Author: Shreya Desai, et al.
Cureus, March 2026
Pectoral nerve blocks are commonly used to provide analgesia for breast and anterior chest-wall surgery. Although PECS I and II blocks are generally considered superficial and relatively safe, local anesthetic may occasionally spread beyond the intended fascial planes and affect portions of the brachial plexus.
This case describes transient motor weakness and sensory loss consistent with an unintended medial cord block following bilateral PECS I and II blocks for augmentation mammoplasty.
Case presentation
A healthy 35-year-old woman underwent bilateral augmentation mammoplasty under general anesthesia with endotracheal intubation.
The operation was performed using a subpectoral, or submuscular, surgical approach and was completed without apparent complications.
At the conclusion of surgery, ultrasound-guided bilateral PECS I and II blocks were performed for postoperative analgesia.
The PECS II injection was performed first, followed by withdrawal of the needle into the more superficial PECS I plane.
Local anesthetic technique
The clinicians prepared a mixture containing:
• 20 mL of 1.3% liposomal bupivacaine
• 20 mL of 0.25% standard bupivacaine
• 20 mL of normal saline
For each side, 15 mL was injected between the pectoralis major and minor muscles for the PECS I block, and an additional 15 mL was injected between the pectoralis minor and serratus anterior muscles for the PECS II block.
The patient initially experienced satisfactory analgesia in the expected chest-wall distribution.
Development of neurologic symptoms
Approximately one hour after block administration, the patient developed new paresthesia and weakness involving the right upper extremity.
Motor examination showed:
• Reduced grip strength
• Weakness of finger abduction and adduction
• Reduced thumb opposition
• Mildly reduced wrist flexion
• Preserved wrist extension
• Preserved elbow flexion and extension
Sensory loss involved:
• The fifth finger
• The medial half of the fourth finger
• The medial forearm
The distribution extended beyond the territory of a single peripheral nerve and was most consistent with involvement of the medial cord of the brachial plexus, primarily affecting the C8-T1 nerve roots.
Reflexes remained intact, and the patient had no evidence of Horner syndrome.
Focused ultrasound examination showed no hematoma, mass, or other compressive lesion.
Management and outcome
The patient was treated conservatively.
An arm sling was provided to protect the weakened extremity, and the patient was counseled that the symptoms were most likely caused by unintended spread of local anesthetic toward the medial cord of the brachial plexus.
She was discharged with instructions for close monitoring and received daily virtual follow-up.
Her neurologic symptoms gradually improved and completely resolved by postoperative day six.
She reported satisfactory surgical-site analgesia and experienced no permanent neurologic deficit.
Relevant anatomy
The PECS I block deposits local anesthetic between the pectoralis major and pectoralis minor muscles.
This interpectoral plane contains the medial and lateral pectoral nerves.
The PECS II block is performed deeper, between the pectoralis minor and serratus anterior muscles, and is intended to anesthetize the lateral branches of the T2-T6 intercostal nerves and provide analgesia to the lateral chest wall.
The interpectoral and deeper pectoral fascial planes communicate with the clavipectoral and axillary fascia.
Because the medial and lateral pectoral nerves originate from the brachial plexus, local anesthetic may potentially track proximally along these nerves or fascial pathways toward the cords of the plexus.
The medial pectoral nerve originates primarily from C8-T1 fibers and is closely associated with the medial cord.
This anatomical relationship provides a plausible pathway for the neurologic pattern observed in this patient.
Role of surgical fascial disruption
In intact anatomy, local anesthetic placed within the PECS fascial planes generally remains confined to the intended compartments.
However, this patient’s blocks were performed after completion of subpectoral breast surgery.
The surgical dissection may have disrupted the normal pectoral fascial barriers that ordinarily limit the spread of local anesthetic.
The authors proposed that postoperative injection into surgically altered tissue allowed the local anesthetic to travel farther toward the axilla and infraclavicular brachial plexus.
The timing of the block may therefore have contributed to the complication.
Injectate volume
The patient received 15 mL in each fascial plane on each side.
