Ruptur Tendon Achilles

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

03Diagnostic Workup

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

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

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.