Treatment of massive brain compression in two dogs

1575875879547blobDr. Vladislav Zlatinov

Central Vet Clinic

Sofia, Bulgaria

 

Introduction

 

This is case series of two dogs with similar advanced brain compression. The aetiology was different, but in both cases there was gradual epidural compression, indeed allowing survival of the patients. The final size of the brain compression lesions in both dogs was impressive and was related to the delayed diagnostic process. Both dogs were successfully treated and followed in next few months post op. Different surgical approaches and techniques were applied, according to the specific needs.

These cases present interest because such large lesions are rarely met in practice, and may be considered untreatable by some veterinary clinicians.

 

 

Case 1

 

Referring Vet: Dr. Evgeni Evtimov

Corresponding authors Dr. Aglika Jordanova (Clinical pathology), Dr. Vladislav Zlatinov (Surgery),Dr Nikola Penchev( Anesthesia)

 

 

Felix, a 7 months old Collie dog was presented for treatment of progressively deteriorating central nervous system dysfunction.

 

The male puppy lives in an apartment; vaccinations and deworming are current, fed on regular dry food diet. Had been with his owner for a month, came from a breeder.

 

The clinical signs had started 3 weeks ago, with unclear manifestation- decreased appetite, lethargy, intermittent fever, unstable walk. The overall body condition of the patient had been appreciated as underdeveloped, and the owner reported the dog is not growing.

Felix had been initially consulted by the referring vet, who had started primary diagnostic and treatment steps. Biochemistry profile, CBC and vector diseases fast serology tests had been done- being normal/ negative, not revealing the specific cause of the condition. Symptomatic antibiotic treatment had been started, without significant improvement. NSAIDs resulted in temporary alleviation of the symptoms – body temperature back to normal, the dog was brighter.

At this point the dog was referred to us to investigate the possible cause of the condition, suspected to be endocrinological.

The dog was found to be lethargic, walking with head positioned low, no pain during head lifting, does not resist opening the jaws, wobbly gait, with normal proprioception of all 4 limbs. body temp.39.0C. The CBC was WNL. Total T4 was normal (16nmol/l). Radiography of limbs and vertebrae showed normal physeal growth for the dog’s age; thus excluding congenital hypothyroidism.

 

Cerebrospinal fluid collection and computer tomography study of the head were suggested, as the symptoms were assessed as central neurological. During the period of owner contemplation, trial course with corticosteroids had been applied. Short-term clinical improvement had been noticed, followed by further decline in the dog’s condition. A bulge on the left side of the head became visible.  After gradual progression of neurological symptoms- dull behaviour, mild head tilt, inactivity, the dog deteriorated profoundly to the status of stupor- severely depressed mental status, barely reacting to stimuli.

 

CT study of the head was performed 14 days after the initial examination at Central Veterinary Clinic (with no anaesthesia needed), revealing dramatic findings. Extensively grown soft tissue “mass” (vs thick fluid accumulation) was found over and under (extra and intracranially) the left parietal and occipital skull calvaria. The outside lesion was more heterogeneous, lobular like, under the temporal fascia. The internal part was homogenous, with clear fluid density, well encapsulated, caudally extending over cerebellar tentorium. It was causing a significant mass effect with compression of the left parietal and occipital cerebellar brain lobes. Dramatic lateral ventricular compression and a falx shift to the right was present.The skull bone in the area was hypertrophied, with aggressive periosteal reaction, mostly extra- cranially. In the cranial left parietal bone, a small concave defect was noticed on 3d reconstruction images.

Fine needle aspiration was done puncturing the extra cranial lesion area. Pus-like  fluid was obtained, cytologically tested, confirming suppurative process.

 

All these findings suggested the main differential diagnosis- massive epidural empyema (abscess), compressing the brain parenchyma and causing profound neurological deficit. The probable cause was bite wound on the head (<=concave defect on the parietal bone).

 

Surgical decompression was suggested and accomplished as an urgent procedure because of the fast deterioration of the patient.

 

Lateral approach to the skull was applied. An abscess cavity with intensively neo-vascularised capsule was found, just under the temporal fascia, Topographically it was within the temporal muscle tissue. After partial capsule resection and copious lavage, the soft tissues were undermined and reflected to expose the lateral (parietal) skull area. Next, rectangular  rostrotentorial craniectomy was accomplished using maxilo-facial mini oscillating saw. Skull sutures and the concave defect (bite area?) were used as reference landmarks to orientate the cuts. The skull bone in the area had reached 1 cm thickness. A fluid filled epidural (over dura mater) cavity was found. It was filled by thick bright yellow purulent fluid. After microbiology and pathohistology sampling, the pus was aspirated and the residual cavity copiously lavaged. Prompt haemostasis was applied, with minimum haemostatic materials left in place.

A fenestrated drain tube was inserted into the empyema  cavity and under the soft tissues. The temporal fascia and the skin were closed routinely over the defect. The drain tube was connected to active vacuum suction system.

