonas, providencia, klebsiella, staphylococcus, and
mycoplasm (Tierney, et al. 2006).
Stones greater than 8mm in diameter qualify for evaluation for shock wave lithotripsy
treatment (Cupisti et al., 1996). Patients with stones larger than 3 cm in diameter may need to
undergo additional procedures to achieve urinary passage of all the fragments (Krysiewicz,
1992). Calcium oxalate stones less than 2 cm diameter can be readily pulverized by shock wave
lithotripsy. Struvite stones also respond well to lithotripsy. However, calcium phosphate stones
and cystine stones are resistant to shock wave lithotripsy (Marberger, et al., 1991).
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Side Effects of Lithotripsy
Although shock wave lithotripsy has largely been considered a benign treatment, over the
last several years many rare, but serious, side effects have been discovered. The following are
rare, but potentially dire side effects of SWL.
One of the first things that should be addressed is the pain associated with shock wave
lithotripsy. In the early 1980’s when the HM-3 lithotripter was first being used, patients had to be
put under general anesthesia because of the pain associated with the shock wave. As the
lithotripters evolved so did the method of pain control during the procedure. Pain control evolved
from general anesthesia, to regional anesthesia to, in some cases, none at all. Recently, a study
was done to compare on a 10 point scale the amount of pain felt on five different procedures
done without anesthesia (SWL, cystoscopy, retrograde ureteral stenting, retrograde pyelography,
and ureteroscopic lithotripsy). Of the five, SWL was rated as the most painful by the patients.
The patients rated the pain as a 6.62/10 (Jeong, Park, Kwak, Oh, & Kim, 2005).
Complications of shock wave lithotripsy (SWL) include bruising of the back of the
patient where the shock waves enter. Although very rare, hepatitis can occur. Hematochezia can
also occur due to damage to the mucosal lining of the colon (Krysiewicz, 1992). Gross hematuria
for the first 24 hours affects nearly everyone receiving lithotripsy (Marberger, et al., 1991). This
is most likely due to tissue and blood vessel damage in the kidney caused by a phenomenon
known as cavitation. Cavitation is damage caused by “microbubbles” that are generated during
the propagation of the shock wave (Delius, Enders, Xuan, Liebich, & Brendel, 1988; Delius et
al., 1988; Krysiewicz, 1992). The energy created by the cavitation has been shown to be
powerful enough to create holes in thin pieces of metal foil (Coleman, Saunders, Crum, &
Dyson, 1987). It is this energy that is used to create the fragmentation of the stone. When the
7
bubbles are formed inside blood vessels, rapid expansion of the bubbles can lead to dilation and
rupture of the vessel wall. Recent evidence also suggests that the collapse of an existing bubble
may cause many smaller bubbles to form. These bubbles in turn can expand and cause additional
damage with each successive shock wave. Additionally, it has been shown that bubbles in large
vessels interacting with shock waves can perforate the vessel (Zhong, Zhou, & Zhu, 2001).
A recent article in the Journal of Emergency Medicine discussed the case of an elderly
man presenting to the emergency department, with the complaint of right flank pain, three hours
after having shockwave lithotripsy to his right kidney. A subcapsular hematoma on his right
kidney was found by CT scan. As many as 30% of patients may develop subcapsular hematomas
post treatment, but it is suggested that less than one percent are associated with pain or
significant bleeding. One of the biggest risk factors for a bleed is hypertension. Hypertension
induces atherosclerotic changes in the vessel walls, resulting in the loss of tensile strength.
Without this tensile strength, the vessel walls are more susceptible to damage by the shock
waves. Hypertension can increase the risk of renal hematomas to 2.7% from less than 0.6%
(Sherman & Dogon, 2006).
Using computerized tomography and magnetic resonance imaging, other studies have
shown that hematomas do occur in 20-25% of patients. These studies also confirm that less than
one percent of patients present symptomatically post treatment with ultrasonographic assessable
hematomas. Routine screening of patients post treatment showed that 4.1% had hematomas
detectable by ultrasound. Patient age is a risk factor for the development of hematomas. As the
patients’ age increased, so did their risk of developing a hematoma. Although it was not
statistically significant, patients treated for caliceal stones were twice as likely to develop
8
hematomas when compared with patients treated for renal pelvic stones (Dhar, Thorton, Karafa,
& Streem, 2004).
