Extracorporeal Shock Wave Lithotripsy (ESWL), also known as Extracorporeal Shock Wave Lithotripsy (ESWL), is the use of extracorporeal shock waves focused on the body to break up the stones, so that they are eliminated from the body with the urine, the importance of this technology, along with CT, MRI, known as the three major medical discoveries of the 20th century. Since the early 80’s when the first extracorporeal lithotriptic machine was introduced by Dornier Company of Germany, millions of cases of extracorporeal lithotripsy treatment have been performed abroad, and it has become the conventional method of choice for the treatment of urolithiasis. Due to the simple operation technique of ESWL, the relatively low price of the equipment and the low entry threshold, large and small hospitals in China have also embarked on extracorporeal lithotripsy equipment. Because of the drive of economic interests, some hospitals at the same time made a lot of improper publicity, especially publicizing the safety of extracorporeal lithotripsy without side effects, treatment on the go, and the treatment process of extracorporeal lithotripsy indications of laxity, resulting in a portion of the patients to appear harm. In order to publicize the rational application of extracorporeal lithotripsy technology and try to avoid complications, the authors refer to Campbell’s Urology and organize the side injuries of extracorporeal shock wave as follows. Extrarenal Injuries Patients with extracorporeal shock wave lithotripsy usually have pain in the posterior lumbar region that is confined close to the site of shock wave entry. It can also cause significant trauma to organs such as the liver and skeletal muscle, as determined by testing bilirubin, lactate dehydrogenase, serum aspartate transferase, and creatine phosphokinase levels within 24 hours of treatment. These parameters begin to decline within 3 to 7 days after shock wave lithotripsy (SWL) treatment and normalize within 3 months. Complications such as gastric and duodenal complications have been reported and are generally recognized as common extrarenal complications of SWL treatment. The lung parenchyma can also suffer damage if it is directly exposed to shock waves. Some patients have developed significant elevations of serum amylase and lipase after lithotripsy, which is a clinically typical manifestation of acute pancreatitis, but no obvious signs of pancreatitis have been found.Blood in the stool secondary to damage to the colonic mucosa immediately after SWL has also been reported.Myocardial infarction, cerebrovascular accidents, and brachial plexus paralysis have also been reported as complications after SWL. In addition, early clinical studies found that shock waves can cause cardiac arrhythmias. As a result many clinicians began treating with higher frequencies, up to 2 Hz.Paterson and colleagues were the first to question the lithotripsy efficacy of increasing the frequency of treatment.Their study showed that increasing the frequency of treatment decreased lithotripsy efficacy, and more recent evidence suggests that increasing the frequency of SWL decreases lithotripsy efficiency. Acute Kidney Injury:Structural and Functional Changes SWL can lead to acute structural changes in the kidneys of most patients treated with SWL. Morphologic studies applying MRI and renal isotope scans have revealed that 63% to 85% of patients treated with SWL exhibit one or more renal injuries within 24 hours of treatment. These values are much higher than the 0.6% incidence of clinical hematomas reported by Chaussy and Schmiedt (1984). The two most common side effects seen in the kidney after SWL are hematuria and intra- or perirenal hematomas. The kidneys are often enlarged with indistinct corticomedullary borders, which is suggestive of acute intrarenal edema; although clinically significant renal edema was found early on in only 1% of SWL-treated patients, more complications were detected when CT and MRI were applied. In addition, studies have found that newer generation lithotripters with smaller focusing areas and higher forward pressures result in a higher incidence of clinical hematomas (3% to 12%). These changes manifest themselves in varying degrees from mild contusions confined to the renal parenchyma to large hematomas, and severe hematomas may present with severe hemorrhage, and this hemorrhage may produce acute renal failure. Typically, perirenal fluid resolves within a few days, whereas subfascial fluid or hemorrhage may persist for 6 weeks to 6 months (or longer) before resolving. Rigatti and colleagues (1989) performed histopathologic studies of patients treated for SWL to detect acute changes in the kidney and surrounding tissues.Renal biopsy specimens obtained within one week after SWL reveal significant tubular, vascular, and interstitial changes confined to the pressure wave plane. Most of the renal vesicles in this region appear ruptured, and the remaining renal units exhibit mild degenerative changes with accumulation of ferritin-containing particles and tubular patterns. Alterations