Portosystemic shunts are anomalies that allow blood returning from the gastrointestinal systems to bypass the liver and pass directly into the systemic circulation. When this occurs, toxins from gastrointestinal tract that are normally cleared by the liver are shunted directly into the systemic circulation. This build-up of these toxins in the bloodstream leads to the clinical signs commonly seen in animals with these shunts. Three categories of clinical signs commonly are associated with the presence of these shunts: neurological, gastrointestinal and urinary. Neurological signs include seizures, head pressing, circling, lethargy and blindness among others- hepatic encephalopathy. Gastrointestinal signs include vomiting, anorexia, weight loss and a reduced rate of growth. Urinary tract signs, including stranguria, pollakiuria and hematuria are generally related to the development of urate cystoliths secondary to the presence of ammonium biurate crystals in the urine.
Contrast CT study with 64 slice scanner was performed with i.v administration of iopamidol solution 370g/ml (contrast agent) in dosage 1ml/kg.
CT findings: There is a abnormal communication between the portal vein and the caudal vena cava using the splenic vein. The portal vein decreases in diameter cranial to the shunt exit and splienic vein is enlarged. The both kidneys are too big and liver is too small.
Diagnosis:
Congenital extrahepatic splienocaval-caval shunt
The treatment consisted of medical and surgical approach. Ten days before the surgery the condition was managed with amoxicillin 12,5 mg/kg p.o q12h for 15, Lactose oral solution 67g/ 100ml in dosage 1ml/kg p.o q12h and hydrolyzed protein food.
The surgery was planned in great teamwork with d-r Kaloyan Voichev in Multidisciplinary Veterinary Clinic Bulgaria. The operation was performed with the kind assistance of the whole team. The operational approach consisted of midline celiotomy and isolation of the shunt from surrounding structures and placement of thin cellophane band surround the vessel.
Max recovered well from the anesthesia and was discharged after 48 hours with amoxicillin 12,5 mg/kg p.o q12h for 10days, Lactose oral solution 67g/100ml in dosage 1ml/kg p.o q12h for 15 days and hydrolyzed protein food. In postoperative period Max was vomiting sporadic within one week, but with good appetite. The vomiting was stopped with maropitant 1mg/kg s.c q 24h for 3 days.
One month after the surgery Max doesn’t show any clinical signs.
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.
Stroke or cerebrovascular accident (CVA) is the most common clinical manifestation of cerebrovascular disease, and can be broadly divided into ischemic stroke and hemorrhagic stroke. CVA are characterized clinically by a per acute or acute onset of focal, asymmetrical and non-progressive brain dysfunction. Next cases show the both type of CVA in dogs.
1st case is about 9 years old female boxer. The dog was referring to the clinic with acute onset of seizures. The results of CBC and Biochemistry were normal and MRI was performed.
Image 1
Image 2
Image 3
Image 4
MRI findings: Intra-axial right piriform lobe and hippocampus lesion with impression of moderate swelling of these portions is present. The cerebral falx is only mildly displaced to the left. There is corresponding low T1 signal intensity in these sections of the brain suggesting edema. There is no enhancement of the lesion after contrast administration. The findings suggest that there is a non-hemorrhagic cerebrovascular accident in right forebrain of the dog.
The 2nd case is about a 8 years old male Cane corso. The dog was present in the clinic with unilateral fore brain deficits and history of epileptic seizures. Biochemistry and CBC were normal and MRI was performed.
Image 5
Image 6
Image 7
Image 8
Image 9
Image 10
MRI findings : There is a well‐delineated T1 iso- to hypointense and T2 hypointense mass lesion with surrounding brain edema in right piriform lobe with a thin peripheral rim of contrast enhancement. There is a mass effect, displacement of the right lateral ventricle and midline shift to the left. This imaging feature is consistent with an acute to subacute intracranial hemorrhage.
Conclusion:
MRI features of Hemorrhagic infarction in dogs may not be distinguishable from hematoma caused by vascular disruption. Imaging characteristics will vary depending on the size, location, and chronicity ofthe hematoma.
Acute 1-3 days T1 iso- to hypointense ; T2 hyperintense
Early subacute >3 days T1 hyperintense ; T2 hypointense
Late subacute >7 days T1 hyperintense ; T2 hyperintense
Chronic > 14 days T1 hypointense ; T2 hypointense
Secondary features : mass effect, surrounding edema, midline shift , ventricular displacement and compression .
MRI features of Nonhemorrhagic Infarction in dogs include mildly T1 hypointense and T2 hyperintense lesion with minimal mass effect involving both gray and white matter on unenhanced MR images. These changes seen in ischemic parenchyma rely on an increase in tissue water content. Gradually, during the acute stage, the T2-weighted image becomes more hyperintense in the ischemic region, particularly over the first 24 hours. These signal changes seen in the first 24-hours are best appreciated in grey matter and are well visualized in deep grey matter structures such as the thalamus or basal ganglia, in addition to cortical grey matter. Gadolinium enhances infarcts because of vascular rupture but does not enhance ischemia or edema.
3 years old male, not castrated British shorthair cat with history of tetraparesis was referred to the clinic for Computed Tomography. Mineral-attenuating endobronchial lesions were detected in Thorax as accidental finings in spinal CT. The finding is specific for broncholitiasis.
