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Worsening after shock wave therapy: what is it due to?
History of shock wave therapy
The first studies by Eisenmenger on electromagnetic generation for the production of shock waves date back to 1961. Since their introduction for the treatment of nephrolithiasis in 1980, shock waves quickly became the treatment of choice and have been part of routine clinical practice in urology for over 30 years. In addition to kidney and gallstones, pancreatic and parotid gland stones have also been treated since the early 1990s. In 1995, kidney stone lithotripsy was approved as a scientifically recognized standard procedure by guidelines for new diagnostic and therapeutic methods. As early as 1996, approximately 100,000 kidney stone lithotripsies were performed nationwide. From the observation of bone apposition in the pelvic bone area following high-energy shock wave treatments, studies began on the possible use of extracorporeal shock waves in the treatment of non-union fractures (pseudoarthrosis). The first publications (Valchanou and Michailov, 1991), followed by German animal and human studies (Schleberger and Senge, 1992), led to an increasing use of high-energy extracorporeal shock waves in the treatment of pseudoarthrosis. Thus, shock waves found their place in the range of orthopedic-surgical therapies in the early 1990s. Regarding the mechanism of action, the original idea was to initiate reparative mechanisms by inducing targeted tissue lesions to stimulate regeneration (mechanical destruction effect). Positive experiences in the treatment of pseudoarthrosis, including the observation of prolonged analgesic effects after shock wave application, led to further development of the method. Shock waves were subsequently used to treat calcific tendinopathy (Loew et al., 1993) and painful soft tissues near bone, such as epicondylitis, epitrochleitis, and heel spurs (Dahmen and Haist, 1995; Rompe et al., 1996). Within a few years, these treatments accounted for the majority of medical shock wave applications, leading to the creation of a new subfield in orthopedic therapy. The lithotripters initially used were soon replaced by devices specifically designed for orthopedic use. These newer devices generally offer a wide energy range and can therefore be used multidirectionally. However, potential in vivo tissue-damaging properties are common to all device types. Two different approaches to the mechanism of action proved decisive for further development of the method:- The causal approach, aimed at eliminating the cause of the disease. In the treatment of pseudoarthrosis, this meant inducing reparative mechanisms to promote bone healing. In calcific tendinopathy of the supraspinatus tendon, the goal was to dissolve the calcific deposit. In both cases, high energy flux densities were used, requiring strong analgesia.
- The symptomatic approach, with a primarily pain-therapeutic background. Analgesia was initially used specifically for shoulder pain and later also for pain in soft tissues near bone (Dahmen and Haist, 1995). These treatments were performed using low energy flux densities and generally did not require local anesthesia. The extent of the analgesic effect could only be measured using indirect (subjective) parameters such as VAS scores and pain scales.
- low-energy radial shock waves (symptomatic), and
- high-energy focused shock waves (causal), for which different mechanisms of action have been hypothesized.
Worsening after shock wave therapy: what causes it?
