A high-volume injection delivers a large volume of fluid, commonly a total injectate of around forty to fifty millilitres, typically thirty to forty millilitres of saline plus local anaesthetic and sometimes a corticosteroid, into the space between a tendon and the fat pad lying against it, intended to separate that tissue plane and disrupt the new blood vessels and accompanying neural structures found in chronic tendinopathy. It is usually written as high-volume image-guided injection (HVIGI), and the principal studied targets are the Achilles tendon, where the injectate is placed between the tendon and Kager's fat pad, and the patellar tendon, where it is placed between the tendon and Hoffa's fat pad, with the evidence more extensive for mid-portion Achilles tendinopathy than for the patellar tendon. It has been proposed in sport and exercise medicine (SEM) as an adjunct for recalcitrant tendinopathy in patients who have already completed a proper loading programme. This page covers the rationale, the technique and what the trial evidence shows.
What is the rationale, and how is it done?
The rationale rests on a well-described observation. In chronic tendinopathy, new blood vessels grow into the tendon from the adjacent fat pad and small nerve fibres accompany them, and the nerve ingrowth is a plausible contributor to pain. Doppler neovascularity is not specific to symptoms and does not establish that these vessels are the pain generator, so it forms part of a proposed rationale rather than proof. Injecting a large volume of fluid into the plane between the tendon and the fat pad is intended to separate the tissue plane and disrupt the neovascular and accompanying neural structures. Two points need to be precise: the injection is extratendinous, placed against the tendon rather than into it, and the mechanism remains proposed rather than proven, although the disappearance of Doppler signal at the end of the procedure is at least consistent with it.
The needle is placed in the interface between the anterior Achilles tendon and Kager's fat pad. Fluid separates the tendon and fat pad planes, consistent with the proposed mechanism.
Technically the procedure is straightforward but needs planning. The tendon is scanned first to assess morphology, support the clinical diagnosis, identify the area of maximum neovascularity, which often corresponds to the thickest part of the tendon, and plan a path; imaging supports the assessment rather than confirming tendinopathy or establishing the pain generator. For the Achilles the patient lies prone and a medial approach is commonly used, after ultrasound identification of the sural nerve, which usually lies laterally, and of the medial neurovascular structures; for the patellar tendon the approach is to the deep surface adjacent to Hoffa's fat pad. A needle of moderate bore is placed in-plane into the interface under ultrasound guidance, and the injectate is delivered through connecting tubing so that syringes can be exchanged without moving the needle, with the needle reoriented during delivery to separate the layers as widely as possible. A common regimen delivers around thirty to forty millilitres of normal saline preceded by roughly ten millilitres of local anaesthetic, giving a total injectate commonly in the region of forty to fifty millilitres, with a corticosteroid included in some protocols. Afterwards the patient rests relatively for a short period and then returns to a progressive loading programme, which remains the core treatment.
Does it work?
The early literature was encouraging and the later literature is more sobering, which is a familiar pattern. Case series and cohort studies reported substantial improvements in pain and function in patients with chronic Achilles and patellar tendinopathy who had already failed loading programmes, alongside a visible reduction in Doppler neovascularity. Those studies were uncontrolled, and in a condition where a painful procedure, a period of relative rest and a supervised loading programme all accompany the injection, an uncontrolled improvement is difficult to attribute to the injectate. The more informative test is a placebo-controlled one, and a double-blind randomised trial in a young active military population compared high-volume injection, with and without corticosteroid, against a small-volume sham injection in chronic Achilles and patellar tendinopathy, with all groups continuing pain-guided progressive loading. The reasonable summary of the current position is that the strongest placebo-controlled trials are negative and benefit over a credible sham has not been established, while a later systematic review that combined less rigorous studies reached a more favourable conclusion, particularly for protocols containing corticosteroid. The evidence is therefore conflicting, with the most rigorous trials negative. On corticosteroid specifically, one placebo-controlled trial found no added benefit, while the heterogeneous wider literature suggests possible early symptom improvement that may reflect the corticosteroid rather than the high-volume mechanism.
Doppler signal typically disappears immediately after the injectate separates the tendon from the fat pad, which is consistent with the proposed mechanism but does not demonstrate clinical benefit, and neovascularity is not specific to symptoms.
That leaves high-volume injection as a treatment to discuss honestly rather than to recommend confidently. Where it is offered, the conditions are the familiar ones: the diagnosis is secure and supported by ultrasound findings including neovascularity, a genuine progressive loading programme has been completed rather than merely attempted, the patient understands that the evidence is limited and inconsistent and that they may pay for no benefit, and the injection is used to enable rehabilitation rather than replace it. Safety should not be assumed simply because saline is the largest component. Recognised risks include procedural pain and post-injection ache, local anaesthetic systemic toxicity given the volumes of anaesthetic used, infection, bleeding, nerve injury, and where a corticosteroid is included the usual tendon-related cautions. Specific points to carry are that the sural nerve should be identified on ultrasound rather than assumed to be avoided by a medial approach alone, and that injectable glucocorticoids carry in-competition anti-doping restrictions. The intervention is non-standard and evidence-limited, so consent should be documented explicitly and outcomes audited where it is offered.
Exam Tips
•High-volume image-guided injection (HVIGI) delivers a total injectate commonly around forty to fifty millilitres, typically thirty to forty millilitres of saline plus local anaesthetic, into the plane between the tendon and the adjacent fat pad.
•The targets are the interface between the Achilles tendon and Kager's fat pad, and between the patellar tendon and Hoffa's fat pad.
•The injection is extratendinous, placed against the tendon rather than into it.
•The proposed mechanism is separation of the tissue plane with disruption of neovascular and accompanying neural structures; Doppler neovascularity is not specific to symptoms and does not prove the pain generator.
•A medial approach is commonly used for the Achilles because the sural nerve usually lies laterally, but the nerve should be identified on ultrasound rather than assumed.
•Uncontrolled series were promising and a later review of less rigorous studies was more favourable, but the strongest placebo-controlled trials are negative, so the evidence is conflicting and progressive loading remains the core treatment.