Ruptur Tendon Achilles
Published on September 10, 2026
Risk Factors
Males 30-50 years old ("weekend warriors"), fluoroquinolone use (ciprofloxacin, levofloxacin), corticosteroid use (systemic or local injection), prior tendinopathy, sudden increase in physical activity, obesity, diabetes, chronic kidney disease, rheumatologic conditions
Etiology
Acute forceful dorsiflexion against a contracted gastrocnemius-soleus complex; degenerative tendinopathy predisposes to rupture at the watershed zone (2-6 cm above the calcaneal insertion)
Presentation
Sudden sharp pain in the posterior ankle/calf during explosive movement (jumping, sprinting, pushing off); patient reports feeling like they were "kicked" or "shot" in the back of the leg; difficulty walking, inability to stand on tiptoes
Classic Exam
Positive Thompson test (squeezing calf fails to produce plantar flexion), palpable gap in the tendon 2-6 cm above the calcaneus, increased passive dorsiflexion on the affected side, loss of plantar flexion strength
Diagnostics
Clinical diagnosis (Thompson test); MRI confirms diagnosis when clinical exam is equivocal; ultrasound is an alternative showing tendon discontinuity with a hypoechoic gap
Management
Surgical repair preferred in young, active patients; nonoperative management (functional bracing with progressive rehabilitation) for older, sedentary patients or those with surgical contraindications; early mobilization regardless of approach
01Pathophysiology
The Achilles tendon is the strongest and thickest tendon in the body, formed by the convergence of the gastrocnemius and soleus muscles. It inserts onto the posterior surface of the calcaneus and functions as the primary plantarflexor of the ankle. Despite its strength, the tendon is vulnerable because of its relatively poor blood supply, particularly in the zone 2 to 6 cm proximal to the calcaneal insertion. This region is called the watershed zone, and it is where the overwhelming majority of ruptures occur.
Rupture typically happens during eccentric loading, meaning the muscle is contracting while simultaneously being stretched. The classic mechanism is a sudden, forceful dorsiflexion of the ankle while the calf muscles are contracting, such as pushing off to sprint, landing from a jump, or suddenly accelerating. The tendon fails because the force exceeds its tensile strength, especially when pre-existing degenerative changes (tendinosis) have weakened the collagen matrix.
Fluoroquinolone antibiotics (ciprofloxacin, levofloxacin) are a high-yield risk factor because they directly impair tenocyte metabolism and promote collagen degradation through matrix metalloproteinase activation. This weakens the tendon structurally. The risk is compounded when fluoroquinolones are combined with corticosteroids, which independently inhibit collagen synthesis and reduce the tendon's ability to repair micro-damage. These two drug classes together are the most commonly tested pharmacologic risk factors.
The reason the patient feels a sudden "pop" or "snap" and describes being "kicked in the calf" is because the acute mechanical failure of the tendon generates a sudden release of stored elastic energy. The palpable gap on exam corresponds to the physical separation of the torn tendon ends, and the inability to plantarflex occurs because the gastrocnemius-soleus complex can no longer transmit force to the foot through the ruptured tendon.
It is important to understand that some residual weak plantarflexion may still be present due to the plantaris, tibialis posterior, peroneal muscles, and toe flexors, which can partially compensate. This is why a patient with a complete rupture may still weakly plantarflex the ankle in a non-weight-bearing position, which can mislead clinicians into missing the diagnosis. The Thompson test eliminates this confusion by testing the integrity of the gastrocnemius-soleus-Achilles unit directly.