Contrary to the assumption that shock waves have no harmful effects, tissue-damaging potential was demonstrated in the 1990s by several scientific studies (Brummer F., 1990; Rompe J.D., 1996; Steinborn M., 1999). However, the rare occurrence of side effects—considered harmless and completely reversible—is one of the main arguments in favor of extracorporeal shock wave therapy. The risk rate is not only significantly lower than that of surgical procedures, but also lower than that associated with local corticosteroid injections or the regular use of NSAIDs. In more recent literature, energy ranges are no longer broadly differentiated; instead, the number of impulses and the energy flux densities used are specifically reported. According to recent publications, substance P appears to be the decisive molecular factor mediating the effects of shock waves. Substance P is a vasoactive neuropeptide found in the neurovesicles of nervous tissue in all mammals. Its release into the synaptic cleft is presumably stimulated by shock wave–induced action potentials. In the central nervous system, substance P can have both inhibitory and activating effects. Peripherally, it is believed to be responsible for plasma extravasation and the proliferation of various cell types, such as stimulation of osteoblasts (leading to healing of pseudoarthrosis) and stimulation of macrophages (leading to degradation of calcium deposits) (Schelling G. et al., 1994). An increase in substance P concentration in tissue immediately after shock wave treatment (initial pain stimulus), followed by a subsequent decrease (long-lasting analgesia), as demonstrated in rats (Maier et al., 2003), explains the theory of hyperstimulation analgesia in the musculoskeletal system at a molecular level. In summary, the effects of shock waves appear to be based on a common molecular mechanism in which substance P likely plays a decisive role. This perspective opens new possibilities for extracorporeal shock wave therapy that were previously not considered.Pain symptoms after shock wave therapy
Per il paziente, la dolorabilità dell'energia meccanica che agisce nell'area, è solitamente in primo piano. Il 70% dei pazienti trattati con alta energia ha sperimentato la terapia come molto dolorosa e in generale, la terapia con energie più elevate richiede un'analgesia più potente. Occasionalmente possono verificarsi petecchie (10% dei casi) nel punto di contatto del macchinario per le onde d'urto, anche se veri e propri ematomi sono molto rari; in entrambe le casistiche, gli effetti indesiderati sono tutti guariti senza conseguenze. For patients, the painful sensation caused by mechanical energy acting on the treated area is usually the main concern. Seventy percent of patients treated with high-energy shock waves reported the therapy as very painful, and in general, higher energy levels require stronger analgesia. Occasionally, petechiae may occur (in about 10% of cases) at the contact point of the shock wave device, although true hematomas are very rare. In all reported cases, these side effects resolved without consequences.- Subcapsular edema and hemorrhages, which may rarely be detected during extracorporeal shock wave therapy, do not represent serious damage. This contrasts with perirenal hematomas—significantly more common in hypertensive patients—which may occur due to insufficient precision of the device or operator during non-orthopedic lithotripsy treatments.
- Some authors have confirmed reports of an increased risk of developing arterial hypertension after shock wave treatment.
- In 25% of cases, temporary swelling of the heel was observed, lasting an average of three and a half days. This may also be considered a consequence of local injections often associated with shock wave therapy.
- Subcutaneous hematomas with an average diameter of 0.5 cm in the coupling area occurred in 15% of treated patients.
- Some patients reported an increase in initial pain during the first three days after treatment. Imaging diagnostics showed no evidence of histological damage to bone or soft tissues. Hematomas at the application site healed without sequelae.
- In addition to a temporary local reduction in plasma flow after focused shock wave therapy, laboratory changes have also been described in the literature. Transient increases in GOT, GPT, γ-GT, LDH, and CK were observed. Based on their physiological cellular localization, their elevation in blood indicates tissue damage of varying degrees.
- The lungs and intestines, as gas-filled cavities, must not be located in the sound path (large impedance jump with possible tissue rupture);
- Nervous tissue should not be treated directly (possible activation of action potentials);
- Blood-thinning medications should be discontinued (increased bleeding risk);
- Pregnant women should not be treated (the effects on fetal tissue have not been adequately studied, and pain-related induction of labor is possible);
- Patients with pacemakers should not be treated (possible cardiac arrhythmias);
- Excessively high energy flux densities should be avoided on tendon tissue (partial tendon necrosis cannot be ruled out);
- Large neurovascular bundles should be avoided within the therapeutic focus;
- Children and adolescents should not be treated (potential damage to growth cartilage cannot be ruled out);
- Tumors must not be located in the sound field;
- The area to be treated must be free of infection.
Frequently asked questions about shock wave therapy
- Do shock waves hurt? It depends. During treatments with medium to high energy levels, patients often perceive pain or discomfort. Local analgesia and individual pain tolerance can influence perception.
- Can pain worsen after shock wave therapy?
- What are the risks or side effects of shock wave therapy?
- Can shock waves cause irreversible damage to bones, tendons, nerves, or blood vessels?
- In which cases should shock wave therapy not be used?