A case in Germany reported the need for removal of the kidney after treatment with
shock wave lithotripsy for a left sided stone. After the lithotripsy treatment, the patient
complained of left flank pain and became increasingly hemodynamicly unstable. Hemodynamic
instability is a state of hypotension resulting in inadequate organ perfusion. A CT and subsequent
surgery revealed that there were multiple lacerations to the kidney and it had to be removed
(May, Gunia, Helke, Seehafer, & Hoschke, 2004).
When treated with shock waves, stones break into smaller pieces that can then be easily
passed in the urine by the patient. If one of the pieces is not small enough to pass it can cause an
obstruction and can cause serious problems. The effective renal plasma flow (ERPF) has been
shown to decrease post treatment, as has the glomerulus filtration rate (GFR). The decrease in
GFR and ERPF has been shown to be transient. However, when associated with obstruction, it
has a chronic effect on renal function, and causes permanent parenchymal damage. Treatment of
an obstruction after lithotripsy must occur quickly to limit the amount of permanent damage
(Sheir & Gad, 2003).
Damage to the parenchyma has been noted even in the absence of obstruction. There
have been several cases of acute renal failure (ARF) following SWL unilaterally. One patient in
Italy developed oligourea two days post treatment with SWL. His serum creatinine had risen to
over 9 mg/dl. Ultrasound revealed no hematomas to the kidneys. Within four weeks his kidney
function returned to normal, indicating a diagnosis of acute tubular necrosis (ATN). It is
postulated that SWL may reduce renal blood flow in both kidneys, not only the one being
treated. With this in mind, renal ischemia can cause tubular damage (Liguori et al., 2004).
9
Renal injury not associated with renal failure occurs in 63-85% of all patients undergoing
SWL, including 30% of patients who have a reduction in plasma flow following treatment. This
damage is caused by inflammation set in motion by parenchymal damage from the SWL. The
inflammation leads to scar formation and permanent kidney damage. One small scale study
showed chronic changes due to scarring of the kidney in seven of twelve patients followed.
Scarring leads to the destruction of the glomerular capillaries and thus loss of function of the
kidney (Evan, Willis, Lingeman, & McAteer, 1998).
Although rare, gastrointestinal injury caused by shockwave lithotripsy is a severe side
effect. One study proposed that as many as 80% of patients undergoing shockwave lithotripsy
develop gastric and duodenal erosions due to the treatment. One case involved a 44 year old man
who, after undergoing SWL, presented in the emergency department with right lower quadrant
pain. A CT of the abdomen showed free air. A laparoscopic procedure showed a perforation in
the cecum. A review of literature by Maker et al showed that only 62 of 3,423 patients who
underwent SWL had documented gastrointestinal complications. Of the 62, only 9 had injuries
that demanded surgical intervention. Small bowel perforations were present in six of the nine
while the other three had colon perforations. There was one case in the review in which the
patient developed an ureterocolic fistula post treatment with shock wave lithotripsy. Pancreatic
hematomas and peripancreatic abscesses were also sited as complications post SWL. The
mechanism for the damage is not known but the theory of cavitation was proposed as the most
plausible. The mechanical damage due to micro-bubble cavitation has been projected as a
possible mechanism; however, chemical damage due to cavitation is also a possible mechanism.
The cavitation has been shown to generate free radicals, highly reactive substances which can
cause cell injury and cell death. Lastly, the position of the patient during the procedure has been
10
used to explain some of the gastrointestinal damage. Patients placed in the prone position have
shown a high incidence of intestinal perforations (Maker & Layke, 2004).
Patients with a stone in the upper portion of the left kidney and enlarged left spleen may
need special attention. A recent case in Germany involved the rupture of a patient’s spleen while
undergoing SWL. Hours after undergoing SWL the patient presented to the emergency
department with low blood pressure, tachycardia, and low hemoglobin levels. A splenectomy
was performed after a CT scan revealed a subcapsular rupture of the patients spleen (Kastelan et
al., 2005).
A 2001 study showed that there is a decline in sperm density, motility and vitality
following SWL for distal ureteral stones. The study compared healthy men who underwent SWL
for distal ureteral stones as compared to healthy men who underwent SWL for more proximal
stones. The impairment, however, was only transient and values returned to normal within 12
weeks (Martinez Portillo et al., 2001).