The authors noted that approximately 10 mL per plane is often sufficient to produce the desired block in intact anatomy.
The larger volume used in this case may have increased pressure within the disrupted fascial planes and promoted proximal spread toward the medial cord.
Injection pressure may also have contributed to transient neuropraxia, potentially explaining why the neurologic symptoms lasted longer than the expected clinical duration of standard local anesthetic alone.
Alternative explanations
Other causes of postoperative upper-extremity weakness were considered.
Positioning-related neuropathy
Perioperative positioning can cause brachial plexus or ulnar nerve injuries, particularly with excessive arm abduction, external rotation, traction, or compression.
However, positioning injuries often appear immediately after surgery and may take considerably longer to resolve.
The delayed onset, broad C8-T1 distribution, and complete recovery within six days were less typical of an isolated positioning injury.
Postoperative hematoma
A hematoma or compressive lesion could produce progressive neurologic deficits.
However, the patient had no swelling, mass effect, progressive pain, or ultrasound evidence of a compressive collection.
Direct surgical nerve injury
A structural nerve injury would generally be expected to cause more persistent symptoms.
The patient’s complete recovery supported a temporary conduction block rather than permanent nerve damage.
Local anesthetic systemic toxicity
Local anesthetic systemic toxicity typically produces systemic neurologic or cardiovascular manifestations, including altered mental status, seizures, arrhythmias, or hemodynamic instability.
The patient developed only a localized neurologic deficit and had no signs of systemic toxicity.
Intraneural injection
An intraneural injection would be more likely to produce a focal and potentially prolonged deficit.
The patchy distribution and eventual full recovery were considered more consistent with proximal local anesthetic spread.
Clinical implications
Although PECS I and II blocks have a favorable safety record, clinicians should recognize that brachial plexus involvement is possible.
Important preventive considerations include:
• Understanding the continuity between the pectoral, clavipectoral, axillary, and infraclavicular fascial planes
• Considering whether surgical dissection has altered normal fascial anatomy
• Using the lowest effective injectate volume
• Carefully observing the spread of local anesthetic under ultrasound
• Avoiding excessive injection pressure
• Reassessing the patient promptly when postoperative arm weakness or sensory loss develops
• Excluding hematoma, surgical injury, positioning injury, and local anesthetic systemic toxicity
Blocks performed after subpectoral surgical dissection may behave differently from blocks performed before surgery because the fascial compartments may no longer restrict local anesthetic spread normally.
Technical optimization
The authors suggest that smaller volumes may reduce the risk of proximal spread, particularly when PECS blocks are performed after surgical disruption of the pectoral planes.
Clinicians may also consider performing the blocks before surgical dissection when clinically appropriate, although the ideal timing and volume require further investigation.
Ultrasound visualization confirms initial needle placement and fascial separation but cannot guarantee that local anesthetic will remain within the intended compartment after injection.
Postoperative neurologic monitoring remains important even when the block appears technically successful.
Important limitations
This was a single case report, and the exact cause of the neurologic deficit could not be proven.
Although the clinical pattern supported unintended medial cord blockade, electrodiagnostic testing was not reported.
Several factors may have contributed simultaneously, including:
• Surgical disruption of the pectoral fascia
• High injectate volume
• Proximal local anesthetic spread
• Injection pressure
• Surgical positioning
Because the symptoms resolved without intervention, it was not possible to determine the precise anatomical route of spread.
Bottom line
PECS I and II blocks can rarely produce unintended brachial plexus involvement.
In this patient, postoperative injection of 15 mL into each PECS plane following subpectoral surgical dissection was followed by transient C8-T1 motor and sensory deficits consistent with medial cord involvement.
The symptoms resolved completely within six days with conservative management.
Clinicians should use meticulous ultrasound-guided technique, select conservative injectate volumes, consider the effect of surgical disruption on fascial anatomy, and promptly evaluate any postoperative upper-extremity neurologic symptoms.
Thank you to Cureus for allowing us to summarize this article.