02Classification and Clinical Manifestation
CLASSIFICATION | DESCRIPTION | CLINICAL FEATURES |
|---|---|---|
Acute rupture | Complete disruption of tendon fibers occurring within 4-6 weeks of injury | Sudden onset posterior ankle/calf pain, audible pop, palpable gap, positive Thompson test, inability to perform single-leg heel rise |
Chronic rupture | Rupture presenting beyond 4-6 weeks, often with retraction and scarring | Persistent weakness in plantarflexion, difficulty with stairs and push-off, tendon gap may be obscured by fibrosis and scar tissue, calf atrophy on the affected side |
Partial rupture | Incomplete disruption of tendon fibers | Pain and swelling at the Achilles region, preserved but weakened plantarflexion, Thompson test may be equivocal or negative, diagnosis often requires imaging |
Insertional rupture | Rupture at or near the calcaneal attachment | Pain localized directly at the heel, associated with Haglund deformity or retrocalcaneal bursitis, may involve avulsion of the calcaneal bone fragment |
PHYSICAL EXAM FINDING | DESCRIPTION | INTERPRETATION |
|---|---|---|
Thompson test (Simmonds test) | With the patient prone and feet hanging off the edge of the table, squeeze the calf | Absent plantarflexion = positive test = ruptured tendon |
Palpable gap | Palpate along the tendon 2-6 cm above the calcaneus | A defect or "sulcus" indicates complete disruption |
Increased passive dorsiflexion | Compare resting ankle position bilaterally | Affected side rests in more dorsiflexion due to loss of tendon tension |
Decreased resting tension (Matles test) | With patient prone, flex both knees to 90 degrees | Affected ankle falls into more dorsiflexion compared to the uninjured side |
Single-leg heel rise | Ask patient to rise onto tiptoes on the affected foot | Inability to perform = loss of functional plantarflexion |
03Diagnostic Workup
TEST | ROLE | KEY FINDINGS |
|---|---|---|
Clinical examination (Thompson test) | Best initial test | Positive Thompson test (no plantarflexion with calf squeeze) is highly sensitive and often sufficient for diagnosis |
Ultrasound | Confirmatory when exam is equivocal; operator-dependent | Hypoechoic gap at the rupture site, loss of normal fibrillar tendon pattern, tendon discontinuity with retraction |
MRI | Most accurate test / Gold standard | Complete disruption of tendon signal, retraction of tendon stumps, surrounding edema; best for evaluating partial tears and chronic ruptures |
Lateral ankle X-ray | Adjunctive | Kager triangle blurring (loss of the normal pre-Achilles fat pad radiolucency), calcaneal avulsion fragment if insertional rupture |
The diagnosis of an acute Achilles tendon rupture is primarily clinical. A well-performed physical examination, centered on the Thompson test, is sufficient to diagnose a complete rupture in most cases. The Thompson test has a sensitivity exceeding 95% for complete ruptures when performed correctly. The combination of a positive Thompson test, a palpable gap, and an appropriate mechanism of injury is considered diagnostic, and imaging is not always necessary before proceeding with treatment.
Ultrasound is the preferred initial imaging modality when the clinical picture is unclear. It is fast, inexpensive, and readily available. It can dynamically assess the tendon during dorsiflexion and plantarflexion, showing real-time tendon discontinuity. The limitation is that it is operator-dependent and may miss partial tears.
MRI is reserved for cases where the diagnosis remains uncertain after clinical exam and ultrasound, or when surgical planning requires detailed assessment of the gap size, degree of retraction, and quality of the remaining tendon tissue. MRI is particularly valuable for partial ruptures and chronic ruptures where scar tissue obscures the clinical exam. On MRI, a complete rupture shows discontinuity of the low-signal tendon on T1-weighted images with surrounding high-signal edema on T2-weighted/STIR sequences.
A lateral ankle radiograph is not diagnostic for soft tissue rupture but may reveal indirect signs. The Kager triangle, the fat-filled space anterior to the Achilles tendon, loses its normal radiolucency and appears blurred when there is hemorrhage and edema from a rupture. An avulsion fracture fragment at the calcaneal insertion points toward an insertional rupture variant.
04Management and Treatment
APPROACH | INDICATION | PROTOCOL |
|---|---|---|
Surgical repair (open) | Young, active patients; athletes; those desiring return to high-level activity | Primary end-to-end repair; postoperative functional bracing with early controlled mobilization |
Surgical repair (percutaneous/minimally invasive) | Alternative to open repair; lower wound complication rate | Tendon reapproximation through small incisions; reduced surgical site infection risk |
Nonoperative (functional rehabilitation) | Older, sedentary patients; patients with surgical contraindications (peripheral vascular disease, diabetes with poor wound healing, immunosuppression) | Initial equinus casting or functional boot (ankle in 20 degrees plantarflexion) for 2 weeks, followed by progressive dorsiflexion adjustments over 6-8 weeks with early weight-bearing |
Chronic rupture repair | Presentation beyond 4-6 weeks with retracted tendon ends | May require tendon reconstruction with V-Y advancement, turndown flap, or flexor hallucis longus (FHL) tendon transfer |
Acute stabilization begins at the time of injury. The ankle should be immobilized in a position of gravity equinus (slight plantarflexion) to approximate the torn tendon ends and reduce the gap. A posterior splint or controlled ankle motion (CAM) boot set in plantarflexion is applied. Weight-bearing is initially restricted, and crutches are provided.
The decision between operative and nonoperative management is one of the most tested concepts. Current evidence shows that both approaches yield similar long-term functional outcomes when nonoperative treatment is paired with an accelerated functional rehabilitation protocol emphasizing early controlled mobilization and progressive weight-bearing. The key distinction is that surgical repair is associated with a lower re-rupture rate (approximately 2-5% surgical vs. 5-15% nonoperative in older protocols), while nonoperative treatment avoids surgical complications such as wound infection, sural nerve injury, and deep vein thrombosis.