of the microvascular system include dilatation of the veins, endothelial injury, and thrombosis.Seitz and colleagues (1991) studied four patients treated with a piezoelectric lithotripter and observed that intra-parenchymal hemorrhagic sites in the corticomedullary junction increased with the number of shock waves, concluding that the visual and histologic manifestations of the kidneys of the four SWL-treated patients correctly reflected the findings of other authors in animal studies. Another way to determine the type and extent of renal injury resulting from SWL is to treat cadaveric kidneys with SWL. These studies clearly elucidate that the amount of clinical treatment can fully result in injury to renal units and small to moderate vascularity within the kidney. The greater the number of shock waves, the greater the damage detected. The acute alteration of renal function in patients with SWL remains unclear, as few studies have followed the changes in the parameters of renal function after SWL.Kaude and colleagues (I985) found that the kidneys of 30% of SWL-treated patients showed an immediate decrease in effective plasma flow. Others have also found a delay in the secretion of contrast medium in the unobstructed kidneys after SWL. The reduction in renal function correlated with the amount of shockwave received. These studies are supported by the following observations:A prospective study was conducted by researchers at the University of Innsbruck, who examined resistance parameters in a group of patients who received a shockwave volume sufficient to break up the stone (average of 2,725 shockwaves received; 16-28 kV, Dorner MFL5000 lithotripter) (Janetscheketal, 1997). . Patients were grouped according to the results of these tests, and those over 60 years of age showed an increase in resistance parameters on the treated side of the kidney immediately after SWL (contralateral normal kidneys did not show any increase). 75% of patients over 60 years of age showed pathologically elevated resistance parameters, and 15 out of 20 had statistically significant increases in resistance parameters at 26 months.Aoki and his coworkers also found that resistance parameters were increased more in the older patients. Aoki and colleagues also found a greater increase in resistance parameters in older patients. 45% of these patients had a sustained increase in resistance parameters, and these patients were also able to develop hypertension. Plasma renin activity was unchanged. Scholars have concluded that there is a significant positive correlation between resistance parameters and blood pressure and that this is a harbinger of underlying renal vascular disease, and that age is a risk factor for long-term complications of SWL. All of the literature cited in this section suggests that renal function is adversely affected, manifesting as an acute response in some patients, and that the primary alteration is a vasoconstrictive response, the latter resulting in decreased renal blood flow and tubular filtration rate. SWL has been reported to lead to significant improvement in renal function in some patients. However, many such patients present with ureteral obstruction prior to treatment, thus misrepresenting these findings. Risk factors can increase the likelihood of acute kidney damage in patients with SWL, and Knapp and colleagues found that the presence of hypertension increased the risk of perinephric hematomas. In particular, patients with suboptimal blood pressure control had the highest incidence of hematoma at the time of SWL.Dhar and colleagues found that the incidence of subperitoneal hematoma increased 2.2-fold for every 10 years of age of the patient after SWL.Newman and Saltzman (1989) corroborated these findings, suggesting that coagulation disorders and thrombocytopenia are more important risk factors for the development of subperitoneal hematomas. Factors. Other risk factors for bleeding are diabetes mellitus, coronary artery disease, and obesity, all of which suggest an association with vascular dysfunction. Chronic renal damage: structural and functional changes Although there is a paucity of information in this area, four potential chronic renal changes can occur after SWL: elevated systemic blood pressure, decreased renal function, increased stone recurrence, and induction of calcium phosphate stone disease. All four effects are associated with the development of scarring from acute injury.Lechevallier and colleagues performed a single-photon emission computed-imaging study of 12 patients undergoing lithotripsy with a piezoelectric lithotripter before and 30 days after SWL. All SWL-treated kidneys showed a decrease in renal function; four of the 12 showed a decrease in local tracer uptake of more than 4%. Peterson and Finlayson first suggested that SWL might be associated with significant alterations in systemic blood pressure, and other investigators have also studied this aspect.Lingeman and colleagues reported that 8.2% of 243 patients with normal blood pressure before SWL developed alterations in blood pressure