Intense post op care was applied in the next 12 hours- blood pressure monitoring and correction with vasopressors, fluid infusion, pain control, i.v. antibiotic therapy. The patient started to improve slowly but steadily- the mental status improved within 24 hours, and the dog was able to stand up on the second day after the surgery. On the fourth day it was stable enough to be discharged from the clinic (still with the active vacuum drainage). The last was removed on the 7th day.  Ultrasound examination rechecks was done on the 10th and 14th days, excluding new fluid accumulation.

 

The microbiology culture test result was negative, but no anaerobic isolation media was available. Just in case of not detected anaerobic infection- 3 weeks course with Clindamycin was prescribed.

The pathology report confirmed the the diagnosis of pyo-granulomatous inflammation with no neoplastic tissue present.

 

Eventually, Felix did full recovery with no infection relapses within the follow up period of 4 months.

 

Case 2

 

Referring Vet: Dr. Milena Pancheva

 

Dr. Vladislav Zlatinov (Surgery), Dr. Antoan Georgiev (Anaesthesia).

 

 

 

Beki, 4 years old female Dalmatian was referred for consultation, regarding the possible treatment  of a huge intra-cranial mass.

The dog had a long history of slowly progressing vestibular signs and eventually obvious ataxic walking  Unfortunately the owners had ignored the problem for several months (> 7 m), because of the mild clinical presentation in the beginning and the good overall condition of the patient. Recently the dog deteriorated- difficult to keep balance during walking and eating. Two seizures  and nocturnal hyper excitement activities were also demonstrated.The dog had already computer tomography study of the head, revealing huge cranial mass. An opinion about euthanasia was already suggested to the owners. Empirical therapy with steroids and antibiotics was already applied before the achievement of the correct diagnosis.

 

During our neurological examination we found: normal mental status and vision, normal cranial and limb segmental reflexes; the menace response reflexes were decreased; body posture revealed broad-based stance. The patient demonstrated obvious ataxia. It was defined as cerebellar one, presented by hypermetria and  swaying, mild intentional head tremors.

We analysed the CT study and found: large hyper-dense oval mass, starting from the region of the occipital bone and engaging the cerebellar tentorium. The mass was protruding extensively into the brain cavity, eccentrically to the right side. Bone lysis and infiltration was evident in the right occipital nuchal area and also cranial to the right nuchal crest. Severe cerebellar compression in cranio-ventral direction was evident. Less severe compression of the occipital cerebral lobes (without lateral vetntricular displacement) was also found.

Despite the large size of the mass, we suggested moderate malignancy of the lesion- smooth, encapsulated margins, homogenous density. Bone neoplasia (osteosarcoma and multilobular osteochondrosarcoma) or meningioma were the most probable diagnosis. Slow progression of mass, made the osteosarcoma less probable. The bone involvement is not typical for meningiomas. Multilobular tumors usually has similar imaging features as presented in the case. Their excision offer good opportunity for long-term tumor control, so a surgical decompression and mass removal was suggested and accomplished in Beki’s case.

 

We approached the skull caudo- laterally, undermining and retracting the overlaying temporal fascia and neck muscles. The tumor mass was found protruding from the bone through osteolysed right occipital and parietal bones.  Using speed burr we created large combined occipital and caudal-lateral craniotomy. Excessive bleeding from the right transverse sinus was anticipated but fortunately not found, because of possible gradual vein obliteration. Despite this, during gradual enlargement of the craniotomy, special precautions was taken not damage the ipsilateral left one.

After exposure the cranium, we attempted to determine the mass borders. The tumor was originating from the cranium bone not invading (just compressing) the nervous tissue. Because of the huge size, en block resection was far from possible, so slow “debulking” mass removal was started.  The brain meninga (dura mater) was not affected by the neoplasia, so tissue direction was amenable.

 

Diffuse, moderate but constant bleeding was met through the whole process of removal small partial tumour masses. Haemostatisis was achieved using Cellulose blood clot inducing products (Surgicel mesh) and intermittent gentle compression. Copious lavage was applied during the whole surgery.

 

To complete the mass removal was a laborious procedure, taking itself about an hour. Finally, immediately  after the decompression a visible brain tissue re-expansion was noticed. After prompt haemostatis (using bone wax and Surgicel materials), the residual craniotomy defect was covered with apposition of the soft tissues over it.

 

In the next 24 h post op period, the dog was was given opioid analgesia, anti-inflammatory doses of steroids and anti oedematous osmotic agent (Manitol).

Indeed, Beki started to recover surprisingly fast- eating on the 12 h post op (on the video). For about 48 h she showed exaggerated ataxia, with difficulties in walking, but the coordination started to improve fast. The patient was discharged from the clinic on the third day pos op, walking reasonably well. Harness supported leash walks were recommended.

No physiotherapy was applied in the recovery time, because the patient coordination improved to normal on the 10th days pos surgery.

 

Patohystology evaluation of the tumor was done. The results was Multi lobular bone tumor. This is a low malignant, well differentiated neoplasia. In short term it can be controlled successfully by surgical resection. Slow reoccurrence could be expected, also long term metaplasia to more aggressive osteosarcoma.

 

Recheck of the patient revealed condition undistinguishable from normal. The follow up period till now is 3 months.

 

 

 

 

Luba Gancheva