Lung tissue is very susceptible to damage by SWL and care is taken to prevent the shock
waves from passing through lung tissue. However, there are cases reported where lung
parenchyma is damaged by SWL. The lung tissue is very sensitive to shock waves, as are the
capillary endothelial cells. The passage of a shock wave through lung tissue causes damage to
both types of cells, resulting in hemoptysis. The damage is often minimal, but cases of death
have been reported (Tiede, Lumpkin, Wass, & long, 2003).
In 2001, Kochanski et al performed experiments on the effect of shock waves on DNA.
Although they were unable to definitively state a mechanism of damage, they reported that
damage was done to DNA in the path of shock waves from an electromagnetic lithotripter. The
11
electromagnetic lithotripter was chosen to prevent damage to the DNA by light from a spark-gap
lithotripter (Kochanski, Mejnartowicz, Latos-Bielenska, Etienne, & Filipczynski, 2001).
Hypertension is a possible side effect of SWL, however, whether or not it is truly a
complication relating to SWL or not is still being debated. In 1987, Lingeman et al and Newman
et al independently published studies showing an increase in the prevalence of hypertension
following SWL (Lingeman & Kulb, 1987; Newman, Williams, Kaude, Peterson, & Thomas,
1987). Lingeman’s study showed new onset hypertension in over eight percent of patients treated
with SWL, and over 15% of patients had a diastolic blood pressure increase. He reported that the
increase in diastolic blood pressure occurred regardless of side of treatment, whether it was
unilateral or bilateral treatment, and regardless of the number of shocks delivered during
treatment. It was theorized that parenchymal damage caused focal scaring in the kidney; which
caused an increase in renin release which in turn caused an increase in blood pressure (Lingeman
& Kulb).
A study published in The Journal of Urology in 1992 contradicted Lingeman’s results.
They stated that the number of patients who had a decrease in blood pressure was greater than
the number of patients that showed an increase in blood pressure. The newer study also showed
that although there was an overall increase in the diastolic blood pressure of patients, it was not
statistically significant. This study did however show that there was a statistically significant
increase in diastolic blood pressure in patients related to the number of shocks received during
treatment. The patients who received a large number of shocks, tended toward having an increase
in their diastolic blood pressure. The authors conceded that the results were with a small number
of patients and that further studies would need to be done with larger groups of patients
(Yokoyama et al., 1992).
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In 1998, a study conducted at the University of Toronto was published in The Journal of
Urology. This study followed 154 patients who were randomized into a control group who were
observed and a treatment group who underwent SWL for the treatment of renal stones. The
groups were then followed on a regular basis for two years. During the two years, two patients in
both the control group and the treated group developed new onset hypertension. This study
showed no change in blood pressure from baseline for either the control group or the group
undergoing SWL (Jewett et al., 1998).
A 2000 British study confirmed the results from the study from the University of Toronto
in 1998. The British study involved 228 patients who were randomized into either a control
group (115 patients) or a treatment group (113 patients). The patients were followed for up to
five years with the average length of follow up being 2.2 years. The study concluded that there
was no statistically significant increase in blood pressure after treatment with shock wave
lithotripsy. The authors did suggest however, that the changes may not show up as meaningful
changes in blood pressure. They proposed that the changes may show up as an increase in
morbidity and mortality from hypertension related causes such as stroke and heart disease (Elves
et al., 2000).
In contrast to the previous two studies which showed no increase in the incidence of
hypertension after treatment with SWL, a study published in The Journal of Urology in 2006
showed an increase in hypertension in patients following treatment with SWL. This study
followed patients 19 years after treatment with SWL for renal and proximal ureteral stones. In
the study, questionnaires were mailed to 578 patients (58.9% responded) who were treated with
SWL in 1985. These patients were matched with a control group who were treated nonsurgically for stones. The rate of hypertension in the treated group was nearly 1.5 times higher
13
than in the non-treated group. The authors noted that the largest increase was within the group
that underwent bilateral SWL (Krambeck et al., 2006).