that required antihypertensive therapy. The average follow-up for this group was 1.5 years, and the annual incidence of hypertension was 5.5%. A study of nearly 1,000 patients at Methodist Hospital in Indiana, USA, found that hypertension may be a long-term complication of SWL.Eterovic and colleagues obtained blood pressure testing and renal vascular resistance data for 30 patients treated for SWL and 30 patients who had pelvic incision for stone removal before treatment and 3 months after stone removal. They found a significant decrease in blood pressure and renal vascular resistance after treatment in patients with pyelotomy for stone removal and no change in SWL-treated patients, suggesting that SWL results respond to the balancing effect of relief of the obstruction and the effect of the SWL-induced lesion on blood pressure.Williams and colleagues found a significant reduction in the effective renal plasma flow fraction present after 17 to 21 months of SWL treatment.Qrestano and colleagues) found that patients treated with more than 2,500 shockwaves had decreased muscle clearance and prolonged delivery of sodium 131l-o-sulfomalonate to the affected kidney 30 days after SWL; similar findings were seen in the contralateral normal kidney of some patients.Lingeman et al. found that patients with isolated kidneys had elevated levels of creatinine at 5 years after SWL (Britaetal, 1990). Another concern is the high rate of stone recurrence after SWL due to residual stones (Pearleetal,1999).Carr and colleagues found that 298 patients with stones removed by SWL treatment developed new stones and compared them with 62 patients treated with PNL. Their data showed a significant increase in the rate of new stone formation within 1 year of SWL.Carr et al. suggested that fine sand-like stone fragments produced by SWL treatment remained in the kidney and gravity caused these fragments to become new stone foci within the renal system. Some studies have found a significant increase in the incidence of calcium phosphate stones over the last 30 years.The attraction of Parks’ study is that when the number of SWL treatments was analyzed for all patients with renal stones, corrected for the number of stones and duration of the disease, patients with calcium phosphate stones received significantly more SWL than patients with idiopathic calcium oxalate stones. In addition, calcium hydrogen phosphate stone components received significantly more SWL than apatite stones. Histopathologic studies of patients with calcium phosphate stones have revealed the presence of progressive tissue changes in the renal cortex and papillae (including interstitial fibrosis, tubular atrophy, glomerular degeneration, and large deposits of light apatite within the medullary collecting system). Although these data do not yet indicate an etiologic and outcome relationship, there is certainly some association between calcium phosphate stones and multiple treatments for SWL. Whereas apatite stones are associated with increased urinary pH, the initial damage to the microvessels located in the renal papillae and the collecting system of SWL found in animal studies could explain why urinary pH is out of control. Biological Effects:Experimental Animal Studies Acute Kidney Injury:Structural and Functional AlterationsAfter the introduction of SWL into the clinic, it was mistakenly assumed that shockwaves did not produce damage and could pass through the body without trauma (ChaussyandFuchs,1986). Subsequent studies have found that SWL can indeed affect the structure and function of organs. By macroscopic examination, acute alterations in the kidneys of dogs and pigs treated with applied clinical shock wave volumes were strikingly similar to those of patients with SWL. These lesions were predictable in advance in terms of size, location, and the type of injury (primarily vascular) that resulted. These changes include hematuria, contusion-like lesions, subperipheral hematomas, hemorrhage, and enlarged kidneys. Perinephric fat is a common site of extensive hemorrhage. Subpericardial hemorrhage may extend along the pericardium or form a detached hematoma. Sites of intra-parenchymal hemorrhage are usually wedge-shaped, with the most severe hemorrhage occurring at the corticomedullary junction. Hematomas located in the renal parenchyma or subperitoneal region can reach a diameter of 0.5 cm, and there can be up to 10 hemorrhages at this site per kidney. Applying extracorporeal shockwave to adult pig kidneys, hemorrhagic lesions can occupy approximately 2% of their functional volume. Larger hematomas appear to compress adjacent tissues, interstitial edema is common, and the diffuse character of the hematoma is responsible for the enlargement of the kidney. The site of the hemorrhage site is typically characterized by rupture of small vessels, including thin-walled veins, small arteries, glomerular capillaries, and peritubular capillaries. Venous thrombosis is often associated with interlobular and arcuate veins at the site of hemorrhage. The absence of endothelial cells, the large number