For surgical repair, the standard technique involves a posteromedial longitudinal incision, debridement of the torn tendon ends, and primary end-to-end repair using a modified Kessler or Krackow suture technique with nonabsorbable suture. Augmentation with the plantaris tendon or periosteal flap may be added. Postoperatively, the patient is placed in a functional brace at 20 degrees of plantarflexion, and controlled motion is initiated within the first 2 weeks.
For nonoperative management, a structured protocol is followed:
Weeks 0-2: Equinus casting or boot locked at 20 degrees plantarflexion; non-weight-bearing.
Weeks 2-4: Boot adjusted to 10 degrees plantarflexion; partial weight-bearing begins.
Weeks 4-6: Boot adjusted to neutral; progressive weight-bearing as tolerated.
Weeks 6-8: Boot weaned; transition to supportive shoe with a heel lift (1-2 cm).
Weeks 8-12 and beyond: Progressive strengthening, calf raises, proprioceptive training, return to sport at 4-6 months.
Contraindications to surgery include peripheral vascular disease, uncontrolled diabetes, active skin infection over the operative site, and significant immunosuppression. For these patients, nonoperative management is mandatory.
For chronic ruptures (beyond 4-6 weeks), the tendon ends have retracted and the gap is often too large for primary repair. Reconstruction options include V-Y advancement of the aponeurosis, a gastrocnemius turndown flap, or a flexor hallucis longus (FHL) tendon transfer. FHL transfer is commonly tested because the FHL tendon lies in close anatomic proximity to the Achilles and provides a functional motor for plantarflexion.
Venous thromboembolism prophylaxis should be considered during the period of immobilization, particularly for patients with additional risk factors such as obesity, prior DVT, or prolonged non-weight-bearing status.
05Differential Diagnosis and Distractors
DIFFERENTIAL | WHY IT IS SIMILAR | KEY DISCRIMINATOR |
|---|---|---|
Achilles tendinopathy (tendinosis) | Posterior ankle/calf pain, tenderness along the Achilles tendon | Gradual onset with activity-related pain (not sudden), no palpable gap, negative Thompson test, no acute loss of plantarflexion; tendon is thickened but intact |
Plantaris tendon rupture | Sudden calf pain during athletic activity, may feel a "pop" | Pain is more medial, full plantarflexion strength preserved, negative Thompson test, no palpable Achilles gap; ultrasound shows intact Achilles with plantaris fluid collection |
Gastrocnemius (medial head) tear ("tennis leg") | Sudden calf pain during push-off or lunging, ecchymosis | Pain and swelling are proximal in the mid-calf at the musculotendinous junction, Thompson test is negative, Achilles tendon is intact on palpation; MRI shows intramuscular hematoma |
Deep vein thrombosis (DVT) | Calf pain, swelling, tenderness | No acute traumatic mechanism, no palpable gap, Homans sign may be present (though unreliable), diffuse calf edema; diagnosed with compression ultrasound showing non-compressible vein |
Retrocalcaneal bursitis | Posterior heel pain, pain with walking | Pain is localized at the calcaneal insertion, no gap, negative Thompson test, associated with Haglund deformity; no sudden event; pain with direct compression of the bursa |
Calcaneal stress fracture | Posterior heel pain with activity | Insidious onset, positive calcaneal squeeze test (medial-lateral compression), negative Thompson test, no palpable gap; MRI shows bone marrow edema in the calcaneus |
06Traps and High-Yield Pearls
The most common trap with Achilles tendon rupture questions is missing the diagnosis because the patient can still weakly plantarflex the ankle. Students often rule out a complete rupture when they read that the patient "can move the foot down slightly." This is the distractor. Accessory plantarflexors (plantaris, tibialis posterior, peroneal muscles, toe flexors) can produce weak motion at the ankle even with a completely ruptured Achilles. The vignette is testing whether you know that the Thompson test, not voluntary plantarflexion, is the definitive bedside test for Achilles tendon integrity.
The second major trap involves the fluoroquinolone association. A vignette may present a middle-aged patient on ciprofloxacin for a urinary tract infection who suddenly develops calf pain during mild activity. The question may frame the scenario subtly, burying the antibiotic history in the medication list. The tested competency is recognizing fluoroquinolone-induced tendon damage as a cause of Achilles rupture, even without a high-energy mechanism.
Another tested concept is the operative vs. nonoperative decision. Questions may present a 70-year-old sedentary patient with diabetes and ask for the next best step. The answer is nonoperative functional rehabilitation, not surgery. Conversely, a 28-year-old competitive athlete will typically be managed surgically to minimize re-rupture risk and optimize return to sport.
Finally, be aware that chronic or missed ruptures are tested differently from acute ones. If the vignette describes a patient presenting weeks after the initial injury with persistent weakness and calf atrophy, the question is likely driving toward advanced reconstruction (FHL tendon transfer), not simple primary repair.