An 11-year-old Mn DSH presented with a three-week history of recurrent, sudden onset blindness and circling, which had responded initially to antimicrobials. The cat was noted as being more subdued than normal. The owners had also noted a swelling over the left side of the skull over the previous two days.
Examination
The cat appeared subdued but responsive, and walked with tentative steps when encouraged, colliding with objects in its path. No circling behaviour was noted. Body temperature was normal (38.2ºC). There was a purulent, discharging sinus tract over the left temporalis muscle. Neurological examination revealed reduced pupillary light responses. There was a reduced menace response in the right eye, and absent response in the left. All other cranial nerves and limb conscious proprioception were considered normal.
Investigations

fig.1 - T2W parasagittal slice of skull showing defect in parietal cortex, with extension of inflammatory process into cerebrum.
Haematology was unremarkable. Biochemistry revealed mild hypokalaemia and a ‘stress’ hyperglycaemia. Blood ammonia and coagulation tests were normal. FeLV/FIV testing was negative. A swab was taken from the swelling on the head, which yielded a moderate growth of Pasteurella multocida. The laboratory elected not to perform antimicrobial sensitivity testing given the predictable pattern of the organism.
MR-scans of the skull were performed (figs. 1 & 2 – click to enlarge) which revealed a high T2W signal area within the subdermal tissues, which extended through a breach in the parietal bone of the calvarium into the left parietal/ temporal lobes. There was slight, peripheral enhancement with gadolinium. FLAIR sequences suggested the brain pathology was focal, expansile encephalitis . In addition, there was coning of the cerebellum, indicative of a raised intracranial pressure.
Treatment
Over the first 24 hours, the cat was stabilised with supportive care, including mannitol and intravenous antibiosis. The following day, repeat neurological examination showed no change in status, and the cat was anaesthetised for exploratory surgery.
Anticipating the use of omentum, a standard, inverted ‘L’ pedicle of the dorsal leaf of the greater omentum was raised via a midline coeliotomy (Ross WE and Pardo AD 1993, fig. 3). The pedicle was exited through a left paracostal incision and the abdomen was closed in a routine manner. The swelling over the skull was explored surgically, and a sinus tract was traced to a defect in the parietal bone, which was filled with granulation tissue (fig. 4). The bone-defect was enlarged with a bur and samples of the underlying meninges and cortex were submitted for histopathology; this revealed a marked, pyohistiocytic, haemorrhagic, nodular, encephalitis with

fig.4 - intraoperative photograph showing soft-tissue removed from parietal bone to reveal defect (tooth-hole).
focal meningeal bony metaplasia. The omental pedicle was tacked lightly into position over the parietal defect to act as a physiological drain (fig. 5). A bridging-incision was created to avoid excessive tunnelling of the pedicle and therefore minimise any risk to its vascular integrity. The craniotomy wound and bridging incision were closed routinely, with staples used to appose the skin (fig 6).
Follow Up
The following day, mentation was still reduced, but the cat was able to track moving objects. Menace and pupillary light responses had returned in both eyes. By 48 hours, appetite was good and mentation was considerably improved. By three days after surgery, all neurological deficits had resolved, and the cat was discharged. Repeat examinations revealed an unremarkable recovery and there had been no recurrence of signs in the 18 months since surgery.
Discussion
This case illustrates the versatility of omental pedicles in case of localised CNS infection that require drainage. Active surgical drains might be used as an alternative, but run an increased risk of nosocomial meningoencephalititis. In addition, local immunogenic properties of the omentum are invaluable in such patients where rapid resolution of sepsis is paramount.
Bacterial CNS infection in otherwise healthy cats is extremely rare (Rusbridge C 2001). Causative organisms may gain access across the blood brain barrier by direct extension (e.g. trauma) or more commonly, adjacent infection such as otitis interna and sinusitis (Sturges BK et al 2006). Alternatively, organisms may enter via bacterial embolization within the brain. This can result from bacterial endocarditis or bacterial penetration of the blood-brain barrier due to a compromised immune system and overwhelming bacteraemia, e.g. FIV/ FeLV infection (Rusbridge C 2001). The findings suggest suppurative meningoencephalititis developed as a result of a penetrating cat bite wound (Weber DJ et al 1984).
To the author’s knowledge, there is little information on the optimal management of feline suppurative meningoencephalitis in the veterinary literature (Barrs et al. 2007). The failure of medical management to effect a significant improvement in the neurological status may reflect the relatively short time frame allowed (Fenner WR 1984). However, it was decided to manage the patient surgically at an early stage in view of the recurrent and progressive nature of the signs. In addition, consideration was given to the MRI-findings; a breach in the integrity of the cranial vault with corresponding evidence of focal pathology within a relatively accessible portion of the brain, togeather with evidence of raised intracranial pressure. The rapid resolution of neurological signs post operatively and the absence of any significant complications would seem to vindicate this approach.
The benefits of omentalising chronic wounds (Hosgood G 1990, Smith BA et al 1995, Brockman DJ et al 1996, Lascelles BDX et al 1998, Heller J 2002, Gray MG 2005), intra-abdominal septic processes (White RAS and Williams JM 1995, Bray JP, White RAS and Williams JM 1997, Campbell BG 2004, Jerram RM et al 2004) and its use for pleural drainage (Williams JM and Niles JD 1999, LaFond E, Weirich WE and Salisbury SK 2002) is well established. In addition, the ability of the omentum to aid in the revascularization and repair of tissues (Hayari L and others 2004, Pap-Szekeres J et al 2005, Kanamori T 2006, Takaba K et al 2006), including CNS lesions (Vatansev C et al 2003, Goldsmith HS, Fonseca Jr A and Porter J 2005) has been demonstrated.
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