of polymorphonuclear leukocytes and activated platelets adhering to the luminal surface of the vessels, and the presence of vasculitis indicate the presence of extensive endothelial disruption in these veins, and damage to the renal units and the vascular system is always first seen in the renal papillae and then in the cortex. Renal units adjacent to the site of apparent hemorrhage show evidence of direct injury due to shock waves and secondary alterations associated with ischemia. These alterations include vacuolar changes in certain cells, tubular dilatation, tubular formation (hyaline tubular, erythrocytic tubular), and mild tubular necrosis. These phenomena demonstrate that both the microvascular system and renal units are sensitive to shock waves and susceptible to damage; however, the primary damage appears to be vascular destruction. The experimental SWL literature’s is not a gap, that is, changes in renal function after shockwave therapy have also been studied.Jaeger and Constantinides (1989) reported a significant decrease in creatinine clearance and an increase in glucose secretion in dogs 1 hr after shockwave.Karlsen and colleagues (1990) found that 2 hr after SWL in dogs hour urine osmolality and urine flow increased, while renal plasma flow decreased by about 1/3. In the early days of lithotripsy, it was known that shock waves could cause a vasoconstrictive response.In a series of studies conducted by Brendel and coworkers in 1987, the application of microvideo techniques revealed that:when a shock wave acted directly on a simple microvascular bed, small arterioles appeared to be acutely spasmodic, while small veins hemorrhage occurs. Vasoconstriction peaked after 20-30 seconds and lasted 4-10 minutes. After vasoconstriction the vessels gradually dilate. These scholars also suggest that vasoconstriction is most pronounced at the peak of pressure generated by the shock wave. Vascular injury may increase ischemic damage to the renal parenchyma.Cohen and colleagues (1998) as well as Brown and colleagues (2000) have found by their studies that clinical doses of shockwaves can lead to peroxidation of renal fat on the treated side and the formation of free radicals. Since SWL can induce a vasoconstrictive response in both kidneys, it is important to focus on the effects of ischemic alterations in both the treated and untreated side of the kidney (Willisetal,1999). Chronic alterations in renal structure after shockwave therapy have been clinically studied.Jaeger and Constantinides (1989) found that the kidney develops alterations such as calcium salt deposits, fibrosis, and cystic changes at the site of acute hemorrhage after 2 weeks of SWL.Newman and colleagues (1987) found permanent morphological alterations in the kidneys of dogs at 30 days after SWL treatment. These changes included diffuse interstitial fibrosis, localized calcification, loss of renal units, dilated veins, hyalinization, and cell-free paralytic scarring from the cortex to the medulla.Morris and colleagues (1991) found a direct relationship between the amount of shock wave and the size of the scar. In addition, Banner and colleagues (1991) treated porcine kidneys by HM3 or EDAP lithotripter and found that their kidneys developed vascularized thylakoid proliferative glomerulopathy after treatment. There was a progressive increase in the deposition of complement C3 and immunoglobulin G on the tethered membranes. Interestingly, these changes occurred in both kidneys and were of similar magnitude, suggesting that SWL results in bilateral injury or similar bilateral changes caused by systemic factors.Delius and colleagues (1990) reported that most of these renal changes could be reversed within a few weeks, with the exception of some large hematomas. These observations suggest that acute intrarenal changes can be categorized as reversible or irreversible. At the same time, clinical doses of SWL always result in irreversible injuries that eventually form scarred areas. Chronic Kidney Injury:Structural and Functional AlterationsOnly a few studies have attempted to clarify the chronic alterations in renal function caused by SWL.Neal and colleagues (1991) treated the kidneys of immature and adult rhesus monkeys with either 15,500 shockwaves at 15 kV or 2,000 shockwaves at 18 kV. Effective renal blood flow remained significantly reduced in the immature rhesus monkeys 6 months after shockwave treatment. In another study, mean arterial blood pressure was significantly higher in immature rabbits than in controls after receiving 1000 to 2000 shock waves for 4 to 8 weeks. In conclusion: ESWL has an important place as a minimally invasive treatment option for urinary tract stones, but it should not be abused, and the current indications are mainly for stones within 2 cm in the kidney and ureter, with a short course of the disease, with onset in about 1-2 weeks, and with the expected number of lithotrips not exceeding 3. The interval between each of these lithotrips should be 10-14 days to allow for a full recovery period from the shockwave damage to the organism.