A Novel Treatment for Acute Complex Regional Pain Syndrome
Complex regional pain syndrome (CRPS) has been called by many names. First coined during the American Civil War by Silas Weir Mitchell, “causalgia” was used to describe the vasomotor and sudomotor symptoms that resulted from nervous injuries.1 It was later hypothesized that the symptomatology resulted from local overstimulation and activation of the sympathetic nervous system, hence the name “reflex sympathetic dystrophy.” More recently, the International Association for the Study of Pain developed the umbrella term complex regional pain syndrome.2 What were formerly known as “reflex sympathetic dystrophy” and “causalgia” are now referred to as CRPS type I and type II, respectively.
The constellation of symptoms that accompany both syndromes is identical; they differ only in the mechanism of the inciting event. CRPS type I (CRPS-I) is initiated by an event associated with no evidence of neurovascular injury, such as a soft-tissue injury or immobilization, whereas CRPS type II (CRPS-II) is associated with documented nerve injury, such as from a gunshot wound.3,4 The main clinical manifestation is pain that is disproportionate to the inciting event that can be debilitating and allodynic.
This report outlines an interesting case of how an adolescent male was cured of CRPS-I using a novel and promising technique.
History and Physical Exam
DP is a 16-year-old white male who presented to the emergency room (ER) with a chief complaint of right leg pain. Upon arrival, the patient stated that he had been playing basketball the day before the onset of symptoms and had experienced a relatively minor fall. There was no significant injury evident from the fall, but the following morning, he had significant pain just below the right prepatellar area, extending down to his ankle and toes.
He described the pain as burning, measuring 10 out of 10 on the visual analog scale, and he did not gain relief with over-the-counter ibuprofen (800 mg twice a day), taken prior to presentation. DP could not bear any weight on his foot or leg and could barely move his toes due to the pain. At this point, the attending physicians ordered tibia/fibula anterior-posterior and lateral radiographs and magnetic resonance imaging (MRI) of his right lower extremity. No acute findings were seen, and his neurovascular bundle was determined to be intact (Figure 1).
He was given a one-time 60 mg dose of oral methylprednisolone as well as hydrocodone/acetaminophen (7.5 mg/325 mg every 4 to 6 hours as needed) for pain and was discharged with a diagnosis of “shin splints.”
On post-injury day 4, the patient’s mother stated that she could feel no pulse in the affected leg, prompting her to have the leg evaluated by a vascular surgeon.
Physical Exam (Day 4)
The vascular surgeon found DP in bed, holding his leg and knee in a semiflexed position and refusing to move his leg. The surgeon performed a physical examination of DP’s right lower extremity, which was cold and diaphoretic, and had a purplish discoloration from the mid-foreleg to the ankle and toes. The shin area and the area of the right lower extremity supplied by the sensory reception of the saphenous nerve was allodynic. He had palpable posterior tibial pulses and monophasic signal by Doppler on the dorsalis pedis artery. Table 1 reviews the patient’s vital signs.
Hyperhidrosis, allodynia, and local vasoconstriction causing a cold limb are classic findings of CRPS due to the hyperstimulation of the sympathetic nervous system.5 With no other physical exam findings better explaining DP’s symptoms, the vascular surgeon diagnosed CRPS-I and referred him to a pain specialist (Table 2).6
Because of the rarity of the condition and acuity of onset, the patient’s mother sought the second opinion of a pediatric surgeon, who found no evidence of connective tissue disorders or immune causes of vasospasm, such as antiphospholipid syndrome, and concurred with the diagnosis.
After determining that DP had no vascular compromise, the specialists referred the patient to an interventional pain specialist who recommended a lumbar sympathetic block. Because the pain was consistent with the dermatomal distribution of the saphenous nerve, the decision was made to continuously block the nerve using a pain ball to decrease the patient’s symptoms. The postganglionic sympathetic efferent nerves also would be anesthetized during the procedure, leading to a decrease in sympathetic tone and vasodilation.
The procedure took place on the 6th day after the patient’s injury. The treatment plan was to have the patient receive an ultrasound-guided continuous adductor canal block to selectively block the saphenous nerve as well as an ultrasound-guided popliteal nerve block (PNB). After informed consent was obtained from both the mother and the patient, intravenous (IV) access was obtained in the patient’s left upper extremity (Figures 2-4).
The procedure was performed with the patient in the supine position, with the right lower extremity slightly flexed and externally rotated to optimize positioning for placing the PNB. The middle third of the patient’s thigh was prepped and draped, and the skin was infiltrated with 2% lidocaine. A 22-gauge, 4-inch ON-Q QuikBloc Over-the-Needle Catheter Set was used for the adductor canal block. The QuikBloc needle was then advanced under ultrasound-guidance inferior to the sartorious muscle and lateral to the neurovascular bundle located in the canal. A 25 mL volume of a 0.2% ropivacaine solution was injected under direct vision. Once the injectate had adequately hydrodissected the fascial plane, the needle was removed, leaving the catheter in place superior to the neurovascular bundle.
The patient was then turned to the left-lateral position for placement of the ultrasound-guided PNB. The area was prepped and skin of the lateral thigh was infiltrated with 2% lidocaine. Under ultrasound-guidance, a 22-gauge Echobright, an echogenic needle, was advanced posterior to the sciatic/popliteal nerve. Local anesthetic (a total volume of 25 mL, including 0.2% ropivacaine and 10 mg of dexamethasone) was deposited superiorly and inferiorly to the nerve. The needle was withdrawn and a bandage was placed over the site of injection.
The patient’s infusion catheter was then connected to an ON-Q continuous infusion device (pain ball) filled with 550 mL of 0.2% ropivacaine. It was set to run continuously at 10 mL per hour.
The patient’s pain pre-procedure was measured at 10 out of 10. Within 15 minutes of receiving the nerve block, he was pain free in the recovery area.