One side effect of SWL that is not being debated is the development of pancreatitis
following SWL. Several cases of acute pancreatitis have been documented after treatment with
SWL (Abe, Nisimura, Osawa, Miura, & Oka, 2000; Hassan & Zietlow, 2002; Hung, Chen, Jan,
& Chen, 2000; Karakayali et al., 2006). One proposed mechanism for the pancreatic damage is
adhesions caused by the SWL (Abe, et at.). Another proposed mechanism for the development of
pancreatitis is cavitation (Hassan & Zietlow,; Hung, Chen, Jan, & Chen, 2000; Karakayali et al.,
2006). That is, the same forces used to break up the stone and that has been linked to hematuria
post-treatment with SWL, is also causing the damage to the pancreas. Damage to the pancreas
could have long term consequences for the patient. It is suggested that diabetes could be a long
term complication to SWL. The mechanism for the development of diabetes is possibly through
the damage done to the pancreas from recurrent bouts of pancreatitis.
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Pancreatitis
Pancreatitis is an inflammation of the pancreas due to the autodigestion of the pancreas
by activated pancreatic enzymes. There are acute and chronic types. The acute type has both a
mild and a more serious form. The more serious form is known as acute hemorrhagic
pancreatitis. Etiologies of pancreatitis include gallstones, alcohol, and hypertriglyceridemia.
There are three phases to acute pancreatitis. First is the activation of the digestive enzymes while
they are still in the pancreas and damage to the acinar cells. Acinar cells comprise greater than
90% of the exocrine cells of the pancreas and are responsible for the production of proteases,
lipases, and amylases. The second phase involves the sequestration of neutrophils in the pancreas
which is the cause of the inflammation seen. The third phase is due to the proteolytic effects of
the pancreatic enzymes on other organs leading to such conditions as systemic inflammatory
response syndrome (SIRS) and acute respiratory distress syndrome (ARDS) (Greenberger,
2005).
Gall stones are regarded as the most common cause of acute pancreatitis. Small stones,
consisting of mostly cholesterol, migrate from the gall bladder into the pancreatic duct and create
an obstruction (Yan & Li, 2006). Experiments have shown that obstruction of the pancreatic duct
changes the pancreatic response to calcium. High intracellular calcium concentrations have been
associated with the premature activation of the pancreatic digestive enzymes. The activated
enzymes are then able to cause damage to the pancreas (Halangk & Lerch, 2004).
Hypertriglyceridemia is another well documented cause of acute pancreatitis. A
triglyceride level of 1,000 to 2,000 mg/dL (values less than 250 mg/dL is considered normal) is
considered a risk factor for developing pancreatitis (Iskandar & Olive, 2004). A patient with
pancreatitis and triglyceride levels greater than 1,000 mg/dL with all other causes of pancreatitis
15
excluded is considered to have pancreatitis due to hypertriglyceridemia (Navarro et al., 2004).
The pancreatitis occurs due to the irritation of the acinar cells as well as the capillaries by free
fatty acids (Fortson, Freedman, & Webster, 1995).
Chronic pancreatitis is a disease state in which the glandular cells of the pancreas are
replaced by scar tissue. The scar tissue forms due to repeated incidents of inflammation.
Recurrent cases of acute pancreatitis can lead to chronic pancreatitis. Within 25 years of the
development of chronic pancreatitis, over 80% of patients develop diabetes (Tierney, McPhee, &
Papadakis, 2006).
Alcohol abuse has long been associated with chronic pancreatitis (Apte & Wilson, 2003;
Fox, 2006). Recent evidence indicates that acute pancreatitis may commonly be due to alcohol
use (Apte & Wilson; Hanck & Whitcomb, 2004; Nordback, Pelli, Lappalainen-Lehto, & Sand,
2005). In 2005, Nordback et al found that the first symptoms of acute pancreatitis often came
after the cessation of alcohol following long term use (Nordback, Pelli, Lappalainen-Lehto, &
Sand, 2005). It has been proposed that the alcohol does not have a direct causative effect in the
development of pancreatitis; however it may just lower the threshold of the disease to some other
contributory agent. The damage to the pancreas may also be due to the toxic effects of the
alcohol on the acinar cells. These cells are responsible for the production of the pancreatic
digestive enzymes. In animal studies, the acinar cells have had mitochondrial damage associated
with alcohol use. With the damage to the mitochondria, and the subsequent decrease in ATP the
acinar cells would have difficulty regulating intracellular calcium (Hanck & Whitcomb).
