Anterior interosseous nerve is a motor branch from median nerve. It innervates three muscles, the flexor pollicis longus, the flexor digitorum profundus, and the pronator quadratus muscles in the forearm. Anterior interosseous nerve syndrome refers to a neuropathy affecting this nerve, to develop weakness of innervated muscles. The etiology can be diverse and the pathophysiology is not clearly documented. We report a case of a 67-year-old male patient with diabetes, who presented symptoms of right thumb and index finger weakness, forearm pain, which was in conclusion diagnosed as anterior interosseous nerve syndrome through electrodiagnostic studies. His anterior interosseous nerve syndrome was revealed as due to fluid extravasation. Fluid extravasation can cause various side effects, and peripheral nerve injury is an uncommon side effect. This is a rare case of anterior interosseous nerve syndrome developed from fluid extravasation.
Anterior interosseous nerve (AIN) is a pure motor branch of the median nerve. AIN arises just below the elbow at the forearm level, and courses distally on the volar side of the interosseous membrane.
Extravasation injury is the damage of subcutaneous or perivascular tissues during intravenous infusion, caused by the efflux of solutions from a vessel into surrounding tissue spaces.
This case study represents a patient who developed AIN syndrome after intravenous fluid injection.
A 67-year-old male with past history of diabetes, visited the outpatient clinic with complaint of edema and pain of right forearm and weakness of right thumb. He could not flex his right thumb and the distal phalanx of right index finger. One week before the visit, he was carried to a local clinic due to hypoglycemic shock, and had intravenous dextrose fluid injection. After the fluid injection, he developed symptoms and signs of right forearm edema, erythema, heating sensation, and pain at the infusion site. On the physical examination, he still had pain on his forearm and edema without clear margin at the volar side of forearm below elbow. Neither heating sensation nor redness was observed, but general induration at the upper region of forearm could be palpated. He had weakness with motor grade 1 on Medical Research Council (MRC) scale in his interphalangeal flexor of right thumb and distal phalanx flexor of right index finger. Also, he could not make an “OK” sign with his right thumb and index finger.
Damage of anterior interosseous nerve was suspected, and nerve conduction studies (NCS) and needle electromyography (EMG) test were performed to confirm the AIN syndrome. NCS and EMG test was performed 15 days after the onset.
The sensory NCS revealed decreased amplitudes of sensory nerve action potentials in bilateral median and ulnar nerves, and the motor NCS revealed decreased conduction velocities in bilateral ulnar, peroneal and tibial nerves (
After confirming the diagnosis, physical therapy of stretching and strengthening exercise was done to recover strength and function. Also, physical modalities of ultrasound, hot pack and interferential current therapy were applied and oral nonsteroidal anti-inflammatory drug was prescribed for pain management. After one month of therapy, the symptoms of forearm edema and pain improved, and the patient showed improvement of muscle strength in interphalangeal joint flexor of thumb and distal phalanx flexor of index finger from MRC scale 1 to 2. He showed spontaneous recovery to some extent without surgical or aggressive interventions.
Peripheral nerve damage is not a common complication of extravasation injury. According to a retrospective analysis of 67 adult patients who developed intravenous catheters related complications, hand was a common site for minor and major complications.
Puhaindran, et al. introduced a case of AIN syndrome in a 42-year old male, after peripherally inserted central catheter insertion into a brachial vein for the administration of intravenous antibiotics.
Even though AIN is a pure motor nerve, and no sensory loss occurs, pain may be present in the forearm. Patients with AIN syndrome are unable to make an “OK” sign with thumb and index finger, due to paralysis of FPL and the radial FDP.
The AIN palsy comprises less than 1% of upper extremity nerve palsies.
Extravasation is not a known common cause for AIN palsy. All fluids can cause tissue damage, but certain substances may cause damage with greater risks. Soft tissue damage due to extravasation depends on the type of the agent, which can be classified as irritants or vesicants. For some known potential causes of severe tissue necrosis, there are parenteral alimentation fluids, antibiotics, calcium, potassium, and sodium bicarbonate solutions.
There are some identified risk factors for extravasations. Patients at risk of extravasation injuries, include those with small, fragile or thrombosed veins increasing the risk of leakage, with chronic diseases, those who are unable to communicate due to confused state or language issues, those on anticoagulants, or those who are obese which makes detection of misplacement difficult, or have undergone multiple intravenous cannulations or venepunctures.
The etiology of tissue damage resulting from extravasation can be categorized into following pathophysiological mechanisms ; vasoconstriction and ischemic necrosis, direct toxicity to the tissue, osmotic damage, extrinsic mechanical compression by large solution volumes, or superimposed infection.
The patient developed anterior interosseous nerve injury after dextrose administration through the median cubital vein. Anatomically, the anterior interosseous nerve accompanies the anterior interosseous artery along the interosseous membrane and supplies the deep muscles on the anterior forearm. The median cubital vein generally runs just below the cubital region, connecting the basilic and cephalic vein. The anterior interosseous nerve lies deeper than the median cubital vein, but it can be assumed that the pressure via extravasation caused injury to the nerve in this case.
