A 68-year-old woman with a history of left-sided breast cancer (treated 5 years ago) now presents with progressive hoarseness and a weak, breathy voice. On laryngoscopy, the left vocal cord is seen in a paramedian position with poor abduction. Additionally, the examiner notes that the left vocal cord appears shorter and sits at a slightly higher level compared to the right. Which nerve is injured, and what is the anatomical explanation for the cord appearing shorter?

Explanation

## Diagnosis: Recurrent Laryngeal Nerve (RLN) Injury ### Clinical Presentation Analysis The patient presents with: - **Progressive hoarseness and weak, breathy voice** — hallmark of vocal cord paralysis - **Left vocal cord in paramedian position with poor abduction** — classic RLN palsy finding - **Cord appears shorter and sits at a slightly higher level** — due to thyroarytenoid muscle paralysis - **History of left breast cancer** — metastatic or treatment-related injury to the left RLN (which loops around the aortic arch on the left side, making it vulnerable to mediastinal/neck pathology) **Key Point:** The combination of **paramedian cord position + poor abduction** is the textbook hallmark of **recurrent laryngeal nerve (RLN) injury**, NOT superior laryngeal nerve (external branch) injury. ### Anatomical Basis: RLN Innervation and Cord Shortening **High-Yield:** The RLN innervates ALL intrinsic laryngeal muscles EXCEPT the cricothyroid. This includes: | Muscle | Innervation | Action | Effect of RLN Paralysis | | --- | --- | --- | --- | | **Posterior cricoarytenoid** | RLN | Abducts vocal cord | Cord cannot abduct → paramedian position | | **Thyroarytenoid** | RLN | Shortens and thickens cord | Cord becomes flaccid, appears **shorter and higher** | | **Lateral cricoarytenoid** | RLN | Adducts vocal cord | Loss of active adduction | | **Interarytenoids** | RLN (bilateral) | Adducts arytenoids | Incomplete glottic closure | **Clinical Pearl:** The **thyroarytenoid muscle** (vocalis) forms the bulk of the vocal cord. When paralyzed by RLN injury, it becomes flaccid and atrophic over time, causing the cord to: 1. Appear **shorter** (loss of muscle bulk and tone) 2. Sit at a **slightly higher level** (loss of downward muscular pull) 3. Remain in a **paramedian position** (unopposed by abductor function) ### Why NOT SLN External Branch Injury? The external branch of the SLN innervates only the **cricothyroid muscle**, which lengthens and tenses the cord. Isolated SLN external branch injury causes: - Loss of pitch control (inability to raise pitch) - Cord in **lateral or paramedian-lateral** position - **Preserved abduction** (posterior cricoarytenoid intact) - Voice fatigue, not true paralysis The stem explicitly states **"poor abduction"** — this is impossible with isolated SLN external branch injury, as abduction is controlled by the posterior cricoarytenoid (RLN-innervated). This finding definitively points to **RLN injury**. ### Clinical Context: Breast Cancer History The left RLN is particularly vulnerable because it loops around the **aortic arch** before ascending to the larynx. Left-sided breast cancer can cause RLN palsy via: - Mediastinal lymph node metastases compressing the nerve - Radiation-induced fibrosis in the neck/mediastinum - Surgical injury during axillary/neck dissection **Warning:** Do NOT confuse the cord appearing "shorter" as exclusive to SLN injury. Thyroarytenoid paralysis (RLN) also causes cord shortening and elevation due to loss of muscle bulk and tone. [cite: Gray's Anatomy 42e Ch 32; Standring S. Gray's Anatomy, 41e; KD Tripathi Essentials of Medical Pharmacology; Last's Anatomy 12e]