Chronic pancreatitis is due to the destruction of the pancreas, often after several attacks
of acute pancreatitis. Patients with chronic pancreatitis have less than 10% of the exocrine
function of their pancreas intact (Greenberger, 2005). An increased risk of pancreatic cancer is
16
associated with chronic pancreatitis due to unwanted cellular proliferation. Up to 80% of the
cases of chronic pancreatitis are associated with heavy alcohol use. However, a predisposition to
chronic pancreatitis is believed to exist to the fact that only 5% to 10% of those who abuse
alcohol develop the disease. There is also a hereditary link to pancreatitis with 80% of the
patients inheriting the gene developing chronic pancreatitis. The prevalence of chronic
pancreatitis is less than 5%. It does however have an association with obesity, insulin resistance
and type 2 diabetes mellitus which are all increasing, therefore one can expect an increase in the
rate of chronic pancreatitis (Fox, 2006).
Current research has shown that smoking causes an increased risk for pancreatitis. It has
been shown that prolonged exposure to nicotine can cause an increase in the accumulation of the
digestive enzymes trypsinogen and chymotypsinogen (Wittel et al., 2006). Laboratory studies
have also shown that nicotine exposure can lead to high intracellular calcium levels
(Maisonneuve et al., 2005). As discussed earlier, high intracellular calcium levels can lead to
activation of the digestive enzymes that are now at higher than normal levels. Unfortunately, for
some the first symptom of pancreatitis is the development of pancreatic insufficiencies such as
steatorrhea or diabetes mellitus (Apte & Wilson, 2003). As eluded to earlier, a study published in
2006 found that diabetes could be a long term complication from SWL. Following is a brief
description of the two types of diabetes as well as commonly accepted etiologies of both types.
17
Diabetes Mellitus
Diabetes mellitus is classically described as two types. Type 1 is the inability of the
pancreas to make insulin while type 2 is explained as a triad of insulin resistance, impaired
insulin secretion, and increased glucose production. Type 1 has two subtypes. Type 1 A is due to
the autoimmune destruction of the insulin producing beta cells of the pancreas. In type 1B
diabetes mellitus, there are no serologic markers indicating autoimmune destruction of the beta
cells; however, the beta cells are destroyed (Powers, 2005). The etiology of type 1 diabetes is
thought to be the combination of genetics and some environmental trigger (Gillespie, 2006; E.
Hathout, W. Beeson, M. Ischander, R. Rao, & J. Mace, 2006; E. H. Hathout, W. L. Beeson, M.
Ischander, R. Rao, & J. W. Mace, 2006; Hirschhorn, 2003; Knip, 2003).
The genetic etiology of type 1 diabetes has several components. One of the most studied
is known as the HLA locus on chromosome 6 (E. H. Hathout, et al, 2006). There are at least 15
other loci that can be attributed to causing type 1 diabetes. There are also two genes associated
with t-cell activation which are being studied as possible factors involved in the autoimmune
response seen in type 1 diabetes (Gillespie, 2006). Twin studies have also provided information
regarding the genetic component to type 1 diabetes. Monozygotic twins are more likely to both
develop type 1 diabetes as compared to dizygotic twins (Hirschhorn, 2003).
Twin studies have also been used as evidence in the fact that there is some environmental
trigger for the susceptible population to develop diabetes. This was shown as only a small
proportion of the susceptible population went on to develop the disease (E. H. Hathout, et al.,
2006; Knip, 2003). The presence of an environmental trigger is also evident when comparing
dizygotic twins with other siblings. Dizygotic twins show a higher rate of diabetes than do
siblings. This can be attributed to the common environment shared by twins (Hirschhorn, 2003).
18
Variability in the incidence of type 1 diabetes in genetically similar populations separated by
geography also lends credence to the theory of an environmental trigger (Hirschhorn). Kathleen
Gillespie notes that currently there is a worldwide increase in the incidence of type 1 diabetes of
about 3% per year. She contributes this rapid rise to some environmental trigger on those having
the susceptible genes (Gillespie, 2006).
Many factors have been found that may be the environmental trigger for type 1 diabetes.
Air pollution was studied and it was found that people exposed to ozone and sulfate had a higher
rate of type 1 diabetes. Passive smoking was more frequent in children with diabetes (30%) than
those without (10%). It has been theorized that the damage done to the beta cells by these
pollutants is due to free radical destruction (Hathout, et al., 2006).
