A 38-year-old woman from Mumbai undergoes elective total hip arthroplasty for severe osteoarthritis. On postoperative day 2, she develops foot drop on the operated side with inability to dorsiflex the ankle and loss of sensation over the dorsum of the foot and lateral leg. Strength in hip extension and knee flexion is preserved. What is the most appropriate next step in management?

Explanation

## Peroneal Nerve Injury Post Hip Arthroplasty ### Clinical Recognition The patient has a **common peroneal nerve (CPN) injury**, evidenced by: - Foot drop (loss of ankle dorsiflexion) - Loss of sensation over dorsum of foot and lateral leg - **Preserved hip extension and knee flexion** (tibial nerve intact) The common peroneal nerve is the **most commonly injured nerve during hip arthroplasty**, accounting for ~60% of iatrogenic lower limb nerve injuries in this setting. ### Mechanism of Injury in Hip Arthroplasty **Key Point:** The common peroneal nerve is vulnerable because it: - Branches from the sciatic nerve at the proximal thigh - Winds around the fibular neck (superficial location) - Can be stretched by hip flexion/adduction during retraction - May be compressed by hematoma, swelling, or tight closure ### Why Conservative Management First? **High-Yield:** The vast majority of postoperative CPN injuries after total hip arthroplasty are **neurapraxia** — a physiological conduction block without axonal disruption — caused by traction, positioning, or mild compression. These injuries have an excellent prognosis for spontaneous recovery over 3–6 months. | Presentation | Likely Cause | Next Step | |---|---|---| | **Immediate (intraop), complete loss** | Direct trauma, transection | Urgent exploration | | **Delayed (24–72 hrs), partial/complete** | Neurapraxia, mild hematoma | **Observation + AFO + serial exam** | | **Progressive worsening >48 hrs** | Expanding hematoma | MRI + surgical consideration | | **No recovery at 3–6 weeks** | Axonotmesis/neurotmesis | EMG + neurosurgery consult | This patient has **delayed onset (postop day 2)** with a stable, non-progressive deficit — the classic presentation of compressive neurapraxia. There is no indication of an expanding hematoma (which would present with worsening deficits, increasing pain, or wound swelling). ### Management Algorithm **Step 1:** Assess for red flags requiring urgent intervention: - Rapidly progressive neurological deficit → suggests expanding hematoma → MRI + surgical evacuation - Intraoperative complete nerve transection → immediate exploration **Step 2:** In the absence of red flags (as in this patient): - Apply **ankle-foot orthosis (AFO)** to prevent equinus contracture and facilitate ambulation - **Serial clinical examination** at 2-week intervals to monitor for recovery or progression - EMG/NCS at 3–6 weeks if no improvement (to characterize injury severity) - Physiotherapy and foot drop management **Clinical Pearl:** Immediate return to OR (Option A) is not indicated without evidence of a surgically correctable lesion (e.g., confirmed hematoma on imaging). MRI (Option C) is reserved for cases with progressive deficits or failure to improve, not as the first step in a stable postoperative neurapraxia. High-dose IV methylprednisolone (Option B) has no evidence base in acute compressive peripheral neuropathy and is not recommended in modern practice (per Campbell's Operative Orthopaedics and AAOS guidelines). **Mnemonic — CPN Injury Features (FOOT DROP):** - **F**oot drop (ankle dorsiflexion loss) - **O**ver dorsum sensation loss - **O**uter leg sensory loss - **T**ibial nerve spared (hip/knee function preserved) - **D**elayed presentation (post-op neurapraxia) - **R**ecovers spontaneously in most cases - **O**bservation + AFO is first-line - **P**eroneal nerve at fibular neck (vulnerable site) ### Why Not Immediate Surgery or MRI? - **Option A (Immediate OR):** No evidence of transection or expanding hematoma; unnecessary re-exploration increases morbidity - **Option B (IV methylprednisolone):** No RCT evidence supports steroids for acute compressive peripheral neuropathy post-arthroplasty; risk of wound complications, infection - **Option C (MRI + neurosurgery):** Appropriate if deficits are progressive or worsening, but not as the initial step in a stable, delayed-onset deficit **High-Yield (per Campbell's Operative Orthopaedics & Harrison's Principles):** Most CPN injuries after hip arthroplasty are neurapraxia with spontaneous recovery. Initial management is **observation with AFO and serial neurological examination**. Imaging and surgical consultation are escalated only if deficits worsen or fail to improve.