Regional Anesthesia and Pain Management Flashcards

A 58-year-old patient undergoing total knee arthroplasty receives an adductor canal block. Postoperatively, he reports adequate analgesia but has significant weakness when attempting to flex his hip against resistance. Which anatomical structure was most likely inadvertently blocked?

Answer: Obturator nerve — posterior division

The obturator nerve's posterior division travels through the adductor magnus and provides motor innervation to the adductor magnus (hip adduction/flexion). When local anaesthetic spreads proximally or posteriorly from an adductor canal injection, it can reach the posterior division of the obturator nerve, causing unexpected hip flexor/adductor weakness. The saphenous nerve within the adductor canal is sensory only; the nerve to vastus medialis causes quadriceps weakness, not hip flexion weakness; and the LFCN is purely sensory.

During a continuous erector spinae plane (ESP) block for thoracic surgery analgesia, you notice the patient develops a T4–T8 dermatomal sensory block but reports pain in the ipsilateral shoulder and anterior chest wall. Which mechanism best explains this analgesic gap?

Answer: Sparing of the lateral cutaneous branches of intercostal nerves T2–T4

The ESP block acts primarily on dorsal and ventral rami via paravertebral spread. However, the lateral cutaneous branches of the upper intercostal nerves (T2–T4) pierce the serratus anterior and supply the anterior and lateral chest wall including pectoral and axillary regions. These branches can be spared if spread is insufficient anteriorly. Phrenic nerve involvement does not explain anterior chest wall pain, and rami communicantes carry visceral afferents, not somatic shoulder/chest pain. The dorsal rami supply the posterior thorax only.

A patient with chronic refractory CRPS type I of the left upper limb is being considered for spinal cord stimulation (SCS). Pre-implant psychological evaluation is normal. Imaging shows the most painful area corresponds to C6–C7 dermatomes. At which vertebral level should the SCS lead tip ideally be positioned to achieve optimal paresthesia coverage?

Answer: C5–C6

For SCS targeting upper limb dermatomes, the lead tip must be positioned rostrally to the target dermatomes because the electrical field stimulates dorsal column fibres travelling cranially. To cover C6–C7 dermatomes, the lead tip is typically placed at C5–C6, as the paresthesias map to approximately 1–2 segments below the electrode position. Positioning at C3–C4 would map coverage too cranially (shoulder/neck), T1–T2 would be too caudal for reliable C6–C7 coverage, and C7–T1 would undershoot the target.

In a patient receiving a high-volume interscalene brachial plexus block with 30 mL of ropivacaine 0.5%, which of the following is the MOST likely serious early complication due to direct anatomical spread rather than systemic toxicity?

Answer: Phrenic nerve palsy causing ipsilateral hemidiaphragm elevation

Phrenic nerve palsy occurs in virtually 100% of interscalene blocks due to the proximity of the phrenic nerve (C3–C5) to the brachial plexus at this level; high volumes reliably spread to the C3–C5 nerve roots. This results in ipsilateral hemidiaphragm paresis, which is generally tolerated in healthy patients but can be life-threatening in those with significant contralateral lung disease. Horner's syndrome (stellate ganglion spread) and hoarseness (recurrent laryngeal nerve) also occur but less consistently and are not as clinically critical. Contralateral hemidiaphragm paresis does not occur via direct spread.

A 70 kg patient undergoing paravertebral block placement for mastectomy receives multiple injections at T1–T5, each with 4 mL of bupivacaine 0.5% with adrenaline 1:200,000. Twenty minutes post-injection she develops palpitations, a blood pressure of 160/100 mmHg, and a heart rate of 115 bpm. The MOST likely explanation for this haemodynamic pattern is:

Answer: Inadvertent intravascular injection of adrenaline via an intercostal vessel

The paravertebral space is highly vascular, containing the intercostal vessels. Even with aspiration, small intravascular injections of adrenaline can go undetected. The haemodynamic profile — hypertension, tachycardia, and palpitations — is the classic signature of IV adrenaline: beta-1 stimulation increases heart rate and contractility, while alpha stimulation raises blood pressure. Bupivacaine toxicity typically causes CNS symptoms (tinnitus, perioral numbness) before haemodynamic collapse and does not cause hypertension. Sympathetic blockade causes hypotension, not hypertension. Pneumothorax causes hypotension and desaturation.

A patient with postherpetic neuralgia (PHN) affecting the right V1 trigeminal dermatome has failed gabapentin, amitriptyline, and topical lidocaine patches at maximum doses. The next most evidence-supported interventional option, according to current guidelines, is:

Answer: High-concentration capsaicin 8% patch applied to the affected area

High-concentration capsaicin 8% (Qutenza) patch has Level A evidence (strong) for PHN across multiple RCTs and meta-analyses, including facial PHN when applied carefully to the V1 distribution avoiding mucous membranes. It desensitises TRPV1 receptors in cutaneous nociceptors, providing months of pain relief after a single 30–60 minute application. Radiofrequency ablation of the trigeminal/Gasserian ganglion carries significant risks (anaesthesia dolorosa, corneal anaesthesia) and is reserved for refractory trigeminal neuralgia, not PHN. Stellate ganglion block has no consistent evidence for PHN. Pulsed RF of peripheral branches lacks robust RCT data for PHN.