Infections have been sited as triggers for diabetes in the susceptible. One infection that
has been identified is enteroviruses, which have been shown to induce diabetes in experimental
animals. Studies have shown that there is an increased risk for developing diabetes for a child
whose mother had an enterovirus infection during pregnancy. Congenital rubella infections have
also been sited as a cause of diabetes (Knip, 2003).
Dietary factors may also be the causative factor in the initiation of the destruction of the
beta cells. Finnish research has shown that a large amount of cow’s milk in childhood was
associated with a higher rate of type 1 diabetes. The foundation for the research into the
relationship between consumption of cow’s milk and diabetes centers around two concepts. The
first is the difference in the proteins that make up cow’s milk as compared to the proteins that
make up human milk. The second is the difference in the amino acid sequence of the bovine
insulin that is present in the cow’s milk and the amino acid sequence of human insulin. A
Swedish study has linked zinc deficiency and type 1 diabetes (Knip, 2003).
19
As the search for the environmental triggers for type1 diabetes continues, some protective
factors have emerged. A Finnish study found that even sporadic supplementation of vitamin D
during infancy can be protective against the development of type1 diabetes (Knip, 2003).
Children who attend daycare and children who are breastfed in infancy have been shown to have
a lower relative risk for developing type1 diabetes (Hathout, et al., 2006).
The triad that describes type 2 diabetes is a summary of interlinked mechanisms. Insulin
resistance is the inability of the cells, especially the skeletal muscle cells and the hepatic cells, to
recognize insulin. The mechanism is unknown; however, it is known that the number of insulin
receptors on the skeletal muscle cells decrease. This decrease in receptors is believed to be due to
the hyperinsulinemia state and the cells down regulation reaction to this state. The defect in
insulin resistance is more likely related to the post receptor pathway. The impaired insulin
secretion is due to the pancreas’ inability to continue to make the high levels of insulin needed to
get cellular response to the insulin. This is because the cells have become resistant to the insulin.
The third leg of the triad is increased gluconeogenesis. This is due to the hepatic cell’s insulin
resistance, and the liver cells inability to recognize the hyperinsulinemia and therefore the
hyperglycemic state on the body. The hepatic cells then begin gluconeogenesis to compensate for
their perceived low blood sugar state (Powers,, 2005) .
The etiology of type 2 diabetes mellitus is not completely understood. There are many
risk factors that are associated with the development of type 2 diabetes. The relationship of
weight and diabetes has been well publicized. A higher risk of diabetes exists amongst those who
are overweight as adults. Losing weight during adulthood has been shown to reduce the risk of
developing diabetes, but not to the same level as those who have never been overweight (Jeffreys
et al., 2006). A Danish study suggests that it is not the overall attained weight that increase the
20
risk of developing diabetes, rather it is the amount of weight gained after the age of 20 (Black et
al., 2005). Rather than looking at a persons’ BMI, an Iranian study suggests that it is better to
compare ones waist/ height ratio to evaluate their risk of developing type 2 diabetes (Hadaegh,
Zabetian, & H. Azizi, 2006).
Smoking increases a person’s risk of developing type 2 diabetes independent of other
risk factors. The weight gain associated with stopping smoking does not increase one’s risk of
diabetes as much as stopping smoking lowers the risk (Patja et al., 2005).
Physical activity level is also associated with the development of type 2 diabetes mellitus.
An increase in physical activity can decrease the risk of developing type 2 diabetes. This
protective effect can be seen regardless of BMI (Hu et al., 2004). Hu et al observed that activity
levels were lower among those who were overweight or obese (Hu et al., 2004). In a study to
determine the effect of lifestyle on the development of diabetes, a group of patients with
impaired glucose tolerance were counseled on weight loss and increasing physical activity. This
group of patients had an overall reduction in the incidence of the development of diabetes of
58% as compared to a control group (Tuomilehto, Lindstrom, Eriksson, & Valle, 2001). Other
characteristics that have been associated with the development of diabetes are a low education
level and a high systolic blood pressure (Bener, Zirie, & Al-Rikabi, 2005).
