NEUROMUSCULAR CASE OF THE MONTH - DECEMBER 2011

Acute onset of left pelvic limb paralysis in an
11-year old male castrated DSH
Contributed by Dr. William B. Thomas
University of Tennessee
Knoxville, TN 37901-1071

Clinical History
Three months prior to examination, this neutered male cat developed signs of urethral obstruction. Treatment included an intramuscular injection of enrofloxacin administered in the left hip region. Within 24 hours the cat developed weakness in the left pelvic limb. The client had noticed no change in the signs since the acute onset.

Physical Examination
General physical examination was unremarkable. Neurological examination revealed an alert cat that dragged the left pelvic limb. There was substantial atrophy of the cranial tibial and gastrocnemius muscles in the affected limb. The cat was unable to flex the stifle and unable to flex or extend the hock. Hip movement and stifle extension were preserved. Proprioceptive positioning was absent. The patellar reflex was exaggerated (3+) and the withdrawal reflex was absent. Deep pain perception was absent distal to the stifle, with the exception of the medial aspect of the limb. No signs of pain were elicited on palpation and manipulation of the spine or affected limb. Femoral pulses were normal bilaterally. The other limbs, cranial nerves, sphincters and tail were normal.

Diagnostic Tests
Routine laboratory tests including CBC, electrolytes, and serum chemistries including creatine kinase (CK) - normal

EMG and NCV - Fibrillation potentials and positive sharp waves were present in the left cranial tibial, gastrocnemius, interosseous, and hamstring muscles (Fig. 1: Electromyogram of the left cranial tibial muscle). Motor NCV could not be elicited on stimulation of the left sciatic nerve at the hip or hock. Motor NCV of the right sciatic nerve was normal (80.6 m/s) with normal amplitude of the M-wave (Fig. 2: Motor nerve conduction study of the unaffected right  sciatic-tibial nerve).

Figure 1. Electromyogram of the left cranial tibial muscle

Figure 2. Motor nerve conduction study of the unaffected right sciatic-tibial nerve

Nerve Biopsy - The left sciatic nerve was surgically explored from the ischium to the stifle with the aid of an operating microscope. No abnormalities were observed or palpated. A fascicular biopsy was obtained from the common peroneal nerve. Semi-thin plastic embedded sections showed severe, end-stage Wallerian degeneration (Fig. 3) with numerous foamy macrophages and large accumulations of macrophages consistent with a granuloma (*). Nerve regeneration was not observed.

Treatment and Outcome
The diagnosis was an injection injury of the left sciatic nerve. The client was instructed in physical therapy of the limb and to watch closely for signs of trauma to the limb, including self-mutilation, which may necessitate amputation.

Comments and Conclusions
The sciatic nerve may be injured by injections due to direct laceration of the nerve, injection of material into the nerve, or secondary inflammation or compression from scarring induced by deposition of the drug close to the nerve.(1) Material injected into the caudal region of the thigh may become dispersed throughout the intermuscular fascial sheaths in the region of the sciatic nerve. (2) A variety of substances, including vehicles for drugs, are capable of damaging the nerve with some more potent than others. In most cases the neurologic deficits are apparent within a few minutes of the injection. A delayed onset suggests a more slowly acting agent and/or the development of perineurial or endoneurial inflammation or fibrosis. There is often intense pain at the time of injury which may persist. There is an associated motor and sensory loss which may be complete or incomplete.

If the complication is noticed immediately, some authors recommend saline injection in the region of the injury in an attempt to dilute the drug and avoid permanent neuropathy. (3). Open surgical irrigation may be more logical. Patients with partial deficits are managed conservatively with vigorous physical therapy, analgesics, and time. (3,4)   The majority of human patients with incomplete deficits caused by injection injury of the sciatic nerve recover spontaneously. (4) If the deficit is complete after several months of observation, surgical exploration is warranted. (3,4). External neurolysis, with or without internal neurolyisis, is often effective in human patients with injection injury of the sciatic nerve. (4) External neurolysis (dissection of the nerve from its bed of scar tissue) is indicated if there is obvious compression from fibrous tissue. Internal neurolysis involves resection of scar tissue from nerve fascicles and may also be necessary to decompress otherwise intact fascicles and improve the chance for recovery. Complete resection of the damaged nerve segment with end-to-end anastamosis or nerve graft may be necessary in a few patients, but the prognosis for recovery is guarded. (4).

Avoiding intramuscular injection into the caudal thigh muscles will prevent injection injuries to the sciatic nerve. Using another site for intramuscular injections, such as the quadriceps or lumbar epaxial muscles is preferable. (2)

NOTE: At follow-up 2 years following the injection incident the cat was doing well and amputation not required.

References
1.    Sunderland S. Causative agents. In: Anonymous nerves and nerve injuries. 2nd edition. Edinburgh: Churchill Livingstone, 1978:145-187.

2.    Autefage A, Fayolle P, Toutain PL. Distribution of material injected intramuscular in dogs. Am J Vet Res 1990;51:901-904.

3.    Kline DG, Hudson Ar. Acute injuries of peripheral nerves. In: Youmans JR (ed). Neurological surgery. 3rd edition. Philadelphia: W.B. Saunders, 1990:2423-2510.

4.   Kline DG, Kim D, Midha R, Harsh C, Tiel R. Management and results of sciatic nerve injuries: a 24-year experience. J Neurosurg 1998;89:13-23.

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