CT :
1
3
2
4
5
CT features: Multifocal mineral-attenuating endobronchial lesions in cranial and middle right and cranial left lung lobe are present. There is mild generalized thickening of the bronchial walls and consolidation of right middle lung lob with regional bronchiectasis
6
7
8
9
10
11
X-rays
1
2
X-ray features: Multiple mineral opacity nodules with irregular margins are present within left and right cranial and right middle lung lobe. The largest of which lies within the right middle lung lobe and interstitial patter in this region is present.
Broncholithiasis is very rare condition in cats and is defined as the presence of calcified or ossified material within the bronchial lumen. Only four cases of broncholithiasis in cats have been reported in the veterinary literature. Normal this condition is associated with lower airway inflammation, but in this case the owner does not report for respiratory problems. Broncholithiasis is an uncommon condition, which should be considered as a differential diagnosis for cats with chronic respiratory disease. Affected cats may develop broncholithiasis secondary to a diffuse inflammatory lower airway disease with mineralisation of secretions in the airways.
8 mounts ,female dog with congenital meningocele and hydrocephalus . The dog is with normal behavior and without neurological deficits.
Meningocele and meningoencephalocele of the skull are congenital deformities. These deformities, which are observed as cyst-like swellings in the median part of the skull cap, occur very rarely. The intracranial material protrudes through a spontaneous cavity, such as the anterior fontanelle , and they are classified as encephalocele, meningocele, or meningoencephalocele according to the cranial bifida.
History: presented for a large firm mass arising from the right side of the calvarium.
Findings: A dense, mineralized mass with a stippled appearance arising from the right side of the calvarium, with an approximate diameter of 6cm.
Because of the dense appearance of the mass, it’s hard to appreciate the degree of underlying osteolysis just with an Xray
A CT scan was recommended to evaluate local invasion.
Diagnostic: the radiological appearance it’s of MLTB (multilobular osteochondrosarcoma)
Discussion: MLTB is an uncommon tumour that arises almost exclusively on the flat bones of the skull, mainly on the calvarium, maxilla and mandible and tend to occur in older medium and large breed dogs, although they have been reported in younger and small breed dogs, and have also been reported in cats. It is slow-growing and locally invasive, often recurring after excision. Metastasis may occur
Findings: Periosteal new bone formation, palisading type, affecting the mandible bilateral.
The tympanic bullae and temporomandibular joints are not affected.
Diagnostic: Craniomandibular osteopathy.
Discussion: Craniomandibular osteopathy is a non-neoplastic, proliferative bone disease that affects primarily the mandible, tympanic bullae, frontal bone and occasionally long bones in dogs of about three to eight months.
The proliferation of new bone of the head and jaws decreases as the endochondral ossification of the long bones slows after 7 to 8 months of age.
Inflammatory polyps that develop at the level of the nasopharynx and the middle ear are non-neoplastic masses which are thought to originate in the epithelial layer of the timpanic bulla or the Eustachian tube. Polyps can also emerge from the epithelium lining the external ear canal in association with otitis.
The etiology of nasopharyngeal polyps is not very clear and congenital pathologies as well as underlining inflammatory diseaseses such as bacterial or viral infections and cronical inflammations are discussed.
Most affected are the cats younger than 3 years of age, but some studies found the average age of the patients to be arround 6-7 years and up to 17,5 years in some cases. The studies citing such advnaced ages implied that polyps developed at a younger age, but remained undiagnosed for a long period.
How to diagnose a nasopharyngeal polyp?
The diagnosis is made based on patient history and clinical examination and confirmed through diagnostic imaging, endoscopy and histopathology.
The clasical clinical signs associated with nasopharyngeal polyps include sneezing andheavy breathing. When a nasopharyngeal polyp reaches a large size (and is located in the nasopharynx) or there are bilateral polyps (extending into the nasal cavities) they cause reduction of the upper airways and are associated with loud breathing noises, nasal discharge, snorring and even vestibular disorders (head tilt, balance disorders). Sometimes nasopharyngeal polyps can be associated with Horner syndrome. Large polyps can lead to difficulties in the act of swallowing and anorexia. Direct or indirect examination (endoscopy and sample retrieval) can be of great help to the clinician in diagnosing this type of pathology (depending on the size and localisation of the polyp). Radiograps (RX), Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) are very good diagnostic tools , providing information about the localisation and size of the polyp and have also a high specificity. Diagnostic imaging can also help differentiate between nasopharyngeal polyps and other pathologies that sometimes similar clinical appearance, such as obstructed or stenotic airways, foreign bodies, neoplasia, thickening or osteolysis of the bullae due to infection. Another advantage when using diagnostic imaging is the ability to assess the regional lymphnodes in order to give a more precise prognosis.
Findings: On plain radiographs there is a plicated appearance of some of the small intestinal loops on the middle side of the abdomen. The content of this intestinal loops it’s mixt gas-fluid, with variably sized and shaped gas bubbles.
pic 3
pic 4
Fallowing contrast medium administration: Delayed gastric emptying time. The bunched and plicated pattern it’s highlighted affectind the duodenum and the jejunum.
Dr Svetoslav Penchev