21
Linking Lithotripsy with Diabetes Mellitus
In 2004, The Mayo Clinic in Rochester, Minnesota completed a 19-year follow up on the
630 patients that had had SWL in 1985 at their facility. It was determined that 578 patients were
still alive at the time. A survey was mailed to them, and 58.9% responded. Patients were
identified who had preexisting renal insufficiency, preexisting obesity (BMI greater than 30), or
preexisting hypertension. A control group was also established. The control group was
established by reviewing charts of patients with nephrolithiasis who were managed nonsurgically. The control group was matched to the experimental group based on age (± 5 years),
sex, and year of presentation (± 1year) (Krambeck et al., 2006).
The experimental group included 218 females and 404 males. Bilateral stones were found
in 57 cases, left sided stones in 384 cases and right sided stones in 295 cases. Eight of the
patients had diabetes prior to undergoing SWL. Postoperative complications were reported by 40
of the patients that responded to the survey. The development of complications was associated
with the number of shocks, voltage, average intensity, total intensity, the number of locations
treated and the number of separate treatments (Krambeck et al., 2006).
The patients treated with SWL who responded to the survey were much more likely to
have developed diabetes than their counterparts in the control group. However, it was noted by
the researchers that there was a significant difference in obesity (BMI>30) for the experimental
group as compared to the control group (p<0.001). The SWL group had a greater percentage of
obese individuals. When BMI was taken into consideration, the risk for developing diabetes
mellitus in the SWL group was 3.75% (p<0.003). It was found that the increased risk existed
regardless of which side the treatment took place (Krambeck et al., 2006).
22
The researchers hypothesized that the increased risk of developing diabetes in the SWL
was due to damage to the pancreatic islet cells. The HM-3 lithotripter is known to have the
pancreas in its shock wave path regardless of the side of treatment. The researchers also noted
that F2 in the HM-3 has a larger cross section than the newer machines. They also found that
obese patients were more likely to develop the disease than the non obese counterparts after
treatment with SWL. Overall it was noted that diabetes development was associated with the
total intensity and the number of shocks received (Krambeck et al., 2006).
The study done by the Mayo Clinic followed patients who were treated with the Dornier
HM-3 lithotripter (HM-3). The HM-3 was the first lithotripter, and although it revolutionized the
way patients were treated, it did have some shortcomings which were eliminated by later
machines. The first problem with the HM-3 was that the focal point of the shock-wave energy
(F2) was not as focused as the machines of today. When using the HM-3 lithotripter, F2 just
needed to be in the vicinity of the stone to work. The newest lithotripters use computers to center
the more focused F2 onto the stone; however this was not the case with the HM-3. When a
patient was being treated with the HM-3, AP and lateral radiographs were obtained and then the
lithotripter was placed at an oblique angle to the patient and the technician made the best
approximation possible to make sure the stone was centered at F2. Taking into consideration
these observations, it is reasonable to see how a patient may suffer damage to other tissues when
being treated with the HM-3 (B. Balduf, personal communication, November 11, 2006).
Short term studies could now be done to follow patients receiving lithotripsy from one of
the newer machines. Serum amylase and lipase levels could be measured post-treatment
revealing if any damage is being done to the pancreas. Future long term studies could be
23
conducted to determine the risk of the development of diabetes following treatment with one of
the newer computer controlled lithotripters.
Lithotripsy is, and will continue to be, a treatment modality for the treatment of
nephrolithiasis. It is important when a physician assistant (PA) is counseling a patient about
treatment options for their kidney stones, that it is not forgotten that there can be serious side
effects. Although lithotripsy has historically been considered a benign treatment, there are rare
but severe side effects. Also, the long term side effects of treatment with lithotripsy are just
coming to light. Diabetes and hypertension are two very serious diseases, and if future studies
confirm the results Krambeck et al. patients need to be made aware.
24
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32
Abstract
In 2006, The Journal of Urology published a 19 year follow-up study on patients who
received shockwave lithotripsy in 1985. This article stated that research showed a correlation
between shockwave lithotripsy and diabetes mellitus.
Google-scholar, Pubmed, and Medline were used to find scientific articles related to
lithotripsy, pancreatitis, and diabetes.
Results of the literature review were that side effects to lithotripsy are rare and usually
mild in nature; however, there are occasionally more serious side effects. One of the more
serious side effects is pancreatitis. It is known that recurrent pancreatitis can lead to diabetes
mellitus. The link between lithotripsy and diabetes mellitus was hypothesized to be due to
damage often done to the pancreas during the procedure. In conclusion, one research paper
published in 2006 found a link between lithotripsy and diabetes; however more research in this
area is needed.