The AIN injury in our case was confirmed by the electrodiagnostic study. However, since the study was performed 15 days after the onset, it had limitations in detecting abnormalities. If follow up electromyography was performed more than three weeks after the injury, further recovery information such as large motor units or polyphasic potentials would have been revealed. Also, electromyography of pronator teres muscle would have been helpful to localize and to rule out more proximal lesions of the median nerve, such as pronator teres syndrome. Another limitation to our case is that no imaging studies were performed. Forearm imaging evaluations such as magnetic resonance imaging, ultrasonography, or computed tomography would have been helpful to confirm nerve compression or soft tissue injury.
This is a case of AIN syndrome which occurred after intravenous fluid injection in a diabetic patient due to extravasation. The peripheral neuropathy could have been caused by direct compression from the fluid or inflammatory reactions. To prevent such neurological injury, special caution is needed when fluid is infused through intravenous line, especially on fragile sites, in high risk patients or with substances with higher risks.
Nerve Conduction Study
Sensory | Stimulation site | Recording site | Latency (ms) | Amplitude(uV) | |
---|---|---|---|---|---|
Rt. Median | Wrist | 3rd finger | 3.1 | 7.9 |
|
Lt. Median | Wrist | 3rd finger | 3.1 | 6.9 |
|
Rt. Ulnar | Wrist | 5th finger | 2.3 | 5.2* | |
Lt. Ulnar | Wrist | 5th finger | 2.3 | 4.6 |
|
Rt. Peroneal | Ankle | Lateral ankle | 2.4 | 4.5 | |
Lt. Peroneal | Ankle | Lateral ankle | 3 | 4.7 | |
Rt. Sural | Calf | Lateral ankle | 3.2 | 6.3 | |
Lt. Sural | Calf | Lateral ankle | 2.3 | 6.7 | |
Rt. Median | Wrist | APB | 3.8 | 10.8 | |
Elbow | APB | 7.9 | 10.5 | 53.7 | |
Lt. Median | Wrist | APB | 3.8 | 10.9 | |
Elbow | APB | 8.0 | 9.4 | 52.4 | |
Rt. Ulnar | Wrist | ADM | 3.0 | 6.0 | |
Below elbow | ADM | 7.2 | 5.7 | 47.6 |
|
Lt. Ulnar | Wrist | ADM | 3.0 | 5.8 | |
Below elbow | ADM | 7.3 | 5.9 | 46.5 |
|
Rt. Peroneal | Ankle | EDB | 4.7 | 5.3 | |
Below fibular head | EDB | 12.5 | 4.7 | 38.5 |
|
Lt. Peroneal | Ankle | EDB | 4.7 | 5.0 | |
Below fibular head | EDB | 12.4 | 4.8 | 38.9 |
|
Rt. Tibial | Ankle | AH | 3.7 | 8.5 | |
Knee | AH | 13.3 | 6.8 | 34.4 |
|
Lt. Tibial | Ankle | AH | 3.7 | 11.7 | |
Knee | AH | 13.2 | 8 | 34.7 |
Rt.: right, Lt.: left, APB: abductor pollicis brevis, ADM: abductor digiti minimi, EDB: extensor digitorum brevis, AH: abductor hallucis.
Abnormal value.
Electromyography Study
Muscle | IA | Fib | PSW | IP |
---|---|---|---|---|
Paravertebral Rt. C5-T1 | Normal | - | - | |
Paravertebral Lt. C5-T1 | Normal | - | - | |
Rt. Deltoid | Normal | - | - | Complete |
Rt. Biceps | Normal | - | - | Complete |
Rt. Triceps | Normal | - | - | Complete |
Rt. FCR | Normal | - | - | Complete |
Rt. APB | Normal | - | - | Complete |
Rt. 1st DI | Normal | - | - | Complete |
Rt. FDP | Increased | + | + | Single |
Rt. FPL | Increased | + | + | Single |
Rt. PQ | Increased | + | + | Single to partial |
Lt. Deltoid | Normal | - | - | Complete |
Lt. Biceps | Normal | - | - | Complete |
Lt. Triceps | Normal | - | - | Complete |
Lt. FCR | Normal | - | - | Complete |
Lt. APB | Normal | - | - | Complete |
Lt. PQ | Normal | - | - | Complete |
Lt. 1st DI | Normal | - | - | Complete |
IA: insertional activity, Fib: fibrillation, PSW: positive sharp wave, IP: interference pattern, Rt.: right, Lt.: left, FCR: flexor carpi radialis, APB: abductor pollicis brevis, DI: dorsal interosseous, FDP: flexor digitorum profundus, FPL: flexor pollicis longus, PQ: pronator quadratus.